Pathophysiology of hepatic coccidiosis in rabbits

Four groups of 5 40-day-old, Eimeria stiedai-naive, New Zealand rabbits were infected with 0 (Group A), 10² (B), 10³ (C) and 10⁴ (D) sporulated oocysts of E. stiedai and observed for 50 days. Serum glutamic pyruvic (GPT) and glutamic oxalacetic (GOT) transaminases, bilirubinemia, lipemia, proteinemia, glycemia, oocyst output, body, carcass and liver weights, and mortality were recorded. Four physiopathological events were identified: (1) a phase of indirect damage to the hepatocytes that takes place during the first 2 weeks of infection and is characterized by increased transaminases; (2) a cholestatic period consequent to the production of oocysts that begins suddenly in the 3rd week, diminishes gradually towards the 7th week, and is characterized by a rise of bilirubinemia and lipemia; (3) a stage of metabolic dysfunction that begins in the 3rd–4th week, intensifies for the next 3 weeks and starts to recover during the 7th week. It is characterized by hypoproteinemia and hypoglycemia; (4) a period of immunodepression characterized by the inability of the heavily infected host to inhibit oocyst production. Apart from the cholestatic phase, the respective pathogenic mechanisms remains to be studied.