Comparative infectivity of Plasmodium falciparum to Anopheles albimanus and Anopheles stephensi

The infectivity of three different clones of the human malaria parasite Plasmodium falciparum to two different natural vector mosquito species, Anopheles albimanus and Anopheles stephensi was investigated. Two of the P. falciparum clones studied (HB3B-B2 and 7G8) established relatively low levels of mature oocyst infection in both mosquito species. In contrast, the third P. falciparum clone investigated (3D7A) did not produce mature oocyst infections in An. albimanus but infected stephensi at a relatively high level. These observations demonstrate the existence of differences between the three malaria parasite clones iii the ability to infect the mosquitoes, and the two mosquito species in their susceptibility to malaria parasite infection. Direct immunofluorescence microscopy and examination of Giemsa-stained histological sections by light microscopy were used to investigate further the development of the P. falciparum 3D7A clone in An. albimanus and An. stephensi. The P. falciparum 3D7A clone formed mature ookinetes within the bloodmeals of both albimanus and An. stephensi. In An. albimanus, these malaria parasite stages subsequently failed to migrate from the bloodmeal and invade the surrounding midgut epithelium suggesting that ookinetes were destroyed within the endoperitrophic space of this mosquito species. The reasons for the disappearance of ookinetes within the endoperitrophic space of An. albimanus were uncertain but were possibly related to the faster time to completion of bloodmeal digestion in this mosquito species compared to An. stephensi. Simultaneous investigation of P. falciparum 3D7A development within An. Stephensi revealed that in this mosquito species ookinetes entered the midgut epithelium via an intracellular route, causing destruction of invaded midgut epithelial cells, and subsequently exited the midgut epithelium by an intercellular route. A general model for the route of ookinete invasion across the midgut epithelium is proposed based upon these observations. Examination of the Giemsa-stained histological sections also provided evidence that regenerative cells within the midgut epithelium of An. stephensi imdergo proliferation and differentiation into midgut epithelial cells following infection with P. falciparum 3D7A, presumably as a mechanism to replace the midgut epithelial cells destroyed as a consequence of ookinete invasion of the midgut epithelium.