Electron microscopic study on the jejunal mucosa in human cholera

Abstract

SUMMARY Small intestinal mucosa obtained from six fasting patientswith cholera byaperoral biopsy technique was studied with the electron microscope. The cultures of their rectal swabs were all positive for Vibrio cholerae. In the absorptive cells, large pseudopod-like cytoplasmic processes with deformed microvilli or without microvilli (blebs) projected into the intestinal lumen from the apical cell surface, interrupting the microvillous border. In the crypts some of the undifferentiated crypt cells possessed pseudopod-like cytoplasmic projections which extended into the crypt lumen. The swelling of mitochondria, the disappearance of their cristae, an increase in the number of vesicles of the Golgi apparatus, and the dilatation and vesiculation of endoplasmic reticulum were observed in the epithelial cells. The apical portion of the cells became oedematous in some of the epithelial cells. Cytoplasmic fragments enclosed by a plasma membrane, desquamated epithelial cells, cytoplasmic organelles, and secretory granules were lying free in the intestinal lumen.Marked irregular widening of the interepithelial spaces in the jejunal mucoa was observed at the midvillous area. Many cystic vacuoles were present in the cytoplasm of epithelial cells. The possibility of fluids being transported from blood vessels to intestinal lumina through the interepithelial spaces, and the significance of these pathological findings in human cholera are discussed in this study.The classic or denudation concept of the intestinal lesion in Asiatic cholera was introduced in 1879 by Virchow (1879), who demonstrated in postmortem studies the loss of mucosa from small bowel villi. This denudation concept was denied by Gangarosa, Beisel, Benyajati, Sprinz, and Piyaratn (1960) and by Fresh, Versage, and Reyes (1964) who performed intestinal biopsies in cholera patients. Several experimental models have become available to study the pathogenesis of human cholera, and produce fluid in response to intraluminal instillation of the organism or to intraluminal administration of cholera toxin. It has been shown that an exotoxin produced by Vibrio cholerae induces not only accumulation of intestinal fluid in various experimental animals but also increases in the vascular permeability in the

Protection and Attachment of Vibrio cholerae Mediated by the Toxin-Coregulated Pilus in the Infant Mouse Model

“…V. cholerae colonization was easier to locate when the epithelial cells were undergoing dramatic denudation, giving a bumpy appearance of the villi. This finding of denudation is consistent with histological and micro-scopic studies of intestinal biopsy specimens from cholera patients (2,12). At 3 h postinoculation, V. cholerae was found attaching to the intestine in a TCP-independent manner.…”

Vascular changes in duodenal mucosa in shigellosis and cholera

“…This in turn paves the way to platelet adhesion and aggregation that initiates hemostasis as platelet endothelial cell adhesion molecule (PECAM-1) and platelet activation-dependent granule external membrane (PADGEM) ad- hesive molecules for platelets are concentrated at the interendothelial cleft (Dejana et al, 1995;Burns et al, 2000). Increased numbers of pinocytic vesicles in the capillary cytoplasm as seen in cholera have been reported earlier in animal models of the disease (Chen et al, 1971;Asakura et al, 1974) and are thought to play a role in the increased secretion.…”

The Arteriolar Vasodilatation Model of Vibrio cholerae Induced Diarrhoeal Disease

“…The absence of dilatation in crypt capillaries and its presence in villus capillaries was proposed [29] to be consistent with fluid secretion from the crypts "which represents the chief site of net fluid loss in cholera". Similar mid villus expansion of inter-epithelial spaces was detected in biopsies from humans [31] but capillary vasodilatation was only confirmed in human studies relatively recently [32], too late to have influenced the consolidation of opinion behind the view based on research after 1971 that secreted fluid came from the enterocytes.…”