Development of glycopeptide-intermediate resistance by Staphylococcus aureus leads to attenuated infectivity in a rat model of endocarditis.

Détails

ID Serval
serval:BIB_1E16B1C38CC4
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Development of glycopeptide-intermediate resistance by Staphylococcus aureus leads to attenuated infectivity in a rat model of endocarditis.
Périodique
Microbial pathogenesis
Auteur(s)
Majcherczyk P.A., Barblan J.L., Moreillon P., Entenza J.M.
ISSN
0882-4010
Statut éditorial
Publié
Date de publication
2008
Peer-reviewed
Oui
Volume
45
Numéro
5-6
Pages
408-414
Langue
anglais
Résumé
Glycopeptide-intermediate resistant Staphylococcus aureus (GISA) are characterized by multiple changes in the cell wall and an altered expression of global virulence regulators. We investigated whether GISA are affected in their infectivity in a rat model of experimental endocarditis. The glycopeptide-susceptible, methicillin-resistant S. aureus M1V2 and its laboratory-derived GISA M1V16 were examined for their ability to (i) adhere to fibrinogen and fibronectin in vitro, (ii) persist in the bloodstream after intravenous inoculation, (iii) colonize aortic vegetations in rats, and (iv) compete for valve colonization by co-inoculation. Both GISA M1V16 and M1V2 adhered similarly to fibrinogen and fibronectin in vitro. In rats, GISA M1V16 was cleared faster from the blood (P < 0.05) and required 100-times more bacteria than parent M1V2 (10(6) versus 10(4)CFU) to infect 90% of vegetations. GISA M1V16 also had 100 to 1000-times lower bacterial densities in vegetations. Moreover, after co-inoculation with GISA M1V16 and M1V2Rif, a rifampin-resistant variant of M1V2 to discriminate them in organ cultures, GISA M1V16 was out-competed by the glycopeptide-susceptible counterpart. Thus, in rats with experimental endocarditis, GISA showed an attenuated virulence, likely due to a faster clearance from the blood and a reduced fitness in cardiac vegetations. The GISA phenotype appeared globally detrimental to infectivity.
Mots-clé
Animals, Anti-Bacterial Agents, Bacterial Adhesion, Disease Models, Animal, Drug Resistance, Bacterial, Endocarditis, Bacterial, Glycopeptides, Mutation, Rats, Staphylococcal Infections, Staphylococcus aureus, Virulence
Pubmed
Web of science
Création de la notice
20/03/2009 15:39
Dernière modification de la notice
20/08/2019 13:54
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