Potential interactions between amphibian immunity, infectious disease and climate change
Article first published online: 24 OCT 2007
Volume 10, Issue 4, pages 420–421, November 2007
How to Cite
Fisher, M. C. (2007), Potential interactions between amphibian immunity, infectious disease and climate change. Animal Conservation, 10: 420–421. doi: 10.1111/j.1469-1795.2007.00148.x
- Issue published online: 24 OCT 2007
- Article first published online: 24 OCT 2007
Environmental conditions can have a great impact on host–pathogen dynamics, and environmental variation has been argued to be a principal driver underlying the emergence of amphibian chytridiomycosis (Pounds et al., 2006). Often, the specific factors that are involved in modulating host/pathogen dynamics are not known; however, they are clearly manifested as changes in the seasonal incidence of the disease. This effect is observed in the seasonal winter cyclicity of human influenza (Viboud, Alonso & Simonsen, 2006) where the change in disease incidence is clear; however, the specific drivers remain cryptic. In order to dissect, model and eventually understand the emergence of infectious disease, we need to know how, and which, environmental factors modulate the disease dynamics. This is possible only when we can dissect the impact of abiotic conditions on the biology, and thus interactions, of the pathogen and its host.
Amphibians are ectotherms, and as such their physiology is uniquely determined by their external environment. Specifically, environmental temperature has a strong effect on the amphibian immune system and components of this system are highly temperature dependent (Raffel et al., 2006). In this case, it is reasonable to expect that the interaction between infectious disease, specifically Batrachochytrium dendrobatidis (Bd), and its amphibian hosts is temperature dependent, an idea that is finding increasing support from environmental studies of this organism (Pounds et al., 2006; Bosch et al., 2007). Woodhams et al. (2007) here present a convincing account of how four different Australian amphibian species show differences in susceptibility to infection by Bd. While such inter-specific differences in susceptibility to Bd are now well documented, Woodhams et al. take the next step and show how these species-level differences correlate with the animals' ability to produce several components of the innate amphibian immune system – specifically antimicrobial peptides and circulating granulocytes. In the light of these findings, it is interesting to ask the question: How are these components of amphibian immunity influenced by the animals environment and how ‘context dependent’ is the susceptibility, and innate immunity, of specific amphibian species to Bd? Answers to these questions are crucial. Woodhams et al. have shown the existence of a species of frog, Limnodynastes tasmaniensis, that is highly resistant to chytridiomycosis and produces peptides with potent anti-Bd activity. However, surviving a Bd infection will be a function of the strength of response that the host can mount, and the growth rate of the pathogen. It is not clear whether animals that have been kept in stable laboratory environments accurately reflect the condition, and thus susceptibility, of animals in nature. Wild amphibians will vary greatly in condition within a cohort, and between years, and this is likely to cause substantial variation in these animals' ability to mount an anti-Bd response. In this case, what appears to be a ‘Bd-resistant’ species in the laboratory may be still at risk in nature – it is generally not possible to make strong statements of conservation relevance from laboratory assays until the findings have been replicated in quasi-natural populations. Therefore, it is first important to replicate Woodhams et al. experiments across a range of temperatures in order to determine whether the four amphibian species here exhibit different temperature optima in their expression of innate immunity; amphibia have likely optimized their fitness in the face of trade-offs between the costs of immunity and the growth rates of parasites, and this could be tested in controlled-temperature environments. Second, it is necessary to determine whether innate immunity varies in natural environments, how this variation is partitioned between individuals and seasons, and whether natural environmental variation in temperature impacts the expression of amphibian species' innate immunity.
These experiments are not simply of academic interest. Rapid climate change is occurring and amphibians that have optimized their immunity to cope with pathogens within specific temperature envelopes may find that their range of anti-pathogen responses is inadequate within our fast-approaching ‘new’ environments. While little data exist on the anti-pathogen response of animals in changing environments, a smoking gun exists showing that global warming is affecting the body condition of common toads in the United Kingdom as a consequence of increases in the animals metabolic rate during hibernation (Reading, 2006). Such physiological stress will likely be directly linked to these animals' ability to mount a successful immune response to infectious disease during their spring emergence, and in the face of cold-tolerant pathogens such as Bd, mortality effects may be non-linearly related to changing temperatures. The study here by Woodhams and colleagues has provided an important insight into the mechanisms that amphibians use to combat infectious disease – the baton that is handed here to the global community is to understand how amphibian immunity is likely to behave under current scenarios of changing climates, and how this is likely to reflect on the dynamics of amphibian species and their pathogens.
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