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Atoxoplasmosis is a parasitic disease primarily of passerine birds, especially canaries, finches, sparrows, grosbeaks, starlings, and mynahs.

It is caused by species of the coccidian protozoan Atoxoplasma, a host-specific parasite. Atoxoplasmaserini, the species found in canaries, is not infectious to sparrows; likewise, the species infecting sparrows is non-infectious to canaries.

The parasite is transmitted via the fecal-oral route. This particular parasite is a special threat to successful species preservation of endangered Bali mynahs.

Following ingestion of sporulatedoocysts and release of sporocysts, the sporocysts of Isospora and Atoxoplasma invade intestinal epithelial cells. Isospora undergoes merogony in the intestinal epithelium, whereas Atoxoplasma enters the blood stream via the vasculature of the small intestine.

Atoxoplasma sporocysts subsequently invade mononuclear leukocytes and undergo asexual division in circulating and tissue lymphocytes, monocytes, and macrophages, as well as in intestinal epithelial cells

The resulting merozoites form microgametes and macrogametes. Gametogony, the sexual stage of the coccidian life cycle, occurs in intestinal epithelial cells. Here the micro- and macrogametes combine to form zygotes, which then undergo multiple fission cycles to produce sporozoites within oocysts.

These unsporulatedoocysts are passed in the feces beginning nine to ten days post-infection and continue to pass for months, long after any clinical signs in the surviving birds have resolved. The oocystssporulate in the environment and are then infective.

Oocysts may be identified by fecal flotation, but atoxoplasma and isosporanoocysts may be difficult to distinguish. Oocysts of both organisms contain two sporocysts with four sporozoites each.

Clinical signs of disease in fledglings are nonspecific and include diarrhea, anorexia, depression, ruffled feathers, ataxia, and hepatic enlargement that may be grossly visible through the living bird’s skin as “black spot”

Mortality rates for atoxoplasmosis approach 80% in young passerines and the disease can devastate an aviary. Adult birds that are shedding oocysts often lack clinical signs, making elimination of the parasite from aviaries difficult.

Patency of infection lasts for up to eight months due to the long life of macrophages in birds and the resultant long-lived pool of merozoites.

Diagnosis of atoxoplasmosis has traditionally been via postmortem examination and histopathology of fledglings that die acutely or by fecal flotation on persistently infected adult birds.

Identification of atoxoplasmaoocysts is notoriously difficult because of structural similarity to those of Isosporaspp and sporadic shedding of the organism by infected birds.

At necropsy, infected birds have hepatomegaly and splenomegaly. Small, white foci are visible grossly on the liver and heart. The intestines may be distended and have translucent walls. Cytologic and histologic specimens reveal granulomatous to lymphohistiocytic inflammation of the heart, spleen, intestine, and liver.

Macrophages may contain atoxoplasmamerozoites. This form of the organism is round to oval, 3-5 m m diameter, cytoplasmic inclusion that causes indentation of the host cell nucleus, giving infected cells a characteristic appearance. Monocytes and lymphocytes containing merozoites may be seen within blood vessels on histologic sections.

Primaquine is reported to suppress tissue forms of the parasite, and sulfachlor has been recommended to reduce oocyst shedding.

Sulfonamides and amprolium, administered to adults before the breeding season and again when chicks are weaned, have also been suggested to reduce chick morbidity..

Sulfachlorpyrazine inhibits the intestinal stages of the parasite life cycle and has been shown to reduce or clear oocyst shedding for as long as it is regularly administered. Toltrazuril may reduce mortality from systemic disease

Diclazuril has been used in passerines other than Bali mynahs to treat toxoplasmosis; it may also prove effective against Atoxoplasma spp.

Effective prophylaxis of and treatment for atoxoplasmosis have not yet been perfected. Reduction of fecal-oral transmission can be achieved by cleaning cages frequently, using screen or hardware cloth cage bottoms to separate birds from infected droppings, and by frequently changing drinking and bathing water to minimize fecal contamination.

Atoxoplasmosis presents a special threat in raising Bali mynahs in captivity due to high chick mortality. The free-ranging Bali Mynah is critically endangered in its native environment in Bali, due in part to poaching activity.

Thus, it is critical to the survival of the Bali mynah that this parasite not be introduced into a naïve free-ranging population, where it could kill wild-bred chicks.

Authors: Sana Majeed *1, Aisha Khatoon1, Zain- Ul- Abidin2,Aneela Amin1, Ashiq Ali1, Fatima Yasin3  

1 Department of Pathology, Faculty of Veterinary Science, University of Agriculture Faisalabad, Pakistan. 2 Veterinary Research Institute, Lahore, Pakistan. 3Department of Parasitology Faculty of Veterinary Science, University of Agriculture Faisalabad, Pakistan.

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