Page:Popular Science Monthly Volume 75.djvu/19

Rh 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 inoculation 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, multiplication is prevented, and the animal escapes severe illness.

The value of hyperleucocytosis as a defensive measure against infection must, probably, always remain greater than its value as a cure for established infection. There are several reasons that make this conclusion 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 chemical agents that provoke hyperleucocytosis than the uninfected organism. And yet we may see the operation of the benign influence of hyperleucocytosis, 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 hyperleucocytosis 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