Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, No.1 Jianshe East Road, Erqi District, Zhengzhou, Henan Province, 450052, China.
Key Clinical Laboratory of Henan Province, Zhengzhou, China.
BMC Infect Dis. 2024 May 10;24(1):486. doi: 10.1186/s12879-024-09376-z.
Recently, linezolid-resistant staphylococci have become an emerging problem worldwide. Understanding the mechanisms of resistance, molecular epidemiology and transmission of linezolid-resistant CoNS in hospitals is very important.
The antimicrobial susceptibilities of all isolates were determined by the microdilution method. The resistance mechanisms and molecular characteristics of the strains were determined using whole-genome sequencing and PCR.
All the strains were resistant to oxacillin and carried the mecA gene; 13 patients (36.1%) had prior linezolid exposure. Most S. epidermidis and S. hominis isolates were ST22 and ST1, respectively. MLST typing and evolutionary analysis indicated most linezolid-resistant CoNS strains were genetically related. In this study, we revealed that distinct CoNS strains have different mechanisms of linezolid resistance. Among ST22-type S. epidermidis, acquisition of the T2504A and C2534T mutations in the V domain of the 23 S rRNA gene, as well as mutations in the ribosomal proteins L3 (L101V, G152D, and D159Y) and L4 (N158S), were linked to the development of linezolid resistance. In S. cohnii isolates, cfr, S158Y and D159Y mutations in the ribosomal protein L3 were detected. Additionally, emergence of the G2576T mutation and the cfr gene were major causes of linezolid resistance in S. hominis isolates. The cfr gene, G2576T and C2104T mutations, M156T change in L3 protein, and I188S change in L4 protein were found in S. capitis isolates.
The emergence of linezolid-resistant CoNS in the environment is concerning because it involves clonal dissemination and frequently coexists with various drug resistance mechanisms.
最近，耐利奈唑烷葡萄球菌已成为全球范围内的一个新兴问题。了解耐利奈唑烷凝固酶阴性葡萄球菌（CoNS）的耐药机制、分子流行病学和传播在医院中非常重要。
采用微量稀释法测定所有分离株的抗菌药敏性。采用全基因组测序和 PCR 方法确定菌株的耐药机制和分子特征。
所有菌株均对苯唑西林耐药，并携带 mecA 基因；13 名患者（36.1%）有先前使用利奈唑胺的暴露史。大多数表皮葡萄球菌和人葡萄球菌分离株分别为 ST22 和 ST1。MLST 分型和进化分析表明，大多数耐利奈唑烷 CoNS 菌株具有遗传相关性。在本研究中，我们揭示了不同的 CoNS 菌株具有不同的利奈唑烷耐药机制。在 ST22 型表皮葡萄球菌中，23S rRNA 基因 V 区的 T2504A 和 C2534T 突变以及核糖体蛋白 L3（L101V、G152D 和 D159Y）和 L4（N158S）的突变与利奈唑烷耐药的发展有关。在科氏葡萄球菌分离株中，检测到核糖体蛋白 L3 中的 cfr、S158Y 和 D159Y 突变。此外，G2576T 突变和 cfr 基因的出现是人葡萄球菌分离株利奈唑烷耐药的主要原因。在头状葡萄球菌分离株中发现了 cfr 基因、G2576T 和 C2104T 突变、L3 蛋白中的 M156T 变化以及 L4 蛋白中的 I188S 变化。
环境中耐利奈唑烷凝固酶阴性葡萄球菌的出现令人担忧，因为它涉及克隆传播，并且经常与各种耐药机制共存。
