alcohol and other poisons, or are exposed to abnormal cold by shaving of the skin, are more subject to certain infections than animals not so treated. If, now, it were found that the blood factors governing resistance fluctuated with these influences, became smaller and less conspicuous when the influences were bad and larger and more efficient when the influences were good, we should then have established an important concrete fact.
But the alexinic activity of the blood varies normally within such wide limits that only maximal changes could be regarded as significant, and it appears that it is only as the fatal termination of certain severe infections are reached—such as experimental anthrax and pneumococcus infections, for example—that the alexinic power falls greatly or disappears altogether. The determination of phagocytic activity outside the body has not thus far been carried out in such a manner as to indicate a functional depression which either precedes immediately or develops in the course of severe infections; although certain infections which take a severe course are characterized by a persistent reduction in the number of leucocytes in the circulating blood. This latter phenomenon must, however, probably be regarded as an effect and not as the cause of the infection. There is, however, known at least one example where paralysis of the phagocytes leads to a fatal infection under conditions in which the normal phagocytes are entirely competent to prevent infection. If to a guinea-pig a small dose of opium be administered and this is followed by the injection of a non-lethal quantity of a culture of the cholera bacillus, death will ensue because the sensitiveness of the phagocytes to the chemical stimulus exerted by the cholera poison has been diminished by the narcotic influence of the opium.
The mean phagocytic value of the blood can, however, be definitely raised by certain agencies, that are at the same time and through the rise in the number of phagocytes produced, useful in warding off and sometimes even in overcoming infection. The means employed to bring about an increase of leucocytes, or to establish a hyperleucocytosis, suffice to maintain the high value for short period relatively only, unless the stimulus is frequently repeated. A cold bath, a sun bath, the injection into the circulation of a number of simple chemical substances—peptone, albumose, nucleinic acid, spermin, pilocarpine—are all followed under physiological conditions by hyperleucocytosis and by a temporary state of increased resistance to bacterial invasion. Moreover, in certain experimental infections, at least, there can thus be aroused a heightened power to overcome established infections—those caused, for example, by the cholera, meningitis and pneumococcus germs. Perhaps the most striking example of the protective influence of hyperleucocytosis is afforded by the experimental infection described under the name of cholera peritonitis of the guinea-pig. If a fatal quantity of cholera germs be injected into the peritoneal cavity of a