Aspectos epidemiológicos y moleculares implicados en la sensibilidad disminuida a la vancomicina en Staphylococcus aureus

Staphylococcus aureus is an opportunistic pathogen that causes disease in humans and animals. Since 1997 there have been worldwide reports of S. aureus with reduced susceptibility to vancomycin (VISA), and strains with heterogeneous resistance (hVISA). The mechanism responsible for this resistance i...

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Autor principal: Di Gregorio, Sabrina Noelia
Otros Autores: Famiglietti, Angela
Formato: Tesis doctoral acceptedVersion
Lenguaje:Español
Publicado: Facultad de Farmacia y Bioquímica 2015
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Acceso en línea:http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_1130
http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_1130.dir/1130.PDF
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Sumario:Staphylococcus aureus is an opportunistic pathogen that causes disease in humans and animals. Since 1997 there have been worldwide reports of S. aureus with reduced susceptibility to vancomycin (VISA), and strains with heterogeneous resistance (hVISA). The mechanism responsible for this resistance is not fully understood. In addittion, detection of hVISA phenotype is difficult in clinical settings.\nThis work describes for the first time the prevalence and molecular characterization of isolates hVISA in a hospital from Argentina. Different methodologies for the detection were evaluated. Additionally, the molecular mechanism probably involved in the reduced susceptibility to vancomycin was studied.\nNo VISA isolate was recovered and hVISA phenotype occurred in 3.3% of S. aureus bacteremia studied. An association between hVISA phenotype and multiple episodes of bacteremia was found, and a combination of methods was proposed to warn of a possible hVISA in those laboratories that can not regularly perform confirmatory methodology.\nThe change in peptidoglycan metabolism of hVISA/VISA strains found in this thesis may be due to diverse genetic changes. Increased IS256 transposition was also associated with this phenotype.