622 Malaria 



native population has had many generations in which to practice "pre- 

 munition" relatively undisturbed by chemotherapy. 



From the practical standpoint, malarial therapy faces two problems 

 (90): suppression of the erythrocytic phase in both clinical prophylaxis 

 and clinical cure of primary attacks and relapses; and the elimination of 

 exo-erythrocytic stages. Solution of the second problem is much the more 

 difficult, but there is no true cure until exo-erythrocytic stages have been 

 eradicated. Suppressive therapy brings relief to the patient, and by elim- 

 inating erythrocytic stages for the moment, temporarily eliminates a 

 source of infection for mosquitoes. However, effective suppressive treat- 

 ment is often followed by relapse, especially in vivax malaria. In terms 

 of modern concepts, such a suppressant has been ineffective against exo- 

 erythrocytic stages. 



Quinine, the traditional malaricidal drug, is a good suppressant, al- 

 though its activity may vary with the strain of parasites and especially 

 so in falciparum, malaria. Atebrin (atabrine, mepacrine, quinacrine) is 

 active against erythrocytic stages of all species, and is valuable also in 

 clinical prophylaxis. Both atebrin and quinine cause morphological 

 changes in trophozoites of P. vivax, as seen in blood films a few hours 

 after treatment (65a), but neither has any marked action on exo-erythro- 

 cytic stages. Chloroquine, which is well tolerated even by infants and is 

 an effective suppressant for vivax, falciparum, and quartan malaria (4, 

 40), also has little effect on exo-erythrocytic stages. Pentaquine, although 

 a poor suppressant, shows apparent activity against E-E stages (62). 

 Plasmochin (pamaquine, plasmoquine) is just a fairly satisfactory sup- 

 pressant for tertian and quartan malaria, but seems to be active against 

 E-E stages (62). However, the effects of plasmochin may vary with the 

 strain, in view of its failure to prevent relapse in mosquito-induced in- 

 fections with the Chesson strain of P. vivax (37). In fairly heavy dosage, 

 plasmochin is said to be an effective prophylactic against P. vivax and P. 

 falciparum (93), but the toxicity of the drug would seem to limit its 

 usefulness for this purpose. Paludrine (proguanil, chloroguanide), which 

 seems to be a fairly good suppressant for vivax and falciparum malaria 

 and is particularly active against pre-erythrocytic forms of P. falciparum 

 (63, 66), has an interesting delayed effect on both species. Gametocytes 

 mature in the treated patient and syngamy occurs after ingestion of 

 gametocytes by the mosquito. However, the resulting oocysts fail to ma- 

 ture in the vector (43, 63). Camoquin, another new drug, seems to be 

 about as good a suppressant as chloroquine and has given excellent re- 

 sults when administered in a single dose for moderate to heavy infections 

 with P. vivax and P. falciparum (49). The advantages of effective treat- 

 ment with a single oral dose are obvious. 



The ideal malaricidal drug Avould be one harmless enough for use in 

 infants, active enough for the prompt suppression of acute infections, 



