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At least 667 records · Page 37Linked to original sources
PubMed2004

Incidence and clinical complications of vancomycin-resistant enterococcus in pediatric stem cell transplant patients.

Vancomycin-resistant enterococcus (VRE) are increasingly important pathogens in stem cell transplant (SCT). In all, 61 pediatric SCT patients had surveillance stool cultures for VRE between July 1999 and November 2002. When VRE was identified, the patients were placed on strict contact isolation. VRE was detected in 15 patients (24.6%). The median age was 3.6 years (range 0.6-18.5 years). Of the 15, 13 (87%) received an allogeneic transplant (six unrelated and seven related). Five of the 15 (33%) colonized patients developed VRE bacteremia. The bacteremia resolved in all five patients after therapy with quinupristin/dalfopristin; three patients required central line removal. Four patients died (38-153 days) post-SCT due to relapse or transplant complication not related to VRE. Of the 11 surviving patients, seven cleared the colonization at a median of 144 days (range 61-198 days) postcolonization. Four patients remain colonized at 68-702 days after the first positive culture. Intestinal colonization with VRE occurred commonly in pediatric SCT patients. Although the morbidity from VRE was not substantial, transplant patients were colonized for prolonged periods. Our results indicate that surveillance for VRE is an effective way to identify colonized patients and may lead to a decrease in transmission to other patients.

Adolescent↗
PubMed1999

Oral dosing of neonatal mice with sucrose reduces infection with Cryptosporidium parvum.

Cryptosporidium parvum is a significant cause of diarrheal disease in humans and economically important livestock species. There is no effective treatment available for this protozoan parasite. Mechanisms of intestinal colonization by C. parvum are not well understood, but it has been suggested that the parasite may utilize a lectin-like receptor. We used an infant mouse model to test whether high sugar concentrations in the intestine would affect in vivo colonization with C. parvum. We found that a single oral dose of sucrose, administered to mice at the time of, or 24 hr before, challenge with C. parvum significantly reduced infection. Significant reduction of infection was also seen in mice given isomaltose. Histologic examination of intestinal sections of mice treated with sucrose or isomaltose, but not other sugars, showed marked vacuolation of the small intestinal epithelium 1 day after treatment. Three days after treatment, tissue appeared normal. Thus, sucrose and, to a lesser extent, isomaltose reduced in vivo colonization with C. parvum and altered epithelial cell morphology in intestines of mice.

Administration, Oral↗
PubMed2004

Long polar fimbriae contribute to colonization by Escherichia coli O157:H7 in vivo.

The contribution of long polar fimbriae to intestinal colonization by Escherichia coli O157:H7 was evaluated in sheep, conventional pigs, and gnotobiotic piglets. E. coli O157:H7 strains with lpfA1 and lpfA2 mutated were recovered in significantly lower numbers and caused fewer attachment and effacement lesions than the parent strain.

Animals↗
PubMed2003

Critical roles for stx2, eae, and tir in enterohemorrhagic Escherichia coli-induced diarrhea and intestinal inflammation in infant rabbits.

Enterohemorrhagic Escherichia coli (EHEC) is a group of food-borne pathogens that can cause diarrhea, colitis, and the hemolytic uremic syndrome (HUS). The importance of several of the proposed EHEC virulence factors lacks experimental verification in animal models. The limitations of current animal models led us to reexamine the infant rabbit model for the study of EHEC pathogenicity. Here, we report that intragastric inoculation of a Shiga toxin 2 (Stx2)-producing E. coli O157:H7 clinical isolate into infant rabbits led to severe diarrhea and intestinal inflammation but no signs of HUS. We constructed a set of isogenic derivatives of this isolate with deletions in several putative virulence genes, including stx(2), eae, tir, and ehxA, to investigate the contribution of individual virulence factors to EHEC pathogenicity. stx(2) increased the severity and duration of EHEC-induced diarrhea. Furthermore, although stx(2) had no role in EHEC intestinal colonization nor was it required for EHEC-induced inflammation, stx(2) altered how the host responded to EHEC infection by promoting heterophilic infiltration of the colonic epithelium and lamina propria. Intragastric inoculation of purified Stx2 also induced inflammation and diarrhea in this model. Diarrhea and intestinal inflammation were also dependent on EHEC colonization, as EHEC derivatives with deletions in eae and tir did not colonize, form attaching and effacing lesions, or develop clinical signs of disease. Our studies indicate that infant rabbits are a useful model for investigation of the intestinal stage of EHEC pathogenesis and suggest that Shiga toxin may play a critical role in causing diarrhea and inflammation in patients infected with EHEC.

Adhesins, Bacterial↗
PubMed1986

Colonization of Syrian hamsters with streptomycin resistant Campylobacter jejuni.

A streptomycin resistant Campylobacter jejuni inoculated per os into two populations of Syrian hamsters (one endemically harboring C. jejuni, the other free of C. jejuni) established chronic colonization of the organism in both groups. Diet, steroid administration, age of hamsters or prior exposure to C. jejuni did not appreciably alter incidence of diarrhea or colonization of C. jejuni. The majority of hamsters sampled during the course of the experiment (1 to 22 weeks) shed streptomycin resistant C. jejuni in the feces. In four hamsters sampled at 14, 17, 19, and 22 weeks, post inoculation, streptomycin resistant C. jejuni were recovered in ileal, cecal, jejunal, duodenal and colonic contents (10(4) to 10(7) colony forming units/gram of intestinal content). The hamster appears to be a potentially useful model for the study of intestinal colonization of enteropathogenic C. jejuni. Hamsters shedding C. jejuni in their feces for extended periods of time should be considered a zoonotic threat to both pet owners and laboratory personnel.

Animals↗
PubMed1989

Effects of fasting and glutathione depletors on the GSH-dependent enzyme system in the gastrointestinal mucosa of the rat.

In rats, the glutathione content of the gastrointestinal mucosa amounted to 50-60% of that of the liver. The GSH-S-transferase activity towards an aryl substrate (CDNB) was low in the stomach, colon and rectum, i.e. 5% of hepatic activity. In the small intestine there was a typical decline of activity from proximal to distal segments. GSH-Peroxidase was much lower in the intestinal mucosa as compared to the stomach and liver, whereas the GSSG-reductase was 2-3 times higher in the gastrointestinal tract in comparison to the liver. Fasting for 24 h significantly decreased the GSH content, GSH-aryltransferase and GSSG-reductase activities in the liver but not in the intestine, where even higher GSH concentrations were found in the proximal segments. L-Buthionine-sulfoximine, an inhibitor of the GSH-synthesis, caused a marked decrease of the GSH levels in the liver, stomach, proximal small intestine, colon and rectum and a concomitant decline in GSSG-reductase activity. Among the GSH-depleting agents, paracetamol exerted the strongest effect, whereas 1,1-dichloroethylene and phorone only decreased the GSH content in the liver and stomach.

Animals↗
PubMed2000

Effect of parenteral antibiotic administration on the establishment of colonization with vancomycin-resistant Enterococcus faecium in the mouse gastrointestinal tract.

A mouse model of intestinal colonization with vancomycin-resistant enterococci (VRE) was used to study the effect of different beta-lactam antibiotics on establishment of VRE colonization. A clinical VanB VRE isolate, Enterococcus faecium C68 (102 or 104 cfu), was inoculated by gastric gavage in conjunction with subcutaneous administration of antibiotics. The MIC of ceftriaxone and ticarcillin against VRE strain C68 is >10,000 microg/mL, and the MIC of piperacillin is 1250 microg/mL. Ceftriaxone and ticarcillin-clavulanate treatment groups developed persistently high levels of stool VRE compared with both the saline and the piperacillin-tazobactam (Pip-Taz) groups (P<.008). The level of stool VRE in the Pip-Taz group did not differ from that for the saline group. Thus, in this mouse model, beta-lactam antibiotics with minimal anti-enterococcal activity promoted establishment of high-level VRE colonization, but Pip-Taz (a beta-lactam antibiotic with more potent activity against VRE) did not.

Animals↗
PubMed2000

Clostridium difficile toxins A and B can alter epithelial permeability and promote bacterial paracellular migration through HT-29 enterocytes.

Clostridium difficile toxins A and B are the widely recognized etiologic agents of antibiotic-associated diseases ranging from diarrhea to pseudomembranous colitis. We hypothesized that C. difficile toxins may alter intestinal epithelial permeability and facilitate bacterial penetration of the intestinal epithelial barrier. Experiments were designed to clarify the effects of C. difficile toxins A and B on the flux of inert particles across HT-29 enterocyte monolayers, and to correlate these results with bacteria-enterocyte interactions. In all experiments, mature, confluent HT-29 cultures were preincubated 16 h with toxin A or B (1-100 ng/mL). To study alterations in epithelial permeability, toxin-treated enterocytes were incubated with 5 pM solutions of 10- and 40-kD inert dextran particles. Toxin A, but not toxin B, was associated with increased dextran flux through enterocyte monolayers. To study bacteria-enterocyte interactions, toxin-treated enterocytes were incubated with 10(8) Salmonella typhimurium, Proteus mirabilis, or Escherichia coli. Although numbers of internalized bacteria were generally unaffected, both toxins were associated with increased bacterial adherence, as well as increased bacterial transmigration through enterocyte monolayers. Bacterial transmigration was significantly greater using toxin A- compared to toxin B-treated enterocytes, consistent with the observation that dextran flux was significantly greater using toxin A- compared to toxin B-treated enterocytes. Thus intestinal colonization with toxigenic C. difficile may facilitate bacterial penetration of the intestinal epithelium by a mechanism involving increased permeability of the intestinal epithelial barrier.

Actins↗
PubMed1999

[Ventilator-associated pneumonia; controversies with respect to diagnosis, pathogenesis, therapy and prevention].

Ventilator-associated pneumonia (VAP) is the most frequent nosocomial infection among intensive care patients; it is associated with increased morbidity and mortality. VAP is always preceded by colonization of the upper respiratory tract with potentially pathogenic micro-organisms. Oropharyngeal colonization is pivotal in the pathogenesis of VAP, while gastric and intestinal colonization appear to be less important than generally believed. The diagnosis is difficult and usually relies on a combination of clinical, microbiological and radiographic criteria. This combination of criteria may have a high sensitivity for VAP, but specificity is low. As a result, many patients receive antibiotics unnecessarily. Bronchoscopic sampling of lower airways can increase specificity, but whether these relatively expensive techniques are cost-effective remains to be established. The best antibiotic therapy for VAP is unknown. General infection control measures remain the cornerstone of infection prevention in each intensive care unit (ICU). Selective digestive decontamination (SDD) was associated with a reduction in the incidence of VAP, but mortality rates remained largely unaffected, and selection of antibiotic-resistant pathogens remains a potential disadvantage. Routine SDD in ICU is discouraged. Decontamination of the oropharynx appears to be equally effective.

Antibiotic Prophylaxis↗
PubMed1994

The Vibrio cholerae acfB colonization determinant encodes an inner membrane protein that is related to a family of signal-transducing proteins.

Vibrio cholerae accessory colonization factor genes (acfA, B, C, and D) are required for efficient intestinal colonization. Expression of acf genes is under the control of a regulatory cascade that also directs the synthesis of cholera toxin and proteins involved in the biogenesis of the toxin-coregulated pilus. The gene for acfB was cloned by using an acfB::TnphoA fusion junction to probe a V. cholerae O395 bacteriophage lambda library. DNA sequence analysis revealed that acfB is predicted to encode a 626-amino-acid protein related to the V. cholerae HlyB and TcpI proteins. These three Vibrio proteins have amino acid sequence similarity in a region highly conserved among bacterial methyl-accepting chemotaxis proteins. Analysis of the predicted AcfB amino acid sequence suggests that this colonization determinant possesses a membrane topology and domain organization similar to those of methyl-accepting chemotaxis proteins. Heterologous expression of acfB in Escherichia coli generates four polypeptide species with apparent molecular masses of 34, 35, 74, and 75 kDa. The 74- and 75-kDa proteins appear to represent modified forms of the full-length AcfB protein. The 34- and 35-kDa polypeptide species most likely correspond to a C-terminal 274-amino-acid polypeptide that results from internal translation initiation of acfB mRNA. Localization studies with AcfB-PhoA hybrid proteins indicate that AcfB resides in the V. cholerae inner membrane. V. cholerae acfB::TnphoA mutants display an altered motility phenotype in semisolid agar. The relationship between AcfB and Vibrio motility and the amino acid similarities between AcfB and chemotaxis signal-transducing proteins suggest that AcfB may interact with the V. cholerae chemotaxis machinery. The data presented in this report provide preliminary evidence that acfB encodes an environmental sensor/signal-transducing protein involved in V. cholerae colonization.

Amino Acid Sequence↗
PubMed1999

Tissue and cell distribution of the multidrug resistance-associated protein (MRP) in mouse intestine and kidney.

The multidrug resistance-associated protein (MRP) that is involved in drug resistance and the export of glutathione-conjugated substrates may not have the same epithelial cell membrane distribution as the P-glycoprotein encoded by the MDR gene. Because intestinal and kidney epithelial cells are polarized cells endowed distinct secreting and absorptive ion and protein transport capacities, we investigated the tissue and cell distribution of MRP in adult mouse small intestine, colon, and kidney by immunohistochemistry. Western blot analyses revealed the 190-kD MRP protein in these tissues. MRP was found in the basolateral membranes of intestinal crypt cells, mainly Paneth cells, but not in differentiated enterocytes. All the cells lining the crypt-villous axis of the colon wall contained MRP. MRP was found in the glomeruli, ascending limb cells, and basolateral membranes of the distal and collecting tubule cells of the kidney but not in proximal tubule cells. Cultured mouse intestinal m-ICcl2 cells and renal distal mpkDCT cells that have retained the features typical of intestinal crypt and renal distal epithelial cells, respectively, also possess MRP in their basolateral membranes. The patterns of subcellular and cellular distribution indicate that MRP may have a specific role in the basolateral transport of endogenous compounds in Paneth, renal distal, and collecting tubule cells.

ATP-Binding Cassette Transporters↗
PubMed2002

[Increased expression of HOXA9 gene in Hirschsprung disease].

OBJECTIVE: Hirschsprung disease is characterized by segmental aganglionosis of the terminal bowel. Neurons of the enteric nervous system arise from neural crest, migrate and colonize intestinal muscle coat where they proliferate and differentiate. The first pathophysiologic hypothesis suggests an absence of neural cell migration. The most recent hypothesis involves disorders of their homing and/or their differentiation due to an altered intestinal microenvironment. PATIENTS AND METHODS: We analyzed the expression of muscle markers and laminin isoforms by immunocytochemistry and of homeotic genes involved in the regionalization of the intestinal mesenchyme during development (HOXA4, HOXA9, HOXD9) by RT-PCR, in colon specimens from two children with Hirschsprung disease (pathological and transition regions) and from healthy adult controls. RESULTS: We showed an increase in HOXA9 gene expression in Hirschsprung disease specimens while HOXA4 and HOXD9 mRNA expressions were unchanged. No significant differences in the muscle markers nor in the laminin isoforms were noted. CONCLUSION: These data suggest that intrinsic dysregulation of the intestinal wall microenvironment could account for the pathophysiology of Hirschsprung disease.

Adult↗
PubMed2004

In vitro studies on the colonization of bovine colonic mucosa by Shiga-toxigenic Escherichia coli (STEC).

This study investigated host-related factors that influence intestinal colonization by Shiga-toxigenic E. coli (STEC). A quantitative colonization assay was developed to comparatively measure attachment of STEC to bovine colonic tissues maintained in vitro. No differences were determined in colonization susceptibility between tissues derived from weaning calves and adult cattle, or for tissues from cattle fed grain and forage-based rations. Substrate conditions designed to represent various intra-enteric environments were tested for their effect on STEC/mucosal interaction. Under conditions corresponding to a well-fed ruminant (high volatile fatty acid and lactate concentrations, low pH), significantly less STEC colonized the mucosal surface of colonic biopsies. These results may help explain why fasted, poorly or intermittently fed cattle and pre-ruminant calves excrete STEC to a greater degree. Studies on the ecology of STEC within the ruminant gut help identify mechanisms to reduce their threat to public health.

Age Factors↗
PubMed1987

Effect of broad-spectrum parenteral antibiotics on "colonization resistance" of intestinal microflora of humans.

Studies with animals have shown that the normal intestinal microflora protects against colonization by new strains ("colonization resistance") and that this protective effect may be related to the anaerobic component of the microflora. However, colonization resistance has not been shown in humans. We administered cefoxitin, piperacillin, cefoperazone, and aztreonam intravenously to healthy subjects for 9 days and monitored the acquisition of new isolates in the fecal flora. Seven of sixteen antibiotic-treated subjects but none of four untreated controls became colonized by gram-negative bacilli. However, there was no correlation between colonization and the particular drug given or the extent of suppression of anaerobes or of any other component of the fecal microflora. Cefoxitin and piperacillin were associated with the greatest increases in the numbers of drug-resistant bacteria and in fecal beta-lactamase content. The results of this study support the concept that colonization resistance occurs in humans and is diminished by antibiotic administration but fail to support the hypothesis that resistance is related to the anaerobic microflora.

Anti-Bacterial Agents↗
PubMed1985

[Ways of reducing mortality in patients with gastric and small and large intestine fistulas].

During 16 years operations were performed on 423 patients with peptic ulcers of anastomoses, in 13 of them the disease was complicated by gastro-intestinal-colonic fistulas. Of 7 patients operated upon during first 11 years four patients died, of 6 patients operated upon during the second period (the last 5 years) there were no lethal outcomes. The less lethality was due to using less traumatic operations and longer preparing the patients for operations.

Colonic Diseases↗
PubMed2001

Characterization of the role of the ToxR-modulated outer membrane porins OmpU and OmpT in Vibrio cholerae virulence.

ToxR, the transmembrane regulatory protein required for expression of virulence factors in the human diarrheal pathogen Vibrio cholerae, directly activates and represses the transcription of two outer membrane porins, OmpU and OmpT, respectively. In an attempt to dissect the role of the OmpU and OmpT porins in viability and virulence factor expression, in-frame chromosomal deletions were constructed in the coding sequences of ompU and ompT of V. cholerae. Two separate deletions were introduced into ompU; the first (small) deletion, Delta ompU1, removed the coding sequence for 84 internal amino acids (aa), while the second (large) deletion, Delta ompU2, removed the coding sequence for the entire amino-terminal 274 aa. The Delta ompU1 strain had a growth defect that could not be complemented by episomal expression of full-length ompU. In contrast, a strain with Delta ompU2 displayed wild-type growth kinetics in rich media, suggesting that this is the true phenotype of a strain lacking OmpU and that the truncated OmpU protein, rather than the absence of OmpU, may be the cause for the Delta ompU1 phenotype. A large deletion removing the coding sequence for the entire N-terminal 273 aa of OmpT (Delta ompT) was also constructed in wild-type as well as Delta toxR and Delta ompU2 strains, and these strains displayed wild-type growth kinetics in rich media. However, the Delta ompU2 strain was deficient for growth in deoxycholate compared to wild-type, Delta ompT, and Delta ompU2 Delta ompT strains, reinforcing a positive role for the OmpU porin and a negative role for the OmpT porin in V. cholerae resistance to anionic detergents. The Delta ompU2, Delta ompT, and Delta ompU2 Delta ompT strains exhibited wild-type levels of in vitro virulence factor expression and resistance to polymyxin B and serum and in vivo colonization levels similar to a wild-type strain in the infant mouse intestine. Our results demonstrate that (i) OmpU and OmpT are not essential proteins, as was previously thought; (ii) these porins contribute to V. cholerae resistance to anionic detergents; and (iii) OmpU and OmpT are not essential for virulence factor expression in vitro or intestinal colonization in vivo.

Adhesins, Bacterial↗