Posted by: oikosasa | May 7, 2013

Top of the pops

One of the most cited papers in Oikos, during 2011 (published 2009 and 2010) is “Life history tradeoffs influence mortality associated with the amphibian pathogen Batrachochytrium dendrobatidis”  Trenton W.J. Garner and co-workers. Here, Trent gives a short summary about the paper and tries to explain why it has been so important.

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The chytridiomycete fungus Batrachochytrium dendrobatidis is a potentially lethal parasite of amphibians considered by many to be a primary factor behind global amphibian declines. It’s been associated with mass mortality and amphibian species decline on four continents and is the subject of a heck of a lot of research effort. However, at the time of the work, almost no published studies had attempted to test hypotheses developed from field observations of infection and mortality, and none had done so using both robust experimental design and multiple life history stages. The study was a real team effort, incorporating the results of extensive field work, multiple experiments and a concerted effort to isolate the parasite from field mortalities. While the results of experiments broadly supported the conclusions derived from field data (infection and death are predominantly related and Batrachochytrium dendrobatidis is likely the cause of post-metamorphic mass mortality events of common toads Bufo bufo in Spain), some previously unconsidered dynamics were revealed. We found that increased mortality was associated with weaker doses of the fungus, but often when infection did not appear to have occurred. We have since shown this to be the case in another amphibian species (Luquet et al 2012 Evolution).

Exactly how the risk of mortality can increase without detectable infection at time of death remains uncertain, but this is certainly different from what is seen in highly susceptible host species, where the burden of infection correlates positively with increased risk of death. As well in our study decoupling of infection from mortality was only detected in larvae. Previous to this, the tadpole stage was primarily overlooked as a stage susceptible to any substantial costs imposed by chytridiomycosis. This is because the parasite requires superficial keratinized tissue to proliferate, and this kind of keratin is only ubiquitously available on host anurans after metamorphosis, when the keratinized stratum corneum is fully developed. I think this may be the most interesting part of the study, that potentially lethal costs may be accrued by a host species even when the tissue that is the primary target for infection is still not fully available to the parasite.

For me one of the most satisfying outcomes of this study has been the ability to export the experimental methodology to other labs, which we have done through our EU-funded project RACE (Risk Assessment of Chytridiomycosis for Europe’s amphibians, http://www.bd-maps.eu). Several researchers in several countries have benefitted from using techniques developed during this study, most importantly several graduate students. We’ve also employed our experimental system to explore relationships between climate change and chytridiomycosis (Garner et al. 2011 Global Change Biology) and investigate the evolution of the fungus itself (Fisher et al. 2009 Mol Ecol, Farrer et al. 2011 PNAS). In doing so, I believe we’ve been able to shine some light on the rather unpredictable and context-dependent relationships between Batrachochytrium dendrobatidis and amphibian hosts that are not highly susceptible to chytridiomycosis, but may still experience the lethal form of the disease.

We use cell culture flasks to house tadpoles individually through metamorphosis. This system allows us to replicate extensively while keeping the individual animal the unit of replication. Replicating treatments 30 or 40 times is easily achievable for most experiments using this approach. Not bad for a vertebrate.

We use cell culture flasks to house tadpoles individually through metamorphosis. This system allows us to replicate extensively while keeping the individual animal the unit of replication. Replicating treatments 30 or 40 times is easily achievable for most experiments using this approach. Not bad for a vertebrate.

 

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