Beta-lactams against methicillin-resistant Staphylococcus aureus.


Autoria(s): Guignard B.; Entenza J.M.; Moreillon P.
Data(s)

2005

Resumo

Methicillin-resistant Staphylococcus aureus (MRSA) have developed resistance to virtually all non-experimental antibiotics. They are intrinsically resistant to beta-lactams by virtue of newly acquired low-affinity penicillin-binding protein 2A (PBP2A). Because PBP2A can build the wall when other PBPs are blocked by beta-lactams, designing beta-lactams capable of blocking this additional target should help solve the issue. Older molecules including penicillin G, amoxicillin and ampicillin had relatively good PBP2A affinities, and successfully treated experimental endocarditis caused by MRSA, provided that the bacterial penicillinase could be inhibited. Newer anti-PBP2A beta-lactams with over 10-fold greater PBP2A affinities and low minimal inhibitory concentrations were developed, primarily in the cephem and carbapenem classes. They are also very resistant to penicillinase. Most have demonstrated anti-MRSA activity in animal models of infection, and two--the carbapenem CS-023 and the cephalosporin ceftopibrole medocaril--have proceeded to Phase II and Phase III clinical evaluation. Thus, clinically useful anti-MRSA beta-lactams are imminent.

Identificador

http://serval.unil.ch/?id=serval:BIB_CDD42C73A259

isbn:1471-4892[print], 1471-4892[linking]

pmid:16095969

doi:10.1016/j.coph.2005.06.002

isiid:000232458600006

Idioma(s)

en

Fonte

Current Opinion in Pharmacology, vol. 5, no. 5, pp. 479-489

Palavras-Chave #Animals; Clinical Trials as Topic; Humans; Methicillin Resistance/drug effects; Penicillin-Binding Proteins/antagonists & inhibitors; Penicillin-Binding Proteins/metabolism; Staphylococcus aureus/drug effects; Staphylococcus aureus/metabolism; beta-Lactams/pharmacokinetics; beta-Lactams/pharmacology
Tipo

info:eu-repo/semantics/review

article