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PubMedDate not supplied

Intestinal colonization and competitive exclusion of Campylobacter fetus subsp. jejuni in young chicks.

Colonization of Campylobacter fetus subsp. jejuni was investigated in monoxenic and holoxenic chicks. In monoxenic chicks, major colonization was found in the crop and ceca, with populations in the ceca consistently reaching 10(9) colony-forming-units/ml of cecal contents over the 28-day test period. Bacteremia was found in most chicks, but no significant gross pathological lesions were detected. In holoxenic chicks, major colonization occurred only in the ceca, and no evidence of bacteremia was detected. Colonization by native gut microflora sharply reduced subsequent colonization by C. fetus subsp. jejuni. The protective mechanism is perhaps the same as that protective against paratyphoid salmonellae and pathogenic strains of Escherichia coli.

Animals↗
PubMed1985

Inhibition of small intestinal colonization of enterotoxigenic Escherichia coli by streptococcus faecium M74 in pigs.

Colonizing and anti E. coli activity of S. faecium M74 was tested by oral inoculation of cesarean derived, colostrum deprived piglets with Streptococcus faecium M74 and subsequently with a heat stable enterotoxin (ST) producing E. coli (O101 : K30 : K99 : NM). Enterotoxin neutralization and co-culture studies were also performed in vitro. Bacterial counts in 10 cm ileal segments, fluorescein antibody stained cryostat sections, as well as 0.5 micron sections from the ilea of the experimental pigs taken 16 hours post exposure to enterotoxic E. coli (ETEC) all indicated that S. faecium M74 could not colonize the ileum of the newborn pigs, in a single high (7 X 10(8) - 3 X 10(10)) dose either in TSB or in milk suspension, in contrast to the ETEC. However, S. faecium given in milk suspension resulted a marked decrease in ileal colonization of ETEC and in weight loss of piglets. In vitro experiments indicated that neither extracellular nor cell-bound products of S. faecium M74 could neutralise ST, but there was a significant reduction of pH in the TSB cultures of S. faecium that was accompanied by a reduction in ETEC counts of the mixed cultures.

Animals↗
PubMed2001

P fimbriae and aerobactin as intestinal colonization factors for Escherichia coli in Pakistani infants.

The carriage rate of a range of virulence genes was compared between resident and transient Escherichia coli strains obtained from the rectal flora of 22 home-delivered Pakistani infants 0-6 months old. Genes for the following virulence factors were assessed using multiplex PCR: P, type 1 and S fimbriae, three P fimbrial adhesin varieties, Dr haemagglutinin, K1 and K5 capsule, haemolysin and aerobactin. The E. coli strains examined here differed from those previously obtained from hosts in Western Europe in a lower prevalence of genes for P, S and type 1 fimbriae, K1 capsule and haemolysin. Nevertheless, genes for P fimbriae, the class II variety of papG adhesin, and aerobactin were significantly more common among resident than transient strains, as previously observed in a Swedish study. The results suggest that P fimbriae and aerobactin, previously implicated as virulence factors for urinary tract infection, might contribute to persistence of E. coli in the normal intestinal microflora.

Adhesins, Bacterial↗
PubMed1977

Intestinal colonization and adhesion by enteroxigenic Escherichia coli: ultrastructural observations on adherence to ileal epithelium of the pig.

Colonization of pig ileum by enterotoxigenic Escherichia coli that were enteropathogenic for pigs but that lacked K88 antigen (K88-) resulted in morphological characteristics similar to those reported for K88+ strains. Strains of enterotoxigenic E. coli from three different K88-serotypes adhered to the villous epithelium. In sections examined by transmission electron microscopy, adherent bacteria were separated from each other and from epithelial microvilli by peribacterial electron-lucent regions. The enterotoxigenic E. coli had appendages that extended into these regions. The appendages were morphologically characteristic for each strain. It is possible that these appendages were pili, polysaccharide K antigens, or structures resulting from some interaction between pili and polysaccharide. Certain pili or pilus-like structures may be virulence attributes that facilitate adhesion of enterotoxigenic E. coli to the intestinal epithelium.

Animals↗
PubMed1994

Occurrence of necrotizing enterocolitis may be dependent on patterns of bacterial adherence and intestinal colonization: studies in Caco-2 tissue culture and weanling rabbit models.

Necrotizing enterocolitis (NEC) is one of the leading causes of death in neonatal intensive care units. The underlying pathophysiology of NEC is poorly defined, although there is a suggestion that bacterial agents play an important role in the process. In this study, we evaluated bacterial isolates from 17 NEC cases and matched asymptomatic control infants. Isolates from NEC patients were no more likely than control isolates to be adherent to enterocytes, as assessed by a Caco-2 cell tissue culture model. Adherent Escherichia coli isolates, from both NEC cases and controls, were able to cause pathologic changes typical of NEC in a weanling rabbit ileal loop model. Adherence of E. coli strains to Caco-2 cells, and subsequent production of disease in weanling rabbits, could be blocked by coinfection with Gram-positive isolates from control children. In contrast, in three of four instances, adherent E. coli from NEC cases retained their adherence and caused illness in rabbits when coinfected with Gram-positive isolates from the homologous child. Our data suggest that patterns of intestinal adherence, as influenced by the underlying intestinal microbial ecology, play a role in the pathophysiology of NEC.

Animals↗
PubMed1991

Prospective study of Clostridium difficile intestinal colonization and disease following single-dose antibiotic prophylaxis in surgery.

A total of 108 volunteers undergoing an elective surgical procedure were randomly given a single 2-g intravenous prophylactic dose of either a cephalosporin or mezlocillin. Stool samples were cultured for Clostridium difficile the day before the operation and later on postoperative days 4, 7, and 14. C. difficile was detected in 23.0% of patients who received a cephalosporin (cefoxitin, 8.3%; cefazolin, 14.3%; cefotetan, 20.0%; ceftriaxone, 25.0%; cefoperazone, 43.7%), in 3.3% of patients given mezlocillin, and in none of 15 control volunteers given no antimicrobial agent. No patient experienced diarrhea.

Adolescent↗
PubMed2003

Effects of diet formulations containing proteins from different sources on intestinal colonization by Campylobacter jejuni in broiler chickens.

The objective of this study was to compare the effects of 3 diet formulations containing different protein sources (animal, plant, and a combination of animal and plant) on the colonization of Campylobacter jejuni in the gastrointestinal tract of broiler chickens. A freshly isolated strain of C. jejuni (biotype IV, serotype HS O:21, O:29, HL untypable) from a broiler chicken was used to infect 3-day-old chicks that had been free of C. jejuni; 0.5 mL of an inoculum containing 10(8) colony-forming units was administered orally. Shedding of the organism was studied, and C. jejuni in the ceca, jejuni, and crop were enumerated by quantitative culture. The isolates recovered from the birds during the study period of 35 d were characterized and confirmed as C. jejuni by the use of standard methods and underwent biotyping, serotyping, antimicrobial susceptibility testing by disk diffusion and the E-test, and flagellin gene typing. A cyclical pattern of shedding of C. jejuni was observed in all the birds. Colonization was highest in the ceca. The ceca of birds receiving plant-protein-based feed had significantly less colonization then the ceca of birds receiving the other types of feed, whereas the differences in colonization of the jejuni and crops were not significant. Characterization by biotyping, serotyping, and flagellin gene typing showed that 95% of the recovered isolates were identical to the strain used for infecting the chicks. However, with the Lior-HL typing scheme, 74% of the recovered isolates were HL untypable. Antimicrobial resistance testing did not reveal significant differences between the infecting strain and the recovered isolates among the different feed groups.

Administration, Oral↗
PubMed1995

Isolation and characterization of the Vibrio cholerae acfA gene, required for efficient intestinal colonization.

The nucleotide sequence of the Vibrio cholerae acfA gene (encoding an accessory colonization factor) has been determined. Sequence analysis revealed the presence of an open reading frame of 215 amino acids with a characteristic signal peptidase I (SPI) cleavage site at the N terminus. Electrophoretic analysis of proteins synthesized by Escherichia coli cells, following T7 promoter/RNA polymerase-directed expression of acfA, revealed a 23-kDa protein corresponding to the mature form of AcfA. The T7 expression system also showed that, in the presence of known SPI inhibitors, a 25-kDa unprocessed form of AcfA is produced.

Amino Acid Sequence↗
PubMedDate not supplied

Modulation of Clostridium perfringens intestinal colonization in infants delivered by caesarean section.

The colonization by Clostridium perfringens was investigated in 19 infants delivered by caesarean section during the two first weeks of life. The pattern of C. perfringens colonization depended upon the feeding. Breast feeding led to the repression of C. perfringens, whereas bottle feeding allowed its maintenance. On the contrary, Bifidobacterium bifidum growth was favoured by breast feeding. However, in one breast-fed infant, B. bifidum was never isolated and C. perfringens decreased. Breast feeding was able to directly modulate C. perfringens numbers. In fact, B. bifidum also had an effect, as demonstrated by the lower mean counts of C. perfringens, in bottle-fed infants carrying the bifidobacteria flora (p = 0.05). None of the bifidobacteria investigated in this study led to the same decrease.

Antibiosis↗
PubMedDate not supplied

[Preventive antibiotic administration for prevention of nosocomial septicemia in very small premature infants (VLBW infants)--preventive vancomycin administration against infections with coagulase negative streptococci--prevention of translocation with oral cefixime therapy in intestinal colonization with pathogenic gram-negative pathogens].

VLBW-infants below 1500 g of birth weight have a quite high risk to acquire a nosocomial sepsis. 20-40% of all infants exhibit signs of nosocomial infection once during neonatal intensive care. The rate of infection is related to technique and amount of used invasive devices as to gestational age. Coagulase-negative staphylococci (CONS) and gram-negative organisms contribute most to these cases of sepsis. In a three phase study we tried to demonstrate the efficacy of different mechanisms to change the rate of nosocomial sepsis. During the first phase a strict hygienical protocol was enforced as isolation, care with sterile gloves and aseptic techniques in introducing and maintaining i.v. lines. In a second phase we started a randomized controlled study of prophylactic vancomycin (10 mg/kg/day in two doses). In a third phase we added an oral antibiotic regime with cefixime for all patients with positive cultures for gramnegative organisms under the hypothesis of translocation from the gut as the way of infection. During the first phase 23.7% of 76 patients enrolled acquired CONS-sepsis, 0.52% gramnegative sepsis. During the second phase (41 patients) 6 patients in the control group acquired CONS-sepsis, none in the vancomycin-group. The rate of gramnegative infections was not different (4 and 3 cases). During the third phase (vancomycin plus cefixime eventually in cases of positive stool cultures) no case of nosocomial sepsis occurred (35 patients, 11 positive cultures). The management used in phase 3 reduced the rate of nosocomial infections in VLBW-infants drastically.

Anti-Infective Agents↗
PubMed2001

Autophagy delays sulindac sulfide-induced apoptosis in the human intestinal colon cancer cell line HT-29.

Autophagy is a major catabolic process allowing the renewal of intracellular organelles by which cells maintain their homeostasis. We have previously shown that autophagy is controlled by two transduction pathways mediated by a heterotrimeric Gi3 protein and phosphatidylinositol 3-kinase activities in the human colon cancer cell line HT-29. Here, we show that 3-methyladenine, an inhibitor of autophagy, increases the sensitivity of HT-29 cells to apoptosis induced by sulindac sulfide, a nonsteroidal anti-inflammatory drug which inhibits the cyclooxygenases. Similarly, HT-29 cells overexpressing a GTPase-deficient mutant of the G(alpha i3) protein (Q204L), which have a low rate of autophagy, were more sensitive to sulindac sulfide-induced apoptosis than parental HT-29 cells. In both cell populations we did not observe differences in the expression patterns of COX-2, Bcl-2, Bcl(XL), Bax, and Akt/PKB activity. However, the rate of cytochrome c release was higher in Q204L-overexpressing cells than in HT-29 cells. These results suggest that autophagy could retard apoptosis in colon cancer cells by sequestering mitochondrial death-promoting factors such as cytochrome c.

Adenine↗
PubMed1979

Dietary Na+ effects on transepithelial transport of NaCl by hen (Gallus domesticus) lower intestine (colon and coprodeum) perfused luminally in vivo.

The colon and coprodeum of anaesthetised laying hens was perfused luminally with solutions of varying compositions, to elucidate the influence of three levels of dietary NaCl and of luminal NaCl concentrations on coprodeal and colonic transport of NaCl. Net Na+ and Cl- absorption rates were increased in response to low dietary Na+ levels and higher luminal NaCl concentrations. Net Na+ absorption was always against the prevailing electrochemical gradient, saturably dependent on luminal Na+ concentrations in low Na+ diet birds, and linearly dependent on luminal concentrations in medium and high Na+ diet birds. Net Cl- absorption was usually down its electrochemical gradient. The Cl- flux rates were strongly linearly dependent on Na+ flux rates, and statistically this relationship could account for all significant variation of Cl- fluxes associated with dietary and perfusate treatments. Transmural electrical potential differences were invariably serosa positive, and partly correlated with Na+ fluxes.

Animals↗
PubMed1979

Transepithelial transport of K+, NH4+, inorganic phosphate and water by hen (Gallus domesticus) lower intestine (colon and coprodeum) perfused luminally in vivo.

The colon and coprodeum of anaesthetised laying hens was perfused luminally with solutions of varying compositions to elucidate the influence of three levels of dietary Na+ and of luminal fluid composition on transport of electrolytes and water. Net rates of secretion of K+ and absorption of NH4+ were increased in response to dietary Na+ depletion and increased luminal Na+ concentrations, but these fluxes were linked to Na+ transport and no dietary or perfusion treatment effects could be detected on them independently of effects on Na+ flux. Similar results were found for Na+-linked water absorption from isosmotic perfusates. Serosal-mucosal net osmotic flow with Na+-free perfusates was significantly reduced by Na+-depletion, but no significant dietary effect could be detected on the serosal-mucosal osmotic permeability coefficient. The reflexion coefficient was effectively unity. Mucosal-serosal inorganic phosphate flux was small. The flux was independent of Na+ flux and dietary Na+ levels, and apparently facilitated by serosalmucosal osmotic flow. The data allowed determination of the absorption/secretion in coprodeum and colon of the ions investigated, as compared to the renal excretion rate.

Ammonium Chloride↗
PubMed2003

Citrobacter rodentium translocated intimin receptor (Tir) is an essential virulence factor needed for actin condensation, intestinal colonization and colonic hyperplasia in mice.

Citrobacter rodentium infection of mice serves as a relevant small animal model to study enterohaemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) infections in man. Enteropathogenic E. coli and EHEC translocate Tir into the host cytoplasmic membrane, where it serves as the receptor for the bacterial adhesin intimin and plays a central role in actin condensation beneath the adherent bacterium. In this report, we examined the function of C. rodentium Tir both in vitro and in vivo. Similar to EPEC, C. rodentium Tir is tyrosine phosphorylated and is essential for actin condensation. Citrobacter Tir and EPEC Tir are functionally interchangeable and both require tyrosine phosphorylation to mediate actin rearrangements. In contrast, Citrobacter Tir supports actin nucleation in EHEC independent of tyrosine phosphorylation, while EHEC Tir cannot replace Citrobacter Tir for this function. This indicates that C. rodentium and EPEC use an actin nucleating mechanism different from EHEC. We also found that Tir is expressed and translocated into mouse enterocytes in vivo by C. rodentium during infections. This represents the first direct demonstration of a type III effector translocated in vivo into a natural host by any pathogen. In addition, we showed that Tir, but not its tyrosine phosphorylation, is essential for C. rodentium to colonize the large bowel and induce attaching/effacing (A/E) lesions and colonic hyperplasia in mice, and that both EPEC Tir and EHEC Tir can substitute for Citrobacter Tir for these activities in vivo. These results thus demonstrate that Tir is an essential virulence factor in this infection model. The data also show that the function of Tir tyrosine phosphorylation and its subsequent actin nucleating activity are not essential for C. rodentium colonization of the mouse gut nor for inducing A/E lesions and colonic hyperplasia, thereby uncoupling colonization and disease from actin condensation for this A/E pathogen.

Actins↗
PubMed2002

Specific proliferative and antibody responses of premature infants to intestinal colonization with nonpathogenic probiotic E. coli strain Nissle 1917.

The aim of this study was to analyze the influence of oral administration of E. coli Nissle 1917 on the systemic humoral and cellular immunity in premature infants. Thirty-four premature infants were colonized with E. coli Nissle 1917 in a randomized, placebo-controlled blinded clinical trial. Stool samples of infants were analyzed repeatedly for the presence of the administered strain. The proliferative response to bacterial antigens of E. coli origin was measured in whole blood of 34 colonized infants and 27 noncolonized controls. E. coli colonization induced a significant increase in the proliferation of blood cells cultivated with bacterial components of E. coli Nissle 1917 and another E. coli strain in colonized infants as compared with noncolonized controls. Significantly higher amounts of specific anti-E. coli Nissle 1917 antibodies (Ab) of immunoglobulin (Ig)A isotype and nonspecific polyclonal IgM were found in the blood of colonized infants compared to noncolonized placebo controls. We concluded that the oral application of E. coli Nissle 1917 after birth significantly stimulates specific humoral and cellular responses and simultaneously induces nonspecific natural immunity.

Administration, Oral↗
PubMed1989

Antibiotic exposure delays intestinal colonization by Clostridium difficile in the newborn.

Two antibiotic regimens commonly used in neonatal intensive care were compared for the rate at which Clostridium difficile appeared in the faeces. Over a nine month period neonates with suspected sepsis admitted to a Special Care Baby Unit (SCBU) were randomly allocated to receive either cefotaxime or penicillin and netilmicin. A contemporaneous group also admitted to SCBU but without sepsis served as non-treated controls. Four hundred and sixteen stool specimens from 158 neonates without diarrhoea were analysed every five to seven days until discharge. The results showed that these antibiotics did not encourage gut colonization by C. difficile, that they might even be protective in this respect and that monotherapy with cefotaxime was no more likely to generate C. difficile overgrowth than the penicillin-aminoglycoside regimen.

Anti-Bacterial Agents↗