Effects of the Host Immune Response on Nematode Infections
Strongyloidesinfections
The host immune response has significant effects on the development of
theS. rattilife cycle. In addition, it has other, apparently direct, effects on
the parasitic females ofStrongyloidesspp., and similar effects are seen in
a range of other parasitic nematodes. ForS. ratti, these effects can be seen
in changes that occur at different times through an infection, which
correlate with the development of an anti-S. rattiimmune response. Thus,
as an infection progresses, worms become shorter and their fecundity
(number of eggs in utero) is reduced (Moqbel and McLaren, 1980);
nematode fecundity is closely related to adult female body size (Skorping
et al., 1991). Concurrently, the worms move posteriorly from the small
intestine to the caecum and colon (Kimuraet al., 1999). Ultrastructural
observations of these worms show degenerate changes in worm tissues. It
is not known whether this damage is a direct effect of the host immune
response (e.g. the action of host molecules or effector cells) or an indirect
result of other, more general (e.g. metabolic stress), effects of the immune
response. As worms move posteriorly in the gut, they appear to be
functionally starved, due to the presence of oral plugs, presumably of host
origin (Moqbel and McLaren, 1980). Thus, here, it is hypothesized that
the reduced ability of worms to feed and the consequent reduction in
available energy result in the observed damage and that this is the basis of
the reduction in fecundity (Moqbel and McLaren, 1980). That these effects
are due to immune responses is demonstrated by the observations that: (i)
the transfer of worms from hosts mounting an immune response to naïve
hosts results in an increase in fecundity (Schadet al., 1997); and (ii)
immune suppression of hosts mounting an immune response results in an
increase in parasite fecundity (Groveet al., 1983; Schadet al., 1984).
Thus, overall, broad aspects of the fitness of nematode infections are
affected by the host immune response. These are usually considered as
manifestations of stresses imposed on the parasites by the host immune
response. However, which particular nematode organ systems, metabolic
pathways or processes are stressed or how these effects are brought about
is not known. Similarly, as discussed above, how the effect of the host
immune response is transduced to affect the sex-determination mecha-
nism and the female-only developmental choice ofS. rattiis not known.
Intuitively, it is envisaged that the host immune response affects
parasitic worms in general, either directly by physically damaging them
or indirectly by interfering with their feeding and nutrient supply or
perhaps by otherwise making their environment generally less hospitable.
These effects are, in turn, manifest as the reduced fitness of infections
(reduced size and fecundity of worms) and, forS. ratti, the change in the
sex ratio and in the developmental choice of female larvae. However, for
S. ratti, it is difficult to see how ‘damage’ to a parasitic female brings about
a change in the sex ratio of her progeny, since this would imply that120 M.E. Viney