[posted 16 July 2004] By Trevor G Marshall, Director, Autoimmunity Research Foundation, Thousand Oaks, California
Re: CFS is a Th1 Immune Disease, Bacterial in Origin We recently established that Sarcoidosis was caused by poorly documented species of antibiotic resistant bacteria which have evolved to infect phagocytes of the immune system. Wirostko, et al, produced TEM photographs of hundreds of these tiny bacteria in the cytoplasm of monocytes, lymphocytes and macrophages in the late 80's. Our recent paper "Sarcoidosis succumbs to antibiotics-implications for autoimmune disease", PMID 15246025, Full text Preprint, explained this phenomenon, and hypothesised that Rheumatoid Arthritis, Lupus and Parkinson's were likely due to a similar Th1 immune pathogenesis.
However, during the last several months, an online CFS community, which can be accessed at Yahoo Health Groups, has found that CFS is indeed also associated with elevated levels of the secosteroid hormone 1,25-dihdroxycholecalciferol, a marker of Th1 inflammatory processes. Further, a significant sample (>50) of these CFS patients have found that that the same protocol of innocuous, oral drugs which we developed to treat Sarcoid inflammation has the ability to put CFS into remission. There still is some uncertainty, due to limited sample size, and lack of controls, but, based on the close resemblence between the progess I have seen in our Sarcoidosis cohort and in the CFS patients I will now state that CFS is a Th1 immune disease, bacterial in origin, and that it responds to the same antibacterial therapy as we developed for sarcoidosis.
The primary difficulty in treating the disease is, like other diseases with pathogens which cannot be cultured (syphilis), the incidence of Jarisch-Herxheimer during the entire recovery process (12-36 months) must be very carefully managed. Competing interests: None declared Source: BMJ.com (http://bmj.bmjjournals.com/cgi/eletters/329/7457/112-b#66977)