Quinolone Resistance of Actinobacillus pleuropneumoniae Revealed through Genome and Transcriptome Analyses

Actinobacillus pleuropneumoniae is a pathogen that infects pigs and poses a serious threat to the pig industry. The emergence of quinolone-resistant strains of A.pleuropneumoniae further limits the choice of treatment. However, the mechanisms behind quinolone resistance in A.pleuropneumoniae remain unclear. The genomes of a ciprofloxacin-resistant strain, A. pleuropneumoniae SC1810 and its isogenic drug-sensitive counterpart were sequenced and analyzed using various bioinformatics tools, revealing 559 differentially expressed genes. The biological membrane, plasmid-mediated quinolone resistance genes and quinolone resistance-determining region were detected. Upregulated expression of efflux pump genes led to ciprofloxacin resistance. The expression of two porins, OmpP2B and LamB, was significantly downregulated in the mutant. Three nonsynonymous mutations in the mutant strain disrupted the water–metal ion bridge, subsequently reducing the affinity of the quinolone–enzyme complex for metal ions and leading to cross-resistance to multiple quinolones. The mechanism of quinolone resistance in A. pleuropneumoniae may involve inhibition of expression of the outer membrane protein genes ompP2B and lamB to decrease drug influx, overexpression of AcrB in the efflux pump to enhance its drug-pumping ability, and mutation in the quinolone resistance-determining region to weaken the binding of the remaining drugs. These findings will provide new potential targets for treatment.

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Bacillus anthracis GrlAV96ATopoisomerase IV, a Quinolone Resistance Mutation That Does Not Affect the Water-Metal Ion Bridge

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.03734-14 ◽

2014 ◽

Vol 58 (12) ◽

pp. 7182-7187 ◽

Cited By ~ 7

Author(s):

Katie J. Aldred ◽

Erin J. Breland ◽

Sylvia A. McPherson ◽

Charles L. Turnbough ◽

Robert J. Kerns ◽

...

Keyword(s):

Bacillus Anthracis ◽

Metal Ion ◽

Resistance Mutation ◽

Drug Binding ◽

Quinolone Resistance ◽

Cross Resistance ◽

Topoisomerase Iv ◽

Content Type ◽

A Subunit ◽

Water Metal

ABSTRACTThe rise in quinolone resistance is threatening the clinical use of this important class of broad-spectrum antibacterials. Quinolones kill bacteria by increasing the level of DNA strand breaks generated by the type II topoisomerases gyrase and topoisomerase IV. Most commonly, resistance is caused by mutations in the serine and acidic amino acid residues that anchor a water-metal ion bridge that facilitates quinolone-enzyme interactions. Although other mutations in gyrase and topoisomerase IV have been reported in quinolone-resistant strains, little is known regarding their contributions to cellular quinolone resistance. To address this issue, we characterized the effects of the V96A mutation in the A subunit ofBacillus anthracistopoisomerase IV on quinolone activity. The results indicate that this mutation causes an ∼3-fold decrease in quinolone potency and reduces the stability of covalent topoisomerase IV-cleaved DNA complexes. However, based on metal ion usage, the V96A mutation does not disrupt the function of the water-metal ion bridge. A similar level of resistance to quinazolinediones (which do not use the bridge) was seen. V96A is the first topoisomerase IV mutation distal to the water-metal ion bridge demonstrated to decrease quinolone activity. It also represents the first A subunit mutation reported to cause resistance to quinazolinediones. This cross-resistance suggests that the V96A change has a global effect on the structure of the drug-binding pocket of topoisomerase IV.

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Investigation of Ciprofloxacin Resistance and Its Mechanisms in Clinical Pseudomonas aeruginosa Isolates

ANKEM Dergisi ◽

10.5222/ankem.2021.022 ◽

2021 ◽

Author(s):

Nilüfer Uzunbayır Akel ◽

Yamaç Tekintaş ◽

Fethiye Ferda Yılmaz ◽

İsmail Öztürk ◽

Mustafa Ökeer ◽

...

Keyword(s):

Pseudomonas Aeruginosa ◽

Efflux Pump ◽

Resistance Mechanisms ◽

Regulatory Genes ◽

Quinolone Resistance ◽

University Hospital ◽

Clinical Samples ◽

Genetic Groups ◽

Ciprofloxacin Resistance ◽

Polymerase Chain

Pseudomonas aeruginosa is one of the most important causes of hospital infections. Although different antibiotic groups are used for the treatment of P.aeruginosa infections, quinolone groups are distinguished by the advantages of oral administration. However, in recent years, resistance against members of this group has made treatment more difficult. The aim of this study was to investigate the epidemiological relationship and possible mechanisms of resistance in ciprofloxacin resistant P. aeruginosa isolates from Ege University Hospital. The identification of P.aeruginosa bacteria isolated from clinical samples in Ege University Medical Faculty Medical Microbiology Laboratory was determined by VITEK MS automated systems by VITEK compact, antimicrobial susceptibility. The epidemiological relationships of the ciprofloxacin resistant isolates were determined by Enterobacterial repetitive intergenic consensus-polymerase chain reaction (ERIC-PCR). The presence of qnrA, qnrB, qnrS, qepA genes, the quinolone resistance genes and nfxB, mexR, the regulatory genes of the efflux pump, was determined by PCR. The phenylalanine-arginine β-naphthylamide (PAβN) assay was used to determine the activation of the efflux pump. Twenty-two isolates (26.5 %) were found resistant to ciprofloxacin. According to the ERIC-PCR results, 11 unrelated clones were detected. Ciprofloxacin minimum inhibitory concentration (MIC) values were decreased 2-64 times in 10 isolates in the presence of PAIN. No ciprofloxacin MIC change was detected in one isolate. The presence of pump regulatory genes was determined in 10 of the 11 representative isolates, while only qnrB of the genes associated with quinolone resistance was detected in seven representative isolates. qnrA, qnrS, qepA genes were not detected in any isolate. Ciprofloxacin resistant P.aeruginosa isolates are isolated from our hospital. It is noteworthy that the isolates belonging to different genetic groups are in circulation in clinics. Basic resistance mechanisms are thought to be efflux pumps and qnrB genes.

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Activities of Newer Fluoroquinolones against Ciprofloxacin-Resistant Streptococcus pneumoniae

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.45.6.1654-1659.2001 ◽

2001 ◽

Vol 45 (6) ◽

pp. 1654-1659 ◽

Cited By ~ 34

Author(s):

Elizabeth A. Coyle ◽

Glenn W. Kaatz ◽

Michael J. Rybak

Keyword(s):

Streptococcus Pneumoniae ◽

Efflux Pump ◽

Specific Area ◽

Cross Resistance ◽

Multidrug Efflux ◽

Multidrug Efflux Pump ◽

Time Curve ◽

Ciprofloxacin Resistance ◽

Derivatives Of

ABSTRACT The incidence of ciprofloxacin resistance in Streptococcus pneumoniae is low but steadily increasing, which raises concerns regarding the clinical impact of potential cross-resistance with newer fluoroquinolones. To investigate this problem, we utilized an in vitro pharmacodynamic model and compared the activities of gatifloxacin, grepafloxacin, levofloxacin, moxifloxacin, and trovafloxacin to that of ciprofloxacin against two laboratory-derived, ciprofloxacin-resistant derivatives of S. pneumoniae (strains R919 and R921). Ciprofloxacin resistance in these strains involved the activity of a multidrug efflux pump and possibly, for R919, a mutation resulting in an amino acid substitution in GyrA. Gatifloxacin, grepafloxacin, levofloxacin, moxifloxacin, and trovafloxacin achieved 99.9% killing of both R919 and R921 in ≤28 h. With respect to levofloxacin, significant regrowth of both mutants was observed at 48 h (P < 0.05). For gatifloxacin, grepafloxacin, moxifloxacin, and trovafloxacin, regrowth was minimal at 48 h, with each maintaining 99.9% killing against both mutants. No killing of either R919 or R921 was observed with exposure to ciprofloxacin. During model experiments, resistance to gatifloxacin, grepafloxacin, moxifloxacin, and trovafloxacin did not develop but the MICs of ciprofloxacin and levofloxacin increased 1 to 2 dilutions for both R919 and R921. Although specific area under the concentration-time curve from 0 to 24 h (AUC0–24)/MIC and maximum concentration of drug in serum (C max)/MIC ratios have not been defined for the fluoroquinolones with respect to gram-positive organisms, our study revealed that significant regrowth and/or resistance was associated with AUC0–24/MIC ratios of ≤31.7 and C max/MIC ratios of ≤3.1. It is evident that the newer fluoroquinolones tested possess improved activity against S. pneumoniae, including strains for which ciprofloxacin MICs were elevated.

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Mutation in 23S rRNA Associated with Macrolide Resistance in Neisseria gonorrhoeae

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.46.9.3020-3025.2002 ◽

2002 ◽

Vol 46 (9) ◽

pp. 3020-3025 ◽

Cited By ~ 104

Author(s):

Lai-King Ng ◽

Irene Martin ◽

Gary Liu ◽

Louis Bryden

Keyword(s):

Neisseria Gonorrhoeae ◽

Promoter Region ◽

Efflux Pump ◽

Macrolide Resistance ◽

23S Rrna ◽

Cross Resistance ◽

E Coli ◽

Single Base Pair ◽

Resistant Strains ◽

Domain V

ABSTRACT Fifty-six azithromycin-resistant (MICs, 2.0 to 4.0 μg/ml) Neisseria gonorrhoeae strains with cross-resistance to erythromycin (MICs, 2.0 to 64.0 μg/ml), isolated in Canada between 1997 and 1999, were characterized, and their mechanisms of azithromycin resistance were determined. Most (58.9%) of them belonged to auxotype-serotype class NR/IB-03, with a 2.6-mDa plasmid. Based on resistance to crystal violet (MICs ≥ 1 μg/ml), 96.4% of these macrolide-resistant strains appeared to have increased efflux. Nine of the eleven strains selected for further characterization were found to have a promoter region mtrR mutation, a single-base-pair (A) deletion in the 13-bp inverted repeat, which is believed to cause overexpression of the mtrCDE-encoded efflux pump. The two remaining macrolide-resistant strains (erythromycin MIC, 64.0 μg/ml; azithromycin MIC, 4.0 μg/ml), which did not have the mutation in the mtrR promoter region, were found to have a C2611T mutation (Escherichia coli numbering) in the peptidyltransferase loop in domain V of the 23S rRNA alleles. Although mutations in domain V of 23S rRNA alleles had been reported in other bacteria, including E. coli, Streptococcus pneumoniae, and Helicobacter pylori, this is the first observation of these mutations associated with macrolide resistance in N. gonorrhoeae.

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Use of an Efflux Pump Inhibitor To Determine the Prevalence of Efflux Pump-Mediated Fluoroquinolone Resistance and Multidrug Resistance in Pseudomonas aeruginosa

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.49.2.565-570.2005 ◽

2005 ◽

Vol 49 (2) ◽

pp. 565-570 ◽

Cited By ~ 94

Author(s):

Jane Kriengkauykiat ◽

Edith Porter ◽

Olga Lomovskaya ◽

Annie Wong-Beringer

Keyword(s):

Pseudomonas Aeruginosa ◽

Multidrug Resistance ◽

Substrate Specificity ◽

Efflux Pump ◽

Fluoroquinolone Resistance ◽

Cross Resistance ◽

Broth Microdilution ◽

Efflux Pump Inhibitor ◽

Broad Substrate Specificity ◽

Resistant Strains

ABSTRACT Fluoroquinolone-resistance in Pseudomonas aeruginosa may be due to efflux pump overexpression (EPO) and/or target mutations. EPO can result in multidrug resistance (MDR) due to broad substrate specificity of the pumps. MC-04,124, an efflux pump inhibitor (EPI) shown to significantly potentiate activity of levofloxacin in P. aeruginosa, was used to examine the prevalence of EPO in clinical isolates. MICs were determined for ciprofloxacin, levofloxacin, moxifloxacin, and gatifloxacin with or without EPI and for other antipseudomonal agents by using broth microdilution against P. aeruginosa isolates from adults (n = 119) and children (n = 24). The prevalence of the EPO phenotype (≥8-fold MIC decrease when tested with EPI) was compared among subgroups with different resistance profiles. The EPO phenotype was more prevalent among levofloxacin-resistant than levofloxacin-sensitive strains (61%, 48/79 versus 9%, 6/64). EPO was present in 60% of fluoroquinolone-resistant strains without cross-resistance, while it was present at variable frequencies among strains with cross-resistance to other agents: piperacillin-tazobactam (86%), ceftazidime (76%), cefepime (65%), imipenem (56%), gentamicin (55%), tobramycin (48%), and amikacin (27%). The magnitude of MIC decrease with an EPI paralleled the frequency of which the EPO phenotype was observed in different subgroups. EPI reduced the levofloxacin MIC by as much as 16-fold in eight strains for which MICs were 128 μg/ml. Efflux-mediated resistance appears to contribute significantly to fluoroquinolone resistance and MDR in P. aeruginosa. Our data support the fact that increased fluoroquinolone usage can negatively impact susceptibility of P. aeruginosa to multiple classes of antipseudomonal agents.

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Prevalence of Ciprofloxacin Resistance Among Gram-Negative Bacilli at a Specialist Hospital in Saudi Arabia

Bangladesh Journal of Medical Science ◽

10.3329/bjms.v11i4.12604 ◽

2012 ◽

Vol 11 (4) ◽

pp. 317-321

Author(s):

Shamweel Ahmad

Keyword(s):

Bacterial Species ◽

Treatment Options ◽

Medical Science ◽

Surrogate Marker ◽

Quinolone Resistance ◽

Cross Resistance ◽

Multi Drug Resistance ◽

Gram Negative ◽

Ciprofloxacin Resistance ◽

Tract Infections

Background: Resistance to antimicrobials of different structural classes including fluoroquinolones has arisen in a multitude of bacterial species both in the community and the hospitals. This may complicate the therapeutic management of infections. Decreased susceptibility to fluoroquinolones arises mainly by singlestep mutations in the gyrA and parC genes, which encode the fluoroquinolones targets, the topoisomerase enzymes, conferring cross resistance to all fluoroquinolones. Accumulation of multiple mutations in several genes confers increasing level of resistance associated with clinical failure. However, even low level resistance can generate therapeutic failure. In 1998, some mobile elements with a potential for the horizontal transfer of the quinolone resistance genes were described. The loci which are responsible for this plasmid-mediated quinolone resistance, which have been designated as qnrA, qnrB and qnrS, have been identified in the Enterobacteriaceae species. Aim: To evaluate the susceptibility pattern of the isolates to various antibiotics and to know the prevalence rate of ciprofloxacin resistance in our hospital. Materials & Methods: A total of 916 gram-negative bacilli (GNB) were isolated from different clinical specimens over a period of nine months, were subjected to antibiotic susceptibility testing. Isolates with resistance or with a decreased susceptibility to ciprofloxacin (£20 mm) were then screened for their minimum inhibitory concentration(MIC) by using the E-test. Results: Out of 916 GNB, 321 (35%) isolates were resistant to ciprofloxacin. The MIC of these isolates ranged from 4 to >32?g/ml.Conclusion: The resistance rate to ciprofloxacin was 35% in our study. Most of the ciprofloxacin resistant isolates were from urinary tract infections (UTI). The ciprofloxacin resistance was also closely associated with multi-drug resistance, thus limiting the treatment options. Ciprofloxacin resistance can be used as a general surrogate marker of multidrug resistance, thus limiting the already restricted treatment options. The considerably high MIC values for ciprofloxacin in this study reflected the extent of the treatment problems for these resistant isolates and a need for the continuous evaluation of the commonly used antibiotics. DOI: http://dx.doi.org/10.3329/bjms.v11i4.12604 Bangladesh Journal of Medical Science Vol. 11 No. 04 Oct12

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Involvement of the AcrAB efflux pump in ciprofloxacin resistance in clinical Klebsiella pneumoniae isolates

Infectious Disorders - Drug Targets ◽

10.2174/1871526520999200905121220 ◽

2020 ◽

Vol 20 ◽

Author(s):

Saeed Khoshnood ◽

Mohsen Heidary ◽

Ali Hashemi ◽

Fatemeh Shahi ◽

Morteza Saki ◽

...

Keyword(s):

Klebsiella Pneumoniae ◽

Bacterial Infections ◽

Efflux Pump ◽

Quinolone Resistance ◽

Diffusion Method ◽

Clinical Samples ◽

Resistant Bacteria ◽

Disk Diffusion Method ◽

Rapd Pcr ◽

Ciprofloxacin Resistance

Background: Increasing prevalence of multiple antibiotic resistance in Klebsiella pneumoniae strains confines the therapeutic options used to treat bacterial infections. Objective: We aimed in this study to investigate the role of AcrAB, qepA efflux pump, and AAC(6′)-Ib-cr enzyme in ciprofloxacin resistance and to detect the RAPD-PCR fingerprint of K. pneumoniae isolates. Methods: In total, 117 K. pneumoniae isolates were collected from hospitalized patients in three hospitals in Tehran, Iran from August 2013 to March 2014. Antimicrobial susceptibility tests were performed by the disk diffusion method. Molecular identification and expression level of encoding quinolone resistance genes, acrA, acrB, qepA, and aac(6')-Ib-cr, was per-formed by PCR and real-time PCR assays, respectively. All the K. pneumoniae isolates containing these genes was used simultaneously for RAPD-PCR typing. Results: Colistin and carbapenems were the most efficient antibiotics against the clinical isolates of K. pneumoniae. PCR assay demonstrated that among the 117 isolates, 110 (94%) and 102 (87%) were positive for acrA and acrB gene, and for qepA and aac(6′)-Ib-cr genes, 5 (4%) and 100 (85%) isolates were detected, respectively. Determination of AcrAB pump expression in 21% of strains demonstrated an increased expression, and the mean increase expression for acrB genes was 0.5-81. The results of RAPD-PCR reflected that in 95% CI, all isolates belong to a clone. Conclusion: A high prevalence of genes encoding quinolone resistance in K. pneumoniae was detected in clinical samples. Therefore, control of infection and prevention of drug-resistant bacteria spread need careful management of medication and identification of resistant isolates.

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Prevalence and characterization of quinolone resistance in Laribacter hongkongensis from grass carp and Chinese tiger frog

Journal of Medical Microbiology ◽

10.1099/jmm.0.059451-0 ◽

2013 ◽

Vol 62 (10) ◽

pp. 1559-1564 ◽

Cited By ~ 11

Author(s):

Ding-Qiang Chen ◽

Ling Yang ◽

Yu-Ting Luo ◽

Min-Jie Mao ◽

Yong-Ping Lin ◽

...

Keyword(s):

Molecular Mechanisms ◽

Efflux Pump ◽

Quinolone Resistance ◽

Efflux Pump Inhibitor ◽

Electrophoretic Patterns ◽

Food Borne ◽

Laribacter Hongkongensis ◽

Resistant Strains

Laribacter hongkongensis is a food-borne bacterium associated with community-acquired gastroenteritis and diarrhoea. Quinolone resistance was recently reported in bacterial isolates from aquatic products, but the molecular mechanisms for resistance were still unknown. In this study, a total of 157 L. hongkongensis strains were isolated from grass carps (n = 443) and Chinese tiger frogs (n = 171). Twenty-one ciprofloxacin-resistant strains were analysed for mutations in quinolone resistance-determining regions (QRDR), acquired quinolone resistance (AQR) genes and the role of efflux pumps in resistance. All QRDR mutations in gyrA (codons 85 and 89) and parC (codons 83 and 231) were found to be closely associated with ciprofloxacin resistance. The AQR gene aac(6′)-Ib-cr was found in 42.9 % (9/21) of the resistant strains, but qnrA, qnrB, qnrC, qnrD, qnrS and qepA were not detected. No significant change of MICs to ciprofloxacin was observed in the presence of an efflux pump inhibitor, indicating the role of efflux pump was probably absent. All 21 ciprofloxacin-resistant strains showed different electrophoretic patterns, which suggested they were not genetically related. These data highlight the importance of QRDR mutations and the AQR gene aac(6′)-Ib-cr during the development of quinolone resistance in a heterogeneous population of L. hongkongensis.

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The prevalence and mechanism of triclosan resistance in Escherichia coli isolated from urine samples in Wenzhou, China

10.21203/rs.3.rs-24751/v2 ◽

2020 ◽

Author(s):

Weiliang Zeng ◽

Wenya Xu ◽

Ye Xu ◽

Wenli Liao ◽

Yajie Zhao ◽

...

Keyword(s):

Efflux Pump ◽

Urine Samples ◽

Cross Resistance ◽

Chain Reaction ◽

E Coli ◽

Resistant Strains ◽

Polymerase Chain ◽

Triclosan Resistance ◽

Encoding Genes

Abstract Background: The widespread application of triclosan contributes to its residual deposition in urine, which provides an environment of long-term exposure to triclosan for the intestinal Escherichia coli. We determined the triclosan and antibiotic resistance characteristics of E. coli strains isolated from urine samples and further investigated the resistance mechanism and molecular epidemic characteristics of triclosan-resistant E. coli isolates. Methods: A total of 200 non-repetitive E. coli strains were isolated from urine samples and then identified. The minimum inhibitory concentrations (MICs) of triclosan and antibiotics, fabI mutation, efflux pump activity, the expression of 14 efflux pump encoding genes, and epidemiological characteristics were determined by the agar dilution method, polymerase chain reaction (PCR), carbonyl cyanide 3-chlorophenylhydrazone (CCCP) inhibition test, quantitative real-time polymerase chain reaction (RT-qPCR), multilocus sequence typing (MLST), and pulse-field gel electrophoresis (PFGE) for all triclosan-resistant isolates. Furthermore, we also investigated the effect of triclosan exposure in vitro on antibiotic susceptibility and the efflux pump encoding gene expressions of triclosan-susceptible strains via serial passage experiments. Results: Of the 200 E. coli isolates, 2.5% (n = 5) were found to be resistant to triclosan, and multidrug resistance (MDR) and cross-resistance phenotypes were noted for these triclosan-resistant strains. The triclosan-sensitive strains also exhibited MDR phenotypes, probably because of the high resistance rate to AMP, CIP, LVX, and GEN. Gly79Ala and Ala69Thr amino acid changes were observed in the triclosan-resistant strains, but these changes may not mediate resistance of E. coli to triclosan, because mutations of these two amino acids has also been detected in triclosan-susceptible strains. Moreover, except for DC8603, all other strains enhanced the efflux pumps activity. As compared with ATCC 25922, except for fabI, increased expressions were noted for all efflux pump encoding genes such as ydcV, ydcU, ydcS, ydcT, cysP, yihV, acrB, acrD, and mdfA among the studied strains with varying PFGE patterns and STs types. Unexpectedly, 5 susceptible E. coli isolates showed rapidly increasing triclosan resistance after exposure to triclosan in vitro for only 12 days, while MDR or cross-resistance phenotypes and the overexpression of efflux pump genes were recorded among these triclosan-induced resistant isolates. Conclusions: This is the first study to report that short-term triclosan exposure in vitro increases triclosan resistance in susceptible E. coli isolates. After acquiring resistance, these strains may present MDR or cross-resistance phenotypes. Moreover, triclosan resistance mainly involves the overexpression of fabI and efflux pumps in E. coli isolates.

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Overexpression of target enzyme gene fabI and efflux pump decrease triclosan susceptibility in Escherichia coli

10.21203/rs.2.21275/v1 ◽

2020 ◽

Author(s):

Weiliang Zeng ◽

Wenya Xu ◽

Ye Xu ◽

Wenli Liao ◽

Yajie Zhao ◽

...

Keyword(s):

Escherichia Coli ◽

Efflux Pump ◽

Close Association ◽

Opportunistic Pathogen ◽

Cross Resistance ◽

Dilution Method ◽

Agar Dilution Method ◽

E Coli ◽

Resistant Strains ◽

Triclosan Resistance

Abstract Background: Escherichia coli isolates, the most opportunistic pathogen in the gut, are responsible for the most acquired infections. Triclosan is an effective disinfectant for inhibits microorganisms, but its widespread use causes its residue in urine, resulting in long-term exposure of E. coli in the intestine to triclosan environment and increasing triclosan resistance. We aim to provide the mechanism of action of E. coli isolates against triclosan and the molecular epidemiological analysis of triclosan-resistant strains.Results: Five triclosan-resistant isolates were screened out from 200 E. coli isolates by agar dilution method by to further study, interestingly, multidrug-resistant and cross-resistance phenotypes were observed in triclosan-resistant strains, but not in susceptible strains, and all except one exhibited an inhibition of efflux pump activity by efflux pump inhibition testing. Furthermore, compared with susceptible E. coli strain ATCC 25922, except fabI, increased expression were also found in efflux pump encoding genes ydcV, ydcU, ydcS, ydcT, cysP, yihV, acrB, acrD and mdfA in studied strains which had different PFGE patterns and STs types.Conclusions: These findings indicated that triclosan resistance in E. coli were mainly involved by overexpression of fabI gene, and there was a close association between overexpression of efflux pump with reducing susceptibility to triclosan. Besides, we described cross-resistance between triclosan and antibiotics may be related to the exposure time of triclosan.

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