The maintenance of tree diversity has been explained by multiple mechanisms. One of the most thoroughly studied is conspecific negative density dependence, in which specialist plant enemies reduce survivorship of seeds, seedlings or saplings located near adult conspecifics. Although there is much support that conspecific negative density dependence occurs in temperate forests, only a subset of the species investigated thus far exhibit this recruitment pattern. It remains unclear what drives differential susceptibility to conspecifics among tree species. Previous investigators have considered shade tolerance and mycorrhizal type (arbuscular mycorrhizal vs. ectomycorrhizal association) as two traits that might explain differential susceptibility to conspecific negative density dependence. Here, we test whether these two plant traits predict susceptibility of tree saplings to conspecific negative density dependence in a temperate hardwood forest using three responses: spatial point patterns of saplings, sapling growth and sapling survival. Spatial patterns of saplings indicate that shade tolerant species are less sensitive to conspecifics than shade intolerant species, but show no differences based on mycorrhizal type. Conversely, shade tolerant saplings exhibit reduced growth, but not survival, when located in areas with high conspecific density. We interpret this finding in light of the conservative functional strategies of shade tolerant species, which typically have low leaf nitrogen levels and slower growth to divert resources to tissue defence against enemies. We found an effect of mycorrhizal type interacting with adult conspecific density, where arbuscular mycorrhizal species show a greater reduction in growth than ectomycorrhizal species in areas dense with conspecifics.
Resistance and tolerance are unique host defence strategies that can limit the impacts of a pathogen on a host. However, for most wildlife–pathogen systems, there are still fundamental uncertainties regarding (a) how changes in resistance and tolerance can affect disease outcomes and (b) the mechanisms underlying resistance and tolerance in host populations. Here, we first compared observed patterns of resistance and tolerance and their effects on disease outcomes among salamander species that are susceptible to infection and mortality from the emerging fungal pathogen We performed multi‐dose We found that resistance and tolerance differed significantly among salamander species, with the most susceptible species being both less resistance and less tolerant of Our study contributes to a broader understanding of resistance and tolerance in host–pathogen systems by showing that differences in host tolerance can significantly affect whether changes in resistance or tolerance have larger effects on disease outcomes, highlighting the need for species and even population‐specific management approaches that target host defence strategies.
A free
- Award ID(s):
- 1814520
- NSF-PAR ID:
- 10452225
- Publisher / Repository:
- Wiley-Blackwell
- Date Published:
- Journal Name:
- Functional Ecology
- Volume:
- 35
- Issue:
- 4
- ISSN:
- 0269-8463
- Page Range / eLocation ID:
- p. 847-859
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Abstract Synthesis . We conclude that the shade tolerance level and the mycorrhizal type of temperate forest saplings may influence how their growth and survival respond to the adult conspecific trees in their neighbourhoods. -
Reguera, Gemma (Ed.)ABSTRACT Mucosal defenses are crucial in animals for protection against pathogens and predators. Host defense peptides (antimicrobial peptides, AMPs) as well as skin-associated microbes are key components of mucosal immunity, particularly in amphibians. We integrate microbiology, molecular biology, network-thinking, and proteomics to understand how host and microbially derived products on amphibian skin (referred to as the mucosome) serve as pathogen defenses. We studied defense mechanisms against chytrid pathogens, Batrachochytrium dendrobatidis (Bd) and B. salamandrivorans (Bsal), in four salamander species with different Batrachochytrium susceptibilities. Bd infection was quantified using qPCR, mucosome function (i.e., ability to kill Bd or Bsal zoospores in vitro ), skin bacterial communities using 16S rRNA gene amplicon sequencing, and the role of Bd-inhibitory bacteria in microbial networks across all species. We explored the presence of candidate-AMPs in eastern newts and red-backed salamanders. Eastern newts had the highest Bd prevalence and mucosome function, while red-back salamanders had the lowest Bd prevalence and mucosome function, and two-lined salamanders and seal salamanders were intermediates. Salamanders with highest Bd infection intensity showed greater mucosome function. Bd infection prevalence significantly decreased as putative Bd-inhibitory bacterial richness and relative abundance increased on hosts. In co-occurrence networks, some putative Bd-inhibitory bacteria were found as hub-taxa, with red-backs having the highest proportion of protective hubs and positive associations related to putative Bd-inhibitory hub bacteria. We found more AMP candidates on salamanders with lower Bd susceptibility. These findings suggest that salamanders possess distinct innate mechanisms that affect chytrid fungi. IMPORTANCE How host mucosal defenses interact, and influence disease outcome is critical in understanding host defenses against pathogens. A more detailed understanding is needed of the interactions between the host and the functioning of its mucosal defenses in pathogen defense. This study investigates the variability of chytrid susceptibility in salamanders and the innate defenses each species possesses to mediate pathogens, thus advancing the knowledge toward a deeper understanding of the microbial ecology of skin-associated bacteria and contributing to the development of bioaugmentation strategies to mediate pathogen infection and disease. This study improves the understanding of complex immune defense mechanisms in salamanders and highlights the potential role of the mucosome to reduce the probability of Bd disease development and that putative protective bacteria may reduce likelihood of Bd infecting skin.more » « less
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Abstract Emerging infectious diseases have caused population declines and biodiversity loss. The ability of pathogens to survive in the environment, independent of their host, can exacerbate disease impacts and increase the likelihood of species extinction. Control of pathogens with environmental stages remains a significant challenge for conservation and effective management strategies are urgently needed.
We examined the effectiveness of managing environmental exposure to reduce the impacts of an emerging infectious disease of bats, white‐nose syndrome (WNS). We used a chemical disinfectant, chlorine dioxide (ClO2), to experimentally reduce
Pseudogymnoascus destructans , the fungal pathogen causing WNS, in the environment. We combined laboratory experiments with 3 years of field trials at four abandoned mines to determine whether ClO2could effectively removeP. destructans from the environment, reduce host infection and limit population impacts.ClO2was effective at killing
P. destructans in vitro across multiple concentrations. In field settings, higher concentrations of ClO2treatment were needed to sufficiently reduce viableP. destructans conidia in the environment.The reduction in the environmental reservoir at treatment sites resulted in lower fungal loads on bats compared to untreated control populations. Survival following treatment was also higher in little brown bats (
Myotis lucifugus ), and trended higher for tricolored bats (Perimyotis subflavus ).Synthesis and applications . Our results highlight that targeted management of sources for environmental transmission can be an effective control strategy for wildlife disease. We found that successfully reducing pathogen in the environment decreased disease severity and increased survival, but required higher treatment exposure than was effective in laboratory experiments, and the effects varied among species. More broadly, our findings have implications for other emerging wildlife diseases with free‐living pathogen stages by highlighting how the degree of environmental contamination can have cascading impacts on hosts, presenting an opportunity for intervention. -
Abstract Understanding parasite transmission in communities requires knowledge of each species' capacity to support transmission. This property, ‘competence’, is a critical currency for modelling transmission under community change and for testing diversity–disease theory. Despite the central role of competence in disease ecology, we lack a clear understanding of the factors that generate competence and drive its variation.
We developed novel conceptual and quantitative approaches to systematically quantify competence for a multi‐host, multi‐parasite community. We applied our framework to an extensive dataset: five amphibian host species exposed to four parasitic trematode species across five ecologically realistic exposure doses. Together, this experimental design captured 20 host–parasite interactions while integrating important information on variation in parasite exposure. Using experimental infection assays, we measured multiple components of the infection process and combined them to produce competence estimates for each interaction.
With directly estimated competence values, we asked which components of the infection process best explained variation in competence: barrier resistance (the initial fraction of administered parasites blocked from infecting a host), internal clearance (the fraction of established parasites lost over time) or pre‐transmission mortality (the probability of host death prior to transmission). We found that variation in competence among the 20 interactions was best explained by differences in barrier resistance and pre‐transmission mortality, underscoring the importance of host resistance and parasite pathogenicity in shaping competence.
We also produced dose‐integrated estimates of competence that incorporated natural variation in exposure to address questions on the basis and extent of variation in competence. We found strong signals that host species identity shaped competence variation (as opposed to parasite species identity). While variation in infection outcomes across hosts, parasites, individuals and doses was considerable, individual heterogeneity was limited compared to among‐species differences. This finding highlights the robustness of our competence estimates and suggests that species‐level values may be strong predictors for community‐level transmission in natural systems.
Competence emerges from distinct underlying processes and can have strong species‐level characteristics; thus, this property has great potential for linking mechanisms of infection to epidemiological patterns.
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Abstract Numerous theoretical models have demonstrated that migration, a seasonal animal movement behaviour, can minimize the risks and costs of parasite infection. Past work on migration–infection interactions assumes migration is the only strategy available to organisms for dealing with the parasite infection, that is they migrate to a different environment to recover or escape from infection. Thus, migration is similar to the non‐spatial strategy of resistance, where hosts prevent infection or kill parasites once infected. However, an alternative defence strategy is to tolerate the infection and experience a lower cost to the infection. To our knowledge, no studies have examined how migration can change based on combining two host strategies (migration and tolerance) for dealing with parasites.
In this paper, we aim to understand how both parasite transmission and infection tolerance can influence the host's migratory behaviour.
We constructed a model that incorporates two host strategies (migration and tolerance) to understand whether allowing for tolerance affects the proportion of the population that migrates at equilibrium in response to infection.
We show that the benefits of tolerance can either decrease or increase the host's migration. Also, if the benefit of migration is great, then individuals are more likely to migrate regardless of the presence of tolerance. Finally, we find that the transmission rate of parasite infection can either decrease or increase the tolerant host's migration, depending on the cost of migration.
These findings highlight that adopting two defence strategies is not always beneficial to the hosts. Instead, a single strategy is often better, depending on the costs and benefits of the strategies and infection pressures. Our work further suggests that multiple host‐defence strategies as a potential explanation for the evolution of migration to minimize the parasite infection. Moreover, migration can also affect the ecological and evolutionary dynamics of parasite–host interactions.