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The pathogenic fungusBatrachochytrium dendrobatidis(Bd)is associated with drastic global amphibian declines. Prophylactic exposure to killed zoospores and the soluble chemicals they produce (Bdmetabolites) can induce acquired resistance toBdin adult Cuban treefrogsOsteopilus septentrionalis. Here, we exposed metamorphic frogs of a second species, the Pacific chorus frogPseudacris regilla, to one of 2 prophylactic treatments prior to liveBdexposures: killedBdzoospores with metabolites, killed zoospores alone, or a water control. Prior exposure to killedBdzoospores with metabolites reducedBdinfection intensity in metamorphic Pacific chorus frogs by 60.4% compared to control frogs. Interestingly,Bdintensity in metamorphs previously exposed to killed zoospores alone did not differ in magnitude relative to the control metamorphs, nor to those treated with killed zoospores plus metabolites. Previous work indicated thatBdmetabolites alone can induce acquired resistance in tadpoles, and so these findings together indicate that it is possible that the solubleBdmetabolites may contain immunomodulatory components that drive this resistance phenotype. Our results expand the generality of this prophylaxis work by identifying a second amphibian species (Pacific chorus frog) and an additional amphibian life stage (metamorphic frog) that can acquire resistance toBdafter metabolite exposure. This work increases hopes that aBd-metabolite prophylaxis might be widely effective across amphibian species and life stages. 

Batrachochytrium dendrobatidis(Bd) is a pathogenic fungus known to infect amphibians and crayfish. In crayfish,Bdcauses gill tissue damage, and in some cases, mortality. Most research has focused on the amphibian-Bdsystem, so to date, little is known about the effects ofBdon the crayfish host. Here, we studied the effects of sublethal exposure toBdand the metabolites produced byBdon crayfishProcambarus allenisurvival, gill damage, and oxygen consumption (as a proxy for mass-specific metabolic rate). Oxygen consumption increased 24 h post-exposure to liveBd, indicative of a stress response, followed by a decrease in oxygen consumption over time (χ²₁= 6.39, p = 0.012). There was no difference in response when comparing the crayfish exposure to liveBdandBd-metabolites alone (χ²₁= 2.70, p = 0.101), indicating that the metabolites may have been the causative agent responsible for the response. Additionally, oxygen consumption decreased with gill damage (tissue recession) inBd-exposed individuals. We found that high doses ofBdcause outright mortality in crayfish, and we show here that sublethalBd-induced inhibition of oxygen consumption could negatively impact crayfish in the field, possibly reducing their overall fitness. More research is needed to understand this understudied host-parasite system. It is essential that we incorporate the disease dynamics associated withBdand crayfish in conservation disease models, as this is the only way to develop comprehensive community-based models.