Saturday, March 7, 2015
An infectious cause to rheumatoid arthritis?
Very little research has been done on the relationship between ureaplasma and mycoplasma infections and their relationship to chronic disease. These organisms are very difficult to find many times as they have many stealth features that allow them to hide intracellularly and in areas of the body that are not easily accessible to clinicians. Also, cultures of these organisms often are unable to identify them and instead identification is only possible with DNA PCR analysis. They are similarly difficult to treat and require long courses of antibiotics as they have the ability to go into a resistant hibernation state.
Many people relate being bit by a tick and subsequently having joint pains or issues with muscle pains or fatigue. Often they test negative for Lyme disease. Mycoplasma can also be transmitted by tick bites. Ureaplasma and mycoplasma can also be transmitted through respiratory contact and sexual contact.
Unfortunately, chronic infections with these organisms can cause irreversible changes in the cellular genetics.
Presence of Mycoplasma fermentans in the bloodstream of Mexican patients with rheumatoid arthritis and IgM and IgG antibodies against whole microorganism.
Gil C1, Rivera A, Bañuelos D, Salinas S, García-Latorre E, Cedillo L.
Increasing evidence incriminates bacteria, especially Mycoplasma fermentans, as possible arthritogenic agents in humans. The purpose of this study was to investigate M. fermentans in the bloodstream of patients with rheumatoid arthritis.
Two hundred and nineteen blood samples from patients with rheumatoid arthritis, systemic lupus erythematosus, antiphospholipid syndrome, and healthy individuals were screened by bacterial culture and direct PCR in order to detect mycoplasmas; IgM and IgG against M. fermentans PG18 were also detected by ELISA and Immunoblotting assays in patients with rheumatoid arthritis and healthy individuals.
Blood samples from patients with antiphospholipid syndrome and healthy individuals were negative for mycoplasma by culture or direct PCR. In blood samples from patients with systemic lupus erythematosus were detected by direct PCR M. fermentans in 2/50 (2%), M. hominis in 2/50 (2%) and U. urealyticum in 1/50 (0.5%). In patients with RA M. fermentans was detected by culture in 13/87 blood samples and in 13/87 by direct PCR, however, there was only concordance between culture and direct PCR in six samples, so M. fermentans was detected in 20/87(23%) of the blood samples from patients with RA by either culture or PCR. Antibody-specific ELISA assay to M. fermentans PG18 was done, IgM was detected in sera from 40/87 patients with RA and in sera of 7/67 control individuals, IgG was detected in sera from 48/87 RA patients and in sera from 7/67 healthy individuals. Antibody-specific immunoblotting to M. fermentans PG18 showed IgM in sera from 35/87 patients with RA and in sera from 4/67 healthy individuals, IgG was detected in sera from 34/87 patients and in sera from 5/67 healthy individuals.
Our findings show that only M. fermentans produce bacteremia in a high percentage of patients with RA. This finding is similar to those reported in the literature. IgM and IgG against M. fermentans PG18 were more frequent in patients with RA than healthy individuals.