Experimental transmission of Cryptosporidium oocyst isolates from mammals, birds and reptiles to captive snakes

Groups of four to five, 3-month-old rat snakes (Elaphe obsoleta) were separately gastrically inoculated with 2.0 × 106 viable oocysts of Cryptosporidium muris (mice and calves), C. muris-like (Bactrian camels), C. wrairi (guinea pigs), C. bailey i (chickens), C. meleagridis (turkeys), Cryptosporidium sp. (turtles, tortoises, chameleons and lizards) and C. serpentis from clinically (fatal case) and subclinically infected snakes. None of the snakes inoculated with oocysts originating from homothermous vertebrates developed infection as determined by histology and serology, whereas all snakes challenged with reptilian oocyst isolates were infected with Cryptosporidium on weeks 6 and 10 post-inoculation (PI). On week 10 PI, the snakes displayed mild to severe, multifocal to widespread, thinning and disorganization of gastric epithelium and nine out of twelve snakes infected by oocysts originating from reptiles other than snakes displayed severe gastric hyperplasia. Three out of ten snakes infected by oocysts originating from snakes had ELISA-detectable Cryptosporidium-specific antibody (Ab) titers on week 6 PI; all snakes were Cryptosporidium-seroconverted on week 10 PI and their serum Ab titer significantly increased. The study demonstrated that Cryptosporidium infections in snakes maintained on the diet of rodents or birds cannot be initiated via ingestion of an infected food item; however, snakes can void ingested oocysts. Lack of host specificity among reptiles to this pathogen, demonstrated for the first time in the present study, indicates that snake-attributed C. serpentis is not distinct from Cryptosporidium sp. infecting reptiles other than snakes, and that clinical manifestations and virulence of Cryptosporidium in snakes is modulated by the species of the host. Housing of snakes with other reptiles can enhance transmission of Cryptosporidium to snakes, and therefore should be avoided.