See the published version of this article at BMC Microbiology.
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Research article
Qingzhong Liu
Shanghai Jiaotong University First People's Hospital
Corresponding Author
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This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Microbiology.
Data on the prevalence of resistance to mupirocin (MUP), fusidic acid (FA) and retapamulin (RET) in methicillin-resistant Staphylococcus aureus (MRSA) from China are still limited. In this study we examined these three antibiotics resistance pheno and geno-typically in 1206 MRSA clinical isolates. Phenotypic MUP, FA and RET resistance was determined by MICs, and genotypically by PCR and DNA sequencing examining genes mupA / B , fusB - D , cfr and vgaA / Av , and mutations in ileS , fusA / E , rplC , and 23S RNA V domain. The genetic characteristics of resistance isolates were conducted by PFGE and MLST. Overall MRSA MUP, FA and RET resistance was low (5.1%, 1.0% and 0.3%, respectively). The mupA was the mechanism of high-level MUP resistance. All low-level MUP resistance isolates possessed an equivocal mutation N213D in IleS, and 2 of them additionally had the reported V588F mutation impacting the Rossman fold. FusA mutations, such as L461K, H457Q, H457Y and V90I, were the primary FA resistance mechanisms among high-level resistance isolates, most of which contained fusC ; however, all low-level resistance strains carried fusB . No resistance mechanisms detected were found among RET resistance isolates. Genetic analysis demonstrated clone spread for MUP resistance isolates. In conclusion, MUP, FA and RET exhibited highly activity against MRSA isolates. Acquired genes and chromosome-borne genes mutations were responsible for MUP and FA resistance, and further investigation is needed to uncover the RET resistance mechanisms. Moreover, the surveillance to MUP in MRSA should be strengthened to prevent resistance increase due to the expansion of clones.
Keywords
Methicillin-resistant Staphylococcus aureus, Mupirocin, Fusidic acid, Retapamulin, Resistance mechanisms, Genetic characteristics
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CURRENT STATUS: Published
Version 1
Posted 24 Jan, 2020
Published
On 29 Jun, 2020
No community comments so far
Editorial decision: Major revision
On 18 Mar, 2020
Reviewer #2 agreed
On 06 Mar, 2020
Review #2 received
Received 06 Mar, 2020
Review #1 received
Received 02 Mar, 2020
Reviewer #1 agreed
On 11 Feb, 2020
Reviewers invited
Invitations sent on 10 Feb, 2020
Editor assigned
On 06 Feb, 2020
Submission checks complete
On 23 Jan, 2020
Editor invited
On 23 Jan, 2020
First submitted
On 20 Jan, 2020
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This preprint is under consideration at BMC Microbiology. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Qingzhong Liu
Shanghai Jiaotong University First People's Hospital
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
Version 1
Posted 24 Jan, 2020
Published
On 29 Jun, 2020
No community comments so far
Editorial decision: Major revision
On 18 Mar, 2020
Reviewer #2 agreed
On 06 Mar, 2020
Review #2 received
Received 06 Mar, 2020
Review #1 received
Received 02 Mar, 2020
Reviewer #1 agreed
On 11 Feb, 2020
Reviewers invited
Invitations sent on 10 Feb, 2020
Editor assigned
On 06 Feb, 2020
Submission checks complete
On 23 Jan, 2020
Editor invited
On 23 Jan, 2020
First submitted
On 20 Jan, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Microbiology.
Data on the prevalence of resistance to mupirocin (MUP), fusidic acid (FA) and retapamulin (RET) in methicillin-resistant Staphylococcus aureus (MRSA) from China are still limited. In this study we examined these three antibiotics resistance pheno and geno-typically in 1206 MRSA clinical isolates. Phenotypic MUP, FA and RET resistance was determined by MICs, and genotypically by PCR and DNA sequencing examining genes mupA / B , fusB - D , cfr and vgaA / Av , and mutations in ileS , fusA / E , rplC , and 23S RNA V domain. The genetic characteristics of resistance isolates were conducted by PFGE and MLST. Overall MRSA MUP, FA and RET resistance was low (5.1%, 1.0% and 0.3%, respectively). The mupA was the mechanism of high-level MUP resistance. All low-level MUP resistance isolates possessed an equivocal mutation N213D in IleS, and 2 of them additionally had the reported V588F mutation impacting the Rossman fold. FusA mutations, such as L461K, H457Q, H457Y and V90I, were the primary FA resistance mechanisms among high-level resistance isolates, most of which contained fusC ; however, all low-level resistance strains carried fusB . No resistance mechanisms detected were found among RET resistance isolates. Genetic analysis demonstrated clone spread for MUP resistance isolates. In conclusion, MUP, FA and RET exhibited highly activity against MRSA isolates. Acquired genes and chromosome-borne genes mutations were responsible for MUP and FA resistance, and further investigation is needed to uncover the RET resistance mechanisms. Moreover, the surveillance to MUP in MRSA should be strengthened to prevent resistance increase due to the expansion of clones.
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