TOXOPLASMOSIS Outli nes Objective TOXOPLASMOSIS Epidemiology Life Cycle and Diagnosis, Prevention and Control Exercise on Topic Learning Outcomes References TOXOPLASMOSIS Toxoplasmosis is a parasitic disease caused by Toxoplasma gondii. Toxoplasmosis is usually spread by eating poorly cooked food that contains cysts, exposure to infected cat feces, and from an infected mother to her baby during pregnancy. Rarely, the disease may be spread by blood transfusion. It can be found in cat feces and undercooked meat, especially venison, lamb, and pork. It can also be transmitted through contaminated water. Toxoplasmosis can be deadly or cause serious birth defects for a fetus if the mother becomes infected. The only known definitive hosts for Toxoplasma gondii are members of family Felidae (domestic cats and their relatives). Unsporulated oocysts are shed in the cat’s feces SYMPTOMS Most people who have toxoplasmosis never have any symptoms at all. People who develop symptoms may experience:a) a fever b) swollen lymph nodes, especially in the neck c) a headache d) muscle aches and pains e) sore throat These symptoms can last for a month or more and usually resolve on their own. Toxoplasmosis is especially serious for people who have weakened immune systems. For these people, they’re at risk of developing:a) Brain inflammation, causing headaches, seizures, confusion and coma. b) a lung infection, causing cough, fever, and shortness of breath c) An eye infection, causing blurry vision and eye pain. TRANSMISSIONS:- a) Drinking contaminated water. b) In rare cases, toxoplasmosis may be transmitted through a blood transfusion or a transplanted organ. c) Congenital transmittance from mother to fetus can also occur. d) Transmission may also occur during the solid organ transplant processor hematogenous stem cell transplants. e) Ingestion of raw or partly cooked meat, especially pork, lamb, or venison containing Toxoplasma cysts: Infection prevalence in countries where undercooked meat is traditionally eaten has been related to this transmission method. Tissue cysts may also be ingested during hand-to-mouth contact after handling undercooked meat, or from using knives, utensils, or cutting boards contaminated by raw meat. f) Ingestion of unwashed fruit or vegetables that have been in contact with contaminated soil containing infected cat feces. g) Ingestion of cat feces containing oocysts: This can occur through hand-to-mouth contact following gardening, cleaning a cat's litter box, contact with children's sandpits; the parasite can survive in the environment for months. h) Ingestion of untreated, unfiltered water through direct consumption or utilization of water for food preparation. i) Ingestion of unpasteurized milk and milk products, particularly goat's milk. j) Ingestion of raw seafood. k) Exposure to infected cat feces PATHOGENESIS: - Most cases of toxoplasmosis in humans are probably acquired by the ingestion of either tissue cysts in infected meat or oocysts in food contaminated with cat feces. Bradyzoites from the tissue cysts or sporozoites released from oocysts penetrate the intestinal epithelial cells and multiply in the intestine. Toxoplasma gondii may spread both locally to mesenteric lymph nodes and to distant organs by invading the lymphatics and blood. Necrosis in intestinal and mesenteric lymph nodes may occur before other organs become severely damaged. Focal areas of necrosis may develop in many organs. The clinical picture is determined by the extent of injury to these organs, especially to vital and vulnerable organs such as the eye, heart, and adrenals. Toxoplasma gondii does not produce a toxin; necrosis is caused by intracellular multiplication of tachyzoites. Control/ Prophylaxis/treatment: - Sulfonamides and pyrimethamine (Daraprim) are two drugs widely used to treat toxoplasmosis in humans. They act synergistically by blocking the metabolic pathway involving p-aminobenzoic acid and the folic-folinic acid cycle, respectively. These two drugs usually are well tolerated by the patient, but sometimes thrombocytopenia, leukopenia, or both may develop. These effects can be overcome without interrupting treatment by administering folinic acid because the vertebrate host can utilize presynthesized folinic acid, whereas T gondii cannot. The commonly used sulfonamides, sulfadiazine, sulfamethazine, and sulfamerazine, are all effective against toxoplasmosis. Generally, any sulfonamide that diffuses across the host cell membrane is useful in antitoxoplasmid therapy. Although these drugs are helpful when given in the acute stage of the disease, usually they will not eradicate infection when active multiplication of the parasite occurs. Because sulfa compounds are excreted within a few hours of administration, they must be administered in daily divided doses. Spiramycin, a drug used in France to treat pregnant women to minimize the effects of congenital toxoplasmosis, is not approved for toxoplasmosis in the United States. As yet, there are no effective drugs to kill tissue cysts. No killed vaccine is currently available to reduce or prevent congenital infections in humans and animals, but a live vaccine using a nonpersistent T gondii strain is available in Europe and New Zealand to reduce abortion in sheep. To prevent T gondii infection, several precautions should be taken. Meat should be cooked to 66°C throughout before eating. Hands should be washed with soap and water after handling meat. Raw meat should never be fed to cats; only dry or canned food or cooked meat should be fed. Cats should be kept indoors and litter boxes changed daily. Cat feces should be flushed down the toilet or burned. Litter pans should be cleaned by immersing them in boiling water. Gloves should be used while working in the garden. Children's sandboxes should be covered when not in use References Baer GM. (ed): The Natural History of Rabies. CRC Press, Boca Raton, 1991 . Campbell JB, Charlton KM (eds): Rabies. Kluwer Acad Publ, Boston, 1988 . Centers for Disease Control: Rabies prevention — United States, 1991. Recommendations of the Immunization Practices Advisory Committee (ACIP). MMWR 40 (RR-3): 1, 1991 . [PubMed] Centers for Disease Control: Compendium of animal rabies control, 1995. MMWR 44 (RR-2): 1, 1995 . [PubMed] Dietzschold B, Kao M, Zheng YM. et al. Delineation of putative mechanisms involved in antibody-mediated clearance of rabies virus from the central nervous system. Proc Natl Acad Sci USA. 1992;89:7252. [PMC free article] [PubMed] Krebs JW, Strine TW, Smith JS. et al. Rabies surveillance in the United States during 1993. J Am Vet Med Assoc. 1994;205:1695. [PubMed] Rupprecht CE, Smith JS. Raccoon rabies: the re-emergence of an epizootic in a densely populated area. Sem Virol. 1994;5:155. Smith JS, Orciari LA, Yager PA. et al. Epidemiologic and historical relationships among 87 rabies virus isolates as determined by limited sequence analysis. J Infect Dis. 1992;166:296. [PubMed] Winkler WG, Bogel K. Control of rabies in wildlife. Sci Am. 1992;266:86. [PubMed] World Health Organization Expert Committee on Rabies: 8th Report. WHO Technical Report Series no. 824.