Abstract

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.

Highlights

  • IntroductionStaphylococcus aureus (MRSA) and vancomycin-resistant enterococci [1]

  • Linezolid belongs to the oxazolidinone antibiotics and is approved for the treatment of severe infections caused by multidrug-resistant Gram-positive pathogens including methicillin-resistantStaphylococcus aureus (MRSA) and vancomycin-resistant enterococci [1]

  • Linezolid resistance was detected in 2.3% of S. aureus isolated from pigs (Table 1)

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Summary

Introduction

Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci [1]. Linezolid interferes with the peptidyltransferase site of the bacterial ribosome. This leads to disruption of protein synthesis and inhibition of bacterial growth [2]. The emergence of linezolid-resistant (LR) staphylococci and enterococci poses a significant and interdisciplinary public health challenge [1]. Mutation in the central loop of domain V of 23S ribosomal ribonucleic acid (rRNA) (C2161T) is the primary mechanism of linezolid resistance. Redundancy of rRNA genes makes it difficult to reach sufficient levels of resistance by a mutation in a single allele [3]. RRNA mutations often negatively affect ribosome functions and are rapidly reversed in the absence of selection [4]

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