850 IMMUNOLOGY 



1, Figs. 1 and 2). When the parasites disappear from the peripheral 

 blood at the time of the crisis, they are not at first phagocytosed, but are 

 filtered out and concentrated in the Billroth cords of the spleen (Pl.'l, 

 Fig. 3). This initial manifestation of acquired immunity probably repre- 

 sents a localization of the parasites due to an antibody, which may be an 

 agglutination, as demonstrated in vitro in P. knowlesi by Eaton (1938), 

 or an attachment of parasites to the macrophages, as found in cultures 

 of P. falciparum by McLay (1922). In a few hours or days the con- 

 centrated parasites are ingested in great numbers by the macrophages 

 (PI. 2, Figs. 1 and 2), owing undoubtedly to an opsonification of the 

 parasites and parasitized red cells by antibody. This antibody probably 

 accounts for the protective property of serum taken from latent infections 

 in avian malaria (Findlay and Brown, 1934), in human malaria (Soti- 

 riades, 1917; Kauders, 1927; Neumann, 1933; and Lorando and Soti- 

 riades, 1937), and in simian malaria (Coggeshall and Kumm, 1938; 

 Coggeshall and Eaton, 1938). The fact that protective antibodies have 

 not always been found (W. H. Taliaferro and L. G. Taliaferro, 1929b 

 and 1934b) led W. H. Taliaferro and Cannon (1936) to suggest that 

 antibodies are produced locally in sufficient quantities to be operative in 

 the specific organs in situ, but not in sufficient quantities to be easily 

 demonstrated in the peripheral blood. A day or two after concentration in 

 the Billroth cords, the parasites are quickly digested except for the ma- 



CAPTION FOR PLATE ON FACING PAGE 



Plate 1. Sluggish phagocytosis of Plaunodium brasiliaiium by macrophages in control 

 of the American monkeys during the acute rise of the malarial infection (Figs. 1 and 2) 

 and the concentration of P. braiilianum in Billroth cords of the spleen at the initiation 

 of the crisis (Fig. 3). X 1450. (From W. H. Taliaferro and P. R. Cannon, "Cellular 

 Reactions during Primary Infections and Superinfections of Plasmodium Brasilianum and 

 Panamanian Monkeys," Journal of Infectious Diseases, LIX {July-August, 1936], 72- 

 125.) 



Figure 1. A Kupffer cell in the liver containing a parasite, an unparasitized erythrocyte, 

 and four small masses of malarial pigment. Acute rise of infection. 



Figure 2. Two macrophages in a Billroth cord in the red pulp of the spleen, containing 

 a small number of residues of parasites, red cells, and malarial pigment. Acute rise of 

 infection. 



Figure 3. Large numbers of parasitized erythrocytes concentrated in Billroth cords of 

 the spleen. Note that parasites are absent from the venous sinus. Also note that the 

 macrophages in the Billroth cords show the sluggish phagocytosis characteristic of the 

 acute rise and that the littoral cells lining the sinus are not phagocytic. Initiation of 

 crisis of infection. 



