Research Article

Prevalence of β-lactamase classes A, C, and D among clinical isolates of Pseudomonas aeruginosa from a tertiary-level hospital in Bangkok, Thailand

Published: September 23, 2016
Genet. Mol. Res. 15(3): gmr8706 DOI: 10.4238/gmr.15038706

Abstract

Pseudomonas aeruginosa is one of the most important causes of nosocomial infection and it has increasing resistance to many antimicrobial agents. β-lactamase production is the most frequent mechanism for β-lactam resistance in P. aeruginosa. We evaluated the prevalence of β-lactamase genes in P. aeruginosa for classes A, C, and D by polymerase chain reaction, and investigated clonal diversity by pulsed-field gel electrophoresis (PFGE). We used the disk diffusion method to test 118 non-duplicate clinical isolates of P. aeruginosa for antimicrobial susceptibility. We identified 51 isolates (43.22%) as multidrug-resistant P. aeruginosa, approximately 44.91% of which were resistant to ceftazidime. β-lactamase genes were found in 80 isolates of P. aeruginosa (67.80%). The genes that encode VEB-1, AmpC, and OXA-10 were detected in 9 (7.62%), 75 (63.56%), and 18 (15.25%) of these isolates, respectively. The genes that encode PER-1, CTX-M, TEM-1 and derivatives, and SHV-1 were not found in any of the P. aeruginosa isolates. We identified 29 different pulsotypes by PFGE. Two predominant pulsotypes were found. In pulsotype 1, OXA- 10, which was co-produced with the AmpC gene, was predominant. Moreover, VEB-1-producing strains were found to be scattered in many pulsotypes, and AmpC-producing strains showed high pulsotype diversity. The prevalence of β-lactamase genes in P. aeruginosa was represented by the genetic heterogeneity of OXA-10, AmpC, and VEB-1. The predominant clone of P. aeruginosa clinical isolates was OXA-10. This raises concern about oxacillinases among P. aeruginosa clinical isolates.

Pseudomonas aeruginosa is one of the most important causes of nosocomial infection and it has increasing resistance to many antimicrobial agents. β-lactamase production is the most frequent mechanism for β-lactam resistance in P. aeruginosa. We evaluated the prevalence of β-lactamase genes in P. aeruginosa for classes A, C, and D by polymerase chain reaction, and investigated clonal diversity by pulsed-field gel electrophoresis (PFGE). We used the disk diffusion method to test 118 non-duplicate clinical isolates of P. aeruginosa for antimicrobial susceptibility. We identified 51 isolates (43.22%) as multidrug-resistant P. aeruginosa, approximately 44.91% of which were resistant to ceftazidime. β-lactamase genes were found in 80 isolates of P. aeruginosa (67.80%). The genes that encode VEB-1, AmpC, and OXA-10 were detected in 9 (7.62%), 75 (63.56%), and 18 (15.25%) of these isolates, respectively. The genes that encode PER-1, CTX-M, TEM-1 and derivatives, and SHV-1 were not found in any of the P. aeruginosa isolates. We identified 29 different pulsotypes by PFGE. Two predominant pulsotypes were found. In pulsotype 1, OXA- 10, which was co-produced with the AmpC gene, was predominant. Moreover, VEB-1-producing strains were found to be scattered in many pulsotypes, and AmpC-producing strains showed high pulsotype diversity. The prevalence of β-lactamase genes in P. aeruginosa was represented by the genetic heterogeneity of OXA-10, AmpC, and VEB-1. The predominant clone of P. aeruginosa clinical isolates was OXA-10. This raises concern about oxacillinases among P. aeruginosa clinical isolates.