The emerging amphibian disease, chytridiomycosis, was unknown even a decade ago. It is now implicated in causing the extinction of more than 100 amphibian species worldwide and is a serious threat to hundreds more, including the mountain yellow-legged frog (Wake and Vredenburg 2008). In fact, chytridiomycosis has now become at least as important a threat to the mountain yellow-legged frog as introduced fish.
Life cycle of the pathogen
Cross-section of the skin of a frog infected with B. dendrobatidis showing many zoosporangia (S), one with a discharge tube (D). From Berger et al. 1998. Proceedings of the National Academy of Sciences, USA 95:9031. Chytridiomycosis is caused by the amphibian chytrid fungus, Batrachochytrium dendrobatidis. This pathogen was first described in 1999 and is the only member of Phylum Chytridiomycota known to infect a vertebrate host. It has a simple life cycle in which a flagellated motile zoospore encysts in keratinized amphibian tissues (skin of adults and juveniles, mouthparts of tadpoles) and forms a zoosporangium. Each zoosporangium subsequently produces zoospores through asexual reproduction. When mature, zoospores are released into the water through a discharge tube. Chytridiomycosis apparently kills amphibians by causing severe disruption of skin functions and associated osmotic imbalance. Although B. dendrobatidis is currently known only to infect amphibians, it is uncertain whether alternative hosts exist, or whether this pathogen can utilize non-living organic matter. In addition, although the only known mode of dispersal for B. dendrobatidis is via the zoospore stage, its rapid spread through even remote and undeveloped areas suggests the existence of other means of dispersal.
B. dendrobatidis and amphibian declines
The cause of the recent emergence of chytridiomycosis in amphibians is unclear. Some scientists have suggested that its emergence is a result of human-mediated spread to areas outside of its native range or of environmental changes such as global warming. Although its historic distribution is not known, the first record of B. dendrobatidis is from an amphibian collected in southern Africa in 1938. B. dendrobatidis subsequently appeared in amphibian populations all around the world. Chytridiomycosis has been linked to amphibian die-offs in many locations, including the United States, Mexico, Central America, South America, Europe, Australia, and New Zealand. Impacts of chytridiomycosis tend to be particularly severe in montane regions characterized by relatively cold temperatures.
It is unclear whether amphibians are able to mount an effective immune response against B. dendrobatidis infection. Like other vertebrates, amphibians defend themselves against infection via both innate and adaptive immune systems. Innate immune defenses are non-specific and do not confer lasting immunity against a pathogen. In addition to typical innate immune responses such as inflammation and cellular activity, the amphibian innate immune system also includes skin peptides and symbiotic skin bacteria, both of which can have powerful antimicrobial properties. The adaptive immune system allows organisms to mount pathogen-specific responses. This targeted response is maintained and can be quickly reactivated if the pathogen is encountered in the future. Vaccinations work by activiting the adaptive immune system and creating permanent protection against the target pathogen. Current research suggests that the adaptive immune system may not confer any protection against B. dendrobatidis, perhaps because B. dendrobatidis is able to evade the adaptive immune system or even suppress adaptive immunity.
Mountain yellow-legged frogs produce numerous antimicrobial skin peptides that strongly inhibit the growth of B. dendrobatidis (Rollins-Smith et al. 2006). In addition, the skin of mountain yellow-legged frogs harbors a community of symbiotic bacteria, some species of which may hinder infection and colonization by B. dendrobatidis (Woodhams et al. 2007; Lam et al. 2010). Laboratory experiments show that the addition of an antifungal bacteria to frog skin reduced chytridiomycosis severity and prevented mortality in mountain yellow-legged frogs (Harris et al. 2009). Field experiments to test whether a bacterial augmentation strategy may be effective at controlling chytridiomycosis are currently being planned. In contrast to results showing that selected components of the mountain yellow-legged frog innative immune system may confer some level of protection against B. dendrobatidis, research has so far failed to demonstrate the involvement of the adaptive immune system. For example, immunization with B. dendrobatidis does not protect mountain yellow-legged frogs from subsequent chytridiomycosis (Stice and Briggs 2010).
Impact on mountain yellow-legged frogs
Within the range of the mountain yellow-legged frog, chytridiomycosis was first detected in 1975 in specimens of Rana muscosa collected just west of Sequoia National Park (Ouellet et al. 2005; originally misidentified as Rana boylii). Chytridiomycosis is now common in R. muscosa and Rana sierrae populations throughout the Sierra Nevada (Fellers et al. 2001; Knapp and Morgan 2006; Rachowicz et al. 2006), and is also present in R. muscosa populations in southern California. B. dendrobatidis strains from throughout the Sierra Nevada are genetically very similar, suggesting recent introduction and spread (Morgan et al. 2007). Chytridiomycosis outbreaks in R. muscosa and R. sierrae populations typically cause mass die-offs of adults and juveniles, and frequently lead to population extinctions (Rachowicz et al. 2006; Vredenburg et al. 2010). However, some mountain yellow-legged frog populations are persisting despite ongoing B. dendrobatidis infections (Briggs et al. 2005; Briggs et al. 2010).
The mechanisms underlying the persistence of mountain yellow-legged frog populations despite chytridiomycosis is the subject of an intense research effort. This effort is investigating the role of between-population differences in frog susceptibility and B. dendrobatidis virulence, as well as environmental factors (e.g., water temperature) that could change the dynamics of the frog-disease interaction. Differential frog susceptibility could result from numerous factors, including variation in frog immune defenses such as antimicrobial skin peptides or symbiotic skin bacteria. Regardless of the mechanism, these persistent frog populations may well be the only hope for preventing the extinction of the mountain yellow-legged frog.