Anthropogenic trade and development have broken down dispersal barriers, facilitating the spread of diseases that threaten Earth's biodiversity. We present a global, quantitative assessment of the amphibian chytridiomycosis panzootic, one of the most impactful examples of disease spread, and demonstrate its role in the decline of at least 501 amphibian species over the past half-century, including 90 presumed extinctions. The effects of chytridiomycosis have been greatest in large-bodied, range-restricted anurans in wet climates in the Americas and Australia. Declines peaked in the 1980s, and only 12% of declined species show signs of recovery, whereas 39% are experiencing ongoing decline. There is risk of further chytridiomycosis outbreaks in new areas. The chytridiomycosis panzootic represents the greatest recorded loss of biodiversity attributable to a disease.

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Amphibian fungal panzootic causes catastrophic and ongoing loss of biodiversity

Globalized infectious diseases are causing species declines worldwide, but their source often remains elusive. We used whole-genome sequencing to solve the spatiotemporal origins of the most devastating panzootic to date, caused by the fungus Batrachochytrium dendrobatidis, a proximate driver of global amphibian declines. We traced the source of B. dendrobatidis to the Korean peninsula, where one lineage, BdASIA-1, exhibits the genetic hallmarks of an ancestral population that seeded the panzootic. We date the emergence of this pathogen to the early 20th century, coinciding with the global expansion of commercial trade in amphibians, and we show that intercontinental transmission is ongoing. Our findings point to East Asia as a geographic hotspot for B. dendrobatidis biodiversity and the original source of these lineages that now parasitize amphibians worldwide.

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Recent Asian origin of chytrid fungi causing global amphibian declines

Infectious diseases affect people, domestic animals and wildlife alike, with many pathogens being able to infect multiple species Fifty years ago, following the wide-scale manufacture and use of antibiotics and vaccines, it seemed that the battle against infections was being won for the human population Since then, however, and in addition to increasing antimicrobial resistance among bacterial pathogens, there has been an increase in the emergence of, mostly viral, zoonotic diseases from wildlife, sometimes causing fatal outbreaks of epidemic proportions Concurrently, infectious disease has been identified as an increasing threat to wildlife conservation A synthesis published in 2000 showed common anthropogenic drivers of disease threats to biodiversity and human health, including encroachment and destruction of wildlife habitat and the human-assisted spread of pathogens Almost two decades later, the situation has not changed and, despite improved knowledge of the underlying causes, little has been done at the policy level to address these threats For the sake of public health and wellbeing, human-kind needs to work better to conserve nature and preserve the ecosystem services, including disease regulation, that biodiversity provides while also understanding and mitigating activities which lead to disease emergence We consider that holistic, One Health approaches to the management and mitigation of the risks of emerging infectious diseases have the greatest chance of successThis article is part of the themed issue 'One Health for a changing world: zoonoses, ecosystems and human well-being'

https://royalsocietypublishing.org/doi/pdf/10.1098/rstb.2016.0167

One health, emerging infectious diseases and wildlife: Two decades of progress?

Discovering that chytrid fungi cause chytridiomycosis in amphibians represented a paradigm shift in our understanding of how emerging infectious diseases contribute to global patterns of biodiversity loss. In this Review we describe how the use of multidisciplinary biological approaches has been essential to pinpointing the origins of amphibian-parasitizing chytrid fungi, including Batrachochytrium dendrobatidis and Batrachochytrium salamandrivorans, as well as to timing their emergence, tracking their cycles of expansion and identifying the core mechanisms that underpin their pathogenicity. We discuss the development of the experimental methods and bioinformatics toolkits that have provided a fuller understanding of batrachochytrid biology and informed policy and control measures.

/pdf/chytrid-fungi-and-global-amphibian-declines-26ry00r14o.pdf

Chytrid fungi and global amphibian declines

Emerging infectious diseases threaten the survival of many species and populations by causing large declines and altering life history traits and population demographics. Therefore, it is imperative to understand how diseases impact wildlife populations so that effective management strategies can be planned. Many studies have focused on understanding the ecology of host/pathogen interactions, but it is equally important to understand the effects on host population genetic structure. In this review, we examined the literature on how infectious diseases influence host population genetic makeup, with a particular focus on whether or not they alter gene flow patterns, reduce genetic variability, and drive selection. Although the results were mixed, there was evidence for all of these outcomes. Diseases often fragmented populations into small, genetically distinct units with limited gene flow among them. In some cases, these isolated populations showed the genetic hallmarks of bottlenecks and inbreeding, but in other populations, there was sufficient gene flow or enough survivors to prevent genetic drift and inbreeding. Direct evidence of diseases acting as selective pressures in wild populations is somewhat limited, but there are several clear examples of it occurring. Also, several studies found that gene flow can impact the evolution of small populations either beneficially, by providing them with variation, or detrimentally, by swamping them with alleles that are not locally adaptive. Thus, differences in gene flow levels may explain why some species adapt while others do not. There are also intermediate cases, whereby some species may adapt to disease, but not at a rate that is meaningful for conservation purposes.

Effects of emerging infectious diseases on host population genetics: a review

Amphibian chytridiomycosis has caused precipitous declines in hundreds of species worldwide. By tracking mountain chicken (Leptodactylus fallax) populations before, during and after the emergence of chytridiomycosis, we quantified the real-time species level impacts of this disease. We report a range-wide species decline amongst the fastest ever recorded, with a loss of over 85% of the population in fewer than 18 months on Dominica and near extinction on Montserrat. Genetic diversity declined in the wild, but emergency measures to establish a captive assurance population captured a representative sample of genetic diversity from Montserrat. If the Convention on Biological Diversity’s targets are to be met, it is important to evaluate the reasons why they appear consistently unattainable. The emergence of chytridiomycosis in the mountain chicken was predictable, but the decline could not be prevented. There is an urgent need to build mitigation capacity where amphibians are at risk from chytridiomycosis.

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Dynamics and genetics of a disease-driven species decline to near extinction: lessons for conservation

Muscle-specific kinase (MuSK) is crucial for acetylcholine receptor (AChR) clustering and thereby neuromuscular junction (NMJ) function. NMJ dysfunction is a hallmark of several neuromuscular diseases, including MuSK myasthenia gravis. Aiming to restore NMJ function, we generated several agonist monoclonal antibodies targeting the MuSK Ig-like 1 domain. These activated MuSK and induced AChR clustering in cultured myotubes. The most potent agonists partially rescued myasthenic effects of MuSK myasthenia gravis patient IgG autoantibodies in vitro. In an IgG4 passive transfer MuSK myasthenia model in NOD/SCID mice, MuSK agonists caused accelerated weight loss and no rescue of myasthenic features. The MuSK Ig-like 1 domain agonists unexpectedly caused sudden death in a large proportion of male C57BL/6 mice (but not female or NOD/SCID mice), likely caused by a urologic syndrome. In conclusion, these agonists rescued pathogenic effects in myasthenia models in vitro, but not in vivo. The sudden death in male mice of one of the tested mouse strains revealed an unexpected and unexplained role for MuSK outside skeletal muscle, thereby hampering further (pre-) clinical development of these clones. Future research should investigate whether other Ig-like 1 domain MuSK antibodies, binding different epitopes, do hold a safe therapeutic promise. 

/pdf/development-and-characterization-of-agonistic-antibodies-273vdf0q.pdf

R. Thomas

Papers

Dynamics and genetics of a disease-driven species decline to near extinction: lessons for conservation

Development and characterization of agonistic antibodies targeting the Ig-like 1 domain of MuSK