Abstract
Mycoplasma hominis is a member of the genus mycoplasma and has only been isolated from humans. It is most frequently isolated from the urogenital tract in the absence of symptoms, but has been isolated from wounds, brain abscess, inflamed joints, blood and placenta from pregnancy with adverse outcomes (especially preterm birth and occasionally term stillbirth). Controversy surrounds whether this organism is a commensal or a pathogen; however, Mycoplasma hominis has been shown to induce preterm birth and foetal lung injury in an experimental primate model as a sole pathogen. These bacteria are known to exist as a parasitic infection, due to a number of missing synthetic and metabolism pathway enzymes from their minimal genome; therefore, the ability to adhere to host cells is important. Here we provide a review that clarifies the different nomenclature (variable adherence-associated antigen and P50) that has been used to investigate the major surface adhesin for this organism, as well as reported mechanisms responsible for turning off its expression. Variation in the structure of this protein can be used to separate strains into six categories, a method that we were able to use to distinguish and characterise 12 UK strains isolated from between 1983 and 2012. We propose that the Vaa should be used in further investigations to determine if commensal populations and those that are associated with disease utilise different forms of this adhesin, as this is under-studied and identification of pathogenic determinants is overdue for this organism.
Highlights
Mycoplasmas are characterised by vastly reduced genomes and are among the smallest of the free-living organisms
Sequence differences have been observed between variable adherence-associated (Vaa) positive (Vaa+) and Vaa negative (Vaa−) variants derived from a single clonal lineage, with a single nucleotide deletion observed in a short tract of adenine residues located 166 nucleotides downstream of the ATG start codon
The Vaa antigen is a major adhesin of M. hominis and displays pronounced mutational variation in size as well as sequence and antigenic variation
Summary
Mycoplasmas are characterised by vastly reduced genomes and are among the smallest of the free-living organisms. Mutation-based phenotypic and genetic variation is a strategy utilised by many pathogenic bacteria and protozoa to adapt to divergent host environments [13] [14] These mutations often affect the surface structures of a pathogen and may change functional aspects of the organism such as adherence, colonisation of the host, or immune evasion. High-frequency mutations, that are distinct from classical regulation of gene expression, are an adaptive tactic that can affect the expression or structure of selected gene products, creating and maintaining repertoires of functionally variant organisms within a population This diversity may contribute in many ways to the survival, propagation, transmission and pathogenic properties of an infectious agent. Despite discovery for more than two decades no comprehensive review of Vaa regulation and expression has been previously undertaken, the importance of Vaa in the pathogenesis and immune evasion of M. hominis infections is still not fully elucidated
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