Mycoplasma - Cause, Co-factor or Commensal in CFS
Bill Paspaliaris
Melbourne Forensic & Diagnostic Services, Albert Street Medical Centre,
372-376 Albert St, East Melbourne, VIC 3002 Australia
(presented at the 1999 ME/CFS Conference in Sydney, Australia)
Mycoplasmas are the smallest free-living organisms known and are distinguished by the absence of a rigid cell wall. There have been 16 species isolated from humans, six of which have the urogenital tract as the main colonisation site and eight of which have the oro-respiratory tract. Interestingly all have different pathogenic potential in humans, some of which have no pathogenic effect and some which are definitely pathogenic.
The most controversial of these species is Mycoplasma fermentans. First isolated in 1952, it has been reported in high incidence in chronic diseases involving abnormal states of the immune system. However, its pathogenic potential is still undecided. In vitro, it has been demonstrated to induce cytokine levels when infected in white blood cells, cause stem cells to turn tumorous, and allow dormant viral infections to activate and replicate at abnormal levels. Recently, M. fermentans membrane-bound proteins have been characterized and have been demonstrated to have monocyte/macrophage activator activity, but their role in disease causation or propagation have yet to be reported.
The aim of our research was to study the presence of M. fermentans in patients with CFS (which is considered a chronic illness involving the immune system) and the possible role of the monocyte/macrophage activator membrane-bound proteins.
Using a sensitive PCR procedure for determination of mycoplasma species DNA, serology, and RT-PCR for expression of M, fermentans monocyte/macrophage activator proteins, M. fermentans DNA was found in a significantly higher portion in the buffy coat layer from patients with CFS (45% of 195) than from asymptomatic individuals (14% of 104). When M. fermentans DNA load was measured it was found to be significantly higher in CFS than in asymptomatic M. fermentans-positive individuals. Interestingly, M. fermentans IgG serology only slightly correlated with differences in the two disease groups.
When M. fermentans monocyte/macrophage activator protein expression was performed from RNA isolated from buffy coat layers of peripheral blood, a striking pattern of differentiation was observed in CFS individuals as compared to asymptomatic individuals. This pattern of expression was only seen in the buffy coat layer of CFS individuals and correlated with increased serum levels of IL-6 and IL-12.
We believe that the expression of M. fermentans monocyte/macrophage activator proteins may be a most useful clinical marker for detecting M. fermentans pathogenicity in chronic illnesses such as CFS.