Soodabeh Rostami1, Ahmad Farajzadeh Sheikh2, Saeed Shoja3, Abbas Farahani2, Mohammad Amin Tabatabaiefar4, Abbas Jolodar5, Raheleh Sheikhi6. 1. Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: srostami1876@gmail.com. 2. Department of Microbiology, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. 3. Infectious and Tropical Diseases Research Center, Hormozgan Health Institute, Hormozgan University of Medical Sciences, Bandar Abbas, Iran. 4. Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. 5. Department of Biomolecular and Biochemistry, School of Veterinary Medicine, Shahid Chamran University, Ahvaz, Iran. 6. Department of Microbiology, Guilan University of Medical Sciences, Rasht, Iran.
Abstract
BACKGROUND: Pseudomonas aeruginosa is an opportunistic pathogen involved in many infections. Carbapenem-resistant P.aeruginosa has emerged as an important cause of infection in different hospitals worldwide. We aimed to determine frequencies of the four main resistance mechanisms [metallo-beta lactamase (MBL) production (blaIMP, blaVIM, blaSPM and blaNDM), overproduction of the MexAB-OprM and MexXY efflux pumps, overproduction of chromosome-encoded AmpC β-lactamase, and reduced OprD expression] in high-level carbapenem-resistant P.aeruginosa isolated from patients with burns. METHODS: In a descriptive study, 107 P. aeruginosa isolates were collected from patients with burn injuries and tested for antibiotic susceptibility, by an E-test for carbapenems, an E-test for metallo-β-lactamase producer isolates, and PCR to detect MBL genes. Furthermore, high-level carbapenem-resistant isolates were tested by real-time PCR for the expression levels of the mexB, mexY, ampC, and oprD genes. RESULTS: Amongst all P. aeruginosa isolates, 78.5%, 46.7%, and 15% were imipenem-, meropenem-, and doripenem-resistant, respectively; 72% of isolates were multidrug-resistant. The blaIMP and blaVIM genes were detected in 17.9% and 1.2% of isolates; respectively. The blaSPM and blaNDM genes were not observed. Among the resistant isolates, mexB overexpression (63.2%) was the most frequent mechanism, followed by mexY overexpression (52.6%), ampC overexpression (36.8%), and reduced oprD expression (21.1%). CONCLUSION: Emerging antimicrobial resistance in burn wound bacterial pathogens is a serious therapeutic challenge for clinicians. In the present study, most of the isolates were MDR. This finding indicated an alarming spread of resistant isolates and suggested that infection control strategies should be considered. Resistance to carbapenems is influenced by several factors, not all of which were evaluated in our study; however, the results showed that production of MBLs and overexpression of the mexB gene were the most frequent mechanisms in carbapenem-resistant isolates.
BACKGROUND:Pseudomonas aeruginosa is an opportunistic pathogen involved in many infections. Carbapenem-resistant P.aeruginosa has emerged as an important cause of infection in different hospitals worldwide. We aimed to determine frequencies of the four main resistance mechanisms [metallo-beta lactamase (MBL) production (blaIMP, blaVIM, blaSPM and blaNDM), overproduction of the MexAB-OprM and MexXY efflux pumps, overproduction of chromosome-encoded AmpC β-lactamase, and reduced OprD expression] in high-level carbapenem-resistant P.aeruginosa isolated from patients with burns. METHODS: In a descriptive study, 107 P. aeruginosa isolates were collected from patients with burn injuries and tested for antibiotic susceptibility, by an E-test for carbapenems, an E-test for metallo-β-lactamase producer isolates, and PCR to detect MBL genes. Furthermore, high-level carbapenem-resistant isolates were tested by real-time PCR for the expression levels of the mexB, mexY, ampC, and oprD genes. RESULTS: Amongst all P. aeruginosa isolates, 78.5%, 46.7%, and 15% were imipenem-, meropenem-, and doripenem-resistant, respectively; 72% of isolates were multidrug-resistant. The blaIMP and blaVIM genes were detected in 17.9% and 1.2% of isolates; respectively. The blaSPM and blaNDM genes were not observed. Among the resistant isolates, mexB overexpression (63.2%) was the most frequent mechanism, followed by mexY overexpression (52.6%), ampC overexpression (36.8%), and reduced oprD expression (21.1%). CONCLUSION: Emerging antimicrobial resistance in burn wound bacterial pathogens is a serious therapeutic challenge for clinicians. In the present study, most of the isolates were MDR. This finding indicated an alarming spread of resistant isolates and suggested that infection control strategies should be considered. Resistance to carbapenems is influenced by several factors, not all of which were evaluated in our study; however, the results showed that production of MBLs and overexpression of the mexB gene were the most frequent mechanisms in carbapenem-resistant isolates.