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O21.1 Mycoplasma Genitalium Infectious Load and Treatment Failure Due to Selected Macrolide Resistance
  1. J Twin1,2,
  2. C Bradshaw3,4,5,
  3. S Garland2,4,
  4. M Bissessor3,
  5. M Chen3,
  6. J Walker4,
  7. C Fairley3,4,
  8. J Hocking4,
  9. S Tabrizi1,2,4
  1. 1Murdoch Childrens Research Institute, Melbourne, Australia
  2. 2Royal Women’s Hospital, Melbourne, Australia
  3. 3Melbourne Sexual Health Centre, Melbourne, Australia
  4. 4University of Melbourne, Melbourne, Australia
  5. 5Monash University, Melbourne, Australia


Background Treatment failure due the development of macrolide resistance seen at Melbourne Sexual Health Centre (MSHC) has risen from 15 to 46% over the last six years (p < 0.01). Macrolide resistance is conferred through point mutations in the M. genitalium 23S rRNA gene. Treatment failure with 1g azithromycin is either due to an infection with a pre-existing resistant strain or development of resistance during treatment, but the mechanism is not yet fully understood.

Methods A subset of M. genitalium positive cases seen at MSHC between 2007–9 (n = 67) and 2012 (n = 70) underwent detection of resistance mutations via high resolution melt analysis, with real-time PCR quantifying M. genitalium infectious load.

Result Of those M. genitalium cases that successfully responded to 1g azithromycin, the pre-treatment median loads for 2007–9 (n = 40) and 2012 (n = 48) were 8.5 x 102 and 1.7 x 103 copies per reaction respectively. For M. genitalium strains that possessed resistance in the pre-treatment sample, the loads were remarkably similar to those successfully treated, with 2.2 x 103 copies per reaction detected for 2007–9 (n = 9) and 5.7 x 103 copies for 2012 (n = 22). However, for M. genitalium cases that appeared to develop resistance following treatment, (ie. mutations only detected in follow-up test of cure sample), there was a significantly higher load detected with 3.1 x 104 copies per reaction for 2007–9 (n = 8) and 1.8 x 104 copies for 2012 (n = 8), when compared to either treatment success cases or those with baseline resistance (one sided p < 0.01).

Conclusions The higher infectious load in pre-treatment M. genitalium cases that developed detectable resistance after 1g of azithromycin compared to those with baseline resistance and those cured raises the possibility that heterotypic resistance and/or induced resistance may be contributing to macrolide failure in M. genitalium. These findings have implications for current recommended treatment for M. genitalium.

  • macrolide resistance
  • Mycoplasma genitalium

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