Amphibian diversity: decimation by disease.

D isease emergence and biodiversity loss are among the most pervasive environmental problems confronting science and society. Widespread and dramatic losses of amphibian populations and species represent the deadly intersection between these issues (1), as illustrated by the work of Lips et al. (2) in this issue of PNAS. Amphibians are one of the most imperiled groups of vertebrates, with nearly half of all species in decline and 100 species extinct or nearly so (3). Although a number of these declines can be linked to habitat loss and land-use changes (4), many of the most rapidly declining species (nearly 50%) occur in areas without obvious environmental changes. Even more disturbing is that affected populations show few signs of recovery, and analyses across species and time confirm the unusual and unidirectional downward trend (5). Since discovery of a chytrid fungus (Batrachochytrium dendrobatidis) pathogenic to amphibians in the mid-1990s (6), increased attention has focused on the pathogen’s role in the death and disappearance of amphibians. Batrachochytrium has been recovered from the skin of dead or dying frogs associated with numerous population declines, particularly from Central America, Australia, and New Zealand (7, 8). Experimental exposure of healthy frogs to chytrid zoospores causes rapid deterioration and death in certain species (6, 9). Although Batrachochytrium cannot explain all enigmatic amphibian population declines, the evidence linking the pathogen to amphibian losses has grown considerably in the last decade, and 60 studies have detailed its origin, pathology, physiology, life cycle, genetic variation, and infection dynamics. Despite enormous progress, the link between Batrachochytrium infection and amphibian population declines has been hindered by data limitations (see ref. 10). During declines in Central America and Australia, for example, little information was available on the changes in chytrid infection prevalence before, during, and after the suspected epidemics or on how prevalence differed between moribund and healthy individuals, which is critical data for evaluating the causal role of infection (10). Collectively, these limitations precluded differentiation between two hypotheses: (i) the infection is entirely novel, spreading among immunologically naı̈ve amphibian populations vs. (ii) it is an endemic infection that has increased in virulence or pathogenicity, likely as the result of environmental changes (11). Without such information, it is impossible to determine whether efforts should focus on slowing the spread of Batrachochytrium or on controlling the environmental cofactors responsible for elevated infection. Finally, pathogens are not supposed to cause host populationor species-level losses because of reduced transmission rates at low host densities, casting doubt as to whether chytrid infection was the cause or a correlate of observed declines.