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Enferm Infecc Microbiol Clin. 2011 Dec;29 Suppl 5:59-65. doi: 10.1016/S0213-005X(11)70045-3.

[Enterococcus: phenotype and genotype resistance and epidemiology in Spain].

[Article in Spanish]

Author information

1
Servicio de Microbiología y Enfermedades Infecciosas, Hospital General Universitario Gregorio Marañón, Madrid, España. ecercenado@terra.es

Abstract

Enterococci are major nosocomial pathogens due to their intrinsic resistance to many antimicrobials as well as to their ability to acquire new mechanisms of resistance. Acquired resistance to beta-lactams is due to PBP5 overproduction or alterations in this protein. Beta-lactamase production is anecdotal. High-level resistance (HLR) to aminoglycosides is due to the production of aminoglycoside-modifying enzymes that delete synergistic killing in association with cell wall-active agents. The most frequent enzyme is AAC(6')- APH(2"), which inactivates all the aminoglycosides most frequently used in clinical practice. Acquired resistance to glycopeptides is due to the acquisition of gene clusters called vanA, vanB, vanD, vanE, vanG, vanL, vanM and vanN. Linezolid resistance is due to ribosomal mutations or to the acquisition of the cfr gene. Some isolates present diminished susceptibility to daptomycin. In Spain, both enterococcal resistance to beta-lactams and HLR to aminoglycosides are high. E. faecalis is almost uniformly susceptible to ampicillin. Enterococcal resistance to glycopeptides is low, with the exception of occasional outbreaks. The new antimicrobials (linezolid, daptomycin, tigecycline) are almost uniformly active against these microorganisms. Because of the wide dissemination of the high-risk clonal complexes CC2 and CC9 (E. faecalis), and CC17 (E. faecium), surveillance studies are required to detect antimicrobial resistance genes as well as to identify high-risk clonal complexes in order to predict future trends in the acquisition of resistance genes.

PMID:
22305671
DOI:
10.1016/S0213-005X(11)70045-3
[Indexed for MEDLINE]

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