Linezolid-resistant Staphylococcus aureus isolated from 2006 through 2008 at six hospitals in Japan

Ikeda-Dantsuji, Yurika; Hanaki, Hideaki; Sakai, Fuminori; Yanagisawa, Chie; Nakae, Taiji; Tomono, Kazunori; Takesue, Yoshio; Honda, Junichi; Nonomiya, Yuriko; Suwabe, Akira; Nagura, Osanori; Yanagihara, Katsunori; Mikamo, Hiroshige; Fukuchi, Kunihiko; Kaku, Mitsuo; Kohno, Shigeru; Yoshida, Koichiro; Niki, Yoshihito

doi:10.1007/s10156-010-0085-1

Cited by 42 publications

(28 citation statements)

References 23 publications

(42 reference statements)

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“…This mutation has been reported in both staphylococci and enterococci (6,15,34,40,59,61,70,71,87,97,101), and a clear correlation between the number of mutated rRNA operons and the linezolid MIC has been found (2,35,59). Most reports of the G2576U mutation in clinical isolates are associated with some form of increased or prolonged linezolid treatment or with high linezolid usage at the local hospital (29,84), underscoring the importance of judicious use of linezolid in clinical settings.…”

Section: Resistance Caused By 23s Rrna Mutationsmentioning

confidence: 97%

Resistance to Linezolid Caused by Modifications at Its Binding Site on the Ribosome

Long

Vester

2012

Antimicrob Agents Chemother

306

195

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Linezolid is an oxazolidinone antibiotic in clinical use for the treatment of serious infections of resistant Gram-positive bacteria. It inhibits protein synthesis by binding to the peptidyl transferase center on the ribosome. Almost all known resistance mechanisms involve small alterations to the linezolid binding site, so this review will therefore focus on the various changes that can adversely affect drug binding and confer resistance. High-resolution structures of linezolid bound to the 50S ribosomal subunit show that it binds in a deep cleft that is surrounded by 23S rRNA nucleotides. Mutation of 23S rRNA has for some time been established as a linezolid resistance mechanism. Although ribosomal proteins L3 and L4 are located further away from the bound drug, mutations in specific regions of these proteins are increasingly being associated with linezolid resistance. However, very little evidence has been presented to confirm this. Furthermore, recent findings on the Cfr methyltransferase underscore the modification of 23S rRNA as a highly effective and transferable form of linezolid resistance. On a positive note, detailed knowledge of the linezolid binding site has facilitated the design of a new generation of oxazolidinones that show improved properties against the known resistance mechanisms. LINEZOLID

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Section: Resistance Caused By 23s Rrna Mutationsmentioning

confidence: 97%

Resistance to Linezolid Caused by Modifications at Its Binding Site on the Ribosome

Long

Vester

2012

Antimicrob Agents Chemother

306

195

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“…The first linezolid-resistant clinical isolate was reported in an MRSA isolate in the USA (Tsiodras et al, 2001). Since then, the occurrence of linezolid-resistant staphylococci has been increasingly reported in the United States (Mendes et al, 2008;Scheetz et al, 2008), Mexico (Mendes et al, 2010a), Japan (Ikeda-Dantsuji et al, 2011), Italy (Bongiorno et al, 2010;Mendes et al, 2010b), Spain (Sánchez García et al 2010;Seral et al, 2011) and Ireland (Kelly et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Identification and characterization of cfr-positive Staphylococcus aureus isolates from community-onset infectious patients in a county hospital in China

Zhao

Zheng

et al. 2015

Journal of Medical Microbiology

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The cfr gene was detected in 14 meticillin-susceptible Staphylococcus aureus isolates recovered from outpatients with community-onset infections in a county hospital in China. The MIC of linezolid was 4 mg ml 21 in eight isolates and 2 mg ml 21 in six isolates. All isolates were susceptible to vancomycin and teicoplanin, but had elevated MICs for penicillin (0.5-128 mg ml 21), chloramphenicol (2-32 mg ml 21), clindamycin (0.5-128 mg ml 21) and erythromycin (4-128 mg ml 21 ). Nine isolates had mutations on domain V of 23S rRNA and/or the ribosomal L proteins that were not located close to the linezolid-binding pocket. Southern blotting experiments demonstrated that the cfr genes in all 14 isolates resided on plasmids. Sequence analysis of the 5.6 kb cfr-carrying plasmid segment revealed 99 % identity to the corresponding sequences in plasmid pSS-01 from animal staphylococci and plasmid pRM-01 from human staphylococci. Five isolates belonged to sequence type (ST)188 and three to ST965; the two ST types were previously reported in isolates of animal origin in some areas of China. These results indicate that the cfr-carrying plasmids in this study are likely of animal origin. The present study shows that cfr-harbouring S. aureus isolates have emerged in some areas of China and that cfr-carrying isolates may be transmitted between animals and humans.

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“…Four S. epidermidis isolates from group I with MICs of Ͼ256 were further investigated by sequencing, but no additional mutations in the 23S rRNA gene or the L3, L4, and L22 genes were found. A correlation between MICs and numbers of mutant alleles has been found after selection of isogenic lines under laboratory conditions (22,23), but the relation is less clear when independent clinical isolates are analyzed (24). The heterogeneity of MICs even among isolates with the same number of mutant alleles suggests that there might be additional unidentified factors affecting linezolid susceptibility.…”

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confidence: 99%

Mechanisms of Linezolid Resistance among Staphylococci in a Tertiary Hospital

et al. 2013

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bThe mechanisms of linezolid resistance among 86 staphylococcal isolates from two intensive care units were investigated. The most frequent was the G2576T mutation in the 23S rRNA (82%). The cfr gene was found in 17% of the isolates, seven S. aureus and eight S. epidermidis isolates. Four of the S. epidermidis isolates had the G2576T mutation and the cfr gene. In four S. haemolyticus isolates, the mechanism could not be identified.

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Linezolid-resistant Staphylococcus aureus isolated from 2006 through 2008 at six hospitals in Japan

Cited by 42 publications

References 23 publications

Resistance to Linezolid Caused by Modifications at Its Binding Site on the Ribosome

Resistance to Linezolid Caused by Modifications at Its Binding Site on the Ribosome

Identification and characterization of cfr-positive Staphylococcus aureus isolates from community-onset infectious patients in a county hospital in China

Mechanisms of Linezolid Resistance among Staphylococci in a Tertiary Hospital

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