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Antigen-Capture Enzyme-Linked Immunosorbent Assay for Specific Detection of Mycoplasma pneumoniae
06:04

Antigen-Capture Enzyme-Linked Immunosorbent Assay for Specific Detection of Mycoplasma pneumoniae

Published on: February 24, 2023

Characterization and molecular analysis of macrolide-resistant Mycoplasma pneumoniae clinical isolates obtained in

Mayumi Matsuoka1, Mitsuo Narita, Norio Okazaki

  • 1Department of Bacterial Pathogenesis and Infection Control, National Institute of Infectious Diseases, Tokyo, Japan.

Antimicrobial Agents and Chemotherapy
|November 25, 2004
PubMed

Insights

Macrolide-resistant Mycoplasma pneumoniae strains are increasingly found in Japan. Genetic analysis revealed specific mutations in the 23S rRNA gene are responsible for erythromycin resistance in these common respiratory pathogens.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antibiotic Resistance

Background:

  • Macrolide antibiotics are crucial for treating Mycoplasma pneumoniae infections.
  • Emergence of macrolide-resistant M. pneumoniae strains poses a significant public health concern.
  • Previous studies indicated occasional macrolide resistance in Japan, necessitating further investigation.

Purpose of the Study:

  • To investigate the prevalence and genetic basis of macrolide (erythromycin) resistance in clinical M. pneumoniae isolates from Japan.
  • To identify specific mutations in the 23S rRNA gene and ribosomal proteins associated with erythromycin resistance.
  • To assess the frequency of these resistance mutations in oral samples from children with respiratory infections.

Main Methods:

  • Isolation and characterization of M. pneumoniae strains from clinical samples in Japan (2000-2003).
  • Determination of erythromycin Minimum Inhibitory Concentrations (MICs) for resistant strains.
  • Nucleotide sequencing of domains II and V of the 23S rRNA gene and ribosomal proteins L4 and L22.
  • Restriction fragment length polymorphism (RFLP) analysis of PCR-amplified 23S rRNA gene domain V from oral samples.

Main Results:

  • 13 out of 76 M. pneumoniae strains exhibited erythromycin resistance (17.1%).
  • High-level resistance (MIC ≥ 256 µg/ml) was observed in 12 strains, with mutations A2063G (10 strains) or A2063C (1 strain) in 23S rRNA domain V.
  • A weakly resistant strain showed a C2617G mutation in 23S rRNA domain V.
  • The A2063G mutation was detected in 24% of PCR-positive oral samples from children with respiratory infections.

Conclusions:

  • Specific point mutations in the 23S rRNA gene, particularly at position 2063, are the primary cause of erythromycin resistance in M. pneumoniae in Japan.
  • Ribosomal proteins L4 and L22, and domain II of 23S rRNA, were not implicated in the observed resistance.
  • Erythromycin-resistant M. pneumoniae infections appear to be prevalent in Japan, highlighting the need for monitoring and alternative treatment strategies.

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