The relationship between acute rheumatism and streptococcal antifibrinolysin.

That haemolytic streptococci of human origin produce a substance capable of liquefying human fibrin was first demonstrated by Tillet and Garner in 1933. The fibrin from patients recently recovered from haemolytic streptococcal infection was in many cases found to be resistant to the action of this fibrinolysin. and confirmed these preliminary observations, and demonstrated antifibrinoly-sin in the blood of about seventy-five per cent. of patients recovering from acute streptococcal infection. The time of appearance of antifibrinolysin in the blood varies in different patients and in different types of infection. Thus Tillett found that in some cases it was present at the time of recovery, but that in others its appearance was delayed for two to four weeks after the acute infection. There was a suggestion that it developed earlier in cases of erysipelas than in those with an acute streptococcal pharyngitis. These observations were confirmed by Myers, Keefer and Holmes (1935), who also showed that the resistance of the plasma to fibrinolysin, once developed, persisted for a varying time, and Spink and Keefer (1936) found that in erysipelas antifibrinoly-sin can be demonstrated from eight to a hundred and fifty days after the attack. Waaler (1936) found that patients with scarlatina did not all develop antifi-brinolysin, and that in those who did, it might first appear from one to five weeks after the infection, similar observations being made by Stuart-Harris (1935, a and b). From this work it is now clear that it is rare for antifibrinolysin to be present in the blood unless the patient has comparatively recently experienced a streptococcal infection. The occasional cases to the contrary can be explained by assuming that the antifibrinolysin has persisted long after the infection to which it is due has been forgotten. Antifibrinolysin ranks with antistreptolysin as one of the antibodies produced as part of the immunity mechanism following infections with haemolytic streptococci. The presence of these antibodies in the blood does not necessarily run parallel, and Stuart-Harris (1935b) has shown that there is no correlation between antistreptolysin and antifibrinolysin except that when the fibrin is completely resistant to fibrinolysin there is usually some rise in the antistreptolysin titre. Shortly after Tillett and Garner's original reports, Hadfield, Magee and Perry (1934) found that the fibrin of many patients in the active stage of acute rheumatism was partially or completely resistant to fibrinolysin. This was regarded as further evidence of the frequent occurrence …