Hepatic neosporosis was reported in a 4-year-old spayed border collie receiving combination immunosuppressive therapy for pemphigus foliaceus for 3 months. The dog presented for progressive lethargy, inappetance, and weakness of 4 days’ duration. Physical examination findings included tachypnea, tachycardia, increased bronchovesicular lung sounds, hepatomegaly, bloody stool, and icteric sclerae. CBC abnormalities included an inflammatory leukogram with a left shift, lymphopenia, and thrombocytopenia. Serum biochemistry panel abnormalities included hyperglycemia and decreased calcium, potassium, sodium, chloride, and albumin. Marked liver enzyme elevation and hyperbilirubinemia were noted. Humane euthanasia was elected; postmortem examination revealed a pale enlarged friable liver and severe vacuolar degeneration and hepatocellular necrosis on histopathology. Also noted were intra- and extracellular protozoa that reacted immunohistochemically with polyclonal antibodies to Neospora caninum, but not Toxoplasma gondii.
N caninum is uncommon in canids and usually manifests as a progressive ascending neuromuscular disorder. Clinical presentation has been previously associated with concomitant cytotoxic and glucocorticoid therapy and age-related immunodeficiency. Bradyzoites or cysts can persist within tissues and experimental evidence has shown recrudescence with administration of glucocorticoids. This case was unusual in its presentation with the liver as the most severely affected organ. Antemortem diagnosis of N caninum includes serology, cytology, histology, and PCR testing. Treatment options include combination therapy with clindamycin, trimethoprim-sulfonamide, and pyrimethamine. Treatment is most successful with slow disease onset, milder clinical signs, and rapid initiation. This case highlights the importance of early detection and treatment of infectious diseases in immunocompromised patients.