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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied sodium-dependent uptake of L-alanine into small intestinal brush border membrane vesicles (BBMV) isolated from piglets 40 h after infection with transmissible gastroenteritis (TGE) virus. Vesicles from TGE-infected pigs and uninfected litter-mate controls showed comparable degrees of enrichment and purity. In BBMV prepared by conventional techniques, [3H]L-alanine "overshoot" (peak uptake/equilibrium uptake) in the presence of a Na gradient was preserved in TGE BBMV, unlike [3H]D-glucose "overshoot," which was reduced. When these experiments were repeated using vesicles of greater purity, initial rates of Na-dependent L-alanine influx were reduced in BBMV from infected piglets under voltage clamped conditions with valinomycin. These studies demonstrate a specific amino acid transport defect in the small intestinal epithelium during acute viral diarrhea. They demonstrate too that brush border L-alanine-Na co-transport, although reduced, is present after viral damage, confirming previous studies that showed additive effects of amino acid and glucose on jejunal epithelial Na+ transport in transmissible gastroenteritis. Our findings support the concept that, in viral enteritis, oral rehydration solutions containing amino acid and glucose have a theoretical advantage over glucose electrolyte solutions because they facilitate brush border Na+ entry by two carrier mechanisms.
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PMID:Diminished brush border membrane Na-dependent L-alanine transport in acute viral enteritis in piglets. 268 49

Three- to four-week-old, just-weaned piglets were infected with transmissible gastroenteritis (TGE) virus and the next day with K88ac+ enterotoxigenic Escherichia coli (ETEC). Histological examination of caudal jejunum and ileum of piglets killed 2-3 days after virus challenge (1-2 days after ETEC infection) revealed severe villus atrophy especially in the jejunum compared with controls (P less than 0.05). Four-5 days after TGE virus infection villus length increased and after 7 days it was near normal. Villi scraped from jejunal and ileal mucosa of the piglets were incubated in vitro with K88ac+ E. coli and the number of bacteria adhering to 250 micron villus brush border was counted. Attachment of bacteria to villi of piglets killed 2-3 days after TGE virus infection was significantly decreased in comparison with adhesion to villi of non-infected piglets or of piglets killed 7 days after the virus infection. Correlation between in vitro adhesion and villus height was 0.6649 (P less than 0.001). The results suggest that the experimentally-induced villus atrophy was attended with a temporarily diminished susceptibility of villus enterocytes to adhesion of K88ac+ E. coli.
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PMID:Effect of experimentally-induced villus atrophy on adhesion of K88ac-positive Escherichia coli in just-weaned piglets. 305 50

A case of prolonged diarrhoea following Escherichia coli 0111 gastroenteritis is reported. Electron microscopy of the jejunal biopsy revealed effacement of the brush border and attachment of bacteria by pedestal formation. Specific activities of brush border enzymes showed marked depression of disaccharidases, zinc-resistant alpha-glucosidase, and alkaline phosphatase. In contrast, marker enzymes for basolateral membranes and endoplasmic reticulum were unaffected. The biochemical changes support the pathogenic mechanism suggested by ultrastructural studies previously reported.
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PMID:Ultrastructural and biochemical changes in human jejunal mucosa associated with enteropathogenic Escherichia coli (0111) infection. 351 Dec 12

The virus of transmissible gastroenteritis produced sprue-like lesions in the small intestines of young pigs. These lesions were characterized by villous shortening, fusing and blunting in the jejunum and ileum. There was decreased height of the brush border and morphologic alteration of the villous epithelial cells from simple columnar to a variable cuboidal type. Accompanying these microscopic lesions were histochemical changes characterized by decreased staining intensity of acid phosphatase, alkaline phosphatase, adenosine triphosphatase, leucine aminopeptidase, succinic dehydrogenase and malic dehydrogenase in the affected intestinal mucosa. The clinical nature of transmissible gastroenteritis in the pig together with the histopathologic and histochemical changes may provide a useful experimental model for obtaining additional basic information on enteric disturbances.
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PMID:Experimental sprue-like small intestinal lesions in pigs. 422 30

Light and electron microscopy findings in the jejunal mucosa of the normal feeder pig and feeder pigs infected with transmissible gastroenteritis (TGE) virus are reported. Villi in the mid jejunum of the normal feeder pig were elongated, finger shaped and covered with a layer of columnar absorptive cells with a well developed and regular brush border. Severe lesions of villous atrophy were present in all jejunal segments of feeder swine killed 96 hours post infection with TGE virus. Atrophic villi were covered by flat to cuboidal cells with a poorly developed brush border in some areas. In other segments, cells varied in appearance from sub-columnar to columnar type of near normal appearance. The ultrastructure of the jejunal absorptive cells in the normal feeder pig was found to be similar to that described for the jejunal cells of other adult mammals. There were no significant indications of high pinocytotic activity. The epithelial cells covering the atrophic villi of TGE infected pigs had a fine structure similar to that described for the crypt cells, ranging in appearance from very immature to moderately differentiated cells. Microvilli were very short, decreased markedly in number and irregular in arrangement. The terminal web was poorly developed. Strands of rough endoplasmic reticulum were markedly diminished and an increase in free ribosomes was noted. The significance of these observations in explaining pathogenesis of TGE in feeder pigs is discussed.
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PMID:Transmissible gastroenteritis in feeder pigs: observations on the jejunal epithelium of normal feeder pigs and feeder pigs infected with TGE virus. 427 43

Rotavirus and enterotoxigenic Escherichia coli (ETEC) are enteropathogens each capable of inducing diarrhoea in some animal species and man. Unstressed young animals develop an age-related resistance to infection with either rotavirus or ETEC which differs for each animal species. The effects of experimental infection of calves, lambs, foals and piglets with rotavirus and ETEC given either alone or in combination, have been examined. In general, dual infections tended to lengthen the period of age susceptibility and increase the severity of gastroenteritis, compared to infection with either agent alone. ETEC caused little or no pathological changes in the small intestine while rotavirus induced moderate inflammatory, morphological and physiological changes including reduced activity of membrane-bound digestive enzymes. In dual infections, mucosal lesions were more severe than those seen after rotavirus infection and ETEC proliferation in the lumen of the small intestine was greater than in animals infected with ETEC alone. Two distinct mechanisms of diarrhoea, presumably, were involved; net fluid hypersecretion into the lumen of the gut mediated by ETEC enterotoxin(s), and brush border maldigestion and malabsorption which was caused by rotavirus infection of the small intestine.
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PMID:The clinical manifestation and pathogenesis of enteritis associated with rotavirus and enterotoxigenic Escherichia coli infections in domestic animals. 636 57

The small intestine of piglets collected during a sudden outbreak of diarrhoeal disease resembling transmissible gastroenteritis (TGE) was examined by light and electron microscopy. The principal histopathological changes were moderate infiltration by mononuclear cells in the lamina propria of the villi and cytoplasmic vacuolation. These were most pronounced in the epithelial cells covering the villous tips. By scanning electron microscopy, the intestinal villi were swollen and the transverse furrows disappeared. Microvilli were reduced in number leaving denuded areas on the brush border of the villous epithelial cells. The ultrastructural changes were restricted to the cytoplasm of affected villous epithelial cells. The cell organelles were missing in rounded areas leaving cleared areas in the cytoplasm. Parallel fascicles and bundles were seen in these areas. Viral particles with an average diameter of 70 nm were found within the dilated apical tubulo-vesicular system, free in the cytoplasm, among the microvilli, or lying free in the intestinal lumen. Viral particles surrounded a non-membrane bound viroplasm in some cases. The negatively stained particles showed a typical coronavirus morphology. These particles were found to be distinct from the known coronaviruses of swine, TGE virus and hemagglutinating encephalomyelitis virus by immune electron microscopy.
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PMID:Ultrastructural changes in the small intestinal epithelium of suckling pigs affected with a transmissible gastroenteritis (TGE)-like disease. 724 29

A case of persistent diarrhea following Escherichia coli O18ab gastroenteritis is reported. Electron microscopy of a biopsy of the small intestine showed effacement of the brush border, attachment of bacteria to the epithelial cells with pedestal formation, and bacteria within the enterocytes. The bacterial isolate was an enteropathogenic E. coli isolate which did not contain the adherence factor (EAF) but possessed the attaching-effacing eae gene, was able to invade HeLa cells in a gentamicin invasion assay, and also invaded rabbit intestinal cells. Results suggest that E. coli organisms of the O18ab serotype may cause diarrhea by an as yet unknown pathogenic mechanism, involving attaching to and effacing of enterocytes followed by invasion of the epithelial cells.
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PMID:Attaching and effacing enteropathogenic Escherichia coli O18ab invades epithelial cells and causes persistent diarrhea. 889 Feb 57

Rotaviruses are nonenveloped viruses that infect enterocytes of the small intestine and cause severe infantile gastroenteritis. It was previously thought that rotavirus exits cells by lysis, but this behavior does not match the local pathogenesis of the virus. In this study, we have investigated the release of the simian rotavirus strain (RRV) from the polarized intestinal Caco-2 cells. We found that RRV is released almost exclusively from the apical pole of Caco-2 cells before any cells lyse. Using confocal laser scanning microscopy and drugs that inhibit vesicular transport, we studied the RRV transport route from the endoplasmic reticulum (ER) to the apical side of intestinal cells. We demonstrated that RRV exits from the ER through a carbonyl cyanide m-chlorophenylhydrazone-sensitive vesicular transport. RRV staining was never found within the Golgi apparatus or lysosomes, suggesting that the RRV intracellular pathway does not involve these organelles. This finding was confirmed by treatment with monensin or NH4Cl, which do not affect release of RRV. Electron microscopic analysis revealed RRV containing small smooth vesicles in the apical area and free virions outside the cell in the brush border, consistent with a vesicular vectorial transport of virus. These results may provide, for the first time, a cellular explanation of the pathogenesis of rotavirus.
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PMID:Rotavirus is released from the apical surface of cultured human intestinal cells through nonconventional vesicular transport that bypasses the Golgi apparatus. 934 79

Rotavirus infection is the most common cause of severe infantile gastroenteritis worldwide. These viruses infect mature enterocytes of the small intestine and cause structural and functional damage, including a reduction in disaccharidase activity. It was previously hypothesized that reduced disaccharidase activity resulted from the destruction of rotavirus-infected enterocytes at the villus tips. However, this pathophysiological model cannot explain situations in which low disaccharidase activity is observed when rotavirus-infected intestine exhibits few, if any, histopathologic changes. In a previous study, we demonstrated that the simian rotavirus strain RRV replicated in and was released from human enterocyte-like Caco-2 cells without cell destruction (N. Jourdan, M. Maurice, D. Delautier, A. M. Quero, A. L. Servin, and G. Trugnan, J. Virol. 71:8268-8278, 1997). In the present study, to reinvestigate disaccharidase expression during rotavirus infection, we studied sucrase-isomaltase (SI) in RRV-infected Caco-2 cells. We showed that SI activity and apical expression were specifically and selectively decreased by RRV infection without apparent cell destruction. Using pulse-chase experiments and cell surface biotinylation, we demonstrated that RRV infection did not affect SI biosynthesis, maturation, or stability but induced the blockade of SI transport to the brush border. Using confocal laser scanning microscopy, we showed that RRV infection induces important alterations of the cytoskeleton that correlate with decreased SI apical surface expression. These results lead us to propose an alternate model to explain the pathophysiology associated with rotavirus infection.
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PMID:Rotavirus infection reduces sucrase-isomaltase expression in human intestinal epithelial cells by perturbing protein targeting and organization of microvillar cytoskeleton. 969 17


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