scholarly journals Dissemination of cfr-mediated linezolid resistance among Staphylococcus species isolated from a teaching hospital in Beijing, China

2018 ◽  
Vol 46 (9) ◽  
pp. 3884-3889 ◽  
Author(s):  
Jiyong Jian ◽  
Liang Chen ◽  
Zeqiang Xie ◽  
Man Zhang

Objective The aim of the present study was to report the dissemination of cfr and fexA genes mediated by linezolid resistance among Staphylococcus species. Methods Three methicillin-resistant staphylococci that were collected from a teaching hospital in Beijing were identified as linezolid-resistant. These three staphylococci were Staphylococcus aureus, S. haemolyticus, and S. cohnii. Mutations in domain V of 23S ribosomal RNA, ribosomal proteins, and the cfr, fexA, and optrA genes were analysed. Results The three isolates had no mutations of 23S ribosomal RNA, but showed mutations in the cfr and fexA genes. Mutations in the gene for ribosomal protein L3, which resulted in the amino acid exchanges Gly108Glu, Ser158Phe, and Asp159Tyr, were identified in S. cohnii X4535. Conclusions This is the first report of the cfr gene in clinical linezolid-resistant methicillin-resistant S. aureus isolated from Beijing. L3 mutations coupled with the cfr and fexA genes may act synergistically. Potential transmissibility of this agent, even without prior exposure to linezolid, may have serious epidemiological repercussions.

Antibiotics ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 769
Author(s):  
Hee Young Kang ◽  
Dong Chan Moon ◽  
Abraham Fikru Mechesso ◽  
Ji-Hyun Choi ◽  
Su-Jeong Kim ◽  
...  

Altogether, 2547 Staphylococcus aureus isolated from cattle (n = 382), pig (n = 1077), and chicken carcasses (n = 1088) during 2010–2017 were investigated for linezolid resistance and were further characterized using molecular methods. We identified linezolid resistance in only 2.3% of pig carcass isolates. The linezolid-resistant (LR) isolates presented resistance to multiple antimicrobials, including chloramphenicol, clindamycin, and tiamulin. Molecular investigation exhibited no mutations in the 23S ribosomal RNA. Nevertheless, we found mutations in ribosomal proteins rplC (G121A) and rplD (C353T) in one and seven LR strains, respectively. All the LR isolates carried the multi-resistance gene cfr, and six of them co-carried the mecA gene. Additionally, all the LR isolates co-carried the phenicol exporter gene, fexA, and presented a high level of chloramphenicol resistance. LR S. aureus isolates represented 10 genotypes, including major genotypes ST433-t318, ST541-t034, ST5-t002, and ST9-t337. Staphylococcal enterotoxin and leukotoxin-encoding genes, alone or in combination, were detected in 68% of LR isolates. Isolates from different farms presented identical or different pulsed-field gel electrophoresis patterns. Collectively, toxigenic and LR S. aureus strains pose a crisis for public health. This study is the first to describe the mechanism of linezolid resistance in S. aureus isolated from food animal products in Korea.


2016 ◽  
Vol 60 (5) ◽  
pp. 3007-3015 ◽  
Author(s):  
Anna C. Shore ◽  
Alexandros Lazaris ◽  
Peter M. Kinnevey ◽  
Orla M. Brennan ◽  
Gráinne I. Brennan ◽  
...  

ABSTRACTLinezolid is often the drug of last resort for serious methicillin-resistantStaphylococcus aureus(MRSA) infections. Linezolid resistance is mediated by mutations in 23S rRNA and genes for ribosomal proteins;cfr, encoding phenicol, lincosamide, oxazolidinone, pleuromutilin, and streptogramin A (PhLOPSA) resistance; its homologuecfr(B); oroptrA, conferring oxazolidinone and phenicol resistance. Linezolid resistance is rare inS. aureus, andcfris even rarer. This study investigated the clonality and linezolid resistance mechanisms of two MRSA isolates from patients in separate Irish hospitals. Isolates were subjected tocfrPCR, PhLOPSAsusceptibility testing, 23S rRNA PCR and sequencing, DNA microarray profiling,spatyping, pulsed-field gel electrophoresis (PFGE), plasmid curing, and conjugative transfer. Whole-genome sequencing was used for single-nucleotide variant (SNV) analysis, multilocus sequence typing, L protein mutation identification,cfrplasmid sequence analysis, andoptrAandcfr(B) detection. Isolates M12/0145 and M13/0401 exhibited linezolid MICs of 64 and 16 mg/liter, respectively, and harbored identical 23S rRNA and L22 mutations, but M12/0145 exhibited the mutation in 2/6 23S rRNA alleles, compared to 1/5 in M13/0401. Both isolates were sequence type 22 MRSA staphylococcal cassette chromosomemectype IV (ST22-MRSA-IV)/spatype t032 isolates, harboredcfr, exhibited the PhLOPSAphenotype, and lackedoptrAandcfr(B). They differed by five PFGE bands and 603 SNVs. Isolate M12/0145 harboredcfrandfexAon a 41-kb conjugative pSCFS3-type plasmid, whereas M13/0401 harboredcfrandlsa(B) on a novel 27-kb plasmid. This is the first report ofcfrin the pandemic ST22-MRSA-IV clone. Differentcfrplasmids and mutations associated with linezolid resistance in genotypically distinct ST22-MRSA-IV isolates highlight that prudent management of linezolid use is essential.


2010 ◽  
Vol 54 (12) ◽  
pp. 5352-5355 ◽  
Author(s):  
Jeffrey B. Locke ◽  
Gracia Morales ◽  
Mark Hilgers ◽  
Kedar G. C. ◽  
Shahad Rahawi ◽  
...  

ABSTRACT Resistance to linezolid (LZD) occurs through mutations in 23S rRNA and ribosomal proteins L3 and L4 or through methylation of 23S rRNA by Cfr. Here we report novel L3 mutations, ΔSer145/His146Tyr and ΔMet169-Gly174, co-occurring with cfr in LZD-resistant Staphylococcus aureus isolates recovered from a hospital outbreak in Madrid, Spain. LZD MIC values (16, 32, or 64 μg/ml) correlated with the presence and severity of the L3 mutation. All isolates had TR-700 (torezolid) MIC values of ≤2 μg/ml.


Pathogens ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 937
Author(s):  
Ramzy B. Anafo ◽  
Yacoba Atiase ◽  
Nicholas T. K. D. Dayie ◽  
Fleischer C. N. Kotey ◽  
Patience B. Tetteh-Quarcoo ◽  
...  

Aim: This study investigated the spectrum of bacteria infecting the ulcers of individuals with diabetes at the Korle Bu Teaching Hospital in Accra, Ghana, focusing on Staphylococcus aureus (S. aureus) and methicillin-resistant S. aureus (MRSA), with respect to their prevalence, factors predisposing to their infection of the ulcers, and antimicrobial resistance patterns. Methodology: This cross-sectional study was conducted at The Ulcer Clinic, Department of Surgery, Korle Bu Teaching Hospital, involving 100 diabetic foot ulcer patients. The ulcer of each study participant was swabbed and cultured bacteriologically, following standard procedures. Antimicrobial susceptibility testing was done for all S. aureus isolated, using the Kirby-Bauer method. Results: In total, 96% of the participants had their ulcers infected—32.3% (n = 31) of these had their ulcers infected with one bacterium, 47.9% (n = 46) with two bacteria, 18.8% (n = 18) with three bacteria, and 1.0% (n = 1) with four bacteria. The prevalence of S. aureus and MRSA were 19% and 6%, respectively. The distribution of the other bacteria was as follows: coagulase-negative Staphylococci (CoNS) (54%), Escherichia coli (24%), Pseudomonas spp. (19%), Citrobacter koseri and Morganella morgana (12% each), Klebsiella oxytoca (11%), Proteus vulgaris (8%), Enterococcus spp. (6%), Klebsiella pneumoniae (5%), Proteus mirabilis and Enterobacter spp. (4%), Klebsiella spp. (2%), and Streptococcus spp. (1%). The resistance rates of S. aureus decreased across penicillin (100%, n = 19), tetracycline (47.4%, n = 9), cotrimoxazole (42.1%, n = 8), cefoxitin (31.6%, n = 6), erythromycin and clindamycin (26.3% each, n = 5), norfloxacin and gentamicin (15.8% each, n = 3), rifampicin (10.5%, n = 2), linezolid (5.3%, n = 1), and fusidic acid (0.0%, n = 0). The proportion of multidrug resistance was 47.4% (n = 9). Except for foot ulcer infection with coagulase-negative Staphylococci, which was protective of S. aureus infection of the ulcers (OR = 0.029, p = 0.001, 95% CI = 0.004–0.231), no predictor of S. aureus, MRSA, or polymicrobial ulcer infection was identified. Conclusions: The prevalence of S. aureus and MRSA infection of the diabetic foot ulcers were high, but lower than those of the predominant infector, coagulase-negative Staphylococci and the next highest infecting agent, E. coli. Diabetic foot ulcers’ infection with coagulase-negative Staphylococci protected against their infection with S. aureus. The prevalence of multidrug resistance was high, highlighting the need to further intensify antimicrobial stewardship programmes.


1988 ◽  
Vol 9 (6) ◽  
pp. 255-260 ◽  
Author(s):  
Nalini Rao ◽  
Sharon Jacobs ◽  
Linda Joyce

AbstractDuring an eight-month period, 25 hospitalized patients became infected or colonized with methicillin-resistant Staphylococcus aureus (MRSA) in a 464-bed acute care, medical-surgical teaching hospital. There were only five cases during the eight months prior to the outbreak period (P < 0.0001). Initial measures, including category-specific isolation and education, did not limit the spread of the outbreak of a strain of MRSA. This prompted institution of additional measures including (1) strict isolation of all infected and colonized cases; (2) prospective microbiological surveillance to detect additional cases; (3) multiple site cultures of identified cases to determine the extent of colonization; (4) employee and environment surveillance; (5) antibiotic decolonization of patients and employees; and (6) educational efforts. The highest number of personnel carriers were noted in one of the critical care units where most of the cases occurred. The decolonization protocol was 100% effective for personnel carriers. The incidence of nosocomial cases of MRSA fell to zero in the five months following the implementation of the strategy. The cost of the entire eradication process was approximately half that of treating a single MRSA bacteremia.


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