Virulence and molecular adaptation of human urogenital mycoplasmas: a review

The pathogenesis of mycoplasmas requires their attachment to the epithelial mucosa membrane of the host cells, followed by colonisation and necrotic destruction of the submucosal tissue. The extent of this pathogenesis depends on the ability of species of Mycoplasma to effectively attach and invade the host’s tissue. In this regard, the cytadherence tip organelle has evolved within the mycoplasmas to accomplish this feat. However, species of Mycoplasma that do not possess the specialized structure remain virulent with the use of surface-membrane lipoproteins. The lipoprotein ligands bind to sulfatides and sialoglycoconjugates on the host’s mucosa membranes. This host-mycoplasma interaction, though poorly studied, appears to have a wide underlying array of complex molecular mechanisms, which after activation trigger cytadherence, immunomodulation and virulence. Mycoplasmas with their highly redundant minimal genomes display dynamic genotypic and phenotypic plasticity; a trait that has allowed them to adapt, persist and survive successfully in adverse niches through circumvention and tempering of the host’s humoral immune response. Additionally, the linkages between the mycoplasmas persistence and chronic inflammatory diseases in humans necessitate examining the host-mycoplasma interaction at the proteogenomic level. This paper provides an overview on the molecular mechanisms involved in cytadherence, surface-membrane antigenic variation and survival strategies of human urogenital mycoplasmas