Conclusions
We have outlined herein a variety of selection pressures and ecological
conditions that could drive the evolution of dishonest signals of
infection and maintain them. Preconditions necessary to foster the
evolution of these traits are met by a variety of animal systems but
these hypotheses have never been considered in depth by theoreticians or
empiricists. Yet, there are numerous plausible conditions where
dishonest signaling of infection could be favored. Where do we go from
here? In truth, almost any contribution would be a novel one.
Empiricists could experimentally impose the traits of infection in
otherwise healthy individuals and compare their performance in staged
interactions with legitimately infected and healthy rivals in
contrasting ecological conditions (e.g., predators +/-, high/low
resources). Likewise, one could evaluate infection-mimicry in terms of
the residuals of a regression of symptoms versus parasite load: do some
individuals appear particularly healthy despite heavy parasite loads
(parasite tolerance) while others seem idiopathically sickly despite low
parasite loads (possible mimics)? How do such individuals fare in terms
of their overall fitness or performance in contrasting contexts, like
acquiring mates, securing fine territories, and so on? Theoreticians
could contribute by analyzing models that link more familiar models of
dishonest signaling with models of the evolution of virulence, optimal
diet theory, animal contests, kin selection, and so on. We freely admit
that this is all, for now, conjecture. Yet, we hope that the
plausibility of the arguments herein will inspire evolutionary
biologists and ecologists alike to consider the possibility of mimicry
within their own study systems and to evaluate their plausibility in
silico.