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With emerging diseases on the rise, there is an urgent need to identify and understand novel mechanisms of prophylactic protection in vertebrate hosts. Inducing resistance against emerging pathogens through prophylaxis is an ideal management strategy that may impact pathogens and their host-associated microbiome. The host microbiome is recognized as a critical component of immunity, but the effects of prophylactic inoculation on the microbiome are unknown. In this study, we investigate the effects of prophylaxis on host microbiome composition, focusing on the selection of anti-pathogenic microbes contributing to host acquired immunity in a model host–fungal disease system, amphibian chytridiomycosis. We inoculated larval Pseudacris regilla against the fungal pathogen Batrachochytrium dendrobatidis ( Bd ) with a Bd metabolite-based prophylactic. Increased prophylactic concentration and exposure duration were associated with significant increases in proportions of putatively Bd -inhibitory host-associated bacterial taxa, indicating a protective prophylactic-induced shift towards microbiome members that are antagonistic to Bd. Our findings are in accordance with the adaptive microbiome hypothesis, where exposure to a pathogen alters the microbiome to better cope with subsequent pathogen encounters. Our study advances research on the temporal dynamics of microbiome memory and the role of prophylaxis-induced shifts in microbiomes contributing to prophylaxis effectiveness. This article is part of the theme issue ‘Amphibian immunity: stress, disease and ecoimmunology’. 

Ivermectin is a broad-spectrum antiparasitic medicine, which is often used as a treatment for parasites or as a prophylaxis. While studies have looked at the long-term effects of Ivermectin on helminths, studies have not considered the long-term impacts of this treatment on host health or disease susceptibility. Here, we tracked the effects of early life Ivermectin treatment in Cuban tree frogs (Osteopilus septentrionalis) on growth rates, mortality, metabolically expensive organ size, and susceptibility toBatrachochytrium dendrobatidis(Bd) infection. One year after exposure, there was no effect of Ivermectin exposure on frog mass (X²₁= 0.904, p = 0.34), but when tracked through the exponential growth phase (~2.5 years) the Ivermectin exposed individuals had lower growth rates and were ultimately smaller (X²₁= 7.78,p= 0.005;X²₁= 5.36,p= 0.02, respectively). These results indicate that early life exposure is likely to have unintended impacts on organismal growth and potentially reproductive fitness. Additionally, we exposed frogs to Bd, a pathogenic fungus that has decimated amphibian populations globally, and found early life exposure to Ivermectin decreased disease susceptibility (disease load:X²₁= 17.57,p= 0.0002) and prevalence (control: 55%; Ivermectin: 22%) over 2 years after exposure. More research is needed to understand the underlying mechanism behind this phenomenon. Given that Ivermectin exposure altered disease susceptibility, proper controls should be implemented when utilizing this drug as an antiparasitic treatment in research studies.

 

Batrachochytrium dendrobatidis(Bd) has been associated with massive amphibian population declines worldwide. Wildlife vaccination campaigns have proven effective for mitigating damage from other pathogens, and there is evidence that adult frogs can acquire resistance to Bd when exposed to killed Bd zoospores and the metabolites they produced.

Here, we investigated whether Cuban treefrogs tadpolesOsteopilus septentrionaliscan gain protection from Bd through exposure to a prophylaxis treatment composed of killed zoospores or soluble Bd metabolites. We used a 2 × 2 factorial design, crossing the presence or absence of killed zoospores with the presence or absence of Bd metabolites. All hosts were subsequently exposed to live Bd to evaluate susceptibility.

Exposure to killed zoospores did not induce a protective response. However, tadpoles exposed to Bd metabolites had significantly lower Bd intensity and prevalence than tadpoles that were not exposed to metabolites.

The metabolites Bd produce pose no risk of Bd infection and therefore make an epidemiologically safe prophylaxis treatment, protecting tadpoles against Bd. This work provides a promising potential for protecting amphibians in the wild as a disease management strategy for controlling Bd‐associated declines.

 

Batrachochytrium dendrobatidis(Bd) is a pathogenic fungus that has devastated amphibian populations globally by causing the disease chytridiomycosis.Batrachochytrium dendrobatidisis capable of infecting non‐amphibian hosts, such as crayfish, and has been detected on reptile and bird species. Given the taxonomic heterogeneity in the known hosts and vectors of Bd, it is likely that there is a diversity of undiscovered non‐amphibian hosts of the fungus.

Here, we investigated whether Bd could survive on freshwater snails (Physella acuta) andCladophoraalgae. We exposed small and large snails (n = 15 snails/size category),Cladophoraalgae (n = 5), and artificial spring water controls (ASW;n = 5) to live Bd. We also maintained Bd‐free control snails (n = 5 snails/size category) in ASW. All treatments were maintained for 7 weeks at 18°C. Mortality was checked three times a week, snails were weighed every 2 weeks, and 7 weeks after exposure, the snails, algae, and water were tested for Bd using quantitative polymerase chain reaction.

We found that Bd did not grow on live snails, algae, or ASW long term. Additionally, live snails (n = 20) collected from Bd‐positive ponds in California were all negative for Bd, as well. Given that we found no Bd on the experimentally exposed or field swabbed snails, snails are probably not a reservoir host of Bd.

While negative results are often not published, Bd is one of the deadliest pathogens on earth; it is essential to know what is and is not capable of maintaining Bd for well‐designed disease models.

 

Heterogeneities in infections among host populations may arise through differences in environmental conditions through two mechanisms. First, environmental conditions may alter host exposure to pathogens via effects on survival. Second, environmental conditions may alter host susceptibility, making infection more or less likely if contact between a host and pathogen occurs. Further, host susceptibility might be altered through acquired resistance, which hosts can develop, in some systems, through exposure to dead or decaying pathogens and their metabolites. Environmental conditions may alter the rates of pathogen decomposition, influencing the likelihood of hosts developing acquired resistance.

The present study primarily tests how environmental context influences the relative contributions of pathogen survival and per capita transmission on host infection prevalence using the amphibian chytrid fungus (Batrachochytrium dendrobatidis; Bd) as a model system. Secondarily, we evaluate how environmental context influences the decomposition of Bd because previous studies have shown that dead Bd and its metabolites can illicit acquired resistance in hosts. We conducted Bd survival and infection experiments and then fit models to discern how Bd mortality, decomposition and per capita transmission rates vary among water sources [e.g. artificial spring water (ASW) or water from three ponds].

We found that infection prevalence differed among water sources, which was driven by differences in mortality rates of Bd, rather than differences in per capita transmission rates. Bd mortality rates varied among pond water treatments and were lower in ASW compared to pond water.

These results suggest that variation in Bd infection dynamics could be a function of environmental factors in waterbodies that result in differences in exposure of hosts to live Bd. In contrast to the persistence of live Bd, we found that the rates of decomposition of dead Bd did not vary among water sources, which may suggest that exposure of hosts to dead Bd or its metabolites might not commonly vary among nearby sites. Ultimately, a mechanistic understanding of the environmental dependence of free‐living pathogens could lead to a deeper understanding of the patterns of outbreak heterogeneity, which could inform surveillance and management strategies.

 

Lethal and sublethal effects of pathogens should theoretically select for host avoidance of these pathogenic organisms. Some amphibians can learn to avoid the pathogenic fungusBatrachochytrium dendrobatidis(Bd) after one infection‐clearance event.

Here, we investigated whether four taxonomically distinct amphibians, Cuban tree frogsOsteopilus septentrionalis, southern toadsAnaxyrus(Bufo)terrestris, greenhouse frogsEleutherodactylus planirostrisand pine woods tree frogsHyla femoralis, exhibited any innate or learned avoidance of Bd on a moist substrate and, if so, what cues they used to identify the fungus.

Cuban tree frogs, pine woods tree frogs and greenhouse frogs did not appear to exhibit detectable innate or learned avoidance of Bd. However, southern toads learned to avoid Bd after only one exposure. Southern toads avoided any treatment containing Bd metabolites but did not avoid treatments that lacked Bd metabolites even when dead zoospores were present.

Bd metabolites appeared to be the cues that amphibians use to avoid Bd. These metabolites may have a distinct smell or may cause discomfort, which would be consistent with a classical or Pavlovian conditioning response.

Synthesis and applications. Not all species of amphibians respond the same way to Bd exposure; some can learn to avoid Bd and the metabolites it produces, while others do not. These findings have important implications for both management practices and policy, and should be considered when developing disease models and conservation plans for amphibians.

 

Climate change might drive species declines by altering species interactions, such as host–parasite interactions. However, few studies have combined experiments, field data, and historical climate records to provide evidence that an interaction between climate change and disease caused any host declines. A recently proposed hypothesis, thethermal mismatch hypothesis, could identify host species that are vulnerable to disease under climate change because it predicts that cool‐ and warm‐adapted hosts should be vulnerable to disease at unusually warm and cool temperatures, respectively. Here, we conduct experiments onAtelopus zeteki, a critically endangered, captively bred frog that prefers relatively cool temperatures, and show that frogs have high pathogen loads and high mortality rates only when exposed to a combination of the pathogenic chytrid fungus (Batrachochytrium dendrobatidis) and high temperatures, as predicted by thethermal mismatch hypothesis. Further, we tested various hypotheses to explain recent declines experienced by species in the amphibian genusAtelopusthat are thought to be associated withB. dendrobatidisand reveal that these declines are best explained by thethermal mismatch hypothesis. As in our experiments, only the combination of rapid increases in temperature and infectious disease could account for the patterns of declines, especially in species adapted to relatively cool environments. After combining experiments on declining hosts with spatiotemporal patterns in the field, our findings are consistent with the hypothesis that widespread species declines, including possible extinctions, have been driven by an interaction between increasing temperatures and infectious disease. Moreover, our findings suggest that hosts adapted to relatively cool conditions will be most vulnerable to the combination of increases in mean temperature and emerging infectious diseases.