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PubMed2006

Diet- and colonization-dependent intestinal dysfunction predisposes to necrotizing enterocolitis in preterm pigs.

BACKGROUND & AIMS: Preterm birth and formula feeding are key risk factors associated with necrotizing enterocolitis (NEC) in infants, but little is known about intestinal conditions that predispose to disease. Thus, structural, functional, and microbiologic indices were used to investigate the etiology of spontaneous NEC development in preterm pigs. METHODS: Piglets were delivered by cesarean section at 92% gestation, reared in infant incubators, and fed infant formula or colostrum every 3 hours (n = 120) until tissue collection at 1-2 days of age. RESULTS: Clinical and histopathologic signs of NEC were observed in 57% of pigs fed FORMULA (26/46) and in 5% of pigs fed COLOSTRUM (2/38) (P < .05). Relative to COLOSTRUM, both healthy and sick FORMULA pigs had reduced intestinal villous heights, enzyme activities, nutrient absorption, and antioxidant levels and higher inducible nitric oxide synthetase activity (P < .05). In healthy pigs, mucosal microbial diversity remained low and diet independent. NEC pigs showed bacterial overgrowth, and a high mucosal density of Clostridium perfringens was detected in some but not all pigs. Germ-free conditions and antiserum against Clostridium perfringens toxin prevented intestinal dysfunction and NEC in formula-fed pigs, whereas the gut trophic factors, epidermal growth factor, and glucagon-like peptide 2 had limited effects. CONCLUSIONS: A subclinical, formula-induced mucosal atrophy and dysfunction predispose to NEC and bacterial overgrowth. The adverse feeding effects are colonization dependent and may be reduced by factors in colostrum that include antibodies against aggressive toxins such as those of Clostridium perfringens.

Animals↗
PubMed1997

Expression of an antigen homologous to the human CO17-1A/GA733 colon cancer antigen in animal tissues.

The CO17-1A/GA733 antigen is associated with human carcinomas and some normal epithelial tissues. This antigen has shown promise as a target in approaches to passive and active immunotherapy of colorectal cancer. The relevance of animal models for studies of immunotherapy targeting this antigen in patients is dependent on the expression of the antigen on normal animal tissues. Immunohistoperoxidase staining with polyclonal rabbit antibodies to the human antigen revealed the human homologue on normal small intestine, colon and liver of mice, rats and non-human primates, whereas mouse monoclonal antibodies to the CO17-1A or GA733 epitopes on the human antigen did not detect the antigen. Polyclonal rabbit antibodies, elicited by the murine antigen homologue derived from recombinant baculovirus-infected insect cells, immunoprecipitated the antigen from mouse small intestine, colon, stomach, kidney and lung. The isolated recombinant murine protein bound polyclonal, but not monoclonal, antibodies to the human CO17-1A/GA733 antigen, and recombinant human antigen bound polyclonal antibodies elicited by the murine antigen homologue. Thus, the antigen homologue expressed by animal tissues is similar, but not identical, to the human antigen. These results have important implications for experimental active and passive immunotherapy targeting the CO17-1A/GA733 antigen.

Animals↗
PubMed1992

Mucin histochemical analysis in the interpretation of Barrett's esophagus. Results of a multicenter study. The Operative Group for the Study of Esophageal Precancer.

A multicentric study of Barrett's esophagus (BE) was started in November 1987 to evaluate (1) the prevalence of BE among subjects undergoing upper gastrointestinal endoscopic examination; (2) the pathologic features of BE; and (3) the correlation between BE and early malignant changes. In 157 of 330 patients who underwent multiple standardized biopsies, BE was confirmed with histologic evaluation. Specialized intestinal-type BE was observed in 84 patients. By applying Alcian blue (pH 2.5)-periodate oxidation-Schiff, high-iron diamine-Alcian blue (pH 2.5), and periodate borohydride-saponification-periodate oxidation-Schiff techniques, the intestinal type of BE was subclassified into colonic and ileal types, both complete and incomplete. Fifty cases had incomplete colonic metaplasia with sulphomucins in the columnar cells and 64 had complete colonic intestinal metaplasia, 49 of them containing O-acetylated sialomucins in the goblet cells. These patients are being included in a short-term follow-up. Dysplasia (six low grade, two high grade) was observed in eight patients in areas of intestinal colonic-type epithelium; in these patients, a complete loss of O-acetylated sialomucins in the dysplastic areas and a remarkable reduction of these mucins in the surrounding tissue were observed. The reduction of O-acetylated sialomucins might indicate relative tissue immaturity, which could represent an early sign of neoplastic dedifferentiation. Therefore, the relevance of O-acetylated sialomucin content in BE, first demonstrated in intestinal type, is now evident, although its biologic importance is being studied.

Adolescent↗
PubMed1987

Bacterial colonization of intestinal urinary conduit diversion: a morphologic and bacteriologic experimental study.

Cutaneous diversion of the urine through intestinal conduits results in bacteriuria with uropathogenic organisms in up to 80% of patients, many of whom suffer pyelonephritis. Analysis of the bacteriologic data from daily sampling at multiple sites and scanning and transmission electron microscopic studies of sequential loop and autopsy specimens in rabbits with functioning colonic conduits indicate that the pyelonephritis evolves in sequential stages of microbial colonization. Using these data on the natural progression of bacterial infection, we can rationally test the ability of strains of bacteria indigenous to the conduit of this animal model to prevent uropathogenic colonization of the conduit.

Animals↗
PubMed2005

The impact of intestinal microflora on serum bilirubin levels.

BACKGROUND/AIMS: Intestinal microflora plays an important role in the pathogenesis of neonatal jaundice by inhibiting enterosystemic circulation of bilirubin. The present study aimed to investigate the influence of intestinal microflora on serum bilirubin levels in hyperbilirubinemic Gunn rats. METHODS: After a baseline phase Gunn rats received oral antibiotics (either clindamycin/neomycine or co-trimethoxazole for four days, phase II). Intestinal colonization was carried out either with a bilirubin-reducing strain of C. perfringens or C. pasteurianum incapable of reducing bilirubin (phase III). Serum bilirubin and fecal bile pigments were determined at the end of each phase. RESULTS: Oral administration of clindamycin/neomycine resulted in the disappearance of fecal urobilinoids. Simultaneously, serum bilirubin increased dramatically (186+/-31 vs. 289+/-35 micromol/l, P=0.004). Intestinal colonization with C. perfringens led to reappearance of fecal urobilinoid production accompanied with a partial decrease of serum bilirubin (289+/-35 vs. 239+/-17 micromol/l, P=0.013), whereas the effect of C. pasteurianum on bile pigment metabolism was negligible. Co-trimethoxazole therapy had no effect on serum and intestinal metabolism of bilirubin. CONCLUSIONS: Intestinal microflora greatly affects intravascular metabolism of bilirubin. Prolonged use of certain antibiotics in man may lead to an increase in serum bilirubin levels, while the enhancement of intestinal catabolism may have an opposite effect.

Animals↗
PubMed1999

Characteristics of polyclonal endemicity of Pseudomonas aeruginosa colonization in intensive care units. Implications for infection control.

We investigated the endemicity of Pseudomonas aeruginosa in intensive care units (ICUs) through analyses of surveillance cultures (from the rectum, stomach, oropharynx, and trachea; n = 1,089), and clinical cultures (n = 2,393) from 297 consecutive patients. Multiple isolates of P. aeruginosa (n = 353) were genotyped. Variables associated with acquisition of respiratory tract colonization (RTC) were tested in a risk factor analysis. The mean daily prevalence of colonization was 34%. On admission, 22 patients had intestinal colonization and 13 had RTC. Twenty patients acquired colonization in the intestinal and 24 in the respiratory tract. Forty-four different genotypes were found; 38 (86%) were isolated from individual patients only. In all, 37 patients had RTC with a total of 38 genotypes: 13 (34%) were colonized on admission, 9 (24%) acquired RTC with a novel genotype during a stay in the ICU, five (13%) acquired colonization from their intestinal tract and three (8%) were colonized via cross-acquisition. In eight patients (21%), no route could be demonstrated for colonization. Antibiotics providing P. aeruginosa with a selective growth advantage were associated with acquired RTC. Endemicity of colonization with P. aeruginosa is characterized by polyclonality, and seems to be maintained by continuous admittance of colonized patients and selection pressure from antibiotics rather than by cross-acquisition.

APACHE↗
PubMed1999

Evaluation of a truncated recombinant flagellin subunit vaccine against Campylobacter jejuni.

A recombinant protein comprising the maltose-binding protein (MBP) of Escherichia coli fused to amino acids 5 to 337 of the FlaA flagellin of Campylobacter coli VC167 was evaluated for immunogenicity and protective efficacy against challenge by a heterologous strain of campylobacter, Campylobacter jejuni 81-176, in two murine models. The sequence of the flaA gene of strain 81-176 revealed a predicted protein which was 98.1% similar to that of VC167 FlaA over the region expressed in the fusion protein. Mice were immunized intranasally with two doses of 3 to 50 microgram of MBP-FlaA, given 8 days apart, with or without 5 microgram of the mutant E. coli heat-labile enterotoxin (LT(R192G)) as a mucosal adjuvant. The full range of MBP-FlaA doses were effective in eliciting antigen-specific serum immunoglobulin G (IgG) responses, and these responses were enhanced by adjuvant use, except in the highest dosing group. Stimulation of FlaA-specific intestinal secretory IgA (sIgA) responses required immunization with higher doses of MBP-FlaA (>/=25 microgram) or coadministration of lower doses with the adjuvant. When vaccinated mice were challenged intranasally 26 days after immunization, the best protection was seen in animals given 50 microgram of MBP-FlaA plus LT(R192G). The protective efficacies of this dose against disease symptoms and intestinal colonization were 81.1 and 84%, respectively. When mice which had been immunized with 50 microgram of MBP-FlaA plus LT(R192G) intranasally were challenged orally with 8 x 10(10), 8 x 10(9), or 8 x 10(8) cells of strain 81-176, the protective efficacies against intestinal colonization at 7 days postinfection were 71.4, 71.4, and 100%, respectively.

Amino Acid Sequence↗
PubMedDate not supplied

[Digestive and cutaneous colonization of Staphylococcus epidermidis in hairless axenic mice].

In order to determine the cutaneous and digestive colonization of S. epidermidis in germ-free HRS mice, several groups of animals were contaminated with this strain according to different methods. The bacterial cutaneous enumerations were performed after preliminary crushing of the cutaneous biopsy. In this study, whatever the method of contamination of germ-free HRS mice, the kinetics of S. epidermidis cutaneous colonization was parallel to the kinetics of intestinal colonization. The isolation of bacteria on skin was possible only when microorganisms were eliminated in faeces (6 h after contamination). During a single experiment, there was only slight variability in colonization, whether intestinal or cutaneous. Some differences could be found from one experiment to another, but all animals in the same trial showed the same cutaneous bacterial count. This experimental model is characterized by an interrelation between the intestinal and cutaneous ecosystems.

Animals↗
PubMed1993

Control of Salmonella and Campylobacter in poultry production. A summary of work at Russell Research Center.

The primary mission of the USDA, Agricultural Research Service, Poultry Microbiological Safety Research Unit is to develop technology preventing commensal intestinal colonization of chickens by human bacterial enteropathogens, including Salmonella and Campylobacter. The different mechanisms of colonization and the wide variety of sources of these pathogens combined with the different factors that affect host susceptibility to colonization indicate that a multifaceted research approach will be required to control Salmonella and Campylobacter during poultry production. The working hypothesis is that only by delivering chickens free of Salmonella or Campylobacter to the processing plant can significant reductions in the number and levels of contamination of chickens leaving the plant with these pathogens be achieved. As the means are developed to substantially reduce or eliminate the intestinal colonization of chickens by these pathogens, the pathogen-free chickens can be delivered to the processing plant, thereby eliminating or at least reducing the prevalence and levels of Salmonella on processed broilers.

Animals↗
PubMed1999

Experimental infection of chickens with Campylobacter jejuni: strains differ in their capacity to colonize the intestine.

Groups of broiler and layer type chickens (25 to 63 d.o.) were inoculated per os with separate isolates of 10 strains of Campylobacter jejuni. Nine of the 10 strains were originally isolated from chickens and one from a dog. The dog strain and five of the chicken isolates could be isolated after inoculation, but four strains were not recovered from cloacal swabs for up to 4 to 16 days after inoculation. However, it was possible to isolate C. jejuni from these birds, from cloacal swabs, when they were inoculated with organisms which had been previously shown to colonize other birds.

Journal Article↗
PubMed2003

Analysis of the Vibrio pathogenicity island-encoded Mop protein suggests a pleiotropic role in the virulence of epidemic Vibrio cholerae.

Epidemic Vibrio cholerae contain a large essential virulence gene cluster called the Vibrio pathogenicity island (VPI). We recently reported that no in vitro difference in virulence was found in El Tor strain N16961 containing a mutation in the VPI-encoded mop gene but this mutant was hypervirulent and reactogenic in rabbit ileal loops. In this paper, we report in vitro studies showing that independent Mop mutants of strain 3083 are significantly attenuated (approximately 40-fold) in cholera toxin (CT) production and have significantly increased motility and biofilm forming ability but appear to be unaffected in TcpA, hemagglutinin protease and hemolysin compared to their parent. The 3083 Mop mutant showed a 100-fold decrease in its in vivo intestinal colonization ability in the infant mouse competition assays. While reverse transcription polymerase chain reaction and phenotypic studies of a mop plasmid in both mutant and wild-type backgrounds suggest Mop is expressed by the plasmid, the differences in CT and biofilm formation could not be restored in any of the mutants. The inability to complement the Mop mutants in trans may be due either to the selection of secondary mutations or to mop possibly being part of an operon. Our findings that Mop is associated with CT, motility, biofilm formation and intestinal colonization support a hypothesis in which Mop has a pleiotropic role in the pathogenesis and persistence of epidemic V. cholerae.

Animals↗
PubMed1989

Taxol toxicity. Epithelial necrosis in the gastrointestinal tract associated with polymerized microtubule accumulation and mitotic arrest.

Taxol, an antineoplastic agent with a novel mechanism of action, is currently undergoing Phase I trials at The Johns Hopkins Hospital, Baltimore. The authors recently observed striking mitotic arrest associated with epithelial necrosis and ulceration in an esophageal biopsy specimen. The biopsy specimen was taken from a patient who received taxol the day before endoscopy. Review of our autopsy files revealed four other cases in which taxol had been administered. Sections of esophagus, stomach, small intestine, colon, liver, skin, bone marrow, and testes were examined for evidence of mitotic arrest. Mitotic arrest was seen in the two patients who underwent autopsy who received taxol less than 11 days before death, whereas the two autopsy patients who received taxol more than 2 weeks before death did not show these changes. Although mitotic arrest was most prominent in the esophagus, it was also found in the stomach, small intestine, colon, liver, and bone marrow. The mitotic arrest was associated with bundling of intermediate filaments and appeared to be secondary to accumulation of polymerized microtubules. These results suggest that taxol induces a transient mitotic arrest associated with cell necrosis.

Adult↗
PubMed2001

EspG, a novel type III system-secreted protein from enteropathogenic Escherichia coli with similarities to VirA of Shigella flexneri.

The function of the rorf2 gene located on the locus of enterocyte effacement (LEE) pathogenicity island of enteropathogenic Escherichia coli (EPEC) has not been described. We report that rorf2 encodes a novel protein, named EspG, which is secreted by the type III secretory system and which is translocated into host epithelial cells. EspG is homologous with Shigella flexneri protein VirA, and the cloned espG (rorf2) gene can rescue invasion in a Shigella virA mutant, indicating that these proteins are functionally equivalent in Shigella. An EPEC espG mutant had no apparent defects in in vitro assays of virulence phenotypes, but a rabbit diarrheagenic E. coli strain carrying a mutant espG showed diminished intestinal colonization and yet diarrheal attack rates similar to those of the wild type. A second EspG homolog, Orf3, is encoded on the EspC pathogenicity islet. The cloned orf3 gene could also rescue invasion in a Shigella virA mutant, but an EPEC espG orf3 double mutant was not diminished in any tested in vitro assays for EPEC virulence factors. Our results indicate that EspG plays an accessory but as yet undefined role in EPEC virulence that may involve intestinal colonization.

Amino Acid Sequence↗
PubMed2006

Mutation accumulation in the intestine and colon of mice deficient in two intracellular glutathione peroxidases.

Mice deficient in two glutathione peroxidases (GPX), Gpx1 and Gpx2, [Gpx1/2-double knockout (DKO) mice] are prone to ileocolitis on a mixed C57BL/6 and 129S1/SvJ (B6.129) genetic background. We reported previously that approximately 25% of B6.129 Gpx1/2-DKO mice develop ileocolonic tumors by 6 to 9 months of age, when their non-DKO littermates [having at least one wild-type (WT) Gpx1 or Gpx2 allele] rarely have inflammation and none have tumors. Because genetic background affects tumor susceptibility, we have generated a B6 Gpx1/2-DKO colony and discovered that these mice have fewer inflammatory cells, milder ileocolitis, and low mortality, and only 2.5% of B6 mice developed tumors. The mutant frequency of a cII reporter gene was about 2- to 3-fold higher in 28-day-old Gpx1/2-DKO and 4-fold higher in 8-month-old Gpx1/2-DKO ileal mucosa than in controls in both genetic backgrounds. In contrast, mutant frequencies in the unaffected B6 liver were not significantly different between WT and Gpx1/2-DKO mice. The mutant frequency of 8-month-old B6.129 Gpx1/2-DKO ileum was 38.94 +/- 15.5(-5), which was not significantly higher than the age-matched B6 ileum, 25.54 +/- 10.33(-5). The mutation spectra analysis has shown that B6 Gpx1/2-DKO ileum had a 3-fold increase in small nucleotide deletions at mononucleotide repeats over control B6, which are a signature mutation associated with oxidative stress. Unexpectedly, B6 Gpx1/2-DKO mice had fewer C to T transitions at CpG dinucleotides than the WT B6 (18.0% versus 40.1%; P < 0.001). Our results suggest that inflammation drives gene mutations, which leads to neoplastic transformation of intestinal epithelium in the B6.129 Gpx1/2-DKO mice but rarely in the B6 Gpx1/2-DKO mice.

Animals↗
PubMed1996

Alterations in Vibrio cholerae motility phenotypes correlate with changes in virulence factor expression.

Motility is thought to contribute to the virulence of Vibrio cholerae, but the role it plays in pathogenesis is not completely understood. To investigate the influence of motility on virulence gene expression and intestinal colonization, we have isolated mutants with altered swarming abilities in soft agar medium. Both spontaneous hyperswarmer (exhibiting faster swarm rates) and spontaneous or transposon-induced nonmotile mutants of strain 0395 were obtained. Surprisingly, we found that two of three classes of hyperswarmer mutants were defective in autoagglutination, a phenotype associated with expression of toxin-coregulated pili (TCP), an essential ToxR-regulated colonization factor of V. cholerae. In contrast, nonmotile mutants exhibited autoagglutination under growth conditions that normally repress this phenotype. Further characterization of mutant strains revealed differences in the expression of other virulence determinants. Class I hyperswarmer mutants were defective in production of TCP, cholera toxin, and a cell-associated hemolysin but showed increased levels of protease and fucose-sensitive hemagglutinin. All nonmotile mutants examined, including those with insertions in a sequence homologous to motB, exhibited increased expression of TCP pilin, cholera toxin, and cell-associated hemolysin but dramatically decreased levels of fucose-sensitive hemagglutinin and HEp-2 adhesins. In general, nonmotile mutants displayed few or no defects in intestinal colonization, while class I hypermotile mutants were highly defective in colonization. These results suggest that the motility phenotype of V. cholerae is tightly coupled to the expression of multiple ToxR-regulated and non-ToxR-regulated virulence determinants.

Agglutination↗
PubMed1995

Vancomycin-resistant enterococci colonizing the intestinal tracts of hospitalized patients.

A point prevalence culture survey was carried out to investigate the prevalence of fecal carriage of vancomycin-resistant enterococci (VRE) among patients admitted to an 800-bed general hospital where no VRE had been isolated previously. Twenty-two of 636 patients (3.5%) were found to be VRE carriers. Eighteen strains were identified as Enterococcus faecium, three were identified as Enterococcus gallinarum, and one was identified as Enterococcus faecalis. The susceptibilities of the enterococci to ampicillin, vancomycin, and teicoplanin were determined by the disk diffusion and the agar dilution methods. High-level resistance (HLR) to gentamicin and streptomycin was determined by the agar screening method. Eighteen strains (82%) were highly resistant to vancomycin, and four strains (18%) were moderately resistant to vancomycin. Five strains were susceptible to teicoplanin (23%; MICs, < or = 8 micrograms/ml). Only one strain (4.5%, E. faecium) showed HLR to gentamicin, and six strains (27%) showed HLR to streptomycin (one E. faecalis and five E. faecium strains). All 18 E. faecium and 1 E. faecalis strain carried the vanA gene, and 3 E. gallinarum strains carried the vanC gene. An epidemiological investigation revealed several risk factors for VRE colonization: hospitalization and duration of stay in the hematology department and prior vancomycin treatment. The study demonstrates that the patient's gastrointestinal tract is a possible reservoir for VRE, even in hospitals where VRE infections have not yet been observed. Therefore, we conclude that infection control precautions and restriction of glycopeptide usage may be key issues in limiting the emergence and spread of nosocomial VRE infections.

Adult↗
PubMed1977

Colonization of porcine small intestine by Escherichia coli: colonization and adhesion factors of pig enteropathogens that lack K88.

The colonizing and adhesive attributes of enterotoxigenic acapsular and/or nonpiliated mutants from K88-negative enteropathogenic Escherichia coli strains were compared with their capsulated and piliated parents (parents were piliated when grown in vitro and in vivo). Acapsular, nonpiliated mutants from three different colonizing strains of enteropathogenic E. coli lost their ability to colonize the ileum of newborn pigs. Acapsular, piliated and capsular, nonpiliated mutants were derived from one of the parental strains (987), and both mutants lacked the ability to colonize the ileum of pigs. The only mutants available from a fourth strain (431) were acapsular and piliated, and they colonized as well as their parents. These data indicate that both capsule and pili are involved in colonization by strain 987. In contrast, capsule is not required for colonization by strain 431, but pili may be.

Animals↗
PubMed1990

Influence of dietary supplementation with Streptococcus faecium M-74 on broiler body weight, feed conversion, carcass characteristics, and intestinal microbial colonization.

Two experiments were conducted to determine the influence of Streptococcus faecium M-74 supplementation of broiler diets. Mixed-sex or male only chicks were used in the experiments. Both experiments consisted of six dietary treatments and four replicates per treatment in a randomized block design. The S. faecium was fed alone for 21, 36, or 44 days or for 44 days with S. faecium supplemented in the water for the first 14 days. In another treatment, S. faecium was fed for 44 days, but the feed was restricted for Days 8 through 13. The S. faecium was also fed in combination with antibacterial products (AP) for 44 days. An additional diet was an unsupplemented basal, and another was supplemented only with AP. In Experiment 1, feed efficiency was significantly better with the basal and diets supplemented with S. faecium than with those diets supplemented with AP or AP and S. faecium. In Experiment 2, BW of broilers at 44 days of age were significantly heavier for broilers receiving S. faecium in the feed and also S. faecium in the water for the first 14 days as compared with broilers receiving AP or AP and S. faecium supplementation. There were no significant differences in carcass yield or composition characteristics. In Experiment 1, the scores representing S. faecium colonies found in the intestinal tract were not influenced by dietary treatment. The ceca had the highest S. faecium score of any of the intestinal tract locations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗