Resistance to β-lactams in enterococci

Paula Gagetti1, Laura Bonofiglio2, Gabriela García Gabarrot3

  • 1Grupo STREP de la Sociedad Argentina de Bacteriología, Micología y Parasitología Clínicas (SADEBAC), División de la Asociación Argentina de Microbiología, Argentina; Servicio Antimicrobianos, Departamento de Bacteriología, Instituto Nacional de Enfermedades Infecciosas (INEI), ANLIS "Dr Carlos G. Malbrán", Ciudad Autónoma de Buenos Aires, Argentina.

Insights

High-level ampicillin resistance in Enterococcus faecium is a growing concern, primarily caused by alterations in the PBP5 protein. This resistance spreads through bacterial clonal expansion and horizontal gene transfer.

Area of Science:

  • Microbiology
  • Antimicrobial Resistance
  • Molecular Biology

Background:

  • Enterococci exhibit intrinsic resistance to antimicrobials and readily acquire new resistance mechanisms.
  • Beta-lactam antibiotics are crucial for treating enterococcal infections, making resistance a significant clinical challenge.
  • Ampicillin resistance is infrequent in Enterococcus faecalis but prevalent in hospital-associated Enterococcus faecium.

Purpose of the Study:

  • To investigate the primary mechanisms driving high-level ampicillin resistance in Enterococcus faecium.
  • To understand the genetic basis and dissemination routes of ampicillin resistance in this pathogen.

Main Methods:

  • Analysis of PBP5 protein production and genetic polymorphisms in ampicillin-resistant Enterococcus faecium isolates.
  • Investigation of clonal spread and horizontal gene transfer as dissemination mechanisms.

Main Results:

  • High-level ampicillin resistance in Enterococcus faecium is predominantly linked to enhanced production of PBP5 and/or mutations in its beta subunit.
  • Both the clonal spread of strains with mutated pbp5 genes and horizontal gene transfer contribute to the dissemination of this resistance.

Conclusions:

  • Alterations in PBP5 are the key drivers of high-level ampicillin resistance in Enterococcus faecium.
  • Understanding these mechanisms and dissemination routes is vital for combating antimicrobial resistance in clinical settings.

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