Association of resistance to trimethoprim/sulphamethoxazole, chloramphenicol and quinolones with changes in major outer membrane proteins and lipopolysaccharide in Burkholderia cepacia

Rajyaguru, Jayshree M.; Muszynski, Michael J.

doi:10.1093/jac/40.6.803

Cited by 17 publications

(14 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, we examined whether OMP expression had been altered in our S. enterica serovar Typhimurium mutants. We also investigated the possible modification of the LPS, since it has been shown in E. coli that LPS alterations could affect the correct folding (6) and trimerization (29,30) of porins and also since quinolone resistance has been associated with changes in the LPSs of gram-negative bacteria such as Burkholderia cepacia (26). Cell envelope modifications in both the OMPs and the LPS, possibly in relation to decreased outer membrane permeability, were found in the fluoroquinolone-selected mutants.…”

Section: Discussionmentioning

confidence: 99%

“…Changes in the cell envelope, including loss of outer membrane porins or alterations of the lipopolysaccharide (LPS), can be partially responsible for decreased susceptibility to a wide range of unrelated antibiotics (5,26). Active efflux systems that act synergistically with the outer membrane could have a high level of participation in the intrinsic and the acquired antibiotic resistance of gram-negative bacteria (16,22).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Evidence for Active Efflux as the Primary Mechanism of Resistance to Ciprofloxacin in Salmonella enterica Serovar Typhimurium

Giraud¹,

Cloeckaert²,

Kerbœuf³

et al. 2000

Antimicrob Agents Chemother

208

180

View full text Add to dashboard Cite

The occurrence of active efflux and cell wall modifications were studied in Salmonella enterica serovar Typhimurium mutants that were selected with enrofloxacin and whose phenotypes of resistance to fluoroquinolones could not be explained only by mutations in the genes coding for gyrase or topoisomerase IV. Mutant BN18/21 exhibited a decreased susceptibility to ciprofloxacin (MIC ‫؍‬ 0.125 g/ml) but did not have a mutation in the gyrA gene. Mutants BN18/41 and BN18/71 had the same substitution, Gly81Cys in GyrA, but exhibited different levels of resistance to ciprofloxacin (MICs ‫؍‬ 2 and 8 g/ml, respectively). None of the mutants had mutations in the parC gene. Evidence for active efflux was provided by a classical fluorimetric method, which revealed a three-to fourfold decrease in ciprofloxacin accumulation in the three mutants compared to that in the parent strain, which was annuled by addition of the efflux pump inhibitor carbonyl cyanide m-chlorophenylhydrazone. In mutant BN18/71, a second fluorimetric method also showed a 50% reduction in the level of accumulation of ethidium bromide, a known efflux pump substrate. Immunoblotting and enzyme-linked immunosorbent assay experiments with an anti-AcrA antibody revealed that the resistance phenotype was strongly correlated with the expression level of the AcrAB efflux pump and suggested that decreased susceptibility to ciprofloxacin due to active efflux probably related to overproduction of this pump could occur before that due to gyrA mutations. Alterations were also found in the outer membrane protein and lipopolysaccharide profiles of the mutants, and these alterations were possibly responsible for the decrease in the permeability of the outer membrane that was observed in the mutants and that could act synergistically with active efflux to decrease the level of ciprofloxacin accumulation.Fluoroquinolones are often the treatment of choice in the cases of life-threatening salmonellosis due to multidrug-resistant strains (4, 27). Salmonella sp. strains that exhibit treatment-compromising resistance to fluoroquinolones are uncommon, but the increasing incidence of strains with decreased susceptibility is a matter of concern (12, 28). In other gramnegative bacteria, such as Escherichia coli, Neisseria gonorrhoeae, or Klebsiella pneumoniae, high-level fluoroquinolone resistance is always associated with the presence of multiple mutations in the quinolone resistance-determining regions (QRDRs) of the genes that code for the intracellular targets of these antibiotics, gyrase (gyrA and gyrB) and topoisomerase IV (parC and parE) (2, 7, 11). For Salmonella enterica serovar Typhimurium, however, we showed in a previous study (9) that fluoroquinolone resistance is not well correlated with the presence of such mutations: highly fluoroquinolone-resistant mutants selected in vitro had no mutations in the genes that code for topoisomerase IV, and some had only one mutation in the gyrA gene, whereas E. coli isolates that exhibited the same level of resistance harbored at leas...

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Evidence for Active Efflux as the Primary Mechanism of Resistance to Ciprofloxacin in Salmonella enterica Serovar Typhimurium

Giraud¹,

Cloeckaert²,

Kerbœuf³

et al. 2000

Antimicrob Agents Chemother

208

180

View full text Add to dashboard Cite

show abstract

“…However, it does not appear clearly from these studies whether such alterations contributed significantly to decreased outer membrane permeability and consecutive quinolone resistance. The role of lipopolysaccharide composition on the accumulation of quinolones has been studied in several bacteria, but it remains unclear, as contradictory results have been obtained [7,13,22,45,47,62]. It has been hypothesised in quinolone-selected Pseudomonas aeruginosa strains that increased amounts of lipopolysaccharide form a permeability barrier which acts preferentially against hydrophilic quinolones [45].…”

Section: Decreased Outer Membrane Permeabilitymentioning

confidence: 99%

Mechanisms of quinolone resistance in Salmonella

Cloeckaert

Chaslus-Dancla

2001

Vet. Res.

View full text Add to dashboard Cite

-As in other Gram-negative bacteria, mechanisms of resistance to quinolones in Salmonella include target gene mutations, active efflux, and decreased outer membrane permeability. However, the exact contribution of these individual mechanisms to resistance, which may nevertheless interplay to reach high-level resistance, has not yet clearly been defined as in other bacteria such as Escherichia coli. This paper reviews the current state of knowledge of quinolone resistance mechanisms in Salmonella by comparison with that of E. coli and future directions of research with particular attention to the recent development of efflux pump inhibitors as possible means of avoiding the emergence and spread of fluoroquinolone resistance.Salmonella / quinolone / resistance / mechanism Résumé -Mécanismes de résistance aux quinolones chez Salmonella. Comme chez les autres bactéries Gram-négatives les mécanismes de résistance aux quinolones chez Salmonella comprennent les mutations dans les gènes cibles, l'efflux actif, et une diminution de la perméabilité de la membrane externe. Cependant la contribution exacte de ces mécanismes individuels, qui peuvent néanmoins interagir pour atteindre des niveaux de résistance élevés, n'a pas encore été clairement définie comme chez d'autres bactéries telle que Escherichia coli. Cette revue présente l'état actuel des connaissances des mécanismes de résistance chez Salmonella par comparaison avec E. coli et des perspectives futures de recherche avec une attention particulière au développement récent d'inhibiteurs de pompes d'efflux comme moyen possible pour éviter l'émergence et la diffusion de la résistance aux fluoroquinolones.Salmonella / quinolone / résistance / mécanisme Vet. Res. 32 (2001) 291-300 291

show abstract

“…However, a proportion of CF patients infected with Bcc can develop "cepacia syndrome," a devastating illness characterized by a fatal acute necrotizing pneumonia that causes rapid and progressive respiratory failure, often leading to the patient's death (22). Intrinsic resistance of Bcc bacteria to many commonly used antibiotics (1) and induction of crossresistance to unrelated antimicrobial agents (40) make it difficult to eradicate these bacteria from CF patients.…”

mentioning

confidence: 99%

Nasal Immunization withBurkholderia multivoransOuter Membrane Proteins and the Mucosal Adjuvant Adamantylamide Dipeptide Confers Efficient Protection against Experimental Lung Infections withB. multivoransandB. cenocepacia

Bertot¹,

Restelli²,

Galanternik

et al. 2007

Infect Immun

View full text Add to dashboard Cite

Association of resistance to trimethoprim/sulphamethoxazole, chloramphenicol and quinolones with changes in major outer membrane proteins and lipopolysaccharide in Burkholderia cepacia

Cited by 17 publications

References 33 publications

Evidence for Active Efflux as the Primary Mechanism of Resistance to Ciprofloxacin in Salmonella enterica Serovar Typhimurium

Evidence for Active Efflux as the Primary Mechanism of Resistance to Ciprofloxacin in Salmonella enterica Serovar Typhimurium

Mechanisms of quinolone resistance in Salmonella

Nasal Immunization withBurkholderia multivoransOuter Membrane Proteins and the Mucosal Adjuvant Adamantylamide Dipeptide Confers Efficient Protection against Experimental Lung Infections withB. multivoransandB. cenocepacia

Contact Info

Product

Resources

About