The Immunophysiology of Serum

The development of edema during the course of acute infectious diseases has been observed in patients for many years. The retention of water and salt during the course of untreated pneumococcal pneumonia was described early in the century (1). The loss of chlorides from the blood and their subsequent excretion in the urine during recovery was shown to be associated with retention by the body of sodium and calcium while potassium and magnesium were excreted normally or in excess. After antipneumococcal horse serum became available for treatment of pneumonia, serum sickness developed frequently in patients during convalescence. The clinical picture of serum disease with edema and fever was shown to be accompanied by the retention of chlorides and water in the body (2). Further investigation of serum disease in human-beings revealed that the clinical symptoms are associated with the appearance in the blood of precipitins against the species of animal in which the therapeutic serum was prepared (3). The appearance of precipitins precedes recovery from the disease by a short interval and is coincident with disappearance of the antigen. These studies indicated that antigen-antibody reactions were of clinical significance in the production of disease in human beings, and that the mechanism was in some way related to that of experimental anaphylaxis in animals. During the course of studies on patients with Rocky Mountain spotted fever, it was observed that alterations in the distribution of body fluids with the development of marked clinical edema reached a maximum just before clinical recovery