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ISME J ; 12(8): 1879-1894, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29599521

RESUMO

Community-acquired (CA)- as opposed to hospital acquired- methicillin-resistant Staphylococcus aureus (MRSA) lineages arose worldwide during the 1990s. To determine which factors, including selective antibiotic pressure, govern the expansion of two major lineages of CA-MRSA, namely "USA300" in Northern America and "European ST80" in North Africa, Europe and Middle-East, we explored virulence factor expression, and fitness levels with or without antibiotics. The sampled strains were collected in a temporal window representing various steps of the epidemics, reflecting predicted changes in effective population size as inferred from whole-genome analysis. In addition to slight variations in virulence factor expression and biofilm production that might influence the ecological niches of theses lineages, competitive fitness experiments revealed that the biological cost of resistance to methicillin, fusidic acid and fluoroquinolones is totally reversed in the presence of trace amount of antibiotics. Our results suggest that low-level antibiotics exposure in human and animal environments contributed to the expansion of both European ST80 and USA300 lineages in community settings. This surge was likely driven by antibiotic (ab)use promoting the accumulation of antibiotics as environmental pollutants. The current results provide a novel link between effective population size increase of a pathogen and a selective advantage conferred by antibiotic resistance.


Assuntos
Farmacorresistência Fúngica , Staphylococcus aureus Resistente à Meticilina/efeitos dos fármacos , África do Norte , Animais , Biofilmes/crescimento & desenvolvimento , Europa (Continente) , Humanos , Staphylococcus aureus Resistente à Meticilina/crescimento & desenvolvimento , Staphylococcus aureus Resistente à Meticilina/patogenicidade , Staphylococcus aureus Resistente à Meticilina/fisiologia , Oriente Médio , América do Norte , Infecções Estafilocócicas/microbiologia , Fatores de Virulência/metabolismo
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