Host Responses to Cryptosporidium Infection

Abstract

Cryptosporidium is a clinically and economically important infection whose pathogenic effect begins with colonization of the intestinal epithelium. Despite intensive efforts, a consistently effective therapy for the infection has yet to be identified. Morbidity and mortality results from ongoing loss of absorptive epithelium, which leads to villous atrophy and malabsorption and release of inflammatory mediators that stimulate electrolyte secretion and diarrhea. With further clarification of the mechanisms underlying enterocyte malfunction in Cryptosporidium infection, it should be possible to design rational nutritional and pharmacologic therapies to enhance nutrient and water absorption, promote the clearance of infected enterocytes, and restore normal villus architecture and mucosal barrier function.

Cryptosporidium parvumIsolate-Dependent Postinfectious Jejunal Hypersensitivity and Mast Cell Accumulation in an Immunocompetent Rat Model

“…Eating disorders have been previously reported in association with well-recognized histological features of Cryptosporidium spp. infection, i.e., loss of VH, edema, and inflammatory infiltration by neutrophils, macrophages, and lymphocytes (3,20). In the present study, small intestine villus atrophy, crypt hyperplasia, and inflammatory cell infiltration were more prominent at day 7 p.i.…”

Introducing Miltefosine as an Anti-cryptosporidial Agent in Immunocompromised Mice

“…The change of the intestinal surface was manifested by villous dystrophy and increased crypt length with cellular infiltration. Several reports similarly described crypt elongation and villous atrophy, and may be accompanied by mixed inflammatory-cell infiltrate in the lamina propria; in areas of severe injury, the epithelial cells showed blunted microvilli [11,27,28]. Twenty days after treatment with miltefosine did not ameliorate undesired result appeared in intestinal morphology with group (IIb), although a decrease in oocysts output percentage has been noticed.…”

Clinical and morphological investigations in a spontaneous cryptosporidium enteritis outbreak in calves

“…This fact, as well as the reported high-degree atrophy of intestinal villi predispose to secondary complications, facilitating the colonisation of other pathogens (Argenzio et al, 1990). The hypothesis is confirmed by the results from a number of animal experimentations (Tzipori et al, 1982;Heine et al, 1984;Argenzio et al, 1990;Moore et al, 1995;Gookin et al, 2002).…”