Pathogenesis of infectious diarrhea: GUT PHYSIOLOGY Part 10

Rotavirus1Rotavirus: In this section, a closer look is taken at the phenomenon of villus shortening and its consequences, and the subsequent host response of villus resynthesis. For this we draw on a multidisciplinary study of a naturally occurring infection of seven-day-old neonatal mice (rotavirus-anti-body free) with the homologous murine epizootic diarrhea of infant mice (EDIM) strain of rotavirus. These studies were carried out from oral challenge (the natural route of infection), through a clinical peak of diarrhea that occurred 72 h after infection to resolution of the infection seven days later.

Quantitative measurements of virus infection in different regions of the gut showed that virus production was biphasic, peaking at 48 h with a second peak at 120 h. Virus was located in the upper regions of mainly mid-small intestinal villi, although the upper and lower small intestines were also infected, but not the colon. Maximal diarrhea did not coincide with peak of virus production. buy asthma inhalers

Transmission and scanning electron microscopic study of changes in gut villi showed constriction of villus bases with edema of the lamina propria, and vacuolation of entero-cytes 24 h after infection, that is before the peak of virus replication. The virus was not by itself inherently cyto-pathic, as was readily demonstrated at later time points in the infection. Enterocyte damage was perceived to be the consequence of tissue hypoxia as discussed below. By 48 h after infection, atrophy of villi occurred — their height being reduced by 50% to 60%. Maximal diarrhea did not coincide with maximal atrophy of villi.

This entry was posted in Diarrhea and tagged Bibrio cholerae, Clostridium difficile, Diarrhea, Escherichia coli, Shigella dysenteri.