Hypothesis: Dynamics of Classical Malaria Epidemics Show Plasmodium falciparum's Survival Strategy

Abstract

Abstract. Areas of marginal transmission can generate enormous lethal falciparum malaria epidemics when factors favoring the parasite shift only slightly. Although usually described in terms of vectorial capacity, medical scientists working in India in the early 20th century came to the conclusion that "an epidemic of relapses" was the key triggering event of malaria epidemics. This explanation has been largely discarded, because the biology of Plasmodium falciparum recrudescence has since been differentiated from P. vivax relapse. Using data from the Punjab in 1908 and Ceylon in 1934-1935, the genesis of malaria epidemics has been re-examined to inform current control efforts. The epidemics were focused geographically depending on recent rainfall or drought. Epidemics arose very suddenly and simultaneously in several places. Malaria spleen surveys indicated very little recent malaria transmission, and blood smears showed very few gametocytes just before the epidemic. Population stress as indicated by high grain prices because of a poor harvest caused by drought the previous year was a risk factor for malaria epidemics. Although increased female Anopheline survival because of increased humidity played an important part in the magnification of the epidemic, it does not explain its genesis. Human population stress triggering a shift toward gametocytogenesis is hypothesized as the key initiation factor for malaria epidemics. Its evolutionary significance may be that it allows the parasite to match the tropical agricultural cycle.

Number and proportion of P.falciparumgametocytes vary from acute infection to chronic parasite carriage despite unaltered sexual commitment rate

“…Our work suggests that gametocytogenesis remains constant as infections progress from recent transmission to chronic carriage, and it is the difference in asexual survival/replication rates that promotes different gametocyte densities, independently of environmental factors. Although it has been suggested that P. falciparum investment in gametocyte production adjusts to host nutrient availability (43), drug pressure (22), transmission intensity (44), and even seasonality (45, 46), results are often inconsistent and potentially affected by the dynamics of asexual parasite growth, without necessarily indicating altered sexual commitment. In Sudan, following the long dry season, gametocyte density estimates have been reported to increase prior to the highest transmission peak (47), suggesting a higher gametocyte investment.…”

“…Although it has been suggested that P. falciparum investment in gametocyte production adjusts to host nutrient availability (54), drug pressure (24), transmission intensity (55), and even seasonality (56, 57), results are often inconsistent and potentially affected by the dynamics of asexual parasite growth, without necessarily indicating altered sexual commitment. In Sudan, following the long dry season, gametocyte density estimates have been reported to increase prior to the highest transmission peak (58), suggesting a higher gametocyte investment.…”