124 RECOVERY FROM INTOXICATIONS 



by supposing that the receptors of the sensitive cells were occupied 

 by the inert toxoid, so that part of the cells would be unable to 

 combine with the true toxin. The subsequent susceptibility he 

 explains by the over-production of new receptors. Now when 

 we consider that in acute disease of natural occurrence the pro- 

 duction of toxin (in cases that recover) is only temporary, and is 

 stopped sooner or later by the destruction of the bacteria, it seems 

 probable that some such process may occur and serve to shorten 

 the period during which the cells are exposed to the action of the 

 toxin. The true toxins are so fragile that it is highly probable 

 that a certain proportion of them are converted into toxoids during 

 or after the process of absorption into the blood-stream, and by 

 occupying their receptors diminish the susceptibility of these cells 

 to the true toxin, which, circulating in the blood, may be dealt 

 with by the leucocytes, liver, or other organs. Afterwards anti- 

 toxin would appear in the blood, but it would have no relation to 

 the early slight immunity of the tissues. 



We may therefore recognize the following stages in the process 

 of recovery from a bacterial intoxication : 



1. In the first the processes are mainly non-specific, the chief 

 being probably leucocytic action ; the dilution of the toxin in the 

 general blood-stream, and its elimination, either in a natural con- 

 dition or after it has undergone some chemical alteration ; the 

 partial destruction and conversion of toxin into toxoids, and sub- 

 sequent " blocking " of side-chains in highly important tissues. 

 In mild cases these may be sufficient for the restoration of health, 

 and no immunity, or the merest trace, may follow. 



2. Where the process lasts longer antitoxin begins to be pro- 

 duced, and in all probability the time which must elapse before 

 this occurs varies greatly in different conditions, depending on : 

 (a) the constitution of the patient, (b) the dose of the toxin, and 

 (c) on the nature of the toxin. Thus, with regard to the last 

 point, it may be remarked that it appears to be extremely 

 difficult to prepare antitoxins to the endotoxins, and it is highly 

 probable that in recovery from such diseases as cholera and 

 typhoid fever the production of antitoxin is slight or absent. 

 Such diseases owe their symptoms mainly to the production of 

 endotoxin, and are combated mainly by the removal of the 

 bacteria which produce them. In the cases in which antitoxin is 

 produced, recovery at this stage depends on its presence, together 

 with the functional efficiency and sufficient numbers of the leuco- 



