PROTEIN SENSITIZATION OR ANAPHYLAXIS 329 



2. This specific proteolytic ferment stored up in the 

 cells of the animal as a result of the first treatment with 

 the protein remains as a zymogen until activated by the 

 reinjection of the same protein. 



3. Our conception of the development of a specific 

 zymogen supposes a rearrangement of the atomic groups 

 of the protein molecules of certain cells, or an alteration 

 of their molecular structure. In other words, we regard 

 the production of the specific zymogen not as the formation 

 of a new body, but as resulting from an alteration in the 

 atomic arrangement within the protein molecule, and a 

 consequent change in its chemism. 



4. Some proteins in developing the specific zymogen 

 produce profound and lasting changes in molecular struc- 

 ture, while the alterations induced by others are slighter 

 and of temporary duration, the molecular structure soon 

 returning to its original condition. 



5. Bacteria and protozoa are living, labile proteins, while 

 egg-white, casein, serum albumin, etc., are stabile proteins. 

 The proteins of one group are in an active, while those of 

 the other are in a resting state, but both are essentially 

 proteins made up of an acid or poisonous chemical nucleus, 

 and basic, non-poisonous groups. Bacterial immunity 

 and protein sensitization, apparently antipodal, are in 

 reality the same, and each consists in developing in the 

 animal body the capability of splitting up specific proteins. 

 If the living protein be split up before it has time to multiply 

 sufficiently to furnish a fatal quantity of the poison, the 

 animal lives and we say it has been immunized. If the 

 stabile protein be introduced into the animal body it 

 leads to the development of a specific proteolytic ferment, 

 and if enough of it to supply a fatal dose be reinjected after 

 this function has been developed, the animal dies. 



6. We are compelled to change our ideas concerning 

 the causation of the lesions of the infectious diseases. 

 Formerly, we believed the structural changes to be due 

 wholly to the living, growing, feeding microorganisms. 

 For instance, we were sure that the intestinal ulcerations 



