by the trypanosomes attaching directly to mechanoreceptors on the
tsetse-fly labrum and physically blocking them, thus impairing their
function (Molyneuxet al., 1979).Vector Reproduction
Vector reproductive behaviour includes mating and oviposition. There
are few reports of either being affected by infection, and changes in the
former are unlikely, because most vectors have mated before they become
infected. Reports of changes in oviposition behaviour are rare, because
oviposition is often used as a measure of egg production and few studies
have assessed the effect of parasites on egg retention as well as
oviposition. However, El Sawafet al. (1994) report thatLeishmania major
andL. infantumcause a significant reduction in both egg retention and
oviposition in the sandflyPhlebotomus papatasi.
Parasite-induced fecundity reduction is reported in diverse parasite–
vector associations, such asLeishmaniaspp. and sandflies, malaria and
mosquitoes and filarial nematodes and mosquitoes and blackflies (Hurd,
1993; Hurdet al., 1995), thus fulfilling one of Poulin’s (1995) criteria for
adaptive manipulation. Although curtailment of reproduction may be a
by-product of manipulation of feeding behaviour, it also occurs when
blood-meal size is not affected by infection.
A. stephensi and A. gambiae are being used to investigate the
mechanisms underlying parasite-induced fecundity reduction caused by
P. yoelii nigeriensis. Infection results in a significant reduction in egg
production and egg hatch rate during an initial gonotrophic cycle after
feeding on an infected host and also during subsequent gonotrophic
cycles, when oocysts are present in the mosquito midgut and when
sporozoites are in the salivary glands (Hogg and Hurd, 1995; Jahan and
Hurd, 1997; Ahmedet al., 1999). Fecundity reduction also occurs in
wild-caughtA. gambiaeinfected withP. falciparum(Hogg and Hurd,
1997). There is considerable physiological evidence to suggest that, in
these associations, fecundity reduction is not a by-product of nutrient
depletion (reviewed by Hurd, 2001). In the fat body of infected females,
the abundance of messenger RNA (mRNA) of the yolk protein precursor,
vitellogenin, is decreased by infection (Ahmed et al., 2001) and, in
the ovaries, cells of the follicular epithelium undergo apoptosis,
thus precipitating the resorption of developing follicles (Hopwoodet al.,
2001). These complex responses to infection may be host or parasite
adaptations (Hurd, 2001).
If vector fecundity reduction is a parasite adaptive strategy, it appears
to have evolved several times among different taxa (Hurd, 1993). This
suggests that fitness benefits must accrue to the parasite from reducing
vector egg production, which, as discussed above, is likely to result in
enhanced vector survivorship over and above that of a vector that sustains
a parasite infection and matures a full batch of eggs (Hurd, 2001).Parasite Manipulation of Vector Behaviour 273