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Intestinal Colonization (intestinal + colonization)
Selected AbstractsEnterobacter sakazakii infection in the newbornACTA PAEDIATRICA, Issue 3 2001B Bar-Oz Enterobacter sakazakii, a Gram-negative bacillus, previously known as "yellow pigmented Enterobacter cloacae," is a rare cause of neonatal infection. We describe the detailed clinical presentation of two cases in whom E. sakazakii was isolated in our neonatal service during the course of 1 mo. These include one case of sepsis and meningitis complicated by cerebral infarction, and one case of sepsis. In addition, three cases of intestinal colonization were identified. The source of the organism was thoroughly sought and was found to be a blender in the milk kitchen that was used for preparation of the reconstituted powdered milk formula. Conclusion: Our paper adds clinical and laboratory information about the disease spectrum caused by this relatively rare organism and emphasizes the importance of a thorough search for the source of the infection. [source] The ToxT-dependent methyl-accepting chemoreceptors AcfB and TcpI contribute to Vibrio cholerae intestinal colonizationFEMS MICROBIOLOGY LETTERS, Issue 2 2010Adriana Paola Chaparro Abstract Vibrio cholerae colonizes the human intestine and causes the acute diarrheal disease cholera. Flagellar-mediated chemotaxis contributes to intestinal colonization as well as infectivity. The virulence-regulatory protein ToxT activates transcription of the genes encoding the major virulence factors cholera toxin and toxin coregulated pilus. ToxT additionally activates transcription of two genes, tcpI and acfB, located within the Vibrio Pathogenicity Island predicted to encode methyl-accepting chemoreceptors. We show that disruption of either tcpI or acfB individually does not noticeably affect V. cholerae intestinal colonization within the infant mouse, but disruption of both tcpI and acfB leads to a decrease in intestinal colonization. These results suggest that TcpI and AcfB may have overlapping or redundant chemotactic functions that contribute to V. cholerae intestinal colonization. [source] INFLUENCE OF ACID ADAPTATION ON THE SURVIVAL OF SALMONELLA ENTERITIDIS AND SALMONELLA TYPHIMURIUM IN SIMULATED GASTRIC FLUID AND IN RATTUS NORVEGICUS INTESTINE INFECTIONJOURNAL OF FOOD SAFETY, Issue 2 2010KARLA JOSEANE PEREZ ABSTRACT The aim of this study was to investigate the influence of acid adaptation in the survival of Salmonella Enteritidis (SE86) and Salmonella Typhimurium (ST99) during exposure to simulated gastric fluid (SGF) and in intestinal infection of Rattus norvegicus. Acid-adapted and nonadapted Salmonella strains were exposed to SGF (pH 1.5) and were inoculated by gavage in adult rats. Results indicated that acid-adapted SE86 survived significantly better (P < 0.05) than nonadapted SE86, nonadapted ST99 and acid-adapted ST99 in SGF. Nonadapted microorganisms were observed in higher counts in feces than acid-adapted strains, while acid-adapted microorganisms demonstrated higher counts in intestine samples, suggesting intestinal invasion capacity. Acid-adapted SE86 was recovered in higher counts from ileum-cecum junction than the other microorganisms. PRACTICAL APPLICATIONS Salmonella Enteritidis has been identified as the most frequent serovar involved with the foodborne outbreaks in Brazil. In Southern Brazil, a specific strain of Salmonella Enteritidis (SE86) has been involved with more than 90% of the salmonellosis occurring in the last years, and the main food vehicle is home-made mayonnaise frequently added with different quantities of vinegar, which can cause acid adaptation in Salmonella cells. The results of this work indicate that SE86 presented higher acid adaptation, which contributed to higher survival rates in simulated gastric fluid and better intestinal colonization. These results could be related to human virulence and the frequent involvement of this strain with foodborne outbreaks in southern Brazil. [source] Delineation of pilin domains required for bacterial association into microcolonies and intestinal colonization by Vibrio choleraeMOLECULAR MICROBIOLOGY, Issue 4 2000Thomas J. Kirn The toxin-co-regulated pilus (TCP), a type 4 pilus that is expressed by epidemic strains of Vibrio cholerae O1 and O139, is required for colonization of the human intestine. The TCP structure is assembled as a polymer of repeating subunits of TcpA pilin that form long fibres, which laterally associate into bundles. Previous passive immunization studies have suggested that the C-terminal region of TcpA is exposed on the surface of the pilus fibre and has a critical role in mediating the colonization functions of TCP. In the present study, we have used site-directed mutagenesis to delineate two domains within the C-terminal region that contribute to TCP structure and function. Alterations in the first domain, termed the structural domain, result in altered pilus stability or morphology. Alterations in the second domain, termed the interaction domain, affect colonization and/or infection by CTX-bacteriophage without affecting pilus morphology. In vitro and in vivo analyses of the tcpA mutants revealed that a major function of TCP is to mediate bacterial interaction through direct pilus,pilus contact required for microcolony formation and productive intestinal colonization. The importance of this function is supported by the finding that intragenic suppressor mutations that restore colonization ability to colonization-deficient mutants simultaneously restore pilus-mediated bacterial interactions. The alterations resulting from the suppressor mutations also provide insight into the molecular interactions between pilin subunits within and between pilus fibres. [source] Preterm birth but not mode of delivery is associated with an increased risk of developing inflammatory bowel disease later in lifeINFLAMMATORY BOWEL DISEASES, Issue 11 2007Barbara Sonntag MD Abstract Background: Exposure to bacterial antigens and other environmental factors in combination with a genetic susceptibility have been implicated in the etiology of inflammatory bowel disease (IBD). As certain perinatal circumstances, e.g., delivery by cesarean section, predispose to a different intestinal colonizations the aim of this analysis was to define a potential influence on the development of IBD in later life. Methods: In a case-control study design, birth data were recorded from patients diagnosed with IBD (Crohn's disease [CD], n = 1096; ulcerative colitis [UC], n = 763) and healthy controls ([C], n = 878) by a self-administered questionnaire. Results: Preterm birth (CD: odds ratio [OR] 1.5 [95% confidence interval 1.1,2.0], UC: OR 1.3 [0.9,1.9]), mother's disease during pregnancy (CD: OR 1.9 [1.3,2.9], UC: OR 1.6 [1.0,2.4]), and disease in the first year of life (CD: OR 2.2 [1.6,2.9], UC: OR 1.7 [1.3,2.3]) are associated with the development of IBD in later life. No significant associations were found for the mode of delivery and breast feeding. In a logistic regression analysis female sex, smoking, appendectomy, maternal IBD, and disease in the first year of life were independently associated with CD. Female sex, appendectomy, and disease in the first year of life were independently associated with UC. Conclusions: Preterm birth and other perinatal circumstances are associated with the development of IBD, of which disease in the first year of life is an independent risk factor in multivariate analysis. (Inflamm Bowel Dis 2007) [source] | |||||||||||||