Sun Young Cho1, Hye Mee Kim2, Doo Ryeon Chung3, So Hyun Kim2, Hee Jae Huh4, Cheol-In Kang5, Kyong Ran Peck5, Nam Yong Lee4, Jae-Hoon Song6. 1. Division of Infectious Diseases, Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea; Center for Infection Prevention and Control, Samsung Medical Center, Seoul, South Korea. 2. Asia Pacific Foundation for Infectious Diseases (APFID), Seoul, South Korea. 3. Division of Infectious Diseases, Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea; Center for Infection Prevention and Control, Samsung Medical Center, Seoul, South Korea; Asia Pacific Foundation for Infectious Diseases (APFID), Seoul, South Korea. Electronic address: dr.chung@samsung.com. 4. Department of Laboratory Medicine and Genetics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. 5. Division of Infectious Diseases, Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea. 6. Division of Infectious Diseases, Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea; Asia Pacific Foundation for Infectious Diseases (APFID), Seoul, South Korea.
Abstract
OBJECTIVES: This study aimed to determine the prevalence of linezolid-resistant (LR) vancomycin-resistant enterococci and to investigate the mechanisms of linezolid resistance with clinical and microbiological characterisation. METHODS: All vancomycin-resistant Enterococcus faecium (VREF) isolated from blood and rectal swab cultures during 2012-2015 were tested for linezolid resistance. LR-VREF isolates were tested for antimicrobial susceptibility, glycopeptide resistance genes and virulence genes. Multilocus sequence typing (MLST) and pulsed-field gel electrophoresis (PFGE) were performed. Isolates were tested for known mechanisms of linezolid resistance. RESULTS: Among 389 VREF isolates, 7 (1.8%) were found to be resistant to linezolid. All LR-VREF isolates carried the vanA gene. Five isolates had both hyl and esp genes. The isolates were susceptible to tigecycline, daptomycin and quinupristin/dalfopristin, except for one isolate with daptomycin resistance. Two LR-VREF isolates recovered from patients with previous linezolid exposure contained the G2576T mutation in 23S rRNA and exhibited high-level resistance to linezolid (MIC>64mg/L). The other five isolates recovered from linezolid-naïve patients revealed no known linezolid resistance mechanism and exhibited low-level resistance to linezolid (MICs=8-16mg/L). Plasmid-mediated genes encoding cfr or optrA were not detected. LR-VREF isolates were represented by six different sequence types, belonging to hospital lineages, and were assigned to seven PFGE types. CONCLUSIONS: The prevalence of LR-VREF in this centre was low. Both linezolid exposure and horizontal transmission appear to be responsible for acquisition of LR-VREF in hospitalised patients. Prudent use of linezolid and improved infection control strategies are needed to limit the spread of LR-VREF.
OBJECTIVES: This study aimed to determine the prevalence of linezolid-resistant (LR) vancomycin-resistant enterococci and to investigate the mechanisms of linezolid resistance with clinical and microbiological characterisation. METHODS: All vancomycin-resistant Enterococcus faecium (VREF) isolated from blood and rectal swab cultures during 2012-2015 were tested for linezolid resistance. LR-VREF isolates were tested for antimicrobial susceptibility, glycopeptide resistance genes and virulence genes. Multilocus sequence typing (MLST) and pulsed-field gel electrophoresis (PFGE) were performed. Isolates were tested for known mechanisms of linezolid resistance. RESULTS: Among 389 VREF isolates, 7 (1.8%) were found to be resistant to linezolid. All LR-VREF isolates carried the vanA gene. Five isolates had both hyl and esp genes. The isolates were susceptible to tigecycline, daptomycin and quinupristin/dalfopristin, except for one isolate with daptomycin resistance. Two LR-VREF isolates recovered from patients with previous linezolid exposure contained the G2576T mutation in 23S rRNA and exhibited high-level resistance to linezolid (MIC>64mg/L). The other five isolates recovered from linezolid-naïve patients revealed no known linezolid resistance mechanism and exhibited low-level resistance to linezolid (MICs=8-16mg/L). Plasmid-mediated genes encoding cfr or optrA were not detected. LR-VREF isolates were represented by six different sequence types, belonging to hospital lineages, and were assigned to seven PFGE types. CONCLUSIONS: The prevalence of LR-VREF in this centre was low. Both linezolid exposure and horizontal transmission appear to be responsible for acquisition of LR-VREF in hospitalised patients. Prudent use of linezolid and improved infection control strategies are needed to limit the spread of LR-VREF.
Authors: András Fodor; Birhan Addisie Abate; Péter Deák; László Fodor; Ervin Gyenge; Michael G Klein; Zsuzsanna Koncz; Josephat Muvevi; László Ötvös; Gyöngyi Székely; Dávid Vozik; László Makrai Journal: Pathogens Date: 2020-06-29