Infection, Allergy and the Pathogenesis of Rheumatic Disease.

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Abstract
Summary The finding of different antibodies (antistreptolysins, etc.) against β-streptococci in serum suggests an etiological connection between these organisms and rheumatic disease. No conclusions can be drawn, however, as to the pathogenetic mechanisms, for the antibodies mentioned are active mainly in immune defence. The more common types of allergy are reviewed and the author discusses different possibilities for streptococcal infections to produce symptoms of rheumatic disease by means of allergic mechanisms. The transient rheumatoids are probably closely related to serum sickness. The first attack of acute rheumatic fever may have a similar allergic background (a form of »seroallergy« according to the terminology of the present author), but it is probable that the main factor is a streptococcal allergy of tuberculin-type — a »microbin allergy« — (the same type that is found in infections with M. tuberculosis, several fungi, etc.). At subsequent relapses the microbin allergy to β-streptococci is the dominating factor and the symptoms in joints, heart etc. may be considered as analogous to the »microbids« often seen in the course of the above-mentioned sensitizing infections. Probably through the action of streptococcus toxin, a sensitization supervenes in the course of time against the body's own proteins (e.g., in articular, periarticular and heart tissue), possibly with the help of different »mediators, « each having affinity for a specific tissue. This »autosensitization« dominates the pathogenesis in the late, chronic phases of rheumatic fever and is probably a main pathogenetic factor from the very beginning in rheumatoid arthritis. In the later phases a sensitization to other streptococci, e.g. of the α and γ groups, or possibly also to other microorganisms, may be an important factor. Research work should be aimed at finding a safe procedure for effective immunization of the patient to all common types of β-streptococci, and if possible, to other groups of streptococci (or other organisms) that may be of importance. Hyposensitization procedures, preferably with very small doses, should be tried out on a much larger scale than hitherto, particularly in rheumatoid arthritis. The importance of autosensitization should be further investigated. More effective antigens for serologic studies, for skin testing and possibly for hyposensitization may be developed through the action of streptococci (or other microbes) on tissue extracts in vitro (or possibly in experimental animals).

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