P. gallinaceum manipulates A. aegypti to increase its own chances of success.[3] Koella et al., 2002 finds that oocysts in the gut increase the volume of each blood meal.[3] This lowers the chances of disgorgement of the parasites into the final host – chicken (Gallus gallus domesticus) – which is important because oocysts can't infect.[3] This prolongs the average duration of oocyst residence in the vector, increasing their chance of successfully maturing to the transmission stage.[3]
On the other hand sporozoites do the opposite: They decrease the volume of meals, increasing the number of meals taken, shortening the time they must continue to be in the vector, and increasing their chance of being successfully disgorged into a final host.[3] Because this is the transmittable (infectious) stage that is desirable.[3]
This appears to generalize to P. gallinaceum and any combination of mosquito and avian.[3]
Virulence factors
Circumsporozoite protein (CSP) is required for host invasion.[4] Warburg et al., 1992 provides a monoclonal antibody against CSP and demonstrates efficacy.[4] The complete inhibition of sporozoite colonization of Aedes aegyptisalivary glands they achieved could be due to the antibody itself blocking contact between the sporozoites and the gland surface, however the antibody's binding is inhibited by a particular CSP motif, suggesting antibody efficacy is due to its anti-CSP effect.[4] This 15-amino acid motif is one found by the original Dame et al., 1984 discovery of CSP which contains the 5-length CSP Region I.[4]: 395–396 [5]
^Brumpt, Emile (1936). "Etude Expérimentale du Plasmodium gallinaceum Parasite de la Poule Domestique. Transmission de ce Germe par Stegomyia fasciata et Stegomyia albopicta" [Experimental Study on the Plasmodium gallinaceum Parasite of the Domesticated Chicken : Transmission of the Pathogen by Stegomyia fasciata and Stegomyia albopicta]. Annales de Parasitologie: 597–620.
