Clinical emergence of inducible macrolide resistance mediated by acquired erm(41) C28T mutation in Mycobacterium

Guiqing He1,2, Shushu Zeng3, Lilla Terezia Banki3

  • 1Department of Infectious Diseases, Wenzhou Central Hospital, The Dingli Clinical College of Wenzhou Medical University, Wenzhou, China.

Insights

Mycobacterium abscessus can develop inducible macrolide resistance during treatment. A point mutation in the erm(41) gene led to resistance in a patient with pulmonary disease, showing in vivo resistance development.

Area of Science:

  • Microbiology
  • Genetics
  • Clinical Medicine

Background:

  • Inducible macrolide resistance in Mycobacterium abscessus is often mediated by the erm(41) T28 allele.
  • This resistance mechanism is considered an intrinsic trait in M. abscessus.

Purpose of the Study:

  • To report a case of M. abscessus pulmonary disease.
  • To document the emergence of inducible macrolide resistance in vivo.
  • To investigate the genetic basis of acquired resistance during therapy.

Main Methods:

  • Case report of a patient with M. abscessus pulmonary disease.
  • Genomic analysis of M. abscessus isolates.
  • Antimicrobial susceptibility testing.

Main Results:

  • The initial M. abscessus isolate carried the erm(41) C28 allele.
  • During prolonged therapy, a de novo C28T point mutation was identified in the erm(41) gene.
  • The isolate developed inducible macrolide resistance.

Conclusions:

  • This case provides the first clinical evidence of inducible erm(41)-mediated resistance arising in vivo.
  • Antimicrobial selective pressure can drive the development of inducible macrolide resistance in M. abscessus.
  • Understanding this mechanism is crucial for managing M. abscessus infections.