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Moderate resistance to penicillin in Neisseria meningitidis

J A Sáez Nieto1, J A Vázquez

  • 1Servicio de Bacteriología, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain. jasaez@isciii.es

Microbiologia (Madrid, Spain)
|November 14, 1997
PubMed

Insights

Meningococcal penicillin resistance has surged globally since the 1980s due to genetic changes in penicillin binding protein 2 (PBP2). This resistance likely stems from Neisseria recombination, impacting treatment strategies.

Area of Science:

  • Microbiology
  • Genetics
  • Epidemiology

Background:

  • Meningococcal resistance to penicillin was rare in Spain before the 1980s.
  • A significant increase in resistant strains was observed between 1985 and 1990 in Spain.
  • Recent reports indicate the emergence of resistant strains in multiple countries.

Purpose of the Study:

  • To investigate the emergence and potential mechanisms of penicillin resistance in Neisseria meningitidis.
  • To understand the genetic basis of altered penicillin susceptibility in meningococci.

Main Methods:

  • Monitoring the frequency of penicillin-resistant Neisseria meningitidis isolates.
  • Investigating the penicillin binding protein 2 (PBP2) in resistant strains.
  • Conducting population genetic studies to identify genetic exchange events.

Main Results:

  • Penicillin resistance in meningococci increased dramatically in Spain from 0.4% in 1985 to 42.6% in 1990.
  • Reduced affinity of penicillin binding protein 2 (PBP2) for penicillin is a key factor in resistance.
  • Similar PBP2 alterations were observed in commensal Neisseria species.
  • Population genetic data suggests that recombination events involving the PBP2 gene, with sequences from commensal Neisseria, followed by clonal spread, are responsible for resistance.

Conclusions:

  • The rise in meningococcal penicillin resistance is linked to genetic modifications in PBP2.
  • Recombination with commensal Neisseria species appears to be the primary mechanism driving this resistance.
  • The findings highlight the dynamic nature of antimicrobial resistance and the need for ongoing surveillance.

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