16.7 Cutaneous chytridiomycosis: an emerging disease of amphibians
Chytridiomycosis is an infectious disease of the skin that affects amphibians worldwide. It is caused by the chytrid fungus Batrachochytrium dendrobatidis, which colonises the epithelium of adult amphibians causing a fatal inflammatory disease.
The disease was only discovered in 1998 (Berger et al., 1998), but it has since been linked to dramatic population declines of amphibian species in western North America, Central America, South America, Australia and Africa. The disease impact in the wild is that in some regions population decline of native amphibian species, already weakened by the effects of pollution and introduced predators, is so devastating as to amount to potential multiple extinction events (Wake & Vredenburg, 2008); not only a loss to the biosphere, but to the pharmaceutical industry too, as amphibians can be an important source of toxins (neurotoxins, vasoconstrictors and pain killers) that could have therapeutic use.
The disease was first described from sick and dead adult amphibians collected from montane rain forests in Queensland (Australia) and Panama (Berger et al., 1998), and this was the first report of parasitism of any vertebrate by a chytrid fungus. Chytrids are ubiquitous in aquatic habitats and moist soil, and are able to degrade cellulose and chitin, and proteins like keratin. Parasitic chytrids are known to infect plants, algae, protists and invertebrates, but B. dendrobatidis colonises the keratinised epithelium of adult amphibians. The pathogen has very low species specificity and causes very high mortality in susceptible populations, so B. dendrobatidis is viewed as a newly emergent pathogen that has reached susceptible amphibian populations in the wild, and has probably been distributed around the world by the pet trade for ‘exotic’ amphibians and freshwater fish (Fisher & Garner, 2007).
So far this remains an amphibian disease and also remains the only example of a chytrid parasite of a vertebrate. Infectious disease is an important component of the population biology of wild animals, as it is one of the balancing factors controlling population size. The occurrence of chytridiomycosis in the wild suggests that Batrachochytrium may have coevolved with some amphibian populations that are in balance with the disease by being tolerant or not susceptible; lowland species of a region, for example, remain unaffected although their highland relatives suffer high mortality. Recent disturbances of rain forest habitats may have introduced the parasite into susceptible amphibian populations in the mountain areas.
The clinical signs of amphibian chytridiomycosis are lethargy, abnormal posture and loss of the animal’s ability to right itself in the water, and sometimes skin lesions, loss of epidermis and ulceration. Haemorrhages can occur in the skin, muscles, or eyes. Death usually occurs a few days after the onset of clinical signs and seems to result from the animal’s inflammatory response to the fungus, either to a toxin or to the aggressive digestion of the epidermal structure by the fungus. This causes epidermal hyperplasia (abnormal proliferation of cells within the skin tissue), which in turn impairs the cutaneous respiration which is essential to the gas balance and osmoregulation of amphibians.
Once established, Batrachochytrium can persist in the keratinised mouthparts of amphibian tadpoles which survive the infection because they are not dependent on cutaneous respiration. This implicates the larval stage as a reservoir host for the pathogen that may enable Batrachochytrium to persist despite reduced populations of adult amphibians. Persistence may be further enhanced by the ability of the chytrid to grow as a saprotroph. Indeed, this capability may greatly increase the impact of the disease and speed up amphibian population decline, and account for the inability of amphibians to recolonise streams in the worst affected areas.
It may seem odd to consider treatments for a disease of frogs, but when faced with the real possibility of threatened extinction of several or even many species, conservation of those species can become a matter of both disease control and treatment of the last few remaining individuals. Some of the more exotic species under threat have been reduced to populations in the range of a few tens or a few hundred adult animals. In practice, conservation at this late stage cannot be done in the wild but it should be feasible to prevent mortalities in captive breeding programmes for these most threatened species.
Proper quarantine procedures on the part of breeders and aquarists could limit or prevent spread of the infection, and some success in clearing the infection in adults has been claimed for treatments with azole antifungal agents. Another apparent cure is to hold the diseased adults at 37ºC for two 8-hour periods, 24 hours apart. The animals have a natural defence in that antimicrobial peptides are produced in glands of the skin and released into skin secretions and the skin is the only organ invaded by the fungus (Rollins-Smith et al., 2002; Zasloff, 2002).
These peptides can kill or inhibit the growth of fungi and are highly effective in inhibiting growth of B. dendrobatidis in suspension culture in vitro. Antimicrobial peptides in the skin secretions could play a role in protection of the skin from initial infection by chytrid zoospores, or protect areas of the skin from disease spreading from adjacent infected areas (Rollins-Smith et al., 2002). However, it is not at all clear whether they offer any promise for treatment of diseased animals or intervention in further spread of this disease.
Updated December 17, 2016