Characterization of linezolid- and methicillin-resistant coagulase-negative staphylococci in a tertiary hospital in China
Abstract Background Recently, linezolid-resistant staphylococci have become an emerging problem worldwide. It is very important to understand the resistance mechanisms, molecular epidemiology and probable transmission of linezolid-resistant CoNS in the hospital. Methods The antimicrobial susceptibilities of all the isolates were determined by the microdilution method. The resistance mechanisms and molecular characteristics of the strains were detected using whole-genome sequencing and PCR. Results All the strains were resistant to oxacillin and carried the mecA gene; 13 patients (36.1%) had received prior linezolid exposure. The majority of the S. epidermidis and S. hominis isolates were ST22 and ST1, respectively. MLST typing and evolutionary analysis indicated that the majority of linezolid-resistant CoNS were genetically related. This study revealed that distinct CoNS strains have different linezolid resistance mechanisms. Among ST22-type S. epidermidis, the acquisition of the T2504A and C2534T mutations in the V domain of the 23S rRNA gene as well as the mutations in the ribosomal proteins L3 (L101V, G152D, and D159Y) and L4 (N158S) were linked to the development of linezolid resistance. In the S. cohnii isolates, the cfr, S158Y and D159Y mutations in the ribosomal protein L3 were found. Additionally, the emergence of the G2576T mutation and the cfr gene were major causes of linezolid resistance in S. hominis isolates.The cfr gene, the G2576T and C2104T mutations, the M156T change in L3, and the I188S change in the L4 protein were found in S. capitis isolates. Conclusion The emergence of linezolid-resistant CoNS in our environment is concerning because it involves clonal dissemination and frequently coexists with various drug resistance mechanisms..
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Preprint| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
ResearchSquare.com - (2024) vom: 22. Feb. Zur Gesamtaufnahme - year:2024 |
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| Sprache: |
Englisch |
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| Beteiligte Personen: |
Liu, Cailin [VerfasserIn] |
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| Links: |
Volltext [kostenfrei] |
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| doi: |
10.21203/rs.3.rs-3927977/v1 |
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| PPN (Katalog-ID): |
XRA042595746 |
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| 245 | 1 | 0 | |a Characterization of linezolid- and methicillin-resistant coagulase-negative staphylococci in a tertiary hospital in China |
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| 520 | |a Abstract Background Recently, linezolid-resistant staphylococci have become an emerging problem worldwide. It is very important to understand the resistance mechanisms, molecular epidemiology and probable transmission of linezolid-resistant CoNS in the hospital. Methods The antimicrobial susceptibilities of all the isolates were determined by the microdilution method. The resistance mechanisms and molecular characteristics of the strains were detected using whole-genome sequencing and PCR. Results All the strains were resistant to oxacillin and carried the mecA gene; 13 patients (36.1%) had received prior linezolid exposure. The majority of the S. epidermidis and S. hominis isolates were ST22 and ST1, respectively. MLST typing and evolutionary analysis indicated that the majority of linezolid-resistant CoNS were genetically related. This study revealed that distinct CoNS strains have different linezolid resistance mechanisms. Among ST22-type S. epidermidis, the acquisition of the T2504A and C2534T mutations in the V domain of the 23S rRNA gene as well as the mutations in the ribosomal proteins L3 (L101V, G152D, and D159Y) and L4 (N158S) were linked to the development of linezolid resistance. In the S. cohnii isolates, the cfr, S158Y and D159Y mutations in the ribosomal protein L3 were found. Additionally, the emergence of the G2576T mutation and the cfr gene were major causes of linezolid resistance in S. hominis isolates.The cfr gene, the G2576T and C2104T mutations, the M156T change in L3, and the I188S change in the L4 protein were found in S. capitis isolates. Conclusion The emergence of linezolid-resistant CoNS in our environment is concerning because it involves clonal dissemination and frequently coexists with various drug resistance mechanisms. | ||
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| 650 | 4 | |a 570 |7 (dpeaa)DE-84 | |
| 700 | 1 | |a Yu, Jing |4 aut | |
| 700 | 1 | |a Chen, Chunguang |4 aut | |
| 700 | 1 | |a Li, Xiaogai |4 aut | |
| 700 | 1 | |a Ye, Yafei |4 aut | |
| 700 | 1 | |a Dong, Yani |4 aut | |
| 700 | 1 | |a Ying, Xinxin |4 aut | |
| 700 | 1 | |a Li, Haijun |4 aut | |
| 700 | 1 | |a Wang, Wanhai |4 aut | |
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