An official website of the United States government
Abstract 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.
more »
« less
Variability in environmental persistence but not per capita transmission rates of the amphibian chytrid fungus leads to differences in host infection prevalence
Abstract 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.
more »
« less
- PAR ID:
- 10446034
- Publisher / Repository:
- Wiley-Blackwell
- Date Published:
- Journal Name:
- Journal of Animal Ecology
- Volume:
- 91
- Issue:
- 1
- ISSN:
- 0021-8790
- Page Range / eLocation ID:
- p. 170-181
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
More Like this
-
-
Abstract Changes to migration routes and phenology create novel contact patterns among hosts and pathogens. These novel contact patterns can lead to pathogens spilling over between resident and migrant populations. Predicting the consequences of such pathogen spillover events requires understanding how pathogen evolution depends on host movement behaviour. Following spillover, pathogens may evolve changes in their transmission rate and virulence phenotypes because different strategies are favoured by resident and migrant host populations. There is conflict in current theoretical predictions about what those differences might be. Some theory predicts lower pathogen virulence and transmission rates in migrant populations because migrants have lower tolerance to infection. Other theoretical work predicts higher pathogen virulence and transmission rates in migrants because migrants have more contacts with susceptible hosts.We aim to understand how differences in tolerance to infection and host pace of life act together to determine the direction of pathogen evolution following pathogen spillover from a resident to a migrant population.We constructed a spatially implicit model in which we investigate how pathogen strategy changes following the addition of a migrant population. We investigate how differences in tolerance to infection and pace of life between residents and migrants determine the effect of spillover on pathogen evolution and host population size.When the paces of life of the migrant and resident hosts are equal, larger costs of infection in the migrants lead to lower pathogen transmission rate and virulence following spillover. When the tolerance to infection in migrant and resident populations is equal, faster migrant paces of life lead to increased transmission rate and virulence following spillover. However, the opposite can also occur: when the migrant population has lower tolerance to infection, faster migrant paces of life can lead to decreases in transmission rate and virulence.Predicting the outcomes of pathogen spillover requires accounting for both differences in tolerance to infection and pace of life between populations. It is also important to consider how movement patterns of populations affect host contact opportunities for pathogens. These results have implications for wildlife conservation, agriculture and human health.more » « less
-
Abstract 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.more » « less
-
Abstract 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.more » « less
-
Abstract In insects and other invertebrates, prior pathogen exposures can improve immune responses and survival to subsequent infections through immune priming. Alternatively, stress and metabolic costs of multiple infections can impair host immunity and survival. The effects of high‐temperature extremes on host–pathogen interactions are not well understood despite the increasing occurrence of heat waves caused by climate change.The response of insects to heat waves and pathogens depends on recent evolutionary history with selective pressures. Domestication of insect pests has occurred in lab colonies of model species, reducing selective pressures for immune and heat stress responses. Lab strains are often used in immunological or heat stress experiments to represent wild field strains, but the efficacy of this approach is seldom evaluated.Using the tobacco hornworm (Manduca sexta), we tested the impact of a heat wave during initial pathogen exposure on survival of a secondary infection withBacillus thuringiensisbacteria. We used a domesticated lab population and a naturally occurring field population ofM. sextato evaluate the impacts of recent domestication on immune and thermal responses.A heat wave during initial infection significantly increased survival of the secondaryB. thuringiensisinfection in the field, but not the lab population ofM. sexta.In the field population, survival of the repeated infection was temperature dependent: exposure to an initial infection event reduced survival of the secondary infection at the control temperature regime, consistent with a stress effect. However, a heat wave during the initial infection event increased survival of the secondary infection, consistent with immune priming effects.The results of this study demonstrate that (a) insect response to thermal stress and pathogens can depend on recent domestication and (b) responses of hosts to repeat pathogen exposures can be temperature‐dependent, suggesting that cross‐talk between the heat stress and immune memory pathways may have important consequences for host–pathogen outcomes under heat wave events. Read the freePlain Language Summaryfor this article on the Journal blog.more » « less
