Mechanisms of Bacterial Resistance to Antibiotics

Dever, Laura Ann; Dermody, Terence S.

doi:10.1001/archinte.1991.00400050040010

Cited by 181 publications

(65 citation statements)

References 138 publications

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“…susceptible versus non-susceptible) of respiratory Streptococcus pyogenes (PY) and Streptococcus pneumoniae (PN) isolates to penicillin and erythromycin following oral consumption of penicillins or cephalosporins [CD: substances with Anatomic Therapeutic Chemical (ATC) code J01C and J01D, respectively] and macrolides or tetracyclines (AF: substances with ATC code J01F and J01A, respectively) [10]. Because resistance to penicillin and erythromycin involves different mechanisms, we did not study penicillin resistance after treatment with AF or erythromycin resistance after treatment with CD [11,12]. Other explanatory variables that were considered to explain an isolate's resistance status were the sampling location (upper respiratory tract, ear, lower respiratory tract or sputum), sex (male or female), preferential reimbursement (yes or no), log(time), age, weight, number of prescription days (for antibiotics in the same treatment group), total dose prescribed (for antibiotics in the same treatment group), whether the patient survived the study (yes or no) and whether the patient was a child (defined as an individual aged <12 years, yes or no).…”

Section: Datamentioning

confidence: 99%

Persistence of antimicrobial resistance in respiratory streptococci

Bruyndonckx

Hens

Aerts

et al. 2017

Journal of Global Antimicrobial Resistance

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A B S T R A C TObjectives: To assess whether persistence of antimicrobial resistance (i.e. non-susceptible resistance status) after treatment with penicillins or cephalosporins versus macrolides or tetracyclines differs and to compare the results obtained using routinely collected data with findings reported in prospective studies. Methods: Routinely collected microbiological data from 14 voluntary participating laboratories (2005) containing information on resistance status and individual antimicrobial consumption patterns (mid 2004-2005) were analysed using a generalised estimating equation (GEE) approach. The link function was adjusted to acknowledge that the proportion of resistant isolates in the population not treated with antibiotics [baseline resistance (BR)] is not necessarily zero. To optimise the comparability of this study with prospective studies, the analysis was repeated after removal of 14 isolates from patients who did not survive 2005. Results: BR estimates were unstable and their confidence intervals were wide, which called for a sensitivity analysis using an adjusted GEE model with three different BR estimates. All models indicated that the proportion of susceptible isolates differed by treatment group and increased significantly over time, with this increase being independent of treatment group. Persistence of resistance after exposure to macrolides or tetracyclines was approximately three times as long as after exposure to penicillins or cephalosporins. Conclusions: Resistance following treatment with macrolides or tetracyclines persists longer than following treatment with penicillins or cephalosporins, which confirms the findings from prospective studies and suggests the use of routinely collected data as a valuable alternative to determine such differences in persistence of resistance.

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Section: Datamentioning

confidence: 99%

Persistence of antimicrobial resistance in respiratory streptococci

Bruyndonckx

Hens

Aerts

et al. 2017

Journal of Global Antimicrobial Resistance

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“…As one of the general resistance mechanisms, antibiotic efflux systems extrude structurally diverse antimicrobial agents out of bacterial cells (6,8,27,29,36). One important family of drug transporters that contribute to multidrug resistance (MDR) in gram-negative bacteria are the resistance-nodulation-cell division (RND) efflux systems, which consist of an inner membrane transporter, a periplasmic fusion protein, and an outer membrane protein (39).…”

mentioning

confidence: 99%

CmeABC Functions as a Multidrug Efflux System in Campylobacter jejuni

Lin

Michel

Zhang

2002

Antimicrob Agents Chemother

479

508

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Campylobacter jejuni, a gram-negative organism causing gastroenteritis in humans, is increasingly resistant to antibiotics. However, little is known about the drug efflux mechanisms in this pathogen. Here we characterized an efflux pump encoded by a three-gene operon (designated cmeABC) that contributes to multidrug resistance in C. jejuni 81-176. CmeABC shares significant sequence and structural homology with known tripartite multidrug efflux pumps in other gram-negative bacteria, and it consists of a periplasmic fusion protein (CmeA), an inner membrane efflux transporter belonging to the resistance-nodulation-cell division superfamily (CmeB), and an outer membrane protein (CmeC). Immunoblotting using CmeABC-specific antibodies demonstrated that cmeABC was expressed in wild-type 81-176; however, an isogenic mutant (9B6) with a transposon insertion in the cmeB gene showed impaired production of CmeB and CmeC. Compared to wild-type 81-176, 9B6 showed a 2-to 4,000-fold decrease in resistance to a range of antibiotics, heavy metals, bile salts, and other antimicrobial agents. Accumulation assays demonstrated that significantly more ethidium bromide and ciprofloxacin accumulated in mutant 9B6 than in wild-type 81-176. Addition of carbonyl cyanide m-chlorophenylhydrazone, an efflux pump inhibitor, increased the accumulation of ciprofloxacin in wild-type 81-176 to the level of mutant 9B6. PCR and immunoblotting analysis also showed that cmeABC was broadly distributed in various C. jejuni isolates and constitutively expressed in wild-type strains. Together, these findings formally establish that CmeABC functions as a tripartite multidrug efflux pump that contributes to the intrinsic resistance of C. jejuni to a broad range of structurally unrelated antimicrobial agents.Bacterial pathogens have evolved multiple mechanisms for resistance to antimicrobial agents, which has greatly compromised the effectiveness of antibiotic treatments and poses a serious threat to public health (13, 17). As one of the general resistance mechanisms, antibiotic efflux systems extrude structurally diverse antimicrobial agents out of bacterial cells (6,8,27,29,36). One important family of drug transporters that contribute to multidrug resistance (MDR) in gram-negative bacteria are the resistance-nodulation-cell division (RND) efflux systems, which consist of an inner membrane transporter, a periplasmic fusion protein, and an outer membrane protein (39). Genetically, many of the RND-type MDR efflux systems or pumps are encoded by a three-gene operon located on the bacterial chromosome (25, 39). However, some efflux pumps, such as AcrAB from Escherichia coli (19), have an outer membrane component that is encoded by a separate gene physically unattached with the other two members on the bacterial chromosome. Expression of these pumps is controlled by regulatory proteins, and their overexpression is usually mediated by mutations in the regulatory elements resulting in an MDR phenotype (27,29,36). Even without overexpression, the MDR efflux pumps ...

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“…Microorganisms can acquire drug resistance via several mechanisms, such as changes in the efficacy of efflux pumps, modification of the cellular target, membrane permeability alterations, and antibiotic degradation (Dever and Dermody, 1991;Tenovor, 2006). This phenomenon occurs by spontaneous mutation in the corresponding gene on the chromosome or through introduction of drug resistance genes from outside of the cell.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Repeated Sodium Hypochlorite Exposure on Chlorine Resistance Development in Escherichia coli O157:H7

Inatsu

Bari

Kitagawa

et al. 2010

FSTR

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Chlorine water has been widely used to reduce viable bacterial contamination on food surfaces and sanitize processing facilities. The emergence and spread of microorganisms with reduced susceptibility to antimicrobial agents is a major public health problem. This in vitro study was designed to evaluate the possibility that E. coli O157:H7 can acquire chlorine resistance and subsequent induction of crossresistance to chlorine water. In addition, the occurrence of spontaneous chlorine resistance mutations or a higher mutation rate introduced by chemical mutations as compared to the standard was also examined. Comparisons of bacterial viability, cellular activity and susceptibility to antibiotics before and after repeated cycles of enrichment cultivation were performed. There were no significant changes observed in bactericidal sensitivity during repeated cultivation in both NTG treated and non-treated cells (n = 6, P > 0.05). There were no significant differences in the activity of cellular respiration enzymes, oxidative stress related gene expression and susceptibility to antibiotics observed in both the NaClO treated samples (n=8, P<0.01) as compared to the control. These results suggested that it might be difficult for E. coli O157:H7 to acquire resistance to chlorine solution even though the bacteria were exposed to NaClO and continued to proliferate.

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Mechanisms of Bacterial Resistance to Antibiotics

Cited by 181 publications

References 138 publications

Persistence of antimicrobial resistance in respiratory streptococci

Persistence of antimicrobial resistance in respiratory streptococci

CmeABC Functions as a Multidrug Efflux System in Campylobacter jejuni

The Effect of Repeated Sodium Hypochlorite Exposure on Chlorine Resistance Development in Escherichia coli O157:H7

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