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.