AM TURK OF THE PROTECTIVE DEFENCES OF THE BODY 167 



Up to the present time the mechanism of the increased production of 

 receptors following the .binding of the haptophore group to the recep- 

 tor has not been experimentally proven. Wassermann, however, 

 believes that he and Bruck have now been successful in this. Although 

 I consider his interpretation as most interesting, yet both this and the 

 reasoning from it are far from proven. 



They employed a tetanus poison kept since 1896. This poison was 

 originally very toxic. In the course of years, however, owing to the 

 damaging influence of this long standing, that is, owing to the action 

 of light, the oxygen of the air, etc., it had become so weak that it was 

 no longer toxic at all. They were able to give a guinea-pig 1 c.c. with- 

 out producing tetanus. Nevertheless, haptophore groups had re- 

 mained intact, as could readily be proved, for this non-poisonous tetanus 

 toxin was still able to bind tetanus antitoxin i. e., thrust-off receptors. 

 When they injected rabbits with this non-poisonous tetanus toxoid in 

 increasing doses, and then examined the blood serum of the animal, 

 they found not a trace of tetanus antitoxin. They considered the absence 

 of antitoxin in this experiment could have either of two causes : 



1. It might be that the toxoid no longer produced any physiological 

 effect whatever in the organism; or 



2. Although it still caused an increase in the receptors in the cells, 

 these increased receptors remained in them, and were not thrust off 

 into the blood. 



In order to decide this question they first determined as nearly as pos- 

 sible the exact quantity of fresh tetanus toxin which constituted a fatal 

 dose for guinea-pigs of a definite size. If, now, the action of the tetanus 

 toxoid was such that in the living organism it was not bound to the 

 receptors, it should be possible to prove this experimentally. 



Their line of reasoning was as follows: Were they to inject first the 

 toxoid, and shortly after, say, in one to two hours, the fresh toxin, they 

 would in such an animal have to increase the fatal dose i. e., they 

 would require more tetanus toxin to kill this animal than an untreated 

 one, because owing to the previous toxoid injection the most sus- 

 ceptible cell receptors had already been occupied. Provided Ehrlich's 

 theory was correct, so that this binding of the toxoid really occurred, 

 the conditions should be entirely different when, instead of injecting 

 the toxin shortly after the toxoid, they waited somewhat longer, one 

 to three days, and then injected the fresh tetanus toxin. For in that 

 case Weigert's law should come into play and the receptors have com- 

 menced to increase in numbers i. e., the organ would now possess 

 more sensitive groups than before. This would have to manifest itself 

 in such fashion that in contrast to the first experiment the fatal dose 

 of fresh tetanus toxin could no\v be decreased; in other words, a small 

 dose would now tetanize the animal in a shorter time. 



As a matter of fact, the experiments yielded results which were 

 exactly like those deduced theoretically as just described. They in- 

 jected a guinea-pig with some of the non-poisonous toxoid, and then, 

 one hour later, with the tetanus toxin. They found that much more 



