Discrepant susceptibility to gentamicin despite amikacin resistance inKlebsiella pneumoniaeby VITEK 2 represents false susceptibility associated with thearmA16S rRNA methylase gene. Issue 10 (October 2017)

• Record Type: Journal Article
• Authors: Ko, Jae‐Hoon; Baek, Jin Yang; Peck, Kyong Ran; Cho, Sun Young; Ha, Young Eun; Kim, So Hyun; Huh, Hee Jae; Lee, Nam Yong; Kang, Cheol‐In; Chung, Doo Ryeon; Song, Jae‐Hoon
• Is Part Of: Journal of medical microbiology. Volume 66:Issue 10(2017)
• Publication Date: 2017-10
• Subjects: gentamicin -- susceptibility -- VITEK 2 -- Klebsiella pneumoniae -- armA; Medical microbiology -- Periodicals; 616.9041
• DOI: 10.1099/jmm.0.000583
• Languages: English
• ISSNs: 0022-2615

Abstract

Abstract : Abstract : Because we experienced gentamicin failure in Klebsiella pneumoniae bacteraemia that was susceptible to gentamicin despite amikacin resistance, as determined by VITEK 2, we evaluated the true susceptibility and mechanism of resistance. We screened 2818 K. pneumoniae isolates during a 1‐year period at a university hospital and reviewed anti‐microbial susceptibility reports using the VITEK 2 system. The minimum inhibitory concentration was substantiated by broth microdilution (BMD), and the presence of 16S rRNA methylase genes and aminoglycoside‐modifying enzymes was also investigated. A total of 131 amikacin‐resistant isolates from 19 patients were gentamicin non‐resistant according to the VITEK 2 system. Among these, we were able to collect isolates from 12 patients (63.2 %), and a single isolate from each patient was tested. Eleven of the gentamicin non‐resistant isolates (91.7 %) showed high‐level resistance to both amikacin and gentamicin by BMD in association with the armA gene. Gentamicin is not an adequate treatment option for amikacin‐resistant K. pneumoniae, even if VITEK 2 reports susceptibility.