What is Hypersensitivity in Rheumatoid Disease?

Hypersensitivity -

* 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.

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.