Potential therapeutic targets for combating Mycoplasma genitalium

Abstract

Mycoplasma genitalium (M. genitalium) has emerged as a sexually transmitted infection (STI) all over the world in the last three decades. It has been identified as a cause of male urethritis, and there is now evidence that it also causes cervicitis and pelvic inflammatory disease in women. However, the precise role of M. genitalium in diseases such as pelvic inflammatory disease, and infertility is unknown, and more research is required. It is a slow-growing organism, and with the advent of the nucleic acid amplification test (NAAT), more studies are being conducted and knowledge about the pathogenicity of this organism is being elucidated. The accumulation of data has improved our understanding of the pathogen and its role in disease transmission. Despite the widespread use of single-dose azithromycin in the sexual health field, M. genitalium is known to rapidly develop antibiotic resistance. As a result, the media frequently refer to this pathogen as the "new STI superbug." Despite their rarity, antibiotics available today have serious side effects. As the cure rates for first-line antimicrobials have decreased, it is now a challenge to determine the effective antimicrobial therapy. In this review, we summarise recent M. genitalium research and investigate potential therapeutic targets for combating this pathogen.

Keywords: Cervicitis; Mycoplasma genitalium; Pelvic inflammatory disease; Sexually transmitted infections; Urethritis.

Fig. 1

General workflow of Drug target identification through comparative genomics approaches

Fig. 2

Schematic representation of the preprotein translocase of E. coli. The cartoon shows the different units of the preprotein translocase including the motor protein SecA which drives preproteins across the membrane via a channel made up of an oligomeric assembly of SecYEG complexes. The SecDFyajC is another heterotrimeric membrane protein complex that stimulates the preprotein translocation. The ribosome contacts the SecYEG complex and SecA protein to facilitates the co-translational insertion of membrane proteins (Veenendaal et al. 2004)

Fig. 3

Restriction-modification (R-M) system as defence mechanism. Incoming foreign DNA, such as phage genomes, is recognised by R-M system for its methylation status. Methylated sequences are recognised as self, but nonmethylated sequences on incoming DNA are recognised as nonself and cleaved by restriction endonuclease (REase). The cognate methyltransferase (MTase) of the R-M system maintains the methylation state at the genomic recognition sites (Vasu and Nagaraja 2013)