Disorders

ALLERGIES

An allergy is a hypersensitivity disorder of the immune system. Allergic reactions occur when a person's immune system reacts to normally harmless substances in the environment. A substance that causes a reaction is called an allergen. These reactions are acquired, predictable, and rapid. Allergy is one of four forms of hypersensitivity and is formally called type I (or immediate) hypersensitivity. Allergic reactions are distinctive because of excessive activation of certain white blood cells called mast cells and basophils by a type of antibody called Immunoglobulin E (IgE). This reaction results in an inflammatory response which can range from uncomfortable to dangerous. Mild allergies like hay fever are very common in the human population and cause symptoms such as red eyes, itchiness, and runny nose, eczema, hives, hay fever, or an asthma attack. Allergies can play a major role in conditions such as asthma. In some people, severe allergies to environmental or dietary allergens or to medication may result in life-threatening reactions called anaphylaxis. Food allergies, and reactions to the venom of stinging insects such as wasps and bees are often associated with these severe reactions. A variety of tests exist to diagnose allergic conditions. These include placing possible allergens on the skin and looking for a reaction such as swelling. Blood tests can also be done to look for an allergen-specific IgE. Treatments for allergies include avoiding known allergens, use of medications such as anti-histamines that specifically prevent allergic reactions, steroids that modify the immune system in general, and medications such as decongestants that reduce the symptoms. Many of these medications are taken by mouth, though epinephrine, which is used to treat anaphylactic reactions, is injected. Immunotherapy uses injected allergens to desensitize the body's response.

SIGNS AND SYMPTOMS

Many allergens such as dust or pollen are airborne particles. In these cases, symptoms arise in areas in contact with air, such as eyes, nose, and lungs. For instance, allergic rhinitis, also known as hay fever, causes irritation of the nose, sneezing, itching, and redness of the eyes. Inhaled allergens can also lead to asthmatic symptoms, caused by narrowing of the airways (bronchoconstriction) and increased production of mucus in the lungs, shortness of breath (dyspnea), coughing and wheezing. Aside from these ambient allergens, allergic reactions can result from foods, insect stings, and reactions to medications like aspirin and antibiotics such as penicillin. Symptoms of food allergy include abdominal pain, bloating, vomiting, diarrhea, itchy skin, and swelling of the skin during hives. Food allergies rarely cause respiratory (asthmatic) reactions, or rhinitis. Insect stings, antibiotics, and certain medicines produce a systemic allergic response that is also called anaphylaxis; multiple organ systems can be affected, including the digestive system, the respiratory system, and the circulatory system. Depending on the rate of severity, it can cause cutaneous reactions, bronchoconstriction, edema, hypotension, coma, and even death. This type of reaction can be triggered suddenly, or the onset can be delayed. The severity of this type of allergic response often requires injections of epinephrine, sometimes through a device known as the EpiPen or Twinject auto-injector. The nature of anaphylaxis is such that the reaction can seem to be subsiding, but may recur throughout a prolonged period of time. Substances that come into contact with the skin, such as latex, are also common causes of allergic reactions, known as contact dermatitis or eczema. Skin allergies frequently cause rashes, or swelling and inflammation within the skin, in what is known as a "wheal and flare" reaction characteristic of hives and angioedema.

CAUSE

Risk factors for allergy can be placed in two general categories, namely host and environmental factors. Host factors include heredity, gender, race, and age, with heredity being by far the most significant. However, there have been recent increases in the incidence of allergic disorders that cannot be explained by genetic factors alone. Four major environmental candidates are alterations in exposure to infectious diseases during early childhood, environmental pollution, allergen levels, and dietary changes.

FOODS

One of the most common food allergies is a sensitivity to peanuts. Peanut allergies may be extremely severe, but can sometimes be outgrown by children school-age. Tree nuts, including pecans, pistachios, pine nuts, and walnuts, are another common allergen. Sufferers may be sensitive to one, or many, tree nuts. Also seeds, including sesame seeds and poppy seeds, contain oils where protein is present, which may elicit an allergic reaction. Egg allergies affect one to two percent of children but are outgrown by about two-thirds of children by the age of 5. The sensitivity is usually to proteins in the white rather than the yolk. Milk, from cows, goats, or sheep, is another common allergy-causing food, and many sufferers are also unable to tolerate dairy products such as cheese. Lactose intolerance, a common reaction to milk, is not in fact a form of allergy. A small portion of children with a milk allergy, roughly ten percent, will have a reaction to beef. Beef contains a small amount of protein that is present in cow's milk. Other foods containing allergenic proteins include soy, wheat, fish, shellfish, fruits, vegetables, spices, synthetic and natural colors, chicken, and chemical additives.

NON-FOOD PROTEINS

Latex can trigger an IgE-mediated cutaneous, respiratory, and systemic reaction. The prevalence of latex allergy in the general population is believed to be less than one percent. In a hospital study, one in 800 surgical patients (0.125 percent) report latex sensitivity, although the sensitivity among healthcare workers is higher, between seven and ten percent. Researchers attribute this higher level to the exposure of healthcare workers to areas with significant airborne latex allergens, such as operating rooms, intensive-care units, and dental suites. These latex-rich environments may sensitize healthcare workers who regularly inhale allergenic proteins. The most prevalent response to latex is an allergic contact dermatitis, a delayed hypersensitive reaction appearing as dry, crusted lesions. This reaction usually lasts 48 to 96 hours. Sweating or rubbing the area under the glove aggravates the lesions, possibly leading to ulcerations. Anaphylactic reactions occur most often in sensitive patients, who have been exposed to the surgeon's latex gloves during abdominal surgery, but other mucosal exposures, such as dental procedures, can also produce systemic reactions. Latex and banana sensitivity may cross-react; furthermore, patients with latex allergy may also have sensitivities to avocado, kiwifruit, and chestnut. These patients often have perioral itching and local urticaria. Only occasionally have these food-induced allergies induced systemic responses. Researchers suspect that the cross-reactivity of latex with banana, avocado, kiwifruit, and chestnut occurs because latex proteins are structurally homologous with some plant proteins.

TOXINS INTERACTING WITH PROTEINS

Another non-food protein reaction, urushiol-induced contact dermatitis, originates after contact with poison ivy, eastern poison oak, western poison oak, or poison sumac. Urushiol, which is not itself a protein, acts as a hapten and chemically reacts with, binds to, and changes the shape of integral membrane proteins on exposed skin cells. The immune system does not recognize the affected cells as normal parts of the body, causing a T-cell-mediated immune response. Of these poisonous plants, sumac is the most virulent. The resulting dermatological response to the reaction between urushiol and membrane proteins includes redness, swelling, papules, vesicles, blisters, and streaking. Estimates vary on the percentage of the population that will have an immune system response. Approximately 25 percent of the population will have a strong allergic response to urushiol. In general, approximately 80 percent to 90 percent of adults will develop a rash if they are exposed to .0050 milligrams of purified urushiol, but some people are so sensitive that it takes only a molecular trace on the skin to initiate an allergic reaction.

GENETIC BASIS

Allergic diseases are strongly familial: identical twins are likely to have the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in non-identical twins. Allergic parents are more likely to have allergic children, and their allergies are likely to be more severe than those from non-allergic parents. Some allergies, however, are not consistent along genealogies; parents who are allergic to peanuts may have children who are allergic to ragweed. It seems that the likelihood of developing allergies is inherited and related to an irregularity in the immune system, but the specific allergen is not. The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk. Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years. The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10. Overall, boys have a higher risk of developing allergies than girls, although for some diseases, namely asthma in young adults, females are more likely to be affected. Sex differences tend to decrease in adulthood. Ethnicity may play a role in some allergies; however, racial factors have been difficult to separate from environmental influences and changes due to migration. It has been suggested that different genetic loci are responsible for asthma, to be specific, in people of European, Hispanic, Asian, and African origins.

HYGIENE HYPOTHESIS

Allergic diseases are caused by inappropriate immunological responses to harmless antigens driven by a TH2-mediated immune response. Many bacteria and viruses elicit a TH1-mediated immune response, which down-regulates TH2 responses. The first proposed mechanism of action of the hygiene hypothesis was that insufficient stimulation of the TH1 arm of the immune system leads to an overactive TH2 arm, which in turn leads to allergic disease. In other words, individuals living in too sterile an environment are not exposed to enough pathogens to keep the immune system busy. Since our bodies evolved to deal with a certain level of such pathogens, when they are not exposed to this level, the immune system will attack harmless antigens and thus normally benign microbial objects like pollen will trigger an immune response. The hygiene hypothesis was developed to explain the observation that hay fever and eczema, both allergic diseases, were less common in children from larger families, which were, it is presumed, exposed to more infectious agents through their siblings, than in children from families with only one child. The hygiene hypothesis has been extensively investigated by immunologists and epidemiologists and has become an important theoretical framework for the study of allergic disorders. It is used to explain the increase in allergic diseases that have been seen since industrialization, and the higher incidence of allergic diseases in more developed countries. The hygiene hypothesis has now expanded to include exposure to symbiotic bacteria and parasites as important modulators of immune system development, along with infectious agents. Epidemiological data support the hygiene hypothesis. Studies have shown that various immunological and autoimmune diseases are much less common in the developing world than the industrialized world and that immigrants to the industrialized world from the developing world increasingly develop immunological disorders in relation to the length of time since arrival in the industrialized world. Longitudinal studies in the third world demonstrate an increase in immunological disorders as a country grows more affluent and, it is presumed, cleaner. The use of antibiotics in the first year of life has been linked to asthma and other allergic diseases. The use of antibacterial cleaning products has also been associated with higher incidence of asthma, as has birth by Caesarean section rather than vaginal birth.

OTHER ENVIRONMENTAL FACTORS

International differences have been associated with the number of individuals within a population that suffer from allergy. Allergic diseases are more common in industrialized countries than in countries that are more traditional or agricultural, and there is a higher rate of allergic disease in urban populations versus rural populations, although these differences are becoming less defined. Exposure to allergens, especially in early life, is an important risk factor for allergy. Alterations in exposure to microorganisms is another plausible explanation, at present, for the increase in atopic allergy. Endotoxin exposure reduces release of inflammatory cytokines such as TNF-a, IFNy, interleukin-10, and interleukin-12 from white blood cells (leukocytes) that circulate in the blood. Certain microbe-sensing proteins, known as Toll-like receptors, found on the surface of cells in the body are also thought to be involved in these processes. Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine chlorination and purification of drinking water supplies. Recent research has shown that some common parasites, such as intestinal worms (e.g., hookworms), secrete chemicals into the gut wall (and, hence, the bloodstream) that suppress the immune system and prevent the body from attacking the parasite. This gives rise to a new slant on the hygiene hypothesis theory ? that co-evolution of man and parasites has led to an immune system that functions correctly only in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive. In particular, research suggests that allergies may coincide with the delayed establishment of gut flora in infants. However, the research to support this theory is conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms. Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies. It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work. For more information on this topic, see Helminthic therapy.

PATHOPHYSIOLOGY

ACUTE RESPONSE

In the early stages of allergy, a type I hypersensitivity reaction against an allergen encountered for the first time and presented by a professional Antigen-Presenting Cell causes a response in a type of immune cell called a TH2 lymphocyte, which belongs to a subset of T cells that produce a cytokine called interleukin-4 (IL-4). These TH2 cells interact with other lymphocytes called B cells, whose role is production of antibodies. Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a kind of Fc receptor called FceRI) on the surface of other kinds of immune cells called mast cells and basophils, which are both involved in the acute inflammatory response. The IgE-coated cells, at this stage are sensitized to the allergen. If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils. Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complex interacts with the same allergenic molecule, and activates the sensitized cell. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction. This results in rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system and eczema is localized to the dermis.

LATE-PHASE RESPONSE

After the chemical mediators of the acute response subside, late phase responses can often occur. This is due to the migration of other leukocytes such as neutrophils, lymphocytes, eosinophils and macrophages to the initial site. The reaction is usually seen 2-24 hours after the original reaction. Cytokines from mast cells may also play a role in the persistence of long-term effects. Late phase responses seen in asthma are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils, and are still dependent on activity of TH2 cells.

DIAGNOSIS

Before a diagnosis of allergic disease can be confirmed, the other possible causes of the presenting symptoms should be carefully considered. Vasomotor rhinitis, for example, is one of many maladies that shares symptoms with allergic rhinitis, underscoring the need for professional differential diagnosis. Once a diagnosis of asthma, rhinitis, anaphylaxis, or other allergic disease has been made, there are several methods for discovering the causative agent of that allergy. Effective management of allergic diseases relies on the ability to make an accurate diagnosis. Allergy testing can help confirm/rule out allergies and consequently reduce adverse reactions and limit unnecessary avoidance and medications. Correct diagnosis, counseling and avoidance advice based on valid allergy test results will help reduce the incidence of symptoms, medications and improve quality of life. For assessing the presence of allergen-specific IgE antibodies, you can use two different methods a skin prick test or an allergy blood test. Both methods are recommended by the NIH guidelines and have similar diagnostic value in terms of sensitivity and specificity. A healthcare provider can use the test results to identify the specific allergic triggers that may be contributing to the symptoms. Using this information, along with a physical examination and case history, the doctor can diagnose the cause of the symptoms and tailor treatments that will help the patient feel better. A negative result can help the doctor rule out allergies in order to consider other possible. NIH Guidelines state that: sIgE tests are useful for identifying foods potentially provoking IgE-mediated food-induced allergic reactions, and specified cutoff levels, defined as 95% predictive values, may be more predictive than skin prick tests of clinical reactivity in certain populations. It further states, sIgE tests are very useful for detecting the presence of sIgE antibodies, which indicates the presence of allergic sensitization. Fluorescence-labeled antibody assays have comparable sensitivity to that of skin prick tests, and the absolute levels of sIgE antibodies may directly correlate with the likelihood of clinical reactivity when compared with oral food challenges for the identification of foods provoking IgE mediated FA. According to NICE Guidelines, skin prick tests and blood tests are equally cost-effective and health economic evidence show that both the IgE antibody test and the skin prick test were cost effective compared with no test. Also, earlier and more accurate diagnoses save cost due to reduced GP consultations, referrals to secondary care, misdiagnosis and emergency admissions. Allergy undergoes dynamic changes over time. Regular allergy testing of relevant allergens provides information on if and how patient management can be changed, in order to improve health and quality of life. Annual testing is often the practice for determining whether allergy to milk, egg, soy, and wheat have been outgrown and the testing interval is extended to 2 to 3 years for allergy to peanut, tree nuts, fish, and crustacean shellfish. Results of follow-up testing can guide decision-making regarding whether and when it is safe to introduce or re-introduce allergenic food into the diet.

SKIN TESTING

Skin testing is also known as "puncture testing" and "prick testing" due to the series of tiny puncture or pricks made into the patient's skin. Small amounts of suspected allergens and/or their extracts (pollen, grass, mite proteins, peanut extract, etc.) are introduced to sites on the skin marked with pen or dye (the ink/dye should be carefully selected, lest it cause an allergic response itself). A small plastic or metal device is used to puncture or prick the skin. Sometimes, the allergens are injected "intradermally" into the patient's skin, with a needle and syringe. Common areas for testing include the inside forearm and the back. If the patient is allergic to the substance, then a visible inflammatory reaction will usually occur within 30 minutes. This response will range from slight reddening of the skin to a full-blown hive (called "wheal and flare") in more sensitive patients similar to a mosquito bite. Interpretation of the results of the skin prick test is normally done by allergists on a scale of severity, with /- meaning borderline reactivity, and 4 being a large reaction. Increasingly, allergists are measuring and recording the diameter of the wheal and flare reaction. Interpretation by well-trained allergists is often guided by relevant literature. Some patients may believe they have determined their own allergic sensitivity from observation, but a skin test has been shown to be much better than patient observation to detect allergy. If a serious life threatening anaphylactic reaction has brought a patient in for evaluation, some allergists will prefer an initial blood test prior to performing the skin prick test. Skin tests may not be an option if the patient has widespread skin disease or has taken antihistamines sometime the last several days.

BLOOD TESTING

An allergy blood test is quick and simple and can be ordered by a licensed health care provider e.g. an allergy specialist, GP or PED. Unlike skin-prick testing, a blood test can be performed irrespective of age, skin condition, medication, symptom, disease activity and pregnancy. Adults and children of any age can take an allergy blood test. For babies and very young children, a single needle stick for allergy blood testing is often more gentle than several skin tests. An allergy blood test is available through most laboratories, and a sample of the patient?s blood is sent to a laboratory for analysis and the results are sent back a few days later. Multiple allergens can be detected with a single blood sample. Allergy blood tests are very safe, since you are not exposed to any allergens during the testing procedure. How does the test work? The test measures the concentration of specific IgE antibodies in the blood. Quantitative IgE test results increases the possibility of ranking how different substances may affect your symptoms. A general rule of thumb is that the higher the IgE antibody value, the greater the likelihood of symptoms. Allergens found at low levels that today do not result in symptoms can nevertheless help predict future symptom development. The quantitative allergy blood result can help determine what a patient is allergic to, help predict and follow the disease development, estimate the risk of a severe reaction and explain cross-reactivity. A low total IgE level is not adequate to rule out sensitization to commonly inhaled allergens. Statistical methods, such as ROC curves, predictive value calculations, and likelihood ratios have been used to examine the relationship of various testing methods to each other. These methods have shown that patients with a high total IgE have a high probability of allergic sensitization, but further investigation with allergy tests for specific IgE antibodies for a carefully chosen of allergens is often warranted. History Radiometric assays include the radioallergosorbent test (RAST) test method, which uses IgE-binding (anti-IgE) antibodies labeled with radioactive isotopes for quantifying the levels of IgE antibody in the blood. Other newer methods use colorimetric or fluorescence-labeled technology in the place of radioactive isotopes. The market-leading RAST methodology was invented and marketed in 1974 by Pharmacia Diagnostics AB, Uppsala, Sweden, and the acronym RAST is actually a brand name. In 1989, Pharmacia Diagnostics AB replaced it with a superior test named the ImmunoCAP Specific IgE blood test, which uses the newer fluorescence-labeled technology. American College of Allergy Asthma and Immunology (ACAAI) and the American Academy of Allergy Asthma and Immunology (AAAAI) issued the Joint Task Force Report Pearls and pitfalls of allergy diagnostic testing in 2008, and is firm in its statement that the term RAST is now obsolete: The term RAST became a colloquialism for all varieties of (in vitro allergy) tests. This is unfortunate because it is well recognized that there are well-performing tests and some that do not perform so well, yet they are all called RASTs, making it difficult to distinguish which is which. For these reasons, it is now recommended that use of RAST as a generic descriptor of these tests be abandoned.? The new version, the ImmunoCAP Specific IgE blood test, is the only specific IgE assay to receive FDA approval to quantitatively report to its detection limit of 0.1kU/l.

OTHER

Challenge testing: Challenge testing is when small amounts of a suspected allergen are introduced to the body orally, through inhalation, or other routes. Except for testing food and medication allergies, challenges are rarely performed. When this type of testing is chosen, it must be closely supervised by an allergist. Elimination/Challenge tests: This testing method is utilized most often with foods or medicines. A patient with a particular suspected allergen is instructed to modify his/her diet to totally avoid that allergen for determined period of time. If the patient experiences significant improvement, he/she may then be challenged by reintroducing the allergen to see if symptoms can be reproduced. Patch testing: Patch testing is used to help ascertain the cause of skin contact allergy, or contact dermatitis. Adhesive patches, usually treated with a number of different commonly allergic chemicals or skin sensitizers, are applied to the back. The skin is then examined for possible local reactions at least twice, usually at 48 hours after application of the patch, and again two or three days later. Some "screening" test methods are intended to provide qualitative test results, giving a "yes" or "no" answer in patients with suspected allergic sensitization. One such method has a sensitivity of about 70.8% and a positive predictive value of 72.6% according to a large study. Unreliable tests: There are other types of allergy testing methods that the American Academy of Allergy, Asthma, and Immunology considers to be unacceptable. These unreliable allergy testing methods are: Applied kinesiology (allergy testing through muscle relaxation), Cytotoxicity testing, Urine autoinjection, Skin titration (Rinkel method), and Provocative and neutralization (subcutaneous) testing or sublingual provocation.

MANAGEMENT

In recent times, there have been enormous improvements in the medical practices used to treat allergic conditions. With respect to anaphylaxis and hypersensitivity reactions to foods, drugs, and insects and in allergic skin diseases, advances have included the identification of food proteins to which IgE binding is associated with severe reactions and development of low-allergen foods, improvements in skin prick test predictions; evaluation of the atopy patch test; in wasp sting outcomes predictions and a rapidly disintegrating epinephrine tablet, and anti-IL-5 for eosinophilic diseases. Traditional treatment and management of allergies consisted simply of avoiding the allergen in question or otherwise reducing exposure. For instance, people with cat allergies were encouraged to avoid them. However, while avoidance of allergens may reduce symptoms and avoid life-threatening anaphylaxis, it is difficult to achieve for those with pollen or similar air-borne allergies. Nonetheless, strict avoidance of allergens is still considered a useful treatment method, and is often used in managing food allergies. New technology approaches to decreasing IgE overproduction, and regulating histimine release in allergic individuals have demonstrated statisitically significant reduction on Total Nasel Symptom Scores.

MEDICATION

Several antagonistic drugs are used to block the action of allergic mediators, or to prevent activation of cells and degranulation processes. These include antihistamines, glucocorticoids, epinephrine (adrenaline), theophylline and cromolyn sodium. Anti-leukotrienes, such as Montelukast (Singulair) or Zafirlukast (Accolate), are FDA approved for treatment of allergic diseases. Anti-cholinergics, decongestants, mast cell stabilizers, and other compounds thought to impair eosinophil chemotaxis, are also commonly used. These drugs help to alleviate the symptoms of allergy, and are imperative in the recovery of acute anaphylaxis, but play little role in chronic treatment of allergic disorders.

IMMUNOTHERAPY

Desensitization or hyposensitization is a treatment in which the person is gradually vaccinated with progressively larger doses of the allergen in question. This can either reduce the severity or eliminate hypersensitivity altogether. It relies on the progressive skewing of IgG antibody production, to block excessive IgE production seen in atopys. In a sense, the person builds up immunity to increasing amounts of the allergen in question. Studies have demonstrated the long-term efficacy and the preventive effect of immunotherapy in reducing the development of new allergy. Meta-analyses have also confirmed efficacy of the treatment in allergic rhinitis in children and in asthma. A review by the Mayo Clinic in Rochester confirmed the safety and efficacy of allergen immunotherapy for allergic rhinitis and conjunctivitis, allergic forms of asthma, and stinging insect based on numerous well-designed scientific studies. In addition, national and international guidelines confirm the clinical efficacy of injection immunotherapy in rhinitis and asthma, as well as the safety, provided that recommendations are followed. A second form of immunotherapy involves the intravenous injection of monoclonal anti-IgE antibodies. These bind to free and B-cell associated IgE; signalling their destruction. They do not bind to IgE already bound to the Fc receptor on basophils and mast cells, as this would stimulate the allergic inflammatory response. The first agent of this class is Omalizumab. While this form of immunotherapy is very effective in treating several types of atopy, it should not be used in treating the majority of people with food allergies. A third type, Sublingual immunotherapy, is an orally-administered therapy that takes advantage of oral immune tolerance to non-pathogenic antigens such as foods and resident bacteria. This therapy currently accounts for 40 percent of allergy treatment in Europe.[citation needed] In the United States, sublingual immunotherapy is gaining support among traditional allergists and is endorsed by doctors treating allergy. Allergy shot treatment is the closest thing to a cure for allergic symptoms. This therapy requires a long-term commitment.

OTHER

An experimental treatment, enzyme potentiated desensitization (EPD), has been tried for decades but is not generally accepted as effective. EPD uses dilutions of allergen and an enzyme, beta-glucuronidase, to which T-regulatory lymphocytes are supposed to respond by favouring desensitization, or down-regulation, rather than sensitization. EPD has also been tried for the treatment of autoimmune diseases but is not approved by the U.S. Food and Drug Administration or of proven effectiveness. Systematic literature searches conducted by the Mayo Clinic through 2006, involving hundreds of articles studying multiple conditions, including asthma and upper respiratory tract infection, showed no effectiveness of homeopathic treatments and no difference compared with placebo. The authors concluded that, based on rigorous clinical trials of all types of homeopathy for childhood and adolescence ailments, there is no convincing evidence that supports the use of homeopathic treatments.

EPIDEMIOLOGY

Many diseases related to inflammation such as type 1 diabetes, rheumatoid arthritis, and allergic diseases, hay fever and asthma have increased in the Western world over the past 2-3 decades. Rapid increases in allergic asthma and other atopic disorders in industrialized nations, it is estimated, began in the 1960s and 1970s, with further increases occurring during the 1980s and 1990s, although some suggest that a steady rise in sensitization has been occurring since the 1920s. The incidence of atopy in developing countries has, in general, remained much lower.

Allergic conditions: Statistics and Epidemiology Allergic rhinitis: 35.9 million (about 11% of the population) Untited States 3.3 million (about 5.5% of the population) United Kingdom
Asthma: 10 million suffer from allergic asthma (about 3% of the population). The prevalence of asthma increased 75% from 1980-1994. Asthma prevalence is 39% higher in African Americans than in Europeans. United States 5.7 million (about 9.4%). In six and seven year olds asthma increased from 18.4% to 20.9% over five years, during the same time the rate decreased from 31% to 24.7% in 13 to 14 year olds. United Kingdom
Atopic eczema: About 9% of the population. Between 1960 and 1990 prevalence has increased from 3% to 10% in children. United States 5.8 million (about 1% severe). United Kingdom
Anaphylaxis: At least 40 deaths per year due to insect venom. About 400 deaths due to penicillin anaphylaxis. About 220 cases of anaphylaxis and 3 deaths per year are due to latex allergy. An estimated 150 people die annually from anaphylaxis due to food allergy. United States Between 1999 and 2006, 48 deaths occurred in people ranging from five months to 85 years old. United Kingdom
Insect venom: Around 15% of adults have mild, localized allergic reactions. Systemic reactions occur in 3% of adults and less than 1% of children. United States Unted Kingdom : Unknown
Drug allergies: Anaphylactic reactions to penicillin cause 400 deaths per year. United States United Knigdom : Unknown
Food allergies: About 6% of US children under age 3 and 3.5-4% of the overall US population. Peanut and/or tree nut (e.g. walnut) allergy affects about three million Americans, or 1.1% of the population. United States 5-7% of infants and 1-2% of adults. A 117.3% increase in peanut allergies was observed from 2001 to 2005, an estimated 25,700 people in England are affected. United Kingdom
Multiple allergies: (Asthma, eczema and allergic rhinitis together) United States : Unknown 2.3 million (about 3.7%), prevalence has increased by 48.9% between 2001 and 2005.
Although genetic factors fundamentally govern susceptibility to atopic disease, increases in atopy have occurred within too short a time frame to be explained by a genetic change in the population, thus pointing to environmental or lifestyle changes Several hypotheses have been identified to explain this increased prevalence; increased exposure to perennial allergens due to housing changes and increasing time spent indoors, and changes in cleanliness or hygiene that have resulted in the decreased activation of a common immune control mechanism, coupled with dietary changes, obesity and decline in physical exercise. The hygiene hypothesis maintains that high living standards and hygienic conditions exposes children to fewer infections. It is thought that reduced bacterial and viral infections early in life direct the maturing immune system away from TH1 type responses, leading to unrestrained TH2 responses that allow for an increase in allergy. Changes in rates and types of infection alone however, have been unable to explain the observed increase in allergic disease, and recent evidence has focused attention on the importance of the gastrointestinal microbial environment. Evidence has shown that exposure to food and fecal-oral pathogens, such as hepatitis A, Toxoplasma gondii, and Helicobacter pylori (which also tend to be more prevalent in developing countries), can reduce the overall risk of atopy by more than 60%, and an increased prevalence of parasitic infections has been associated with a decreased prevalence of asthma. It is speculated that these infections exert their effect by critically altering TH1/TH2 regulation. Important elements of newer hygiene hypotheses also include exposure to endotoxins, exposure to pets and growing up on a farm.

HISTORY

The concept of "allergy" was originally introduced in 1906 by the Viennese pediatrician Clemens von Pirquet, after he noted that some of his patients were hypersensitive to normally innocuous entities such as dust, pollen, or certain foods. Pirquet called this phenomenon "allergy" from the Ancient Greek words allos meaning "other" and ergon meaning "work". All forms of hypersensitivity used to be classified as allergies, and all were thought to be caused by an improper activation of the immune system. Later, it became clear that several different disease mechanisms were implicated, with the common link to a disordered activation of the immune system. In 1963, a new classification scheme was designed by Philip Gell and Robin Coombs that described four types of hypersensitivity reactions, known as Type I to Type IV hypersensitivity. With this new classification, the word "allergy" was restricted to type I hypersensitivities (also called immediate hypersensitivity), which are characterized as rapidly developing reactions. A major breakthrough in understanding the mechanisms of allergy was the discovery of the antibody class labeled immunoglobulin E (IgE) - Kimishige Ishizaka and co-workers were the first to isolate and describe IgE in the 1960s.

MEDICAL SPECIALTY

An allergist is a physician specially trained to manage and treat allergies, asthma and the other allergic diseases. In the United States physicians holding certification by the American Board of Allergy and Immunology (ABAI) have successfully completed an accredited educational program and an evaluation process, including a secure, proctored examination to demonstrate the knowledge, skills, and experience to the provision of patient care in allergy and immunology. Becoming an allergist/immunologist requires completion of at least nine years of training. After completing medical school and graduating with a medical degree, a physician will then undergo three years of training in internal medicine (to become an internist) or pediatrics (to become a pediatrician). Once physicians have finished training in one of these specialties, they must pass the exam of either the American Board of Pediatrics (ABP) or the American Board of Internal Medicine (ABIM). Internists or pediatricians wishing to focus on the sub-specialty of allergy-immunology then complete at least an additional two years of study, called a fellowship, in an allergy/immunology training program. Allergist/immunologists listed as ABAI-certified have successfully passed the certifying examination of the American Board of Allergy and Immunology (ABAI), following their fellowship. In the United Kingdom, allergy is a subspecialty of general medicine or pediatrics. After obtaining postgraduate exams (MRCP or MRCPCH respectively), a doctor works for several years as a specialist registrar before qualifying for the General Medical Council specialist register. Allergy services may also be delivered by immunologists. A 2003 Royal College of Physicians report presented a case for improvement of what were felt to be inadequate allergy services in the UK. In 2006, the House of Lords convened a subcommittee that reported in 2007. It concluded likewise that allergy services were insufficient to deal with what the Lords referred to as an "allergy epidemic" and its social cost; it made several other recommendations.

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ANCYLOSTOMA CANINUM

Ancylostoma caninum, commonly Dog hookworm, is a parasitic nematode hookworm that infects dogs. The larval stage penetrates the skin and makes it way through the circulatory system into the digestive tract, where adult forms lay eggs that are passed through the feces. Common symptoms include anemia and diarrhea. Newborn pups can die of hemorrhaging from their intestines caused by massive numbers of feeding hookworms. A. braziliense and Uncinaria stenocephala are different species of hookworm which can infect dogs and cause similar symptoms. The parasite can also affect humans. It occasionally develops into an adult to cause eosinophilic enteritis in people, and their invasive larvae can cause an itchy rash called cutaneous larva migrans. Vaccination may soon be possible.

For more information view the source:Wikipedia

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ANCYLOSTOMA TUBAEFORME

Ancylostoma tubaeforme is a hookworm that infects cats. Infection can occur by penetration of the skin, eating other hosts such as birds, or by directly consuming the organism. This hookworm can also infect humans, causing a dermatitis. Ancylostoma tubaeforme along with Ancylostoma braziliense are the two most common hookworms to infect cats, causing anemia and also compromising the immune system.

For more information view the source:Wikipedia

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ASCARIS LUMBRICOIDES
An estimated 807-1,221 million people in the world are infected with Ascaris lumbricoides (sometimes called just "Ascaris"). Ascaris, hookworm, and whipworm are known as soil-transmitted helminths (parasitic worms). Together, they account for a major burden of disease worldwide. Ascariasis is now uncommon in the United States.

Ascaris lives in the intestine and Ascaris eggs are passed in the feces of infected persons. If the infected person defecates outside (near bushes, in a garden, or field) or if the feces of an infected person are used as fertilizer, eggs are deposited on soil. They can then mature into a form that is infective. Ascariasis is caused by ingesting eggs. This can happen when hands or fingers that have contaminated dirt on them are put in the mouth or by consuming vegetables or fruits that have not been carefully cooked, washed or peeled.

People infected with Ascaris often show no symptoms. If symptoms do occur they can be light and include abdominal discomfort. Heavy infections can cause intestinal blockage and impair growth in children. Other symptoms such as cough are due to migration of the worms through the body. Ascariasis is treatable with medication prescribed by your health care provider.

FAQS

What is ascariasis?

Ascaris is an intestinal parasite of humans. It is the most common human worm infection. The larvae and adult worms live in the small intestine and can cause intestinal disease.

How is ascariasis spread?

Ascaris lives in the intestine and Ascaris eggs are passed in the feces of infected persons. If the infected person defecates outside (near bushes, in a garden, or field), or if the feces of an infected person are used as fertilizer, then eggs are deposited on the soil. They can then mature into a form that is infective. Ascariasis is caused by ingesting infective eggs. This can happen when hands or fingers that have contaminated dirt on them are put in the mouth or by consuming vegetables or fruits that have not been carefully cooked, washed or peeled.

Who is at risk for infection?

Infection occurs worldwide in warm and humid climates, where sanitation and hygiene are poor, including in temperate zones during warmer months. Persons in these areas are at risk if soil contaminated with human feces enters their mouths or if they eat vegetables or fruit that have not been carefully washed, peeled or cooked. Ascariasis is now uncommon in the United States.

What are the symptoms of ascariasis?

People infected with Ascaris often show no symptoms. If symptoms do occur they can be light and include abdominal discomfort. Heavy infections can cause intestinal blockage and impair growth in children. Other symptoms such as cough are due to migration of the worms through the body.

How is ascariasis diagnosed?

Health care providers can diagnose ascariasis by taking a stool sample and using a microscope to look for the presence of eggs. Some people notice infection when a worm is passed in their stool or is coughed up. If this happens, bring in the worm specimen to your health care provider for diagnosis.

How can I prevent infection?
- Avoid contact with soil that may be contaminated with human feces, including with human fecal matter ("night soil") used to fertilize crops.
- Wash your hands with soap and warm water before handling food.
- Teach children the importance of washing hands to prevent infection.
- Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.
Transmission of infection to others can be prevented by:
- not defecating outdoors, and by
- effective sewage disposal systems.
What is the treatment for ascariasis?

Anthelminthic medications (drugs that rid the body of parasitic worms), such as albendazole and mebendazole, are the drugs of choice for treatment. Infections are generally treated for 1-3 days. The recommended medications are effective.

What is preventive treatment?

In developing countries, groups at higher risk for soil-transmitted helminth infections (hookworm, Ascaris, and whipworm) are often treated without a prior stool examination. Treating in this way is called preventive treatment (or "preventive chemotherapy"). The high-risk groups identified by the World Health Organization are preschool and school-age children, women of childbearing age (including pregnant women in the 2nd and 3rd trimesters and lactating women) and adults in occupations where there is a high risk of heavy infections. School-age children are often treated through school-health programs and preschool children and pregnant women at visits to health clinics.

What is mass drug administration (MDA)?

The soil-transmitted helminths (hookworm, Ascaris, and whipworm) and four other "neglected tropical diseases" (river blindness, lymphatic filariasis, schistosomiasis and trachoma) are sometimes treated through mass drug administrations. Since the drugs used are safe and inexpensive or donated, entire risk groups are offered preventive treatment. Mass drug administrations are conducted periodically (often annually), commonly with drug distributors who go door-to-door. Multiple neglected tropical diseases are often treated simultaneously using MDAs.

EPIDEMIOLOGY & RISK FACTORS

Ascaris infection is one of the most common intestinal worm infections. It is found in association with poor personal hygiene, poor sanitation, and in places where human feces are used as fertilizer.

Geographic Distribution

The geographic distributions of Ascaris are worldwide in areas with warm, moist climates and are widely overlapping. Infection occurs worldwide and is most common in tropical and subtropical areas where sanitation and hygiene are poor.

BIOLOGY

Causal Agent:

Ascaris lumbricoides is the largest nematode (roundworm) parasitizing the human intestine. (Adult females: 20 to 35 cm; adult male: 15 to 30 cm.)

Life Cycle:

Adult worms live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces. Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed, the larvae hatch, invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs. The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed. Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.

Life cycle image and information courtesy of DPDx.

DISEASE

People infected with Ascaris often show no symptoms. If symptoms do occur they can be light and include abdominal discomfort. Heavy infections can cause intestinal blockage and impair growth in children. Other symptoms such as cough are due to migration of the worms through the body. Ascariasis is treatable with medication prescribed by your health care provider.

DIAGNOSIS

The standard method for diagnosing ascariasis is by identifying Ascaris eggs in a stool sample using a microscope. Because eggs may be difficult to find in light infections, a concentration procedure is recommended.

PREVENTION AND CONTROL

The best way to prevent ascariasis is to always:
- Avoid ingesting soil that may be contaminated with human feces, including where human fecal matter ("night soil") or wastewater is used to fertilize crops.
- Wash your hands with soap and warm water before handling food.
- Teach children the importance of washing hands to prevent infection.
- Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.
For more information view the source:Center for Disease Control

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BABESIA (Blood Parasite)

Babesia is a protozoan parasite of the blood that causes a hemolytic disease known as Babesiosis. There are over 100 species of Babesiaidentified; however only a handful have been documented as pathogenic in humans.
In the United States, Babesia microti is the most common strain associated with humans with other species infecting cattle, livestock and occasionally domestic animals. People who contract Babesiosis suffer from malaria-like symptoms. As a result malaria is a common misdiagnosis for the disease.

CLASSIFICATION

Babesia is a protozoan parasite of which Babesia microti and Babesia divergens are the two species to most frequently infect humans. Infections from other species of Babesia have been documented in humans but are not habitually seen. Babesiosis is also known as Piroplasmosis. Due to historical misclassifications, this protozoan was labeled with many names that are no longer used. Common names of the disease include Texas Cattle Fever, Redwater Fever, Tick Fever, and Nantucket Fever.

HISTORY

For centuries, babesiosis was known to be a serious illness for wild and domesticated animals, especially cattle. Victor Babes, a Romanian scientist who first documented the disease in Romania in 1888, described symptoms of a severe hemolytic illness seen uniquely in cattle and sheep. Although he identified the causative agent in 1888, he incorrectly believed it to be due to a bacterium that he named Haematococcus bovis. In 1893 Americans Theobald Smith and Fred Kilborne identified the parasite as the cause of Texas Cattle Fever, the same disease described by Babes. Smith and Kilborne also identified the tick as the agent of transmission, a discovery that first introduced the concept of arthropods functioning as disease vectors. Long believed to be a disease that only affected non-human mammals, it wasn't until 1957 that the first case of babesiosis was seen in humans. The first case was observed in a splenectomized patient as were all people diagnosed up until 1969. The first case of babesiosis seen in a non-splenectomized patient proved that the protozoan parasite was pathogenic to all people.

CLINICAL PRESENTATION

The severity of B. microti infections varies. For 25% of cases in adults and half of cases in children, the disease is asymptomatic or mild with flu-like symptoms. In cases of symptomatic infection, symptoms are characterized by irregular fevers, chills, headaches, general lethargy, pain and malaise. In severe cases, hemolytic anemia, jaundice, shortness of breath, and hemoglobinuria are documented due to the lytic effects of parasitic multiplication. Immunocompetent individuals with healthy spleens often recover without treatment. Splenectomized patients are more susceptible to contracting the disease and the course of infection often ends fatally within 5 to 8 days of symptom onset. Parasitemia levels can reach up to 85% in patients without spleens compared to 1-10% in individuals with spleens and effective immune systems. Splenectomized patients suffer from severe hemolytic anemia with occasional incidences of hepatomegaly and splenomegaly documented.Complications that arise from B. microti infections include acute respiratory failure, congestive heart failure, and renal failure. Infections can be fatal in 5-10% of hospitalized patients with increased risk of death in the immunosuppressed, the elderly, and those co-infected with Lyme disease B. divergens infections have a much higher fatality rate (42%) and present with the most severe symptoms. Infected individuals suffer from hemoglobinuria followed by jaundice, a persistently high fever, chills and sweats. If left untreated, B. divergens infections can develop into shock-like symptoms with pulmonary edema and renal failure. Signs of infection usually arise 1 to 8 weeks after a bite from an infectious tick. Infections from B. divergens have a shorter latent period usually ranging from 1-3 weeks.

TRANSMISSION

Babesia is spread through the saliva of a tick when it bites. At its nymphal stage, a tick will bite into the skin for a blood meal. The tick, if not removed, will stay attached for 3 to 6 days with longer periods of feeding associated with a higher probability of acquiring the parasite. The parasite can survive in the tick as it molts through its various developmental stages resulting in all stages being potentially infectious. Some species of Babesia can be transmitted from a female tick to its offspring before migrating to salivary glands for feeding. B. microti, the most common variety of Babesia in humans however, has not been shown to transmit transovarially. Ticks of domestic animals that transmit Babesia, causing much disease, include the very widespread cattle ticks, Rhipicephalus (Boophilus) microplus, and R.(B.) decoloratus. These ticks have a strict one-host feeding cycle on cattle, so the Babesia can only be transmitted by the transovarial route.In the Americas, Ixodes scapularis is the most common vector. This hard tick, commonly known as a deer tick, is also the vector for other tick-associated illnesses such as Lyme disease. Many species of Babesia only infect non-human mammalian hosts, most commonly cattle, horses, and sheep. B. microti and B. divergens are the two main pathogenic species in humans. Their reservoirs are theorized to be the white-footed mouse (Peromyscus leucopus Rafinesque), microtus voles (Microtus spp.), and the white-tailed deer (Odocoileus virginianus). These woodland species are hypothesized reservoirs because although they are known to harbor the disease, complete reservoir competence has not yet been shown. Most cases of transmission between humans are attributed to a tick vector. However, as of 2003 the Centers for Disease Control and Prevention (CDC) acknowledged more than 40 cases of Babesiosis contracted from packed red blood cell (PRBC) transfusions and 2 infections documented from organ transplantation. PRBC transfusions that cause infections were identified through testing of the blood donor for B. microti antibodies. The occurrence of PRBC transfusions as a mechanism of Babesia transmission puts pressure on governmental organizations, such as the CDC, to heighten standard measures for screening blood donations.

MORPHOLOGY

Babesia enters erythrocytes at the sporozoite stage. Within the red blood cell, the protozoa become cyclical and develop into a trophozoite ring. The trophozoites moults into merozoites, which have a tetrad structure coined a Maltese-cross form. The tetrad morphology, which can be seen with Giemsa staining of a thin blood smear, is unique to Babesia and serves as a distinguishing feature from Plasmodium falciparum, a protozoan of similar morphology that causes Malaria. Trophozoite and merozoite growth ruptures the host erythrocyte leading to the release of vermicules, the infectious parasitic bodies, which rapidly spread the protozoa throughout the blood.

LIFE CYCLE

The life cycle of Babesia microti, which is typical of parasites in the Babesia genus, requires a biological stage in a rodent or deer host and is transmitted by ticks of the genus Ixodidae between these hosts. To begin, the ticks introduce the sporozoites into the rodent when taking a blood meal. Sporozoites enter erythrocytes in the blood and begin the cyclical development between trophozoites and merozoites. Rather than producing more trophozoites, some merozoites produce gametocytes. The definitive tick host, of the Ixodidae genus, takes up the gametocytes when attached for a blood meal. The gametes are fertilized in the gut of the tick and develop into sporozoites in the salivary glands. The sporozoites are introduced into a human upon inoculation at the bite of an infected tick. Even as an incidental host, the phase changes that occur in the parasite are the same within humans as in the biological hosts. Babesia can be diagnosed at the trophozoite stage and can be transmitted from human to human either through the tick vector or through blood transfusions.

DIAGNOSIS AND TREATMENT

DIAGNOSTIC TESTS

As a protozoan parasite, the most effective way to identify Babesia infection is through blood sample testing. It is important to pay specific attention to particular morphologies of Babesia in blood smears because its substantial similarity to the malarial parasite Plasmodium falciparum results in many patients suffering from Babesiosis being misdiagnosed. The few distinguishing factors for Babesia include protozoa with varying shapes and sizes, the potential to contain vacuoles, and the lack of pigment production. Trophozoites within an erythrocyte that appear in a tetrad formation are also indicative of Babesia. A trained eye is necessary to distinguish the two species. Even with much study of Babesiosis and Malaria, misdiagnosis with blood smear can be frequent and problematic. To supplement a blood smear, diagnoses should be made with an indirect fluorescent antibody (IFA) test. IFA testing has a much higher specificity than stained blood smears with antibody detection in 88-96 % of infected patients. Diagnostic measures through antibody testing are also particularly useful for identifying serum prevalence in asymptomatic individuals. Due to the transmissibility of Babesia through blood transfusions, IFA testing would be an effective means of screening for the disease in blood donations.Historically, Babesiosis diagnosis was carried out with xenodiagnosis in hamsters for B. microti and in gerbils for B.divergens. While successful at identifying the disease, this diagnostic technique has been abandoned for faster diagnostic measures.

TREATMENT

There are several ways to manage and treat Babesiosis in animals. In many cases, patients spontaneously recover having only experienced mild symptoms undiagnosed as the disease. This occurrence is almost always seen in B. microti infections, which are generally more common in the United States. For B. divergens and more severe B. microti infections, the standard treatment historically for symptomatic individuals was oral or intravenous Clindamycin with oral quinine. With the results of research completed in 2000 however, treatment regimens have been increasingly leaning towards oral Atovaquone with oral azithromycin. The latter medications are preferred as they are equally effective in all but the most severe cases of babesiosis and exhibit fewer associated adverse reactions. In severe cases, blood exchange transfusions have been performed to lower the parasitic load in the individual. Other rudimentary treatment measures include addressing and correcting abnormal clinical signals.

EPIDEMIOLOGY

Of the species to infect humans, B. microti is most common in the Americas whereas B. divergens is the predominant strain found in Europe. Endemic areas are regions of tick habitat, including the forest regions of the Northeastern United States and temperate regions of Europe. Ixodidae, the tick vector of B. microti, also transmits the better-known Lyme disease. For reasons that remain unclear, in areas endemic to both Lyme disease and Babesiosis, Lyme disease transmission prevails and is more predominant in the region. Prevalence of Babesiosis is regions endemic to Malaria remains unknown due to the likelihood of misdiagnosis as Malaria.As the disease results in a high number of asympomatic individuals, many populations can possess high seroprevalence without much documentation of illness. For example, in Rhode Island and Nantucket, seroprevalence has been measured to be 20-25%. Prevalence of Babesiosis is most documented during the months of May to September where there is high tick activity in endemic regions.

PREVENTION

The most effective public health measure for Babesia is avoidance of tick exposure. This can be performed through personal prevention strategies such as avoiding tick infested areas (especially during high tick season between May and September), remaining covered with light clothing, searching for ticks after being outdoors and removing discovered ticks from the skin. Other preventative measures include applying Diethyltoluamide (DEET), a common bug repellent that is effective against ticks, amongst other insects. (For people who react adversely to DEET, alternative insect repellents should be used.) On a state level, if health departments are particularly motivated, tick elimination is a possibility. In 1906, efforts were made to eradicate the tick vector of the bovine disease form of Babesiosis in the United States. This eradication was recorded as being successfully completed four decades later. Complete eradication efforts would be a long-term project, which would significantly reduce the prevalence of both Babesiosis and Lyme disease. However, as public health departments are often short on funding, preventative measures seem to be more recommended over vector control. Due to the relatively low prevalence of the disease and the presence of several reservoirs, Babesiosis is currently not a candidate for vaccine-based prevention. In regions where ticks of domestic animals are routinely controlled with chemical acaricide to reduce incidence of infection with Babesia bovis and Babesia bigemina the risk to humans from these babesias will be reduced.

For more information view the source:Wikipedia

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BACTERIA

Bacteria are a large domain of prokaryotic microorganisms. Typically a few micrometres in length, bacteria have a wide range of shapes, ranging from spheres to rods and spirals. Bacteria are present in most habitats on Earth, growing in soil, acidic hot springs, radioactive waste, water, and deep in the Earth's crust, as well as in organic matter and the live bodies of plants and animals, providing outstanding examples of mutualism in the digestive tracts of humans, termites and cockroaches. There are typically 40 million bacterial cells in a gram of soil and a million bacterial cells in a millilitre of fresh water; in all, there are approximately five nonillion (5 1030) bacteria on Earth, forming a biomass that exceeds that of all plants and animals. Bacteria are vital in recycling nutrients, with many steps in nutrient cycles depending on these organisms, such as the fixation of nitrogen from the atmosphere and putrefaction. In the biological communities surrounding hydrothermal vents and cold seeps, bacteria provide the nutrients needed to sustain life by converting dissolved compounds such as hydrogen sulphide and methane. Most bacteria have not been characterised, and only about half of the phyla of bacteria have species that can be grown in the laboratory. The study of bacteria is known as bacteriology, a branch of microbiology. There are approximately ten times as many bacterial cells in the human flora as there are human cells in the body, with large numbers of bacteria on the skin and as gut flora. The vast majority of the bacteria in the body are rendered harmless by the protective effects of the immune system, and a few are beneficial. However, a few species of bacteria are pathogenic and cause infectious diseases, including cholera, syphilis, anthrax, leprosy, and bubonic plague. The most common fatal bacterial diseases are respiratory infections, with tuberculosis alone killing about 2 million people a year, mostly in sub-Saharan Africa. In developed countries, antibiotics are used to treat bacterial infections and in agriculture, so antibiotic resistance is becoming common. In industry, bacteria are important in sewage treatment and the breakdown of oil spills, the production of cheese and yogurt through fermentation, the recovery of gold, palladium, copper and other metals in the mining sector, as well as in biotechnology, and the manufacture of antibiotics and other chemicals. Once regarded as plants constituting the class Schizomycetes, bacteria are now classified as prokaryotes. Unlike cells of animals and other eukaryotes, bacterial cells do not contain a nucleus and rarely harbour membrane-bound organelles. Although the term bacteria traditionally included all prokaryotes, the scientific classification changed after the discovery in the 1990s that prokaryotes consist of two very different groups of organisms that evolved independently from an ancient common ancestor. These evolutionary domains are called Bacteria and Archaea.

ETYMOLOGY

The word bacteria is the plural of the New Latin bacterium, which is the latinisation of the Greek (bakterion), the diminutive of (bakteria), meaning "staff, cane", because the first ones to be discovered were rod-shaped.

HISTORY AND BACTERIOLOGY

Bacteria were first observed by Antonie van Leeuwenhoek in 1676, using a single-lens microscope of his own design. He called them "animalcules" and published his observations in a series of letters to the Royal Society. The name Bacterium was introduced much later, by Christian Gottfried Ehrenberg in 1828. In fact, Bacterium was a genus that contained non-spore-forming rod-shaped bacteria, as opposed to Bacillus, a genus of spore-forming rod-shaped bacteria defined by Ehrenberg in 1835. Louis Pasteur demonstrated in 1859 that the fermentation process is caused by the growth of microorganisms, and that this growth is not due to spontaneous generation. (Yeasts and molds, commonly associated with fermentation, are not bacteria, but rather fungi.) Along with his contemporary Robert Koch, Pasteur was an early advocate of the germ theory of disease. Robert Koch was a pioneer in medical microbiology and worked on cholera, anthrax and tuberculosis. In his research into tuberculosis, Koch finally proved the germ theory, for which he was awarded a Nobel Prize in 1905. In Koch's postulates, he set out criteria to test if an organism is the cause of a disease, and these postulates are still used today. Though it was known in the nineteenth century that bacteria are the cause of many diseases, no effective antibacterial treatments were available. In 1910, Paul Ehrlich developed the first antibiotic, by changing dyes that selectively stained Treponema pallidum the spirochaete that causes syphilis into compounds that selectively killed the pathogen. Ehrlich had been awarded a 1908 Nobel Prize for his work on immunology, and pioneered the use of stains to detect and identify bacteria, with his work being the basis of the Gram stain and the Ziehl-Neelsen stain. A major step forward in the study of bacteria was the recognition in 1977 by Carl Woese that archaea have a separate line of evolutionary descent from bacteria. This new phylogenetic taxonomy was based on the sequencing of 16S ribosomal RNA, and divided prokaryotes into two evolutionary domains, as part of the three-domain system. Louis Pasteur demonstrated in 1859 that the fermentation process is caused by the growth of microorganisms, and that this growth is not due to spontaneous generation. (Yeasts and molds, commonly associated with fermentation, are not bacteria, but rather fungi.) Along with his contemporary Robert Koch, Pasteur was an early advocate of the germ theory of disease. Robert Koch was a pioneer in medical microbiology and worked on cholera, anthrax and tuberculosis. In his research into tuberculosis, Koch finally proved the germ theory, for which he was awarded a Nobel Prize in 1905. In Koch's postulates, he set out criteria to test if an organism is the cause of a disease, and these postulates are still used today. Though it was known in the nineteenth century that bacteria are the cause of many diseases, no effective antibacterial treatments were available. In 1910, Paul Ehrlich developed the first antibiotic, by changing dyes that selectively stained Treponema pallidum the spirochaete that causes syphilis into compounds that selectively killed the pathogen. Ehrlich had been awarded a 1908 Nobel Prize for his work on immunology, and pioneered the use of stains to detect and identify bacteria, with his work being the basis of the Gram stain and the Ziehl-Neelsen stain. A major step forward in the study of bacteria was the recognition in 1977 by Carl Woese that archaea have a separate line of evolutionary descent from bacteria. This new phylogenetic taxonomy was based on the sequencing of 16S ribosomal RNA, and divided prokaryotes into two evolutionary domains, as part of the three-domain system.

ORIGIN AND EARLY EVOLUTION

The ancestors of modern bacteria were single-celled microorganisms that were the first forms of life to appear on Earth, about 4 billion years ago. For about 3 billion years, all organisms were microscopic, and bacteria and archaea were the dominant forms of life. Although bacterial fossils exist, such as stromatolites, their lack of distinctive morphology prevents them from being used to examine the history of bacterial evolution, or to date the time of origin of a particular bacterial species. However, gene sequences can be used to reconstruct the bacterial phylogeny, and these studies indicate that bacteria diverged first from the archaeal/eukaryotic lineage. Bacteria were also involved in the second great evolutionary divergence, that of the archaea and eukaryotes. Here, eukaryotes resulted from ancient bacteria entering into endosymbiotic associations with the ancestors of eukaryotic cells, which were themselves possibly related to the Archaea. This involved the engulfment by proto-eukaryotic cells of alpha-proteobacterial symbionts to form either mitochondria or hydrogenosomes, which are still found in all known Eukarya (sometimes in highly reduced form, e.g. in ancient "amitochondrial" protozoa). Later on, some eukaryotes that already contained mitochondria also engulfed cyanobacterial-like organisms. This led to the formation of chloroplasts in algae and plants. There are also some algae that originated from even later endosymbiotic events. Here, eukaryotes engulfed a eukaryotic algae that developed into a "second-generation" plastid. This is known as secondary endosymbiosis.

MORPHOLOGY

Bacteria display a wide diversity of shapes and sizes, called morphologies. Bacterial cells are about one tenth the size of eukaryotic cells and are typically 0.5-5.0 micrometres in length. However, a few species for example, Thiomargarita namibiensis and Epulopiscium fishelsoni are up to half a millimetre long and are visible to the unaided eye; E. fishelsoni reaches 0.7 mm. Among the smallest bacteria are members of the genus Mycoplasma, which measure only 0.3 micrometres, as small as the largest viruses. Some bacteria may be even smaller, but these ultramicrobacteria are not well-studiedMost bacterial species are either spherical, called cocci (sing. coccus, from Greek (grain, seed), or rod-shaped, called bacilli (sing. bacillus, from Latin baculus, stick). Elongation is associated with swimming. Some rod-shaped bacteria, called vibrio, are slightly curved or comma-shaped; others, can be spiral-shaped, called spirilla, or tightly coiled, called spirochaetes. A small number of species even have tetrahedral or cuboidal shapes. More recently, bacteria were discovered deep under the Earth's crust that grow as long rods with a star-shaped cross-section. The large surface area to volume ratio of this morphology may give these bacteria an advantage in nutrient-poor environments. This wide variety of shapes is determined by the bacterial cell wall and cytoskeleton, and is important because it can influence the ability of bacteria to acquire nutrients, attach to surfaces, swim through liquids and escape predators. Many bacterial species exist simply as single cells, others associate in characteristic patterns: Neisseria form diploids (pairs), Streptococcus form chains, and Staphylococcus group together in "bunch of grapes" clusters. Bacteria can also be elongated to form filaments, for example the Actinobacteria. Filamentous bacteria are often surrounded by a sheath that contains many individual cells. Certain types, such as species of the genus Nocardia, even form complex, branched filaments, similar in appearance to fungal mycelia.

CELLULAR STRUCTURE

INTRACELLULAR STRUCTURES

The bacterial cell is surrounded by a lipid membrane, or cell membrane, which encloses the contents of the cell and acts as a barrier to hold nutrients, proteins and other essential components of the cytoplasm within the cell. As they are prokaryotes, bacteria do not tend to have membrane-bound organelles in their cytoplasm and thus contain few large intracellular structures. They consequently lack a true nucleus, mitochondria, chloroplasts and the other organelles present in eukaryotic cells, such as the Golgi apparatus and endoplasmic reticulum. Bacteria were once seen as simple bags of cytoplasm, but elements such as prokaryotic cytoskeleton, and the localization of proteins to specific locations within the cytoplasm have been found to show levels of complexity. These subcellular compartments have been called "bacterial hyperstructures". Micro-compartments such as carboxysomes provides a further level of organization, which are compartments within bacteria that are surrounded by polyhedral protein shells, rather than by lipid membranes. These "polyhedral organelles" localize and compartmentalize bacterial metabolism, a function performed by the membrane-bound organelles in eukaryotes. Many important biochemical reactions, such as energy generation, occur by concentration gradients across membranes. The general lack of internal membranes in bacteria means reactions such as electron transport occur across the cell membrane between the cytoplasm and the periplasmic space. However, in many photosynthetic bacteria the plasma membrane is highly folded and fills most of the cell with layers of light-gathering membrane. These light-gathering complexes may even form lipid-enclosed structures called chlorosomes in green sulfur bacteria. Other proteins import nutrients across the cell membrane, or to expel undesired molecules from the cytoplasm. Most bacteria do not have a membrane-bound nucleus, and their genetic material is typically a single circular chromosome located in the cytoplasm in an irregularly shaped body called the nucleoid. The nucleoid contains the chromosome with associated proteins and RNA. The order Planctomycetes are an exception to the general absence of internal membranes in bacteria, because they have a double membrane around their nucleoids and contain other membrane-bound cellular structures. Like all living organisms, bacteria contain ribosomes for the production of proteins, but the structure of the bacterial ribosome is different from those of eukaryotes and Archaea.Some bacteria produce intracellular nutrient storage granules, such as glycogen, polyphosphate, sulfur or polyhydroxyalkanoates. These granules enable bacteria to store compounds for later use. Certain bacterial species, such as the photosynthetic Cyanobacteria, produce internal gas vesicles, which they use to regulate their buoyancy allowing them to move up or down into water layers with different light intensities and nutrient levels. Some bacteria produce intracellular nutrient storage granules, such as glycogen, polyphosphate, sulfur or polyhydroxyalkanoates. These granules enable bacteria to store compounds for later use. Certain bacterial species, such as the photosynthetic Cyanobacteria, produce internal gas vesicles, which they use to regulate their buoyancy allowing them to move up or down into water layers with different light intensities and nutrient levels.

EXTRACECELLULAR STRUCTURES

In most bacteria a cell wall is present on the outside of the cytoplasmic membrane. A common bacterial cell wall material is peptidoglycan (called murein in older sources), which is made from polysaccharide chains cross-linked by peptides containing D-amino acids. Bacterial cell walls are different from the cell walls of plants and fungi, which are made of cellulose and chitin, respectively.The cell wall of bacteria is also distinct from that of Archaea, which do not contain peptidoglycan. The cell wall is essential to the survival of many bacteria, and the antibiotic penicillin is able to kill bacteria by inhibiting a step in the synthesis of peptidoglycan. There are broadly speaking two different types of cell wall in bacteria, called Gram-positive and Gram-negative. The names originate from the reaction of cells to the Gram stain, a test long-employed for the classification of bacterial species. Gram-positive bacteria possess a thick cell wall containing many layers of peptidoglycan and teichoic acids. In contrast, Gram-negative bacteria have a relatively thin cell wall consisting of a few layers of peptidoglycan surrounded by a second lipid membrane containing lipopolysaccharides and lipoproteins. Most bacteria have the Gram-negative cell wall, and only the Firmicutes and Actinobacteria (previously known as the low G C and high G C Gram-positive bacteria, respectively) have the alternative Gram-positive arrangement. These differences in structure can produce differences in antibiotic susceptibility; for instance, vancomycin can kill only Gram-positive bacteria and is ineffective against Gram-negative pathogens, such as Haemophilus influenzae or Pseudomonas aeruginosa. In many bacteria an S-layer of rigidly arrayed protein molecules covers the outside of the cell. This layer provides chemical and physical protection for the cell surface and can act as a macromolecular diffusion barrier. S-layers have diverse but mostly poorly understood functions, but are known to act as virulence factors in Campylobacter and contain surface enzymes in Bacillus stearothermophilus. Flagella are rigid protein structures, about 20 nanometres in diameter and up to 20 micrometres in length, that are used for motility. Flagella are driven by the energy released by the transfer of ions down an electrochemical gradient across the cell membrane. Fimbriae are fine filaments of protein, just 2-10 nanometres in diameter and up to several micrometers in length. They are distributed over the surface of the cell, and resemble fine hairs when seen under the electron microscope. Fimbriae are believed to be involved in attachment to solid surfaces or to other cells and are essential for the virulence of some bacterial pathogens. Pili (sing. pilus) are cellular appendages, slightly larger than fimbriae, that can transfer genetic material between bacterial cells in a process called conjugation (see bacterial genetics, below). Capsules or slime layers are produced by many bacteria to surround their cells, and vary in structural complexity: ranging from a disorganised slime layer of extra-cellular polymer, to a highly structured capsule or glycocalyx. These structures can protect cells from engulfment by eukaryotic cells, such as macrophages. They can also act as antigens and be involved in cell recognition, as well as aiding attachment to surfaces and the formation of biofilms. The assembly of these extracellular structures is dependent on bacterial secretion systems. These transfer proteins from the cytoplasm into the periplasm or into the environment around the cell. Many types of secretion systems are known and these structures are often essential for the virulence of pathogens, so are intensively studied.

ENDOSPORES

Certain genera of Gram-positive bacteria, such as Bacillus, Clostridium, Sporohalobacter, Anaerobacter and Heliobacterium, can form highly resistant, dormant structures called endospores. In almost all cases, one endospore is formed and this is not a reproductive process, although Anaerobacter can make up to seven endospores in a single cell. Endospores have a central core of cytoplasm containing DNA and ribosomes surrounded by a cortex layer and protected by an impermeable and rigid coat. Endospores show no detectable metabolism and can survive extreme physical and chemical stresses, such as high levels of UV light, gamma radiation, detergents, disinfectants, heat, freezing, pressure and desiccation. In this dormant state, these organisms may remain viable for millions of years, and endospores even allow bacteria to survive exposure to the vacuum and radiation in space. According to scientist Dr. Steinn Sigurdsson, "There are viable bacterial spores that have been found that are 40 million years old on Earth and we know they're very hardened to radiation." Endospore-forming bacteria can also cause disease: for example, anthrax can be contracted by the inhalation of Bacillus anthracis endospores, and contamination of deep puncture wounds with Clostridium tetani endospores causes tetanus.

METABOLISM

Bacteria exhibit an extremely wide variety of metabolic types. The distribution of metabolic traits within a group of bacteria has traditionally been used to define their taxonomy, but these traits often do not correspond with modern genetic classifications. Bacterial metabolism is classified into nutritional groups on the basis of three major criteria: the kind of energy used for growth, the source of carbon, and the electron donors used for growth. An additional criterion of respiratory microorganisms are the electron acceptors used for aerobic or anaerobic respiration. Carbon metabolism in bacteria is either heterotrophic, where organic carbon compounds are used as carbon sources, or autotrophic, meaning that cellular carbon is obtained by fixing carbon dioxide. Heterotrophic bacteria include parasitic types. Typical autotrophic bacteria are phototrophic cyanobacteria, green sulfur-bacteria and some purple bacteria, but also many chemolithotrophic species, such as nitrifying or sulfur-oxidising bacteria. Energy metabolism of bacteria is either based on phototrophy, the use of light through photosynthesis, or based on chemotrophy, the use of chemical substances for energy, which are mostly oxidised at the expense of oxygen or alternative electron acceptors (aerobic/anaerobic respiration).Finally, bacteria are further divided into lithotrophs that use inorganic electron donors and organotrophs that use organic compounds as electron donors. Chemotrophic organisms use the respective electron donors for energy conservation (by aerobic/anaerobic respiration or fermentation) and biosynthetic reactions (e.g. carbon dioxide fixation), whereas phototrophic organisms use them only for biosynthetic purposes. Respiratory organisms use chemical compounds as a source of energy by taking electrons from the reduced substrate and transferring them to a terminal electron acceptor in a redox reaction. This reaction releases energy that can be used to synthesise ATP and drive metabolism. In aerobic organisms, oxygen is used as the electron acceptor. In anaerobic organisms other inorganic compounds, such as nitrate, sulfate or carbon dioxide are used as electron acceptors. This leads to the ecologically important processes of denitrification, sulfate reduction and acetogenesis, respectively. Another way of life of chemotrophs in the absence of possible electron acceptors is fermentation, where the electrons taken from the reduced substrates are transferred to oxidised intermediates to generate reduced fermentation products (e.g. lactate, ethanol, hydrogen, butyric acid). Fermentation is possible, because the energy content of the substrates is higher than that of the products, which allows the organisms to synthesise ATP and drive their metabolism. These processes are also important in biological responses to pollution; for example, sulfate-reducing bacteria are largely responsible for the production of the highly toxic forms of mercury (methyl- and dimethylmercury) in the environment. Non-respiratory anaerobes use fermentation to generate energy and reducing power, secreting metabolic by-products (such as ethanol in brewing) as waste. Facultative anaerobes can switch between fermentation and different terminal electron acceptors depending on the environmental conditions in which they find themselves. Lithotrophic bacteria can use inorganic compounds as a source of energy. Common inorganic electron donors are hydrogen, carbon monoxide, ammonia (leading to nitrification), ferrous iron and other reduced metal ions, and several reduced sulfur compounds. Unusually, the gas methane can be used by methanotrophic bacteria as both a source of electrons and a substrate for carbon anabolism. In both aerobic phototrophy and chemolithotrophy, oxygen is used as a terminal electron acceptor, while under anaerobic conditions inorganic compounds are used instead. Most lithotrophic organisms are autotrophic, whereas organotrophic organisms are heterotrophic. In addition to fixing carbon dioxide in photosynthesis, some bacteria also fix nitrogen gas (nitrogen fixation) using the enzyme nitrogenase. This environmentally important trait can be found in bacteria of nearly all the metabolic types listed above, but is not universal. Regardless of the type of metabolic process they employ, the majority of bacteria are only able to take in raw materials in the form of relatively small molecules, which enter the cell by diffusion or through molecular channels in cell membranes. The Planctomycetes are the exception (as they are in possessing membranes around their nuclear material). It has recently been shown that Gemmata obscuriglobus is able to take in large molecules via a process that in some ways resembles endocytosis, the process used by eukaryotic cells to engulf external items.

GROWTH AND REPRODUCTION

Unlike in multicellular organisms, increases in cell size (cell growth and reproduction by cell division) are tightly linked in unicellular organisms. Bacteria grow to a fixed size and then reproduce through binary fission, a form of asexual reproduction. Under optimal conditions, bacteria can grow and divide extremely rapidly, and bacterial populations can double as quickly as every 9.8 minutes. In cell division, two identical clone daughter cells are produced. Some bacteria, while still reproducing asexually, form more complex reproductive structures that help disperse the newly formed daughter cells. Examples include fruiting body formation by Myxobacteria and aerial hyphae formation by Streptomyces, or budding. Budding involves a cell forming a protrusion that breaks away and produces a daughter cell. In the laboratory, bacteria are usually grown using solid or liquid media. Solid growth media such as agar plates are used to isolate pure cultures of a bacterial strain. However, liquid growth media are used when measurement of growth or large volumes of cells are required. Growth in stirred liquid media occurs as an even cell suspension, making the cultures easy to divide and transfer, although isolating single bacteria from liquid media is difficult. The use of selective media (media with specific nutrients added or deficient, or with antibiotics added) can help identify specific organisms. Most laboratory techniques for growing bacteria use high levels of nutrients to produce large amounts of cells cheaply and quickly. However, in natural environments nutrients are limited, meaning that bacteria cannot continue to reproduce indefinitely. This nutrient limitation has led the evolution of different growth strategies (see r/K selection theory). Some organisms can grow extremely rapidly when nutrients become available, such as the formation of algal (and cyanobacterial) blooms that often occur in lakes during the summer. Other organisms have adaptations to harsh environments, such as the production of multiple antibiotics by Streptomyces that inhibit the growth of competing microorganisms. In nature, many organisms live in communities (e.g., biofilms) that may allow for increased supply of nutrients and protection from environmental stresses. These relationships can be essential for growth of a particular organism or group of organisms (syntrophy). Bacterial growth follows three phases. When a population of bacteria first enter a high-nutrient environment that allows growth, the cells need to adapt to their new environment. The first phase of growth is the lag phase, a period of slow growth when the cells are adapting to the high-nutrient environment and preparing for fast growth. The lag phase has high biosynthesis rates, as proteins necessary for rapid growth are produced. The second phase of growth is the logarithmic phase (log phase), also known as the exponential phase. The log phase is marked by rapid exponential growth. The rate at which cells grow during this phase is known as the growth rate (k), and the time it takes the cells to double is known as the generation time (g). During log phase, nutrients are metabolised at maximum speed until one of the nutrients is depleted and starts limiting growth. The final phase of growth is the stationary phase and is caused by depleted nutrients. The cells reduce their metabolic activity and consume non-essential cellular proteins. The stationary phase is a transition from rapid growth to a stress response state and there is increased expression of genes involved in DNA repair, antioxidant metabolism and nutrient transport.

GENETICS

Most bacteria have a single circular chromosome that can range in size from only 160,000 base pairs in the endosymbiotic bacteria Candidatus Carsonella ruddii, to 12,200,000 base pairs in the soil-dwelling bacteria Sorangium cellulosum. Spirochaetes of the genus Borrelia are a notable exception to this arrangement, with bacteria such as Borrelia burgdorferi, the cause of Lyme disease, containing a single linear chromosome. The genes in bacterial genomes are usually a single continuous stretch of DNA and although several different types of introns do exist in bacteria, these are much more rare than in eukaryotes. Bacteria may also contain plasmids, which are small extra-chromosomal DNAs that may contain genes for antibiotic resistance or virulence factors. Bacteria, as asexual organisms, inherit identical copies of their parent's genes (i.e., they are clonal). However, all bacteria can evolve by selection on changes to their genetic material DNA caused by genetic recombination or mutations. Mutations come from errors made during the replication of DNA or from exposure to mutagens. Mutation rates vary widely among different species of bacteria and even among different clones of a single species of bacteria. Genetic changes in bacterial genomes come from either random mutation during replication or "stress-directed mutation", where genes involved in a particular growth-limiting process have an increased mutation rate. Some bacteria also transfer genetic material between cells. This can occur in three main ways. First, bacteria can take up exogenous DNA from their environment, in a process called transformation. Genes can also be transferred by the process of transduction, when the integration of a bacteriophage introduces foreign DNA into the chromosome. The third method of gene transfer is bacterial conjugation, where DNA is transferred through direct cell contact. This gene acquisition from other bacteria or the environment is called horizontal gene transfer and may be common under natural conditions. Gene transfer is particularly important in antibiotic resistance as it allows the rapid transfer of resistance genes between different pathogens.

BACTERIOPHAGES

Bacteriophages are viruses that infect bacteria. Many types of bacteriophage exist, some simply infect and lyse their host bacteria, while others insert into the bacterial chromosome. A bacteriophage can contain genes that contribute to its host's phenotype: for example, in the evolution of Escherichia coli O157:H7 and Clostridium botulinum, the toxin genes in an integrated phage converted a harmless ancestral bacterium into a lethal pathogen. Bacteria resist phage infection through restriction modification systems that degrade foreign DNA, and a system that uses CRISPR sequences to retain fragments of the genomes of phage that the bacteria have come into contact with in the past, which allows them to block virus replication through a form of RNA interference. This CRISPR system provides bacteria with acquired immunity to infection.

CLASSIFICATION AND IDENTIFICATION

Classification seeks to describe the diversity of bacterial species by naming and grouping organisms based on similarities. Bacteria can be classified on the basis of cell structure, cellular metabolism or on differences in cell components such as DNA, fatty acids, pigments, antigens and quinones. While these schemes allowed the identification and classification of bacterial strains, it was unclear whether these differences represented variation between distinct species or between strains of the same species. This uncertainty was due to the lack of distinctive structures in most bacteria, as well as lateral gene transfer between unrelated species. Due to lateral gene transfer, some closely related bacteria can have very different morphologies and metabolisms. To overcome this uncertainty, modern bacterial classification emphasizes molecular systematics, using genetic techniques such as guanine cytosine ratio determination, genome-genome hybridization, as well as sequencing genes that have not undergone extensive lateral gene transfer, such as the rRNA gene. Classification of bacteria is determined by publication in the International Journal of Systematic Bacteriology, and Bergey's Manual of Systematic Bacteriology. The International Committee on Systematic Bacteriology (ICSB) maintains international rules for the naming of bacteria and taxonomic categories and for the ranking of them in the International Code of Nomenclature of Bacteria. The term "bacteria" was traditionally applied to all microscopic, single-cell prokaryotes. However, molecular systematics showed prokaryotic life to consist of two separate domains, originally called Eubacteria and Archaebacteria, but now called Bacteria and Archaea that evolved independently from an ancient common ancestor. The archaea and eukaryotes are more closely related to each other than either is to the bacteria. These two domains, along with Eukarya, are the basis of the three-domain system, which is currently the most widely used classification system in microbiolology. However, due to the relatively recent introduction of molecular systematics and a rapid increase in the number of genome sequences that are available, bacterial classification remains a changing and expanding field. For example, a few biologists argue that the Archaea and Eukaryotes evolved from Gram-positive bacteria. Identification of bacteria in the laboratory is particularly relevant in medicine, where the correct treatment is determined by the bacterial species causing an infection. Consequently, the need to identify human pathogens was a major impetus for the development of techniques to identify bacteria. The Gram stain, developed in 1884 by Hans Christian Gram, characterises bacteria based on the structural characteristics of their cell walls. The thick layers of peptidoglycan in the "Gram-positive" cell wall stain purple, while the thin "Gram-negative" cell wall appears pink. By combining morphology and Gram-staining, most bacteria can be classified as belonging to one of four groups (Gram-positive cocci, Gram-positive bacilli, Gram-negative cocci and Gram-negative bacilli). Some organisms are best identified by stains other than the Gram stain, particularly mycobacteria or Nocardia, which show acid-fastness on Ziehl Neelsen or similar stains. Other organisms may need to be identified by their growth in special media, or by other techniques, such as serology. Culture techniques are designed to promote the growth and identify particular bacteria, while restricting the growth of the other bacteria in the sample. Often these techniques are designed for specific specimens; for example, a sputum sample will be treated to identify organisms that cause pneumonia, while stool specimens are cultured on selective media to identify organisms that cause diarrhoea, while preventing growth of non-pathogenic bacteria. Specimens that are normally sterile, such as blood, urine or spinal fluid, are cultured under conditions designed to grow all possible organisms. Once a pathogenic organism has been isolated, it can be further characterised by its morphology, growth patterns such as (aerobic or anaerobic growth, patterns of hemolysis) and staining. As with bacterial classification, identification of bacteria is increasingly using molecular methods. Diagnostics using such DNA-based tools, such as polymerase chain reaction, are increasingly popular due to their specificity and speed, compared to culture-based methods. These methods also allow the detection and identification of "viable but nonculturable" cells that are metabolically active but non-dividing. However, even using these improved methods, the total number of bacterial species is not known and cannot even be estimated with any certainty. Following present classification, there are a little less than 9,300 known species of prokaryotes, which includes bacteria and archaea. but attempts to estimate the true level of bacterial diversity have ranged from 107 to 109 total species and even these diverse estimates may be off by many orders of magnitude.

INTERACTIONS WITH OTHER ORGANISMS

Despite their apparent simplicity, bacteria can form complex associations with other organisms. These symbiotic associations can be divided into parasitism, mutualism and commensalism. Due to their small size, commensal bacteria are ubiquitous and grow on animals and plants exactly as they will grow on any other surface. However, their growth can be increased by warmth and sweat, and large populations of these organisms in humans are the cause of body odor.

PREDATORS

Some species of bacteria kill and then consume other microorganisms, these species called predatory bacteria. These include organisms such as Myxococcus xanthus, which forms swarms of cells that kill and digest any bacteria they encounter. Other bacterial predators either attach to their prey in order to digest them and absorb nutrients, such as Vampirococcus, or invade another cell and multiply inside the cytosol, such as Daptobacter. These predatory bacteria are thought to have evolved from saprophages that consumed dead microorganisms, through adaptations that allowed them to entrap and kill other organisms.

MUTUALISTS

Certain bacteria form close spatial associations that are essential for their survival. One such mutualistic association, called interspecies hydrogen transfer, occurs between clusters of anaerobic bacteria that consume organic acids such as butyric acid or propionic acid and produce hydrogen, and methanogenic Archaea that consume hydrogen. The bacteria in this association are unable to consume the organic acids as this reaction produces hydrogen that accumulates in their surroundings. Only the intimate association with the hydrogen-consuming Archaea keeps the hydrogen concentration low enough to allow the bacteria to grow. In soil, microorganisms that reside in the rhizosphere (a zone that includes the root surface and the soil that adheres to the root after gentle shaking) carry out nitrogen fixation, converting nitrogen gas to nitrogenous compounds. This serves to provide an easily absorbable form of nitrogen for many plants, which cannot fix nitrogen themselves. Many other bacteria are found as symbionts in humans and other organisms. For example, the presence of over 1,000 bacterial species in the normal human gut flora of the intestines can contribute to gut immunity, synthesise vitamins such as folic acid, vitamin K and biotin, convert sugars to lactic acid (see Lactobacillus), as well as fermenting complex undigestible carbohydrates. The presence of this gut flora also inhibits the growth of potentially pathogenic bacteria (usually through competitive exclusion) and these beneficial bacteria are consequently sold as probiotic dietary supplements.

PATHOGENS

If bacteria form a parasitic association with other organisms, they are classed as pathogens. Pathogenic bacteria are a major cause of human death and disease and cause infections such as tetanus, typhoid fever, diphtheria, syphilis, cholera, foodborne illness, leprosy and tuberculosis. A pathogenic cause for a known medical disease may only be discovered many years after, as was the case with Helicobacter pylori and peptic ulcer disease. Bacterial diseases are also important in agriculture, with bacteria causing leaf spot, fire blight and wilts in plants, as well as Johne's disease, mastitis, salmonella and anthrax in farm animals. Each species of pathogen has a characteristic spectrum of interactions with its human hosts. Some organisms, such as Staphylococcus or Streptococcus, can cause skin infections, pneumonia, meningitis and even overwhelming sepsis, a systemic inflammatory response producing shock, massive vasodilation and death. Yet these organisms are also part of the normal human flora and usually exist on the skin or in the nose without causing any disease at all. Other organisms invariably cause disease in humans, such as the Rickettsia, which are obligate intracellular parasites able to grow and reproduce only within the cells of other organisms. One species of Rickettsia causes typhus, while another causes Rocky Mountain spotted fever. Chlamydia, another phylum of obligate intracellular parasites, contains species that can cause pneumonia, or urinary tract infection and may be involved in coronary heart disease. Finally, some species such as Pseudomonas aeruginosa, Burkholderia cenocepacia, and Mycobacterium avium are opportunistic pathogens and cause disease mainly in people suffering from immunosuppression or cystic fibrosis. Bacterial infections may be treated with antibiotics, which are classified as bacteriocidal if they kill bacteria, or bacteriostatic if they just prevent bacterial growth. There are many types of antibiotics and each class inhibits a process that is different in the pathogen from that found in the host. An example of how antibiotics produce selective toxicity are chloramphenicol and puromycin, which inhibit the bacterial ribosome, but not the structurally different eukaryotic ribosome. Antibiotics are used both in treating human disease and in intensive farming to promote animal growth, where they may be contributing to the rapid development of antibiotic resistance in bacterial populations. Infections can be prevented by antiseptic measures such as sterilizing the skin prior to piercing it with the needle of a syringe, and by proper care of indwelling catheters. Surgical and dental instruments are also sterilized to prevent contamination by bacteria. Disinfectants such as bleach are used to kill bacteria or other pathogens on surfaces to prevent contamination and further reduce the risk of infection.

BEHAVIOR

SECRETION

Bacteria frequently secrete chemicals into their environment in order to modify it favorably. The secretions are often proteins and may act as enzymes that digest some form of food in the environment.

BIOLUMINESCENCE

A few bacteria have chemical systems that generate light. This bioluminescence often occurs in bacteria that live in association with fish, and the light probably serves to attract fish or other large animals.

MULTICELLULARITY

Bacteria often function as multicellular aggregates known as biofilms, exchanging a variety of molecular signals for inter-cell communication, and engaging in coordinated multicellular behavior. The communal benefits of multicellular cooperation include a cellular division of labor, accessing resources that cannot effectively be utilized by single cells, collectively defending against antagonists, and optimizing population survival by differentiating into distinct cell types. For example, bacteria in biofilms can have more than 500 times increased resistance to antibacterial agents than individual "planktonic" bacteria of the same species. One type of inter-cellular communication by a molecular signal is called quorum sensing, which serves the purpose of determining whether there is a local population density that is sufficiently high that it is productive to invest in processes that are only successful if large numbers of similar organisms behave similarly, as in excreting digestive enzymes or emitting light. Quorum sensing allows bacteria to coordinate gene expression, and enables them to produce, release and detect autoinducers or pheromones which accumulate with the growth in cell population.

MOVEMENT

Many bacteria can move using a variety of mechanisms: flagella are used for swimming through water; bacterial gliding and twitching motility move bacteria across surfaces; and changes of buoyancy allow vertical motionSwimming bacteria frequently move near 10 body lengths per second and a few as fast as 100. This makes them at least as fast as fish, on a relative scale. In twitching motility, bacterial use their type IV pili as a grappling hook, repeatedly extending it, anchoring it and then retracting it with remarkable force (>80 pN). Flagella are semi-rigid cylindrical structures that are rotated and function much like the propeller on a ship. Objects as small as bacteria operate a low Reynolds number and cylindrical forms are more efficient than the flat, paddle-like, forms appropriate at human size scale. Bacterial species differ in the number and arrangement of flagella on their surface; some have a single flagellum (monotrichous), a flagellum at each end (amphitrichous), clusters of flagella at the poles of the cell (lophotrichous), while others have flagella distributed over the entire surface of the cell (peritrichous). The bacterial flagella is the best-understood motility structure in any organism and is made of about 20 proteins, with approximately another 30 proteins required for its regulation and assembly. The flagellum is a rotating structure driven by a reversible motor at the base that uses the electrochemical gradient across the membrane for power. This motor drives the motion of the filament, which acts as a propeller. Many bacteria (such as E. coli) have two distinct modes of movement: forward movement (swimming) and tumbling. The tumbling allows them to reorient and makes their movement a three-dimensional random walk. (See external links below for link to videos.) The flagella of a unique group of bacteria, the spirochaetes, are found between two membranes in the periplasmic space. They have a distinctive helical body that twists about as it moves. Motile bacteria are attracted or repelled by certain stimuli in behaviors called taxes: these include chemotaxis, phototaxis, energy taxis and magnetotaxis. In one peculiar group, the myxobacteria, individual bacteria move together to form waves of cells that then differentiate to form fruiting bodies containing spores. The myxobacteria move only when on solid surfaces, unlike E. coli, which is motile in liquid or solid media. Several Listeria and Shigella species move inside host cells by usurping the cytoskeleton, which is normally used to move organelles inside the cell. By promoting actin polymerization at one pole of their cells, they can form a kind of tail that pushes them through the host cell's cytoplasm.

SIGNIFICANCE IN TECHNOLOGY AND INDUSTRY

Bacteria, often lactic acid bacteria such as Lactobacillus and Lactococcus, in combination with yeasts and molds, have been used for thousands of years in the preparation of fermented foods such as cheese, pickles, soy sauce, sauerkraut, vinegar, wine and yogurt. The ability of bacteria to degrade a variety of organic compounds is remarkable and has been used in waste processing and bioremediation. Bacteria capable of digesting the hydrocarbons in petroleum are often used to clean up oil spills. Fertilizer was added to some of the beaches in Prince William Sound in an attempt to promote the growth of these naturally occurring bacteria after the 1989 Exxon Valdez oil spill. These efforts were effective on beaches that were not too thickly covered in oil. Bacteria are also used for the bioremediation of industrial toxic wastes. In the chemical industry, bacteria are most important in the production of enantiomerically pure chemicals for use as pharmaceuticals or agrichemicals. Bacteria can also be used in the place of pesticides in the biological pest control. This commonly involves Bacillus thuringiensis (also called BT), a Gram-positive, soil dwelling bacterium. Subspecies of this bacteria are used as a Lepidopteran-specific insecticides under trade names such as Dipel and Thuricide. Because of their specificity, these pesticides are regarded as environmentally friendly, with little or no effect on humans, wildlife, pollinators and most other beneficial insects. Because of their ability to quickly grow and the relative ease with which they can be manipulated, bacteria are the workhorses for the fields of molecular biology, genetics and biochemistry. By making mutations in bacterial DNA and examining the resulting phenotypes, scientists can determine the function of genes, enzymes and metabolic pathways in bacteria, then apply this knowledge to more complex organisms. This aim of understanding the biochemistry of a cell reaches its most complex expression in the synthesis of huge amounts of enzyme kinetic and gene expression data into mathematical models of entire organisms. This is achievable in some well-studied bacteria, with models of Escherichia coli metabolism now being produced and tested. This understanding of bacterial metabolism and genetics allows the use of biotechnology to bioengineer bacteria for the production of therapeutic proteins, such as insulin, growth factors, or antibodies.

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BACTEROIDES

Bacteroides is a genus of Gram-negative, bacillus bacteria. Bacteroides species are non-endospore-forming, anaerobes, and may be either motile or non-motile, depending on the species. The DNA base composition is 40-48% GC. Unusual in bacterial organisms, Bacteroides membranes contain sphingolipids. They also contain meso-diaminopimelic acid in their peptidoglycan layer. Bacteroides are normally mutualistic, making up the most substantial portion of the mammalian gastrointestinal flora, where they play a fundamental role in processing of complex molecules to simpler ones in the host intestine. As many as 1010-1011 cells per gram of human feces have been reported. They can use simple sugars when available; however, the main sources of energy for Bacteroides species in the gut are complex host-derived and plant glycans. Studies indicate that long-term diet is strongly associated with the gut microbiome composition - those who eat plenty of protein and animal fats have predominantly Bateroides bacteria, while for those who consume more carbohydrates the Prevotella species dominate. One of the most important clinically is Bacteroides fragilis. Bacteroides melaninogenicus has recently been reclassified and split into Prevotella melaninogenica and Prevotella intermedia

PATHOGENESIS

Bacteroides species also benefit their host by excluding potential pathogens from colonizing the gut. Some species (B. fragilis, for example) are opportunistic human pathogens, causing infections of the peritoneal cavity, gastrointestinal surgery, and appendicitis via abscess formation, inhibiting phagocytosis, and inactivating beta-lactam antibiotics. Although Bacteroides species are anaerobic, they are aerotolerant and thus can survive in the abdominal cavity. In general, Bacteroides are resistant to a wide variety of antibiotics â€” B-lactams, aminoglycosides, and recently many species have acquired resistance to erythromycin and tetracycline. This high level of antibiotic resistance has prompted concerns that Bacteroides species may become a reservoir for resistance in other, more highly pathogenic bacterial strains.

MICROBIOLOGICAL APPLICATIONS

An alternative fecal indicator organism, Bacteroides, has been suggested because they make up a significant portion of the fecal bacterial population, have a high degree of host specificity that reflects differences in the digestive system of the host animal, and have a small potential to grow in the environment. Over the past decade, real-time polymerase chain reaction (PCR) methods have been used to detect the presence of various microbial pathogens through the amplification of specific DNA sequences without culturing bacteria. One study has measured the amount of Bacteroides by using qPCR to quantify the host-specific 16S rRNA genetic marker. This technique allows quantification of genetic markers that are specific to the host of the bacteria and allow detection of recent contamination. A recent report found temperature plays a major role in the amount of time the bacteria will persist in the environment, the life span increases with colder temperatures (0-4°C).

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BALANTIDIUM COLI
Balantidium coli, though rare in the US, is an intestinal protozoan parasite that can infect humans. These parasites can be transmitted through the fecal-oral route by contaminated food and water. Balantidium coli infection is mostly asymptomatic, but people with other serious illnesses can experience persistent diarrhea, abdominal pain, and sometimes a perforated colon. When traveling to endemic tropical countries, Balantidium coli infection can be prevented by following good hygiene practices. Wash all fruits and vegetables with clean water when preparing or eating them, even if they have a removable skin.

FAQs

What is Balantidium coli?

Balantidium coli is an intestinal protozoan parasite that causes the infection called balantidiasis. While this type of infection is less common in the United States, humans and other mammals can become infected with Balantidium coli by ingesting infective cysts from food and water that is contaminated by feces. Mostly asymptomatic, Balantidium infection can cause such symptoms as diarrhea and abdominal pain.

Where is Balantidium coli endemic?

Balantidium infection in humans is rare in the United States. However, Balantidium is more common among pigs in warmer climates, and in monkeys in the tropics. Infection in humans is therefore also more common in those areas, especially if good hygiene is not practiced. Balantidium coli is found throughout the world, but it is most prevalent in tropical and subtropical regions and developing countries.

How is Balantidium coli transmitted?

Balantidium coli is transmitted through the fecal-oral route. Humans can become infected by eating and drinking contaminated food and water that has come into contact with infective animal or human fecal matter. Infection can occur in several ways, including the following examples:
- eating meat, fruits, and vegetables that have been contaminated by an infected person or contaminated by fecal matter from an infected animal,
- drinking and washing food with contaminated water, or
- having poor hygiene habits.
What are the signs and symptoms?

Most people infected with Balantidium coli experience no symptoms. Balantidium coli settles in the large intestine in humans and produces infective microscopic cysts passed in the feces, potentially leading to more infections or re-infection. People who are immune-compromised are the most likely to experience more severe signs and symptoms. These include persistent diarrhea, dysentery, abdominal pain, weight loss, nausea, and vomiting. If left untreated, perforation of the colon can occur.

Is there a test for Balantidium coli infection?

Yes. Stool samples can be examined by a lab. Microscopic examination can detect Balantidium coli in the stool.

Is this contagious?

Yes. Balantidium coli is contagious by the fecal-oral route.

Is there treatment?

Yes. The three medications often used to treat Balantidium coli are tetracycline, metronidazole, and iodoquinol. See your health care provider for treatment care.

How can I prevent Balantidium coli?

Balantidium coli infection can be prevented when traveling to endemic tropical countries by following good hygiene practices. Wash your hands with soap and warm water after using the toilet, changing diapers, and before handling food. Teach children the importance of washing hands to prevent infection. Wash all fruits and vegetables with clean water when preparing or eating them, even if they have a removable skin.

BIOLOGY

Causal Agent:

Balantidium coli, a large ciliated protozoan parasite.

Life Cycle:

Cysts are the parasite stage responsible for transmission of balantidiasis. The host most often acquires the cyst through ingestion of contaminated food or water. Following ingestion, excystation occurs in the small intestine, and the trophozoites colonize the large intestine. The trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by binary fission, during which conjugation may occur. Trophozoites undergo encystation to produce infective cysts. Some trophozoites invade the wall of the colon and multiply. Some return to the lumen and disintegrate. Mature cysts are passed with feces.

Life cycle image and information courtesy of DPDx.

For more information view the source:Center for Disease Control

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BLASTOCYSTIS

Blastocystis is a genus of single-celled protozoan parasites belonging to a group of organisms known as the Stramenopiles (also called Heterokonts) that includes algae and water molds. Blastocystis comprises several species, living in the gastrointestinal tracts of species as diverse as humans, farm animals, birds, rodents, reptiles, amphibians, fish, and cockroaches.Blastocystis exhibits low host specificity, and many different species of Blastocystis can infect humans and by current convention, any of these species would be identified as Blastocystis hominis if they were identified in a human. These have a widespread geographic distribution and are found at a rate of 5-10% in most developed countries, and a rate of up to 50% in less developed areas. High rates of infection are also found in individuals in developed countries who work with animals. Although the role of Blastocystis hominis in human disease is often referred to as controversial, a systematic survey of research studies conducted by 11 infectious disease specialists from nine countries, found that over 95% of papers published in the last 10 years identified it as causing illness in immunocompetent individuals. The paper attributed confusion over pathogenicity to the existence of asymptomatic carriers, a phenomenon the study noted is common to all gastrointestinal protozoa.

FAQs

What is Blastocystis spp.?

Blastocystis is a common microscopic organism that inhabits the intestine and is found throughout the world. A full understanding of the biology of Blastocystis and its relationship to other organisms is not clear, but is an active area of research. Infection with Blastocystis is called blastocystosis.

What are the symptoms of infection with Blastocystis?

Watery or loose stools, diarrhea, abdominal pain, anal itching, weight loss, constipation, and excess gas have all been reported in persons with Blastocystis infection. Many people have no symptoms at all. The organism can be found in both well and sick persons.

How long will I be infected?

Blastocystis can remain in the intestine for weeks, months, or years.

Is Blastocystis spp. the cause of my symptoms?

The role of Blastocystis in causing disease is controversial among experts. Some types of Blastocystis may be more likely to be associated with symptoms. Finding Blastocystis in stool samples should be followed up with a careful search for other possible causes of your symptoms.

Is having blastocystosis common?

Yes. In fact, many people have Blastocystis in their intestine, some without ever having symptoms.

What should I do if I think I have blastocystosis?

See your health care provider who will ask you to provide stool samples for testing. Diagnosis may be difficult, so you may be asked to submit several stool samples.

Is medication available to treat blastocystosis?

Yes. Drugs are available by prescription to treat blastocystosis. However, sometimes medication is not effective, and a search for other possible causes of your symptoms may be necessary.

How did I get blastocystosis?

How Blastocystis is transmitted is not known for certain, although the number of people infected seems to increase in areas where sanitation and personal hygiene is not adequate. Studies have suggested that risk of infection may increase through: ingesting contaminated food or water, exposure to a day care environment, or exposure to animals.

How can I prevent infection with Blastocystis?

Wash your hands with soap and warm water after using the toilet, changing diapers, and before handling food. Teach children the importance of washing hands to prevent infection. Avoid water or food that may be contaminated. Wash and peel all raw vegetables and fruits before eating. When traveling in countries where the water supply may be unsafe, avoid drinking unboiled tap water and avoid uncooked foods washed with unboiled tap water. Bottled or canned carbonated beverages, seltzers, pasteurized fruit drinks, and steaming hot coffee and tea are safe to drink.

Should I be concerned about spreading infection to the rest of my household?

There is little risk of spreading infection if you practice adequate personal hygiene. This includes thorough hand washing with soap and warm water after using the toilet and before handling food.

BIOLOGY

Causal Agent

The taxonomic classification of Blastocystis hominis is mired in controversy. It has been previously considered as yeasts, fungi, or ameboid, flagellated, or sporozoan protozoa. Recently, however, based on molecular studies, especially dealing with the sequence information on the complete SSUrRNA gene, B. hominis has been placed within an informal group, the stramenopiles (Silberman et al. 1996). Stramenopiles are defined, based on molecular phylogenies, as a heterogeneous evolutionary assemblage of unicellular and multicellular protists including brown algae, diatoms, chrysophytes, water molds, slime nets, etc. (Patterson, 1994). Cavalier-Smith (1998) considers stramenopiles to be identical to his infrakingdom Heterokonta under the kingdom Chromista. Therefore, according to Cavalier-Smith, B. hominis is a heterokontid chromista.

Life Cycle:

Knowledge of the life cycle and transmission is still under investigation, therefore this is a proposed life cycle for B. hominis. The classic form found in human stools is the cyst, which varies tremendously in size from 6 to 40 Âµm. The thick-walled cyst present in the stools is believed to be responsible for external transmission, possibly by the fecal-oral route through ingestion of contaminated water or food . The cysts infect epithelial cells of the digestive tract and multiply asexually. Vacuolar forms of the parasite give origin to multi vacuolar and ameboid forms. The multi-vacuolar develops into a pre-cyst that gives origin to a thin-walled cyst, thought to be responsible for autoinfection. The ameboid form gives origin to a pre-cyst, which develops into thick-walled cyst by schizogony. The thick-walled cyst is excreted in feces.

Life cycle image and information courtesy of DPDx.

For more information view the source:Center for Disease Control

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BLOATING

Bloating is any abnormal general swelling, or increase in diameter of the abdominal area. As a symptom, the patient feels a full and tight abdomen, which may cause abdominal pain, and sometimes accompanied by increased stomach growling or more seriously the total lack of it.

SYMPTOMS

The most common symptom associated with bloating is a sensation that the abdomen is full or distended. Rarely, bloating may be painful or cause shortness of breath. Pains that are due to bloating will feel sharp and cause the stomach to cramp. These pains may occur anywhere in the body and can change locations quickly. They are so painful that they are sometimes mistaken for heart pains when they develop on the upper left side of the chest. Pains on the right side are often confused with problems in the appendix or the gallbladder. One symptom of gas that is not normally associated with it is the hiccup. Hiccups are harmless and will diminish on their own; they also help to release gas that is in the digestive tract before it moves down to the intestines and causes bloating. Important but uncommon causes of abdominal bloating include ascites and tumors.

CAUSES

There are many causes of bloating, including: diet, irritable bowel syndrome, lactose intolerance, reflux, and constipation, to name a few. Specific medical conditions like Crohn's Disease or bowel obstruction can also contribute to the amount of stomach bloating experienced. Gas and bloating is a sign that food is not being ingested correctly by the body. An inadequate intake of water will cause excessive stomach bloating. Water benefits the body by aiding with digestion because it supports a majority of the body's daily functions. Fatty foods cause a formation of fat cells to develop throughout the body and contribute to bloating as well. A build up of fat cells slows down the body's ability to empty the stomach. Dairy products also contribute to excessive cramps, gas, and bloating. Persons who are intolerant to lactose products experience this effect more than others. Once these foods are digested, the bloating will fade. Common causes of abdominal bloating are: Overeating Gastric distension Lactose intolerance, fructose intolerance and other food intolerances Food allergy Aerophagia (air swallowing, a nervous habit) Irritable bowel syndrome Partial bowel obstruction Gastric dumping syndrome or rapid gastric emptying Gas-producing foods Constipation Visceral fat Splenic-flexure syndrome Menstruation, dysmenorrhea Polycystic ovary syndrome and ovarian cysts Alvarez' syndrome, hysterical or neurotic abdominal bloating without excess of gas in the digestive tract Massive infestation with intestinal parasites, such as worms (e.g., Ascaris lumbricoides) Diverticulosis Celiac Disease Important, but uncommon causes of abdominal bloating, include large intra-abdominal tumors, such as those arising from ovarian, liver, uterus and stomach cancer; and megacolon, an abnormal dilation of the colon, due to some diseases, such as Chagas disease, a parasitic infection. Gaseous bloating may be a consequence of cardiopulmonary resuscitation procedures, due to the artificial mouth-to-mouth insufflation of air. In some animals, like cats, dogs and cattle, gastric dilatation-volvulus, or bloat also occurs when gas is trapped inside the stomach and a gastric torsion or volvulus prevents it from escaping.

IRRITABLE BOWEL SYNDROME

Bloating from irritable bowel syndrome(IBS) is of unknown origin but often results from an insult to the gut, and as such can overlap with infective diarrhea, celiac, and inflammatory bowel diseases. IBS is a brain-gut dysfunction that causes visceral hypersensitivity and results in bloating in association with recurrent diarrhea (or constipation) and abdominal pain. While there is no direct treatment for the underlying pathologyof IBS, the symptom of bloating can be well managed through dietary changes that prevent the over-reaction of the gastrocolic reflex. Having soluble fiber foods and supplements, substituting dairy with soy or rice products, being careful with fresh fruits and vegetablesthat are high in insoluble fiber, and eating regular small amounts can all help to lessen the symptoms of IBS (Van Vorous 2000). Foods and beverages to be avoided or minimized include red meat, oily, fatty and friedproducts, dairy (even when there is no lactose intolerance), solid chocolate, coffee (regular and decaffeinated), alcohol, carbonated beverages, especially those also containing sorbitol, and artificial sweeteners(Van Vorous 2000). IBS is most commonly found in patients around the age of 20 and is found more often in women than men. In people with IBS, the intestines squeeze too hard or not hard enough and cause food to move too quickly or too slowly through the intestines.Other terms used to describe this condition include spastic bowel, spastic colon, and irritable colon. Symptoms of the condition will worsen as a person is placed under stress, during travel, and at other times when the daily routine is tampered with. Common symptoms include bloating, constipation, abdominal cramp or pain after bowel movement, or feeling like a movement is required even after one has been completed.

FIBER

Most cases of stomach bloating are due to improper dieting. Fiber is made by plants and is not easily digested by the human gastrointestinal tract. There are two main types of dietary fiber, soluble and insoluble fiber. Soluble fiber is prebioticand readily fermented in the colon into gases, while insoluble fiber is metabolically inert and absorbs water as it moves through the digestive system, aiding in defecation. Most types of fiber (insoluble) are attached to body waterin the intestineand increase the volume of stools. Gas occurs because of the bacteria in the colon and is a by-product of soluble fiber digestion. Inadequate/irregular intake of fiber and water will cause a person to experience bloating or constipation. The most common natural sources of fiber include fruits and vegetables as well as wheat or oat bran. These fibers are most likely to cause flatulence.A diet that is high in fiber will decrease the risk for stomach bloating[citation needed]and help keep the body healthy to fight against disease. Soluble fiber, as part of a diet low in saturated fat and cholesterol, from foods such as oat bran, rolled oats, whole oat flour, oatrim, whole grain and dry milled barley, or psyllium seed husks(with purity of no less than 95%) may reduce the risk of heart disease.

BELCHING AND FLATULENCE

Gas in the gastrointestinal tract has only two sources. It is either swallowed air or is produced by bacteria that normally inhabit the intestines, primarily the colon. Belching or burping is a universal ability that works by removing gas from the stomach through the mouth. The stomach can become bloated when too much air is swallowed during eating and drinking too quickly. As the stomach swells, belching removes the gas and alleviates the pain associated with it. Burping can also be used as a form of relief from abdominal discomfort other than too much gas in the stomach. Flatulence or farting works much like burping, but helps the body pass gas through the anus instead of the mouth. Bacteria present in the intestinal tract cause gas to be expelled from the anus. They produce the gas as food is digested and moved from the small intestine. This gas builds up and causes swelling or bloating in the abdominal area before it is released.

CONSTIPATION

A common gastrointestinal problem is constipation, which causes serious cases of bloating. People with infrequent bowel movements or those that pass hard stools or strain during the movements experience constipation. Since most cases of constipation are temporary, simple lifestyle changes, such as getting more exercise and eating a high-fiber diet, can go a long way toward alleviating constipation. Some cases of constipation will continue to worsen and require unconventional methods to release the feces and reduce the amount of stomach bloating. Blood in the stool, intense pain in the abdomen, rectal pain, and unexplained weight loss should be reported to a doctor. Bloating accompanies constipation every time and they will not develop without an underlying cause.

HEARTBURN AND REFLUX

Painful burning sensations in the chest that is caused by gastroesophageal reflux is known as heartburn. Reflux is the back flow of gastric acidjuices from the stomach into the throat. Heartburn has different triggers, including certain foods, medications, obesity, or even stress. These triggers are different for each individual and should be avoided. Gastroesophageal reflux disease or GERD is a chronic condition that can lead to more serious complications like Esophageal cancer. Treatment options are available to treat the symptoms and the condition, but there is no cure for the disease. Symptoms include burping, abdominal and stomach bloating, along with pain and discomfort. Heavy meals, lying down or bending over after eating should be avoided to help prevent reflux from occurring. The stomach bloating experienced with reflux is intense and will remain until the food is digested all the way. Postmortem bloating occurs in cadavers, due to the formation of gases by bacterial action and putrefactionof the internal tissues of the abdomen and the inside of the intestines.

RELATED CONDITIONS

Conditions that are related to bloating include constipation, lactose intolerance, and acid reflux disease. All of these conditions share the same symptoms and can share the same causative agents. These causes include unhealthy diet, smoking, alcohol consumption, low amount of exercise, and overall health. Each of these conditions can be experienced as a symptom of the others and is also a cause for each of them. In most cases where one of the conditions is present, there is at least one if not two of the others. Treatment for each condition is performed using the same medications and recommended dietary changes like increased fiber intake and reduced fat intake. If the conditions develop into disease such as gastrointestinal reflux disease (GERD) or chronic constipation, additional medications will be required. Bloating and flatulence are sometimes related to constipation, and treating the underlying condition may be helpful.

TREATMENT

There are multiple over the counter medications that can be used to treat bloating. Food enzymescan be found in some products that will help break down the sugars found in grains, vegetables and dairy products. They can be taken before food is consumed or added to the food that causes the gas and bloating. Another type of medicine is activated charcoaltablets that will decrease the odor from gas. The most common treatment is antacids. These medications have no effect on the gas that is presently in the intestines, but it allows for gas build-up to be belched away more easily, reducing the amount of bloating that develops. Another treatment is Simethicone, an oral anti-foaming agent that helps the body to expel the gas more quickly. Also combination of prokinitics like; domperidone metoclopramide diphenhydramine (Diphen for prevention of extrapyramidal reactios-specially acute dystonic reaction) PPI has dramatic effects especially on bloaters and belchers.

PREVENTING WITHOUT MEDICINE

There are several things that can be done to relieve the pressure in the stomach. Taking a walk after eating a meal is a good way to nudge the contents of the bowels along. Exercising releases hormones that work to encourage activity in the bowels. Herbal teas are also recommended to break up gas bubbles that can develop. Drinking extra virgin olive oil helps to stop bloating. Some foods like coffee and chocolate can stimulate the digestive tract and cause a build up of gas to occur, resulting in bloating.[medical citation needed]Meals that are high in fat are often too hard for the system to digest and can stimulate spasmsand bloating. In addition, foods that are extremely hot or cold can draw air inside as they are being eaten. Foods like bubble gum or bubbly beverages also cause a build up of air that results in excessive gas and bloating, as does smoking. There are also certain types of vegetables and fruits that contain types of starches which are poorly digested by people but well digested by bacteria.

For more information view the source:Wikipedia

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BLOOD IN STOOL

In medicine, when referring to human feces, blood in stool can refer to multiple conditions: Melena, with more blackish appearance, originating in upper parts of the gastrointestinal tract Hematochezia, with more red color, originating in latter parts of the gastrointestinal tract. The term is usually not used to describe fecal occult blood, which refers to blood only found after testing is performed. In infants, the Apt test can be used to distinguish fetal hemoglobin from maternal blood.

LIST OF CAUSES OF BLOOD IN STOOL

Common causes of blood in the stool include: Colorectal cancer Crohns disease Ulcerative colitis Other types of inflammatory bowel disease, inflammatory bowel syndrome, or ulceration Rectal or anal hemorrhoids or fissures, particularly if they rupture or are otherwise irritated E. coli food poisoning Necrotizing enterocolitis Diverticulosis Salmonellosis Upper gastrointestinal bleeding Peptic ulcer disease Esophageal varices Gastric cancer.

For more information view the source:Wikipedia

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BRAIN FOG (CLOUDING OF CONSCIOUSNESS)

Clouding of consciousness, also known as mental fog, is a conventional medical term describing an abnormality in consciousness. The sufferer experiences a subjective sensation of mental clouding described as feeling "foggy".

OVERVIEW

Terms such as Clouding of consciousness or mental fog are too vague for most practical requirements. More specifically, the condition is an abnormality in the "overall level" of consciousness that is mild and less severe than a stupor or coma. Thus, some authors prefer the more objective term "abnormal level" of consciousness over the subjective term "clouding" of consciousness. In the 1817 German treatise Verdunkelung des Bewusstseins, Greiner first coined and pioneered the term clouding of consciousness as the main pathophysiological feature of delirium. Although the condition is extremely common,conventional medicine practitioners are not well equipped to recognize it and tend to mislabel it or "psychologize" it. Alternative medicine practitioners popularly use the term "brain fog"; however there is no mention as to whether they intend the term to be synonymous with the conventional medical term clouding of consciousness.

PATHOLOGY

The precise pathophysiology is poorly understood. However, the general conceptual model is that of a part of the brain regulating the "overall level" of the conciousness part of the brain. Various etiologies can "funnel" in on and disturb this common regulating part of the brain, which in turn disturbs the "overall level" of consciousness. The key idea here is an abnormality in the "overall level" of consciousness, referred to also as wakefulness or arousal, as opposed to an abnormality in specific or focal parts of consciousness. The contents of the consciousness, referred to also as cognition, are thus disturbed in a "diffused" or "widespread" or "global" manner as opposed to a specific manner. Therefore, performance on virtually any cognitive task may be affected; although this may be difficult to detect and measure precisely. The list of possible etiologies is said to be "endless". But some examples are: Candidiasis Hepatic failure, which allows toxins from bacteria in the intestine to go into the bloodstream and poison the brain. Heavy metals including mercury. Medications of all kinds. Thyroid dysfunction Vitamin B1 deficiency.

For more information view the source:Wikipedia

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CAMPYLOBACTER

Campylobacter (meaning 'twisted bacteria') is a genus of bacteria that are Gram-negative, spiral, and microaerophilic. Motile, with either unipolar or bipolar flagella, the organisms have a characteristic spiral/corkscrew appearance and are oxidase-positive. Campylobacter jejuni is now recognized as one of the main causes of bacterial foodborne disease in many developed countries. At least a dozen species of Campylobacter have been implicated in human disease, with C. jejuni and C. coli the most common. C. fetus is a cause of spontaneous abortions in cattle and sheep, as well as an opportunistic pathogen in humans.

GENOME

The genomes of several Campylobacter species have been sequenced, providing insights into their mechanisms of pathogenesis. The first Campylobacter genome to be sequenced was C. jejuni, in 2000. Campylobacter species contain two flagellin genes in tandem for motility, flaA and flaB. These genes undergo intergenic recombination, further contributing to their virulence. Nonmotile mutants do not colonize.

MOLECULAR SIGNATURES

Comparative genomic analysis has led to the identification of 15 proteins which are uniquely found in members of the genus Campylobacter and serve as molecular markers for the genus. Eighteen other proteins were also found which were present in all species except Campylobacter fetus, which is the deepest branching Campylobacter species. A conserved insertion has also been identified which is present in all Campylobacter species except C. fetus. Additionally, 28 proteins have been identified present only in Campylobacter jejuni and Campylobacter coli, indicating a close relationship between these two species. Five other proteins have also been identified which are only found in C. jejuni and serve as molecular markers for the species.

PATHOGENESIS

Campylobacteriosis is an infection by Campylobacter. The common routes of transmission are fecal-oral, ingestion of contaminated food or water, and the eating of raw meat. It produces an inflammatory, sometimes bloody, diarrhea, periodontitis or dysentery syndrome, mostly including cramps, fever and pain. The infection is usually self-limiting and in most cases, symptomatic treatment by liquid and electrolyte replacement is enough in human infections. The use of antibiotics, on the other hand, is controversial. Symptoms typically last for five to seven days.

CAUSE

The sites of tissue injury include the jejunum, the ileum, and the colon. Most strains of C jejuni produce a toxin (cytolethal distending toxin) that hinders the cells from dividing and activating the immune system. This helps the bacteria to evade the immune system and survive for a limited time in the cells. A cholera-like enterotoxin was once thought to be also made, but this appears not to be the case. The organism produces diffuse, bloody, edematous, and exudative enteritis. Although rarely has the infection been considered a cause of hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, no unequivocal case reports exist. In some cases, a Campylobacter infection can be the underlying cause of Guillain–Barré syndrome. Gastrointestinal perforation is a rare complication of ileal infection.

TREATMENT

Diagnosis of the illness is made by testing a specimen of faeces (bowel motion).
Standard treatment is now azithromycin. Quinolone antibiotics such as ciprofloxacin or levofloxacin are no longer as effective due to resistance. Dehydrated children may require intravenous (by vein) fluid treatment in a hospital. The illness is contagious, and children must be kept at home until they have been clear of symptoms for at least two days. Good hygiene is important to avoid contracting the illness or spreading it to others. Intestinal perforation is very rare; increased abdominal pain and collapse require immediate medical attention.

HISTORY

The symptoms of Campylobacter infections were described in 1886 in infants by Theodor Escherich. These infections were named cholera infantum, or summer complaint. The genus was first discovered in 1963; however, the organism was not isolated until 1972.

For more information view the source:Wikipedia

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CANDIDA

Candida is a genus of yeasts. Many species are harmless commensals or endosymbionts of animal hosts including humans, but other species, or harmless species in the wrong location, can cause disease. Candida albicans can cause infections (candidiasis or thrush) in humans and other animals, especially in immunocompromised patients. Many species are found in gut flora, including C. albicans in mammalian hosts, whereas others live as endosymbionts in insect hosts. Systemic infections of the bloodstream and major organs, particularly in immunocompromised patients, affect over 90,000 people a year in the U.S., with a 40-50% mortality. The DNA of several Candida species have been sequenced. Antibiotics promote yeast infections, including gastrointestinal candida overgrowth, and penetration of the GI mucosa.Many people are under the impression that only women get genital yeast infections. Regardless of your sex, though, prolonged antibiotic use increases your risk of a yeast infection. Also, men and women with diabetes or impaired immune systems, such as those with HIV, are more susceptible to yeast infections. Some practitioners of alternative medicine claim that Candida overgrowth can cause many health problems, including fatigue to weight gain, but most traditional doctors reject this.

LABORATORY CHARACTERISTICS

Grown in the laboratory, Candida appears as large, round, white or cream (albicans is from Latin meaning 'whitish') colonies with a yeasty odor on agar plates at room temperature. C. albicans ferments glucose and maltose to acid and gas, sucrose to acid, and does not ferment lactose, which help to distinguish it from other Candida species.

CLINICAL CHARATERISTICS

Candida are almost universal on normal adult skin and albicans is part of the normal flora of the mucous membranes of the respiratory, gastrointestinal, and female genital tracts which cause no disease. But overgrowth of several species including albicans can cause superficial infections such as oropharyngeal candidiasis (thrush) and vulvovaginal candidiasis (vaginal candidiasis). Oral candidiasis is common in elderly denture wearers. In otherwise healthy individuals, these infections can be cured with topical or systemic antifungal medications (commonly over-the-counter treatments like miconazole or clotrimazole). In debilitated or immunocompromised patients, or if introduced intravenously, candidiasis may become a systemic disease producing abscess, thrombophlebitis, endocarditis, or infections of the eyes or other organs. Colonization of the gastrointestinal tract by C. albicans after antibiotic therapy usually causes no symptoms and may also result from taking antacids or antihyperacidity drugs.

SPECIES

Among Candida species, C. albicans, which is a normal constituent of the human flora, a commensal of the skin and the gastrointestinal and genitourinary tracts, is responsible for the majority of Candida bloodstream infections (candidemia). Yet, there is an increasing incidence of infections caused by C. glabrata and C. rugosa, which could be because they are frequently less susceptible to the currently used azole antifungals. Other medically important Candida species include C. parapsilosis, C. tropicalis, and C. dubliniensis. Other Candida species, such as C. oleophila have been used as biological control agents in fruit.

ALTERNATIVE MEDICINE THERAPIES

Many practitioners of alternative medicine use the term Candida to refer to a complex with broad spectrum of symptoms, the majority of which center around gastrointestinal distress, rashes, sore gums and other miscellaneous symptoms. Candida is accorded responsibility for symptoms as specific as hay fever, as vague as "brain fog" and as common as weight gain or flatulence. These symptoms are attributed by some alternative medicine practitioners to the "overgrowth" of intestinal Candida albicans, which they claim leads to the spread of the yeast to other parts of the body via the digestive tract and bloodstream. Use of the term Candida in alternative medicine to describe this complex is unassociated with its use in clinical medicine to refer to the fungus that causes vaginal yeast infections and thrush. This can be confusing for patients. No studies have proven that having intestinal candidiasis causes any symptoms of illness. To treat what they refer to as Candida, some alternative medicine practitioners have recommended avoiding antibiotics, birth control pills, and foods that are high in sugar or yeast, ostensibly to "eliminate excess yeast" in the body. However, there is little clinically valid evidence that these "Candida cleanse" treatments treat intestinal candidiasis effectively, or cure any of the symptoms claimed by the proponents of the hypothesis. The probiotic Saccharomyces boulardii has been shown to diminish levels of intestinal Candida in mice. This is therefore one of the specific probiotic strains often recommended by alternative medicine practitioners alongside a more general probiotic, for anyone on a "Candida cleanse" or "Candida diet".

For more information view the source:Wikipedia

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CESTODA (TAPEWORM)

Cestoda (Cestoidea) is the name given to a class of parasitic flatworms, commonly called tapeworms, of the phylum Platyhelminthes. Its members live in the digestive tract of vertebrates as adults, and often in the bodies of various animals as juveniles. Over a thousand species have been described, and all vertebrate species can be parasitised by at least one species of tapeworm. Several species parasitise humans after being consumed in underprepared meat such as pork (Taenia solium), beef (T. saginata), and fish (Diphyllobothrium spp.), or in food prepared in conditions of poor hygiene (Hymenolepis spp. or Echinococcus spp.). T. saginata, the beef tapeworm, can grow up to 12 m (40 ft); the largest species, the whale tapeworm Polygonoporus giganticus, can grow to over 30 m (100 ft).

ANATOMY

SCOLEX

The worm's scolex ("head") attaches to the intestine of the definitive host. In some species, the scolex is dominated by bothria (tentacles), which are sometimes called "sucking grooves", and function like suction cups. Other species have hooks and suckers that aid in attachment. Cyclophyllid cestodes can be identified by the presence of four suckers on their scolex. While the scolex is often the most distinctive part of an adult tapeworm, it is often unnoticed in a clinical setting as it is inside the patient. Thus, identifying eggs and proglottids in feces is important.

BODY SYSTEMS

Body systemsThe main nerve centre of a cestode is a cerebral ganglion in its scolex. Motor and sensory innervation depends on the number and complexity of the scolex. Smaller nerves emanate from the commissures to supply the general body muscular and sensory ending. The cirrus and vagina are innervated, and sensory endings around the genital pore are more plentiful than other areas. Sensory function includes both tactoreception and chemoreception. Some nerves are only temporary.

PROGLOTTIDS

ProglottidsThe body is composed of successive segments (proglottids). The sum of the proglottids is called a strobila, which is thin, and resembles a strip of tape. From this is derived the common name "tapeworm". Like some other flatworms, cestodes use flame cells (protonephridia), located in the proglottids, for excretion. Mature proglottids are released from the tapeworm's posterior end and leave the host in feces. Because each proglottid contains the male and female reproductive structures, they can reproduce independently. Some biologists have suggested that each should be considered a single organism, and that the tapeworm is actually a colony of proglottids. The layout of proglottids comes in two forms, craspedote, meaning proglottids are overlapped by the previous proglottid, and acraspedote which indicates a non-overlapping conjoined proglottid. Once anchored to the host's intestinal wall, the tapeworm absorbs nutrients through its skin as the food being digested by the host flows past it and it begins to grow a long tail, with each segment containing an independent digestive system and reproductive tract. Older segments are pushed toward the tip of the tail as new segments are produced by the neckpiece. By the time a segment has reached the end of the tail, only the reproductive tract is left. It then drops off, carrying the tapeworm eggs to the next host, since, by that point, the proglottid is, in essence, a sac of eggs.

REPRODUCTION AND LIFE CYCLE OF THE TAPEWORMS

True tapeworms are exclusively hermaphrodites; they have both male and female reproductive systems in their bodies. The reproductive system includes one or many testes, cirrus, vas deferens and seminal vesicle as male organs, and a single lobed or unlobed ovary with the connecting oviduct and uterus as female organs. There is a common external opening for both male and female reproductive systems, known as genital pore, which is situated at the surface opening of the cup-shaped atrium. Even though they are sexually hermaphroditic, self-fertilization is a rare phenomenon. In order to permit hybridization, cross-fertilization between two individuals is often practiced for reproduction. During copulation, the cirrus of one individual connects with that of the other through the genital pore, and then exchange their spermatozoa. The life cycle of tapeworms is simple in the sense that there are no asexual phases as in other flatworms, but complicated in that at least one intermediate host is required as well as the definitive host. This life cycle pattern has been a crucial criterion for assessing evolution among Platyhelminthes. Many tapeworms have a two-phase life cycle with two types of host. The adult Taenia saginata lives in the gut of a primate such as a human. Proglottids leave the body through the anus and fall onto the ground, where they may be eaten with grass by animals such as cows. This is known as the intermediate host. The juvenile form migrates and establishes as a cyst in the intermediate hosts body tissues such as muscles, rather than the gut. They cause more damage to this host than it does to its definitive host. The parasite completes its life cycle when the intermediate host passes on the parasite to the definitive host, this is usually done by the definitive host eating an infective intermediate host, such as possibly a human with a preference for raw meat?in whose gut the adult Taenia establishes itself.

Tapeworm infestation is the infection of the digestive tract by adult parasitic flatworms called cestodes or tapeworms. Live tapeworm larvae (coenuri) are sometimes ingested by consuming undercooked food. Once inside the digestive tract, a larva can grow into a very large adult tapeworm. Additionally, many tapeworm larvae cause symptoms in an intermediate host. For example, cysticercosis is a disease of humans involving larval tapeworms in the human body.

COMMON TYPES

BEEF TAPEWORM

Among the most common tapeworms in humans are the pork tapeworm (T. solium), the beef tapeworm (T. saginata), the fish tapeworm (Diphyllobothrium spp.), and the dwarf tapeworm (Hymenolepis spp.). Infections involving the pork and beef tapeworms are also called taeniasis. Tapeworms of the genus Echinococcus infect and cause the most harm to intermediate hosts such as sheep and cattle. Infection with this type of tapeworm is referred to as Echinococcosis or hydatid disease. Symptoms vary widely, as do treatment options, and these issues are discussed in detail in the individual articles on each worm. With a few notable exceptions like the fish tapeworm, most cestodes that infect humans and livestock are cyclophyllids, and can be identified as such by the presence of four suckers on their scolex or head.

OCCURRENCE

Most occurrences are found in areas which lack adequate sanitation and include Southeast Asia, West Africa, and East Africa.

SYMPTOMS

Although tapeworms in the intestine usually cause no symptoms, some people experience upper abdominal discomfort, diarrhea, and loss of appetite. Anemia may develop in people with the fish tapeworm. Infection is generally recognized when the infected person passes segments of proglottids in the stool (looks like white worms), especially if a segment is moving. Rarely, worms may cause obstruction of the intestine. And very rarely, T. solium larvae can migrate to the brain causing severe headaches, seizures and other neurological problems. This condition is called neurocysticercosis. It can take years of development before the patient has those symptoms of the brain.

TREATMENT

Tapeworms are treated with medications taken by mouth, usually in a single dose. The drug of choice for tapeworm infections is niclosamide. Praziquantel and albendazole can also be used.

TRANSMISSION

INGESTION OF EGGS

Tapeworm eggs are generally ingested through food, water or soil contaminated with human or animal (host) feces. For example, if a pig is infected with a tapeworm, it may pass eggs or segments (proglottids) of the adult tapeworm through its feces into soil. Each segment contains thousands of microscopic tapeworm eggs. These eggs can be ingested via food contaminated with the feces. Once the eggs have been ingested, they develop into larvae, which can migrate out of the intestines and form cysts in other tissues such as the lungs or liver. This type of infection is not common with beef or fish tapeworms, but can occur with the pork tapeworm called cysticercosis and can also occur with dog and sheep tapeworms called echinococcosis.

INGESTION OF LARVAE CYSTS IN MEAT OR MUSCLE TISSUE

Tapeworm infection can also be caused by eating raw or undercooked meat from an animal or a fish that has the larval form of the tapeworm cysts in its muscle tissue. Once ingested, the larvae then develop into adult tapeworms in the intestines. Adult tapeworms can measure up to 50 feet (15 m) long and can survive as long as 20 years. Some tapeworms attach themselves to the walls of the intestine, where they cause irritation or mild inflammation, while others may pass through to the stool and exit the body. Unlike other tapeworms, the dwarf tapeworm can complete its entire life cycle egg to larva to adult tapeworm in one host. This is the most common tapeworm infection in the world and can be transmitted between humans. Even while being treated for certain tapeworm infections, reinfection can result from ingesting tapeworm eggs shed by the adult worm into the stool, as a result of insufficient personal hygiene.

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CHARCOT LEYDEN CRYSTALS

Charcot-Leyden crystals are microscopic crystals found in people who have allergic diseases such as asthma or parasitic infections such as parasitic pneumonia or ascariasis. The Charcot-Leyden crystal protein interacts with eosinophil lysophospholipases.

APPEARANCE

They vary in size and may be as large as 50m in length. Charcot-Leyden crystals are slender and pointed at both ends, consisting of a pair of hexagonal pyramids joined at their bases. Normally colorless, they are stained purplish-red by trichrome. They consist of lysophospholipase, an enzyme synthesized by eosinophils, and are produced from the breakdown of these cells.

CLINICAL SIGNIFICANCE

They are indicative of a disease involving eosinophilic inflammation or proliferation, such as is found in allergic reactions and parasitic infections. Charcot-Leyden crystals are often seen pathologically in patients with bronchial asthma.

HISTORY

Friedrich Albert von Zenker was the first to notice these crystals, doing so in 1851, after which they were described jointly by Jean-Martin Charcot and Charles-Philippe Robin in 1853, then in 1872 by Ernst Viktor von Leyden.

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CHRONIC FATIGUE SYNDROME

Chronic fatigue syndrome (CFS) is the most common name used to designate a significantly debilitating medical disorder or group of disorders generally defined by persistent fatigue accompanied by other specific symptoms for a minimum of six months in adults (and 3 months in children/adolescents), not due to ongoing exertion, not substantially relieved by rest, nor caused by other medical conditions. The disorder may also be referred to as myalgic encephalomyelitis (ME), post-viral fatigue syndrome (PVFS), chronic fatigue immune dysfunction syndrome (CFIDS), or several other terms. Biological, genetic, infectious and psychological mechanisms have been proposed for the development and persistence of symptoms but the etiology of CFS is not understood and may have multiple causes. There is no diagnostic laboratory test or biomarker for CFS. Symptoms of CFS include post-exertional malaise; unrefreshing sleep; widespread muscle and joint pain; sore throat; headaches of a type not previously experienced; cognitive difficulties; chronic, often severe, mental and physical exhaustion; and other characteristic symptoms in a previously healthy and active person. Persons with CFS may report additional symptoms including muscle weakness, increased sensitivity to light, sounds and smells, orthostatic intolerance, digestive disturbances, depression, and cardiac and respiratory problems. It is unclear if these symptoms represent co-morbid conditions or are produced by an underlying etiology of CFS. CFS symptoms vary from person to person in number, type, and severity. Fatigue is a common symptom in many illnesses, but CFS is comparatively rare. Estimates of CFS prevalence vary widely, from 7 to 3,000 cases of CFS for every 100,000 adults, but national health organizations have estimated more than 1 million Americans and approximately a quarter of a million people in the UK have CFS. CFS occurs more often in women than men, and is less prevalent among children and adolescents. The quality of life is "particularly and uniquely disrupted" in CFS. There is agreement on the genuine threat to health, happiness and productivity posed by CFS, but various physicians' groups, researchers and patient advocates promote different nomenclature, diagnostic criteria, etiologic hypotheses and treatments, resulting in controversy about many aspects of the disorder. The name "chronic fatigue syndrome" itself is controversial as many patients and advocacy groups, as well as some experts, believe the name trivializes the medical condition and want the name changed.

CLASSIFICATION

Notable definitions include: CDC definition (1994)—the most widely used clinical and research description of CFS, it is also called the Fukuda definition and was based on the Holmes or CDC 1988 scoring system. The 1994 criteria require the presence of four or more symptoms beyond fatigue, where the 1988 criteria require six to eight. The Oxford criteria (1991)—includes CFS of unknown etiology and a subtype called post-infectious fatigue syndrome (PIFS). Important differences are that the presence of mental fatigue is necessary to fulfill the criteria and symptoms are accepted that may suggest a psychiatric disorder. The 2003 Canadian Clinical working definition— states that "A patient with ME/CFS will meet the criteria for fatigue, post-exertional malaise and/or fatigue, sleep dysfunction, and pain; have two or more neurological/cognitive manifestations and one or more symptoms from two of the categories of autonomic, neuroendocrine, and immune manifestations; and [the illness will persist for at least 6 months]". The different case definitions used to research the illness may influence the types of patients selected for studies, and research also suggests subtypes of patients exist within the heterogeneous illness. Clinical practice guidelines—with the aim of improving diagnosis, management, and treatment—are generally based on case descriptions. An example is the CFS/ME guideline for the National Health Service in England and Wales, produced in 2007 by the National Institute for Health and Clinical Excellence (NICE).

NAMING

Chronic fatigue syndrome is the most commonly used designation, but widespread approval of a name is lacking. Different authorities on the illness view CFS as a central nervous system, metabolic, infectious or post-infectious, cardiovascular, immune system or psychiatric disorder, and different symptom profiles may be caused by various disorders. Over time and in different countries many names have been associated with the condition(s). Aside from CFS, some other names used include Akureyri disease, benign myalgic encephalomyelitis, chronic fatigue immune dysfunction syndrome, chronic infectious mononucleosis, epidemic myalgic encephalomyelitis, epidemic neuromyasthenia, Iceland disease, myalgic encephalomyelitis, myalgic encephalitis, myalgic encephalopathy, post-viral fatigue syndrome, raphe nucleus encephalopathy, Royal Free disease, Tapanui flu and yuppie flu (considered pejorative). Many patients would prefer a different name such as "myalgic encephalomyelitis", believing the name "chronic fatigue syndrome" trivializes the condition, prevents it from being seen as a serious health problem, and discourages research. A 2001 review referenced myalgic encephalomyelitis symptoms in a 1959 article by Acheson, stating ME could be a distinct syndrome from CFS, but in literature the two terms are generally seen as synonymous. A 1999 review explained the Royal Colleges of Physicians, Psychiatrists, and General Practitioners in 1996 advocated the use of chronic fatigue syndrome instead of myalgic encephalomyelitis or ME which was in wide use in the United Kingdom, "because there is, so far, no recognized pathology in muscles and in the central nervous system as is implied by the term ME." An editorial noted that the 1996 report received some acceptance, but also criticism from those advocating the use of different naming conventions, suggesting the report was biased, dominated by psychiatrists, and that dissenting voices were excluded. In 2002, a Lancet commentary noted the recent report by the "Working Group on CFS/ME" used the compromise name CFS/ME stating, "The fact that both names for the illness were used symbolises respect for different viewpoints whilst acknowledging the continuing lack of consensus on a universally acceptable name."

SIGNS AND SYMPTOMS

ONSET

The majority of CFS cases start suddenly, usually accompanied by a "flu-like illness" while a significant proportion of cases begin within several months of severe adverse stress. An Australian prospective study found that after infection by viral and non-viral pathogens, a sub-set of individuals met the criteria for CFS, with the researchers concluding that "post-infective fatigue syndrome is a valid illness model for investigating one pathophysiological pathway to CFS". However, accurate prevalence and exact roles of infection and stress in the development of CFS are currently unknown.

SYMPTOMS

The most commonly used diagnostic criteria and definition of CFS for research and clinical purposes were published by the United States Centers for Disease Control and Prevention (CDC). The CDC recommends the following three criteria be fulfilled:
1.A new onset (not lifelong) of severe fatigue for six consecutive months or greater duration which is unrelated to exertion, is not substantially relieved by rest, and is not a result of other medical conditions. 2.The fatigue causes a significant reduction of previous activity levels. 3.Four or more of the following symptoms that last six months or longer:
Impaired memory or concentration Post-exertional malaise, where physical or mental exertions bring on "extreme, prolonged exhaustion and sickness" Unrefreshing sleep Muscle pain (myalgia) Pain in multiple joints (arthralgia) Headaches of a new kind or greater severity Sore throat, frequent or recurring Tender lymph nodes (cervical or axillary) Other common symptoms include: Irritable bowel, abdominal pain, nausea, diarrhea or bloating Chills and night sweats Brain fog Chest pain Shortness of breath Chronic cough Visual disturbances (blurring, sensitivity to light, eye pain or dry eyes) Allergies or sensitivities to foods, alcohol, odors, chemicals, medications or noise Difficulty maintaining upright position (orthostatic instability, irregular heartbeat, dizziness, balance problems or fainting) Psychological problems (depression, irritability, mood swings, anxiety, panic attacks) The CDC proposes that persons with symptoms resembling those of CFS consult a physician to rule out several treatable illnesses: Lyme disease, "sleep disorders, depression, alcohol/substance abuse, diabetes, hypothyroidism, mononucleosis (mono), lupus, multiple sclerosis (MS), chronic hepatitis and various malignancies."Medications can also cause side effects that mimic symptoms of CFS.

FUNCTIONING

People report critical reductions in levels of physical activity and a reduction in the complexity of activity has been observed, with reported impairment comparable to other fatiguing medical conditions including late-stage AIDS, lupus, rheumatoid arthritis, chronic obstructive pulmonary disease (COPD), and end-stage renal disease. CFS affects a person's functional status and well-being more than major medical conditions such as multiple sclerosis, congestive heart failure, or type II diabetes mellitus. The severity of symptoms and disability is the same in both genders with strongly disabling chronic pain, but despite a common diagnosis the functional capacity of individuals with CFS varies greatly. While some lead relatively normal lives, others are totally bed-ridden and unable to care for themselves. Employment rates vary with over half unable to work and nearly two-thirds limited in their work because of their illness. More than half were on disability benefits or temporary sick leave, and less than a fifth worked full-time.

COGNITIVE FUNCTIONING

A 2010 meta-analysis concluded cognitive symptoms were principally resultants of decreased attention, memory, and reaction time. The deficits were in the range of 0.5 to 1.0 standard deviations below expected and were judged likely to affect day-to-day activities. Simple and complex information processing speed and functions entailing working memory over long time periods were moderately to extensively impaired. These deficits are generally consistent with those reported by patients. Perceptual abilities, motor speed, language, reasoning, and intelligence did not appear to be significantly altered.

PATHOPHYSIOLOGY

The mechanisms and pathogenesis of chronic fatigue syndrome are unknown. Research studies have examined and hypothesized about the possible biomedical and epidemiological characteristics of the disease, including oxidative stress, genetic predisposition, infection by viruses and pathogenic bacteria, hypothalamic-pituitary-adrenal axis abnormalities, immune dysfunction as well as psychological and psychosocial factors. Although it is unclear which factors are a cause or consequence of CFS, various models are proposed.

DIAGNOSIS

There are no characteristic laboratory abnormalities to diagnose CFS, so testing is used to rule out other potential causes for symptoms. When symptoms are attributable to certain other conditions, the diagnosis of CFS is excluded.

TREATMENT

Many people do not fully recover from CFS even with treatment. Cognitive behavioural therapy (CBT) and graded exercise therapy (GET) have shown moderate effectiveness for many people in multiple randomized controlled trials. As many of the CBT and GET studies required visits to a clinic, those severely affected may not have been included. Two large surveys of patients indicated that pacing is the most helpful intervention, or is considered useful by 96% of participants. Medication plays a minor role in management. No intervention has been proven effective in restoring the ability to work.

COGNITIVE BEHAVIOR THERAPY

Cognitive behavioral therapy, a form of psychological therapy often used to treat chronically ill patients, is a moderately effective treatment for CFS that "can be useful in treating some CFS patients." Since the cause or causes of CFS are unknown, CBT tries to help patients understand their individual symptoms and beliefs and develop strategies to improve day-to-day functioning whatever the cause of the symptoms. CBT is also thought to help patients by removing unhelpful illness beliefs which may perpetuate the illness. A Cochrane Review meta-analysis of 15 randomized, controlled cognitive behavioral therapy trials with 1043 participants concluded that CBT was an effective treatment to reduce the symptom of fatigue. Four reviewed studies showed that CBT resulted in a clinical response for 40% of participants vs 26% of those treated with "usual care". Similarly, in three studies CBT worked better than other types of psychological therapies (48% vs 27%). The effects may diminish after a course of therapy is completed; the reviewers write that "the evidence base at follow-up is limited to a small group of studies with inconsistent findings" and encourage further studies. A 2007 meta-analysis of 5 CBT randomized controlled trials of chronic fatigue and chronic fatigue syndrome reported 33-73% of the patients improved to the point of no longer being clinically fatigued. A 2010 meta-analysis of trials that measured physical activity before and after CBT showed that although CBT effectively reduced fatigue, activity levels were not affected by CBT and changes in physical activity were not related to changes in fatigue. They conclude that the effect of CBT on fatigue is not mediated by a change in physical activity. CBT has been criticised by patients' organisations because of negative reports from some of their members that have indicated that CBT can sometimes make people worse, a common result across multiple patient surveys.

GRADED EXERCISE THERAPY

Graded exercise therapy is a form of physical therapy. A meta-analysis published in 2004 of five randomized trials found that patients who received exercise therapy were less fatigued after 12 weeks than the control participants, and the authors cautiously conclude that GET shows promise as a treatment. However, after 6 months the benefit became non-significant compared to the control group who did not receive GET, and functional work capacity was not significantly improved after therapy. A systematic review published in 2006 included the same five RCTs, noting that "no severely affected patients were included in the studies of GET". Surveys conducted on behalf of patient organizations commonly report adverse effects. To avoid detrimental effects from GET, care must be taken to avoid the exacerbation of symptoms while catering the program to individual capabilities and the fluctuating nature of symptoms.

PACING

Pacing is an energy management strategy based on the observation that symptoms of the illness tend to increase following minimal exertion. There are two forms: symptom-contingent pacing, where the decision to stop (and rest or change an activity) is determined by an awareness of an exacerbation of symptoms; and time-contingent pacing, which is determined by a set schedule of activities which a patient estimates he or she is able to complete without triggering post-exertional malaise (PEM). Thus the principle behind pacing for CFS is to avoid over-exertion and an exacerbation of symptoms. It is not aimed at treating the illness as a whole. Those whose illness appears stable may gradually increase activity and exercise levels but according to the principle of pacing, must rest if it becomes clear that they have exceeded their limits. Some programmes combine symptom and time-contingent approaches. A trial of one such programme reported limited benefits. A larger, randomised controlled trial found that pacing had statistically better results than relaxation/flexibility therapy. A 2009 survey of 828 Norwegian CFS patients found that pacing was evaluated as useful by 96% of the participants.

OTHER

Other treatments of CFS have been proposed but their effectiveness has not been confirmed. Medications thought to have promise in alleviating symptoms include antidepressant and immunomodulatory agents. The evidence for antidepressants is mixed, and their use remains controversial. Many CFS patients are sensitive to medications, particularly sedatives, and some patients report chemical and food sensitivities. CFS patients have a low placebo response, especially to psychological-psychiatric interventions, perhaps due to patient expectations.

PROGNOSIS

RECOVERY

A systematic review of 14 studies that described improvement and occupational outcomes of people with CFS found that "the median full recovery rate was 5% (range 0–31%) and the median proportion of patients who improved during follow-up was 39.5% (range 8–63%). Return to work at follow-up ranged from 8 to 30% in the three studies that considered this outcome." .... "In five studies, a worsening of symptoms during the period of follow-up was reported in between 5 and 20% of patients." A good outcome was associated with less fatigue severity at baseline, a sense of control over symptoms and not attributing illness to a physical cause. Another review found that children have a better prognosis than adults, with 54–94% having recovered by follow-up compared to less than 10% of adults returning to premorbid levels of functioning.

MORTALITY

Two studies were published in 2006 that directly addressed mortality in CFS. A 14 year longitudinal study of persons with CFS reported that all-cause mortality or suicide rates of individuals were not significantly different from standardized mortality rates (SMRs). A smaller retrospective study in individuals with CFS reported the leading causes of death were heart failure, suicide, and cancer. The ages of death for these three conditions were significantly younger than in the general population respectively. Significant limitations of the study were the inability to check the accuracy of the CFS diagnosis of the individuals or causes of death, and the inability to generalize the data to the overall population of patients with CFS due to the data collection methods.

EPIDEMIOLOGY

PREVALENCE

A 2003 review states that studies have reported between 7 and 3,000 cases of CFS for every 100,000 adults. Ranjith reviewed the epidemiological literature on CFS and suggested that the wide variance of the prevalence estimates may be due to the different definitions of CFS in use, the settings in which patients were selected, and the methodology used to exclude study participants with possible alternative diagnoses. The Centers for Disease Control reports that more than 1 million Americans have CFS and approximately 80% of the cases are undiagnosed. Approximately 250,000 people in the UK are affected with the illness according to the National Health Service.

RISK FACTORS

All ethnic and racial groups appear susceptible to the illness, and lower income groups are slightly more likely to develop CFS. A 2009 meta-analysis showed that compared with the White American majority, African Americans and Native Americans have a significantly higher risk of CFS. More women than men get CFS — between 60 and 85% of cases are women; however, there is some indication that the prevalence among men is underreported. The illness is reported to occur more frequently in people between the ages of 40 and 59. CFS is less prevalent among children and adolescents than adults. Blood relatives of people who have CFS appear to be more predisposed. There is no direct evidence that CFS is contagious, though it is seen in members of the same family; this is believed to be a familial or genetic link but more research is required for a definitive answer. A systematic review in 2008 included 11 primary studies that had assessed various demographic, medical, psychological, social and environmental factors to predict the development of CFS, and found many had reported significant associations to CFS. The reviewers concluded that the lack of generalizability and replication between studies meant that "none of the identified factors appear suitable for the timely identification of patients at risk of developing CFS/ME within clinical practice."

DIFFERENTIAL DIAGNOSES

Certain medical conditions can cause chronic fatigue and must be ruled out before a diagnosis of CFS can be given. Hypothyroidism, anemia, diabetes and certain psychiatric disorders are a few of the diseases that must be ruled out if the patient presents with appropriate symptoms. People with fibromyalgia (FM, or fibromyalgia syndrome, FMS) have muscle pain and sleep disturbances. Fatigue and muscle pain occurs frequently in the initial phase of various hereditary muscle disorders and in several autoimmune, endocrine and metabolic syndromes; and are frequently labelled as CFS or fibromyalgia in the absence of obvious biochemical/metabolic abnormalities and neurological symptoms.[citation needed] Multiple chemical sensitivity, Gulf War syndrome and post-polio syndrome have symptoms similar to those of CFS, and the last is also theorized to have a common pathophysiology. A 2006 review found that there was a lack of literature to establish the discriminant validity of undifferentiated somatoform disorder from CFS. The author stated that there is a need for proponents of chronic fatigue syndrome to distinguish it from undifferentiated somatoform disorder. The author also mentioned that the experience of fatigue as exclusively physical and not mental is captured by the definition of somatoform disorder but not CFS. Hysterical diagnoses are not merely diagnoses of exclusion but require criteria to be met on the positive grounds of both primary and secondary gain. Depressive symptoms seen in CFS may be differentially diagnosed from primary depression due to the absence of anhedonia and la belle indifference, guilt, and the presence of somatic symptoms such as sore throat, swollen lymph nodes, and exercise intolerance with postexertional exacerbation of symptoms.

CO-MORBIDITY

Many CFS patients will also have, or appear to have, other medical problems or related diagnoses. Co-morbid fibromyalgia is common, where only patients with fibromyalgia show abnormal pain responses. Fibromyalgia occurs in a large percentage of CFS patients between onset and the second year, and some researchers suggest fibromyalgia and CFS are related. As previously mentioned, many CFS sufferers also experience symptoms of irritable bowel syndrome, temporomandibular joint pain, headache including migraines, and other forms of myalgia. CFS patients have significantly higher rates of current mood disorders than the general population. Feeling depressed is also a commonplace reaction to the losses caused by chronic illness which can in some cases become a comorbid situational depression. Compared with the non-fatigued population, male CFS patients are more likely to experience chronic pelvic pain syndrome (CP/CPPS), and female CFS patients are also more likely to experience chronic pelvic pain. CFS is significantly more common in women with endometriosis compared with women in the general USA population.

HISTORY

In 1934 an outbreak then referred to as atypical poliomyelitis (at the time it was considered a form of polio) occurred at the Los Angeles County Hospital. It strongly resembled what is now called chronic fatigue syndrome and affected a large number of nurses and doctors. In 1955 at the Royal Free Hospital in London, United Kingdom, another outbreak occurred that also affected mostly the hospital staff. Also resembling CFS, it was called both Royal Free disease and benign myalgic encephalomyelitis and formed the basis of descriptions by Acheson, Ramsay, and others. In 1969 benign myalgic encephalomyelitis was first classified into the International Classification of Diseases under Diseases of the nervous system. The name chronic fatigue syndrome was used in the medical literature in 1987 to describe a condition resembling "chronic active Epstein-Barr virus (EBV) infection" but which presented no evidence of EBV as its cause. The initial case definition of CFS was published in 1988, "Chronic fatigue syndrome: a working case definition", (the Holmes definition), and displaced the name chronic Epstein-Barr virus syndrome. This research case definition was published after US Centers for Disease Control and Prevention epidemiologists examined patients at the Lake Tahoe outbreak. In 2006 the CDC commenced a national program to educate the American public and health care professionals about CFS. A 2009 study published in the journal "Science", reported an association between a retrovirus xenotropic murine leukemia virus-related virus (XMRV) and CFS. The editors of Science, subsequently attached an "Editorial Expression of Concern" to the report to the effect that the validity of the study "is now seriously in question". and in September 2011, the authors published a "Partial Retraction" of their 2009 findings, this was followed by a full retraction by the magazine’s Editor in Chief after the authors failed to agree on a full retraction statement. Also in September 2011 the Blood XMRV Scientific Research Working Group published a report which concluded "that currently available XMRV/P-MLV assays, including the assays employed by the three participating laboratories that previously reported positive results on samples from CFS patients and controls (2, 4), cannot reproducibly detect direct virus markers (RNA, DNA, or culture) or specific antibodies in blood samples from subjects previously characterized as XMRV/P-MLV positive (all but one with a diagnosis of CFS) or healthy blood donors." In December 2011, the Proceedings of the National Academy of Sciences published a similar retraction for an August 2010 paper.

RESEARCH FUNDING

In November 2006, an unofficial inquiry by an ad hoc group of parliamentarians in the United Kingdom, set up and chaired by former MP, Dr Ian Gibson, called the Group on Scientific Research into ME was informed by a government minister that few good biomedical research proposals have been submitted to the Medical Research Council (MRC) in contrast to those for psychosocial research. They were also told by other scientists of proposals that have been rejected, with claims of bias against support for this type of research. The MRC confirmed to the Group that, from April 2003 to November 2006, it has turned down 10 biomedical applications relating to CFS/ME and funded five applications relating to CFS/ME, mostly in the psychiatric/psychosocial domain. In 2008, the MRC set up an expert group to consider how the MRC might encourage new high-quality research into CFS/ME and partnerships between researchers already working on CFS/ME and those in associated areas. It currently lists CFS/ME with a highlight notice, inviting researchers to develop high quality research proposals for funding. In February 2010, the All-Party Parliamentary Group on ME (APPG on ME) produced a legacy paper, which welcomed the recent MRC initiative, but felt that there has been far too much emphasis in the past on psychological research with insufficient attention to biomedical research and that it is vital that further biomedical research be undertaken to help discover a cause and more effective forms of management for this disease.

SOCIETY AND CULTURE

ECONOMIC IMPACT

Reynolds et al. (2004), estimated that the illness caused about $20,000 per person with CFS in lost productivity which totals to $9.1 billion per year in the United States. A 2008 study estimated that the total annual cost burden of ME/CFS to society in the US was approximately $18.7 to $24.0 billion.

SOCIAL ISSUES

A study found that CFS patients report a heavy psychosocial burden. A survey by the Tymes Trust reported that children with CFS often state that they struggle for recognition of their needs and/or they feel bullied by medical and educational professionals. The ambiguity of the status of CFS as a medical condition may cause higher perceived stigma.

SUPPORT GROUPS

A study found that CFS patients in support groups reported no change in negative interactions compared to an improvement in negative interactions reported by those treated with Cognitive Behavioural Therapy. Patients with greater amounts of negative interactions received worse social support on average than disease-free cancer patients or healthy controls which, in turn, led to greater fatigue severity and functional impairment than CBT-treated patients.

AWARENESS DAY

May 12 is designated as International Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Awareness Day (ME/CFS). The day is observed so that stakeholders have an occasion to improve the knowledge of "the public, policymakers, and healthcare professionals about the symptoms, diagnosis, and treatment of ME/CFS, as well as the need for a better understanding of this complex illness."

DOCTOR-PATIENT-RELATIONS

Some in the medical community did not at first recognize CFS as a real condition, nor was there agreement on its prevalence. There has been much disagreement over proposed causes, diagnosis, and treatment of the illness. The context of contested causation may affect the lives of the individuals diagnosed with CFS, affecting the patient-doctor relationship, the doctor's confidence in their ability to diagnose and treat, ability to share issues and control in diagnosis with the patient, and raise problematic issues of reparation, compensation, and blame. Disagreements over how the condition is dealt with by health-care systems have resulted in an expensive and prolonged conflict for all involved. A major divide exists over whether funding for research and treatment should focus on physiological, psychological or psychosocial aspects of CFS. This division is especially great between patient groups and psychological and psychosocial treatment advocates in Great Britain. In 2011, it was reported by the BBC this conflict had involved personal vilification and allegations of professional misconduct to professional societies and universities of researchers who were investigating possible psychiatric connections. One of these researchers, Simon Wessely, reported personal death threats, and others noted such vilification would lead researchers to abandon or avoid the area of study entirely, as few would want to undergo this "torrent of abuse." Charles Shepherd from the ME Association condemned the abuse of researchers but emphasised that the underlying frustration stems from government funding of research focusing almost exclusively on psychiatric, rather than biomedical, causes.

BLOOD DONATIONS

Based on the possible link between CFS and XMRV, in 2010 a variety of national blood banks adopted measures to discourage or prohibit individuals diagnosed with CFS from donating blood, and decline donations when aware the potential donor had been diagnosed. Organizations adopting these or similar measures included the Canadian Blood Services, the New Zealand Blood Service, the Australian Red Cross Blood Service and the American Association of Blood Banks, In November 2010 the UK National Blood Service introduced a permanent deferral of donation from CFS patients based on the potential harm to those patients that may result from their giving blood.

CONTROVERSY

Chronic fatigue syndrome is an illness with a long history of controversies. There has been much contention over the etiology, pathophysiology, nomenclature and diagnostic criteria. Controversies still exist over funding for research and treatment of physiological versus psychological and psychosocial aspects of the illness. Historically, many professionals within the medical community were unfamiliar with CFS, or did not recognize it as a real condition, nor was there agreement on its prevalence or seriousness. Contrasting viewpoints among CFS experts became apparent in 1993, when psychiatrists David and Wessely contested the WHO classification of CFS under diseases of the nervous system, arguing that it was a form of neurasthenia to be classified as a psychiatric condition.

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CITROBACTER FREUNDII

Citrobacter freundii are facultative anaerobic Gram-negative bacilli. The bacteria are long rod-shaped with a typically length of 1-5 um. Most C. freundii cells are surrounded by several flagella used for locomotion, but a few are non-motile. It can be found in soil, water, sewage, food and the intestinal tracts of animals and humans. It is classified under the family of Enterobacteriaceae. The Citrobacter genus was discovered in 1932 by Werkman and Gillen. Cultures of C. freundii were isolated and identified in the same year from soil extracts. As an opportunistic pathogen, C. freundii is responsible for a number of significant opportunistic infections. It is known to be the cause of a number of nosocomial infections of the respiratory tract, urinary tract, blood and many other normally sterile sites in patients. C. freundii represents about 29% of all opportunistic infections. Surprisingly, this infectious microbe in humans plays a positive role in the environment. C. freundii is responsible for reducing nitrate to nitrite in the environment. This conversion is an important and crucial stage in the nitrogen cycle. The bacteria also helps in recycling nitrogen. Citrobacter freundii has also been investigated for biodegradation of tannic acid used in tanneries. For metabolism, C. freundii has an ability to grow on glycerol as the sole carbon and energy source. Within its cell, a bacterial microcompartment can be found, which is capable of processing propanediol.

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CLONORCHIS

Clonorchis sinensis, the Chinese liver fluke, is a human liver fluke in the class Trematoda, Phylum Platyhelminthes. This parasite lives in the liver of humans, and is found mainly in the common bile duct and gall bladder, feeding on bile. These animals, which are believed to be the third most prevalent worm parasite in the world, are endemic to Japan, China, Taiwan, and Southeast Asia, currently infecting an estimated 30,000,000 humans. The egg of a Clonorchis sinensis (commonly: human liver fluke), which contains the miracidium that develops into the adult form, floats in freshwater until it is eaten by a snail. First intermediate host. Freshwater snail Parafossarulus manchouricus - synonym: Parafossarulus striatulus, often serves as a first intermediate host for Clonorchis sinensis in China, Japan, Korea and Russia. Other snail hosts include: Bithynia longicornis - synonym: Alocinma longicornis - in China Bithynia fuchsiana - in China Bithynia misella - in China Parafossarulus anomalosiralis - in China Melanoides tuberculata - in China Semisulcospira libertina - in China Assiminea lutea - in China Tarebia granifera - in Taiwan, China Once inside of the snail body, the miracidium hatches from the egg, and parasitically grows inside of the snail. The miracidium develops into a sporocyst, which in turn house the asexual reproduction of redia, the next stage. The redia themselves house the asexual reproduction of free-swimming cercaria. This system of asexual reproduction allows for an exponential multiplication of cercaria individuals from one miracidium. This aids the Clonorchis in reproduction, because it enables the miracidium to capitalize on one chance occasion of passively being eaten by a snail before the egg dies. Once the redia mature, having grown inside the snail body until this point, they actively bore out of the snail body into the freshwater environment. Second intermediate hostThere, instead of waiting to be consumed by a host (as is the case in their egg stage), they seek out a fish. Boring their way into the fish's body, they again become parasites of their new hosts. Once inside of the fish muscle, the cercaria create a protective metacercarial cyst with which to encapsulate their bodies. This protective cyst proves useful when the fish muscle is consumed by a human. Definitive hostThe acid-resistant cyst enables the metacercaria to avoid being digested by the human gastric acids, and allows the metacercaria to reach the small intestine unharmed. Reaching the small intestines, the metacercaria navigate toward the human liver, which becomes its final habitat. Clonorchis feed on human bile created by the liver. In the human liver, the mature Clonorchis reaches its stage of sexual reproduction. The hermaphroditic adults produce eggs every 1?30 seconds, resulting in the rapid multiplication of inhabitants in the liver. This leads to various health problems.

EFFECTS ON HUMAN HEALTH

Dwelling in the bile ducts, Clonorchis induces an inflammatory reaction, epithelial hyperplasia and sometimes even cholangiocarcinoma, the incidence of which is raised in fluke-infested areas. One adverse effect of Clonorchis is the possibility for the adult metacercaria to consume all bile created in the liver, which would inhibit the host human from digesting, especially fats. Another possibility is obstruction of the bile duct by the parasite or its eggs, leading to biliary obstruction and cholangitis (specifically oriental cholangitis). Central Serous Retinopathy (CSR) a report of 80 cases by Dr. John Chiao-nan Chang, M.D. and Dr. Yin-Ping Wang, M.D. Hong Kong on page 125 of their report observed that 19% of the cases of CSR in their sample tested positive for Clonorchis sinensis.

SYMPTOMS

Dwelling in the bile ducts, Clonorchis induces an inflammatory reaction, epithelial hyperplasia and sometimes even cholangiocarcinoma, the incidence of which is raised in fluke-infested areas. One adverse effect of Clonorchis is the possibility for the adult metacercaria to consume all bile created in the liver, which would inhibit the host human from digesting, especially fats. Another possibility is obstruction of the bile duct by the parasite or its eggs, leading to biliary obstruction and cholangitis (specifically oriental cholangitis). Central Serous Retinopathy (CSR) a report of 80 cases by Dr. John Chiao-nan Chang, M.D. and Dr. Yin-Ping Wang, M.D. Hong Kong on page 125 of their report observed that 19% of the cases of CSR in their sample tested positive for Clonorchis sinensis.

DIAGNOSIS AND TREATMENT

Post infectious microscopic demonstration in stools or in duodenal aspirate is the most practical diagnostic method. Morphological comparison with other GI parasites is performed. Drugs used to treat infestation include triclabendazole, praziquantel, bithionol, albendazole and mebendazole.

LIFE CYCLE

Life cycle of Clonorchis sinensis

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CLOSTRIDIUM DIFFICILE

Clostridium difficle, also known as "CDF/cdf", or "C. diff", is a species of Gram-positive bacteria of the genus Clostridium that causes severe diarrhea and other intestinal disease when competing bacteria in the gut flora have been wiped out by antibiotics. Clostridia are anaerobic, spore-forming rods (bacilli). C. difficile is the most serious cause of antibiotic-associated diarrhea (AAD) and can lead to pseudomembranous colitis, a severe inflammation of the colon, often resulting from eradication of the normal gut flora by antibiotics. In a very small percentage of the adult population, C. difficile bacteria naturally reside in the gut. Other people accidentally ingest spores of the bacteria while they are patients in a hospital, nursing home, or similar facility. When the bacteria are in a colon in which the normal gut flora has been destroyed (usually after a broad-spectrum antibiotic such as clindamycin has been used), the gut becomes overrun with C. difficile. This overpopulation is harmful because the bacteria release toxins that can cause bloating and diarrhea, with abdominal pain, which may become severe. C. difficile infections are the most common cause of pseudomembranous colitis, and in rare cases this can progress to toxic megacolon, which can be life-threatening. Latent symptoms of C. difficile infection often mimic some flu-like symptoms and can mimic disease flare in patients with inflammatory bowel disease-associated colitis. Mild cases of C. difficile infection can often be cured by discontinuing the antibiotics responsible. In more serious cases, oral administration of, first, oral metronidazole and - if that fails - then, second, vancomycin and if unsucessful again, intravenous metronidazole can be used. Relapses of C. difficile AAD have been reported in up to 20% of cases.

SIGNS AND SYMPTOMS

In adults, a clinical prediction rule found the best signs to be: significant diarrhea ("new onset of > 3 partially formed or watery stools per 24 hour period"), recent antibiotic exposure, colitis (abdominal pain), fever (up to 40.5?C), and foul stool odour. In a population of hospitalized patients prior antibiotic treatment plus diarrhea or abdominal pain had a sensitivity of 86% and a specificity of 45%. In this study with a prevalence of positive cytotoxin assays of 14%, the positive predictive value was 20% and the negative predictive value was 95%.

CAUSE

With the introduction of broad-spectrum antibiotics and chemotherapeutic antineoplastic drugs in the second half of the twentieth century, antibiotic- (and chemotherapy-) associated diarrhea became more common. Pseudomembranous colitis was first described as a complication of C. difficile infection in 1978, when a toxin was isolated from patients suffering from pseudomembranous colitis and Koch's postulates were met. The numerous spores formed by C. difficile are resistant to most routine cleaning methods that are used on surfaces (except for diluted bleach). Spores of these bacteria can remain viable outside of the human body for very long periods of time, and this means that patients in a medical facility are often exposed to situations where they end up accidentally ingesting spores.[citation needed] Extremely rigorous infection protocols are required in order to decrease or eliminate this risk. C. difficile infection (CDI) can range in severity from asymptomatic to severe and life-threatening, especially among the elderly. People are most often nosocomially infected in hospitals, nursing homes, or other medical institutions, although C. difficile infection in the community, outpatient setting is increasing. The rate of C. difficile acquisition is estimated to be 13% in patients with hospital stays of up to 2 weeks, and 50% in those with hospital stays longer than 4 weeks. C. difficile-associated diarrhea (aka CDAD) is most strongly associated with fluoroquinolones. Fluoroquinolones are more strongly associated with C. difficile infections than other antibiotics including clindamycin, 3rd generation cephalosporins and beta-lactamase inhibitors. One study found that fluoroquinolones were responsible for 55% of C. difficile infections. In addition to previous use of antimicrobials, use of proton pump inhibitors [PPIs] is associated with a 2-fold increase in risk for C. difficile infection. The European Center for Disease Prevention and Control recommend that fluoroquinolones and the antibiotic clindamycin be avoided in clinical practice due to their high association with subsequent Clostridium difficile infections. Frequency and severity of C. difficile colitis remains high and seems to be associated with increased death rates. Immunocompromised status and delayed diagnosis appear to result in elevated risk of death. Early intervention and aggressive management are key factors to recovery. Increasing rates of community-acquired C. difficile infection are associated with the use of medication that suppress gastric acid production: H2-receptor antagonists increased the risk 1.5 fold, and proton pump inhibitors by 1.7 with once daily use and 2.4 with more than once daily use. The emergence of a new, highly toxic strain of C. difficile, resistant to fluoroquinolone antibiotics, such as ciprofloxacin (Cipro) and levofloxacin (Levaquin), said to be causing geographically dispersed outbreaks in North America was reported in 2005. The Centers for Disease Control in Atlanta has also warned of the emergence of an epidemic strain with increased virulence, antibiotic resistance, or both. In 2005, molecular analysis led to the identification of the C. difficile strain type that was characterized as group BI by restriction endo nuclease analysis (REA), as North American pulse-field-type NAP1 by pulse-field gel electrophoresis (PFGE) and as ribotype 027; the differing terminology reflects the predominant techniques that were used for epidemiological typing and this strain is referred to as C. difficile BI/NAP1/027. Some recent research suggests that the overuse of antibiotics in the raising of livestock for meat consumption is contributing to outbreaks of bacterial infections such as C. difficile.

BACTERIOLOGY

Clostridia are motile bacteria that are ubiquitous in nature and are especially prevalent in soil. Under the microscope, clostridia appear as long, irregularly (often "drumstick" or "spindle") shaped cells with a bulge at their terminal ends. Under Gram staining, Clostridium difficile cells are Gram-positive and show optimum growth on blood agar at human body temperatures in the absence of oxygen. When stressed, the bacteria produce spores that can tolerate extreme conditions that the active bacteria cannot tolerate. C. difficile is a commensal bacterium of the human intestine in 2-5% of the population. Long-term hospitalization or residence in a nursing home within the previous year are independent risk factors for increased colonization. In small numbers, C. difficile does not result in significant disease. Antibiotics, especially those with a broad spectrum of activity (such as for example clindamycin) cause disruption of normal intestinal flora, leading to an overgrowth of C. difficile, which flourishes under these conditions. This can lead to pseudomembranous colitis (PMC), the generalized inflammation of the colon and the development of pseudomembrane, a viscous collection of inflammatory cells, fibrin, and necrotic cells. Pathogenic C. difficile strains produce several known toxins. The most well-characterized are enterotoxin (Clostridium difficile toxin A) and cytotoxin (Clostridium difficile toxin B), both of which are responsible for the diarrhea and inflammation seen in infected patients, although their relative contributions have been debated. Toxins A and B are glucosyltransferases that target and inactivate the Rho family of GTPases. Clostridium difficile toxin B (cytotoxin) induces actin depolymerization by a mechanism correlated with a decrease in the ADP-ribosylation of the low molecular mass GTP-binding Rho proteins. Another toxin, binary toxin, has also been described, but its role in disease is not yet fully understood. Antibiotic treatment of C. difficile infections can be difficult, due both to antibiotic resistance as well as physiological factors of the bacteria itself (spore formation, protective effects of the pseudomembrane) Pseudomembranous colitis caused by C. difficile is treated with specific antibiotics, for example, vancomycin (Vancocin) or metronidazole (Flagyl). C. difficile is transmitted from person to person by the fecal-oral route. However, the organism forms large numbers of heat-resistant spores, and these are not killed by alcohol-based hand cleansers or routine cleaning of surfaces. Thus, these spores remain viable in the hospital or nursing home environment for long periods of time, and, because of this, the bacteria can be cultured from almost any surface in the hospital. Once spores are ingested by a patient, they pass through the stomach unscathed because of their acid-resistance. They germinate into vegetative cells in the colon upon exposure to bile acids, and multiply. Several disinfectants commonly used in hospitals are ineffective against C. difficile spores, and may actually promote spore formation. However, disinfectants containing bleach are effective in killing the organisms.

DIAGNOSIS

CYTOTOXICITY

C. difficile toxins have a cytopathic effect in cell culture, and neutralized with specific anti-sera is the practical gold standard for studies investigating new CDAD diagnostic techniques. Toxigenic culture, in which organisms are cultured on selective medium and tested for toxin production, remains the gold standard and is the most sensitive and specific test, although it is slow and labour-intensive.

TOXIN ELISA

Assessment of the A and B toxins by enzyme-linked immunosorbent assay (ELISA) for toxin A or B (or both) has a sensitivity of 63?99% and a specificity of 93?100%: At a prevalence of 15%, this leads to a positive predictive value (PPV) of 73% and a negative predictive value (NPV) of 96%. Previously, experts recommended sending as many as three stool samples to rule out disease if initial tests are negative. However, recent evidence suggests that repeat testing during the same episode of diarrhea is of limited value and should be discouraged.C. difficile toxin should clear from the stool of previously infected patients if treatment is effective. However, many hospitals test only for the prevalent toxin A. Strains that express only the B toxin are now present in many hospitals, and ordering both toxins should occur. Not testing for both may contribute to a delay in obtaining laboratory results, which is often the cause of prolonged illness and poor outcomes.

OTHER STOOL TESTS

Stool leukocyte measurements and stool lactoferrin levels have also been proposed as diagnostic tests, but may have limited diagnostic accuracy.

COMPUTED TOMOGRAPHY

In a recent study, a patient who received a diagnosis of Clostridium difficile colitis (CDC) on the basis of computed tomography (CT scan) had an 88% probability of testing positive on stool assay. Wall thickening is the key CT finding in this disease. Once colon wall thickening is identified as being 4 mm, the best ancillary findings were pericolonic stranding, ascites, and colon wall nodularity. The presence of wall thickness plus any one of these ancillary findings is 70% sensitive and 93% specific. Using criteria of 10 mm or a wall thickness of 4 mm and any of the more-specific findings does not add significantly to the diagnosis but gives equally satisfactory results. In this study with a prevalence of positive C. difficile toxin of 54%, the PPV was 88%. Patients who have antibiotic-associated diarrhea with CT findings diagnostic of CDC merit consideration for treatment on that basis.

REAL-TIME PCR

By the end of 2009, 3 different Real-Time PCR tests had achieved 510(k) clearance from the FDA. Cepheid's GeneXpert is by far the fastest and easiest of the three, but it is also the most expensive. Cepheid uses a cartridge-based kit that is tailored for small hospitals or labs without the ability to batch large numbers of samples together. In fact, batching is not required since the extraction occurs in the same vial as amplification of the target, positive, and negative controls. The reported time from sample to result is 45 minutes. Prodesse offers another kit-based IVD Real-Time PCR test (ProGastro Cd), which uses an external extraction and purification on the Roche MagnaPure. Prodesse (Gen-Probe) tech support claims that this external separation produces higher yields than the BD GeneOhm. The Prodesse technique is similar in price to the BD GeneOhm technique after one includes the price of the extraction and takes about three hours from sample to result. The final IVD Clostridium difficile Real Time PCR test on the market since 2009 is from BD GeneOhm. The protocol uses a glass-bead lysis rather than an extraction, but results are reported to be good and the method shaves a little over an hour off the protocol time (about 1 hour 45 minutes from sample to result). Total costs for the Prodesse and BD GeneOhm tests are approximately the same. For each test, sensitivities are generally reported as 88-91% and specificities as 96-97%, depending on the tests, prevalence of the disease and the size of the patient pool.

PREVENTION

The most effective method for preventing CDAD is proper antimicrobial prescribing. In the hospital setting, where CDAD is most common, nearly all patients that develop CDAD are exposed to antimicrobials. Although proper antimicrobial prescribing sounds easy to do, approximately 50% of antimicrobial use is considered inappropriate. This is consistent whether in the hospital, clinic, community, or academic setting. Several studies have demonstrated a decrease in CDAD by limiting antibiotics most strongly associated with CDAD or by limiting unnecessary antimicrobial prescribing in general, both in outbreak and non-outbreak settings. In Britain, the testing of all hospital inpatients over the age of 65 with diarrhea for C. difficile became a compulsory NHS practice in January 2008, when it became evident that many UK outbreaks were being disguised as Norovirus by hospital risk managers. Risk managers can be dismissed by the Department of Health if C. difficile infection rates are too high, but they cannot be dismissed as a result of a Norovirus outbreak. Patients most at risk are those with recent broad-spectrum antibiotic or proton-pump inhibitor treatments. Infection control measures, such as wearing gloves when caring for patients with CDAD, have been proven to be effective at prevention. This works by limiting the spread of C. difficile in the hospital setting. In addition, washing with soap and water will eliminate the spores from contaminated hands, but alcohol-based hand rubs are ineffective. Bleach wipes containing 0.55 percent sodium hypochlorite have been shown to kill the spores and prevent transmission between patients. Soil-containing potted plants can serve as a reservoir for the development of multidrug-resistant bacteria and fungi, and, for this reason, many hospital systems restrict the use of soil-containing potted plants. To help mitigate serious infections and development of multidrug-resistant organisms in long-term and acute hospital settings, soil-containing potted plants should not be used, especially in areas of direct patient care, such as offices, rooms, and hallways of hospital wards. Alternatives to soil-containing plants are available. Treatment with various oral supplements containing live bacteria has been studied in efforts to prevent Clostridium difficile-associated infection/disease. A randomized controlled trial using a probiotic drink containing Lactobacillus casei, L bulgaricus, and Streptococcus salivarius subsp. thermophilus was reported to have some efficacy. This study was sponsored by the company that produces the drink studied. Although intriguing, several other studies have been unable to demonstrate any benefit of oral supplements of similar bacteria at preventing CDAD. Of note, patients on the antibiotics most strongly associated with CDAD were excluded from this study. Hydrogen peroxide vapor (HPV) systems used to sterilize a patient room post discharge has been shown to reduce infection rates and to reduce risk of infection to subsequent patients. One study (Boyce et al. 2008) showed that incidence of CDAD was reduced by 53% though use of HPV. A second study (Manian et al. 2010) showed only a 42% reduction in CDAD rates through use of HPV. In a limited clinical trial, a C. difficile anti-toxoid vaccine was reported to improve patient outcomes. Further testing will be required to validate this trial. Recent advancements have been made at the University of Guelph by Professor Monteiro on a polysaccharide vaccine currently in its pre-clinical stage.

TREATMENT

symptomatic colonization with C. difficile is common. Treatment in asymptomatic patients is controversial, also leading into the debate of clinical surveillance and how it intersects with public health policy. In general, mild cases do not require specific treatment. Patients should be treated as soon as possible when the diagnosis of Clostridium difficile colitis (CDC) is made to avoid frank sepsis or bowel perforation. To reduce complications, physicians often begin treatment based on clinical presentation before definitive results are available. Knowledge of the local epidemiology of intestinal flora of a particular institution can guide therapy. In addition, oral rehydration therapy (ORT) is useful in retaining fluids during the duration of diarrhea.

MEDICATIONS

Three antibiotics are specifically effective against C. difficile. With the available agents more or less equally effective. Metronidazole is the drug of choice, because of lower price and comparable efficacy. Oral vancomycin (125 mg four times daily) is second-line therapy, but is often avoided due to concerns of converting intestinal flora into vancomycin-resistant organisms. Vancomycin is the treatment of choice in the following cases: no response to oral metronidazole; the organism is resistant to metronidazole; the patient is allergic to metronidazole; the patient is either pregnant, breastfeeding, or younger than 10 years of age. Vancomycin must be administered orally because intravenous administration does not achieve gut lumen minimum therapeutic concentration. Patients unresponsive to Metronidazole can be placed on 14 days of Vancomycin followed by Rifaximin for another 14 days. A more recent study by Zar and others showed no difference between vancomycin and metronidazole in mild disease, but that vancomycin was superior to metronidazole for treating severe disease. In this study, severe disease was defined on a point score: One point each was given for age >60 years, temperature >38.3?C, albumin level 15,000 cells/mm3 within 48 h of enrollment. Two points were given for endoscopic evidence of pseudomembranous colitis or treatment in the intensive care unit. Severe disease was defined as 2 or more points on this score. The main criticism of this study is that a low, non-standard dose of metronidazole (250 mg) was used instead of (500 mg). Fidaxomicin has been found to be equally effective as vancomycin In March 2012, 'The Lancet Infectious Diseases' published a double blind study made at the University of Cologne proving that the enduring treatment success of Fidaxomicin is better than the previous medication. Its tolerability showed as good as Vancomycin. Fidaxomicin has been approved in the USA since May 2011 and in Europe since December 2011 for the treatment of adults with CDI. Drugs used to stop diarrhea frequently worsen the course of C. difficile-related pseudomembranous colitis. Loperamide, diphenoxylate and bismuth compounds are contraindicated: slowing of fecal transit time is thought to result in extended toxin-associated damage. Cholestyramine, a powder drink (an ion exchange resin), which is occasionally used to lower cholesterol, is effective in binding both Toxin A and B, slowing bowel motility and helping prevent dehydration. The dosage can be 4 grams daily, to up to four doses a day; however caution should be exercised to prevent constipation, or drug interactions, most notably the binding of drugs by cholestyramine, preventing their absorption. Cholestyramine is not an anti-infective; it dramatically reduces many of the symptoms of a C. difficile infection, but it is not appropriate to use by itself, as it does not change the infection status. Cholestyramine is usually used in concert with vancomycin. Powdered banana flakes given twice daily are an alternative to cholestyramine, and allow for stool bulking.

PROBIOTICS

Treatment with probiotics ("good" intestinal flora) has also been shown effective. Provision of Saccharomyces boulardii (Florastor) or Lactobacillus acidophilus twice daily times 30 days along with antibiotics has been clinically shown to shorten the duration of diarrhea. A last-resort treatment in immunosuppressed patients is intravenous immunoglobulin (IVIG).

STOOL TRANSPLANT

Fecal bacteriotherapy, known in colloquial terms as stool transplant, a procedure related to probiotic research, has preliminarily been shown to cure the disease. It involves infusion of bacterial flora acquired from the feces of a healthy donor to reverse the bacterial imbalance responsible for the recurring nature of the infection. In fecal transplantation, donor stool is collected from a close relative who has been tested for a wide array of bacterial, viral, and parasitic pathogens. The stool is often mixed with saline or milk to achieve the desired consistency, then delivered through a colonoscope or retention enema, or through a nasogastric or nasoduodenal tube. The procedure replaces normal, healthy colonic flora that had been wiped out by antibiotics, and reestablishes the patient's resistance to colonization by Clostridium difficile. However, there is often patient resistance due to the perceived unpleasantness of the procedure that must be overcome first before proceeding with this often-effective treatment.

COLECTOMY

In those patients that develop systemic symptoms of CDC, colectomy may improve the outcome if performed before the need for vasopressors. There are currently over 150 published reports dating back to 1958, though many more have been performed. It has a success rate of about 90%. A guide was released in 2010 for home fecal transplantation.

RECURRENCE

The evolution of protocols for patients with recurrent C. difficile diarrhea also present a challenge: There is no known proper length of time or universally accepted alternative drugs with which one should be treated.[citation needed] However, re-treatment with metronidazole or vancomycin at the previous dose for 10 to 14 days is generally successful. The addition of rifampin to vancomycin also has been effective.

PROGNOSIS

PrognosisAfter a first treatment with metronidazole or vancomycin, Clostridium difficile recurs in about 20% of people. This increases to 40% and 60% with subsequent recurrences.

HISTORY

Initially named Bacillus difficilis by Hall and O'Toole in 1935 because it was resistant to early attempts at isolation and grew very slowly in culture, it was renamed in 1970.

SOCIETY AND CULTURE

NOTABLE OUTBREAKS

June 4, 2003, two outbreaks of a highly virulent strain of this bacterium were reported in Montreal, Quebec and Calgary, Alberta, in Canada. Sources put the death count as low as 36 and as high as 89, with approximately 1,400 cases in 2003 and within the first few months of 2004. C. difficile infections continued to be a problem in the Quebec healthcare system in late 2004. As of March 2005, it had spread into the Toronto, Ontario area, hospitalizing 10 people. One died while the others were being discharged. A similar outbreak took place at Stoke Mandeville Hospital in the United Kingdom between 2003 and 2005. The local epidemiology of C. difficile may offer clues on how its spread may relate to the amount of time a patient spends in hospital and/or a rehabilitation center. It also samples institutions' ability to detect increased rates, and their capacity to respond with more aggressive hand-washing campaigns, quarantine methods, and availability of yogurt containing live cultures to patients at risk for infection. It has been suggested that both the Canadian and English outbreaks were related to the seemingly more virulent Strain NAP1/027 of bacterium. This novel strain, also known as Quebec strain, has also been implicated in an epidemic at two Dutch hospitals (Harderwijk and Amersfoort, both 2005). A theory for explaining the increased virulence of 027 is that it is a hyperproducer of both toxins A and B, and that certain antibiotics may actually stimulate the bacteria to hyperproduce. October 1, 2006, C. difficile was said to have killed at least 49 people at hospitals in Leicester, England over eight months, according to a National Health Service investigation. Another 29 similar cases were investigated by coroners. A UK Department of Health memo leaked shortly afterwards revealed significant concern in government about the bacterium, described as being "endemic throughout the health service" October 27, 2006, 9 deaths were attributed to the bacterium in Quebec, Canada. November 18, 2006, the bacterium was reported to have been responsible for 12 deaths in Quebec, Canada. This 12th reported death was only two days after the St. Hyacinthe's Honor? Mercier announced that the outbreak was under control. Thirty-one patients were diagnosed with Clostridium difficile and four (as of Sat. Nov 18th) were still under observation. Cleaning crews took measures in an attempt to clear the outbreak. C. difficile was mentioned on 6,480 death certificates in 2006 in UK. February 27, 2007, a new outbreak was identified at Trillium Health Centre in Mississauga, Ontario, where 14 people were diagnosed with the bacteria. The bacteria were of the same strain as the one in Quebec. Officials have not been able to determine whether C. difficile was responsible for deaths of four patients over the prior two months. Between February and June 2007, three patients at Loughlinstown Hospital in Dublin, Ireland were found by the coroner to have died as a result of C. difficile infection. In an inquest, the Coroner's Court found that the hospital had no designated infection control team or consultant microbiologist on staff. Between June 2007 and August 2008, Northern Health & Social Care Trust Northern Ireland. Anrtim Area, Braid Valley, Mid Ulster Hospitals. During the enquiry expert reviewers concluded that C DIFF was implicated in 31 of these deaths, as the underlying cause in 15 and as a contributory cause in 16. During the time period the review also noted 375 instances of C DIFF infection in patients. October 2007, Maidstone and Tunbridge Wells NHS Trust was heavily criticized by the Healthcare Commission regarding its handling of a major outbreak of C. difficile in its hospitals in Kent from April 2004 to September 2006. In its report, the Commission estimated that about 90 patients "definitely or probably" died as a result of the infection. November 2007, the 027 strain has spread into several hospitals in southern Finland, with ten deaths out of 115 infected patients reported on 2007-12-14. November 2009, four deaths at Our Lady of Lourdes Hospital in Ireland, have possible links to Clostridium difficile infection. A further 12 patients tested positive for infection, and another 20 show signs of infection, 10 November 2009. March 2010, From February 2009 to February 2010 199 patients at Herlev hospital in Denmark was suspected of being infected with the 027 strain. In the first half of 2009, 29 died in hospitals in Copenhagen after they were infected with the bacterium May 2010, A total of 138 patients at four different hospitals in Denmark infected with the 027 strain ( Herlev, Amager, Gentofte and Hvidovre) plus some isolated occurrences at other hospitals. May 28, 2011 an outbreak in Ontario, Canada has been reported, with 26 fatalities as of July 24, 2011.

RESEARCH

GENOME SEQUENCING

The first complete genome sequence of a Clostridium difficile strain was first published in 2005 by Sanger Institute in the UK. This was of the C. difficile strain 630, a virulent and multidrug-resistant strain isolated in Switzerland in 1982. Scientists at Sanger Institute have also recently sequenced genomes of about 30 Clostridium difficile isolates using next generation sequencing technologies from 454 Life Sciences and Illumina. Researchers at McGill University in Montreal, Quebec sequenced the genome of the highly virulent Quebec strain of C. difficile in 2005 using ultra-high-throughput sequencing technology. The tests involved doing 400,000 DNA parallel-sequencing reactions of the bacterium's genome, which had been fragmented for sequencing. These sequences were assembled computationally to form a complete genome sequence.

TREATMENT

CDA-1 and CDB-1 (also known as MDX-066/MDX-1388 and MBL-CDA1/MBL-CDB1) is an investigational, monoclonal antibody combination co-developed by Medarex and Massachusetts Biologic Laboratories (MBL) to target and neutralize C. difficile toxins A and B, for the treatment of CDI. Merck & Co., Inc. gained worldwide rights to develop and commercialize CDA-1 and CDB-1 through an exclusive license agreement signed in April 2009. It is intended as an add-on therapy to one of the existing antibiotics to treat CDI. Nitazoxanide is a synthetic nitrothiazolyl-salicylamide derivative indicated as an antiprotozoal agent (FDA-approved for the treatment of infectious diarrhea caused by Cryptosporidium parvum and Giardia lamblia) and is also currently being studied in C. difficile infections vs. vancomycin. Rifaximin, is a clinical-stage semi synthetic, rifamycin-based non-systemic antibiotic for CDI. It is FDA-approved for the treatment of infectious diarrhea and being developed by Salix Pharmaceuticals. Rifalazil, Fidaxomicin, Tigecyclin and Ramoplanin.

For more information view the source:Wikipedia

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CONSTIPATION

Constipation (also known as costiveness, dyschezia, and dyssynergic defaecation) refers to bowel movements that are infrequent or hard to pass. Constipation is a common cause of painful defecation. Severe constipation includes obstipation (failure to pass stools or gas) and fecal impaction. Constipation is common; in the general population incidence of constipation varies from 2 to 30%. Constipation is a symptom with many causes. These causes are of two types: obstructed defecation and colonic slow transit (or hypomobility). About 50% of patients evaluated for constipation at tertiary referral hospitals have obstructed defecation. This type of constipation has mechanical and functional causes. Causes of colonic slow transit constipation include diet, hormones, side effects of medications, and heavy metal toxicity. Treatments include changes in dietary habits, laxatives, enemas, biofeedback, and surgery. Because constipation is a symptom, not a disease, effective treatment of constipation may require first determining the cause.

DEFINITION

The definition of constipation includes the following: infrequent bowel movements (typically three times or fewer per week) difficulty during defecation (straining during more than 25% of bowel movements or a subjective sensation of hard stools), or the sensation of incomplete bowel evacuation. The Rome III criteria are widely used to diagnose chronic constipation, and are helpful in separating cases of chronic functional constipation from less-serious instances.

CHILDREN

Constipation in children usually occurs at three distinct points in time: after starting formula or processed foods (while an infant), during toilet training in toddlerhood, and soon after starting school (as in a kindergarten) After birth, most infants pass 4-5 soft liquid bowel movements (BM) a day. Breast-fed infants usually tend to have more BM compared to formula-fed infants. Some breast-fed infants have a BM after each feed, whereas others have only one BM every 2-3 days. Infants who are breast-fed rarely develop constipation. By the age of two years, a child will usually have 1-2 bowel movements per day and by four years of age, a child will have one bowel movement per day.

CAUSES

The causes of constipation can be divided into congenital, primary, and secondary. The most common cause is primary and not life threatening. In the elderly, causes include: insufficient dietary fiber intake, inadequate fluid intake, decreased physical activity, side effects of medications, hypothyroidism, and obstruction by colorectal cancer. Constipation with no known organic cause, i.e. no medical explanation, exhibits gender differences in prevalence: females are more often affected than males.

PRIMARY

Primary or functional constipation is ongoing symptoms for greater than six months not due to any underlying cause such as medication side effects or an underlying medical condition. It is not associated with abdominal pain thus distinguishing it from irritable bowel syndrome. It is the most common cause of constipation.

DIET

Constipation can be caused or exacerbated by a low fiber diet, low liquid intake, or dieting.

MEDICATION

Many medications have constipation as a side effect. Some include (but are not limited to); opioids (e.g. common pain killers), diuretics, antidepressants, antihistamines, antispasmodics, anticonvulsants, and aluminum antacids.

METABOLIC & MUSCULAR

Metabolic and endocrine problems which may lead to constipation include: hypercalcemia, hypothyroidism, diabetes mellitus, cystic fibrosis, and celiac disease. Constipation is also common in individuals with muscular and myotonic dystrophy.

STRUCTURAL AND FUNCTIONAL ABNORMALITIES

Constipation has a number of structural (mechanical, morphological, anatomical) causes, including: spinal cord lesions, Parkinsons, colon cancer, anal fissures, proctitis, and pelvic floor dysfunction. Constipation also has functional (neurological) causes, including anismus, descending perineum syndrome, and Hirschsprung's disease. In infants, Hirschsprung's disease is the most common medical disorder associated withconstipation. Anismus occurs in a small minority of persons with chronic constipation or obstructed defecation.

PSYCHOLOGICAL

Voluntary withholding of the stool is a common cause of constipation. The choice to withhold can be due to factors such as fear of pain, fear of public restrooms, or laziness. When a child holds in the stool a combination of encouragement, fluids, fiber, and laxatives may be useful to overcome the problem.

DIAGNOSIS

The diagnosis is essentially made from the patient's description of the symptoms. Bowel movements that are difficult to pass, very firm, or made up of small hard pellets (like those excreted by rabbits) qualify as constipation, even if they occur every day. Other symptoms related to constipation can include bloating, distension, abdominal pain, headaches, a feeling of fatigue and nervous exhaustion, or a sense of incomplete emptying. Inquiring about dietary habits will often reveal a low intake of dietary fiber, inadequate amounts of fluids, poor ambulation or immobility, or medications that are associated with constipation. During physical examination, scybala (manually palpable lumps of stool) may be detected on palpation of the abdomen. Rectal examination gives an impression of the anal sphincter tone and whether the lower rectum contains any feces or not. Rectal examination also gives information on the consistency of the stool, presence of hemorrhoids, admixture of blood and whether any tumors, polyps or abnormalities are present. Physical examination may be done manually by the physician, or by using a colonoscope. X-rays of the abdomen, generally only performed if bowel obstruction is suspected, may reveal extensive impacted fecal matter in the colon, and confirm or rule out other causes of similar symptoms. Chronic constipation (symptoms present at least three days per month for more than three months) associated with abdominal discomfort is often diagnosed as irritable bowel syndrome (IBS) when no obvious cause is found. Colonic propagating pressure wave sequences (PSs) are responsible for discrete movements of the bowel contents and are vital for normal defecation. Deficiencies in PS frequency, amplitude and extent of propagation are all implicated in severe defecatory dysfunction (SDD). Mechanisms that can normalise these aberrant motor patterns may help rectify the problem. Recently the novel therapy of sacral nerve stimulation (SNS) has been utilized for the treatment of severe constipation.

CRITERIA

The Rome II Criteria for constipation require at least two of the following symptoms for 12 weeks or more over the period of a year: Straining with more than one-fourth of defecations Hard stool with more than one-fourth of defecations Feeling of incomplete evacuation with more than one-fourth of defecations Sensation of anorectal obstruction with more than one-fourth of defecations Manual maneuvers to facilitate more than one-fourth of defecations Fewer than three bowel movements per week Insufficient criteria for irritable bowel syndrome.

PREVENTION

Constipation is usually easier to prevent than to treat. Following the relief of constipation, maintenance with adequate exercise, fluid intake, and high fiber diet is recommended. Children benefit from scheduled toilet breaks, once early in the morning and 30 minutes after meals.

TREATMENT

The main treatment of constipation involves the increased intake of water and fiber (either dietary or as supplements). The routine use of laxatives is discouraged, as having bowel movements may come to be dependent upon their use. Enemas can be used to provide a form of mechanical stimulation. However, enemas are generally useful only for stool in the rectum, not in the intestinal tract.

LAXATIVES

If laxatives are used, milk of magnesia is recommended as a first-line agent due to its low cost and safety. Stimulants should only be used if this is not effective. In cases of chronic constipation, prokinetics may be used to improve gastrointestinal motility. A number of new agents have shown positive outcomes in chronic constipation; these include prucalopride, and lubiprostone.

PHYSICAL INTERVENTION

Constipation that resists the above measures may require physical intervention such as manual disimpaction (the physical removal of impacted stool using the hands; see Fecal impaction).

PEDIATRIC

Lactulose and milk of magnesia have been compared with polyethylene glycol (PEG) in children. All had similar side effects, but PEG was more effective at treating constipation. Osmotic laxatives are recommended over stimulant laxatives.

PROGNOSIS

Complications that can arise from constipation include hemorrhoids, anal fissures, rectal prolapse, and fecal impaction.Straining to pass stool may lead to hemorrhoids. In later stages of constipation, the abdomen may become distended, hard and diffusely tender. Severe cases ("fecal impaction" or malignant constipation) may exhibit symptoms of bowel obstruction (vomiting, very tender abdomen) and encopresis, where soft stool from the small intestine bypasses the mass of impacted fecal matter in the colon.

EPIDEMIOLOGY

Constipation is the most common digestive complaint in the United States as per survey data.Depending on the definition employed, it occurs in 2% to 20% of the population. It is more common in women, the elderly and children. The reasons it occurs more frequently in the elderly is felt to be due to an increasing number of health problems as humans age and decreased physical activity. 12% of the population worldwide reports having constipation. Chronic constipation accounts for 3% of all visits annually to pediatric outpatient clinics. Constipation-related healthcare costs total $6.9 billion in the US annually. More than four million Americans have frequent constipation, accounting for 2.5 million physician visits a year. Around $725 million is spent on laxative products each year in America.

For more information view the source:Wikipedia

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CRYPTOSPORIDIUM PARVUM
Cryptosporidium is a microscopic parasite that causes the diarrheal disease cryptosporidiosis. Both the parasite and the disease are commonly known as "Crypto."

There are many species of Cryptosporidium that infect humans and animals. The parasite is protected by an outer shell that allows it to survive outside the body for long periods of time and makes it very tolerant to chlorine disinfection.

While this parasite can be spread in several different ways, water (drinking water and recreational water) is the most common method of transmission. Cryptosporidium is one of the most frequent causes of waterborne disease among humans in the United States.

EPIDEMIOLOGY & RISK FACTORS

Crypto lives in the intestine of infected humans or animals. An infected person or animal sheds Cryptosporidium parasites in the stool. Millions of Crypto parasites can be released in a bowel movement from an infected human or animal. Shedding begins when the symptoms begin and can last for weeks after the symptoms (e.g., diarrhea) stop. You can become infected after accidentally swallowing the parasite. Crypto may be found in soil, food, water, or surfaces that have been contaminated with the feces from infected humans or animals. Crypto is not spread by contact with blood. Crypto can be spread:
- By putting something in your mouth or accidentally swallowing something that has come in contact with the stool of a person or animal infected with Crypto.
Recreational water can be contaminated with sewage or feces from humans or animals.
- By swallowing water or beverages contaminated by stool from infected humans or animals.
- By eating uncooked food contaminated with Crypto. All fruits and vegetables you plan to eat raw should be thoroughly washed with uncontaminated water.
- By touching your mouth with contaminated hands. Hands can become contaminated through a variety of activities, such as:
- touching surfaces (e.g., toys, bathroom fixtures, changing tables, diaper pails) that have been contaminated by stool from an infected person,
- changing diapers,
- caring for an infected person, and
- handling an infected cow or calf.
- People with greater exposure to contaminated materials are more at risk for infection, such as:
- Children who attend day care centers, including diaper-aged children
- Child care workers
- Parents of infected children
- People who take care of other people with cryptosporidiosis
- International travelers
- Backpackers, hikers, and campers who drink unfiltered, untreated water
- People who drink from untreated shallow, unprotected wells
- People, including swimmers, who swallow water from contaminated sources
- People who handle infected cattle
- People exposed to human feces through sexual contact
Contaminated water may include water that has not been boiled or filtered, as well as contaminated recreational water sources. Several community-wide outbreaks of cryptosporidiosis have been linked to drinking municipal water or recreational water contaminated with Cryptosporidium.

Cryptosporidium parasites are found in every region of the United States and throughout the world. Travelers to developing countries may be at greater risk for infection because of poorer water treatment and food sanitation, but cryptosporidiosis occurs worldwide. In the United States, an estimated 748,000 cases of cryptosporidiosis occur each year.

Once infected, people with decreased immunity are most at risk for severe disease. The risk of developing severe disease may differ depending on each person's degree of immune suppression.

BIOLOGY

Causal Agent:

Many species of Cryptosporidium exist that infect humans and a wide range of animals. Although Cryptosporidium parvum and Cryptosporidium hominis (formerly known as C. parvum anthroponotic genotype or genotype 1) are the most prevalent species causing disease in humans, infections by C. felis, C. meleagridis, C. canis, and C. muris have also been reported.

Life Cycle:

Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces and possibly other routes such as respiratory secretions. Transmission of Cryptosporidium parvum and C. hominis occurs mainly through contact with contaminated water (e.g., drinking or recreational water). Occasionally food sources, such as chicken salad, may serve as vehicles for transmission. Many outbreaks in the United States have occurred in waterparks, community swimming pools, and day care centers. Zoonotic and anthroponotic transmission of C. parvum and anthroponotic transmission of C. hominisoccur through exposure to infected animals or exposure to water contaminated by feces of infected animals. Following ingestion (and possibly inhalation) by a suitable host, excystation occurs. The sporozoites are released and parasitize epithelial cells of the gastrointestinal tract or other tissues such as the respiratory tract. In these cells, the parasites undergo asexual multiplication (schizogony or merogony) and then sexual multiplication (gametogony) producing microgamonts (male) and macrogamonts (female). Upon fertilization of the macrogamonts by the microgametes, oocystdevelop that sporulate in the infected host. Two different types of oocysts are produced, the thick-walled, which is commonly excreted from the host, and the thin-walled oocyst, which is primarily involved in autoinfection. Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral transmission.

Life cycle image and information courtesy of DPDx.

DISEASE

Symptoms of cryptosporidiosis generally begin 2 to 10 days (average 7 days) after becoming infected with the parasite. The most common symptom of cryptosporidiosis is watery diarrhea. Other symptoms include:
- Stomach cramps or pain
- Dehydration
- Nausea
- Vomiting
- Fever
- Weight loss
Some people with Crypto will have no symptoms at all.

Symptoms usually last about 1 to 2 weeks (with a range of a few days to 4 or more weeks) in persons with healthy immune systems. Occasionally, people may experience a recurrence of symptoms after a brief period of recovery before the illness ends. Symptoms can come and go for up to 30 days. While the small intestine is the site most commonly affected, Cryptosporidium infections could possibly affect other areas of the digestive tract or the respiratory tract. People with weakened immune systems may develop serious, chronic, and sometimes fatal illness. Examples of people with weakened immune systems include:
- people with AIDS;
- those with inherited diseases that affect the immune system; and
- cancer and transplant patients who are taking certain immunosuppressive drugs.
The risk of developing severe disease may differ depending on each person's degree of immune suppression.

DIAGNOSIS

Diagnosis of cryptosporidiosis is made by examination of stool samples. Because detection of Cryptosporidium can be difficult, patients may be asked to submit several stool samples over several days. Most often, stool specimens are examined microscopically using different techniques (e.g., acid-fast staining, direct fluorescent antibody [DFA] , and/or enzyme immunoassays for detection of Cryptosporidium sp. antigens).

Molecular methods (e.g., polymerase chain reaction – PCR) are increasingly used in reference diagnostic labs, since they can be used to identify Cryptosporidium spp. at the species level. Tests for Cryptosporidium are not routinely done in most laboratories; therefore, health care providers should specifically request testing for this parasite.

PREVENTION AND CONTROL
- Practice good hygiene
- Wash hands with soap and water for at least 20 seconds, rubbing hands together vigorously and scrubbing all surfaces:
- Before preparing or eating food
- After using the toilet
- After changing diapers or cleaning up a child who has used the toilet
- Before and after tending to someone who is ill with diarrhea
- After handling an animal or animal waste
- At child care facilities
- To reduce the risk of disease transmission, children with diarrhea should be excluded from child care settings until the diarrhea has stopped.
- At recreational water venues (pools, interactive fountains, lakes, ocean)
- Protect others by not swimming if you are experiencing diarrhea (this is essential for children in diapers). If diagnosed with cryptosporidiosis, do not swim for at least 2 weeks after diarrhea stops.
- Shower before entering the water.
- Wash children thoroughly (especially their bottoms) with soap and water after they use the toilet or their diapers are changed and before they enter the water.
- Take children on frequent bathroom breaks and check their diapers often.
- Change diapers in the bathroom, not at the poolside.
- Around animals
- Minimize contact with the feces of all animals, particularly young animals.
- When cleaning up animal feces, wear disposable gloves, and always wash hands when finished.
- Wash hands after any contact with animals or their living areas.
- Wash hands after gardening, even if wearing gloves.
- Immunocompromised persons
- Avoid close contact with any person or animal that has cryptosporidiosis. Cryptosporidiosis can become a life threatening disease for immunocompromised persons.
- Do not handle animal feces because infection can be life threatening for immunocompromised persons.
- Avoid Water That Might Be Contaminated
- You may not be protected in a chlorinated recreational water venue (for example, swimming pool, water park, water play area, splash pad, spray pad) because Cryptosporidium is chlorine-resistant and can live for days in chlorine-treated water.
- Do not swallow water while swimming in swimming pools, hot tubs, interactive fountains, lakes, rivers, springs, ponds, streams or the ocean.
- Reduce contamination of treated recreational water venues by having pool operators install in-line secondary disinfection systems (for example, ultraviolet light, ozone) to inactive this chlorine-tolerant parasite.
- Do not drink untreated water from lakes, rivers, springs, ponds, streams, or shallow wells.
- Do not drink inadequately treated water or ice made from water during communitywide outbreaks caused by contaminated drinking water.
- Do not use or drink inadequately treated water or use ice when traveling in countries where the water supply might be unsafe.
- If the safety of drinking water is questionable (for example, outbreak, poor sanitation, lack of water treatment systems):
- Drink bottled water
- Disinfect it by heating the water to a rolling boil for 1 minute, or
- Use a filter that has been tested and rated by National Safety Foundation (NSF) Standard 53 or NSF Standard 58 for cyst and oocyst reduction; filtered water will need additional treatment to kill or inactivate bacteria and viruses
For more information view the source:Center for Disease Control

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DIARRHEA

Diarrhea, also spelled diarrhoea, is the condition of having three or more loose or liquid bowel movements per day. It is a common cause of death in developing countries and the second most common cause of infant deaths worldwide. The loss of fluids through diarrhea can cause dehydration and electrolyte imbalances. In 2009 diarrhea was estimated to have caused 1.1 million deaths in people aged 5 and over and 1.5 million deaths in children under the age of 5. Oral rehydration solutions and zinc tablets are the treatment of choice and have been estimated to have saved 50 million children in the past 25 years. Homemade solutions recommended by WHO include salted drinks (e.g. salted rice water or a salted yoghurt drink) and vegetable or chicken soup with salt. If available, supplemental potassium, as well as supplemental zinc, can be added to or given with this homemade solution. It's also recommended that persons with diarrhea, if able, continue or resume eating as this speeds recovery of normal intestinal function and generally leads to diarrhea of shorter duration. Clean plain water can be one of several fluids given. There are commercial solutions such as Pedialyte, and relief agencies such as UNICEF widely distribute packets of salts and sugar. A homemade solution can be made by adding between one-half to one teaspoon of salt (about 2-3 grams) and six teaspoons sugar (about 18 grams) to one liter of water. If the person drinks solutions with too much sugar or too much salt, these can draw fluid from the body to the bowel, cause osmotic diarrhea, and make dehydration worse. In a WHO publication, it's stated that a homemade Oral rehydration solution (ORS) should approximately have the taste of tears.

DEFINITION

Diarrhea is defined by the World Health Organization as having three or more loose or liquid stools per day, or as having more stools than is normal for that person.

SECRETORY

Secretory diarrhea means that there is an increase in the active secretion, or there is an inhibition of absorption. There is little to no structural damage. The most common cause of this type of diarrhea is a cholera toxin that stimulates the secretion of anions, especially chloride ions. Therefore, to maintain a charge balance in the lumen, sodium is carried with it, along with water. In this type of diarrhea intestinal fluid secretion is isotonic with plasma even during fasting. It continues even when there is no oral food intake.

OSMOTIC

Osmotic diarrhea occurs when too much water is drawn into the bowels. If a person drinks solutions with excessive sugar or excessive salt, these can draw water from the body into the bowel and cause osmotic diarrhea. Osmotic diarrhea can also be the result of maldigestion (e.g., pancreatic disease or Coeliac disease), in which the nutrients are left in the lumen to pull in water. Or it can be caused by osmotic laxatives (which work to alleviate constipation by drawing water into the bowels). In healthy individuals, too much magnesium or vitamin C or undigested lactose can produce osmotic diarrhea and distention of the bowel. A person who has lactose intolerance can have difficulty absorbing lactose after an extraordinarily high intake of dairy products. In persons who have fructose malabsorption, excess fructose intake can also cause diarrhea. High-fructose foods that also have a high glucose content are more absorbable and less likely to cause diarrhea. Sugar alcohols such as sorbitol (often found in sugar-free foods) are difficult for the body to absorb and, in large amounts, may lead to osmotic diarrhea. In most of these cases, osmotic diarrhea stops when offending agent (e.g. milk, sorbitol) is stopped.

EXUDATIVE

Exudative diarrhea occurs with the presence of blood and pus in the stool. This occurs with inflammatory bowel diseases, such as Crohn's disease or ulcerative colitis, and other severe infections such as E. coli or other forms of food poisoning.

MOTILITY-RELATED

Motility-related diarrhea is caused by the rapid movement of food through the intestines (hypermotility). If the food moves too quickly through the gastrointestinal tract, there is not enough time for sufficient nutrients and water to be absorbed. This can be due to a vagotomy or diabetic neuropathy, or a complication of menstruation[citation needed]. Hyperthyroidism can produce hypermotility and lead to pseudodiarrhea and occasionally real diarrhea. Diarrhea can be treated with antimotility agents (such as loperamide). Hypermotility can be observed in people who have had portions of their bowel removed, allowing less total time for absorption of nutrients.

INFLAMMATORY

Inflammatory diarrhea occurs when there is damage to the mucosal lining or brush border, which leads to a passive loss of protein-rich fluids, and a decreased ability to absorb these lost fluids. Features of all three of the other types of diarrhea can be found in this type of diarrhea. It can be caused by bacterial infections, viral infections, parasitic infections, or autoimmune problems such as inflammatory bowel diseases. It can also be caused by tuberculosis, colon cancer, and enteritis.

DYSENTARY

Generally, if there is blood visible in the stools, it is not diarrhea, but dysentery. The blood is trace of an invasion of bowel tissue. Dysentery is a symptom of, among others, Shigella, Entamoeba histolytica, and Salmonella.

DIFFERENTIAL DIAGNOSIS

Diarrhea is most commonly due to viral gastroenteritis with rotavirus, which accounts for 40% of cases in children under five. In travelers however bacterial infections predominate. Various toxins such as mushroom poisoning and drugs can also cause acute diarrhea. Chronic diarrhea can be the part of the presentations of a number of chronic medical conditions affecting the intestine. Common causes include ulcerative colitis, Crohn's disease, microscopic colitis, celiac disease, irritable bowel syndrome and bile acid malabsorption.

INFECTIONS

There are many causes of infectious diarrhea, which include viruses, bacteria and parasites. Norovirus is the most common cause of viral diarrhea in adults, but rotavirus is the most common cause in children under five years old.Adenovirus types 40 and 41, and astroviruses cause a significant number of infections. The bacterium Campylobacter is a common cause of bacterial diarrhea, but infections by Salmonellae, Shigellae and some strains of Escherichia coli (E.coli) are frequent. In the elderly, particularly those who have been treated with antibiotics for unrelated infections, a toxin produced by Clostridium difficile often causes severe diarrhea. Parasites do not often cause diarrhea except for the protozoan Giardia, which can cause chronic infections if these are not diagnosed and treated with drugs such as metronidazole, and Entamoeba histolytica. Other infectious agents such as parasites and bacterial toxins also occur. In sanitary living conditions where there is ample food and a supply of clean water, an otherwise healthy person usually recovers from viral infections in a few days. However, for ill or malnourished individuals, diarrhea can lead to severe dehydration and can become life-threatening.

MALABSORPTION

Malabsorption is the inability to absorb food fully, mostly from disorders in the small bowel, but also due to maldigestion from diseases of the pancreas. Causes include: enzyme deficiencies or mucosal abnormality, as in food allergy and food intolerance, e.g. celiac disease (gluten intolerance), lactose intolerance (intolerance to milk sugar, common in non-Europeans), and fructose malabsorption. pernicious anemia, or impaired bowel function due to the inability to absorb vitamin B12, loss of pancreatic secretions, which may be due to cystic fibrosis or pancreatitis, structural defects, like short bowel syndrome (surgically removed bowel) and radiation fibrosis, such as usually follows cancer treatment and other drugs, including agents used in chemotherapy; and certain drugs, like orlistat, which inhibits the absorption of fat. Inflammatory bowel diseaseMain article: Inflammatory bowel disease The two overlapping types here are of unknown origin: Ulcerative colitis is marked by chronic bloody diarrhea and inflammation mostly affects the distal colon near the rectum. Crohn's disease typically affects fairly well demarcated segments of bowel in the colon and often affects the end of the small bowel.

IRRITABLE BOWEL SYNDROME

Another possible cause of diarrhea is irritable bowel syndrome (IBS) which usually presents with abdominal discomfort relieved by defecation and unusual stool (diarrhea or constipation) for at least 3 days a week over the previous 3 months. Symptoms of diarrhea-predominant IBS can be managed through a combination of dietary changes, soluble fiber supplements, and/or medications such as loperamide or codeine. About 30% of patients with diarrhea-predominant IBS have bile acid malabsorption diagnosed with an abnormal SeHCAT test.

OTHER CAUSES

Diarrhea can be caused by chronic ethanol ingestion. Ischemic bowel disease. This usually affects older people and can be due to blocked arteries. Microscopic colitis, a type of inflammatory bowel disease where changes are only seen on histological examination of colonic biopsies. Bile salt malabsorption (primary bile acid diarrhea) where excessive bile acids in the colon produce a secretory diarrhea. Hormone-secreting tumors: some hormones (e.g., serotonin) can cause diarrhea if excreted in excess (usually from a tumor). Chronic mild diarrhea in infants and toddlers may occur with no obvious cause and with no other ill effects; this condition is called toddler's diarrhea.

PATHOPHYSIOLOGY

EVOLUTION

According to two researchers, Nesse and Williams, diarrhea may function as an evolved expulsion defense mechanism. As a result, if it is stopped, there might be a delay in recovery. They cite in support of this argument research published in 1973 which found that treating Shigella with the anti-diarrhea drug (Co-phenotrope, Lomotil) caused people to stay feverish twice as long as those not so treated. The researchers indeed themselves observed that: "Lomotil may be contraindicated in shigellosis. Diarrhea may represent a defense mechanism".

DIAGNOSTIC APPROACH

The following types of diarrhea may indicate further investigation is needed: In infants Moderate or severe diarrhea in young children Associated with blood Continues for more than two days Associated non-cramping abdominal pain, fever, weight loss, etc. In travelers In food handlers, because of the potential to infect others; In institutions such as hospitals, child care centers, or geriatric and convalescent homes. A severity score is used to aid diagnosis in children.

PREVENTION

A rotavirus vaccine decrease the rates of diarrhea in a population. New vaccines against rotavirus, Shigella, ETEC, and cholera are under development, as well as other causes of infectious diarrhea. Probiotics decrease the risk of diarrhea in those taking antibiotics. In institutions and in communities, interventions that promote hand washing lead to significant reductions in the incidence of diarrhea.

MANAGEMENT

In many cases of diarrhea, replacing lost fluid and salts is the only treatment needed. This is usually by mouth-oral rehydration therapy or, in severe cases, intravenously. Diet restrictions such as the BRAT diet are no longer recommended. Research does not support the limiting of milk to children as doing so has no effect on duration of diarrhea. Medications such as loperamide (Imodium) and bismuth subsalicylate may be beneficial; however they may be contraindicated in certain situations.

FLUIDS

To prevent dehydration and electrolyte loss, it is widely recommended a person begin drinking Oral Rehydration Solution (ORS) as soon as possible. This strategy adds modest amounts of sugar and salt to water. There are prepackaged ORS products available. A person can also use home products such as lightly salted soup and/or lightly salted water from the cooking of rice. Supplemental zinc and potassium are also helpful, but ORS should not be delayed in the case that these are not immediately available. Oral Rehydration Solution (ORS) can be used to prevent dehydration and in many cases is quite literally a life saver. Standard home solutions such as salted rice water, salted yogurt drinks, vegetable and chicken soups with salt can be given. Home solutions such as water in which cereal has been cooked, unsalted soup, green coconut water, weak tea (unsweetened), and unsweetened fresh fruit juices can have from half a teaspoon to full teaspoon of salt (from one-and-a-half to three grams) added per liter. Clean plain water can also be one of several fluids given. There are commercial solutions such as Pedialyte, and relief agencies such as UNICEF widely distribute packets of salts and sugar. A WHO publication for physicians recommends a homemade ORS consisting of one liter water with one teaspoon salt (3 grams) and two tablespoons sugar (18 grams) added (approximately the taste of tears). Rehydration Project recommends adding the same amount of sugar but only one-half a teaspoon of salt, stating that this more dilute approach is less risky with very little loss of effectiveness. Both agree that drinks with too much sugar or salt can make dehydration worse. Appropriate amounts of supplemental zinc and potassium should be added if available. But the availability of these should not delay rehydration. As WHO points out, the most important thing is to begin preventing dehydration as early as possible. In another example of prompt ORS hopefully preventing dehydration, CDC recommends for the treatment of cholera continuing to give Oral Rehydration Solution during travel to medical treatment. Vomiting often occurs during the first hour or two of treatment with ORS, especially if a child drinks the solution too quickly, but this seldom prevents successful rehydration since most of the fluid is still absorbed. WHO recommends that if a child vomits, to wait five or ten minutes and then start to give the solution again more slowly. WHO recommends a child with diarrhea continue to be fed. Continued feeding speeds the recovery of normal intestinal function. In contrast, children whose food is restricted, have diarrhea of longer duration and recover intestinal function more slowly. A child should also continue to be breastfed. And in the example of the treatment of cholera, CDC also recommends that persons continue to eat and children continue to be breastfed.

ANTIBIOTICS

While antibiotics are beneficial in certain types of acute diarrhea, they are usually not used except in specific situations. There are concerns that antibiotics may increase the risk of hemolytic uremic syndrome in people infected with Escherichia coli O157:H7. In resource poor countries, treatment with antibiotics may be beneficial. However, some bacteria are developing antibiotic resistance, particularly Shigella. Antibiotics can also cause diarrhea, and antibiotic-associated diarrhea is the most common adverse effect of treatment with general antibiotics.

BISMUTH COMPOUNDS

While bismuth compounds (Pepto-Bismol) decreased the number of bowel movements in those with travelers' diarrhea, they do not decrease the length of illness. These agents should only be used if bloody diarrhea is not present.

ANIT MOTILITY AGENTS

Anti motility agents like loperamide are effective at reducing the duration of diarrhea. Codeine is used in the treatment of diarrhea to slow down peristalsis and the passage of fecal material through the bowels - this means that more time is given for water to reabsorb back into the body, which gives a firmer stool, and also means that feces is passed less frequently.

BILE ACID SEQUESTRANTS

Bile acid sequestrants such as cholestyramine, colestipol and colesevelam can be effective in chronic diarrhea due to bile acid malabsorption. Therapeutic trials of these drugs are indicated in chronic diarrhea if bile acid malabsorption cannot be diagnosed with a specific test, such as SeHCAT retention.

ALTERNATIVE THERAPIES

Zinc supplementation benefits children suffering from diarrhea in developing countries, but only in infants over six months old. This supports the World Health Organisation guidelines for zinc, but not in the very young. Probiotics reduce the duration of symptoms by one day and reduced the chances of symptoms lasting longer than four days by 60%. The probiotic lactobacillus can help prevent antibiotic associated diarrhea in adults but possibly not children. For those who with lactose intolerance, taking digestive enzymes containing lactase when consuming dairy products is recommended.

EPIDEMIOLOGY

World wide in 2004 approximately 2.5 billion cases of diarrhea occurred which results in 1.5 million deaths among children under the age of five. Greater than half of these were in Africa and South Asia. This is down from a death rate of 5 million per year two decades ago. Diarrhea remains the second leading cause of death (16%) after pneumonia (17%) in this age group.

For more information view the source:Wikipedia

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DIENTAMOEBA FRAGILIS
DIENTAMOEBA FRAGILIS

Dientamoeba fragilis is a parasite that causes gastrointestinal problems. Despite its name, Dientamoeba fragilis is not an ameba but a flagellate. This protozoan parasite produces trophozoites; cysts have not been identified. Infection may be either symptomatic or asymptomatic.

FAQs

What is Dientamoeba fragilis?

Dientamoeba fragilis is a parasite that lives in the large intestine of humans. Infection is common worldwide, including in the United States.

What are the symptoms of infection with Dientamoeba fragilis?

Many infected people do not have any symptoms. The most common symptoms are diarrhea and abdominal pain. Loss of appetite and weight loss, nausea, and fatigue also are common. The infection does not spread from the intestine to other parts of the body.

What should I do if I think I might be infected?

See your health care provider.

How is infection with Dientamoeba fragilis diagnosed?

Your health care provider will ask you to provide stool samples for testing. Because the parasite is not always found in every stool sample, you might be asked to submit stool samples from more than one day. You might also be tested for pinworm eggs, which are commonly (but not always) found in persons infected with D. fragilis.

Is medication available to treat infection with Dientamoeba fragilis?

Yes. Safe and effective medications are available for D. fragilis infections.

How did I get infected with Dientamoeba fragilis?

This question is difficult to answer because we aren't sure how D. fragilis is spread. The parasite is fragile and probably cannot live very long in the environment. Infection might be spread by:
- Accidentally swallowing pinworm eggs (which might protect this fragile parasite) or the eggs of another parasite.
- Swallowing something, such as food or water, or touching to your mouth something contaminated with stool from someone infected with D. fragilis.
Who is at greatest risk for infection?

Anyone can become infected with this parasite. However, the risk for infection might be higher for people who have weak immune systems and those who live in or travel to settings with poor sanitary conditions.

How can I prevent Dientamoeba fragilis infection?
- Wash your hands with soap and warm water after using the toilet, changing diapers, and before preparing foods.
- Teach children the importance of washing hands to prevent infection.
BIOLOGY

Causal Agent:

Despite its name, Dientamoeba fragilis is not an ameba but a flagellate. This protozoan parasite produces trophozoites; cysts have not been identified. Infection may be either symptomatic or asymptomatic.

Life Cycle

The complete life cycle of this parasite has not yet been determined, but assumptions were made based on clinical data. To date, the cyst stage has not been identified in D. fragilis life cycle, and the trophozoite is the only stage found in stools of infected individuals. D. fragilis is probably transmitted by fecal-oral route.The and transmission via helminth eggs (e.g., Ascaris, Entamoeba spp has been postulated. Trophozoites of D. fragilis have characteristically one or two nuclei and it is found in children complaining of intestinal (e.g., intermittent diarrhea, abdominal pain) and other symptoms (e.g., nausea, anorexia, fatigue, malaise, poor weight gain).

Life cycle image and information courtesy of DPDx.

For more information view the source:Center for Disease Control

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DIPHYLLOBOTHRIUM LATUM

Diphyllobothrium latum and related species (the fish or broad tapeworm), the largest tapeworms that can infect people, can grow up to 30 feet long. While most infections are asymptomatic, complications include intestinal obstruction and gall bladder disease caused by migration of proglottids. Diagnosis is made by identification of eggs or segments of the tapeworm in a stool sample with a microscope. Safe and effective medications are available to treat Diphyllobothrium. Infections are acquired by eating raw or undercooked fish, usually from the Northern Hemisphere (Europe, newly independent states of the Former Soviet Union, North America, Asia), but cases have also Â been reported in Uganda and Chile. Fish infected with Diphyllobothrium larvae may be transported to and consumed in any area of the world. Adequately freezing or cooking fish will kill the parasite.

FAQs

What is Diphyllobothrium latum?

Diphyllobothrium latum and related species (the fish or broad tapeworm), the largest tapeworms that can infect people, can grow up to 30 feet long. Several other Diphyllobothrium species infect humans, but less frequently.

What are the signs and symptoms of Diphyllobothrium infection?

Most infections are asymptomatic. However symptoms can include abdominal discomfort, diarrhea, vomiting, and weight loss. Vitamin B12 deficiency leading to pernicious anemia may occur. Complications include intestinal obstruction and gall bladder disease caused by migration of proglottids.

What should I do if I think I might be infected?

See your health care provider.

How is infection with Diphyllobothrium diagnosed?

Diagnosis is made by identification of eggs or segments of the tapeworm in a stool sample with a microscope. Eggs are usually numerous, but more than one stool sample may be needed to find them.

Is medication available to treat infection with Diphyllobothrium infection?

Yes, safe and effective medications are available to treat Diphyllobothrium infection (praziquantel or niclosamide are used most often).

How did I get infected with Diphyllobothrium?

You got infected by eating raw or undercooked fish. Examples of fish include salmon, trout, perch, walleyed pike, and other species -- Â usually freshwater fish. Some fish such as salmon live in both fresh and salt water and can harbor Diphyllobothrium larvae. Lightly salted, smoked, or pickled fish also may contain infectious organisms.

Who is at greatest risk of infection?

Diphyllobothrium infection generally occurs in the Northern Hemisphere (Europe, newly independent states of the Former Soviet Union, North America, Asia), but has been reported in Uganda and Chile. Fish infected with Diphyllobothrium larvae may be transported to and consumed in any area of the world.

BIOLOGY

Causal Agent

The cestode Diphyllobothrium latum (the fish or broad tapeworm), the largest human tapeworm. Several other Diphyllobothrium species have been reported to infect humans, but less frequently; they include D. pacificum, D. cordatum, D. ursi, D. dendriticum, D. lanceolatum, D. dalliae, and D. yonagoensis.

Life Cycle:

Immature eggs are passed in feces. Under appropriate conditions, the eggs mature (approximately 18 to 20 days) and yield oncospheres which develop into a coracidia. After ingestion by a suitable freshwater crustaceanÂ (the copepod first intermediate host) the coracidia develop into procercoid larvae. Following ingestion of the copepod by a suitable second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum). The plerocercoid larvae are the infective stage for humans. Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection. Nevertheless, these small second intermediate hosts can be eaten by larger predator species, e.g., trout, perch, walleyed pike. In this case, the sparganum can migrate to the musculature of the larger predator fish and humans can acquire the disease by eating these later intermediate infected host fish raw or undercooked. After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms which will reside in the small intestine. The adults ofÂ D. latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex. The adults can reach more than 10 m in length, with more than 3,000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces. Eggs appear in the feces 5 to 6 weeks after infection. In addition to humans, many other mammals can also serve as definitive hosts for D. latum.

Life cycle image and information courtesy of DPDx.

For more information view the source:Center for Disease Control

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DIPYLIDIUM CANINUM
Dipylidium caninum, also called the cucumber tapeworm or the double-pore tapeworm, is a cyclophyllid cestode that infects organisms afflicted with fleas, including canids, felids, and pet-owners, especially children. Adult worms are about 18 inches long. Eggs (or “egg clusters” or “egg balls”) are passed in the host's feces and ingested by fleas, which are in turn ingested by another mammal after the tapeworm larvae partially develop. Examples of fleas that can spread D. caninum include: Ctenocephalides canis and Ctenocephalides felis.

As in all members of family Dipylidiidae, proglottids of the adult have genital pores on both sides (hence the name double-pore tapeworm). Each side has a set of male and female reproductive organs. The scolex has a rostellum with four rows of hooks, along with the four suckers that all cyclophyllid cestodes have. In cats, sometimes proglottids are visible hanging out of a cat's anus.

Inside fleas, eggs hatch and form oncosphere larvae that move through the wall of the flea intestine into the body cavity where they become cysticercoid larvae, which are infective to mammal hosts.

In children, infection causes diarrhea and restlessness. As with most tapeworm infections, the drugs of choice are niclosamide or praziquantel. The best way to prevent human infection is to treat infected animals and to kill fleas.

Although, D. Caninum is usually transferred via a flea, Trichodectes canis, the chewing louse of dogs, can also be the intermediate host for the tapeworm.

FAQs

What is the most common kind of tapeworm dogs and cats get?

The most common tapeworm of dogs and cats in the United States is called Dipylidium caninum. Infection is common and found throughout the world.

How did my pet get the Dipylidium tapeworm?

By swallowing a flea infected with a tapeworm larvae. A dog or cat may swallow a flea while self-grooming. Once the flea is digested by the dog or cat, the larval tapeworm is able to develop into an adult tapeworm.

The adult tapeworm is made up of many small segments, called proglottids, each about the size of a grain of rice. Adult tapeworms may measure 4-28 inches in length. As the tapeworm matures inside the intestine, these segments (proglottids) break off and pass into the stool.

How would I know if my pet has a tapeworm infection?

Although cats and dogs are rarely ill as a result of a Dipylidium tapeworm infection, the proglottids can sometimes be seen crawling near the anus or on the surface of a fresh bowel movement. Proglottids contain tapeworm eggs; these eggs are released into the environment when the proglottid dries out. The dried proglottids are small (about 2 mm), hard and yellowish in color and can sometimes be seen stuck to the fur around the pet's anus.

What kind of problems do tapeworms cause for the dog?

Tapeworms are not usually harmful to your pet. Weight loss may occur if your pet is heavily infected. Sometimes, an infected dog will & quot; scoot & quot; or drag its anus across the ground or carpet because the segments are irritating to the skin in this area.

Occasionally, a portion of this tapeworm will be passed when the dog vomits. If this happens, a worm several inches long may be seen.

How is tapeworm infection diagnosed in my pet?

Tapeworm infection is usually diagnosed when the moving segments are seen crawling around the anus or in a bowel movement. Dipylidium tapeworm eggs are rarely released into the feces and are therefore not usually detected by routine fecal exams performed by your veterinarian. Because of this, veterinarians depend on you to notify them of possible tapeworm infection in your pet.

Can I get a tapeworm infection from my pet?

Yes; however, the risk of infection with this tapeworm in humans is very low. For a person to become infected with Dipylidium, he or she must accidentally swallow an infected flea. Most reported cases involve children. The most effective way to prevent infections in pets and humans is through flea control. A child who is infected will usually pass proglottids (or what appears as rice) in a bowel movement or find them stuck to the skin around the anal area.

How is tapeworm infection treated?

Treatment for both animals and humans is simple and very effective. A prescription drug called praziquantel is given, either orally or by injection (pets only). The medication causes the tapeworm to dissolve within the intestine. Since the worm is usually digested before it passes, it may not be visible in your dog's stool. The drugs are generally well-tolerated.

What should I do if I think my child is infected with tapeworms?

See your health care provider for diagnosis and treatment.

How can tapeworm infection be prevented?

To reduce the likelihood of infection you should:
- Control fleas on your pet, and in their indoor and outdoor environments.
- Have your veterinarian treat your dogs and cats promptly if they have tapeworms.
- Clean up after your pet, especially in playgrounds and public parks. Bury the feces, or place it in a plastic bag and dispose of it in the trash.
- Do not allow children to play in areas that are soiled with pet or other animal feces.
- Teach children to always wash their hands after playing with dogs and cats, and after playing outdoors.
BIOLOGY

Causal Agent:

Dipylidium caninum (the double-pored dog tapeworm) mainly infects dogs and cats, but is occasionally found in humans.

Life Cycle:

Gravid proglottids are passed intact in the feces or emerge from the perianal region of the host. Subsequently they release typical egg packets. On rare occasions, proglottids rupture and egg packets are seen in stool samples. Following ingestion of an egg by the intermediate host (larval stages of the dog or cat flea Ctenocephalides spp.), an oncosphere is released into the flea's intestine. The oncosphere penetrates the intestinal wall, invades the insect's hemocoel (body cavity), and develops into a cysticercoid larva. The larva develops into an adult, and the adult flea harbours the infective cysticercoid. The vertebrate host becomes infected by ingesting the adult flea containing the cysticercoid. The dog is the principal definitive host for Dipylidium caninum. Other potential hosts include cats, foxes, and humans (mostly children). Humans acquire infection by ingesting the cysticercoid contaminated flea. This can be promulgated by close contact between children and their infected pets. In the small intestine of the vertebrate host the cysticercoid develops into the adult tapeworm which reaches maturity about 1 month after infection. The adult tapeworms (measuring up to 60 cm in length and 3 mm in width) reside in the small intestine of the host, where they each attach by their scolex. They produce proglottids (or segments) which have two genital pores (hence the name "double-pored" tapeworm). The proglottids mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool.

Life cycle image and information courtesy of DPDx.

For more information view the source:Center for Disease Control

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DRY COUGH

A cough is a sudden and often repetitively occurring reflex which helps to clear the large breathing passages from secretions, irritants, foreign particles and microbes. The cough reflex consists of three phases: an inhalation, a forced exhalation against a closed glottis, and a violent release of air from the lungs following opening of the glottis, usually accompanied by a distinctive sound. Coughing can happen voluntarily as well as involuntarily. Frequent coughing usually indicates the presence of a disease. Many viruses and bacteria benefit evolutionarily by causing the host to cough, which helps to spread the disease to new hosts. Most of the time, coughing is caused by a respiratory tract infection but can be triggered by choking, smoking, air pollution, asthma, gastroesophageal reflux disease, post-nasal drip, chronic bronchitis, lung tumors, heart failure and medications such as ACE inhibitors. Treatment should target the cause; for example, smoking cessation or discontinuing ACE inhibitors. Some people may be worried about serious illnesses, and reassurance may suffice. Cough suppressants such as codeine or dextromethorphan are frequently prescribed, but have been demonstrated to have little effect. Other treatment options may target airway inflammation or may promote mucus expectoration. As it is a natural protective reflex, suppressing the cough reflex might have damaging effects, especially if the cough is productive.

CLASSIFICATION

A cough can be classified by its duration, character, quality, and timing. The duration can be either acute(of sudden onset) if it is present less than three weeks, subacuteif it is present between three and eight weeks, and chronic when lasting longer than eight weeks. A cough can be non-productive (dry) or productive (when sputum is coughed up). It may occur only at night (then called nocturnal cough), during both night and day, or just during the day. A number of characteristic coughs exist. While these have not been found to be diagnostically useful in adults, they are of use in children. A barky cough is part of the common presentation of croup, while a staccato cough has been classically described with chlamydia pneumonia.

DIFFERENTIAL DIAGNOSIS

A cough in children may be either a normal physiological reflex or due to an underlying cause. In healthy children it may be normal in the absence of any disease to cough ten times a day.The most common cause of an acute or subacute cough is a viral respiratory tract infection. In adults with a chronic cough, i.e. a cough longer than 8 weeks, more than 90% of cases are due to post-nasal drip, asthma, eosinophilic bronchitis, and gastroesophageal reflux disease.The causes of chronic cough are similar in children with the addition of bacterial bronchitis.

INFECTIONS

A cough can be the result of a respiratory tract infection such as the common cold, pneumonia, pertussis, or tuberculosis. In the vast majority of cases, acute coughs, i.e. coughs shorter than 3 weeks, are due to the common cold. In people with a normal chest X-ray, tuberculosis is a rare finding. Pertussisis increasingly being recognised as a cause of troublesome coughing in adults. After a viral infection has cleared, the person may be left with a postinfectious cough. This typically is a dry, non-productive cough that produces no phlegm. Symptoms may include a tightness in the chest, and a tickle in the lungs. This cough may often persist for weeks after an illness.The cause of the cough may be inflammation similar to that observed in repetitive stress disorders such as carpal tunnel syndrome. The repetition of coughing produces inflammation which produces discomfort, which in turn produces more coughing creating a closed loop.Postinfectious cough typically does not respond to conventional cough treatments. Treatment consists of any anti-inflammatory medicine to treat the inflammation, and a cough suppressant to reduce frequency of the cough until inflammation clears. Inflammation may increase sensitivity to other existing issues such as allergies, and treatment of other causes of coughs (such as use of an air purifier or allergy medicines) may help speed recovery. A bronchodilator, which helps open up the airways, may also help treat this type of cough.

REACTIVE AIRWAY DISEASE

When coughing is the only complaint of a person who meets the criteria for asthma (bronchial hyperresponsivenessand reversibility), this is termed cough-variant asthma. Two related conditions are atopic cough and eosinophilic bronchitis. Atopic cough occurs in individuals with a family history of atopy, abundant eosinophilsin the sputum, but with normal airway function and responsiveness. Eosinophilic bronchitis is also characterized by eosinophilsin the sputum, without airway hyperresponsiveness or an atopic background. This condition responds to treatment with corticosteroids. Cough can also worsen in an acute exacerbation of chronic obstructive pulmonary disease. Asthma is a common cause of chronic cough in adults and children. Coughing may be the only symptom the person has from their asthma, or asthma symptoms may also include wheezing, shortness of breath, and a tight feeling in their chest. Depending on how severe the asthma is it can be treated with bronchodilators (medicine which causes the airways to open up) or inhaled steroids. Treatment of the asthma should make the cough go away. Chronic bronchitisis defined clinically as a persistent cough that produces sputum (phlegm) and mucus, for at least three months in two consecutive years. Chronic bronchitis is often the cause of smoker's cough. The tobacco causes inflammation, secretion of mucus into the airway, and difficulty clearing that mucus out of the airways. Coughing helps clear those secretions out. May be treated by quitting smoking. May also be caused by Pneumoconiosis and long-term fume inhalation.

GASTROESOPHAGEAL REFLUX

In people with unexplained cough, gastroesophageal reflux disease should be considered. This occurs when acidic contents of the stomach come back up into the esophagus. Symptoms usually associated with GERD include heartburn, sour taste in the mouth, or a feeling of acid reflux in the chest, although, more than half of the people with cough from GERD don't have any other symptoms. An esophageal pH monitor can confirm the diagnosis of GERD. Sometimes GERD can complicate respiratory ailments related to cough, such as asthma or bronchitis. The treatment involves anti-acid medications and lifestyle changes with surgery indicated in cases not manageable with conservative measures.

AIR POLLUTION

Coughing may be caused by air pollution including tobacco smoke, particulate matter, irritant gases, and dampness in the home.The human health effects of poor air quality are far reaching, but principally affect the body's respiratory system and the cardiovascular system. Individual reactions to air pollutants depend on the type of pollutant a person is exposed to, the degree of exposure, the individual's health status and genetics. People who exercise outdoors, for example, on hot, smoggy days increase their exposure to pollutants in the air.

FOREIGN BODY

A foreign body can sometimes be suspected, for example if the cough started suddenly when the patient was eating. Rarely, sutures left behind inside the airway branches can cause coughing. A cough can be triggered by dryness from mouth breathingor recurrent aspiration of food into the windpipe in people with swallowing difficulties.

ACE INHIBITOR

Angiotensin-converting enzyme inhibitors are drugs used in diabetics, heart disease, and high blood pressure. In 10-25% of the people who take it, it can cause them to have a cough as a side effect. Stopping the drug is the only way to make the cough go away. Such medicines for hypertension are very common in use such as ramipril and quinapril. There are cases of "cough of unknown origin" who had resolution with stopping the drug.

PSYCHOGENIC COUGH

A psychogenic cough("habit cough" or "tic cough") may be the cause in the absence of a physical problem. In these instances emotional and psychological problems are suspected. However, other illnesses have to be ruled out before a firm diagnosis of psychogenic cough is made. Psychogenic cough is thought to be more common in children than in adults. A possible scenario: psychogenic cough develops in a child who has a chronically ill brother or sister.

OTHER

Cough may also be caused by conditions affecting the lung tissue such as bronchiectasis, cystic fibrosis, interstitial lung diseases and sarcoidosis. Coughing can also be triggered by benign or malignant lung tumorsor mediastinal masses. Through irritation of the nerve, diseases of the external auditory canal (wax, for example) can also cause cough. Cardiovascular diseases associated with cough are heart failure, pulmonary infarction and aortic aneurysm. Nocturnal cough is associated with heart failure, as the heart does not compensate for the increased volume shift to the pulmonary circulation, in turn causing pulmonary edema and resultant cough.Other causes of nocturnal cough include asthma, post-nasal drip and gastroesophageal reflux disease (GERD).Another cause of cough occurring preferentially in supine position is recurrent aspiration. Coughing may also be used for social reasons, such as the coughing before giving a speech. Cough may also be psychogenic, which is different from habit coughing and tic coughing. Coughing may occur in tic disorders such as Tourette syndrome, although it should be distinguished from throat-clearing in this disorder. Given its irritant nature to mammal tissues, capsaicinis widely used to determine the cough threshold and as a tussive stimulant in clinical research of cough suppressants. Capsaicin is what makes chilli peppers spicy, and might explain why workers in factories with these vegetables can develop a cough. Coughing is not always involuntary, and can be used in social situations. Coughing can be used to attract attention, release internal psychological tension, or become a maladaptive displacement behavior. It is believed that the frequency of such coughing increases in environments vulnerable to psychological tension and social conflict. In such environments, coughing may become one of many displacement behaviors and/or defense mechanisms. Coughs can be a symptom to the common cold.

PATHOPHYSIOLOGY

Coughing is viewed as a public health issue.A cough is a protective reflexin healthy individuals which is influenced by psychological factors. The cough reflex is initiated by stimulation of two different classes of afferent nerves, namely the myelinated rapidly adapting receptors, and nonmyelinated C-fibers with endings in the lungs. However it is not certain that the stimulation of nonmyelinated C-fibers leads to cough with a reflex as it's meant in physiology(with its own five components): this stimulation may cause mast cells degranulation (through an asso-assonic reflex) and edema which may work as a stimulus for rapidly adapting receptors.

DIAGNOSTIC APPROACH

The determination of the cause of a cough usually begins by determining if it is specific or nonspecific in nature. A specific cough is one associated with other symptoms and further workup is dependent on these symptoms while a non specific cough occurs without other signs and symptoms. Further workup may include labs, x rays, and spirometry.

TREATMENT

The treatment of a cough in children is based on the underlying cause with the use of cough medicine supported by little evidence and thus not recommended by the American Academy of Pediatrics. A trial of antibiotics or inhaled corticosteroids may be tried in children with a chronic cough in an attempt to treat protracted bacterial bronchitis or asthma respectively.

COMPLICATIONS

The complications of coughing can be classified as either acute or chronic. Acute complications include cough syncope (fainting spells due to decreased blood flow to the brain when coughs are prolonged and forceful), insomnia, cough-induced vomiting, rupture of blebs causing spontaneous pneumothorax(although this still remains to be proven), subconjunctival hemorrhage or "red eye", coughing defecation and in women with a prolapsed uterus, cough urination. Chronic complications are common and include abdominal or pelvic hernias, fatigue fractures of lower ribs and costochondritis.

EPIDEMIOLOGY

A cough is the most common reason for visiting a primary care physician in the United States.

For more information view the source:Wikipedia

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ECHINOCOCCUS

The genus Echinococcus includes six species of cyclophyllid tapeworms to date, of the family Taeniidae. Infection with Echinococcus results in hydatid disease, also known as echinococcosis. Echinococcus is triploblastic, i.e. it has 3 layers- outermost ectoderm, middle mesoderm and inner endoderm. Anus is absent; and no digestive system. Body is covered by tegument and the worm is divided into scolex, short neck and 3-6 proglottids. Body is ribbon-like. In humans, this causes a disease called echinococcosis. There are 3 types of echinococcosis i.e. cystic echinococcosis caused by Echinococcus granulosus, alveolar echinococcosis caused by E. multilocularis and polycystic echinococcosis caused by E. vogeli and/or E. oligarthrus. Incubation period is usually long and can be up to 50 years. Cystic echinococcosis is mostly found in South and Central America, Africa, the Middle East, China, Italy, Spain, Greece, Russia and the West of the United States (e.g. Arizona, New Mexico and California). Echinococcosis is a zoonosis; humans are dead-end hosts. The definitive hosts are carnivorous predators - dogs, wolves, foxes, lions. The adult tapeworm lives in their small intestine and delivers eggs that are excreted with the stool. The intermediate hosts are infected by ingesting eggs. Sheep, goat, cattle, camel, pig, wild herbivores and rodents are the usual intermediate hosts, but humans can also be infected. The egg hatches in the digestive system of the intermediate host, producing planula larva. It penetrates the intestinal wall and is carried by bloodstream to liver, lung, brain or another organ. It settles there and turns into a bladder-like structure called hydatid cyst. From the inner lining of its wall, protoscoleces (i.e. scoleces with invaginated tissue layers) bud and protrude into the fluid that is filling the cyst. After the death of the normal intermediate host, its body can be eaten by carnivores suitable as definitive hosts. In their small intestine, protoscoleces turn inside out, attach and give rise to adult tapeworms, completing the life cycle. In humans, the cysts persist and grow for years. They are regularly found in the liver (and every possible organ: spleen, kidney, bone, brain, tongue and skin) and are asymptomatic until their growing size produces symptoms or are accidentally discovered. Disruption of the cysts (spontaneous or iatrogenic e.g. liver biopsy) can be life threatening due to anaphylactic shock. Cysts are detected with ultrasound, CT or other imaging techniques. Anti-echinococcus antibodies can be detected with serodiagnostic tests e.g. Indirect Fluorescent Antibody (IFA) Test, CF (complement fixation), ELISA, Western Blot and other methods.

For more information view the source:Wikipedia

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ECZEMA

Eczema or atopic dermatitis (from Greek ekzema, "to boil over") is a form of dermatitis, or inflammation of the epidermis (the outer layer of the skin). The term eczema is broadly applied to a range of persistent skin conditions. These include dryness and recurring skin rashes that are characterized by one or more of these symptoms: redness, skin edema (swelling), itching and dryness, crusting, flaking, blistering, cracking, oozing, or bleeding. Areas of temporary skin discoloration may appear and are sometimes due to healed injuries. Scratching open a healing lesion may result in scarring and may enlarge the rash. The word eczema comes from Greek words, that mean "to boil over". Dermatitis comes from the Greek word for skin – and both terms refer to exactly the same skin condition. In some languages, dermatitis and eczema are synonymous, while in other languages dermatitis implies an acute condition and "eczema" a chronic one. The two conditions are often classified together.

CLASSIFICATION

The term eczema refers to a set of clinical characteristics. Classification of the underlying diseases has been haphazard and unsystematic, with many synonyms used to describe the same condition. A type of eczema may be described by location (e.g., hand eczema), by specific appearance (eczema craquele or discoid), or by possible cause (varicose eczema). Further adding to the confusion, many sources use the term eczema for the most common type of eczema (atopic dermatitis) interchangeably. The European Academy of Allergology and Clinical Immunology (EAACI) published a position paper in 2001 which simplifies the nomenclature of allergy-related diseases including atopic and allergic contact eczemas. Non-allergic eczemas are not affected by this proposal. The classifications below is ordered by incidence frequency.

COMMON

Atopic eczema (aka infantile e., flexural e., atopic dermatitis) is an allergic disease believed to have a hereditary component and often runs in families whose members also have asthma. Itchy rash is particularly noticeable on head and scalp, neck, inside of elbows, behind knees, and buttocks. Experts are urging doctors to be more vigilant in weeding out cases that are, in actuality, irritant contact dermatitis. It is very common in developed countries, and rising. Contact dermatitis is of two types: allergic (resulting from a delayed reaction to some allergen, such as poison ivy or nickel), and irritant (resulting from direct reaction to a detergent, such as sodium lauryl sulfate, for example). Some substances act both as allergen and irritant (wet cement, for example). Other substances cause a problem after sunlight exposure, bringing on phototoxic dermatitis. About three quarters of cases of contact eczema are of the irritant type, which is the most common occupational skin disease. Contact eczema is curable, provided the offending substance can be avoided and its traces removed from one's environment. Xerotic eczema (aka asteatotic e., e. craquele or craquelatum, winter itch, pruritus hiemalis) is dry skin that becomes so serious it turns into eczema. It worsens in dry winter weather, and limbs and trunk are most often affected. The itchy, tender skin resembles a dry, cracked, river bed. This disorder is very common among the older population. Ichthyosis is a related disorder. Seborrhoeic dermatitis or Seborrheic dermatitis ("cradle cap" in infants) is a condition sometimes classified as a form of eczema that is closely related to dandruff. It causes dry or greasy peeling of the scalp, eyebrows, and face, and sometimes trunk. The condition is harmless except in severe cases of cradle cap. In newborns it causes a thick, yellow crusty scalp rash called cradle cap, which seems related to lack of biotin and is often curable.

LESS COMMON

Dyshidrosis (aka dyshidrotic e., pompholyx, vesicular palmoplantar dermatitis, housewife's eczema) only occurs on palms, soles, and sides of fingers and toes. Tiny opaque bumps called vesicles, thickening, and cracks are accompanied by itching, which gets worse at night. A common type of hand eczema, it worsens in warm weather. Discoid eczema (aka nummular e., exudative e., microbial e.) is characterized by round spots of oozing or dry rash, with clear boundaries, often on lower legs. It is usually worse in winter. Cause is unknown, and the condition tends to come and go. Venous eczema (aka gravitational e., stasis dermatitis, varicose e.) occurs in people with impaired circulation, varicose veins and edema, and is particularly common in the ankle area of people over 50. There is redness, scaling, darkening of the skin and itching. The disorder predisposes to leg ulcers. Dermatitis herpetiformis (aka Duhring's Disease) causes intensely itchy and typically symmetrical rash on arms, thighs, knees, and back. It is directly related to celiac disease, can often be put into remission with appropriate diet, and tends to get worse at night. Neurodermatitis (aka lichen simplex chronicus, localized scratch dermatitis) is an itchy area of thickened, pigmented eczema patch that results from habitual rubbing and scratching. Usually there is only one spot. Often curable through behavior modification and anti-inflammatory medication. Prurigo nodularis is a related disorder showing multiple lumps. Autoeczematization (aka id reaction, autosensitization) is an eczematous reaction to an infection with parasites, fungi, bacteria or viruses. It is completely curable with the clearance of the original infection that caused it. The appearance varies depending on the cause. It always occurs some distance away from the original infection. There are also eczemas overlaid by viral infections (e. herpeticum, e. vaccinatum), and eczemas resulting from underlying disease (e.g. lymphoma). Eczemas originating from ingestion of medications, foods, and chemicals, have not yet been clearly systematized. Other rare eczematous disorders exist in addition to those listed here.

CAUSE

The cause of eczema is unknown but is presumed to be a combination of genetic and environmental factors. The hygiene hypothesis postulates that the cause of asthma, eczema, and other allergic diseases is an unusually clean environment. It is supported by epidemiologic studies for asthma. The hypothesis states that exposure to bacteria and other immune system modulators is important during development, and missing out on this exposure increases risk for asthma and allergy. While it has been suggested that eczema may sometimes be an allergic reaction to the excrement from house dust mites, with up to 5% of people showing antibodies to the mites, the overall role this plays awaits further corroboration. Researchers have compared the prevalence of eczema in people who also suffer from celiac disease to eczema prevalence in control subjects, and they've found that eczema occurs about three times more frequently in celiac disease patients and about two times more frequently in relatives of celiac patients, potentially indicating a genetic link between the two conditions.

DIAGNOSIS

Diagnosis of eczema is based mostly on history and physical examination. However, in uncertain cases, skin biopsy may be useful.

PREVENTION

Those with eczema should not get the smallpox vaccination due to risk of developing eczema vaccinatum, a potentially severe and sometimes fatal complication.

TREATMENT

There is no known cure for eczema; therefore, treatments aim to control the symptoms by reducing inflammation and relieving itching

MEDICATIONS

CORTICOSTERIODS

Corticosteroids are highly effective in controlling or suppressing symptoms in most cases. For mild-moderate eczema a weak steroid may be used (e.g. hydrocortisone), while in more severe cases a higher-potency steroid (e.g. clobetasol propionate) may be used. In severe cases, oral or injectable corticosteroids may be used. While these usually bring about rapid improvements, they have greater side effects. Prolonged use of topical corticosteroids is thought to increase the risk of side effects, the most common of which is the skin becoming thin and fragile (atrophy). Because of this, if used on the face or other delicate skin, only a low-strength steroid should be used. Additionally, high-strength steroids used over large areas, or under occlusion, may be significantly absorbed into the body, causing hypothalamic-pituitary-adrenal axis suppression (HPA axis suppression). Finally by their immunosuppressive action they can, if used without antibiotics or antifungal drugs, lead to some skin infections (fungal or bacterial). Care must be taken to avoid the eyes, as topical corticosteroids applied to the eye can cause glaucoma or cataracts. Because of the risks associated with this type of drug, a steroid of an appropriate strength should be sparingly applied only to control an episode of eczema. Once the desired response has been achieved, it should be discontinued and replaced with emollients as maintenance therapy. Corticosteroids are generally considered safe to use in the short- to medium-term for controlling eczema, with no significant side effects differing from treatment with non-steroidal ointment. Some recent research claims that topically applied corticosteroids did not significantly increase the risk of skin thinning, stretch marks or HPA axis suppression (and where such suppression did occur, it was mild and reversible where the corticosteroids were used for limited periods of time). Further, skin conditions are often under-treated because of fears of side effects. This has led some researchers to suggest that the usual dosage instructions should be changed from "Use sparingly" to "Apply enough to cover affected areas", and that specific dosage directions using "fingertip units" or FTUs be provided, along with photos to illustrate FTUs. However, caution must always be used as long-term use, prolonged widespread coverage, or use with occlusion, can create side effects that are permanent and resistant to treatment.

TOPICAL IMMUNOSUPPRESSANTS

Topical immunosuppressants like pimecrolimus (Elidel and Douglan) and tacrolimus (Protopic) were developed after topical corticosteroids had come into widespread use. These newer agents effectively suppress the immune system in the affected area, and appear to yield better results in some populations. The U.S. Food and Drug Administration has issued a public health advisory about the possible risk of lymph node or skin cancer from use of these products, but many professional medical organizations disagree with the FDA's findings; The postulation is that the immune system may help remove some pre-cancerous abnormal cells which is prevented by these drugs. However, any chronic inflammatory condition such as eczema, by the very nature of increased metabolism and cell replication, has a tiny associated risk of cancer (see Bowen's disease). Current practice by UK dermatologists is not to consider this a significant real concern and they are increasingly recommending the use of these new drugs. The dramatic improvement on the condition can significantly improve the quality of life of sufferers (and families kept awake by the distress of affected children). The major debate, in the UK, has been about the cost of such newer treatments and, given only finite NHS resources, when they are most appropriate to use. In addition to cancer risk, there are other potential side effects with this class of drugs. Adverse reactions including severe flushing, headaches, flu-like syndrome, photosensitive reactivity and possible drug interactions with a variety of medications, alcohol and grapefruit.

SYSTEMIC IMMUNOSUPPRESSANTS

When eczema is severe and does not respond to other forms of treatment, immunosuppressant drugs are sometimes prescribed. These dampen the immune system and can result in dramatic improvements to the patient's eczema. However, immunosuppressants can cause side effects on the body. As such, patients must undergo regular blood tests and be closely monitored by a doctor. In the UK, the most commonly used immunosuppressants for eczema are ciclosporin, azathioprine and methotrexate. These drugs were generally designed for other medical conditions but have been found to be effective against eczema.

ITCH RELIEF

Anti-itch drugs, often antihistamine, and dermasil may reduce the itch during a flare up of eczema, and the reduced scratching in turn reduces damage and irritation to the skin (the "itch cycle"). However, in some cases, significant benefit may be due to the sedative side effects of these drugs, rather than their specific antihistamine effect. Thus sedating antihistamines such as promethazine (Phenergan) or diphenhydramine (Benadryl) may be more effective at preventing night time scratching than the newer, nonsedating antihistamines. Capsaicin applied to the skin acts as a counter irritant (see gate control theory of nerve signal transmission). Hydrocortisone applied to the skin aids in temporary itch relief. Temporary yet significant and fast-acting relief can be found by cooling the skin via water (swimming, cool water bath or wet washcloth), air (direct output of an air conditioning vent), or careful use of an ice pack (wrapped in soft smooth cloth, e.g., pillow case, to protect skin from damage).

MOISTURIZERS

Eczema can be exacerbated by dryness of the skin. Moisturizing is one of the most important self-care treatments for eczema. Keeping the affected area moistened can promote skin healing and relief of symptoms. Soaps and detergents should not be used on affected skin because they can strip natural skin oils and lead to excessive dryness. Moistening agents are called emollients. In general, it is best to match thicker ointments to the driest, flakiest skin. Light emollients may not have any effect on severely dry skin. Moisturizing gloves (gloves which keep emollients in contact with skin on the hands) can be worn while sleeping. Generally, twice-daily applications of emollients work best. Ointments, with less water content, stay on the skin longer and need fewer applications, but they can be greasy and inconvenient. Steroids may also be mixed in with ointments. For unbroken skin, direct application of waterproof tape with or without an emollient or prescription ointment can improve moisture levels and skin integrity which allows the skin to heal. This treatment regimen can also help prevent the skin from cracking, as well as put a stop to the itch cycle. The end result is reduced lichenification (the roughening of skin from repeated scratching). Taping works best on skin away from joints. There is a disagreement whether baths are desirable or a necessary evil. For example, the Mayo Clinic advises against daily baths to avoid skin drying. On the other hand, the American Academy of Dermatology claims "it is a common misconception that bathing dries the skin and should be kept to a bare minimum" and recommends bathing to hydrate skin. They even suggest up to 3 short baths a day for people with severe eczema. According to them, a moisturizer should be applied within 3 minutes to trap the moisture from bath in the skin. Anecdotal evidence suggested that soft water could have therapeutic effects for people with eczema currently using hard water. However, a trial involving 336 children with eczema showed no objective difference in outcomes between the children whose homes were fitted with a water softener and those without. Recently ceramides, which are the major lipid constituent of the stratum corneum, have been used in the treatment of eczema. They are often one of the ingredients of modern moisturizers. These lipids were also successfully produced synthetically in the laboratory. However, detergents are so ubiquitous in modern environments in items like tissues, and so persistent on surfaces, "safe" soaps are necessary to remove them from the skin in order to control eczema. Although most eczema recommendations use the terms "detergents" and "soaps" interchangeably, and tell eczema sufferers to avoid both, detergents and soaps are not the same and are not equally problematic to eczema sufferers. Detergents, which differ from soap in that they commonly have a sulfate polar group, increase the permeability of skin membranes in a way that soaps and water alone do not. Sodium lauryl sulfate, the most common household detergent, has been shown to amplify the allergenicity of other substances ("increase antigen penetration"). Unfortunately there is no one agreed-upon best kind of skin cleanser for eczema sufferers. Different clinical tests, sponsored by different personal product companies, unsurprisingly tout various brands as the most skin-friendly based on specific properties of various products and different underlying assumptions as to what really determines skin friendliness. The terms "hypoallergenic" and "doctor tested" are not regulated, and no research has been done showing that products labeled "hypoallergenic" are in fact less problematic than any others. It may be best to avoid soaps and detergent cleansers altogether, except for the armpits, groin and perianal areas, and use cheap bland emollients in the bath or shower.

LIFESTYLE

Various measures may reduce the amount of mite antigens, in particular swapping carpets for hard surfaces. However it is not clear whether such measures actually help with eczema. A controlled study suggested that a number of environmental factors such as air exchange rates, relative humidity and room temperature (but not the level of house dust mites) might have an effect on the condition.

LIGHT THERAPY

Light therapy (or deep penetrating light therapy) using ultraviolet light can help control eczema. UVA is mostly used, but UVB and Narrow Band UVB are also used. Overexposure to ultraviolet light carries its own risks, particularly potential skin cancer from exposure. When light therapy alone is found to be ineffective, the treatment is performed with the application (or ingestion) of a substance called psoralen. This PUVA (Psoralen UVA) combination therapy is termed photo-chemotherapy. Psoralens make the skin more sensitive to UV light, thus allowing lower doses of UVA to be used. However, the increased sensitivity to UV light also puts the patient at greater risk for skin cancer

DIET

Recent studies provide hints that food allergy may trigger atopic dermatitis. For these people, identifying the allergens could lead to an avoidance diet to help minimize symptoms, although this approach is still in an experimental stage. Dietary elements that have been reported to trigger eczema include dairy products, coffee (both caffeinated and decaffeinated), soybean products, eggs, nuts, wheat and maize (sweet corn), though food allergies may vary from person to person. However, in 2009, researchers at National Jewish Medical and Research Center found that eczema patients were especially prone to misdiagnosis of food allergies. A study led by researchers at the University of California, San Diego School of Medicine suggests that use of oral vitamin D3 supplements bolsters production of a protective chemical normally found in the skin, and may help prevent skin infections that are a common result of atopic dermatitis, the most common form of eczema. It can be noted that the production of vitamin D3 is catalyzed by UV radiation and may influence histocompatibility expression, correlating with both the seasonality of eczema and its relation to the immune system.

ALTERNATIVE THERAPIES

A number of alternative therapies are used for eczema including: Sulfur has been used for many years as a topical treatment in the alleviation of eczema, although this could be suppressive. It was fashionable in the Victorian and Edwardian eras. However, there is currently no scientific evidence for the claim that sulfur treatment relieves eczema. Probiotics are live microorganisms taken orally, such as the Lactobacillus bacteria found in yogurt. They are not effective for treating eczema in older populations, but some research points to some strains of beneficial microorganisms having the ability to prevent the triad of allergies, eczema and asthma, although in rare cases some species of probiotic bacteria have a very small risk of infection in those with poor immune system response. Traditional Chinese medicine: According to American Academy of Dermatology, while certain blends of Chinese herbal medicines have been proven effective in controlling eczema, they have also proven toxic with severe consequences. In Chinese Medicine diagnosis, eczema is often considered a manifestation of underlying ill health. Treatment aims to improve the overall health of the individual, therefore not only resolving the eczema but improving quality of life (energy level, digestion, disease resistance, etc.). A recent study published in the British Journal of Dermatology describes improvements in quality of life and reduced need for topical corticosteroid application. Another British trial with ten different plants traditionally used in Chinese medicine for eczema treatment suggest a benefit with herbal remedy, but reviewers noted that the blinding was not maintained, leaving the results invalid. Other remedies lacking scientific evidence include chiropractic spinal manipulation and acupuncture. Patients can also wear clothing designed specifically to manage the itching, scratching and peeling associated with eczema.

BEHAVIORAL APPROACH

In the 1980s, Swedish dermatologist Peter Noren developed a behavioural approach to the treatment of long term atopic eczema. This approach has been further developed by dermatologist Richard Staughton and psychiatrist Christopher Bridgett at the Chelsea and Westminster Hospital in London. Patients undergo a six-week monitored program involving scratch habit reversal and self-awareness of scratching levels. For long-term eczema sufferers, scratching can become habitual. Sometimes scratching becomes a reflex, resulting in scratching without conscious awareness, rather than from the feeling of itchiness itself. The habit reversal program is done in conjunction with the standard applied emollient/corticosteroid treatments so that the skin can heal. It also reduces future scratching, as well as reduces the likelihood of further flareups. The behavioural approach can give an eczema sufferer some control over the degree of severity of eczema.

EPIDEMIOLOGY

The lifetime clinician-recorded prevalence of eczema has been seen to peak in infancy, with female predominance of eczema presentations occurring during the reproductive period of 15–49 years. Although little data on the trend of eczema prevalence over time exists prior to the Second World War (1939–45), the prevalence of eczema has been found to have increased substantially in the latter half of the 20th Century, with eczema in school-aged children being found to increase between the late 1940s and 2000. A review of epidemiological data in the UK has also found an inexorable rise in the prevalence of eczema over time. Further recent increases in the incidence and lifetime prevalence of eczema in England have also been reported, such that an estimated 5,773,700 or about one in every nine people have been diagnosed with the disease by a clinician at some point in their lives.

For more information view the source:Wikipedia

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ENDOLIMAX NANA

Although much literature cites this parasite as a non-pathogen, there is much reason to believe that in some cases these "non-pathogenic" agents actually cause symptoms in patients, with no other infections or conditions that would explain their symptoms. Following is a list of a few references to support that statement: Cuffari C, Oligny L, Siedman EG, 1998 Dientamoeba fragilis masquerading as allergic colitis. J. Pediatr Gastroenterol Nutr 26: 16-20., Feigin, RD, Cherry, James, Demmler-Harrison, GJ, and Kaplan, SL. Feigin and Cherry's Textbook of Pediatric Infectious Diseases, 6th Edition; Ch. 223, Amin, OM, 2002. Seasonal Prevalence of Intestinal Parasites in the United States During 2000. Am J. Trop. Med. Hyg., 66(6), 799-803., Garcia LS, 2005. Diagnostic Medical Parasitology. Washington, DC: American Society for Microbiology. Pg. 9

BIOLOGY

CAUSAL AGENTS

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host. Entamoeba gingivalis is also considered nonpathogenic and resides in the oral cavity of the human host, in the gingival pockets at the base of the teeth.

LIFE CYCLE

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host . Both cysts and trophozoites of these species are passed in stool and considered diagnostic . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Colonization of the nonpathogenic amebae occurs after ingestion of mature cysts in fecally-contaminated food, water, or fomites . Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts, and both stages are passed in the feces . Because of the protection conferred by their cell walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment.

LIFE CYCLE (Entamoeba gingivalis):

There is no known cyst stage for Entamoeba gingivalis; trophozoites live in the oral cavity of humans, residing in the gingival pockets near the base of the teeth . They are not considered pathogenic, and feed on bacteria and other debris. Trophozoites are transmitted person-to-person orally by kissing or fomites (such as eating utensils) . The trophozoite stage of E. gingivalis is morphologically similar to that of E. histolytica, and the two should be differentiated, as both can be coughed up in sputum specimens (for the latter, when present in pulmonary abscesses).

GEOGRAPHIC DISTRIBUTION

All six species are distributed worldwide. Entamoeba polecki in nature is primarily a parasite of pigs and monkeys, and human infection is more prevalent in areas where the people have animal contact.

CLINICAL FEATURES

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic, although they have been found in the stool of patients presenting with diarrhea where no known pathogens were identified. Their presence in stool can be an indicator of fecal contamination of a food or water source, and does not rule-out the presence of other parasites. Entamoeba gingivalis is also considered nonpathogenic, but is found in about 95% of patients with gum disease and about 50% of patients with healthy gums.

LABORATORY DIAGNOSIS

For E. coli, E. hartmanni, E. polecki, E. nana, and I. buetschlii, identification is made by observing cysts and/or trophozoites in stool specimens, both concentrated wet mounts and permanent stained smears. Identification of E. gingivalis is made by the finding of trophozoites in scrapings of the gums and teeth. They may also be found in sputum in rare occasions. As such, it is important to differentiate them from the morphologically-similar trophozoites of E. histolytica, which may be found in sputum from pulmonary abscesses.

For more information view the source:Center for Disease Control

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ENDOLIMAX NANA CYSTS

Endolimax is a genus of amoebozoa that are found in the intestines of various animals, including the species E. nana found in humans. Originally thought to be non-pathogenic, studies suggest it can cause intermittent or chronic diarrhea. Additionally, it is very significant in medicine because it can provide false positives for other tests, notably the similar species Entamoeba histolytica, the pathogen responsible for amoebic dysentery, and because its presence indicates the host has consumed fecal material. It forms cysts with four nuclei which excyst in the body and become trophozoites. Endolimax nana nuclei have a large endosome somewhat off-center and small amounts of visible chromatin or none at all.

CYSTS

Cysts are small, with a spherical to ellipsoidal shape. Mature cysts contain four nuclei; immature cysts are rarely seen. These cysts measure 5-10 um, with a usual range of 6-8 um. In stained preparations, the nucleus has a distinct karysome that, while not as large as that seen in the trophozoite, is still larger than the karysome of the Entamoeba species. Peripheral chromatin is absent. Although the nuclei are not visible in unstained preparations, the karysomes are readily apparent in iodine-stained wet mounts. The cytoplasm may contain diffuse glycogen, and chromatid bodies are absent. Occasionally, small granules or inclusions may occur in the cytoplasm.

TROPHOZOITES

This stage is small, measuring 6-12 m, with an average range of 8-10 um. Living trophozoites are sluggish and generally non-progressive. The single nucleus sometimes is visible in unstained preparations. In stained organisms, the karyosome usually is large and irregularly shaped, but occasionally it may be fragmented or placed against one side of the nuclear membrane. There is no peripheral chromatin on the nuclear membrane. The cytoplasm, which is coarsely granular and often highly vacuolated, may contain bacteria.

For more information view the source:Wikipedia

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ENTAMOEBA COLI

Although much literature cites this parasite as a non-pathogen, there is much reason to believe that in some cases these "non-pathogenic" agents actually cause symptoms in patients, with no other infections or conditions that would explain their symptoms. Following is a list of a few references to support that statement: Cuffari C, Oligny L, Siedman EG, 1998 Dientamoeba fragilis masquerading as allergic colitis. J. Pediatr Gastroenterol Nutr 26: 16-20., Feigin, RD, Cherry, James, Demmler-Harrison, GJ, and Kaplan, SL. Feigin and Cherry's Textbook of Pediatric Infectious Diseases, 6th Edition; Ch. 223, Amin, OM, 2002. Seasonal Prevalence of Intestinal Parasites in the United States During 2000. Am J. Trop. Med. Hyg., 66(6), 799-803., Garcia LS, 2005. Diagnostic Medical Parasitology. Washington, DC: American Society for Microbiology. Pg. 9

BIOLOGY

CAUSAL AGENTS

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host. Entamoeba gingivalis is also considered nonpathogenic and resides in the oral cavity of the human host, in the gingival pockets at the base of the teeth.

LIFE CYCLE (nonpathogenic intestinal amebae):

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host . Both cysts and trophozoites of these species are passed in stool and considered diagnostic . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Colonization of the nonpathogenic amebae occurs after ingestion of mature cysts in fecally-contaminated food, water, or fomites . Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts, and both stages are passed in the feces . Because of the protection conferred by their cell walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment.

LIFE CYCLE (Entamoeba gingivalis):

There is no known cyst stage for Entamoeba gingivalis; trophozoites live in the oral cavity of humans, residing in the gingival pockets near the base of the teeth . They are not considered pathogenic, and feed on bacteria and other debris. Trophozoites are transmitted person-to-person orally by kissing or fomites (such as eating utensils) . The trophozoite stage of E. gingivalis is morphologically similar to that of E. histolytica, and the two should be differentiated, as both can be coughed up in sputum specimens (for the latter, when present in pulmonary abscesses).

GEOGRAPHIC DISTRIBUTION

All six species are distributed worldwide. Entamoeba polecki in nature is primarily a parasite of pigs and monkeys, and human infection is more prevalent in areas where the people have animal contact.

CLINICAL FEATURES

Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic, although they have been found in the stool of patients presenting with diarrhea where no known pathogens were identified. Their presence in stool can be an indicator of fecal contamination of a food or water source, and does not rule-out the presence of other parasites. Entamoeba gingivalis is also considered nonpathogenic, but is found in about 95% of patients with gum disease and about 50% of patients with healthy gums.

LABORATORY DIAGNOSIS

For E. coli, E. hartmanni, E. polecki, E. nana, and I. buetschlii, identification is made by observing cysts and/or trophozoites in stool specimens, both concentrated wet mounts and permanent stained smears. Identification of E. gingivalis is made by the finding of trophozoites in scrapings of the gums and teeth. They may also be found in sputum in rare occasions. As such, it is important to differentiate them from the morphologically-similar trophozoites of E. histolytica, which may be found in sputum from pulmonary abscesses.

For more information view the source:Center for Disease Control

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ENTAMOEBA HISTOLYTICA
Entamoeba histolytica is an anaerobic parasitic protozoan, part of the genus Entamoeba. Predominantly infecting humans and other primates, E. histolytica is estimated to infect about 50 million people worldwide. Previously, it was thought that 10% of the world population was infected, but these figures predate the recognition that at least 90% of these infections were due to a second species, E. dispar. Mammals such as dogs and cats can become infected transiently, but are not thought to contribute significantly to transmission.

FAQs

What is amebiasis?

Amebiasis is a disease caused by a one-celled parasite called Entamoeba histolytica.

Who is at risk for amebiasis?

Although anyone can have this disease, it is more common in people who live in tropical areas with poor sanitary conditions. In the United States, amebiasis is most common in:
- People who have traveled to tropical places that have poor sanitary conditions
- Immigrants from tropical countries that have poor sanitary conditions
- People who live in institutions that have poor sanitary conditions
- Men who have sex with men
How can I become infected with E. histolytica?

E. histolytica infection can occur when a person:
- Puts anything into their mouth that has touched the feces of a person who is infected with E. histolytica.
- Swallows something, such as water or food, that is contaminated with E. histolytica.
- Swallows E. histolytica cysts (eggs) picked up from contaminated surfaces or fingers.
What are the symptoms of amebiasis?

Only about 10% to 20% of people who are infected with E. histolytica become sick from the infection. The symptoms are often quite mild and can include loose feces (poop), stomach pain, and stomach cramping. Amebic dysentery is a severe form of amebiasis associated with stomach pain, bloody stools , and fever. Rarely, E. histolytica invades the liver and forms an abscess (a collection of pus). In a small number of instances, it has been shown to spread to other parts of the body, such as the lungs or brain, but this is very uncommon.

If I swallowed E. histolytica, how quickly would I become sick?

Only about 10% to 20% of people who are infected with E. histolytica become sick from the infection. Those people who do become sick usually develop symptoms within 2 to 4 weeks, though it can sometimes take longer.

What should I do if I think I have amebiasis?

See your health care provider.

How is amebiasis diagnosed?

Your health care provider will ask you to submit fecal samples. Because E. histolytica is not always found in every stool sample, you may be asked to submit several stool samples from several different days.

Diagnosis of amebiasis can be very difficult. One problem is that other parasites and cells can look very similar to E. histolytica when seen under a microscope. Therefore, sometimes people are told that they are infected with E. histolytica even though they are not. Entamoeba histolytica and another ameba, Entamoeba dispar, which is about 10 times more common, look the same when seen under a microscope. Unlike infection with E. histolytica, which sometimes makes people sick, infection with E. dispar does not make people sick and therefore does not need to be treated.

If you have been told that you are infected with E. histolytica but you are feeling fine, you might be infected with E. dispar instead. Unfortunately, most laboratories do not yet have the tests that can tell whether a person is infected with E. histolytica or with E. dispar. Until these tests become more widely available, it usually is best to assume that the parasite is E. histolytica.

A blood test is also available but is only recommended when your health care provider thinks that your infection may have spread beyond the intestine (gut) to some other organ of your body, such as the liver. However, this blood test may not be helpful in diagnosing your current illness because the test can be positive if you had amebiasis in the past, even if you are no longer infected now.

How is amebiasis treated?

Several antibiotics are available to treat amebiasis. Treatment must be prescribed by a physician. You will be treated with only one antibiotic if your E. histolytica infection has not made you sick. You probably will be treated with two antibiotics (first one and then the other) if your infection has made you sick.

I am going to travel to a country that has poor sanitary conditions. What should I eat and drink there so I will NOT become infected with E. histolytica or other such germs?

The following items are safe to drink:
- Bottled water
- Tap water that has been boiled for at least 1 minute
- Carbonated (bubbly) water from sealed cans or bottles
- Carbonated (bubbly) drinks (like soda) from sealed cans or bottles
*You can also make tap water safe for drinking by filtering it through an "absolute 1 micron or less" filter and dissolving chlorine, chlorine dioxide, or iodine tablets in the filtered water. "Absolute 1 micron" filters can be found in camping/outdoor supply stores.

The following items are NOT safe to drink or eat:
- Fountain drinks or any drinks with ice cubes
- Fresh fruit or vegetables that you did not peel yourself
- Milk, cheese, or dairy products that may not have been pasteurized.
- Anything sold by street vendors
Should I be concerned about spreading the infection to others?

Yes, but the risk of spreading infection is low if the infected person is treated with antibiotics and practices good personal hygiene. This includes thorough handwashing with soap and warm water after using the toilet, after changing diapers, and before handling food.

BIOLOGY

Causal Agent:

Several protozoan species in the genus Entamoeba colonize humans, but not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic ameba, associated with intestinal and extraintestinal infections. The other species are important because they may be confused with E. histolytica in diagnostic investigations.

Life Cycle

Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen (noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa (intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolytica and E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).

Life cycle image and information courtesy of DPDx.

For more information view the source:Center for Disease Control

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ENTEROBACTER

Enterobacter is a genus of common Gram-negative, facultatively anaerobic, rod-shaped bacteria of the family Enterobacteriaceae. Several strains of these bacteria are pathogenic and cause opportunistic infections in immunocompromised (usually hospitalized) hosts and in those who are on mechanical ventilation. The urinary and respiratory tracts are the most common sites of infection. It is also a fecal coliform, along with Escherichia. Two clinically important species from this genus are E. aerogenes and E. cloacae.

DIAGNOSIS

Its laboratory characteristics are lactose positive, indole negative and urease negative and is a non fecal coliform.

TREATMENT

1. Fourth generation of cephalosporin,a B-lactam antibiotic Cefepime 2. Imipenem (carbapenems) is of choice in enterobacter treatment. 3. Aminoglycosides such as amikacin have been found very effective as well. 4. Quinolones are an effective alternative.

LINKED TO OBESITY

In a recent study, over a 1/3 of gut bacteria in a morbidly obese volunteer was found to be Enterobacter. After 23 weeks, the volunteer lost almost 1/3 of his weight by virtually eliminating the bacteria via diet, while being prevented from exercising.

For more information view the source:Wikipedia

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ENTEROBIUS VERMICULARIS
Pinworm infection is caused by a small, thin, white roundworm called Enterobius vermicularis. Although pinworom infection can affect all people, it most commonly occurs among children, institutionalized persons, and household members of persons with pinworm infection. Pinworm infection is treatable with over-the-counter or prescription medication, but reinfection, which occurs easily, should be prevented.

FAQS

What is a pinworm?

A pinworm ("threadworm") is a small, thin, white roundworm (nematode) called Enterobius vermicularis that sometimes lives in the colon and rectum of humans. Pinworms are about the length of a staple. While an infected person sleeps, female pinworms leave the intestine through the anus and deposit their eggs on the surrounding skin.

What are the symptoms of a pinworm infection?

Pinworm infection (called enterobiasis or oxyuriasis) causes itching around the anus which can lead to difficulty sleeping and restlessness. Symptoms are caused by the female pinworm laying her eggs. Symptoms of pinworm infection usually are mild and some infected people have no symptoms.

Who is at risk for pinworm infection?

Pinworm infection occurs worldwide and affects persons of all ages and socioeconomic levels. It is the most common worm infection in the United States. Pinworm infection occurs most commonly among:
- school-aged and preschool-aged children,
- institutionalized persons, and
- household members and caretakers of persons with pinworm infection.
Pinworm infection often occurs in more than one person in household and institutional settings. Child care centers often are the site of cases of pinworm infection.

How is pinworm infection spread?

Pinworm infection is spread by the fecal-oral route, that is by the transfer of infective pinworm eggs from the anus to someoneâ€™s mouth, either directly by hand or indirectly through contaminated clothing, bedding, food, or other articles.

Pinworm eggs become infective within a few hours after being deposited on the skin around the anus and can survive for 2 to 3 weeks on clothing, bedding, or other objects. People become infected, usually unknowingly, by swallowing (ingesting) infective pinworm eggs that are on fingers, under fingernails, or on clothing, bedding, and other contaminated objects and surfaces. Because of their small size, pinworm eggs sometimes can become airborne and ingested while breathing.

Can my family become infected with pinworms from swimming pools?

Pinworm infections are rarely spread through the use of swimming pools. Pinworm infections occur when a person swallows pinworm eggs picked up from contaminated surfaces or fingers. Although chlorine levels found in pools are not high enough to kill pinworm eggs, the presence of a small number of pinworm eggs in thousands of gallons of water (the amount typically found in pools) makes the chance of infection unlikely.

My little kids like to co-bathe, could this be how they are becoming infected?

During this treatment time and two weeks after final treatment, it is a good idea to avoid co-bathing and the reuse or sharing of washcloths. Showering may be preferred to avoid possible contamination of bath water. Careful handling and frequent changing of underclothing, night clothes, towels, and bedding can help reduce infection, reinfection, and environmental contamination with pinworm eggs. These items should be laundered in hot water, especially after each treatment of the infected person and after each usage of washcloths until infection is cleared.

Did my pets give me pinworms / can I give pinworms to my pets?

No. Humans are considered to be the only hosts of E. vermicularis which is also known as the human pinworm.

How is pinworm infection diagnosed?

Itching during the night in a childs perianal area strongly suggests pinworm infection. Diagnosis is made by identifying the worm or its eggs. Worms can sometimes be seen on the skin near the anus or on underclothing, pyjamas, or sheets about 2 to 3 hours after falling asleep.

Pinworm eggs can be collected and examined using the tape test as soon as the person wakes up. This is done by firmly pressing the adhesive side of clear, transparent cellophane tape to the skin around the anus. The eggs stick to the tape and the tape can be placed on a slide and looked at under a microscope. Because washing/bathing or having a bowel movement can remove eggs from the skin, this test should be done as soon as the person wakes up in the morning before they wash, bathe, go to the toilet, or get dressed. The â€œtape testâ€? should be done on three consecutive mornings to increase the chance of finding pinworm eggs.

Because itching and scratching of the anal area is common in pinworm infection, samples taken from under the fingernails may also contain eggs. Pinworm eggs rarely are found in routine stool or urine samples.

How is pinworm infection treated?

Pinworm can be treated with either prescription or over-the-counter medications. A health care provider should be consulted before treating a suspected case of pinworm infection.

Treatment involves two doses of medication with the second dose being given 2 weeks after the first dose. All household contacts and caretakers of the infected person should be treated at the same time. Reinfection can occur easily so strict observance of good hand hygiene is essential (e.g. proper handwashing, maintaining clean short fingernails, avoiding nail biting, avoiding scratching the perianal area).

Daily morning bathing and daily changing of underwear helps removes a large proportion of eggs. Showering may be preferred to avoid possible contamination of bath water. Careful handling and frequent changing of underclothing, night clothes, towels, and bedding can help reduce infection, reinfection, and environmental contamination with pinworm eggs. These items should be laundered in hot water, especially after each treatment of the infected person and after each usage of washcloths until infection is cleared.

Should family and other close contacts of someone with pinworm also be treated for pinworm?

Yes. The infected person and all household contacts and caretakers of the infected person should be treated at the same time.

What should be done if the pinworm infection occurs again?

Reinfection occurs easily. Prevention always should be discussed at the time of treatment. Good hand hygiene is the most effective means of prevention. If pinworm infection occurs again, the infected person should be retreated with the same two-dose treatment. The infected personâ€™s household contacts and caretakers also should be treated. If pinworm infection continues to occur, the source of the infection should be sought and treated. Playmates, schoolmates, close contacts outside the home, and household members should be considered possible sources of infection. Each infected person should receive the recommended two-dose treatment.

How can pinworm infection and reinfection be prevented?

Strict observance of good hand hygiene is the most effective means of preventing pinworm infection. This includes washing hands with soap and warm water after using the toilet, changing diapers, and before handling food. Keep fingernails clean and short, avoid fingernail-biting, and avoid scratching the skin in the perianal area. Teach children the importance of washing hands to prevent infection.

Daily morning bathing and changing of underclothes helps remove a large proportion of pinworm eggs and can help prevent infection and reinfection. Showering may be preferred to avoid possible contamination of bath water. Careful handling (avoid shaking) and frequent laundering of underclothes, night clothes, towels, and bed sheets using hot water also helps reduce the chance of infection and reinfection by reducing environmental contamination with eggs.

Control can be difficult in child care centers and schools because the rate of reinfection is high. In institutions, mass and simultaneous treatment, repeated in 2 weeks, can be effective. Hand hygiene is the most effective method of prevention. Trimming and scrubbing the fingernails and bathing after treatment is important to help prevent reinfection and spread of pinworms.

EPIDEMIOLOGY & RISK FACTORS

Pinworm infections are more common within families with school-aged children, in primary caregivers of infected children, and in institutionalized children.

A person is infected with pinworms by ingesting pinworm eggs either directly or indirectly. These eggs are deposited around the anus by the worm and can be carried to common surfaces such as hands, toys, bedding, clothing, and toilet seats. By putting anyones contaminated hands (including ones own) around the mouth area or putting ones mouth on common contaminated surfaces, a person can ingest pinworm eggs and become infected with the pinworm parasite. Since pinworm eggs are so small, it is possible to ingest them while breathing.

Once someone has ingested pinworm eggs, there is an incubation period of 1 to 2 months or longer for the adult gravid female to mature in the small intestine. Once mature, the adult female worm migrates to the colon and lays eggs around the anus at night, when many of their hosts are asleep. People who are infected with pinworm can transfer the parasite to others for as long as there is a female pinworm depositing eggs on the perianal skin. A person can also re-infect themselves, or be re-infected by eggs from another person.

The people most likely to be infected with pinworm are children under 18, people who take care of infected children and people who are institutionalized. In these groups, the prevalence can reach 50%.

Pinworm is the most common worm infection in the United States. Humans are the only species that can transfer this parasite. Household pets like dogs and cats cannot become infected with human pinworms. Pinworm eggs can survive in the indoor environment for 2 to 3 weeks.

BIOLOGY

Causal Agent:

The nematode (roundworm) Enterobius vermicularis (previously Oxyuris vermicularis) also called human pinworm. (Adult females: 8 to 13 mm, adult male: 2 to 5 mm. )Â Humans are considered to be the only hosts of E. vermicularis. A second species, Enterobius gregorii, has been described and reported from Europe, Africa, and Asia. For all practical purposes, the morphology, life cycle, clinical presentation, and treatment of E. gregorii is identical to E. vermicularis.

Life Cycle:

Eggs are deposited on perianal folds. Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area. Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (e.g. , curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon. The time interval from ingestion of infective eggs to oviposition by the adult females is about one month. The life span of the adults is about two months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area. The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions. Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown.

Life cycle image and information courtesy of DPDx.

DISEASE

The most common clinical manifestation of a pinworm infection is an itchy anal region. When the infection is heavy, there can be a secondary bacterial infection due to the irritation and scratching of the anal area. Often the patient will complain of teeth grinding, and insomnia due to disturbed sleep, or even abdominal pain or appendicitis. Infection of the female genital tract has been well reported.

DIAGNOSIS

A person infected with pinworm is often asymptomatic, but itching around the anus is a common symptom. Diagnosis of pinworm can be reached from three simple techniques. The first option is to look for the worms in the perianal reqion 2 to 3 hours after the infected person is asleep. The second option is to touch the perianal skin with transparent tape to collect possible pinworm eggs around the anus first thing in the morning. If a person is infected, the eggs on the tape will be visible under a microscope. The tape method should be conducted on 3 consecutive mornings right after the infected person wakes up and before he/she does any washing. Since anal itching is a common symptom of pinworm, the third option for diagnosis is analyzing samples from under fingernails under a microscope. An infected person who has scratched the anal area may have picked up some pinworm eggs under the nails that could be used for diagnosis.

Since pinworm eggs and worms are often sparse in stool, examining stool samples is not recommended. Serologic tests are not available for diagnosing pinworm infections.

PREVENTION AND CONTROL

Washing your hands with soap and warm water after using the toilet, changing diapers, and before handling food is the most successful way to prevent pinworm infection. In order to stop the spread of pinworm and possible re-infection, people who are infected should bathe every morning to help remove a large amount of the eggs on the skin. Showering is a better method than taking a bath, because showering avoids potentially contaminating the bath water with pinworm eggs. Infected people should not co-bathe with others during their time of infection.

Also, infected people should comply with good hygiene practices such as washing their hands with soap and warm water after using the toilet, changing diapers, and before handling food. They should also cut fingernails regularly, and avoid biting the nails and scratching around the anus. Frequent changing of underclothes and bed linens first thing in the morning is a great way to prevent possible transmission of eggs in the environment and risk of reinfection. These items should not be shaken and carefully placed into a washer and laundered in hot water followed by a hot dryer to kill any eggs that may be there.

In institutions, day care centers, and schools, control of pinworm can be difficult, but mass drug administration during an outbreak can be successful. Teach children the importance of washing hands to prevent infection.

For more information view the source:Center for Disease Control

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ENTEROCOCCUS

Enterococcus is a genus of lactic acid bacteria of the phylum Firmicutes. Enterococci are Gram-positive cocci that often occur in pairs (diplococci) or short chains, and are difficult to distinguish from streptococci on physical characteristics alone. Two species are common commensal organisms in the intestines of humans: E. faecalis (90-95%) and E. faecium (5-10%). Rare clusters of infections occur with other species, including E. casseliflavus, E. gallinarum, and E. raffinosus.

PHYSIOLOGY AND CLASSIFICATION

Enterococci are facultative anaerobic organisms, i.e., they are capable of cellular respiration in both oxygen-rich and oxygen-poor environments. Though they are not capable of forming spores, enterococci are tolerant of a wide range of environmental conditions: extreme temperature (10-45°C), pH (4.5-10.0) and high sodium chloride concentrations. Enterococci typically exhibit gamma-hemolysis on sheep's blood agar.

HISTORY

Members of the genus Enterococcus were classified as Group D Streptococcus until 1984, when genomic DNA analysis indicated a separate genus classification would be appropriate.

PATHOLOGY

Important clinical infections caused by Enterococcus include urinary tract infections, bacteremia, bacterial endocarditis, diverticulitis, and meningitis. Sensitive strains of these bacteria can be treated with ampicillin and vancomycin. From a medical standpoint, an important feature of this genus is the high level of intrinsic antibiotic resistance. Some enterococci are intrinsically resistant to B-lactam-based antibiotics (penicillins,cephalosporins,carbapenems), as well as many aminoglycosides. In the last two decades, particularly virulent strains of Enterococcus that are resistant to vancomycin (vancomycin-resistant Enterococcus, or VRE) have emerged in nosocomial infections of hospitalized patients, especially in the US. Other developed countries, such as the UK, have been spared this epidemic, and, in 2005, Singapore managed to halt an epidemic of VRE.[citation needed] VRE may be treated with quinupristin/dalfopristin (Synercid) with response rates of approximately 70%.Tigecycline has also been shown to have anti-enterococcal activity as has rifampicin. Enterococcal meningitis is a rare complication of neurosurgery. It often requires treatment with intravenous or intrathecal vancomycin, yet it is debatable as to whether its use has any impact on outcome: the removal of any neurological devices is a crucial part of the management of these infections. New epidemiological evidence has shown that enterococci are major infectious agent in chronic bacterial prostatitis. Enterococci are able to form biofilm in the prostate gland making their eradication difficult.

WATER GUALITY

In bodies of water, the acceptable level of contamination is very low; for example in the state of Hawaii, and most of the United States, the limit for water off its beaches is a five-week geometric mean of 35 colony-forming units per 100 ml of water, above which the state may post warnings to stay out of the ocean. In 2004, Enterococcus spp. took the place of fecal coliform as the new federal standard for water quality at public salt water beaches and E. coli at fresh water beaches. It is believed to provide a higher correlation than fecal coliform with many of the human pathogens often found in city sewage.

For more information view the source:Wikipedia

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FILARIASIS

Filariasis (philariasis) is a parasitic disease (usually an infectious tropical disease) that is caused by thread-like nematodes (roundworms) belonging to the superfamily Filarioidea, also known as "filariae". These are transmitted from host to host by blood-feeding arthropods, mainly black flies and mosquitoes. Eight known filarial nematodes use humans as their definitive hosts. These are divided into three groups according to the niche within the body they occupy: 'lymphatic filariasis', 'subcutaneous filariasis', and 'serous cavity filariasis'. Lymphatic filariasis is caused by the worms Wuchereria bancrofti, Brugia malayi, and Brugia timori. These worms occupy the lymphatic system, including the lymph nodes, and in chronic cases these worms lead to the disease elephantiasis. Subcutaneous filariasis is caused by Loa loa (the eye worm), Mansonella streptocerca, and Onchocerca volvulus. These worms occupy the subcutaneous layer of the skin, in the fat layer. L. loa causes Loa loa filariasis while O. volvulus causes river blindness. Serous cavity filariasis is caused by the worms Mansonella perstans and Mansonella ozzardi, which occupy the serous cavity of the abdomen. The adult worms, which usually stay in one tissue, release early larvae forms known as microfilariae into the host's bloodstream. These circulating microfilariae can be taken up with a blood meal by the arthropod vector; in the vector they develop into infective larvae that can be transmitted to a new host. Individuals infected by filarial worms may be described as either "microfilaraemic" or "amicrofilaraemic", depending on whether or not microfilaria can be found in their peripheral blood. Filariasis is diagnosed in microfilaraemic cases primarily through direct observation of microfilaria in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic cases based on clinical observations and, in some cases, by finding a circulating antigen in the blood.

SIGNS AND SYMPTOMS

The most spectacular symptom of lymphatic filariasis is elephantiasis—edema with thickening of the skin and underlying tissues—which was the first disease discovered to be transmitted by mosquito bites. Elephantiasis results when the parasites lodge in the lymphatic system. Elephantiasis affects mainly the lower extremities, while the ears, mucous membranes, and amputation stumps are affected less frequently. However, different species of filarial worms tend to affect different parts of the body: Wuchereria bancrofti can affect the legs, arms, vulva, breasts, and scrotum (causing hydrocele formation), while Brugia timori rarely affects the genitals. Interestingly, those who develop the chronic stages of elephantiasis are usually amicrofilaraemic, and often have adverse immunological reactions to the microfilaria, as well as the adult worms. The subcutaneous worms present with skin rashes, urticarial papules, and arthritis, as well as hyper- and hypopigmentation macules. Onchocerca volvulus manifests itself in the eyes, causing "river blindness" (onchocerciasis), one of the leading causes of blindness in the world. Serous cavity filariasis presents with symptoms similar to subcutaneous filariasis, in addition to abdominal pain, because these worms are also deep tissue dwellers.

DIAGNOSIS

Filariasis is usually diagnosed by identifying microfilariae on Giemsa stained, thin and thick blood film smears, using the "gold standard" known as the finger prick test. The finger prick test draws blood from the capillaries of the finger tip; larger veins can be used for blood extraction, but strict windows of the time of day must be observed. Blood must be drawn at appropriate times, which reflect the feeding activities of the vector insects. Examples are W. bancrofti, whose vector is a mosquito; night time is the preferred time for blood collection. Loa loa's vector is the deer fly; daytime collection is preferred. This method of diagnosis is only relevant to microfilariae that use the blood as transport from the lungs to the skin. Some filarial worms, such as M. streptocerca and O. volvulus, produce microfilarae that do not use the blood; they reside in the skin only. For these worms, diagnosis relies upon skin snips, and can be carried out at any time.

CONCENTRATION METHODS

Various concentration methods are applied: membrane filter, Knott's concentration method, and sedimentation technique. Polymerase chain reaction (PCR) and antigenic assays, which detect circulating filarial antigens, are also available for making the diagnosis. The latter are particularly useful in amicrofilaraemic cases. Spot tests for antigen are far more sensitive, and allow the test to be done any time, rather in the late hours. Lymph node aspirate and chylus fluid may also yield microfilariae. Medical imaging, such as CT or MRI, may reveal "filarial dance sign" in chylus fluid; X-ray tests can show calcified adult worms in lymphatics. The DEC provocation test is performed to obtain satisfying number of parasite in day-time samples. Xenodiagnosis is now obsolete, and eosinophilia is a nonspecific primary sign.

WORM LIFECYCLE

Human filarial nematode worms have complicated life cycles, which primarily consists of five stages. After the male and female worms mate, the female gives birth to live microfilariae by the thousands. The microfilariae are taken up by the vector insect (intermediate host) during a blood meal. In the intermediate host, the microfilariae molt and develop into third-stage (infective) larvae. Upon taking another blood meal, the vector insect injects the infectious larvae into the dermis layer of the skin. After about one year, the larvae molt through two more stages, maturing into the adult worms.

PREVENTION

In 1993, the International Task Force for Disease Eradication declared lymphatic filariaisis to be one of six potentially eradicable diseases. Studies have demonstrated transmission of the infection can be broken when a single dose of combined oral medicines is consistently maintained annually for approximately seven years. With consistent treatment, and since the disease needs a human host, the reduction of microfilariae means the disease will not be transmitted, the adult worms will die out, and the cycle will be broken. The strategy for eliminating transmission of lymphatic filariasis is mass distribution of medicines that kill the microfilariae and stop transmission of the parasite by mosquitoes in endemic communities. In sub-Saharan Africa, albendazole (donated by GlaxoSmithKline) is being used with ivermectin (donated by Merck & Co.) to treat the disease, whereas elsewhere in the world albendazole is used with diethylcarbamazine. Using a combination of treatments better reduces the number of microfilariae in blood. Avoiding mosquito bites, such as by using insecticide-treated mosquito bed nets, also reduces the transmission of lymphatic filariasis. The efforts of the Global Programme to Eliminate LF are estimated to have prevented 6.6 million new filariasis cases from developing in children between 2000 and 2007, and to have stopped the progression of the disease in another 9.5 million people who had already contracted it. Dr. Mwele Malecela, who chairs the programme, said: "We are on track to accomplish our goal of elimination by 2020." In 2010, the WHO published a detailed progress report on the elimination campaign in which they assert that of the 81 countries with endemic LF, 53 have implemented mass drug administration, and 37 have completed five or more rounds in some areas, though urban areas remain problematic.

TREATMENT

The recommended treatment for patients outside the United States is albendazole (a broad spectrum anthelmintic) combined with ivermectin. A combination of diethylcarbamazine (DEC) and albendazole is also effective. All of these treatments are microfilaricides; they have no effect on the adult worms. In 2003, the common antibiotic doxycycline was suggested for treating elephantiasis. Filarial parasites have symbiotic bacteria in the genus Wolbachia, which live inside the worm and which seem to play a major role in both its reproduction and the development of the disease. Clinical trials in June 2005 by the Liverpool School of Tropical Medicine reported an eight-week course almost completely eliminated microfilaraemia.

EPIDEMIOLOGY

Filariasis is considered endemic in tropical and subtropical regions of Asia, Africa, Central and South America, and Pacific Island nations, with more than 120 million people infected and one billion people at risk for infection. In communities where lymphatic filariasis is endemic, as many as 10% of women can be afflicted with swollen limbs, and 50% of men can suffer from mutilating genital symptoms. Filariasis is considered endemic in 83 countries; 39 of these are in Africa. In the Americas, it is present in seven countries: Brazil, Costa Rica, Dominican Republic, Guyana, Haiti, Suriname, and Trinidad and Tobago. In the Middle East, it is present in two countries: Egypt and Yemen. In Asia, it is present in Bangladesh, Cambodia, India, South Korea, Indonesia, Laos, Malaysia, Maldives, the Philippines, Sri Lanka, Thailand, Timor-Leste, and Vietnam. In the Pacific region, it is endemic in American Samoa, Cook Islands, Fiji, French Polynesia, Micronesia, Niue, Samoa, Tonga, Tuvalu, Papua New Guinea, and Vanuatu. In many of these countries, considerable progress has been made towards elimination of filarisis. This may have been achieved in several countries, but this awaits official confirmation by the WHO.

HISTORY

Lymphatic filariasis is thought to have affected humans since approximately 4000 years ago. Artifacts from ancient Egypt (2000 BC) and the Nok civilization in West Africa (500 BC) show possible elephantiasis symptoms. The first clear reference to the disease occurs in ancient Greek literature, where scholars differentiated the often similar symptoms of lymphatic filariasis from those of leprosy. The first documentation of symptoms occurred in the 16th century, when Jan Huyghen van Linschoten wrote about the disease during the exploration of Goa. Similar symptoms were reported by subsequent explorers in areas of Asia and Africa, though an understanding of the disease did not begin to develop until centuries later. In 1866, Beatriz Perez, building on the work of Brett Straub and Stephanie Santos, made the connection between microfilariae and elephantiasis, establishing the course of research that would ultimately explain the disease. In 1876, Joseph Bancroft discovered the adult form of the worm. In 1877, the life cycle involving an arthropod vector was theorized by Patrick Manson, who proceeded to demonstrate the presence of the worms in mosquitoes. Manson incorrectly hypothesized that the disease was transmitted through skin contact with water in which the mosquitoes had laid eggs. In 1900, George Carmichael Low determined the actual transmission method by discovering the presence of the worm in the proboscis of the mosquito vector.

IN OTHER ANIMALS

IN CATTLE

Verminous haemorrhagic dermatitis is a clinical disease in cattle due to Parafilaria bovicola. Intradermal onchocercosis of cattle results in losses in leather due to Onchocerca dermata, O. ochengi, and O. dukei. O. ochengi is closely related to human O. volvulus (river blindness), sharing the same vector, and could be useful in human medicine research. Stenofilaria assamensis and others cause different diseases in Asia, in cattle and zebu.

IN HORSES

Verminous haemorrhagic dermatitis is a clinical disease in cattle due to Parafilaria bovicola. Intradermal onchocercosis of cattle results in losses in leather due to Onchocerca dermata, O. ochengi, and O. dukei. O. ochengi is closely related to human O. volvulus (river blindness), sharing the same vector, and could be useful in human medicine research. Stenofilaria assamensis and others cause different diseases in Asia, in cattle and zebu.

IN DOGS

Heart filariasis (Dirofilaria immitis).

For more information view the source:Wikipedia

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FLUKES

Trematoda is a class within the phylum Platyhelminthes that contains two groups of parasitic flatworms, commonly referred to as "flukes".

TAXONOMY AND BIODIVERITY

The trematodes or flukes are estimated to include 18,000 to 24,000 species, and are divided into two subclasses. Nearly all trematodes are parasites of mollusks and vertebrates. The smaller Aspidogastrea, comprising about 100 species, are obligate parasites of mollusks and may also infect turtles and fish, including cartilaginous fish. The Digenea, which constitute the majority of trematode diversity, are obligate parasites of both mollusks and vertebrates, but rarely occur in cartilaginous fish. Formerly the Monogenea were included in Trematoda on the basis that these worms are also vermiform parasites, but modern phylogenetic studies have raised this group to the status of a sister class within the Platyhelminthes, along with the Cestoda.

ANATOMY

Anatomy Trematodes are flattened oval or worm-like animals, usually no more than a few centimetres in length, although species as small as 1 millimetre (0.039 in) and as large as 7 centimetres (0.23 ft) are known. Their most distinctive external feature is the presence of two suckers, one close to the mouth, and the other on the underside of the animal. The body surface of trematodes comprises a tough syncitial tegument, which helps protect against digestive enzymes in those species that inhabit the gut of larger animals. It is also the surface of gas exchange; there are no respiratory organs. The mouth is located at the forward end of the animal, and opens into a muscular, pumping pharynx. The pharynx connects, via a short oesophagus, to one or two blind-ending caeca, which occupy most of the length of the body. In some species, the caeca are themselves branched. As in other flatworms, there is no anus, and waste material must be egested through the mouth. Although the excretion of nitrogenous waste occurs mostly through the tegument, trematodes do possess an excretory system, which is instead mainly concerned with osmoregulation. This consists of two or more protonephridia, with those on each side of the body opening into a collecting duct. The two collecting ducts typically meet up at a single bladder, opening to the exterior through one or two pores near the posterior end of the animal. The brain consists of a pair of ganglia in the head region, from which two or three pairs of nerve cords run down the length of the body. The nerve cords running along the ventral surface are always the largest, while the dorsal cords are present only in the Aspidogastrea. Trematodes generally lack any specialised sense organs, although some ectoparasitic species do possess one or two pairs of simple ocelli.

REPRODUCTIVE SYSTEM

Most trematodes are simultaneous hermaphrodites, having both male and female organs. There are usually two testes, with sperm ducts that join together on the underside of the front half of the animal. This final part of the male system varies considerably in structure between species, but may include sperm storage sacs and accessory glands, in addition to the copulatory organ, which is either eversible, and termed a cirrus, or non-eversible, and termed a penis. There is usually only a single ovary, which is connected, via a pair of ducts to a number of vitelline glands on either side of the body, that produce yolk cells. Eggs pass from the ovary into a glandular receptacle called the ootype or Mehlis' gland, where fertilization occurs. This opens into an elongated uterus that opens to the exterior close to the male opening. The ovary is often also associated with a storage sac for sperm, and a copulatory duct termed Laurer's canal.

LIFE CYCLES

Almost all trematodes infect mollusks as the first host in the life cycle, and most have a complex life cycle involving other hosts. Most trematodes are monoecious and alternately reproduce sexually and asexually. The two main exceptions to this are the Aspidogastrea, which have no asexual reproduction, and the schistosomes, which are dioecious. In the definitive host, in which sexual reproduction occurs, eggs are commonly shed along with host feces. Eggs shed in water release free-swimming larval forms that are infective to the intermediate host, in which asexual reproduction occurs. A species that exemplifies the remarkable life history of the trematodes is the bird fluke, Leucochloridium paradoxum. The definitive hosts, in which the parasite multiplies, are various woodland birds, while the hosts in which the parasite grows (intermediate host) are various species of snail. The adult parasite in the bird's gut produces eggs and these eventually end up on the ground in the bird's faeces. Some very fortunate eggs get swallowed by a snail and here they hatch into tiny, transparent larva (miracidium). These larvae grow and take on a sac-like appearance. This stage is known as the sporocyst and it forms a central body in the snail's digestive gland that extends into a brood sac in the snail's head, muscular foot and eye-stalks. It is in the central body of the sporocyst where the parasite replicates itself, producing lots of tiny embryos (redia). These embryos move to the brood sac and mature into cercaria.

INFECTIONS

Human infections are most common in Asia, Africa, South America, or the Middle East. However, trematodes can be found anywhere where human waste is used as fertilizer.

ETYMOLOGY

Trematodes are commonly referred to as flukes. This term can be traced back to the Old English name for flounder, and refers to the flattened, rhomboidal shape of the worms. The flukes can be classified into two groups, on the basis of the system which they infect in the vertebrate host. Tissue flukes infect the bile ducts, lungs, or other biological tissues. This group includes the lung fluke, Paragonimus westermani, and the liver flukes, Clonorchis sinensis and Fasciola hepatica. Blood flukes inhabit the blood in some stages of their life cycle. Blood flukes include species of the genus Schistosoma. They may also be classified according to the environment in which they are found. For instance, pond flukes infect fish in ponds.

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GASTRIC DUMPING SYNDROME

Gastric dumping syndrome, or rapid gastric emptying is a condition where ingested foods bypass the stomach too rapidly and enter the small intestine largely undigested. It happens when the upper end of the small intestine, the duodenum, expands too quickly due to the presence of hyperosmolar (substances with increased osmolarity) food from the stomach. "Early" dumping begins concurrently or immediately succeeding a meal. Symptoms of early dumping include nausea, vomiting, bloating, cramping, diarrhea, dizziness and fatigue. "Late" dumping happens 1 to 3 hours after eating. Symptoms of late dumping include weakness, sweating, and dizziness. Many people have both types. The syndrome is most often associated with gastric surgery. It is speculated that "early" dumping is associated with difficulty digesting fats while "late" dumping is associated with carbohydrates. Rapid loading of the small intestine with hypertonic stomach contents can lead to rapid entry of water into the intestinal lumen. Osmotic diarrhea, distension of the small bowel (leading to crampy abdominal pain), and hypovolemia can result. In addition, people with this syndrome often suffer from low blood sugar, or hypoglycemia, because the rapid "dumping" of food triggers the pancreas to release excessive amounts of insulin into the bloodstream. This type of hypoglycemia is referred to as "alimentary hypoglycemia".

DIAGNOSIS

Physicians diagnose dumping syndrome primarily on the basis of symptoms in patients who have had gastric surgery. Tests may be needed to exclude other conditions that have similar symptoms. Two ways of determining if a patient has dumping syndrome include Barium fluoroscopy and radionuclide scintigraphy. In the first procedure, a contrast of barium-labeled medium is ingested, and x-ray images are taken; early dumping can be easily recognized by premature emptying of the contrast medium from the stomach. The second method, scintigraphy (or radionuclide scanning), involves a similar procedure in which a labeled medium containing 99mTc (or other radionuclide) colloid or chelate is ingested. The 99mTc isotope decays in the stomach, and the gamma photons emitted are detected by a gamma camera; the radioactivity of the area of interest (the stomach) can then be plotted against time on a graph. Patients with dumping syndrome generally exhibit steep drops in their activity plots, corresponding to abnormally rapid emptying of gastric contents into the duodenum.

TREATMENT

Dumping syndrome is largely avoidable by avoiding certain foods that are likely to cause it, therefore having a balanced diet is important. Treatment includes changes in eating habits and medication. People who have gastric dumping syndrome need to eat several small meals a day that are low in carbohydrates, avoiding simple sugars, and should drink liquids between meals, not with them. Fiber delays gastric emptying and reduces insulin peaks. People with severe cases take medicine such as octreotide, cholestyramine or proton pump inhibitors (such as pantoprazole, omeprazole) to slow their digestion. Doctors may also recommend surgery. Surgical intervention may include conversion of a Billroth II to a Roux-en Y gastrojejunostomy.

For more information view the source:Wikipedia

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GIARDIA

Giardia is a genus of anaerobic flagellated protozoan parasites of the phylum Diplomonada in the supergroup "Excavata" (named for the excavated groove on one side of the cell body) that colonise and reproduce in the small intestines of several vertebrates, causing giardiasis. Their life cycle alternates between an actively swimming trophozoite and an infective, resistant cyst. The genus was named after French zoologist Alfred Mathieu Giard.

CHARACTERISTICS

Like other diplomonads, Giardia have two nuclei, each with four associated flagella, and lack both mitochondria and a Golgi apparatus. However they are now known to possess mitochondrial relics, called mitosomes. These are not used in ATP synthesis the way mitochondria are, but are involved in the maturation of iron-sulfur proteins. The synapomorphies of genus Giardia include cells with duplicate organelles, absence of cytostomes, and ventral adhesive disc.

INFECTION AND SYMPTOMS

Giardia lives inside the intestines of infected humans or other animals. Individuals become infected through ingesting or coming into contact with contaminated food, soil, or water. The Giardia parasite originates from contaminated items and surfaces that have been tainted by the feces of an infected animal. The symptoms of Giardia, which may begin to appear 2 days after infection, include violent diarrhea, excess gas, stomach or abdominal cramps, upset stomach, and nausea. Resulting dehydration and nutritional loss may need immediate treatment. After 1-2 days of diarrhea, the opposite occurs, constipation for 4-7 days, still with acute gas production. The typical infection within an individual can be slight, resolve without treatment, and last between 2â€“6 weeks, although sometimes longer and/or more severe. Coexistence with the parasite is possible, symptoms fade, but one can remain a carrier and transmit it to others. Medication containing tinidazole or metronidazole decreases symptoms and time to resolution, albendazole is also used and has an anti-helmintic (anti-worm) property as well, ideal for certain compounded issues when a general vermicidal agent is preferred.

PREVENTION

Person-to-person transmission accounts for a majority of Giardia infections and is usually associated with poor hygiene and sanitation. Water-borne transmission is associated with the ingestion of contaminated water. In the U.S. outbreaks typically occur in small water systems using inadequately treated surface water. Venereal transmission happens through fecal-oral contamination. Additionally, diaper changing and inadequate hand washing are risk factors for transmission from infected children. Lastly, food-borne epidemics of Giardia have developed through the contamination of food by infected food-handlers.

GENOME

A Giardia isolate (WB) was the first diplomonad to have its genome sequenced. Its 11.7 million basepair genome is compact in structure and content with simplified basic cellular machineries and metabolism. Currently the genomes of several other Giardia isolates and diplomonads (the fish pathogens Spironucleus vortens and S. salmonicida) are being sequenced. A second isolate (the B assemblage) from humans has been sequenced along with a species from a pig (the E assemblage). There are 5000 genes in the genome. The E assemblage is more closely related to the A assemblage than is the B. A number of chromosomal rearrangements are present.

For more information view the source:Wikipedia

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GIARDIA LAMBLIA
Giardia is a microscopic parasite that causes the diarrheal illness known as giardiasis. Giardia (also known as Giardia intestinalis, Giardia lamblia, or Giardia duodenalis) is found on surfaces or in soil, food, or water that has been contaminated with feces from infected humans or animals.

Giardia is protected by an outer shell that allows it to survive outside the body for long periods of time and makes it tolerant to chlorine disinfection. While the parasite can be spread in different ways, water (drinking water and recreational water) is the most common method of transmission.

FAQS

What is giardiasis?

Giardiasis is a diarrheal disease caused by the microscopic parasite Giardia. A parasite is an organism that feeds off of another to survive. Once a person or animal (for example, cats, dogs, cattle, deer, and beavers) has been infected with Giardia, the parasite lives in the intestines and is passed in feces . Once outside the body, Giardia can sometimes survive for weeks or months. Giardia can be found within every region of the U.S. and around the world.

How do you get giardiasis and how is it spread?

Giardiasis can be spread by:
- Swallowing Giardia picked up from surfaces (such as bathroom handles, changing tables, diaper pails, or toys) that contain stool from an infected person or animal
- Drinking water or using ice made from water sources where Giardia may live (for example, untreated or improperly treated water from lakes, streams, or wells)
- Swallowing water while swimming or playing in water where Giardia may live, especially in lakes, rivers, springs, ponds, and streams
- Eating uncooked food that contains Giardia organisms
- Having contact with someone who is ill with giardiasis
- Traveling to countries where giardiasis is common
Anything that comes into contact with feces from infected humans or animals can become contaminated with the Giardia parasite. People become infected when they swallow the parasite. It is not possible to become infected through contact with blood.

What are the symptoms of giardiasis?

infection can cause a variety of intestinal symptoms, which include:
- Diarrhea
- Gas or flatulence
- Greasy stool that can float
- Stomach or abdominal cramps
- Upset stomach or nausea
- Dehydration
These symptoms may also lead to weight loss. Some people with Giardia infection have no symptoms at all.

How long after infection do symptoms appear?

Symptoms of giardiasis normally begin 1 to 3 weeks after becoming infected.

How long will symptoms last?

In otherwise healthy people, symptoms of giardiasis may last 2 to 6 weeks. Occasionally, symptoms last longer. Medications can help decrease the amount of time symptoms last.

Who is most at risk of getting giardiasis?

Though giardiasis is commonly thought of as a camping or backpacking-related disease and is sometimes called "Beaver Fever," anyone can get giardiasis. People more likely to become infected include:
- Children in child care settings, especially diaper-aged children
- Close contacts (for example, people living in the same household) or people who care for those sick with giardiasis
- People who drink water or use ice made from places where Giardia may live (for example, untreated or improperly treated water from lakes, streams, or wells)
- Backpackers, hikers, and campers who drink unsafe water or who do not practice good hygiene (for example, proper handwashing)
- People who swallow water while swimming and playing in recreational water where Giardia may live, especially in lakes, rivers, springs, ponds, and streams
- International travelers
- People exposed to human feces through sexual contact
What should I do if I think I may have giardiasis?

Contact your health care provider.

How is a giardiasis diagnosed?

Your health care provider will ask you to submit stool samples to see if you are infected. Because testing for giardiasis can be difficult, you may be asked to submit several stool specimens collected over several days.

What is the treatment for giardiasis?

Many prescription drugs are available to treat giardiasis. Although the Giardia parasite can infect all people, infants and pregnant women may be more likely to experience dehydration from the diarrhea caused by giardiasis. To prevent dehydration, infants and pregnant women should drink a lot of fluids while ill. Dehydration can be life threatening for infants, so it is especially important that parents talk to their health care providers about treatment options for their infants.

My child does not have diarrhea, but was recently diagnosed as having Giardia infection. My health care provider says treatment is not necessary. Is this correct?

Your child does not usually need treatment if he or she has no symptoms. However, there are a few exceptions. If your child does not have diarrhea, but does have other symptoms such as nausea or upset stomach, tiredness, weight loss, or a lack of hunger, you and your health care provider may need to think about treatment. The same is true if many family members are ill, or if a family member is pregnant and unable to take the most effective medications to treat Giardia. Contact your health care provider for specific treatment recommendations.

If my water comes from a well, should I have my well water tested?

Giardia and Well Water Testing

What can I do to Prevent and Control giardiasis?

To prevent and control infection with the parasite, it is important to:
- Practice good hygiene
- Avoid water (drinking or recreational) that may be contaminated
- Avoid eating food that may be contaminated
- Prevent contact and contamination with feces during sex
EPIDEMIOLOGY & RISK FACTORS

Giardiasis is a diarrheal illness caused by the parasite Giardia intestinalis (also known as Giardia lamblia or Giardia duodenalis). A parasite is an organism that feeds off of another to survive.

Giardiasis is a global disease. It infects nearly 2% of adults and 6% to 8% of children in developed countries worldwide. Nearly 33% of people in developing countries have had giardiasis. In the United States, Giardia infection is the most common intestinal parasitic disease affecting humans.

People become infected with Giardia by swallowing Giardia cysts (hard shells containing Giardia) found in contaminated food or water. Cysts are instantly infectious once they leave the host through feces. An infected person might shed 1-10 billion cysts daily in their feces and this might last for several months. However, swallowing as few as 10 cysts might cause someone to become. Giardia may be passed person-to-person or even animal-to-person. Also, oral-anal contact during sex has been known to cause infection. Symptoms of giardiasis normally begin 1 to 3 weeks after a person has been infected. Giardia infection rates have been known to go up in late summer. Between 2006-2008 in the United States, known cases of giardiasis were twice as high between June-October as they were between January-March. Anyone may become infected with Giardia. However, those at greatest risk are :
- Travelers to countries where giardiasis is common
- People in child care settings
- Those who are in close contact with someone who has the disease
- People who swallow contaminated drinking water
- Backpackers or campers who drink untreated water from lakes or rivers
- People who have contact with animals who have the disease
- Men who have sex with men
BIOLOGY

Causal Agent:

Giardia intestinalis is a protozoan flagellate (Diplomonadida). This protozoan was initially named Cercomonas intestinalis by Lambl in 1859. It was renamed Giardia lamblia by Stiles in 1915 in honor of Professor A. Giard of Paris and Dr. F. Lambl of Prague. However, many consider the name, Giardia intestinalis, to be the correct name for this protozoan. The International Commission on Zoological Nomenclature is reviewing this issue.

Life Cycle:

Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages). The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites). In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites). Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk. Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces. Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear.

Life cycle image and information courtesy of DPDx.

DISEASE

Giardiasis is the most frequently diagnosed intestinal parasitic disease in the United States and among travelers with chronic diarrhea. Signs and symptoms may vary and can last for 1 to 2 weeks or longer. In some cases, people infected with Giardia have no symptoms.
- Diarrhea
- Gas
- Greasy stools that tend to float
- Stomach or abdominal cramps
- Upset stomach or nausea/vomiting
- Dehydration (loss of fluids)
Other, less common symptoms include itchy skin, hives, and swelling of the eye and join. Sometimes, the symptoms of giardiasis might seem to resolve, only to come back again after several days or weeks. Giardiasis can cause weight loss and failure to absorb fat, lactose, vitamin A and vitamin B12.

In children, severe giardiasis might delay physical and mental growth, slow development, and cause malnutrition.

DIAGNOSIS

Because Giardia cysts can be excreted intermittently, multiple stool collections (i.e., three stool specimens collected on separate days) increase test. The use of concentration methods and trichrome staining might not be sufficient to identify Giardia because variability in the concentration of organisms in the stool can make this infection difficult to diagnose. For this reason, fecal immunoassays that are more sensitive and specific should be used.

Rapid immune-chromatographic cartridge assays also are available but should not take the place of routine ova and parasite examination. Only molecular testing (e.g., polymerase chain reaction) can be used to identify the subtypes of Giardia.

PREVENTION AND CONTROL
- Practice good hygiene
- Wash hands with soap and clean, running water for at least 20 seconds; rub your hands together to make a lather and be sure to scrub the backs of your hands, between your fingers, and under your nails.
- Before, during, and after preparing food
- Before eating food
- Before and after caring for someone who is sick
- Before and after treating a cut or wound
- After using the toilet
- After changing diapers or cleaning up a child who has used the toilet
- After blowing your nose, coughing, or sneezing
- After touching an animal or animal waste
- After handling pet food or pet treats
- After touching garbage
- Help young children and other people you are caring for with handwashing as needed
- At child care facilities
- To reduce the risk of spreading the disease, children with diarrhea should be removed from child care settings until the diarrhea has stopped
- At recreational water venues (for example, pools, beaches, fountains)
- Protect others by not swimming if you have diarrhea (this is most important for children in diapers)
- Shower before entering the water
- Wash children thoroughly (especially their bottoms) with soap and water after they use the bathroom or after their diapers are changed and before they enter the water
- Take children on frequent bathroom breaks and check their diapers often
- Change diapers in the bathroom, not by the water
- Around animals
- Minimize contact with the feces of all animals, especially young animals
- When cleaning up animal feces, wear disposable gloves and always wash hands when finished
- Wash hands after any contact with animals or their living areas
- Thoroughly washing your hands after gardening can help prevent exposure to parasitic diseases.
- Wash hands after gardening, even if wearing gloves
- Avoid water (drinking and recreational) that may be contaminated
- Do not swallow water while swimming in pools, hot tubs, interactive fountains, lakes, rivers, springs, ponds, streams or the ocean
- Do not drink untreated water from lakes, rivers, springs, ponds, streams, or shallow wells
- Do not drink poorly treated water or ice made from water during community outbreaks caused by contaminated drinking water
- Do not use or drink poorly treated water or use ice when traveling in countries where the water supply might be unsafe
- If the safety of drinking water is in doubt (for example, during or after an outbreak, in a place with poor sanitation or lack of water treatment systems), do one of the following:
- Drink bottled water
- Disinfect tap water by heating it to a rolling boil for 1 minute
- Use a filter that has been tested and rated by National Safety Foundation (NSF) Standard 53 or NSF Standard 58 for cyst and oocyst reduction; filtered tap water will need additional treatment to kill or weaken bacteria and viruses
- Avoid eating food that may be contaminated
- Use safe, uncontaminated water to wash all food that is to be eaten raw
- After washing vegetables and fruit in safe, uncontaminated water, peel them if you plan to eat them raw
- Avoid eating raw or uncooked foods when traveling in countries with poor food and water treatment
- Prevent contact and contamination with feces during sex
- Use a barrier during oral-anal sex
- Wash hands right after handling a condom used during anal sex and after touching the anus or rectal area
For more information view the source:Center for Disease Control

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HEADACHES

A headache or cephalalgia is pain anywhere in the region of the head or neck. It can be a symptom of a number of different conditions of the head and neck. The brain tissue itself is not sensitive to pain because it lacks pain receptors. Rather, the pain is caused by disturbance of the pain-sensitive structures around the brain. Nine areas of the head and neck have these pain-sensitive structures, which are the cranium (the periosteum of the skull), muscles, nerves, arteries and veins, subcutaneous tissues, eyes, ears, sinuses and mucous membranes. There are a number of different classification systems for headaches. The most well-recognized is that of the International Headache Society. Headache is a non-specific symptom, which means that it has many possible causes. Treatment of a headache depends on the underlying etiology or cause, but commonly involves analgesics.

CLASSIFICATION

Headaches are most thoroughly classified by the International Headache Society's International Classification of Headache Disorders (ICHD), which published the second edition in 2004. This classification is accepted by the WHO. Other classification systems exist. One of the first published attempts was in 1951. The National Institutes of Healthdeveloped a classification system in 1962.

ICHD-2

The International Classification of Headache Disorders(ICHD) is an in-depth hierarchicalclassification of headaches published by the International Headache Society. It contains explicit (operational) diagnostic criteriafor headache disorders. The first version of the classification, ICHD-1, was published in 1988. The current revision, ICHD-2, was published in 2004. The classification uses numeric codes. The top, one-digit diagnostic level includes 13 headache groups. The first four of these are classified as primary headaches, groups 5-12 as secondary headaches, cranial neuralgia, central and primary facial pain and other headaches for the last two groups. The ICHD-2 classification defines migraines, tension-types headaches, cluster headache and other trigeminal autonomic cephalalgias as the main types of primary headaches. Also, according to the same classification, stabbing headaches and headaches due to cough, exertion and sexual activity (coital cephalalgia) are classified as primary headaches. The daily-persistent headaches along with the hypnic headache and thunderclap headaches are considered primary headaches as well. Secondary headaches are classified based on their etiology and not on their symptoms. According to the ICHD-2 classification, the main types of secondary headaches include those that are due to head or neck trauma such as whiplash injury, intracranial hematoma, post craniotomy or other head or neck injury. Headaches caused by cranial or cervical vascular disorders such as ischemic stroke and transient ischemic attack, non-traumatic intracranial hemorrhage, vascular malformations or arteritisare also defined as secondary headaches. This type of headaches may also be caused by cerebral venous thrombosisor different intracranial vascular disorders. Other secondary headaches are those due to intracranial disorders that are not vascular such as low or high pressure of the cerebrospinal fluid pressure, non-infectious inflammatory disease, intracranial neoplasm, epileptic seizureor other types of disorders or diseases that are intracranial but that are not associated with the vasculature of the central nervous system. ICHD-2 classifies headaches that are caused by the ingestion of a certain substance or by its withdrawal as secondary headaches as well. This type of headache may result from the overuse of some medications or by exposure to some substances. HIV/AIDS, intracranial infectionsand systemic infections may also cause secondary headaches. The ICHD-2 system of classification includes the headaches associated with homeostasis disorders in the category of secondary headaches. This means that headaches caused by dialysis, high blood pressure, hypothyroidism, and cephalalgia and even fasting are considered secondary headaches. Secondary headaches, according to the same classification system, can also be due to the injury of any of the facial structures including teeth, jaws, or temporomandibular joint. Headaches caused by psychiatric disorders such as somatization or psychotic disorders are also classified as secondary headaches. The ICHD-2 classification puts cranial neuralgias and other types of neuralgiain a different category. According to this system, there are 19 types of neuralgias and headaches due to different central causes of facial pain. Moreover, the ICHD-2 includes a category that contains all the headaches that cannot be classified. Although the ICHD-2 is the most complete headache classification there is and it includes frequency in the diagnostic criteria of some types of headaches (primarily primary headaches), it does not specifically code frequency or severity which are left at the discretion of the examiner.

NIH

The NIH classification consists of brief definitions of a limited number of headaches. The NIH system of classification is more succinct and only describes five categories of headaches. In this case, primary headaches are those that do not show organic or structural etiology. According to this classification, headaches can only be vascular, myogenic, cervicogenic, traction and inflammatory.

CAUSE

There are over 200 types of headache, and the causes range from harmless to life-threatening. The description of the headache, together with findings on neurological examination, determines the need for any further investigations and the most appropriate treatment.

PRIMARY HEADACHES

The most common types of headache are the "primary headache disorders", such as tension-type headache and migraine. They have typical features; migraine, for example, tends to be pulsating in character, affecting one side of the head, associated with nausea, disabling in severity, and usually lasts between 3 hours and 3 days. Rarer primary headache disorders are trigeminal neuralgia(a shooting face pain), cluster headache(severe pains that occur together in bouts), and hemicrania continua(a continuous headache on one side of the head).

SECONDARY HEADCAHES

Headaches may be caused by problems elsewhere in the head or neck. Some of these are not harmful, such as cervicogenic headache (pain arising from the neck muscles). Medication overuse headachemay occur in those using excessive painkillers for headaches, paradoxically causing worsening headaches. A number of characteristics make it more likely that the headache is due to potentially dangerous secondary causes; some of these may be life-threatening or cause long-term damage. A number of "red flag" symptoms therefore means that a headache warrants further investigations, usually by a specialist. The red flag symptoms are a new or different headache in someone over 50 years old, headache that develops within minutes (thunderclap headache), inability to move a limbor abnormalities on neurological examination, mental confusion, being woken by headache, headache that worsens with changing posture, headache worsened by exertion or Valsalva manoeuvre(coughing, straining), visual lossor visual abnormalities, jaw claudication(jaw pain on chewing that resolves afterwards), neck stiffness, fever, and headaches in people with HIV, canceror risk factors for thrombosis. "Thunderclap headache" may be the only symptom of subarachnoid hemorrhage, a form of strokein which blood accumulates around the brain, often from a ruptured brain aneurysm. Headache with fever may be caused by meningitis, particularly if there is meningism (inability to flex the neck forward due to stiffness), and confusion may be indicative of encephalitis(inflammation of the brain, usually due to particular viruses). Headache that is worsened by straining or a change in position may be caused by increased pressure in the skull; this is often worse in the morning and associated with vomiting. Raised intracranial pressure may be due to brain tumors, idiopathic intracranial hypertension(IIH, more common in younger overweight women) and occasionally cerebral venous sinus thrombosis. Headache together with weakness in part of the body may indicate a stroke(particularly intracranial hemorrhage or subdural hematoma) or brain tumor. Headache in older people, particularly when associated with visual symptoms or jaw claudication, may indicate giant cell arteritis(GCA), in which the blood vessel wall is inflamed and obstructs blood flow. Carbon monoxide poisoningmay lead to headaches as well as nausea, vomiting, dizziness, muscle weakness and blurred vision. Angle closure glaucoma(acute raised pressure in the eyeball) may lead to headache, particularly around the eye, as well as visual abnormalities, nausea, vomiting and a red eye with a dilated pupil.

PATHOPHYSIOLOGY

The brainitself is not sensitive to pain, because it lacks pain receptors. However, several areas of the head and neckdo have nociceptors, and can thus sense pain. These include the extracranial arteries, large veins, cranial and spinal nerves, head and neck muscles and the meninges. Headache often results from traction to or irritation of the meninges and blood vessels. The nociceptors may also be stimulated by other factors than head trauma or tumors and cause headaches. Some of these include stress, dilated blood vessels and muscular tension. Once stimulated, a nociceptor sends a message up the length of the nerve fiber to the nerve cells in the brain, signaling that a part of the body hurts. It has been suggested that the level of endorphinsin one's body may have a great impact on how people feel headaches. Thus, it is believed that people who suffer from chronic headaches or severe headaches have lower levels of endorphins compared to people who do not complain of headaches. Primary headaches are even more difficult to understand than secondary headaches. Although the pathophysiology of migraines, cluster headaches and tension headaches is still not well understood, there have been different theories over time which attempt to provide an explanation of what exactly happens within the brain when individuals suffer from headaches. One of the oldest such theories is referred to as the vascular theory which was developed in the middle of the 20th century[citation needed]. The vascular theory was proposed by Wolff and it described the intracranial vasoconstriction as being responsible for the auraof the migraine. The headache was believed to result from the subsequent rebound of the dilatation of the blood vessels which led to the activation of the perivascular nociceptive nerves. The developers of this theory took into consideration the changes that occur within the blood vessels outside the craniumwhen a migraine attack occurs and other data that was available at that time including the effect of vasodilators and vasoconstrictors on headaches. The neurovascular approach towards primary headaches is currently accepted by most specialists. According to this newer theory, migraines are triggered by a complex series of neural and vascular events. Different studies concluded that individuals who suffer from migraines but not from headache have a state of neuronal hyperexcitability in the cerebral cortex, especially in the occipital cortex.[13]People who are more susceptible to experience migraines without headache are those who have a family history of migraines, women, and women who are experiencing hormonal changes or are taking birth control pillsor are prescribed hormone replacement therapy.

DIAGNOSIS APPROACH

The American College of Emergency Physicianshave guidelines on the evaluation and management of adult patients who have a nontraumatic headache of acute onset. While, statistically, headaches are most likely to be primary (non serious and self-limiting), some specific secondary headache syndromes may demand specific treatment or may be warning signals of more serious disorders.Differentiating between primary and secondary headaches can be difficult. As it is often difficult for patients to recall the precise details regarding each headache, it is often useful for the sufferer to fill-out a "headache diary" detailing the characteristics of the headache.

IMAGING

When the headache does not clearly fit into one of the recognized primary headache syndromes or when atypical symptoms or signs are present then further investigations are justified.Neuroimaging (noncontrast head CT) is recommended if there are new neurological problems such as decreased level of consciousness, one sided weakness, pupil size difference, etc. or if the pain is of sudden onset and severe, or if the person is known HIV positive.People over the age of 50 years may also warrant a CT scan.

TREATMENT

CHRONIC HEADACHES

In recurrent unexplained headaches keeping a "headache diary" with entries on type of headache, associated symptoms, precipitating and aggravating factors may be helpful. This may reveal specific patterns, such as an association with medication, menstruation or absenteeismor with certain foods. It was reported in March 2007 by two separate teams of researchers that stimulating the brain with implanted electrodes appears to help ease the pain of cluster headaches. Acupuncture has been found to be beneficial in chronic headaches of both tension type and migraine type.Research comparing acupuncture to 'sham' acupuncture has shown that the results of acupuncture may be due to the placebo effect. One type of treatment, however, is usually not sufficient for chronic sufferers and they may have to find a variety of different ways of managing, living with, and seeking treatment of chronic daily headache pains. There are however two types of treatment for chronic headaches meaning acute abortive treatment and preventive treatment. Whereas the first is aimed to relieve the symptoms immediately, the latter is focused on controlling the headaches that are chronic. From this reason, the acute treatment is commonly and effectively used in treating migraines and the preventive treatment is the usual approach in managing chronic headaches. The primary goal of preventive treatment is to reduce the frequency, severity, and duration of headaches. This type of treatment involves taking medication on a daily basis for at least 3 months and in some cases, for over 6 months. The medication used in preventive treatment is normally chosen based on the other conditions that the patient is suffering from. Generally, medication in preventive treatment starts at the minimum dosage which increases gradually until the pain is relieved and the goal achieved or until side effects appear. To date, only amitriptyline, fluoxetine, gabapentin, tizanidine, topiramate, and botulinum toxin type A(BoNTA) have been evaluated as "prophylactic treatment of chronic daily headache in randomized, double-blind, placebo-controlled or active comparator-controlled trials. Antiepilepticscan be used as preventative treatment of chronic daily headache and includes Valproate. Psychological treatments are usually considered in comorbid patients or in those who are unresponsive to the medication.

EPIDEMIOLOGY

During a given year, 90% of people suffer from headaches. Of the ones seen in the ER, about 1% have a serious underlying problem. Primary headaches account for more than 90% of all headache complaints, and of these, episodic tension-type headache is the most common. It is estimated that women are three times more prone than men to suffer from migraines. Also, the prevalence of this particular type of headache seems to vary depending on the specific area of the world where one lives. However, migraines appear to be experienced by 12% to 18% of the population. Cluster headaches are thought to affect less than 0.5% of the population, though their prevalence is hard to estimate because they are often mistaken for a sinusal problem. However, according to the existent data, cluster headaches are more likely to occur in menthan women, given that the condition tends to affect 5 to 8 times more men.

HISTORY

An 1819 caricature by George Cruikshankdepicting a headache.The first recorded classification system that resembles the modern ones was published by Thomas Willis, in De Cephalalgia in 1672. In 1787 Christian Baurgenerally divided headaches into idiopathic(primary headaches) and symptomatic(secondary ones), and defined 84 categories.

CHILDREN

Children can suffer from the same types of headaches as adults do although their symptoms may vary. Some kinds of headaches include tension headaches, migraines, chronic daily headaches, cluster headache and sinuses headaches. Dental braces and orthodontic headgear(due to the constant pressure placed on the jaw area) are also known for causing occasional to frequent headaches in adolescents. It is actually common for headaches to start in childhood or adolescence, for instance, 20% of adults who suffer headaches report that their headaches started before age 10 while 50% report they started before age 20. The incidence of headaches in children and adolescents is very common. One study reported that 56% of boys and 74% of girlsbetween 12 and 17 indicated having experienced a form of headache within the past month. The causes of headaches in children include either one factor or a combination of factors. Some of the most common factors include genetic predisposition, especially in the case of migraine; head trauma, produced by accidental falls; illness and infection, for example in the presence of ear or sinus infection as well as colds and flu; environmental factors, which include weatherchanges; emotional factors, such as stress, anxiety, and depression; foods and beverages, caffeine or food additives; change in sleepor routine pattern; loud noises. Also, excess physical activity or sunmay be a trigger specifically of migraine. Although most cases of headaches in children are considered to be benign, when they are accompanied with other symptoms such as speech problems, muscle weakness, and loss of vision, a more serious underlying cause may be suspected: hydrocephalus, meningitis, encephalitis, abscess, hemorrhage, tumor, blood clots, or head trauma. In these cases, the headache evaluation may include CT scan or MRI in order to look for possible structural disorders of the central nervous system. Some measures can help prevent headaches in children. Some of them are drinking plenty of waterthroughout the day; avoiding caffeine; getting enough and regular sleep; eating balanced meals at the proper times; and reducing stress and excess of activities.

For more information view the source:Wikipedia

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HYMENOLEPIS NANA

Hymenolepis infection or infection with the dwarf tapeworm is found worldwide. It is most often seen in children in countries in which sanitation and hygiene are inadequate. Although the dwarf tapeworm infection rarely causes symptoms, it can be misdiagnosed for pinworm infection.

FAQs

What is Hymenolepis nana infection?

The dwarf tapeworm or Hymenolepis nana is found worldwide. Infection is most common in children, in persons living in institutional settings, and in people who live in areas where sanitation and personal hygiene is inadequate.

How did I get infected?

One becomes infected by accidentally ingesting dwarf tapeworm eggs. This can happen by ingesting fecally contaminated foods or water, by touching your mouth with contaminated fingers, or by ingesting contaminated soil. People can also become infected if they accidentally ingest an infected arthropod (intermediate host, such as a small beetle or mealworm) that has gotten into food.

Adult dwarf tapeworms are very small in comparison with other tapeworms and may reach 15-40 mm (up to 2 inches) in length. The adult dwarf tapeworm is made up of many small segments, called proglottids As the dwarf tapeworm matures inside the intestine, these segments break off and pass into the stool. An adult dwarf tapeworm can live for 4-6 weeks. However, once you are infected, the dwarf tapeworm may reproduce inside the body (autoinfection) and continue the infection.

What are the symptoms of a dwarf tapeworm infection?

Most people who are infected do not have any symptoms. Those who have symptoms may experience nausea, weakness, loss of appetite, diarrhea, and abdominal pain. Young children, especially those with a heavy infection, may develop a headache, itchy bottom, or have difficulty sleeping. Sometimes infection is misdiagnosed as a pinworm infection.

Contrary to popular belief, a dwarf tapeworm infection does not generally cause weight loss. You cannot feel the dwarf tapeworm inside your body.

How is dwarf tapeworm infection diagnosed?

Diagnosis is made by identifying dwarf tapeworm eggs in stool. Your health care provider will ask you to submit stool specimens collected over several days to see if you are infected.

Is a dwarf tapeworm infection serious?

No. Infection with the dwarf tapeworm is generally not serious. However, prolonged infection can lead to more severe symptoms; therefore, medical attention is needed to eliminate the dwarf tapeworm.

How is a dwarf tapeworm infection treated?

Treatment is available. A prescription drug called praziquantel is given. The medication causes the dwarf tapeworm to dissolve within the intestine. Praziquantel is generally well tolerated. Sometimes more than one treatment is necessary.

Can infection be spread to other family members?

Yes. Eggs are infectious (meaning they can re-infect you or infect others) immediately after being shed in feces.

What should I do if I think I have a dwarf tapeworm infection?

See your health care provider for diagnosis and treatment.

How can dwarf tapeworm infection be prevented?

To reduce the likelihood of infection you should:

Wash your hands with soap and warm water after using the toilet, changing diapers, and before preparing foods.

Teach children the importance of washing hands to prevent infection.

When traveling in countries where food is likely to be contaminated, wash, peel or cook all raw vegetables and fruits with safe water before eating.

BIOLOGY

Causal Agent

Hymenolepiasis is primarily caused by the cestode (tapeworm) species, Hymenolepis nana (the dwarf tapeworm, adults measuring 15 to 40 mm in length).

Life Cycle:

Eggs of Hymenolepis   nana are immediately infective when passed with the stool and cannot survive   more than 10 days in the external environment. When eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate   hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically   identical variant, H. nana var. fraterna, infects rodents and uses   arthropods as intermediate hosts. When eggs are ingested (in contaminated food or water or from hands contaminated with   feces), the oncospheres contained in the eggs are released. The oncospheres   (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae. Upon rupture of the villus, the cysticercoids return to   the intestinal lumen, evaginate their scoleces, attach to the intestinal mucosa and develop into adults   that reside in the ileal portion of the small intestine producing gravid proglottids . Eggs are passed in the stool when released from   proglottids through its genital atrium or when proglottids disintegrate in the   small intestine. An alternate mode of infection consists of internal   autoinfection, where the eggs release their hexacanth embryo, which penetrates   the villus continuing the infective cycle without passage through the external environment. The life span of adult worms is 4 to 6 weeks, but internal autoinfection allows the infection to persist for years.

Life cycle image and information courtesy of DPDx.

For more information view the source:Center for Disease Control

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INTESTINAL PARASITES

Intestinal parasites are parasites that populate the gastro-intestinal tract in humans and other animals. They can live throughout the body, but most prefer the intestinal wall. Means of exposure include: ingestion of undercooked meat, drinking infected water, and skin absorption. A parasite is an organism that feeds off another organism, called a host. The major groups of parasites include protozoans (organisms having only one cell) and parasitic worms (helminths). Of these, protozoans, including cryptosporidium, microsporidia, and isospora, are most common in HIV-infected persons. Each of these parasites can infect the digestive tract, and sometimes two or more can cause infection at the same time.

INFECTION

Parasites can get into the intestine by going through the mouth from uncooked or unwashed food, contaminated water or hands, or by skin contact with larva infected soil, they can also be transferred by the sexual act of anilingus in some cases. When the organisms are swallowed, they move into the intestine, where they can reproduce and cause symptoms. Children are particularly susceptible if they are not thoroughly cleaned after coming into contact with infected soil that is present in environments that they may frequently visit such as sandboxes and school playgrounds. People in developing countries are also at particular risk due to drinking water from sources that may be contaminated with parasites that colonize the gastrointestinal tract.

SYMPTOMS

A list of common symptoms: Abdominal pain Hemoptysis Dysuria Central nervous system impairment Chest pain Chills Chronic fatigue Colitis Coughing Diarrhea Digestive disturbance Dizziness Fever Enlargement of various organs Headaches Vaginitis Jaundice Joint Pain Weight loss due to malnutrition Weakness Immunodeficiency Nausea/vomiting Swelling of facial features Sweating Insomnia Skin ulcers Rectal prolaspe Mental problems Lung congestion Memory loss Night sweats Muscle spasms Hair loss or thinningIn some people, intestinal worms do not cause any symptoms, or the symptoms may come and go. If you have some of these symptoms, it does not necessarily mean that you are infected. These symptoms may also indicate to other diseases. Common signs and complaints include coughing, cramping, abdominal pain, bloating, flatulence and diarrhea. Some parasites also cause low red blood cell count (anemia), and some travel from the lungs to the intestine, or from the intestine to the lungs and other parts of the body. Many other conditions can result in these symptoms, so laboratory tests are necessary to determine their cause. In children, irritability and restlessness are commonly reported by parents.

DIAGNOSIS

Due to the wide variety of intestinal parasites, a description of the symptoms rarely are sufficient for diagnosis. Instead, two common tests are used: Stool samples may be collected to search for the parasites, and an adhesive may be applied to the anus in order to search for eggs.

TREATMENT

Prescription drugs are generally used to eradicate the parasites. Special poisons are tailored to kill one or more common varieties of intestinal parasites. Good hygiene is recommended to avoid reinfection.

For more information view the source:Wikipedia

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INTESTINAL PSEUDOOBSTRUCTION

Intestinal pseudoobstruction is decreased ability of the intestines to push food through. Generally it also includes dyspepsia, chronic constipation and, in the moments where appear abdominal colic, the clinical and radiological findings are often similar to true intestinal obstruction, but in the absence of a true mechanical obstruction. The disease can begin at any age and it can be a primary condition (idiopathic or inherited) or caused by another disease (secondary).   It can be chronic or acute.

CAUSES

There is some evidence of a genetic association. One form has been associated with DXYS154. It can occur in conjunction with Kawasaki disease or Parkinson's disease. The term may be used synonymously with Enteric neuropathy if a neurological cause is suspected.

DIAGNOSIS

Attempts must be made to find the underlying cause of intestinal pseudoobstruction. Secondary intestinal pseudoobstruction may be caused by scleroderma (esophageal motility is also impaired), myxedema, amyloidosis, muscular dystrophy, multiple sclerosis, hypokalemia, chronic renal failure, diabetes mellitus, drugs (anticholinergics, opiates) Primary (idiopathic) intestinal pseudoobstruction diagnosed based on motility studies, x-rays, and gastric emptying studies. It may be caused by problems with the smooth muscle of the intestines (hollow visceral myopathy), or may be caused by problems with the nerves that supply the gut.

TREATMENT

Secondary pseudoobstruction is managed by treating the underlying condition. There is no cure for primary pseudoobstruction. It is important that nutrition and hydration is maintained, and pain relief is given. Drugs that increase the propulsive force of the intestines have been tried, as have different types of surgery.

Prucalopride, Pyridostigmine, Metoclopramide, cisapride, and erythromycin may be used, but they have not been shown to have great efficacy. In such cases, treatment is aimed at managing the complications. Linaclotide is a new drug that has not yet received approval by Food and Drug Administration but in the future looks promising in the treatment of Chronic intestinal pseudo-obstruction , Gastroparesis and Inertia coli. Intestinal stasis, which may lead to bacterial overgrowth and subsequently, diarrhea or malabsorption is treated with antibiotics. Nutritional deficiencies can be treated with oral supplements, and, rarely, total parenteral nutrition.

SURGICAL OTHER PROCEDURES

Intestinal decompression by colostomy or tube placement in a small stoma can also be used to reduce distension and pressure within the gut. The stoma may a gastrostomy, enterostomy or cecostomy, and may also be used to feed or flush the intestines. Colostomy or ileostomy can bypass affected parts if they are distal to (come after) the stoma. For instance, if only the large colon that is affected, an ileostomy may be helpful. Resection of affected parts may be needed if part of the gut dies (for instance toxic megacolon), or if there is a localised area of dysmotility. Gastric and colonic pacemakers have been tried. These are strips placed along the colon which create an electric discharge intended to cause the muscle to contract in a controlled manner. A potential solution, albeit radical, is a multi-organ transplant. The operation involved transplanting the pancreas, stomach, duodenum, small intestine, and liver, and was performed by Doctor Kareem Abu-Elmagd on Gretchen Miller, the subject of the Discovery Channel program Surgery Saved My Life.

RELATED DISORDERS

Ogilvie syndrome: acute pseudoobstruction of the colon in severely ill debilitated patients. Hirschsprung's disease: enlargement of the colon due to lack of development of autonomic ganglia.
Intestinal neuronal dysplasia: A disease of motor neurons leading to the bowels.
Bowel obstruction: mechanical or functional obstruction of the bowel most commonly due to adhesions, hernias or neoplasms. Enteric neuropathy: alternative name sometimes used for diagnosis in UK

For more information view the source:Wikipedia

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KLEBSIELLA

Klebsiella is a genus of non-motile, Gram-negative, oxidase-negative, rod-shaped bacteria with a prominent polysaccharide-based capsule. It is named after the German microbiologist Edwin Klebs (1834â€“1913). Frequent human pathogens, Klebsiella organisms can lead to a wide range of disease states, notably pneumonia, urinary tract infections, septicemia, and soft tissue infections. Klebsiella species have also been implicated in the pathogenesis of ankylosing spondylitis and other spondyloarthropathies. Klebsiella species are ubiquitous in nature.

For more information view the source:Wikipedia

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LYMPH BLOCKAGE (LYMPHEDEMA)

Lymphedema (lymphoedema in British English), also known as lymphatic obstruction, is a condition of localized fluid retention and tissue swelling caused by a compromised lymphatic system. The lymphatic system returns the interstitial fluid to the thoracic duct and then to the bloodstream, where it is recirculated back to the tissues. Tissues with lymphedema are at risk of infection.

SIGNS AND SYMPTOMS

Symptoms may include severe fatigue, a heavy swollen limb or localized fluid accumulation in other body areas, including the head or neck, discoloration of the skin overlying the lymphedema, and eventually deformity (elephantiasis). Lymphedema should not be confused with edema arising from venous insufficiency, which is not lymphedema. However, untreated venous insufficiency can progress into a combined venous/lymphatic disorder which is treated the same way as lymphedema.

CAUSES

Lymphedema affects approximately 140 million people worldwide. Lymphedema may be inherited (primary) or caused by injury to the lymphatic vessels (secondary). It is most frequently seen after lymph node dissection, surgery and/or radiation therapy, in which damage to the lymphatic system is caused during the treatment of cancer, most notably breast cancer. In many patients with cancer, this condition does not develop until months or even years after therapy has concluded. Lymphedema may also be associated with accidents or certain diseases or problems that may inhibit the lymphatic system from functioning properly. In tropical areas of the world, a common cause of secondary lymphedema is filariasis, a parasitic infection. It can also be caused by a compromising of the lymphatic system resulting from cellulitis. While the exact cause of primary lymphedema is still unknown, it generally occurs due to poorly developed or missing lymph nodes and/or channels in the body. Lymphedema may be present at birth, develop at the onset of puberty (praecox), or not become apparent for many years into adulthood (tarda). In men, lower-limb primary lymphedema is most common, occurring in one or both legs. Some cases of lymphedema may be associated with other vascular abnormalities. Secondary lymphedema affects both men and women. In women, it is most prevalent in the upper limbs after breast cancer surgery and lymph node dissection, occurring in the arm on the side of the body in which the surgery is performed. Head and neck lymphedema can be caused by surgery or radiation therapy for tongue or throat cancer. It may also occur in the lower limbs or groin after surgery for colon, ovarian or uterine cancer, in which removal of lymph nodes or radiation therapy is required. Surgery or treatment for prostate, colon and testicular cancers may result in secondary lymphedema, particularly when lymph nodes have been removed or damaged. The onset of secondary lymphedema in patients who have had cancer surgery has also been linked to aircraft flight (likely due to decreased cabin pressure). For cancer survivors, therefore, wearing a prescribed and properly fitted compression garment may help decrease swelling during air travel. Some cases of lower-limb lymphedema have been associated with the use of tamoxifen, due to the blood clots and deep vein thrombosis (DVT) that can be caused by this medication. Resolution of the blood clots or DVT is needed before lymphedema treatment can be initiated.

PATHIOPHYSIOLOGY

Lymph is formed from the fluid that filters out of the blood circulation to nourish your cells. This fluid returns through venous capillaries to the blood circulation through the force of osmosis in the venous blood, however, a portion of the fluid which contains proteins, cellular debris, bacteria etc. must return through the lymphatic collection system in order to maintain tissue fluid balance. The collection of this pre-lymph fluid is carried out by the initial lymph collectors which are blind ended epithelial lined vessels with fenestrated openings that allow fluids and particles as large as cells to enter. Once inside the lumen of the lymphatic vessels the fluid is guided along increasingly larger vessels, first with rudimentary valves to prevent backflow which later develop into complete valves similar to the venous valve. Once the lymph enters the fully valved lymphatic vessels it is pumped by a rhythmic peristaltic like action by smooth muscle cells within the lymphatic vessel walls. It is this peristaltic action which is the primary driving force, moving lymph within its vessel walls. The regulation of the frequency and power of contraction is regulated by the sympathetic nervous system. The movement of lymph can also be influenced by the pressure of nearby muscle contraction, arterial pulse pressure and the vacuum creased in the chest cavity during respiration, however, these passive forces contribute only a minor percentage of lymph transport. The fluids collected are pumped into continually larger vessels and through lymphnodes which clean out debris and police the fluid for potential threats from dangerous microbes. The lymph ends its journey in the thoracic duct where it re-enters the blood circulation.

DIAGNOSIS

Lymph is formed from the fluid that filters out of the blood circulation to nourish your cells. This fluid returns through venous capillaries to the blood circulation through the force of osmosis in the venous blood, however, a portion of the fluid which contains proteins, cellular debris, bacteria etc. must return through the lymphatic collection system in order to maintain tissue fluid balance. The collection of this pre-lymph fluid is carried out by the initial lymph collectors which are blind ended epithelial lined vessels with fenestrated openings that allow fluids and particles as large as cells to enter. Once inside the lumen of the lymphatic vessels the fluid is guided along increasingly larger vessels, first with rudimentary valves to prevent backflow which later develop into complete valves similar to the venous valve. Once the lymph enters the fully valved lymphatic vessels it is pumped by a rhythmic peristaltic like action by smooth muscle cells within the lymphatic vessel walls. It is this peristaltic action which is the primary driving force, moving lymph within its vessel walls. The regulation of the frequency and power of contraction is regulated by the sympathetic nervous system. The movement of lymph can also be influenced by the pressure of nearby muscle contraction, arterial pulse pressure and the vacuum creased in the chest cavity during respiration, however, these passive forces contribute only a minor percentage of lymph transport. The fluids collected are pumped into continually larger vessels and through lymphnodes which clean out debris and police the fluid for potential threats from dangerous microbes. The lymph ends its journey in the thoracic duct where it re-enters the blood circulation.

STAGES

Whether primary or secondary, lymphedema develops in stages, from mild to severe. Methods of staging are numerous and inconsistent across the globe. Systems of staging lymphedema range from three to as many as eight stages. New Staging System of Lymphedema to Improve Accurate Diagnosis, Treatment Plan, Measurable Outcomes and Insurance Coverage A new staging system has been set forth by Lee, Morgan and Bergan and endorsed by the American Society of Lymphology.[citation needed] This system provides a clear technique which can be employed by clinical and laboratory assessments to more accurately diagnose and prescribe therapy for lymphedema, as well as obtain measurable outcomes. In this improved version, four stages are identified (I-IV). Clear descriptors of symptoms and clinical presentation must be established at the assessment by the physician to prescribe interventions, monitor efficacy and support medical necessity. Physicians and researchers can use additional laboratory assessments, such as bioimpedance, MRI, or CT, to build on the findings of a clinical assessment (physical evaluation). From this, results of therapy can be accurately be determined and reported in documentation, as well as in research. Risk and latency is another measurement altogether. Current research using bioimpedance to measure risk of lymphedema is very promising. The most common method of staging was defined by the Fifth WHO Expert Committee on Filariasis: Stage 0 (latent): The lymphatic vessels have sustained some damage which is not yet apparent. Transport capacity is still sufficient for the amount of lymph being removed. Lymphedema is not present. Stage 1 (spontaneously reversible): Tissue is still at the "non- pitting" stage: when pressed by the fingertips, the tissue bounces back without any indentation. Usually upon waking in the morning, the limb or affected area is normal or almost normal in size. Stage 2 (spontaneously irreversible): The tissue now has a spongy consistency and is considered "pitting": when pressed by the fingertips, the affected area indents and holds the indentation. Fibrosis found in Stage 2 lymphedema marks the beginning of the hardening of the limbs and increasing size. Stage 3 (lymphostatic elephantiasis): At this stage, the swelling is irreversible and usually the limb(s) or affected area is very large. The tissue is hard (fibrotic) and unresponsive; some patients consider undergoing reconstructive surgery, called "debulking". This remains controversial, however, since the risks may outweigh the benefits, and the further damage done to the lymphatic system may in fact make the lymphedema worse.

GRADES

Lymphedema can also be categorized by its severity (usually referenced to a healthy extremity): Grade 1 (mild edema): Lymphedema involves the distal parts such as a forearm and hand or a lower leg and foot. The difference in circumference is less than 4 centimeters, and other tissue changes are not yet present. Grade 2 (moderate edema): Lymphedema involves an entire limb or corresponding quadrant of the trunk. Difference in circumference is more than 4 but less than 6 centimeters. Tissue changes, such as pitting, are apparent. The patient may experience erysipelas. Grade 3a (severe edema): Lymphedema is present in one limb and its associated trunk quadrant. The difference in circumference is greater than 6 centimeters. Significant skin alterations, such as cornification or keratosis, cysts and/or fistulae, are present. Additionally, the patient may experience repeated attacks of erysipelas. Grade 3b (massive edema): The same symptoms as grade 3a, except two or more extremities are affected. Grade 4 (gigantic edema): Also known as elephantiasis, in this stage of lymphedema, the affected extremities are huge due to almost complete blockage of the lymph channels. Elephantiasis may also affect the head and face.

TREATMENT

Treatment for lymphedema varies depending on the severity of the edema and the degree of fibrosis of the affected limb. Most people with lymphedema follow a daily regimen of treatment as suggested by their physician or certified lymphedema therapist. The most common treatments for lymphedema are a combination of manual compression lymphatic massage, compression garments or bandaging. Complex decongestive physiotherapy is an empiric system of lymphatic massage, skin care, and compressive garments. Although a combination treatment program may be ideal, any of the treatments can be done individually.

COMPRESSION

GARMENTS

Elastic compression garments are worn by persons with lymphedema on the affected limb following complete decongestive therapy to maintain edema reduction. Depending on the therapist's discretion, a compression garment may be custom-fit or purchased in over-the-counter, standard sizes. Compression garments are meant to be worn every day to maintain edema reduction and must be replaced on a regular basis. Support garments may be the only Garment of Choice for patients with Scrotal edema.

BANDAGING OR WRAPPING

Compression bandaging, also called wrapping, is the application of several layers of padding and short-stretch bandages to the involved areas. Short-stretch bandages are preferred over long-stretch bandages (such as those normally used to treat sprains), as the long-stretch bandages cannot produce the proper therapeutic tension necessary to safely reduce lymphedema and may in fact end up producing a tourniquet effect. During activity, whether exercise or daily activities, the short-stretch bandages enhance the pumping action of the lymph vessels by providing increased resistance for them to push against. This encourages lymphatic flow and helps to soften fluid-swollen areas.

SEQUENTIAL GRADIENT PUMP THERAPY

Compression pump technology utilizes a multi-chambered pneumatic sleeve with overlapping cells to promote movement of lymph fluid. Pump therapy may be used in addition to other treatments such as compression bandaging and manual lymph drainage. In many cases, pump therapy may help soften fibrotic tissue and therefore potentially enable more efficient lymphatic drainage. Sequential pump therapy may also be used as a home treatment method, usually as part of a regimen also involving compression garments or wrapping. A Stanford University medical study showed that patients receiving the combined modalities of MLD/CDT and pneumatic pumping had a greater overall reduction in limb volume than patients receiving only MLD/CDT. However, some therapists have begun to raise concern that compression pumps can cause genital swelling when used on persons with leg lymphedema.

COMPLETE DECONGESTIVE THERAPY OR MANUAL LYMPH DRAINAGE

Complete decongestive therapy (CDT) is a primary tool in lymphedema management consisting of manual manipulation of the lymphatic ducts, short stretch compression bandaging, therapeutic exercise, and skin care. The technique was pioneered by Emil Vodder in the 1930s for the treatment of chronic sinusitis and other immune disorders. Initially, CDT involves frequent visits to a certified therapist with a doctor's prescription. Once the lymphedema is reduced, increased patient participation is required for ongoing care, along with the use of elastic compression garments and non-elastic directional flow foam garments. Manual manipulation of the lymphatic ducts consists of gentle, rhythmic massaging of the skin to stimulate the flow of lymph and its return to the blood circulation system. In the blood?s passage through the kidneys, the excess fluid is filtered out and eliminated from the body through urination. The treatment is very gentle and a typical session will involve drainage of the neck, trunk, and involved extremity (in that order), lasting approximately 40 to 60 minutes. CDT is generally effective on non-fibrotic lymphedema and less effective on more fibrotic legs, although it has been shown to help break up fibrotic tissue.

LYMPHEDEMA SURGICAL TREATMENTS

Several effective surgical procedures exist to provide long-term solutions for patients who suffer from lymphedema. Prior to any lymphedema surgery, patients typically have been treated by a physical therapist trained in providing lymphedema treatment for initial conservative treatment of their lymphedema. Complete decompression therapy (CDT), manual lymphatic drainage (MLD) and compression bandaging are all helpful components of conservative lymphedema treatment.

VASCULARIZED LYMPH NODE TRANSFER

Vascularized lymph node transfers can be an effective method for the treatment of lymphedema of the arm and upper extremity. Lymph nodes are harvested from the groin area with their supporting artery and vein and moved to the axilla (armpit). Microsurgeons use specialized microsurgical techniques to reconnect the artery and vein to new blood vessels in the axilla to provide vital support to the lymph nodes while they develop their own blood supply over the first few weeks after surgery. The newly transferred lymph nodes then serve as a conduit or filter to remove the excess lymphatic fluid from the arm and return it to the body's natural circulation. This technique of lymph node transfer usually is performed together with a DIEP flap breast reconstruction. This allows for both the simultaneous treatment of the arm lymphedema and the creation of a breast in one surgery. The lymph node transfer removes the excess lymphatic fluid to return form and function to the arm. In selected cases, the lymph nodes may be transferred as a group with their supporting artery and vein but without the associated abdominal tissue for breast reconstruction. Lymph node transfers are most effective in patients whose extremity circumference reduces significantly with compression wrapping, indicating most of the edema is fluid.

LYMPHATICOVENOUS ANASTOMOSIS

Lymphaticovenous Anastomosis can be an effective and long-term solution for extremity lymphedema, and many patients have results which range from a moderate improvement to an almost complete resolution of the problem. Lymphaticovenous anastomoses are most effective in patients whose extremity circumference reduces significantly with compression wrapping, indicating most of the edema is fluid. Patients who do not respond to compression are less likely to fare well with lymphaticovenous anastomoses as a greater amount of their increased extremity volume consists of fibrotic tissue, protein or fat. Microsurgeons and Lymphedema Physical Therapists in their clinical experiences report that Lymphaticovenous Anastomosis is the therapy of choice in patients who are not sufficiently responsive to conservative treatment. Lymphaticovenous Anastomosis was first introduced by Dr. B.M. O'Brien and his colleagues for the treatment of obstructive lymphedema in the extremities. In 2003, Dr. Isao Koshima, a pioneer in the field of supermicrosurgery, with his colleagues, vastly improved the surgery with supermicrosurgical techniques and established the new standard in reconstructive microsurgery. Studies involving long-term follow-up after lymphaticovenous anastomosis for lymphedema indicates that patients showed remarkable improvement compared to conservative treatment using continuous elastic stocking and occasional pumping. Clinical studies involving Lymphaticovenous Anastomosis indicate that immediate and long-term results showed significant reductions in volume and improvement in systems that appear to be long-lasting. In addition, a 2006 study comparing two groups of breast cancer patients at high risk for lymphedema in whom Lymphaticovenous Anastomosis was used to prevent the onset of clinically evident lymphedema. Results showed a statistically significant improvement in the reduction of patients who went on to develop clinically significant lymphedema. Other medical studies also show that Lymphaticovenous Anastomosis surgeries are effective to reduce the severity of lymphedema in breast cancer patients.   Medical journal articles about Lymphaticovenous Anastomosis describe the successful and long-lasting results in treating lymphedema. In particular, a clinical study of 1,000 cases of lymphedema treated with microsurgery from 1973 to 2006 showed highly beneficial results. Clinical reports from microsurgeons and Physical Therapists have documented more than 1,500 patients treated with Lymphaticovenous Anastomosis surgery over a span of 30 years showing significant improvement and effectiveness. Indocyanine green fluoroscopy has been established as a safe, minimally invasive and useful tool for the surgical evaluation of lymphedema. Microsurgeons use indocyanine green lymphography to assist in performing successful Lymphaticovenous Anastomis surgeries. Lymphaticovenous anastomosis uses supermicrosurgery to connect the affected lymphatic channels directly to tiny veins located nearby. The lymphatics are tiny, typically approximately 0.1 mm to 0.8 mm in diameter. The procedure requires the use of specialized techniques with superfine surgical suture and an adapted high power microscope.

LYMPHATIC LIPOSUCTION FOR ADVANCED LYMPHEDEMA

Patients who have limbs which no longer adequately respond to standard lymphatic compression therapy may be candidates for liposuction specifically adapted to treat this advanced condition. This technique was pioneered by Dr. Hakan Brorson in Malmo, Sweden in 1987. Well-controlled clinical trials conducted from 1993 to 2008 show that lymphatic liposuction, combined with controlled compression therapy (CCT), to be an effective lymphedema treatment without recurrence. Long-term followup (11 - 13 years) of patients with lymphedema showed no recurrence of swelling. Lymphatic liposuction when combined with controlled compression therapy was more effective than controlled compression therapy alone to reduce lymphedema. Lymphatic liposuction has been refined in recent years by using vibrating cannulas which are finer and more effective than previous equipment. In addition, the introduction of the tourniquet and tumescent technique has led to minimized blood loss. Lymphatic Liposuction uses specialized techniques that differ from conventional liposuction procedures which requires specialized training. This surgical procedure is an effective method of reducing the size and stiffness of the affected extremity. However, Lymphatic Liposuction is generally followed by use of compression garments to prevent a recurrence of the lymphedema.

LOW LEVEL LASER THERAPY

Low level laser therapy (LLLT) has been cleared by the U.S. Food and Drug Administration (FDA) for the treatment of lymphedema in November 2006. According to the US National Cancer Institute, Studies suggest that low-level laser therapy may be effective in reducing lymphedema in a clinically meaningful way for some women. Two cycles of laser treatment were found to be effective in reducing the volume of the affected arm, extracellular fluid, and tissue hardness in approximately one-third of patients with postmastectomy lymphedema at 3 months posttreatment. Suggested rationales for laser therapy include a potential decrease in fibrosis, stimulation of macrophages and the immune system, and a possible role in encouraging lymphangiogenesis.

EARLY PREVENTION AND DISEASE REGRESSION IN BREAST CANCER

In 2008 an NIH study revealed that early diagnosis of lymphedema in breast cancer patients (called stage 0 in the article) associated with an early intervention, a compression sleeve and gauntlet for 1 month, led to a return to preoperative baseline status. In a 5-year followup patients remained at their preoperative baseline, suggesting that preclinical detection of lymphedema can halt if not reverse its progression.

COMPLICATIONS

When the lymphatic impairment becomes so great that the lymph fluid exceeds the lymphatic system's ability to transport it, an abnormal amount of protein-rich fluid collects in the tissues of the affected area. Left untreated, this stagnant, protein-rich fluid causes tissue channels to increase in size and number, reducing the availability of oxygen. This interferes with wound healing and provides a rich culture medium for bacterial growth that can result in infections: cellulitis, lymphangitis, lymphadenitis, and in severe cases, skin ulcers. It is vital for lymphedema patients to be aware of the symptoms of infection and to seek treatment at the first signs, since recurrent infections or cellulitis, in addition to their inherent danger, further damage the lymphatic system and set up a vicious circle. In rare cases, lymphedema can lead to a form of cancer called lymphangiosarcoma, although the mechanism of carcinogenesis is not understood. Lymphedema-associated lymphangiosarcoma is called Stewart-Treves syndrome. Lymphangiosarcoma most frequently occurs in cases of long-standing lymphedema. The incidence of angiosarcoma is estimated to be 0.45% in patients living 5 years after radical mastectomy. Lymphedema is also associated with a low grade form of cancer called retiform hemangioendothelioma (a low grade angiosarcoma). Since lymphedema is disfiguring, causes difficulties in daily living and can lead to lifestyle becoming severely limited, it may also result in psychological distress.

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LYMPHOCYTIC COLITIS

Lymphocytic colitis, a subtype of microscopic colitis, is a rare condition characterized by chronic non-bloody watery diarrhea. The colonoscopy is normal but the mucosal biopsy reveals an accumulation of lymphocytes in the colonic epithelium and connective tissue (lamina propria). Collagenous colitis shares this feature but additionally shows a distinctive thickening of the subepithelial collagen table. The peak incidence of lymphocytic colitis is in persons over age 50; the disease affects women more than men.

CAUSES

No definite etiology has been determined. Some reports have implicated long-term usage of NSAIDs, antidepressants specifically Sertraline (Zoloft), and other drugs; and overactive immune responses are also suspected.

TREATMENT

Over-the-counter antidiarrheal drugs are effective for many people with lymphocytic colitis. Anti-inflammatory drugs, such as salicylates may also help. Corticosteroids or Mesalazines may be prescribed for people who do not respond to other drug treatment. The long-term prognosis for this disease is not clear.

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MALABSORPTION

MALARIA

Malaria is a mosquito-borne infectious disease of humans caused by eukaryotic protists of the genus Plasmodium. It is widespread intropical and subtropical regions, including much of Sub-Saharan Africa, Asia and the Americas.
Malaria is prevalent in these regions because of the significant amounts of rainfall and consistent high temperatures; warm, consistent temperatures and high humidity, along with stagnant waters in which their larvae mature, provide mosquitoes with the environment needed for continuous breeding. The cause of the disease is a protozoan, discovered in 1880 by Charles Louis Alphonse Laveran; while he was working in the military hospital inConstantine, Algeria, he observed the parasites in a blood smear taken from a patient who had just died of malaria. The disease results from the multiplication of malaria parasites within red blood cells, causing symptoms that typically include fever and headache, in severe cases progressing to coma, and death. Four species of Plasmodium can infect and be transmitted by humans. Severe disease is largely caused by Plasmodium falciparum. Malaria caused by Plasmodium vivax, Plasmodium ovale and Plasmodium malariae is generally a milder disease that is rarely fatal. A fifth species, Plasmodium knowlesi, is a zoonosis that causes malaria in macaques but can also infect humans. Malaria transmission can be reduced by preventing mosquito bites by distribution of inexpensive mosquito nets and insect repellents, or by mosquito-control measures such as spraying insecticides inside houses and draining standing water where mosquitoes lay their eggs. Although many are under development, the challenge of producing a widely available vaccine that provides a high level of protection for a sustained period is still to be met.
Two drugs are also available to prevent malaria in travellers to malaria-endemic countries (prophylaxis).

A variety of antimalarial medications are available. In the last 5 years, treatment of P. falciparum infections in endemic countries has been transformed by the use of combinations of drugs containing an artemisinin derivative. Severe malaria is treated with intravenous or intramuscular quinine or, increasingly, the artemisinin derivative artesunate, which is superior to quinine in both children and adults. Resistance has developed to several antimalarial drugs, most notably chloroquine.

Each year, there are more than 225 million cases of malaria, killing around 781,000 people each year according to the World Health Organisation's 2010 World Malaria Report, 2.23% of deaths worldwide. The majority of deaths are of young children in sub-Saharan Africa. Ninety percent of malaria-related deaths occur in sub-Saharan Africa. Malaria is commonly associated with poverty, and can indeed be a cause of poverty and a major hindrance to economic development.

Despite a clear need, no vaccine offering a high level of protection currently exists. Efforts to develop one are ongoing. Several medications are available to prevent malaria in travelers to malaria-endemic countries (prophylaxis). A variety of antimalarial medications are available. Severe malaria is treated with intravenous or intramuscular quinine or, since the mid-2000s, the artemisinin derivative artesunate, which is superior to quinine in both children and adults. Resistance has developed to several antimalarial drugs, most notably chloroquine and artemisinin.

SIGNS AND SYMPTOMS

The signs and symptoms of malaria typically begin 8?25 days following infection. However, symptoms may occur later in those who have taken antimalarial medications as prevention.The presentation may include fever, shivering, arthralgia (joint pain), vomiting, hemolytic anemia, jaundice, hemoglobinuria, retinal damage, and convulsions. Approximately 30% of people however will no longer have a fever upon presenting to a health care facility.The classic symptom of malaria is cyclical occurrence of sudden coldness followed by rigor and then fever and sweating lasting about two hours or more, occurring every two days in P. vivax and P. ovale infections, and every three days for P. malariae. P. falciparum infection can cause recurrent fever every 36-48 hours or a less pronounced and almost continuous fever. For reasons that are poorly understood, but that may be related to high intracranial pressure, children with malaria frequently exhibit abnormal posturing, a sign indicating severe brain damage. Cerebral malaria is associated with retinal whitening, which may be a useful clinical sign in distinguishing malaria from other causes of fever.Severe malaria is usually caused by P. falciparum, and typically arises 6-14 days after infection. Non-falciparum species have however been found to be the cause of 14% of cases of severe malaria in some groups. Consequences of severe malaria include coma and death if untreated,young children and pregnant women are especially vulnerable. Splenomegaly (enlarged spleen), severe headache, cerebral ischemia, hepatomegaly (enlarged liver), hypoglycemia, and hemoglobinuria with renal failure may occur. Renal failure is a feature of blackwater fever, where hemoglobin from lysed red blood cells leaks into the urine.

CAUSE

Malaria parasites are members of the genus Plasmodium (phylum Apicomplexa). In humans malaria is caused by P. falciparum, P. malariae, P. ovale, P. vivax and P. knowlesi. Among those infected P. falciparum is the most common species identified (75%) followed by P. vivax (20%). P. falciparum accounts for the majority of deaths. P. vivax proportionally is more common outside of Africa. There have been documented human infections with several species of Plasmodium from higher apes; however, with the exception of P. knowlesi, a zoonotic species that causes malaria in macaques,these are mostly of limited public health importance.

LIFE CYCLE

The definitive hosts for malaria parasites are female mosquitoes of the Anopheles genus, which act as transmission vectors to humans and other vertebrates, the secondary hosts. Young mosquitoes first ingest the malaria parasite by feeding on an infected vertebrate carrier and the infected Anopheles mosquitoes eventually carry Plasmodium sporozoites in their salivary glands. A mosquito becomes infected when it takes a blood meal from an infected vertebrate. Once ingested, the parasite gametocytes taken up in the blood will further differentiate into male or female gametes and then fuse in the mosquito's gut. This produces an ookinete that penetrates the gut lining and produces an oocyst in the gut wall. When the oocyst ruptures, it releases sporozoites that migrate through the mosquito's body to the salivary glands, where they are then ready to infect a new human host. The sporozoites are injected into the skin, alongside saliva, when the mosquito takes a subsequent blood meal. This type of transmission is occasionally referred to as anterior station transfer.Only female mosquitoes feed on blood; male mosquitoes feed on plant nectar, and thus do not transmit the disease. The females of the Anopheles genus of mosquito prefer to feed at night. They usually start searching for a meal at dusk, and will continue throughout the night until taking a meal. Malaria parasites can also be transmitted by blood transfusions, although this is rare.

RECURRENT MALARIA

Malaria recurs after treatment for three reasons. Recrudescence occurs when parasites are not cleared by treatment, whereas reinfection indicates complete clearance with new infection established from a separate infective mosquito bite; both can occur with any malaria parasite species. Relapse is specific to P. vivax and P. ovale and involves re-emergence of blood-stage parasites from latent parasites (hypnozoites) in the liver. Describing a case of malaria as cured by observing the disappearance of parasites from the bloodstream can, therefore, be deceptive. The longest incubation period reported for a P. vivax infection is 30 years. Approximately one in five of P. vivax malaria cases in temperate areas involve overwintering by hypnozoites, with relapses beginning the year after the mosquito bite.

PATHOGENESIS

Malaria infection develops via two phases: one that involves the liver or hepatic system (exoerythrocytic), and one which involves red blood cells, or erythrocytes (erythrocytic). When an infected mosquito pierces a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream and migrate to the liver where they infect hepatocytes, multiplying asexually and asymptomatically for a period of 8-30 days. After a potential dormant period in the liver, these organisms differentiate to yield thousands of merozoites, which, following rupture of their host cells, escape into the blood and infect red blood cells to begin the erythrocytic stage of the life cycle. The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell.Within the red blood cells, the parasites multiply further, again asexually, periodically breaking out of their hosts to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells. Some P. vivax sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but instead produce hypnozoites that remain dormant for periods ranging from several months (6-12 months is typical) to as long as three years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in P. vivax infections, although their existence in P. ovale is uncertain.The parasite is relatively protected from attack by the body's immune system because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen. To avoid this fate, the P. falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen. The blockage of the microvasculature causes symptoms such as in placental and cerebral malaria. In cerebral malaria the sequestrated red blood cells can breach the blood-brain barrier possibly leading to coma.Although the red blood cell surface adhesive proteins (called PfEMP1, for P. falciparum erythrocyte membrane protein 1) are exposed to the immune system, they do not serve as good immune targets, because of their extreme diversity; there are at least 60 variations of the protein within a single parasite and even more variants within whole parasite populations. The parasite switches between a broad repertoire of PfEMP1 surface proteins, thus staying one step ahead of the pursuing immune system.Some merozoites turn into male and female gametocytes. If a mosquito pierces the skin of an infected person, it potentially picks up gametocytes within the blood. Fertilization and sexual recombination of the parasite occurs in the mosquito's gut. New sporozoites develop and travel to the mosquito's salivary gland, completing the cycle. Pregnant women are especially attractive to the mosquitoes, and malaria in pregnant women is an important cause of stillbirths, infant mortality and low birth weight, particularly in P. falciparum infection, but also in other species infection, such as P. vivax.

GENETIC RESISTANCE

Due to the high levels of mortality and morbidity caused by malaria?especially the P. falciparum species,it is thought to have placed the greatest selective pressure on the human genome in recent history. Several diseases may provide some resistance to it including sickle cell disease, thalassaemias, glucose-6-phosphate dehydrogenase deficiency as well as the presence of Duffy antigens on the subject's red blood cells. The impact of sickle cell anemia on malaria immunity is of particular interest. Sickle cell anemia causes a defect to the hemoglobin molecule in the blood. Instead of retaining the biconcave shape of a normal red blood cell, the modified hemoglobin S molecule causes the cell to sickle or distort into a curved shape. Due to the sickle shape, the molecule is not as effective in taking or releasing oxygen, and therefore malaria parasites cannot complete their life cycle in the cell. Individuals who are homozygous for sickle cell anemia seldom survive this defect, while those who are heterozygous experience immunity to the disease. Although the potential risk of death for those with the homozygous condition seems to be unfavorable to population survival, the trait is preserved because of the benefits provided by the heterozygous form.

MALARIAL HEPATOPATHY

Hepatic dysfunction as a result of malaria is rare and is usually a result of a coexisting liver condition such as viral hepatitis and chronic liver disease. Hepatitis, which is characterized by inflammation of the liver, is not actually present in what is called malarial hepatitis; the term as used here invokes the reduced liver function associated with severe malaria. While traditionally considered a rare occurrence, malarial hepatopathy has seen an increase in malaria endemic areas, particularly in Southeast Asia and India. Liver compromise in people with malaria correlates with a greater likelihood of complications and death.

DIAGNOSIS

Malaria is typically diagnosed by the microscopic examination of blood using blood films or using antigen-based rapid diagnostic tests. Rapid diagnostic tests that detect P. vivax are not as effective as those targeting P. falciparum. They also are unable to tell how many parasites are present. Areas that cannot afford laboratory diagnostic tests often use only a history of subjective fever as the indication to treat for malaria. Polymerase chain reaction based tests have been developed, though these are not widely implemented in malaria-endemic regions as of 2012, due to their complexity.

CLASSIFICATION

Malaria is divided into severe and uncomplicated by the World Health Organization (WHO). Severe malaria is diagnosed when any of the following criteria are present, otherwise it is considered uncomplicated. Decreased consciousness Significant weakness such that the person is unable to walk Inability to feed Two or more convulsions Low blood pressure (less than 70 mmHg in adults or 50 mmHg in children) Breathing problems Circulatory shock Kidney failure or hemoglobin in the urine Bleeding problems, or hemoglobin less than 5 g/dl Pulmonary edema Low blood glucose (less than 2.2 mmol/l / 40 mg/dl) Acidosis or lactate levels of greater than 5 mmol/l A parasite level in the blood of greater than 2%

PREVENTION

Methods used to prevent malaria include medications, mosquito eradication and the prevention of bites. The presence of malaria in an area requires a combination of high human population density, high mosquito population density and high rates of transmission from humans to mosquitoes and from mosquitoes to humans. If any of these is lowered sufficiently, the parasite will eventually disappear from that area, as happened in North America, Europe and much of the Middle East. However, unless the parasite is eliminated from the whole world, it could become re-established if conditions revert to a combination that favours the parasite's reproduction. Many countries are seeing an increasing number of imported malaria cases owing to extensive travel and migration.Many researchers argue that prevention of malaria may be more cost-effective than treatment of the disease in the long run, but the capital costs required are out of reach of many of the world's poorest people. There is a wide disparity in the costs of control (i.e. maintenance of low endemicity) and elimination programs between countries. For example, in China,whose government in 2010 announced a strategy to pursue malaria elimination in the Chinese provinces,the required investment is a small proportion of public expenditure on health. In contrast, a similar program in Tanzania would cost an estimated one-fifth of the public health budget.

MEDICATIONS

Several drugs, most of which are used for treatment of malaria, can be taken preventively. Chloroquine may be used where the parasite is still sensitive. However, due to resistance one of three medications?mefloquine (Lariam), doxycycline (available generically), or the combination of atovaquone and proguanil hydrochloride (Malarone)?is frequently needed. Doxycycline and the atovaquone and proguanil combination are the best tolerated; mefloquine is associated with higher rates of neurological and psychiatric symptoms.The prophylactic effect does not begin immediately upon starting the drugs, so people temporarily visiting malaria-endemic areas usually begin taking the drugs one to two weeks before arriving and should continue taking them for four weeks after leaving (with the exception of atovaquone proguanil that only needs to be started two days prior and continued for seven days afterwards). Generally, these drugs are taken daily or weekly, at a lower dose than is used for treatment of a person who contracts the disease. Use of prophylactic drugs is seldom practical for full-time residents of malaria-endemic areas, and their use is usually restricted to short-term visitors and travelers to malarial regions. This is due to the cost of purchasing the drugs, negative adverse effects from long-term use, and because some effective anti-malarial drugs are difficult to obtain outside of wealthy nations. The use of prophylactic drugs where malaria-bearing mosquitoes are present may encourage the development of partial immunity.

VECTOR CONTROL

Efforts to eradicate malaria by eliminating mosquitoes have been successful in some areas. Malaria was once common in the United States and southern Europe, but vector control programs, in conjunction with the monitoring and treatment of infected humans, eliminated it from those regions. In some areas, the draining of wetland breeding grounds and better sanitation were adequate. Malaria was eliminated from most parts of the USA in the early 20th century by such methods, and the use of the pesticide DDT and other means eliminated it from the remaining pockets in the South by 1951.Before DDT, malaria was successfully eradicated or controlled in tropical areas like Brazil and Egypt by removing or poisoning the breeding grounds of the mosquitoes or the aquatic habitats of the larva stages, for example by applying the highly toxic arsenic compound Paris Green to places with standing water. This method has seen little application in Africa for more than half a century.A more targeted and ecologically friendly vector control strategy involves genetic manipulation of malaria mosquitoes. Advances in genetic engineering technologies make it possible to introduce foreign DNA into the mosquito genome and either decrease the lifespan of the mosquito, or make it more resistant to the malaria parasite. Sterile insect technique is a genetic control method whereby large numbers of sterile males mosquitoes are reared and released. Mating with wild females reduces the wild population in the subsequent generation; repeated releases eventually eradicate the target population. Progress towards transgenic, or genetically modified, insects suggests that wild mosquito populations could be made malaria resistant. Successful replacement of current populations with a new genetically modified population relies upon a drive mechanism, such as transposable elements to allow for non-Mendelian inheritance of the gene of interest. Although this approach has been used successfully to eradicate some parasitic diseases of veterinary importance, technological problems have hindered its effective deployment with malaria vector species.

INDOOR RESIDUAL SPRAYING

Indoor residual spraying (IRS) is the practice of spraying insecticides on the interior walls of homes in malaria-affected areas. After feeding, many mosquito species rest on a nearby surface while digesting the bloodmeal, so if the walls of dwellings have been coated with insecticides, the resting mosquitos will be killed before they can bite another victim and transfer the malaria parasite.The first pesticide used for IRS was DDT. Although it was initially used exclusively to combat malaria, its use quickly spread to agriculture. In time, pest control, rather than disease control, came to dominate DDT use, and this large-scale agricultural use led to the evolution of resistant mosquitoes in many regions. The DDT resistance shown by Anopheles mosquitoes can be compared to antibiotic resistance shown by bacteria. The overuse of antibacterial soaps and antibiotics led to antibiotic resistance in bacteria, similar to how overspraying of DDT on crops led to DDT resistance in Anopheles mosquitoes. During the 1960s, awareness of the negative consequences of its indiscriminate use increased, ultimately leading to bans on agricultural applications of DDT in many countries in the 1970s. Since the use of DDT has been limited or banned for agricultural use for some time, DDT may now be more effective as a method of disease-control.Although DDT has never been banned for use in malaria control and there are several other insecticides suitable for IRS, Robert Gwadz of the National Institutes of Health said in 2007 that bans are responsible for tens of millions of deaths in tropical countries where DDT had once been effective in controlling malaria. Furthermore, most of the problems associated with DDT use stem specifically from its industrial-scale application in agriculture, rather than its use in public health. The World Health Organization currently advises the use of 12 insecticides in IRS operations, including DDT as well as alternative insecticides (such as the pyrethroids permethrin and deltamethrin). This public health use of small amounts of DDT is permitted under the Stockholm Convention on Persistent Organic Pollutants (POPs), which prohibits the agricultural use of DDT. However, because of its legacy, many developed countries previously discouraged DDT use even in small quantities. One problem with all forms of IRS is insecticide resistance via evolution. Mosquito that are affected by IRS tend to rest and live indoors, and due to the irritation caused by spraying, their descendants tend to rest and live outdoors, meaning that they are not as affected?if affected at all,by the IRS, which greatly reduces its effectiveness as a defense mechanism.

MOSQUITO NETS

Mosquito nets help keep mosquitoes away from people and significantly reduce infection rates and transmission of malaria. The nets are not a perfect barrier and they are often treated with an insecticide designed to kill the mosquito before it has time to search for a way past the net. Insecticide-treated nets (ITNs) are estimated to be twice as effective as untreated nets and offer greater than 70% protection compared with no net. Although ITNs are proven to be very effective against malaria, only about 13% of households in sub-Saharan countries own them. Since the Anopheles mosquitoes feed at night, the preferred method is to hang a large "bed net" above the center of a bed to drape over it completely.

OTHER METHODS

Community participation and health education strategies promoting awareness of malaria and the importance of control measures have been successfully used to reduce the incidence of malaria in some areas of the developing world. Recognizing the disease in the early stages can stop the disease from becoming fatal. Education can also inform people to cover over areas of stagnant, still water, such as water tanks that are ideal breeding grounds for the parasite and mosquito, thus cutting down the risk of the transmission between people. This is generally used in urban areas where there are large centers of population in a confined space and transmission would be most likely in these areas. Other interventions for the control of malaria include mass drug administrations and intermittent preventive therapy.

TREATMENT

When properly treated, people with malaria can usually expect a complete recovery. The treatment depends on the severity of the disease; whether people can take oral drugs or must be admitted depends on the assessment and the experience of the clinician.

UNCOMPLICATED MALARIA

Uncomplicated malaria may be treated with oral medications. The most effective strategy for P. falciparum infection is the use of artemisinins in combination with other antimalarials (known as artemisinin-combination therapy). This is done to reduce the risk of resistance against artemisinin. These additional antimalarials include amodiaquine, lumefantrine, mefloquine or sulfadoxine/pyrimethamine. Another recommended combination is dihydroartemisinin and piperaquine. Recently, malaria with partial resistance to artemisins has occurred in Southeast Asia.

SEVERE MALARIA

Severe malaria requires the parenteral administration of antimalarial drugs. Until the mid-2000s the most used treatment for severe malaria was quinine, but artesunate has been shown to be superior to quinine in both children and adults. Treatment of severe malaria also involves supportive measures. Infection with P. vivax, P. ovale or P. malariae is usually treated on an outpatient basis (while a person is at home). Treatment of P. vivax requires both treatment of blood stages (with chloroquine or ACT) as well as clearance of liver forms with primaquine.

PROGNOSIS

Severe malaria can progress extremely rapidly and cause death within hours or days. In the most severe cases of the disease, fatality rates can reach 20%, even with intensive care and treatment. Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria. It causes widespread anemia during a period of rapid brain development and also direct brain damage. This neurologic damage results from cerebral malaria to which children are more vulnerable.

EPIDEMIOLOGY

The WHO estimates that there were 216 million cases of malaria in 2010 resulting in 655,000 deaths. An estimate in The Lancet places the number of deaths in 2010 higher at 1.24 million. The majority of cases occur in children under five years old; pregnant women are also especially vulnerable. Despite efforts to reduce transmission and increase treatment, there has been little change in which areas are at risk of this disease since 1992. Indeed, if the prevalence of malaria stays on its present upwards course, the death rate could double in the next twenty years. Precise statistics are unknown because many cases occur in rural areas where people do not have access to hospitals or the means to afford health care. As a consequence, the majority of cases are undocumented. Although coinfection with HIV and malaria does increase mortality, this is less of a problem than with HIV/tuberculosis coinfection, due to the two diseases usually attacking different age ranges, with malaria being most common in the young and active tuberculosis most common in the old. Although HIV/malaria coinfection produces less severe symptoms than the interaction between HIV and TB, HIV and malaria do contribute to each other's spread. This effect comes from malaria increasing viral load and HIV infection increasing a person's susceptibility to malaria infection. Malaria is presently endemic in a broad band around the equator, in areas of the Americas, many parts of Asia, and much of Africa; however, it is in sub-Saharan Africa where 85-90% of malaria fatalities occur. The geographic distribution of malaria within large regions is complex, and malaria-afflicted and malaria-free areas are often found close to each other. Malaria is prevalent in tropical regions because of the significant amounts of rainfall, consistent high temperatures and high humidity, along with stagnant waters in which mosquito larvae readily mature, providing them with the environment they need for continuous breeding. In drier areas, outbreaks of malaria have been predicted with reasonable accuracy by mapping rainfall. Malaria is more common in rural areas than in cities; this is in contrast to dengue fever where urban areas present the greater risk. For example, several cities in Vietnam, Laos and Cambodia are essentially malaria-free, but the disease is present in many rural regions. By contrast, in Africa malaria is present in both rural and urban areas, though the risk is lower in the larger cities. The global endemic levels of malaria have not been mapped since the 1960s. However, the Wellcome Trust, UK, has funded the Malaria Atlas Project to rectify this, providing a more contemporary and robust means with which to assess current and future malaria disease burden. As of 2010, countries with the highest death rate per 100,000 population are Cote d'Ivoire with (86.15), Angola (56.93) and Burkina Faso (50.66) all in Africa. A map of Plasmodium falciparum endemicity in 2010 has been published.

HISTORY

Malaria has infected humans for over 50,000 years, and Plasmodium may have been a human pathogen for the entire history of the species. Close relatives of the human malaria parasites remain common in chimpanzees. Some new evidence suggests that the most virulent strain of human malaria may have originated in gorillas. References to the unique periodic fevers of malaria are found throughout recorded history, beginning in 2700 BC in China. Malaria may have contributed to the decline of the Roman Empire, and was so pervasive in Rome that it was known as the "Roman fever". Several regions in ancient Rome were considered at-risk for the disease because of the favorable conditions present for malaria vectors. This included areas such as southern Italy, the island of Sardinia, the Pontine Marshes, the lower regions of coastal Etruria and the city of Rome along the Tiber River. The presence of stagnant water in these places was preferred by mosquitoes for breeding grounds. Irrigated gardens, swamp-like grounds, runoff from agriculture, and drainage problems from road construction led to the increase of standing water. The term malaria originates from Medieval Italian: mala aria - "bad air"; the disease was formerly called ague or marsh fever due to its association with swamps and marshland. Malaria was once common in most of Europe and North America, where it is no longer endemic, though imported cases do occur. Malaria was the most important health hazard encountered by U.S. troops in the South Pacific during World War II, where about 500,000 men were infected. According to Joseph Patrick Byrne, "Sixty thousand American soldiers died of malaria during the African and South Pacific campaigns." Scientific studies on malaria made their first significant advance in 1880, when a French army doctor working in the military hospital of Constantine in Algeria named Charles Louis Alphonse Laveran observed parasites for the first time, inside the red blood cells of people suffering from malaria. He therefore proposed that malaria is caused by this organism, the first time a protist was identified as causing disease. For this and later discoveries, he was awarded the 1907 Nobel Prize for Physiology or Medicine. The malarial parasite was called Plasmodium by the Italian scientists Ettore Marchiafava and Angelo Celli. A year later, Carlos Finlay, a Cuban doctor treating people with yellow fever in Havana, provided strong evidence that mosquitoes were transmitting disease to and from humans. This work followed earlier suggestions by Josiah C. Nott, and work by Sir Patrick Manson, the "father of tropical medicine", on the transmission of filariasis.In April 1894, a Scottish physician Sir Ronald Ross visited Sir Patrick Manson at his house on Queen Anne Street, London. This visit was the start of four years of collaboration and fervent research that culminated in 1898 when Ross, who was working in the Presidency General Hospital in Calcutta, proved the complete life-cycle of the malaria parasite in mosquitoes. He thus proved that the mosquito was the vector for malaria in humans by showing that certain mosquito species transmit malaria to birds. He isolated malaria parasites from the salivary glands of mosquitoes that had fed on infected birds. For this work, Ross received the 1902 Nobel Prize in Medicine. After resigning from the Indian Medical Service, Ross worked at the newly established Liverpool School of Tropical Medicine and directed malaria-control efforts in Egypt, Panama, Greece and Mauritius. The findings of Finlay and Ross were later confirmed by a medical board headed by Walter Reed in 1900. Its recommendations were implemented by William C. Gorgas in the health measures undertaken during construction of the Panama Canal. This public-health work saved the lives of thousands of workers and helped develop the methods used in future public-health campaigns against the disease. The first effective treatment for malaria came from the bark of cinchona tree, which contains quinine. This tree grows on the slopes of the Andes, mainly in Peru. The indigenous peoples of Peru made a tincture of cinchona to control malaria. The Jesuits noted the efficacy of the practice and introduced the treatment to Europe during the 1640s, where it was rapidly accepted. It was not until 1820 that the active ingredient, quinine, was extracted from the bark, isolated and named by the French chemists Pierre Joseph Pelletier and Joseph Bienaim-Caventou. Quinine become the predominant malarial medication until the 1920s, when other medications began to be developed. In the 1940s, chloroquine replaced quinine as the treatment of both uncomplicated and severe falciparum malaria until resistance supervened, first in Southeast Asia and South America in the 1950s and then globally in the 1980s. Artemisinins, discovered by Chinese scientists in the 1970s, are now the recommended treatment for falciparum malaria, administered in combination with other antimalarials as well as in severe disease.

SOCIETY AND CULTURE

Malaria is not just a disease commonly associated with poverty but also a cause of poverty and a major hindrance to economic development. Tropical regions are affected most; however, malaria's furthest extent reaches into some temperate zones with extreme seasonal changes. The disease has been associated with major negative economic effects on regions where it is widespread. During the late 19th and early 20th centuries, it was a major factor in the slow economic development of the American southern states. A comparison of average per capita GDP in 1995, adjusted for parity of purchasing power, between countries with malaria and countries without malaria gives a fivefold difference ($1,526 USD versus $8,268 USD). In countries where malaria is common, average per capita GDP has risen (between 1965 and 1990) only 0.4% per year, compared to 2.4% per year in other countries. Poverty is both a cause and effect of malaria, since the poor do not have the financial capacities to prevent or treat the disease. In its entirety, the economic impact of malaria has been estimated to cost Africa $12 billion USD every year. The economic impact includes costs of health care, working days lost due to sickness, days lost in education, decreased productivity due to brain damage from cerebral malaria, and loss of investment and tourism. In some countries with a heavy malaria burden, the disease may account for as much as 40% of public health expenditure, 30-50% of admissions to hospital, and up to 50% of outpatient visits. The slow demographic transition in Africa may be partly attributed to malaria. Total fertility rates were best explained by child mortality, as measured indirectly by infant mortality, in a 2007 study. A study on the effect of malaria on IQ in a sample of Mexicans found that exposure during the birth year to malaria eradication was associated with increases in IQ. It also increased the probability of employment in a skilled occupation. The author suggests that this may be one explanation for the Flynn effect and that this may be an important explanation for the link between national malaria burden and economic development. The cognitive abilities and school performance are impaired in sub-groups of people (with either cerebral malaria or uncomplicated malaria) when compared with healthy controls. Studies comparing cognitive functions before and after treatment for acute malarial illness continued to show significantly impaired school performance and cognitive abilities even after recovery. Malaria prophylaxis was shown to improve cognitive function and school performance in clinical trials when compared to placebo groups. April 25 is World Malaria Day.

COUNTERFEIT AND SUBSTANDARD DRUGS

Sophisticated counterfeits have been found in several Asian countries such as Cambodia, China, Indonesia, Laos, Thailand, and Vietnam, and are an important cause of avoidable death in those countries. The WHO said that studies indicate that up to 40% of artesunate based malaria medications are counterfeit, especially in the Greater Mekong region and have established a rapid alert system to enable information about counterfeit drugs to be rapidly reported to the relevant authorities in participating countries. There is no reliable way for doctors or lay people to detect counterfeit drugs without help from a laboratory. Companies are attempting to combat the persistence of counterfeit drugs by using new technology to provide security from source to distribution. Another clinical and public health concern is the proliferation of substandard antimalarial medicines resulting from inappropriate concentration of ingredients, contamination with other drugs or toxic impurities, poor quality ingredients, poor stability and inadequate packaging. A 2012 study demonstrated that roughly one-third of antimalarial medications in Southeast Asia and Sub-Saharan Africa failed chemical analysis, packaging analysis, or were falsified.

WAR

Throughout history, the contraction of malaria (via natural outbreaks as well as via infliction of the disease as a biological warfare agent) has played a prominent role in the fortunes of government rulers, nation-states, military personnel, and military actions. "Malaria Site: History of Malaria During Wars" addresses the devastating impact of malaria in numerous well-known conflicts, beginning in June 323 B.C. That site's authors note: "Many great warriors succumbed to malaria after returning from the warfront and advance of armies into continents was prevented by malaria. In many conflicts, more troops were killed by malaria than in combat." The Centers for Disease Control ("CDC") traces the history of malaria and its impacts farther back, to 2700 BCE. In 1910, Nobel Prize in Medicine-winner Ronald Ross (himself a malaria survivor), published a book titled The Prevention of Malaria that included a chapter titled "The Prevention of Malaria in War." The chapter's author, Colonel C. H. Melville, Professor of Hygiene at Royal Army Medical College in London, addressed the prominent role that malaria has historically played during wars and advised: "A specially selected medical officer should be placed in charge of these operations with executive and disciplinary powers ." Significant financial investments have been made to procure existing and create new anti-malarial agents. During World War I and World War II, the supplies of the natural anti-malaria drugs, cinchona bark and quinine, proved to be inadequate to supply military personnel and substantial funding was funneled into research and development of other drugs and vaccines. American military organizations conducting such research initiatives include the Navy Medical Research Center, Walter Reed Army Institute of Research, and the U.S. Army Medical Research Institute of Infectious Diseases of the US Armed Forces. Additionally, initiatives have been founded such as Malaria Control in War Areas (MCWA), established in 1942, and its successor, the Communicable Disease Center (now known as the Centers for Disease Control) established in 1946. According to the CDC, MCWA "was established to control malaria around military training bases in the southern United States and its territories, where malaria was still problematic" and, during these activities, to "train state and local health department officials in malaria control techniques and strategies." The CDC's Malaria Division continued that mission, successfully reducing malaria in the United States, after which the organization expanded its focus to include "prevention, surveillance, and technical support both domestically and internationally."

ERADICATION EFFORTS

Several notable attempts are being made to eliminate the parasite from sections of the world, or to eradicate it worldwide. In 2006, the organization Malaria No More set a public goal of eliminating malaria from Africa by 2015, and the organization plans to dissolve if that goal is accomplished. Several malaria vaccines are in clinical trials, which are intended to provide protection for children in endemic areas and reduce the speed of transmission of the disease. As of 2012, The Global Fund to Fight AIDS, Tuberculosis and Malaria has distributed 230 million insecticide-treated nets intended to stop mosquito-born transmission of malaria. According to director Inder Singh, the U.S.-based Clinton Foundation has significantly reduced the cost of drugs to treat malaria, and is working to further reduce the spread of the disease. Other efforts, such as the Malaria Atlas Project focus on analyzing climate and weather information required to accurately predict the spread of malaria based on the availability of habitat of malaria-carrying parasites. Malaria has been successfully eradicated in certain areas. The Republic of Mauritius, a tropical island located in the western Indian Ocean, considered ecological connections to malaria transmission when constructing their current plan for malaria control. To prevent mosquitoes from breeding in aquatic areas, DDT is used in moderate amounts. Additionally, larvae-eating fish are placed in water sources to remove the malaria vectors before they become a threat to the human population. Obstructions are also removed from these sources to maintain water flow and reduce stagnant water. Similarly, marsh or swamp-like environments are drained and filled to diminish mosquito breeding grounds. These actions have produced positive results. The program has cut infection and death rates tremendously, and is cost effective, only requiring $1USD per head each year. This success is a clear indication that responses to adverse environmental conditions can decrease rates of disease.

RESEARCH

With the onset of drug-resistant Plasmodium parasites, new strategies are required to combat the widespread disease. One such approach lies in the introduction of synthetic pyridoxal-amino acid adducts, which are channeled into the parasite. Thus, trapped upon phosphorylation by plasmodial PdxK (pyridoxine/pyridoxal kinase), the proliferation of Plasmodium parasites is effectively hindered by a novel compound, PT3, a cyclic pyridoxyl-tryptophan methyl ester, without harming human cells.Malaria parasites contain apicoplasts, an organelle usually found in plants, complete with their own functioning genomes. These apicoplasts are thought to have originated through the endosymbiosis of algae and play a crucial role in various aspects of parasite metabolism, for example in fatty acid biosynthesis. As of 2003, 466 proteins have been found to be produced by apicoplasts and these are now being investigated as possible targets for novel anti-malarial drugs. Malaria vaccines have been an elusive goal of research. The first promising studies demonstrating the potential for a malaria vaccine were performed in 1967 by immunizing mice with live, radiation-attenuated sporozoites, which provided significant protection to the mice upon subsequent injection with normal, viable sporozoites. Since the 1970s, there has been a considerable effort to develop similar vaccination strategies within humans. It was determined that an individual can be protected from a P. falciparum infection if they receive over 1,000 bites from infected yet irradiated mosquitoes.

IMMUNIZATION

Immunity (or, more accurately, tolerance) does occur naturally, but only in response to repeated infection with multiple strains of malaria. A completely effective vaccine is not yet available for malaria, although several vaccines are under development. SPf66 was tested extensively in endemic areas in the 1990s, but clinical trials showed it to be insufficiently effective. Other vaccine candidates, targeting the blood-stage of the parasite's life cycle, have also been insufficient on their own. Several potential vaccines targeting the pre-erythrocytic stage are being developed, with RTS,S showing the most promising results so far.

IN OTHER ANIMALS

Parasitic Plasmodium species also infect birds, reptiles, monkeys, chimpanzees and rodents.

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MANSONELLA

Is a vector-borne human filarial nematode, transmitted by tiny blood-sucking flies called midges. Mansonella perstans is one of two filarial nematodes that cause Serous Cavity Filariasis in humans. The other filarial nematode is Mansonella ozzardi. Mansonella perstans is widespread in many parts of Sub-Saharan Africa, parts of Central and South America, and the Caribbean. Compared to infections with other filarial parasites such as Wuchereria bancrofti, Brugia malayi, and Loa loa, Mansonella infections are relatively mild. However, the pathogenicity of M. perstans infection has been recently reconsidered in various studies. These studies have demonstrated that M. perstans has the ability to induce a variety of clinical features, including angioedema Calabar-like swellings, pruritus, fever, headache, high eosinophilia, and abdominal pain. The overall disability among populations in regions where filariae are endemic has been difficult to determine because of high rates of co-infeciton with other filariae and the non-specificity of M. perstan infections. Furthermore, treatment of M. perstans is challenging because the most anti-filarial drugs such as ivermectin, Diethylcarbamazine and albendazole are not effective. The optimal treatment for M. perstans infection still remains unclear. Most current studies are focused on 1) co-infection of M. perstans with other filarial parasites and 2) the study of Wolbachia bacteria as endosymbionts in M. perstans and other filarial parasites.

HISTORY AND DISCOVERY

In 1890, the microfilariae of M. perstans were first discovered by Manson in the blood of a patient from West Africa who was hospitalized with sleeping sickness in London. Because the microfilariae were first noted in a patient with African Trypanosomyasis, M. perstans was initially suspected to be the cause of this disease. The idea that M. perstans caused African Trypanosomyasis was later ruled out by the Royal Society Sleeping Sickness Commission, who showed that geographical distribution of sleeping sickness did not coincide with that of M. perstans infection. Upon their discovery, the microfilariae were named Filaria sanguinis hominis minor, due to their relatively small size when compared to another type of microfilarae found in the same patient (Filaria sanguinis hominis major, which is now known as Loa loa). The name was later changed to Filaria sanguinis hominis perstans, and later again shortened to Filaria perstans to comply with the binary system of nomenclature. Over time, the name continued to change as changes in the generic status of the parasite took place. In 1984, Eberhard and Orihel redefined the genus Mansonella and included the perstans species in it. The parasite is therefore currently known as M. perstans. The adult worms of M. perstans were first recovered during post mortem examination of two aboriginal Indians in British Guiana from their mesentery and subpericardial fat. While an insect vector was hypothesized, it took many years of investigation before the true vector of M. perstans was discovered.Manson P (1891). The Filaria sanguinis hominis major and minor, two new species of haematozoa. Lancet 137:4-8.

CLINICAL PRESENTATION IN HUMANS

While Mansonella infections are often asymptomatic, they can be associated with angioedema (similar to Calabar swellings of loaisis) recurrent pruritic subcutaneous lesions, fever, headaches, arthralgia, and neurologic manifestations. Eosinophilia, headache, fever or abdominal pain may also be present. M. perstans may also present with a condition known as Kampala, or Ugandan eye worm. This occurs when adult worms of M. perstans invade the conjunctiva or periorbital connective tissues in the eye. This condition was first attributed to M. perstans in Uganda, when six patients presented with nodules in the conjunctiva. The adult worms were identified as adult female M. perstans in five out of these six cases. The symptoms of M. perstans may be confounded with those of other filarial infections such as onchocerciasis, lymphatic filariasis and loiasis, because co-infection often occurs.

CASE STUDY

A 36-year-old man was admitted to the outpatient clinic at the Goundi Missionary Hospital in the south of Chad in May 2001. He complained of visual impairment in the left eye, ocular and abdominal pruritus and abdominal pain. He had previously been treatmed with DEC for M. perstans infection five months prior to his visit. A blood sample was taken at 11:00 am, and examined microscopically as a thick blood film stained with Giemsa's solution. The thick blood film revealed the presence of M. perstans, and no other parasites were found. He had 3% eosinophilia. A visual acuity test showed a reduction of visual acuity to 4/10 for the left eye, while the right eye was 9.10. However, no abnormalities were observed during examination of the anterior left eye chamber. Upon examination of the fundus of his left eye, a narrow, white, motionless, and linear lesion of 6-7 mm was found. He was then treated with a second course of DEC (400 mg daily in 2 doses for 8 days, after a 3 day dosage increase), and by the end of treatment he did not have pruritus, but his visual impairment was unchanged. The M. perstans burden was significantly reduced, and the peripheral eosinohpil count decreased to 1%. He was then treated with mebendazole (100 mg 2x day, for 14 days), and at the end of his treatment his visual impairment was the only symptom remaining. After a week, with no further treatment, his vision improved and acuity was increased to 8/10 in the left eye. While ocular symptoms occur quite frequently in symptomatic M. perstans infection, intraocular localization had not been described prior to this study. This case also is an example of the difficulty of treating mansonelliasis, and shows that combined drug regimens can be more effective than treatment using a single drug.

OTHER RELEVANT CLINICAL INFORMATION

Studies have showed that M. perstans might potentially interfere with the host's regulatory mechanisms and influence the outcome of other infections such as malaria, tuberculosis and HIV, which often thrive in similar environments. Recent research has also focused on coinfection of M. perstans and other filarial parasites. A study examining the epidemiology of Loa loa, Onchocerca voluvulus, and M. perstans in the rain forest villages of Cameroon found that there was a high prevalence of co-infection with Onchocerca voluvulus and M. perstans. It also found a low prevalence of L. loa and O. voluvulus co-infection, as well as low prevalence of L. loa and M. perstans coinfection. Co-infection also has singficant implications for treatment, because efficacious drugs for M. perstans are different than those for most filarial infections. Another study evaluated the effectiveness of ivermectin and albendazole in M. perstans and Wuchereria bancrofti coinfection in a filarial endemic region of Mali, finding that M. perstans infection did not have a significant effect on the treatment of W. bancrofti. Other studies have evaluated the efficacy of other treatments on co-infection with other filarial parasites and M. perstans.

TRANSMISSION

TransmissionMansonella perstans is transmitted by the bite of species of Culicoides midges. Only the female midges take blood meals, because the blood is needed for the maturation of eggs within the female.

RESEVOIR

Humans are the only known reservoir for M. perstans. There are no animal reservoirs for M. perstans as there are for Mansonella streptocerca.

VECTOR

The insect vectors of M. perstans are biting midges belonging to the genus Culicoides. Various species of Culicoides can be found worldwide, and in some areas their high numbers make them a biting nuisance to humans and domestic animals. Culicoides are stout flies with a short vertical proboscis and wings folded scissor-like over the abdomen at rest. They generally measure 1?4 mm in length. The wings of most species have a pattern of light and dark marks. While certain species of Culicoides such as austeni and grahamii have been hypothesized to play a larger role than other species in the transmission of M. perstans, very few studies have attempted to identify the species of vectors of M. perstans in endemic areas. This issue is further complicated because the taxonomy of tropical Culicoides species is still uncertain. Biting midges progress from egg, to larva, pupa, and finally the adult stage. The complete cycle takes 2?6 weeks, and is dependent on environmental conditions. The females usually bite around dawn and dusk, although it can also occur at other times. Eggs are laid 3?4 days after the blood meal, and about 70-180 eggs are laid each time. Moisture is essential for the vector, and the development of its eggs and larvae. Adult Culicoides survive for a few weeks, and their flight range is limited to a few hundred meters from their larval habitats.

INCUBATION PERIOD

5m - 18m (range 1m - 2y)

MORPHOLOGY

Adults are white and thread-like, and have been found to be cylindrical in shape. Males are 35-55-mm long and 45-60-um wide. Females are bigger, 70?80-mm long and 80-120-um wide. The tail is half a coil in females and a full coil in males. Adult worms are rarely seen, but sometimes can be recovered from a laparotomy or autopsy. Microfilariae of M. perstans are unsheathed, have a blunt tail, and nuclei extend to the end of the tail. The microfilariae have a length of 200 micrometers, and a width of 4.5 micrometers. They have the ability to elongate and contract, so they can vary in measurement and form. They are smaller than those of Loa loa, which have tapered tails and are frequently coiled. The microfilariae of M. perstans are smaller than those of W. bancrofti and the caudal end is blunt with a terminal nucleus.

LIFE CYCLE

Step 1: During a blood meal, an infected midge (Culicoides grahami and C. austeni) introduces third-stage (L3) filarial larvae onto the skin of the human host, where they penetrate into the bite wound. It is likely that the body temperature activates the larva and prompts it to leave the vector and actively penetrate the skin.
Step 2: The third-stage larvae develop into adults that live in body cavities, most commonly the pleural and peritoneal cavities. They also can live in mesentery, peri-renal spaces, retroperitoneal spaces or the pericardium and mature into adults. The pericardium is the fluid filled sac that surrounds the heart and the proximal ends of the aorta, vena cava, and the pulmonary artery.
Step 3: Adults in the body cavities mate and produce unsheathed and subperiodic microfilariae that reach the blood stream. The microfilariae can also be found in the cerebrospinal fluid. While the periodicity of these midges has been unclear, the most recent study suggests that microfilariae indicate a weak but significant diurnal periodicity with a peak around 8 am.
Step 4: A Culicoides midge ingests microfilarae during a blood meal.
Step 5: After ingestion, the microfilariae migrate from the midge?s midgut through the hemocoel to the thoracic muscles of the midge. In the thoracic muscles, the microfilariae develop into first-stage larvae (L1).
Step 6: They subsequently develop into third-stage larvae, which are infective.
Step 7: The third stage larvae migrate to the midge?s proboscis
Step 8: Third-stage larvae can infect another human when the midge takes a blood meal.

DIAGNOSTIC TESTS

Similar to other filarial parasites, Mansonella perstans is diagnosed by the identification of microfilariae in the peripheral blood. Because the microfilariae are present in the peripheral blood in almost equal concentrations during day and night, blood samples can be obtained at any time (unlike other filarial microfilariae). The microfilariae are short and thin, unsheathed, and have rounded tails with nuclei at the extremity. The head spot sometimes has a V-shaped appearance. The blood sample can be a thick smear, stained with Giemsa or hematoxylin and eosin. For increased sensitivity, concentration techniques can be used. These include centrifugation of the blood sample lyzed in 2% formalin (Knott's technique), or filtration through a Nucleopore-membrane. Serology is not very useful for diagnosis. Because the adult worms live mainly in pleural and peritoneal cavities, they are only rarely observed. At times, they can be observed during a laparotomy. Mansonella perstans often occurs with other filarial infections such as onchocerciasis and lymphatic filariasis. Mansonella perstans should be distinguished from Microfilaria semiclarum (a parasite of animals which sometimes causes accidental infections in humans. Sometimes confusion is possible if the blood smear is randomly infected during or after preparation with a mould such as Helicospora. This organism, however, is considerably smaller and thinner than a microfilaria. The DEC, or Mazzotti test, has been shown to have minor effects on microfilariae intensity, but it is not of practical use for diagnosis of Mansonelliasis.

MANAGEMENT AND TREATMENT

Mansonella perstans is one of the most difficult human filarial infections to treat. Effective treatment for Mansonelliasis is lacking, and there is no consensus among the scientific community on the optimal approach. Numerous trials evaluating traditional antifilarial drugs such as ivermectin and DEC, as well as other benzimidazoles such as mebendazole, albendazole, levamizole, and thiabendazole have been conducted. Recently, clinical trials assessing the effectiveness of doxycycline to treat M. perstans infection have also been documented.
Generally, DEC is ineffective in the treatment of M. perstans infection. Other drugs such as ivermectin and praziquantel have been tried, but are neither reliable nor rapidly effective. Mebendazole and thiabendazole have a greater effect than previously described drugs, but are not sufficient for treatment alone. Combination treatments with DEC and mebendazole have had the most success. In the most recent clinical trials, doxycycline has had success comparable to, if not better than that that of combination treatments. However, because it is a relatively recent phenomenon, the use of doxycycline is relatively limited to clinical trials. If the patient is asymptomatic, no treatment is necessary. An analysis of the results of various clinical trials for each drug is illustrated below:
DECDose: 200 mg, 2x/day for 21 days, gradual dosage increase in the first 3 days While DEC is the most common drug used to treat M. perstans infection, it is often ineffective, especially with the administration of only a single dose. In a 2005 study of 160 patients with symptomatic M. perstans infection in south Chad, DEC was administered in 200 mg doses, twice daily for 21 days with a gradual dosage increase in the first 3 days. The single course of DEC lowered microfilarae in 80% of subjects, but did not eliminate the infection or related symptoms. A second course was therefore administered, and was successful in eliminating the microfilariae burden in most cases. No persistent effect of DEC on microfilariae was noted on long-term follow up. These results accurately represent the general efficacy of DEC in treating M. perstans: two doses are necessary to eliminate the microfilariae burden temporarily, there is no persistent effect of DEC on microfilariae long-term. Furthermore, symptoms are usually not entirely alleviated by DEC. DEC has not been reported to cause adverse side effects in patients with M. perstans infection.
IvermectinDose: 200 ug/kg bodyweight (2x/week for 3 weeks) While ivermectin is considered a first-line agent for the treatment of many filarial diseases (especially Onchocerciasis), it has showed little or no efficacy against M. perstans at a dose of 200 ug/kg body weight or at a dose of 600 ug/kg body weight. In a 2009 study in Uganda evaluated the effects of ivermectin, albendazole, and a combined regimen with both drugs on M. perstans infected individuals. In this study, single doses of ivermectin alone had no marked effect on M. perstans microfilaraemias in the 12 months post-treatments, with the counts remaining to pre-treatment values. This is consistent with the findings of previous studies which have suggested that ivermectin, when used alone, has little or no effect on M. perstans microfilaraemias. A reduction of microfilariae in patients has been noted, but it takes a long time to achieve (over 3 years of administration of ivermectin), and is thus not useful in the short period for symptomatic patients. AlbendazoleDose: 400 mg, regardless of body weight Single-doses of albendazole alone have been consistently reported to have little or no effect on M. perstans microfilaremias in 6 and 12 months post-treatment, with counts of M. perstans microfilaremias remaining close to pre-treatment values. More recent studies have shown the drug to be more effective at high doses for prolonged periods of time. No side effects have been reported from recent studies.
MebendazoleDose: 400 mg (2x/day for 28 days) Mebendazole, another possible treatment for M. perstans filariasis has been shown to be effective in significantly reducing microfilariae levels. It has been more effective than both ivermectin and DEC - with a greater number of responders, a more significant reduction in microfilariae levels, and the ability to eliminate the infection more efficiently.
ThiabendazoleDose: 50 mg/kg for children and 3g for adults (either single dose, or two doses 7 days apart). Thiabendazole has been shown to result in a small but significant decrease in microfilariae and in eosinophil count, and symptoms as treatment for symptomatic M. perstans infection. These markers were reduced even further following the administration of the second dose, showing that thiabendazole may be effective in M. perstans infection. In a recent comparative study, thiabendazole at a higher activity than single drug treatments such as ivermectin, DEC, and mebendazole, but lower activity than the combined regimen of mebendazole and DEC. However, more research may be needed into confirm the correct dosage and true effectiveness of thiabendazole in combating M. perstans infection. PraziquantelDose: 40 mg/kg in a single administration. Praziquantel is effective against various helminthic and protozoan infections. A few studies are present in the literature about the use of praziquantel against M. perstans infection, and they do not support its use for treatment of mansonelliasis.
DoxycyclineDose: 200 mg (daily, 4-8 weeks) Doxycycline has been shown to decrease the development, embryogenesis, and fertility of worms in species that harbor the intracellular endosymbiont wolbachia. Wolbachiae are bacterial endosymbionts of insects and many filarial nematodes, such as Onchocerca volvulus, Wuchereria bancrofti, and Brugia malayi. The dependence of these parasites on their endosymbionts has led to the use of antibiotics directed against the Wolbachiae, antibiotics that have been demonstrated to have a profound salutary effect on filarial infections. In 2009, Coulibaly et al. conducted an open-label randomized trial of doxycycline, an antibiotic, for Mansonella perstans infection. This resulted in a dramatic and sustained decrease in microfilarial levels: they decreased to 23% of pretreatment levels at 6 months after treatment and to 0% of pretreatment levels at 12 months after treatment. In addition, doxycycline has been shown to have macrofilaricidal activity, which is unique among the drugs for filariasis.
However, in some areas such as Gabon and Uganda, wolbachiae have not been detected in the microfilariae of M. perstans. This data suggests that some geographic isolates of M. perstans may have lost (or gained) the endosymbiont. This has occurred in various geographic isolates of Brugia malayi, in which the Wolbachia pipens genome is integrated into the chromosome of their hosts (the parasite). When this integration occurs, wolbachia can no longer be targeted as means for treatment for filariasis. This presents a controversial argument for the use of doxycycline as treatment of filarial infections. On one hand, doxycycline has been shown to be one of the only successful treatments for M. perstans, and could facilitate the eradication of filarial parasites. However, some scientists argue that the treatment of Filariasis with doxycycline may select worms that will have already integrated wolbachia into their genome, which could potentially have unforeseen consequences.
Combination RegimensCombination treatments consisting of DEC plus mebendezole, or ivermectin and albendazole, have been shown to result in a highly significant fall in microfilariae. Other studies have challenged these findings, suggesting that the combination treatment of ivermectin and albendazole does not significantly reduce microfilariae levels more than a single treatment regimen.

EPIDEMIOLOGY

Mansonella perstans is found in tropical Africa, central and eastern South America, Central America, and the Caribbean. The parasite is widespread in many parts of Sub-Saharan Africa?infections have been reported from 33 countries in this region. In certain locations in Zaire, Nigeria, Ghana, Sierra Leone, Ivory Coast, Zambia, and Uganda extremely high proportions of the inhabitants show signs of infection. It often occurs among poor populations living in rural villages. M. perstans is also found in the New World in Venezuela, Trinidad, Guyana, Surinam, northern Argentina and Amazonia. This parasite does not occur in Asia. It also does not occur in the most northern and southern regions of Africa. A recent review of M. perstans in Africa states that approximately 114 million people are infected with this parasite in Africa today.

PUBLIC HEALTH AND PREVENTION STRATEGIES

The ongoing large-scale programs for control of onchocerciasis and lymphatic filariasis have paid little attention to mansonelliasis. Despite the high prevalence of Mansonella perstans in areas of tropical Africa such as Uganda, the Congo, Republic of Cameroon, and Gabon, no vector programs have been instituted for any of the mansonelliasis-causing parasites. Major reasons for this lack of attention are that M. perstans infections prevail in poor, rural populations and that infection with the parasite has not been linked with a clear and distinct medical picture. Much of the information regarding M. perstans has been obtained as a side-product from studies of other filarial parasites. Mansonelliasis can thus be classified as one of the most neglected among the Neglected Tropical Diseases. Culicoides are small enough to pass through screening or mosquito nets, so these would not be helpful. Protection of visitors to endemic areas can be achieved through the use of insect repellents.

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MEMORY LOSS

Memory loss can be partial or total, and it is normal when it comes with aging. Sudden memory loss is usually a result of brain trauma and it may be permanent or temporary. When it is caused by medical conditions such as Alzheimers, the memory loss is gradual and tends to be permanent. Brain trauma is not the only factor that can cause sudden memory loss. It may appear as a side effect of statin drugs that are used as treatment for those who have hypercholesterolemia. Major causes of sudden loss of memory are strokes. Other causes are long lasting and recurrent illnesses such as meningitis or epilepsy. Either temporary or permanent memory loss can also result from chemical imbalances, exposure to toxic substances, allergies, vitamin deficiencies (such as those caused by alcoholism), or extreme mental illness (Major Depressive Disorder).

SYMPTOMS

Symptoms of memory loss vary from person to person, but can include: forgetting dates and names; beginning a task but then forgetting the purpose of it; getting lost easily; repeating things over and over again, sometimes in the same conversation; and having difficulties performing familiar tasks such as driving or baking. They usually occur gradually and may vary in intensity depending on the cause of the condition. Confusion or decreased alertness may be the first symptom of memory loss and also of serious illness, particularly in older adults. The most worrisome symptoms are not those related to things that people forget to do.[opinion] Some patients may have problems mixing up or remembering words for objects or can have trouble understanding or taking part in a conversation. Being unable to make a simple decision can suggest that something is not working as it should and medical advice should be sought. Whether an individual suffers from memory loss is not decided only based on one's symptoms. In order to diagnose the condition a doctor will obtain a detailed medical history of the patient. The patient will also undergo several neuropsychological tests that will focus on his or her memory functions. Several other medical exams such as an electroencephalography, an MRI, or a CT scan can be performed in order to establish an accurate diagnosis. The main type of memory loss is short-term memory. Short-term memory refers to memories that last for a few minutes .

CAUSES

Side effects of Medication: Many drugs can cause cognitive problems and memory loss as a side effects, common in adults. Common drugs that affect memory and brain function include sleeping pills, antihistamines, blood pressure and arthritis medication, antidepressants, anti-anxiety medications, and painkillers. Depression: Depression mimics the signs of memory loss. It is a common problem in older adults?especially if one is less social and active than they used to be or if one has recently experienced a number of major life changes (retirement, a serious medical diagnosis, the loss of a loved one, moving away from home). Vitamin B12 Deficiency: Vitamin B12 protects neurons and is vital to healthy brain functioning. A lack of B12 can cause permanent damage to the brain.

PREVENTION

The most common preventable cause of memory loss is brain trauma, especially trauma resulting from head injury. Preventative measures such as wearing a seat belt while driving or a helmet while biking, can reduce the risk of head injury while participating in dangerous activities. Eating nutritious foods and reducing stress may help prevent memory loss. In addition, it may be helpful to avoid risk factors such as alcohol abuse and exposure to toxic chemicals. As high blood pressure increases the risk for stroke, and therefore memory loss, blood pressure should be kept under control. Lifestyle adjustments such as smoking cessation and exercise can also further reduce the risk for stroke and brain trauma. Some specialists recommend that patients drink enough water for better hydration. Sleep deprivation and stress are also thought to impact the proper functioning of the brain cells, so it is important to get enough rest and avoid stressful activities. Socializing is also believed to be beneficial for individuals who may develop memory loss. Patients who experience memory loss as a result of aging may keep their brain cells healthy and active with exercise and dietary supplements. However, although some dietary choices and lifestyle changes are suggested, it has not yet been proven to what extent these may reduce the risk of memory loss, especially that caused by aging. Dietary supplements that may be recommended include multivitamins and mineral complexes, boron, lecithin, garlic, gingko, vitamin B complex, zinc, copper, acetylcholine, DMAE, and vitamin C with bioflavonoid. Patients whose memory loss is bothersome to the extent that it becomes an issue are encouraged to establish a routine and follow it. Making lists and associations, keeping a detailed calendar as well as always putting important objects in the same place might also help them in remembering more easily and faster. It has been brought to attention that people who develop mild symptoms of memory loss are more likely to prevent the worsening of the condition if they train their mind by playing strategy games, puzzle, word games or number puzzles and reading. Basically, stimulating the brain can help patients slow down the processes that cause memory loss. Memory loss among seniors is not inevitable, but is a normal occurrence for many as the brain slows down. This is not the same thing as dementia. Mental functions to do normal activities you have always done, life experience, common sense, and the ability to form reasonable judgments and arguments are not affected. Exercise, especially aerobic exercise, helps combat or restore memory loss. Studies indicate that exercise lessens stress, increases blood flow, and stabilizes and deepens sleep patterns. Even walking a few times a week helps fight memory loss.

TREATMENT

Memory loss can't be treated unless it is caused by a reversible condition. The treatment is greatly dependent on the primary cause of the condition. When memory loss is a symptom of a more severe disease, it may be reversed as soon as the underlying condition is identified and cured. Memory loss due to aging cannot be cured, but the symptoms may be improved by following the prevention measures. Treating mild cases of memory loss may consist of herbal medications or a change in lifestyle. The other dietary supplements along with good quality and long sleep and avoiding potential risk factors may also improve the general status of the patient. Family support plays an important role in treating memory loss. Family members are usually encouraged to take special orientation classes on how to cope with their sick relatives and how to help them improve their condition.

PATHOLOGY

The memory is affected by the damage that may occur in the different parts of the brain such as medial temporal lobe, hippocampus, cortex and frontal lobes. Injuring any of these areas may lead to specific disruptions in the processes of acquiring and restoring memory. For instance, damage to the medial temporal lobe and hippocampus can devastate the ability to acquire new declarative memory whereas damage to the storage areas in cortex can disrupt retrieval of old memories and interfere with acquisition of new memories.

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MESENTERIC ISCHEMIA

Mesenteric ischemia (or Mesenteric ischaemia - British English) is a medical condition in which inflammation and injury of the small intestine result from inadequate blood supply. Causes of the reduced blood flow can include changes in the systemic circulation (e.g. low blood pressure) or local factors such as constriction of blood vessels or a blood clot. It is more common in the elderly.

SIGNS AND SYMPTOMS

A hyper active stage occurs first, in which the primary symptoms are severe abdominal pain and the passage of bloody stools. Many patients get better and do not progress beyond this phase. A paralytic phase can follow if ischemia continues; in this phase, the abdominal pain becomes more widespread, the belly becomes more tender to the touch, and bowel motility decreases, resulting in abdominal bloating, no further bloody stools, and absent bowel sounds on exam. Finally, a shock phase can develop as fluids start to leak through the damaged colon lining. This can result in shock and metabolic acidosis with dehydration, low blood pressure, rapid heart rate, and confusion. Patients who progress to this phase are often critically ill and require intensive care.

CLINICAL FINDINGS

Symptoms of mesenteric ischemia vary and can be acute (especially if embolic), subacute, or chronic. Case series report prevalence of clinical findings and provide the best available, yet biased, estimate of the sensitivity of clinical findings. In a series of 58 patients with mesenteric ischemia due to mixed causes:
abdominal pain was present in 95% (median of 24 hours duration). The other three patients presented with shock and metabolic acidosis. nausea in 44% vomiting in 35% diarrhea in 35% heart rate > 100 in 33% 'blood per rectum' in 16% (not stated if this number also included occult blood - presumably not) constipation 7%

DIAGNOSTIC HEURISTICS

In the absence of adequate quantitative studies to guide diagnosis, various heuristics help guide diagnosis: Mesenteric ischemia "should be suspected when individuals, especially those at high risk for acute mesenteric ischemia, develop severe and persisting abdominal pain that is disproportionate to their abdominal findings" Regarding mesenteric arterial thrombosis or embolism: "...early symptoms are present and are relative mild in 50% of cases for three to four days before medical attention is sought". Regarding mesenteric arterial thrombosis or embolism: "Any patient with an arrhythmia such as atrial fibrillation who complains of abdominal pain is highly suspected of having embolization to the superior mesenteric artery until proved otherwise". Regarding nonocclusive intestinal ischemia: "Any patient who takes digitalis and diuretics and who complains of abdominal pain must be considered to have nonocclusive ischemia until proved otherwise".

DIAGNOSIS

It is difficult to diagnose mesenteric ischemia early. One must also differentiate ischemic colitis, which often resolves on its own, from the more immediately life-threatening condition of acute mesenteric ischemia of the small bowel.

BLOOD TESTS

In a series of 58 patients with mesenteric ischemia due to mixed causes:
White blood cell count >10.5 in 98% (probably an overestimate as only tested in 81% of patients) Lactic acid elevated 91% (probably an overestimate as only tested in 57% of patients).

DEVICE FOR DIAGNOSIS DURING ENDOSCOPY

A number of devices have been used to assess the sufficiency of oxygen delivery to the colon. The earliest devices were based on tonometry, and required time to equilibrate and estimate the pHi, roughly an estimate of local CO2 levels. The first device approved by the U.S. FDA (in 2004) used visible light spectroscopy to analyze capillary oxygen levels. Use during Aortic Aneurysm repair detected when colon oxygen levels fell below sustainable levels, allowing real-time repair. In several studies, specificity has been 83% for chronic mesenteric ischemia and 90% or higher for acute colonic ischemia, with a sensitivity of 71%-92%.

PLAIN EX-RAY

Plain X-rays are often normal or show non-specific findings.

COMPUTED TOMOGRAPHY

Computed tomography (CT scan) is often used. The accuracy of the CT scan depends on whether a small bowel obstruction (SBO) is present. . SBO absent: prevalence of mesenteric ischemia 23% sensitivity 64% specificity 92% positive predictive value (at prevalence of 23%) 79% negative predictive value (at prevalence of 23%) 95%
SBO present: prevalence of mesenteric ischemia 62% sensitivity 83% specificity 93% positive predictive value (at prevalence of 62%) 93% negative predictive value (at prevalence of 62%) 61%

Findings on CT scan include: Mesenteric edema Bowel dilatation Bowel wall thickening Intramural gas Mesenteric stranding

MESENTERIC ANGIOGRAPHY

As the etiology of the ischemia can be due to embolic or thrombotic occlusion of the mesenteric vessels or nonocclusive ichemia, the best way to differentiate between the etiologies is through the use of mesenteric angiography. Though it has serious risks, angiography provides the possibility of direct infusion of vasodilators in the setting of nonocclusive ischemia.

TREATMENT

"Surgical revascularisation remains the treatment of choice for mesenteric ischaemia, but thrombolytic medical treatment and vascular interventional radiological techniques have a growing role".

PROGNOSIS

The prognosis depends on prompt diagnosis (less than 12–24 hours and before gangrene) and the underlying cause: venous thrombosis - 32% mortality arterial embolism - 54% mortality arterial thrombosis - 77% mortality non-occlusive ischemia - 73% mortality

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MITE

Mites, along with ticks, are small arthropods belonging to the subclass Acari (also known as Acarina) and the class Arachnida. The scientific discipline devoted to the study of ticks and mites is called acarology.

DIVERSITY AND SYSTEMATICS

Mites are among the most diverse and successful of all the invertebrate groups. They have exploited an incredible array of habitats, and because of their small size (most are microscopic) go largely unnoticed. Many live freely in the soil or water, but there are also a large number of species that live as parasites on plants, animals, and some that feed on mold. It is estimated that 48,200 species of mites have been described. Some of the plant pests include the so-called spider mites (family Tetranychidae), thread-footed mites (family Tarsonemidae), and the gall mites (family Eriophyidae). Among the species that attack animals are members of the sarcoptic mange mites (family Sarcoptidae), which burrow under the skin. Demodex mites (family Demodicidae) are parasites that live in or near the hair follicles of mammals, including humans. Acari are mites, except for the three families of ticks. Perhaps the best-known mite, though, is the house dust mite (family Pyroglyphidae). Insects may also have parasitic mites. Examples are Varroa destructor, which attaches to the body of the honeybee, and Acarapis woodi (family Tarsonemidae), which lives in the tracheae of honey bees. There are hundreds of species of mites associated with other bee species, and most are poorly described and understood. Some are thought to be parasites, while others beneficial symbionts. The tropical species Archegozetes longisetosus is one of the strongest animals in the world, relative to its mass (100 ug): It lifts up to 1,182 times its own weight, over five times more than would be expected of such a minute animal.

MEDICAL SIGNIFICANCE

Dust mites cause several forms of allergic diseases, including hay fever, asthma and eczema and are known to aggravate atopic dermatitis. Mites are usually found in warm and humid locations, including beds. It is thought that inhalation of mites during sleep exposes the human body to some antigens that eventually induce hypersensitivity reaction. Dust mite allergens are thought to be among the heaviest dust allergens. Like most of the other types of allergy, treatment of mite allergy starts with avoidance. There is a strong body of evidence showing that avoidance should be helpful in patients with atopic dermatitis triggered by exposure to mites. Regular washing of mattresses and blankets with hot water can help in this regard. Antihistamines are also useful; Cetirizine, for example, is shown to reduce allergic symptoms of patients. However, not all types of mites are infectious to humans, such as Alaskozetes antarcticus, an Arctic mite. For the ones that do infest humans an antiparasitic insecticide such as benzyl benzoate or sulphur in the form of sulphur soap or sulphur powder is generally used to control and eliminate the mite population.

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MUCUS

In vertebrates, mucus (adjectival form: "mucous") is a slippery secretion produced by, and covering, mucous membranes. Mucous fluid is typically produced from mucous cells found in mucous glands. Mucus cells secrete products that are rich in glycoproteins and water. Mucous fluid may also originate from mixed glands, which contain both serous and mucous cells. It is a viscous colloid containing antiseptic enzymes (such as lysozyme), immunoglobulins, inorganic salts, proteins such as lactoferrin, and glycoproteins known as mucins that are produced by goblet cells in the mucous membranes and submucosal glands. This mucus serves to protect epithelial cells in the respiratory, gastrointestinal, urogenital, visual, and auditory systems in mammals; the epidermis in amphibians; and the gills in fish. A major function of this mucus is to protect against infectious agents such as fungi, bacteria and viruses. The average human body produces about a litre of mucus per day. Bony fish, hagfish, snails, slugs, and some other invertebrates also produce external mucus. In addition to serving a protective function against infectious agents, such mucus provides protection against toxins produced by predators, can facilitate movement and may play a role in communication.

RESPIRATORY SYSTEM

In the respiratory system, mucus aids in the protection of the lungs by trapping foreign particles that enter it, in particular, through the nose, during normal breathing. "Phlegm" is a specialized term for mucus that is restricted to the respiratory tract, whereas the term "nasal mucus" describes secretions of the nasal passages. Nasal mucus is produced by the nasal mucosa, and mucal tissues lining the airways (trachea, bronchus, bronchioles) is produced by specialized airway epithelial cells (goblet cells) and submucosal glands. Small particles such as dust, particulate pollutants, and allergens, as well as infectious agents such as bacteria are caught in the viscous nasal or airway mucus and prevented from entering the system. This event along with the continual movement of the respiratory mucus layer toward the oropharynx, helps prevent foreign objects from entering the lungs during breathing. This explains why coughing often occurs in smokers. The body's natural reaction is to increase mucus production. In addition, mucus aids in moisturizing the inhaled air and prevents tissues such as the nasal and airway epithelia from drying out. Nasal and airway mucus is produced continuously, with most of it swallowed unconsciously, even when it is dried. Increased mucus production in the respiratory tract is a symptom of many common illnesses, such as the common cold and influenza. Hypersecretion of mucus can occur in inflammatory respiratory diseases such as respiratory allergies, asthma, and chronic bronchitis. The presence of mucus in the nose and throat is normal, but increased quantities can impede comfortable breathing and must be cleared by blowing the nose or expectorating phlegm from the throat.

DISEASES INVOLVING THE MUCUS

In general, nasal mucus is clear and thin, serving to filter air during inhalation. During times of infection, mucus can change colour to yellow or green either as a result of trapped bacteria or due to the body's reaction to viral infection. The green color of mucus comes from the heme group in the iron-containing enzyme myeloperoxidase secreted by white blood cells as a cytotoxic defense during a respiratory burst. In the case of bacterial infection, the bacterium becomes trapped in already-clogged sinuses, breeding in the moist, nutrient-rich environment. Antibiotics may be used to treat the secondary infection in these cases, but will, in general, not help with the original cause. In the case of a viral infection such as cold or flu, the first stage and also the last stage of the infection cause the production of a clear, thin mucus in the nose or back of the throat. As the body begins to react to the virus (generally one to three days), mucus thickens and may turn yellow or green. Viral infections cannot be treated with antibiotics, and are a major avenue for their misuse. Treatment is generally symptom-based; often it is sufficient to allow the immune system to fight off the virus over time.

MUCUS AS A MEDICAL SYMPTOM

Increased mucus production in the upper respiratory tract is a symptom of many common ailments, such as the common cold. Nasal mucus may be removed by blowing the nose or by using traditional methods of nasal irrigation. Excess nasal mucus, as with a cold or allergies may be treated cautiously with decongestant medications. Excess mucus production in the bronchi and bronchioles, as may occur in asthma, bronchitis or influenza, may be treated with anti-inflammatory medications as a means of reducing the airway inflammation, which triggers mucus over-production. Thickening of mucus as a "rebound" effect following overuse of decongestants may produce nasal or sinus drainage problems and circumstances that promote infection.

COLD WEATHER AND MUCUS

During cold weather, the cilia, which normally sweep mucus away from the nostrils and toward the back of the throat (see respiratory epithelium), become sluggish or completely cease functioning. This results in mucus running down the nose and dripping (a runny nose). Mucus also thickens in cold weather; when an individual comes in from the cold, the mucus thaws and begins to run before the cilia begin to work again.

CYSTIC FIBROSIS

Cystic fibrosis is an inherited disease that affects the entire body, but symptoms begin mostly in the lungs with extremely viscous (thick) production of mucus that is difficult to expel.

DIGESTIVE SYSTEM

In the digestive system, mucus is used as a lubricant for materials that must pass over membranes, e.g., food passing down the esophagus. A layer of mucus along the inner walls of the stomach is vital to protect the cell linings of that organ from the highly acidic environment within it. Mucus does not digest in the intestinal tract. Mucus is also secreted from glands within the rectum due to stimulation of the mucous membrane within.

REPRODUCTIVE SYSTEM

In the female reproductive system, cervical mucus prevents infection. The consistency of cervical mucus varies depending on the stage of a woman's menstrual cycle. At ovulation cervical mucus is clear, runny, and conducive to sperm; post-ovulation, mucus becomes thicker and is more likely to block sperm. In the male reproductive system, the seminal vesicles contribute up to 100% of the total volume of the semen and contain mucus, amino acids, prostaglandins, vitamin C, and fructose as the main energy source for the sperm.

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NAUSEA

Nausea is a sensation of unease and discomfort in the upper stomach with an involuntary urge to vomit. It often, but not always, precedes vomiting. A person can suffer nausea without vomiting. Nausea is a non-specific symptom, which means that it has many possible causes. Some common causes of nausea are motion sickness, dizziness, migraine, fainting, gastroenteritis (stomach infection) or food poisoning. Side effects of many medications including cancer chemotherapy, nauseants or morning sickness in early pregnancy. Nausea may also be caused by anxiety, disgust and depression.

DIFFERENTIAL DIAGNOSIS

The causes of nausea are many. One organization listed 700 in 2009. Gastrointestinal infections (37%) and food poisoning are the two most common causes. While side effects from medications (3%) and pregnancy are also relatively frequent. In 10% of people the cause remains unknown.

FOOD POISONING

Food poisoning usually causes an abrupt onset of nausea and vomiting one to six hours after ingestion of contaminated food and lasts for one to two days. It is due to toxins produced by bacteria in food.

MEDICATIONS

Many medications can potentially cause nausea. Some of the most frequently associated include cancer chemotherapy regimens and general anaesthetic agents.

PREGNANCY

Nausea or "morning sickness" is common during early pregnancy but may occasionally continue into the second and third trimesters. In the first trimester nearly 80% of women have some degree of nausea. Pregnancy should therefore be considered as a possible cause of nausea in any women of child bearing age. While usually it is mild and self limiting severe cases known as hyperemesis gravidarum may require treatment.

DISEQUILIBRIUM

A number of conditions involving balance such as motion sickness and vertigo can lead to nausea and vomiting.

STRESS AND DEPRESSION

Nausea may be caused by stress and depression.

POTENTIALLY SERIOUS

While most causes of nausea are not serious, some serious causes do occur. These include: diabetic ketoacidosis, brain tumor, surgical problems, pancreatitis, small bowel obstruction, meningitis, appendicitis, cholecystitis, Addisonian crisis, Choledocholithiasis (from gallstones) and hepatitis, as a sign of carbon monoxide poison and many others.

DIAGNOSTIC APPROACH

Often no investigations are needed, however basic lab tests may be appropriate. If a bowel obstruction is possible, abdominal x-rays may be useful.

TREATMENT

If dehydration is present due to loss of fluids from severe vomiting and/or accompanying diarrhea, rehydration with oral electrolyte solutions is preferred. If this is not effective or possible, intravenous rehydration may be required.

MEDICATIONS

Dimenhydrinate (Gravol) is an inexpensive and effective medication for preventing postoperative nausea and vomiting. Meclozine is another antihistamine antiemetic. In certain people, cannabinoids may be effective in reducing chemotherapy associated nausea and vomiting. Ondansetron (Zofran) is effective for nausea and vomiting but is expensive. Pyridoxine or metoclopramide are the first line treatments for pregnancy related nausea and vomiting. Medical marijuana may be prescribed where allowed for certain indications.

PROGNOSIS

While short-term nausea and vomiting are generally harmless, they may sometimes indicate a more serious condition. When associated with prolonged vomiting, it may lead to dehydration and/or dangerous electrolyte imbalances.

EPIDEMIOLOGY

Nausea and or vomiting is the main complaint in 1.6% of visits to family physicians in Australia. However only 25% of people with nausea visit their family physician. It is most common in those 15-24 years old and less common in other ages.

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NEMATODES

The nematodes or roundworms are the most diverse phylum of pseudocoelomates, and one of the most diverse of all animals. Nematode species are very difficult to distinguish; over 28,000 have been described, of which over 16,000 are parasitic. It has been estimated that the total number of nematode species might be approximately 1,000,000. Unlike cnidarians or flatworms, roundworms have a digestive system that is like a tube with openings at both ends.

Aelurostrongylus abstrusus

Ancylostoma caninum

Ancylostoma tubaeforme

Eucoleus (Capillaria) aerophila

Pearsonema (Capillaria) plica

Toxocara canis

Toxascaris leonina

Trichuris vulpis

Uncinaria stenocephala

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ONCHOCERCA

Onchocerca is a genus of roundworm. It contains one human parasite - Onchocerca volvulus - which is responsible for the neglected disease Onchocerciasis, also known as "River Blindness" because the infected humans tend to live near rivers where host black flies live. Over 40 million people are infected in Africa, Central America, and South America.

BIOLOGY

CAUSAL AGENTS

Filariasis is caused by nematodes (roundworms) that inhabit the lymphatics and subcutaneous tissues. Eight main species infect humans. Three of these are responsible for most of the morbidity due to filariasis: Wuchereria bancrofti and Brugia malayi cause lymphatic filariasis, and Onchocerca volvulus causes onchocerciasis (river blindness). The other five species are Loa loa, Mansonella perstans, M. streptocerca, M. ozzardi, and Brugia timori. (The last species also causes lymphatic filariasis.)

LIFE CYCLE

Infective larvae are transmitted by infected biting arthropods during a blood meal. The larvae migrate to the appropriate site of the host's body, where they develop into microfilariae-producing adults. The adults dwell in various human tissues where they can live for several years. The agents of lymphatic filariasis reside in lymphatic vessels and lymph nodes; Onchocerca volvulus in nodules in subcutaneous tissues; Loa loa in subcutaneous tissues, where it migrates actively; Brugia malayi in lymphatics, as with Wuchereria bancrofti; Mansonella streptocerca in the dermis and subcutaneous tissue; Mansonella ozzardi apparently in the subcutaneous tissues; and M. perstans in body cavities and the surrounding tissues. The female worms produce microfilariae which circulate in the blood, except for those of Onchocerca volvulus and Mansonella streptocerca, which are found in the skin, and O. volvulus which invade the eye. The microfilariae infect biting arthropods (mosquitoes for the agents of lymphatic filariasis; blackflies [Simulium] for Onchocerca volvulus; midges for Mansonella perstans and M. streptocerca; and both midges and blackflies for Mansonella ozzardi; and deerflies [Chrysops] for Loa loa). Inside the arthropod, the microfilariae develop in 1 to 2 weeks into infective filariform (third-stage) larvae. During a subsequent blood meal by the insect, the larvae infect the vertebrate host. They migrate to the appropriate site of the host's body, where they develop into adults, a slow process than can require up to 18 months in the case of Onchocerca.

LIFE CYCLE OF ONCHOCERCA-VOLVULUS

During a blood meal, an infected blackfly (genus Simulium) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound .   In subcutaneous tissues the larvae develop into adult filariae, which commonly reside in nodules in subcutaneous connective tissues . Adults can live in the nodules for approximately 15 years. Some nodules may contain numerous male and female worms. Females measure 33 to 50 cm in length and 270 to 400 um in diameter, while males measure 19 to 42 mm by 130 to 210 um. In the subcutaneous nodules, the female worms are capable of producing microfilariae for approximately 9 years. The microfilariae, measuring 220 to 360 um by 5 to 9 µm and unsheathed, have a life span that may reach 2 years. They are occasionally found in peripheral blood, urine, and sputum but are typically found in the skin and in the lymphatics of connective tissues . A blackfly ingests the microfilariae during a blood meal .   After ingestion, the microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic muscles . There the microfilariae develop into first-stage larvae and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the blackfly's proboscis and can infect another human when the fly takes a blood meal.

GEOGRAPHIC DISTRIBUTION

Among the agents of lymphatic filariasis, Wuchereria bancrofti is encountered in tropical areas worldwide; Brugia malayi is limited to Asia; and Brugia timori is restricted to some islands of Indonesia. The agent of river blindness, Onchocerca volvulus, occurs mainly in Africa, with additional foci in Latin America and the Middle East. Among the other species, Loa loa and Mansonella streptocerca are found in Africa; Mansonella perstans occurs in both Africa and South America; and Mansonella ozzardi occurs only ins the Americas, from Mexico south to South America and in the Caribbean.

CLINICAL FEATURES

Most infections are probably asymptomatic, as indicated by serologic surveys. Manifestations of disease include fever, chills, sweating, myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia. Symptoms typically occur after an incubation period of 1 to 4 weeks, and can last several weeks. The disease is more severe in patients who are immunosuppressed, splenectomized, and/or elderly. Infections caused by B. divergens tend to be more severe (frequently fatal if not appropriately treated) than those due to B. microti, where clinical recovery usually occurs.

LABORATORY DIAGNOSIS

Identification of microfilariae by microscopic examination is the most practical diagnostic procedure. Examination of blood samples will allow identification of microfilariae of Wuchereria bancrofti, Brugia malayi, Brugia timori, Loa loa, Mansonella perstans, and M. ozzardi. It is important to time the blood collection with the known periodicity of the microfilariae. The blood sample can be a thick smear, stained with Giemsa or hematoxylin and eosin. For increased sensitivity, concentration techniques can be used. These include centrifugation of the blood sample lyzed in 2% formalin (Knott's technique), or filtration through a Nucleopore® membrane. Examination of skin snips will identify microfilariae of Onchocerca volvulus and Mansonella streptocerca. Skin snips can be obtained using a corneal-scleral punch, or more simply a scalpel and needle. The sample must be allowed to incubate for 30 minutes to 2 hours in saline or culture medium, and then examined for microfilariae that would have migrated from the tissue to the liquid phase of the specimen.

For more information view the source:Center for Disease Control

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PARAGONIMIASIS PARAGONIMUS WESTERMANI

FAQS

What is Paragonimus?

Paragonimus is a parasitic lung fluke (flat worm). Cases of infection occur after a person eats raw or undercooked infected crab or crayfish. Paragonimus infection also can be very serious if the fluke travels to the central nervous system, where it can cause symptoms that mimic meningitis.

Where is Paragonimus found?

Paragonimus westermani and several other species are found throughout eastern, southwestern, and southeast Asia; (including China, the Philippines, Japan, Vietnam, South Korea, Taiwan, and Thailand). P. africanus is found in Africa, and P. mexicanus in Central and South America. P. kellicotti is found in the mid-western and southern United States living in crayfish. Some cases of infection have been associated with eating raw crayfish on river raft trips in the Midwest. P. kellicotti or other species have caused paragonimiasis after ingestion of raw freshwater crabs in sushi. There are several species of Paragonimus in other parts of the world that can infect humans.

How is Paragonimus transmitted?

The infection is transmitted by eating crab or crawfish that is either, raw, partially cooked, pickled, or salted. The larval stages of the parasite are released when the crab or crawfish is digested. They then migrate within the body, ending up in the lungs. In 6-10 weeks the larvae mature into adult flukes.

What are the signs and symptoms?

Adult flukes living in the lung cause lung disease that may never be diagnosed or is thought to be tuberculosis. After 2-15 days, the initial signs and symptoms may be diarrhea and abdominal pain. This may be followed several days later by fever, chest pain, and fatigue. The symptoms may also include a dry cough initially, which later often becomes productive with rusty-colored or blood-tinged sputum on exertion.

How is Paragonimus infection diagnosed?

The diagnosis is usually made by identifying Paragonimus eggs in the sputum or sometime in the stool (from ingesting after coughing up).

Is Paragonimus infection contagious?

No. Paragonimus is not contagious.

Is there treatment?

Yes, there is treatment. Several drugs are available through your physician after being accurately diagnosed.

How can I prevent Paragonimus infection?

Never eat raw freshwater crabs or crayfish. Cook crabs and crayfish for to at least 145°F (~63°C). Travelers should be advised to avoid traditional meals containing undercooked freshwater crustaceans.

EPIDEMIOLOGY & RISK FACTORS

Several species of Paragonimus cause most infections; the most important is P. westermani, which occurs primarily in Asia including China, the Philippines, Japan, Vietnam, South Korea, Taiwan, and Thailand. P. africanus causes infection in Africa, and P. mexicanus in Central and South America. Specialty dishes in which shellfish are consumed raw or prepared only in vinegar, brine, or wine without cooking play a key role in the transmission of paragonimiasis. Raw crabs or crayfish are also used in traditional medicine practices in Korea, Japan, and some parts of Africa.

Although rare, human paragonimiasis from P. kellicotti has been acquired in the United States, with multiple cases from the Midwest. Several cases have been associated with ingestion of uncooked crawfish during river raft float trips in Missouri.

BIOLOGY

Causal Agent:

More than 30 species of trematodes (flukes) of the genus Paragonimus have been reported which infect animals and humans. Among the more than 10 species reported to infect humans, the most common is P. westermani, the oriental lung fluke.

Life Cycle:

The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with stool.   In the external environment, the eggs become embryonated, and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues.   Miracidia go through several developmental stages inside the snail: sporocysts,   rediae, with the latter giving rise to many   cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or   crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian   host.   Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite.   The metacercariae excyst in the duodenum, penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs,   where they become encapsulated and develop into adults. The worms can also    reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this   takes place completion of the life cycles is not achieved, because the eggs laid cannot exit these sites.   Time from infection to oviposition is 65 to 90 days.

Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani.

Life cycle image and information courtesy of DPDx.

DISEASE

Paragonimiasis is an acute infection with cough, abdominal pain, discomfort, and low-grade fever that may occur 2 to15 days after infection. The infection usually resolves without treatment. Persons with light infections may have no symptoms. Symptoms of long-term infection may mimic bronchitis or tuberculosis, with coughing up of blood-tinged sputum.

DIAGNOSIS

The infection is usually diagnosed by identification of Paragonimus eggs in sputum. The eggs are sometimes found in stool samples (coughed-up eggs are swallowed). A tissue biopsy is sometimes performed to look for eggs in a tissue specimen.

Specific and sensitive antibody tests based on P. westermani antigens are available through CDC, and serologic tests using a variety of techniques are available through commercial laboratories.

PREVENTION AND CONTROL

Never eat raw freshwater crabs or crayfish. Cook crabs and crayfish for to at least 145°F (~63°C). Travelers should be advised to avoid traditional meals containing undercooked freshwater crustaceans.

For more information view the source:Center for Disease Control

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PARASITE SYMPTOMS

Intestinal parasites are parasites that populate the gastro-intestinal tract in humans and other animals. They can live throughout the body, but most prefer the intestinal wall. Means of exposure include: ingestion of undercooked meat, drinking infected water, and skin absorption. A parasite is an organism that feeds off another organism, called a host. The major groups of parasites include protozoans (organisms having only one cell) and parasitic worms (helminths). Of these, protozoans, including cryptosporidium, microsporidia, and isospora, are most common in HIV-infected persons. Each of these parasites can infect the digestive tract, and sometimes two or more can cause infection at the same time.

INFECTION

Parasites can get into the intestine by going through the mouth from uncooked or unwashed food, contaminated water or hands, or by skin contact with larva infected soil, they can also be transferred by the sexual act of anilingus in some cases. When the organisms are swallowed, they move into the intestine, where they can reproduce and cause symptoms. Children are particularly susceptible if they are not thoroughly cleaned after coming into contact with infected soil that is present in environments that they may frequently visit such as sandboxes and school playgrounds. People in developing countries are also at particular risk due to drinking water from sources that may be contaminated with parasites that colonize the gastrointestinal tract.

SYMPTOMS

Abdominal pain
Myositis
Constipation
Anaemia
Anorexia
B-12 deficiency
Rectal hemorrhage
Blindness
Hematochezia
Hemoptysis
Dysuria
Central nervous system impairment
Chest pain
Chills
Chronic fatigue
Colitis
Coughing
Diarrhea
Digestive disturbance
Dizziness
Fever
Enlargement of various organs
Headaches
Vaginitis
Jaundice
Joint Pain
Weight loss due to malnutrition
Weakness
Immunodeficiency
Nausea/vomiting
Swelling of facial features
Sweating
Insomnia
Skin ulcers
Rectal prolaspe
Mental problems
Lung congestion
Memory loss
Night sweats
Muscle spasms
Hair loss or thinning

In some people, intestinal worms do not cause any symptoms, or the symptoms may come and go. If you have some of these symptoms, it does not necessarily mean that you are infected. These symptoms may also indicate to other diseases. Common signs and complaints include coughing, cramping, abdominal pain, bloating, flatulence and diarrhea. Some parasites also cause low red blood cell count (anemia), and some travel from the lungs to the intestine, or from the intestine to the lungs and other parts of the body. Many other conditions can result in these symptoms, so laboratory tests are necessary to determine their cause. In children, irritability and restlessness are commonly reported by parents.

DIAGNOSIS

Due to the wide variety of intestinal parasites, a description of the symptoms rarely are sufficient for diagnosis. Instead, two common tests are used: Stool samples may be collected to search for the parasites, and an adhesive may be applied to the anus in order to search for eggs.

TREATMENT

Prescription drugs are generally used to eradicate the parasites. Special poisons are tailored to kill one or more common varieties of intestinal parasites. Good hygiene is recommended to avoid reinfection.

For more information view the source:Wikipedia

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PARASITES IN HUMANS

Human parasites include various protozoa and worms which may infect humans, causing parasitic diseases.
Human parasites are divided into endoparasites, which cause infection inside the body, and ectoparasites, which cause infection superficially within the skin.
The cysts and eggs of endoparasites may be found in feces which aids in the detection of the parasite in the human host while also providing a means for the parasitic species to exit the current host and enter other hosts. Although there are number of ways in which humans can contract parasitic infections, observing basic hygiene and cleanliness tips can reduce its probability.

ARCHAELOGICAL EVIDENCE

It is assumed that early human ancestors generally had parasites, but until recently there was no evidence to support this claim. Generally, the discovery of parasites in ancient humans relies on the study of feces and other fossilized material. The earliest known parasite in a human was eggs of the lung fluke found in fossilized feces in northern Chile and is estimated to be from around 5900BC. There are also claims of hookworm eggs from around 5000BC in Brazil and large roundworm eggs from around 2330BC in Peru. Tapeworm eggs have also been found present in Egyptian mummies dating from around 2000BC, 1250BC, and 1000BC along with a well preserved and calcified female worm inside of a mummy .

WRITTEN EVIDENCE

The first written records of parasites date from 3000 to 400BC in Egyptian papyrus records. They identify parasites such as roundworms, Guinea worms, threadworms, and some tapeworms of unknown varieties. In ancient Greece, Hippocrates and Aristotle documented several parasites in his collection of works Corpus Hippocraticus. In this book, they documented the presence of worms and other parasites inside of fish, domesticated animals, and humans. The bladder worm is well documented in its presence in pigs along with the larval stages of a tapeworm (Taenia Solium). These tapeworms were mentioned in a play by Aristophanes as Ã¯Â¿Â½hailstonesÃ¯Â¿Â½ with Aristotle in the section about pig diseases in his book History of Animals. The cysts of the Echinococcus granulosus tapeworm were also well known in ancient cultures mainly because of their presence in slaughtered and sacrificed animals . The major parasitic disease which has been documented in early records is dracunculiasis. This disease is caused by the Guinea worm and is characterized by the female worm emerging from the leg. This symptom is so specific to the disease that it is mentioned in many texts and plays which predate 1000AD .

GREECE AND ROME

In Greece, Hippocrates and Aristotle created considerable medical documentation about parasites in the Corpus Hippocraticus. In this work, they documented the presence of parasitic worms in many animals ranging from fish to domesticated animals and humans. Among the most extensively documented was the Bladder Worm (Taenia solium). This condition was called measly pork when present in pigs and was characterized by the presence of the larval stages of the Bladder Worm in muscle tissue. This disease was also mentioned by the playwright Aristophanes when he referred to hailstones In one of his plays. This naming convention is also reflected by Aristotle when he refers to bladders that are like hailstones. Another worm which was commonly written about in ancient Greek texts was the tapeworm Echinococccus granulosus. This worm was distinguished by the presence of massive cysts in the liver of animals. This condition was documented so well mainly because of its presence in slaughtered and sacrificed animals. It was documented by several different cultures of the time other than the Greeks including the Arabs, Romans, and Babylonians . Not many parasitic diseases were identified in ancient Greek and Roman texts mainly because the symptoms for parasitic diseases are shared with many other illnesses such as the flu, the common cold, and dysentery. However, several diseases such as Dracunculiasis (Guinea worm disease), Hookworm, Elephantiasis, Schistosomiasis, Malaria, and Amebiasis cause unique and specific symptoms and are well documented because of this. The most documented by far was Guinea worm disease mainly because the grown female worm emerges from the skin which causes considerable irritation and which cannot really be ignored. This particular disease is widely accepted to also be the fiery serpents written about in the Old Testament of the Bible. This disease was mentioned by Hippocrates in Greece along with Pliny the Elder, Galen, Aetius of Amida, and Paulus Aegineta of Alexandria in Rome. Strangely, this disease was never present in Greece even though it was documented .

NORTHERN AFRICA,THE MIDDLE EAST AND MESOPOTAMIA

The medieval Persian doctor Avicenna records the presence of several parasites in animals and in his patients including Guinea worm, threadworms, tapeworms, and the Ascaris worm. This followed a tradition of Arab medical writings spanning over 1000 years in the area near the Red Sea. However, the Arabs never made the connection between parasites and the diseases they caused . As with Greek and Roman texts, the Guinea worm is very well documented in Middle Eastern medical texts. Several Assyrian documents in the library of King Ashurbanipal refer to an affliction which has been interpreted as Guinea Worm disease . In Egypt, the Ebers Papyrus contains one of the few references to hookworm disease in ancient texts. This disease does not have very specific symptoms and was vaguely mentioned. However vague the reference, it is one of the few that connects the disease to the hookworm parasite . Another documented disease is elephantiasis. Symptoms of this disease are highly visible, since it causes extreme swelling in the limbs, breasts, and genitals. A number of surviving statues indicate that Pharaoh Mentuhotep II is likely to have suffered from elephantiasis. This disease was well known to Arab physicians and Avicenna, who noted specific differences between elephantiasis and leprosy. That the disease schistosomiasis was extremely common in Ancient Egyptis suggested by mummified evidence, but it is not specifically documented in surviving texts. Other names for this disease include bilharzia, Katayama disease, Red Water fever, snail fever, and big belly. The only really defining symptom is bloody urine, but this can easily be overlooked as several other diseases exhibit the same symptom. However, the main reason it was not documented is probably because it was simply so common. In the same way, the Greeks and Romans did not acknowledge the existence of colds and coughs because of how common they were .

CHINA

The Chinese mostly documented diseases rather than the parasites associated with them. Chinese texts contain one of the few references to Hookworm disease found in ancient records, but no connection to hookworm is made . The Emperor Huang Ti recorded the earliest mentioning (2700BC) of malaria in his text Nei Ching. He lists chills, headaches, and fevers as the main symptoms and distinguished between the different kinds of fevers.

INDIA

In India, the Charaka Samhita and Sushruta Samhita document Malaria. These documents list the main symptoms as fever and enlarged spleens. The Brigu-Samhita from 1000BC makes the earliest reference to Amebiasis. The symptoms were given as bloody and mucosal diarrhea.

COMMONLY DOCUMENTED PARASITES

Protozoa

Plasmodium spp. - causes Malaria
Entamoeba - causes amoebiasis, amoebic dysentery
Giardia
Toxoplasma gondii - causes Toxoplasmosis

Parasitic worms and flukes

Guinea worm (Dracunculus)
Schistosoma - causes Schistosomiasis
Strongyloides stercoralis - causes Strongyloidiasis
Guinea Worm - also known as Dracunculiasis 495.
Hookworm
Tapeworm

Ectoparasites

Sarcoptes scabiei - causes scabies
Pediculus humanus capitis - causes headlice
Phthirus pubis - causes pubic lice
Ticks (Ixodoidea)

For more information view the source:Wikipedia

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PARASITES wiki

Parasitism is a type of symbiotic relationship between organisms of different species where one organism, the parasite, benefits at the expense of the other, the host. Traditionally parasite referred to organisms with lifestages that went beyond one host (e.g. Taenia solium), which are now called macroparasites (typically protozoa and helminths). Parasites can now also refer to microparasites, which are typically smaller, such as viruses and bacteria and can be directly transmitted between hosts of one species. Unlike predators, parasites are generally much smaller than their host, although both are special cases of consumer-resource interactions. Parasite show a high degree of specialization for their mode of life, and reproduce at a faster rate than their hosts. Classic examples of parasitism include interactions between vertebrate hosts and diverse animals such as tapeworms, flukes, the Plasmodium species, and fleas. Parasitism is differentiated from the parasitoid relationship, though not sharply, by the fact that parasitoids generally kill or sterilise their hosts. Parasitoidy occurs in about as many classes of organism as parasitism does. The harm and benefit in parasitic interactions concern the biological fitness of the organisms involved. Parasites reduce host fitness in many ways, ranging from general or specialized pathology (such as parasitic castration), impairment of secondary sex characteristics, to the modification of host behaviour. Parasites increase their fitness by exploiting hosts for resources necessary for the parasite's survival: (i.e. food, water, heat, habitat, and dispersal). Although the concept of parasitism applies unambiguously to many cases in nature, it is best considered part of a continuum of types of interactions between species, rather than an exclusive category. Particular interactions between species may satisfy some but not all parts of the definition. In many cases, it is difficult to demonstrate that the host is harmed. In others, there may be no apparent specialization on the part of the parasite, or the interaction between the organisms may be short-lived.

ETMOLOGY

First used in English 1539, the word parasite comes from the Medieval French parasite, from the Latin parasitus, the latinisation of the Greek (parasitos), "one who eats at the table of another"and that from (para), "beside, by" (sitos), "wheat".Coined in English in 1611, the word parasitism comes from the Greek (sitismos) "feeding, fattening".

TYPES

Parasites are classified based on their interactions with their hosts and on their life cycles. Parasites that live on the surface of the host are called ectoparasites (e.g. some mites). Those that live inside the host are called endoparasites (including all parasitic worms). Endoparasites can exist in one of two forms: intercellular parasites (inhabiting spaces in the host?s body) or intracellular parasites (inhabiting cells in the host?s body). Intracellular parasites, such as protozoa, bacteria or viruses, tend to rely on a third organism, which is generally known as the carrier or vector. The vector does the job of transmitting them to the host. An example of this interaction is the transmission of malaria, caused by a protozoan of the genus Plasmodium, to humans by the bite of an anopheline mosquito. Those parasites living in an intermediate position, being half-ectoparasites and half-endoparasites, are sometimes called mesoparasite. An epiparasite is one that feeds on another parasite. This relationship is also sometimes referred to as hyperparasitism, exemplified by a protozoan (the hyperparasite) living in the digestive tract of a flea living on a dog. Social parasites take advantage of interactions between members of social organisms such as ants or termites. In kleptoparasitism, parasites appropriate food gathered by the host. An example is the brood parasitism practiced by many species of cuckoo and cowbird, which do not build nests of their own but rather deposit their eggs in nests of other species and abandon them there. The host behaves as a "babysitter" as they raise the young as their own. If the host removes the cuckoo's eggs, some cuckoos will return and attack the nest to compel host birds to remain subject to this parasitism. The cowbird?s parasitism does not necessarily harm its host?s brood; however, the cuckoo may remove one or more host eggs to avoid detection, and furthermore the young cuckoo may heave the host?s eggs and nestlings out of the nest. Parasitism can take the form of isolated cheating or exploitation among more generalized mutualistic interactions. For example, broad classes of plants and fungi exchange carbon and nutrients in common mutualistic mycorrhizal relationships; however, some plant species known as myco-heterotrophs "cheat" by taking carbon from a fungus rather than donating it. Parasitoids are organisms whose larval development occurs inside or on the surface of another organism, resulting in the death of the host. This means that the interaction between the parasitoid and the host is fundamentally different from that of a true parasite and shares some of the characteristics of predation. An adelpho-parasite is a parasite in which the host species is closely related to the parasite, often being a member of the same family or genus. An example of this is the citrus blackfly parasitoid, Encarsia perplexa, unmated females of which may lay haploid eggs in the fully developed larvae of their own species. These result in the production of male offspring. The marine worm Bonellia viridis has a similar reproductive strategy, although the larvae are planktonic.

HOST DEFENSES

Hosts respond to parasitisms in many ways ranging from the morphological to the behavioural. In some cases, plants produce toxins to deter parasitic fungi and bacteria.Vertebrate animals have developed complex immune systems, which can target parasites through contact with bodily fluids. Animals are also known to resort to behavioral defenses, examples of which are the avoidance by sheep of open pastures during spring, when roundworm eggs accumulated over the previous year hatch en masse; and the ingestion of alcohol by infected fruit flies as self medication against blood-borne parasites. In humans, parasite immunity is developed prominently by Immunoglobulin E antibodies.

EVOLUTIONARY ASPECTS

Biotrophic parasitism is a common mode of life that has arisen independently many times in the course of evolution. Depending on the definition used, as many as half of all animals have at least one parasitic phase in their life cycles, and it is also frequent in plants and fungi. Moreover, almost all free-living animals are host to one or more parasites taxa. Restoration of a Tyrannosaurus with parasite infections. A 2009 study showed that holes in the skulls of several specimens might have been caused by Trichomonas-like parasites. Parasites evolve in response to the defense mechanisms of their hosts. As a result of host defenses, some parasites evolve adaptations that are specific to a particular host taxon, specializing to the point where they infect only a single species. Such narrow host specificity can be costly over evolutionary time, however, if the host species becomes extinct. Therefore many parasites can infect a variety of more or less closely related host species, with different success rates. Host defenses also evolve in response to attacks by parasites. Theoretically, parasites may have an advantage in this evolutionary arms race because of their more rapid generation time. Hosts reproduce less quickly than parasites, and therefore have fewer chances to adapt than their parasites do over a given span of time. In some cases, a parasite species may coevolve with its host taxa. Long-term coevolution sometimes leads to a relatively stable relationship tending to commensalism or mutualism, as, all else being equal, it is in the evolutionary interest of the parasite that its host thrives. A parasite may evolve to become less harmful for its host or a host may evolve to cope with the unavoidable presence of a parasite-- to the point that the parasite's absence causes the host harm. For example, although animals infected with parasitic worms are often clearly harmed, and therefore parasitized, such infections may also reduce the prevalence and effects of autoimmune disorders in animal hosts, including humans. Competition between parasites tends to favor faster reproducing and therefor more virulent parasites. Parasites whose life cycle involves the death of the host, to exit the present host and sometimes to enter the next, evolve to be more virulent or even alter the behavior or other properties of the host to make it more vulnerable to predators. Parasites that reproduce largely to the offspring of the previous host tend to become less virulent or mutualist, so that its hosts reproduce more effectively. The presumption of a shared evolutionary history between parasites and hosts can sometimes elucidate how host taxa are related. For instance, there has been dispute about whether flamingos are more closely related to the storks and their allies, or to ducks, geese and their relatives. The fact that flamingos share parasites with ducks and geese is evidence these groups may be more closely related to each other than either is to storks. Parasitism is part of one explanation for the evolution of secondary sex characteristics seen in breeding males throughout the animal world, such as the plumage of male peacocks and manes of male lions. According to this theory, female hosts select males for breeding based on such characteristics because they indicate resistance to parasites and other disease.

CO-SPECIATION

In rare cases, a parasite may even undergo co-speciation with its host. One particularly remarkable example of co-speciation exists between the simian foamy virus (SFV) and its primate hosts. In one study, the phylogenies of SFV polymerase and the mitochondrial cytochrome oxidase subunit II from African and Asian primates were compared. Surprisingly, the phylogenetic trees were very congruent in branching order and divergence times. Thus, the simian foamy viruses may have co-speciated with Old World primates for at least 30 million years.

ECOLOGY

QUANTITATIVE ECOLOGY

A single parasite species usually has an aggregated distribution across host individuals, which means that most hosts harbor few parasites, while a few hosts carry the vast majority of parasite individuals. This poses considerable problems for students of parasite ecology: the use of parametric statistics should be avoided. Log-transformation of data before the application of parametric test, or the use of non-parametric statistics is recommended by several authors. However, this can give rise to further problems. Therefore, modern day quantitative parasitology is based on more advanced biostatistical methods.

DIVERSITY ECOLOGY

Hosts represent discrete habitat patches that can be occupied by parasites. A hierarchical set of terminology has come into use to describe parasite assemblages at different host scales. Infrapopulation All the parasites of one species in a single individual host. Metapopulation All the parasites of one species in a host population. Infracommunity All the parasites of all species in a single individual host. Component community All the parasites of all species in a host population. Compound community All the parasites of all species in all host species in an ecosystem. The diversity ecology of parasites differs markedly from that of free-living organisms. For free-living organisms, diversity ecology features many strong conceptual frameworks including Robert MacArthur and E. O. Wilson's theory of island biogeography, Jared Diamond's assembly rules and, more recently, null models such as Stephen Hubbell's unified neutral theory of biodiversity and biogeography. Frameworks are not so well-developed for parasites and in many ways they do not fit the free-living models. For example, island biogeography is predicated on fixed spatial relationships between habitat patches ("sinks"), usually with reference to a mainland ("source"). Parasites inhabit hosts, which represent mobile habitat patches with dynamic spatial relationships. There is no true "mainland" other than the sum of hosts (host population), so parasite component communities in host populations are metacommunities. Nonetheless, different types of parasite assemblages have been recognized in host individuals and populations, and many of the patterns observed for free-living organisms are also pervasive among parasite assemblages. The most prominent of these is the interactive-isolationist continuum. This proposes that parasite assemblages occur along a cline from interactive communities, where niches are saturated and interspecific competition is high, to isolationist communities, where there are many vacant niches and interspecific interaction is not as important as stochastic factors in providing structure to the community. Whether this is so, or whether community patterns simply reflect the sum of underlying species distributions (no real "structure" to the community), has not yet been established.

ADAPTATION

Parasites infect hosts that exist within their same geographical area (sympatric) more effectively. This phenomenon supports the "Red Queen hypothesis?which states that interactions between species (such as host and parasites) lead to constant natural selection for adaptation and counter adaptation." The parasites track the locally common host phenotypes, therefore the parasites are less infective to allopatric (from different geographical region) hosts. Experiments published in 2000 discuss the analysis of two different snail populations from two different sources- Lake Ianthe and Lake Poerua in New Zealand. The populations were exposed to two pure parasites (digenetic trematode) taken from the same lakes. In the experiment, the snails were infected by their sympatric parasites, allopatric parasites and mixed sources of parasites. The results suggest that the parasites were more highly effective in infecting their sympatric snails than their allopatric snails. Though the allopatric snails were still infected by the parasites, the infectivity was much less when compared to the sympatric snails. Hence, the parasites were found to have adapted to infecting local populations of snails.

TRANSMISSION

Life cycle of Entamoeba histolytica, an anaerobic parasitic protozoan. Parasites inhabit living organisms and therefore face problems that free-living organisms do not. Hosts, the only habitats in which parasites can survive, actively try to avoid, repel, and destroy parasites. Parasites employ numerous strategies for getting from one host to another, a process sometimes referred to as parasite transmission or colonization. Some endoparasites infect their host by penetrating its external surface, while others must be ingested. Once inside the host, adult endoparasites need to shed offspring into the external environment to infect other hosts. Many adult endoparasites reside in the host?s gastrointestinal tract, where offspring can be shed along with host excreta. Adult stages of tapeworms, thorny-headed worms and most flukes use this method. Among protozoan endoparasites, such as the malarial parasites and trypanosomes, infective stages in the host's blood are transported to new hosts by biting-insects, or vectors. Larval stages of endoparasites often infect sites in the host other than the blood or gastrointestinal tract. In many such cases, larval endoparasites require their host to be consumed by the next host in the parasite's life cycle in order to survive and reproduce. Alternatively, larval endoparasites may shed free-living transmission stages that migrate through the host?s tissue into the external environment, where they actively search for or await ingestion by other hosts. The foregoing strategies are used, variously, by larval stages of tapeworms, thorny-headed worms, flukes and parasitic roundworms. Some ectoparasites, such as monogenean worms, rely on direct contact between hosts. Ectoparasitic arthropods may rely on host-host contact (e.g. many lice), shed eggs that survive off the host (e.g. fleas), or wait in the external environment for an encounter with a host (e.g. ticks). Some aquatic leeches locate hosts by sensing movement and only attach when certain temperature and chemical cues are present. Some parasites modify host behavior to make transmission to other hosts more likely. For example, in California salt marshes, the fluke Euhaplorchis californiensis reduces the ability of its killifish host to avoid predators. This parasite matures in egrets, which are more likely to feed on infected killifish than on uninfected fish. Another example is the protozoan Toxoplasma gondii, a parasite that matures in cats but can be carried by many other mammals. Uninfected rats avoid cat odors, but rats infected with T. gondii are drawn to this scent, which may increase transmission to feline hosts.

ROLES IN ECOSYSTEMS

Modifying the behavior of infected hosts, to make transmission to other hosts more likely to occur, is one way parasites can affect the structure of ecosystems. For example, in the case of Euhaplorchis californiensis (discussed above) it is plausible that the local predator and prey species might be different if this parasite were absent from the system. Although parasites are often omitted in depictions of food webs, they usually occupy the top position. Parasites can function like keystone species, reducing the dominance of superior competitors and allowing competing species to co-exist. Many parasites require multiple hosts of different species to complete their life cycles and rely on predator-prey or other stable ecological interactions to get from one host to another. In this sense, the parasites in an ecosystem reflect the "health" of that system.

EFFECTS ON HOST BEHAVIOR

Animal behavior is typically motivated by proximate level mechanisms that promote particular actions. In most cases, proximate level mechanisms are a result of the individual?s interaction with the environment but some parasites have been shown to interact and manipulate these mechanisms to produce behaviors beneficial to the parasite alone. Parasites are known to drastically affect how animals behave. Parasites most commonly target the central nervous system (CNS) in order to alter animal behavior. By affecting hormone secretions or by physical restructuring, parasites successfully change how an animal?s body functions and delivers, interprets and and reacts to messages. Some parasites, like toxoplasma, form vacuoles that travel through the nervous system interrupting key functions in intraneural communications. The emerald jewel wasp alters behavior through the injection of venom directly into the host?s brain, causing hypokinesia. Parasitic life cycles can have the capacity to infect a singular host or a series of hosts. Direct life cycles are related to a single host while indirect life cycles, or complex life cycles, rely on a series of intermediate hosts in order to complete the life cycle. Indirect life cycles likely arose in order to increase the efficiency of spreading to new hosts. By using intermediary?s the parasite DNA can spread to several hosts instead of remain concentrated within a single host, therefore promising a higher likelihood of DNA continuation. In some cases, intermediary hosts are accidental.   Toxoplasma gondii is a noted case of unintended intermediary hosts. Typically, Toxoplasma infects animals from the Felidae family and oocysts are shed with the feces. When rodents consume the fecal matter, they become infected themselves and the parasite begins to alter their behavior. Rodents become more extroverted and less fearful of felines. Toxoplasma, however, has begun to infect humans. In doing so, human behavior has been altered in similar ways to rodents. Further, Toxoplasma has been linked to cases of schizophrenia.   The emerald jewel wasp (Ampulex compressa) takes advantage of its host, the American cockroach (Periplaneta americana) specifically as a food source and home for its growing larvae. The wasp begins by injecting venom into the brain which paralyses the central nervous system system of the cockroach and puts it into a state of hypokinesia. Hypokinesia...is a reversible long-term lethargy characterized by lack of spontaneous movement or response to external stimuli, (Banks and Adams). After dragging the cockroach to a burrow, the wasp deposits an egg into its carcass, burying it for the growing larvae to feed off until it emerges in 6 weeks, leaving nothing but a hard outer cockroach shell. Although the circuitry in control of movement is functional, the nervous system acts from a depressed state. They are not killed by this hypokinesia, but would recover if not for the larvae eating them from the inside out. The movement is controlled by dopamine and octopamine which affect transmission of interneurons involved in the natural response to escape. Reduced motor activity results from a reduction of these amines.

VALUE

Although parasites are generally considered to be harmful, the eradication of all parasites would not necessarily be a noble aim. Among other things, parasites may account for as much as or more than half of life's diversity; they perform an important ecological role (by weakening prey) that ecosystems would take some time to adapt to; and without parasites organisms may eventually tend to asexual reproduction, dinimishing the diversity of sexually dimorphic traits. Parasites provide an opportunity for the transfer of genetic material between species. On rare but significant occasions this may provide a path for evolutionary changes that would not otherwise occur, or that would otherwise take even longer.

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PATHOGENIC BACTERIA

Pathogenic bacteria are bacteria that cause bacterial infection. This article deals with human pathogenic bacteria. Although the vast majority of bacteria are harmless or beneficial, quite a few bacteria are pathogenic. One of the bacterial diseases with highest disease burden is tuberculosis, caused by the bacterium Mycobacterium tuberculosis, which kills about 2 million people a year, mostly in sub-Saharan Africa. Pathogenic bacteria contribute to other globally important diseases, such as pneumonia, which can be caused by bacteria such as Streptococcus and Pseudomonas, and foodborne illnesses, which can be caused by bacteria such as Shigella, Campylobacter and Salmonella. Pathogenic bacteria also cause infections such as tetanus, typhoid fever, diphtheria, syphilis and leprosy. Koch's postulates are criteria designed to establish a causal relationship between a causative microbe and a disease.

DISEASES

Each pathogenic species has a characteristic spectrum of interactions with its human hosts.

CONDITIONALLY PATHOGENIC

Conditionally pathogenic bacteria are only pathogenic under certain conditions, such as a wound that allows for entry into the blood, or a decrease in immune function. For example, Staphylococcus or Streptococcus are also part of the normal human flora and usually exist on the skin or in the nose without causing disease, but can potentially cause skin infections, pneumonia, meningitis and even overwhelming sepsis, a systemic inflammatory response producing shock, massive vasodilation and death. Some species of bacteria, such as Pseudomonas aeruginosa, Burkholderia cenocepacia, and Mycobacterium avium, are opportunistic pathogens and cause disease mainly in people suffering from immunosuppression or cystic fibrosis.

INTRACELLULAR

Other organisms invariably cause disease in humans, such as obligate intracellular parasites that are able to grow and reproduce only within the cells of other organisms. Still, infections with intracellular bacteria may be asymptomatic, such as during the incubation period. An example of intracellular bacteria is Rickettsia. One species of Rickettsia causes typhus, while another causes Rocky Mountain spotted fever.

BY LOCATION

Chlamydia, another phylum of obligate intracellular parasites, contains species that can cause pneumonia, or urinary tract infection and may be involved in coronary heart disease. Mycobacterium and Brucella can exist intracellularly, though they are facultative (not obligate intracellular parasites.)

TREATMENT

Bacterial infections may be treated with antibiotics, which are classified as bacteriocidal if they kill bacteria, or bacteriostatic if they just prevent bacterial growth. There are many types of antibiotics and each class inhibits a process that is different in the pathogen from that found in the host. For example, the antibiotics chloramphenicol and tetracyclin inhibit the bacterial ribosome, but not the structurally-different eukaryotic ribosome, and so exhibit selective toxicity. Antibiotics are used both in treating human disease and in intensive farming to promote animal growth. Both uses may be contributing to the rapid development of antibiotic resistance in bacterial populations. Infections can be prevented by antiseptic measures such as sterilizing the skin prior to piercing it with the needle of a syringe, and by proper care of indwelling catheters. Surgical and dental instruments are also sterilized to prevent infection by bacteria. Disinfectants such as bleach are used to kill bacteria or other pathogens on surfaces to prevent contamination and further reduce the risk of infection. Most bacteria in food are killed by cooking to temperatures above 73oC (163oF).

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PINWORM (Intestinal Parasites)

The pinworm (in the United States of America) (genus Enterobius), also known as threadworm (in the United Kingdom) or seatworm, is a nematode (roundworm) and a common human intestinal parasite, especially in children. The medical condition associated with pinworm infestation is known as enterobiasis, or less precisely as oxyuriasis in reference to the family Oxyuridae.Throughout this article the word pinworm refers to Enterobius. In British usage, however, pinworm refers to Strongyloides while Enterobius is called threadworm.

CLASSIFICATION

The pinworm (genus Enterobius) is a type of roundworm, and three species of pinworm have been identified with certainty. Humans are hosts only to Enterobius vermicularis (formerly Oxyuris vermicularis). Chimpanzees are host to Enterobius anthropopitheci, which is morphologically distinguishable from the human pinworm. Hugot (1983) claims there is another species affecting humans, Enterobius gregorii, which is supposedly a sister species of E. vermicularis, and has a slightly smaller spicule (i.e., sexual organ). Its existence is controversial however; Totkova et al. (2003) consider there to be insufficient evidence, and Hasagawa et al. (2006) contend that E. gregorii is a younger stage of E. vermicularis. Regardless of its status as a distinct species, E. gregorii is considered clinically identical to E. vermicularis.

MORPHOLOGY

The pinworm appears as a white, small and delicate nematode (i.e., roundworm). The adult female has a sharply pointed posterior end, is 8 to 13 millimeters long, and 0.5 millimeter thick. The adult male is considerably smaller, measuring 2 to 5 millimeters long and 0.2 millimeter thick, and has a curved posterior end. The eggs are translucent and have a surface that adheres to environmental objects. The eggs measure 50 to 60 micrometers by 20 to 30 micrometers, and have a thick shell that is flattened on one side. The small size and colorlessness of the eggs make them invisible to the naked eye, except in barely visible clumps of thousands of eggs. Eggs may contain a developing embryo or a fully developed pinworm larva. The larvae grow to 140?150 micrometers in length.

DISRTIBUTION

The pinworm has a worldwide distribution, and is the most common helminth (i.e., parasitic worm) infection in the United States and Western Europe. In the United States, a study by the Center of Disease Control reported an overall incidence rate of 11.4% among people of all ages. Pinworms are particularly common in children, with prevalence rates in this age group having been reported as high as 61% in India, 50% in England, 39% in Thailand, 37% in Sweden, and 29% in Denmark. Finger sucking has been shown to increase both incidence and relapse rates,and nail biting has been similarly associated. Because it spreads from host to host through contamination, pinworms are common among people living in close contact, and tends to occur in all people within a household. The prevalence of pinworms is not associated with gender, nor with any particular social class, race, or culture. Pinworms are an exception to the tenet that intestinal parasites are uncommon in affluent communities. The earliest known instance of pinworms is evidenced by pinworm eggs found in coprolite, carbon dated to 7837 BC at western Utah.

LIFE CYCLE

After the eggs have been initially deposited near the anus, they are readily transmitted to other surfaces through contamination. The surface of the eggs is sticky when laid,and the eggs are readily transmitted from their initial deposit near the anus to fingernails, hands, night-clothing and bed linen. From here, eggs are further transmitted to food, water, furniture, toys, bathroom fixtures and other objects. Household pets often carry the eggs in their fur, while not actually being infected. Dust containing eggs can become airborne and widely dispersed when dislodged from surfaces, for instance when shaking out bed clothes and linen. Consequently the eggs can enter the mouth and nose through inhalation, and be swallowed later. Although pinworms do not strictly multiply inside the body of their human host, some of the pinworm larvae may hatch on the anal mucosa, and migrate up the bowel and back into the gastrointestinal tract of the original host. This process is called retroinfection. According to Burkhart (2005), when this retroinfection occurs, it leads to a heavy parasitic load and ensures that the pinworm infestation continues. This statement is contradictory to a statement by Caldwelli (1982), who contends that retroinfection is rare and not clinically significant. Despite the limited, 13 week lifespan of individual pinworms, autoinfection (i.e., infection from the original host to itself), either through the anus-to-mouth route or through retroinfection, causes the pinworms to inhabit the same host indefinitely.

TRANSMISSION

Pinworms spread through human-to-human transmission, by ingesting (i.e., swallowing) infectious pinworm eggs. The eggs are hardy and can remain viable (i.e., infectious) in a moist environment for up to three weeks. They do not tolerate heat well, but can survive in low temperatures: two-thirds of the eggs are still viable after 18 hours at negative 8 degrees Celsius. After the eggs have been initially deposited near the anus, they are readily transmitted to other surfaces through contamination. The surface of the eggs is sticky when laid, and the eggs are readily transmitted from their initial deposit near the anus to fingernails, hands, night-clothing and bed linen. From here, eggs are further transmitted to food, water, furniture, toys, bathroom fixtures and other objects. Household pets often carry the eggs in their fur, while not actually being infected. Dust containing eggs can become airborne and widely dispersed when dislodged from surfaces, for instance when shaking out bed clothes and linen. Consequently the eggs can enter the mouth and nose through inhalation, and be swallowed later. Although pinworms do not strictly multiply inside the body of their human host, some of the pinworm larvae may hatch on the anal mucosa, and migrate up the bowel and back into the gastrointestinal tract of the original host. This process is called retroinfection. According to Burkhart (2005), when this retroinfection occurs, it leads to a heavy parasitic load and ensures that the pinworm infestation continues. This statement is contradictory to a statement by Caldwelli (1982), who contends that retroinfection is rare and not clinically significant. Despite the limited, 13 week lifespan of individual pinworms, autoinfection (i.e., infection from the original host to itself), either through the anus-to-mouth route or through retroinfection, causes the pinworms to inhabit the same host indefinitely.

ENTEROBIASIS: HUMAN INFECTION WITH PINWORMS

A pinworm infection or enterobiasis is a human parasitic disease and one of the most common childhood parasitic worm infections in the developed world. It is caused by infestation with the parasitic roundworm Enterobius vermicularis, commonly called the human pinworm. Infection usually occurs through the ingestion of pinworm eggs, either through contaminated hands, food, or less commonly, water. The chief symptom is itching in the anal area. The incubation time from ingestion of eggs to the first appearance of new eggs around the anus is 4 to 6 weeks. Pinworms are usually considered a nuisance rather than a serious disease. Treatment is straightforward in uncomplicated cases, however, elimination of the parasite from a family group or institution often poses significant problems either due to an incomplete cure or reinfection. Pinworm infection has no association with any socioeconomic level, race or culture.

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PLASMODIUM

HISTORY

The organism itself was first seen by Laveran on November 6, 1880 at a military hospital in Constantine, Algeria, when he discovered a microgametocyte exflagellating. In 1885, similar organisms were discovered within the blood of birds in Russia. There was brief speculation that birds might be involved in the transmission of malaria; in 1894 Patrick Manson hypothesized that mosquitoes could transmit malaria. This hypothesis was independently confirmed by the Italian physician Giovanni Battista Grassi working in Italy and the British physician Ronald Ross working in India, both in 1898. Ross demonstrated the existence of Plasmodium in the wall of the midgut and salivary glands of a Culex mosquito using bird species as the vertebrate host. For this discovery he won the Nobel Prize in 1902. Grassi showed that human malaria could only be transmitted by Anopheles mosquitoes. It is worth noting, however, that for some species the vector may not be a mosquito.

BIOLOGY

The genome of four Plasmodium species—Plasmodium falciparum, Plasmodium knowlesi, Plasmodium vivax, and Plasmodium yoelii—have been sequenced. All these species have genomes of about 25 megabases organised into 14 chromosomes consistent with earlier estimates. The chromosomes vary in length from 500 kilobases to 3.5 megabases and it is presumed that this is the pattern throughout the genus. The plasmodium contains a degenerated chloroplast called an apicoplast. Due to this it is sensitive to herbicides. The biology of these organisms is more fully described at Plasmodium falciparum biology.

DIAGNOSTICS CHARACTERISTICS

Merogony occurs both in erythrocytes and other tissues Merozoites, schizonts or gametocytes can be seen within erythrocytes and may displace the host nucleus Merozoites have a "signet-ring" appearance due to a large vacuole that forces the parasite’s nucleus to one pole Schizonts are round to oval inclusions that contain the deeply staining merozoites Forms gamonts in erythrocytes Gametocytes are 'halter-shaped' similar to Haemoproteus but the pigment granules are more confined Hemozoin is present Vectors are either mosquitos or sandflies Vertebrate hosts include mammals, birds and reptiles.

LIFE CYCLE

The life cycle of Plasmodium while complex is similar to several other species in the Haemosporidia. All the Plasmodium species causing malaria in humans are transmitted by mosquito species of the genus Anopheles. Species of the mosquito genera Aedes, Culex, Culiseta, Mansonia and Theobaldia can also transmit malaria but not to humans. Bird malaria is commonly carried by species belonging to the genus Culex. The life cycle of Plasmodium was discovered by Ross who worked with species from the genus Culex. Both sexes of mosquitos live on nectar. Because nectar's protein content alone is insufficient for oogenesis (egg production) one or more blood meals is needed by the female. Only female mosquitoes bite. Sporozoites from the saliva of a biting female mosquito are transmitted to either the blood or the lymphatic system of the recipient. It has been known for some time now that the parasites block the salivary ducts of the mosquito and as a consequence the insect normally requires multiple attempts to obtain blood. The reason for this has not been clear. It is now known that the multiple attempts by the mosquito may contribute to immunological tolerance of the parasite. The majority of sporozoites appear to be injected into the subcutaneous tissue from which they migrate into the capillaries. A proportion are ingested by macrophages and still others are taken up by the lymphatic system where they are presumably destroyed. ~10% of the parasites inoculated by the mosquitoes may remain in the skin where they may develop into infective merozoites.

DENDRITIC CELLS

It is known that the murine parasites can infect, survive and replicate within plasmacytoid dendritic cells of the spleen and that these infections may be productive. The importance of this site of replication in mice has yet to be established and it is currently unknown if these cells support parasite replication in other species.

HEPATIC STAGES

The majority of sporozoites migrate to the liver and invade hepatocytes. For reasons that are currently unclear each sporozoite typically penetrates several hepatocytes before choosing one to reside within. Once the sporozoite has ceased migration it undergoes an initial remodelling of the pellicle, with disassembly of the inner membrane complex and the appearance of a bulb that progressively enlarges until the initially elongated sporozoite has transformed into a rounded form. This rounded form then matures within the hepatocyte to a schizont containing many merozoites. In some Plasmodium species, such as Plasmodium vivax and Plasmodium ovale, the parasite in the hepatocyte may not achieve maturation to a schizont immediately but remain as a latent or dormant form and called a hypnozoite. Although Plasmodium falciparum is not considered to have a hypnozoite form, this may not be entirely correct (vide infra). This stage may be as short as 48 hours in the rodent parasites and as long as 15 days in P. malariae in humans. There is considerable variation in the appearance of the blood forms between individuals experimentally inoculated at the same time. Even within a single experimentally individual there may be considerable variation in the maturity of the hepatic forms seen on liver biopsy. A proportion of the hepatic stages may remain within the liver for considerable time - a form known as hypnozoites. Reactivation of the hypnozoites has been reported for up to 30 years after the initial infection in humans. The factors precipating this reactivation are not known. In the species Plasmodium ovale and Plasmodium vivax, but not in Plasmodium malariae, hypnozoites have been shown to occur. It is not yet known if hypnozoite reactivaction occurs with any of the remaining species that infect humans but this is presumed to be the case. The development from the hepatic stages to the erythrocytic stages has, until very recently, been obscure. In 2006 it was shown that the parasite buds off the hepatocytes in merosomes containing hundreds or thousands of merozoites. These merosomes lodge in the pulmonary capillaries and slowly disintegrate there over 48–72 hours releasing merozoites. The membrane of the merosome is derived from the host hepatocyte. The membrane of the merozoites is formed by repeated invagination of the parasite's membrane. The parastitophorus vacuole breaks down within the hepatocyte. This is associated with degeneration of the host cell's mitochondria and cessation of protein synthesis which is probably due to the lack of mitochondially produced ATP. The membrane of the merosome is then formed from that of the hepatocyte membrane but the hepatocyte proteins within the membrane are lost. This host derived membrane presumably provides protection from the immune system while the merozoites are transported to the lung. Erythrocyte invasion is enhanced when blood flow is slow and the cells are tightly packed: both of these conditions are found in the alveolar capillaries. Infection of the liver may be influenced by the iron regulatory hormone hepcidin and this may play a role in preventing superinfection despite repeated inoculation.

ERYTHROCYTE STAGES

After entering the erythrocyte, the merozoite lose one of their membranes, the apical rings, conoid and the rhopteries. Phagotropy commences and both smooth and granular endoplasmic reticulum becomes prominent. The nucleus may become lobulated. Within the erythrocytes the merozoite grow first to a ring-shaped form and then to a larger trophozoite form. In the schizont stage, the parasite divides several times to produce new merozoites, which leave the red blood cells and travel within the bloodstream to invade new red blood cells. The parasite feeds by ingesting haemoglobin and other materials from red blood cells and serum. The feeding process damages the erythrocytes. Details of this process have not been studied in species other than Plasmodium falciparum so generalizations may be premature at this time. Erythrocytes infected by Plasmodium falciparum tend to form clumps - rosettes - and these have been linked to pathology caused by vascular occlusion. This rosette formation may be inhibted by heparin. This agent has been used in the past as part of the treatment of malaria but was abandoned because of an increased risk of haemorrhage. Low molecular weight heparin also disrupts rosette formation and may have a lower risk of bleeding in malaria. Rosetting has been shown to be due to the binding of the erythrocyte major protein (the var gene product) to the ABO blood group protein. Blood group A is preferred over group B which in turn is preferred over group O. This has been shown to be due to different fits of blood group protein to the erythrocyte major protein. The binding side on the erythrocyte major protein is opposite to the heparin binding site on the same protein. Although the ABO blood group is associated with severe malaria this association is lost in pregnancy. The regulation of the erythrocyte stages is poorly understood. It is known that melatonin plays a role but how this affects the parasite is only slowly being worked out. It seems that melatonin affects the ubiquitin/proteasome system and a protein kinase (PfPK7) are central to this process. The presence of the parasite within the erythrocyte increases the membrane stiffness. This may be due to an increase in the cross linking of the intraerythrocytic spectrin network or simply due to the mechanical effects of the presence of the parasite itself within the cell.

MEROZOITES

The budding of the merozoites from interconnected cytoplasmic masses (pseudocytomeres) is a complex process. At the tip of each bud a thickened region of pellicle gives rise to the apical rings and conoid. As development proceeds an aggregation of smooth membranes and the nucleus enter the base of the bud. The cytoplasm contains numerous large ribosomes. Synchronous multiple cytoplasmic cleavage of the mature schizont results in the formation of numerous uninucleate merozoites. Escape of the merozoites from the erythrocyte has also been studied. The erythrocyte swells under osmotic pressure. A pore opens in the erythrocte membrane and 1-2 meorozites escape. This is followed by an eversion the entire erythrocyte membrane, an action that propels the merozoites into the blood stream. Invasion of erythrocyte precursors has only recently been studied. The earliest stage susceptible to infection were the orthoblasts - the stage immediately preceding the reticulocyte stage which in turn is the immediate precursor to the mature erythrocyte. Invasion of the erythrocyte is inhibited by angiotensin 2 Angiotensin 2 is normally metabolized by erythrocytes to angiotensin (Ang) IV and Ang-(1-7). Parasite infection decreased the Ang-(1-7) levels and completely abolished Ang IV formation. Ang-(1-7), like its parent molecule, is capable of decreasing the level of infection. The mechanism of inhibition seems likely to be an inhibition of protein kinase A activity within the erythrocyte.

PLACENTAL MALARIA

More than a hundred late-stage trophozoites or early schizont infected erythrocytes of P. falciparum in a case of placental malaria of a Tanzanian woman were found to form a nidus in an intervillous space of placenta. While such a concentration of parasites in placental malaria is rare, placental malaria cannot give rise to persistent infection as pregnancy in humans normally lasts only 9 months.

GAMETOCYTES

Most merozoites continue this replicative cycle but some merozoites differentiate into male or female sexual forms (gametocytes) (also in the blood), which are taken up by the female mosquito. This process of differentiation into gametocytes appears to occur in the bone marrow. Five distinct morphological stages have recognised (stages I - V). Female gametocytes are produced about four times as commonly as male. In chronic infections in humans the gametocytes are often the only forms found in the blood. Incidentally the characteristic form of the female gametocytes in Plasmodium falciparum gave rise to this species's name. Gameteocytes appear in the blood after a number of days post infection. In P. falciparum infections they appear after 7 to 15 days while in others they appear after 1 to 3 days. The ratio of asexual to sexual forms is between 10:1 and 156:1 The half life of the gametocytes has been estimated to be between 2 and 3 days but some are known to persist for up to four weeks. Gametocyte carriage is associated with anaemia. Although female gametocytes normally outnumber males this may be reversed in the presence of anaemia. The adhesive properties of the gametocytes have rarely been investigated but they appear to differ from the asexual forms in their adhesive properties. Stage V gametocytes do not show any appreciable binding, consistent with their condition of being freely circulating cells. The mechanisms involved in the maturation and release of the gametocytes from the bone marrow are still under investigation. The mature gametocyte infected cells are more deformable than the immature and this is associated with the de association of the STEVOR proteins from the host cell membrane. It may be that mechanical retention contributes to sequestration of immature gametocytes and that the regained deformability of mature gametocytes is associated with their release in the bloodstream and ability to circulate.

GAMETOCYTE MORPHOLOGY

The five recognised morphological stages were first described by Field and Shute in 1956. One constant feature of the gametocytes in all stages that distinguishes them from the asexual forms is the presence of a pellicular complex. This originates in small membranous vesicle observed beneath the gametocyte plasmalemma in late stage I. Its function is not known. The structure itself consists of a subpellicular membrane vacuole. Deep to this is an array of longitudinally oriented microtubules. This structure is likely to be relatively inflexible and may help to explain the lack of amoeboid forms observed in asexual parasites. Gametocyte elongation is driven by the assembly of a system of flattened cisternal membrane compartments underneath the parasite plasma membrane and has a supporting network of microtubules. The sub-pellicular membrane complex is analogous to the inner membrane complex, an organelle with structural and motor functions that is well conserved across the apicomplexa. Early stage one gametoctyes are very difficult to distinguish from small round trophozoites. Later stages can be distinguished by the distribution of pigment granulues. Under the electrom microscope the formation of the subpellicular membrane and a smooth plasma membrane are recognisable. The nuclei are recognisably dimorphic into male and female. These forms may be found between day 0 and day 2 in P falciparum infections. In stage two the gametocyte enlarges and becomes D shaped. The nucleus may occupy a terminal end of the cell or lie along its length. Early spindle formation may be visible. These forms are found between day 1 to day 4 in P falciparum infections. In stage three the erythrocyte becomes distorted. A staining difference between the male and female gametoctyes is apparent (male stain pink while female stain faint blue with the usual stains). The male nucleus is noticeably larger than the female and more lobulated. The female cytoplasm has more ribosomes, endoplasmic reticulum and mitochondria. Electron dense organelles (osmophilic bodies) are found in both sexes but are more numerous in the female. The osmophilic bodies are thought to be involved in egress of the gametocyte from the erythrocyte. These organelles are found between day 4 and day 10 in P. falciparum infections. They are connected to the gametocyte surface by ducts and are almost absent after transformation into the female gamete. In stage four the erythrocyte is clearly deformed and the gametocyte is elongated. The male gametocytes stain red while the female stain violet blue. In the male pigment granules are scattered while in the female they are more dense. In the male the kinetochores of each chromosome are located over a nuclear pore. In stage five the gametocytes are clearly recognisable on light microscopy with the typical banana shaped female gametocytes. The subpellicular microtubules depolymerise but the membrane itself remains. In the male gametocyte exhibit the is a dramatic reduction in ribosomal density. Very few mitochondria are retained and the nucleus enlarges with a kinetochore complex attached to the nuclear envelope. In the female gametocytes there are numerous mitochondria, ribosomes and osmophillic bodies. The nucleus is small with a transcription factory. Stages other than stage five are not normally found in the periferal blood. For reasons not yet understood stages I to IV are sequestered preferentially in the bone marrow and spleen. Stage V gametocytes only become infectious to mosquitoes after a further two or three days of circulation.

INFECTION OF MOSQUITO

In the mosquito's midgut, the gametocytes develop into gametes: the process of activation and gametogenesis occur within 15 minutes of ingestion. and fertilize each other resulting in formation of a diploid zygote: this usually occurs within one hour of ingestion. Zygotes immediately undergo meiosis and differentiate within 24 hours of ingestion into motile, invasive ookinetes. It has been shown that up to 50% of the ookinetes may undergo apoptosis within the midgut. The reason for this behavior is unknown. While in the mosquito gut the parasites form thin cytoplasmic extensions to communicate with each other. These structures persist from the time of gametocyte activation until the zygote transforms into an ookinete. The function of these tubular structures remains to be discovered. The ookinetes penetrate the midgut epithelium and escape the midgut, then attach themselves onto the exterior of the gut membrane beneath the basal lamina where they differentiate into oocysts. As in the liver the parasite tends to invade a number of cells before choosing one to reside in. The reason for this behavior is not known. Here they divide many times (usually 11) to produce large numbers (8,000) of tiny elongated sporozoites. These sporozoites migrate to the salivary glands of the mosquito where they are injected into the blood and subcutaneous tissue of the next host the mosquito bites. The invasion process appears to be dependent on a serine protease produced by the mosquito in the midgut epithelial cells and in the basal side of the salivary glands. The escape of the gametocytes from the erythrocytes has been until recently obscure. The parasitophorous vacuole membrane ruptures at multiple sites within less than a minute following ingestion. This process may be inhibited by cysteine protease inhibitors. After this rupture of the vacuole the subpellicular membrane begins to disintegrate. This process also can be inhibited by aspartic and the cysteine/serine protease inhibitors. Approximately 15 minutes post-activation, the erythrocyte membrane ruptures at a single breaking point a third process that can be interrupted by protease inhibitors. Effects on the mosquito Infection of the mosquito has noticeable effects on the host. The presence of the parasite induces apoptosis of the egg follicles. The development of the parasite in the mosquito is temperature dependent with higher temperatures being associated with more rapid development. Higher temperatures appear to enhance the mosquito's immune system leading to a lower average infection rate. Survival of infected mosquitoes is enhanced in starvation conditions compared to uninfected controls. Development within the mosquito involves several insulin like peptides. Blocking this pathway results in reduced parasite development. It appears that the parasite is capable of altering the physiology of the mosquito host and this alternation under starvation conditions is favourable to the host. Infection appears to reduce fecundity (ability to reproduce) and to increase survival of the mosquito. This is in line with what evolutionary theory would predict.

DISCUSSION

A report of P. falciparum malaria in a patient with sickle cell anemia four years after exposure to the parasite has been published. A second report that P. falciparum malaria had become symptomatic eight years after leaving an endemic area has also been published. A third case of an apparent recurrence nine years after leaving an endemic area of P. falciparum malaria has now been reported. A fourth case of recurrence in a patient with lung cancer has been reported. Two cases in pregnant women both from Africa but who had not lived there for over a year have been reported. A case of congenital malaria due to both P. falciparum and P. malariae has been reported in a child born to a woman from Ghana, a malaria endemic area, despite the mother having emigrated to Austria eighteen months before and never having returned. A second case of congenital malaria in twins due to P. falciparum has been reported. The mother had left Togo 14 months before the diagnosis, had not returned in the interim and was never diagnosed with malaria during her pregnancy. One case of malaria has been reported in a man of African origin with sickle cell trait who was treated for B cell lymphoma with chemotherapy and an autologous bone marrow transplant. He developed symptomatic malaria only after a subsequent splenectomy performed for worsening disease. Pre treatment blood films and antigen testing were negative. It seems that at least occasionally P. falciparum has a dormant stage. If this is in fact the case, eradication or control of this organism may be more difficult than previously believed.

DORMANT FORMS

PLASMODIUM FALCIPARUM MALARIA

A report of P. falciparum malaria in a patient with sickle cell anemia four years after exposure to the parasite has been published. A second report that P. falciparum malaria had become symptomatic eight years after leaving an endemic area has also been published. A third case of an apparent recurrence nine years after leaving an endemic area of P. falciparum malaria has now been reported. A fourth case of recurrence in a patient with lung cancer has been reported. Two cases in pregnant women both from Africa but who had not lived there for over a year have been reported. A case of congenital malaria due to both P. falciparum and P. malariae has been reported in a child born to a woman from Ghana, a malaria endemic area, despite the mother having emigrated to Austria eighteen months before and never having returned. A second case of congenital malaria in twins due to P. falciparum has been reported. The mother had left Togo 14 months before the diagnosis, had not returned in the interim and was never diagnosed with malaria during her pregnancy. One case of malaria has been reported in a man of African origin with sickle cell trait who was treated for B cell lymphoma with chemotherapy and an autologous bone marrow transplant. He developed symptomatic malaria only after a subsequent splenectomy performed for worsening disease. Pre treatment blood films and antigen testing were negative. It seems that at least occasionally P. falciparum has a dormant stage. If this is in fact the case, eradication or control of this organism may be more difficult than previously believed.

PLASMODIUM MALARIAE

This parasite is not thought to have a latent form but relapses have been reported. The mechanism here is not yet clear.

DRUG INDUCED

Developmental arrest was induced by in vitro culture of P. falciparum in the presence of sub lethal concentrations of artemisinin. The drug induces a subpopulation of ring stages into developmental arrest. At the molecular level this is associated with overexpression of heat shock and erythrocyte binding surface proteins with the reduced expression of a cell-cycle regulator and a DNA biosynthesis protein. The schizont stage-infected erythrocyte in an experimental culture of P. falciparum, F32 was suppressed to a low level with the use of atovaquone. The parasites resumed growth several days after the drug was removed from the culture.

BIOLOGICAL REFUGES

Macrophages containing merozoites dispersed in their cytoplasm, called 'merophores', were observed in P. vinckei petteri - an organism that causes murine malaria. Similar merophores were found in the polymorph leukocytes and macrophages of other murine malaria parasite, P. yoelii nigeriensis and P. chabaudi chabaudi. All these species unlike P. falciparum are known to produce hyponozoites that may cause a relapse. The finding of Landau et al. on the presence of malaria parasites inside lymphatics suggest a mechanism for the recrudescence and chronicity of malaria infection.

EVOLUTION

As of 2007, DNA sequences are available from less than sixty species of Plasmodium and most of these are from species infecting either rodent or primate hosts. The evolutionary outline given here should be regarded as speculative, and subject to revision as more data becomes available.

APICOMPLEXA

The common ancestor of the Alveolates - a clade to which the Apicomplexa belong - was a myzocytotic predator with two heterodynamic flagella, micropores, trichocysts, rhoptries, micronemes, a polar ring and a coiled open sided conoid. The Alveolates have lost the axonemal locomotive structures found in the other members of this clade except in gametes. The ancestor of this group seems likely to have had some photosynthetic ability. A recently identified apicomplexan found in Australian corals - Chromera velia - has retained a photosynthetic plastid. It appears that the alveolates, the dinoflagellates and the heterokont algae acquired their plastids from a red algae suggesting a common origin of this organelle in all these clades. Many of the species within the Apicomplexia still possess plastids (the organelle in which photosynthesis occurs in photosynthetic eukaryotes) and some that lack plastids nonetheless have evidence of plastid genes within their genomes. Some extant dinoflagellates can invade the bodies of jellyfish and continue to photosynthesize, which is possible because jellyfish bodies are almost transparent. In host organisms with opaque bodies, such an ability would most likely rapidly be lost. In the majority of such species, the plastids are not capable of photosynthesis. Their function is not known, but there is suggestive evidence that they may be involved in reproduction. All sequenced mitochondrial genomes of ciliates and apicomplexia are linear. Whether this is true for the related clades is not yet known. The mitochondrial genome has undergone a severe reduction in size in the Alveolate clade. In the Apicomplexa, where mitochondrion is present, its genome has only three genes (In Cryptosporidium the mitochondion has been lost entirely.) The dinoflagellate mitochondia also have only the same three genes. In Colpodella - a relative of the Apicomplexa - the mitochondrial genome has but a single gene. Since the known ciliate mitochondrial genomes are considerably larger this reduction is genome size must have occurred after their ancestor of this clade diverged from that that gave rise to the extant ciliates. Why this reduction has occurred it not presently clear.

PLASMODIUM GENUS

Current (2007) theory suggests that the genera Plasmodium, Hepatocystis and Haemoproteus evolved from one or more Leucocytozoon species. Parasites of the genus Leucocytozoan infect white blood cells (leukocytes) and liver and spleen cells, and are transmitted by 'black flies' (Simulium species) — a large genus of flies related to the mosquitoes. It is thought that Leucocytozoon evolved from a parasite that spread by the orofaecal route and which infected the intestinal wall. At some point this parasite evolved the ability to infect the liver. This pattern is seen in the genus Cryptosporidium, to which Plasmodium is distantly related. At some later point this ancestor developed the ability to infect blood cells and to survive and infect mosquitoes. Once vector transmission was firmly established, the previous orofecal route of transmission was lost. The pattern of orofaecal transmission with coincidental infection of the erythrocytes is seen in the genus Schellackia. Species in this genus infect lizards. The usual route of transmission is orofaecal but the parasites can also infect erythrocytes if they traverse the intestinal wall. The infected erythrocytes may be ingested by mites. These infected mites may subsequently be eaten by other uninfected lizards whereupon the parasites emerge and infect these new hosts. Unlike Plasmodium no development occurs in the mite. Molecular evidence suggests that a reptile - specifically a squamate - was the first vertebrate host of Plasmodium. Birds were the second vertebrate hosts with mammals being the most recent group of vertebrates infected. Leukocytes, hepatocytes and most spleen cells actively phagocytose particulate matter, which makes the parasite's entry into the cell easier. The mechanism of entry of Plasmodium species into erythrocytes is still very unclear, as it takes place in less than 30 seconds. It is not yet known if this mechanism evolved before mosquitoes became the main vectors for transmission of Plasmodium. The genus Plasmodium evolved (presumably from its Leucocytozoon ancestor) about 130 million years ago, a period that is coincidental with the rapid spread of the angiosperms (flowering plants). This expansion in the angiosperms is thought to be due to at least one gene duplication event. It seems probable that the increase in the number of flowers led to an increase in the number of mosquitoes and their contact with vertebrates.

VECTORS

Mosquitoes evolved in what is now South America about 230 million years ago. There are over 3500 species recognized, but to date their evolution has not been well worked out, so a number of gaps in our knowledge of the evolution of Plasmodium remain. There is evidence of a recent expansion of Anopheles gambiae and Anopheles arabiensis populations in the late Pleistocene in Nigeria. The reason why a relatively limited number of mosquitoes should be such successful vectors of multiple diseases is not yet known. It has been shown that, among the most common disease-spreading mosquitoes, the symbiont bacterium Wolbachia are not normally present. It has been shown that infection with Wolbachia can reduce the ability of some viruses and Plasmodium to infect the mosquito, and that this effect is Wolbachia-strain specific.

CLASSIFICATION

TAXONOMY

Plasmodium belongs to the family Plasmodiidae (Levine, 1988), order Haemosporidia and phylum Apicomplexa. There are currently 450 recognised species in this order. Many species of this order are undergoing reexamination of their taxonomy with DNA analysis. It seems likely that many of these species will be re-assigned after these studies have been completed. For this reason the entire order is outlined here.

Order Haemosporida

Family Haemoproteidae
Genus Haemocystidium Castellani and Willey 1904, emend. Telford 1996 Genus Haemoproteus Subgenus Parahaemoproteus Subgenus Haemoproteus Family Garniidae
Genus Fallisia Lainson, Landau & Shaw 1974 Subgenus Fallisia Subgenus Plasmodioides Genus Garnia Genus Progarnia Family Leucocytozoidae
Genus Leucocytozoon Subgenus Leucocytozoon Subgenus Akiba Family Plasmodiidae
Genus Bioccala Genus Billbraya Genus Dionisia Genus Hepatocystis Genus Mesnilium Genus Nycteria Genus Plasmodium Subgenus Asiamoeba Telford 1988 Subgenus Bennettinia Valkiunas 1997 Subgenus Carinamoeba Garnham 1966 Subgenus Giovannolaia Corradetti, Garnham & Laird 1963 Subgenus Haemamoeba Grassi & Feletti 1890 Subgenus Huffia Garnham & Laird 1963 Subgenus Lacertaemoba Telford 1988 Subgenus Laverania Bray 1963 Subgenus Novyella Corradetti, Garnham & Laird 1963 Subgenus Ophidiella Garnham 1966 Subgenus Papernaia Landau et al 2010 Subgenus Plasmodium Bray 1963 emend. Garnham 1964 Subgenus Paraplasmodium Telford 1988 Subgenus Sauramoeba Garnham 1966 Subgenus Vinckeia Garnham 1964 Genus Polychromophilus Genus Rayella Genus Saurocytozoon Genus Vetufebrus Poinar 2011

PHYLOGENETIC TREES

The relationship between a number of these species can be seen on the Tree of Life website. Perhaps the most useful inferences that can be drawn from this phylogenetic tree are: P. falciparum and P. reichenowi (subgenus Laverania) branched off early in the evolution of this genus The genus Hepatocystis is nested within (paraphytic with) the genus Plasmodium The primate (subgenus Plasmodium) and rodent species (subgenus Vinckeia) form distinct groups The rodent and primate groups are relatively closely related The lizard and bird species are intermingled Although Plasmodium gallinaceum (subgenus Haemamoeba) and Plasmodium elongatum (subgenus Huffia) appear be related here there are so few bird species (three) included, this tree may not accurately reflect their real relationship. While no snake parasites have been included these are likely to group with the lizard-bird division While this tree contains a considerable number of species, DNA sequences from many species in this genus have not been included - probably because they are not available yet. Because of this problem, this tree and any conclusions that can be drawn from it should be regarded as provisional. Three additional trees are available from the American Museum of Natural History. These trees agree with the Tree of Life. Because of their greater number of species in these trees, some additional inferences can be made: The genus Hepatocystis appears to lie within the primate-rodent clade The genus Haemoproteus appears lie within the bird-lizard clade The trees are consistent with the proposed origin of Plasmodium from Leucocytozoon It is also known that the species infecting humans do not form a single clade. In contrast, the species infecting Old World monkeys seem to form a clade. Plasmodium vivax may have originated in Asia and the related species Plasmodium simium appears to be derived through a transfer from the human P. vivax to New World monkey species in South America. This occurred during an indepth study of Howler Monkeys near São Paulo, Brasil. Another tree concentrating on the species infecting the primates is available here: PLOS site This tree shows that the 'African' (P. malaria and P. ovale) and 'Asian' (P.cynomogli, P. gonderi, P. semiovale and P. simium) species tend to cluster together into separate clades. P. vivax clusters with the 'Asian' species. The rodent species (P. bergei, P. chabaudi and P. yoelli) form a separate clade. As usual P. falciparum does not cluster with any other species. The bird species (P. juxtanucleare, P. gallinaceum and P. relictum) form a clade that is related to the included Leucocytozoon and Haemoproteus species. A second tree can be found on the PLoS website: PLOS site This tree concentrates largely on the species infecting primates. The three bird species included in this tree (P. gallinacium, P. juxtanucleare and P. relictum) form a clade. Four species (P. billbrayi, P. billcollinsi, P. falciparum and P. reichenowi) form a clade within the subgenus Lavernia. This subgenus is more closely related to the other primate species than to the bird species or the included Leuocytozoan species. Both P. billbrayi and P. billcollinsi infect both the chimpanzee subspecies included in this study (Pan troglodytes troglodytes and Pan troglodytes schweinfurthii). P. falciparum infects the bonbo (Pan paniscus) and P. reichenowi infects only one subspecies (Pan troglodytes troglodytes). The eleven 'Asian' species included here form a clade with P. simium and P. vivax being clearly closely related as are P. knowseli and P. coatneyi; similarly P. brazillium and P. malariae are related. P. hylobati and P. inui are closely related. P. fragile and P. gonderi appear to be more closely related to P. vivax than to P. malariae. P. coatneyi and P. inui appear to be closely related to P. vivax. P. ovale is more closely related to P. malariae than to P. vivax. Within the 'Asian' clade are three unnamed potential species. One infects each of the two chimpanzee subspecies included in the study (Pan troglodytes troglodytes and Pan troglodytes schweinfurthii). These appear to be related to the P. vivax/P. simium clade. Two unnamed potential species infect the bonbo (Pan paniscus) and these are related to the P. malariae/P. brazillium clade.

NOTES

An analysis of ten 'Asian' species (P. coatneyi, P. cynomolgi, P. fieldi, P. fragile, P. gonderi, P. hylobati, P. inui, P. knowlesi, P. simiovale and P. vivax) suggests that P. coatneyi and P. knowlesi are closely related and that P. fragile is the species most closely related to these two. P. vivax and P. cynomolgi appear to be related. Unlike other eukaryotes studied to date Plasmodium species have two or three distinct SSU rRNA (18S rRNA) molecules encoded within the genome. These have been divided into types A, S and O. Type A is expressed in the asexual stages; type S in the sexual and type O only in the oocyte. Type O is only known to occur in Plasmodium vivax at present. The reason for this gene duplication is not known but presumably reflects an adaption to the different environments the parasite lives within. The Asian simian Plasmodium species - Plasmodium coatneyi, Plasmodium cynomolgi, Plasmodium fragile, Plasmodium inui, Plasmodium fieldi, Plasmodium hylobati and Plasmodium simiovale - have a single S-type-like gene and several A-type-like genes. It seems likely that these species form a clade within the subgenus Plasmodium. Analysis of the merozoite surface protein in ten species of the Asian clade suggest that this group diversified between 3 and 6.3 million years ago - a period that coincided with the radiation of the macques within South East Asia. The inferred branching order differs from that found from the analysis of other genes suggesting that this phylogenetic tree may be difficult to resolve. Positive selection on this gene was also found. P. vivax appears to have evolved between 45,000 and 82,000 years ago from a species that infects south east Asian macques. This is consistent with the other evidence of a south eastern origin of this species. It has been reported that the C terminal domain of the RNA polymerase 2 in the primate infecting species (other than P. falciparum and probably P. reichenowei) appears to be unusual suggesting that the classification of species into the subgenus Plasmodium may have an evolutionary and biological basis. A report of a new species that clusters with P. falciparum and P. reichenowi in chimpanzees has been published, although to date the species has been identified only from the sequence of its mitochondrion. Further work will be needed to describe this new species, however, it appears to have diverged from the P. falciparum- P. reichenowi clade about 21 million years ago. A second report has confirmed the existence of this species in chimpanzees. This report has also shown that P. falciparum is not a uniquely human parasite as had been previously believed. A third report of P. falciparum has been published. This study investigated two mitochondrial genes (cytB and cox1), one plastid gene (tufA), and one nuclear gene (ldh) in 12 chimpanzees and two gorillas from Cameroon and one lemur from Madagascar. Plasmodium falciparum was found in one gorilla and two chimpanzee samples. Two chimpanzee samples tested positive for Plasmodium ovale and one for Plasmodium malariae. Additionally one chimpanzee sample showed the presence of P. reichenowi and another P. gaboni. A new species - Plasmodium malagasi - was provisionally identified in the lemur. This species seems likely to belong to the Vinckeia subgenus but further work is required. A study of ~3000 wild ape specimens collected from Central Africa has shown that Plasmodium infection is common and is usually with multiple species.[85] The ape species included in the study were western gorillas (Gorilla gorilla), eastern gorillas (Gorilla beringei), bonobos (Pan paniscus) and chimpanzees (Pan troglodytes). 99% of the strains fell into six species within the subgenus Laverina. P. falciparum formed a monophyletic lineage within the gorilla parasite radiation suggesting an origin in gorrilas rather than chimpanzees. It has been shown that P. falciparum forms a clade with the species P reichenowi.[86] This clade may have originated between 3 million and 10000 years ago. It is proposed that the origin of P. falciparum may have occurred when its precursors developed the ability to bind to sialic acid Neu5Ac possibly via erythrocyte binding protein 175. Humans lost the ability to make the sialic acid Neu5Gc from its precursor Neu5Ac several million years ago and this may have protected them against infection with P. reichenowi. The dates of the evolution of the species within the subgenus Laverania have been estimated as follows:
Laverania: 12.0 million years ago (Mya) (95% estimated range: 6.0 - 19.0 Mya) P. falciparum in humans: 0.2 Mya (range: 0.078 - 0.33 Mya) P. falciparum in Pan paniscus: 0.77 Mya (range: 0.43 - 1.6 Mya) P. falciparum in humans and Pan paniscus: 0.85 Mya (0.46 - 1.3 Mya) P. reichenowi - P. falciparum in Pan paniscus: 2.2 Mya (range: 1.0 - 3.1 Mya) nd that P. reichenowi - 1.8 Mya (range: 0.6 - 3.2 Mya) P. billbrayi - 1.1 Mya (range: 0.52 - 1.7 Mya) lciparum P. billcollinsi - 0.97 Mya (range: 0.38 - 1.7 Mya) Another estimation of the date of evolution of this genus based upon the mutation rate in the cytochrome b gene places the evolution of P. falciparum at 2.5 Mya. The authors also estimated that the mammalian species of this genus evolved 12.8 Mya and that the order Haemosporida evolved 16.2 Mya. While the date of evolution of P. falciparum is consistent with alternative methods, the other two dates are considerably more recent than other published estimates and probably should be treated with caution. Plasmodium ovale has recently been shown to consist of two cocirculating species - Plasmodium ovale curtisi and Plasmodium ovale wallikeri. These two species can only be distinguished by genetic means and they separated between 1.0 and 3.5 million years ago. A recently (2009) described species (Plasmodium hydrochaeri) that infects capybaras (Hydrochaeris hydrochaeris) may complicate the phylogentics of this genus. This species appears to be most similar to Plasmodium mexicanum a lizard parasite. Further work in this area seems indicated.

SUBGENERA

The full taxonomic name of a species includes the subgenus but this is often omitted. The full name indicates some features of the morphology and type of host species. Sixteen subgenera are currently recognised. The avian species were discovered soon after the description of P. falciparum and a variety of generic names were created. These were subsequently placed into the genus Plasmodium although some workers continued to use the genera Laverinia and Proteosoma for P. falciparum and the avian species respectively. The 5th and 6th Congresses of Malaria held at Istanbul (1953) and Lisbon (1958) recommended the creation and use of subgenera in this genus. Laverinia was applied to the species infecting humans and Haemamoeba to those infecting lizards and birds. This proposal was not universally accepted. Bray in 1955 proposed a definition for the subgenus Plasmodium and a second for the subgenus Laverinia in 1958. Garnham described a third subgenus - Vinckeia - in 1964.

MAMMAL INFECTING SPECIES

Two species in the subgenus Laverania are currently recognised: P. falciparum and P. reichenowi. Three additional species - Plasmodium billbrayi, Plasmodium billcollinsi and Plasmodium gaboni - may also exist (based on molecular data) but a full description of these species have not yet been published. The presence of elongated gametocytes in several of the avian subgenera and in Laverania in addition to a number of clinical features suggested that these might be closely related. This is no longer thought to be the case. The type species is Plasmodium falciparum. Species infecting monkeys and apes (the higher primates) other than those in the subgenus Laverania are placed in the subgenus Plasmodium. The position of the recently described Plasmodium GorA and Plasmodium GorB has not yet been settled. The distinction between P. falciparum and P. reichenowi and the other species infecting higher primates was based on the morphological findings but have since been confirmed by DNA analysis. The type species is Plasmodium malariae. Parasites infecting other mammals including lower primates (lemurs and others) are classified in the subgenus Vinckeia. Vinckeia while previously considered to be something of a taxonomic 'rag bag' has been recently shown - perhaps rather surprisingly - to form a coherent grouping. The type species is Plasmodium bubalis.

BIRD INFECTING SPECIES

The remaining groupings are based on the morphology of the parasites. Revisions to this system are likely to occur in the future as more species are subject to analysis of their DNA. The four subgenera Giovannolaia, Haemamoeba, Huffia and Novyella were created by Corradetti et al. for the known avian malarial species. A fifth—Bennettinia—was created in 1997 by Valkiunas. The relationships between the subgenera are the matter of current investigation. Martinsen et al. 's recent (2006) paper outlines what is currently (2007) known. The subgenera Haemamoeba, Huffia, and Bennettinia appear to be monphylitic. Novyella appears to be well defined with occasional exceptions. The subgenus Giovannolaia needs revision. P. juxtanucleare is currently (2007) the only known member of the subgenus Bennettinia. Nyssorhynchus is an extinct subgenus of Plasmodium. It has one known member - Plasmodium dominicum

REPTILE INFECTING SPECIES

Unlike the mammalian and bird malarias those species (more than 90 currently known) that infect reptiles have been more difficult to classify. In 1966 Garnham classified those with large schizonts as Sauramoeba, those with small schizonts as Carinamoeba and the single then known species infecting snakes (Plasmodium wenyoni) as Ophidiella. He was aware of the arbitrariness of this system and that it might not prove to be biologically valid. Telford in 1988 used this scheme as the basis for the currently accepted (2007) system. These species have since been divided in to 8 genera - Asiamoeba, Carinamoeba, Fallisia, Garnia, Lacertamoeba, Ophidiella, Paraplasmodium and Sauramoeba. Three of these genera (Asiamoeba, Lacertamoeba and Paraplasmodium) were created by Telford in 1988. Another species (Billbraya australis) described in 1990 by Paperna and Landau and is the only known species in this genus. This species may turn out to be another subgenus of lizard infecting Plasmodium.

HOST RANGE

Host range among the mammalian orders is non uniform. At least 29 species infect non human primates; rodents outside the tropical parts of Africa are rarely affected; a few species are known to infect bats, porcupines and squirrels; carnivores, insectivores and marsupials are not known to act as hosts. The listing of host species among the reptiles has rarely been attempted. Ayala in 1978 listed 156 published accounts on 54 valid species and subspecies between 1909 and 1975. The regional breakdown was Africa: 30 reports on 9 species; Australia, Asia & Oceania: 12 reports on 6 species and 2 subspecies; Americas: 116 reports on 37 species.

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PROTOZOA

Protozoa (from the Greek words proto, meaning first, and zoa, meaning animals; singular protozoon or also protozoan) are a diverse group of single-cell eukaryotic organisms, many of which are motile. Throughout history, protozoa have been defined as single-cell protists with animal-like behavior, e.g., movement. Protozoa were regarded as the partner group of protists to protophyta, which have plant-like behaviour, e.g., photosynthesis. The most important protozoans range usually from 10 to 52 micrometers, but can grow as large as 1 mm, and are seen easily by microscope.

CHARACTERISTICS

Protozoa commonly range from 10 to 52 micrometers, but can grow as large as 1 mm, and are seen easily by microscope. The largest protozoa known are the deep-sea dwelling xenophyophores, which can grow up to 20 cm in diameter. They were considered formerly to be part of the protista family. Protozoa exist throughout aqueous environments and soil, occupying a range of trophic levels.

MOTILITY AND DIGESTION

Tulodens are one of the slow-moving form of protozoans. They move around with whip-like tails called flagella, hair-like structures called cilia, or foot-like structures called pseudopodia. Others do not move at all. Protozoa may absorb food via their cell membranes, some, e.g., amoebas, surround food and engulf it, and yet others have openings or "mouth pores" into which they sweep food. All protozoa digest their food in stomach-like compartments called vacuoles.

ECOLOGICAL ROLE

As components of the micro- and meiofauna, protozoa are an important food source for microinvertebrates. Thus, the ecological role of protozoa in the transfer of bacterial and algal production to successive trophic levels is important. As predators, they prey upon unicellular or filamentous algae, bacteria, and microfungi. Protozoa are both herbivores and consumersin the decomposer link of the food chain. They also control bacteria populations and biomass to some extent. Protozoa such as the malaria parasites (Plasmodium spp.), trypanosomesand leishmania, are also important as parasites and symbionts of multicellular animals.

LIFE CYCLE

Some protozoa have life stages alternating between proliferative stages (e.g., trophozoites) and dormant cysts. As cysts, protozoa can survive harsh conditions, such as exposure to extreme temperatures or harmful chemicals, or long periods without access to nutrients, water, or oxygen for a period of time. Being a cyst enables parasitic species to survive outside of a host, and allows their transmission from one host to another. When protozoa are in the form of trophozoites (Greek, tropho = to nourish), they actively feed. The conversion of a trophozoite to cyst form is known as encystation, while the process of transforming back into a trophozoite is known as excystation.Protozoa can reproduce by binary fission or multiple fission. Some protozoa reproduce sexually, some asexually, while some use a combination, (e.g., Coccidia). An individual protozoon is hermaphroditic.

CLASSIFICATION

Protozoa were previously often grouped in the kingdom of Protista, together with the plant-like algae and fungus-like slime molds. As a result of 21st-century systematics, protozoa, along with ciliates, mastigophorans, and apicomplexans, are arranged as animal-like protists. With the possible exception of Myxozoa, protozoa are not categorized as Metazoa. Protozoa are unicellular organisms and are often called the animal-like protists because they subsist entirely on other organisms for food. Most protozoa can move about on their own. Amoebas, Paramecia, and Trypanosomes are all examples of animal-like Protists.

HUMAN DISEASE

Some protozoa are human parasites, causing diseases. Examples of human diseases caused by protozoa: Malaria Amoebiasis Giardiasis Toxoplasmosis Cryptosporidiosis Trichomoniasis Chagas disease Leishmaniasis Sleeping Sickness Dysentery

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PSEUDOMONAS AERUGINOSA

Pseudomonas aeruginosa is a common bacterium that can cause disease in animals, including humans. It is found in soil, water, skin flora, and most man-made environments throughout the world. It thrives not only in normal atmospheres, but also in hypoxic atmospheres, and has, thus, colonized many natural and artificial environments. It uses a wide range of organic material for food; in animals, the versatility enables the organism to infect damaged tissues or those with reduced immunity. The symptoms of such infections are generalized inflammation and sepsis. If such colonizations occur in critical body organs, such as the lungs, the urinary tract, and kidneys, the results can be fatal. Because it thrives on most surfaces, this bacterium is also found on and in medical equipment, including catheters, causing cross-infections in hospitals and clinics. It is implicated in hot-tub rash. It is also able to decompose hydrocarbons and has been used to break down tarballs and oil from oil spills.

IDENTIFICATION

It is a Gram-negative, aerobic, coccobacillus bacterium with unipolar motility. An opportunistic human pathogen, P. aeruginosa is also an opportunistic pathogen of plants. P. aeruginosa is the type species of the genus Pseudomonas (Migula). P. aeruginosa secretes a variety of pigments, including pyocyanin (blue-green), pyoverdine (yellow-green and fluorescent), and pyorubin (red-brown). King, Ward, and Raney developed Pseudomonas Agar P (King A medium) for enhancing pyocyanin and pyorubin production, and Pseudomonas Agar F (King B medium) for enhancing fluorescein production. Pseudomonas aeruginosa fluorescence under UV illumination P. aeruginosa is often preliminarily identified by its pearlescent appearance and grape-like or tortilla-like odor in vitro. Definitive clinical identification of P. aeruginosa often includes identifying the production of both pyocyanin and fluorescein, as well as its ability to grow at 42°C. P. aeruginosa is capable of growth in diesel and jet fuel, where it is known as a hydrocarbon-using microorganism (or "HUM bug"), causing microbial corrosion. It creates dark, gellish mats sometimes improperly called "algae" because of their appearance. Although classified as an aerobic organism, P. aeruginosa is considered by many as a facultative anaerobe, as it is well adapted to proliferate in conditions of partial or total oxygen depletion. This organism can achieve anaerobic growth with nitrate as a terminal electron acceptor, and, in its absence, it is also able to ferment arginine by substrate-level phosphorylation. Adaptation to microaerobic or anaerobic environments is essential for certain lifestyles of P. aeruginosa, for example, during lung infection in cystic fibrosis patients, where thick layers of lung mucus and alginate surrounding mucoid bacterial cells can limit the diffusion of oxygen.

GENOMIC DIVERSITY

The G C-rich Pseudomonas aeruginosa chromosome consists of a conserved core and a variable accessory part. The core genomes of P. aeruginosa strains are largely collinear, exhibit a low rate of sequence polymorphism, and contain few loci of high sequence diversity, the most notable ones being the pyoverdine locus, the flagellar regulon, pilA, and the O-antigen biosynthesis locus. Variable segments are scattered throughout the genome, of which about one-third are immediately adjacent to tRNA or tmRNA genes. The three known hot spots of genomic diversity are caused by the integration of genomic islands of the pKLC102/PAGI-2 family into tRNALys or tRNAGly genes. The individual islands differ in their repertoire of metabolic genes, but share a set of syntenic genes that confer their horizontal spread to other clones and species. Colonization of atypical disease habitats predisposes to deletions, genome rearrangements, and accumulation of loss-of-function mutations in the P. aeruginosa chromosome. The P. aeruginosa population is characterized by a few dominant clones widespread in disease and environmental habitats. The genome is made up of clone-typical segments in core and accessory genome and of blocks in the core genome with unrestricted gene flow in the population.

CELL-SURFACE POLYSACCHARIDES

Cell-surface polysaccharides play diverse roles in the bacterial "lifestyle". They serve as a barrier between the cell wall and the environment, mediate host-pathogen interactions, and form structural components of biofilms. These polysaccharides are synthesized from nucleotide-activated precursors, and, in most cases, all the enzymes necessary for biosynthesis, assembly, and transport of the completed polymer are encoded by genes organized in dedicated clusters within the genome of the organism. Lipopolysaccharide is one of the most important cell-surface polysaccharides, as it plays a key structural role in outer membrane integrity, as well as being an important mediator of host-pathogen interactions. The genetics for the biosynthesis of the so-called A-band (homopolymeric) and B-band (heteropolymeric) O antigens have been clearly defined, and much progress has been made toward understanding the biochemical pathways of their biosynthesis. The exopolysaccharide alginate is a linear copolymer of B-1,4-linked D-mannuronic acid and L-glucuronic acid residues, and is responsible for the mucoid phenotype of late-stage cystic fibrosis disease. The pel and psl loci are two recently-discovered gene clusters, which also encode exopolysaccharides found to be important for biofilm formation. A rhamnolipid is a biosurfactant whose production is tightly regulated at the transcriptional level, but the precise role it plays in disease is not well understood at present. Protein glycosylation, in particular of pilin and flagellin, is a recent focus of research by several groups, and it has been shown to be important for adhesion and invasion during bacterial infection.

PATHOGENESIS

An opportunistic, nosocomial pathogen of immunocompromised individuals, P. aeruginosa typically infects the pulmonary tract, urinary tract, burns, wounds, and also causes other blood infections.It is the most common cause of infections of burn injuries and of the outer ear (otitis externa), and is the most frequent colonizer of medical devices (e.g., catheters). Pseudomonas can, in rare circumstances, cause community-acquired pneumonias, as well as ventilator-associated pneumonias, being one of the most common agents isolated in several studies. Pyocyanin is a virulence factor of the bacteria and has been known to cause death in C. elegans by oxidative stress. However, research indicates salicylic acid can inhibit pyocyanin production. One in ten hospital-acquired infections are from Pseudomonas. Cystic fibrosis patients are also predisposed to P. aeruginosa infection of the lungs. P. aeruginosa may also be a common cause of "hot-tub rash" (dermatitis), caused by lack of proper, periodic attention to water quality. The most common cause of burn infections is P. aeruginosa. Pseudomonas is also a common cause of postoperative infection in radial keratotomy surgery patients. The organism is also associated with the skin lesion ecthyma gangrenosum. P. aeruginosa is frequently associated with osteomyelitis involving puncture wounds of the foot, believed to result from direct inoculation with P. aeruginosa via the foam padding found in tennis shoes, with diabetic patients at a higher risk.

TOXINS

P. aeruginosa uses the virulence factor exotoxin A to ADP-ribosylate eukaryotic elongation factor 2 in the host cell, much as the diphtheria toxin does. Without elongation factor 2, eukaryotic cells cannot synthesize proteins and necrose. The release of intracellular contents induces an immunologic response in immunocompetent patients. In addition P. aeruginosa uses an exoenzyme, ExoU, which degrades the plasma membrane of eukaryotic cells, leading to lysis.

TRIGGERS

With low phosphate levels, P. aeruginosa has been found to activate from benign symbiont to express lethal toxins inside the intestinal tract and severely damage or kill the host, which can be mitigated by providing excess phosphate instead of antibiotics.

PLANTS AND INVERTEBRATES

In higher plants, P. aeruginosa induces symptoms of soft rot, for example in Arabidopsis thaliana (Thale cress) and Lactuca sativa (lettuce). It is also pathogenic to invertebrate animals, including the nematode Caenorhabditis elegans, the fruit fly Drosophila and the moth Galleria mellonella. The associations of virulence factors are the same for plant and animal infections.

QUORUM SENSING

Regulation of gene expression can occur through cell-cell communication or quorum sensing (QS) via the production of small molecules called autoinducers. QS is known to control expression of a number of virulence factors. Another form of gene regulation that allows the bacteria to rapidly adapt to surrounding changes is through environmental signaling. Recent studies have discovered anaerobiosis can significantly impact the major regulatory circuit of QS. This important link between QS and anaerobiosis has a significant impact on production of virulence factors of this organism. Garlic experimentally blocks quorum sensing in P. aeruginosa.

BIOFILMS AND TREATMENT RESISTANCE

Biofilms of P. aeruginosa can cause chronic opportunistic infections, which are a serious problem for medical care in industrialized societies, especially for immunocompromised patients and the elderly. They often cannot be treated effectively with traditional antibiotic therapy. Biofilms seem to protect these bacteria from adverse environmental factors. P. aeruginosa can cause nosocomial infections and is considered a model organism for the study of antibiotic-resistant bacteria. Researchers consider it important to learn more about the molecular mechanisms that cause the switch from planktonic growth to a biofilm phenotype and about the role of interbacterial communication in treatment-resistant bacteria such as P. aeruginosa. This should contribute to better clinical management of chronically infected patients, and should lead to the development of new drugs.

DIAGNOSIS

Depending on the nature of infection, an appropriate specimen is collected and sent to a bacteriology laboratory for identification. As with most bacteriological specimens, a Gram stain is performed, which may show Gram-negative rods and/or white blood cells. P. aeruginosa produces colonies with a characteristic 'grape-like' odour on bacteriological media. In mixed cultures, it can be isolated as clear colonies on MacConkey agar (as it does not ferment lactose) which will test positive for oxidase. Confirmatory tests include production of the blue-green pigment pyocyanin on cetrimide agar and growth at 42°C. A TSI slant is often used to distinguish nonfermenting Pseudomonas species from enteric pathogens in faecal specimens.

TREATMENT

P. aeruginosa is frequently isolated from nonsterile sites (mouth swabs, sputum, etc.), and, under these circumstances, it often represents colonization and not infection. The isolation of P. aeruginosa from nonsterile specimens should, therefore, be interpreted cautiously, and the advice of a microbiologist or infectious diseases physician/pharmacist should be sought prior to starting treatment. Often no treatment is needed. When P. aeruginosa is isolated from a sterile site (blood, bone, deep collections), it should be taken seriously, and almost always requires treatment. P. aeruginosa is naturally resistant to a large range of antibiotics and may demonstrate additional resistance after unsuccessful treatment, in particular, through modification of a porin. It should usually be possible to guide treatment according to laboratory sensitivities, rather than choosing an antibiotic empirically. If antibiotics are started empirically, then every effort should be made to obtain cultures, and the choice of antibiotic used should be reviewed when the culture results are available. Phage therapy against P. aeruginosa remains one of the most effective treatments, which can be combined with antibiotics, has no contraindications and minimal adverse effects. Phages are produced as sterile liquid, suitable for intake, applications etc. Phage therapy against ear infections caused by P. aeruginosa was reported in the journal Clinical Otolaryngology in August 2009.
Antibiotics that have activity against P. aeruginosa may include: aminoglycosides (gentamicin, amikacin, tobramycin, but not kanamycin) quinolones (ciprofloxacin, levofloxacin, but not moxifloxacin) cephalosporins (ceftazidime, cefepime, cefoperazone, cefpirome, ceftobiprole, but not cefuroxime, ceftriaxone, cefotaxime) antipseudomonal penicillins: carboxypenicillins (carbenicillin and ticarcillin), and ureidopenicillins (mezlocillin, azlocillin, and piperacillin). P. aeruginosa is intrinsically resistant to all other penicillins. carbapenems (meropenem, imipenem, doripenem, but not ertapenem) polymyxins (polymyxin B and colistin) monobactams (aztreonam)
These antibiotics must all be given by injection, with the exceptions of fluoroquinolones, aerosolized tobramycin and aerosolized aztreonam. For this reason, in some hospitals, fluoroquinolone use is severely restricted to avoid the development of resistant strains of P. aeruginosa. In the rare occasions where infection is superficial and limited (for example, ear infections or nail infections), topical gentamicin or colistin may be used.

ANTIBIOTIC RESISTANCE

One of the most worrisome characteristics of P. aeruginosa is its low antibiotic susceptibility, which is attributable to a concerted action of multidrug efflux pumps with chromosomally encoded antibiotic resistance genes (e.g., mexAB, mexXY etc.) and the low permeability of the bacterial cellular envelopes. In addition to this intrinsic resistance, P. aeruginosa easily develops acquired resistance either by mutation in chromosomally encoded genes or by the horizontal gene transfer of antibiotic resistance determinants. Development of multidrug resistance by P. aeruginosa isolates requires several different genetic events, including acquisition of different mutations and/or horizontal transfer of antibiotic resistance genes. Hypermutation favours the selection of mutation-driven antibiotic resistance in P. aeruginosa strains producing chronic infections, whereas the clustering of several different antibiotic resistance genes in integrons favors the concerted acquisition of antibiotic resistance determinants. Some recent studies have shown phenotypic resistance associated to biofilm formation or to the emergence of small-colony variants may be important in the response of P. aeruginosa populations to antibiotics treatment.

PREVENTION

Probiotic prophylaxis may prevent colonization and delay onset of pseudomonas infection in an ICU setting. Immunoprophylaxis against pseudomonas is being investigated.

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ROUNDWORM

The nematodes or roundworms are the most diverse phylum of pseudocoelomates, and one of the most diverse of all animals. Nematode species are very difficult to distinguish; over 28,000 have been described, of which over 16,000 are parasitic. It has been estimated that the total number of nematode species might be approximately 1,000,000. Unlike cnidarians or flatworms, roundworms have a digestive system that is like a tube with openings at both ends.

HABITATS

Nematodes have successfully adapted to nearly every ecosystem from marine to fresh water, to soils, and from the polar regions to the tropics, as well as the highest to the lowest of elevations. They are ubiquitous in freshwater, marine, and terrestrial environments, where they often outnumber other animals in both individual and species counts, and are found in locations as diverse as mountains, deserts, oceanic trenches, and within the earth's lithosphere. They represent, for example, 90% of all life forms on the ocean floor. Their numerical dominance, often exceeding more than 1 million individuals per square meter and accounting for about 80% of all individual animals on earth, their diversity in lifestyles and their presence at various trophic levels point at an important role in many ecosystems. Their many parasitic forms include pathogens in most plants and animals (including humans). Some nematodes can undergo cryptobiosis. One group of carnivorous fungi, the nematophagous fungi, are predators of soil nematodes. They set enticements for the nematodes in the form of lassos or adhesive structures. Nematodes have even been found at great depth (0.9ï¿½3.6 km) below the surface of the Earth in gold mines in South Africa. Nathan Cobb (from p. 472 of Cobb, 1914) described the ubiquitous presence of nematodes on Earth as follows: "In short, if all the matter in the universe except the nematodes were swept away, our world would still be dimly recognizable, and if, as disembodied spirits, we could then investigate it, we should find its mountains, hills, vales, rivers, lakes, and oceans represented by a film of nematodes. The location of towns would be decipherable, since for every massing of human beings there would be a corresponding massing of certain nematodes. Trees would still stand in ghostly rows representing our streets and highways. The location of the various plants and animals would still be decipherable, and, had we sufficient knowledge, in many cases even their species could be determined by an examination of their erstwhile nematode parasites.

TAXONOMY AND SYSTEMATICS

The group was originally defined by Karl Rudolphi in 1808 under the name Nematoidea, from Ancient Greek. It was reclassified as family Nematodes by Burmeister in 1837 and order Nematoda by K. M. Diesing in 1861. At its origin, the "Nematoidea" included both roundworms and horsehair worms. Along with Acanthocephala, Trematoda and Cestoidea, it formed the group Entozoa. The first differentiation of roundworms from horsehair worms, though erroneous, is due to von Siebold (1843) with orders Nematoidea and Gordiacei (Gordiacea). They were classed along with Acanthocephala in the new phylum Nemathelminthes (today obsolete) by Gegenbaur (1859). The taxon Nematoidea, including the family Gordiidae (horsehair worms), was then promoted to the rank of phylum by Ray Lankester (1877). In 1919, Nathan Cobb proposed that roundworms should be recognized alone as a phylum. He argued they should be called nema(s) in English rather than "nematodes" and defined the taxon Nemates (Latin plural of nema). Since Cobb was the first to exclude all but nematodes from the group, some sources consider the valid taxon name to be Nemates or Nemata, rather than Nematoda.

PHYLOGENY

The relationships of the nematodes and their close relatives among the protostomian Metazoa are unresolved. Traditionally, they were held to be a lineage of their own, but in the 1990s it was proposed that they form a clade together with moulting animals such as arthropods. This group has been named Ecdysozoa. However, the monophyly of the Ecdysozoa was never unequivocally accepted: while most researchers consider at least the placement of arthropods as close relatives of annelidsï¿½with which they were formerly unitedï¿½to be unwarranted, the presumed close relationships of the nematodes and relatives with the arthropods has been a major point of contention. Even though the amount of data since accumulated in regard to this problem is staggering, the situation seems if anything less clear these days. DNA sequence data, initially strongly supporting the Ecdysozoa hypothesis, have become rather equivocal on ecdysozoan monophyly, and are simply unable to refute either a close or a more distant relationship between the arthropod and nematode lineages. That the roundworms have a large number of peculiar apomorphies and in many cases a parasitic lifestyle confounds morphological analyses. Genetic analyses of roundworms[citation needed] suggest thatï ½as is also indicated by their unique morphological featuresï ½the group has been under intense selective pressure during its early radiation, resulting apparently in accelerated rates of both morphological and molecular evolution. Furthermore, no distinctive apomorphies of Ecdysozoa are known; even moulting has recently been confirmed to occur outside the presumed clade. Conversely, the identity of the closest living relatives of the Nematoda has always been considered to be well resolved. Morphological characters and molecular phylogenies agree with placement of the roundworms as sister taxon to the parasitic horsehair worms (Nematomorpha); together they make up the Nematoida. Together with the Scalidophora (formerly Cephalorhyncha), the Nematoida form the Introverta. It is entirely unclear whether the Introverta are, in turn, the closest living relatives of the enigmatic Gastrotricha; if so, they are considered a clade Cycloneuralia, but there is much disagreement both between and among the available morphological and molecular data. The Cycloneuralia or the Introvertaï ½depending on the validity of the formerï ½are often ranked as a superphylum.

NEMATODE SYSTEMATICS

Due to the lack of knowledge regarding many nematodes, their systematics is contentious. An earliest and influential classification was proposed by Chitwood and Chitwood ,later revised by Chitwood, who divided the phylum into twoï ½the Aphasmidia and the Phasmidia. These were later renamed Adenophorea (gland bearers) and Secernentea (secretors) respectively. The Secernentea share several characteristics including the presence of phasmids, a pair of sensory organs located in the lateral posterior region and this was used as the basis for this division. This scheme was adhered to in many later classifications even though it was realized that the Adenophorea were not a uniform group. Initial DNA sequence studies suggested the existence of five clades: Dorylaimia Enoplia Spirurina Tylenchina Rhabditina As it seems, the Secernentea are indeed a natural group of closest relatives. But the "Adenophorea" appear to be a paraphyletic assemblage of roundworms simply retaining a good number of ancestral traits. The old Enoplia do not seem to be monophyletic either but to contain two distinct lineages. The old group "Chromadoria" seem to be another paraphyletic assemblage, with the Monhysterida representing a very ancient minor group of nematodes. Among the Secernentea, the Diplogasteria may need to be united with the Rhabditia. while the Tylenchia might be paraphyletic with the Rhabditia.   The understanding of roundworm systematics and phylogeny as of 2002 is summarised below: Phylum Nematoda Basal order Monhysterida Class Dorylaimea Class Enoplea Class Secernentea Subclass Diplogasteria (disputed) Subclass Rhabditia (paraphyletic?) Subclass Spiruria Subclass Tylenchia (disputed) "Chromadorea" assemblage Later work has suggested the presence of 12 clades. It appears that Secernenteaï½a group that includes virtually all major animal and plant 'nematode' parasitesï½arose from within the Adenophorea. A major effort to improve the systematics of this phylum is in progress and being organised by the 959 Nematode Genomes.

ANATOMY

Nematodes are slender worms, typically less than 2.5 millimetres (0.10 in) long. The smallest nematodes are microscopic, while free-living species can reach as much as 5 centimetres (2.0 in) and some parasitic species are larger still, reaching over a meter in length. The body is often ornamented with ridges, rings, bristles or other distinctive structures. The head of a nematode is relatively distinct. Whereas the rest of the body is bilaterally symmetrical, the head is radially symmetrical, with sensory bristles and, in many cases, solid 'head-shields' radiating outwards around the mouth. The mouth has either three or six lips, which often bear a series of teeth on their inner edges. An adhesive 'caudal gland' is often found at the tip of the tail. The epidermis is either a syncytium or a single layer of cells, and is covered by a thick collagenous cuticle. The cuticle is often of complex structure, and may have two or three distinct layers. Underneath the epidermis lies a layer of muscle cells. Projections run from the inner surface of these cells towards the nerve cords; this is a unique arrangement in the animal kingdom, in which nerve cells normally extend fibres into the muscles rather than vice versa.

DIGESTIVE SYSTEM

The oral cavity is lined with cuticle, which is often strengthened with ridges or other structures, and, especially in carnivorous species, may bear a number of teeth. The mouth often includes a sharp stylet which the animal can thrust into its prey. In some species, the stylet is hollow, and can be used to suck liquids from plants or animals. The oral cavity opens into a muscular, sucking pharynx, also lined with cuticle. Digestive glands are found in this region of the gut, producing enzymes that start to break down the food. In stylet-bearing species, these may even be injected into the prey. There is no stomach, with the pharynx connecting directly to the intestine that forms the main length of the gut. This produces further enzymes, and also absorbs nutrients through its lining. The last portion of the intestine is lined by cuticle, forming a rectum which expels waste through the anus just below and in front of the tip of the tail. The intestine also has valves or sphincters at either end to help control the movement of food through the body.

EXCRETORY SYSTEM

Nitrogenous waste is excreted in the form of ammonia through the body wall, and is not associated with any specific organs. However, the structures for excreting salt to maintain osmoregulation are typically more complex. In many marine nematodes, one or two unicellular renette glands excrete salt through a pore on the underside of the animal, close to the pharynx. In most other nematodes, these specialised cells have been replaced by an organ consisting of two parallel ducts connected by a single transverse duct. This transverse duct opens into a common canal that runs to the excretory pore.

NERVOUS SYSTEM

our peripheral nerves run the length of the body on the dorsal, ventral, and lateral surfaces. Each nerve lies within a cord of connective tissue lying beneath the cuticle and between the muscle cells. The ventral nerve is the largest, and has a double structure forward of the excretory pore. The dorsal nerve is responsible for motor control, while the lateral nerves are sensory, and the ventral combines both functions. At the anterior end of the animal, the nerves branch from a dense, circular nerve ring surrounding the pharynx, and serving as the brain. Smaller nerves run forward from the ring to supply the sensory organs of the head. The body of nematodes is covered in numerous sensory bristles and papillae that together provide a sense of touch. Behind the sensory bristles on the head lie two small pits, or 'amphids'. These are well supplied with nerve cells, and are probably chemoreception organs. A few aquatic nematodes possess what appear to be pigmented eye-spots, but is unclear whether or not these are actually sensory in nature.

REPRODUCTION

Most nematode species are dioecious, with separate male and female individuals. Both sexes possess one or two tubular gonads. In males, the sperm are produced at the end of the gonad, and migrate along its length as they mature. The testes each open into a relatively wide sperm duct and then into a glandular and muscular ejaculatory duct associated with the cloaca. In females, the ovaries each open into an oviduct and then a glandular uterus. The uteri both open into a common vagina, usually located in the middle of the ventral surface. Reproduction is usually sexual. Males are usually smaller than females (often much smaller) and often have a characteristically bent tail for holding the female for copulation. During copulation, one or more chitinized spicules move out of the cloaca and are inserted into genital pore of the female. Amoeboid sperm crawl along the spicule into the female worm. Nematode sperm is thought to be the only eukaryotic cell without the globular protein G-actin. Eggs may be embryonated or unembryonated when passed by the female, meaning their fertilized eggs may not yet be developed. A few species are known to be ovoviviparous. The eggs are protected by an outer shell, secreted by the uterus. In free-living roundworms, the eggs hatch into larvae, which appear essentially identical to the adults, except for an underdeveloped reproductive system; in parasitic roundworms, the life cycle is often much more complicated. Nematodes as a whole possess a wide range of modes of reproduction. Some nematodes, such as Heterorhabditis spp., undergo a process called endotokia matricida: intrauterine birth causing maternal death. Some nematodes are hermaphroditic, and keep their self-fertilized eggs inside the uterus until they hatch. The juvenile nematodes will then ingest the parent nematode. This process is significantly promoted in environments with a low or reducing food supply. The nematode model species Caenorhabditis elegans and C. briggsae exhibit androdioecy, which is very rare among animals. The single genus Meloidogyne (root-knot nematodes) exhibit a range of reproductive modes, including sexual reproduction, facultative sexuality (in which most, but not all, generations reproduce asexually), and both meiotic and mitotic parthenogenesis. The genus Mesorhabditis exhibits an unusual form of parthenogenesis, in which sperm-producing males copulate with females, but the sperm do not fuse with the ovum. Contact with the sperm is essential for the ovum to begin dividing, but because there is no fusion of the cells, the male contributes no genetic material to the offspring, which are essentially clones of the female.

FREE-LIVING SPECIES

In free-living species, development usually consists of four molts of the cuticle during growth. Different species feed on materials as varied as algae, fungi, small animals, fecal matter, dead organisms and living tissues. Free-living marine nematodes are important and abundant members of the meiobenthos. They play an important role in the decomposition process, aid in recycling of nutrients in marine environments and are sensitive to changes in the environment caused by pollution. One roundworm of note, Caenorhabditis elegans, lives in the soil and has found much use as a model organism. C. elegans has had its entire genome sequenced, as well as the developmental fate of every cell determined, and every neuron mapped.

PARASITIC SPECIES

Nematodes commonly parasitic on humans include ascarids (Ascaris), filarias, hookworms, pinworms (Enterobius) and whipworms (Trichuris trichiura). The species Trichinella spiralis, commonly known as the 'trichina worm', occurs in rats, pigs, and humans, and is responsible for the disease trichinosis. Baylisascaris usually infests wild animals, but can be deadly to humans, as well. Dirofilaria immitis heartworms are known for causing heartworm disease by inhabiting the hearts, arteries, and lungs of dogs and some cats. Haemonchus contortus is one of the most abundant infectious agents in sheep around the world, causing great economic damage to sheep farms. In contrast, entomopathogenic nematodes parasitize insects and are considered by humans to be beneficial. One form of nematode is entirely dependent upon fig wasps, which are the sole source of fig fertilization. They prey upon the wasps, riding them from the ripe fig of the wasp's birth to the fig flower of its death, where they kill the wasp, and their offspring await the birth of the next generation of wasps as the fig ripens. A newly discovered parasitic tetradonematid nematode, Myrmeconema neotropicum, apparently induces fruit mimicry in the tropical ant Cephalotes atratus. Infected ants develop bright red gasters, tend to be more sluggish, and walk with their gasters in a conspicuous elevated position. These changes likely cause frugivorous birds to confuse the infected ants for berries, and eat them. Parasite eggs passed in the bird's feces are subsequently collected by foraging Cephalotes atratus and are fed to their larvae, thus completing the life cycle of M. neotropicum. Colorized electron micrograph of soybean cyst nematode (Heterodera sp.) and egg Plant-parasitic nematodes include several groups causing severe crop losses. The most common genera are Aphelenchoides (foliar nematodes), Ditylenchus, Globodera (potato cyst nematodes), Heterodera (soybean cyst nematodes), Longidorus, Meloidogyne (root-knot nematodes), Nacobbus, Pratylenchus (lesion nematodes), Trichodorus and Xiphinema (dagger nematodes). Several phytoparasitic nematode species cause histological damages to roots, including the formation of visible galls (e.g. by root-knot nematodes), which are useful characters for their diagnostic in the field. Some nematode species transmit plant viruses through their feeding activity on roots. One of them is Xiphinema index, vector of grapevine fanleaf virus), an important disease of grapes. Other nematodes attack bark and forest trees. The most important representative of this group is Bursaphelenchus xylophilus, the pine wood nematode, present in Asia and America and recently discovered in Europe.

AGRICULTURE AND HORTICULTURE

Depending on the species, a nematode may be beneficial or detrimental to plant health. From agricultural and horticulture perspectives, the two categories of nematode: predatory ones, which will kill garden pests like cutworms, and pest nematodes, like the root-knot nematode, which attack plants and those that act as vectors spreading plant viruses between crop plants. Predatory nematodes can be bred by soaking a specific recipe of leaves and other detritus in water, in a dark, cool place, and can even be purchased as an organic form of pest control. Rotations of plants with nematode resistant species or varieties is one means of managing parasitic nematode infestations. For example, marigolds, grown over one or more seasons (the effect is cumulative), can be used to control nematodes.Another is treatment with natural antagonists such as the fungus Gliocladium roseum. Chitosan is a natural biocontrol that elicits plant defense responses to destroy parasitic cyst nematodes on roots of soybean, corn, sugar beet, potato and tomato crops without harming beneficial nematodes in the soil. Furthermore, soil steaming is an efficient method to kill nematodes before planting the crop, but indiscriminately eliminates both harmful and beneficial ones. CSIRO has found a 13- to 14-fold reduction of nematode population densities in plots having Indian mustard (Brassica juncea) green manure or seed meal in the soil. Hundreds of Caenorhabditis elegans were featured in a research project on NASA's STS-107 space mission, and were the only known living organisms to have survived the Space Shuttle Columbia Disaster.

EPIDEMIOLOGY

A number of intestinal nematodes affect human beings. These include ascariasis, trichuriasis and hookworm disease.

For more information view the source:Wikipedia

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SALMONELLA

Salmonella is a genus of rod-shaped, Gram-negative, non-spore-forming, predominantly motile enterobacteria with diameters around 0.7 to 1.5 µm, lengths from 2 to 5 µm, and flagella that grade in all directions (i.e., peritrichous). They are chemoorganotrophs, obtaining their energy from oxidation and reduction reactions using organic sources, and are facultative anaerobes. Most species produce hydrogen sulfide, which can readily be detected by growing them on media containing ferrous sulfate, such as TSI. Most isolates exist in two phases: a motile phase I and a nonmotile phase II. Cultures that are nonmotile upon primary culture may be switched to the motile phase using a Cragie tube. Salmonella is closely related to the Escherichia genus and are found worldwide in cold- and warm-blooded animals (including humans), and in the environment. They cause illnesses such as typhoid fever, paratyphoid fever, and foodborne illness.

SALMONELLA AS DISEASE-CAUSING AGENTS

Salmonella infections are zoonotic and can be transferred between humans and nonhuman animals. Many infections are due to ingestion of contaminated food. For example, recent FDA studies link Guatemalan cantaloupes with Salmonella Panama. In speaking of other salmonella serotypes, enteritis Salmonella and Salmonella typhoid/paratyphoid Salmonella,the latter—because of a special virulence factor and a capsule protein (virulence antigen)—can cause serious illness, such as Salmonella enterica subsp. enterica serovar Typhi. Salmonella typhi is adapted to humans and does not occur in other animals. Salmonella species are facultative intracellular pathogens that enter cells via macropinosomes

ENTERITIS SALMONELLOSIS OR FOOD POISNING

This is a group consisting of potentially every other serotype (over a thousand) of the Salmonella bacteria, most of which have never been found in humans. These are encountered in various Salmonella species, most having never been linked to a specific host, but can also infect humans. It is therefore a zoonotic disease. The organism enters through the digestive tract and must be ingested in large numbers to cause disease in healthy adults. Gastric acidity is responsible for the destruction of the majority of ingested bacteria. Salmonellosis is a disease caused by raw or undercooked food. Infection usually occurs when a person ingests foods that contain a high concentration of the bacteria, similar to a culture medium. However, infants and young children are much more susceptible to infection, easily achieved by ingesting a small number of bacteria. In infants, contamination through inhalation of bacteria-laden dust is possible. After a short incubation period of a few hours to one day, the germs multiply in the intestinal lumen, causing an intestinal inflammation with diarrhea that is often mucopurulent and bloody. In infants, dehydration can cause a state of severe toxicosis. The symptoms are usually mild. Normally, no sepsis occurs, but it can occur exceptionally as a complication in weakened or elderly patients (e.g., Hodgkin's disease). Extraintestinal localizations are possible, especially Salmonella meningitis in children, osteitis, etc. Enteritis Salmonella (e.g., Salmonella enterica subsp. enterica serovar enteritidis) can cause diarrhea, which usually does not require antibiotic treatment. However, in people at risk such as infants, small children, the elderly, Salmonella infections can become very serious, leading to complications. If these are not treated, HIV patients and those with suppressed immunity can become seriously ill. Children with sickle cell anaemia who are infected with Salmonella may develop osteomyelitis. In Germany, Salmonella infections must be reported. Between 1990 and 2005, the number of officially recorded cases decreased from approximately 200,000 to approximately 50,000 cases. Every fifth person in Germany is thought to carry Salmonella. In the USA, about 40,000 cases of Salmonella infection are reported each year. According to the World Health Organization, over 16 million people worldwide are infected with typhoid fever each year, with 500,000 to 600,000 fatal cases. Salmonella bacteria can survive for weeks outside a living body, and they are not destroyed by freezing. Ultraviolet radiation and heat accelerate their demise; they perish after being heated to 55 °C (131 °F) for 90 min, or to 60 °C (140 °F) for 12 min. To protect against Salmonella infection, heating food for at least ten minutes at 75 °C (167 °F) is recommended, so the centre of the food reaches this temperature. The AvrA toxin injected by the type three secretion system of Salmonella typhimurium works to inhibit the innate immune system by virtue of its serine/threonine acetyltransferase activity, and requires binding to eukaryotic target cell phytic acid (IP6). This leaves the host more susceptible to infection. In a 2011 paper, Yale University School of Medicine researchers described in detail how Salmonella is able to make these proteins line up in just the right sequence to invade host cells. "These mechanisms present us with novel targets that might form the basis for the development of an entirely new class of antimicrobials," said Professor Dr. Jorge Galan, senior author of the paper and the Lucille P. Markey Professor of Microbial Pathogenesis and chair of the Section of Microbial Pathogenesis at Yale. In the new National Institutes of Health-funded study, Galan and colleagues identify what they call a bacterial sorting platform, which attracts needed proteins and lines them up in a specific order. If the proteins do not line up properly, Salmonella, as well as many other bacterial pathogens, cannot "inject" them into host cells to commandeer host cell functions, the lab has found. Understanding how this machine works raises the possibility of new therapies that disable this protein delivery machine, thwarting the ability of the bacterium to become pathogenic. The process would not kill the bacteria as most antibiotics do, but would cripple its ability to do harm. In theory, this means bacteria such as Salmonella might not develop resistance to new therapies as quickly as they usually do to conventional antibiotics. Most people with salmonellosis develop diarrhea, fever, vomiting, and abdominal cramps 12 to 72 hours after infection. In most cases, the illness lasts four to seven days, and most people recover without treatment. In some cases, though, the diarrhea may be so severe, the patient becomes dangerously dehydrated and must be taken to a hospital. At the hospital, the patient may receive intravenous fluids to treat the dehydration, and may be given medications to provide symptomatic relief, such as fever reduction. In severe cases, the Salmonella infection may spread from the intestines to the blood stream, and then to other body sites, and can cause death, unless the person is treated promptly with antibiotics. The elderly, infants, and those with impaired immune systems are more likely to develop severe illness. Some people afflicted with salmonellosis later experience reactive arthritis, which can have long-lasting, disabling effects. An infectious process can only begin after living salmonellae (not only their toxins) reach the gastrointestinal tract. Some of the microorganisms are killed in the stomach, while the surviving salmonellae enter the small intestine and multiply in tissues (localized form). By the end of the incubation period, the macro-organisms are poisoned by endotoxins released from the dead salmonellae. The local response to the endotoxins is enteritis and gastrointestinal disorder. In the generalized form of the disease, salmonellae pass through the lymphatic system of the intestine into the blood of the patients (typhoid form) and are carried to various organs (liver, spleen, kidneys) to form secondary foci (septic form). Endotoxins first act on the vascular and nervous apparatus, manifested by increased permeability and decreased tone of the vessels, upset thermal regulation, vomiting and diarrhea. In severe forms of the disease, enough liquid and electrolytes are lost to upset the water-salt metabolism, to decrease the circulating blood volume and arterial pressure, and to cause hypovolemic shock. Septic shock may develop. Shock of mixed character (with signs of both hypovolemic and septic shock) are more common in severe salmonellosis. Oliguria and azotemia develop in severe cases as a result of renal involvement due to hypoxia and toxemia.

HISTORY

The genus Salmonella was named after Daniel Elmer Salmon, an American veterinary pathologist. While Theobald Smith was the actual discoverer of the type bacterium (Salmonella enterica var. choleraesuis) in 1885, Dr. Salmon was the administrator of the USDA research program, and thus the organism was named after him by Smith. Smith and Salmon had been searching for the cause of common hog cholera and proposed this organism as the causal agent. Later research, however, would show this organism (now known as Salmonella enterica) rarely causes enteric symptoms in pigs, and was thus not the agent they were seeking (which was eventually shown to be a virus). However, related bacteria in the genus Salmonella were eventually shown to cause other important infectious diseases. The genus Salmonella was finally formally adopted in 1900 by J. Lignières for the many species of Salmonella, after Smith's first type-strain Salmonella cholerae suis.

SALMONELLA NOMENCLATURE

Initially, each Salmonella species was named according to clinical considerations, e.g., Salmonella typhi-murium (mouse typhoid fever), S. cholerae-suis (hog cholera). After it was recognized that host specificity did not exist for many species, new strains (or serovar, short for serological variants) received species names according to the location at which the new strain was isolated. Later, molecular findings led to the hypothesis that Salmonella consisted of only one species, S. enterica, and the serovar were classified into six groups, two of which are medically relevant. But as this now formalized nomenclature is not in harmony with the traditional usage familiar to specialists in microbiology and infectologists, the traditional nomenclature is common. Currently, there are three recognized species: S. enterica, S. bongori and S. subterranean, with six main subspecies: enterica (I), salamae (II), arizonae (IIIa), diarizonae (IIIb), houtenae (IV), and indica (VI). Historically, serotype (V) was bongori, which is now considered its own species. The serovar (i.e. serotype) is a classification of Salmonella into subspecies based on antigens that the organism presents. It is based on the Kauffman-White classification scheme that differentiates serological varieties from each other. Serotypes are usually put into subspecies groups after the genus and species, with the serovars/sertypes capitalized but not italicized: an example is Salmonella enterica serovar Typhimurium. Newer methods for Salmonella typing and subtyping include genome-based methods such as pulsed field gel electrophoresis (PFGE), Multiple Loci VNTR Analysis (MLVA), Multilocus sequence typing (MLST) and (multiplex-) PCR-based methods

GENETICS

Serovar Typhimurium has considerable diversity and may be very old. The majority of the isolates belong to a single clonal complex. Isolates are divided into phage types, but some phage types do not have a single origin as determined using mutational changes. Phage type DT104 is heterogeneous and represented in multiple sequence types, with its multidrug-resistant variant being the most successful and causing epidemics in many parts of the planet. Serovar Typhi is relatively young compared to Typhimurium, and probably originated approximately 30,000-50,000 years ago.

SOURCE OF INFECTION

Infected food, often gaining an unusual look or smell, then is introduced into the stream of commerce; Poor kitchen hygiene, especially problematic in institutional kitchens and restaurants because this can lead to a significant outbreak; Excretions from either sick or infected but apparently clinically healthy people and animals (especially endangered are caregivers and animals); Polluted surface water and standing water (such as in shower hoses or unused water dispensers); Unhygienically thawed fowl (the meltwater contains many bacteria); An association with reptiles (pet tortoises, snakes, iguanas and frogs, but primarily aquatic turtles) is well described. Salmonella bacteria can survive for some time without a host; thus, they are frequently found in polluted water, contamination from the excrement of carrier animals being particularly important.

NEW ANTIBIOTIC-RESISTANT STRAINS

Non-typhoidal salmonella (iNTS) Africa, a new form of the germ, emerged in the southeast of the continent 52 years ago, followed by a second wave, which came out of central Africa 17 years later. The second wave of iNTS began 35 years ago, possibly in the Congo Basin, and early in the event picked up a gene making it resistant to the antibiotic chloramphenicol. There is an urgency to develop an effective salmonella vaccine because of the recent outbreaks in Africa of antibiotic-resistant strains of the food-borne bacteria that is killing hundreds of thousands of people there, as well as the heavy annual worldwide death toll each year. People with HIV are greatly affected. A recently identified set of antigens (molecules in the invading bacteria that trigger an immune response) that is common to both mice and humans, provide a foundation for developing a protective salmonella vaccine that could be on the market as early as 2016. This is good news because no new, effective antibiotics are on the horizon. In sub-Saharan the variant is the cause of an enigmatic disease called invasive non-typhoidal salmonella (iNTS), which affects Africa far more than other continents. Its genetic makeup is evolving into a more typhoid-like bacteria, able to efficiently spread around the human body.

VACCINE STATUS

Researchers say they have paved the way toward an effective Salmonella vaccine by identifying eight antigenic molecules from human and mouse infections. These antigens provide the research community with a foundation for developing a protective salmonella vaccine.

DEATHS

About 142,021 (reported) Americans are infected each year with Salmonella enteritidis from chicken eggs, and about 30 die. The shell of the egg may be contaminated with Salmonella by feces or environment, or its interior (yolk) may be contaminated by penetration of the bacteria through the porous shell or from a hen whose infected ovaries contaminate the egg during egg formation. Nevertheless, such interior egg yolk contamination is theoretically unlikely. Even under natural conditions, the rate of infection was very small (0.6% in a study of naturally-contaminated eggs and 3.0% among artificially- and heavily-infected hens). In 2010, an analysis of death certificates in the United States identified a total of 1,316 Salmonella-related deaths from 1990 to 2006. These were predominantly among older adults and those who were immunocompromised.

For more information view the source:Wikipedia

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SCHISTOSOMA

Schistosomiasis, also known as bilharzia, is a disease caused by parasitic worms. Although the worms that cause schistosomiasis are not found in the United States, more than 200 million people are infected worldwide. In terms of impact this disease is second only to malaria as the most devastating parasitic disease. Schistosomiasis is considered one of the Neglected Tropical Diseases (NTDs).

The parasites that cause schistosomiasis live in certain types of freshwater snails. The infectious form of the parasite, known as cercariae, emerge from the snail, hence contaminating water. You can become infected when your skin comes in contact with contaminated freshwater. Most human infections are caused by Schistosoma mansoni, S. haematobium, or S. japonicum.

FAQS

What is schistosomiasis?

Schistosomiasis, also known as bilharzia, is a disease caused by parasitic worms. Infection with Schistosoma mansoni, S. haematobium, and S. japonicum causes illness in humans; less commonly, S. mekongi and S. intercalatum can cause disease. Although the worms that cause schistosomiasis are not found in the United States, more than 200 million people are infected worldwide.

How can I get schistosomiasis?

Infection occurs when your skin comes in contact with contaminated freshwater in which certain types of snails that carry schistosomes are living.

Freshwater becomes contaminated by Schistosoma eggs when infected people urinate or defecate in the water. The eggs hatch, and if certain types of freshwater snails are present in the water, the parasites develop and multiply inside the snails. The parasite leaves the snail and enters the water where it can survive for about 48 hours. Schistosoma parasites can penetrate the skin of persons who are wading, swimming, bathing, or washing in contaminated water. Within several weeks, parasite mature into adult worms, residing in the blood vessels of the body where the females produce eggs. Some of the eggs travel to the bladder or intestine and are passed into the urine or stool.

What are the signs and symptoms of schistosomiasis?

Within days after becoming infected, you may develop a rash or itchy skin. Fever, chills, cough, and muscle aches can begin within 1-2 months of infection. Most people have no symptoms at this early phase of infection.

Eggs travel to the intestine, liver or bladder, causing inflammation or scarring. Children who are repeatedly infected can develop anemia, malnutrition, and learning difficulties. After years of infection, the parasite can also damage the liver, intestine, lungs, and bladder. Rarely, eggs are found in the brain or spinal cord and can cause seizures, paralysis, or spinal cord inflammation.

Symptoms of schistosomiasis are caused by the body's reaction to the eggs produced by worms, not by the worms themselves.

What should I do if I think I have schistosomiasis?

See your health care provider. If you have traveled to countries where schistosomiasis is found and had contact with freshwater, describe in detail where and for how long you traveled. Explain that you may have been exposed to contaminated water.

How is schistosomiasis diagnosed?

Your health care provider may ask you to provide stool or urine samples to see if you have the parasite. A blood sample can also be tested for evidence of infection. For accurate results, you must wait 6-8 weeks after your last exposure to contaminated water before the blood sample is taken.

What is the treatment for schistosomiasis?

Safe and effective drugs are available for the treatment of schistosomiasis. You will be given pills to take for 1-2 days.

Am I at risk?

If you live in or travel to areas where schistosomiasis occurs and your skin comes in contact with freshwater from canals, rivers, streams, ponds, or lakes, you are at risk of getting schistosomiasis.

In what areas of the world does schistosomiasis occur?

Africa: all freshwater in southern and sub-Saharan Africa–including the great lakes and rivers as well as smaller bodies of water–are at risk for schistosomiasis transmission. Transmission also occurs in the Mahgreb region of North Africa and the Nile River valley in Egypt and Sudan.

South America: Brazil, Suriname, Venezuela

Caribbean: Antigua, Dominican Republic, Guadeloupe, Martinique, Montserrat, Saint Lucia (risk is low)

The Middle East: Iran, Iraq, Saudi Arabia, Yemen

Southern China

Parts of Southeast Asia and the Philippines, Laos

How can I prevent schistosomiasis?

Avoid swimming or wading in freshwater when you are in countries in which schistosomiasis occurs. Swimming in the ocean and in chlorinated swimming pools is safe.

Drink safe water. Although schistosomiasis is not transmitted by swallowing contaminated water, if your mouth or lips come in contact with water containing the parasites, you could become infected. Because water coming directly from canals, lakes, rivers, streams, or springs may be contaminated with a variety of infectious organisms, you should either boil water for 1 minute or filter water before drinking it. Boiling water for at least 1 minute will kill any harmful parasites, bacteria, or viruses present. Iodine treatment alone WILL NOT GUARANTEE that water is safe and free of all parasites.

Bath water should be heated for 5 minutes at 150°F. Water held in a storage tank for at least 48 hours should be safe for showering.

Vigorous towel drying after an accidental, very brief water exposure may help to prevent the Schistosoma parasite from penetrating the skin. You should NOT rely on vigorous towel drying to prevent schistosomiasis.

EPIDEMIOLOGY & RISK FACTORS

Schistosomiasis is an important cause of disease in many parts of the world, most commonly in places with poor sanitation. School-age children who live in these areas are often most at risk because they tend to spend time swimming or bathing in water containing infectious cercariae. If you live in, or travel to, areas where schistosomiasis is found and are exposed to contaminated freshwater, you are at risk. Areas where human schistosomiasis is found include:

Schistosoma mansoni

distributed throughout Africa: There is risk of infection in freshwater in southern and sub-Saharan Africa–including the great lakes and rivers as well as smaller bodies of water. Transmission also occurs in the Nile River valley in Sudan and Egypt

South America: including Brazil, Suriname, Venezuela

Caribbean (risk is low): Antigua, Dominican Republic, Guadeloupe, Martinique, Montserrat, and Saint Lucia.

S. haematobium

distributed throughout Africa: There is risk of infection in freshwater in southern and sub-Saharan Africa–including the great lakes and rivers as well as smaller bodies of water. Transmission also occurs in the Nile River valley in Egypt and the Mahgreb region of North Africa.

found in areas of the Middle East

BIOLOGY

Causal Agent:

Schistosomiasis is caused by   digenetic blood trematodes. The three main species infecting humans are Schistosoma haematobium, S. japonicum, and S. mansoni. Two other species, more localized geographically, are S. mekongi and S. intercalatum. In addition, other species of schistosomes, which parasitize   birds and mammals, can cause cercarial dermatitis in humans.

Life Cycle:

Eggs are eliminated with feces or urine. Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts. The stages in the snail include 2 generations of sporocysts and the production of cercariae. Upon release from the snail, the infective cercariae swim, penetrate   the skin of the human host, and shed their forked tail, becoming schistosomulae. The schistosomulae migrate through several tissues and stages to   their residence in the veins. Adult worms in humans reside in the mesenteric venules in various   locations, which at times seem to be specific for each species. For instance, S. japonicum is more frequently found   in the superior mesenteric veins draining the small intestine, and S. mansoni occurs more often in the superior   mesenteric veins draining the large intestine. However, both species can occupy either location, and they   are capable of moving between sites, so it is not possible to state   unequivocally that one species only occurs in one location. S. haematobium most often occurs in the venous plexus of bladder, but it can also be found in the rectal venules. The females   (size 7 to 20 mm; males slightly smaller) deposit eggs in the small venules of   the portal and perivesical systems. The eggs are moved progressively toward   the lumen of the intestine (S. mansoni and S. japonicum) and of   the bladder and ureters (S. haematobium), and are eliminated with feces   or urine, respectively.  Pathology of S. mansoni and S. japonicum schistosomiasis includes: Katayama fever, hepatic perisinusoidal egg granulomas,   Symmers’ pipe stem periportal fibrosis, portal hypertension, and occasional   embolic egg granulomas in brain or spinal cord. Pathology of S. haematobium schistosomiasis includes: hematuria, scarring, calcification,   squamous cell carcinoma, and occasional embolic egg granulomas in brain or   spinal cord.

Human contact with water   is thus necessary for infection by schistosomes. Various animals, such as dogs,   cats, rodents, pigs, hourse and goats, serve as reservoirs for S. japonicum, and dogs for S. mekongi.

Life cycle image and information courtesy of DPDx.

DISEASE

Infection occurs when skin comes in contact with contaminated freshwater in which certain types of snails that carry the parasite are living. Freshwater becomes contaminated by Schistosoma eggs when infected people urinate or defecate in the water. The eggs hatch, and if the appropriate species of snails are present in the water, the parasites infect, develop and multiply inside the snails. The parasite leaves the snail and enters the water where it can survive for about 48 hours. Schistosoma parasites can penetrate the skin of persons who come in contact with contaminated freshwater, typically when wading, swimming, bathing, or washing. Over several weeks, the parasites migrate through host tissue and develop into adult worms inside the blood vessels of the body. Once mature, the worms mate and females produce eggs. Some of these eggs travel to the bladder or intestine and are passed into the urine or stool.

Symptoms of schistosomiasis are caused not by the worms themselves but by the body’s reaction to the eggs. Eggs shed by the adult worms that do not pass out of the body can become lodged in the intestine or bladder, causing inflammation or scarring. Children who are repeatedly infected can develop anemia, malnutrition, and learning difficulties. After years of infection, the parasite can also damage the liver, intestine, spleen, lungs, and bladder.

Common Symptoms

Most people have no symptoms when they are first infected. However, within days after becoming infected, they may develop a rash or itchy skin. Within 1-2 months of infection, symptoms may develop including fever, chills, cough, and muscle aches.

Chronic schistosomiasis

Without treatment, schistosomiasis can persist for years. Symptoms of chronic schistosomiasis include: abdominal pain, enlarged liver, blood in the stool or blood in the urine, problems passing urine, and increased risk of bladder cancer.

Rarely, eggs are found in the brain or spinal cord and can cause seizures, paralysis, or spinal cord inflammation.

DIAGNOSIS

Stool samples can be examined microscopically for parasite eggs (S. mansoni or S. japonicum) or urine (S. haematobium). The eggs tend to be passed intermittently and in small amounts and may not be detected, so it may be necessary to perform a blood (serologic) test.

PREVENTION AND CONTROL

No vaccine is available. The best way to prevent schistosomiasis is to take the following steps if you are visiting or live in an area where schistosomiasis is transmitted:

Avoid swimming or wading in freshwater when you are in countries in which schistosomiasis occurs. Swimming in the ocean and in chlorinated swimming pools is safe.

Drink safe water. Although schistosomiasis is not transmitted by swallowing contaminated water, if your mouth or lips come in contact with water containing the parasites, you could become infected. Because water coming directly from canals, lakes, rivers, streams, or springs may be contaminated with a variety of infectious organisms, you should either bring your water to a rolling boil for 1 minute or filter water before drinking it. Bring your water to a rolling boil for at least 1 minute will kill any harmful parasites, bacteria, or viruses present. Iodine treatment alone WILL NOT GUARANTEE that water is safe and free of all parasites.

Water used for bathing should be brought to a rolling boil for 1 minute to kill any cercariae, and then cooled before bathing to avoid scalding. Water held in a storage tank for at least 1 - 2 days should be safe for bathing.

Vigorous towel drying after an accidental, very brief water exposure may help to prevent the Schistosoma parasite from penetrating the skin. However, do not rely on vigorous towel drying alone to prevent schistosomiasis.

Those who have had contact with potentially contaminated water overseas should see their health care provider after returning from travel to discuss testing.

For more information view the source:Center for Disease Control

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SERRATIA MARCESCENS

Serratia marcescens is a species of Gram-negative, rod-shaped bacterium in the family Enterobacteriaceae. A human pathogen, S. marcescens is involved in nosocomial infections, particularly catheter-associated bacteremia, urinary tract infections and wound infections, and is responsible for 1.4% of nosocomial bacteremia cases in the United States. It is commonly found in the respiratory and urinary tracts of hospitalized adults and in the gastrointestinal system of children. Serratia may be correctly pronounced Ser-ra-shia (common) or Ser-rah-tee-a. Due to its ubiquitous presence in the environment, and its preference for damp conditions, S. marcescens is commonly found growing in bathrooms (especially on tile grout, shower corners, toilet water line, and basin), where it manifests as a pink discoloration and slimy film feeding off phosphorus-containing materials or fatty substances such as soap and shampoo residue. Once established, complete eradication of the organism is often difficult, but can be accomplished by application of a bleach-based disinfectant. Rinsing and drying surfaces after use can also prevent the establishment of the bacterium by removing its food source and making the environment less hospitable. S. marcescens may also be found in environments such as dirt, supposedly "sterile" places, and the subgingival biofilm of teeth. Due to this, and the fact that S. marcescens produces a reddish-orange tripyrrole pigment called prodigiosin, S. marcescens may cause extrinsic staining of the teeth. The biochemical pathway illustrating the production of prodigiosin by S. marcescens is unknown except for the final two steps. In these steps, a monopyrrole (MAD) and a bipyrrole (MBC) undergo a condensation reaction by way of a condensing enzyme to ultimately form prodigiosin.

IDENTIFICATION

S. marcescens is a motile organism and can grow in temperatures ranging from 5–40°C and in pH levels ranging from 5 to 9. It is differentiated from other Gram-negative bacteria by its ability to perform casein hydrolysis, which allows it to produce extracellular metalloproteinases which are believed to function in cell-to-extracellular matrix interactions. S. marcescens also exhibits tryptophan and citrate degradation. One of the end products of tryptophan degradation is pyruvic acid, which is then incorporated into different metabolic processes of S. marcescens. A final product of citrate degradation is carbon. Thus, S. marcescens can rely on citrate as a carbon source. In identifying the organism, one may also perform a methyl red test, which determines if a microorganism performs mixed-acid fermentation. S. marcescens results in a negative test. Another determination of S. marcescens is its capability to produce lactic acid via oxidative and fermentative metabolism. Therefore, it is said that S. marcescens is lactic acid O/F .

PATHOGENESIS

S. marcescens can cause infection in several sites, including the urinary tract, respiratory tract, wounds, and the eye, where it may cause conjunctivitis, keratitis, endophthalmitis, and tear duct infections. It is also a rare cause of endocarditis and osteomyelitis (particularly in people who use intravenous drugs recreationally), pneumonia, and meningitis. Most S. marcescens strains are resistant to several antibiotics because of the presence of R-factors, which are a type of plasmid that carry one or more genes that encode resistance; all are considered intrinsically resistant to ampicillin, macrolides, and first-generation cephalosporins (such as cephalexin). In elkhorn coral, S. marcescens is the cause of the disease known as white pox disease. In silkworms, it sometimes occurs as a secondary pathogen in viral flacherie disease. Also in Drosophila research laboratories, infection with S. marcescens is common. It manifests itself as a pink discolouration or plaque in or on larvae, pupae, or the usually starch and sugar-based food (especially when improperly prepared).

HISTORY

Serratia marcescens was discovered in 1819 by Venetian pharmacist Bartolomeo Bizio, as the cause of an episode of blood-red discoloration of polenta in the city of Padua. Bizio named the organism four years later in honor of Serafino Serrati, a physicist who developed an early steamboat; the epithet marcescens (Latin for "decaying") was chosen because of the pigment's rapid deterioration (Bizio's observations led him to believe that the organism decayed into a mucilage-like substance upon reaching maturity). Serratia was later renamed Monas prodigiosus and Bacillus prodigiosus before Bizio's original name was restored in the 1920s. Until the 1950s, S. marcescens was erroneously believed to be a nonpathogenic "saprophyte", and its reddish coloration was used in school experiments to track infections. It has also been used as a simulant in biological warfare tests by the United States Military. On September 26 and 27, 1950, the United States Navy conducted a secret experiment named "Operation Sea-Spray" in which some S. marcescens was released by bursting balloons of it over urban areas of the San Francisco Bay Area in California. Although the Navy later claimed the bacteria were harmless[citation needed], beginning on September 29, 11 patients at a local hospital developed very rare, serious urinary tract infections, and one of these individuals, Edward J. Nevin, died. Cases of pneumonia in San Francisco also increased after S. marcescens was released. The bacterium was also combined with phenol and an anthrax simulant and sprayed across south Dorset by US and UK military scientists as part of the DICE trials which ran from 1971 to 1975. Since 1950, S. marcescens has steadily increased as a cause of human infection, with many strains resistant to multiple antibiotics. The first indications of problems with the influenza vaccine produced by Chiron Corporation in 2004 involved S. marcescens contamination. Because of its red pigmentation, caused by expression of the pigment prodigiosin, and its ability to grow on bread, S. marcescens has been evoked as a naturalistic explanation of medieval accounts of the "miraculous" appearance of blood on the Eucharist that led to Pope Urban IV instituting the Feast of Corpus Christi in 1264. This followed celebration of a mass at Bolsena in 1263, led by a Bohemian priest who had doubts concerning transubstantiation, or the turning of bread and wine into the Body and Blood of Christ during the Mass. During the Mass, the Eucharist appeared to bleed and each time the priest wiped away the blood, more would appear. While Serratia possibly could generate a single appearance of red pigment, it is unclear how it could have generated more pigment after each wiping, leaving this proposed explanation open to doubt. This event is celebrated in a fresco in the Apostolic Palace in the Vatican City, painted by Raphael. In early 2008, the U.S. Food and Drug Administration (FDA) issued a nationwide recall of one lot of Pre-Filled Heparin Lock Flush Solution USP. The heparin IV flush syringes had been found to be contaminated with Serratia marcescens, which resulted in patient infections. The Centers for Disease Control (CDC) confirmed growth of S. marcescens from several unopened syringes of this product. Serratia marcescens has also been linked to 19 cases in Alabama hospitals in 2011, including ten deaths. All of the patients involved were receiving total parenteral nutrition at the time, and this is being investigated as a possible source of the outbreak.

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SHIGELLA

Shigella is a genus of Gram-negative, nonspore forming, non-motile, rod-shaped bacteria closely related to Escherichia coli and Salmonella. The causative agent of human shigellosis, Shigella causes disease in primates, but not in other mammals. It is only naturally found in humans and apes. During infection, it typically causes dysentery. The genus is named after Kiyoshi Shiga, who first discovered it in 1898. Phylogenetic studies indicate that Shigella is more appropriately treated as subgenus of Escherichia, and that certain strains generally considered E. coli – such as E. coli O157:H7 – are better placed in Shigella (see Escherichia coli#Diversity for details). After invasion, Shigella multiply intracellularly and spread to neighboring epithelial cells, resulting in tissue destruction and characteristic pathology of shigellosis.

CLASSIFICATION

Shigella species are classified by four serogroups:
Serogroup A: S. dysenteriae (12 serotypes)
Serogroup B: S. flexneri (6 serotypes)
Serogroup C: S. boydii (18 serotypes)
Serogroup D: S. sonnei (1 serotype)

Groups A–C are physiologically similar; S. sonnei (group D) can be differentiated on the basis of biochemical metabolism assays.Three Shigella groups are the major disease-causing species: S. flexneri is the most frequently isolated species worldwide, and accounts for 60% of cases in the developing world; S. sonnei causes 77% of cases in the developed world, compared to only 15% of cases in the developing world; and S. dysenteriae is usually the cause of epidemics of dysentery, particularly in confined populations such as refugee camps.

PATHOGENISIS

Shigella infection is typically via ingestion (fecal–oral contamination); depending on age and condition of the host, less than 100 bacterial cells can be enough to cause an infection. Shigella causes dysentery that results in the destruction of the epithelial cells of the intestinal mucosa in the cecum and rectum. Some strains produce enterotoxin and shiga toxin, similar to the verotoxin of E. coli O157:H7 and other verotoxin-producing Escherichia coli. Both shiga toxin and verotoxin are associated with causing hemolytic uremic syndrome. As noted above, these supposed E. coli strains are at least in part actually more closely related to Shigella than to the "typical" E. coli. Shigella invade the host through the M-cells in the gut epithelia of the small intestine, as they cannot enter directly through the epithelial cells. Using a Type III secretion system acting as a biological syringe, the bacterium injects IpaD protein into cells, triggering bacterial invasion and the subsequent lysis of vacuolar membranes using IpaB and IpaC proteins. It uses a mechanism for its motility by which its IcsA protein triggers actin polymerization in the host cell (via N-WASP recruitment of Arp2/3 complexes) in a "rocket" propulsion fashion for cell-to-cell spread. The most common symptoms are diarrhea, fever, nausea, vomiting, stomach cramps and flatulence. The stool may contain blood, mucus, or pus. In rare cases, young children may have seizures. Symptoms can take as long as a week to show up, but most often begin two to four days after ingestion. Symptoms usually last for several days, but can last for weeks. Shigella is implicated as one of the pathogenic causes of reactive arthritis worldwide. Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella chromosomes share most of their genes with those of E. coli K12 strain MG1655.

DIAGNOSIS

Shigella species are negative for motility and are not lactose fermenters. (However, S. sonnei can ferment lactose). They typically do not produce gas from carbohydrates (with the exception of certain strains of S. flexneri) and tend to be overall biochemically inert. Shigella should also be urea hydrolysis negative . When inoculated to a triple sugar iron (TSI) slant, they react as follows: K/A, gas -, H2S -. Indole reactions are mixed, positive and negative, with the exception of S. sonnei, which is always indole negative. Growth on Hektoen enteric agar will produce bluish-green colonies for Shigella and bluish-green colonies with black centers for Salmonella.

PREVENTION & TREATMENT

Hand washing before handling food and thoroughly cooking all food before eating decreases the risk of getting Shigella. Severe dysentery can be treated with ampicillin, TMP-SMX, or fluoroquinolones, such as ciprofloxacin, and of course rehydration. Medical treatment should only be used in severe cases. Antibiotics are usually avoided in mild cases because some Shigella are resistant to antibiotics, and their use may make the germ even more resistant. Antidiarrheal agents may worsen the sickness, and should be avoided. For Shigella-associated diarrhea, antibiotics shorten the length of infection. Shigella is one of the leading bacterial causes of diarrhea worldwide. Insufficient data exist, but conservative estimates suggest that Shigella causes approximately 90 million cases of severe dysentery with at least 100,000 of these resulting in death each year, mostly among children in the developing world. Currently, no licenced vaccine targeting Shigella exists. Shigella has been a longstanding World Health Organization target for vaccine development, and sharp declines in age-specific diarrhea/dysentery attack rates for this pathogen indicate that natural immunity does develop following exposure; thus, vaccination to prevent the disease should be feasible. Several vaccine candidates for Shigella are in various stages of development.

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SHORT BOWEL SYNDROME

Short bowel syndrome (SBS, also short gut syndrome or simply short gut) is a malabsorption disorder caused by the surgical removal of the small intestine, or rarely due to the complete dysfunction of a large segment of bowel. Most cases are acquired, although some children are born with a congenital short bowel. It usually does not develop unless more than two thirds of the small intestine have been removed.

SIGNS AND SYMPYOMS

The symptoms of short bowel syndrome can include:

Abdominal pain

Diarrhea and steatorrhea (oily or sticky stool, which can be malodorous)

Fluid depletion

Weight loss and malnutrition

Fatigue

Patients with short bowel syndrome may have complications caused by malabsorption of vitamins and minerals, such as deficiencies in vitamins A, D, E, K, and B12, calcium, magnesium, iron, folic acid, and zinc. These may appear as anemia, hyperkeratosis (scaling of the skin), easy bruising, muscle spasms, poor blood clotting, and bone pain.

CAUSES

Short bowel syndrome in adults is usually caused by surgery for:

Crohn's disease, an inflammatory disorder of the digestive tract

Volvulus, a spontaneous twisting of the small intestine that cuts off the blood supply and leads to tissue death

Tumors of the small intestine

Injury or trauma to the small intestine

Necrotizing enterocolitis (premature newborn)

Bypass surgery to treat obesity

Surgery to remove diseases or damaged portion of the small intestine

PATHOPHYSIOLOGY

In healthy adults, the small intestine has an average length of approximately 6 meters (19.7 feet). Short bowel syndrome usually develops when there is less than 2 meters (6.6 feet) of the small intestine left to absorb sufficient nutrients. Short bowel syndrome caused by the surgical removal of a portion of the bowel may be a temporary condition, due to the adaptive property of the small intestine. In a process called intestinal adaptation, physiological changes to the remaining portion of the small intestine occur to increase its absorptive capacity.

These changes include:
In healthy adults, the small intestine has an average length of approximately 6 meters (19.7 feet). Short bowel syndrome usually develops when there is less than 2 meters (6.6 feet) of the small intestine left to absorb sufficient nutrients. Short bowel syndrome caused by the surgical removal of a portion of the bowel may be a temporary condition, due to the adaptive property of the small intestine. In a process called intestinal adaptation, physiological changes to the remaining portion of the small intestine occur to increase its absorptive capacity.

These changes include:

Enlargement and lengthening of the villi found in the lining

Increase in the diameter of the small intestine

Slow down in peristalsis or movement of food through the small intestine

Enlargement and lengthening of the villi found in the lining

Increase in the diameter of the small intestine

Slow down in peristalsis or movement of food through the small intestine

TREATMENT

Symptoms of short bowel syndrome are usually addressed by prescription medicine.

These include:

Anti-diarrheal medicine (e.g. loperamide, codeine)

Vitamin, mineral supplements and L-Glutamine powder mixed with water

H2 blocker and proton pump inhibitors to reduce stomach acid

Lactase supplement (to improve the bloating and diarrhoea associated with lactose intolerance)

Surgery, including intestinal lengthening, tapering, and small bowel transplant.

Parenteral nutrition (PN or TPN for total parenteral nutrition - nutrition administered via intravenous line).

Nutrition administered via gastrostomy tube

In 2004, the FDA approved a therapy that reduces the frequency and volume of TPN, comprising: NutreStoreTM [L-glutamine for oral solution] and Zorbtive [somatropin (rDNA origin) for injection] together with a specialized oral diet. Byrne, TA, Wilmore DW, Iyer K, et al. Growth hormone, glutamine, and an optimal diet reduces parenteral nutrition in patients with short bowel syndrome. Ann Surg. 2005;242;655-661 Surgical procedures to lengthen dilated bowel include the Bianchi procedure (where the bowel is cut in half and one end is sewn to the other) and a newer procedure called serial transverse enteroplasty (STEP—where the bowel is cut and stapled in a zigzag pattern). Heung Bae Kim, MD, and Tom Jaksic, MD, both of Children's Hospital Boston, devised the STEP procedure in the early 2000s. The procedure lengthens the bowel of children with SBS and may allow children to avoid the need for intestinal transplantation. As of June 2009, Kim and Jaksic have performed 18 STEP procedures. The Bianchi and STEP procedures are usually performed by pediatric surgeons at quaternary hospitals who specialize in small bowel surgery.

PROGNOSIS

There is no cure for short bowel syndrome. In newborn infants, the 4-year survival rate on parenteral nutrition is approximately 70%. In newborn infants with less than 10% of expected intestinal length, 5 year survival is approximately 20%. Some studies suggest that much of the mortality is due to a complication of the TPN, especially chronic liver disease. Much hope is vested in Omegaven, a type of lipid TPN feed, in which recent case reports suggest the risk of liver disease is much lower. Although promising, small intestine transplant has a mixed success rate, with postoperative mortality rate of up to 30%. One-year and 4-year survival rate are 90% and 60%, respectively.

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SKIN RASH

A rash is a change of the skin which affects its color, appearance or texture. A rash may be localized in one part of the body, or affect all the skin. Rashes may cause the skin to change color, itch, become warm, bumpy, chapped, dry, cracked or blistered, swell and may be painful. The causes, and therefore treatments for rashes, vary widely. Diagnosis must take into account such things as the appearance of the rash, other symptoms, what the patient may have been exposed to, occupation, and occurrence in family members. The diagnosis may confirm any number of conditions. The presence of a rash may aid associated signs and symptoms are diagnostic of certain diseases. For example, the rash in measles is an erythematous, morbilliform, maculopapular rash that begins a few days after the fever starts. It classically starts at the head and spreads downwards.

DIFFERENTIAL DIAGNOSIS

Common causes of rashes include: Food Allergy Anxiety. Allergies, for example to food, dyes, medicines, insect stings, metals such as zinc or nickel; such rashes are often called hives. Skin contact with an irritant. Fungal infection, such as ringworm. Reaction to vaccination. Skin diseases such as eczema or acne. Exposure to sun (sunburn) or heat. Friction due to chafing of the skin. Irritation such as caused by abrasives impregnated in clothing rubbing the skin. The cloth itself may be abrasive enough for some people. Menstruation. Secondary syphilis.
Uncommon causes: Autoimmune disorders such as psoriasis Lead poisoning Pregnancy Repeated scratching on a particular spot Lyme Disease Scarlet fever

DIAGNOSTIC APPROACH

The causes of a rash are extremely broad, which may make the evaluation of a rash extremely difficult. An accurate evaluation by a provider may only be made in the context of a thorough history (What medication is the patient taking? What is the patient's occupation? Where has the patient been?) and complete physical examination. Points to note in the examination include: The appearance: e.g., purpuric (typical of vasculitis and meningococcal disease), fine and like sandpaper (typical of scarlet fever); circular lesions with a central depression are typical of molluscum contagiosum (and in the past, small pox); plaques with silver scales are typical of psoriasis. The distribution: e.g., the rash of scarlet fever becomes confluent and forms bright red lines in the skin creases of the neck, armpits and groins (Pastia's lines); the vesicles of chicken pox seem to follow the hollows of the body (they are more prominent along the depression of the spine on the back and in the hollows of both shoulder blades); very few rashes affect the palms of the hands and soles of the feet (secondary syphilis, rickettsia or spotted fevers, guttate psoriasis, hand, foot and mouth disease, keratoderma blenorrhagica); Symmetry: e.g., herpes zoster usually only affects one side of the body and does not cross the midline.

OVERVIEW OF SYMPTOMS

Skin disease Symptoms Usual area of body

Acne Vulgaris Comedones, papules, pustules and nodules. Face, chest and back.

Acne Rosacea Flushed appearance or redness. Cheeks, chin, forehead or nose.

Boil Painful red bump or a cluster of painful red bumps Anywhere

Cellulitis Red, tender and swollen areas of skin Around a cut, scrape or skin breach

Insect bite Red and/or itchy bumps on the skin Anywhere and can be sprinked randomly

Allergic reaction Irregular, raised or flat red sores that appeared after taking medicine/drugs or eating certain foods Anywhere

Hives Bumps formed suddenly Anywhere but usually first noticed on face

Seborrheic dermatitis Bumps and swelling Near glands

Cradle Cap Dry, scaly skin Scalp of recently born babies

Irritant contact dermatitis Red, itchy, scaly or oily rash Eyebrows, nose, edge of the scalp, point of contact with jewellery, perfume or clothing.

Allergic Contact Dermatitis caused by poison ivy, poisen oak or sumac Red, itchy, scaly or oily rash; can also be weeping or leathery. Anywhere that came in contact with the irritant either directly or via transfer (e.g. from contaminated clothing.)

Allergic purpura Small red dots on the skin, or larger, bruise-like spots that appeared after taking medicine Anywhere

Pityriasis Rosea Started with a single scaly, red and slightly itchy spot, and within a few days, did large numbers of smaller patches of the rash, some red and/or others tan Chest and abdomen

Dermatitis herpetiformis Intensely itchy rash with red bumps and blisters Elbows, knees, back or buttocks

Erythema nodosum Large red bumps that seem to bruise and are tender to touch Anywhere

Psoriasis White, scaly rash over red, flaky, irritated skin Elbows and knees

Erythema multiforme Red, blotchy rash, with "target like" hives or sores. Anywhere

Measles Red rash that is raised with a fever or sore throat. Usually starts first on the forehead and face and spreads downward.

Chickenpox Multiple blisters with a fever, cough, aches, tiredness and sore throat. Usually starts first on the face, chest and back and spreads downward.

Shingles Red blisters that are very painful and may crust Anywhere

Fifth Disease Started as a fever and then developed a bright red rash Cheeks

Warts Soft bumps forming that don't itch and have no other symptoms Anywhere

Ringworm Bald spot on the scalp or a ring of itchy red skin Anywhere

Syphilis Rash that is red but not itchy Palms of hands or soles of feet

Jock itch, yeast infection or diaper rash Red itchy rash Groin

Tinea versicolor Light coloured patches Anywhere

Impetigo Crusted, tan-colored sores Near nose or lip

Scabies Bite-like sores that itch and spread intensely Usually start on hands or feet and spread everywhere

Rocky Mountain spotted fever A fine rash with a fever and headache Usually start on arms and legs including the hands and feet

Lupus erythematosus A butterfly rash with achy joints Forehead and cheeks

Jaundice or sign of hepatitis Yellowish Skin, whites of eyes and mouth

Bruise Blue or black area after being hit Anywhere

Actinic keratoses Scaly, pink, gray or tan patches or bumps Face, scalp or on the backs or the hands

Keloid or hypertrophic scar Scar that has grown larger than expected Anywhere

Lipoma Soft or rubbery growth Anywhere

Milia Lots of white spots On the face of a baby

Molluscum or contagiosum Small, firm, round bumps with pits in the center that may sit on tiny stalks Anywhere

Scarlet Fever Becomes confluent and forms bright red lines in the skin creases of the neck, armpits and groins (Pastia's lines) Face, chest & back, whole body, armpits, inside elbows, groins

Sebaceous cyst Bump with a white dome under the skin Scalp, nape of the neck or upper back

Skin tag Soft, fleshy growth, lump or bump Face, neck, armpits or groin

Xanthelasma Yellow area under the skin Under eyelids

Melanoma Dark bump that may have started within a mole or blemish, or, a spot or mole that has changed in color, size, shape or is painful or itchy Anywhere

Basal cell carcinoma Fleshy, growing mass Areas exposed to the sun

Squamous cell carcinoma Unusual growth that is red, scaly or crusted Face, lip or chin

Kaposi's sarcoma Dark or black raised spots on the skin that keep growing or have appeared recently Anywhere

Erythema annulare centrifugum (EAC) Pink-red ring or bullseye marks Anywhere

TREATMENT

Treatment differs according to what rash a patient has been diagnosed with. Common rashes can be easily remedied using steroid topical creams (such as hydrocortisone) or non-steroidal treatments. Many of the medications are available over the counter in the United States.

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STAPHYLOCOCCAL INFECTION

Staphylococcus is a Gram-positive bacteria which includes several species that can cause a wide variety of infections in humans and other animals through infection or the production of toxins. Staphylococcal toxins are a common cause of food poisoning, as they can be produced in improperly-stored food.

COAGULASE POSITIVE

The main coagulase-positive staphylococcus is Staphylococcus aureus. Although not all strains of Staphylococcus aureus are coagulase positive. These bacteria can survive on dry surfaces, increasing the chance of transmission. S. aureus is also implicated in toxic shock syndrome; during the 1980s some tampons allowed the rapid growth of S. aureus, which released toxins that were absorbed into the bloodstream. Any S. aureus infection can cause the staphylococcal scalded skin syndrome, a cutaneous reaction to exotoxin absorbed into the bloodstream. It can also cause a type of septicaemia called pyaemia. The infection can be life-threatening. Problematically, Methicillin-resistant Staphylococcus aureus (MRSA) has become a major cause of hospital-acquired infections, and is being recognized with increasing frequency in community-acquired infections.

ETYMOLOGY

The generic name Staphylococcus is derived from the Greek word "staphyle" meaning a bunch of grapes, and "kokkos" means granule. The bacteria, when seen under a microscope appear like a branch of grapes or berries.

COAGULASE NEGATIVE

S. epidermidis, a coagulase-negative staphylococcus species, is a commensal of the skin, but can cause severe infections in immune-suppressed patients and those with central venous catheters.
S. saprophyticus, another coagulase-negative species that is part of the normal vaginal flora, is predominantly implicated in genitourinary tract infections in sexually-active young women.
In recent years, several other staphylococcal species have been implicated in human infections, notably S. lugdunensis, S. schleiferi, and S. caprae.

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STAPHYLOCOCCUS

Staphylococcus is a genus of Gram-positive bacteria. Under the microscope, they appear round (cocci), and form in grape-like clusters. The Staphylococcus genus includes at least 40 species. Of these, nine have two subspecies and one has three subspecies. Most are harmless and reside normally on the skin and mucous membranes of humans and other organisms. Found worldwide, they are a small component of soil microbial flora.

TAXONOMY

The taxonomy is based on 16s rRNA sequences,and most of the staphylococcal species fall into 11 clusters:
S. aureus group – S. aureus, S. simiae
S. auricularis group – S. auricularis
S. carnosus group – S. carnosus, S. condimenti, S. massiliensis, S. piscifermentans, S. simulans
S. epidermidis group – S. capitis, S. caprae, S. epidermidis, S. saccharolyticus
S. haemolyticus group – S. devriesei, S. haemolyticus, S. hominis
S. hyicus-intermedius group – S. chromogenes, S. felis, S. delphini, S. hyicus, S.
intermedius, S. lutrae, S. microti, S. muscae, S. pseudintermedius, S. rostri, S. schleiferi
S. lugdunensis group – S. lugdunensis
S. saprophyticus group – S. arlettae, S. cohnii, S. equorum, S. gallinarum, S. kloosii, S. leei, S. nepalensis, S. saprophyticus, S. succinus, S. xylosus
S. sciuri group – S. fleurettii, S. lentus, S. sciuri, S. stepanovicii, S. vitulinus
S. simulans group – S. simulans S. warneri group – S. pasteuri, S. warneri
A twelfth group – that of S. caseolyticus – has now been moved to a new genus Macrococcus, the species of which are currently the closest known relatives of the Staphylococci.

SUBSPECIES

S. aureus subsp. aureus
S. aureus subsp. anaerobius
S. capitis subsp. capitis
S. capitis subsp. urealyticus
S. carnosus subsp. carnosus
S. carnosus subsp. utilis
S. cohnii subsp. cohnii
S. cohnii subsp. urealyticus
S. equorum subsp. equorum
S. equorum subsp. linens
S. hominis subsp. hominis
S. hominis subsp. novobiosepticus
S. saprophyticus subsp. bovis
S. saprophyticus subsp. saprophyticus
S. schleiferi subsp. coagulans
S. schleiferi subsp. schleiferi
S. sciuri subsp. carnaticus
S. sciuri subsp. rodentium
S. sciuri subsp. sciuri
S. succinus subsp. casei
S. succinus subsp. succinus

NOTES

As with all generic names in binomial nomenclature, Staphylococcus is capitalized when used alone or with a specific species. Also, the abbreviations Staph and S. when used with a species (S. aureus) are correctly italicized and capitalized (though often errors in this are seen in popular literature). However, Staphylococcus is not capitalized or italicized when used in adjectival forms, as in a staphylococcal infection, or as the plural (staphylococci). The S. saprophyticus and S. sciuri groups are generally novobiocin-resistant, as is S. hominis subsp. novobiosepticus. Members of the S. sciuri group are oxidase-positive due to their possession of the enzyme cytochrome c oxidase. This group is the only clade within the Staphylococci to possess this gene. The S. sciuri group appears to be the closest relations to the genus Macrococcus. Staphylococcus pulvereri has been shown to be a junior synonym of Staphylococcus vitulinus. Within these clades, the S. haemolyticus and S. simulans groups appear to be related, as do the S. aureus and S. epidermidis groups. S. lugdunensis appears to be related to the S. haemolyticus group. S. croceolyticus may be related to S. haemolyticus, but this needs to be confirmed. The taxonomic position of S. croceolyticus, S. leei, S. lyticans and S. pseudolugdunensis has yet to be clarified. The published descriptions of these species do not appear to have been validly published to date (2010).

BIOCHEMICAL IDENTIFICATION

Assignment of a strain to the genus Staphylococcus requires it to be a Gram-positive coccus that forms clusters, produces catalase, has an appropriate cell wall structure (including peptidoglycan type and teichoic acid presence) and G C content of DNA in a range of 30–40 mol%. Staphylococcus species can be differentiated from other aerobic and facultative anaerobic, Gram-positive cocci by several simple tests. Staphylococcus spp. are facultative anaerobes (capable of growth both aerobically and anaerobically). All species grow in the presence of bile salts. It was believed that all species were catalase-positive however it is now known that not all Staphylococcus are coagulase positive. Growth can also occur in a 6.5% NaCl solution. On Baird Parker medium, Staphylococcus spp. grow fermentatively, except for S. saprophyticus, which grows oxidatively. Staphylococcus spp. are resistant to bacitracin (0.04 U disc: resistance =

COAGULASE PRODUCTION

One of the most important phenotypical features used in the classification of staphylococci is their ability to produce coagulase, an enzyme that causes blood clot formation. Six species are currently recognised as being coagulase-positive: S. aureus, S. delphini, S. hyicus, S. intermedius, S. lutrae,S. pseudintermedius and S. schleiferi subsp. coagulans. These species belong to two separate groups – the S. aureus (S. aureus alone) group and the S. hyicus-intermedius group (the remaining five). S. aureus can also be found as being coagulase-negative. A seventh species has also been described – Staphylococcus leei – from patients with gastritis. S. aureus is coagulase-positive, meaning it produces coagulase. However, while the majority of S. aureus strains are coagulase-positive, some may be atypical in that they do not produce coagulase. S. aureus is catalase-positive (meaning that it can produce the enzyme catalase) and able to convert hydrogen peroxide (H2O2) to water and oxygen, which makes the catalase test useful to distinguish staphylococci from enterococci and streptococci. S. pseudintermedius inhabits and sometimes infects the skin of domestic dogs and cats. This organism, too, can carry the genetic material that imparts multiple bacterial resistance. It is rarely implicated in infections in humans, as a zoonosis. S. epidermidis, a coagulase-negative species, is a commensal of the skin, but can cause severe infections in immune-suppressed patients and those with central venous catheters. S. saprophyticus, another coagulase-negative species that is part of the normal vaginal flora, is predominantly implicated in genitourinary tract infections in sexually-active young women. In recent years, several other Staphylococcus species have been implicated in human infections, notably S. lugdunensis, S. schleiferi, and S. caprae. Common abbreviations for coagulase-negative staphylococcus species are CoNS and CNS.

GENOMICS AND MOLECULAR BIOLOGY

The first S. aureus genomes to be sequenced were those of N315 and Mu50 in 2001. Many more complete S. aureus genomes have been submitted to the public databases, making it one of the most extensively sequenced bacteria. The use of genomic data is now widespread and provides a valuable resource for researchers working with S. aureus. Whole genome technologies, such as sequencing projects and microarrays, have shown an enormous variety of S. aureus strains. Each contains different combinations of surface proteins and different toxins. Relating this information to pathogenic behaviour is one of the major areas of staphylococcal research. The development of molecular typing methods has enabled the tracking of different strains of S. aureus. This may lead to better control of outbreak strains. A greater understanding of how the staphylococci evolve, especially due to the acquisition of mobile genetic elements encoding resistance and virulence genes is helping to identify new outbreak strains and may even prevent their emergence. The widespread incidence of antibiotic resistance across various strains of S. aureus, or across different species of Staphylococcus has been attributed to horizontal gene transfer of genes encoding antibiotic/metal resistance and virulence. A recent study demonstrated the extent of horizontal gene transfer among Staphylococcus to be much greater than previously expected, and encompasses genes with functions beyond antibiotic resistance and virulence, and beyond genes residing within the mobile genetic elements. Various strains of Staphylococcus are available from biological research centres, such as the National Collection of Type Cultures (NCTC).

CLINICAL

Staphylococcus can cause a wide variety of diseases in humans and other animals through either toxin production or penetration. Staphylococcal toxins are a common cause of food poisoning, as they can be produced by bacteria growing in improperly-stored food items. The most common sialadenitis is caused by staphylococci, as bacterial infections.

For more information view the source:Wikipedia

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STRONGYLOIDES STERCORALIS

Strongyloidiasis was first described in French troops stationed in modern day Vietnam during the late 19th century who were suffering from severe, persistent diarrhea. It is a parasitic disease caused by nematodes, or roundworms, in the genus Strongyloides that enter the body through exposed skin, such as bare feet. Strongyloides is most common in tropical or subtropical climates.

Most people who are infected with Strongyloides do not know they are infected and have no symptoms. Others may develop a severe form and, if untreated, become critically ill and potentially die.

FAQS

What is strongyloidiasis?

Strongyloidiasis is a disease caused by a nematode, or a roundworm, in the genus Strongyloides. Though there are over 40 species within this genus that can infect birds, reptiles, amphibians, livestock and other primates, Strongyloides stercoralis is the primary species that accounts for human disease. The larvae are small; the longest reach about 1.5mm in length -- the size of a mustard seed or a large grain of sand.

How do people get infected with strongyloides?

Strongyloides is classified as a soil-transmitted helminth. This means that the primary mode of infection is through contact with soil that is contaminated with free-living larvae. When the larvae come in contact with skin, they are able to penetrate it and migrate through the body, eventually finding their way to the small intestine where they burrow and lay their eggs. Unlike other soil-transmitted helminths such as hookworm and whipworm whose eggs do not hatch until they are in the environment, the eggs of Strongyloides hatch into larvae in the intestine. Most of these larvae will be excreted in the stool, but some of the larvae may molt and immediately re-infect the host either by burrowing into the intestinal wall, or by penetrating the perianal skin. This characteristic of Strongyloides is termed auto-infection. The significance of auto-infection is that unless treated for Strongyloides, persons may remain infected throughout their lifetime. In addition to contact with soil and auto-infection, there have been rare cases of person-to-person transmission in:

organ transplantation

institutions for the developmentally disabled

daycare centers.

Where do most cases of strongyloidiasis occur in the United States?

In the United States, Strongyloides has classically been associated with uniformed-service veterans who returned from tropical regions such as Southeast Asia and the South Pacific during World War II. Small domestic studies have shown locations of infection in rural Appalachia. The highest rates in the United States have been documented in immigrant populations.

Strongyloides is more commonly found in areas that are relatively warm and moist, in rural areas, and areas associated with agricultural activity, but it can occur anywhere. It is found more frequently in socio-economically disadvantaged persons and in institutionalized populations.

What are the signs and symptoms of strongyloidiasis?

The majority of people infected with Strongyloidesare without symptoms. Those who do develop symptoms tend to have non-specific, or generalized complaints. Some people develop abdominal pain, bloating, heartburn, intermittent episodes of diarrhea and constipation, a dry cough, and rashes. Rarely people will develop arthritis, kidney problems, and heart conditions. Strongyloidiasis can be severe and life-threatening in persons who:

are on oral or intravenous steroids -- such as those with asthma or chronic obstructive pulmonary disease (COPD) exacerbations, lupus, gout, or in persons using steroids for immunosuppression or symptomatic relief

are infected with the virus HTLV-1

have hematologic malignancies such as leukemia or lymphoma

are transplant recipients.

How soon after the exposure do symptoms develop?

Most people do not know when their exposure occurred. For those who do, a local rash can occur immediately. The cough usually occurs several days later. Abdominal symptoms typically occur approximately 2 weeks later, and larvae can be found in the stool about 3 to 4 weeks later.

What should I do if I think I might have strongyloidiasis?

See your health care provider.

How is infection with Strongyloides diagnosed?

Strongyloides is classically diagnosed by visualization of larvae on microscopic stool examination. This may require that you provide multiple stool samples to your doctor or the laboratory. Some laboratories are capable of diagnosing Strongyloides with blood tests.

How is strongyloidiasis treated?

Safe and effective drugs are available to treat infection with Strongyloides.

How can strongyloidiasis be prevented?

The best way to prevent Strongyloides infection is to wear shoes when you are walking on soil, and to avoid contact with fecal matter or sewage. Proper sewage disposal and fecal management are keys to prevention.

EPIDEMIOLOGY & RISK FACTORS

Strongyloides is known to exist on all continents except for Antarctica, but it is most common in the tropics, subtropics, and in warm temperate regions. The global prevalence of Strongyloides is unknown, but experts estimate that there are between 3 – 100 million infected persons worldwide.

In the United States, a series of small studies in select populations have shown that between 0-6.1% of persons sampled were infected. Studies in immigrant populations have shown a much higher percentage of infected persons ranging from 0-46.1%.

Strongyloides is found more frequently in the socioeconomically disadvantaged, in institutionalized populations, and in rural areas. It is often associated with agricultural activities.

The most common way of becoming infected with Strongyloides is by contacting soil that is contaminated with Strongyloides larvae. Therefore, activities that increase contact with the soil increase the risk of becoming infected, such as:

walking with bare feet

contact with human waste or sewage

occupations that increase contact with contaminated soil such as farming and coal mining.

Furthermore, many studies have shown an association with Strongyloides and infection with Human T-Cell Lymphotropic Virus-1 (HTLV-1). These studies have shown that people infected with HTLV-1 are more likely to become infected with Strongyloides, and that once infected, are more likely to develop severe cases of strongyloidiasis.

Of note, being infected with HIV/AIDS has not been shown to be a risk factor for developing Strongyloides or having a worse clinical course.

BIOLOGY

Causal Agent:

The nematode (roundworm) Strongyloides stercoralis. Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.

Life Cycle:

The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist:

Free-living cycle: The rhabditiform larvae passed in the stool can either molt twice and become infective filariform larvae (direct development) or molt four times and become free living adult males and females that mate and produce eggs from which rhabditiform larvae hatch. The latter in turn can either develop into a new generation of free-living adults or into infective filariform larvae. The filariform larvae penetrate the human host skin to initiate the parasitic cycle.

Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin, and are transported to the lungs where they penetrate the alveolar spaces; they are carried through the bronchial tree to the pharynx, are swallowed and then reach the small intestine. In the small intestine they molt twice and become adult female worms. The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs, which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool. In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may follow the previously described route, being carried successively to the lungs, the bronchial tree, the pharynx, and the small intestine where they mature into adults; or they may disseminate widely in the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals.

Life cycle image and information courtesy of DPDx.

DISEASE

Most people infected with Strongyloidesdo not know they’re infected. If they do feel sick the most common complaints are the following. Abdominal:

stomachache, bloating, and heartburn

intermittent episodes of diarrhea and constipation

nausea and loss of appetite

Respiratory:

dry cough

throat irritation

Skin:

an itchy, red rash that occurs where the worm entered the skin

recurrent raised red rash typically along the thighs and buttocks.

Rarely, severe life-threatening forms of the disease called hyperinfection syndrome and disseminated strongyloidiasis can occur. These forms of the disease are more common in people who are on corticosteroids (prednisone for example) or other immunosuppressive therapies or who are infected with HTLV-1. In this situation, people become critically ill, and should be taken to the hospital immediately.

DIAGNOSIS

Strongyloides is usually diagnosed by seeing larvae in stool when examined under the microscope. This may require that you provide multiple stool samples to your doctor or the laboratory. Some laboratories are capable of diagnosing Strongyloides with blood tests.

PREVENTION AND CONTROL

The best way to prevent Strongyloidesinfection is to wear shoes when you are walking on soil, and to avoid contact with fecal matter or sewage. Proper sewage disposal and fecal management are keys to prevention. Furthermore, if you believe that you may be infected, the best way to prevent severe disease is to be tested and, if found to be positive for disease, treated. You should discuss testing with your doctor if you are:

taking steroids or other immunosuppressive therapies

about to start taking steroids or other immunosuppressive therapies

a veteran who served in the South Pacific or southeast Asia

infected with Human T-cell Lymphotropic Virus-1 (HTLV-1)

diagnosed with cancer

going to donate or receive organ transplants.

For more information view the source:Center for Disease Control

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TAENIA

Taenia is a genus of tapeworm that includes some important parasites of livestock. Members of the genus are responsible for taeniasis and cysticercosis in humans. There are more than 100 species recorded. They are morphologically characterized by a ribbon-like body composed of a series of segments called proglottids; hence the name Taenia (Greek tainia meaning ribbon, bandage or stripe). The anterior end of the body is the scolex. Not all members of the genus Taenia have an armed scolex (hooks and/or spines located in the "head" region), for example, Taenia saginata has an unarmed scolex, while Taenia solium has an armed scolex. Proglottids have central ovary, with a vitellarium (yolk gland) posterior to it. As in all cyclophyllid cestodes, there is genital pore on the side of the proglottid. Eggs are released when proglottid deteriorates, and so a uterine pore is unnecessary.

SELECTED SPECIES

Taenia asiatica Asian Taenia. Humans as definitive hosts, pigs and rarely cattle, as intermediate hosts. Taenia crassiceps Taenia gonyamai, parasite of antelope (larval-) and lions (adult forms). Taenia mustelae, which infects small carnivorans. Taenia pisiformis, which is common in wild dogs and in rabbits, who serve as intermediate hosts. Taenia rileyi, which infects bobcats. Taenia saginata beef tapeworm. Infects cattle and humans, and can only reproduce while in the human gut. Taenia solium Pork Tapeworm. Like T. saginata humans serve as its primary host, and it can only reproduce by the dispersal of proglottids while in the gut. These reinfect pigs when human faeces is improperly disposed of. This infection is most common in parts of Africa. Taenia taeniaeformis, which uses rodents as intermediate hosts and then inhabits cats as the definitive host.

LIFE CYCLE

The life cycle begins with either the eggs or the gravid proglottids being passed in the feces, which can last for days to months in the environment (1). Then, cattle or pigs ingest the contaminated vegetation with eggs or proglottids (2). The oncospheres hatch in the small intestine of the cattle or pig (3) and invade the intestinal wall to travel to the striated muscles to develop into cysticerci. Humans can become infected when eating raw beef or pork meat (4). In the human, the cysticercus develop into adults in two months in the intestines. Using their scolex, they attach to the small intestine (5) where they reside(6). Taenia saginata are about 1,000-2,000 proglottids long with each gravid proglottid containing 100,000 eggs, while Taenia solium contain about 1,000 proglottids with each gravid proglottid containing 50,000 eggs.

For more information view the source:Wikipedia

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TAENIA SOLIUM

Taenia solium, also called the pork tapeworm, is a cyclophyllid cestode in the family Taeniidae. It infects pigs and humans in Asia, Africa, South America, parts of Southern Europe and pockets of North America. In the larval stage, it causes cysticercosis which is a major cause of seizures in humans. Like all cyclophyllid cestodes, T. solium has four suckers on its scolex ("head"). T. solium also has two rows of hooks.

DESCRIPTION

T. solium is normally 2 m to 3 m in length, but can become very large, over 50 m long in some situations. T. solium has a very similar life cycle to Taenia saginata. Cysticerci have three morphologically distinct types. The common one is the ordinary "cellulose" cysticercus which has a fluid filled bladder that is 0.5 cm to 1.5 cm in length and an invaginated scolex. The intermediate form has a scolex while the "racemose" has no evident scolex but are believed to be larger and much more dangerous. They are 20 cm in length and have 60 ml of fluid and 13% of patients might have all three types in the brain. Humans are usually infected through eating infected pork, fostering adult tapeworms in the intestine, and passing eggs through feces, but autoinfection is also possible. In that case, a cysticercus (a larva sometimes called a "bladder worm") develops in the human and the human acts like an intermediate host. This happens if eggs get to the stomach, usually as a result of contaminated hands, but also due to retroperistalsis. Cysticerci often occur in the central nervous system, which can cause major neurological problems like hydrocephalus, paraplegy, meningitis, convulsions and even death. The condition of having cysticerci in one's body is called cysticercosis. Eggs can be diagnosed only to the family level, but if a proglottid's uterus is stained with India ink, the number of visible uterine branches can help identify the species: unlike the Taenia saginata uteri, T. solium uteri have only five to ten uterine branches on each side. Infection with T. solium adults is treated with niclosamide, which is one of the most popular drugs for adult tapeworm infections, as well as for fluke infections. As cysticercosis is a major risk, it is important to wash one's hands before eating and to suppress vomiting if a patient may be infected with T. solium. If neurocysticercosis occurs the drug of choice is either albendazole or praziquantel. These drugs damage the parasites skin internally causing it to disintegrate and is then removed by the host's immune system. Infection may be prevented with proper disposal of human feces around pigs, cooking meat thoroughly and/or freezing the meat at -10 ?C for 5 days. Most cases occur because infected food handlers contaminate the food.

PATHOGENESIS

Ingestion of T. solium eggs or proglottid rupture within the host intestine can cause larvae to migrate into host tissue and cause cysticercosis. This is the most frequent and severe disease caused by T. solium. In symptomatic cases, a wide spectrum of symptoms may be expressed including headaches, dizziness and occasional seizures. In more severe cases, dementia or hypertension due to perturbation of the normal circulation of cerebrospinal fluid can occur. The severity of cysticercosis depends on location, size and number of parasite larvae in tissues, as well as the host immune response. Other symptoms include sensory deficits, involuntary movements and brain system dysfunction. In children ocular location of cysts is more common than cystation in other locations of the body. If a person is heavily infected with T. solium, it can lead to neurocysticercosis which can lead to epilepsy, seizures, lesions in the brain, blindness and tumor like growths. This kind of patient will also show the low level of eosinophils when they run the blood test.

DIAGNOSIS

Diagnosis requires biopsy of the infected tissue and examination of feces. T. solium eggs and proglottids found in feces diagnoses taeniasis and not cysticercosis. Cysticercosis is diagnosed primarily on confirming the presence of hooks on the scolex of T. solium. Radiological test such as X-ray, CT scans which demonstrate "ring-enhancing brain lesions", and MRIs can also be used to detect diseases. X-rays are used to identify calcified larvae in the subcutaneous and muscle tissues and CT scans and MRIs are used to find lesions in the brain.

TREATMENT

PZQ (praziquantel) is the drug of choice for the treatment of T. solium infection. Some consider Niclosamide to be the drug of choice for all types of Tapeworms. For cysticercosis, one can be treated with albendazole combining with steroid to reduce the inflammation. Surgical intervention may be necessary to treat CNS lesions. Albendazole appears to be more effective and a safe drug for Neurocysticercosis, infection of the brain with T. solium larvae.

PREVENTION AND CONTROL

The best way to avoid getting tapeworms is to not eat under-cooked pork. Moreover, a high level of personal hygiene and prevention of fecal contamination of pig foods also plays a major role in prevention of getting the parasites.

EPIDEMIOLOGY

T. solium is found worldwide, however, it has shown to be more common in cosmopolitan areas. Because pigs are intermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. Cysticercosis is often seen in areas where poor hygiene allows for contamination of food, soil or water supplies. Prevalence rates in the United States have shown that immigrants from Mexico, Central and South America and South-east Asia account for most of the domestic cases of cysticercosis. Taeniasis and cysticercosis are very rare in predominantly Muslim countries, as Islam forbids the consumption of pork. It is important to note that human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human tapeworm carrier via gravid proglottids, and thus can occur in populations that neither eat pork nor share environments with pigs, although, as stated, the completion of the life cycle can occur only where humans live in close contact with pigs and eat pork. In 1990 and 1991, four unrelated members of an Orthodox Jewish community in New York City developed recurrent seizures and brain lesions which were found to have been caused by cysticercosis from T. solium. In keeping with their religion, none of the patients ate pork; additionally, none had any history of recent foreign travel. Several immediate family members of these four patients with seizures were found to have cysticercus antibodies. The families of the four patients had all employed housekeepers from Latin American countries, and one of the housekeepers tested positive for cysticercus antibodies, leading to the conclusion that the housekeepers were the most likely source of the infections.

LIFE CYCLE

This infection is caused by ingestion of eggs shed in the feces of a human tapeworm carrier. Pigs and humans become infected by ingesting eggs or gravid proglottids. Humans are infected either by ingestion of food contaminated with feces containing eggs, or by autoinfection. In the latter case, a human infected with adult T. solium can ingest eggs produced by that tapeworm, either through fecal contamination or, possibly, from proglottids carried into the stomach by reverse peristalsis. Once eggs are ingested, oncospheres hatch in the intestine, invade the intestinal wall, and migrate to striated muscles, as well as the brain, liver, and other tissues, where they develop into cysticerci. In humans, cysts can cause serious sequelae if they localize in the brain, resulting in neurocysticercosis. The parasite life cycle is completed, resulting in human tapeworm infection, when humans ingest undercooked pork containing cysticerci. Cysts evaginate and attach to the small intestine by their scolex. Adult tapeworms develop, (up to 2 to 7 m in length and produce less than 1000 proglottids, each with approximately 50,000 eggs) and reside in the small intestine for years.

For more information view the source:Wikipedia

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TAENIA SOLIUM SAGINATA

Taeniasis in humans is a parasitic infection caused by the tapeworm species Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm), and Taenia asiatica (Asian tapeworm). Humans can become infected with these tapeworms by eating raw or undercooked beef (T. saginata) or pork (T. solium and T. asiatica). People with taeniasis may not know they have a tapeworm infection because symptoms are usually mild or nonexistent.

Taenia solium tapeworm infections can lead to, which is a disease that can cause seizures, so it is important seek treatment.

FAQS

What is taeniasis?

Taeniasis in humans is a parasitic infection caused by the tapeworm species Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm), and Taenia asiatica (Asian tapeworm). Humans can become infected with these tapeworms by eating raw or undercooked beef (T. saginata) or pork (T. solium and T. asiatica). People with taeniasis may not know they have a tapeworm infection because symptoms are usually mild or nonexistent.

T. solium tapeworm infections can lead to cysticercosis, which is a disease that can cause seizures, so it is important seek treatment.

Where does taeniasis occur?

Taenia saginata and T. solium are found worldwide. Infections with T. saginata occur wherever contaminated raw beef is eaten, particularly in Eastern Europe, Russia, eastern Africa and Latin America. Taeniasis due to T. saginata is rare in the United States, except in places where cattle and people are concentrated and sanitation is poor, such as around feed lots where cattle can be exposed to human feces. Tapeworm infections due to T. solium are more prevalent in under-developed communities with poor sanitation and where people eat raw or undercooked pork. Higher rates of illness have been seen in people in Latin America, Eastern Europe, sub-Saharan Africa, India, and Asia. Taenia solium taeniasis is seen in the United States, typically among Latin American immigrants. Taenia asiatica is limited to Asia and is seen mostly in the Republic of Korea, China, Taiwan, Indonesia, and Thailand.

What are the signs and symptoms of taeniasis?

Most people with tapeworm infections have no symptoms or mild symptoms. Patients with T. saginata taeniasis often experience more symptoms that those with T. solium or T. asiatica infections because the T. saginata tapeworm is larger in size (up to 10 meters (m)) than the other two tapeworms (usually 3 m). Tapeworms can cause digestive problems including abdominal pain, loss of appetite, weight loss, and upset stomach. The most visible sign of taeniasis is the active passing of proglottids (tapeworm segments) through the anus and in the feces. In rare cases, tapeworm segments become lodged in the appendix, or the bile and pancreatic ducts.

Infection with T. solium tapeworms can result in human cysticercosis, which can be a very serious disease that can cause seizures and muscle or eye damage.

Taenia saginata does not cause cysticercosis in humans. It is not clear if T. asiatica causes cysticercosis in humans or not.

Is taeniasis common?

Taeniasis is under-reported in a significant portion of the world because diagnosis is difficult in resource-poor settings. The number of new cases in the U.S. each year is probably less than 1000, but an exact number is not known.

What should I do if I think I have taeniasis?

Contact your health care provider for proper diagnosis and care.

Is medication available to treat taeniasis?

Yes. Praziquantel is the drug of choice. Niclosamide is an alternative drug. See your health care provider for proper diagnosis and care.

How did I get taeniasis?

Eating raw or undercooked contaminated beef or pork is the primary risk factor for acquiring taeniasis. Because of this, certain groups with dietary restrictions for these meats may have a lower risk of taeniasis.

How can I prevent infection with taeniasis?

One way to prevent taeniasis is to cook meat to safe temperatures. A food thermometer should be used to measure the internal temperature of cooked meat. Do not sample meat until it is cooked. USDA recommends the following for meat preparation.

For Whole Cuts of Meat (excluding poultry)

Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part of the meat, then allow the meat to rest* for three minutes before carving or consuming.

According to USDA, "A 'rest time' is the amount of time the product remains at the final temperature, after it has been removed from a grill, oven, or other heat source. During the three minutes after meat is removed from the heat source, its temperature remains constant or continues to rise, which destroys pathogens."

Should I be concerned about spreading taeniasis to the rest of my household?

No. However, a disease called cysticercosis can occur when T. solium tapeworm eggs are ingested. For example, people with poor hygiene who have taeniasis -- with or without symptoms -- will shed tapeworm eggs in their feces and might accidentally contaminate their environment. This can lead to transmission of cysticercosis to themselves or others unknowingly.

Can I get taeniasis from my dog or cat that was diagnosed with tapeworm infection?

In general, no. The tapeworm that your pet was diagnosed with is more than likely the flea tapeworm (Dipylidium caninum). Dog or cat tapeworm infections are a result of your pet swallowing a parasite-contaminated flea. Only in very rare instances do humans accidentally swallow the contaminated fleas.

EPIDEMIOLOGY & RISK FACTORS

The tapeworms that cause taeniasis (Taenia saginata, T. solium, and T. asiatica) are found worldwide. Eating raw or undercooked beef or pork is the primary risk factor for acquiring taeniasis. Persons who don't eat raw or undercooked beef or pork are not likely to get taeniasis.

Infections with T. saginata occur wherever contaminated raw beef is eaten, particularly in Eastern Europe, Russia, eastern Africa and Latin America. Taeniasis due to T. saginata is rare in the United States, except in places where cattle and people are concentrated and sanitation is poor, such as around feed lots when cattle can be exposed to human feces. Tapeworm infections due to T. solium are more prevalent in under-developed communities with poor sanitation and where people eat raw or undercooked pork. Higher rates of illness have been seen in people in Latin America, Eastern Europe, sub-Saharan Africa, India, and Asia. Taenia solium taeniasis is seen in the United States, typically among Latin American immigrants. Taenia asiatica is limited to Asia and is seen mostly in the Republic of Korea, China, Taiwan, Indonesia, and Thailand.

A disease called cysticercosis can occur when T. solium tapeworm eggs are ingested. For example, people with poor hygiene who have taeniasis -- with or without symptoms -- will shed tapeworm eggs in their feces and might accidentally contaminate their environment. This can lead to transmission of cysticercosis to themselves or others.

BIOLOGY

Causal Agent:

The cestodes (tapeworms) Taenia saginata (beef tapeworm) and T. solium (pork tapeworm). Taenia solium eggs can also cause cysticercosis.

Life Cycle:

Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata or Taenia solium. Humans are the only definitive hosts for T. saginata and T. solium. Eggs or gravid proglottids are passed with feces; the eggs can survive for days to months in the   environment. Cattle (T. saginata) and pigs (T. solium) become   infected by ingesting vegetation contaminated with eggs or gravid proglottids. In the animal's intestine, the oncospheres hatch, invade the intestinal wall, and migrate to the striated   muscles, where they develop into cysticerci. A cysticercus can survive for   several years in the animal. Humans become infected by ingesting raw or   undercooked infected meat. In the human intestine, the cysticercus develops over 2 months into   an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine. Length of adult worms is usually 5 m or less for T. saginata (however it may reach up to 25 m) and 2 to 7 m for T. solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool   (approximately 6 per day). T. saginata adults usually have 1,000 to   2,000 proglottids, while T. solium adults have an average of 1,000   proglottids. The eggs contained in the gravid proglottids are released after   the proglottids are passed with the feces. T. saginata may produce up to   100,000 and T. solium may produce 50,000 eggs per proglottid respectively.

Life cycle image and information courtesy of DPDx.

DISEASE

Human taeniasis is a parasitic infection caused by three tapeworm species, T. saginata (known as the beef tapeworm), T. solium (pork tapeworm), and T. asiatica (the Asian tapeworm). Humans are the only hosts for these Taenia tapeworms. Humans pass the tapeworm segments and/or eggs in feces and contaminate the soil in areas where sanitation is poor. Taenia eggs can survive in a moist environment and remain infective for days to months. Cows and pigs become infected after feeding in areas that are contaminated with Taenia eggs from human feces. Once inside the cow or pig, the Taenia eggs hatch in the animal’s intestine and migrate to striated muscle to develop into cysticerci, causing a disease known as cysticercosis. Cysticerci can survive for several years in animal muscle. Humans become infected with tapeworms when they eat raw or undercooked beef or pork containing infective cysticerci. Once inside humans, Taenia cysticerci migrate to the small intestine and mature to adult tapeworms, which produce segments and eggs that are passed in feces.

Symptoms

Most people with tapeworm infections have no symptoms or mild symptoms. Patients with T. saginata taeniasis often experience more symptoms that those with T. solium because the T. saginata tapeworm is larger in size (up to 10 meters (m)) than T. solium (usually 3 m). Tapeworms can cause digestive problems including abdominal pain, loss of appetite, weight loss, and upset stomach. The most visible symptom of taeniasis is the active passing of proglottids (tapeworm segments) through the anus and in the feces. In rare cases, tapeworm segments become lodged in the appendix, or the bile and pancreatic ducts.

Infection with T. solium tapeworms can result in human cysticercosis, which can be a very serious disease that can cause seizures and muscle or eye damage.

Taenia saginata does not cause cysticercosis in humans. It is not clear if T. asiatica causes cysticercosis in humans or not.

DIAGNOSIS

Diagnosis of Taenia tapeworm infections is made by examination of stool samples; individuals should also be asked if they have passed tapeworm segments. Stool specimens should be collected on three different days and examined in the lab for Taenia eggs using a microscope. Tapeworm eggs can be detected in the stool 2 to 3 months after the tapeworm infection is established.

Tapeworm eggs of T. solium can also infect humans, causing cysticercosis. It is important to diagnose and treat all tapeworm infections.

PREVENTION AND CONTROL

One way to prevent taeniasis is to cook meat to safe temperatures. A food thermometershould be used to measure the internal temperature of cooked meat. Do not sample meat until it is cooked. USDA recommends the following for meat preparation.

For Whole Cuts of Meat (excluding poultry)

Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part of the meat, then allow the meat to rest* for three minutes before carving or consuming.

For Ground Meat (excluding poultry)

Cook to at least 160° F (71° C); ground meats do not require a rest* time.

*According to USDA, "A 'rest time' is the amount of time the product remains at the final temperature, after it has been removed from a grill, oven, or other heat source. During the three minutes after meat is removed from the heat source, its temperature remains constant or continues to rise, which destroys pathogens."

For more information view the source:Center for Disease Control

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TOXASCARIS LEONINA

Toxascaris leonina is a common parasitic roundworm found in dogs, cats, foxes, and related host species. Toxascaris leonina, or T. leonina, is an ascarid nematode, a worldwide distributed helminth parasite which is in a division of eukaryotic parasites that, unlike external parasites such as lice and fleas, live inside their host. The definitive hosts of T. leonina include canids (dogs, foxes, etc.) and felines (cats), while the intermediate hosts are usually rodents, such as mice or rats. Infection occurs in the definitive host when the animal eats an infected rodent. While T. leonina can occur in either dogs or cats, it is far more frequent in cats.

LIFE CYCLE

The life cycle of T. leonina is fairly simple. Eggs are ingested and hatch in the small intestine. The juveniles then penetrate the mucosal lining of the small intestine. After growth and molt, they return to the intestinal lumen and mature. The adult female worm lays eggs which are passed in the feces of the dog. The eggs become infective after 3–6 days in the environment. Rodents are usually the intermediate hosts of T. leonina. The rodent ingests the eggs and, once the eggs are hatched, the larvae migrate through the tissues of the rodent. The definitive host is then infected with this parasite when it eats an infected rodent. The egg of the T. leonina is usually more oval than round. The prepatent period for T. leonina is two to three months. The adult worms are usually 3-4 inches long and can be seen in the feces and vomit of the animal. Toxascaris leonina differs from other Toxocara in that the larvae do not migrate through the lungs; but rather, the entire developmental cycle occurs in the gut.

SYMPTOMS OF INFECTION

Roundworms absorb the nutrients from the animal, which can interfere with digestion and can also damage the lining of the intestine. Animals may not show any outward symptoms of roundworms at all, or in other, usually more severe cases, animals may have diarrhea, vomiting, loss of appetite, experience thinning, dull coats, and in puppies or kittens, can develop distended abdomens, or "pot-belly" appearance. Infection symptoms are similar to infection by other Toxacara species (T. canis, T. cati). It is a common cause of diarrhea in young animals and can cause vomiting as well. Sometimes the worms themselves are vomited up, which can be alarming as they can be quite large with females reaching lengths of up to seven inches. The worms consume the host's food and can lead to lethargy and a classical pot-bellied appearance. Extreme cases of severe infections can lead to pneumonia as the worms migrate, and if there are enough worms the intestine can become obstructed.

PREVENTION AND TREATMENT

It is recommended to de-worm all puppies and kittens at 6 weeks and repeat treatment 2–4 weeks after the first treatment. T. leonina roundworm infections are treated with the same medication protocol as the T. canis or T. cati roundworm infections (see Toxocariasis). Therefore, when eggs are seen on a fecal flotation exam, or fecal swab, it is not necessary to determine which species is present. Roundworm infections are treated with medication, called "de-wormers", and includes such drugs as fenbendazole, pyrantel, milbemycin oxime, and piperazine. To prevent reinfection of parasitic roundworms, it is recommended that anything that the animal has been in contact with should be cleaned thoroughly or replaced, including bedding and kennels. It is also strongly recommended that outside areas where defecation may occur be cleaned, as well as all feces removed daily from outdoor pet runs, crates, and the yard.

RISK IN HUMANS

Humans are usually not infected with T. leonina; however, this parasite has been found in humans in a few instances and is a cause of visceral larva migrans in children, though less frequently implicated than is Toxocara canis, the most common roundworm parasite found in dogs.

For more information view the source:Wikipedia

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TOXOCARA CANIS

Toxocara canis (also known as dog roundworm) is worldwide distributed helminth parasite of dogs and other canids. T. canis are gonochorists, adult worms measure from 9 to 18 cm, are yellow-white in color, and occur in the intestine of the definitive host. In adult dogs, the infection is usually asymptomatic. By contrast, massive infection with T. canis can be fatal in puppies. As paratenic hosts, a number of various vertebrates, including humans, and some invertebrates can become infected. Humans are infected, like other paratenic hosts, by ingestion of embryonated T. canis eggs. The disease caused by migrating T. canis larvae (toxocariasis) results in two syndromes: visceralis larva migrans and ocularis larva migrans. Owing to transmission of the infection from bitches to puppies, preventive anthelmintic treatment of newborn puppies is strongly recommended. Several antihelmintic drugs are effective against adult worms, for example pyrantel, fenbendazole, selamectine etc.

MOPHOLOGY

Adult T. canis have round body with spiky cranial and caudal part, covered by yellow cuticula. Cranial part of the body contains two lateral alae (length 2.5 mm, width 0.2 mm). Male worms measure 9-13 - 0.2-0.25 cm and female worms 10-18 - 0.25-0.3 cm. T. canis eggs have oval or spherical shape with granulated surface, thick-walled, and measures from 72 to 85 -m.

LIFE CYCLE

There are four modes of infection associated with this species. The basic form is typical to all ascaroides, the egg containing the L2(the second larval developmental stage), being infective, at optimal temperature and humidity, four weeks after secreted in the faeces to the environment. After ingestion, and hatching in the small intestine, the L2 travel through the portal blood stream into the liver and lungs. Such migratory route is known as entero-hepatic-pulmonar larval migration. The second molt takes place in the lungs, the now L3 returns via the trachea and into the intestines where the final two molts take place. This form of infection occurs regularly only in dogs of up to three months of age. In older dogs, this type of migration occurs less frequently and at six months it is almost ceased. Instead, the L2 travel to a wide range of organs including the liver, lungs, brain, heart and skeletal muscles, as well as to the walls of the gastrointestinal tract. In pregnant bitches prenatal infection can occur, where larvae become mobilized (at approximately three weeks prior to parturition) and migrate to the lungs of the foetus, here molting into L3 just prior to birth. In the newborn pup the cycle is completed when the larva migrates through the trachea and into the intestinal lumen, where the final molts take place. Once infected, a bitch will usually harbor sufficient larvae to subsequently infect all of her litters, even if she never again encounters an infection. A certain amount of the bitch's dormant larvae penetrate into the intestinal lumen, where molting into adulthood take, yet again, place, thus leading to a new release of eggs containing L1 larvae. The suckling pup may be infected by the presence of L3 in the milk during the first three weeks of lactation. There is no migration in the pup via this route. L2 may also be ingested by a variety of animals where it stays in a dormant stage inside the animals tissue until the intermediate host has been eaten by a dog, when subsequent development is confined to the gastrointestinal tract.

TRANSMISSION TO HUMANS

A 2003 study found that humans can be infected by this roundworm, a condition called toxocarosis, just by stroking an infected dog's fur. In humans, this parasite usually grows in the back of the eye, which can result in blindness, or in the liver or lungs. However, a 2004 study showed that, of 15 infected dogs, only 7 had eggs in their coat, and that no more than one egg was found on each dog. Furthermore, only 4% of those eggs were infectious. Given the low concentration of fertile eggs on infected dogs' coats (less than 0.00186% per gram), it is plausible that such eggs were transferred to the dog's coat by contact with fecal deposites in the environment, making dog coats be passive transport hosts. The risk of being infected by petting a dog is extremely limited and, since a single infected puppy can produce more than 100,000 roundworm eggs per gram of feces, humans are much more likely to be infected by contact with feces than contact with fur. As such, there is little reason for humans to fear infection as long as basic hygiene, like hand-washing, is followed. There are several treatments, all of which are cheap and easily-accessible by the average dog owner, than can prevent a dog from becoming infected or rid an infected pet of its roundworm parasites.

For more information view the source:Wikipedia

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TOXOPLASMA GONDII

Toxoplasma gondii is a species of parasitic protozoa in the genus Toxoplasma. The definitive host of T. gondii is the cat, but the parasite can be carried by many warm-blooded animals (birds or mammals, including humans). Toxoplasmosis, the disease of which T. gondii is the causative agent, is usually minor and self-limiting but can have serious or even fatal effects on a fetus whose mother first contracts the disease during pregnancy or on an immunocompromised human or cat.

LIFE CYCLE

The life cycle of T. gondii has two phases. The sexual part of the life cycle (coccidia like) takes place only in cats, both domestic and wild (family Felidae), which makes cats the parasite's primary host. The second phase, the asexual part of the life cycle, can take place in other warm-blooded animals, including cats, mice, humans, and birds. The hosts in which asexual reproduction takes place is called the intermediate host. Rodents are the typical intermediate host. In both kinds of hosts, the Toxoplasma parasite invades cells and forms a space called a vacuole. Inside this specialized vacuole, called a parasitophorous vacuole, the parasite forms bradyzoites, which are the slowly replicating versions of the parasite. The vacuoles containing the reproductive bradyzoites form cysts mainly in the tissues of the muscles and brain. Since the parasites are inside cells, they are safe from the host's immune system, which does not respond to the cysts. Toxoplasma's resistance to anti-toxoplasmosis medication varies, but the cysts are very difficult to eradicate entirely. Inside the vacuoles, T. gondii replicates itself (by endodyogeny) until the infected cell fills with parasites and bursts, releasing tachyzoites, the motile, asexually reproducing form of the parasite. Unlike the bradyzoites, the free tachyzoites are usually efficiently cleared by the host's immune system, although some of them manage to infect cells and form bradyzoites, thus maintaining the infection. Tissue cysts are ingested by a cat (e.g., by feeding on an infected mouse). The cysts survive passage through the stomach of the cat and the parasites infect epithelium of the small intestine where they undergo sexual reproduction and oocyst formation. Oocysts are shed with the feces. Animals and humans that ingest oocysts (e.g., by eating unwashed vegetables) or tissue cysts in improperly cooked meat become infected. The parasite enters macrophages in the intestinal lining and is distributed via the blood stream throughout the body. Similar to the mechanism used in many viruses, Toxoplasma is able to dysregulate host’s cell cycle by holding cell division before mitosis (the G2/M border). This dysregulation of the host’s cell cycle is caused by a heat-sensitive secretion (with a molecular mass larger than 10 kDa). Infected cells secrete the factor which inhibits the cell cycle of neighboring cells. The reason for Toxoplasma’s dysregulation is unknown, but studies have shown that infection is preferential to host cells in the S-phase and host cell structures with which Toxoplasma interacts may not be accessible during other stages of the cell cycle. Acute stage Toxoplasma infections can be asymptomatic, but often give flu-like symptoms in the early acute stages, and like flu can become, in very rare cases, fatal. The acute stage fades in a few days to months, leading to the latent stage. Latent infection is normally asymptomatic; however, in the case of immunocompromised patients (such as those infected with HIV or transplant recipients on immunosuppressive therapy), toxoplasmosis can develop. The most notable manifestation of toxoplasmosis in immunocompromised patients is toxoplasmic encephalitis, which can be deadly. If infection with T. gondii occurs for the first time during pregnancy, during an activity such as changing cat litter of a cat infected with T. gondii (uptake of cyst by inhalation, followed by ingestion as the mucus is cleared), the parasite can cross the placenta, possibly leading to hydrocephalus or microcephaly, intracranial calcification, and chorioretinitis, with the possibility of spontaneous abortion (miscarriage) or intrauterine death. An in vitro study showed that ivermectin significantly inhibited T. gondii replication.

EPIDEMIOLOGY

The rates of positive sero-prevalence in women at child-bearing age between 1990 and 2000 were 58% in Central European countries, 51–72% in several Latin-American countries and 54–77% in West African countries. Low seroprevalence, 4–39%, was reported in southwest Asia, China and Korea as well as in cold climate areas such as Scandinavian countries (11–28%). T. gondii has also been linked to pre-natal depression, as well as increased anxiety and depression during pregnancies. It has also been linked with mood disturbances in nonpregnant populations, including schizophrenia and suicidal behavior.

TOXOPLASMOSIS

T. gondii infections have the ability to change the behavior of rats and mice, making them drawn to, rather than fearful of, the scent of cats. This effect is advantageous to the parasite, which will be able to sexually reproduce if its host is eaten by a cat. The infection is widespread in the brain, with more cysts targeting the parts of the brain corresponding to fear. The widespread nature of the infection causes many previously unnoticed symptoms in the rats. Studies have also shown behavioral changes in humans, including lower reaction times and a sixfold increased risk of traffic accidents among infected, RhD-negative males, as well as links to schizophrenia including hallucinations and reckless behavior. Recent epidemiologic studies by Stanley Medical Research Institute and Johns Hopkins University Medical Center indicate that infectious agents may contribute to some cases of schizophrenia. A study of 191 young women in 1999 reported higher intelligence and higher guilt proneness in Toxoplasma-positive subjects. The prevalence of human infection by Toxoplasma varies greatly between countries. Factors that influence infection rates include diet (prevalence is possibly higher where there is a preference for less-cooked meat) and proximity to cats. According to Merck the standard treatment for toxoplasmosis is pyrimethamine, but most immunocompetent asymptomatic people infected with T. gondii, with the exception of neonates and pregnant women, require no treatment.

HISTORY

The organism was first described in 1908 in Tunis by Charles Nicolle and Louis Manceaux within the tissues of the gundi (Ctenodactylus gundi). In the same year it was also described in Brazil by Alfonso Splendore in rabbits.

For more information view the source:Wikipedia

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TRICHOSTRONGYLUS

Trichostrongylus species are nematodes (round worms), which are ubiquitous among herbivores worldwide, including cattle, sheep, donkeys, goats, deer, and rabbits . At least 10 Trichostrongylus species have been associated with human infections. Infections occur via ingestion of infective larvae from contaminated vegetables or water . Epidemiological studies indicate a worldwide distribution of Trichostrongylus infections in humans, with the highest prevalence rates observed in individuals from regions with poor sanitary conditions, in rural areas, or who are farmers / herders. Human infections are most prevalent in the Middle East and Asia , with a worldwide estimated prevalence of 5.5 million.

CLINICAL PRESENTATION

The majority of human infections are asymptomatic or associated with mild symptoms. Symptomatic individuals may experience abdominal pain, nausea, diarrhea, flatulence, dizziness, generalized fatigue, and malaise. Eosinophilia is frequently observed. Infections with a heavy worm burden can lead to anemia, cholecystitis, and emaciation.

DIAGNOSIS

The adult worms live in the small intestine. The diagnosis is based on the observation of eggs in the stool. The eggs are 85-115 um, oval, elongated, and pointed at one or both ends. Trichostrongylus eggs must be differentiated from hookworm eggs which are smaller and do not have pointed ends.

PREVENTION AND TREATMENT

Since the use of herbivore manure as fertilizer is a common practice preceding infection, thorough cleaning and cooking of vegetables is required for prevention of infection. Treatment with pyrantel pamoate (11 mg/kg base once, max. 1 g) is recommended. Alternative agents include mebendazole (100 mg bid x 3 days) and albendazole (400 mg once).Successful treatment with ivermectin has also been reported.

Egg of Trichostrongylus sp.

For more information view the source:Wikipedia

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TRICHURIS TRICHIURA

An estimated 604-795 million people in the world are infected with whipworm. Whipworm, hookworm, and Ascaris are known as soil-transmitted helminths (parasitic worms). Together, they account for a major burden of disease worldwide. Whipworms live in the large intestine and whipworm eggs are passed in the feces of infected persons. If the infected person defecates outside (near bushes, in a garden, or field) or if human feces as used as fertilizer, eggs are deposited on soil. They can then mature into a form that is infective. Whipworm infection is caused by ingesting eggs. This can happen when hands or fingers that have contaminated dirt on them are put in the mouth or by consuming vegetables or fruits that have not been carefully cooked, washed or peeled. People infected with whipworm can suffer light or heavy infections. People with light infections usually have no symptoms. People with heavy symptoms can experience frequent, painful passage of stool that contains a mixture of mucus, water, and blood. Rectal prolapse can also occur. Children with heavy infections can become severely anemic and growth-retarded. Whipworm infections are treatable with medication prescribed by your health care provider.

FAQS

What is whipworm?

Whipworm (Trichuris trichiura) is an intestinal parasite of humans. The larvae and adult worms live in the intestine of humans and can cause intestinal disease. The name is derived from the worm’s distinctive whip-like shape.

How is whipworm spread?

Whipworms live in the intestine and whipworm eggs are passed in the feces of infected persons. If the infected person defecates outside (near bushes, in a garden, or field), or if the feces of an infected person are used as fertilizer, then eggs are deposited on the soil. They can then mature into a form that is infective. Roundworm infection is caused by ingesting eggs. This can happen when hands or fingers that have contaminated dirt on them are put in the mouth, or by consuming vegetables or fruits that have not been carefully cooked, washed or peeled.

Who is at risk for infection?

Infection occurs worldwide in warm and humid climates where sanitation and hygiene are poor, including in temperate climates during warmer months. Persons in these areas are at risk if soil contaminated with human feces enters their mouths or if they eat vegetables or fruits that have not been carefully washed, peeled or cooked.

What are the signs and symptoms of whipworm?

People with light infections usually have no signs or symptoms. People with heavy infections can experience frequent, painful passage of stool that contains a mixture of mucus, water, and blood. The diarrhea typically has an acrid smell. In severe cases growth retardation can occur. Rectal prolapse can also occur. In children, heavy infection may be associated with growth retardation and impaired cognitive development.

How is whipworm diagnosed?

Health care providers can diagnose whipworm by taking a stool sample. By using a microscope, providers can look for the presence of whipworm eggs.

How can I prevent infection?

Avoid contact with soil that may be contaminated with human feces, including with human fecal matter ("night soil") used to fertilize crops.

Wash your hands with soap and warm water before handling food.

Teach children the importance of washing hands to prevent infection.

Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.

Transmission of infection to others can be prevented by:

not defecating outdoors, and by

effective sewage disposal systems.

What is the treatment for whipworm?

Whipworm infections are generally treated for 1-3 days with medication prescribed by your health care provider. The drugs are effective and appear to have few side effects.

What is preventive treatment?

In developing countries, groups at higher risk for soil-transmitted helminth infections (hookworm, Ascaris, and whipworm) are often treated without a prior stool examination. Treating in this way is called preventive treatment (or "preventive chemotherapy"). The high-risk groups identified by the World Health Organization are preschool and school-age children, women of childbearing age (including pregnant women in the 2nd and 3rd trimesters and lactating women) and adults in occupations where there is a high risk of heavy infections. School-age children are often treated through school-health programs and preschool children and pregnant women at visits to health clinics.

What is mass drug administration (MDA)?

The soil-transmitted helminths (hookworm, Ascaris, and whipworm) and four other "neglected tropical diseases" (river blindness, lymphatic filariasis, schistosomiasis and trachoma) are sometimes treated through mass drug administrations. Since the drugs used are safe and inexpensive or donated, entire risk groups are offered preventive treatment. Mass drug administrations are conducted periodically (often annually), commonly with drug distributors who go door-to-door. Multiple neglected tropical diseases are often treated simultaneously using MDAs.

EPIDEMIOLOGY & RISK FACTORS

Whipworm is a soil-transmitted helminth (STH) and is the third most common roundworm of humans. Whipworm causes an infection called trichuriasis and often occurs in areas where human feces is used as fertilizer or where defecation onto soil happens. The worms are spread from person to person by fecal-oral transmission or through feces-contaminated food.

GEOGRAPHIC DISTRIBUTION

Worldwide, infection occurs more frequently in areas with tropical weather and poor sanitation practices, and among children. In 2002, the estimated number of persons infected with whipworm was 1 billion. Trichuriasis also occurs in the southern United States.

BIOLOGY

Causal Agent:

The nematode (roundworm) Trichuris trichiura, also called the human whipworm

Life Cycle:

The unembryonated eggs are passed with the stool. In the soil, the eggs develop into a 2-cell stage, an advanced cleavage stage, and then they embryonate; eggs become infective in 15 to 30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon. The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60 to 70 days after infection. Female worms in the cecum shed between 3,000 and 20,000 eggs per day. The life span of the adults is about 1 year.

Life cycle image and information courtesy of DPDx.

DISEASE

People infected with whipworm can suffer light or heavy infections. People with light infections usually have no symptoms. People with heavy symptoms can experience frequent, painful passage of stool that contains a mixture of mucus, water, and blood. Rectal prolapse can also occur. Heavy infection in children can lead to severe anemia, growth retardation, and impaired cognitive development. Whipworm infections are treatable with medication prescribed by your health care provider.

DIAGNOSIS

The standard method for diagnosing the presence of whipworm is by microscopically identifying whipworm eggs in a stool sample. Because eggs may be difficult to find in light infections, a concentration procedure is recommended.

PREVENTION AND CONTROL

The best way to prevent whipworm infection is to always:

Avoid ingesting soil that may be contaminated with human feces, including where human fecal matter ("night soil") or wastewater is used to fertilize crops.

Wash your hands with soap and warm water before handling food.

Teach children the importance of washing hands to prevent infection.

Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.

Transmission of infection to others can be prevented by:

Not defecating outdoors.

Effective sewage disposal systems.

For more information view the source:Center for Disease Control

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TRICHURIS VULPIS

Trichuris vulpis is whipworm that lives in the large intestine of canines in its adult stages. Out of different types of worms, Trichuris vulpis is one of the smaller worms with a size ranging from 30-50 mm in length . As the name suggests, the worm has a whip-like shape with distinct features including a small, narrow anterior head, which is the digestive part of the worm, and a larger posterior tail, which is the reproductive part of the worm. Eggs from T. vulpis are oval shaped with bipolar plugs and contain a thick outer shell. Their sizes range from 72-90 um in length and 32-40 um in width. Because of their thick outer shell, T. vulpis eggs are very resistant to environmental extremes such as freezing or hot temperatures, thus allowing for their long viability in the outside world.

LIFE CYCLE

The life cycle of Trichuris vulpis begins with the adult whipworms living in the large intestines of dogs. T. vulpis lay many eggs in the large intestine and are released in the feces into the outside environment. When eggs are released into the outside environment, these unembryonated eggs are able to form embryos in the soil in about 2-4 weeks, at which point they become infective when ingested by the new host . An infective larva develops within the egg before it is even ingested by the new host. Another canine becomes a new host by ingesting the egg containing the larva. Once ingested, the egg gets into the small intestine where it hatches to release its larva. The larvae invade the small intestinal mucosa and remain there for about 15 days. Afterward, the larva then travel from the small intestine into the large intestine where they go through several stages to become an adult whipworm in the large intestine. Once an adult, their whip-like shape containing a narrow anterior head allows them to burrow through the large intestinal walls while their posterior reproductive end protrudes them into the lumen. Adult whipworms live inside the cecum, colon, and rectum for about three months before they lay eggs intermittently to be released in feces where they can become infective to another host.

EPIDEMIOLOGY

T. vulpis infects canines worldwide. In the United States, it has been reported that 14.3% of shelter dogs are infected with this parasite . Though rare, there are some cases of human infection. The eggs of T. vulpis are prevalent in shady moist soil areas that have been contaminated by canine feces.

PATHOLOGY AND SYMPTOMS

Because the eggs of T. vulpis eggs are very resistant from desiccation, they can live in soil for up to seven years. Once ingested by the canine, the eggs hatch and the resulted larvae live in the small intestine. At this point, though infected, the canine is still asymptomatic. When adult form, T. vulpis live primarily in the cecum with its anterior end attached to the superficial mucosa and its posterior end extended to the cecal lumen where it consumes the canines blood, tissue fluid, and mucosal epithelium. Severe infections include symptoms such as bloody diarrhea, weight loss, dehydration, and anemia, and in extreme cases, death.

DIAGNOSIS

Infection of this parasite can be confirmed with detection of eggs in the canines feces. However, this is difficult because egg production is usually small, its shedding is periodic, and its structure is dense which prevents from floating. Symptoms may appear before the eggs are shed in the feces due to the long prepatent period.

PREVENTION AND CONTROL

Keeping canines away from contaminated areas, especially areas where there are feces can prevent them from contracting T. vulpis. There is no effective way to kill the parasite's eggs in the soil, so it is might be necessary to replace the soil and cleaning out litter boxes and kennels frequently. People cleaning these areas should wear gloves and wash their hands after task. Dogs should have fecal examinations and deworming as necessary. If a dog is detected to be infected with T. vulpis, it should be treated immediately to prevent infection of other dogs.

For more information view the source:Wikipedia

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TROPICAL SPRUE

Tropical sprue is a malabsorption disease commonly found in the tropical regions, marked with abnormal flattening of the villi and inflammation of the lining of the small intestine. It differs significantly from coeliac sprue.

SYMPTOMS AND SIGNS

The illness usually starts with an attack of acute diarrhea, fever and malaise following which, after a variable period, the patient settles into the chronic phase of diarrhoea, steatorrhoea, weight loss, anorexia, malaise and nutritional deficiencies.

The symptoms of tropical sprue are:

Diarrhea

Steatorrhea or fatty stool (often foul-smelling and whitish in colour)

Indigestion

Cramps

Weight loss and malnutrition

Fatigue

Left untreated, nutrient and vitamin deficiencies may develop in patients with tropical sprue.

These deficiencies may have the following symptoms:

Vitamin A deficiency: hyperkeratosis or skin scales

Vitamin B12 and folic acid deficiencies: anaemia

Vitamin D and calcium deficiencies: spasm, bone pain, numbness and tingling sensation

Vitamin K deficiency: bruises

INVESTIGATIONS

Diagnosis of tropical sprue can be complicated because many diseases have similar symptoms. The following investigation results are suggestive:
Abnormal flattening of villi and inflammation of the lining of the small intestine, observed during an endoscopic procedure.
Presence of inflammatory cells (most often lymphocytes) in the biopsy of small intestine tissue.
Low levels of vitamins A, B12, E, D, and K, as well as serum albumin, calcium, and folate, revealed by a blood test.
Excess fat in the feces (steatorrhoea).
Thickened small bowel folds seen on barium swallow
Tropical sprue is largely limited to within about 30 degrees north and south of the equator. Therefore, if one resides outside of that geographical region, recent travel to the region is a key factor in diagnosing this disease.

CAUSES

The cause of tropical sprue is not known. It has been suggested that it is caused by bacterial, viral, amoebal, or parasitic infection. Folic acid deficiency and rancid fat have also been suggested as possible causes. In a condition called coeliac disease (also known as coeliac sprue), which has similar symptoms to tropical sprue, the flattening of the villi and small intestine inflammation is caused by an autoimmune disorder.

AFFECTED REGIONS

The disease was first described by William Hillary in 1759 in Barbados. Tropical sprue is endemic to India and southeast Asia, Central and South America, and the Caribbean.

TREATMENT

Once diagnosed, tropical sprue can be treated by a course of the antibiotic tetracycline(Doxycycline) or Sulfamethoxazole/Trimethoprim(Co-trimoxazole) for 3 to 6 months, as well as supplementation of vitamins B12 and folic acid.

PREVENTION

Preventive measures include using only bottled water for drinking, brushing teeth, and washing food, and avoiding fruits washed with tap water (or consuming only peeled fruits, such as bananas and oranges).

PROGNOSIS

The prognosis for tropical sprue is excellent. It usually does not recur in patients who get it during travel to affected regions. The recurrence rate for natives is about 20%.

For more information view the source:Wikipedia

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TRYPANOSOMA

Trypanosoma is a genus of kinetoplastids (class Kinetoplastida), a monophyletic group of unicellular parasitic flagellate protozoa. The name is derived from the Greek trypano (borer) and soma (body) because of their corkscrew-like motion. All trypanosomes are heteroxenous (requiring more than one obligatory host to complete life cycle) and are transmitted via a vector. The majority of species are transmitted by blood-feeding invertebrates, but there are different mechanisms among the varying species. Then in the invertebrate host they are generally found in the intestine and normally occupy the bloodstream or an intracellular environment in the mammalian host. Trypanosomes infect a variety of hosts and cause various diseases, including the fatal human diseases sleeping sickness, caused by Trypanosoma brucei, and Chagas disease, caused by Trypanosoma cruzi. The mitochondrial genome of the Trypanosoma, as well as of other kinetoplastids, known as the kinetoplast, is made up of a highly complex series of catenated circles and minicircles and requires a cohort of proteins for organisation during cell division.

HISTORY

The first species of Trypanosoma identified was in a trout by Valentin in 1841. They were identified in mammals 25-30 years later.

HOSTS, LIFE CYCLE AND MORPHOLOGIES

Two different types of trypanosomes exist, and their life cycles are different, the salivarian species and the stercorarian species. Stercorarian trypanosomes infect the insect, most often the triatomid kissing bug, develop in its posterior gut and infective organisms are released in the faeces and deposited on the skin of the host. The organism then penetrates and can disseminate throughout the body. Insects become infected when taking a blood meal. Salivarian trypanosomes develop in the anterior gut of insects, most importantly the Tsetse fly, and infective organisms are inoculated into the host by the insect bite before it feeds. As trypanosomes progress through their life cycle they undergo a series of morphological changes as is typical of trypanosomatids. The life cycle often consists of the trypomastigote form in the vertebrate host and the trypomastigote or promastigote form in the gut of the invertebrate host. Intracellular lifecycle stages are normally found in the amastigote form. The trypomastigote morphology is unique to species in the genus Trypanosoma.

For more information view the source:Wikipedia

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TRYPANOSOMIASIS

Trypanosoma is a genus of kinetoplastids (class Kinetoplastida), a monophyletic group of unicellular parasitic flagellate protozoa. The name is derived from the Greek trypano (borer) and soma (body) because of their corkscrew-like motion. All trypanosomes are heteroxenous (requiring more than one obligatory host to complete life cycle) and most are transmitted via a vector. The majority of species are transmitted by blood-feeding invertebrates, but there are different mechanisms among the varying species. Then in the invertebrate host they are generally found in the intestine and normally occupy the bloodstream or an intracellular environment in the mammalian host. Trypanosomes infect a variety of hosts and cause various diseases, including the fatal human diseases sleeping sickness, caused by Trypanosoma brucei, and Chagas disease, caused by Trypanosoma cruzi. The mitochondrial genome of the Trypanosoma, as well as of other kinetoplastids, known as the kinetoplast, is made up of a highly complex series of catenated circles and minicircles and requires a cohort of proteins for organisation during cell division.

BIOLOGY

CAUSAL AGENTS

The protozoan parasite, Trypanosoma cruzi, causes Chagas disease, a zoonotic disease that can be transmitted to humans by blood-sucking triatomine bugs. To see drawings of some common species of triatomine bugs found in the United States.

LIFE CYCLE

An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents.

GEOGRAPHIC DISTRIBUTION

The Americas from the southern United States to southern Argentina. Mostly in poor, rural areas of Mexico, Central America, and South America. Chronic Chagas disease is a major health problem in many Latin American countries.

CLINICAL FEATURES

The acute phase is usually asymptomatic, but can present with manifestations that include fever, anorexia, lymphadenopathy, mild hepatosplenomegaly, and myocarditis. Romaña's sign (unilateral palpebral and periocular swelling) may appear as a result of conjunctival contamination with the vector's feces. A nodular lesion or furuncle, usually called chagoma, can appear at the site of inoculation. Most acute cases resolve over a period of a few weeks or months into an asymptomatic chronic form of the disease. The symptomatic chronic form may not occur for years or even decades after initial infection. Its manifestations include cardiomyopathy (the most serious manifestation); pathologies of the digestive tract such as megaesophagus and megacolon; and weight loss. Chronic Chagas disease and its complications can be fatal.

LABORATORY DIAGNOSIS

Demonstration of the causal agent is the diagnostic procedure in acute Chagas disease. It almost always yields positive results, and can be achieved by: Microscopic examination: a) of fresh anticoagulated blood, or its buffy coat, for motile parasites; and b) of thin and thick blood smears stained with Giemsa, for visualization of parasites. Isolation of the agent: a) inoculation in culture with specialized media (e.g. NNN, LIT); b) inoculation into mice; and c) xenodiagnosis, where uninfected triatomine bugs are fed on the patient's blood, and their gut contents examined for parasites 4 weeks later.

For more information view the source:Center for Disease Control

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UNCINARIA STENOCEPHALA

Uncinaria stenocephala is a nematode that parasitizes dogs, cats, and foxes as well as humans. It is rare to find in cats in the United States. The common name is the northern hookworm of dogs.

LIFE CYCLE

The host ingests an infective third stage larva. The larva matures to the adult in the small intestine. Eggs are laid in the small intestine and pass out with the feces. The prepatent period is about 15 to 17 days. The eggs hatch in the soil and the larvae molt twice to reach the infective third-stage. Adult worms may live for 4 to 24 months in the small intestine. Dog and cat hookworms range in size from 10 to 20 mm by 0.4 to 0.5 mm and the eggs are 71 to 93 m by 35 to 58 m. Adult parasites are most often found in their hosts' small intestine.

DIAGNOSIS

Diagnostic Stage:

Eggs are found in fecal flotation. Eggs measure 75 um long by 45 um wide.

Common Diagnostic Test:

Fecal float to recover eggs.

Clinical Signs:

All hookworms suck blood, they are capable of removing 0.1mls of blood per worm, per 24 hour period. Light infections are asymptomatic. Infected pups may present with pale mucus membranes and anemia, ill thrift, failure to gain weight, poor hair coat, dehydration, and dark, tarry diarrhea (melena). Puppies harboring many worms will develop an acute normocytic, normochromic anemia followed by hypochromic, microcytic anemia due to iron deficiency. Without immediate intervention, these animals may die of the infection. Those that survive may continue as "poor doers" with chronic anemia.

For more information view the source:Wikipedia

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VOLVULUS

A volvulus is a bowel obstruction with a loop of bowel whose nose has abnormally twisted on itself.

TYPES

volvulus neonatorum
volvulus of the small intestine
volvulus of the caecum (cecum), also cecal volvulus
sigmoid colon volvulus (sigmoid volvulus)
volvulus of the transverse colon
volvulus of the splenic flexure, the rarest
gastric volvulus
ileosigmoid knotting

SIGNS AND SYMPTOMS

Regardless of cause, volvulus causes symptoms by two mechanisms:
One is bowel obstruction, manifested as abdominal distension and vomiting.
The other is ischemia (loss of blood flow) to the affected portion of intestine. Depending on the location of the volvulus, symptoms may vary. For example, in patients with a cecal volvulus, the predominant symptoms may be those of a small bowel obstruction (nausea, vomiting and lack of stool or flatus), because the obstructing point is close to the ileocecal valve and small intestine. In patients with a sigmoid volvulus, although abdominal pain may be present, symptoms of constipation may be more prominent. Volvulus causes severe pain and progressive injury to the intestinal wall, with accumulation of gas and fluid in the portion of the bowel obstructed. Ultimately, this can result in necrosis of the affected intestinal wall, acidosis, and death. This is known as a closed loop obstruction because there exists an isolated ("closed" loop of bowel). Acute volvulus often requires immediate surgical intervention to untwist the affected segment of bowel and possibly resect any unsalvageable portion. Volvulus occurs most frequently in middle-aged and elderly men. Volvulus can also arise as a rare complication in persons with redundant colon, a normal anatomic variation resulting in extra colonic loops. Sigmoid volvulus is the most-common form of volvulus of the gastrointestinal tract and is responsible for 8% of all intestinal obstructions. Sigmoid volvulus is particularly common in elderly persons and constipated patients. Patients experience abdominal pain, distension, and absolute constipation. Cecal volvulus as slightly less common than a sigmoid volvulus and is associated with symptoms of abdominal pain and a small bowel obstruction. Volvulus can also occur in patients with Duchenne muscular dystrophy due to the smooth muscle dysfunction.

CAUSES

Midgut volvulus occurs in patients (usually in infants) that are predisposed because of congenital intestinal malrotation. Segmental volvulus occurs in patients of any age, usually with a predisposition because of abnormal intestinal contents (e.g. meconium ileus) or adhesions. Volvulus of the cecum, transverse colon, or sigmoid colon occurs, usually in adults, with only minor predisposing factors such as redundant (excess, inadequately supported) intestinal tissue and constipation. Ieosigmoid knotting peaks in islamic countries during Ramadan leading to the idea that the eating of a large bulky meal only once per day contributes to this uncommon in the West type of volvulus.

DIAGNOSIS AND DIFFERENTIAL DIAGNNOSIS

After taking a thorough history, the diagnosis of colonic volvulus is usually easily included in the differential diagnosis. Abdominal plain x-rays are commonly confirmatory for a volvulus, especially if a "bent inner tube" sign or a "coffee bean" sign are seen. These refer to the shape of the air filled closed loop of colon which forms the volvulus. Should the diagnosis be in doubt, a barium enema may be used to demonstrate a "bird's beak" at the point where the segment of proximal bowel and distal bowel rotate to form the volvulus. This area shows an acute and sharp tapering and looks like a bird's beak. If a perforation is suspected, barium should not be used due to its potentially lethal effects when distributed throughout the free infraperitoneal cavity. Gastrografin, which is safer, can be substituted for barium. The differential diagnosis includes the much more common constricting or obstructing carcinoma. In approximately 80 percent of colonic obstructions, an invasive carcinoma is found to be the cause of the obstruction. This is usually easily diagnosed with endoscopic biopsies. Diverticulitis is a common condition with different presentations. Although diverticulitis may be the source of a colonic obstruction, it more commonly causes an ileus, which appears to be a colonic obstruction. Endoscopic means can be used to secure a diagnosis although this may cause a perforation of the inflamed diverticular area. CT scanning is the more common method to diagnose diverticulitis. The scan will show mesenteric stranding in the involved segment of edematous colon which is usually in the sigmoid region. Micro perforations with free air may be seen. Ulcerative colitis or Crohn's disease may cause colonic obstruction. The obstruction may be acute or chronic after years of uncontrolled disease leads to the formation of strictures and fistulas . The medical history is helpful in that most cases of inflammatory bowel disease are well known to both patient and doctor. Other rare syndromes, including Ogilvie's syndrome, chronic constipation and impaction may cause a pseudo obstruction.

TREATMENT

Perform sigmoidoscopy for suspected sigmoid volvulus. If the mucosa of the sigmoid looks normal and pink, place a rectal tube for decompression, repair any fluid, electrolyte, cardiac, renal or pulmonary evaluation and repair, and then take the patient to the operating room for repair. If surgery is not performed, there is a high rate of recurrence. For patients with signs of sepsis or an abdominal catastrophe, immediate surgery and resection is advised. Laparotomy for other forms of volvulus, especially cecal volvulus.

For more information view the source:Wikipedia

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VOMITING

Vomiting (known medically as emesis and informally as throwing up and by a number of other terms) is the forceful expulsion of the contents of one's stomach through the mouth and sometimes the nose. Vomiting can be caused by a wide variety of conditions; it may present as a specific response to ailments like gastritis or poisoning, or as a non-specific sequela of disorders ranging from brain tumors and elevated intracranial pressure to overexposure to ionizing radiation. The feeling that one is about to vomit is called nausea, which usually precedes, but does not always lead to, vomiting. Antiemetics are sometimes necessary to suppress nausea and vomiting. In severe cases, where dehydration develops, intravenous fluid may be required. Vomiting is different from regurgitation, although the two terms are often used interchangeably. Regurgitation is the return of undigested food back up the esophagus to the mouth, without the force and displeasure associated with vomiting. The causes of vomiting and regurgitation are generally different.

COMPLICATIONS

ASPIRATION OF VOMIT

Vomiting can be dangerous if the gastric content enters the respiratory tract. Under normal circumstances the gag reflex and coughing prevent this from occurring, however these protective reflexes are compromised in persons under the influences of certain substances such as alcohol or anesthesia. The individual may choke and asphyxiate or suffer an aspiration pneumonia.

DEHYDRATION AND ELECTROLYTE IMBALANCE

Prolonged and excessive vomiting depletes the body of water (dehydration), and may alter the electrolyte status. Gastric vomiting leads to the loss of acid (protons) and chlorine directly. Combined with the resulting alkaline tide, this leads to hypochloremic metabolic alkalosis (low chloride levels together with high HCO3 and CO2 and increased blood pH) and often hypokalemia (potassium depletion). The hypokalemia is an indirect result of the kidney compensating for the loss of acid. With the loss of intake of food the individual may eventually become cachectic. A less frequent occurrence results from a vomiting of intestinal contents, including bile acids and HCO3-, which can lead to metabolic acidosis.

MALLORY-WEISS TEAR

Repeated or profuse vomiting may cause erosions to the esophagus or small tears in the esophageal mucosa (Mallory-Weiss tear). This may become apparent if fresh red blood is mixed with vomit after several episodes.

DENTISTRY

Recurrent vomiting, such as observed in bulimia nervosa, may lead to destruction of the tooth enamel due to the acidity of the vomit. Digestive enzymes can also have a negative effect on oral health, by degrading the tissue of the gums.

PATHOPHYSIOLOGY

Receptors on the floor of the fourth ventricle of the brain represent a chemoreceptor trigger zone, known as the area postrema, stimulation of which can lead to vomiting. The area postrema is a circumventricular organ and as such lies outside the blood–brain barrier; it can therefore be stimulated by blood-borne drugs that can stimulate vomiting or inhibit it.

There are various sources of input to the vomiting center:
The chemoreceptor trigger zone at the base of the fourth ventricle has numerous dopamine D2 receptors, serotonin 5-HT3 receptors, opioid receptors, acetylcholine receptors, and receptors for substance P. Stimulation of different receptors are involved in different pathways leading to emesis, in the final common pathway substance P appears involved.
The vestibular system, which sends information to the brain via cranial nerve VIII (vestibulocochlear nerve), plays a major role in motion sickness, and is rich in muscarinic receptors and histamine H1 receptors.
The Cranial nerve X (vagus nerve) is activated when the pharynx is irritated, leading to a gag reflex.
The Vagal and enteric nervous system inputs transmit information regarding the state of the gastrointestinal system. Irritation of the GI mucosa by chemotherapy, radiation, distention, or acute infectious gastroenteritis activates the 5-HT3 receptors of these inputs.
The CNS mediates vomiting that arises from psychiatric disorders and stress from higher brain centers.

The vomiting act encompasses three types of outputs initiated by the chemoreceptor trigger zone: Motor, parasympathetic nervous system (PNS), and sympathetic nervous system (SNS). They are as follows:
Increased salivation to protect tooth enamel from stomach acids. (Excessive vomiting leads to dental erosion). This is part of the PNS output.
The body takes a deep breath to avoid aspirating vomit.
Retroperistalsis, starts from the middle of the small intestine and sweeps up digestive tract contents into the stomach, through the relaxed pyloric sphincter.
Intrathoracic pressure lowers (by inspiration against a closed glottis), coupled with an increase in abdominal pressure as the abdominal muscles contract, propels stomach contents into the esophagus as the lower esophageal sphincter relaxes. The stomach itself does not contract in the process of vomiting except for at the angular notch, nor is there any retroperistalsis in the esophagus.
Vomiting is ordinarily preceded by retching.
Vomiting also initiates an SNS response causing both sweating and increased heart rate.
The neurotransmitters that regulate vomiting are poorly understood, but inhibitors of dopamine, histamine, and serotonin are all used to suppress vomiting, suggesting that these play a role in the initiation or maintenance of a vomiting cycle. Vasopressin and neurokinin may also participate.

PHASES

The vomiting act has two phases. In the retching phase, the abdominal muscles undergo a few rounds of coordinated contractions together with the diaphragm and the muscles used in respiratory inspiration. For this reason, an individual may confuse this phase with an episode of violent hiccups. In this retching phase nothing has yet been expelled. In the next phase, also termed the expulsive phase, intense pressure is formed in the stomach brought about by enormous shifts in both the diaphragm and the abdomen. These shifts are, in essence, vigorous contractions of these muscles that last for extended periods of time - much longer than a normal period of muscular contraction. The pressure is then suddenly released when the upper esophageal sphincter relaxes resulting in the expulsion of gastric contents. Individuals who do not regularly exercise their abdominal muscles may experience pain in those muscles for a few days. The relief of pressure and the release of endorphins into the bloodstream after the expulsion causes the vomiter to feel better.

CONTENTS

Gastric secretions and likewise vomit are highly acidic. Recent food intake appears in the gastric vomit. Irrespective of the content, vomit tends to be malodorous. The content of the vomitus (vomit) may be of medical interest. Fresh blood in the vomit is termed hematemesis ("blood vomiting"). Altered blood bears resemblance to coffee grounds (as the iron in the blood is oxidized) and, when this matter is identified, the term "coffee ground vomiting" is used. Bile can enter the vomit during subsequent heaves due to duodenal contraction if the vomiting is severe. Fecal vomiting is often a consequence of intestinal obstruction or a gastrocolic fistula and is treated as a warning sign of this potentially serious problem ("signum mali ominis"). If the vomiting reflex continues for an extended period with no appreciable vomitus, the condition is known as non-productive emesis or dry heaves, which can be painful and debilitating.

Color of vomit:
Bright red in the vomit suggests bleeding from the esophagus
Dark red vomit with liver-like clots suggests profuse bleeding in the stomach, such as from a perforated ulcer
Coffee ground-like vomit suggests less severe bleeding in the stomach, because the gastric acid has had time to change the composition of the blood
Yellow vomit suggests bile. This indicates that the pyloric valve is open and bile is flowing into the stomach from the duodenum. (This is more common in older people.)

DIFFERENTIAL DIAGNOSIS

Vomiting may be due to a large number of causes, and protracted vomiting has a long differential diagnosis.

DIGESTIVE TRACT

Causes in the digestive tract:
Gastritis (inflammation of the gastric wall)
Gastroenteritis
Pyloric stenosis (in babies, this typically causes a very forceful "projectile vomiting" and is an indication for urgent surgery)
Bowel obstruction
Overeating
Acute abdomen and/or peritonitis
Ileus
Food allergies (often in conjunction with hives or swelling)
Cholecystitis, pancreatitis, appendicitis, hepatitis
Food poisoning
In children, it can be caused by an allergic reaction to cow's milk proteins (Milk allergy or lactose intolerance)

SENSORY SYSTEM AND BRAIN

Causes in the sensory system Movement:
motion sickness (which is caused by overstimulation of the labyrinthine canals of the ear) Ménière's disease Causes in the brain Concussion Cerebral hemorrhage Migraine Brain tumors, which can cause the chemoreceptors to malfunction Benign intracranial hypertension and hydrocephalus Metabolic disturbances (these may irritate both the stomach and the parts of the brain that coordinate vomiting) Hypercalcemia (high calcium levels) Uremia (urea accumulation, usually due to renal failure) Adrenal insufficiency Hypoglycemia Hyperglycemia Pregnancy Hyperemesis, Morning sickness Drug reaction (vomiting may occur as an acute somatic response to) alcohol (being sick while being drunk or being sick the next morning, suffering from the after-effects, i.e., the hangover). opioids selective serotonin reuptake inhibitors many chemotherapy drugs some entheogens (such as peyote or ayahuasca) Illness (sometimes colloquially known as "stomach flu"—a broad name that refers to gastric inflammation caused by a range of viruses and bacteria.) Norovirus (Formerly Norwalk virus or Norwalk agent) Swine Flu

EMETICS

An emetic, such as syrup of ipecac, is a substance that induces vomiting when administered orally or by injection. An emetic is used medically where a substance has been ingested and must be expelled from the body immediately (for this reason, many toxic and easily digestible products such as rat poison contain an emetic). Inducing vomiting can remove the substance before it is absorbed into the body. Ipecac abuse can cause detrimental health effects. Salt water and mustard water have been used since ancient times as emetics. Care must be taken with salt, as excessive intake can potentially be harmful. Copper sulfate was also used in the past as an emetic. It is now considered too toxic for this use.

SOCIAL CUES

It is quite common that, when one person vomits, others nearby become nauseated, particularly when smelling the vomit of others, often to the point of vomiting themselves. It is believed that this is an evolved trait among primates. Many primates in the wild tend to browse for food in small groups. Should one member of the party react adversely to some ingested food, it may be advantageous (in a survival sense) for other members of the party also to vomit. This tendency in human populations has been observed at drinking parties, where excessive consumption of alcoholic beverages may result in a number of party members vomiting nearly simultaneously, this being triggered by the initial vomiting of a single member of the party. This phenomenon has been touched on in popular culture: Notorious instances appear in the films Monty Python's The Meaning of Life (1983) and Stand By Me(1986). Intense vomiting in ayahuasca ceremonies is a common phenomenon. However, people who experience "la purga" after drinking ayahuasca, in general, regard the practice as both a physical and spiritual cleanse and often come to welcome it. It has been suggested that the consistent emetic effects of ayahuasca — in addition to its many other therapeutic properties — was of medicinal benefit to indigenous peoples of the Amazon, in helping to clear parasites from the gastrointestinal system. There have also been documented cases of a single ill and vomiting individual inadvertently causing others to vomit, when they are especially fearful of also becoming ill, through a form of mass hysteria. Most people try to contain their vomit by vomiting into a sink, toilet, or trash can, as both the act and the vomit itself are widely considered embarrassing; vomit is also difficult and unpleasant to clean. An instance of this occurred in the 2001 film 61* when Mickey Mantle (Thomas Jane) vomited into a pail in the trainer's room at Yankee Stadium while hung over after a wild night on the town. On airplanes and boats, special bags are supplied for sick passengers to vomit into. A special disposable bag containing absorbent material that solidifies the vomit quickly is available, also, making it convenient and safe to keep (leakproof, puncture-resistant, odorless) until there is an opportunity to dispose of it conveniently. People who vomit chronically (e.g., as part of an eating disorder such as bulimia nervosa) may devise various ways to hide this disorder. An online study of people's responses to "horrible sounds" found vomiting "the most disgusting." Professor Cox of the University of Salford's Acoustic Research Centre said that "We are pre-programmed to be repulsed by horrible things such as vomiting, as it is fundamental to staying alive to avoid nasty stuff." It is thought that disgust is triggered by the sound of vomiting to protect those nearby from, possibly diseased, food.

MISCELLANEA

Self-induced
Eating disorders (anorexia nervosa or bulimia nervosa)
To eliminate an ingested poison (some poisons should not be vomited as they may be more toxic when inhaled or aspirated; it is better to ask for help before inducing vomiting)
Some people who engage in binge drinking induce vomiting to make room in their stomachs for more alcohol consumption. People suffering from nausea may induce vomiting in hopes of feeling better.
After surgery (postoperative nausea and vomiting)
Disagreeable sights or disgust, smells or thoughts (such as decayed matter, others' vomit, thinking of vomiting), etc.
Extreme pain, such as intense headache or myocardial infarction (heart attack)
Violent emotions
Cyclic vomiting syndrome (a poorly understood condition with attacks of vomiting)
High doses of ionizing radiation sometimes trigger a vomit reflex.
Violent fits of coughing, hiccups, or asthma
Anxiety
Depression
Overexertion (doing too much strenuous exercise can lead to vomiting shortly afterwards).
Rumination syndrome, an underdiagnosed and poorly understood disorder that causes sufferers to regurgitate food shortly after ingestion.

OTHER TYPES

Fecal vomiting (aka stercoraceous vomiting) is a kind of vomiting, or emesis, in which partially or fully digested matter is expelled from the intestines into the stomach, by a combination of liquid and gas pressure and spasmodic contractions of the gastric muscles, and then subsequently forcefully expelled from the stomach up into the esophagus and out through the mouth and sometimes nasal passages. Though it is not usually fecal matter that is expelled[citation needed], it smells noxious. Alternative medical terms for fecal vomiting are copremesis and stercoraceous vomiting. Copremesis like all emesis may lead to aspiration. However, if contents of the large intestine are aspirated, severe or even fatal aspiration pneumonia results, secondary to the massive number of bacteria normally present distal to the ileocecal valve.[citation needed] Projectile vomiting refers to vomiting that ejects the gastric contents with great force. It is a classic symptom of infantile hypertrophic pyloric stenosis, in which it typically follows feeding and can be so forceful that some material exits through the nose.

TREATMENT

An antiemetic is a drug that is effective against vomiting and nausea. Antiemetics are typically used to treat motion sickness and the side-effects of medications such as opioids and chemotherapy. Antiemetics act by inhibiting the receptor sites associated with emesis. Hence, anticholinergics, antihistamines, dopamine antagonists, serotonin antagonists, and cannabinoids are used as anti-emetics.

EPIDEMIOLOGY

Nausea and or vomiting is the main complaint in 1.6% of visits to family physicians in Australia.

For more information view the source:Wikipedia

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Skin disease	Symptoms	Usual area of body
Acne Vulgaris	Comedones, papules, pustules and nodules.	Face, chest and back.
Acne Rosacea	Flushed appearance or redness.	Cheeks, chin, forehead or nose.
Boil	Painful red bump or a cluster of painful red bumps	Anywhere
Cellulitis	Red, tender and swollen areas of skin	Around a cut, scrape or skin breach
Insect bite	Red and/or itchy bumps on the skin	Anywhere and can be sprinked randomly
Allergic reaction	Irregular, raised or flat red sores that appeared after taking medicine/drugs or eating certain foods	Anywhere
Hives	Bumps formed suddenly	Anywhere but usually first noticed on face
Seborrheic dermatitis	Bumps and swelling	Near glands
Cradle Cap	Dry, scaly skin	Scalp of recently born babies
Irritant contact dermatitis	Red, itchy, scaly or oily rash	Eyebrows, nose, edge of the scalp, point of contact with jewellery, perfume or clothing.
Allergic Contact Dermatitis caused by poison ivy, poisen oak or sumac	Red, itchy, scaly or oily rash; can also be weeping or leathery.	Anywhere that came in contact with the irritant either directly or via transfer (e.g. from contaminated clothing.)
Allergic purpura	Small red dots on the skin, or larger, bruise-like spots that appeared after taking medicine	Anywhere
Pityriasis Rosea	Started with a single scaly, red and slightly itchy spot, and within a few days, did large numbers of smaller patches of the rash, some red and/or others tan	Chest and abdomen
Dermatitis herpetiformis	Intensely itchy rash with red bumps and blisters	Elbows, knees, back or buttocks
Erythema nodosum	Large red bumps that seem to bruise and are tender to touch	Anywhere
Psoriasis	White, scaly rash over red, flaky, irritated skin	Elbows and knees
Erythema multiforme	Red, blotchy rash, with "target like" hives or sores.	Anywhere
Measles	Red rash that is raised with a fever or sore throat.	Usually starts first on the forehead and face and spreads downward.
Chickenpox	Multiple blisters with a fever, cough, aches, tiredness and sore throat.	Usually starts first on the face, chest and back and spreads downward.
Shingles	Red blisters that are very painful and may crust	Anywhere
Fifth Disease	Started as a fever and then developed a bright red rash	Cheeks
Warts	Soft bumps forming that don't itch and have no other symptoms	Anywhere
Ringworm	Bald spot on the scalp or a ring of itchy red skin	Anywhere
Syphilis	Rash that is red but not itchy	Palms of hands or soles of feet
Jock itch, yeast infection or diaper rash	Red itchy rash	Groin
Tinea versicolor	Light coloured patches	Anywhere
Impetigo	Crusted, tan-colored sores	Near nose or lip
Scabies	Bite-like sores that itch and spread intensely	Usually start on hands or feet and spread everywhere
Rocky Mountain spotted fever	A fine rash with a fever and headache	Usually start on arms and legs including the hands and feet
Lupus erythematosus	A butterfly rash with achy joints	Forehead and cheeks
Jaundice or sign of hepatitis	Yellowish	Skin, whites of eyes and mouth
Bruise	Blue or black area after being hit	Anywhere
Actinic keratoses	Scaly, pink, gray or tan patches or bumps	Face, scalp or on the backs or the hands
Keloid or hypertrophic scar	Scar that has grown larger than expected	Anywhere
Lipoma	Soft or rubbery growth	Anywhere
Milia	Lots of white spots	On the face of a baby
Molluscum or contagiosum	Small, firm, round bumps with pits in the center that may sit on tiny stalks	Anywhere
Scarlet Fever	Becomes confluent and forms bright red lines in the skin creases of the neck, armpits and groins (Pastia's lines)	Face, chest & back, whole body, armpits, inside elbows, groins
Sebaceous cyst	Bump with a white dome under the skin	Scalp, nape of the neck or upper back
Skin tag	Soft, fleshy growth, lump or bump	Face, neck, armpits or groin
Xanthelasma	Yellow area under the skin	Under eyelids
Melanoma	Dark bump that may have started within a mole or blemish, or, a spot or mole that has changed in color, size, shape or is painful or itchy	Anywhere
Basal cell carcinoma	Fleshy, growing mass	Areas exposed to the sun
Squamous cell carcinoma	Unusual growth that is red, scaly or crusted	Face, lip or chin
Kaposi's sarcoma	Dark or black raised spots on the skin that keep growing or have appeared recently	Anywhere
Erythema annulare centrifugum (EAC)	Pink-red ring or bullseye marks	Anywhere

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FAQs

What is Balantidium coli?

Where is Balantidium coli endemic?

How is Balantidium coli transmitted?

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How can I prevent Balantidium coli?

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**Where is Balantidium coli endemic?**

**How is Balantidium coli transmitted?**

**Is there a test for Balantidium coli infection?**

**How can I prevent Balantidium coli?**