The Why Files The Science Behind The News Fri, 19 Dec 2014 18:21:04 +0000 en-US hourly 1 Europe: Return of the carnivores! Thu, 18 Dec 2014 19:33:24 +0000 More »]]>
Europe: Return of the carnivores!
A Eurasian lynx with a thick fur coat perches on a mossy, downed tree trunk, gazing toward a distant object, looking ready to strike.
The Eurasian lynx is Europe’s largest cat. The new study finds them abundant in Finland, Sweden and Norway, the Baltics, Balkans and Romania.
Copyright: Miha Krofel, Slovenia

A surprising new study shows that four big carnivores (brown bear, lynx, wolverine and wolf) are doing quite nicely in Europe, thank you very much, even without the wilderness protection that benefits some large predators in the United States.

“We find that in Europe we have twice as many wolves as in the lower 48 (American) states, on half the land area, with two times the human population density,” says Guillaume Chapron of the Swedish University of Agricultural Sciences, the corresponding author of the new study.

In Europe, as in North America, large carnivores face ingrained hostility. It’s not just their ferocity, but also their need for a large range and lots of meat that makes them natural competitors.

Photo of two fuzzy wolf pups standing in the sun in a grassy opening
Wolf pups photographed in front of their den in western Poland.
Credit: Robert W. Myslajek

Add it up, and both Europe and the United States had severe losses of carnivore populations by the 1960s.

Wilderness reserves and national parks in North America are intended to separate animals from people, but the new study points to other ways to ensure predator survival. “If we had followed the North American model of wilderness in Europe, we would not have predators, because in Europe everything is developed, we have roads everywhere,” Chapron says.

The study, “shows that this coexistence, this ‘land sharing,’ does not just work in a particular context, it is working on a continental scale,” says Chapron. “It’s possible to have predators living in a human-dominated landscape, and this is unexpected.”

Predator stomping grounds
Four maps showing the spread of large carnivores across Europe, with images of a bear, wolf, lynx and wolverine. Bears, lynx and wolverines appear concentrated in Fennoscandinavia, and wolves reside primarily across the Balkan countries and eastern Europe.
Location of bear, wolf, lynx and wolverine populations across Europe between 2010 and 2012; permanent populations shown in dark orange, and occasional sightings shown in light orange.

The 1970s: A turnaround

Photo of a wolverine standing on an overturned tree near a pond with lily pads.
Wolverines are adapted to living in the snow. This one is near a pond in Finland.

The same environmental awareness that sparked the Endangered Species Act (ESA) in the United States in the 1970s also affected Europe, Chapron says. “In Europe … we have our own ESA and habitat directives that protect wildlife and wildlife habitat.” Member states of the European Union are obligated to restore wildlife populations and habitat, he says. “The willingness of society to have a good relationship with wildlife has been a key reason why this has turned into a success story.”

Photo of three wolves greeting one another in a forest opening. Wolves do eat livestock, and in Europe (much as in the United States), problem wolves can be shot even though they are protected.
Highly intelligent and cooperative, the wolf pack forms a hunting machine with a large territory.
Copyright: Miha Krofel, Slovenia

Of the four predators, the oft-feared wolf has staged the most dramatic recovery, Chapron says. Since the 1950s and ’60s, wolves have become more numerous in Finland and Poland, and breeding populations have returned to Sweden, France, Germany and Norway. “The wolf was never deliberately reintroduced in Europe,” Chapron says. “The wolf has done all of this naturally.”

The territory of European wolves has, on average, 37 people per square kilometer. (That’s 103 per square mile, or about the same density as the state of Alabama.) “That clearly shows the wolf can live in places with people; they don’t need a totally empty landscape,” Chapron says.

Although the findings are encouraging for those who see predators as necessary to a healthy ecosystem, “This coexistence is not a peaceful love story,” says Chapron. “With carnivores, there will always be conflicts. They are big, they eat the wrong type of meat, including meat we would like to eat. The goal is not to have no conflict at all, because I don’t think that’s possible.”

– David J. Tenenbaum

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Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. Recovery of large carnivores in Europe’s modern human-dominated landscapes, Guillaume Chapron et al, Science, 19 December 2014.
  2. Europe’s large carnivore initiative webpage.
  3. The status of large carnivores in Europe, 2013.
  4. Why should we care about carnivores in North America?
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Happy holidays: Inventions we need now! Thu, 11 Dec 2014 20:11:21 +0000 More »]]>
Happy holidays: Inventions we need now!

Can’t decide if you want a scarf or a fruitcake? Aim higher! The Why Files cooked up a science-lab wish list for the season. Let’s meet ‘n greet The Why Files big four inventions for a happier, healthier tomorrow!

Pie in sky? Why not stash carbon dioxide in the basement?

Three-dimensional diagram of rock layers underlying CO2 injection wells, where liquefied carbon is pumped below "cap" rocks into oil, coal and gas reserves, as well as unusable aquifers.
Adopting a method used to increase flow of oil to the surface, carbon capture and storage places liquefied carbon dioxide from coal plants deep beneath Earth’s surface, in porous rock formations under dense “cap” rocks that should permanently hold the carbon. But how much testing is needed to assure permanence?

The problem: Carbon dioxide – the king of the greenhouse gases – is warming the climate and raising sea level.

The holiday gift: A technology called “carbon capture and storage” (CCS) has panacea scrawled all over it: Solve the problem of fossil-fuel carbon dioxide by capturing the gas at the generating station. Inject it deep into the ground, where it will — we hope — solidify into stone.

Because carbon dioxide injections mobilize oil in partly-spent oil fields, this pollutant is worth money. Oil recovery is the goal of 20 of 27 CCS projects now operating or being built. The other seven will inject the gas into deep rock formations beneath a cap rock.

CCs is difficult, and expensive: the budget for the flagship U.S. effort, the Kemper-IGCC project in Mississippi, has ballooned from $2.4 billion to $5.6 billion. The plant is scheduled to start in May, 2015, one year late, and to pipe its carbon dioxide to an oil field.

A steel plant in the United Arab Emirates is expected to start injecting 800,000 tons of carbon dioxide for oil recovery in 2015.

The upshot: CCS is unproven, and even a rapid move toward a safe, affordable technology will not come close to solving our climate woes. More research is needed. If the goal is to store carbon underground, it may even be cheaper to leave petroleum, natural gas and coal where it is.

Universal flu vaccine

The problem: Influenza keeps evolving, so we need a new flu shot every year, and it doesn’t always work.

Black and white photograph of nurses donned with surgical masks hefting an infected flu victim on a stretcher into a Red Cross ambulance.
The Motor Corps of the St. Louis chapter of the American Red Cross on ambulance duty during the influenza epidemic. In 1918 and 1919, in the aftermath of World War I, influenza killed 50 to 100 million around the world.
Photo: October 1918 Influenza archive

The holiday gift: Influenza viruses evolve to battle the immune system. Immunity to last year’s virus fails against this year viruses, so we need an annual vaccination containing viruses expected in the coming flu season, and predictions are chancy. So flu researchers dream of a universal vaccine that would protect against any virus strain, even a deadly flu like H5N1. Now, some of the obstacles have become clear — and perhaps surmountable, says Thomas Friedrich, a virologist and associate professor in the School of Veterinary Medicine at the University of Wisconsin-Madison. These three improvements would go a long way toward improving protection against flu.

Generate “broadly neutralizing” antibodies. The flu shot induces antibodies, immune molecules that block structures the virus uses to infect cells. Because the antibodies are targeted against strains present in the vaccine, the virus is forced to evolve to “escape” the vaccine. Researchers have recently found people and animals with antibodies that neutralize most flu strains, even bird flu. Still to come: ways to induce these broad antibodies with a vaccine.

Recruit additional “arms” of the immune response: Currently, vaccines induce antibodies that recognize fast-evolving parts of the virus. T cells and non-neutralizing antibodies that recognize static elements could be effective against many strains, if we are able to stimulate them with vaccine.

Make vaccines faster: It takes almost a year to grow vaccine in chicken eggs — after next year’s strains are selected. Vaccine producers are adopting modern cellular and molecular biology techniques that hasten this process, but the pace remains slow.

The upshot: A universal vaccine will not arrive tomorrow, but progress is likely with good funding.

Better antibiotics on the horizon?

False-colored, electron microscope image of the spherical "staph" virus being engulfed by voracious white blood cells.
Scanning electron micrograph of a human neutrophil ingesting MRSA (methicillin-resistant staph aureus), a drug-resistant “superbug.”

The problem: Abuse of antibiotics, in human health and animal agriculture, has caused a resistance crisis. When antibiotics kill susceptible bacteria, the bugs evolve toward resistance.”Super-bugs” are emerging from India, where babies are routinely injected with strong antibiotics, which helps accelerate the very infections they are intended to save.

The holiday gift: Antibiotics that work without killing bacteria. The idea is not to be nice to pathogens, but to avoid causing resistance to evolve.

Quorum sensing: Many bacteria release “I-am-here” chemical that their own species can detect. Once the microbes are numerous enough to withstand immune attack (when they reach their “quorum”), their behavior can change from harmless to hateful, as they secrete toxins or tissue-destroying enzymes, or form a biofilm that protects from harm. At UW-Madison, Helen Blackwell is investigating the signals of quorum sensing in an effort to trick bacteria into thinking that their numbers are small so they remain harmless. She says such a tactic could avoid the antibiotic-resistance paradigm. Because the bacteria are not killed, there is no selective pressure for resistance.

Interrupting the cell cycle: Another way to monkey-wrench the microbial menaces occurs when bacteria multiply and break proteins using enzymes called proteases. “When the environment becomes damaging, these proteases selectively target particular proteins to stop cell division so the bacteria can focus instead on repair until the stress is over,” explains “Peter Chien, of the University of Massachusetts Amherst. “Understanding how bacteria use these machines at the cellular and molecular level could reveal avenues for discovery of new drugs to treat infectious diseases.”

Madison (Wis.) Metropolitan Sewerage District distributes biosolids — the remains left after sewage is processed — to nearby farms. The district injects its liquid fertilizer-soil conditioner into the soil, minimizing runoff and odor. Rollover to see the injection machine being filled: Notice the tidy bucket that catches spills during the transfer?
1992 photos courtesy David Tenenbaum

The upshot: Learning to mess with the bacterial signals could sidestep the evolved-resistance problem. But don’t count bacteria out. They outnumber us, and they will do anything to come out on top.

Recycle and save soil!

The problem: Soil, the basis of civilization, is easily damaged by erosion, over-cropping, and other abuses. Gardeners compost organic scraps, and municipalities compost the “biosolids” left after biological treatment of sewage. About 60 percent (4 million dry tons) of U.S. biosolids was applied to land after treatment in 2004. It’s time to recycle the 40 percent that was buried or burned.

The gift: Biosolids, when used with care, improve soil’s structure, water retention and nutrient content, while reducing erosion and replacing conventional fertilizers.

Biosolids are the leftovers from sewage, and they can carry toxic metals or pharmaceuticals, but when done correctly, biosolids are more thoroughly analyzed than the conventional fertilizer used on farmland. Biosolids are so effective they can even restore tailings piles at abandoned mines — which leach toxic metals as rainfall and sulfates in the rock form sulfuric acid.

The upshot: More recycling would be better, but the mistaken “don’t defecate on our food” movement is strong. Yet caution is needed. Fear-mongering will only be fed by errors and short-cuts that cause soil or water pollution.

– David J. Tenenbaum

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Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. ‘Superbugs’ Kill India’s Babies and Pose an Overseas Threat
  2. High Cost Hinders Progress of Carbon Capture As Climate-Change Fix
  3. Potential “universal” influenza vaccine tested at FDA.
  4. Biosolids May Help Fight Global Warming.
  5. Superbugs to kill ‘more than cancer‘ by 2050.
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The deadly jolt of the electric eel Fri, 05 Dec 2014 14:38:51 +0000 More »]]>
The deadly jolt of the electric eel
Photo of an electric eel, set on a white background, its smooth body coiled, 2 tiny fins at front, no fins on top;  with a tiny tail fin.
The electric eel (Electrophorus electricus) has three uses for the electric field it generates.
Courtesy Kenneth Catania, Vanderbilt University

Long before the first battery, the electric eel was an ambassador from the unknown world of electricity. So Kenneth Catania, a professor of biology at Vanderbilt University who has just published a study on the hunting behavior of the eel, was a bit surprised that nobody had studied exactly how the eel attacks its prey.

While teaching about eels, he says, “I got fascinated by their behavior. Under high-speed video — no-one had done that as far as I can tell — the prey were completely immobilized about 3 milliseconds after the eel began its electric attack.”

When the eel’s specialized muscle cells created an electric field in the water, “I imagined the prey would twitch,” Catania says, “but it completely froze up, which suggests this was caused by involuntary muscle contraction, which is pretty much how a Taser works.”

With its prey immobilized, the eel mounts “an incredibly fast, explosive strike,” says Catania. And even though the fish muscle cells must devote energy to generating current, “There was no indication in its behavior that suggests they had lost a substantial amount of movement. I thought, and others thought, the electric eel could lazily swim up, shock and consume the prey.”

All things considered, Catania says the eels “are quite a formidable predator.” In its native Amazon Basin, “Fishermen really don’t like them, and there are historic accounts of people who study eels who have slipped, been shocked and immobilized.”

Photograph of an elderly fisherman in a hand-carved canoe floating on the muddy waters of the Amazon.
The electric eel thrives in the shallow, murky waters of the Amazon Basin, where it locates hidden prey with low-energy electric discharges.
Photo: Shutterstock.

A three-step “dance of doom”

But the shocks are only the final step in a sophisticated, three-prong attack. Electrically speaking, the eels use:

A form of low-voltage (think electric sonar) to detect prey in its muddy environment.

A different, low-voltage signal that elicits a twitch from nearby prey that makes waves that the eel’s pressure sensors can detect.

The immobilizing jolt at a frequency of 400 hertz. At 600 volts, it’s more than four times the voltage of household current. The attack causes tetanus — a widespread explosion of muscular activity that turns the fish into a rigid, helpless dinner.

“It’s a very sophisticated animal,” says Catania. “It’s got eyes, and even though a lot of people say they are mostly blind, the ones I study clearly are paying attention visually. They have passive electrical receptors and active electrical receptors; they can probe with electricity, and have that high-voltage immobilizing discharge. And they are incredibly sensitive to slight water movement, which will cause them to attack almost immediately.”

A large electric eel captures a fish during its high-voltage discharge. The clicking sound represents the electric signal in the water; notice how the frequency changes before and after the attack. The slower clicks are used to detect prey, not immobilize it.
Courtesy Kenneth Catania

“First, you become my slave. Then you die!”

Perhaps the most astonishing part of the story is how the eel seizes control of the prey’s nervous system. In part of the experiment, Catania removed the brain and spinal cord from the prey fish, and saw that the electric attack nonetheless caused its muscles to fire by activating nerves linking the spinal cord to the muscles. “There is a remarkably tight correspondence between eel’s output and the muscles,” Catania says.

Photo of brilliant blue wasp yanking a cockroach’s antennae, leading the insect to the wasp’s lair.
It’s a cruel world: The emerald cockroach wasp converts its prey into zombies — for the benefit of the wasp’s larvae.

Other predators enslave their prey. For example, the emerald cockroach wasp injects its eggs and disables the cockroach’s nervous system, forcing the roach, zombie-like, to carry the wasp’s larvae until the larvae eats it alive. The rabies virus turns dogs aggressive to help the virus spread before its host dies. “But nothing I know of works as fast” as the electric eel, says Catania.

Photo of an electric eel’s head bent upward to face a small, silver fish moments before the prey is swallowed
This electric eel is attacking a fish that been immobilized by the eel’s high-voltage output.
Courtesy Kenneth Catania

If it’s so powerful, why doesn’t the electric eel shock itself? “I’ve not found any obvious explanation,” says Catania. “Presumably there is some way of projecting the electricity through a path of least resistance that does not include its own brain.”

Creating all that electric energy does tire the fish, Catania adds. “You can see, over time, that the frequency of the pulses does slow down.”

All-electric alliance

The electric eel Electrophorus electricus is one of hundreds of fish that create electric current for defense, predation, navigation and communication. A new study by University of Wisconsin-Madison researchers shows that all six electric fish lineages use essentially the same genes and cellular pathways to make the electric organ. “What is amazing is that the electric organ arose independently six times in the course of evolutionary history,” says Lindsay Traeger, a UW-Madison graduate student and a co-lead author of the report.

Some scientific advances rely on new instrumentation or theories, but not the current (heh-heh!) study. Instead, the hunting behavior of the electric eel was hiding in plain sight. “Maybe it sounded open and shut,” Catania says, when asked why the eel’s electric secret was not unraveled before now. “What was there to know if eel shocked the heck out of its prey? But it turned out to be far more interesting than you could have imagined.”

– David J. Tenenbaum

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Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. The shocking predatory strike of the electric eel, Kenneth Catania, Science, 5 December, 2014.
  2. Sequencing electric eel genome unlocks shocking secrets.
  3. Eel muscle could be the first step towards human-generated electricity.
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Eating to extinction (Happy Thanksgiving, bird eaters!) Thu, 27 Nov 2014 13:33:27 +0000 More »]]>
Eating to extinction (Happy Thanksgiving, bird eaters!)
A prone man  aims shotgun, resting on log, at 3 turkeys; an Indian guide crouches behind him.
1890 lithograph by Rufus Fairchild Zogbaum, Harry T. Peters “America on Stone” Lithography Collection

Sept. 1, 1914: The passenger pigeon goes extinct after billions were shot to feed hungry urban markets during the preceding century.

Nov. 27, 2014: Thanksgiving, the day we gobble gobblers (AKA turkeys) and wonder: Is the original Thanksgiving meat now extinct? Hint: It’s not the wild turkey.

The turkey, supposedly the focus of the Pilgrim’s first feasts, was eliminated across much of its wild realm by over-hunting and habitat destruction. These days, after extensive restoration efforts, the wild turkey is easy to find (though reputedly difficult to hunt).

But we’ve learned that the heath hen, a smaller bird that was more common in the Northeast during Pilgrim times, was more likely the focus of the feeding frenzy in those first feasts. If so, the true “Thanksgiving turkey” went extinct in 1932.

Thanksgiving ruminations: Remembering the birds we ate ’til they were gone!

ird with striped feathers seen in profile,  with crest on its head.

Heath Hen

Ornithologist and conservationist Stanley Temple at the University of Wisconsin-Madison, says “Many people, myself included, believe the Pilgrim Thanksgiving meal was not turkey but the heath hen.” The area had few turkeys, but the many heath hens “were intensely hunted and very good to eat. I don’t think anyone would argue against overkill, over-hunting as the major cause of their demise.” By the late 19th century, heath hens were only found on Martha’s Vineyard, an island only 50 miles from the Pilgrim’s colony at Plymouth, Mass. Even though a large preserve was created for them, heath hens were battered by predatory birds, a catastrophic fire during nesting season and possibly diseases carried by poultry. Eventually, low fertility and other symptoms of inbreeding depression appeared, and the birds died out in 1932.
Feathered game of the Northeast, by Walter H. Rich
Mid-1800s wood block engraving of 9 hunters shooting an enormous swarm of passenger pigeons; some birds fall, and hunters collect them from the ground.

Passenger Pigeon

In 1871, hundreds of millions of passenger pigeons nested across 850 square miles of central Wisconsin, and eyewitnesses reported that almost every tree held dozens of nests. So if any bird seemed extinction-proof, it was this one, but later in the century, squads of “pigeoners” travelling the new railroads shotgunned these colonial-nesting birds and stuffed their carcasses into barrels for shipment to Eastern and Midwestern cities. “Martha,” the last of her species, died in a Cincinnati zoo in 1914.
A plump dodo, with huge bill, in profile, before other extinct birds


The dodo, a pigeon-family bird that lived and died on the island of Mauritius in the Indian Ocean, has come to symbolize both death (“dead as a dodo”) and extinction. The island lacked mammals, so the bird was unfamiliar with their rapacious ways, making it easy prey for hungry sailors who arrived in 1598. The dodo was gone by 1662, or perhaps a few years later. With such a quick extinction, it’s impossible to know precisely the bird’s appearance or behavior, but it was about one meter tall and apparently not fearful enough for its own good. A wide range of other animals on Mauritius went extinct, including the Mauritian duck and the Round Island burrowing boa. And although the dodo came to exemplify the idea that people could eat birds to extinction, introduced monkeys, rats and cats may have played a bigger role, says Temple.
“Edward’s Dodo,” painted by Roelant Savery, in 1626 Public Domain
Photo: Short, squat pigeon with wings flexed; tail feathers are bright pink, breast pinkish-white, bird has band on leg.

Pink Pigeon

A relative of the dodo shows how a bird can resist extermination through clever chemistry. The pink pigeon ate tropical fruits loaded with toxic alkaloids and was the only pigeon species on Mauritius not hunted to extinction. “Once the report got out that you would became deathly ill if you ate the pink pigeon, it survived,” says Temple, a professor emeritus of wildlife ecology. As a young ornithologist on Mauritius, Temple had a taste of the pigeon’s menacing meals. “Whenever I saw a bird feeding on something, I would pluck a piece of fruit and touch it to my tongue,” he says. “I saw a pigeon eat several fruits and picked one on the tip of my tongue, and most of my throat and mouth went numb, like I’d been shot with Novocain.” Although the pink pigeon survived, and hundreds live in captivity, it is endangered by habitat loss.
Illustration of long-legged, long-beaked birds on a rock and grass; one bird lies on its back, presumably dead

Eskimo curlew

The Eskimo curlew almost certainly met its demise via a hungry market. Possibly the most numerous migratory bird in North America, their numbers plummeted in the late 1800s after market hunters targeted them as the supply of passenger pigeons petered out. Large flocks of curlews migrated south along the Eastern Seaboard to the Caribbean and South America, then back north through Texas and the Great Plains, where, according to some accounts, millions were slaughtered annually. Although the species hasn’t been seen, officially, since the 1960s, occasional sightings are claimed.
Painting by John James Audubon
Illustration of three waterfowl -- a black and white male, brown female and juvenile -- wading in chilly waters and perched on floating ice.

Labrador duck

Cold winters in New York spelled trouble for the hapless Labrador duck, which wintered along the New England coast and Long Island Sound. Wintering waterfowl were a big source of meat supplied to New York City markets. Although the Labrador duck wasn’t the tastiest tidbit on the menu, its conspicuous plumage made it an easy target. The last one was seen on Long Island Sound in 1875.
Illustrated by J.G. Keulemans, Rowley’s Ornithological Miscellany Vol II
Drawing of two large ostrich-like birds in a tropical landscape, unaware of the looming Maori hunter brandishing a spear from behind a tree. 

Giant moa

When Polynesian settlers called the Maori landed on the islands of New Zealand around 1280, they encountered several endemic species of moas: large, wingless cousins of the ostrich. Confined to islands, and never knowing humans, the moas were easy prey for the Maori. Even the topographically and ecologically diverse landscape of New Zealand couldn’t curb the hunters’ excess success. Radiocarbon dating shows all species of moa were hunted to extinction within 200 years of Maori arrival. Not a single species in the moa genus survived the 15th century, not even these 12-foot-tall giants.
From Extinct Monsters: A popular account of some of the larger forms of ancient animal life, by Rev. H. N. Hutchinson, 1896.

Add it up, and you have to start wondering about the birds we love to eat. How much “love” is too much love? Lest you argue that we have learned from our history, Temple points to the bluefin tuna — a heavily fished delicacy of the sea that is, he suspects, headed for extinction. “You could superimpose the trajectory of the passenger pigeon’s decline on this modern day example, which we are exploiting with deadly efficiency,” he says. “It reminds me of the passenger pigeon, where the simple answer is that we killed ‘em and ate ‘em.”

– David J. Tenenbaum & Kevin D. Barrett

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Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. Dodo, a lá Wiki.
  2. Pacific island birds: 1,000 species gone!
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Bankers: dishonest when banking is on their minds? Thu, 20 Nov 2014 15:28:34 +0000 More »]]>
Bankers: dishonest when banking is on their minds!

Be honest: Do you look at banking and other financial institutions and imagine the swishing sound of billions of dollars and euros flushing down the drain? Lies, thefts and frauds are not getting any scarcer grow among the people who handle money, so we ask:

Flyer on a metal pole carries image of a smirking Bob Diamond, reading, 'I've got your money, and I'm keeping it! Why isn't Bob Diamond in prison?'
When a bank pays interest on your savings account, or charges interest on a loan, who sets the interest rate? The bank, usually based on Libor (London interbank offered rate). So tempers flared when major London-based bank Barclay’s was caught rigging Libor. Former Barclay’s CEO Bob Diamond resigned in 2012, and the company handed over a $435 million settlement to U.S. and British authorities. On Nov. 19, 2014, National Public Radio reported that the Federal Reserve is talking with European authorities about finding a replacement for Libor. The same day, we learned that “ANZ, one of Australia’s biggest banks, has suspended seven traders as part of an inquiry into the potential rigging of key interbank interest rates.”
Photo: duncan c

Who takes? What gives?

The august scientific journal Nature took a stab at explaining the apparent rise in financial cheating with a study by three researchers at the University of Zurich (a banking capital!) who looked at 120 employees of an anonymous international bank. The study rested on the concept of “salience,” the idea that behavior is affected by thoughts and values that happen to be present in our minds.

The question was, are bankers less honest when the thoughts and values associated with banking are running through their minds?

Who takes?

The study was built around a coin-flip experiment. Participants were told which side would win, and asked to report the result after each of 10 flips. Wins were worth $20 apiece. Statistics were the only way for the testers to know if the subject was being honest — in the long run, close to 50 percent of the flips should be heads, so any deviation from 50-50 marked dishonesty.

In the control situation, the bankers were asked a series of generic questions about their lives; in the experimental situation, some of the question were intended to raise the salience of banking, such as, “What is your function at the bank?”

 Man-on-the-street -shot of a worried man in a navy suit amid press cameras and reporters.
Wall Street billionaire Raj Rajaratnam was convicted on five counts of conspiracy and nine counts of securities fraud in 2011, and is serving an 11 year sentence. According to Preet Bharara, the federal prosecutor who put him away, “Rajaratnam was among the best and the brightest — one of the most educated, successful and privileged professionals in the country. Yet, like so many others recently, he let greed and corruption cause his undoing.”
Photo: GalleryHip

Bankers responded honestly, essentially stating that half the throws were winners — unless the thoughts of banking were raised. But after the banking prompts, 58.2 percent of their responses were winners — a result that is not possible given the random results of flipping a coin many times. Close to 10 percent of the primed bankers reported a win on every throw, a result that would be expected in about 1 percent of the 120 cases!

What gives?

Why are bankers honest — but only until they are reminded that they work in a bank? The cause seems to lie in the bank culture or values, says author Ernst Fehr, a professor of economics, who commented in a conference call that the spate of banking and financial scandals “raise question of whether the business culture in banks is favoring, or tolerating, fraud, to a larger degree than business culture in other industries.”

The researchers wrote that after being reminded of their profession, subjects were significantly more likely to “endorse the statement that social status is primarily determined by financial success.” That endorsement, they added, “is positively correlated with the reported number of successful outcomes.” Recall that an excessive number of successes involved what we call cheating.

The authors continued that their findings “substantiate current concerns about the influence of materialistic values in the banking sector,” especially since the simple recognition that one is a banker, “may have increased dishonesty through an increase in materialistic values.”

It’s not that bank management is telling employees to be dishonest, “it’s the opposite,” Fehr said. But does not seem to be getting through, he added. “I believe that … what is thought to be implicitly okay is what is showing up here.”

Photo of a smiling white-collar hand-cuffed man escorted from a building by London police officers.
Convicted of fraudulent trading in 2011, Kweku Adoboli’s work at Swiss megabank UBS’s London office cost the company $2.3 billion in losses, called at the time “UK’s biggest fraud.” Billions aside, the conviction also unveiled an atmosphere of negligence and profit-hounding at UBS, leading to the resignation of the bank’s CEO, Oswald Gruebel, and an investigation by the Financial Services Authority. Adoboli has appealed his conviction.

When money talks, can we answer?

Co-author Michel Maréchal, an assistant professor of economics at Zurich, added that “those in the experimental group who most strongly endorse the materialist statement have a positive relationship with dishonesty.” Occupational norms in the banking industry, he added, “put a greater employee emphasis on dishonesty and materialism.”

What can be done, given that financial businesses commonly encourage employees with financial incentives, which the authors said could play a role in the outbreak of cheating.

Recall that the study found that, until being primed to think about banking, these bank employees “are basically honest, so it’s really the cultural aspect, the unwritten norms and values that prevail in the company that seem to make them more dishonest, and that is something we can change,” said Fehr.

Incentives may offer one basis for fighting dishonesty, Fehr said, since any incentive “can be an incentive for being dishonest… and the stronger it is, the bigger is the problem. We don’t argue for removing all incentives, but maybe we should reduce the strength of these incentives.”

A second fix may reside in trying to counter the professional norms with pledges or standards, a tactic that is being tested to battle fraud among taxpayers and insurance claimants.

– David J. Tenenbaum

1 2 3 4

Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. Business culture and dishonesty in the banking industry, Alain Cohn, Ernst Fehr & Michel André Maréchal, Nature (online 19 November, 2014).
  2. What science tells us about why we lie.
  3. Convicted of felonies, banks are allowed to stay in business.
  4. What’s so significant about Barclays Bank lying about the interest rate they paid on loans?
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Volcanoes: How they work, what they do Thu, 13 Nov 2014 15:51:14 +0000 More »]]>
Volcanoes: How they work; what they do
bright orange and black crusty-looking lava flows over wire fence
The slow burn in Hawaii: Lava from a lobe in the forest below the P?hoa, Hi., cemetery burst past a property-line fence on Fri., Oct 31, 2014.

Rock is flowing once again on Hawaii’s big island, where geologic change is not a matter of centuries and millennia, but rather of hours and days. Every square inch of these Hawaiian islands owes its existence to a hot spot that conduits molten rock from deep inside Earth to the surface.

Pelé, the god of the volcano, is a hungry god, and as volcano Kilauea oozes red-hot rock, the village of Pahoa watches the lava push closer. Families on the volcano side of town have already packed for evacuation if necessary.

Volcanoes can do much worse than ooze into the backyard and seize territory. On Sept. 27, Ontake, Japan’s second-tallest volcano, erupted without warning, killing at least 56 in that island nation’s worst volcanic tragedy since 1902. Earthquakes, caused by the movement of molten rock, or magma, usually precede eruptions, but little magma moved before the steam explosion at Ontake, so the government issued no warning.

September 27, 2014: white smoke rising from Mount Ontake as the volcano erupts in Nagano prefecture, central Japan. The unexpected eruption killed at least 56 people at the popular hiking spot.

Kilauea’s rock chemistry is not conducive to explosive eruptions, and more inclined to slow-moving oozes. You can walk up to the molten lava. As the cherry-red surface cools to a brittle, glassy, black rock, you hear the unforgettable crinkly, crackly noise of a planet changing shape.

The rare opportunity to watch terra firma forming in Hawaii is misleading: most of the planet’s crust was once rock — magma — that emerged from the deeps and cooled million or billions of years ago. Some estimates say that 80 percent Earth’s cold, hard surface originated as molten rock.

Energetic but enigmatic

Volcanoes are awesome reminders that Earth is not a boring, static hunk of rock, but rather a living planet that coalesced from a hot cloud of gas and dust about 4.5 billion years ago. The skin cooled as heat from the surface radiated to space. But the high-temperature rock inside was insulated by the crust, and actually has gained heat from radioactive decay and gravitational energy.

In short, we’re sitting on a ball of fiery rock wrapped in a dozen kilometers or two of cool rock.

cross-section of volcano

Diagram illustrating the inner-workings of a volcano, highlighting the flow of magma through canals and out the top
Volcanoes typically consist of a deep magma chamber, a central vent that passes magma and a crater at the summit, usually the result of an eruption or a collapse of the vent. Side vents are also common. (If a magma chamber fails to erupt and cools instead, it can solidify into a large, subterranean hunk of igneous rock called a pluton.)
Graphic: USGS

That’s unstable. Heat rises. Hot substances are less dense than colder ones, so magma is always looking for an escape hatch through the crust. And since heat is a form of energy, rising magma brings up oodles of energy — enough to power cataclysmic explosions. Enough to reshape the face of the planet.

Volcano plumbing

Volcanoes don’t just appear anywhere. They require places where

* deep hot rock rises above intra-oceanic “hot spots;” these magma pipelines fuel volcanoes on Hawaii and Reunion Island; or

* water-rich ocean crust is subducted into much hotter mantle rocks at the edges of tectonic plates.

To understand volcanoes, you need to know the Ring of Fire, where most of them are located. The Ring is located where tectonic plates meet and denser ocean crust sinks beneath the lighter continental crust.

That’s the process of subduction, and it’s the major source of magma.

Map of the Pacific Ocean, showing tectonic plate boundaries and locations of major volcanoes, most of which lie on the boundary of the Pacific plate.
Most volcanoes are in the “Ring of Fire” around the perimeter of the Pacific Ocean.

One hundred kilometers deep in a subduction zone, the sinking crust carries seawater under fantastic pressure (about 30,000 times atmospheric pressure) and temperature (1,000° Celsius) into the earth’s hot mantle. When this water mixes with hot mantle rock, the rock melts. (Just as salt melts ice on your sidewalk by lowering its melting point, water lowers the melting point of mantle rock by hundreds of degrees.)

Diagram of an ocean-continental plate boundary, showing the sliding of the ocean floor beneath the continent, feeding back to the mantle and uplifting volcanoes.
At subduction zones, the oceanic slab sinks below the continent, bringing water and rock to the mantle and powering volcanoes. Ocean floors form when massive outflows of lava at the mid-oceanic ridges solidify and spread. The ocean floors act as slow-motion conveyor belts, moving toward the continents, where they dive underground and disappear. Strings of volcanoes in the Andes, Cascades, Aleutians and so on across the Ring of Fire mark the subduction zones.
Graphic: USGS

The mantle rock melts, and becomes less dense than surrounding rocks, so they rise through the surrounding solid mantle by convection, eventually reaching a magma chamber a few kilometers below the volcanic vent. As the magma continues rising, falling pressure liberates high-pressure gas that was trapped inside it, vapor bubbles expand and eventually rupture, and the volcano can erupt explosively.

Volcano structures

Volcano structure is dependent on the geologic setting and chemistry of the emerging magma.

Satellite image looking down on a towering Chilean volcano, topped in snow.
Villarrica, in the Southern Andes in Chile, is one of the few volcanoes with an active lava lake in its crater summit.
By Jesse Allen and Robert Simmon – NASA Earth Observatory. Licensed under Public domain via Wikimedia Commons

Composite volcanoes are built of alternating layers of ash and lava. These so-called stratovolcanoes, including Mt. Fuji in Japan, Vesuvius and Stromboli in Italy, and Villarrica in Chile, fulfill the stereotypical volcanic cone.

Shield volcanoes are born from multiple vents that emit flowing (not exploding) lava. Mauna Loa on Hawaii, standing 10 kilometers from ocean floor to summit, is a classic shield volcano. Shield volcanoes typically form over an oceanic hot spot, not at a subduction zone.

A lava dome is built by eruptions of viscous, non-explosive andesitic or dacitic lava.

A cinder cone is built from basaltic ash and lapilli — sand to golf-ball-sized ballistic fragments that pile up around a volcanic vent.

A caldera is a ring-shaped depression surrounded by steep cliffs. A caldera forms when a magma chamber spews out its molten rock, and the mountain above it collapses.

Volcano flavors

All volcanoes, in one way or another, represent a leak in the Earth’s crust that allows magma to ooze or burst out. Many types of rock can be released, and some flows can threaten locations so distant that the volcano is just innocuous scenery at the horizon.

Photograph of a domed mountain void of vegetation, its image reflected by a glassy lake in the foreground.
At center, Domo Maule is a dome built of dacitic lava more than 100,000 years ago. Arrow points to reddish rhyodacite lava flow that wrapped around the Domo and flowed into Laguna del Maule, Chile, in the past few thousand years.
Photo: The Why Files
Photo taken above the clouds of a series of enormous volcanic cones and crates; two are spewing smoke.
Mt. Bromo, Java, Indonesia smolders in the foreground, with Mt. Semeru in back. Bromo’s caldera (note wall at left) encloses several younger, daughter cones.
Visual of the relationship between explosiveness and silica content in volcanically-sourced rocks.
The mineral composition of molten rock determines its eruptive behavior. Higher silica content allows a rock to trap more water and forms the most explosive lava.
Graphic: The Why Files

Volcanic Violence Slide Show Rated R

Click to view slideshow.
Pyroclastic flow: USGS, Mud flow: Javier Rubilar

Big dangers

As rising populations run out of safe places to live in volcano country, sooner or later volcanoes will write headlines of havoc. The dying was already under way 2,000 years ago, when Mt. Vesuvius erupted and buried Pompeii in 79 CE. Today, three million people in Naples, Italy, live in the shadow of Vesuvius.

Plenty of other cities face grave volcanic threats. At the western edge of the Ring of Fire, for example, densely crowded Japan, Philippines and Indonesia are all studded with active volcanoes.

For example, Mexico City, the world’s largest metropolis, is just 55 kilometers from Popocatépetl, a 5,465-meter giant that’s erupted about 17 times since Columbus “discovered” the New World.

Photo of Roman ruins in late-afternoon light; an immense volcano looms behind.
Mt. Vesuvius, destroyer of Pompeii (whose ruins appear in foreground), poses a grievous threat to Naples.
Photo: Pattie

For perspective, eruptions like Mount St. Helens, which emitted one cubic kilometer of ash in 1980, happen every decade or so. Krakatau, Indonesia, 1883, put out about 20 times as much stuff. Such event is expectable roughly once in a century.

But consider the 3,000-cubic-kilometer eruption about 75,000 years ago of Mount Toba (also in Indonesia), which likely affected the global climate for years. These volcanic “super-eruptions” can effect the climate and economy of an entire hemisphere, yet we have no human experience of what signals volcanoes might emit before such mega-eruptions.

It’s a principle of geology: What happened before can happen again. So get this straight. Gargantuan eruptions are rare. But gargantuan eruptions can happen.

Map of western Washington State, showing the location of Mt. Ranier and it's attributed "hazard zones" of potential mud and debris flows off the mountain. The paths cut through several towns and suburbs.
If the past repeats itself, these areas near Seattle, Wash., could be affected by debris flows, lahars, lava flows or pyroclastic flows from majestic Mount Rainier.

Perilous predictions

Volcanoes are fascinating in their own right, but the big money is trying to anticipate, even predict, eruptions. The record is spotty, as emphasized by Ontake’s unexpected and deadly eruption on Sept. 27, but steady progress in understanding the chemistry and dynamics of volcanoes should improve matters.

To reduce the surprise quotient for volcanoes, scientists look at:

* Geologic history: How regular and frequent were this volcano’s past eruptions? Based on the composition of the erupted magma, how explosive were the eruptions? How did past eruptions change the landscape? How far away were the effects felt?

* Deformation of Earth’s surface: Before eruption, rising magma may change the surface above the magma chamber. Broad deformation indicates deep magma, while more focused deformation signifies shallow magma that may be more likely to erupt in the near future.

* Gas emissions: Rising magma releases gases like water, carbon dioxide and sulfur dioxide. The timing and intensity of these gases hints at the magma’s composition and location.

* Chemical and physical structure of the magma: Scientists are fascinated by crystals present in a “mush” in some magma reservoirs capable of super-eruptions. If the crystals vanish or change composition, could that trigger an eruption?

* Earthquakes: Rising magma must bust through rock, and the resulting quakes may be the best single indication of magma movement and near-term eruption.

* Gravity: Magma is hotter, and therefore, less dense than the same rock at lower temperatures.

* Electrical conductivity: Changes in underground electrical conductivity can reveal the presence of hot water or molten rock at shallow depths.

Photo of the view across a crystal blue lake towards a volcanically shaped landscape.
Laguna del Maule, a volcanic complex in the Southern Andes, is the result of about 20 millennia of intense volcanic action. This land surface here is rising faster than any place on Earth — about 25 centimeters per year. A full-bore scientific investigation here showcases the techniques that can be used to understand what the volcano is doing. In the past, this volcanic field has produced eruptions many times larger than Krakatau, and capable of devastating large parts of Chile, Argentina, and the downwind southern hemisphere including Australia and New Zealand. The 2011 eruption of Cordon Caulle in Chile (at 41° S latitude), closed airports in Brisbane, Sydney, Melbourne, Auckland and Buenos Aires.
Photo: Laguna del Maule, Chile, The Why Files
Image of four geologists adjusting equipment on rocky ground; one inspects the gear and the other three prep a tripod for reading gravitational changes.
On a field of broken igneous rock, University of Wisconsin-Madison geophysicists set up a station to measure gravity. The satellite dish feeds a high-precision GPS instrument that measures the altitude of a reference rock, which will hold an ultra-sensitive instrument to measure gravity. A change in gravity indicates a change in rock density underground, a clue that magma is rising.
Photo: Laguna del Maule, Chile, The Why Files

Although scientists do not claim that the volcano prediction problem is near solution, some incremental gains are evident. In 1991, for example, the lessons of Mount St. Helens were tested when the ground began shaking around Mount Pinatubo in the Philippines.

A collaboration of U.S. and Filipino volcanologists watched, waited, and eventually made an accurate warning. The Philippine government evacuated tens of thousands of residents, saving massive casualties. Although gigantic mud flows and ash deposits lead to the closing of two major U.S. military bases, few lives were lost during the largest eruption of the 20th century.

– David J. Tenenbaum

1 2 3 4 5

Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. USGS volcanic activity and alert center.
  2. Slow-moving lava from Kilauea volcano burns down first Hawaiian house.
  3. How long will Kilauea Volcano’s June 27 flow last?
  4. U.S. Geological Survey’s Hawaiian and Cascades volcano observatories.
  5. Incredible footage of Japan’s Mount Ontake erupting.
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Imperiled species reproduces in a quiet refuge Thu, 06 Nov 2014 19:34:00 +0000 More »]]>
Imperiled species reproduces in a quiet refuge
Head-on photo of a white rhino looking inquisitively at the camera
Why does the white rhino breed in the Fossil Rim Wildlife Center? The answer could be blowing in the wind. Sound, like sight and scent, affects animal behavior – but scientists are only now starting to focus on sound in captive environments.
Photo: Fossil Rim Wildlife Center

Many zoos and wildlife parks have replaced cages with more natural enclosures, but they may be paying less attention than they should to sound, says Suzi Wiseman, a graduate student in environmental geography at Texas State University-San Marcos.

At last week’s meeting of the Acoustical Society of America, Wiseman reported on sound and the white rhinoceros at a Texas game park. She says she chose the site because it is one the few parks that can actually breed white rhinos in captivity, indicating that they are healthier and/or happier than the average captive rhino.

One reason, she says, may be the rural location of their home, the Fossil Rim Wildlife Center. But how, exactly, does that good ol’ rural life help?

One possibility is sound, says Wiseman, who has just finished preliminary exams for a Ph.D. that she expects shortly.

White rhinos, natives of tropical and subtropical savannahs and grasslands, “Have the most sensitive hearing of all animals, according to animal trackers,” Wiseman says.

Typical night sounds at Fossil Rim Wildlife Center

Colorized graph of sound frequency over time from the Fossil Rim Wildlife Center shows different sound events, like bird chirps, coyote yips and rhino grunts. Quieter sounds are blue; louder sounds are red and yellow.
Click this frequency spectrogram to listen to a nighttime cascade of animal calls. After a quiet period, noise from a car turns on a symphony of animals, starting with birds and coyotes. A rhino chimes in, briefly. If you add persistent human noise, like people working or an engine, the animal symphony halts but the distressed rhinos vocalize more.
Courtesy Susan Wiseman

You can take the rhino out of the wild, but can you take the wild out of the rhino?

Concerned that rhinos, which have huge territories and can run 35 mph, spend too much time standing around at zoos looking bored, Wiseman several years ago started “enrichment practices,” playing audio recordings and watching for a response. “In the Texas summer,” she says, “I played the sound of a storm rolling in, and they jumped up and started looking around and sniffing the air. I played a bird call, and they started poking their heads into the bushes, looking for birds. I played frog calls, and they went over to the moat and looked at the water.”

But when she played zoo sounds, like a child crying, “I got a fairly disinterested response.”

When we commented that these experiments seemed pretty straightforward, Wiseman responded, “I was astonished that nobody had thought to do this.”

Rhino radio review: We don’t dig that techno beat!

In her report last week, Wiseman described an exhaustive program to measure the full panoply of sound, stretching beyond the optimal human range of 20 to 20,000 hertz to:

Infrasound: vibrations slower than a person with perfect hearing can detect

Ultrasound: vibrations above the 20,000 limit to human hearing

Geosound: vibrations in the Earth made by wind, traffic and footfalls

Photo of five white rhinos huddled together on a pasture, two lying down.
Above: White-rhino cows and calves relax at the Texas refuge.
Below: The landscape surrounding Fossil Rim Wildlife Center has little of the artificial sound that can distress zoo animals, but even a slamming door or an auto can change the soundscape and alter animal behavior.
Panoramic view of Fossil Rim Wildlife Center shows an open, sprawling woodland and pastureland characteristic of central Texas countryside

Daddy sang bass

We asked how low a rhino could hear, and Wiseman admitted, “It’s controversial. Rhinos have been recorded in the literature vocalizing down to 4 or 5 hertz … but there are indications that it’s a great deal lower than that. Some say infrasound is just a byproduct of their large size, but if an animal vocalizes at a particular frequency, and has most of the energy in their call at low frequency, I assume they can hear that frequency. The hard part is proving it.”

Infrasonic noise, she points out, “tends to be pretty typical in urban areas,” due to traffic and other concomitants of development.

In the future, Wiseman wants to record soundscapes at zoos and other captive environments and compare animal health in different environments. “Where they are healthier, and what is the sound like?”

Typically, acoustic studies look at volume and pitch. But Wiseman probed more deeply, saying, “I think this is the first study that used broad-based measurements to look at the whole soundscape.”

She looked, for example, at entropy — a ten-dollar term for variations in sound frequency and energy. “We know humans respond poorly to a fluctuating sound, and we know animals respond to a sudden noise out of nowhere.” Sirens vary quickly in pitch and intensity and are designed to grab our attention – and create an emotional response. “The point is you get stressed out if the sound moves,” Wiseman says.

A sound idea?

To gauge response to the sound, Wiseman suggests measuring stress hormones in urine. “We might be able to play back a positive sound track to rhinos and see if the stress hormones go down.”

If the research continues to support the importance of sound to captive-animal health, zoos will be able to adapt, Wiseman says. 50 years ago, she notes, zoo relied on cages, but “now all of them have improved. I hope soundscapes might be another area for improvement.”

Among her suggestions:

Using embankments or fences to block noise and rubber mats to insulate against severe ground vibration

Building a waterfall to create white noise that masks stressful noise

Silencing back-up alarms on zoo vehicles (“I’m sure a lot of animals don’t like that”)

Switching off equipment when possible

Zoos “are doing a wonderful job with the facilities they have,” Wiseman says, “but if they are surrounded by freeways….”

Knowledge is power, Wiseman contends. “Are there particular frequency ranges associated with particular problems? Which species are sensitive to these frequencies? Maybe we can move them to another location with less noise.”

– David J. Tenenbaum

1 2 3 4 5

Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. White rhino
  2. Visit the Fossil Rim website; better yet, tour the grounds.
  3. Vietnamese ‘rhino horn traffickers’ charged in South Africa.
  4. David Beckham, Yao Ming and Prince William have a message about rhino horn trafficking.
  5. Rare Northern white rhinos on the brink of extinction.
]]> 0
Stem cell advance Fri, 31 Oct 2014 14:27:10 +0000 More »]]>
Stem cell advance
Artist's drawing of the eye cross-section showing the detail of the lens' engineering and the pigment layer that surrounds the retina.
Photoreceptors in the retina detect light and send nerve signals to the brain. The retinal pigment epithelium keeps the photoreceptors healthy. When it dies in age-related macular degeneration, the light detectors die as well. A new study that implanted new RPE cells raises new hope for stem-cell therapy.

A field long on promise and short on healing was energized on Oct. 15, 2014, when The Lancet reported on the transplant of retinal cells into 18 people who were blind because cells had died in the center of the retina.

The study focused on safety, but the hints that the transplant worked fed a desperate hunger for progress on stem cells — the long-awaited “spare parts” that may someday revolutionize medicine. Getting the story precisely backwards, CNN headlined “Stem cells help nearly blind see”, then proceeded to explain that “Researchers say that human embryonic stem cells have restored the sight of several nearly blind patients — and that their latest study shows the cells are safe to use long-term.”

Macular degeneration can destroy central vision; roll over image to see how a person afflicted with AMD might see these kids.

In fact, the experts we talked to were optimistic about the safety issue — a huge hurdle for stem cells — but less sanguine about the “getting the blind to see” aspect.

So, how much progress are we making in stem cells, in the clinic and the laboratory?

The clinic part is easy: The U.S. Food and Drug Administration has not approved any non-experimental transplant of cells derived from the most versatile stem cells. These are the embryonic stem cells (ESC) that sparked all the attention 16 years ago, when they were first isolated by Jamie Thomson at the University of Wisconsin-Madison.

The laboratory part is promising, but more complex.

Stem cells stem from what?

A pluripotent a stem cell can develop into any type of human cells, including neurons, muscle and blood cells. Roll over image to see how the stem cell differentiates into various developmental pathways as cells become more specialized.

The cells replaced in the Lancet study, called retinal pigment epithelium, came from ESCs. The RPE provides essential metabolic support to photoreceptors — the cells that convert light into nerve impulses.

Patients in the Lancet study had either dry age-related macular degeneration (AMD) or Stargardt’s macular dystrophy, which affects younger people. In both diseases, the RPEs die, which kills the photoreceptors. The dying starts at the center of vision, causing blindness exactly where detailed vision is most needed.

Each patient received three RPE-cell injections to one eye.

The diseases chosen illustrate the type of condition most appropriate to early human tests of pluripotent stem cells, says William Murphy, co-director of the Stem Cell and Regenerative Medicine Center at UW-Madison. “You need a substantial, unsolved clinical problem like AMD, ALS (Lou Gehrig’s disease) or spinal cord injury.”

“The new study was important from the basis of safety,” says David Gamm, an associate professor of ophthalmology and visual sciences at UW-Madison, and an expert in retinal stem cell biology and cell-based therapies, “but I think it’s difficult to read too much into the efficacy data.”


The examiner and the patient both knew which eye was treated (“you can’t fake that,” Gamm says) and patients may try harder on vision tests with that eye after the transplant;

After repeated eye-chart testing, AMD patients may learn to use surviving retinal regions; and

The procedure replaced the RPE, not the photoreceptors. Because those light-sensitive cells in the center of vision are dead, the treatment at best could have “awoken photoreceptors on the edge of the lesion that are not dead but are not working because they don’t have the RPE,” Gamm explains.

Transplanting retinal cells may sound like a magic bullet, “But it’s not like putting a new carburetor into a car,” says Gamm. Eyes in advanced cases of both diseases are like “a beat-up engine. A lot of those not-so-subtle details were not discussed” in the article.

The study was more convincing on the safety issue, Gamm says, “but unfortunately that often does not get the attention it should get. The patients were followed for a median of 22 months, and nothing like the formation of tumors was seen, or cells getting to the wrong place. These are all important aspects of the study and were done well. I would flip the order of priority on the study to the safety aspect. That’s the part that will advance the field.”

Stem cell research: the output

Graph of stem cell publications from 1996 to 2012. The growth was exponential in the early 2000s followed by an apparent leveling after 2010, though more publications on iPSCs may drive higher growth.
Stem cell researchers are cranking out publications. Between 2008 and 2012, stem cell publication output grew at a 7 percent compound rate, while the total of all subjects grew at a 3 percent compound rate. The bulk of literature in the past two decades focused on non-human embryonic stem cells, but recent advances in reprogramming human adult cells have spawned a cascade of iPSC publications.
Graphic (with slight modification) from Research Trends

But if the retinal cell transplant was the most impressive clinical trial to date, how much longer must we wait?

How long?

For people with untreatable disease, the 16 years since the discovery of human embryonic stem cells amounts to forever. But it’s fair to say that when ESCs were first isolated, they resembled a gang of trouble-prone youths more than a disciplined cadre of bio-workers.

Their unlimited capacity to form any cell type gave embryonic stem cells plenty of potential for mischief, so the first step in putting them to work was to decipher the biochemical cues that guide stem cells into useful occupations.

For comparison, how does the timeline stack up against monoclonal antibodies, identical molecules that trigger or block specific biological processes? Monoclonals were dubbed a “magic bullet” when they were discovered in the early 1980s, but “It took 20-plus years for first therapies,” says Derek Hei, director of Waisman Biomanufacturing at UW-Madison’s Waisman Center.

A moon-suited scientist peers through goggles into a microscope viewfinder, looking at a gel sample in a plastic tray.
Stem cells being produced under the “good manufacturing practices” needed for cell therapy experiments were examined in a clean room at the University of Wisconsin-Madison.

Today, Hei says, monoclonals have finally become “a mainstay of biotechnology,” used in treating cancer and autoimmune diseases like psoriasis and arthritis. “You can look for a similar timeline with cell therapy [derived from pluripotent stem cells].”

Even though biomedical technology has advanced rapidly since the 1980s, stem cells are “significantly more complex” than monoclonals, Hei says. “Cells can differentiate, integrate and replace dead cells, can secrete factors to help other cells survive, and it would not surprise me if it takes 30 years from the initial discovery, to where we have pluripotent stem cells becoming mainstream therapy.”

Nonetheless, Hei was pleased with the latest results. “You don’t really understand all the potential risks and technical issues until you start developing therapy. You will learn things in the first clinical trials that you can’t learn in animal studies.” It’s safe to assume that unanticipated problems will need to be solved, he adds.

The other uses

Research specialist Lia Thornberry Kent worked under a fume hood dispensing a feeder solution for stem cell cultures in the Thomson laboratory at the University of Wisconsin-Madison. Second image: lab manager Jessica Antosiewicz removed a tray of stem cell cultures from an incubator.
2005 Photos: Jeff Miller, University Communications, UW-Madison

Even as Thomson’s epic 1998 discovery focused attention on the blockbuster potential of “spare body parts,” he and his colleagues already envisioned other jobs for the versatile stem cells.

Testing new drugs on a variety of human cells in a dish “is the immediate application” for stem cells, says Su-Chun Zhang, a professor of neuroscience at UW-Madison. Since the discovery of induced pluripotent stem cells (iPSCs) in 2007, researchers can grow cells from patients with various diseases, adds Zhang, a world expert on developing neural cells from stem cells. Having millions of cells, each carrying the donor’s disease, enables use of “high-throughput” screening to test thousands of potential drugs in robotic equipment.

William Murphy, a biomedical engineer at UW-Madison, says “Industry has been ramping up screening,” especially now that they can buy ready-made offspring of iPSCs. “I don’t think iPSCs or ESCs have replaced the current drug-discovery system, broadly, but in particular areas, there are quite a lot of pilot studies to try understand” how to screen drugs against diseased stem cells.

Further technological development is needed to ease high-throughput screening, Zhang says. “We need ways to handle the cells in a uniform way, to put the chemical on, and do this as simply as possible.” If it works, rapid screening of highly specialized cells “could be quite dramatic, can potentially shorten the process of discovery and increase the likelihood of success for a new drug.”

ALS is a fatal degeneration of the motor nerves that signal muscles to contract, and Zhang has already begun screening for a drug to stop an aberrant protein that he recently discovered as a root of ALS.

But he says researchers could benefit from a more sophisticated model-in-a-dish. Since the nerves do not operate in isolation, an ideal model would include nerve cells joined to muscle cells. “That is currently not available, due to complexity,” Zhang says. For one thing, when a nerve cell in a dish signals “contract!” to a muscle cell, the contraction can cause them to jump right out of the dish. “We are still trying to figure out a way to build such a system,” Zhang says, “but we are not there yet.

Making life easy for the robots, he adds, is a “pure technology issue.”

Challenge remain

All of which is to say that pluripotent stem cells are a work in progress, especially in in terms of the ultimate pay-off: treating disease by replacing broken parts. Here are some critical areas for improvement:

Photo of a wheelchair-bound man with an assisted breathing device, his wife looks on from the background next to a handicap-accessible van
Jim Cassidy, a Gulf War veteran, suffers from ALS, a fatal neurodegenerative disease that affects motor function. ALS is one key target for experimental therapy with cells derived from stem cells.

Getting absolute control. “We know [controlling] differentiation is a challenge going forward for all applications,” says Murphy. “We have to specify, standardize the target cell for transplanting; have to know what is going in. Standardization will be an ongoing area of focus for the next five to 10 years. It’s a move from scientific discovery to engineering.”

Cell maturity: How much is enough? Some situations require that mature cells be transplanted, says Murphy, who explains that partly developed pancreatic cells would not release insulin. But to replace cartilage in osteoarthritis, a slightly immature cartilage-forming cell is better, since very mature cells don’t make that essential friction reducer. Immaturity is also valuable for neural-cell transplants, says Zhang. “If you move a mature cell, it will die. A young neuron in a hospitable location will connect to the right place. If it projects to the wrong place, that creates problems.”

Getting to maturity. Even fully differentiated cells derived from pluripotent stem cells may perform like fetal cells, not adult ones. Heart muscle cells, for example, can have the pulse and pumping force of a fetal heart. “We have to find ways to rapidly mature cells so they mimic the properties of an adult,” Murphy says. “It’s a giant challenge facing the field, how to get a maturation process that typically takes years and do it in days or weeks in a dish. The kitchen sink is being thrown at this problem.”

Getting realistic. Cells don’t live in isolation and flat dishes of a single cell type are gross simplifications of a real organ. Therefore, researchers are developing “organoids” that fuse multiple cell types to screen drugs and model diseases. Gamm has generated in-dish combinations of the eye’s retinal pigment epithelium and photoreceptor cells, and Murphy is developing a simple simulation of brain tissue. By recreating a disease in a dish, he says, “We can start testing the mechanism of disease progression, and compounds that influence the disease, but there are no simple technologies yet that can form organoids that are amenable to high-throughput screening.”

Photo of robotic equipment with hundreds of pipette dispensers used to inject biological and chemical compounds for multi-sampling research.
High-throughput screening uses robotic liquid handling and assay detection in 96-and 384-well plates. Under automation, more than 100,000 potential drugs or 18,000 bits of human RNA that may silence gene expression can be tested with minimal labor.

On the bright side

Finally, we return our story to its roots — a study of the safety of transplanting cells to treat age-related macular degeneration. As we neared publication, Cellular Dynamics Inc., received a $1.2 million grant from the National Institutes of Health to grow retinal cells for AMD transplant experiments scheduled for 2017 or ’18.

Black and white electron microscope image of a cell colony showing thousands of stem cells.
This colony of Induced pluripotent stem cell colony was created from skin cells. iPSCs have become a focus of stem cells work because, among other reasons, they can carry a disease that afflicted their donors.
Image: Newswise

Another source of optimism is the growing recognition that developing cells heed chemical signals from their neighbors. “If you want to create a tissue structure in a dish, you might think the cells would have to be individually placed using external manipulation,” says Murphy, “but it turns out for some applications, cells have the capability” to find their proper location.

“If you provide them with the right surrounding conditions, stem-cell self-assembly can build complex structures, tissues, even organs,” says Murphy. “I don’t think anyone would have anticipated that, but it’s tremendously useful.”

Bringing stem cells to the clinic has been a long struggle, but Murphy admits to “cautious enthusiasm. There remains a great deal of potential for treatment, but there are real technical and regulatory hurdles that have to be passed.”

Stem cell products transplanted into the retina may or may not have restored vision in the recent study, says ophthalmologist Gamm, but the study was still a watershed. “You have taken cells derived from embryonic stem cells and put them into the retina, and did not hurt anybody; that’s good. It’s possible there may have been a limited positive effect on vision, and there was no negative. This was major, very positive.”

– David J. Tenenbaum

2 3 4 5 6

Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. Human embryonic stem cell-derived retinal pigment epithelium in patients with age-related macular degeneration and Stargardt’s macular dystrophy… Steven D Schwartz et al, The Lancet, Published online October 15, 2014
  2. Stem Cell and Regenerative Medicine Center at UW-Madison
  3. The ALS Association advocacy homepage, trumpeting support for ALS research.
  4. The ethical, legal and political minefield of stem cell research
  5. Nasal cells allow paralyzed man to walk again
  6. Stem cell research trends
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Cold-War exclusive: Cuban lizards invade Florida Thu, 23 Oct 2014 22:05:57 +0000 More »]]>
Cold-War exclusive: Cuban lizards invade Florida

A new study of lizards along Florida’s Atlantic Coast shows that a long- lasting genetic change — evolution — can occur in just 20 generations. Scientists have seen evolution among microbes or fruitflies in the lab, but demonstrating a change in gene structure is more difficult for larger organisms living beyond the lab.

For decades, native Anolis carolinensis lizards have lived on islands built of sediment dredged during construction of the Intracoastal Waterway. In the 1940s, the closely related Cuban brown anole lizard (Anolis sagrei) entered Florida. Since the Cuban outcompetes the native for food and habitat, A. carolinensis lizards began moving higher into the vegetation.

The situation provided a natural experiment, says Yoel Stuart, a post-doctoral fellow at the University of Texas. Stuart is first author of new study in Science showing that this competition forced a change in native-lizard behavior and foot structure.

The behavior change started within months of the Cuban’s arrival. The change in the genes that control the size and build of foot pads needed to hold onto branches happened within two decades.

Photo of a small fish next to an underwater insect with translucent, trumpet-like mouth parts extended; fish has maneuvered out of range.

Ecologists at Loberg Lake, Alaska were lucky enough to watch evolution in the wild. Notice the fast-moving stickleback fish dodging the dragonfly larva’s sticky lower lip? After this lake’s native sticklebacks were exterminated in 1982, marine sticklebacks with body armor replaced them. Within a decade, almost all of the sticklebacks were lean and armorless because small, fast freshwater predators like the dragonfly larva were feasting on the armored stickleback’s slow-moving young. Within a decade, evolution changed the sticklebacks. In this case, lean and agile beat tough and spiky. Photo: Bob Armstrong

A natural experiment

A brown lizard shows off its bright orange, mate-attracting 'dewlap' hanging from its chin.

Anolis sagrei, the Cuban invader, during a courtship display called dewlapping.
Photo: Todd Campbell, University of Tampa

Plants and animals, including the native anole lizard, took up residence after the artificial islands were created 60 or more years ago. Competition began with the arrival of the Cuban lizard in the 1990s.

During a 1995 survey, co-author Todd Campbell, an associate professor of biology at the University of Tampa, located six islands with only the native lizards, measured the height of their perches, then released Cubans on three of those islands. Within three months, the natives were roosting higher in the trees — but only on islands with the introduced Cubans.

Both lizard species eat insects and compete for territory, says Stuart. The competition “is a little bit of everything; they fight, eat one another and eat each other’s food.”

Was the native’s choice to cede the lower elevations to the Cubans a simple behavior change, or was it associated with a genetic change — evolution? Higher branches are smaller, and higher leaves tend to be slicker, and so before investigating the genetics, the researchers predicted that the lizards would enlarge the toepads that give them such a good grip.

The observations for the new report began in 2010, when Campbell, Stuart and their colleagues compared six islands containing both species to five islands housing only natives. Again they noticed the different perching height, and also noticed that toepads on the natives were larger than before.

So far, so good. But what about genetics? After all, environment and behavior can have physical effects with no alteration of the genetic code. “Professional tennis players have a longer serving arm, likely because of tens of thousands of serves,” says Stuart. With the lizards, “There might be some plastic changes that occur during growth that cause them to have different sized toepad just because they are living in trees, but this is not evolved.”

left hind foot of Anolis carolinensis

A scan of the left hind foot of Anolis carolinensis, the native lizard under study. Toepad measurements were taken on the expanded scales (lamellae) at the end of the longest toe. The lamellae improve the grip while climbing.
Courtesy Yoel Stuart

Aerial photo of eastern Florida where several islands line single file offshore where a deep canal was dredged.

The lizard study was performed on these “dredge spoil” islands in Mosquito Lagoon on Florida’s Atlantic Coast.
Photo: Todd Campbell, University of Tampa


To test whether the enlargement was genetic, the researchers raised individuals from both the invaded and native-only islands in a controlled environment. “We found those differences maintained in the lab, which suggests that the population has evolved,” Stuart says.

Finally, using advanced sequencing, the researchers compared the displaced natives, and concluded that the larger toepads had evolved on each of the six islands they shared with the Cubans.

We remarked that 20 generations or less seemed a short time for an evolutionary change, and Stuart responded that biologists “are tending to realize that if selection is strong, it’s possible to detect evolution rather quickly.”

Finding a way to enter an environmental niche — like the upper branches — “is a really good way of partitioning resources, building up the number of species that can live in a community, and allowing species to coexist,” Stuart says.

Stuart wrote that if the same rate of change in the standard deviation (a statistical gauge of variations in data) in the toepads were applied to men, “a back of the envelope calculation” showed that “the average U.S. male would be the height of an NBA shooting guard or small forward” after 20 generations.

– David J. Tenenbaum
1 2 3 4

Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. Rapid evolution of a native species following invasion by a congener, Y. E. Stuart et al, Science, 24 October, 2014.
  2. Lizard evolution virtual lab!
  3. Rapid evolution of green-backed lizards in the South Adriatic Sea.
  4. Stickleback evolution with flash video.
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Ebola on the march! Thu, 16 Oct 2014 19:28:18 +0000 More »]]>
Ebola on the march!

UNITED NATIONS — Schools have shut down, elections have been postponed, mining and logging companies have withdrawn, farmers have abandoned their fields. The Ebola virus ravaging West Africa has renewed the risk of political instability in a region barely recovering from civil war, United Nations officials said Tuesday, hours after the World Health Organization reported that new cases could reach 10,000 a week by December — 10 times the current rate. New York Times, Oct. 14, 2014

Ebola has spread to a second Texas health care worker, and the World Health Organization has predicted a frightening climb in new infections. Health authorities are scrambling to contain a highly infectious disease that kills through massive bleeding.

In the absence of a prompt and effective response, the director of the UN’s Ebola Emergency Response Mission, Anthony Banbury warned that the world faces “an entirely unprecedented situation.”

Woman in lab coat smiles at camera; a stack of Petri dishes is on her desk.
Caitlin Pepperell, an assistant professor of medical microbiology at UW-Madison, investigates evolution in the tuberculosis bacterium. “People tend to conflate fitness and virulence,” she says. Virulence measures the ability to cause severe disease or death. Fitness is the ability to infect new hosts.
Credit Terri Watters

As the global response lumbers onward and thousands die, we started wondering about the “classic dogma” of infectious disease: Pathogens become less virulent — less deadly — over time since live hosts spread infections better than dead ones. The rapid and mysterious disappearance of the Black Death (bubonic plague) from Europe in the middle ages helped raise the question: After killing as many as 200 million in Europe between 1346 and 1353, did the Yersinia pestis bacterium lose its “will to kill,” in the interests of its own survival?

The comforting dogma is backed by some evidence — and rebutted by plenty of counter-examples, as we’ll see.

Evolution is a numbers game, and this comforting dogma could allow us to think that deadly Ebola will lose its grip over time, as evolutionary pressures “persuade” the virus to sheath its claws. As many as 70 percent of West African Ebola patients are dying, far more than previously reported. The original source of infection is likely a virus-infected bat butchered and eaten by some unlucky African.

It’s a nice notion that pathogens “always evolve towards less virulence,” Lone Simonsen, a research professor in global health at George Washington University wrote to us.  “But this is in fact not necessarily what will happen, as it depends on how the changes affect its transmissibility in the human host.”

1804 painting of Napoleon visiting his plague-infected soldiers after a battle; hospital is in a mosque.
Plague, and its Middle Ages outbreak Black Death, were caused by the bacterium Yersinia pestis, spread by fleas on rats. Several outbreaks occurred between the 6th and early 19th centuries, including one in the Middle East. Here, French emperor Napoleon Bonaparte visits hospitalized troops in Jaffa (present-day Israel) in 1799, during his Egyptian campaign.
Image: Antoine-Jean Gros – Bonaparte visitant les pestiférés de JaffaPublic Domain

Transmissibility is the gauge of evolutionary “fitness,” but the discussion of pathogen evolution can get “pretty muddy,” says Caitlin Pepperell, an assistant professor of medical microbiology at the University of Wisconsin-Madison. “People tend to conflate two concepts: fitness and virulence. Virulence has to do with whether it kills you or makes you extremely sick.” Fitness concerns the ability to infect others and expand its own population.

Some things have been around for a long time, and are adapted to the host,” either through the host’s immunity, or the development of a symbiotic relationship, says Ann Palmenberg, a common-cold expert and professor of biochemistry at UW-Madison. “Cytomegalovirus infects virtually everybody on earth, 99 percent, but it does not cause a lot of damage.”

Cytomegalovirus infections are usually unnoticed, except in people with weak immune systems. Pregnant women can pass an active infection to their newborns.

Following the dogma- more evidence

A second virus with minimal symptoms is herpes simplex. “Herpes simplex causes a genital infection that will not hurt you much, but will be transmissible,” says Palmenberg. “I assume it was much more virulent and killed people initially and then the virus thought, ‘Hey, it’s much better if I stay alive longer.'”

Photo of healthcare workers strapping on personal protective equipment, including rubber gloves, face masks and body suits
An Ebola epicenter in eastern Sierra Leone bordering Guinea, was quarantined at the beginning of August and remains chained by the outbreak.
District of Kailahun, European Commission DG ECHO

There are many ways that viruses can adapt to be transmissible, Palmenberg says. “You don’t have to spread by lysing [dissolving] the cell; shedding a low amount over a long period [as with HIV] is a much better evolutionary strategy.”

The host-microbe relationship can be unstable, Palmenberg says. Most of the countless bacteria in your gut are benign or beneficial, “but you get the occasional outbreak” of disease if they acquire disease-causing genes.

During the infection and replication process, “RNA viruses,” including Ebola and HIV, insert DNA into host cells that force those cells to make new virus particles. Each human cell carries proof of an ancient stalemate between mammals and ancient RNA viruses, or retroviruses, Palmenberg says: “One-third of your genome is retrovirus,” Palmenberg says. These RNA viruses infected our ancestors but instead of killing them, merged into their genome and became part of their descendants — of us.

Counterexamples — flouting the dogma

Pathogen virulence does not always abate over time. For example, a 2013 study found that the West Nile Virus strain that reached New York in 1999 and a recently discovered “lineage 2″ version have both evolved toward greater virulence over the past 300 or 400 years. 1

West Nile, transmitted by mosquitoes, can cause fatal brain infections.

Concerning lineage 2, now found in Greece, Italy and Russia, the researchers reported, “As the virus has spread and continued to evolve, it appears to have become more virulent leading to increased numbers of cases of avian, equine and human disease.”

plane spraying insecticide, city skyline in background with orange sky
A flight crew douses the Gulf Coast with pesticide to kill mosquitoes that spread West Nile virus. The virus has not become more moderate during its 15-year residency in the Western Hemisphere.

In some pathogens, disease is almost an afterthought — harmful to the host and neutral to the virus. For example, the bacteria Streptococcus pneumoniae (the most common cause of meningitis acquired outside the hospital) is carried in the throat in healthy people. The bacterium may sit idly by as it competes with other bacteria for a niche in the throat, Pepperell says. But if its invasive genes activate, the bacteria can enter the blood stream and cause significant disease which does not, however, help it infect new hosts, which it easily achieves from its position in the throat or nose. “We probably don’t really understand the driver of virulence in those organisms,” Pepperell concludes. “This is not a case where it has evolved to reduced virulence.”

In many cases, however, causing disease can boost fitness — measured by the number of new infections. Cholera and other diarrheal diseases, for example, are spread by infected stools that are a by-product of infection.

Similarly, the bacterium that causes tuberculosis needs to be transmitted via coughing, Pepperell says. In this case, as with cholera and Ebola, high virulence translates into high fitness.

kid installing mosquito netting inside red brick room
Not waiting for malaria to defang itself; dedicated bed nets trump evolution. The “classic dogma” — that pathogens tend to lose their bite over time — is “More a mis-reading of the data than a fairy tale,” says Eddie Holmes of the University of Sydney. “There are certainly many instances where this has happened, but also many cases where virulence has not changed much through time and even cases where it increases. For example, malaria has been in humans for millennia and there is no evidence that this it is less nasty now than it was in the past.”

Ebola is largely spread by contact with infected blood, and evolving toward lower virulence would reduce its frightening and frighteningly dangerous bleeding. “This is a theoretical example of lower virulence linked to  lower transmissibility, and therefore not a likely evolutionary path for the virus to take,” Simonsen says.

Lessons from HIV

More than 30 years ago, another fearsome virus emerged from the African bush. HIV, which causes the immune disease AIDS, descended from SIV, a monkey virus. Since 1981, AIDS has killed about 36 million people.

Has the heavily-studied HIV undergone significant evolution, and if so, in what direction?

Photo of cut sections of wild animals from the Congo bush being sold for meat; offerings include alligator and small deer.
Bushmeat for sale at the Moutuka Nunene market in Democratic Republic Congo. The first Ebola outbreak in 1976 was traced to consumption of forest-dwelling animals in the DRC; the new pandemic in West Africa may be traced to flying bushmeat — bats.

There is some evidence that some HIV strains cause varying levels of disease, says Thomas Friedrich, an associate professor of pathobiological sciences at UW-Madison, and head of virology services at the Wisconsin National Primate Research Center. “In evolutionary terms, HIV has not had a long time to evolve toward a peaceful coexistence with humans, if it is ever going to do that. If we let nature take its course, over one-half million years, the virus could or could not co-evolve with the host to make it less pathological.”

HIV evolves in every patient, Friedrich said, as it struggles to survive attacks from the host immune system. “During the natural history of the infection of one person, we see evidence of adaptation to evade immune detection.” This evolutionary ability also enables HIV to evade drugs.

False-color image of roughly-knobbed, red T cell dotted with tiny particles representing the HIV virus.
Scanning electron micrograph of HIV agents (yellow) infecting a T cell (red). T cells play a vital role in the immune system; attacking T cells results in destruction of the immune system that marks AIDS.

The AIDS crisis gave a shot in the arm to all aspects of virology, and one in particular seems applicable to the Ebola crisis, says David O’Connor, a professor in the UW-Madison School of Medicine and Public Health. The drug used with some success on a few Ebola patients, ZMapp, contains three antibodies. Antibodies, delivered by the immune system or as medicine, can block the attachment points that a virus needs to infect a cell. With HIV, and likely with Ebola as well, a single antibody will quickly fail due to genetic changes in the virus — evolution. However, a “triple cocktail” of drugs, which is the standard treatment for HIV, has a better chance of success. “The three antibodies are going to synergize, and reduce the viral replication, without causing resistance to emerge,” O’Connor says.

That’s the case with AIDS, and the hope with Ebola. We won’t know for sure until more of the difficult-to-manufacture ZMapp becomes available.

False-color image of the Ebola virus showing long, sinuous tentacle-like structures.
This colorized transmission electron micrograph reveals some of the fine structure in a particle of Ebola virus.
Created by CDC microbiologist Cynthia Goldsmith: CDC Global

How variable is Ebola?

As we discuss viral evolution, we wonder: Is Ebola evolving now, and if so, in what direction? The only genetic study of the current outbreak documented variations among 300 base pairs in a genome containing 18,000 base pairs.

Whether that’s a lot or a little, “is a bit like a Rorschach test for scientists,” said O’Connor. “The real question is how many of these genetic changes are meaningful and are likely to rise up to dominate an individual’s virus population,” O’Connor says. “For example, how many of these could alter the shape of the virus to protect it from the immune system? Of the 300 base pairs [“letters” in the alphabet of RNA] with variation, there are only about 20 that could both change the shape of the virus and are found in more than 5 percent of viruses in an infected person. To me, that’s not a lot of changes given how much Ebola replicates.”

Pathogen evolution, in this case, is pretty straightforward: What doesn’t kill them makes them stronger. The pathogens that escape the immune attack are those that have some trick to evade attack. When these viruses or bacteria multiply, their offspring are likewise resistant.

As mentioned, Ebola is composed of RNA rather than DNA, and “While we have evidence from other RNA viruses that a single base pair change can change the the structure or function of the virus,” O’Connor says, “the vast majority of single base-pair changes will only modestly affect the ability of the virus to replicate, in one way or another, positive or negative.”

Viruses that are unstable and frequently change shape are difficult to vaccinate against, but Ebola seems fairly stable, says O’Connor. “The issue of enormous diversity, over time, and in different populations, is probably the biggest single obstacle to a universal HIV or influenza vaccine. With Ebola, that does not seem as formidable an obstacle.”

A preliminary test of a candidate Ebola vaccine on 20 human volunteers began Oct. 13 at the Walter Reed Army Institute of Research in Silver Spring, Md.

Making sense yet?

We started with the fantasy that Ebola would quickly abate, following its predecessors in its effort to stay alive, but we’ve learned that many factors affect whether a pathogen benefits by becoming more or less virulent, or staying pretty much as it is.

One more wrinkle: Not all changes in deadliness reflect a change in pathogen genetics; changes in medicine, the environment, host immune systems and human behavior and economics can all play a role. The recent Ebola outbreaks in Africa occurred in villages with few connections to the outside world, and they burned themselves out, says Pepperell, the tuberculosis researcher. “If you have a small, poorly connected population, the virus is going to disappear with a high mortality rate.”

Once Ebola appeared in Monrovia, Liberia, and other cities in West Africa, the picture changed, she adds. “If you have a huge, well connected population, you will not run out of hosts quickly, and the selection pressure to soften the virulence is not very strong, and there is no advantage to evolving toward less virulence.”

Pepperell adds that, “People who are not strong on evolutionary biology tend to think that everything that evolves is driven by advantageous mutations that increase in frequency, but many modes of evolution are neutral. Some aspects of bacterial physiology are really driven by chance.”

The classic dogma is, “A vast oversimplification,” Pepperell concludes. “The evolutionary strategies employed by different pathogens are different from each other, and I don’t think you can make one simple rule to apply to all of them.”

Edward Holmes of the University of Sydney, who has studied the evolution of viruses used to attack the hordes of rabbits that over-ran Australia in the last century, wrote us to say that the path of pathogen change, “All depends on the relationship between virulence and transmission, and which is (a) very poorly understood and (b) differs between each pathogen. In short, predicting how virulence will evolve in the long-term (or even the short-term) is very difficult and often little more than speculation.”

Having heard all these criticisms of the dogma, there still is a grain of truth, says Palmenberg, a researcher into the common cold virus. “I think this is true of any host parasite relationship. If the parasite is so effective that it kill all its hosts, it will have killed itself. That has probably occurred millions and millions of times in evolution, but it’s an end game.”

In a sense, she adds, the pathogen will recognize, “‘Oh *$&^^#%#(, we have killed ourselves!’ The only examples we have in nature are those that were successful [in reducing virulence].”

None of which tells us how Ebola will end up if control efforts fail. It could simmer down, or it could run rampant. “There are Ebola-related viruses that are not as pathogenic, in the same family,” Palmenberg says, “but there is no way of saying who is right and who is wrong. Ebola will be what it will be; we can’t predict the endpoint. Even if Ebola kills all humans on earth, it will still have rats and bats that may count as hosts.”

Moral of the story: Don’t wait for evolution to save us. Unless a vaccine makes a dramatic appearance, we’ll need to do the hard work of controlling this deadly virus.

– David J. Tenenbaum

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Kevin Barrett, project assistant; Terry Devitt, editor; S.V. Medaris, designer/illustrator; David J. Tenenbaum, feature writer


  1. Molecular evolution of lineage 2 West Nile virus, Allison R. McMullen et al, Journal of General Virology (2013), 94, 318–325
  2. RNA Virus Evolution: A Guide for the Perplexed, Eddie Holmes, University of Sydney (Australia).
  3. Black death in Europe
  4. Q & A on NPR with the co-discoverer of ebola.
  5. New ebola cases may soon reach 10,000 a week, officials predict.
  6. Ebola: The longer the outbreak, the greater the risk of mutation.
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