Role of phenotypic diversity in pathogenesis of avian mycoplasmosis

Abstract

The interactions between avian mycoplasmas and their host cells are far more complex than might be anticipated from their apparent structural and functional simplicity. Phenotypic diversity in the form of reversible phase variation, antigenic variation or size variation is an adaptive mechanism that enables avian mycoplasmas to survive in a hostile and highly evolved host. Despite significant similarities between major membrane antigens of Mycoplasma gallisepticum and Mycoplasma synoviae, the molecular mechanisms that mediate phenotypic variation in these two pathogens are completely different. Throughout the years, these mechanisms have evolved side by side with their host immune system and provided mycoplasmas the capacity to colonize, invade and persist in an intricate host. In this article, recent advances in the understanding of the molecular mechanisms of phenotypic variation are reviewed, and implications of such variation in pathogenesis of the disease and development of vaccines and diagnostic assays are outlined.

An assessment of opportunities to dissect host genetic variation in resistance to infectious diseases in livestock

“…At present, there is no published evidence regarding the genetic control of host response to Mycoplasma spp. infection, although information has been published on the pathogen genomics and on molecular mechanisms of phenotypic variation in pathogenesis (Noormohammadi, 2007). At present, this is not a target pathogen for OG.…”

Decreased production in broiler breeders due to tendon rupture by Mycoplasma synoviae

“…Nevertheless, this agent can also cause infectious synovitis (Cobb, 2011). In both cases, infection with M. synoviae might result in significant losses due to decreased egg production, growth and hatchability rates, and downgrading of carcasses at slaughter due to airsacculitis and arthritis lesions (Fiorentin et al, 2003;Kleven, 2003;Noormohammadi, 2007;Peebles et al, 2011). In recent years, the occurrence of arthropathic and amyloidogenic strains of M. synoviae, as well as of strains that induce eggshell apex abnormalities and egg production losses, has increased economic impact of this pathogen Landman and Feberwee, 2008;Catania et al, 2010).…”

Diversity of Expressed vlhA Adhesin Sequences and Intermediate Hemagglutination Phenotypes in Mycoplasma synoviae

“…Sequential integration of different pseudogene sequences can further result in the formation of chimeric alleles. The selective pressure of anti-VlhA antibodies in vivo is proposed to perpetuate lineages of M. synoviae that each express a different allele of vlhA as an antigen-diversifying mechanism to evade the adaptive immune system of the host (1,30,31,32).Although the specific receptor(s) engaged by VlhA remains unknown, cytadherence is mediated by sialylated moieties on the host cell surface. It has been known for a long time that receptor desialylation reduces or abolishes cytadherence by M. synoviae (22), but it was only recently discovered that adjacent to the vlhA locus, M. synoviae encodes an extracellular sialidase whose specific activity differs quantitatively among strains in a stable pattern correlated with strain virulence (26).…”

“…Sequential integration of different pseudogene sequences can further result in the formation of chimeric alleles. The selective pressure of anti-VlhA antibodies in vivo is proposed to perpetuate lineages of M. synoviae that each express a different allele of vlhA as an antigen-diversifying mechanism to evade the adaptive immune system of the host (1,30,31,32).…”

“…Cytadherence mediated by its primary adhesin VlhA is a precursor to virulence (30). Posttranslational cleavage of full-length VlhA produces the peptides MSPA (carboxy-terminal portion of VlhA) and MSPB (amino-terminal portion) (Fig.…”