THERAPEUTIC IMMUNIZATION IN MAN 467 



stance is formed in the body fluids to prevent their action as far as 

 we know. Immunity in such cases, then, is not an antitoxic immu- 

 nity in any sense of the word ; it is rather an antibacterial immunity 

 in which the disease is prevented or cured only when complete de- 

 struction of the bacteria has taken place. If an animal or a human 

 being is prophylactically immunized against diseases of this kind 

 (typhoid, cholera, etc.), it is easy to see that an increased presence 

 of antibacterial substances, bactericidal or opsonic, in the circulation 

 would serve efficiently and rapidly in disposing of the small numbers 

 of invading micro-organisms which ordinarily enter the body in spon- 

 taneous infections. And, indeed, experience has shown that prophy- 

 lactic immunization can be successfully carried out in the case of 

 cholera, typhoid fever, plague, and other diseases which are suffi- 

 ciently prevalent endemically or epidemically to justify prophylaxis 

 on an extensive scale. 



However, when in diseases of this kind the body is already exten- 

 sively infected and has begun, as is usually the case, to respond spon- 

 taneously with the formation of specific antibodies, it has been a 

 matter of doubt whether or not passive immunization, that is, the 

 introduction of specific antibodies in the form of the serum of a 

 highly immunized animal, is therapeutically of value. Indeed, it 

 has been feared that the use of such sera may even be harmful in 

 that the sudden introduction of large amounts of bactericidal sub- 

 stances might lead to a sudden liberation of large quantities of poi- 

 sonous products and consequent rapid toxemia. 



The conditions in such cases are exceedingly complex and many 

 gaps exist in our knowledge concerning them. The bacteria when 

 invading the body, immediately enter into conflict with the protective 

 forces, as we have stated in the chapter on Infection. If a consider- 

 able degree of resistance exists, let us say as the result of preceding 

 immunization or a recent attack of the disease, there is a rapid 

 destruction of the bacteria, probably by active phagocytosis. It has 

 been shown by Bordet in the case of cholera and more recently by 

 Gay with typhoid, that injection of the organisms into immunized 

 animals is followed by prompt and high leukocytosis, whereas sim- 

 ilar injections into normal animals usually induce a temporary leuko- 

 penia. When the invaded animal is not particularly resistant the 

 bacteria may accumulate and, as in the case of pneuraococci and 

 streptococci, develop phagocytosis-resisting properties (capsule forma- 

 tion, etc.) ; or, as in the case of typhoid bacilli, there may be an 

 immediate liberation of toxic substances (anaphylatoxins) by reac- 

 tion between bacterial cell and blood plasma, w r hich can induce leuko- 

 penia, and by this means the organisms may be protected from 

 phagocytic destruction. Experience with curative sera in all of the 

 conditions of this class has yielded promising results only when the 

 cases have been treated with the sera at early stages of the disease, 



