696 INFECTION BY THE BLOOD PROTOZOA 



or later, however, as the acquired resistance is built up, a large proportion of the parasites 

 are killed. There may then be a temporary relapse, but eventually the destruction of the 

 parasites equalizes or exceeds the number produced by reproduction, and the chronic period 

 or low grade of blood infection ensues. In time, the destruction becomes so great that no 

 parasites can be found in the blood (latent period) , but their presence can be demonstrated 

 by Whitmore's technique. This continues until some condition, such as the injection of 

 adrenalin, temporarily stops the destruction and the parasites accumulate again, causing a 

 relapse. 



Ross and Thomson (igiob) have made a very precise enumerative study of 

 infections of human malaria. From their work and the general observations 

 of other workers, it seems probable that the course of infection of both P. vivax, 

 the benign tertian parasite, and P. malariae, the quartan parasite, is very similar to 

 that of bird malaria. On the other hand, it is difficult to analyze the effects of resist- 

 ance in P. falciparum, the parasite of malignant tertian fever, as well as of certain 

 avian malarial parasites, because schizogony does not occur in the peripheral blood. 



Although there is no conclusive evidence as to the defense mechanism involved 

 in the destruction of the malaria parasites to such a great degree at the crisis and 

 to a lesser extent throughout the remainder of the infection, a number of recent 

 investigations on bird malaria have a bearing on this point. It seems very probable 

 from the work of Ben Harel (1923), and from the well-established fact that an en- 

 larged spleen containing many parasites occurs after the crisis, that the wandering 

 mononuclears and fixed-tissue phagocytes of the spleen and other organs ingest the 

 parasites at the crisis and during the latent infection. Furthermore, the author and 

 L. G. Taliaferro have shown (1927) that if a large number of washed parasitized cells 

 are injected intravenously into an infected canary during the latent period, they are 

 quickly removed from the circulation (probably by the phagocytes), whereas in a 

 normal canary they are not removed but steadily increase in numbers until the death 

 of the canary or until a crisis ensues (Fig. 11). One very interesting feature in this 

 work is that the parasites are being removed from the peripheral blood continuously 

 — a fact which is not in accord with Bass and Johns' (191 2) assumption that the great- 

 est hazard is when the parasite is passing from one cell to another. Evidently, there 

 is some factor in the blood stream of the infected bird which afifects either the para- 

 sites or the phagocytes or both. All attempts to show that this factor is an antibody 

 have failed. The author and L. G. Taliaferro have been unable either to sensitize 

 infected red cells with serum from infected birds in the latent period or to obtain a 

 passive transfer of the lethal factor. This might be taken to indicate that the para- 

 sites simply injure the red cells to such a degree that they are phagocyted, but such 

 an assumption is not tenable because the same infected cells are not phagocyted by 

 the normal uninfected bird. The failure to obtain evidence of an antibody together 

 with the recent work of Hegner and MacDougall (1926) and MacDougall (1927) 

 suggests that the factor which kills the parasites or which makes the parasite-red- 

 cell combination phagocytable is connected with the simpler serum constituents. 

 Hegner and MacDougall have found that increasing the blood sugar by feeding solu- 

 tions of glucose brings about conditions favorable to the accumulation of the parasites 

 in the blood, whereas decreasing the blood sugar by injecting insulin prt)bably inhibits 



