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PubMed2001

Bacterial infection promotes colon tumorigenesis in Apc(Min/+) mice.

The Min mouse, which has a germ line mutation in 1 allele of the Apc tumor suppressor gene, is a model for the early steps in human colorectal cancer. Helicobacter pylori infection, a known risk factor for gastric cancer in humans, causes chronic inflammation and increased epithelial cell proliferation in the stomach. Infection with the bacterium Citrobacter rodentium is known to increase epithelial cell proliferation and to promote chemically initiated tumors in the colon of mice. Min mice infected with C. rodentium at 1 month of age were found to have a 4-fold increase in the number of colonic adenomas at 6 months of age, compared with uninfected Min mice. Most of the colonic adenomas in the infected Min mice were in the distal colon, where C. rodentium-induced hyperplasia occurs. These data demonstrate that bacterial infection promotes colon tumor formation in genetically susceptible mice.

Adenoma↗
PubMed2005

Colonic bacterial infection abrogates eosinophilic pulmonary disease.

Induction of immunity to one pathogen in the lungs modifies the microenvironment and alters immunopathological changes that result from a second, unrelated pulmonary infection. However, it is unclear whether immunity generated at distant sites also affects lung immune responses. Here, we show that infection with the gut-restricted bacterium Citrobacter rodentium modifies immunopathological changes that result from pulmonary Cryptococcus neoformans infection. Th2 cytokine-driven pulmonary eosinophilia induced by C. neoformans infection was reduced, and the enhanced Th1 cytokine environment afforded more-rapid clearance of the fungus in C. rodentium-immune mice. The activated and intraepithelial (CD103+) T cell populations that expand after C. neoformans infection were diminished in C. rodentium-immune mice. T cell cross-reactivity was absent, but cross-reactive antibodies were detected. It is of importance to the "hygiene hypothesis" that these data indicate that an immune response induced by a gut-restricted pathogen can modify the immune outcome after pulmonary infection, suggesting that cell-phenotype modifications occur across mucosal sites.

Animals↗
PubMed2006

Bacterial genetic determinants of non-O157 STEC outbreaks and hemolytic-uremic syndrome after infection.

Although O157:H7 Shiga toxin-producing Escherichia coli (STEC) are the predominant cause of hemolytic-uremic syndrome (HUS) in the world, non-O157:H7 serotypes are a medically important cause of HUS that are underdetected by current diagnostic approaches. Because Shiga toxin is necessary but not sufficient to cause HUS, identifying the virulence determinants that predict severe disease after non-O157 STEC infection is of paramount importance. Disease caused by O157:H7 STEC has been associated with a 26-gene pathogenicity island known as O island (OI) 122. To assess the public-health significance of this pathogenicity island, we examined the association between OI122 genes and outbreaks and HUS after non-O157 STEC infection. We found that a subset of OI122 genes is independently associated with outbreaks and HUS after infection with non-O157 STEC. The presence of multiple virulence genes in non-O157 serotypes strengthened this association, which suggests that the additive effects of a variable repertoire of virulence genes contribute to disease severity. In vivo, Citrobacter rodentium mutants lacking outbreak- and HUS-associated genes were deficient for virulence in mice; in particular, nleB mutant bacteria were unable to cause mortality in mice. The present study shows that virulence genes associated epidemiologically with outbreaks and HUS after non-O157 STEC infection are pivotal to the initiation, progression, and outcome of in vivo disease.

Animals↗
PubMed2002

CTX-m-3 beta-lactamase-producing Escherichia coli from Greece.

An Escherichia coli clinical strain resistant to all beta-lactams except carbapenems was isolated in a Greek hospital. Analysis of beta-lactamase content by isoelectric focusing, PCR assays specific for various bla genes, and DNA sequencing showed that the strain produced TEM-1, a Citrobacter freundii AmpC-related cephalosporinase, and CTX-M-3. The blaCTX.M-3 gene was carried by a 120-kb plasmid that was readily transferable to a susceptible E. coli host.

Citrobacter freundii↗
PubMed2004

Accelerating bacterial identification by infrared spectroscopy by employing microarray deposition of microorganisms.

A microarray method for the deposition of bacteria onto an agar slide was developed to accelerate the formation of microcolonies. Representative microarrays each consisting of 40 micro-spots of five replicates of eight foodborne bacteria (Yersinia enterocolitica, Staphylococcus aureus, Salmonella typhimurium, Listeria monocytogenes, Enterobacter cloacae, Citrobacter freundii, Klebsiella pneumoniae, and Escherichia coli) were printed on a Brain Heart Infusion (BHI) agar slide using a contact micro-spotting robotic system. Within 3 h, sufficient bacterial cells were obtained to allow accurate identification of the microorganism by infrared spectroscopy. This approach allows a "complete-in-a-single-day" analysis of a large array of samples.

Bacteria↗
PubMedDate not supplied

Hydrolytic rate at low drug concentration as a limiting factor in resistance to newer cephalosporins.

Hydrolysis kinetics of two cephalosporinases from Citrobacter freundii and Proteus vulgaris having different affinities for cefotaxime and ceftazidime was assessed in studies with cefotaxime, ceftazidime, BMY-28142, and imipenem. The two cephalosporinase genes were cloned into strains of Escherichia coli. The production of these cephalosporinases in strains of E. coli, as well as in the derepressed mutants of C. freundii and P. vulgaris, caused a decrease in susceptibility to the newer cephalosporins. The difference in the rate of hydrolysis at a 0.1 microM concentration of substrate adequately explains the difference in antibacterial activity between cefotaxime and BMY-28142 against E. coli strains with the two cephalosporinases. The results indicate that hydrolysis rate at low substrate concentration, rather than binding with beta-lactams, would be a limiting factor in resistance. The low affinity of cephalosporinases for BMY-28142 means high stability of the agent to the enzymes at low concentration. Furthermore, outer membrane permeability affects the susceptibility of E. coli to cephalosporins synergistically with hydrolysis by cephalosporinases.

Cefotaxime↗
PubMedDate not supplied

Mechanism of inhibition of chromosomal beta-lactamases by third-generation cephalosporins.

The kinetic interactions of the beta-lactamase from Enterobacter cloacae 908 R with ceftriaxone, cefotaxime, and ceftazidime have been examined in detail. With all of these cephalosporins, there is an initial rapid reaction involving opening of the beta-lactam that then decreases to a slower steady-state rate (kss) of beta-lactam hydrolysis (at 37 degrees C: ceftriaxone, kss = 0.044 s-1; cefotaxime, kss = 0.033 s-1; ceftazidime, kss = 0.011 s-1). More than stoichiometric quantities of beta-lactam are cleaved during the rapid phase, during which there is accumulation of a transiently stable cephalosporin-enzyme complex whose rate of breakdown is slower than the overall rate of hydrolysis. Qualitatively similar behavior is observed with the E. cloacae M6300 beta-lactamase. These observations eliminate the possibility that the reaction follows a simple linear kinetic scheme. A branched kinetic scheme in which an initially formed acyl intermediate partitions between deacylation and elimination of the 3' substituent is proposed to explain the data. Investigations of the interaction of ceftriaxone with the chromosomally encoded beta-lactamases from Citrobacter freundii, Providencia rettgeri, Morganella morganii, Pseudomonas aeruginosa, and Escherichia coli show that the partitioning behavior of E. cloacae beta-lactamases is atypical. All of the data, however, clearly demonstrate that it is a physical impossibility for cephalosporin trapping to contribute to bacterial resistance phenotypes.

Cefotaxime↗
PubMedDate not supplied

Plasmid-mediated beta-lactamase (TEM-7) involved in resistance to ceftazidime and aztreonam.

TEM-7, a novel TEM-type beta-lactamase (pI 5.41) encoded on a plasmid of approximately 85 kilobases, was found in a clinical isolate of Citrobacter freundii. Strains containing this enzyme exhibited decreased susceptibility to ceftazidime (64-fold) and aztreonam (16-fold) but not to other third-generation cephalosporins. Addition of a beta-lactamase inhibitor--clavulanic acid, sulbactam, or YTR 830--restored normal susceptibility to associated compounds such as ampicillin, piperacillin, ceftazidime, and aztreonam. DNA-DNA hybridization of an intragenic probe of TEM-1 occurred with a 19-kilobase EcoRI fragment of the plasmid encoding TEM-7. A TEM-2 derivative, TEM-201, with characteristics similar to those of TEM-7 was selected spontaneously in the presence of ceftazidime in vitro.

Aztreonam↗
PubMedDate not supplied

Plasmid-mediated resistance to third-generation cephalosporins caused by point mutations in TEM-type penicillinase genes.

Infections due to strains of Klebsiella pneumoniae, Escherichia coli, and Citrobacter freundii resistant to third-generation cephalosporins have been observed recently in France and the Federal Republic of Germany. This resistance phenotype is due to the production of new plasmid-mediated, broad-substrate-range beta-lactamases designated TEM-3 to TEM-7. DNA-DNA hybridization analysis with a probe specific for TEM-1 indicated that the corresponding genes blaT-3 to blaT-7 were variants of the structural genes for TEM-type beta-lactamases. In the present studies, a 2.5-kilobase BamHI plasmid DNA fragment encoding TEM-3 was cloned in E. coli, and the entire nucleotide sequence of blaT-3 was determined. The deduced amino acid sequence of TEM-3 differed in two positions from that of the TEM-2 enzyme: lysine (TEM-3) was substituted for glutamic acid (TEM-2) at residue 104 and serine (TEM-3) for glycine (TEM-2) at residue 238 in the numbering system of Ambler. Spontaneous mutants of TEM penicillinases with increased activity against third-generation cephalosporins were obtained in vitro by selection on cefotaxime or ceftazidime. It therefore appears that mutations in TEM-type beta-lactamases contribute to resistance to new-generation cephalosporins.

Amino Acid Sequence↗
PubMed1978

A comparative study of the activity of cefamandole and other cephalosporins and analysis of the beta-lactamase stability and synergy of cefamandole with aminoglycosides.

The antibacterial activity of cefamandole against 445 clinical isolates was investigated and compared with the activity of other known cephalosporins (cephalothin, cephaloridine, cephalexin, and cefazolin) and of two penicillins (ampicillin and carbenicillin). Cefamandole was the most active antibiotic against isolates of Citrobacter, Enterobacter, and Shigella, and its activity against Staphylococcus aureus, Bacteroides, and some members of the Enterobacteriaceae was comparable to that of the other antibiotics tested. The stability of cefamandole with respect to beta-lactamase was investigated and compared with that of cephalothin, cefazolin, and cephalexin. Cefamandole was stable with respect to the beta-lactamases of Enterobacter and some other members of the Enterobacteriaceae. No significant correlation was found between the antibacterial activity and the beta-lactamase stability of cefamandole, except with Enterobacter. The synergistic activity of cefamandole combined with gentamicin or amikacin was demonstrated by killing-curve techniques, isobolograms, and susceptibility data. Although 12%--46% of the isolates were synergistically inhibited by either combination, antagonism was not observed. No correlation between the hydrolysis of cefamandole by beta-lactamase and the synergistic activity of cefamandole combined with amikacin was demonstrated.

Acinetobacter↗
PubMed1979

Lethal effect of complement and lysozyme on polymyxin-treated, serum-resistant gram-negative bacilli.

When genetically serum-resistant Escherichia coli, Klebsiella pneumoniae, and Citrobacter freundii, but not Pseudomonas aeruginosa or Proteus mirabilis, were exposed to polymyxin B, they became susceptible to the bactericidal action of normal human and rabbit sera. In constrast, beta-lactam and aminoglycoside antibiotics did not render any serum-resistant bacteria serum-sensitive. Synergy between polymyxin B and the serum bactericidal system could be demonstrated by the addition of polymyxin B to bacteria in vitro, as well as to bacilli in serum from rabbits injected with the antibiotic. Polymyxin B-treated bacteria were killed by normal, lysozyme-depleted, C2-deficient, and hypogammaglobulinemic sera, but not by heated or C6-deficient sera. These findings indicate that polymyxin B-treated bacteria can be killed via the alternative complement pathway. However, C3 and C3b were detected on the surface of serum-resistant E. coli, regardless of whether the bacteria had been treated with polymyxin B. This observation suggests that a change in susceptibility to the alternative complement pathway was not the only explanation for the acquired serum sensitivity. Polymyxin B may also affect a step in the complement sequence beyond the activation of C3, a step that is apparently blocked in serum-resistant gram-negative bacteria.

Animals↗
PubMed1984

Incidence of trimethoprim-sulfamethoxazole-resistant enterobacteriaceae among transplant recipients.

Of 114 recipients of pancreatic, renal, and bone marrow transplants who were given trimethoprim-sulfamethoxazole (TMP-SMZ) for antimicrobial prophylaxis, 44 (39%) had a total of 52 fecal isolates of TMP-SMZ-resistant gram-negative bacilli. In most of these 44 patients, the resistant isolate was found at a concentration of greater than or equal to 10(6) organisms/ml of feces. Escherichia coli was the most frequent of the isolates, and Citrobacter freundii was the next most frequent. Eight of the 114 transplant recipients had gram-negative bacteremia; in six of these eight patients, a TMP-SMZ-resistant gram-negative bacillus was the etiologic agent of bacteremia. Four of the latter six patients had stool cultures analyzed prior to the detection of bacteremia; all four had high concentrations (greater than or equal to 10(8)/ml) of fecal TMP-SMZ-resistant E. coli one to 20 days before they were found to have E. coli bacteremia. In each of these instances, the E. coli isolates from the stool and the blood had similar antibiograms. These findings indicated that resistance to TMP-SMZ is becoming more prevalent and that the screening of patients for the presence of fecal TMP-SMZ-resistant Enterobacteriaceae prior to initiation of long-term therapy with this antimicrobial agent may be worthwhile.

Bone Marrow Transplantation↗
PubMed1983

Comparative activity of cefotetan on Escherichia coli K12 possessing plasmid-mediated beta-lactamases.

The antibacterial activity of cefotetan, a new cephamycin, was compared with that of cephalothin, cefoxitin, cefamandole, cefoperazone and cefotaxime on 12 substrains of Escherichia coli K12 BM13 harbouring single and multi-copy plasmids coding for plasmid-mediated beta-lactamases TEM, SHVI, OXA-I and OXA-III. The 99% inhibitory concentrations (IC99) for the recipient strain were increased in proportion to the enzyme activity in the case of cefamandole and cefoperazone. In contrast, the activity of cefoxitin, cefotaxime and cefotetan was not significantly modified. Since these enzymes are responsible for the resistance of Enterobacteriaceae in the great majority of clinical isolates, cefotetan can be expected to be fully active against strains producing them. Cefotetan was not hydrolysed by chromosomal cephalosporinase and it was active against Enterobacter, Citrobacter and Morganella strains producing a low level of enzyme but hyperproducing variants were highly resistant to cefotetan.

Anti-Bacterial Agents↗
PubMed1983

The origin and properties of beta-lactamase satellite bands seen in isoelectric focusing.

Citrobacter diversus 2046E and Branhamella catarrhalis 2001E each produce a constitutive, chromosomally mediated broad-spectrum beta-lactamase. Isoelectric focusing of both enzymes revealed patterns of multiple 'satellite' bands. The principal satellite bands of each enzyme were isolated and characterized. Individual bands of each enzyme gave similar substrate profiles, molecular weights and responses to inhibitors to one another. The results support the theory that satellite bands are due to the loss and/or modification of specific amino acid residues resulting in biologically active molecules with altered nett charges.

Anti-Bacterial Agents↗
PubMed1985

Application of in-vitro models: development of resistance.

The development of chromosomal beta-lactam resistance of Escherichia coli, Enterobacter cloacae and Citrobacter freundii was observed by following the bacterial kill-kinetics in an in-vitro model simulating human serum antibiotic concentrations. From sensitive Escherichia coli cells mutants arose resistant to aminopenicillins, and to first and second generation cephalosporins, whereas with the Ent. cloacae and Citro. freundii mutants were also resistant to cefotaxime. Resistant mutants from all three species could also be selected on antibiotic-containing agar plates. With E. coli they occurred in two steps, the first mutation being stable but the second mutation reverting spontaneously. In Ent. cloacae, and apparently also in Citro. freundii, the mutation changes the cephalosporinase production from an inducible to a constitutive one. The different mutation rates, and the rate was extremely high for some Ent. cloacae strains, were correlated with a corresponding reduction of viable cell count and with the time of re-growth observed in the model.

Anti-Bacterial Agents↗
PubMed1986

Synergy of amoxycillin combined with clavulanate and YTR 830 in experimental infections in mice.

YTR 830, a new beta-lactamase inhibitor, is synergistic with amoxycillin in vitro against a number of beta-lactamase-producing organisms. The combination of amoxycillin-YTR 830 was compared to amoxycillin-clavulanate in the treatment of experimental Staphylococcus aureus, Citrobacter freundii and Proteus mirabilis infections in mice. Both combinations were synergistic with amoxycillin against all three test organisms. The amoxycillin-clavulanate combination was superior against S. aureus and C. freundii while amoxycillin-YTR 830 was more effective against P. mirabilis. The difference in efficacy between the two drug combinations appears to relate to the degree of protection afforded the animals by the beta-lactamase inhibitor alone. YTR 830 is a promising new agent and should undergo further investigation.

Amoxicillin↗
PubMed1986

The effects on beta-lactam susceptibility of phenotypic induction and genotypic derepression of beta-lactamase synthesis.

We have compared the ability of beta-lactam antibiotics to induce beta-lactamase synthesis and antagonize the in-vitro activity of other beta-lactams and also to select mutants with derepressed beta-lactamase synthesis amongst representative Gram-negative bacilli that produce inducible beta-lactamases. Both imipenem and cefoxitin were potent inducers of beta-lactamase and were able to antagonize the activity of other beta-lactams against isolates of Enterobacter cloacae, Citrobacter freundii and Pseudomonas aeruginosa when the two beta-lactams were present simultaneously. However, there was no antagonism for any compound against any of the organisms when the imipenem or cefoxitin was removed immediately before susceptibility to the other compounds was measured. Cefotaxime was a less potent inducer of beta-lactamase and failed to antagonize the activity of other compounds, even when present concurrently with them. Neither imipenem nor cefoxitin induced beta-lactamase synthesis in a strain of Escherichia coli, nor did they antagonize the activity of other beta-lactams against this strain. Imipenem was compared with cefotaxime and cefoxitin as an agent for the selection of beta-lactam-resistant variants. Resistant variants were obtained from isolates of Ent. cloacae, C. freundii and P. aeruginosa when cefotaxime or cefoxitin was used as the selective agent. Most of them synthesized beta-lactamase constitutively and showed reduced susceptibility to a wide range of beta-lactams, but not to imipenem. Variants with reduced susceptibility to imipenem were obtained only from the two isolates of P. aeruginosa. They did not show cross resistance to other beta-lactams and were not distinguishable from the parent strains in beta-lactamase production.

Anti-Bacterial Agents↗