The consensus of opinion among bacteriologists is that, of the aerobes found in acute appendicitis and acute appendicitis associated with spreading peritonitis or a local abscess formation, Bacterium coli and various strains of streptococci play the leading rôles. The precise rôle of the anaerobes has been a controversial subject. The work of Dudgeon and Sargent in 1905 (4) may be regarded as detrimental to the advancement of our knowledge of the etiologic factors operating in spreading peritonitis. These men were so positive in their assertion that anaerobes play no part in the toxemia of peritonitis that they impressed even such leaders and molders of medical opinion as Murphy and Deaver. It is only recently that the importance of the anaerobes in this disease has been suspected, especially of Clostridium welchii (5).

The results obtained in carrying out tests for the presence of antitoxin for the toxin of Clostridium welchii in the blood of patients who were convalescing or had recovered from acute appendicitis, active or quiescent pelvic peritonitis, and spreading peritonitis, the result of a ruptured appendix, indicate that a major percentage of these patients recovered from spreading peritonitis, not only because of the surgical and medical measures instituted, but also because of their immunologic response to infection with Clostridium welchii. We feel that this indicates that Clostridium welchii plays an important rôle in spreading peritonitis of appendiceal origin. Although our series of cases is small, the percentage of individuals who develop sufficient antitoxin in their blood serum, after recovering from an attack of appendiceal peritonitis, to protect pigeons against the toxin is high enough to support this statement. In 10 apparently normal adults used as controls, the incidence of antitoxin in the blood serum was zero; in 9 patients convalescing or recovered from acute unperforated appendicitis, the incidence of demonstrable antitoxin in the blood serum was 22.2 per cent; in 15 patients with active or quiescent pelvic peritonitis the incidence of demonstrable antitoxin was 46.6 per cent and in 28 patients suffering with or recovered from spreading peritonitis secondary to acute perforative appendicitis, the incidence of demonstrable antitoxin in the blood serum was 69 per cent.

Furthermore, we have been using perfringens antitoxin in the treatment of cases of spreading peritonitis following perforative appendicitis with results which are encouraging and which will be reported later.

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