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PubMed2000

Altered expression of the ToxR-regulated porins OmpU and OmpT diminishes Vibrio cholerae bile resistance, virulence factor expression, and intestinal colonization.

The transmembrane transcriptional activators ToxR and TcpP modulate expression of Vibrio cholerae virulence factors by exerting control over toxT, which encodes the cytoplasmic transcriptional activator of the ctx, tcp, and acf virulence genes. However, ToxR, independently of TcpP and ToxT, activates and represses transcription of the genes encoding two outer-membrane porins, OmpU and OmpT. To determine the role of ToxR-dependent porin regulation in V. cholerae pathogenesis, the ToxR-activated ompU promoter was used to drive ompT transcription in a strain lacking OmpU. Likewise, the ToxR-repressed ompT promoter was used to drive ompU transcription in a strain lacking both ToxR and OmpT. This strategy allowed the generation of a toxR(+) strain that expresses OmpT in place of OmpU, and a toxR(-) strain that expresses OmpU in place of OmpT. Growth rates in the presence of bile salts and other anionic detergents were retarded for the toxR(+) V. cholerae expressing OmpT in place of OmpU, but increased in toxR(-) V. cholerae expressing OmpU in place of OmpT. Additionally, the toxR(+) V. cholerae expressing OmpT in place of OmpU expressed less cholera toxin and toxin-coregulated pilus, and this effect was shown to be caused by reduced toxT transcription in this strain. Finally, the toxR(+) V. cholerae expressing OmpT in place of OmpU was approximately 100-fold reduced in its ability to colonize the infant-mouse intestine. Our results indicate that ToxR-dependent modulation of the outer membrane porins OmpU and OmpT is critical for V. cholerae bile resistance, virulence factor expression, and intestinal colonization.

Adhesins, Bacterial↗
PubMed1978

[Restrictive artificial mechanisms in prevention of late complications after small intestine-colon anastomosis].

The experiments on 30 dogs proved that reduplication and semi-invagination serve as restrictive mechanisms before small intestine-colon anastomosis. These procedures slow dowm the evacuation of intestinal contents, interfere with small intestine-colonic outflow, improve digestion and absorption, contribute to the shortening of the time needed for compensation, provide better late results of the right hemicolonectomy.

Animals↗
PubMed1996

Surveillance of intestinal colonization and of infection by vancomycin-resistant enterococci in hospitalized cancer patients.

OBJECTIVE: To study epidemiologic features of and risk factors for intestinal colonization and infection by vancomycin-resistant enterococci (VRE) in cancer patients. METHODS: During a 41-month period, over 7600 fecal samples and all samples from sterile sites from hospitalized cancer patients were screened for VRE. Species were identified and isolates analyzed by pulsed-field gel electrophoresis (PFGE) of SmaI DNA restriction fragments. Antibiotic resistance was characterized by MIC determinations, and polymerase chain reaction for vanA, vanB, and vanC1 genes. Plasmid contents were analyzed before and after PstI and HindIII restriction, and by Southern hybridization with a vanA probe. Two case-control studies were performed to identify risk factors for colonization or infection by VRE, respectively. RESULTS: Eighty-two isolates were recovered from 81 patients. Most (72%) isolates were Enterococcus faecium VanA/vanA, with 37 different PFGE types, each of which was found in only one to four patients, except for type P1, which was found in 20 patients hospitalized over a 3-month period in the pediatric wards. Plasmid analysis suggested that only two types of plasmid were carrying gene vanA, as part of a transposon related to transposon Tn 1546 from reference strain E. faecium BM4147. Seventy-seven patients were colonized during the study period. Six of them became infected. Four patients were infected but not colonized. Only one patient died during the course of infection, but intestinal colonization persisted for months in the survivors. Case-control analysis revealed that cephalosporin treatment was a significant risk factor for colonization. No significant risk factor for infection was found in colonized patients. CONCLUSION: Colonization by VRE was mostly endemic and the colonized patients were not often infected. However, when clustered cases of colonization occurred, they were then associated with an increased rate of infection.

Journal Article↗
PubMed1985

Motility as an intestinal colonization factor for Campylobacter jejuni.

The colonization of the intestinal tract of suckling mice by Campylobacter jejuni was examined by orally challenging the mice with a wild-type strain and several nonmotile mutant strains which were isolated after treating the wild-type strain with mutagens. The wild-type strain had colonized the lower portion of the small intestine, the caecum and the colon 2 d after inoculation. Two nonmotile strains, one of which (M8) had lost all the flagellar structure including the filament, the hook and the basal structure, and the other (M1) which had lost only the filament region, were both cleared from the intestinal tract 2 d after challenge. Another nonmotile strain (M14), which had a complete flagellar structure like that of the wild-type strain, did not colonize and was cleared from the intestinal tract like the other nonmotile and nonflagellated strains. One atypically motile strain (M5), which had a shorter flagellar filament than that of the wild-type strain, colonized the intestinal tract only when mice were challenged with a large inoculum. None of the mice challenged with either the wild-type or any of the mutant strains showed signs of illness. We concluded that motility is an important factor in the colonization of the intestinal tract of suckling mice by C. jejuni.

Adhesiveness↗
PubMed1983

Intestinal colonization of infant hamsters with Clostridium difficile.

Infant hamsters of different ages were examined for their susceptibility to enteric Clostridium difficile colonization. Intragastric administration of C. difficile to infant hamsters resulted in multiplication of the organism in the intestinal tracts of animals 4 to 12 days old; hamsters younger or older were resistant to C. difficile intestinal colonization. Toxicity to the colonized animals could not be demonstrated despite cytotoxin titers in some infant hamsters comparable to titers found in the intestinal tracts of adult hamsters with C. difficile-associated intestinal disease. When introduced into 4-day-old hamsters, C. difficile colonized the intestinal tract and remained at high levels until the animals were 13 days old, at which time the presence of intestinal C. difficile could no longer be demonstrated. The number of C. difficile required to colonize the intestinal tracts of 50% of 7-day-old hamsters was 18 viable cells. On the other hand, 10(8) viable cells of C. difficile failed to colonize the intestinal tracts of healthy, non-antibiotic-treated adult hamsters.

Aging↗
PubMedDate not supplied

Bacterial contamination of enteral nutrient solutions: intestinal colonization and sepsis in mice after ingestion.

Contaminated enteral nutrient solution (ENS) was used to assess the risks of intestinal colonization and invasive sepsis using normal mice. Dilute Osmolite containing 10(6) Group B Streptococci/ml given for 2 to 10 consecutive days resulted in the detection of organisms by rectal washing sampling and in the recovery of 10(3) to 10(4) organisms from the cecum, large intestine, and rectum. Only 10(1) organisms survived in the small intestine. Colonization, or the persistence of organisms for 10 days after exposure, was produced after 2 days of ingestion in 44% of animals and in 100% after exposure for 5 days. There were 39 septic deaths. During the 7-day ingestion interval 15 died and 24 died within 10 days after exposure. The risk of sepsis was highest for young mice. Ways to minimize bacterial contamination of ENS intended for administration to patients are discussed.

Age Factors↗
PubMed2025

Genomic and phenotypic insights into ST164 blaNDM-1-positive Acinetobacter baumannii from intestinal colonization in China.

BACKGROUND: Carbapenem-resistant Acinetobacter baumannii (CRAB) poses a critical global threat, especially in ICUs. Yet, reports on ST164 CRAB harboring blaNDM-1 remain scarce. This study investigates two clinical CRAB isolates, L4773hy and L4796hy, derived from intestinal colonization in Hangzhou, China, focusing on their phenotypic and genomic characteristics as well as the broader transmission of ST164 A. baumannii. METHODS: Bacterial identification was performed using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF) mass spectrometry. Antimicrobial susceptibility was assessed via agar and broth microdilution. Whole-genome sequencing employed Illumina NovaSeq 6000 and Oxford Nanopore platforms. Resistance genes, insertion elements, transposons, and integrons were detected using ResFinder, PlasmidFinder, VFDB, ISFinder, pdifFinder, and IntegronFinder. Strains were typed by MLST, and a phylogenetic tree was constructed with kSNP3.0. Genetic environment diagrams were generated using Easyfig 2.2.5. RESULTS: Two blaNDM-1-carrying A. baumannii isolates exhibiting extensive resistance to carbapenems, cephalosporins, and fluoroquinolones. Whole-genome sequencing and genetic environment analysis revealed the presence of a conserved structural sequence (ISAba14-ISAba14-aphA-ISAba125-blaNDM-1-bleMBL) on their chromosomes. Phylogenetic and clonal dissemination analysis showed that ST164 CRAB is primarily distributed in China and exhibits clonal spread. Pathogenicity studies indicated that blaNDM-1-positive ST164 strains have enhanced survival under immune pressure but do not display increased virulence in infection models. CONCLUSION: This study provides the genomic and phenotypic characterization of intestinally colonized ST164 blaNDM-1 positive CRAB in Hangzhou, China. The elucidation of the genetic environment of blaNDM-1 further confirms the clonal dissemination of ST164 isolates, highlighting the importance of enhanced surveillance and infection control measures to mitigate the spread of these multidrug-resistant pathogens.

Acinetobacter baumannii↗
PubMed1988

Effects of clindamycin and metronidazole on the intestinal colonization and translocation of enterococci in mice.

The intestinal colonization and translocation of enterococci was studied in mice treated intramuscularly with metronidazole or clindamycin, with or without oral streptomycin. Treatment with metronidazole resulted in selective elimination of strictly anaerobic cecal bacteria, with a 100-fold increase in the numbers of aerobic and facultative gram-negative bacilli and a 10,000-fold increase in the numbers of aerobic and facultative gram-positive species. Clindamycin had a similar effect on the cecal flora except that the numbers of aerobic and facultative gram-positive bacteria decreased at least 10-fold. The predominating gram-positive species in the cecal flora or metronidazole-treated mice was an enterococcus, but this organism could not be recovered from the ceca of clindamycin-treated mice. Translocating bacteria (primarily gram-negative enteric bacteria) were recovered from the mesenteric lymph nodes of the majority of mice given metronidazole or clindamycin. Gram-positive bacteria were not recovered from the mesenteric lymph nodes of 20 clindamycin-treated mice, whereas 26% of 19 metronidazole-treated mice had translocating enterococci. With addition of streptomycin to the metronidazole and clindamycin regimens, mice treated with metronidazole-streptomycin became colonized predominantly with an enterococcus, and this was the only translocating species recovered from 13% of 23 mice; however, enterococci could not be detected in the ceca of clindamycin-streptomycin-treated mice, and Bacillus spp. were recovered from the mesenteric lymph nodes of 8% of 24 mice, reflecting the composition of the cecal flora. The apparent elimination of enterococci from the ceca of clindamycin and clindamycin-streptomycin-treated mice was inconsistent with the observation that the average (n=6) peak levels of clindamycin in blood and ceca were 25 and 21 microgram/ml, respectively, whereas the in vitro MIC was 128 microgram/ml. However, this apparent in vivo activity of clindamycin against enterococci was not evident in mice given 10(9) oral enterococci; the concentrations of cecal enterococci in both clindamycin-streptomycin- and metronidazole-streptomycin-treated mice were 10(10) to 10(11) enterococci per g, with translocating enterococci recovered from approximately half of these antibiotic-treated mice. Thus antibiotic therapy with metronidazole, clindamycin, metronidazole-streptomycin, and clindamycin-streptomycin resulted in a wide variation in the cecal population levels and translocation frequencies of enterococci. This variation appeared to be related to the discrepancy between the in vivo and in vitro activities of clindamycin against enterococci.

Animals↗
PubMed1994

Relationship between intestinal colonization of Bifidobacterium bifidum in infants and the presence of exogenous and endogenous growth-promoting factors in their stools.

The relationship between the intestinal colonization of a test strain of Bifidobacterium bifidum requiring human milk growth-promoting factors in vitro and the presence of growth-promoting factors either in the stools of human neonates or in their diet was investigated. Thirty-one infants were inoculated with a single dose of this strain within the first 8 d of life. Spores of a strictly thermophilic Bacillus admixed with the B. bifidum inoculum were used as transit marker, and the fecal population levels of both strain B. bifidum and the transit marker were recorded within 6 d after inoculation. Strain B. bifidum was found in the predominant flora of six neonates. It was eliminated more quickly than the transit marker from the stools of 17 neonates. Its population remained at a low level in the remaining eight neonates. Amounts of B. bifidum growth-promoting factor in the infant stools were not significantly different whether they harbored strain B. bifidum at a high population level or not. Although these amounts were significantly higher in infants fed human milk containing B. bifidum growth-promoting factor than in infants fed formula milk without B. bifidum growth-promoting factor, strain B. bifidum became established in one of the 18 infants fed human milk and in five of the 13 formula-fed infants. No relationship could be found between the population levels of strain B. bifidum and those of facultatively anaerobic streptococci and enterobacteria already present on d 0 and 1. These results clearly show that no relationship exists between the intestinal colonization of B. bifidum and the amounts of exogenous or endogenous growth-promoting factors found in stools.

Administration, Oral↗
PubMed1999

Salmonella landau as a live vaccine against Escherichia coli O157:H7 investigated in a mouse model of intestinal colonization.

The present study was performed to assess the potential of a humoral mucosal immune response directed against the O157 antigen of Escherichia coli O157:H7 to prevent intestinal colonization by the pathogen. To this end, mice were gavaged with inocula of Salmonella landau, a Salmonella strain that naturally expresses the O157 antigen. Salmonella landau was avirulent for mice. Despite this, mice exposed to S. landau developed high titres of serum and coproantibodies against the O157 antigen. These mice, compared with controls, demonstrated some ability to resist transient intestinal colonization by an oral inoculum of an isolate of E. coli O157:H7. These findings suggest that a local immune response directed against the O157 antigen might increase host resistance to this pathogen.

Administration, Oral↗
PubMed2003

Deletion of a Vibrio cholerae ClC channel results in acid sensitivity and enhanced intestinal colonization.

ClC chloride channels are found in all three kingdoms of life though little is known about their functions in prokaryotes. Here we investigated the role of a Vibrio cholerae ClC channel in acid resistance and intestinal colonization. The putative V. cholerae ClC channel was found to confer mild resistance to acid when pH was adjusted with HCl, but not with other acids. Surprisingly, a ClC channel deletion mutant exhibited enhanced intestinal colonization in infant mice.

Acids↗
PubMed2006

Contribution of AIDA-I to the pathogenicity of a porcine diarrheagenic Escherichia coli and to intestinal colonization through biofilm formation in pigs.

In order to evaluate the role of the AIDA-I of porcine diarrheagenic Escherichia coli strain PD20 serogroup O143 (AIDA-I(+), STb(+)), a mutant strain PD20M (AIDA-I(-), STb(+)) was generated from strain PD20 by an allelic exchange procedure. In addition, the full-length aidA gene was reintroduced into strain PD20M to generate the complemented strain PD20C (pTaidA, AIDA-I(+), STb(+)). A non-pathogenic E. coli strain PD71 was used as negative control. Each strain was inoculated to newborn pigs via stomach tube. Severity of diarrhea was evaluated clinically and intestinal colonization was assessed by histology, immunohistochemistry (IHC), and transmission electron microscopy (TEM) including immunogold electron microscopy (IGEM). The adhesion pattern to HeLa cells, bacterial auto-aggregation and biofilm formation were evaluated in vitro. Pigs infected with strains PD20 or PD20C developed diarrhea 16 and 28h after inoculation, respectively, in contrast to pigs infected with strains PD20M or PD71. Histology, IHC, TEM and IGEM examinations showed heavy bacterial colonization with biofilm formation in the large intestine, and marked in vivo expression of AIDA-I protein in pigs infected with strains PD20 or PD20C in contrast to pigs infected with strains PD20M or PD71. The in vitro assays showed marked diffuse adherence to HeLa cells, enhanced bacterial auto-aggregation and significant biofilm formation (p<0.05) by the AIDA-I(+) strains, when compared to AIDA-I(-) strains. These results demonstrate that expression of AIDA-I is essential for intestinal colonization and in vitro bacterial autoaggregation and biofilm formation. Thus, AIDA-I may be considered a significant virulence determinant in development of diarrhea caused by porcine diarrheagenic AIDA-I(+)E. coli PD20 in piglets.

Adhesins, Escherichia coli↗
PubMed2005

Enterococcal surface protein Esp does not facilitate intestinal colonization or translocation of Enterococcus faecalis in clindamycin-treated mice.

Enterococcal surface protein (Esp) is a cell wall-associated protein of Enterococcus faecalis that has been identified as a potential virulence factor. We used a mouse model to examine whether Esp facilitates intestinal colonization or translocation of E. faecalis to mesenteric lymph nodes. After clindamycin treatment, similar levels of high-density colonization were established after orogastric inoculation of an E. faecalis isolate containing the esp gene within a large pathogenicity island and an isogenic mutant created by allelic replacement of the esp gene with a chloramphenicol resistance cassette (P=0.7); translocation to mesenteric lymph nodes was detected in 3 of 12 (25%) mice in both groups. Isogenic mutants of FA2-2 (a plasmid-free derivative of E. faecalis strain JH2) with or without the esp gene failed to establish colonization of clindamycin-treated mice. These results suggest that Esp does not facilitate intestinal colonization or translocation of E. faecalis.

Animals↗
PubMed1992

Asymptomatic intestinal colonization by pathogenic Entamoeba histolytica in amebic liver abscess: prevalence, response to therapy, and pathogenic potential.

Since the application of isoenzyme electrophoresis to the study of Entamoeba histolytica, the prevalence and natural history of asymptomatic intestinal colonization in patients with amebic liver abscess (ALA) has not been addressed. We prospectively evaluated this enteric phase in 50 patients with ALA, using two dosage regimens of metronidazole. The overall prevalence of asymptomatic colonization was 72% (36/50). All these isolates, without exception, proved to express pathogenic zymodemes. Despite a 100% clinical response of the hepatic lesions, failure to eradicate the organism from the bowel occurred in 20 of these 36 subjects. During longitudinal posttreatment surveillance, three carriers returned with second bouts of invasive disease: one with dysentery and two with liver abscesses. Thus, in patients with ALA, there is a high prevalence of intestinal colonization with exclusively pathogenic strains, and treatment with metronidazole frequently results in a continued carrier state. These carriers have a propensity for developing recurrent invasive disease and constitute a public health hazard.

Adult↗
PubMed1979

A nosocomial outbreak of infections due to multiply resistant Proteus mirabilis: role of intestinal colonization as a major reservoir.

An outbreak of nosocomial infections involving an unusual strain of multiply resistant Proteus mirabilis (phage type 8888) occurred in 15 patients, 14 of whom were in the surgical intensive care unit at that time. No common source of infection was identified, and person-to-person transmission was the most likely mode of spread. Case-control analysis indicated a significantly increased risk infection related to length of hospital stay (P less than 0.005), number of operations (P less than 0.005), proximity to another case (P less than 0.01), number of antibiotics received (P less than 0.02), and use of a respirator (P less than 0.01). Only the number of operations (P less than 0.01) and proximity to another case (P less than 0.05) remained significant risk factors when related parameters were controlled by multivariate analysis. Thirteen of 14 patients prospectively cultured were colonized by the epidemic organism in the intestinal tract, while rectal carriage preceded infection by the same strain in at least four patients. These data suggest that intestinal colonization may have been an important reservoir for this outbreak, and the findings may explain the unduly prolonged course of intrahospital spread as well as the difficulty encountered in the eradication and control of the outbreak.

Cross Infection↗
PubMed2006

Antibiotic regimens and intestinal colonization with antibiotic-resistant gram-negative bacilli.

The intestinal tract provides an important reservoir for antibiotic-resistant gram-negative bacilli, including Enterobacteriaceae species, Pseudomonas aeruginosa, and Acinetobacter baumannii. Selective pressure exerted by antibiotics plays a crucial role in the emergence and dissemination of these pathogens. Many classes of antibiotics may promote intestinal colonization by health care-associated gram-negative bacilli, because the organisms are often multidrug resistant. Antibiotics may inhibit colonization by gram-negative pathogens that remain susceptible, but the benefits of this effect are often limited because of the emergence of resistance. Antibiotic formulary alterations and standard infection control measures have been effective in controlling outbreaks of colonization and infection with antibiotic-resistant gram-negative pathogens. Additional research is needed to clarify the role of strategies such as selective decontamination of the digestive tract and decontamination of environmental surfaces and of patients' skin and wounds.

Animals↗
PubMed1997

Endogenous antibody production to botulinum toxin in an adult with intestinal colonization botulism and underlying Crohn's disease.

A patient with obstruction of the terminal ileum from Crohn's disease developed complete paralysis in week 1 of hospitalization. Features initially suggested Guillain-Barre syndrome, but botulinum toxin was identified in serum and stool specimens from week 1 and type A toxin-producing Clostridium botulinum in stool specimens from weeks 3 to 19, confirming botulism due to intestinal colonization. In week 19, the inflamed small bowel was resected, and C. botulinum disappeared from the stool. In week 31, the patient was able to breath without assistance. Testing for an active immune response with neutralizing antibodies to C. botulinum at week 19 was positive; these antibodies remained at a protective level for >1 year. Intestinal colonization botulism, rare in adults, should be considered for patients with descending paralysis, especially those with a preceding alteration in small bowel function. An active immune response to botulinum toxin with production of protective antibodies has not been demonstrated previously in a patient with botulism and may have contributed to this patient's recovery.

Aged↗