Parasite-mediated enhancement of transmission by haematophagous insects
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Blood-sucking arthropods are vectors for a variety of parasites and pathogens, including many that infect man and his domestic animals. Infective stages are imbibed during blood feeding and their life cycle is completed when they are transferred back to their vertebrate host during another blood-feeding episode. Transmission of vector-borne parasites is therefore dependent upon contact between hosts and haematophagous arthropods. In order for blood feeding to occur, a vector performs a series of behaviour patterns that are initiated in response to both endogenous and exogenous triggers; the latter including odour signals from the host. If the host is infected these signals may change in ways that makes them more attractive to the vector of the parasite. In addition, infection-induced lethargy in the host may make blood feeding less risky and blood that has fewer erythrocytes is easier to imbibe. When vectors are infected several aspects of blood-feeding behaviour may be changed in ways that increase host contact or facilitate feeding. Mosquitoes infected with rodent malarias have been shown to exhibit increased response to host odours, to have a lower blood volume threshold at which they cease feeding and to show increased feeding persistence in the face of host-defensive behaviour. Increased feeding persistence is also observed in Leishmania-infected sand flies, as is increased biting behaviour. The latter is due to blockage of the gut with promastigote secretory gel. Vector infections also alter mechanisms that combat host haemostasis, such as the mosquito anti-platelet aggregation factor, apyrase. This causes additional probing attempts when sporozoite infections are present. The evidence that some vector-transmitted parasites and pathogens increase transmission prospects by altering the blood-feeding process suggests that they are manipulating the host or the vector. Host contact determines the spread of infection thus information concerning parasite-induced changes in haematophagy needs to be incorporated into epidemiological models.