The Beta Streptococcal Theory of Rheumatic Fever in the Modern Treatment of the Condition

Summary We have reviewed the long and varied story of the investigations into the cause of rheumatic fever, starting from the days when it was confidently thought to be a simple disease syndrome following K och 's postulates, like many other diseases the germ being thought to be 8 non‐haemolytic diplo‐ or streptococcus, up to the present day when one of the most authorative British journals, The Luncet , states dogmatically in the first sentence of its primary leading article on July 12th, 1952: “Acute rheumatic fever is a complication of a group A beta streptococcal infection of the throat of a susceptible person”, and goes on to discuss the mechanisms possible to bring this about. With our present knowledge only two possible explanations are tenable, first that the phenomenon of rheumatic fever is due to a changed body reaction to certain products of the beta streptococcus, or secondly that the beta streptococcus prepares the body for an unknown virus or actually carries the virus to the patient. The second hypothesis appeals to the general critic who has not studied the subject very closely, and feels unconvinced of the former hypothesis. But no such virus has been found, nor are there any reasons leading workers in this field even to suspect such an unusual agent of disease, nor if one was suspected would its association with the beta streptococcus be any easier to explain than the antigen‐antibody or changed‐body‐reaction hypothesis which now holds the field among the majority of workers who have studied the condition minutely. Indeed the reverse is the case and there ip even some animal experimental evidence to show how the mechanism of the disease may work. M uilphy and S wift (22) for instance have demonstrated microscopic lesions in the hearts of rabbits resembling closely those of rheumatic fever in the human, in animals which had been repeatedly injected intradermally with group A beta haemolytic streptococci. Previously R ich et al . (25) had shown that lesions could be produced in animals which were similar to those of rheumatic carditis as a result of anaphylactic hypersensitivity. We admit that ultimate proof of this hypothesis must await either the complete confirmation of MURPW and SWIFT'S line of experiments or the isolation of a definite antigen obtained from the beta streptococcus capable of causing the rheumatic fever reaction. In the meantime, however, we submit that the evidence of the association of the beta haemolytic streptococcus and acute rheumatic fever is overwhelming and that if this is accepted and made the basis of therapy we are confident that the disease can be prevented if the streptococcal infection can be prevented. This means that active measures in general to prevent beta streptococcal pharyngitis, particularly in semi‐isolated communities, will lower the incidence of first attacks of rheumatic fever, and prevent almost altogether recurrences. Further we ourselves believe that if the antigen‐antibody theory is accepted as a working hypothesis, the actual attack itself can be modified by the proper administration of drugs belonging to the salicylate group and hormones of the suprarenal cortex. We have also shown that the latter agents should not be used alone, but their therapy should be combined with an attack upon the antigen (the beta streptococcus) by means of prolonged treatment with antibiotics, and that when this is carried out marked amelioration of the rheumatic fever process can be obtained.