After experimental inoculation in cats, T. foetus organisms colonize the ileum, cecum, and colon, reside in close contact with the epithelium, and are associated with transient diarrhea that is exacerbated by coexisting cryptosporidiosis but not treatment with prednisolone.

Cryptosporidium meleagridis oocysts, originally isolated from droppings of commercial turkey poults with increased mortality due to viral (reovirus) hepatitis and enteritis, were treated with peracetic acid to kill companion bacteria and viruses and then propagated by passage in young turkeys. Thirty-eight 5-day-old large white turkey poults were inoculated by crop gavage with 500,000 cryptosporidial oocysts and compared with 40 uninoculated poults. Cryptosporidial oocysts shedding began 3 days postinoculation (PI), peaked on day 4 PI, and persisted at a low level for the duration of the 21-day trial. Low to moderate cryptosporidial infections of the ileal mucosa (days 3, 6, and 15 PI), cecal mucosa (days 3, 6, and 21 PI), and bursa of Fabricius (days 6, 12, 15 and 21 PI) were found on histopathological examination. There were no differences in mean body weights between the inoculated and uninoculated groups, and no mortality or clinical signs of disease were seen in either group.

Fecal smears from 112 avian necropsy accessions representing 431 birds were stained with auramine O and examined for Cryptosporidium oocysts by fluorescence microscopy. Stained Cryptosporidium oocysts fluoresced bright yellow-green and were easily differentiated from extraneous material by their uniform small size (approx. 5 micron) and morphology. The rates of cryptosporidia-positive accessions were 27.3% (9/33) of broilers, 10% (3/30) of broiler breeders, and 5.9% (1/17) of layers. Further analyses of available data for various risk factors that may have influenced rates of cryptosporidia-positive samples in broilers, broiler breeders, and layers failed to show significant relationships. However, it was apparent that positive samples were clustered within accessions and not scattered throughout the population sampled. This survey also resulted in the first reported identification of Cryptosporidium oocysts from a budgerigar, macaw, and tundra swan.

Specific-pathogen-free chickens orally inoculated at 4 days of age with a moderately pathogenic vaccine strain of infectious bursal disease virus (IBDV) and/or at 5 days of age with Cryptosporidium baileyi oocysts remained free of overt clinical signs throughout a 16-day period postinoculation (PI). The prepatency period for C. baileyi oocyst shedding was shorter in chickens receiving higher numbers of oocysts, but once shedding was detected, there were no obvious differences in shedding patterns among groups receiving 10(3) through 10(6) oocysts. On days 8 and 16 PI, cryptosporidia were located primarily in the bursae of Fabricius. IBDV exposure was associated with bursal follicle atrophy, whereas C. baileyi infection resulted in bursal epithelial hypertrophy and hyperplasia, mild follicle atrophy, and heterophil infiltration of the bursal mucosa. Examination of experimental groups of 30 birds each indicated that concurrent infection with both agents resulted in more severe bursal lesions, more infected birds, and greater numbers of cryptosporidia in infected tissues. At the termination of the trial, 16 days PI, Cryptosporidium infection was associated with a 6% decrease in mean body weight compared with controls.

No clinical signs, gross lesions, or increased mortality were observed in specific-pathogen-free chickens orally inoculated at 5 days of age with Cryptosporidium baileyi, reovirus 2035, reovirus 2408, or combinations of these agents. Weight gain of chickens inoculated with only reovirus 2408 was depressed 0-8 days postinoculation (PI) (P less than 0.01) but not for the 21-day period PI. Weight gain of chickens inoculated with only reovirus 2035 was not affected. Cryptosporidium baileyi infection significantly depressed weight gain 8-14 days PI but not for the entire 21-day period PI. Weight gain of chickens infected with both C. baileyi and reovirus 2035 was significantly depressed 0-14 days PI and for the entire 21-day period PI. Dual infection with C. baileyi and either reovirus appeared to promote shedding of both agents. Cryptosporidia were found principally in the rectum 2-10 days PI and in the bursa of Fabricius 6-10 days PI. Reovirus infection did not cause any microscopic lesions and did not modify lesions caused by C. baileyi infection.