Additional audio editing by Matt Largey form Boston’s WBUR radio station.

If you make it right, it’ll even float.

Each year, the American Society of Civil Engineers (ASCE) puts on the National Concrete Canoe Competition, for which engineering undergraduates formulate, troubleshoot, sift, mix, and cast concrete canoes. Then they race them.

More than 250 ASCE student chapters from the U.S. and Canada compete in the regional competitions. But the competition is as stiff as the stone they race; only a handful of teams make it to nationals. To win, students must not only craft a stone canoe and paddle it speedily down a river–they also need to earn top scores for the canoe design, technical write-up, and oral presentation.

Wentworth Institute of Technology in Boston, MA made their canoe debut in 2005. They started out with a bang—taking regionals, and winning 17^th place in the national competition. Since then though, it’s been a challenge: in 2006, they took third in the regional challenge and won fifth in 2007. But since then, they haven’t placed.

But this time, headed up by sophomore Joe Jazwicz, Wentworth’s canoe club team is starting earlier, running more cement experiments, and busting out the creativity.

It’s a crew race—engineer-style.

For many western fly-fishermen, climate change is hitting too close to the snow-fed trout rivers they call home: trout populations are declining throughout the interior west as water temperatures rise, habitat ranges shift and buckle, and stream ecosystems collapse. In fact, recent studies conducted by federal agencies and trout conservation groups predict that by century’s end climate change will decrease suitable trout habitat in the American west by 50 percent or more. Indeed, the impacts of climate change on trout are as clear and chilling as the water in which the fish have tenaciously survived since the Pleistocene, one million years ago.

Less clear, however, is how waning trout populations will impact the state and local economies that derive millions of dollars from trout-related recreation every year. Local trout shops, guides, and outfitters rely on the health and stability of trout fisheries. However, climate change has increased the frequency and intensity of winter flooding, summer drought, and forest fires. And it is unclear if these businesses will be able to adjust quickly enough to compensate.

Climate change for trout begins high above their river residences. Mountain snow pack, a frozen, natural reservoir of the cold, clear water that nourishes trout streams and their piscine populace is decreasing. The chief cause is a rapid rise in western air temperatures. According to the Rocky Mountain Climate Organization, a non-profit coalition of businesses and environmental groups, the five-year average temperature for Montana, Wyoming, Idaho, and Colorado is two degrees higher today than it was in those states a century ago.

As the air warms, precipitation patterns change. More snow now falls as rain in the winter, which leads to smaller mountain snow packs. Normally, snow pack melts incrementally during the spring and summer, providing rivers a constant supply of cold, clear water. But smaller average snow packs mean that western states are not getting the mountain water storage they need to maintain stream flows during the year. Bruce Farling, Executive Director of Montana Trout Unlimited, says that for eight of the last ten years Montana has seen below average stream flows. On top of that, he says, severe droughts, which plague nearly every western state, are preventing beleaguered streams from being naturally replenished by spring and summer rains.

Decreased stream flows directly affect trout, which depend on cold water to survive. Less water means less suitable habitat for fish because shallow water heats up faster. “All salmonids (a family that includes trout, salmon, and whitefish) have pretty limited temperature ranges,” somewhere between 50 and 65 degrees Fahrenheit, says Jeffrey Kershner, Director of the United States Geological Survey’s (USGS) Northern Rocky Mountain Science Center in Bozeman, Montana. At these temperatures, water contains enough dissolved oxygen for adult trout to respire or “breathe” and for young trout to develop. Beyond 60 degrees, however, dissolved oxygen decreases, and trout begin to suffocate.

Ominously, climate models indicate that surface water temperature in many western rivers and streams will increase if air temperatures rise beyond 5.4 degrees Fahrenheit. In fact, scientists predict a rise in average air temperatures anywhere from 5-10 degrees by the end of the century, according to the NRDC.

Dwindling snow packs indirectly influence trout populations as well. Consistent supplies of snow pack runoff helps reduce the frequency and intensity of forest fires. “When forests dry out, wildfire activity picks up,” says Jack Williams, Senior Scientist for Trout Unlimited. “This can have some serious ramifications for trout fisheries.” Intense forest fires burn away the vegetation that anchors soil and sediment in place. This liberated sediment can enter streams in large quantities and muddy up the clear, oxygenated water that trout eggs require for development.  Streams containing more than 15 to 20 percent of fine sediments like silt or clay, Williams says, threaten trout eggs. “The sediment gets into spaces between gravel and the eggs die from lack of oxygen.”

As diminished snow packs melt earlier and faster, many western states now experience more frequent and powerful spring and winter flooding. These floods are the combined result of rapidly melting snow pack and increased winter rains when there should be snow. They can devastate fall-spawning species like brown and bull trout, which lay their eggs in river gravel during the fall to over-winter for a few months before hatching in the spring. Frequent and intense winter and spring flooding effectively scours the eggs from the river bottom, killing the un-hatched fish in a roil of sediment and stones.

As trout populations suffer, however, so too will the trout angler’s experience and all of the businesses inspired and supported by that experience.   According to the American Sport Fishing Association, the country’s 40 million anglers produce nearly $50 billion in retail sales a year. In 2002, Colorado sport fishing supported more than 10,000 jobs and generated nearly $800 million for the state. And in Montana, angling produces nearly $300 million dollars for the state, annually.

Most of this money is generated during the summer when vacationing tourists seek refuge from their sweltering cities and flock to the cool, trout-filled rivers of the Rocky Mountains. But as the West warms, peak trout fishing season shifts to months when people can’t take vacation. “Most out-of-state anglers are geared to fishing June through September,” says Dave Kumlien, outfitter and owner of Troutfitters fly shop in Bozeman, Montana. “You might have a handful of hard core guys who can come and fish earlier but most people just can’t do that.”

This seasonal shift is largely the result of prolonged and widespread summer fishing closures on western rivers. These closures are instituted by the Department of Fish, Wildlife, and Parks (FWP) when water temperatures exceed the thermal limits of a river’s trout population. From 2001 to 2007, the FWP ordered161 fishing closures in Montana alone.

In July of 2007, for instance, hundreds of rainbow and brown trout died when temperatures in Yellowstone National Park’s Firehole River reached 82 degrees Fahrenheit. The event prompted a highly publicized river closure that many guides say deterred potential clients. That’s because river closures, which generally begin in the afternoon, force anglers to begin their day well before the sun comes up. This is a problem for guides whose clients would rather cancel their trips than get up at 5:00 a.m. to accommodate closures.

Other fishermen will cut their trips in half.  But “Half days equal less tackle and less equipment which means less money coming in,” Kumlien says.  In addition, the quality of fishing in rivers warm enough to warrant closures is generally poor since the thermally stressed trout are sluggish and weak. Consequently, summer tourists cancel their trips and truck their rods to cooler, Canadian waters where trout are in better shape. This adversely impacts western fly-fishing businesses that depend on the summer tourism to keep them financially healthy during the off-season.

Changes in insect hatches also promote a seasonal shift. The emergence of mayflies, a primary trout food, coincides with the tail end of peak runoff and, Williams says, the insects have been shown to emerge earlier in warmer water. So, as rivers warm and runoff peaks sooner, mayflies that normally hatch in June and July are now emerging in March and April. “When popular hatches shift to these earlier months”, says Kumlien, “people don’t come in the same numbers they used to and you have fewer guides and outfitters running around.”

Ultimately, climate related changes restrict trout habitat, and less habitat means fewer fish. Over time, trout will retreat to higher, cooler tributaries to escape the starving flows of the West’s progressively tepid main stems. As a result, easily accessible and heavily-fished rivers like the Madison in Montana and the North Platte in Wyoming may empty of fish and, hence, fishermen. Over time, guides and their clients may have to travel farther to find fish. And because the higher elevation streams to which trout populations will move are narrow, steep, and more difficult to access, outfitters may be pushed out of the float-fishing business.  Similarly, prolonged drought, violent runoff and flooding will make boat access to floatable rivers more challenging.

Scientists are only just beginning to quantify the economic impacts associated with climate change; so much is left to speculation.  But the trout that swim beneath the West’s imperiled rivers and the anglers who cast feathered trickery upon them can’t wait for calculation. “If we wait for hard and fast numbers to act it’s going to be too late,” says Farling.

Williams believes the best way to mitigate climate change impacts on trout and their associated economies is to manage river systems responsibly; to ensure that trout are not forgotten in our rush to seize water for irrigation, recreation, and cities.  “One of the most important things we can do,” he says, “is to make sure river systems are in good quality. Because those that are in good shape can withstand the disturbances associated with climate change and they will be able to bounce back.”

After all, fly-fishing is not simply a past time. For many western states, it is a way of life, a western heritage built on blue-ribbon trout streams and supported by family-owned fly-shops and outfitters. Protecting these businesses and the millions of dollars that trout angling generates begins by protecting the resource: the beautiful and boisterous beasts caught in the swift current of a changing climate.

To learn more about western fisheries and trout conservation click here!

Viruses are mindlessly competent, ruthlessly efficient, and so simple they blur the line between life and non-life. Yet we humans, despite our elaborate nervous systems and thousands of genes, can barely keep pace.

Modern technology has allowed us to begin combating viral infections, but many still afflict our daily lives. These are not necessarily the diseases that overwhelm our news headlines—rather, they’re the chicken pox, the seasonal flu, and the common cold. Sometimes, they’re the viruses we didn’t even know we carried. So how about a moment of respect for these tiny, beautiful plagues of daily life?

The Flu

We’re bigger, brainier, and have technology on our side—but we still can’t stamp out influenza. Every year, those microscopic sacs of 11 genes manage to evade and elude us.

The inner workings of the influenza virus. Photo credit: CDC/Dan Higgins/Douglas Jordan. http://phil.cdc.gov/phil/details.asp

The key to influenza’s repeated success stems from two proteins studding the outside surface of the viral particles: hemagglutinin (H) and neuraminidase (N). When the body mounts a defense against the virus, it remembers those proteins so that the next time, it can catch the virus before it wreaks havoc. Unfortunately for us, influenza has a few tricks up its membranous sleeves. It is advantageously sloppy as it copies and proofreads its genetic material. Sometimes, it sticks adenine where there ought to be a cytosine, or a guanine where there ought to have been a thymine. These little changes add up. By the time the next flu season rolls around, the face of the virus has morphed into something a little less recognizable.

But influenza’s most stunning shapeshifting comes about through a process called antigenic shift. When this happens, the virus shuffles its genetic deck to create a new incarnation of itself, unknown to vaccine-makers and immune systems alike. Shift happens for two reasons: First, influenza viruses store their genetic information not in one long strand, but in eight separate segments. When it infects a cell, those segments are dumped out for replication. Second, some animals—like pigs—can be infected by multiple versions of flu simultaneously, like swine, avian and human. If that happens, and if those viruses all happen to go after the same cell, then they can swap out genetic information and recombine into a whole new strain.

Our T cells never had a chance.

Respiratory viruses have little difficulty getting around, despite their lack of limbs. A sneeze is worth a few million virions.Photo credit: Tim Vickers/CDC, via Wikicommons. http://commons.wikimedia.org/wiki/File:Sneeze.JPG

The Common Cold

Almost everyone in their lifetime will contract some form of the common cold—hence the descriptive common.  Technically though, the ‘cold’ covers a spectrum of minor pathogens. Some people might contract the rhinovirus or maybe the coronavirus. But five to ten percent will get the adenovirus: a misery-inducing, fever-producing virus that just happens to be one of the most studied viral vectors in biomedical research.

Viral vectors provide scientists a chance to turn the table on our microscopic invaders, making them work for us.  In essence, parts of another less manipulable or more dangerous virus like Ebola are inserted into the genetic code of the vector virus. The Ebola-flavored vector enters the body and revs up the host defense system. The end result: immunity not only to those cold proteins, but to those key pieces of Ebola.

There are many faces to the beautifully geometric adenovirus particle--twenty, to be precise. The viral shell is arranged as a twenty-sided icosahedron, made up of an elaborate latticework of about 252 different subunit. Photo credit: CDC/Dr. G. William Gary Jr. http://phil.cdc.gov/phil/details.asp

Lots of viruses can serve as vectors, but the adenovirus holds a special place in the heart of many a geneticist. Of all the vectors out there, the adenovirus genome has been so well picked apart that tweaking its code has become old hat. By now, it has appeared in more human clinical trials than any other vector so far. It’s a small virus, so it doesn’t have as many proteins to compete with the added antigens, unlike the pox or herpes virus vectors. But it’s still large enough to comfortably fit two to three antigens without becoming unstable. The adenovirus also stays in the body for a long time—up to ten days—without necessarily killing all the cells it enters. That means the immune system can take a long, hard look at the foreign antigens.

The Viruses in our Genes

Most diseases make themselves known as they set up shop in a person’s cells. But there’s a class of viruses so indelibly everyday that few people ever realize they’re infected. From conception to death, human endogenous retroviruses (HERV) make up eight percent of our genomes.

Retroviruses act opposite the typical genetic cycle. Instead of transcribing from DNA to RNA to protein, they reverse transcribe their RNA into DNA, and then integrate it into our DNA. In a generic cell, that integration only goes so far. But if the retrovirus happens to infect an egg or sperm cell (and doesn’t kill or cripple the fetus that results from that cell), then its legacy can continue indefinitely. But that said, millions of years spent traveling down our ancestry has rendered most of these now-endogenous retroviruses defunct. It’s as though someone jammed an image into a Xerox machine and let it mash around for a few million years. After a while, the image gets a little screwy. Still, just because they’re defective doesn’t necessarily mean they’re out of the picture. Some retroviruses have been key to our evolution. They’re critical to the existence of the placenta and they maximize how well we digest our starches. But some, like the HERV-K family still produce virus-like particles and proteins. HERV-K members have been found in various cancers, but it’s not clear why yet. In fact, over the years, retroviral genes have been tied to all sorts of problems, including cancers, diabetes and lupus. But again, no one knows for sure whether and how much they cause or exacerbate these conditions.

The Chicken Pox

Up until the 1995 vaccine program went into effect, chickenpox was about as common as puberty. Except that, unlike puberty, it sometimes came back. The virus, varicella zoster, belongs to the same family as genital and oral herpes, but with less stigma. It usually makes a single (spotty) appearance during its host’s childhood, then goes dormant for decades–waiting for an encore. Same virus, different diagnosis: shingles.

How it does this is a bit of a mystery. However, the varicella zoster community has pieced together a tale to the best of their ability, and it goes something like this: As a patient scratches through the throes of chickenpox, th­e virus sneaks through an open sore and hitches a ride back to the heart of a spinal cell. There, instead of going into its usual hijack-replicate routine, it allows the cell’s defense mechanism to kick in. The cell coats the invader with little proteins called histones, which wrap the DNA around themselves so tightly that transcription grinds to a halt. The virus goes dormant.

Nearly a lifetime later though, the virus suddenly revs up the protein-making machinery, hijacks its host, and kicks off a new breakout. The only difference is that this time, the pox only shows up in the one span of skin that the infected nerve covers. Just what sets off this revival remains unclear—it could be old age, or a weakened immune system from disease, or something else. But one thing’s for sure:  it’s the perfect strategy. The virus runs through one generation and then lays low for a few decades. By the time it reactivates, a whole new generation of children await, just yearning to hug their be-shingled grandparents.

Link to Google Map of Turbidity on the University of Cincinnati's website

Dozens of molecules with scary-sounding names, but nearly always in quantities so small that they’re deemed safe by the Environment Protection Agency.

For some molecules, the name may indeed be more scary than the molecule itself, and for some we don’t really know yet–there are no restricted levels on all possible contaminants. In any case, there is one relatively cheap way to improve your drinking water even further, by buying an NSF-approved home filter.

Tip-Top tap waters

I turns out you should worry more about the water from a hand-pump in the National Park campground than about the one flowing out of the tap in a big city. Smaller utilities and water from wells sometimes come closer to the allowed limit for some contaminants, because they may not afford to invest in expensive equipment.

Link to Google Map on the University of Cincinnati's website

Still, a study by the University of Cincinnati and Procter & Gamble researchers found all tested waters to be within federal health limits, and therefore safe to drink: “I believe the overall picture for US drinking water quality in the US is good,” says lead author Scott Dyer of Procter & Gamble. (Note: Procter & Gamble markets the “PUR” line of home water filters, one of the main brands on the market with “BRITA.”)

The authors of the study started looking at many utilities around Cincinnati, including some supplying water to only a hundred homes. They then enlarged the study, but to be make it relevant to more people, they focused on 77 urban areas in the US.

Find out if your city is one of these 77.

Note that the concentrations used are reported by the utilities themselves–as required by federal regulation–and date back to 2004-2006. The report took into account 392 water utilities that serve 62% of the population.

Costs and benefits

You wouldn’t fill your bathtub with spring water. Yet you flush drinking water down your toilets, use it for washing clothes, dishes and your skin. It would be even more irresponsible to ask for all that water to be absolutely pure. All drinking waters are exposed to contaminants, whether from pipes, bottles or contact with the environment. Purifying beyond a certain point is counterproductive: both useless and prohibitively expensive.

A more cheaper solution is to use a filter at home, and treat only that water which you are going to drink. A filter containing what is called “activated carbon” and “ion-exchange resins” is the easiest, most affordable solution to raise your drinking water quality above federal standards.

Link to the results for Boston on the University of Cincinnati's webpage

If you find out that your tap water (on the right is a diagram of the results for Boston) contains high levels of some unwanted contaminants, you may consider getting a filter that removes the incriminated contaminants. Just make sure it is NSF-certified and doesn’t rob your water of its healthy minerals (most filters won’t).

What’s good for you is not good for your dishwasher

You should drink water that is free from microbes and various organic molecules seeping from farms and factories. Yet you do want some of the minerals–not lead or arsenic, but at least calcium and magnesium.

When spring water contains lots of minerals it’s called mineral water. With minerals such as calcium and magnesium, water is beneficial to your heart. Even companies that bottle tap water after purifying it also often add some of these minerals back–check the labels to see how much. Don’t get too crazy about this, though: with a balanced diet, you should get a lot of these minerals from food rather than from water.

The simpler and cheaper way is to drink tap water: when tap water contains lots of calcium and magnesium, it is called hard. So if you live in an area with hard tap water, by all means, drink it! A proper filter shouldn’t remove these healthy minerals.

On the other hand, if the water in your area is hard, you may want to install a water softener on the pipes that feed your dishwasher and other appliances, because the calcium and magnesium in hard water clogs these.

“I can see clearly now the rain is gone”

“One cannot tell if water is safe just because it appears clear or tastes good,” says Rick Andrew from the National Science Foundation.

#1 Bubbles: Your water may appear cloudy, but colorless. Most likely, the pressure in the mains has increased so that minuscule bubbles form when the waters exits your tap and reaches normal pressure.

Bottom Line: Leave your glass aside for a minute or two and see if the bubbles coalesce and finally clear up. If that’s the case, you’re fine, but if the cloudiness remains and is accompanied with color, go to step #2.

#2 Soil: Heavy rains may have caused soil runoff, or maybe there’s repair work being done on the water mains: the little submarines floating in your glass are soil particles, and they may have brought microbes along for a ride.

Bottom Line: You may see soil particles, but you can’t see germs, so check item #7. You may also want to get a filter.

#3 Iron: Iron oxide can seep into some wells and color the water a rusty brown-orange and give it a metallic taste. To avoid this nuisance, federal standards recommend an upper limit on the iron content of water.

Bottom Line: Utilities have no obligation to follow the federal standards for taste, only those for health. There is no clear associated risk with iron–which is why water in some rural areas can taste funny–but if iron is leaching from a mine, there may be other metals around (see #8).

#4 Algae: Algae present in lakes and stream can give an unpleasant flavor to drinking water, if your water comes from reservoirs as opposed to wells.

Bottom Line: The presence of algae mostly causes an unpleasant odor, but it can also be accompanied by bacteria (see #7).

Not just a matter of taste

#5 Chlorine: Chlorine is added to disinfect tap water: water leaving the treatment plant without chlorine wouldn’t be so safe during its trip through the water mains. But chlorine brings an unpleasant taste and can produce unwanted byproducts that affect the nervous system, irritate the eyes or nose and increase the chances of cancer and anemia.

Bottom Line: You can use a home filter to remove chlorine and its byproducts right before you drink–just don’t leave the water standing for days, and pay attention to seasonal variations in waterborne germs (see #7).

#6 Copper: Corrosion attacks pipes, and copper may slowly dissolve into the water. This gives a metallic taste and even a blue-green color to your water. It can also upset your digestion, or even damage your liver and kidneys in the longer term.

Bottom Line: More recent pipes made out of PVC avoid the problem with copper, older ones containing lead may be worse (see #8).

Tasteless

#7 Microbes: Germs in human or animal excrement can trigger gastro-intestinal illnesses. Spikes in bacteria concentration may also stem from the seasonal blooming of algae on which some bacteria feed in lakes and streams. In areas that rely on surface water as opposed to groundwater, these bacteria can end up in tap water.

Bottom Line: In general, utilities will solve the safety issue, but make the flavor one worse–by adding chlorine to get rid of germs (see #5).

#8 Lead: If the pipes in your area are old and contain lead, this metal can find its way into your water–even if it was removed properly at the plant. Lead can delay a child’s development and affect an adult’s kidneys and blood pressure. Even though old water systems are more likely to have lead pipes, the tests reported by utilities may not reflect that since they’re often performed upstream at the plant.

Bottom Line: Pipe quality varies, and it is impossible to test the water in every single house. This may be a good reason to install a filter, unless you can convince someone to replace the pipes in your area (see #6).

Link to Google Map for Nitrate on the University of Cincinnati's website

#9 Residue from fertilizer and septic tanks: These produce nitrites and nitrates which can affect infants, leading to shortness of breath and blue-baby syndrome and possibly death. On the map drawn by the University of Cincinnati – Procter & Gamble team, these concentrations are clearly high in a teardrop-shaped region from Nebraska to Ohio, says team researcher Scott Dyer from Procter & Gamble, who explains this by fertilizers seeping into the cornbelt’s water table.

Bottom Line: As for many other contaminants, you can use a filter to remove most of it.

Everything you ever wanted to know about tap water

There are many other compounds to pay attention to. For instance, perchlorate, which is used in explosive and rocket fuel to provide extra oxygen, has been found in some tap waters. The Environmental Working Group’s Nneka Leiba is hoping that the EPA will enforce an upper limit on perchlorate concentrations in drinking water. She mentions 141 unregulated compounds found in tap water for which she would like to see standards enacted–yet for most of these, it is unclear what effect they have on our health, if any.

The Environmental Working Group’s report is a few years older than that of the University of Cincinnati, but it lists many more communities, and separates them according to 39,751 utilities, so you can find yours instead of reading about a city average. It also lists a broader range of compounds, including unregulated ones.

If you still cannot locate your utility, try via the EPA’s website.

Video by Meredith Sorensen and Rachel Leah Blumenthal

Click here to visit the DHART website.

Structure of an Ebola viral particle revealed via transmission electron micrograph. Photo credit: CDC/ Frederick Murphy.

It began in Kikyo, a remote village in western Uganda’s Bundibugyo district, during the twilight days of August. People grew ill with headache, fever, bloody diarrhea, and vomiting. Then they died. In mid-November, a young Ugandan doctor named Jonah Kule rode his motorcycle to the village to investigate. Witnesses say he suspected cholera, possibly typhoid. He sent blood samples from patients to international laboratories for testing. On November 29th, the same day that the U.S. Centers for Disease Control (CDC) identified the virus as Ebola, Kule developed a headache and checked into Mulago Hospital. Five days later, he died. That outbreak lasted nearly three more months, officially ending February 20, 2008.

Ebola may have faded from the spotlight of public attention it enjoyed during the mid- 90s, but that doesn’t mean it went away. Quite the opposite: the number of recorded major outbreaks has more than doubled since 2000. Researchers continue to investigate the virus, but licensed therapies and vaccines still escape them. Meanwhile, patient care during outbreaks remains limited, hampered by a lack of detailed clinical information, inadequate resources, and fear.

A complex and lethal virus, Ebola kills up to 90 percent of its victims. Five known strains exist, each named for their place of origin: Zaire, Sudan, Reston, Cote d’Ivoire and—as of 2007—Bundibuygo. Contrary to popular belief, fewer than 50% of Ebola patients experience massive bleeding, says Dr. Thomas Geisbert, Director of the Boston University National Emerging Infectious Diseases Laboratories. The disease actually closely mimics a condition called septic shock: the virus causes excessive clotting, blocking normal blood circulation and exhausting coagulating factors. The blood, with nowhere else to go, damages the internal walls of the blood vessels as it pushes against them from the inside. Major organs, starved of critical oxygen and nutrients, begin to fail.

Two nurses stand by an Ebola victim under their care during the first 1976 outbreak in Kinshasa, Zaire. Photo credit: CDC/Dr. Lyle Conrad, courtesy of wikicommons.

When Ebola first emerged in the summer of 1976, it took the world by surprise. No one knew where it had come from, what it was, or how to treat it. The World Health Organization (WHO) and an international commission descended on outbreak sites in the Sudan and Zaire (now the Democratic Republic of the Congo). Medical personnel quarantined patients and stopped the use of unsterilized needles while investigative teams set out to discover the source of the virus. They never found their answer, but within three months, the outbreaks ended as suddenly as they began. Over the next 20 years, the world watched with horrified fascination as another five major outbreaks erupted in sub-Saharan Africa, infecting 1105 individuals, of whom 802 would die.

Ebola’s macabre effects and unknown origins lent the disease a dark glamour that captured the public’s imagination. In 1994, Richard Preston published his sensationalized account of Ebola’s history, The Hot Zone, which shot to the top of the bestsellers list; a year later, the movie Outbreak fueled the public’s growing fascination with virulent disease. When a major outbreak erupted in Kikwit, Democratic Republic of Congo (formerly Zaire) that same year, Ebola had become if not quite a household word, then certainly a familiar one. Heavy media coverage allowed the public to watch— captivated—as WHO, Doctors without Borders and other organizations again leapt into the fray. But as the virus burned out six months later, the urgency passed and public interest waned. Ebola faded once again into the inscrutable African jungle.

But Ebola has come back. The past nine years have seen more major outbreaks than the twenty years following the virus’ debut. In 2000, the largest outbreak to date occurred in Uganda, killing more than half of the 425 patients over four months. The following October, Ebola appeared simultaneously in Gabon and the Republic of the Congo, lingering in both nations for about seven months. Two more outbreaks occurred in quick succession in the Republic of Congo, and another flared briefly in the Sudan, dying out in the summer of 2004. Then the virus withdrew for three years, before resurfacing in 2007 in Uganda and the Democratic Republic of the Congo. The most recent outbreak, again in the Democratic Republic of the Congo, was declared Christmas day 2008, ending only a few months ago this year in February. Researchers aren’t certain why so many outbreaks have occurred recently. Part of it may be that more healthcare workers are aware of Ebola and more likely to test for it. “I would guess that if you’d looked for Ebola in the Congo in that part of Africa 40 or 50 years ago, you’d have found it,” Geisbert says.

Red Cross members disinfect the body of an Ebola patient during the 1995 Kikwit outbreak. Photo credit: CDC/Ethleen Lloyd.

But some of the rise is likely genuine. Increased logging brings workers deeper into the rainforests and closer to the bats believed to harbor the virus. And should people return to their villages infected, few if any hospitals are equipped to readily counter the virulent fever. War and economic turmoil have decimated what healthcare infrastructure existed in the areas most frequently afflicted with the disease. “It’s hard to understand how they could deal with Ebola in a setting like that,” says Bill Johnston, president of the Jane Goodall Institute, which conducts health and education programs in the Sub-Sahara.

Meanwhile, the hunt for an Ebola vaccine continues. New approaches target specific proteins on the outer surface of the Ebola virus, called glycoproteins, which help the virus attach to and invade cells. The trick is getting the glycoprotein safely into someone’s body and stimulating their immune response enough to build resistance to Ebola. The National Institutes of Health (NIH), CDC, and other research teams shuttle the protein into the body by piggybacking it onto less deadly viruses, like the common cold. The cold virus enters the body and starts replicating, so the person’s immune system mounts an assault not only on the cold, but also on the accompanying Ebola protein. This model looked promising and even passed human safety trials—but 40-60 percent of the world’s population has already had a cold, so their immune systems would remember and destroy that virus before ever addressing the Ebola glycoproteins tagging along. Less common viruses are more effective because they don’t have that problem—but they carry potentially greater risks to immunocompromised patients. (In otherwise healthy people though, these vaccines appear to be safe: earlier this year, after a contaminated needle-stick injury, a Hamburg researcher safely tolerated a glycoprotein vaccine based on the vesicular stomatitis virus, part of the rabies family of viruses). Other avenues target critical genes in the Ebola replication system like VP-30, but that work is still in its infancy. Licensed, FDA-approved Ebola vaccines remain at least several years away, but “this isn’t a function of how brilliant the scientists are that work on it,” warns Dr. Gigi Kwik Gronvall, a Senior Associate at the Center for Biosecurity at the University of Pittsburgh Medical Center. “It’s a function of how difficult the virus is.”

New drug therapies for infected patients are also under development. Unfortunately, like vaccines, these are highly experimental. These newer therapies focus on stopping the excessive coagulation that Ebola causes. If the clots don’t form, then the body’s organs can get the nutrients they need to function, and stopped-up blood won’t leak out of increasingly damaged blood vessels. But even the most successful approaches save only about 30 percent of test monkeys. “There’s never going to be a magic bullet,” Geisbert says.

A doctor cares for an Ebola patient in a Yambuku, Zaire hospital theatre-cum-ICU in the first 1976 outbreak. Photo credit: CDC/Dr. Lyle Conrad.

In contrast to the progress made in laboratories, overall patient survival has remained relatively unchanged. The typical outbreak setting—rural Sub-Sahara—is rudimentary at best. Running water and electricity and even basic medical equipment are rare luxuries. Healthcare workers risk themselves with every patient they treat; a lethal dose of Ebola is as low as one virus particle—a needlestick injury contains many times that amount, says Dr. James Strong, hemorrhagic fever researcher with the Public Health Agency of Canada. Cultural differences add another dimension: indigenous populations fear foreign aid workers, who arrive in protective suits to whisk the ill away to isolation wards. Panicked, many flee—spreading the disease.

Yet inadequate clinical information poses the greatest obstacle to improved care. “It’s like with SARS. Even though any one hospital only saw a few patients, when you put it all together, you can say: here’s what the potassium levels are in SARS, here’s the kidney function.” says Dr. Daniel Bausch, a professor of tropical diseases at Tulane University. But, he adds, you don’t get that if it’s not systematically collected—as is the case with Ebola.

That may change. In the fall of 2006, an international group of experts in hemorrhagic fevers and healthcare met at the Public Health Agency of Canada in Winnipeg to discuss the need for improved care and research during outbreaks. In November of 2008, WHO convened an informal gathering of many of the same experts, including Bausch, to explore the possibility of establishing a clinical outbreak network. The consensus reached emphasized education and information—creating, for example, a standardized data collection strategy that could be implemented across a broad region. When an outbreak ends, researchers can take stock: what was done and what worked. Then experts could devise improved treatment strategies and decrease case-fatality ratios, earning the trust of their patients.

Although WHO’s meeting was purely a preliminary gathering of ideas and opinions, it’s a start. Ebola shows no signs of disappearing anytime soon, and although vaccines and therapeutics will ease the burden, they won’t be available for several years; the practicalities of patient care and research remain a priority. “If you think about it, you’re challenged not only to take care of the patient, but also to learn as much as you can about the disease in the same setting,” Bausch says. “The clinical and the clinical research part of it go hand in hand.”

Video by Jennifer Berglund and Julia Darcey

Mud Flow

WATER- Here’s Mud in Your Eye: Mud volcanoes may sound absurd, but these underground pools of pressurized mud can be just as dangerous as their fiery cousins. In May 2006, drilling company PT Lapindo Brantas chose to drill for natural gas in East Java, Indonesia despite warnings from geologists that their find was on a fault line. The company drilled down to nearly 9,300 feet, cracking through the limestone above an undetected highly pressurized mud reservoir. Even then, disaster might have been averted had the company not illegally decided to forgo the standard a protective steel cage to stabilize the area. The mud quickly fractured its casing and a fountain of hot mud swept down to the nearby villages, forcing over one and a half million people to flee their homes. The mud volcano continues to pump out around 100,000 feet of mud every day and will continue to do so for another 30 years. Despite attempts by the company to blame an earthquake from two days before and 200 miles away from the volcano, they were eventually fined $278 million for their shortsighted arrogance. Currently, the company is trying to declare bankruptcy to avoid paying.

Road to Centralia

FIRE- Feel the Burn: Pennsylvania was long a hub of coal mining, but after the mines were exhausted, the local towns were left with deep caverns under the Earth.  Many towns, including Centralia, used nearby abandoned mines as landfills. Every year, the town firemen would set the landfill on fire as a cleaning measure.  To contain the fire, layers of trash were sperated by layers of clay. Unfortunately, the town forgot te clay one year and in May 1962, a deliberate fire set in an abandoned strip mine used as a landfill spread underground. Soon, the fire spread to the remaining coal seams under the town, making every attempt to put it out futile. The fire released carbon monoxide and other poisonous gases into the town as well as creating dangerous sinkholes. The town was officially evacuated in 1981 although there are still a few diehards living in the fiery ghost-town. Scientists estimate the fire will continue to burn for another 250 years.

Life in the Dust Bowl

EARTH- Dust Follows the Plow: In the late 19th century, many farmers believed that agricultural activity on semi-arid plains leads to increased rainfall and more fertile soil. The “rain follows the plow” theory (based on limited, circumstantial evidence) was used as justification by the United States government when it gave away thousands of grassy, unproductive prairie to farmers in the beginning of the twentieth century. Thousands of families took the government up on the offer, and plowed over the grass that protected the soil from drying out. Without the grass to hold the soil and keep it moist, the soil rapidly became dust. The notorious Midwestern winds then whipped up the dust into enormous storms so that during the 1930’s; the drought plaguing the area only grew worse. If that wasn’t enough, whatever crops were left got eaten up in a jackrabbit and grasshopper population boom. At the same time, tarantulas, black widow spiders, and centipede numbers also grew enormously. Unsurprisingly, over half a million Americans fled the situation to seek jobs in the West. The lessons of the Dust Bowl are still being taught. Today there are several candidates for new dust bowls around the world, especially in China and Africa, and no guarantee it won’t happen again.

Great Sparrow Campaign

AIR- Sparrow Sorrow: When Mao Zedong and the Communist Party took over China, they announced a series of social and economic plans jointly called the Great Leap Forward. One of the first to be implemented in 1958 was the Four Pests campaign, a concentrated attack on the most problematic pest animals: mosquitoes, flies, rats… and sparrows. Prompted by the sparrows’ grain seed eating habits, the Chinese government encouraged people to drive sparrows off with pots and pans, destroy nests, kill nestlings, and otherwise get rid of the perceived menace. But in their zeal to destroy the sparrows, the fact that sparrows mainly eat insects, not grain was forgotten. The result: a veritable plague of locusts devouring crops. This disaster, compounded by other Great Leap Forward projects (encouraging farmers to start their own personal steel furnaces, implementing new farming techniques based on very flawed Soviet science) led to the Great Chinese Famine, also known as the time when 30 million peasants starved to death.