A study on detection of extended-spectrum beta-lactamases (ESBLs) and comparison of various phenotypic methods of AmpC detection in Pseudomonas aeruginosa from various clinical isolates in a tertiary care teaching hospital

Introduction: Pseudomonas aeruginosa is one of the major etiological agents of nosocomial infection. They are difficult to treat as the majority of them exhibit varying degrees of innate resistance. Acquired resistance is mediated by the production of chromosomal and plasmid-mediated AmpC beta-lactamases, extended-spectrum beta-lactamases (ESBLs), and metallo-beta-lactamases (MBLs). Objectives: This study was conducted for the detection of ESBLs and the comparison of various phenotypic methods of AmpC beta-lactamases (both inducible and plasmid-mediated) from various clinical isolates of Pseudomonas aeruginosa. Materials and Methods: A prospective study was conducted for a period of 6 months from January 2014 to June 2014. Isolates of Pseudomonas aeruginosa were tested for ESBLs by combined disk diffusion method using ceftazidime/ceftazidime+clavulanic acid (CAZ+CAC). Inducible AmpC beta-lactamases were detected by both ceftazidime-imipenem antagonism test (CIAT) and cefotaxime/cefoxitin (CTX/CX) inducible disk diffusion test. Plasmid-mediated AmpC were detected using AmpC disk test and ethylenediaminetetraacetic acid (EDTA) disk test. All the isolates were tested for cefepime resistance. Results: Out of 116 Pseudomonas aeruginosa isolates, 70 were ceftazidime-resistant. While ESBLs were observed in 67 out of 70 isolates, 36 were positive for inducible AmpC by both the methods. Plasmid-mediated AmpC were detected in only 8 isolates. All the 70 strains showed resistance to cefepime. Conclusions: High prevalence of ESBL and chromosomal-mediated AmpC was observed in Pseudomonas aeruginosa. Both the inducible disk diffusion tests (CIAT, CTX/CX) were equally effective in the detection of inducible AmpC. As Pseudomonas is one of the major nosocomial pathogens, such high resistance poses a grave threat.