142 ANAPHYLAXIS 



clear that the susceptible cells would become even more liable to 

 attack by the toxin. 



Probably belonging to the same order of cellular hypersuscepti- 

 bility is also the increased susceptibility of the tubercular organism 

 to the introduction of tuberculin in doses which in the normal 

 individual produce no reaction whatever. We may here imagine 

 that in tubercular foci, sessile receptors are present in large numbers 

 which possess a greater affinity for the tubercular antigen (tuber- 

 culin) than do the receptors of any normal cells, and that these 

 receptors eagerly take up the corresponding antigen, when this is 

 introduced from without. The specific reaction which then takes 

 place we can conceive to be due to an interaction between antigen 

 (tuberculin) and antibody (receptor), with the consequent produc- 

 tion of toxic products and their action upon the cells in question. 

 This view is supported by the discovery on the part of Wassermann 

 and Bruck that tubercular organs actually contain specific sub- 

 stances which will combine with tubercular antigen, as can be 

 demonstrated with the complement fixation method (which see). 



Richet's Early Investigations. A marked impetus to the study of 

 hypersusceptibility was then given by certain observations of Richet 

 (1902). This investigator found that the intravenous injection into 

 dogs of extracts made from the tentacles of certain actinise pro- 

 duced marked toxic symptoms (excitement, bloody diarrhea, and 

 subnormal temperature), which appear after a certain interval, then 

 increase in severity during the first two days, and lead to a fatal 

 issue only at the expiration of the third day. Post mortem he found 

 marked congestion of the viscera (stomach, intestines, liver, and 

 kidneys), and he accordingly termed the toxic principle in question 

 actinocongestin. He further ascertained that very curiously the 

 immediate repetition of a fatal dose of the poison never produced 

 sudden death, but that the end was invariably delayed until the 

 expiration of the third day. If now an animal is injected with a 

 non-fatal dose of the poison, and after recovery from its effects is 

 reinjected with an amount which in an animal that had previously 

 not been injected would produce no deleterious effects whatever 

 (such as one-twentieth of the original quantity), most serious 

 symptoms develop at once and the animal dies within twelve to 

 twenty-four hours. In a concrete case 0.08 gram was used in the 

 first injection without producing any vomiting, while a reinjection 



