Abstract
Carvacrol is a herbal antimicrobial agent with in vitro activity against several bacterial pathogens. However, multidrug resistant strains of Pseudomonas aeruginosa are resistant to herbal antimicrobial compounds including carvacrol. Resistance of P. aeruginosa to carvacrol is not well studied. This study was aimed to identify the gene(s) associated with carvacrol resistance, thus to understand its mechanisms in P. aeruginosa. A herbal drug resistant strain was isolated from a hospital environment. Carvacrol sensitive mutant was generated using transposon mutagenesis. The inactivated gene in the mutant was identified as mexA, which is part of the mexAB-oprM operon. Inactivation of the mexA gene resulted in a >31-fold reduction in MIC of carvacrol, whereas a >80-fold reduction was observed in the presence of drug efflux inhibitor phenylalanine-arginine β-naphthylamide (PAβN). The parental herbal-resistant strain was completely killed within 3 h of incubation in the presence of carvacrol and PAβN. The mexA inactivation did not affect the resistance to other herbal compounds used. The results demonstrate that resistance to carvacrol in P. aeruginosa is mediated by the MexAB-OprM efflux pump.
Highlights
Pseudomonas aeruginosa is a Gram-negative bacteria present ubiquitously in nature and is one of the major causative agents of the nosocomial infections worldwide (Lederberg, 2000; Quartin et al, 2013)
Pseudomonas aeruginosa is intrinsically resistant to many antimicrobial agents which can be mediated by restricted uptake of antimicrobials through the outer membrane, by expression of Carvacrol Tolerance in Pseudomonas aeruginosa efflux pumps and/or by the action of drug degrading enzymes (Li et al, 2015)
The sequence matched with the sequence of the mexA gene of P. aeruginosa PAO1 strain with 100% identity (Supplementary Figure S4) suggesting that mexA gene was inactivated by the insertion of the transposon
Summary
Pseudomonas aeruginosa is a Gram-negative bacteria present ubiquitously in nature and is one of the major causative agents of the nosocomial infections worldwide (Lederberg, 2000; Quartin et al, 2013). This organism produces a broad range of virulence factors and is associated with a variety of infections (Tang et al, 1996; Lamont et al, 2002). Pseudomonas aeruginosa is intrinsically resistant to many antimicrobial agents which can be mediated by restricted uptake of antimicrobials through the outer membrane, by expression of Carvacrol Tolerance in Pseudomonas aeruginosa efflux pumps and/or by the action of drug degrading enzymes (Li et al, 2015). The MexAB-OprM system is responsible for the resistance to quinolones, macrolides, novobiocin, chloramphenicol, tetracyclines, lincomycin, and β-lactam antibiotics (Li et al, 1995; Masuda et al, 2000)
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