Malaria 601 



Coast, Nigeria, Sierra Leone, Uganda, West Africa), from Palestine, 

 western South America, and the Philippines. However, ovale malaria 

 seems to be rare wherever it has been found. The ecology of the Plas- 

 modhirn-Anopheles complex is not yet known well enough to explain 

 these differences in distribution, although the biothermal range of the 

 parasites may be a factor in some cases. P. vivax, for instance, apparently 

 does not develop in Anopheles quadrimaculatus at temperatures much 

 above 30° (111), whereas such temperatures seem to be satisfactory for 

 P. falciparum. 



The evolutionary relationships of human malarial parasites and those 

 of apes are suggested by the apparent morphological identity of P. vivax, 

 P. falciparum, and P. malariae with P. schxuetzi Brumpt, P. reichenowi 

 Sluiter and Swellengrebel, and P. rodhaini Brumpt. In fact, it is debatable 

 whether these parasites of apes are specifically different from those of man. 

 Apparent physiological differentiation does indicate that P. vivax and 

 P. falciparum and their homologues in apes are distinct strains. P. 

 schxuetzi (85, 88, 89) and P. reichenoivi (6, 88) have failed to infect 

 artificially inoculated men, and P. falciparum has not infected chimpan- 

 zees under similar conditions (71). P. vivax, upon inoculation into 

 chimpanzees, occasionally produces a subpatent infection which persists 

 for several weeks without loss of virulence for man (85). The differentia- 

 tion of P. malariae and P. rodhaini seems to be less marked. Inoculation 

 of P. rodhaini into man has led to mild symptoms of quartan malaria and 

 the appearance of parasites showing the characteristics of P. malariae 

 (86). Strains of P. malariae also have proven infective for chimpanzees, 

 in which they retain their virulence for man (87). 



THE LIFE-CYCLE OF MALARIAL 

 PARASITES 



Exo-erythrocytic phase 



For many years protozoologists were puzzled by the failure to 

 find malarial parasites early in an infection. The rather abrupt appear- 

 ance of parasites later on led to a suspicion, expressed clearly by Grassi 

 in 1900 and later by James (54), that sporozoites develop outside the 

 blood before invading erythrocytes. The confirmatory evidence is now 

 conclusive. 



Experimental inoculations have indicated that parasites disappear 

 from the blood soon after introduction of sporozoites, are absent for 

 some time, and then suddenly reappear. Blood transfusions, within 7-30 

 minutes after inoculation of sporozoites, have transferred P. vivax and 

 P. falciparum to the recipients. Transfusions made after more than 30 

 minutes have given negative results (42). The blood does not become 

 infective again until about the eighth day with P. vivax (25, 42) and 



