Croaking Frogs: The global amphibian decline has been attributed, among other causes, to an amphibian skin disease chytridiomycosis caused by the fungus Batrachochytrium dendrobatidis . However, how this pathogen causes mortality has been unclear. Voyles et al. (p. 582 ) show that this superficial skin infection may lead to cardiac failure owing to changes caused by lowered ion transport through the skin and consequent electrolyte reduction in the blood.

Panzootic chytrid fungus out of Asia: Species in the fungal genus Batrachochytrium are responsible for severe declines in the populations of amphibians globally. The sources of these pathogens have been uncertain. O'Hanlon et al. used genomics on a panel of more than 200 isolates to trace the source of the frog pathogen B. dendrobatidis to a hyperdiverse hotspot in the Korean peninsula (see the Perspective by Lips). Over the past century, the trade in amphibian species has accelerated, and now all lineages of B. dendrobatidis occur in traded amphibians; the fungus has become ubiquitous and is diversifying rapidly. Science , this issue p. 621 ; see also p. 604

Mounting evidence implicates the disease chytridiomycosis, caused by the fungus Batrachochytrium dendrobatidis, in global amphibian declines and extinctions. While the virulence of this disease has been clearly demonstrated, there is, as yet, no mechanistic explanation for how B. dendrobatidis kills amphibians. To investigate the pathology of chytridiomycosis, blood samples were collected from uninfected, aclinically infected and clinically diseased amphibians and analyzed for a wide range of biochemical and hematological parameters. Here, we show that green tree frogs Litoria caerulea with severe chytridiomycosis had reduced plasma osmolality, sodium, potassium, magnesium and chloride concentrations. Stable plasma albumin, hematocrit and urea levels indicated that hydration status was unaffected, signifying depletion of electrolytes from circulation rather than dilution due to increased water uptake. We suggest that B. dendrobatidis kills amphibians by disrupting normal epidermal functioning, leading to osmotic imbalance through loss of electrolytes. Determining how B. dendrobatidis kills amphibians is fundamental to understanding the host-pathogen relationship and thus the population declines attributed to B. dendrobatidis. Understanding the mechanisms of mortality may also explain interspecific variation in susceptibility to chytridiomycosis.

Mounting an immune response to fight disease is costly for an organism and can reduce investment in another life-history trait, such as reproduction. The terminal investment hypothesis predicts that an organism will increase reproductive effort when threatened by disease. The reproductive fitness of amphibians infected with the deadly fungal pathogenBatrachochytrium dendrobatidis(Bd) is largely unknown. In this study, we explored gametogenesis in two endangered and susceptible frog species,Pseudophryne corroboreeandLitoria verreauxii alpina.Gametogenesis, both oogenesis and spermatogenesis, increased when animals were experimentally infected withBd. InP. corroboree, infected males have thicker germinal epithelium, and a larger proportion of spermatocytes. InL. v. alpina, infected males had more spermatic cell bundles in total, and a larger proportion of spermatozoa bundles. In femaleL. v. alpina, ovaries and oviducts were larger in infected animals, and there were more cells present within the ovaries. Terminal investment has consequences for the evolution of disease resistance in declining species. If infected animals are increasing reproductive efforts and producing more offspring before succumbing to disease, it is possible that population-level selection for disease resistance will be minimized.

Amphibian chytridiomycosis, caused by infection with Batrachochytrium dendrobatidis (Bd), is the most devastating vertebrate disease on record. Reservoir hosts are likely to be important in the Bd‐amphibian system because many amphibian species can carry infections without experiencing mortality. However, while a variety of reservoirs have been proposed, few have been empirically demonstrated to act as competent reservoir hosts. In this study, we investigate whether the common eastern froglet, Crinia signifera, a non‐declining species that is widespread in eastern Australia, is a reservoir host for Bd infection. We conducted a long‐term, large‐scale field survey to investigate disease dynamics in C. signifera at sites where four sympatric, threatened anuran species have severely declined. We also monitored Bd‐infected C. signifera in the laboratory to determine susceptibility and survivorship. Finally, we assessed population age structure to investigate disease impact in the wild. We found that C. signifera is a competent reservoir host, maintaining high prevalence and infection intensities in the wild and in the laboratory, with no signs of sub‐lethal effects or clinical disease. In the wild, the modal age is 4 years with individuals living up to 6 years, indicating that adults can survive across multiple years despite high infection prevalence and intensity. The occurrence of C. signifera at sites with remnant populations of threatened species likely contributes to ongoing disease impact in declining species decades after the arrival of Bd. The presence of C. signifera at sites where threatened species have become extinct inhibits effective reintroductions, and we recommend avoiding sites with high reservoir host abundance when planning reintroductions.