positively correlated with the gametocyte density, which the authors
interpreted in terms of facultative LMC and which relies on one major
assumption: that gametocyte densities increase with the number of
coinfecting clones. When there are multiple clones present, the parasite
clones are expected to adjust their sex ratio in response to local
conditions: single clone infections produce low gametocytaemia and LMC
predicts the maintenance of a female bias; multiple clone infections result
in a higher gametocytaemia and there is a facultative switch to a more
equal sex ratio. This requires that coinfecting clones are able to estimate
the number of coinfecting clones, which they could do using any number
of cues, as long as the cues vary in intensity according to the number of
clones present. In mouse malaria, coinfection resulted in significantly
increased anaemia independent of parasitaemia in mixed rather than
single infections, with an accompanying increase in gametocytaemia and
infectiousness to mosquitoes (Taylor et al., 1997, 1998). Here clones
may be responding to haematological cues, which vary according to
coinfecting clone number. In contrast, mixed-strain infections of
Plasmodium gallinaceum in their chicken hosts did not result in
an increase in anaemia, gametocytaemia or sex ratio. Rather, the
gametocytaemia reflected the asexual reproduction rate, which differed
between the individual strains, and the sex ratio, as discussed below,
altered with the host’s haematological response to the infection. Despite
these apparently contradictory results, which probably reflect differences
in the host–parasite systems and, most notably, the differing immune
systems of the vertebrate hosts, all suggest that changes in the blood
environment play a significant role in parasite sexuality (production of
gametocytes or sex ratio) and hence transmission. Both asexual growth
rates and anaemia are considerably influenced by the host immune
response to infection. Although the former reflects the parasite-
virulence/host-resistance relationship, the role of immunity in malaria-
induced anaemia is poorly understood. Anaemia is not only the result of
red blood-cell haemolysis by parasites, but is also a mechanism (perhaps
autoimmune), at least in some host–parasite interactions, by which the
host controls the infection: many malaria parasite species are only able
to infect mature red blood cells and not young ones (reticulocytes).
The intricate relationship between haematology and immunology will
determine how host quality varies. How multiple clones affect each other
via their individual effects on host quality is implicit to malaria research
and yet remains poorly understood. That parasites do use haematological
cues to increase reproductive success does, however, seem to be the case,
as discussed next.Host quality and mating assurance
The second selection-based explanation for fluctuating sex ratios
concerns the effect of a varying habitat (blood) on reproductive success –212 R.E.L. Paul