Rapid Emergence and Evolution of Staphylococcus aureus Clones Harboring fusC-Containing Staphylococcal Cassette Chromosome Elements

February 23, 2017 at 7:51 am

Antimicrobial Agents and Chemotherapy April 2016 V.60 N.4 P.2359-2365

Sarah L. Baines, Benjamin P. Howden, Helen Heffernan, Timothy P. Stinear, Glen P. Carter, Torsten Seemann, Jason C. Kwong, Stephen R. Ritchie, and Deborah A. Williamson

aDoherty Applied Microbial Genomics, Department of Microbiology & Immunology, The University of Melbourne at The Doherty Institute for Infection and Immunity, Melbourne, Australia

bMicrobiological Diagnostic Unit Public Health Laboratory, Department of Microbiology & Immunology, The University of Melbourne at The Doherty Institute for Infection and Immunity, Melbourne, Australia

cInfectious Diseases Department, Austin Health, Melbourne, Australia

dInstitute of Environmental Science and Research, Wellington, New Zealand

eVictorian Life Sciences Computation Initiative, The University of Melbourne, Melbourne, Australia

fSchool of Medical Sciences, University of Auckland, Auckland, New Zealand

The prevalence of fusidic acid (FA) resistance among Staphylococcus aureus strains in New Zealand (NZ) is among the highest reported globally, with a recent study describing a resistance rate of approximately 28%.

Three FA-resistant S. aureus clones (ST5 MRSA, ST1 MSSA, and ST1 MRSA) have emerged over the past decade and now predominate in NZ, and in all three clones FA resistance is mediated by the fusC gene. In particular, ST5 MRSA has rapidly become the dominant MRSA clone in NZ, although the origin of FA-resistant ST5 MRSA has not been explored, and the genetic context of fusC in FA-resistant NZ isolates is unknown.

To better understand the rapid emergence of FA-resistant S. aureus, we used population-based comparative genomics to characterize a collection of FA-resistant and FA-susceptible isolates from NZ. FA-resistant NZ ST5 MRSA displayed minimal genetic diversity and represented a phylogenetically distinct clade within a global population model of clonal complex 5 (CC5) S. aureus.

In all lineages, fusC was invariably located within staphylococcal cassette chromosome (SCC) elements, suggesting that SCC-mediated horizontal transfer is the primary mechanism of fusC dissemination.

The genotypic association of fusC with mecA has important implications for the emergence of MRSA clones in populations with high usage of fusidic acid. In addition, we found that fusC was colocated with a recently described virulence factor (tirS) in dominant NZ S. aureus clones, suggesting a fitness advantage.

This study points to the likely molecular mechanisms responsible for the successful emergence and spread of FA-resistant S. aureus.

PDF

http://aac.asm.org/content/60/4/2359.full.pdf

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Entry filed under: Antimicrobianos, Bacterias, Bacteriemias, Biología Molecular, Epidemiología, Infecciones emergentes, Metodos diagnosticos, Resistencia bacteriana, Sepsis, Update.

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