Ookinete destruction within the mosquito midgut lumen explains Anopheles albimanus refractoriness to Plasmodium falciparum (3D7A) oocyst infection.
Bottom Line: Similar densities of macrogametes/zygotes, and immature retort-form and mature ookinetes were found within the bloodmeals of both mosquito species.However, in A. albimanus, ookinetes were seldom associated with the peritrophic matrix, and were neither observed in the ectoperitrophic space nor the midgut epithelium.Vital staining of the immature retort-form and mature ookinetes found within the luminal bloodmeal, demonstrated that a significantly greater proportion of these malaria parasite stages were non-viable in A. albimanus compared with A. stephensi.
Affiliation: Wellcome Trust Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, Sir Graeme Davies Building, University of Glasgow, Glasgow, UK. email@example.comShow MeSH
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Mentions: Combining the data from the different experimental feeds reported above, ookinete and oocyst mortality rates within different compartments of the midgut were calculated for the P. falciparum clone 3D7A in A. albimanus and A. stephensi (Fig. 5). In A. albimanus, less than 1% of ookinetes forming within the bloodmeal attained the peritrophic matrix, while none survived to enter the ectoperitrophic space, indicating that all ookinetes forming within the bloodmeal were lost within the endoperitrophic space (Fig. 5). In A. stephensi, approximately 72.1% of all ookinetes forming within the bloodmeal were lost within the endoperitrophic space and failed to attain the peritrophic matrix; 8.6% were lost between penetration of the peritrophic matrix and entry into the midgut epithelium; and 8.0% were lost during invasion of the midgut epithelium. The remaining 11.2% of all ookinetes forming within the bloodmeal successfully transformed into oocysts on the basal surface of the midgut epithelium (Fig. 5). The inferred mortality of ookinetes during invasion of the midgut epithelium (approximately 40%) is quantitatively proportional to the previously reported number of morphologically-abnormal midgut epithelial cells not associated with detectable malaria parasites, consistent with the loss of these malaria parasites through lysis during or after invasion of midgut epithelial cells (Baton and Ranford-Cartwright, 2004).
Affiliation: Wellcome Trust Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, Sir Graeme Davies Building, University of Glasgow, Glasgow, UK. firstname.lastname@example.org