The life cycle is relatively simple, with ingestion of oocysts, followed by proteolytic activation of sporozoites. These enter and multiply in intestinal epithelium and associated lymph nodes to form rapidly multiplying tachyzoites which then disseminate and form bradyzoites in the brain, lover, striated muscle and remain viable for the life of the host. Bradyzoites are indistinguishable from sporozoites except using periodic acid-Schiff's reagent. Definitive hosts are infected by ingesting bradyzoites in tissue or oocysts passed in the feces.
Species which are pathogenic to dogs include:
- Toxoplasma gondii
Dogs are normally infected with T. gondii by ingestion of tissue cysts in meat, but spread via semen and transplacental transmission also occur, with tachyzoites isolated from the brain of pups born from infected bitches.
In adult dogs, T. gondii is usually nonpathogenic, and recrudescence is the primary concern in coexisting disease such as distemper, or immunocompromised dogs with immune-mediated disease, or receiving cyclosporin, cyclophosphamide or prednisolone. Furthermore, another special feature of this evolutionarily successful parasite is the fact that it usually causes asymptomatic infections and in most cases does not kill immunocompetent hosts. However, without sufficient therapy, reactivation of T. gondii in immunocompromised individuals frequently results in death of the host.
Symptoms are more common in younger dogs, where disseminated toxoplasmosis may present as acute fever, hepatitis, pneumonia and ulcerative dermatitis. Neurological diseases such as acute protozoal polyradiculoneuritis (as is observed with N. caninum), myositis, hindlimb paresis, chorioretinitis, seizures and death have been reported.
Diagnosis is based on presenting clinical signs, fecal examination for oocysts (usually unreliable), ELISA detection of T. gondii antibodies in tissue samples, light microscopy identification of tachyzoites in CSF or other tissues and PCR assays for species identification.
A differential diagnosis in deaths associated with neonatal acute pup deaths would include canine herpesvirus and canine distemper virus. Other protozoan parasites and some bacteria can cause similar symptoms and must be excluded as a possible cause, including Neospora caninum, Leishmania spp, Giardia spp and Brucella spp.
The recommended drug of choice in treatment is clindamycin (10 - 50 mg/kg orally for 2 - 4 weeks), with aggressive supportive therapy in acutely ill pups.
Dogs of any age with neurological signs have a more guarded prognosis.
- Brain Bank
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