Ultrastructural Changes in the Intestine of Suckling Rabbits Infected with Cholerogenic and Non-Cholerogenic nonO1/nonO139 Vibrio cholerae Strains.

We performed an electron microscopic study of the small intestine of suckling rabbits infected with cholerogenic and non-cholerogenic strains nonO1/nonO139 Vibrio cholerae. Cholerogenic strain induced mostly hydropic degeneration of the epithelium typical of cholera toxin effect, while non-cholerogenic strain induced the formation of lacunae along the borders of adjacent epithelial cells typical of hemagglutinin/protease effect. In both cases, reduction of microvilli, destruction of intracellular organelles, two types of mitochondrial reaction (condensation and swelling with destruction of cristae), appearance of myelin figures, defects in the capillary walls, and activation of pinocytosis were observed. These data confirm our previous assumption on interchangeability of different pathogenic factors of Vibrio cholerae, including nonO1/nonO139 strains.

Ultrastructural evidence of invasive activity of Vibrio cholerae.

The development of experimental cholera in suckling rabbits is associated with typical cholerogenic syndrome: the presence of Vibrio cholerae in the blood, bile (in 60 and 70% cases, respectively), small and large intestine (in 100% cases). Simultaneously with enterocyte desquamation and increased permeability of the blood-enterocyte barrier, the vibrios are released into villous stroma and then into the microcirculatory bed. the zot toxin is involved in the mechanism of Vibrio cholerae invasion, the corresponding gene is present in the genome of the studied strain.

Ultrastructural changes in small intestinal lipofibroblasts of suckling rabbits with experimental cholera.

Ultrastructural analysis of the jejunum in suckling rabbits showed that lipofibroblasts localized in the submucosa and adjacent to crypts contain lipid inclusions (granules) with typical "melting" surface. Lipofibroblasts contained moderately widened cisternae of the granular endoplasmic reticulum and few mitochondria with dense matrix and poorly developed cristae. Experimental cholera was usually accompanied by a decrease in the number of lipid inclusions, and only in some cases by accumulation of lipid material. Our results suggest that the material accumulated in granules plays a role in the pathogenesis of cholera.

Ultrastructural changes in smooth muscle cells of the small intestine in suckling rabbits with experimental cholera.

Ultrastructural study of the small intestine in suckling rabbits with experimental cholera revealed involvement of the inner and outer smooth muscle layers into the pathological process. Smooth muscle cells were characterized by vacuolar and fatty degeneration and focal colliquative necrosis. Apoptosis played little role in gastrointestinal motility disturbances. The presence of considerable amounts of fluid in intestinal loops reflects peristaltic dysfunction due to generalized damage to smooth muscle cells.

Ultrastructural peculiarities of intranuclear inclusions in some target cells during endotoxin shock.

Intranuclear inclusions detected in hepatic, renal, and cerebral cells during endotoxemia can be subdivided into true and pseudo inclusions. True inclusions have filamentous and crystalline structure and are rarely found in control animals. However, the number of true inclusions increases during pathology and can serve as a marker of molecular pathology in the cells provoked by endotoxin.

Ultrastructural changes in the nephron and renal protein cleaving function in suckling rabbits with experimental cholera.

Immature nephrons and the presence of a proteolytic system mediating extracellular protein digestion in the epithelium of proximal tubules are characteristic features of renal cortical ultrastructure in intact 10-12-day-old suckling rabbits. Cholera infection is accompanied by intensive cleavage of exogenous protein, which starts in podocytes and is completed in the cytoplasm of the proximal tubule epitheliocytes. Overload to nephron associated (in addition to urine production) with intensive extracellular hydrolysis impairs nephrothelium reactivity and increases its vulnerability to cholera exo- and endotoxins and their mediators.