How llamas' unusual antibodies might help in the fight against HIV/AIDS

Llamas contribute to the fight against AIDS. Credit: Nika Stropakke, CC-BY

Most vaccines work by inducing an immune response characterized by neutralizing antibodies against the respective pathogen. An effective HIV vaccine has remained elusive so far, but researchers have continued to make progress, often employing innovative methods. A study published on December 18th in PLOS Pathogens reports that a combination of antibodies from llamas can neutralize (destroy) a wide range of circulating HIV viruses.

After initial disappointment that HIV vaccine candidates were unable to elicit neutralizing antibodies, researchers found that some HIV-infected individuals did produce such antibodies. The current challenge is therefore to find safe and effective vaccine formulations (as opposed to HIV infection) that trigger the development of neutralizing antibodies that can recognize and prevent infection with all or most circulating HIV subtypes.

Many known neutralizing antibodies are directed against a specific part of the virus that binds to the CD4 receptor on the human target cells, and structural biology studies indicated that the site is a narrow groove. Antibodies in most mammals are relatively large proteins made up of two copies of two different individual parts (or chains), and bulkiness might be one reason why neutralizing antibodies are rare. Llamas are a notable exception: besides the common four-chain antibodies they also produce smaller ones made up of only two of the four chains. Robin Weiss, an HIV expert, and Theo Verrips, a llama antibody expert, therefore started working with this unconventional research animal.

Laura McCoy (working with Weiss at University College London, UK) led an international group of researchers to test immunization protocols and the resulting immune response in llamas. Having previously identified one particular HIV neutralizing llama antibody, for this study the researchers immunized two additional llamas and identified a total of three new neutralizing antibodies. The four HIV neutralizing llama antibodies target different parts of the CD4-binding site of the virus, and the researchers could show that when used in combination, rather than interfering with each other, they are more potent and can neutralize all of the 60 different HIV strains tested.

To understand how the llama immunization--which included two sets of four sequential vaccine injections per animal--worked, the researchers sequenced many copies of antibody-coding genes from blood cells collected after the first set of immunizations and after a further four rounds of vaccination. They also looked at the "naïve" antibody repertoire from seven llamas that had not been vaccinated. The results suggest that the neutralizing antibodies were not part of the pre-immunization repertoire, nor were they detectable after the first vaccination round. Rather, they were generated as immune cells repeatedly encountered the vaccine and responded by maturing specific antibodies that can recognize it.

While it is encouraging that broadly neutralizing antibodies were found in all of the immunized llamas, they are present only at low concentrations in the blood, and so fail to meet the goal for a protective HIV vaccine. Nonetheless, the researchers conclude that the llama model has allowed them to examine the generation of four broadly neutralizing antibodies induced by vaccination, which has not been possible in any other species.

Source: PLOS.

Experimental Ebola vaccine appears safe, prompts immune response

A 39-year-old woman, the first participant enrolled in VRC 207, receives a dose of the investigational NIAID/GSK Ebola vaccine at the NIH Clinical Center in Bethesda, Md. on September 2. Credit: NIAID

An experimental vaccine to prevent Ebola virus disease was well-tolerated and produced immune system responses in all 20 healthy adults who received it in a Phase 1 clinical trial conducted by researchers from the National Institutes of Health. The candidate vaccine, which was co-developed by the NIH's National Institute of Allergy and Infectious Diseases (NIAID) and GlaxoSmithKline (GSK), was tested at the NIH Clinical Center in Bethesda, Maryland. The interim results are reported online in advance of print in the New England Journal of Medicine.

"The unprecedented scale of the current Ebola outbreak in West Africa has intensified efforts to develop safe and effective vaccines, which may play a role in bringing this epidemic to an end and undoubtedly will be critically important in preventing future large outbreaks," said NIAID Director Anthony S. Fauci, M.D. "Based on these positive results from the first human trial of this candidate vaccine, we are continuing our accelerated plan for larger trials to determine if the vaccine is efficacious in preventing Ebola infection."

The candidate NIAID/GSK Ebola vaccine was developed collaboratively by scientists at the NIAID Vaccine Research Center (VRC) and at Okairos, a biotechnology company acquired by GSK. It contains segments of Ebola virus genetic material from two virus species, Sudan and Zaire. The Ebola virus genetic material is delivered by a carrier virus (chimpanzee-derived adenovirus 3 or cAd 3) that causes a common cold in chimpanzees but causes no illness in humans. The candidate vaccine does not contain Ebola virus and cannot cause Ebola virus disease.

The trial enrolled volunteers between the ages of 18 and 50. Ten volunteers received an intramuscular injection of vaccine at a lower dose and 10 received the same vaccine at a higher dose. At two weeks and four weeks following vaccination, the researchers tested the volunteers' blood to determine if anti-Ebola antibodies were generated. All 20 volunteers developed such antibodies within four weeks of receiving the vaccine. Antibody levels were higher in those who received the higher dose vaccine.

The investigators also analyzed the research participants' blood to learn whether the vaccine prompted production of immune system cells called T cells. A recent study by VRC scientist Nancy J. Sullivan, Ph.D., and colleagues showed that non-human primates inoculated with the candidate NIAID/GSK vaccine developed both antibody and T-cell responses, and that these were sufficient to protect vaccinated animals from disease when they were later exposed to high levels of Ebola virus.

The experimental NIAID/GSK vaccine did induce a T-cell response in many of the volunteers, including production of CD8 T cells, which may be an important part of immune protection against Ebola viruses. Four weeks after vaccination, CD8 T cells were detected in two volunteers who had received the lower dose vaccine and in seven of those who had received the higher dose.

"We know from previous studies in non-human primates that CD8 T cells played a crucial role in protecting animals that had been vaccinated with this NIAID/GSK vaccine and then exposed to otherwise lethal amounts of Ebola virus," said Julie E. Ledgerwood, D.O., a VRC researcher and the trial's principal investigator. "The size and quality of the CD8 T cell response we saw in this trial are similar to that observed in non-human primates vaccinated with the candidate vaccine."

There were no serious adverse effects observed in any of the volunteers, although two people who received the higher dose vaccine did develop a briefly lasting fever within a day of vaccination.

Source: NIH/National Institute of Allergy and Infectious Diseases

Using power of computers to harness human genome may provide clues into Ebola virus

Ramaswamy Narayanan, Ph.D., professor in the Charles E. Schmidt College of Science at Florida Atlantic University.

Ramaswamy Narayanan, Ph.D., professor in the Charles E. Schmidt College of Science at Florida Atlantic University, is working to blend the power of computers with biology to use the human genome to remove much of the guesswork involved in discovering cures for diseases.

In an article titled "Ebola-Associated Genes in the Human Genome: Implications for Novel Targets," published in the current MedCrave Online Journal of Proteomics and Bioinformatics, Narayanan describes how key genes that are present in our cells could be used to develop drugs for this disease.

"Bioinformatics is a powerful tool to help us understand biological data," said Narayanan whose research has focused in this field for more than a decade. "We are mining the human genome for Ebola virus association to develop an understanding of the human proteins involved in this disease for subsequent research and development, and to potentially create a pipeline of targets that we can test and evaluate."

Ebola virus disease is a major healthcare challenge facing the globe today and if left unchecked could become a pandemic. A limited knowledgebase exists about the Ebola virus and companies are hastening to develop vaccines and other forms to treat and cure the virus. There are no FDA-approved drugs, and developing vaccines or antibodies and testing them in clinical trials is an arduous process that takes considerable time. Currently, patients infected with Ebola are only able to receive supportive care such as fluid replacement, nutritional support, pain control, and blood pressure maintenance. In some cases, patients may be fortunate enough to be treated with experimental drugs.

Narayanan's work has helped to identify numerous FDA-approved drugs already used for many other diseases including anti-inflammatory drugs, anticoagulants, cancer, HIV, statins and hormones, which could potentially be used to add to the current supportive care for patients with the Ebola virus.

"With the high mortality rate of this disease, the world urgently needs new ways to treat patients," said Narayanan. "The ability to use drugs that are already approved by the FDA could provide clinicians with more options to treat Ebola patients, rather than just relying on supportive measures like fluid replacement or antibiotics."

According to the World Health Organization (WHO), Ebola virus disease (EVD) is a severe, often fatal illness in humans. The virus is transmitted to people from wild animals and spreads in the human population through human-to-human transmissions. The evolving knowledge of this disease is prompting appropriate attention locally and globally. The 2014 Ebola epidemic has affected multiple countries in West Africa with some cases observed in Europe and the United States.

Source: Florida Atlantic University

Researchers ferret out a flu clue

Professor Michael Jennings, Deputy Director of the Institute for Glycomics. Credit: Image courtesy of Griffith University

Research that provides a new understanding as to why ferrets are similar to humans is set to have major implications for the development of novel drugs and treatment strategies.

Published in the journal Nature Communications, the research is a collaboration between Professor Michael Jennings and other researchers from the Institute for Glycomics, Griffith University and collaborators at the University of Queensland and the University of Adelaide.

The team has shown for the first time that ferrets share a mutation that was previously thought to be unique to humans, among the mammals. This helps to explain why the molecular characteristics of ferrets so uniquely mimic human susceptibility, severity and transmission of influenza A virus strains.

Professor Michael Jennings, Deputy Director of the Institute for Glycomics, says these findings open up a completely novel approach to tackling human diseases from influenza through to cancer.

"For over 80 years we've known that ferrets are uniquely susceptible to human influenza A virus, but the precise reason was unknown," Professor Jennings said.

"We have shown that ferrets have a mutation in a gene required to make a crucial sugar called sialic acid. Most animals can make two types of sialic acid. Ferrets, like humans can make only one. Different flu strains have preferences for the type of sialic acid they bind to cause infection. Because ferrets can only make the human form of this sugar, they are naturally "humanized" for the receptors recognised by human strains of the flu virus."

Source: Griffith University

Flu virus key machine: First complete view of structure revealed

The complete structure allows researchers to understand how the polymerase uses host cell RNA (red) to kick-start the production of viral messenger RNA. Credit: © EMBL/P.Riedinger

Scientists looking to understand -- and potentially thwart -- the influenza virus now have a much more encompassing view, thanks to the first complete structure of one of the flu virus' key machines. The structure, obtained by scientists at EMBL Grenoble, allows researchers to finally understand how the machine works as a whole, and could prove instrumental in designing new drugs to treat serious flu infections and combat flu pandemics.

If you planned to sabotage a factory, a recon trip through the premises would probably be much more useful than just peeping in at the windows. Scientists looking to understand -- and potentially thwart -- the influenza virus have now gone from a similar window-based view to the full factory tour, thanks to the first complete structure of one of the flu virus' key machines. The structure, obtained by scientists at the European Molecular Biology Laboratory (EMBL) in Grenoble, France, allows researchers to finally understand how the machine works as a whole. Published in two papers in Nature, the work could prove instrumental in designing new drugs to treat serious flu infections and combat flu pandemics.

The machine in question, the influenza virus polymerase, carries out two vital tasks for the virus. It makes copies of the virus' genetic material -- the viral RNA -- to package into new viruses that can infect other cells; and it reads out the instructions in that genetic material to make viral messenger RNA, which directs the infected cell to produce the proteins the virus needs. Scientists -- including Cusack and collaborators -- had been able to determine the structure of several parts of the polymerase in the past. But how those parts came together to function as a whole, and how viral RNA being fed in to the polymerase could be treated in two different ways remained a mystery.

"The flu polymerase was discovered 40 years ago, so there are hundreds of papers out there trying to fathom how it works. But only now that we have the complete structure can we really begin to understand it," says Stephen Cusack, head of EMBL Grenoble, who led the work.

Using X-ray crystallography, performed at the European Synchrotron Radiation Facility (ESRF) in Grenoble, Cusack and colleagues were able to determine the atomic structure of the whole polymerase from two strains of influenza: influenza B, one of the strains that cause seasonal flu in humans, but which evolves slowly and therefore isn't considered a pandemic threat; and the strain of influenza A -- the fast-evolving strain that affects humans, birds and other animals and can cause pandemics -- that infects bats.

"The high-intensity X-ray beamlines at the ESRF, equipped with state-of-the-art Dectris detectors, were crucial for getting high quality crystallographic data from the weakly diffracting and radiation sensitive crystals of the large polymerase complex," says Cusack. "We couldn't have got the data at such a good resolution without them."

The structures reveal how the polymerase specifically recognises and binds to the viral RNA, rather than just any available RNA, and how that binding activates the machine. They also show that the three component proteins that make up the polymerase are very intertwined, which explains why it has been very difficult to piece together how this machine works based on structures of individual parts.

Although the structures of both viruses' polymerases were very similar, the scientists found one key difference, which showed that one part of the machine can swivel around to a large degree. That ability to swivel explains exactly how the polymerase uses host cell RNA to kick-start the production of viral proteins. The swivelling component takes the necessary piece of host cell RNA and directs it into a slot leading to the machine's heart, where it triggers the production of viral messenger RNA.

Now that they know exactly where each atom fits in this key viral machine, researchers aiming to design drugs to stop influenza in its tracks have a much wider range of potential targets at their disposal -- like would-be saboteurs who gain access to the whole production plant instead of just sneaking looks through the windows. And because this is such a fundamental piece of the viral machinery, not only are the versions in the different influenza strains very similar to each other, but they also hold many similarities to their counterparts in related viruses such as lassa, hanta, rabies or ebola.

The EMBL scientists aim to explore the new insights this structure provides for drug design, as well as continuing to try to determine the structure of the human version of influenza A, because although the bat version is close enough that it already provides remarkable insights, ultimately fine-tuning drugs for treating people would benefit from/require knowledge of the version of the virus that infects humans. And, since this viral machine has to be flexible and change shape to carry out its different tasks, Cusack and colleagues also want to get further snapshots of the polymerase in different states.

"This doesn't mean we now have all the answers," says Cusack, "In fact, we have as many new questions as answers, but at least now we have a solid basis on which to probe further."

Source: European Molecular Biology Laboratory (EMBL)

Study may help slow the spread of flu

A false color image of an influenza virus particle, or “virion.” Credit: Centers for Disease Control/Cynthia Goldsmith

An important study conducted in part at the Department of Energy's SLAC National Accelerator Laboratory may lead to new, more effective vaccines and medicines by revealing detailed information about how a flu antibody binds to a wide variety of flu viruses.

The flu virus infects millions of people each year. While for most this results in an unproductive and uncomfortable week or two, the flu also contributes to many deaths in the average flu season. And while vaccines are effective in preventing the flu, they require almost yearly reformulation to keep up with the constantly changing virus.

At SSRL and APS, a team of researchers from The Scripps Research Institute, Fujita Health University and Osaka University studied both samples of flu virus components and an anti-flu antibody. The antibody, called F045-092, was already known to neutralize the flu by connecting to the region of the flu virus that binds to host cells, so it can no longer bind to its target and cause infection.

"There are patches of the virus that are more hypervariable than others," said Peter Lee, a postdoctoral research associate at The Scripps Research Institute and first author of the paper. "But the flu always binds to host cells within the same region, and so that binding site needs to be functionally conserved. That makes it a site of vulnerability."

The team used the X-ray beams at SLAC's Stanford Synchrotron Radiation Lightsource (SSRL) and Argonne National Laboratory's Advanced Photon Source (APS), both DOE Office of Science User Facilities, to view the structure of the antibody bound to one subtype of the flu virus called H3N2. They discovered that the antibody inserts a loop into the binding site of the virus, which would otherwise attach to a receptor in a host cell. Additional experimental data showed that F045-092 binds a wide variety of strains and subtypes, including all H3 avian and human viruses from 1963 to 2011 that were tested.

This understanding of the antibody's structural details and binding modes offers new insight for future structure-based drug discovery and novel avenues for designing future vaccines.
But the only way to achieve those goals is for many groups of scientists to work together, Lee said. "Our lab is very focused on the structure of the virus and antibodies, while there are lots of other labs focused on everything from small protein design to vaccine design," he said. "Hopefully we can use this structural information and join together as one big team to tackle the flu."

Source: SLAC National Accelerator Laboratory

Flu at the zoo and other disasters: Experts help animal exhibitors prepare for the worst

After experiencing power outages during a 2007 ice storm in Springfield, Mo., Dickerson Park Zoo officials improved their backup power and heating systems to keep animals -- like Henry, pictured here -- safe and warm. Credit: Dickerson Park Zoo

Here are three disaster scenarios for zoo or aquarium managers: One, a wildfire lunges towards your facility, threatening your staff and hundreds of zoo animals. Two, hurricane floodwaters pour into your basement, where thousands of exotic fish and marine mammals live in giant tanks. Three, local poultry farmers report avian influenza (bird flu) in their chickens, a primary source of protein for your big cats.

What do you do?

These are among the many potential disasters the managers of zoos and aquariums ponder in their emergency preparedness drills and plans. But these stories are not just worst-case scenarios: The events described above actually happened, and the aftermath -- often heroic, and sometimes tragic -- depended in large part on the institutions' preparedness training, planning and forethought in calmer times.

When bad weather strikes or illness invades, zoos and aquariums are among the most vulnerable facilities affected, said University of Illinois veterinarian Yvette Johnson-Walker, a clinical epidemiologist who contributes to emergency response training efforts at animal exhibitor institutions. She is a clinical instructor in the department of veterinary clinical medicine at Illinois, and lead author of a new paper on emergency preparedness at zoos and aquariums in the journal Homeland Security & Emergency Management.

Some animals are likely to suffer if the electricity goes out for long, she said. Others are large, skittish and dangerous under normal conditions.

Training caretakers and keepers to minimize their own risks while attending to their animals in an emergency is a challenge, but leads to the best outcomes, she said.

In 2012, Johnson-Walker joined forces with Yvonne Nadler, a project manager with the Zoo and Aquarium All Hazards Preparedness Response and Recovery Center, to bring vital emergency training to accredited animal exhibitor institutions in Illinois, Indiana and Missouri. This effort, funded by the U.S. Department of Agriculture and supported by the Association of Zoos & Aquariums, has since expanded, providing training to staff from zoos and aquariums in 23 states.

The trainings, dubbed "Flu at the Zoo," focus on avian influenza, a viral disease that spread in the 2000s among wild and captive birds and also infected hundreds of people, primarily in Asia, Africa and the Middle East. Bird flu serves as a useful model scenario to help train participants in basic preparedness skills.

One such skill is familiarity with the Incident Command System (ICS), a framework developed by firefighters and adopted by the Federal Emergency Management Agency (FEMA) that allows first responders to quickly set up their emergency response operation and assign vital tasks. The ICS has long been used by public safety, law enforcement and public health entities involved in emergency response.

"We wanted zoos and aquariums to have a seat at the table when there's planning for how we're going to respond to emergencies, and to be able to fit into the system, know who to talk to and how to communicate," Johnson-Walker said.

It's also important to recognize the other responders and understand their roles, she said. If the event involves a disease like bird flu, the USDA, FEMA, National Institutes of Health, state veterinarian, state and federal wildlife services, public health authorities, veterinary organizations, police, hospitals and perhaps even local poultry operations will be involved in the response. Knowing who does what can speed communication in a crisis.

Planning also helps managers make best use of the limited supplies or equipment they have on hand, Nadler said.

"There are certain types of livestock trailers, for example, that can be adapted to moving big cats," she said. "Is that your preferred method of movement? Of course it isn't, but in an emergency that might be your only option."

One beneficiary of the emergency training, Melinda Arnold, knows firsthand the value of preparedness. Arnold is public relations director for Friends of the Zoo, affiliated with Dickerson Park Zoo in Springfield, Missouri. The zoo suffered a blackout during a 2007 ice storm that shut off power for most of the city for several days.

"We did have backup generators," Arnold said. "The greatest problem with the generators was that those fueling stations in town that did have gas didn't have power, so they couldn't pump the gas."

Zoo staff had to travel many miles outside of the affected area with gas cans to collect gas to run the backup generators, she said.

"Now we have some propane-powered backups," Arnold said.

A more recent incident at the zoo, the accidental death of a zookeeper in 2013, caused Dickerson Park Zoo officials to re-evaluate all of their safety protocols. Even though the zookeeper had decades of experience and was guarded by a protective barrier, a skittish elephant rushed him at an unguarded moment, and he fell and was trampled to death.
"It made us step back, not only in our elephant management but in all areas of the zoo, and look at our safety procedures and points of contact with dangerous animals and evaluate those safety conditions and make improvements," Arnold said.

The preparedness plans, drills, discussions and training all help zoos and aquariums reassess their procedures, even those that seem to be safe after decades of operations and no major incidents, she said.

Source: University of Illinois at Urbana-Champaign

Mapping bats could help stop Ebola's spread

Fruit bats (Pteropodidae) are considered the likely host of the Ebola virus. Credit: Satit Srihin

In the fight against Ebola, mapping fruit bat habitats could be one important step, says a geoinformatics researcher at Sweden's Royal Institute of Technology.

Like the Black Death that ravaged medieval Europe, the Ebola virus' progress through remote areas of West Africa is enabled by lack of understanding about the disease, including its causes and transmission.

Mapping technology however will give responders to the crisis in Africa the upper hand in stopping the spread of the deadly disease, says Skog, a researcher in geoinformatics at Sweden's KTH Royal Institute of Technology.

Skog's research has produced a method that medical professionals can use to visualise the geographical distribution of a disease over time. In his research, Skog has explored the relationship between geography and disease distribution in major epidemics of the past, including the Black Death, the Russian Flu pandemic of 1889, the Asiatic Influenza of 1957 and the swine flu. He says the historical data provides a basis for predicting the course of future epidemics and pandemics.

"My research and method can also be used to report the current state of a pandemic, or predict how extensive the spread will be. And where the disease will strike next," Skog says.

In fact, the way in which Black Death spread during the mid 14th, century bears a no small resemblance to today's Ebola epidemic, he says. Both diseases were hosted by small mammals -- black rats and fruit bats, respectively. But ultimately it was humans that enabled its spread.

"The Black Death was very much depending on total lack of knowledge regarding the etiology of the disease and how to avoid further transmission," Skog says. "That is also the case for the mainly remote locations where Ebola now is spread."

Fruit bats are believed to be the natural hosts of Ebola. These bats are among the creatures that residents of rural West Africa hunt for "bush meat." The disease is also spread by the droppings of the bat, and it is believed to have spread to other types of bush meat, as well as monkeys and pigs that are raised for slaughter.

"The local population is getting part of their nourishment from bush hunting, leading to contact with the virus that is transmitted via body fluids," Skog says, suggesting that closer study of the fruit bat could provide vital answers.

"A guess of mine is that the number of infected fruit bats is a determining factor for an Ebola outbreak," he says. "Are there any known factors that may have changed the ecosystem in favor of the bats? Are the bats affected by the virus too? Do fruit bats always carry the Ebola virus or is the virus fatal to them as well? If so the percentage of infected bats will vary over the years also depending on the immunology of the species."

There are a number of geoinformation technology options available to public health organizations that have sent field crews to respond to the crisis. These, Skog says, including equipping field workers with hand-held GPS devices that feed a central database with data and findings regarding locations of bodies, possible infections and diagnosed cases personnel.

"The data can easily be centrally monitored and used for decisions and policies to mitigate the spread," he says. "Using satellite imagery, population centers can be localized. Collected disease data can also be compared and analysed with environmental and climatologic data to support other efforts to control the spread."

For instance, assuming that fruit bats are the reservoir for the ebola virus, Skog says it would be of interest to find out if the first detected cases in an outbreak are located in or close to a fruit bat habitat. "If the environmental and climatologic parameters for fruit bat habitats can be defined, there is a chance these habitats could be mapped using existing map data and satellite or airborne imagery," he says.

"Then risk areas could be monitored and preventive measures could be performed by health authorities. If the natural reservoir is in fact some other animal, positioning the first cases in each outbreak would still give a clue about what to look for."

Source: KTH The Royal Institute of Technology

In a rapidly changing north, new diseases travel on the wings of birds

When polar bears (Ursus maritimus) meet glaucous gulls (Larus hyperboreaus) over the remains of a bowhead whale (Balaena mysticetus), they may be sharing more than a meal. As the warming climate brings animals into new proximity, parasites, viruses, and bacteria can find opportunities to spread to new and naïve hosts, sometimes jumping from birds to mammals, and from marine ecosystems to land ecosystems. Credit: USGS

When wild birds are a big part of your diet, opening a freshly shot bird to find worms squirming around under the skin is a disconcerting sight. That was exactly what Victoria Kotongan saw in October, 2012, when she set to cleaning two of four spruce grouse (Falcipennis canadensis) she had taken near her home in Unalakleet, on the northwest coast of Alaska. The next day, she shot four grouse and all four harbored the long, white worms. In two birds, the worms appeared to be emerging from the meat.

Kotongan, worried about the health of the grouse and the potential risk to her community, reported the parasites to the Local Environmental Observer Network, which arranged to have the frozen bird carcasses sent to a lab for testing. Lab results identified the worms as the nematode Splendidofilaria pectoralis, a thinly described parasite previously observed in blue grouse (Dendragapus obscurus pallidus) in interior British Columbia, Canada. The nematode had not been seen before so far north and west. Though S. pectoralis is unlikely to be dangerous to people, other emerging diseases in northern regions are not so innocuous.

Animals are changing their seasonal movements and feeding patterns to cope with the changing climate, bringing into close contact species that rarely met in the past. Nowhere is this more apparent than the polar latitudes, where warming has been fastest and most dramatic. Red foxes are spreading north into arctic fox territory. Hunger is driving polar bears ashore as sea ice shrinks. Many arctic birds undertake long migratory journeys and have the mobility to fly far beyond their historical ranges, or extend their stay in attractive feeding or nesting sites.

With close contact comes a risk of infection with the exotic parasites and microorganisms carried by new neighbors, and so disease is finding new territory as well. Clement conditions extend the lifecycles of disease carrying insects, and disease-causing organisms. Migratory birds can take infectious agents for rides over great distances. In November 2013, Alaska Native residents of St. Lawrence Island, in the Bering Sea, alerted wildlife managers to the deaths of hundreds of crested auklets, thick-billed murres, northern fulmars and other seabirds, caused by an outbreak of highly contagious avian cholera (Pasteurella multocida).

"It's the first time avian cholera has shown up in Alaska," said Caroline Van Hemert, a wildlife biologist with the U.S. Geological Survey in Anchorage, Alaska. "St. Lawrence Island is usually iced in by November, but last year we had a warm fall and winter in Alaska. We don't know for sure that open water, climate, and high-densities of birds contributed to the outbreak, but it coincided with unusual environmental conditions."

Circumstantial evidence collected by researchers and local observers is pointing toward a surge of infectious disease in the northern latitudes, but scanty baseline data makes interpretation of current trends uncertain. Van Hemert and colleagues review the state of our knowledge of emerging disease in northern birds and effects on wildlife and human health, discussing strategies for cooperative programs to fill in information gaps in the December issue of Frontiers in Ecology and the Environment.

Source:  Ecological Society of America