848 IMMUNOLOGY 



curve is extraneous to the present discussion, but is interesting because 

 of the stiletto-hke peaks it shows at each sporulation. Some work on the 

 infection after the crisis has been done on human malaria by Bohm 

 (1918), Knowles and Das Gupta (1930), and Sinton et al. (1931). 



Throughout the developed infection, an equilibrium is established 

 between the number of parasites killed and the number produced. Later, 

 the defensive factors are usually successful in suppressing the parasites 

 arising by reproduction, so that latency ensues. Latency may last for 

 years, but may be interrupted by relapses. Although there is no unanimity 

 of opinion on the mechanism of relapse, the best evidence indicates that 

 it represents simply the removal of the defensive factors, so that the 

 parasites, which are continuously reproducing at a constant rate, reaccu- 

 mulate in the blood. The relapse may be fatal, or the defensive factors 

 may again materialize and successfully suppress it. Accordingly, the 

 severity of the relapse depends upon its extent and upon the length of 

 time the defensive factors are removed. These statements are substanti- 

 ated by work on P. cathemerium and P. brasilianum, references for which 

 have already been given. 



Koch (1899) believed that immunity persisted after complete re- 

 covery, but Wasielewski (1901) suggested, and subsequent workers 

 have supported the conclusion, that parasites remain in small numbers 

 for longer periods than was at first supposed and that this latent infection 

 accounts for the long continued immunity (see Thomson, 1933, review; 

 Chopra and Mukherjee, 1936; Sergent, 1936). More recently, Nauck 

 and Malamos (1935) and Coggeshall (1938) have shown that a certain 

 amount of immunity is retained after complete cure of P. knowlesi. 



Acquired immunity to malaria can be demonstrated not only by the 

 crisis, recovery from initial infection, and recovery from relapse, but by 

 superinfection. Such immunity is usually species-specific or even strain- 

 specific in human, simian, and avian infections. A series of investigators, 

 beginning with Koch (1899), have worked on this aspect of the subject 

 (for literature and for especial work, see W. H. Taliaferro and L. G. 

 Taliaferro, 1929a, 1934c; Gingrich, 1932; Mulligan and Sinton, 1935; 

 M. F. Boyd et al, 1936; Manwell, 1938; Redmond, 1939; and Manwell 

 and Goldstein, 1939). The work on human malaria has been recorded 

 chiefly as a result of the use of therapeutic infections in the treatment 

 of paresis (see Mulligan and Sinton, 1933a). W. H. Taliaferro and 



