Host fertility is often curtailed as a result of parasitic infection.
The hypothesis that this may confer an adaptive advantage upon the sym
bionts if nutrients are directed from reproduction and made available
for host/parasite maintenance is explored. The suggestion is made that
an understanding of the mechanisms underlying the pathophysiology of
fecundity reduction may shed light upon the evolutionary implications
of this strategy for both parasite and host. To illustrate this the do
wn-regulation of egg production is explored with reference to a partic
ular model system, the association between metacestodes of the rat tap
eworm, Hymenolepis diminuta and the mealworm beetle, Tenebrio molitor.
Several aspects of host reproductive behaviour and physiology are aff
ected by infection in this association, including vitellogenesis. Meta
cestodes directly inhibit the fat body synthesis of vitellogenin in a
stage-specific, density-dependent manner. This inhibition is likely to
be orchestrated by a modulator molecule, produced by the parasite. In
the ovarian follicles, juvenile hormone III binding to a specific fol
licular membrane-binding protein is inhibited in infected beetles, res
ulting in the down-regulation of a cascade of events which enables vit
ellogenin to pass into the developing oocyte. Data to support the prop
osed existence of a parasite-induced antigonadotrophin, of host origin
, are discussed. Evidence that similar mechanisms operate in Plasmodiu
m-infected anopheline mosquitoes and Onchocerca-infected blackflies is
presented in support of the possibility that a parasite-induced reduc
tion in host reproductive fitness is an adaptive strategy and an asses
sment of who is manipulating whom is made.