IMMUNITY TO TOXINS IIQ 



tion, in spite of the presence in the blood of amounts of antitoxin 

 sufficient to neutralize the toxin many times over. Similar appear- 

 ances may be seen in animals in which death from acute intoxica- 

 tion does not occur. Thus, in two horses which were treated at 

 the same time for the production of diphtheria antitoxin, one 

 showed but little sign of the action of the toxin, and improved in 

 general health during the treatment it developed only 5 units of 

 antitoxin per cubic centimetre of serum ; the other suffered severely 

 in general health, and had ultimately to be killed it developed 

 70 units per cubic centimetre. Similar phenomena are often met 

 with, and, as a general rule (to which there are numerous excep- 

 tions), the presence of a large amount of antitoxin in the blood 

 indicates susceptibility rather than immunity. The facts of the 

 later stages of antitoxin-formation may also be borne in mind. 

 Sooner or later in the history of any antitoxin horse there comes a 

 time when the amount of antitoxin begins to diminish, and would, 

 in all probability, disappear entirely if the injections were con- 

 tinued ; yet these horses are extremely resistant to the action of 

 toxin more so, in fact, than animals with much antitoxin in the 

 blood. The degree of immunity, therefore, is not measured by 

 the amount of antitoxin in the blood, and we might argue that the 

 two are not related in any way. This, however, is absurd, in 

 view of the ascertained action of antitoxin in neutralizing the 

 effects of toxin in vitro, or of protecting against a dose surely fatal. 

 We may consider the role of antitoxin under two heads : (i) in 

 immunity, and (2) in recovery from disease. 



Considering first the question why an animal dies in spite of the 

 presence of an excess of antitoxin in the blood, we must regard 

 the simplest and most probable explanation as one on which the 

 toxin-antitoxin molecule is looked upon as dissociable. This is 

 always the case on Arrhenius and Madsen's theory of the inter- 

 action of the two substances, whilst on the colloid theory the dis- 

 sociation only takes place for a short time after the compound has 

 formed, the union between the two substances gradually becoming 

 firmer and firmer. On this supposition the failure of antitoxin is 

 readily explicable : the two substances unite, and the inert mole- 

 cule is formed ; this dissociates, and the toxin-molecules, which 

 happen to be set free in the neighbourhood of susceptible cells, 

 unites with them. The removal of some of the molecules of toxin 

 allows more dissociation to take place, and ultimately the whole of 

 this substance is passed on to the tissues. We must assume that 



