Basic Concept of Rheumatic Mechanism

Taken from a lecture by the rheumatologist who pioneered antibiotic therapy, the late Thomas McPherson Brown, M.D., spoken at the Huntsville, Alabama Family Practice Center.

Rheumatoid arthritis represents a form of bacterial hypersensitivity with the responsible antigen derived primarily from mycoplasma and/or bacterial L-forms. Mycoplasma are tissue-invisible microorganisms of infinitely minute particle size. They are known to produce arthritis in swine, chickens, turkeys, rats, mice, sheep and cattle. They promote a high degree of tissue hypersensitivity in a manner comparable to the tubercule bacillus, the brucella organism and the ß-hemolytic streptococcus.

The above diagram illustrates what's going on in the rheumatoid patient and where treatment should focus.

The organisms listed in the diagram: bacteria, spirocytes, protoplasm, L-forms and mycoplasmas, can all contribute to an antigen pool which can be sensitizing to the patient. The mycoplasmas can interfere with the whole genetic code by inactivating the patient's DNA which could thus explain some of the crippling effects of these diseases.

At a certain point - like lightening striking - some emotional phenomenon, injury or other environmental trigger can kick off the release of proteolytic enzymes with ensuing rheumatic signs and symptoms. This enzyme release is developed by nature to suppress the bacterial antecedents and antigen formation. This is why it's there, and if you take it away with corticosteroids, the patient loses the immune system's ability to protect them from infection and opens up the possibility for getting into greater trouble in the long run.

Presently, arthritis treatment deals with symptomatic control, but not in the area of antigen suppression. There is no way you can expect RA to go into remission with the use of plaquenil or gold or other standard remedies because they sensitize the patient, eventually build up to toxic levels and have to be stopped. To target antigen, you must start with something that's relatively benign in order to respond to the hypersensitive state.

Penicillamine does not have any effect on mycoplasma or L-forms of bacteria, but it does have an effect on DNAse, which mycoplasmas produce.

What is Hypersensitivity in Rheumatoid DiseaseHypersensitivity

* is a bacterial allergy - In all microbial hypersensitivity states, the causative agent goes underground as the tissue reactivity becomes manifest; it is a bacterial allergy. The existence of rheumatoid arthritis appears to require at least two components - a long-standing, antigenic challenge and a tissue reactive potential capable of responding to this precise stimulus.

* is a cell-mediated response - Mycoplasmas produce their pathogenic effect in man, not by the classical methods of invasion and rapid tissue destruction, but by creating a cell-mediated response resulting from long-standing cellular parasitism with gradual sensitization of the host through intermittent antigen release from the cells.

* is antimicrobial - A hypersensitive state itself is designed to suppresses the microbial antigen replication; e.g. the sputum of the asthmatic is generally sterile; the pleural fluid of tuberculosis pleurisy with effusion is usually devoid of culturable tubercle bacilli. In this highly reactive state, little medication is needed to further control the disease, and if too much is given, the body will react against the medication itself, defeating the purpose of the treatment.

* makes culturing the organism difficult - In hypersensitivity states, the causative organisms have become equally difficult to culture or identify in tissues while the disease process dependent on these agents remains highly active. They have a high degree of affinity for joint tissues. Man and the gorilla appear to be the most advanced in this form of reactivity opposing virus invasion.

* doesn't fit Koch's Postulates

* treatment is opposite that of standard infections - Effective treatment in each instance has evolved to be the converse of the treatment of standard infection. The dosage of the medication is relatively low instead of high; it is generally interrupted instead of sustained; and the treatment is usually long-term.

* symptoms include: loss of appetite, excessive fatigue, increased pain in areas where pain was decreasing, and increased fluid retention.

*Second page references:

TMcP Brown, HW Clark, JS Bailey, Natural Occurence of Rheumatoid Arthritis in Great Apes - A New Animal Model, Proceedings. of the Zoological Society of Philadelphia Centennial Symposium on Science and Research, November 1974; 43-79.

HW Clark, JS Bailey, TMcP Brown, Medium-Dependent Properties of Mycoplasmas, Diagn Microbiol Infect Dis, 1985; 3: 283-294.

TMcP Brown, Guidelines for Infectious Hypersensitivity Approach to the Treatment of Rheumatoid Disease, lecture notes.

* The treatment goal is direct suppression of antigen (in early disease) or suppression of antigen mimicry through tying up receptor sites (late disease / auto-immunity) with a dose of medication low enough to avoid exacerbation of the hypersensitivity state.

* A probing patient history may reveal a triggering event such as an injury, chemical sensitivity or illness. Finding such a trigger may provide information on a contributing antigenic source. Testing for organisms can be helpful in confirming the involvement of a pathogen in the disease process.

* Apparently unrelated infections such as dental problems and sinus infection complicate the antigen pool and compromise an already stressed immune system.

* A second infection can be a cofactor in the disease and an additional source of antigen: e.g. strep, chlamydia, candida, or chronic sinus or bladder infections. Treat focal infections first or concurrently.

* A washout period of several weeks to a month prior to beginning antibiotic therapy is preferable; however not all patients will be able to tolerate such a step. In those who opt for the washout, low dose prednisone may be used temporarily to help control inflammation and pain medications can help keep pain to a manageable level.

* Pursue treatment long enough (in early disease) to eventually suppress antigen formation or to interrupt chronic process (in late disease) to allow the host's immune system to dominate.

* Long term disease may require lifetime treatment.

* Treatment histories of >20-30 years currently exist with disease control and no negative side effects from the antibiotics

* Patients need to maintain a healthy life style with balanced meals, exercise, active stress reduction and adequate sleep in order to support the immune system.

* Vitamins and supplements which strengthen the immune ??system are helpful.

* Daily NSAIDs are necessary to suppress inflammation and increase the effectiveness of the antibiotic by allowing it to penetrate the inflammatory barrier.

* Acidophilus supplements will help maintain a normal bowel flora and counter an overgrowth of candida.

* To strengthen muscles and increase joint stability, rehabilitation should begin as soon as the disease shows signs of quieting, also decreasing the chances of joint disfigurement. Massage may be begun immediately to relieve trigger points in soft tissue adjacent to irritated joints, to retard contractures and provide pain relief.

* Treatment response is generally slow and subtle although some patients see an immediate lessening of pain. Six months to a year is not an unusual time required for significant improvement.

* It is not unusual to see a preliminary worsening (Herxheimer reaction) when antibiotics are begun or when treat-ment adjustments are made. The severity of the reaction is usually dose related. Although uncomfortable, this reaction is a sign the offending organism is being reached and is a good sign.

* Laboratory parameters can improve before clinical improvement is seen or vice versa. Treatment of an infection with antibiotic therapy is supported by fall a in RF and acute phase reactants.

* Depression, memory loss and mood swings are symptoms of the disease, possibly due to accumulation of antigen.

* Some generics are ineffective; brand names are more costly but strongly recommended. Adding d.a.w. to the prescription will insure the patient receives the brand name of the drug.

(*For references, see above)