Abstract
Mycoplasma pneumoniae is one of the major pathogens responsible for pneumonia in children. Modern molecular genetics has advanced both the management and the epidemiologic study of this disease. Despite these advancements, macrolide resistance remains a global threat in the management of M. pneumoniae infection, for which the genetic background remains unrevealed. In this study, the result of whole genome analysis of 20 sequence type 3 (ST3) M. pneumoniae strains were examined to investigate the gene(s) associated with macrolide resistance. Overall, genetic similarities within M. pneumoniae, and especially ST3, were very high (over 99.99 %). Macrolide resistant ST3 strains shared 20 single nucleotide polymorphisms, of which one gene (mpn085) was found to be associated with resistance. BLAST comparison of M. pneumoniae revealed regular tandem repeat number variabilities between macrolide-susceptible and resistant strains for genes coding the Type I restriction-modification (R-M) system of subunit S (HsdS). Of the ten known HsdS genes, macrolide resistance was determined by the unique tandem repeat of mpn085 and mpn285. In conclusion, the use of whole genome sequencing (WGS) to target macrolide resistance in M. pneumoniae indicates that the determinant of macrolide resistance is variabilities in the tandem repeat numbers of the type I R-M system in subunit S.
Highlights
Mycoplasma pneumoniae is one of the major pathogens responsible for pneumonia in children [1]
We investigated the whole genomes of 20 M. pneumoniae strains that are currently known to belong to sequence type 3 in respect of the existence of macrolide resistance
Comparative Genomics-Coding of DNA Sequences with Identical Functions Based on the gene annotation of the Rapid Annotations using Subsystems Technology (RAST) and SEED, BLAST comparisons were applied to ascertain the differences between four macrolide susceptible strains [19,20]
Summary
Mycoplasma pneumoniae is one of the major pathogens responsible for pneumonia in children [1]. There is increasing evidence of the associations between macrolide resistance and the development of M. pneumoniae-related extra-pulmonary diseases, as well as progression to prolonged and more serious lung disease [5,6,7]. Despite this situation, current knowledge concerning the mechanism of macrolide resistance is limited. Previous studies have proven an association between the 23s rRNA point mutation and macrolide resistance and the correlation has been verified by laboratory experiments [8]. Molecular genetics have revealed that certain strains are associated with macrolide resistance [3,9,10]. Discovering the genetic basis of macrolide resistance is likely to benefit the scientific community in terms of clinical treatment because of the ongoing increase in this form of resistance
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