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Stenotrophomonas maltophilia intestinal colonization in hospitalized oncology patients with diarrhea.

A 6-week surveillance study was performed to determine the prevalence of Stenotrophomonas maltophilia intestinal colonization among patients hospitalized in an oncology unit who developed diarrhea. Ninety-two stool samples obtained from 41 patients were cultured, and 4 patients (4 [9.5%] of 41 patients) had cultures that were positive for S. maltophilia. After controlling for duration of diarrhea, patients colonized with S. maltophilia had received a greater number of different types of antibiotics than noncolonized patients (5 vs. 3 different drugs; P=.04).

Anti-Bacterial Agents↗

Mycotoxin fumonisin B1 increases intestinal colonization by pathogenic Escherichia coli in pigs.

Fumonisin B(1) (FB(1)) is a mycotoxin that commonly occurs in maize. FB(1) causes a variety of toxic effects in different animal species and has been implicated as a contributing factor of esophageal cancers in humans. In the present study, we examined the effect of dietary exposure to FB(1) on intestinal colonization by pathogenic Escherichia coli associated with extraintestinal infection. Three-week-old weaned pigs were given FB(1) by gavage as a crude extract or as a purified toxin at a dose of 0.5 mg/kg of body weight daily for 6 days. On the last day of the toxin treatment, the pigs were orally inoculated with an extraintestinal pathogenic E. coli strain. All animals were euthanized 24 h later, necropsies were performed, and tissues were taken for bacterial counts and light microscopic examination. Ingestion of FB(1) had only a minimal effect on animal weight gain, did not cause any macroscopic or microscopic lesions, and did not change the plasma biochemical profile. However, colonization of the small and large intestines by an extraintestinal pathogenic E. coli strain was significantly increased. Our results show that FB(1) is a predisposing factor to infectious disease and that the pig can be used as a model for the study of the consequences of ingesting mycotoxin-contaminated food.

Administration, Oral↗

Bifidobacteria and human health: regulatory effect of indigenous bifidobacteria on Escherichia coli intestinal colonization.

Bifidobacteria are assumed to exert colonization resistance to enteric pathogens. We associated C3H germfree mice with either Bifidobacterium longum or Escherichia coli or both strains and studied how they settled in the gut and the lymphoid organs as well as their effect on mucus composition. Within 24 hE. coli colonized the gut of germfree or B. longum ex-germfree mice. In contrast,B. longum was established in the intestine of E. coli ex-germfree mice only 1 month after inoculation whereas it colonized the germfree gut within 24 h. Although B. longum did not exert colonization resistance to E. coli, the establishing of bifidobacteria in the gut partly prevented changes in the E. coli cell wall. After colonization of the germfree or B. longum mono-associated mice, E. coli lipopolysaccharide exhibited a higher concentration of Kdo and the O-antigen side chain disappeared. A reduction in Kdo content was observed within 1 month in E. coli-B. longum diassociated mice whereas it remained at a high level in E. coli mono-associated mice. Association in a second step with B. longum led to Kdo reduction. Changes in E. coli LPS might be related to mucus modification. Inoculation of either bacterium led to a slow increase in mucus protein content which was however twice as high after E. coli implantation. Inoculation of B. longum in a second step led to a reduction in protein content before B. longum colonized the intestine at a high level suggesting that the protein concentration in the mucus was controlled by the host itself. A new glycoprotein of 200-230 kDa detected during the period preceeding colonization seemed to be broken down by B. longum. The resulting end product might participate in the restoration of E. coli LPS. Finally,B. longum inoculation led to the disappearance of E. coli from kidneys, liver, spleen and lung. The organs were cleared of E. coli before B. longum highly colonized the intestine suggesting that high intestinal colonization by B. longum was not required. Regulation of E. coli invasion seemed to depend on the ability of B. longum to stimulate the immune system.

Journal Article↗

[Maternal lactation. II. Intestinal colonization in breast fed newborn infants].

Twenty-three low birth weight infants were studied to establish the role that breast milk plays in the intestinal colonization of the preterm infant, and in the control of epidemic diarrhea due to enteropathogenic E. coli, in nurseries. Twelve of these case were fed breast milk in bottles, and eleven with "humanized" powder cow's milk (NAN M.R.). Bacteriologic studies of feces were performed daily during the first 18 days of life. In 5 cases given breast milk, and in 8 receiving cow's milk, Staphylococcus aureus was isolated. Enteropathogenic E. coli was found in 3 cases with breast milk and in 6 with cow's milk. The finding of other non-pathogenic strains, was similar for both groups, except in the case of Proteus, that was found in 10 cases with breast milk, and in only 3 cases with cow's milk. Breast milk was unable to avoid the colonization by E. coli and in one case, was unable to eradicate this germ. None of the cases fed breast milk had diarrhea, including the three cases with E. coli. In another group, 4 cases developed severe acute diarrhea, due to enteropathogenic E. coli followed by 2 deaths. The results seem to point out that although colonization by enteropathogenic strains of E. coli is not completely avoided, these strains do not cause disease when these infants are fed breast milk.

Asepsis↗

Transcriptional regulation through RfaH contributes to intestinal colonization by Escherichia coli.

The Escherichia coli regulatory protein RfaH contributes to efficient colonization of the mouse gut. Extraintestinal pathogenic (ExPEC) as well as non-pathogenic probiotic E. coli strains rapidly outcompeted their isogenic rfaH mutants following oral mixed infections. LPS-core and O-antigen side-chain as well as capsular polysaccharide synthesis are among the E. coli virulence factors affected by RfaH. In respect of colonization, deep-rough LPS mutants (waaG) but not capsular (kps) mutants were shown to behave similarly to rfaH mutants. Furthermore, alteration in the length of O-antigen side-chains did not modify colonization ability either indicating that it was the regulatory effect of RfaH on LPS-core synthesis, which affected intestinal colonization. Loss of RfaH did not significantly influence adhesion of bacteria to cultured colon epithelial cells. Increased susceptibility of rfaH mutants to bile salts, on the other hand, suggested that impaired in vivo survival could be responsible for the reduced colonization capacity.

Animals↗

Intestinal colonization with Enterobacteriaceae in Pakistani and Swedish hospital-delivered infants.

Rectal cultures from Swedish and Pakistani hospital-delivered newborn infants were analysed regarding the early acquisition of enterobacteria. Swedish infants were delivered vaginally, Pakistani infants were delivered either vaginally or by caesarean section. The Swedish infants were all breast-fed, whereas breastfeeding was incomplete and often started late among the Pakistani infants. Both groups of Pakistani infants were more rapidly colonized with enterobacteria than were the Swedish infants. Cultures from Swedish infants seldom yielded more than one kind of enterobacteria; E. coli and Klebsiella were most frequently isolated. E. coli dominated in both Pakistani groups, but especially caesarean section delivered infants were in addition often colonized with Proteus, Klebsiella, Enterobacter or Citrobacter species. Breastfeeding from the first day of life reduced colonization with Klebsiella/Enterobacter/Citrobacter. The results suggest that environmental exposure, delivery mode and early feeding habits all influence the early intestinal colonization with enterobacteria.

Breast Feeding↗

Morphology of intestinal colonization of Yersinia enterocolitica serovar O3 in mice.

The present study was made to know the morphology of the initial invasion and lesions involved in the intestinal colonization of Yersinia enterocolitica serovar O3 in the epithelium of Peyer's patches of mice. Microfold (M) cells formed a specific structure like a pseudopodium and the bacteria were observed on the surface of the pseudopodium-like structure 4 hr after oral administration of serovar O3. The colonies of serovar O3 were observed in the epithelium and the lamina propria of the Peyer's patches dome region, and the bacteria grown in the Peyer's patches were in direct contact with the lumen without covered with the host tissue 24 hr after the administration.

Animals↗

Immunocytochemical and enzyme histochemical localization of kallikrein-like enzymes in colon, intestine, and stomach of rat and cat.

Kallikrein was localized in goblet (or mucous) cells of rat colon and in rat and cat small intestine and stomach by two immunocytochemical techniques. A kallikrein-like enzyme was also localized by enzyme histochemistry in mast cells of colon, intestine, and stomach of the cat, where they appeared to be associated with blood vessels in the lamina propria. The mast cell enzyme, however, was not detected by immunocytochemistry using antibodies to kallikrein. Modification in the enzyme histochemical procedure (pH, fixation) yielded positive results for a kallikrein-like protease in goblet cells of the intestine and colon. The possible physiological and pathological significance of kallikrein-like enzyme in the gastrointestinal tract and elsewhere is discussed.

Animals↗

Intestinal colonization of rats following experimental infection with Campylobacter jejuni.

Oral infection of rats with 10(6)-10(8) colony forming units per ml of Campylobacter jejuni resulted in prompt intestinal colonization. Campylobacter jejuni was recovered from rat faecal samples for four months post infection. The colonized rats did not succumb to clinical diarrhoea or pyrexia. The resistance of rats to C. jejuni clinical infection and their ability to shed the organism for protracted periods, make rats potential source of zoonotic campylobacteriosis.

Animals↗

The role of Klebsiella pneumoniae urease in intestinal colonization and resistance to gastrointestinal stress.

The first step in nosocomial infections due to Klebsiella pneumoniae is colonization of the patient's gastrointestinal (GI) tract. In a previous work, signature-tagged mutagenesis was used in a murine model to identify 13 genes required for efficient colonization, two of which were involved in urea metabolism. The role of urease was further investigated by the construction and analysis of an isogenic urease-deficient mutant. The behavior of both the wild-type strain and the urease-deficient mutant was tested under hostile conditions, reproducing stresses encountered in the GI environment. The wild-type strain had an acid tolerance response (ATR) to inorganic acid, was resistant to organic acids (38.5% survival) and was able to survive concentrations of bile encountered in vivo. The absence of urease did not affect the resistance of K. pneumoniae to acid and bile stresses, but the enhanced adhesion response to Int-407 cells after exposure to bile observed with the wild-type strain was no longer detected with the urease mutant. When tested in the murine intestinal colonization model, both strains were mainly recovered in the large intestine parts, and the mutant was impaired in its colonization capacities, but only when tested in competition with the wild-type strain. These findings emphasize the prominent role played by metabolic function in the colonization process of such a complex ecosystem as the host GI tract.

Acids↗

In vivo effect of cadmium chloride on intestinal colonization of rats by Campylobacter jejuni.

Campylobacter jejuni (10(8) C.F.U) fed intragastrically unto 18 laboratory rats (white whiskers) resulted in colonization of the 18 rats intestines and their eventual excretion of the organism for four months post infection. When 10(8) CFU of C. jejuni was mixed with 10 mu/ml of cadmium chloride (CdCl2) and fed immediately to another set of 18 rats, colonization of rats intestines was greatly reduced and C. jejuni was recovered from two (11%) out of 18 rats and the faeces were positive for C. jejuni for a maximum of 29 days. Six control rats given 1 ml of phosphate buffered saline (PBS) and a second set of another six control animals given 1 ml of PBS containing 10 micrograms/ml of CdCl2 gave negative result for C. jejuni throughout the experiment. This work depicts an in vivo effect of CdCl2 on C. jejuni and may be of importance in the control of C. jejuni colonization in experimental animals.

Administration, Oral↗

[Inventory relating to roentgen diagnostics of the gastro-intestinal tract (especially of the small intestine, colon, and biliary tract) (author's transl)].

The article describes the authors' experience in their Department in Nijmegen (Holland) with the various types of x-ray equipment: in gastroenterology--especially in the examination of the small intestine, colon, and the bile ducts--and also within the framework of a general roentgenology diagnostics section. Problems of cost are also considered, relating on the one hand to the equipment required in an examination room, and on the other hand to gastroenterological examination. In conclusion, the authors suggest the most suitable type of apparatus to be acquired for a particular purpose.

Digestive System↗

Metronidazole may inhibit intestinal colonization with Clostridium difficile.

PURPOSE: Antibiotics suppress normal gut flora, allowing overgrowth of acquired or native Clostridium difficile, with release of toxins that cause mucosal inflammation. Oral metronidazole is used to treat antibiotic-associated colitis (pseudomembranous colitis). This study was designed to determine whether oral metronidazole, as part of preoperative bowel preparation, prevents or decreases incidence of antibiotic-associated colitis after elective colonic and rectal procedures. METHODS: Eighty-two patients (40 men) were prospectively, randomly assigned to receive one of two oral antibiotic regimens before colorectal surgery. All patients underwent mechanical bowel preparation with polyethylene glycol-electrolyte lavage solution before administration of oral antibiotics. Group 1 (n = 42) patients received three doses (1 g/dose) of neomycin and erythromycin. Group 2 (n = 40) patients received three doses (1 g/dose) of neomycin and metronidazole. Both groups received one preoperative and three postoperative doses of intravenous cefotetan (2 g/dose). Both groups had stool samples tested for C. difficile toxin in the preoperative and postoperative periods by enzyme-linked immunoabsorbent assay or by tissue culture cytotoxicity. Patients with preoperative stool studies positive for C. difficile were excluded from the study. RESULTS: Treatment groups were not different for age, gender, or surgical procedure. Mean age +/- 1 standard deviation was 67.6 +/- 13.6 (range, 34-94) years in Group 1 and 62.1 +/- 13.5 (range, 35-84) years in Group 2 (P = 0.069). Mean length of hospital stay +/- 1 standard deviation was 9.76 +/- 4.9 (range, 4-28) days for Group 1 and 8.05 +/- 2.6 (range, 3-14) days for Group 2 (P = 0.053). Five patients in Group 1 (neomycin and erythromycin) and one patient in Group 2 (neomycin and metronidazole) had positive stool studies for C. difficile. Relative risk of colonization with C. difficile in Group 1 was 4.76 times that in Group 2 (95 percent confidence interval, 0.581, 39). This difference was not statistically significant (P = 0.202). There were no significant differences in C. difficile colonization rates with respect to age, length of stay, or gender. CONCLUSIONS: This study suggests that there may be a clinical association between use of metronidazole preoperatively and inhibition of intestinal colonization by C. difficile in this patient population undergoing colonic and rectal surgery.

Adult↗

A 53 kDa protein of Vibrio cholerae classical strain 0395 involved in intestinal colonization.

Mutants of Vibrio cholerae 01 strain 0395 (classical) mutated in genes encoding secretory or cell surface proteins were induced by TnphoA mutagenesis and were selected as blue colonies on L-agar plates containing 5-bromo-4-chloro-3-indolyl phosphate. Southern analysis of the total DNA from blue colonies showed that all mutants had TnphoA insertion in genomic DNA. These mutants were analysed for adherence, colonization and protein profile. Adherence to freshly isolated rabbit intestinal discs was affected in some mutants. The less adhesive mutants were examined for colonization of the intestine of infant mice. One mutant, designated T-87, was extremely poor at colonization and less diarrhaegenic than the parent strain. Analysis of T-87 by SDS-PAGE revealed that two proteins of 53 and 38 kDa were lacking. The 38 kDa protein was identified as OmpU. The 53 kDa protein was extracellular and cells treated with anti-53-kDa antibodies could not colonize the gut of infant mice. The expression of the 53 and 38 kDa proteins in T-87 was dependent of the growth medium. The data suggest that T-87 is mutated in a regulatory gene which regulates the expression of proteins involved in intestinal colonization.

Animals↗

Competitive exclusion of intestinal colonization of Escherichia coli in chicks.

A native gut microflora of chickens that protected chicks against Salmonella was evaluated against six pathogenic strains of Escherichia coli using similar methodology. Nalidixic-acid-resistant forms of the E. coli strains were derived for use in seeder-bird and individual-bird challenge tests. A substantial degree of exclusion of intestinal colonization of each of the six pathogenic strains of E. coli was secured in chicks that had been treated with native gut microflora. E. coli appeared to colonize chiefly the crop and cecum. Native gut microflora limited to a much lesser degree the "normal" E. coli present in the intestinal tract of test chicks. The mechanism of protection appears to be similar to that for Salmonella: native gut microflora and E. coli competed for sites of attachment.

Animals↗

Efficacy of oral ramoplanin for inhibition of intestinal colonization by vancomycin-resistant enterococci in mice.

Ramoplanin is a glycolipodepsipeptide antibiotic with activity against gram-positive bacteria that is in clinical trials for prevention of vancomycin-resistant Enterococcus (VRE) bloodstream infections and treatment of Clostridium difficile diarrhea. Orally administered ramoplanin suppresses VRE intestinal colonization, but recurrences after discontinuation of treatment have frequently been observed. We used a mouse model to examine the efficacy of ramoplanin for inhibition of VRE colonization and evaluated the etiology of recurrences of colonization. Eight days of treatment with ramoplanin (100 microg/ml) in drinking water suppressed VRE to undetectable levels, but 100% of mice developed recurrent colonization; a higher dose of 500 microg/ml in water was associated with recurrent colonization in 50% of mice. Two of eight (25%) mice treated with the 100-microg/ml dose of ramoplanin had low levels of VRE in their cecal tissues on day 8 despite undetectable levels in stool and cecal contents. Mice that received prior ramoplanin treatment did not develop VRE overgrowth when challenged with 10(7) CFU of oral VRE 1, 2, or 4 days later. In communal cages, rapid cross-transmission and overgrowth of VRE was observed among clindamycin-treated mice; ramoplanin treatment effectively suppressed VRE overgrowth in such communal cages. Ramoplanin treatment promoted increased density of indigenous Enterobacteriaceae and overgrowth of an exogenously administered Klebsiella pneumoniae isolate. These results demonstrate the efficacy of ramoplanin for inhibition of VRE colonization and suggest that some recurrences occur due to reexpansion of organisms that persist within the lining of the colon. Ramoplanin treatment may be associated with overgrowth of gram-negative bacilli.

Administration, Oral↗

Use of a selective medium with potassium tellurite to follow intestinal colonization of hospitalized patients by drug-resistant Enterobacteriaceae.

Nosocomial infections are a relevant factor in complicating the recovery of patients interned for even minor causes. In a attempt to determine their origin it is crucial to consider that their origin is of an endogenous nature. Looking for an accessible expression of intestinal colonization we analyzed fecal samples from 3 separate groups of hospital patients collected after different lengths of time. For practical reasons one group was studied prospectively and two other groups (patients hospitalized for up to 7 days and patients hospitalized for more than 7 days) were compared to one another. We looked for the emergence of tellurite resistance among Enterobacteriaceae using a selective medium, MacConkey potassium tellurite (MCPT). The frequency of prospectively studied patients with tellurite resistant strains was significantly greater after 7 days of hospitalization. For the two other groups, patients with more than 7 days of hospitalization showed a significant increase of bacterial species and of strains with new antimicrobial resistance markers. High molecular weight plasmids were detected in some of these strains. These data show that the MCPT medium is a useful tool for the investigation of bowel colonization in hospitalized patients by drug-resistant Enterobacteriaceae.

Adult↗