We currently live in an era of mass extinction, where many species around the world are at high risk of being lost forever, and among these species, amphibians are at much higher risk of extinction than any other (Wake and Vrendenburg, 2008). This comes from a combination of many factors, including climate change, habitat destruction and human land use, the presence of invasive species, and as we’ll be looking at here: the fungal infection chytridiomycosis.
Chytridiomycosis is a skin disease caused by a chytrid fungus, either Batrachochytrium dendrobatidis (Bd), or Batrachochytrium salamandrivorans (Bsal). Though these fungi may be small, they are a big deal when it comes to the health and stability of amphibian populations. They have been implicated for the heavy decline or even outright extinction of a large number of amphibian species, making it potentially the most impactful wildlife disease known (Scheele et al., 2014). These fungi have a number of traits that make it easy for them to spread to amphibians. One such trait is the ability to reside within a host without causing infection, using it as a reservoir from which it can spread to more vulnerable species (Fisher, 2017). This can be seen in the example of the midwife toad and alpine newt, which are carriers for Bsal, and can lead to infection of fire salamander populations.
|Figure 1: Potential pathways for the spread of Bsal in Europe, from Fisher 2017.|
The zoospores of these fungi also have two forms which contribute to their spread among amphibian population. The first is the motile aquatic form, which allows them to establish infection during the tadpole stage (Fisher, 2017). The second is the non-motile form, called an encysted spore, which has a thick cell wall, and are highly resilient. These encysted spores are capable of persisting in the environment while retaining their infectiousness, without needing a host at all for a long period of time. And if that wasn’t enough, it could be the case that birds can act as carriers for these encysted spores, bringing the fungus to new locations and further contributing to the spread of disease over larger distances. As noted by Fisher et al. (2017), it really does seem like amphibians really are in peril from a perfect pathogen. But what exactly do these fungal infections do to amphibians that make it such a problem?
Amphibians are cutaneous respirators. They “breathe” through their skin, allowing them to maintain the correct osmotic balance of electrolytes and water within the body. This is what makes chytrid fungi such a unique threat to amphibians. To other organisms the development of a cutaneous chytrid infection is usually not a big deal, but to amphibians it can directly interfere with their ability to respire (Voyles et al., 2009). The ensuing loss of electrolytes impairs the ability of the heart to function, blood flow to the rest of the body is reduced, and cardiac arrest leads to death as a result of complete collapse of the circulatory system. However, even before that occurs, the now physically impaired and lethargic individual is likely to become a victim of predation or a combination of other stressors as well. As an example of the potential severity of this disease, fire salamanders in the Netherlands that were infected with Bsal experienced a mortality rate of over 96% (Fisher, 2017). A very morbid and unfortunate situation our amphibian friends find themselves in.
Normally, the mucus layer present on the skin of amphibians contains a number of antimicrobial peptides and lysozymes, as well as symbiotic bacteria which all contribute to innate defenses against invading pathogens (Rollins-Smith et al., 2011). Amphibians have also shown to be capable of developing an acquired immune response to chytrid fungi after exposure, with some even developing Bd specific antibodies. So then why is chytridiomycosis such a problem for amphibians? The answer appears to be because chytrid fungi are capable of suppressing immune responses in many species before these defenses are capable of protecting against infection (Ellison et al., 2014). Other environmental stressors can also interfere with the ability of amphibians to mount an appropriate immune defense. Lack of food resources, temperature stress, or exposure to chemicals like pesticides can all increase the likelihood of fungal infection (Rollins-Smith et al., 2011). Furthermore, the amphibian life cycle itself can impair the ability of an individual to resist infection. When a tadpole undergoes metamorphosis into an adult, the immune system also goes through a drastic transition to maturity. This period of time provides an opening for infection to develop while the defenses of the amphibian aren’t at full capacity. Ultimately, this means that the ability for a species of amphibian to defend against chytrid fungi varies heavily based on the level of innate and acquired defenses mounted, the health of the habitat, the climate, and what part of the life cycle the species in question is in.
It is abundantly clear that amphibian populations are in great danger as a result of this disease outbreak, so the obvious follow-up question is what can we do about this ongoing threat? While there is no silver bullet for stopping chytridiomycosis outright, there are a number of potentially promising forms of intervention that could help to bring mortality rates down to less extreme levels. In short-term or small scales, the direct treatment of individuals with antifungals is shown to be an effective method of temporarily controlling an outbreak, but more long-term measures are needed to ensure success in restoring populations (Garner et al., 2016). Scheele et al. (2014) provide a framework of three potential classes of action to protect amphibians from fungal infection. The first class is Environmental Manipulation. As mentioned previously, there are a number of environmental factors that influence the chance of successful infection. Reducing the presence chemical pollutants can reduce stress on amphibian populations are lower infection rates. The creation of warm regions in the habitat, such as warm pools of water, areas of high sun exposure to bask in, or the introduction of artificial heat sources can also allow species to initiate behavioural fever, raising their body temperature to levels that are no longer ideal for chytrid fungi to survive. Finally, methods such as bio-augmentation, which involves introducing microbes with the ability to inhibit chytrid fungi to the environment, can potentially provide an ecosystem-wide treatment, so long as proper testing is done to ensure that this will not negatively impact the environment in any way.
Artificial ponds for the captive breeding of the endangered Pseudophryne corroboree.
(Figure 2 from Scheele et al., 2014)
When manipulation is not a reasonable solution, the Amphibian Introduction class is next in line. This involves the translocation of amphibian populations to refugia: environments that are ideal for the species, but poor for chytrid fungus. This method does require that it is ensured that this translocation will not cause any impacts in the new environment. Alternatively, captive bred amphibians can be added to wild populations in order to increase the buffering capacity of the ecosystem, allowing higher likelihood of survival for a population even after an chytrid epidemic. Finally, failing the previous two classes, the last class is Ex-Situ Conservation, which involves keeping colonies in captivity. Infected individuals are treated with chemicals or heat to kill the fungus, and individuals are bred in order to improve resistance among the population while maintaining genetic diversity (Scheele et al. 2014).
While these treatments are still in development and have not been used in proper field tests yet, they definitely have the potential to rescue amphibian populations. However, the fact remains that many amphibians around the world are critically imperilled, so there is clear need for feasibility research as soon as possible if we want to prevent any more extinctions. The loss of mass amounts of amphibians could lead to huge impacts on many ecosystems around the world, and it is all but guaranteed to happen unless we take action.
Ellison AR et al. 2014. Fighting a Losing Battle: Vigorous Immune Response Countered by Pathogen Suppression of Host Defenses in the Chytridiomycosis-Susceptible Frog Atelopus zeteki. G3-Genes Genom Genet 4(7): 1275-1289.
Fisher MC. 2017. Ecology: In peril from a perfect pathogen. Nature 544(7650): 300-301.
Garner TWJ et al. 2016. Mitigating amphibian chytridiomycoses in nature. Philos T Roy Soc B 371(1709).
Rollins-Smith LA et al. 2011. Amphibian Immune Defenses against Chytridiomycosis: Impacts of Changing Environments. Integr Comp Biol 51(4): 552-562.
Scheele BC et al. 2014. Interventions for Reducing Extinction Risk in Chytridiomycosis-Threatened Amphibians. Conserv Biol 28(5): 1195-1205.
Voyles J, et al. 2009. Pathogenesis of Chytridiomycosis, a Cause of Catastrophic Amphibian Declines. Science 326(5952): 582-585.
Wake DB and Vredenburg VT. 2008. Are we in the midst of the sixth mass extinction? A view from the world of amphibians. P Natl Acad Sci USA 105(1): 1466-1473.