228 ANAPHYLAXIS 



If for the second injection only a small dose of serum is administered, or it is intro- 

 duced intraperitoneally instead of intravenously, acute death does not result and the 

 picture is similar to that given by the anaphylactic dog (Pfeiffer and Mita). The 

 guinea-pigs become very restless, move about continuously and are very easily fright- 

 ened. Their hair becomes raised, and isolated clonic muscular contractions may be 

 observed. Continuous hiccough sets in and evacuation of urine and f eces, first formed 

 and later fluid occurs. The abdominal muscles become spastically rigid and at times a 

 severe pruritus of the skin probably exists. Following this transient period of excita- 

 tion the animals enter into a stage of depression. They stagger about or fall to one side 

 and remain for hours as if paralyzed; breathing is slow and superficial. In the midst of 

 these symptoms the temperature falls abruptly, often as many as 7 to 13 C. Death 

 is due to a paralysis of the peripheral blood-vessels and takes place usually in one to 

 two hours, sometimes four to eight hours, being always preceded by Cheyne-Stokes 

 respiration. 



The symptoms of the anaphylactic shock simulate very closely 

 Relation to those occasioned by peptone poisoning, as seen after intra- 

 Peptone venous injection of Witte's peptone, for example. Biedl and 

 img ' Kraus thus considered that anaphylaxis was a manifestation 

 of peptone poisoning. They believed that through immunization with 

 proteids, antibodies of a ferment nature were stimulated, and that these 

 split up the proteids into peptones. According to these authors, animals 

 exposed to peptone poisoning become hypersensitive, and vice versa, 

 animals that recover from an anaphylactic attack withstand poisoning by 

 peptones. The production of anaphylatoxin in vitro, and the demonstra- 

 tion by Pfeiffer that peptone is formed in the test-tube during this process, 

 further added to the support of their theory. 



This hypothesis cannot as yet be definitely accepted. In 

 Toxopeptid. the first place Manwaring was unable to confirm the experi- 

 ment that recovery of an animal from an anaphylactic shock 

 renders it refractory toward future peptone poisoning. Furthermore, 

 M. Wassermann and Keysser mixed kaolin + inactive immune serum + 

 complement and obtained a poison which caused the same disturbances as 

 anaphylatoxin. Since kaolin is no proteid and cannot be split up, the 

 anaphylactic symptoms in this instance cannot be due to a peptone as a 

 split product of the antigen. 



M. Wassermann and Keysser have a different conception of the nature of anaphy- 

 laxis. The antigen serves in a physical chemical capacity to fix the amboceptor. By 

 the addition of complement the amboceptor is broken up with the formation of "Toxo- 

 peptids," and it is these which stimulate the anaphylactic phenomena. Passive 

 anaphylaxis is explained by the passive transmission of the specific amboceptors; the 

 antigen itself plays no chemical role; it is not split up. The difference between ana- 

 phylaxis and immunity lies in that in the former the complement under cover of 

 the antigen digests the amboceptor alone, while in the state of immunity the strength 

 and number of amboceptors are very much greater and the activity of the complement 

 extends not only to the amboceptor but also to the secondarily attached antigen. 



