RESISTANCE TO INFECTIOUS DISEASE 15 



guinea-pig, symptoms of poisoning quickly set in and death results in 

 a few hours. A study of the conditions present in the peritoneal cavity 

 shows that the bacteria have developed freely, that some have been broken 

 up and disintegrated, and that very few preserved phagocytes can be 

 found. Examination of the blood reveals that the number of leucocytes 

 in the general circulation has been reduced ; and all the evidences point 

 to the conclusion that not only has phagocytosis not taken place, but 

 that there has been a general destruction of leucocytes produced by the 

 cholera poison. If, however, there be introduced into the peritoneal 

 cavity of a guinea-pig twelve to twenty-four hours prior to the inocula- 

 tion of the cholera bacilli, a small amount of sterile salt solution, or 

 bouillon, or one of the other chemicals mentioned, which procedure will 

 bring into the peritoneum a considerable number of leucocytes at the 

 same time that it causes a rise of leucocytes in the circulating blood, 

 then the cholera germs are quickly taken up by the phagocytes, multi- 

 plication is prevented, and the animal escapes severe illness. 



The value of hyperleucocytosis as a defensive measure against infec- 

 tion must, probably, always remain greater than its value as a cure for 

 established infection. There are several reasons that make this con- 

 clusion probable : the capacity of the blood is increased in the direction 

 of destroying bacteria without being augmented at the same time in the 

 direction of neutralizing bacterial poisons; the organism that is 

 already severely poisoned by infection reacts less certainly to the chemi- 

 cal agents that provoke hyperleucocytosis than the uninfected organism. 

 And yet we may see the operation of the benign influence of hyper- 

 leucocytosis, associated with an increased passage of alexin-containing 

 lymph through the vessels, upon certain local infections at least, in the 

 results of measures that determine an augmented supply of blood to a 

 diseased part; in the mechanical hyperemias produced through posture 

 or superheated air; the influence (in part) of tuberculin injections; 

 and the effects of poultices and embrocations, of counter-irritants, and 

 of certain of the phenomena of local inflammation. 



The facts at our command point to the great potential power of the 

 normal organism to resist infection and indicate that the normal 

 body possesses the capacity, on demand, to increase this power beyond 

 the mean value, chiefly by opposing intending infection by hyper- 

 leucocytosis and also, probably, by the strengthening of its plasmatic 

 defensive action through the additional soluble alexin substances 

 thrown off by the augmented leucocytes. This defensive mechanism 

 acts in the same manner on all bacterial invaders and is not specially 

 adapted for any one or group of bacteria. The form of activity is 

 strictly non-specific. 



Let us now ask ourselves if in overcoming infectious disease, which 

 luckily the organism is frequently able to accomplish, the mechanism 

 put into operation is similar and only more intense than the one we 

 have considered for warding off infection ? The answer to this question 



