Shio-Shin Jean1, Wen-Sen Lee2, Kuan-Jen Bai3, Carlos Lam1, Chin-Wang Hsu4, Kwok-Woon Yu5, Chun-Hsing Liao6, Feng-Yi Chang7, Wen-Chien Ko8, Jiunn-Jong Wu9, Yen-Hsu Chen10, Yao-Shen Chen11, Jien-Wei Liu12, Min-Chi Lu13, Cheng-Yi Liu14, Ray-Jade Chen15, Po-Ren Hsueh16. 1. Department of Emergency Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. 2. Division of Infectious Diseases, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. 3. Department of Pulmonary, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; Department of Critical Care Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. 4. Department of Emergency and Critical Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. 5. Department of Internal Medicine, Pathology, and Laboratory Medicine, Taipei Veterans General Hospital, National Yang-Ming University, Taipei, Taiwan. 6. Department of Internal Medicine, Far Eastern Memorial Hospital, Taipei, Taiwan. 7. Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center (NDMC), Taipei, Taiwan. 8. Department of Internal Medicine, National Cheng-Kung University Hospital, Tainan, Taiwan. 9. School of Medical Technology, National Cheng-Kung University College of Medicine, Tainan, Taiwan. 10. Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan; Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. 11. Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan. 12. Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung Medical College, Kaohsiung, Taiwan. 13. Department of Laboratory Medicine and Internal Medicine, Chung Shan Medical and Dental University, Taichung, Taiwan. 14. Division of Infectious Diseases, Department of Internal Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. 15. Department of Emergency Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan; Department of Critical Care Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. 16. Department of Laboratory Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan; Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan. Electronic address: hsporen@ntu.edu.tw.
Abstract
BACKGROUND: The data on susceptibility of important cephalosporins against four Enterobacteriaceae members producing potential extended-spectrum β-lactamase (ESBL) collected from Taiwanese intensive care units are lacking. METHODS: Minimum inhibitory concentrations (MICs) of cefotaxime, ceftazidime, and cefepime were determined using agar dilution method, against Escherichia coli (n = 344), Klebsiella pneumoniae (n = 359), Enterobacter cloacae (n = 103), and Proteus mirabilis (n = 78). Susceptibilities of these isolates to three cephalosporins were assessed according to MIC breakpoints recommended by the Clinical and Laboratory Standards Institute (CLSI) and the European Committee on Antimicrobial Susceptibility Testing (EUCAST) in 2013. The double-disk synergy test using disks containing cefepime (30 μg) with or without clavulanate (10 μg) was applied to confirm production of ESBL for isolates with cephalosporin MIC ≥ 2 μg/mL. RESULTS: A total of 175 isolates were verified as ESBL producers. The rates of cefepime susceptibility among the ESBL-producing isolates, according to CLSI (EUCAST) criteria, were 56.7% (22.4%) for E. coli, 61.3% (12.0%) for K. pneumoniae, 57.9% (31.6%) for E. cloacae, and 71.4% (7.1%) for P. mirabilis. Using different cefepime MIC breakpoints (MICs ≥ 16 μg/mL recommended by CLSI criteria and ≥ 2 μg/mL by EUCAST criteria) to define nonsusceptibility, we found that both criteria were poorer at predicting ESBL producers among K. pneumoniae and E. cloacae than among the other two species. In addition, we also found that the cefepime MIC level of 1.0 μg/mL best distinguished non-ESBL- from ESBL-producing K. pneumoniae and E. cloacae. CONCLUSION: To detect ESBLs, CLSI should revise the cefepime MIC breakpoint against Enterobacteriaceae.
BACKGROUND: The data on susceptibility of important cephalosporins against four Enterobacteriaceae members producing potential extended-spectrum β-lactamase (ESBL) collected from Taiwanese intensive care units are lacking. METHODS: Minimum inhibitory concentrations (MICs) of cefotaxime, ceftazidime, and cefepime were determined using agar dilution method, against Escherichia coli (n = 344), Klebsiella pneumoniae (n = 359), Enterobacter cloacae (n = 103), and Proteus mirabilis (n = 78). Susceptibilities of these isolates to three cephalosporins were assessed according to MIC breakpoints recommended by the Clinical and Laboratory Standards Institute (CLSI) and the European Committee on Antimicrobial Susceptibility Testing (EUCAST) in 2013. The double-disk synergy test using disks containing cefepime (30 μg) with or without clavulanate (10 μg) was applied to confirm production of ESBL for isolates with cephalosporin MIC ≥ 2 μg/mL. RESULTS: A total of 175 isolates were verified as ESBL producers. The rates of cefepime susceptibility among the ESBL-producing isolates, according to CLSI (EUCAST) criteria, were 56.7% (22.4%) for E. coli, 61.3% (12.0%) for K. pneumoniae, 57.9% (31.6%) for E. cloacae, and 71.4% (7.1%) for P. mirabilis. Using different cefepime MIC breakpoints (MICs ≥ 16 μg/mL recommended by CLSI criteria and ≥ 2 μg/mL by EUCAST criteria) to define nonsusceptibility, we found that both criteria were poorer at predicting ESBL producers among K. pneumoniae and E. cloacae than among the other two species. In addition, we also found that the cefepime MIC level of 1.0 μg/mL best distinguished non-ESBL- from ESBL-producing K. pneumoniae and E. cloacae. CONCLUSION: To detect ESBLs, CLSI should revise the cefepime MIC breakpoint against Enterobacteriaceae.