Abstract

Cryptosporidiurn sp. are coccidian parasites of the family Cryptosporidiidae and were first recognized in the gastric glands of mice by Tyzzer in 1907.9 Since that time, cryptosporidiosis has been reported in a wide variety of vertebrates. Several reports have been published describing cryptosporidiosis in animals and humans with other concurrent disease processes including canine distemper in a dog,4 rotavirus and coronavirus infection in calves,6 generalized toxoplasmosis and cytomegalovirus infection in humans,*Jo and specific immunologic deficiencies of horses and human^.^,^ This communication describes cryptosporidiosis in a weanling male Golden hamster that had concurrent lesions of proliferative ileitis. The hamster died without clinical signs. Several hamsters from the same group had died previously with clinical signs and intestinal lesions compatible with proliferative ileitis. The animals were obtained from a commercial supplier and were housed in conventional stainless steel cages. They were maintained on a diet of commercial pelleted hamster ration and given water ad libitum. No experimental manipulations had been done. Grossly, the hamster was thin and markedly dehydrated. There was moderate to marked thickening and reddening of the distal ileum and proximal colon. Multiple yellow foci that often extended transmurally were visible from the serosa of the colon. Sections of ileum and colon were fixed in 10% formalin and processed routinely for light microscopy. Several formalin-fixed sections of colon were also post-fixed in 2.5% glutaraldehyde and processed for transmission electron microscopy. Intestinal lesions similar to those described previously for proliferative ileitis] were seen by light microscopy both in the ileum and colon but were most severe in the colon. These changes included hyperplasia of crypt and villous epithelial cells and formation of false diverticula that extended transmurally. Bacteria in large numbers were seen within the apical cytoplasm of enterocytes in epon-embedded, toluidine blue-stained, 1 pm histosections. Many round basophilic organisms (1 to 3 pm in diameter), compatible with Cryptosporidiurn sp., were visible along the enterocyte microvillous borders (Fig. 1). It was not possible to clearly demonstrate lesions that may have resulted from Ctyptosporidiurn sp. infection because of the more prominent manifestations of proliferative ileitis. Ultrastructurally, Cryptosporidiurn sp. in various endogenous stages were present embedded in or lying above the microvillous surface of enterocytes (Fig. 2). Stages observed included trophozoites, first and second generation schizonts, macrogametes, microgametes, and oocysts. Numerous bacterial profiles were present within the apical cytoplasm of

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