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Toxoplasmosis is a disease caused by the protozoan parasite Toxoplasma gondii (T. gondii). T. gondii is commonly found in backyard and free range chickens worldwide. However, clinical disease rarely occurs in chickens, and they are generally considered to be resistant to clinical toxoplasmosis. There have only been a few documented reports of clinical toxoplasmosis in chickens.
Felids (wild and domestic cats, bobcats, ocelots, pumas, and Asian leopards) are an essential part of the life cycle of T. gondii. Therefore, domestic cats are frequently infected with the organism, and will shed it's eggs (called oocysts) in their feces (by the millions), contaminating the surrounding environment. T. gondii oocysts are very hardy and will remain in the environment for years---well after the cat's feces has decomposed. Chickens become infected by ingestion of these oocysts from the environment.
Documented Toxoplasmosis Outbreaks in Chickens
Three out of a flock of 14 backyard chickens were infected with T. gondii in Illinois. The observed clinical signs were: torticollis (wry neck), inability to stand and lateral recumbency prior to death. The remaining 11 flock members showed no signs of disease.
Case 1: Toxoplasmosis in a Geese Fatal disseminated Toxoplasma gondii infection was diagnosed in 2 captive magpie geese from a zoo in Texas. Both geese died suddenly, without apparent clinical signs. Lesions associated with T. gondii tachyzoites were seen in lungs, pancreas, liver, adrenals, bursa of Fabricius, spleen, brain, and kidneys. Toxoplasmic pneumonia and hepatitis were considered to be the primary cause of death. An unusual feature was the presence of numerous tissue cysts in hepatocytes of both geese. The diagnosis was confirmed immunohistochemically. Antibodies to T. gondii were found in 2 of 11 other geese from the zoo examined using the modified agglutination test. Ref
Case 2: Toxoplasmosis in a Mixed backyard Three chickens on a farm in Illinois developed neurological signs. One of these chickens was examined postmortem and it had non-suppurative encephalitis with numerous Toxoplasma gondii tachyzoites and tissue cysts. The identity of the protozoa was confirmed immunohistochemically by staining with T. gondii specific antibodies, and by transmission electron microscopy. Viable T. gondii was isolated from all tissues. Ref
Case 3: Toxoplasmosis in a Red lory Toxoplasmosis was diagnosed in a 3-week-old red lory. Grossly, there was hepatomegaly and pulmonary consolidation. The salient microscopic lesions were multifocal necrotizing mycocarditis, interstitial pneumonia with multifocal necrosis and vasculitis, and multifocal necrotizing hepatitis with periacinar hepatocellular necrosis. Toxoplasma gondii-like organisms were observed in lung, heart, and liver by light and electron microscopy. The organisms in tissues stained with anti-T. gondii serum using an immunohistochemical method. Ref
Case 4: Toxoplasmosis in a Guinea fowl Two of seven birds lost out of approximately 20 guinea fowl present in a flock in the United States were diagnosed with toxoplasmosis. Birds reportedly exhibited lethargy prior to death. Necropsy examinations were performed on two of the dead birds. There were no gross lesions; however, intralesional protozoan cysts suggestive of T. gondii were observed microscopically. One of two guinea fowl demonstrated dramatic microscopic pathology consisting of variable multifocal necrosis, fibrin exudation, and inflammation of spleen, lung, and heart associated with protozoa cysts and tachyzoites compatible with toxoplasmosis. The bone marrow also exhibited multifocal necrosis and fibrin exudation, as well as marked erythroid and lesser granulocytic hyperplasia with intralesional protozoan cysts. The diagnosis of toxoplasmosis was confirmed with immunohistochemistry and PCR. Ref
Case 5: Toxoplasmosis in a Chickens and guinea fowl 22 of a flock of 47 domestic chickens and 29 guinea fowl in Brazil started showed clinical signs of lethargy, anorexia, and neurological signs over a clinical course of 24-72 h, and 15 died. Epidemiological data were obtained through fieldwork performed at the chicken farm and necropsies of six birds. Gross lesions were absent at necropsy, and histopathological findings included inflammatory infiltrate of macrophages, lymphocytes, and plasma cells and necrosis in several tissues associated with intralesional Toxoplasma gondii. Immunohistochemistry for T. gondii was positive. Additionally, restriction fragment length polymorphism (RFLP) analysis with 11 markers (SAG1, SAG2 (5'3'SAG2 and alt. SAG2), SAG3, BTUB, GRA6, c22-8, c29-2, L358, PK1, Apico, and CS3) and microsatellite (MS) analysis with 15 markers (TUB2, W35, TgMA, B18, B17, M33, IV.1, XI.1, N60, N82, AA, N61, N83, M48, and M102) were performed. PCR-RFLP revealed T. gondii genotype ToxoDB-PCR-RFLP #280, and MS analysis also showed a unique genotype. Ref