Chytridiomycosis in Amphibians

Overview of the emerging infectious disease Chytridiomycosis in amphibian populations

By: Megan Potter

Amphibian populations have been declining worldwide at an alarming rate for the past three decades, especially in Australia and North, Central and Latin America (2). Scientists believe that the population decline is due to multiple factors from habitat loss to climate change and even environmental chemicals. However, there is emerging evidence that the amphibian population decline could also be due to the infectious disease chytridiomycosis, caused by the chytrid fungus Batrachochytrium dendrobatidis (1). 

Blue Poison Dart Frog

The chytrid fungus B. dendrobatidis got its name from the blue poison dart frog (Dendrobates azureus).  This fungus is found in the phylum Chytridiomycota and lives exclusively in the water or in moist environments. The chytrids are one of the oldest and most primitive types of fungi and until recently were considered members of the Kingdom Protista. The B. dendrobatidis life cycle has two main stages:  motile, which are waterborne zoospores, used for dispersal and a stationary thallus, which develops into a zoosporangium for asexual reproduction (3).

Chytrid Life Cycle

           In the motile stage, which lasts only twenty-four hours, the waterborne zoospores (3-5 μm in diameter with a posterior flagellum) attach and encyst in amphibian adult epithelial cells (3). Zoospores can also encyst in the keratinizing epidermis of tadpole mouthparts. The zoospores will colonize the cells of the stratum corneum, the outermost layer of the epidermis consisting of dead cells that lack nuclei and organelles, this layer of skin also contains the cytoskeletal protein keratin, which keeps the skin hydrated (1). With the zoospores ability to replicate away from vascularized layers of skin, that contain macrophages, the B. dendrobatidis pathogen can be hidden from cells of the amphibian’s adaptive immune system (2). When the zoospores encyst they re-absorb their flagellum and develop fine branching rhizoids and will eventually develop into a stationary thallus. The thallus will form single non-dividing mature zoosporangia, this development is known as momocentric (3). The cytoplasm of the zoosporangia will start to cleave and formation of flagellated zoospores occurs. The release of the zoospores to the external environment is done through a discharge tube which points toward the hosts exposed skin surface.

            There are certain adaptations of B. dendrobatidis that suggest it has evolved to live in skin. One of the adaptations is the fact that it invades and grows in living epidermal cells that contain prekeratin and completes its development in dead superficial cells that are completely keratinized; which shows that keratinizing epidermis is a requirement for B. dendrobatidis when it occurs as a parasite (1,3). A second adaptation is that the discharge tubes have the ability to merge with and dissolve the epidermal cell membrane and orient themselves towards the external environment, how this is done is still not know (3). A third adaptation of B. dendrobatidis is that thalli found in the skin of infected frogs were clustered together instead of uniformly distributed (2). This suggests that transmission of B. dendrobatidis is done over short distances, for example, from one area of the skin to the next. Another adaptation is the shift in B. dendrobatidis life history, it’s optimal range is between 17-23°C but it can also survive in lower temperature ranges between 7-10°C, if the temperature gets higher then 30°C the B. dendrobatidis strain will die (1).

            Signs of chytridiomycosis disease in infected frogs usually occur in individuals that contain the highest loads of zoospores. The primary sign is epidermal hyperplasia and hyperkeratosis, which is the enlargement and thickening of the stratum corneum (1). This thickening of the epidermis can cause a reduction in the plasma electrolyte concentrations and lead to the deterioration of cardiac electrical functioning, which could lead to cardiac arrest in amphibian species. A few other symptoms for chytridiomycosis are laziness, lack of appetite, cutaneous erythema (redness of skin), irregular skin sloughing, abnormal posture, and loss of righting reflex (1).  B. dendrobatidis has been identified in skin that has been molted from amphibians. It has also been hypothesized by some, that by increasing the sloughing of skin (especially in higher temperatures) that it assists amphibians in shedding and clearing the infection from their system.

            The skins of many amphibians are also associated with anti-microbial peptides (AMP), which are produced by epidermal granular glands and secreted at the skin surface. The AMPs are thought to be a first-line defense against B. dendrobatidis infections (4). The diversity of AMPs among amphibian species is quite remarkable, related species will share families of peptides but no overlap is seen in individual peptides from one species to another. The fact that AMPs have such a species-specific potency could explain why certain wild amphibians have a resistance to chytridiomycosis (5). For example, the AMP of temporin A, a member of the temporin family, is produced by many species of the genus Rana, suggesting that this peptide can penetrate the cells membranes. It is able to do this because of its α-helical conformation, which is important for its effectiveness against B. dendrobatidis (6). It has been shown that the amphibian immune system has the capacity to develop some protection against the fungus and its possible mortality. However, more work is still needed on AMPs and other possible mechanisms used by amphibian species that are immune to chytridiomycosis.

 The chytrid fungus B. dendrobatidis was just recently included as a notifiable pathogen by the World Organization for Animal Health (OIE), because of its high global impact and its threat to biodiversity. The decline in amphibians caused by B. dendrobatidis has been described by some as the most extreme loss of biodiversity due to a disease in recorded history.

Work Cited

1. Voyles, J; Erica B. Rosenblum, and Lee Berger. (2011) Interactions between Batrachochytrium dendrobatidis and its amphibian hosts: a review of pathogenesis and immunity. Microbes and Infection. 13, 25-32

2. Rollins-Smith, L.A. and Conlon, J.M. (2005) Antimicrobial peptide defenses against

            Chytridiomycosis, an emerging infectious disease of amphibian populations. Dev.

            Comp. Immunol. 29, 589-598

3. Berger, Lee, et al. (2005) Life cycle stages of the amphibian chytrid Batrachochytrium dendrobatidis. Dis. Aquat. Org. 68, 51-63

4. Rollins-Smith, L.A., et al. (2002) Antimicrobial peptide defenses against pathogens associated with global amphibian declines. Dev. Comp. Immunol. 26, 63-72

5. Conlon J.M, et al. (2004) Antimicrobial peptides from ranid frogs: taxonomic and phylogenetic markers and a potential source of new therapeutic agents. Biochem. Biophys. 1696, 1-14

6. Rollins-Smith, L.A., et al. (2003) Activities of temporin family peptides against the chytrid fungus (Batrachochytrium dendrobatidis) associated with global amphibian declines. Antimicrob. Agents Chemother. 47, 1157-60