Febbuabt 12, 1909] 



SCIENCE 



245 



tion is set in motion. The cause of this 

 interesting negative phase is not well 

 understood, but it lies closely at hand to 

 ascribe it to neutralization of the normal 

 antibodies by the antigen, or to its effect 

 on the antibody-forming cells. There is 

 good reason to believe, especially on clin- 

 ical grounds, that the general resistance to 

 the specific infection is lowered in the neg- 

 ative phase, although certain experimental 

 results indicate that the opposite may be 

 the case. 



Blood serum may contain antigens 

 causing the production of antibodies for 

 its homologous corpuscles; thus, the injec- 

 tion of antidiphtheric horse serum is fol- 

 lowed by a wave-like rise and fall of the 

 lysin, agglutinin and opsonin for horse 

 corpuscles in the blood of the patient, the 

 highest point being reached usually about 

 the tenth day. Undoubtedly these anti- 

 genic substances are derived from disin- 

 tegration of the corpuscles. 



Serum and other protein mixtures also 

 induce the formation of specific precipi- 

 tating substances in suitable animals. 

 Whether the specific precipitin test for 

 protein material, now extensively used for 

 the identification of blood and in the solu- 

 tion of allied problems, will prove of 

 service also in the study of pure proteins, 

 remains to be seen. 



In several acute infectious diseases the 

 course of the formation of new opsonin 

 for the infecting agent, in the typical at- 

 tack, terminating promptly in recovery 

 without complications, shows a marked 

 general resemblance to the opsonin or 

 antibody curve after a single antigen in- 

 jection in the normal animal. It also 

 bears definite and constant relations to 

 the clinical phenomena. During the early 

 stages when the symptoms are pronounced 

 there is a negative phase, and then as the 

 symptoms begin to subside the opsonin 

 curve rises above normal, reaching the 



highest point several days after the onset, 

 followed by a gradual subsidence. This is 

 true of the pneumococcus opsonin in pneu- 

 monia, of the opsonin for the diphtheria 

 bacillus in diphtheria, of the streptococcus 

 opsonin in erysipelas, and also of the op- 

 sonin for the diplococcus of mumps in 

 that disease. The curve is typical as well 

 for the streptococcus in scarlet fever, indi- 

 cating clearly that this organism unques- 

 tionably plays a definite role in scarlet 

 fever whatever its actual causative relation 

 to the disease may be. In pneumonia the 

 greatest rise in the leukocytosis appears to 

 precede somewhat the highest rise of the 

 opsonin. In all these diseases the typical 

 wave-like opsonin curve is modified by the 

 development of complications of various 

 kinds and at the onset of which it com- 

 monly undergoes a distinct depression. In 

 rapidly fatal cases, for instauce of pneu- 

 monia, the opsonic curve or index may not 

 return from the primary depression but 

 sink lower and lower. In prolonged in- 

 fections, general as well as local, there oc- 

 cur irregular fluctuations and in chronic, 

 more or less stationary cases, the opsonic 

 index is often subnormal. At this time 

 further details can not be given. My 

 chief point is to make clear the close asso- 

 ciation between recovery and the wave-like 

 rise of the opsonin and, as a result of the 

 immunization, in all likelihood also of other 

 antibodies in the typical attack of acute 

 so-called self-limited infections. In some 

 of the diseases the opsonin is the only anti- 

 body that we can measure readily with our 

 present means. As I have stated, intra- 

 phagocytic destruction of pneumococci 

 and streptococci takes place in the pres- 

 ence of fresh leukocytes and opsonic serum, 

 whereas either alone constitutes a good 

 medium for these bacteria. Taking these 

 facts into account, it seems to me that the 

 wave-like course of the opsonin in pneu- 

 monia and in acute streptococcus infec- 



