2025, Vol. 6, Issue 2, Part C

Background: Amp C β-lactamases are clinically important cephalosporinases that offers resistance to Penicillin, first, second and third generation Cephalosporin, Monobactams and β-lactamase inhibitor but susceptible to fourth generation Cephalosporins and Carbapenem antibiotics. This study aims to detect the prevalence of plasmid mediated bla FOX-CIT gene among phenotypically confirmed p Amp C beta lactamase producing Enterobacteriaceae in skin and soft tissue exudates in a tertiary care hospital.

Materials and Methods: A total of 685 cefotaxime resistant Enterobacteriaceae samples identified from skin and soft tissue infection by Standard Microbiological Laboratory procedures were screened for Cefoxitin resistance by disk diffusion method as per CLSI 2024 guidelines. A total 122 consecutive non-replicate cefoxitin resistant isolates were subjected to Cefoxitin-Cloxacillin double disk synergy confirmatory test (CC-DDS). Molecular genotyping by Conventional Multiplex PCR for bla FOX-CIT gene was done for the phenotypically confirmed isolates.

Results: Out of the total 122 Cefoxitin resistant isolates, 69(56.5%) isolates were Escherichia coli, 48 (39.3%) isolates were Klebsiella pneumoniae, 3(2.4%) isolates were Proteus mirabilis and 2 isolates (1.63%) were Citrobacter koseri. Majority of the samples were from Department of surgery. Out of those 122 isolates 55 (45.1%) isolates were positive for double disk synergy test which were then subjected to genotypic confirmation by Conventional Multiplex PCR method. Among the total 55 isolates 14 (58.3%) were detected with FOX-CIT gene.

Conclusion: Early and accurate detection of p Amp C β-lactamase producers through combined phenotypic and genotypic methods is vital to guide appropriate therapy and to limit the worsening of resistance. Therefore it is significant to have strict infection control measures, establishing antimicrobial stewardship and continuous surveillance in hospital facilities to prevent the inappropriate use of antibiotics and emergence of antimicrobial resistance.