Efflux pumps and biofilm formation by both methicillin-resistant and methicillin-sensitive Staphylococcus aureus strains

Aggarwal, Shifu ; Singh, Durg Vijai

Abstract

Staphylococcus aureus is the primary cause of nosocomial infections. It produces potent toxins and causes superficial lesions, systemic diseases, and several toxaemic syndromes. In this study, we determined the role of efflux pump in conferring resistance to fluoroquinolones in the biofilm of methicillin resistant Staphylococcus aureus (MRSA) and methicillin sensitive S. aureus (MSSA) strains. We selected five strains of S. aureus comprising three methicillin sensitive strains, including ATCC25923, and two strains of methicillin resistant S. aureus. Thioridazine, chlorpromazine, carbonyl cyanide 3-chloro-phenylhydrazone and reserpine showed activity against MSSA strains. Whereas, thioridazine and chlorpromazine were active against MRSAstrains too. Thioridazine and chlorpromazine showed a significant decrease in biofilm formation of MSSA strain 2493, and MRSA strain UC1079 compared to the control strain ATCC25923. Thioridazine showed a similar effect on MSSA strain N297214 and MRSA strain N307002. Four to eight-fold increase was found in the expression of efflux pump genes with ethidium bromide, ciprofloxacin, and moxifloxacin in these strains. However, a decrease in the expression of norB, norC, abcA and mepA was observed in MSSA, and MRSA strains with thioridazine, chlorpromazine and naringenin. This study, thus demonstrate that the major facilitator superfamily, multidrug and toxin compound extrusion, and ATP binding cassette family of efflux pumps play an essential role in developing antibiotic resistance and biofilm formation. It is the first report on existence of efflux pump genes in biofilm beside antibiotic resistance for fluoroquinolones in MRSA and MSSA strains, which need further characterization

Keyword(s)

Antibiofilm agent, Antimicrobial resistance, Efflux pump inhibitors, fluoroquinolones, Gene expression, MATE family, MDR pump, Nosocomial infection

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