Aim and Objectives: The significant nosocomial pathogen Pseudomonas aeruginosa is inherently resistant to several medications. Metallo-beta-lactamases (MBLs) are a specific type of carbapenemase, belonging to class B enzymes. MBL producing Pseudomonas aeruginosa are a significant concern due to their ability to hydrolyze a wide range of beta-lactams, including carbapenems and has far higher mortality rates. Aim of the present study is to detect and evaluate the presence of carbapenemase-producing Pseudomonas aeruginosa isolates from clinical specimens using phenotypic methods in a tertiary care hospital setting. Also to assess the prevalence of carbapenemase-producing P. aeruginosa in the hospital’s clinical setting.
Materials and Methods: In the current investigation, Pseudomonas aeruginosa isolates have been identified using standard biochemical reactions and an antibiotic susceptibility test. The imipenem disk diffusion method was employed as a screening test to select suspected MBL producers. The strains were further confirmed by imipenem-(Ethylene diamine tetra acetic acid) EDTA combined disc method and imipenem- EDTA double disc synergy test.
Result: Out all 50 isolates Pseudomonas aeruginosa, 14 (28%) produced MBL, while 36 (72%) did not. The DDST (Double Disk Synergy Test) and CDST (Combined Disc Synergy Test) techniques had respective sensitivity levels of 78.5% & 92.8%. Compared to isolates of Pseudomonas aeruginosa that do not produce MBL, those that exhibit high levels of resistance to ceftazidime and all other antibiotics. The isolates that produced MBL are 100% resistant to ciprofloxacin, tobramycin and meropenem, followed by imipenem (92.8%) & gentamicin (85.7%).
Conclusion: According our study, P. aeruginosa that produced MBL exhibited the greatest degrees of fluoroquinolone, aminoglycoside, and carbapenem resistance. This implies that the gene that produces MBL have co-resistance to quinolones, aminoglycosides, and other antibiotic families. Prompt evidence that rules out carbapenemases guides clinicians to more optimal therapeutic selections based on local phenotypic profiling of non-carbapenemase-producing, carbapenem-resistant P. aeruginosa. Also, rapid confirmation and differentiation among the various classes of carbapenemases is key to the initiation of early effective therapy.
Keywords: Carbapenemase, Drug Resistance, Pseudomonas aeruginosa
