Submitted to: Veterinary Clinics of North America
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 20, 2009
Publication Date: March 1, 2010
Repository URL:http://hdl.handle.net/10113/46923 Citation: Wyatt, C.R., Riggs, M.W., Fayer, R. 2010. Cryptosporidiosis in Neonatal Calves. Veterinary Clinics of North America. 26(1):89-103.
Interpretive Summary: Cryptosporidiosis in calves is a widespread and ongoing problem, primarily because of the high morbidity associated with the infection. Recent studies suggest that nearly 100 percent of dairy calves acquire cryptosporidiosis during the first month of life. This article summarizes current knowledge of the host-parasite interactions associated with cryptosporidiosis. The infection process in the intestine, the pathology and physiology of the disease process, and the immune responses initiated in the calf to control the infection are discussed. Methods for diagnosing C. parvum infection, treatments that have been tried, and management controls are also examined.
Cattle are subject to infections with 4 principal species of Cryptosporidium. C. parvum is found in a high percentage of monogastric calves, especially from 1-3 weeks of age, but in relatively few calves after weaning or in mature cattle. This species is often associated with diarrhea, sometimes severe, and occasionally associated with mortality. Oocysts containing 4 infectious sporozoites are excreted in feces and initiate infection via contaminated feed and water. After ingestion of oocysts sporozoites are released and bind via their anterior end to the luminal membrane of enterocytes between microvilli followed by host cell actin polymerization and remodeling with protrusion of the host cell microvillous membrane leading to engulfment and encapsulation of the invading sporozoites. This results in an intracellular but extracytosolic, epicellular localization in a parasitophorous vacuole at the apical region of the host cell surface immediately beneath the plasma membrane. A multimembranous feeder organelle subsequently forms, connecting the parasite with, and providing access to, the host cell cytoplasm for acquisition of essential nutrients and substrates. The molecular mechanisms and biochemical signaling pathways involved in these initial host cell-sporozoite interactions and subsequent life cycle development are described. Infection in calves leads to villous atrophy and a reduction in total surface area of the intestinal mucosa resulting from accelerated loss of mature, absorptive villous enterocytes and microvillous atrophy resulting in a maldigestion-malabsorption type diarrhea. Innate immunity is insufficient to clear C. parvum infection. After exposure to C. parvum, cattle develop both humoral and cell-mediated responses. T lymphocytes are important in adaptive immune responses. There are neither vaccines nor approved or highly efficacious drugs for prevention or treatment of cryptosporidiosis in cattle.