Toxoplasmosis

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Toxoplasmosis is an infection with Toxoplasma gondii. Symptoms range from a lack of up to a benign lymphadenopathy (a mononucleosis-like disease) or a life-threatening CNS disease or involvement of other organs in immunocompromised people. Encephalitis can develop in patients with AIDS and low CD4 counts. In congenital infection may lead to a retinochoroiditis, seizures and mental retardation. The diagnosis is made by serologic tests, histology, or PCR. Treatment is usually with pyrimethamine plus either sulfadiazine or clindamycin. In a retinochoroiditis additional corticosteroids are given.

A human exposure to Toxoplasma occurs everywhere often where there are cats; an estimated 15% of US residents are seropositive. The risk of disease, however, is very low, except for fetuses infected in utero, and people who are immune compromised or are.

Toxoplasmosis is an infection with Toxoplasma gondii. Symptoms range from a lack of up to a benign lymphadenopathy (a mononucleosis-like disease) or a life-threatening CNS disease or involvement of other organs in immunocompromised people. Encephalitis can develop in patients with AIDS and low CD4 counts. In congenital infection may lead to a retinochoroiditis, seizures and mental retardation. The diagnosis is made by serologic tests, histology, or PCR. Treatment is usually with pyrimethamine plus either sulfadiazine or clindamycin. In a retinochoroiditis additional corticosteroids are given. A human exposure to Toxoplasma occurs everywhere often where there are cats; an estimated 15% of US residents are seropositive. The risk of disease, however, is very low, except for fetuses infected in utero, and people who are immune compromised or are. Pathophysiology T. gondii is ubiquitous in birds and mammals. It is an obligate intracellular pathogen that reproduces asexually in the form of tachyzoites within the cytoplasm of nucleated cells. (. Life cycle of Toxoplasma gondii) develops an immune response of the host, the proliferation of tachyzoites comes to a standstill, and are formed tissue cysts; the cysts persist at rest for years, particularly in the brain and muscles. The ruhendne Toxoplasma forms within the cysts are called Bradyzoites. Sexual reproduction of T. gondii occurs only in the digestive tract of cats; the oocysts produced are excreted in the feces and can remain infectious in moist soil for months. Life cycle of Toxoplasma gondii. The only known definitive hosts for T. gondii are members of the family Felidae (cats and their relatives). 1a. Oocysts are shed in cat feces. High numbers are repelled, but usually only for 1-2 weeks. Oocysts need 1-5 days to become infectious. 1b. Cats be reinfected by the inclusion of sporulated oocysts. 2. soil, water, plant material or cat litter contaminated with oocysts. Intermediate hosts in nature (eg. As birds, rodents, wild, animals that are bred for human consumption), after the inclusion of infected materials (uncooked or poorly cooked meat, contaminated with cat feces, which is older than 48 hours) infected. 3. oocysts develop shortly after admission to tachyzoites. 4. tachyzoites may spread in the body and form tissue cysts in neural and muscle tissue. 5. Cats become infected after ingestion of intermediate hosts containing tissue cysts. 6a. People can infect by eating not completely undercooked meat containing tissue cysts. 6b. People can by the ingestion of food or water contaminated with cat feces or by the inclusion of materials (eg., Ground), which are contaminated with feces or other infected by contact with cat litter. 7. Rarely, human infections through blood transfusions or organ transplants. 8. Rarely occurs transplacental transmission from the mother to the fetus. 9. In the human host parasites form tissue cysts, most commonly in skeletal muscle, the myocardium, the brain and the eyes. These cysts can persist throughout the life of the host and reactivate when the host is immunocompromised. An infection can occur by ingestion of oocysts receiving tissue cysts The transplacental transmission is unusual. Blood transfusion or organ transplantation The most common type of infection is oral intake of oocysts from cat feces with contaminated food or water. However, an infection can also occur by eating raw or not fully-cooked, gewebezystenhaltigem meat, usually lamb, pork, rarely beef. After taking oocytes or tissue cysts tachyzoites are released and spread throughout the body. This acute infection is followed by the development of a protective immune response and the formation of tissue cysts in many organs. The cysts can reactivate, primarily in immunocompromised patients. Toxoplasmosis reactivated at 30-40% of AIDS -Patients who are not taking adequate prophylaxis, the widespread use of trimethoprim-sulfamethoxazole for Pneumocystis prophylaxis has led to a dramatic decline in incidence. Toxoplasmosis can be transmitted placenta when the mother becomes infected during pregnancy or if a previous infection is reactivated by immunosuppression. The transmission of Toxoplasma to a fetus is in immunocompetent women who were previously infected with toxoplasmosis, extremely rare. A transfer may be by transfusion of whole blood units or leukocytes, or by transplantation of an organ from a seropositive donor. In otherwise healthy people, it can lead to reactivation of a congenital or acquired infection in the retina. A previously resolved infection protects against reinfection. Symptoms and complaints infections can manifest themselves in different ways. Acute toxoplasmosis CNS toxoplasmosis Congenital toxoplasmosis Ocular toxoplasmosis Disseminated diseases or diseases outside the CNS in immunocompromised patients acute toxoplasmosis Acute infection is usually asymptomatic, but 10-20% of patients develop bilateral, insensitive cervical or axillary lymphadenopathy. A few of them also have easy flu-like syndrome of fever, malaise, myalgia, hepatosplenomegaly, and less commonly, pharyngitis, which can mimic an infectious mononucleosis. There is often an atypical lymphocytosis, mild anemia, leukopenia, and mildly elevated liver enzymes. The syndrome can persist for weeks, but usually runs selbstlimitierend.ZNS toxoplasmosis Most patients with AIDS or other immune compromised patients who develop toxoplasmosis, present with encephalitis and a ring-reinforced intracranial mass lesion. The risk is greatest in people with a CD4 count <50 / ul; Toxoplasma encephalitis is rare when the CD4 count is> 200 / ul. In these patients are usually headache, altered mental status, seizures, coma, fever and sometimes focal neurological deficits such as motor or sensory loss, cranial nerve paralysis, blurred vision and partial seizures vor.Kongenitale toxoplasmosis This form is based on an acquired by the mother during pregnancy primary (often asymptomatic) infection. Women who have been infected before fertilization transferred, usually no Toxoplasma to the fetus as long as the infection is not reactivated by one place during pregnancy immunosuppression. There may be spontaneous abortions, stillbirths and birth defects. The percentage of surviving born with toxoplasmosis fetus depends on when the maternal infection was acquired; it increases by 15% in the 1st trimester up to 30% during the 2nd and up to 60% in 3.Trimester. Diseases in newborns can, especially if they are acquired in early pregnancy, lost heavily. Symptoms include jaundice, rash, hepatosplenomegaly and the characteristic tetrad of abnormalities: bilateral retinochoroiditis, cerebral calcifications, hydrocephalus or microcephaly and psychomotor retardation. The prognosis is unfavorable. Many children with a less severe infection and most children of mothers who were infected in the third trimester of pregnancy, appear healthy at birth, but are at high risk, months or even years and decades later, seizures, mental retardation, retinochoroiditis or other symptoms entwickeln.Okuläre toxoplasmosis This form occurs mostly through a reactivated congenital infection into existence, often during the teenage age, and at 20 years of age, but rarely occurs in an acquired infection. Focal necrotizing retinitis and a secondary granulomatous inflammation of the choroid occur and can lead to eye pain, blurred vision and sometimes blindness. Relapses are häufig.Disseminierte infection outside the CNS diseases outside the eye and central nervous system are far less common and occur mainly in severely immunocompromised patients. They may be associated with pneumonia, myocarditis, polymyositis, diffuse maculopapular rash, high fever, chills and fatigue. In a toxoplasmosis pneumonitis diffuse interstitial infiltrates can cause a rapidly progressive consolidation and respiratory failure, while a endarteritis may cause infarction of small lung segments. Myocarditis, in which frequently occur mostly asymptomatic conduction disturbances can rapidly lead to cardiac insufficiency. Untreated disseminated infections are usually fatal. Diagnosis Serological tests At CNS involvement, CT or MRI and lumbar puncture The diagnosis is usually made serologically by an indirect fluorescent antibody (IFA) test or enzyme immunoassay (EIA) for IgG and IgM antibodies (see table: interpretation of serological tests of Toxoplasma *). During the first 2 weeks of an acute disease-specific IgM antibodies, however, reach its highest value within 4-8 weeks and ultimately fall below the detection limit, may remain detectable for up to 18 months after an acute infection appear. IgG antibodies more slowly rise, reach after 1-2 months to max and can remain high and stable for months to years. Assays for Toxoplasma IgM lacks specificity. Interpretation of serological tests of Toxoplasma * IgG IgM Interpretation Negative Negative No evidence of infection negative questionable Maybe early infection or false-positive IgM result Negative Positive Maybe acute infection or false-positive IgM results Questionable negative Undecided questionable questionable Undecided questionable positive acute infection may Hated It infection for> 1 year positive questionable infection possibly for> 1 year or false positive IgM results may Positive Positive recent infection in the last 12 months or false-positive IgM result * Except in infants Adapted by Centers for Disease Control and Prevention (CDC): Toxoplasmosis: Antibody detection. Available on http://www.cdc.gov/dpdx/toxoplasmosis/dx.html; called last January 24, 2014. The diagnosis of acute toxoplasmosis during pregnancy and the fetus or newborn can be difficult, and it is recommended with an expert consultation. If the patient is pregnant and IgG and IgM positive, IgG avidity test should be performed. High avidity antibody in the first 12-16 weeks of pregnancy include essentially of an acquired infection during pregnancy. But a low IgG Aviditätsergebnis can not be interpreted as indicating a recent infection, as some patients have a persistent low IgG avidity for many months after infection. The suspected recent infection in a pregnant woman should be confirmed before an intervention by tests in a reference laboratory for toxoplasmosis. If the patient has a clinical disease, corresponding to a toxoplasmosis, but the IgG titer is low, 2-3 weeks later should a subsequent titers show an increase in antibody titer when the disease was caused by an acute toxoplasmosis, unless , the host is severely immune compromised. In general, the detection of specific IgM antibodies in newborns suggests a congenital infection. Maternal IgG antibodies cross the placenta but IgM antibodies do not. The detection of toxoplasmaspezifischen IgA antibodies is more sensitive in congenitally infected neonates as IgM. It is available only with special reference laboratories and it is usually necessary that the IgA antibodies are requested with the clinical request specifically and explicitly. An expert should be consulted if a fetal or congenital infection is suspected. Toxoplasma can occasionally be detected histologically. Tachyzoites that are present during acute infection, take the dyes at a Giemsa or Wright stain, but can be hard to find in routine tissue sections. The detection of tissue cysts not allowed the differentiation between an acute and a chronic infection. Toxoplasma needs of other intracellular pathogens such. be as Histoplasma, Trypanosoma cruzi and Leishmania, distinguished. In various reference laboratories PCR-based DNA evidence of parasites from blood, cerebrospinal fluid or amniotic fluid are available. The preferred method for the diagnosis of toxoplasmosis during pregnancy, the PCR-based analysis of amniotic fluid. In suspected CNS -Toxoplasmose should in the patients an MRI, a CT with contrast or both, and in addition a lumbar puncture lumbar puncture (spinal tap) is performed if no evidence of increased intracranial pressure are present. The MRI is more sensitive than CT. MRI and CT typically have single or multiple round, ring enhanced lesions. Although these lesions are not pathognomonic, is their presence in AIDS patients with CNS symptoms is an indication for chemotherapy against T. gondii. The CSF may be positive for lymphocytic pleocytosis and the protein level may be increased. An acute infection should be suspected in immunocompromised patients if the IgG is positive. However, in AIDS patients with toxoplasmosis encephalitis IgG antibody levels are usually low to medium high and IgG antibodies sometimes lacking; IgM antibodies are not present. When the suspected diagnosis of toxoplasmosis is correct, it should come within 7-14 days to a clinical and radiological improvement. If symptoms get worse in the first week or not improve until the end of the second week, a brain biopsy should be considered. An eye disease is diagnosed based on the appearance of the eye lesions, symptoms, course of disease and the results of serological tests. Therapy pyrimethamine plus. Sulfadiazine (if the treatment is indicated) no treatment is required in most immunocompetent patients when no visceral disease is present or persist severe symptoms. No specific therapy is, however, indicated for acute toxoplasmosis in newborns, pregnant women and immunocompromised patients. The most effective treatment in immunocompetent patients is pyrimethamine plus. Sulfadiazine. The dosage of pyrimethamine is 100 mg on Day 1, then 25 to 100 mg of 1 times a day for 2-4 weeks in adults (2 mg / kg po for 2 days, then 1 mg / kg 1 times daily in children, maximum 25 mg daily). The dosage for sulfadiazine is 1-1.5 g p.o. 4 times a day in adults for 2-4 weeks (25-50 mg / kg four times daily in children). Higher doses of pyrimethamine are used in HIV-infected patients with CNS toxoplasmosis. A loading dose of 200 mg pyrimethamine is administered on the first day, then 50-100 mg daily plus sulfadiazine for at least 6 weeks. In patients who have or develop a hypersensitivity to sulfonamide clindamycin is 600 to 800 mg po 3 times daily given with pyrimethamine instead sulfonamide. Another option is atovaquone 1500 mg every 12 hours plus pyrimethamine. Antiretroviral treatment should be optimized in patients with AIDS. Relapses of toxoplasmosis are common in patients with AIDS and a suppressive therapy should be continued indefinitely until the CD4 count rises and> 200 / ul stays and patients remain symptom free. A bone marrow suppression caused by pyrimethamine may by leucovorin (also called folinic acid, but not folic acid or folate, which would antagonize the therapeutic effect of pyrimethamine) should be minimized, but the complete blood counts should be monitored weekly. The dosage is 10-25 mg p.o. 1 times daily (7.5 mg in children). Patients with ocular toxoplasmosis also be administered corticosteroids. The treatment of pregnant women with primary infection can reduce the incidence of fetal infection. In pregnant women in the first trimester of pregnancy Spiramycin 1 g p.o. applied three times or four times a day to reduce a transmission safe (available from the FDA [telephone 301-827-2335]), but is less effective than spiramycin pyrimethamine plus. sulfonamide and does not cross the placental barrier. Spiramycin is passed until the end of the first trimester detected fetal infection or excluded. If it has not come to a transmission, spiramycin can be continued until birth. If the fetus is infected, pyrimethamine administered excl. Sulfadiazine. Pyrimethamine is a potent teratogen and should not be used in the first trimester. The consultation of an expert in infectious diseases is recommended. Congenitally infected infants should be treated with pyrimethamine and sulfadiazine every 2-3 days 1 times a day for one year. Small children should also during the administration of pyrimethamine leucovorin received and for 1 wk. after pyrimethamine was stopped, to prevent bone marrow suppression. Prevention is important to have a thorough hand washing (preferably a hygienic hand disinfection) after handling of raw meat, ground or from cat litter. Foods that may have been potentially contaminated with cat feces should be avoided. Meat should to about 73.9 ° -76.7 ° C are heated (165 ° -170 ° F). Chemoprophylaxis is recommended for HIV-positive patients with IgG-positive T. gondii serology test if the number of CD4 + cells drops to <100 / ul. One tablet double-strength trimethoprim / sulfamethoxazole 1 times a day, which is also prophylactically against Pneumocystis jirovecii is recommended. (Editor's note: The permanent dosage is 3-4 tablets cotrimoxazole forte [800/160 mg] per week, so for example, a tablet, depending on the days Monday, Wednesday and Friday..) A tablet of double thickness 3 times a week is an alternative. If the patient trimethoprim-sulfamethoxazole can not tolerate dapsone plus pyrimethamine and leucovorin is recommended. Atovaquone with or without pyrimethamine and leucovorin can also be used. Chemoprophylaxis continues until the CD4 counts are> 200 / ul for ? 3 months. Important points T. gondii reproduces only in the intestinal tract of cats; most infections result from direct or indirect contact with cat feces, but they can also be purchased through the placenta from mother to child or through the ingestion of poorly cooked meat containing cysts. About 15% of the US population have been infected, but symptomatic disease is rare and occurs mainly in fetuses infected in the womb, and in people who are immunocompromised, on. Acute infection is usually asymptomatic, but 10-20% of patients have manifestations similar to those of mononucleosis. Immunocompromised patients present with encephalitis usually before and have reinforced ring intracranial lesions, which can be seen on MRI or CT. The diagnosis is made by serological tests (on IgG-and IgM antibodies), histology, or PCR. Especially for newborns, pregnant women and immunocompromised Patiente treatment is indicated; Pyrimethamine plus sulfadiazine is used.

Health Life Media Team

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