Mycoplasma fermentans as a Commensal
September 1, 2000 3 minutes read
Mycoplasma fermentans as a Commensal
abstract & commentary
Synopsis: Mycoplasma fermentans appears to be a common commensal organism.
Source: Ainsworth JG, et al. Detection of Mycoplasma fermentans in healthy students and patients with congenital immunodeficiency. J Infect 2000;40:138-140.
Mycoplasma fermentans gained some notoriety several years ago when it was suggested to be a major cofactor in HIV infection. M. fermentans had previously been associated with a wide range of diseases including seronegative arthritis, acute respiratory disease, and nongonococcal arthritis. Since culture of mycoplasmas is laborious and probably less than 100% sensitive, DNA amplification technology using polymerase chain reaction (PCR) has revolutionized the study of mycoplasma.
What is needed in the study of M. fermentans is an understanding of the true epidemiology of the organism. In this study from a group of British investigators who have been publishing on this organsim for years, medical students were used as healthy controls. A second group of 19 patients had common variable immunodeficiency. Samples for DNA amplification from both groups included throat, urine, and peripheral blood mononuclear cells (PBMCs).
PCR analysis produced the following results: for the student group of 62 throat samples, 11 (18%) were positive; of 46 urine samples, 17% were positive. For students who provided both a urine and throat sample, 27% were positive, but only four were positive at both sites. Of the 19 immune deficiency patients, only one was PCR positive in the throat, and three were positive in urine. Three of these four positive patients were receiving gamma globulin therapy. None of the immune deficiency patients had PCR-positive PBMC.
Comment by Joseph F. John, MD
This study suggests further studies in pathologic states to determine the presence of M. fermentans DNA. Ainsworth and colleagues feel that the presence in tissue of M. fermentans DNA indicates invasiveness. On the contrary, perhaps organisms of such low pathogenicity can exist in tissue without giving rise to disease. There are some reasonably good animal models for Mycoplasma infection and perhaps with new DNA array technology, a pathologic role can be detected.
Mycoplasmas may be much more widely distributed on mucosal surfaces than previously appreciated. Serological responses to the different species combined with DNA amplification technology will help resolve the commensal vs. the pathologic role. One of the species of mycoplasmas, M. incognitans, has been associated by some with chronic fatigue syndrome (CFS). Some private labs have developed PCR testing for M. incognitans. Innocent enough perhaps, but there is a long-standing view from some that chronic mycoplasma infection is either the cause or one cause of CFS. Some patients seeing that they are positive for M. incognitans testing, succumb to the seduction of long-term tetracycline therapy, assuming such therapy will eradicate the suspicious mycoplasma and cure the CFS. Unfortunately, CFS is probably not explainable with any one microorganism hypothesis. That is not to say that each and every opportunistic infection in CFS should not be understood or studied. Yet, as Ainsworth et al have shown in the current study, mycoplasmas are probably ubiquitous and understanding their pathogenic side will take time and innovative methods.
Until many further studies are conducted, the current study lends caution to earlier work suggesting that the presence of M. fermentans indicates disease. Both normal medical students and people with common variable immunodeficiency have M. fermentans at some mucosal sites. The next several years should prove interesting for the study of the cell walless bacterial agents, including M. fermentans.
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