Efflux pump genes and chlorhexidine resistance: Clue for Klebsiella pneumoniae infections in intensive care units, Egypt

Abstract

One of the serious and growing challenges for infection control programs worldwide is hospital acquired infections. Klebsiella pneumoniae is considered the second most common cause of hospital-acquired Gram-negative blood stream infections. Chlorhexidine is a topical antiseptic agent, widely used in different applications in hospitals. Healthcare associated infection rates were lower after chlorhexidine-containing detergent hand washing when compared with using plain soap or an alcohol-based hand rinse. Intensive exposure of hospital pathogens to biocides may result in the emergence of resistance not just to the biocides but also to antibiotics. We aimed to investigate the susceptibility of multi-drug resistant K. pneumoniae isolates to chlorhexidine and to correlate chlorhexidine susceptibility and its association with both the efflux pump genes (cepA, qacDE, qacE), and resistance to later-generation anti-Gram negative antibiotics. Fifty-six strains of K. pneumoniae were isolated from blood specimens in intensive care units, Suez Canal University Hospital, Ismailia, Egypt. Antibiotic sensitivity profiles were determined by disc diffusion method. Minimal inhibitory concentration (MICs) of 1% chlorhexidine was assessed by the agar dilution method. The effect of efflux pumps was determined by repeating the susceptibility in the presence of the efflux pump inhibitor carbonyl cyanide m-chlorophenyl hydrazone (CCCP) (10 mg/L). Polymerase chain reaction (PCR) was used for identifying efflux pump genes. The MICs of chlorhexidine ranged from 4-256 mg/L. Most isolates carried the cepA gene. The MICs of chlorhexidine was significantly reduced on addition of CCCP. Carriage of efflux pump gene cepA affect chlorhexidine susceptibility in ICU related K. pneumoniae infections.