The ileal crypt ultrastructural changes accompanying cryptosporidiosis in type 1 diabetic mouse model versus dexamethasone-immunocompromised mouse model

Cryptosporidiosis is an enteric infection caused by Cryptosporidium spp. The severity of the disease depends mainly on the immune status of the host. The infection is self-limited in immunocompetent individuals but in immunocompromised patients, it can be severe and threatening. To provide new insights into a better understanding of the pathogenesis of the infection and the impact of immune modulation on the course of the disease, we used 4 groups of Swiss-Albino mice; dexamethasone (DEX) group, the diabetic group, the DEX-infected group, and the diabetic-infected group. The blood glucose levels, oocyst shedding, mortality rates, and ultrastructural changes among study groups were observed and documented. The diabetic groups showed hyperglycemia while the DEX-infected group showed significantly higher oocyst shedding rates compared to the diabetic-infected group (P > 0.005). At the end of the experiment, the DEX groups showed higher mortality rates. Regarding the ultrastructural ileal crypt changes recorded in all groups, the DEX-infected group showed the severest changes with significantly lower numbers of Paneth cells, depletion of Paneth cell granules, and increased number of apoptotic crypt bodies significantly (P > 0.005) compared to the diabetic-infected group. On the contrary, the diabetic-infected group showed a significant expansion of Paneth cells with an increased number of granules and a significantly decreased number of apoptotic crypt bodies (P > 0.005). However, both models failed to control the infection properly highlighting the importance of early diagnosis and treatment of suspected immunocompromised cases.