Triclosan resistance in clinical isolates of Acinetobacter baumannii

The susceptibility to triclosan of 732 clinical Acinetobacter baumannii isolates obtained from 25 hospitals in 16 cities in China from December 2004 to December 2005 was screened by using an agar dilution method. Triclosan MICs ranged between 0.015 and 16 mg l−1, and the MIC90 was 0.5 mg l−1, lower than the actual in-use concentration of triclosan. Twenty triclosan-resistant isolates (MICs ≥1 mg l−1) were characterized by antibiotic susceptibility, clonal relatedness, fabI mutation, fabI expression, and efflux pump phenotype and expression to elucidate the resistance mechanism of A. baumannii to triclosan. The resistance rates of triclosan-resistant isolates to imipenem, levofloxacin, amikacin and tetracycline were higher than those of triclosan-sensitive isolates. Triclosan resistance was artificially classified as low level (MICs 1–2 mg l−1) or high level (MICs ≥4 mg l−1). High-level triclosan resistance could be explained by a Gly95Ser mutation of FabI, whilst wild-type fabI was observed to be overexpressed in low-level resistant isolates. Active efflux did not appear to be a major reason for acquired triclosan resistance, but acquisition of resistance appeared to be dependent on a background of intrinsic triclosan efflux.

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Impact of an Intervention to Control Imipenem-Resistant Acinetobacter baumannii and Its Resistance Mechanisms: An 8-Year Survey

Frontiers in Microbiology ◽

10.3389/fmicb.2020.610109 ◽

2021 ◽

Vol 11 ◽

Cited By ~ 1

Author(s):

Lida Chen ◽

Pinghai Tan ◽

Jianming Zeng ◽

Xuegao Yu ◽

Yimei Cai ◽

...

Keyword(s):

Drug Resistance ◽

Acinetobacter Baumannii ◽

Bacterial Resistance ◽

Efflux Pump ◽

Resistance Mechanism ◽

Resistance Mechanisms ◽

Multi Drug Resistance ◽

Minimal Inhibitory Concentrations ◽

Resistance Rates ◽

The Impact

BackgroundThis study aimed to examine the impact of an intervention carried out in 2011 to combat multi-drug resistance and outbreaks of imipenem-resistant Acinetobacter baumannii (IRAB), and to explore its resistance mechanism.MethodsA total of 2572 isolates of A. baumannii, including 1673 IRAB isolates, were collected between 2007 and 2014. An intervention was implemented to control A. baumannii resistance and outbreaks. Antimicrobial susceptibility was tested by calculating minimal inhibitory concentrations (MICs), and outbreaks were typed using pulsed-field gel electrophoresis (PFGE). Resistance mechanisms were explored by polymerase chain reaction (PCR) and whole genome sequencing (WGS).ResultsFollowing the intervention in 2011, the resistance rates of A. baumannii to almost all tested antibiotics decreased, from 85.3 to 72.6% for imipenem, 100 to 80.8% for ceftriaxone, and 45.0 to 6.9% for tigecycline. The intervention resulted in a decrease in the number (seven to five), duration (8–3 months), and departments (five to three) affected by outbreaks; no outbreaks occurred in 2011. After the intervention, only blaAMPC (76.47 to 100%) and blaTEM–1 (75.74 to 96.92%) increased (P < 0.0001); whereas blaGES–1 (32.35 to 3.07%), blaPER–1 (21.32 to 1.54%), blaOXA–58 (60.29 to 1.54%), carO (37.50 to 7.69%), and adeB (9.56 to 3.08%) decreased (P < 0.0001). Interestingly, the frequency of class B β-lactamase genes decreased from 91.18% (blaSPM–1) and 61.03% (blaIMP–1) to 0%, while that of class D blaOXA–23 increased to 96.92% (P < 0.0001). WGS showed that the major PFGE types causing outbreaks each year (type 01, 11, 18, 23, 26, and 31) carried the same resistance genes (blaKPC–1, blaADC–25, blaOXA–66, and adeABC), AdeR-S mutations (G186V and A136V), and a partially blocked porin channel CarO. Meanwhile, plasmids harboring blaOXA–23 were found after the intervention.ConclusionThe intervention was highly effective in reducing multi-drug resistance of A. baumannii and IRAB outbreaks in the long term. The resistance mechanisms of IRAB may involve genes encoding β-lactamases, efflux pump overexpression, outer membrane porin blockade, and plasmids; in particular, clonal spread of blaOXA–23 was the major cause of outbreaks. Similar interventions may also help reduce bacterial resistance rates and outbreaks in other hospitals.

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Widespread Occurrence of Possible Antibiotic Efflux Mechanism in Multidrug Resistant Intestinal E. coli Strains Isolated from Healthy Human Subjects in Bangladesh

Bangladesh Journal of Microbiology ◽

10.3329/bjm.v30i1-2.28454 ◽

2016 ◽

Vol 30 (1-2) ◽

pp. 55-59

Author(s):

M Hasibur Rahman ◽

Jamil Mahmud ◽

Md Mahamudul Haque ◽

Farzana Tarannum Tuli ◽

Nazneen Jahan ◽

...

Keyword(s):

Ethidium Bromide ◽

Efflux Pump ◽

Human Subjects ◽

Agar Plate ◽

Multidrug Resistant ◽

Dilution Method ◽

Agar Dilution Method ◽

Healthy Human ◽

Efflux Mechanism ◽

High Level

A total of 50 isolates of Escherichia coli obtained from healthy adult human subjects were studied and tested for possible presence of efflux mechanism in resistance determination and possible correlation of plasmids with resistance.Minimal inhibitory concentration (MIC) of the antibiotics amoxicillin, azithromycin, ciprofloxacin, chloramphenicol and tetracycline were determined by agar dilution method with or without the H+/K+ proton pump inhibitor omeprazole. Plasmids were extracted by rapid alkaline plasmid extraction method and analyzed by agarose gel electrophoresis. Many strains showed 5 10 fold reduction of MIC values in the presence of omeprazole; a few strains showed up to 100-fold MIC reduction. Plasmid analysis of these 50 isolates revealed the presence of both plasmidless and plasmid containing strains, the latter with plasmid number varying from one to seven. However, the plasmids apparently had no relationship with high level antibiotic tolerance as indicated by the observation that some plasmidless strains had very high MIC values, while other strains containing several plasmids had very low MIC. Decrease in MIC in the presence of omeprazole apparently indicates existence of an efflux mechanism. Evidence of the efflux of ethidium bromide was noted in some strains that had been grown in ethidium bromide containing agar plate with and without omeprazole. These results suggest that reduction of MIC caused by omeprazole may be related to possible inhibition of efflux pump activity by omeprazole in the isolates studied.Bangladesh J Microbiol, Volume 30, Number 1-2,June-Dec 2013, pp 55-59

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Triclosan Can Select for an AdeIJK-Overexpressing Mutant of Acinetobacter baumannii ATCC 17978 That Displays Reduced Susceptibility to Multiple Antibiotics

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.03074-14 ◽

2014 ◽

Vol 58 (11) ◽

pp. 6424-6431 ◽

Cited By ~ 26

Author(s):

Dinesh M. Fernando ◽

Wayne Xu ◽

Peter C. Loewen ◽

George G. Zhanel ◽

Ayush Kumar

Keyword(s):

Acinetobacter Baumannii ◽

Efflux Pump ◽

Resistant Mutant ◽

Dilution Method ◽

Gene Encoding ◽

Content Type ◽

Resistance Nodulation Division ◽

Triclosan Resistance ◽

Encoding Genes ◽

Multiple Antibiotics

ABSTRACTIn order to determine if triclosan can select for mutants ofAcinetobacter baumanniiATCC 17978 that display reduced susceptibilities to antibiotics, we isolated a triclosan-resistant mutant,A. baumanniiAB042, by serial passaging ofA. baumanniiATCC 17978 in growth medium supplemented with triclosan. The antimicrobial susceptibility of AB042 was analyzed by the 2-fold serial dilution method. Expression of five different resistance-nodulation-division (RND) pump-encoding genes (adeB,adeG,adeJ,A1S_2818, andA1S_3217), two outer membrane porin-encoding genes (carOandoprD), and the MATE family pump-encoding geneabeMwas analyzed using quantitative reverse transcriptase (qRT) PCR.A. baumanniiAB042 exhibited elevated resistance to multiple antibiotics, including piperacillin-tazobactam, doxycycline, moxifloxacin, ceftriaxone, cefepime, meropenem, doripenem, ertapenem, ciprofloxacin, aztreonam, tigecycline, and trimethoprim-sulfamethoxazole, in addition to triclosan. Genome sequencing ofA. baumanniiAB042 revealed a116G→V mutation infabI, the gene encoding the target enzyme for triclosan. Expression analysis of efflux pumps showed overexpression of the AdeIJK pump, and sequencing ofadeN, the gene that encodes the repressor of theadeIJKoperon, revealed a 73-bp deletion which would cause a premature termination of translation, resulting in an inactive truncated AdeN protein. This work shows that triclosan can select for mutants ofA. baumanniithat display reduced susceptibilities to multiple antibiotics from chemically distinct classes in addition to triclosan resistance. This multidrug resistance can be explained by the overexpression of the AdeIJK efflux pump.

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Overexpression of the adeB Efflux Pump Gene in Tigecycline-Resistant Acinetobacter baumannii Clinical Isolates and Its Inhibition by (+)Usnic Acid as an Adjuvant

Antibiotics ◽

10.3390/antibiotics10091037 ◽

2021 ◽

Vol 10 (9) ◽

pp. 1037

Author(s):

Nagaraju Bankan ◽

Fathimunnisa Koka ◽

Rajagopalan Vijayaraghavan ◽

Sreekanth Reddy Basireddy ◽

Selvaraj Jayaraman

Keyword(s):

Acinetobacter Baumannii ◽

Efflux Pump ◽

Resistance Mechanism ◽

Usnic Acid ◽

Pcr Analysis ◽

Dilution Method ◽

High Morbidity ◽

Efflux Pump Inhibitor ◽

Acinetobacter Species ◽

Pump Activity

Acinetobacter species are among the most life-threatening Gram-negative bacilli, causing hospital-acquired infections, and they are associated with high morbidity and mortality. They show multidrug resistance that acts via various mechanisms. In Acinetobacter baumannii, efflux pump-mediated resistance to many antimicrobial compounds, including tigecycline, has been widely reported. Natural compounds have been used for their various pharmacological properties, including anti-efflux pump activity. The present study aimed to evaluate the efflux pump-mediated resistance mechanism of Acinetobacter baumannii and the effect of (+)Usnic acid as an efflux pump inhibitor with tigecycline. For detecting the efflux pump activity of tigecycline-resistant Acinetobacter baumannii isolates, microbroth dilution method and real-time quantitative reverse transcription–polymerase chain reaction was used. (+)Usnic acid was added to tigecycline and tested by the checkerboard method to evaluate its efficacy as an efflux pump inhibitor. qRT-PCR analysis was carried out to show the downregulation of the efflux pump in the isolates. Out of 42 tigecycline-resistant Acinetobacter baumannii isolates, 19 showed efflux pump activity. All 19 strains expressed the adeB gene. (+)Usnic acid as an adjuvant showed better efficacy in lowering the minimum inhibitory concentration compared with the conventional efflux pump inhibitor, carbonyl cyanide phenylhydrazone.

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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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Prevalence and characterization of extended spectrum beta-lactamase-producing Enterobacter cloacae strains in Algeria

The Journal of Infection in Developing Countries ◽

10.3855/jidc.3127 ◽

2013 ◽

Vol 7 (11) ◽

pp. 804-811 ◽

Cited By ~ 5

Author(s):

Sabrina Nedjai ◽

Abouddihaj Barguigua ◽

Nassima Djahmi ◽

Loubna Jamali ◽

Khalid Zerouali ◽

...

Keyword(s):

Enterobacter Cloacae ◽

Dilution Method ◽

Agar Dilution Method ◽

Extended Spectrum Beta Lactamase ◽

Agar Dilution ◽

Synergy Test ◽

High Level ◽

Genomic Typing ◽

Microbiological Data

Introduction: Expended spectrum β-lactamase (ESBL)-producing Enterobacter cloacae is an important nosocomial pathogen. In this study, the prevalence and the molecular epidemiology of ESBL producing E. cloacae strains isolated from various hospitals in Annaba, Algeria were investigated. Methodology: The study involved 63 isolates of E. cloacae obtained during 2009 at the four hospitals in Annaba. The detection of ESBL was performed using the double-disk synergy test and the combined disk test. Minimum inhibitory concentrations (MICs) were determined using the agar dilution method. The presence of blaCTX-M, blaSHV, blaTEM, and blaDHA β-lactamase genes was evaluated by PCR, and genomic typing was determined by pulsed-field gel electrophoresis (PFGE) analysis. The clinical and microbiological data were entered into the EpiI Info database. Results: Thirty isolates (47.6%) had an ESBL phenotype. BlaCTX-M group1 (76%); blaTEM (70%) were the most prevalent, followed by blaDHA (16.6%) and blaSHV (10%). Eighteen strains expressed at least two bla genes. MICs revealed a high level of resistance to cefotaxime, ceftazidime, and cefepime. PFGE revealed an epidemic clonal dissemination of these isolates. Various risk factors associated with the occurrence of ESBL-producing E. cloacae were detected. Conclusions: A higher frequency of ESBL-producing isolates and a diversity of β-lactamases were detected among ESBL-producing E. cloacae; these resulted from an epidemic clonal dissemination and high transference of ESBL genes between bacteria in hospital settings. Strict measures will be required to control the further spread of these pathogens in hospital settings.

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Efflux-Related Resistance to Norfloxacin, Dyes, and Biocides in Bloodstream Isolates of Staphylococcus aureus

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.00430-07 ◽

2007 ◽

Vol 51 (9) ◽

pp. 3235-3239 ◽

Cited By ~ 122

Author(s):

Carmen E. DeMarco ◽

Laurel A. Cushing ◽

Emmanuel Frempong-Manso ◽

Susan M. Seo ◽

Tinevimbo A. A. Jaravaza ◽

...

Keyword(s):

Gene Expression ◽

Staphylococcus Aureus ◽

Efflux Pump ◽

Resistance Mechanism ◽

Efflux Pump Inhibitor ◽

Qrt Pcr ◽

Reverse Transcription Pcr ◽

Environmental Surfaces ◽

Genes Encoding ◽

High Level

ABSTRACT Efflux is an important resistance mechanism in Staphylococcus aureus, but its frequency in patients with bacteremia is unknown. Nonreplicate bloodstream isolates were collected over an 8-month period, and MICs of four common efflux pump substrates, with and without the broad-spectrum efflux pump inhibitor reserpine, were determined (n = 232). A reserpine-associated fourfold decrease in MIC was considered indicative of efflux. Strains exhibiting efflux of at least two of the four substrates were identified (“effluxing strains” [n = 114]). For these strains, MICs with or without reserpine for an array of typical substrates and the expression of mepA, mdeA, norA, norB, norC, and qacA/B were determined using quantitative real-time reverse transcription-PCR (qRT-PCR). A fourfold or greater increase in gene expression was considered significant. The most commonly effluxed substrates were ethidium bromide and chlorhexidine (100 and 96% of effluxing strains, respectively). qRT-PCR identified strains overexpressing mepA (5 [4.4%]), mdeA (13 [11.4%]), norA (26 [22.8%]), norB (29 [25.4%]), and norC (19 [16.7%]); 23 strains overexpressed two or more genes. Mutations probably associated with increased gene expression included a MepR-inactivating substitution and norA promoter region insertions or deletions. Mutations possibly associated with increased expression of the other analyzed genes were also observed. Effluxing strains comprised 49% of all strains studied (114/232 strains), with nearly half of these overexpressing genes encoding MepA, MdeA, and/or NorABC (54/114 strains). Reduced susceptibility to biocides may contribute to persistence on environmental surfaces, and efflux of drugs such as fluoroquinolones may predispose strains to high-level target-based resistance.

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Detection of OXA-181/OXA-48 carbapenemase producing Enterobacteriaceae in Bangladesh

Ibrahim Medical College Journal ◽

10.3329/imcj.v9i2.28853 ◽

2016 ◽

Vol 9 (2) ◽

pp. 45-51 ◽

Cited By ~ 1

Author(s):

Rehana Khatun ◽

SM Shamsuzzaman

Keyword(s):

Health Concern ◽

Dilution Method ◽

Agar Dilution Method ◽

College Hospital ◽

Medical College ◽

Epidemiological Monitoring ◽

Diffusion Technique ◽

Genes Encoding ◽

High Level ◽

Phenotypic Tests

Carbapenem resistant Enterobacteriaceae (CRE) is becoming a major public health concern globally. Detection of carbapenem hydrolyzing enzyme carbapenemase in Enterobacteriaceae is important to institute appropriate therapy and to initiate preventive measures. This study was designed to determine the presence of carbapenemase producers among the CRE isolated from patients at Dhaka Medical College Hospital, Bangladesh. Twenty-nine CRE strains detected by disk diffusion technique were included in the study. Minimum inhibitory concentration of imipenem and tigecycline was determined by agar dilution method. Carbapenemase production was phenotypically detected by Modified Hodge test while MBL producers were detected by combined disk and double disk synergy tests. Genes encoding blaNDM-1, blaOXA-181, blaOXA-48, blaKPC, blaCTX-M-15, blaOXA-1-group were identified by polymerase chain reaction (PCR). Out of 29 CRE, nineteen (65.6%) were positive for carbapenemase by any of the three phenotypic tests namely MHT, CD or DD tests. Those 19 isolates were also positive either for blaNDM-1 or blaOXA-181/blaOXA-48 by PCR. Of the 19 PCR positive isolates, the rate of positivity for blaNDM- 1, blaOXA-181/blaOXA-48 and blaNDM-1+ blaOXA-181/blaOXA-48 was 73.7% (14/19), 57.9% (11/19) and 31.6% (6/19) respectively. Both blaOXA-181 and blaOXA-48 co-existed. All the carbapenemase producing organisms harboured blaCTX-M-15 except one C. freundii strain. The rate of resistance to different classes of antibiotics ranged from 63.2% to 100% except colistin and tigecycline. Organisms positive for OXA-181/OXA-48 had a low level of resistance to carbapenem (MIC 1 - 4 ì g/ml) while with NDM-1 had high level resistance to imipenem (MICs 16 - ? 32 ì g/ ml). Out of 19 carbapenemase positive isolates, 12 (63.16%) were extensively drug-resistant (XDR) and were only sensitive to tigecycline and colistin. The result of this study showed the presence of blaOXA-181/ blaOXA-48, blaNDM-1 positive strains in Bangladesh and colistin and tigecycline were the most effective drugs against carbapenemase producing Enterobacteriaceae (CPE). Epidemiological monitoring of carbapenemase producing organisms in Bangladesh is important to prevent their dissemination.Ibrahim Med. Coll. J. 2015; 9(2): 45-51

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RamA, a transcriptional regulator conferring florfenicol resistance in Leclercia adecarboxylata R25

Folia Microbiologica ◽

10.1007/s12223-020-00816-2 ◽

2020 ◽

Vol 65 (6) ◽

pp. 1051-1060

Author(s):

Cong Cheng ◽

Yuanyuan Ying ◽

Danying Zhou ◽

Licheng Zhu ◽

Junwan Lu ◽

...

Keyword(s):

Resistance Gene ◽

Efflux Pump ◽

Gene Knockout ◽

Regulatory Gene ◽

Resistance Mechanism ◽

Agricultural Practice ◽

The Novel ◽

Inappropriate Use ◽

Rnd Efflux Pump ◽

High Level

AbstractDue to the inappropriate use of florfenicol in agricultural practice, florfenicol resistance has become increasingly serious. In this work, we studied the novel florfenicol resistance mechanism of an animal-derived Leclercia adecarboxylata strain R25 with high-level florfenicol resistance. A random genomic DNA library was constructed to screen the novel florfenicol resistance gene. Gene cloning, gene knockout, and complementation combined with the minimum inhibitory concentration (MIC) detection were conducted to determine the function of the resistance-related gene. Sequencing and bioinformatics methods were applied to analyze the structure of the resistance gene-related sequences. Finally, we obtained a regulatory gene of an RND (resistance-nodulation-cell division) system, ramA, that confers resistance to florfenicol and other antibiotics. The ramA-deleted variant (LA-R25ΔramA) decreased the level of resistance against florfenicol and several other antibiotics, while a ramA-complemented strain (pUCP24-prom-ramA/LA-R25ΔramA) restored the drug resistance. The whole-genome sequencing revealed that there were five RND efflux pump genes (mdtABC, acrAB, acrD, acrEF, and acrAB-like) encoded over the chromosome, and ramA located upstream of the acrAB-like genes. The results of this work suggest that ramA confers resistance to florfenicol and other structurally unrelated antibiotics, presumably by regulating the RND efflux pump genes in L. adecarboxylata R25.

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Identification and Characterization of TriABC-OpmH, a Triclosan Efflux Pump of Pseudomonas aeruginosa Requiring Two Membrane Fusion Proteins

Journal of Bacteriology ◽

10.1128/jb.00850-07 ◽

2007 ◽

Vol 189 (21) ◽

pp. 7600-7609 ◽

Cited By ~ 73

Author(s):

Takehiko Mima ◽

Swati Joshi ◽

Margarita Gomez-Escalada ◽

Herbert P. Schweizer

Keyword(s):

Pseudomonas Aeruginosa ◽

Membrane Fusion ◽

Fusion Proteins ◽

Efflux Pump ◽

Divalent Cations ◽

Constitutive Expression ◽

Multiple Copies ◽

High Level ◽

Triclosan Resistance ◽

Membrane Fusion Proteins

ABSTRACT Pseudomonas aeruginosa achieves high-level (MIC > 1 mg/ml) triclosan resistance either by constitutive expression of MexAB-OprM, an efflux pump of the resistance nodulation cell division (RND) family, or expression of MexCD-OprJ, MexEF-OprN, and MexJK-OpmH in regulatory mutants. A triclosan-resistant target enzyme and perhaps other mechanisms probably act synergistically with efflux. To probe this notion, we exposed the susceptible Δ(mexAB-oprM) Δ(mexCD-oprJ) Δ(mexEF-oprN) Δ(mexJK) Δ(mexXY) strain PAO509 to increasing triclosan concentrations and derived a resistant strain, PAO509.5. This mutant overexpressed the PA0156-PA0157-PA0158 pump, which only effluxed triclosan, but not closely related compounds, antibiotics, and divalent cations, and was therefore renamed TriABC. Constitutive expression of the triABC operon was due to a single promoter-up mutation. Deletion of two adjacent genes, pcaR and PA0159, encoding transcriptional regulators had no effect on expression of this operon. TriABC is the only P. aeruginosa RND pump which contains two membrane fusion proteins, TriA and TriB, and both are required for efflux pump function. Probably owing to tight transcriptional coupling of the triABC genes, complementation of individual mutations was only partially achievable. Full complementation was only observed when a complete triABC operon was provided in trans, either in single or multiple copies. TriABC associated with OpmH, but not OprM, for assembly of a functional triclosan efflux pump. TriABC is the fifth RND pump in P. aeruginosa shown to efficiently efflux triclosan, supporting the notion that efflux is the primary mechanism responsible for this bacterium's high intrinsic and acquired triclosan resistance.

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