SPOROZOA 1127 



The leucocytes, although increased during paroxysm, are soon 

 diminished so that leucopenia is characteristic of the disease ; in 

 addition, there is a relative increase in the mononuclear leucocytes. 

 The loss of hemoglobin is very great, yet is quickly recovered from 

 during convalescence. 



In fatal cases of aestivo-autumnal fever a striking feature is the 

 presence of innumerable infected red cells in the capillaries of the 

 brain or abdominal viscera. A smear from a pigmented brain may 

 show a capillary thrombus made up of infected erythrocytes, most of 

 them showing the sporulatmg stage. In deaths after repeated ma- 

 larial attacks the kidneys will show, in addition to the presence of 

 many parasites, a marked chronic diffuse nephritis, one of the most 

 important sequelae of the disease. 



Immunity. The disease is strictly confined to human beings, as 

 none of the lower animals are susceptible ; there appears to be some 

 racial and acquired immunity, although it is incomplete; in native 

 settlements the number of children showing parasites in the blood is 

 much greater than the number of adults, yet the latter are not abso- 

 lutely immune; one attack certainly gives no protection against a 

 new infection. The evidence from different regions is quite con- 

 flicting in regard to immunity and has been most plausibly explained 

 in this way ; where the disease prevails throughout the year there is 

 a constant reinfection and under this stimulus the body is able to 

 keep up an immunity strong enough to kill off the parasites before 

 any symptoms arise; in other regions, however, where malaria is a 

 seasonal disease, the constant stimulus is lacking and there is less 

 evidence of immunity. It has also been noted that the three varieties 

 of the disease are distinct, and that no immunity against the whole 

 group is obtained by an infection with one species. 



Since many mild cases recover without treatment, it is apparent 

 that some little immunity is produced by an infection, yet it is tem- 

 porary and does not protect against repeated relapses. Before the 

 days of radical treatment with quinine, relapses were the rule and 

 were considered an essential feature of the disease (Manneberg). 



Clinical experience teaches that relapses occur when treatment 

 has been insufficient, and especially after fatigue, getting wet and 

 catching cold, or after over-heating in the tropical sun, and par- 

 ticularly after a sea voyage or a long journey. They may continue 

 to occur in a region free from malaria, for about three years ; in a 

 malarial region it is difficult to differentiate between relapses and 



