The ileal crypt ultrastructural changes accompanying cryptosporidiosis in type 1 diabetic mouse model versus...

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.