Detection of Extended-spectrum Beta-lactamases (ESBLs), Carbapenemase, Metallo-beta-lactamase Production Bacteria and Antibiotic Susceptibility Pattern in Hospitalized Patients with Ventilator-associated Pneumonia

摘要

Background: Due to the increase in microbial resistance, nosocomial multidrug resistance infections, including ventilator-associated pneumonia (VAP), are presently one of the main causes of death in hospitals since they are difficult to treat.Objectives: This study aimed to investigate the bacterial etiology of VAP and their microbial resistance pattern in Dezful Hospital, southwest of Iran.Methods: In this cross-sectional study, 131 bacterial isolates were isolated from the respiratory secretions of the patients with VAP in ICU wards. Antibiotic susceptibility testing (AST) of all isolates was carried out after the identification. Then the extended-spectrum beta-lactamases (ESBLs), carbapenemase, and metallobetalactamase were identified by phenotyping and genotyping.Results: The most frequent isolates were Staphylococcus aureus (30.5), Acinetobacter baumannii (25.2), and Klebsiella pneumoniae (24.4). All strains of S. aureus were sensitive to vancomycin, ticoplanin, quinupristin-dalfopristin, and linezolid. Escherichia coli and Klebsiella showed high resistance to cephalosporins. More than 93 of Acinetobacter isolates were resistant to carbapenem and quinolones. The overall prevalence of ESBLs and carbapenemase producing bacteria were 80.43 and 73.6, respectively. The most frequent ESBLs gene was blaCTX-M gene (78.3) followed by blaAMP-Cgene (67.5), blaSHV gene (64.8), and blaTEM gene (54).Conclusions: In sum, there was a possibility that the treatment of nosocomial multidrug resistant infections such as VAP would become a major challenge. Therefore, it was recommended that AST results should always be considered when selecting the ap-propriate treatment regimen. Furthermore, it was found important to emphasize the principles of antibiotic stewardship and to constantly monitor the pattern of microbial susceptibility.