[vc_row][vc_column width=”2/3″][text_output]Imagine trying to solve a jigsaw puzzle with 6,500 pieces, all of which are dramatically different, scattered throughout the world on every continent and apt to change shape in response to a varying environment. That kind of complexity is at the root of what scientists face as they piece together a comprehensive picture of the fungal disease Batrachochytrium dendrobatidis (Bd, or chytrid), even as it continues to decimate populations of amphibians around the globe.
“Part of why the amphibian disease crisis is such a crisis is because we have thousands of amphibian species all over the world with very different life histories living in different environments,” says Dr. Anna Savage, molecular evolution postdoctoral fellow with the Smithsonian Conservation Biology Institute and assistant professor at the University of Central Florida. “There are just so many unique combinations of conditions leading to different disease outcomes in a thousand different scenarios.”
A number of researchers, including Savage, are turning to a field that has not traditionally focused on amphibians—that of genetics—to start to solve the puzzle of chytrid: how it has evolved, how it spreads, how (and why) its strains vary, how it affects each frog species and individual differently, where it came from and, most importantly, how to stop its deadly global rampage.
THE EMERGING DISEASE TRIFECTA
When Savage set out to work on her dissertation, she focused on looking at the differences in the immune system genes between Lowland leopard frogs (Rana yavapaiensis) that effectively fight off chytrid and those that succumb to it. Conservationists and population managers could then translocate individuals with the identified “good genes” or even breed for those genes in captive populations. This idea, however, gets complicated quickly, Savage says.
“Although we have actually found some genetic variants that we know in the lab are associated with very high survival rates against Bd infections, we don’t necessarily want to just breed that genotype into every population,” she says. “That could erase other local adaptations that help fight off other pathogens. We don’t have enough information to say that would be the right thing to do.”
So now Savage has changed her focus, expanding her scope beyond DNA variance. Today her research looks at gene expression—the combination of genes in an individual frog that gets turned on or off—while the frog mounts an immune response to fight off chytrid. Specifically, Savage and colleagues are looking at the intersection of three factors that can manipulate the on and off switch: the genetic diversity of the individual frog, the environment in which that frog lives and the genes of the pathogen infecting the frog.
The collection of the results from these kinds of studies could be tremendous. Conservationists could turn to a database or catalog that outlines the genetic and environmental factors that may make a specific population of frogs more or less susceptible to chytrid. It could also help conservationists at the start of an endemic, such as the recent discovery of chytrid in Madagascar, determine where to focus their efforts.
“Eventually we’ll be able to say the specific things that you should do as a population manager or conservationist to promote the right environmental conditions to help your specific populations fight off disease,” Savage says. Until that time, the most important thing conservationists can do for amphibians is protect their habitat, she adds.
“The more protected habitat a population has, the more breeding success it will have,” Savage says. “The bigger your effective population size, the more genetic diversity you have in a population. And the more genetic diversity you have, the better you are at fighting off pathogens.”
LOOKING BACK AND LOOKING BEYOND
Like Savage, Dr. Erica Bree Rosenblum, assistant professor at the University of California at Berkeley, is interested not only in the host’s genes, but the genetic make-up of chytrid itself. Her pathogen work revolves not only around identifying the particular genes chytrid needs to successfully attack its host, but also on answering basic questions about the fungal disease: where did it come from, where geographically has it had a longer history, where has it spread more quickly, what pathways has it travelled and what about its genome allows it to evolve so rapidly.
“What we call Bd has a lot of diversity inside of it,” Rosenblum says. “Recognizing that complexity is critically important so we do not assume there will be a one-size-fits-all conservation strategy. For example, our conservation strategies are going to be different in places where Bd has had a longer history than in places where it is a new arrival.”
This type of research is about more than benefiting amphibians, Rosenblum says, especially as emerging infectious diseases are on the rise globally. Researchers studying white-nose syndrome in bats, for example, have been able to mobilize quicker, in part, because of the lessons the amphibian community has learned about fungal disease.
“What we learn about a particular emerging infectious disease becomes part of the collective database to inform how we will respond to wildlife disease threats in general over the next century,” says Rosenblum.
Are researchers optimistic that their efforts today will help solve the puzzle of these emerging infectious diseases in time to stop some species from going extinct? Yes and no, Rosenblum says.
“I am troubled by what is likely to happen to amphibian biodiversity over the next 50–100 years,” she says. “I think many people who work in the field are concerned about the state of biodiversity on the planet and humans’ role in that capacity. But, even so, I would say there are a few rays of hope.”
By Lindsay Renick Mayer
Photo: Researcher Anna Savage © Connor Mallon, Smithsonian National Zoo.[/text_output][/vc_column][vc_column width=”1/3″]
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