High-Level Aminoglycoside Resistance and β-Lactamase Production in Enterococci at a Tertiary Care Hospital in India

• Published in: Japanese Journal of Infectious Diseases Vol. 62; no. 2; pp. 158 - 159
• Main Authors: Agarwal, Jyotsna, Kalyan, Rajkumar, Singh, Mastan
• Format: Journal Article
• Language: English
• Published: Japan National Institute of Infectious Diseases 30-03-2009
• Subjects: Aminoglycosides - pharmacology; Anti-Bacterial Agents - pharmacology; Bacterial Proteins - biosynthesis; beta-Lactamases - biosynthesis; beta-Lactams - pharmacology; Drug Resistance, Bacterial; Enterococcus; Enterococcus - drug effects; Enterococcus - isolation & purification; Gram-Positive Bacterial Infections - microbiology; Hospitals; Humans; India; Microbial Sensitivity Tests; India
• ISSN: 1344-6304; 1884-2836
• DOI: 10.7883/yoken.JJID.2009.158

Enterococci, a family of important opportunistic pathogens, exhibits intrinsic resistance to a number of antimicrobial agents in addition to acquired multidrug resistance. The present study was conducted to determine whether enterococci at a tertiary care hospital in India exhibit high-level aminoglycoside resistance and β-lactamase production. Enterococci were isolated from various clinical specimens and identified phenotypically. High-level resistance (HLR) to gentamicin, kanamycin, and streptomycin was determined by disc diffusion tests. β-lactamase production was detected using three methods: iodometric, acidometric, and chromogenic β-lactamase assays. Among the 86 enterococci isolated, 34 were found to have HLR to one or more aminoglycosides; HLR to kanamycin was most common. Vancomycin resistance was present in four of the isolates. Only one enterococcus produced β-lactamase, and it was sensitive to ampicillin on routine disc diffusion testing. β-lactamase production among enterococci, though not very common, may be missed on routine susceptibility testing. Frequent occurrence of HLR to kanamycin makes amikacin a poor choice for inclusion in combination therapy with cell wall-active agents.