Assessment of Genotypic Macrolide Resistance among Mycoplasma pneumoniae Infections in Children in Singapore.

Dear Editor, Mycoplasma pneumoniae belongs to the class Mollicutes and is a small bacterium without a cell wall that is a common cause of community-acquired pneumonia in adults and children. Due to its unique physical structure, M. pneumoniae is resistant to cell wall-targeting agents, such as beta-lactam antibiotics. Therefore, the antibiotics of choice for the treatment of suspected M. pneumoniae infections, particularly for children, are the macrolides, with their main class representative being erythromycin. Alternatives for treatment include the tetracyclines and fluoroquinolones. Reduced susceptibility or resistance of M. pneumoniae to macrolide antibiotics has been described; this is the consequence of point mutations in domain V (peptidyltransferase region) of the 23S rRNA gene.1,2 The most common mutation is the substitution of adenine with guanine (A2063G) at base position 2063 (M. pneumoniae numbering, equivalent to base position 2058 in Escherichia coli).3 This mutation has been found associated with a 103-fold to >105-fold elevation of the minimum inhibitory concentration (MIC) of erythromycin as compared to susceptible strains.4 Less common mutations occur at positions 2063 (A→T, A→C), 2064 (A→G, A→C), 2067 (A→G) and 2617 (the latter not studied in this work). These mutations reduce the affinity of macrolides for the ribosome,4,5 thereby reducing their efficacy. Macrolide resistance due to erm genes or enzymes that inactivate macrolides have not been detected thus far in M. pneumoniae.2 Studies conducted from 2011 onwards in Japan, South Korea and China have demonstrated alarmingly high levels of macrolide resistance (ranging from 63% to 98%) in M. pneumoniae strains.2 On the other hand, macrolide resistance in M. pneumoniae from Europe, North America and Australia has been less common (ranging from 0% to 26%).2 The prevalence of macrolide resistance in M. pneumoniae in Singapore or its neighbouring countries in South-east Asia is currently unknown. Thus, we sought to determine the prevalence of genotypic macrolide resistance in M. pneumoniae among clinical specimens submitted for diagnostic purposes at a paediatric hospital in Singapore. We used PCR primers published by Wolff et al6 to amplify a region that encompasses the mutations at positions 2063, 2064 and 2067 that account for more than 99% of macrolide resistance in published works.2