microplastics in your shellfish

the human microbiome

WATCH: Raindrops Catapult Bacteria Into The Air, And It's Beautiful

When you step outside after a big rainstorm and take a deep whiff of that fresh, earthy smell, you're mostly smelling a chemical called geosmin.

It's a byproduct of bacteria and fungi. And something about rain lofts the chemical — and sometimes the organisms themselves — into the air, a process that not only helps release that earthy smell but may, in very rare conditions, spread diseases.

Somehow raindrops launch tiny living things off the ground.

Wind can pick bacteria up from the ground and bring into the sky, sometimes settling in clouds thousands of feet above us. Sea spray can also send bacteria flying. The mystery has been, how does rain do it?

Now, mechanical engineers writing Wednesday in the journal Nature Communications say they've figured it out. It has to do with tiny bubbles.

Using high-speed cameras and fluorescent dye, the researchers filmed drops of water as they fell on different types of soil infused with bacteria. They watched as the drops delicately catapulted the microbes into the air. WATCH!

Washing clothes releases thousands of microplastic particles into environment

More than 700,000 microscopic fibres could be released into waste water during each use of a domestic washing machine, with many of them likely to pass through sewage treatment and into the environment, according to new research.

A study by Plymouth University examined the mass, abundance and size of fibres present in waste effluent following washes of synthetic fabrics at standard temperatures of 30˚C and 40˚C.

It found hundreds of thousands of tiny synthetic particles could be released in each wash, confirming earlier work at Plymouth University that the washing of clothes is a major source of microscopic fibres within the aquatic environment.

The research, published in Marine Pollution Bulletin, was led by PhD student Imogen Napper in conjunction with Professor Richard Thompson, who is a leading international expert on microplastics and marine debris having worked in the field for more than 20 years.

For the study, a series of polyester, acrylic and polyester-cotton items were washed at 30˚C and 40˚C using various combinations of detergent and fabric conditioner. Fibres were then extracted from the waste effluent and examined using an electron microscope to determine the typical size and any differences in mass and abundance among treatments.

The research found that laundering an average washing load of 6kg could release an estimated 137,951 fibres from polyester-cotton blend fabric, 496,030 fibres from polyester and 728,789 from acrylic. The polyester-cotton blend was consistently found to shed fewer fibres than both the other fabric types, regardless of the differing treatments, however the addition of bio-detergents or conditioners tended to release more fibres.

Professor Thompson, who leads the International Marine Litter Research Unit at Plymouth University, recently gave both written and oral evidence to the microplastics inquiry held by the House of Commons Environmental Audit Committee, which led to recommendations for a ban on the use of microbeads in cosmetics. read more

When People Ate People, A Strange Disease Emerged

Most of the world didn't know anyone lived in the highlands of Papua New Guinea until the 1930s, when Australian gold prospectors surveying the area realized there were about a million people there.

When researchers made their way to those villages in the 1950s, they found something disturbing. Among a tribe of about 11,000 people called the Fore, up to 200 people a year had been dying of an inexplicable illness. They called the disease kuru, which means "shivering" or "trembling."

Once symptoms set in, it was a swift demise. First, they'd have trouble walking, a sign that they were about to lose control over their limbs. They'd also lose control over their emotions, which is why people called it the "laughing death." Within a year, they couldn't get up off the floor, feed themselves or control their bodily functions.

Many locals were convinced it was the result of sorcery. The disease primarily hit adult women and children younger than 8 years old. In some villages, there were almost no young women left.

"They were obsessed with trying to save themselves because they knew demographically that they were on the brink of extinction," says Shirley Lindenbaum, a medical anthropologist with the City University of New York.

But what was causing it? That answer eluded researchers for years. After ruling out an exhaustive list of contaminants, they thought it must be genetic. So in 1961, Lindenbaum traveled from village to village mapping family trees so researchers could settle the issue.

But Lindenbaum, who continues to write about the epidemic, knew it couldn't be genetic, because it affected women and children in the same social groups, but not in the same genetic groups. She also knew that it had started in villages in the north around the turn of the century, and then moved south over the decades.

Lindenbaum had a hunch about what was going on, and she turned out to be right. It had to do with funerals. Specifically, it had to do with eating dead bodies at funerals.

In many villages, when a person died, they would be cooked and consumed. It was an act of love and grief.

As one medical researcher described, "If the body was buried it was eaten by worms; if it was placed on a platform it was eaten by maggots; the Fore believed it was much better that the body was eaten by people who loved the deceased than by worms and insects."

Women removed the brain, mixed it with ferns, and cooked it in tubes of bamboo. They fire-roasted and ate everything except the gall bladder. It was primarily adult women who did so, says Lindenbaum, because their bodies were thought to be capable of housing and taming the dangerous spirit that would accompany a dead body.

"So, the women took on the role of consuming the dead body and giving it a safe place inside their own body — taming it, for a period of time, during this dangerous period of mortuary ceremonies," says Lindenbaum.

But women would occasionally pass pieces of the feast to children. "Snacks," says Lindenbaum. "They ate what their mothers gave them," she says, until the boys hit a certain age and went off to live with the men. "Then, they were told not to touch that stuff."

Finally, after urging from researchers like Lindenbaum, biologists came around to the idea that the strange disease stemmed from eating dead people. The case was closed after a group at the U.S. National Institutes of Health injected infected human brain into chimpanzees, and watched symptoms of kuru develop in the animals months later. The group, which won a Nobel Prize for the findings, dubbed it a "slow virus."

But it wasn't a virus — or a bacterium, fungus, or parasite. It was an entirely new infectious agent, one that had no genetic material, could survive being boiled, and wasn't even alive.

As another group would find years later, it was just a twisted protein, capable of performing the microscopic equivalent of a Jedi mind trick, compelling normal proteins on the surface of nerve cells in the brain to contort just like them. The so-called "prions," or "proteinaceous infectious particles," would eventually misfold enough proteins to kill pockets of nerve cells in the brain, leaving the cerebellum riddled with holes, like a sponge.

The process was so odd that some compared it to Dr. Jekyll's transformation to Mr. Hyde: "the same entity but in two manifestations — a 'kind', innocuous one and a 'vicious', lethal one." npr

WATCH: Bacteria Invade Antibiotics And Transform Into Superbugs

The Evolution of Bacteria on a "Mega-Plate" Petri Dish from Harvard Medical School on Vimeo.

npr

If you've ever wanted to watch a superbug evolve before your very eyes, you're in luck. Researchers filmed an experiment that created bacteria a thousand times more drug-resistant than their ancestors. In the time-lapse video, a white bacterial colony creeps across an enormous black petri dish plated with vertical bands of successively higher doses of antibiotic.

The colony pauses when it hits the first band of antibiotic, creating a stark border between the white colony and the black petri dish. Then the bacteria start to edge their way into the toxic soup. More dots appear and they start growing, racing to the next, stronger band of antibiotic. The bacteria are evolving. After almost two weeks of real time have passed, they've become resistant to the strongest antibiotic and completely taken over the kitchen-table-sized petri dish.

We know dangerous bacteria are getting stronger all the time and that it's our fault because of our excessive and indiscriminate use of antibiotics. Each year, 23,000 people in the U.S. die as a result of superbug infections. But we typically don't get to see superbugs created.

For most people, evolution is just conceptual, says Tami Lieberman, an evolutionary microbiologist at MIT. She and her Ph.D. adviser, Roy Kishony at Harvard Medical School, wanted something that would make the evolution of superbugs seem more concrete. "The goal was to see evolution, not to abstract it," she says.

Their video and report were published Thursday in the journal Science.

Look, Ma! No Mitochondria

Scientists have found a microbe that does something textbooks say is impossible: It's a complex cell that survives without mitochondria.

Mitochondria are the powerhouses inside eukaryotic cells, the type of complicated cell that makes up people, other critters and plants and fungi. All eukaryotic cells contain a nucleus and little organelles — and one of the most famous was the mitochondrion.

"They were considered to be absolutely indispensable components of the eukaryotic cell and the hallmark of the eukaryotic cell," says Anna Karnkowska, a researcher in evolutionary biology at the University of British Columbia in Vancouver. Karnkowska and her colleagues describe their new find in a study published online Thursday in the journal Current Biology.

Mitochondria have their own DNA, and scientists believe they were once free-living bacteria that got engulfed by primitive, ancient cells that were evolving to become the complex life forms we know and love today.

For decades, researchers have tried to find eukaryotic cells that don't have mitochondria — and for a while they thought they'd found some. One example is Giardia, a human gut parasite that causes diarrhea. It was considered to be a kind of living fossil because it had a nucleus but didn't seem to have acquired mitochondria. But additional studies on Giardia and other microbes showed that actually, the mitochondria were there.

"It turned out that all of them actually had some kind of remnant mitochondrion," says Karnkowska, who notes that mitochondria perform key jobs in the cell beyond just generating power.

A biggie is assembling iron-sulfur clusters for certain proteins, which is thought to be a mitochondrial function that's really essential. So even if a microbe powers itself in a different way and has a limited form of the organelle that isn't the same as the mitochondria found in people, Karnkowska says, "it's still a mitochondrion and it has some important function for the cell."

That kind of vestigial mitochondrion is what she expected to find when she was a researcher at Charles University in Prague and started investigating a particular gut microbe that had been isolated from a researcher's pet chinchilla.

After she and her colleagues sequenced the gut microbe's genome, however, they found no trace that it made any mitochondrial proteins at all. "So that's a great surprise for us," she says. "That should theoretically kill the cell — it shouldn't exist."

What they learned is that instead of relying on mitochondria to assemble iron-sulfur clusters, these cells use a different kind of machinery. And it looks like they acquired it from bacteria.

The researchers say this is the first example of any eukaryote that completely lacks mitochondria.

Michael Gray, a biochemist at Dalhousie University in Halifax, Nova Scotia, says the researchers have made a "compelling" case that they have a bona fide eukaryote without any vestige of a mitochondrion; he calls the finding "unprecedented."

"The observation is significant, in that it clearly demonstrates that a eukaryote can still be a eukaryote without having a mitochondrion," he tells Shots via email.

However, the results do not negate the idea that the acquisition of a mitochondrion was an important and perhaps defining event in the evolution of eukaryotic cells, he adds.

That's because it seems clear that this organism's ancestors had mitochondria that were then lost after the cells acquired their non-mitochondrial system for making iron-sulfur clusters.

"This is not the missing link of eukaryotic evolution," agrees Mark Van Der Giezen, a researcher in evolutionary biochemistry at the University of Exeter in the United Kingdom.

Still, he says, it is an example of how flexible life is.

"It lives in an area without oxygen and therefore can get rid of a lot of biochemistry that you and I would need in our cells to survive," says Van Der Giezen. "This organism managed to adapt in such a way that it could lose an organelle, which every textbook will tell you is an essential feature of eukaryotes. That's pretty amazing. It shows you that life is extremely creative in finding a way to eke out an existence." npr

Meet The Tiny Critters Thriving In Your Carpet, Kitchen And Bed

With the weather warming, it's the season for spring cleaning. But before you reach for the broom and mop, consider who else is sharing your home. The variety of uninvited guests in your dustpan may surprise you.
A recent study published in the journal PeerJ took up the challenge of cataloging the large numbers of tiny animals — arthropods — that live in modern human dwellings. In 50 houses in and around Raleigh, N. C., the research team found about a hundred different species of arthropods in each home. The tally included familiar types — like flies, spiders and ants — but also some species that are less well known, such as gall wasps and book lice.

Grains of uncooked rice dwarf this book louse. Though book lice thrive in most human homes, they largely go unnoticed.

npr

This Plastic-Eating Bacterium Might Help Deal With Waste One Day

Plastic makes great food packaging. It's waterproof and flexible. And best of all, it's impervious to all known bacteria – until now. Researchers have found a bacterium in the debris fields around a recycling plant in Japan that can feed off a common type of plastic used in clothing, plastic bottles and food packaging.

The bacterium is a new species called Ideonella sakaiensis, named for the Japanese city Sakai where it was found growing on plastic debris made from a type of plastic called PET or polyethylene terephthalate. "It's the most unique thing. This bacterium can degrade PET and then make their body from PET," says Shosuke Yoshida, a microbiologist at Kyoto University and lead author on the study published in Science on Thursday.

Most plastics are insurmountable obstacles for microbes because plastics are large chains of repeating molecules called polymers. The entire chain is far larger than the individual microbe. "So the organism can't take it inside the cell to metabolize it," says John Coates, a microbiologist at the University of California, Berkeley who was not involved with the work. Imagine a baby trying to eat an enormous pizza from the middle. It can't do it. The pie is too big.

But Ideonella sakaiensis, which we here at NPR have decided to call "the polymer chomper," has two enzymes that can slice and dice the plastic polymer into smaller pieces. In other words, the baby gets a pizza cutter. The bacterium can then take the pieces and eat them, eventually converting the plastic into carbon dioxide and water.

After Yoshida and his colleagues isolated the polymer chomper, they were able to watch it disintegrate a plastic film in about six weeks. It would be great if we could culture the bacteria, spray landfills down with them and let them deal with our mountains of plastic refuse. But alas, that may never happen. "It grows very fast," Yoshida explains, "but it's likely not so useful in the field" because it chomps very slowly.

And if getting rid of our plastic waste were so easy, Coates notes, the bacterium would likely have already been found in landfills and anywhere you find mounds of plastic waste.

But with more research, Coates thinks that the bacterium might be engineered for such a purpose. "It's certainly a move in the right direction. Having an organism that seems to be capable of biodegrading these components directly will help us develop a bioremediation technology," he says. Certain species of fungi have been found to be able to degrade plastics before – though none have been converted to landfill-munching purposes. The polymer chomper offers new hope, Coates says, because bacteria are easier to work with and engineer. npr

echinoid spine terminology

thefossilforum.com

Our Parasites And Vermin Reveal Secrets Of Human History

They look like tiny tubes with stumpy legs. They can nestle snugly into pores, right at the base of small hairs. And there are probably hundreds on your face.

The harmless mite Demodex folliculorum, seen here in an electron microscope image, lives in the follicles of eyelashes.

We're taking about Demodex folliculorum, the mite that calls your hair follicles home. "Probably if you've ever gotten a gross gunky plug out of a nose pore, that's what it looks like," says Michelle Trautwein, an evolutionary biologist at the California Academy of Sciences. "When you get to know them, they're actually pretty adorable."

Trautwein and her colleagues have peeled the mites off microscope slides that they super-glued to their faces. They've scraped the little guys off people's foreheads with the curved end of a bobby pin. They've even ferreted out the insects' DNA from tiny spatulas of face grease." They've probably been with us since the origin of our species," she says.

And Trautwein thinks the mites could help answer questions about human migrations through history, perhaps more than genetics or archaeology could alone because of how they're shared among humans.

The mites are the latest in a not-so-regal lineage of parasites and vermin that could help pin down how human ancestors behaved and moved across the continents. When archaeological evidence is scant or human genetic data is too messy, sometimes these millennia-old frenemies — from rats to tapeworms — are the next best option.

"You don't share them with strangers when you give them a hug hello," she says of the mites. They're mostly shared between sexual partners and members of the same nuclear family. Because of that tight bond, the mites can be a pretty good measure of where people came from.

In an exploratory study published this month in Proceedings of the National Academy of Sciences, the researchers collected mites from the faces of about 70 people with different origins, most of them living in the U.S., and sequenced the mites' mitochondrial DNA. They found that people from different continents harbor different varieties of mites on their faces. Even generations after a family leaves one geographic region for another, Trautwein and her colleagues found, their descendants can retain those original mite populations. Think of them as family heirlooms.

"Basically, as all humans evolved in Africa our mites evolved with us," says Trautwein. "And as populations became isolated they evolved into their own lineages, just like humans did."

"They are potentially gross and they do infect us and take things from us, but to understand ourselves, it's a really great potential tool to use," says George Perry, an anthropologist and biologist at Pennsylvania State University who was not involved with the study. "It's an amazing, largely untapped area to learn about our own history."

Perry's group is researching how tapeworms, which live in the intestines of mammals, could help show when hominins — human ancestors and their relatives — started consistently eating meat. The archaeological evidence is pretty meager — just a few scratched up animal bones from a couple of million years ago. It's assumed that human ancestors first got tapeworms when they domesticated pigs and cows sometime in the last 12,000 years and started routinely eating undercooked meat, which is how the worms would transfer over.

But, he says, the three species of tapeworm that currently inhabit humans are actually most similar to those of lions and hyenas. Perry says the similarity suggests that hominins picked them up long before the domestication of herbivores, when they were consistently chowing down on the same animals as lions and hyenas. He's now studying tapeworm adaptations to heat stress to see if it yields hints about when humans started cooking meat.

Rodents also have been useful tools in piecing together human travel routes. Rats helped corroborate the hypothesis that indigenous Taiwanese people first colonized Polynesia about 3,000 years ago. There isn't much evidence left of the first generations of people to colonize New Zealand, but there is archaeological evidence of a rat population that arrived on the island and was well established by about 700 years ago. That suggests that humans brought them there on their boats.

Lice might take the cake when it comes to vermin that have revealed the most snippets of human history. Scientists have used louse DNA to determine when human ancestors lost their fur and started wearing clothes. Human ancestors picked up pubic lice from gorilla ancestors some 4 million years ago, meaning that by that point the islands of head hair and pubic hair were far enough apart to provide two different environments for their parasite guests. This change suggests to anthropologists that our modern way of regulating body temperature may have come about early in our evolutionary history. (It also suggests some unexpected cavorting between gorilla and human ancestors.)

DNA analysis showed that body lice diverged genetically from head lice somewhere between 30,000 and 114,000 years ago, giving archaeologists a minimum date for when people first started wearing clothes. Before clothes, there wouldn't have been an environment separate enough for a group of lice to inhabit and evolve separately from the ones on people's heads.

"We're really just a habitat for all sorts of natural life," says Trautwein. "People think that evolution and wildlife are these remote things, but it's happening all over us."

If it weren't, pieces of deep human history might still be hidden. npr

teeny tiny fish vertebrae

estimating 0.25 - 1mm across

toxoplasma gondii

Toxoplasma gondii, a parasitic protozoan, afflicts cats and other mammals. Acute toxoplasmosis produces flu-like symptoms and has been linked to behavioral changes in humans. npr

Algae bloom toxins may make Florida’s manatees and sea turtles susceptible to deadly accidents

Fond of a range of marine and freshwater vegetation such as turtle grass and eelgrass, the Florida manatee spends most of its waking hours grazing in shallow water. Its gentle motions and 3 to 5 mile-per-hour swimming speeds belie the fact that many of these endangered mammals survive under the stress of repeated, low-dose poisoning. The source: red tides and massive algae blooms that produce an array of deadly toxins. Blooms often blanket the submerged plants they eat causing the manatees to swallow the toxins along with their food or inhale it as they breathe.

New research by scientists from the Smithsonian Marine Station in Fort Pierce, Fla.; James Cook University in Townsville, Australia and the Florida Fish and Wildlife Conservation Commission, has shown that manatees and green sea turtles (both herbivores) from Florida live with low-levels of a number of algae-produced toxins in their bodies and digestive systems. Sampling muscle and liver tissues and stomach and intestine contents from 14 dead manatees and 13 dead green sea turtles washed ashore in Florida between December 2003 and February 2006, the researchers found most of the specimens had been exposed to sub-lethal levels of the harmful algal bloom toxins: brevetoxin, okadaic acid and saxitoxin.

Together, the cumulative impact of these toxins could potentially impair the health and fitness of the animals, the researchers write, making them susceptible to accidental death by reducing their ability to evade boats and fishing lines, or withstand periods of cold weather. Many of the turtles in the study had been severely damaged in accidents, such as fishing-line entangled flippers, cut and cracked shells and boat-propeller wounds.

Florida is a hotspot for harmful algae blooms with more than 70 potentially harmful algal species identified in its waters. “There are many catalysts for these blooms, such as changes in temperature, salinity, turbidity and nutrient run-off,” explains Angela Capper, principle author of the study from the Smithsonian Marine Station and James Cook University. “Some blooms are successive, i.e. when one bloom dies off it provides the nutrients for a subsequent bloom of another harmful species.” The manatees in the study were collected on the Gulf Coast of Florida where red tides are prevalent and the turtles were collected from Florida’s Atlantic Coast.

“Animals are not only exposed to lethal doses of toxins during bloom periods but, also, due to toxin circulating through food webs, for weeks or months after a bloom has dissipated, prolonging the risk to marine animals,” the researchers write. Multiple species of algae also may bloom at the same time, exposing the animals to different toxins simultaneously.–John Barrat smithsonian

“Dietary exposure to harmful algae bloom (HAB) toxins in the endangered manatee (Trichechus manatus latirostris) and green sea turtle (Chelonia mydas) in Florida, USA”was published in the Journal “Harmful Algae” in July 2013.

Oysters May Serve as Link in Transmission of Norovirus

Oysters appear to be an important link in the transmission of norovirus among humans, according to new research from China.

Norovirus — better known as “cruise-ship flu,” “stomach flu” or “winter vomiting flu” — is one of the world’s most common causes of gastrointestinal distress. Although most patients recover after a few days of misery, and sometimes ruined vacations, the virus can be lethal to infants, older adults and people with weak immune systems.

It is highly infectious — especially in confined environments like ships — but exactly how it is transmitted has been a mystery. The unwashed hands of food workers have been blamed. But recently, scientists at North Carolina State built a “vomiting machine” that showed tiny infectious droplets of vomit can fly through the air to infect other people, just as droplets from a sneeze do.

In the current study, published last month in Applied and Environmental Microbiology, researchers analyzed the genetic sequences of 1,077 samples of noroviruses found in oysters. Some sequences had been stockpiled in genetic databases since 1983.

The scientists found that 80 percent of the known human noroviruses matched those found in oysters. The majority of the matches were in oysters from coastal waters, more likely to be contaminated with human sewage.

Noroviruses mutate very quickly, as do influenza viruses, and big outbreaks usually begin after a new strain emerges. There was a “convergence” between new strains circulating in oysters and those circulating in humans, the researchers also found.

Yongjie Wang, a food science specialist at Shanghai Ocean University and lead author of the study, concluded that oysters were an important reservoir for human noroviruses — a place where they can hide between outbreaks and mutate. They also can be transmitted back to humans, presumably when oysters are eaten raw.

A way to detect noroviruses in oyster flesh and in the beds where they grow needs to be developed, Dr. Wang said. nytimes

Gasping for air: nutrients, warming trigger ocean oxygen deficit

“When you can’t breathe, nothing else matters,” once a tagline of the American Lung Association, today it might easily describe what is happening in many areas of the ocean. Hypoxia, the lack of oxygen in our estuaries, coastal and deep ocean waters, is on the rise and endangering marine life around the world. Its causes are a complex mix of excess nutrients and our warming world. Agriculture, human waste, and rising levels of atmospheric CO2 underlie these changes.

Denise Breitburg, senior scientist at the Smithsonian Environmental Research Center in Edgewater, Md. near the Chesapeake Bay, answers a few questions about marine hypoxia.

Breitburg and Lisa Levin of the Scripps Institute of Oceanography were co-authors of a recent article on ocean deoxygenation in the journal Nature Climate Change.

Q: Where does hypoxia occur in the ocean?

Breitburg: It occurs in estuaries, along our coasts and in the deep ocean.

In estuaries, the areas where fresh and salt water meet, and in some coastal waters, hypoxia is caused by overstimulation of algal growth by nutrients from human activities, primarily agriculture and human waste. Some nutrients are OK but large amounts result in too much algae. Algae that aren’t consumed by animals die and decompose in great quantities. Decomposition depletes the oxygen in the water causing low-oxygen zones. Basically, many microbes use oxygen and release carbon dioxide when they respire, just like people do when they breathe.

A truck applies nutrient rich liquid manure to a farm field, some of which will end up in streams, estuaries and the ocean. (Photo courtesy Chesapeake Bay Program)

In the deep ocean, deoxygenation is mainly a natural phenomenon. Oxygen is mixed into the water at the surface but once you reach a certain depth you no longer get much benefit from that mixing. In addition, organic matter produced near the ocean surface can wind up sinking to bottom waters. Microbial decomposition of this organic matter depletes the deep oxygen and creates large deoxygenated zones.

Coastal and open-ocean hypoxia have long been regarded by scientists as distinct, but our world is highly interconnected. For example, there is some evidence that nutrient enrichment from human activities, a known cause of coastal hypoxia, could also increase deeper water low oxygen zones. Some systems, such as the Gulf of St. Lawrence, experience hypoxia that appears to be caused both by nutrients coming from land and the inflow of deep oceanic water that is naturally low in oxygen.

Oxygen is mixed into the ocean at the surface, but beyond a certain depth there is no benefit from this surface mixing. (Flickr photo by David Robertson)

Q: Do deep water hypoxic zones stay down deep?

Breitburg: No. Deep areas of low oxygen water become a problem when they upwell near shore, bringing their very low oxygen waters right up to the shallows. The upwelling also brings nutrients to the surface, which is one reason we have incredibly productive fisheries along the west coasts of many continents including North America, South America and Africa.

Upwelling of deep ocean water is caused when a combination of persistent longshore winds and the earth’s rotation push coastal surface water out to sea. In response, deep water moves up to bathe the continental shelves in hypoxic water that is also more acidic than open ocean surface water. Warming atmospheric temperatures very definitely affect wind patterns that cause this upwelling.

Continental margins, shelves and estuaries around the world that were previously well oxygenated, now experience hypoxia either seasonally or episodically. For example, upwelling is creating seasonal dead zones on the inner Oregon Shelf.

A phytoplankton bloom is visible off the coast of Argentina, just south of the Rio de la Plata estuary (visible in the top of the image). (Photo Credit: Jeff Schmaltz, MODIS Land Rapid Response Team at NASA GSFC | NASA Earth Observatory)

Q: What happens to marine animals during these events?

Breitburg. Animals like bivalves, worms or corals that can’t easily swim away from areas of low oxygen are especially vulnerable, but even fish that are strong swimmers can be trapped and killed. Low oxygen levels in oceanic and estuarine waters can alter food webs, growth rates, and make organisms more susceptible to disease. If a low-oxygen event is severe or long-lasting, it can have a devastating impact on a region. This can translate into a loss of the ocean resources humans depend on.

Q: Would removing nutrients from estuaries help?

Breitburg: It’s not a matter of trying to get nutrients out of the estuaries or the ocean. It’s a matter of trying to reduce what we are putting in. If we turn the spigot off, these systems will, over time, clean themselves up. In some cases it would be very quick, maybe a few years, not necessarily hundreds or thousands.

There are a lot of efforts worldwide to reduce nutrients going into estuaries and other coastal waters. Some of them have been very successful. Some are making slow incremental progress. Overloading a system with nutrients is a problem that is much better to prevent than to try to correct.

Algae blooms are often referred to as red tides because of their red color in the water. Red tides, like this one in La Jolla, Calif., can form as a result of nutrient pollution. (Flickr photo by Alejandro Díaz)

smithsonianscience.si.edu

The Microbes on the Handprint of an 8-Year-Old After Playing Outside

We all know our bodies are home to countless millions of bacteria and microorganisms, but without seeing them with our bare eyes it’s almost impossible to comprehend. This petri dish handprint created by Tasha Sturm of Cabrillo College, vividly illustrates the variety of bacteria found on her 8-year-old son’s hand after playing outdoors. The print itself represents several days of growth as different yeasts, fungi, and bacteria are allowed to incubate.

It’s safe to say almost everything you see growing in this specimen is harmless and in many cases even beneficial to a person’s immunity, but it just goes to show why we sometimes it’s good to wash our hands. Sturm discusses in detail how she made the print in the comments of this page. (via Ziya Tong)

Can You Protect Your Tummy From Traveler's Diarrhea?

It goes by many names: Delhi belly. Montezuma's revenge. The Aztec two-step.But doctors use one not-so-glamorous term: traveler's diarrhea.

If you're visiting a place this summer with less than ideal sewage disposal — maybe a resort in Mexico or a village in Rajasthan — chances are your GI tract will give you trouble at least once ... maybe twice ... maybe continuously.

There are just about as many misconceptions and myths about traveler's diarrhea as there are names for it. So we're here to try and set the record straight — or a least discuss what's known and not known.

We dove into the literature and talked to two pioneers in the field to figure out what causes Montezuma to take revenge, what precautions might work and what to do when your tummy starts to rumble.

1. I'm sick because the food has "different" bacteria in it that my GI tract isn't accustomed to. FALSE.

Hop on a red-eye flight from New York to New Delhi, and in 24 hours you'll literally have "Delhi belly." About half the bacteria species in your gut will switch from those typically found in New Yorkers to those found in New Delhi residents, says Dr. Bradley Connor, who directs The New York Center for Travel And Tropical Medicine.

"But that's not what makes you sick," Connor says. Those bacteria are the "good guys." They're the bacteria that help you digest food and tune your immune system.

Problems arise when you accidentally pick up a "bad guy" — a pathogenic bacteria, Connor says. These bacteria would make you sick anywhere in the world, even here in the U.S. They're just more common in developing countries because they're found in raw sewage.

2. If I keep eating the local cuisine for a month or so, I'll build up immunity to the bacteria. FALSE.

Shlim has spent 30 years studying travelers' illnesses in Nepal. He found that long-term trekkers and expats will eventually build up immunity to diarrhea-causing bacteria. But it takes years, not weeks or months.

3. Washing my hands will keep me from getting sick. FALSE.

Sure, a quick wash with antibacterial soap will knock out bad E. coli. But that's unlikely to cut your risk of getting sick, Shlim says.

"You can never really be against hand-washing," he says. "But the fact is that it usually takes a high quantity of bacteria, sometimes in the millions, to overcome your stomach acid. So just the random bacteria you get on your hands, I think is unlikely to make you sick."

4. If I avoid certain types of foods, I won't get sick. MAYBE.

The major source of all traveler's diarrhea is contaminated food and water at restaurants, Shlim says. Avoiding the bad water is easy — just buy bottled water, boil it or treat ityourself. But the food part is trickier.

Many travelers swear by the old saying "boil it, cook it, peel it or forget it."

But scientific studies don't really back it up. One meta-analyses of seven studies didn't find a connection between getting bacterial diarrhea and eating raw vegetables or unpeeled fruits. But it did find a link between illness and foods that sat around at room temperature for a while.

5. If I get sick, I should take an antibiotic. MAYBE.

Ten years ago, standard advice from travel clinics was clear-cut: Take a pack of Cipro on your trip and pop a pill at the first rumbles in your belly. Back in 2006, I was given that exact advice from a clinic in Berkeley.

Now the advice is a bit more nuanced. Travel doctors don't recommend taking antibiotics for mild or moderate cases of diarrhea — and definitely not as a preventive measure.

"Your body will naturally fight off bacterial diarrhea in three to seven days," Shlim says.

But if you're running to the bathroom several times a day — or have bloody stools — then Shlim recommends a quick dose of antibiotics. "You'll feel much better in six to 24 hours." npr for the full responses....