Batrachochytrium dendrobatidis - The Link Between Climate Change and Amphibians

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Fig 1. Illustration shows a cross-sectional view of a Batrachochytrium dendrobatidis zoospore. The spore type responsible for the infectious disease called chytridiomycosis. [1]

By Scott Upton

Batrachochytrium dendrobatidis(Bd) is a pathogen primarily found in amphibians, and it’s presence can have devastating effects on amphibian populations. Bd is responsible for causing chytridiomycosis, or chytrid, in amphibians all across the world in response to rising global temperatures (Fig. 1) [1]. Bd can be found on all continents in which amphibians are present and as of 2019, Bd has been found to infect 1,015 of 1,854 species (54%) and has lead to the decline of 6.5% of all amphibian species and the extinction of 90 species [2]. Bd has been given the nickname “the doomsday fungus” in response to its incredible ability to reduce biodiversity and its ability to produce mass extinction of species. At the time, Bd is said to have led to the largest reduction of biodiversity of any species of vertebrates in the world [2]. Unfortunately, this fungus is not slowing down any time soon and its effects will continue to devastate amphibian populations as long as temperatures continue to fluctuate [2].

Recent studies on climate change have suggested that the frequency of temperature fluctuations will continue to rise without warning [3]. Global climate change and its effects on infectious diseases has proven to be one of the most formidable ecological challenges in modern history. With that being said, there has been controversy over whether or not climate change and the increase in infectious diseases are directly linked without the addition of other factors. Despite controversy of the two being directly linked, the combination of climate change and infectious diseases are creating significant declines in biodiversity as well as extinction across amphibian populations. Both Bd and amphibians are sensitive to the results of climate change, but Bd is able to outperform amphibians when the performance gap between the pathogen and host is at its greatest; this can be called the thermal mismatch hypothesis [4]. This hypothesis suggests that hosts who are adapted to cooler environments will be more susceptible to chytridiomycosis in unusually warm conditions. Similarly, hosts who are adapted to warmer temperatures are more susceptible to chytridiomycosis in unusually colder temperatures. Scientists may be able to mitigate the effects of chytridiomycosis on amphibian populations by further studying Bd in terms of host interactions and comparing it to temperature fluctuations. With that being said, mother nature has a strange way of correcting human influence on the environment and amphibians may be able to avoid the risks Bd poses by adapting to unusual environments.

Global Distribution and Origin of Batrachochytrium dendrobatidis

Fig 2. Global distribution of differnt Batrachochytrium dendrobatidis(Bd) lineages including Batrachochytrium salamandrivorans (Bsal), another severe fungus that causes chytridiomycosis. [2]

There has been debate on how Bd has risen to the forefront of amphibian declines, but two competing hypotheses have shed light on how Bd has become a global issue among amphibians. The first hypothesis, the “endemic pathogen hypothesis” (EPH), suggests that Bd led to an outbreak in mutualistic amphibians in which the virulence of the pathogen created imbalanced infection rates as a result of global climate change [2]. The second hypothesis, the “novel pathogen hypothesis” (NPH), suggests that chytridiomycosis consequentially emerged from global trade routes and invaded weak ecosystems [2]. Africa was initially thought to be the origin of chytridiomycosis due to the fact that skin samples of African clawed frogs (Xenopus laevis) revealed the presence of Bd in 1938 [5]. The NPH is thought to have led to the introduction of Bd into amphibian populations due to decades of global trading of African clawed frogs. Recent genomic studies have revealed that genetic diversity has significantly decreased in the African clawed frogs, but high allelic diversity has been maintained in North American bullfrogs despite both species being ravished by the chytrid fungus [5]. This suggests that Bd may not have origins in Africa, rather that Bd infections in amphibians can be carried across continents with global trade, supporting the NPH. Early genome sequencing of Bd across globally distributed sites experiencing chytridiomycosis revealed strikingly similar patterns in which several lineages were identified. BdGPL, BdCAPE,BdCH, and BdAsia1-3 strains were all identified and labeled based on geographic distribution (Fig. 2) [2]. BdGPL was the only globally distributed lineage, and it has been found on four continents (Fig. 2) [2]. BdCAPE was given its name based on its distribution across Cape regions of Southern Africa, and BdCH was found in isolated regions of Switzerland (Fig. 2) [2]. Lastly, BdAsia1-3 strains are obviously found throughout Asian amphibian populations and are now considered to be the origin of chytridiomycosis [2].

The commercial global trade of amphibians continues to transfer the fungus between populations across the globe, however new studies have revealed Bd’s origins can be dated back to Eastern Asia in the 20th century [6]. Analysis of over 200 hosts insinuated that the species BdAsia1 had originated in Korea and is considered the ancestral population of Bd [6]. BdAsia1 is thought to have emerged approximately 150 years ago due to mitochondrial DNA analyses and dating [6]. Resistance to the fungus has led to little decline in Asain amphibian populations in recent years, suggesting that the amphibians who were exposed 150 years ago have developed stable responses to the pathogen.

In order to halt the transmission of Bd, amphibian trading must be put to a halt in order to preserve biodiversity in amphibian species as well as prevent further extinction. As long as trading continues, Bd will continue to expand across the globe affecting the few ecosystems in which the pathogen is not yet prevalent. Not only will Bd continue to devastate amphibian populations, a related pathogen that is functionally different called Batrachochytrium salamandrivorans (Bsal) has begun to threaten salamander populations [3]. Both mitigation and prevention of trading must be the response to chytrid fungus because it will continue to travel across the globe and new strains of the pathogen, such as Bsal, will begin to devastate similar species.

Effects of Chytridiomycosis

Fig 3. Trends of survival over 108 days of four different Australian frog species exposed to Batrachochytrium dendrobatidis . Shapes on each line represent mortality of a single amphibian. [7].

Chytridiomycosis is able to travel from host to host via flagellar motility that targets the susceptible skin of amphibians. Infections begin when zoospores land on the amphibian's skin, reabsorb their flagella, and form a new cell wall within the host [8]. The pathogen then moves from the surface of the skin into the stratum granulosum to grow, then into the stratum corneum to mature. In the stratum corneum, Bd grows to full size, infects healthy cells, and forms a zoosporangium which creates more zoospores and multiplies the infection rate [9].

In some species such as Rana catesbeiana (American bullfrog species), chytridiomycosis is somewhat harmless and infected hosts are often unscathed by the fungus. These individuals who do not experience any symptoms are called ‘carrier species’, but the pathogen is still able to spread to other organisms through these asymptomatic carriers. However when susceptible hosts become infected, the chytrid fungus attacks the keratin in the superficial epidermal layer of the skin. Tadpoles primarily only have keratin in their mouths so when they become infected, Bd can cause interferences with feeding and nutrient uptake, but Bd often has nonlethal effects on tadpoles. On the other hand, adult amphibians' skin is full of keratin and they face more lethal consequences than those in the pre-metamorphic stage. Bd causes the skin to thicken and harden which leads to significant consequences for post-metamorphic amphibians. Frogs and other amphibians have unique skin that is responsible for regulating gas and water exchange as well as respiration. So when the pathogen causes the epidermis to thicken, the organisms suffer the consequences of dehydration, suffocation, and improper thermoregulation. The most significant response to a Bd infection is hyperplasia. Hyperplasia causes epidermal cells to swell and die at rapid rates within the skin of amphibians. This triggers a response in the body to begin shedding the dead layers of the skin in order to try and get rid of the pathogen, but this defense system is often fatal. Oftentimes, the rate of skin regeneration is quicker than the rate of shedding, leading to the buildup of multiple layers of skin that can create improper ion transportation and osmotic imbalance [10]. If Bd impaires ion transportation, the endocrine responses that usually balance ion transport will begin to elevate glucocorticoid responses which results in immune suppression [8]. Once immune suppression occurs, the amphibian can either no longer fight off the pathogen, or the body will go into cardiac arrest, both results are consequently fatal. Cardiac arrest is the primary cause of death in amphibians infected with Bd .

An experiment conducted in 2007 compared the effects Bd in respect to mortality rate. The scientists exposed four species (Lit. caerulea, Lit. chloris, M. fasciolatus and Limnodynastes tasmaniensis) of Australian anurans (78 total individuals) to Bd and recorded mortality rates up until 108 days of exposure (Fig. 3) [7]. The results showed that of the four species of frogs exposed, only Limnodynastes tasmaniensis had a mortality rate of 0% in which all 18 frogs exposed survived after 18 days (Fig. 3) [7]. Lit. caerulea and M. fasciolatus experienced a mortality rate of 5% in which only 1 of 20 individuals in each species survived the 108 days of exposure, and lastly, Lit. chloris experienced a mortality rate of 35% in which 7 of 20 individuals survived 108 days (Fig. 3) [7]. The median survival time of Lit. chloris and M. fasciolatus were 21.5 and 26.8 days, and the median survival time of Lit. caerulea was approximately 9 days [7]. Based on the data, Limnodynastes tasmaniensis can be classified as a ‘carrier species’ due to the fact that every frog survived the 108 day trial with little to no symptoms. As previously explained, asymptomatic carriers of Bd are still able to expose less fortunate species to the effects of Bd and spread the pathogen. Interestingly enough Lit. chloris showed signs of an adaptive immune response to the pathogen because around 50 to 70 days of exposure there was a plateau in which no deaths occured (Fig. 3) [7]. This is interesting because despite the plateau, Lit. chloris individuals ended up dying in the following 35 days [7]. This is a promising sign for amphibians because there is clearly an adaptive immune response in certain species that are able to fend off the pathogen, and maybe species such as Lit. chloris will eventually be able to outperform the pathogen and prevent biodiversity loss and extinction.

How Climate Change Effects Pathogen and Host Infections

Fig 4. The thermal mismatch hypothesis in isolation. Parasites (red lines) generally have broader thermal performance curves than hosts (blue lines). Parasite growth on hosts is not dependent on how the parasite performs in isolation, rather it is determined by the temperatures at which the parasite is able to outperform the host. For amphibians who are adapted to cooler temperatures, maximum parasitic growth is expected to be prevalent at moderately warmer temperatures. Conversely, warm adapted amphibians experience maximum parasitic growth at cooler temperatures. [11]

As previously explained in the introduction, climate change models have shown that the magnitude of temperature fluctuations will continue to increase, and the warming of the globe over the last century or so will only speed up this process [12]. Many studies and models have revealed that climate change and infectious diseases are independently able to reduce biodiversity in certain species, however few studies have revealed evidence that climate change and infectious diseases interact together in order to reduce biodiversity of species [11]. Comparing temperature fluctuations in terms of pathogen and host performance can create a valuable framework for understanding how climate change and infectious diseases create a decline in biodiversity.

The thermal mismatch hypothesis proposes the idea that infectious diseases are likely to occur at temperatures where the performance gap between pathogen and host is at its greatest [4]. Both pathogen and host are adapted to their specific environmental temperatures, but when temperatures begin to fluctuate, infectious diseases are often able to outperform their host because they typically have a broader range of temperatures in which they can thrive in comparison to hosts (Fig. 4) [4]. This suggests that hosts who are adapted to cooler temperatures will be susceptible to infection when temperatures begin to fluctuate and rise and vice versa [11]. The chytrid fungus Bd grows best primarily in moderately warm and cooler temperatures; based on 235 species of globally distributed amphibians, warm and cool adapted amphibians had the highest Bd prevalence in cool and warm temperatures, further supporting the thermal mismatch hypothesis (Fig. 4) [4].

Cohen et. al conducted two experiments: A temperature gradient experiment in which Atelopus zeteki (Panamanian Golden frogs) were exposed to Bd zoospores at five different temperatures (14°, 18°, 22°, 26°, and 28°C) as well as a control group with no Bd exposure, and a temperature shift experiment in which Bd infected frogs were acclimated to 20°C and then exposed to temperatures of 17°C, 23°C, or 26°C [11]. The results in the temperature gradient experiment showed that the control group that was not exposed to Bd experienced no effects from temperature fluctuation, but temperature fluctuations to Bd infected frogs significantly increased mortality rate [11]. At the two highest temperatures, 26°C and 28°C, mortality rate rose to 69% and 78% respectively after a week of Bd exposure, however at the two coldest temperatures, 14°C and 18°C, there was only a mortality rate of 6% after a week of Bd exposure [11]. In the temperature shift experiment, host mortality rate due to Bd exposure correlated with temperature fluctuations. Exposed frogs that experienced temperature fluctuations were found to have larger Bd concentrations compared to exposed frogs who did not experience temperature fluctuations [11].

Defense Against Batrachochytrium dendrobatidis

Fig 5. Diagram showing the immune defense systems against Bd in the skin. Secreted mucus contains antimicrobial peptides, antibodies, and inhibitory bacteria. Dermal and epidermal layers contain macrophages, helpful bacteria, and lymphocytes. [8]

Mother nature is extremely resilient and multiple amphibian species are developing immune defense systems as well as bacteria in their skin that are capable of defeating the pathogen. For example, the African clawed frogs (Xenopus laevis), who were once thought to be the origin of the chytrid fungus, have developed mucus full of antibodies capable of binding to Bd [8]. The mucus they secrete contains antimicrobial peptides and lysozymes that defend against Bd (Fig. 5) [8]. When the pathogen attaches to epidermal cells in the stratum corneum, the cells are flooded with macrophages, lymphocytes, and neutrophils which attempt to reduce swelling caused by Bd (Fig. 5) [8]. The mucous and granular glands found in amphibian skin produce bioactive peptides including neuropeptides and antimicrobial peptides that play a role in defense against predators as well as microbes (Fig. 5) [13]. In granular glands, epithelial cell nuclei fuse to form a syncytium filled with granules which are packed with defensive peptides [14]. The granular glands contain myoepithelial cells which release the peptides and after release, the glands are able to restore the peptide contents. Amphibian antimicrobial peptides have the ability to form an amphipathic α-helix which is able to disturb pathogenetic membranes and it is an important defense mechanism against Bd [15]. A number of less frequently exposed species seem to lack this antimicrobial peptide response, which typically results in fatalities.

In addition to immune defense systems, the skin and mucous glands contain symbiotic bacteria which help defend against Bd. Janthinobacterium lividum is an anti-fungal bacteria found in the skin of amphibians and it has been proven to inhibit the growth of Bd [16]. Amphibians who are continuously exposed to Bd have higher levels of bacteria that inhibit Bd in their skin compared to those who are infrequently exposed. It has been found that pretreatment with Janthinobacterium lividum protects certain species of amphibians from untreated Bd infections [16]. Species such as the African clawed frog have been exposed to Bd for about 100 years, insinuating that repetitive exposure has altered their immune response systems to be able to fend off the pathogen [5]. African clawed frogs possess two important peptides that act synergistically with other natural defense systems, such as macrophages and lymphocytes, in order to terminate the pathogen [8]. However in less frequently exposed species, an adaptive lymphocyte-mediated immune response is often unable to fight off the pathogen due to the fact that Bd zoospores release factors that are able to inhibit lymphocyte mediated responses.[8] In order to fight off the pathogen, less frequently exposed amphibian species must be able to suppress the inhibitive factors that zoospores release [8].


As previously explained, there has been little research conducted comparing climate change and parasite-host interactions. More studies must be conducted in order to have a clear understanding that infectious diseases and climate change are not just casual links, rather that they are interdependent and increase linearly [11]. At the present time, in order to halt global Bd infection rates across amphibian populations, stricter policies must be implemented regarding global amphibian trade as well as preventing an increase in climate change.

Further exposure to Bd may allow amphibians to evolve and adapt to the challenges that chytridiomycosis presents. Evidence that immune responses as well as helpful bacteria in the skin are beginning to have noticeable effects against Bd is promising for amphibian populations. Although progress is being made, there are many unanswered questions that are crucial to understanding how Bd and the immune system interact. As of now, it is yet to be determined how Bd is able to inhibit the hosts autoimmune responses, and if or how skin bacteria can be an effective barrier against the pathogen [8]. Continued research must be done on asymptomatic carriers in order to understand how they can fight the effects of Bd.


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Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2021, Kenyon College.