High clonal diversity in erythromycin-resistant Streptococcus pneumoniae invasive isolates in Madrid, Spain (2000-07)

Elia Gómez G de la Pedrosa1, Fernando Baquero, Elena Loza

  • 1Servicio de Microbiología, Hospital Ramón y Cajal y CIBER en Epidemiología y Salud Pública (CIBERESP), Madrid, Spain.

Abstract

Insights

Erythromycin resistance in Streptococcus pneumoniae is rising globally. The study found that erm(B) and erm(B) plus mef(A) resistance genes are widespread in diverse S. pneumoniae clones, potentially driving further antibiotic resistance evolution.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Epidemiology

Background:

  • Erythromycin resistance in Streptococcus pneumoniae is a growing global health concern.
  • Understanding the genetic basis and population structure of resistant strains is crucial for effective treatment strategies.

Purpose of the Study:

  • To investigate the erythromycin resistance determinants and population structure of Streptococcus pneumoniae isolates from blood cultures.
  • To analyze the genetic diversity and distribution of resistance genes within these isolates.

Main Methods:

  • Screening of erythromycin resistance determinants using Polymerase Chain Reaction (PCR).
  • Multilocus sequence typing (MLST) and quantitative clonal diversity analysis using mathematical indexes (diversity ratio, Simpson, Selander-Levin, Shannon).

Main Results:

  • The erm(B) gene was the predominant resistance determinant (74.3%), followed by erm(B) plus mef(A) (17.9%) and mef(A) (7.7%).
  • A polyclonal population structure was observed in resistant strains, including international clones like Spain(9V)-3, Spain(6B)-2, and Denmark(14)-32.
  • High genetic diversity and distribution were noted, especially in clones carrying erm(B) and erm(B) plus mef(A).

Conclusions:

  • Erythromycin resistance determinants erm(B) and erm(B) plus mef(A) are present in multiple Streptococcus pneumoniae bacteraemic clones.
  • The polyclonal structure of these resistant strains may facilitate the further evolution and spread of antibiotic resistance.

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