Distribution of Class A Extended-Spectrum β-Lactamases Among Pseudomonas aeruginosa Clinical Strains Isolated from Ardabil Hospitals

Background: Currently, the emergence of extended-spectrum β-lactamase (ESBL)-producing bacteria is becoming a major threat to patients in the hospital and community. Such enzymes have been recently detected in Pseudomonas aeruginosa, but there is no epidemiological data on the prevalence of ESBL-producing clinical isolates in the hospitals of Ardabil City (Iran). Objectives: This study aimed to determine the phenotypic and genotypic prevalence of class A ESBL-producing P. aeruginosa strains in Ardabil City. Methods: A total of 120 clinical isolates of P. aeruginosa collected from Ardabil hospitals were used in this study. Phenotypic detection of class A ESBL-producing P. aeruginosa isolates was performed using a double-disk synergy test. In addition, the detection of class A ESBL-encoding genes, including Pseudomonas extended resistant (PER), Vietnamese extended-spectrum β-lactamase (VEB), temoniera (TEM), sulfhydryl variable (SHV), cefotaximase (CTX-M), guyana extended-spectrum β-lactamase (GES), and Pseudomonas-specific enzyme (PSE), was performed using the polymerase chain reaction (PCR). Results: The prevalence of class A ESBL-producing P. aeruginosa strains was 8.3% (10 out of 120) based on the double-disk synergy test. However, 40% (48 out of 120) of these isolates were found to carry genes encoding class A ESBLs based on PCR. Among 48 class A ESBL-positive strains, the prevalence of PSE, TEM, VEB, CTX-M, and PER genes were 64.6% (31/48), 25% (12/48), 4.2% (2/48), 4.2% (2/48), and 2% (1/48), respectively. However, the frequency of other class A ESBL genes (SHV and GES genes) was 0%. Conclusions: Our results confirmed the presence of class A ESBL-producing P. aeruginosa strains in the hospital environment of Ardabil. On the other hand, the use of molecular tests can be a more precise and reliable method than phenotypic ones to identify these resistant strains and prevent the emergence of antibiotic resistance and ensuing treatment failure.