Antibody Formation in Cases of Lobar Pneumonia Treated with Sulfathiazole.

Early in 1940'we published a report (1) on antibody formation in cases of lobar pneumonia treated with sulfapyridine. In nineteen treated cases of pneumococcus pneumonia repeatedly studied during the acute phase of the disease and during convalescence, an excess of type-specific antibody was only demonstrated in the serum of four. In the past it has often been shown that spontaneous recovery from lobar pneumonia is associated, in the great majority of instances, with the appearance of an excess of antibody in the patient's serum, and this phenomenon has been generally regarded as an essential part of the mechanism of spontaneously occurring crisis. Our failure to demonstrate antibodies in fifteen out of nineteen cases suggested to us that sulfapyridine had supplanted, at least to some degree, this portion of the immune process. We did not believe that antibody-production ceased to exist in treated cases, but rather that it proceeded at a lower rate, probably because the stimulus to antibody formation was lessened as a result of the action of the drug on the invading organism. Our technique for the demonstration of excess antibody throughout the series studied was the precipitin reaction with type-specific polysaccharide. While this paper was in press, two similar studies were published. Wood and Long (2) reported the appearance of mouse-protective antibodies in the serum of ten out of eleven treated patients recovering from lobar pneumonia but pointed out that in seven of these cases antibody appeared after the time of " essential recovery." Subsequently, Finland and his associates (3) reported a large series of cases of pneumococcus pneumonia in which mouse-protective antibodies and agglutinins were sought. They concluded as a result of these studies that "the antibody response of patients with pneumococcic pneumonia treated with sulfapyridine, as far as could be determined, was comparable in every respect to that resulting from spontaneous recovery." It will be observed that these results were not in accord with our findings. None of these investigators, however, used the same technique as we did-to wit, the precipitin reaction. It is our belief that the precipitin reaction, as Heidelberger and Kendall (4) have pointed out, is probably less sensitive than the other methods, but that it is more clear-cut and more specific. Unfortunately, at the time our paper was written, we had no control series of our own in which untreated patients were studied by the same technique, although such was present in the literature (5). As will be observed, the results which we obtained in patients treated with sulfathiazole, as opposed to sulfapyridine, using precisely the same technique, were almost diametrically different, and therefore constitute a very satisfactory control of the method. Before sulfathiazole was introduced, eleven additional sulfapyridine-treated cases were studied in the same manner as those reported in the original paper. Including one doubtful reaction, only four of these showed precipitins during convalescence. Adding these to the original series, we have then a total of thirty cases of pneumococcus pneumonia treated with sulfapyridine; of these twenty-two, or nearly seventy-five per cent, recovered from the disease without the appearance of an excess of antibody in the blood serum as demonstrated by the precipitin reaction. The chief purpose of the present communication is to describe the results which we obtained when an exactly similar study was made of patients treated with sulfathiazole.