IMMUNITY TO TOXINS 121 



particles are taken up by these cells. Further, the injection of 

 toxin into an animal which already contains antitoxin in the blood 

 brings about a more or less marked leucocytosis. It is true that 

 the local leucocytosis brought about by the injection of neutral 

 mixtures of the two may be but slight, but we must remember 

 that substances in a state of solution are quickly absorbed and 

 carried to the lymph glands or bloodvessels, in either of which 

 situations leucocytes occur in plenty. Further, there are always 

 some leucocytes in the tissues, and the number may be sufficient 

 to deal with the amount of toxin-antitoxin injected, which, con- 

 sidered as mere weight, is always very small. 



The effect of antitoxin on the toxin of B. pyocyaneus may also be 

 cited as a phenomenon capable of explanation on this supposition. 

 A few lethal doses of toxin are fully neutralized by antitoxin, the 

 law of multiple proportions holding up to a certain point. When, 

 however, more than ten lethal doses are injected the law does not 

 hold, and no amount of antitoxin will avert the fatal issue. Here 

 we must assume that the antitoxin has but a slight affinity for the 

 toxin, so that dissociation takes place rapidly, and the ultimate 

 cause of the destruction of the toxin to be leucocytic activity. 

 The single lethal dose is just more than the leucocytes can deal 

 with ; but when antitoxin is injected simultaneously the leucocytes 

 have time to come into action, and the toxin, gradually set free by 

 dissociation, is dealt with in detail instead of in a single dose. 

 There are, however, limits to this process, and when more than 

 ten lethal doses are present fully combined with toxin we must 

 imagine that dissociation goes on so rapidly that more toxin than 

 one lethal dose is set free before the toxin-antitoxin molecules can 

 be taken up. If this explanation is highly theoretical, it seems 

 the best that is available at present. 



The difference between the effect of toxin in animals with anti- 

 toxin in the blood, but otherwise normal, and its effect in animals 

 in the early stage of antitoxin formation, is explicable if we regard 

 the hypersensitiveness as occurring in the leucocytes themselves 

 as well as in the tissues. When antitoxin is injected into a normal 

 animal, the leucocytes of which are functionally active, the con- 

 ditions for the immediate destruction of the inert molecule are 

 present, and no dissociated toxin gains access to the susceptible 

 tissues. But in hypersensitive animals the leucocytes will be 

 unable to deal with the molecule, or will perhaps be killed by toxin 

 liberated by dissociation taking place within their protoplasm, and 



