PCR amplification of the gene can be used to predict the sensitivity of complex strains to clarithromycin.

A worldwide increase in the () complex has been observed. Therefore, the aim of the present study was to investigate the diversity of the and (41) genes, both of which are associated with macrolide sensitivity in the complex. The current study also examined the efficacy of mass spectrometry as an alternative to molecular testing to classify subspecies of the complex. A total of 14 strains of the complex were obtained, and based on conventional analyses using housekeeping genes, 57% were determined to be subsp. , 43% were subsp. , and none were identified as subsp. . However, depending on the strain, it was not always possible to distinguish between the subspecies by mass spectrometry. Consequently, PCR products for the and (41) genes were directly sequenced. Overall, 7.1% of the strains were identified to have a mutation, and 92.9% carried a T at position 28 of (41). Results presented here suggest that the principal cause of treatment failure for complex infections is inducible macrolide resistance encoded by the (41) gene. From a strictly pragmatic standpoint, the phenotypic function of a putative (41) gene is the most important piece of information required by clinicians in order to prescribe an effective treatment. Although PCR amplification of (41) is not sufficient to differentiate between the complex subspecies, PCR can be easily and efficiently used to predict the sensitivity of members of the complex to clarithromycin.