on an SP-treated host, we observe both a significant increase in the number of oocysts in the midgut, 43 and a drastic decrease in both sporozoite prevalence (-30%) and burden (-80%) compared to the 44 untreated controls. We discuss the potential mechanisms underlying these seemingly contradictory 45 results and contend that, provided the results are translatable to human malaria, the potential 46 epidemiological and evolutionary consequences of the current preventive use of SP in malaria-endemic 47 countries could be substantial. 48 Keywords: transmission-blocking interventions, vaccines, antimalarial drugs, avian malaria 49 50 throughout the world. Over the last century, these synthetic antimalarials, have replaced traditional 53 herbal remedies such as the (quinine-containing) bark of the South American cinchona trees and the 54 (artemisin-containing) Chinese drug qinghao. Broadly speaking, four major synthetic antimalarial drug 55 classes exist for the treatment of malaria: (i) quinolines (chloroquine, mefloquine), which owe their 56 origins to quinine, interfere with the ability of Plasmodium detoxify hematin, a toxic compound 57 resulting from the degradation of the haemoglobin; (ii) antifolates (pyrimethamine, sulfadoxine, 58 proguanil), so-called because they disturb the folate pathway of Plasmodium, thereby interfering with 59 its DNA and amino-acid synthesis; (iii) atovaquone which interferes with the parasite's mitochondrial 60 electron transport, and (iv) artemisinin derivatives (artemether, artesunate), the most potent and 61 effective anti-malarials to date, which exert their anti-malarial action by perturbing redox homeostasis 62 and the haematin detoxification in the parasite (Müller and Hyde, 2010). 63Although the prime purpose for developing these antimalarials is obviously to prevent or cure 64 the infection of the patients, it has become rapidly obvious that they can also be used to reduce the 65 prevalence of the disease in the population by reducing the onward transmission of the parasite by the 66 vector (Sinden et al., 2012;Wadi et al., 2019). The transmission-blocking effect of antimalarial drugs 67 can take place in three different, albeit non-exclusive, ways. Firstly, drugs may be able to kill, arrest 68 the maturation, alter the sex ratio or reduce the infectivity of gametocytes, the sexual stages of the 69 parasite that are present in the blood and are responsible for the transmission to the mosquito. 70 Secondly, drugs may be able to hinder the development of the parasite within the mosquito. 71Plasmodium development inside the mosquito is complex and involves the fusion of male and female 72 gametocytes to form a zygote, the passage of the mobile zygote through the midgut wall to form an 73 oocyst that grows, undergoing successive mitosis, ruptures and releases thousands of sporozoites that 74 migrate to the salivary glands. Antimalarial drugs, or their metabolites, can find their way to the 75 mosquito midgut where they can block the parasite either directly, by being toxic to any ...