Submitted to: Journal of Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/3/2007
Publication Date: 8/30/2008
Citation: Dubey, J.P., Crutchley, C. 2008. Toxoplasmosis in wallabies (macropus rufogriseus, macropus eugenii ): blindness, treatment with atovaquone, and isolation of toxoplasma gondii. Journal of Parasitology. 94:929-933. Interpretive Summary: Toxoplasma gondii is a single-celled parasite of all warm-blooded hosts worldwide. It causes mental retardation and loss of vision in children, and abortion in livestock. Cats are the main reservoir of T. gondii because they are the only hosts that can excrete the resistant stage (oocyst) of the parasite in the feces. Humans become infected by eating undercooked meat from infected animals and food and water contaminated with oocysts. Toxoplasmosis causes mortality in many species of animals in the zoos, especially wallabies.Scientists at the Beltsville Agricultural Research Center and from Pennsylvania report characteristics of Toxoplasma isolates and treatment of wallabies for toxoplasmosis. The results will be of interest to biologists, parasitologists, and veterinarians
Technical Abstract: Australasian marsupials, especially wallabies are highly susceptible to clinical toxoplasmosis. Three wallabies (1Tammar, Macropus eugenii no.1, and 2 Bennett’s, Macropus rufogriseus, no.2 and 3) imported from New Zealand to Pennsylvania were diagnosed to have toxoplasmosis after arrival in the US. Wallaby no.1 was ill on arrival, died 3 mo later, and T. gondii was isolated by bioassay of macropod tissues in mice. Wallaby no. 2 and 3 developed acute toxoplasmosis 4 mo after arrival in the US. Diagnosis was based on seroconversion, development of high antibody titers to T. gondii in the modified agglutination test, and clinical signs. Treatment of these wallabies with a combination of pyrimethamine, sulfadimethoxine, leucovorin calcium, and vitamin E, failed to prevent progression of the disease. Both wallabies developed neurological signs and blindness. Death was imminent when treatment with atovaquone was initiated. Treatment with atovaquone (100 mg/kg, oral, every 24 hr), along with 10 ml peanut oil to facilitate absorption, restored health. Clinical improvement was seen within 24 hr and vision was improving by 1 wk, and their reproductive capacity returned. No signs of toxicity were found in the dams or joeys after 6-mo treatment. Three yr after initial treatment, the wallabies were examined at necropsy (1 died of unrelated causes and the other was killed because of pain associated with recurrence of blindness) and their tissues were bioassayed for viable T. gondii. Toxoplasma gondii was not isolated from the wallaby no.2. Viable T. gondii was isolated from the brain of wallaby no.3 but lesions were not found in histological sections of its tissues. Another Bennett’s wallaby (no. 4, born and raised in Pennsylvania) was successfully treated with atovaquone for 3 mo; T. gondii was isolated from the brain of this wallaby killed 5 yr later. A joey born to wallaby no.2 and sired by wallaby no.4, developed clinical signs simulating toxoplasmosis; T. gondii was isolated from the brain of this wallaby when killed at 4-yr of age. Genotyping of these 3 T. gondii isolates using PCR-RFLP marker SAG2 revealed that 3 of the 4 isolates were genotype III. This is the first success in treating acute toxoplasmosis in wallabies, and the first isolation and genetic typing of T. gondii from wallabies in the US.