The progress of an infection is usually associated with marked changes in the serum proteins. There may be an increase in the percentage of the total protein during some stage of the infection, and there is usually a change in the albumin-globulin ratio with an increase in the total globulins. This rise may antedate the development of any resistance by a considerable period of time.

The non-protein constituents of the blood show fluctuations with a tendency to rise as the infection progresses.

The process of immunization is in almost all instances associated with a definite increase in the globulins of the blood, and in some cases with a complete inversion of the normal albumin-globulin ratio. This may be produced both by living and dead organisms and by bacterial endotoxins. Massive doses usually result in an upset which shows no tendency to right itself during the period of observation.

A rise in the globulins has been shown to occur long before the animal develops immune bodies in any appreciable concentration; and where the globulin curve and antibody curve appear to parallel one another, it can be shown by a careful analysis of both curves that there is a definite lack of correspondence at various periods of the experiment.

Animals possessing a basic immunity show a more rapid rise in the globulin curve following inoculation.

There is no parallelism between the leukocytic reaction and the globulin reaction. During periods of leukopenia the globulins may be as high as during the period of a leukocytosis.

Bacterial endotoxins produce as striking an increase in the serum globulins as do living and killed bacteria. This would seem to indicate that a bacterial invasion of the organism is not absolutely essential for the globulin changes, and that the toxogenic factor in infection and immunity must play a part in the production of the changes noted.

Inflammatory irritants injected intraperitoneally also result in a globulin increase. In this case the changes produced may best be explained by the toxogenic effect produced by the protein split products resulting from the inflammatory condition.

Intraperitoneal injections of killed bacteria give rise to a more rapid increase in the serum globulins. The rapidity of the response following intraperitoneal as compared with intravenous injections doubtless stands in intimate relationship to the neutralizing power possessed by the blood serum and perhaps to the more extensive surface of absorption following injection by the intraperitoneal route.

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