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Macrolide-resistant pneumococcal endocarditis and epidural abscess that develop during erythromycin therapy
Jay C Butler1, Jeffrey L Lennox, Linda K McDougal
1Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, Alaska 99508, USA. Jbutler@cdc.gov
Abstract:
Suppurative complications of Streptococcus pneumoniae infections have become uncommon in the antibiotic era. We report a case of pneumococcal bacteremia and pneumonia complicated with epidural abscess and endocarditis in which macrolide resistance (the MLS(B) phenotype) emerged during erythromycin therapy. Genetic determinants known to mediate the most common mechanisms of macrolide resistance (methylation of the 23S rRNA and antibiotic efflux) were not detected by polymerase chain reaction or DNA hybridization. Sequence analysis of the DNA encoding the 23S rRNA of the macrolide-resistant isolate from the patient demonstrated the replacement of adenine by thymine at position 2058 (A2058T) in 2 of 4 alleles. Clinicians should be alert to the possibility of the emergence of resistance during macrolide therapy for community-acquired pneumonia, particularly if suppurative complications of pneumococcal infection are suspected.
Insights
Emergence of macrolide resistance in Streptococcus pneumoniae during erythromycin treatment is rare but possible. A novel A2058T mutation in 23S rRNA caused resistance, complicating pneumonia and bacteremia.
Area of Science:
- Infectious Diseases
- Microbiology
- Genetics
Background:
- Suppurative complications from Streptococcus pneumoniae infections are infrequent in the current antibiotic era.
- Macrolide antibiotics are commonly used for community-acquired pneumonia.
Observation:
- A patient with pneumococcal bacteremia and pneumonia developed an epidural abscess and endocarditis.
- Macrolide resistance (MLS(B) phenotype) emerged during erythromycin therapy.
Findings:
- Standard genetic mechanisms for macrolide resistance (23S rRNA methylation, antibiotic efflux) were absent.
- Sequence analysis revealed a novel A2058T mutation in the 23S rRNA gene of the resistant isolate.
Implications:
- Clinicians must consider the potential for emergent macrolide resistance during treatment for community-acquired pneumonia.
- This case highlights a new mechanism of macrolide resistance in Streptococcus pneumoniae.
- Vigilance is crucial, especially when suppurative complications are suspected.
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