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See the Ugly Beauty That Lives in a Toxic Cave

Norman Pace collects samples of a microbial mat.
Microbiologist Norman Pace collects a sample of a brainy-looking mat made of microbes (called a vermiculation) that coats the ceiling of Sulphur Cave.
Photograph by Norman R. Thompson

Lurking below the quaint ski town of Steamboat Springs, Colorado, lies a cave belching deadly gases. Its ceiling is dotted with snottites, dangling blobs that look like thick mucus and drip sulfuric acid strong enough to burn holes through T-shirts. And the whole place is covered in slime.

So why would anyone want to go there?

“Being in the cave reminded me of being inside a huge organism—as if I had been swallowed by some gigantic, alien monster from deep in the ocean or from outer space,” says photographer Norman Thompson.

Thompson joined a small group of scientists who are among the few people to ever explore Sulphur Cave, and who found it eerily beautiful, and brimming with strange life. As shown in National Geographic’s exclusive video below, along with spiders and insects, the cave holds sulfur-breathing microbes and a new species of blood-red worm.

EXCLUSIVE VIDEO: Clumps of newly discovered blood-red worms thrive in Sulfur Cave, which contains levels of toxic gases so lethal that any human who enters unprotected could quickly die.

“In a sense, we really were inside of an organism,” Thompson says, “or perhaps more accurately, an ecosystem. Because the cave is a colony of organisms, living together in a lightless ecosystem, powered not by sunlight, but by the sulfur coming from deep within the Earth.”

Inside the Belly

To enter the 180-foot-long (54 meters) cave, the intrepid scientists had to squeeze into a pit entrance, a hole in the ground that skiers might glide right past. And if you happen to visit without special equipment, you ought to glide past. Otherwise, the cave’s gases could knock you unconscious in a jiffy.

“It’s sort of foreboding,” says David Steinmann, a cave biologist at the Denver Museum of Nature and Science. “You have to climb and crawl down a wet muddy slop that’s stinky and smells like rotten eggs.”

A snottite found in a sulphur cave.
Snottites are thick, mucus-like blobs formed by bacteria growing in a sulfur cave.
Photograph by Norman R. Thompson

“It’s belching toxic gases,” Steinmann says, “and in the winter you can see steam coming out. You have to stoop down and squeeze through to get into the first room. Once you’re in there, it’s totally dark.”

But when the team brought in lights, they found that the cave is also lovely, in its own way. Crystals made of gypsum glitter on walls, and a small stream washes across the floor. Long tendrils made of more microbial colonies wave in the water’s flow.

Thompson photographed the cave twice, entering only after scientists had aired out the crevice using large fans—appropriately, the kind normally used to flush out underground sewers. “Even with the poisonous air flushed out by the fan, the cave still stunk of sulfur,” he says.

Such sulfur-filled caves are rare, with some found in Mexico and Italy. The high levels of sulfur that create the gas in Colorado’s Sulphur Cave come from deep within the earth. The cave is formed in travertine, a type of stone formed by deposits from streams and mineral springs.

Hydrogen sulfide gas, which gives the cave its rotten-egg smell, can be deadly at high concentrations. Yet life thrives inside the cave despite both the hydrogen sulfide and carbon dioxide up to four times levels that could kill a human.

Wormy Wonders

The biggest surprise was the blood-red worms found in the cave. “There’s a hell of a lot of worms in there!” says Norm Pace, emeritus professor of microbiology at the University of Colorado Boulder.

Worms in Sulphur Cave, Steamboat Springs, Colorado. These worms are believed to live on the chemical energy in the sulfur in the cave, similar to the way tube worms live in a world without light at the bottom of the ocean. Also visible on the left side of the image are streamers—colonies of microorganism, similar to those seen in hot springs in Yellowstone National Park. Photograph by Norman R. Thompson
These worms in Colorado’s Sulphur Cave are believed to live on the chemical energy in the sulfur in the cave, similar to deep-ocean tube worms. On the left are streamers—colonies of microorganisms similar to those in hot springs in Yellowstone National Park.
Photograph by Norman R. Thompson

The small worms live clumped together on the cave floor, where they’re probably making a living by grazing on the bacteria growing in wet spots, Pace says.

They’re also intensely red, much like the famous Riftia worms found at deep-sea vents, which are also rich in hydrogen sulfide. Pace has studied life in the vents and expected the cave ecosystem to be similar. It wasn’t, exactly. The ocean worms have special structures called trophosomes filled with bacteria that are able to live on hydrogen sulfide; essentially they “breathe” it. The worms rely on the bacteria to do this, so Pace was surprised that so far, the team hasn’t found a special home for bacteria inside the Sulphur Cave worms.

As for the cave worms’ bright red color, it probably comes from high levels of hemoglobin and related compounds that protect the worm from hydrogen sulfide. Steinmann and his colleagues described the worms this year in the journal Zootaxa.

They named it Limnodrilus sulphurensis, in honor of the sulfur that powers the base of the food chain in this otherwise deadly environment.

“It took over a year for the sulfur smell to gradually air out from my cave coveralls,” Thompson says. But would he go back? He’s still drawn by its strange beauty he says, so yes— “in a heartbeat.”

 

Correction: The cave is 180 feet long, not deep. This has been updated, and I  deleted a sentence about organic matter in the cave’s travertine—the cave’s sulfur comes mainly from geothermal activity, with microbial breakdown of organic matter as an additional, but minor, source. A clarifying sentence has been added. —EE (updated 6/15)

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This Plant Bleeds Sweet Nectar To Recruit Ant Bodyguards

A bittersweet nightshade plant, Solanum dulcamara.
A bittersweet nightshade plant, Solanum dulcamara.
Photograph by Joel Sartore

Six years ago, Anke Steppuhn noticed that the bittersweet nightshade, when attacked by slugs and insects in a greenhouse, would bleed. Small droplets would exude from the wounds of its part-eaten leaves. At the same time, Steppuhn and her colleagues saw that the wild plants were often covered in ants.

These facts are connected. Steppuhn’s team from the Free University of Berlin, including student Tobias Lortzing, have since discovered that the droplets are a kind of sugary nectar, which the beleagured nightshade uses to summon ants. The ants, in return for their sweet meals, attack the pests that are destroying the plant. And this discovery provides important clues about the evolution of more intimate partnerships between ants and plants.

Acacia trees, for example, are masters at recruiting ant bodyguards. The insects protect the trees from plant-eaters and even prune back invading vines. In return the trees provide them with shelter in the form of swollen thorns, snack stations that look like orange berries, and drinks in the form of nectar. The latter come from small green lumps called extrafloral nectaries, which the ants sip from.

Some 4,000 species of plants have extrafloral nectaries, which vary considerably in their shape. Some are obvious structures, like those of the acacia. Others are mere pits or hollows. But whatever their form, their benefits are invaluable. They are not only ant rewards, but also ant concentrators.

“Ants often appear to be whimsically inefficient plant defence agents,” says Elizabeth Pringle from the Max Planck Institute for Chemical Ecology. “They wander to and fro, haphazardly nipping at anything that happens to be in their way, which gives plenty of time for something with a hard exoskeleton and wings, like an adult flea beetle, to escape and happily land somewhere else to feed. But concentrate lots of ants around a sugar source, and pretty soon nothing soft and slow stands a chance. This is the value of extrafloral nectaries.”

The bittersweet nightshade’s oozing droplets have almost all the characteristics of extrafloral nectaries. It’s a sweet liquid, obviously. But Lortzing showed that it’s not just fluid that passively leaks from a damaged leaf. When he cut the nightshade with a clean scalpel, the nectar droplets didn’t appear. They did emerge, however, if Lortzing first coated his scalpel in jasmonic acid—a hormone that plants release upon insect attack.

Sweet nectar oozes from a wounded bittersweet nightshade.
Sweet nectar oozes from a wounded bittersweet nightshade.
Photograph by Tobias Lortzing

He also showed that the nectar is chemically distinct from the plant’s actual sap—full of sweet sucrose, and deficient in almost everything else. Clearly, it is actively produced and secreted by the plant.

Why?

To find out, the team added droplets of either sucrose or water to wild undamaged nightshades. After a month, they saw that the sucrose-treated plants were patrolled by more ants, and had suffered half as much damage to their leaves. To their surprise, the ants even seemed to protect the nightshades against slugs. That’s new. Ants have been known to defend plants against other insects and mammals, but never before slugs or snails.

More bizarrely, the ants didn’t seem to attack adult flea beetles—the nightshade’s greatest enemies. They seemed like poor defenders, until Steppuhn’s team realised that the ants were focused not on the beetle adults, but on their larvae. The larvae hatch from eggs in the soil, climb up the nightshade’s shoots, and bury themselves in its stem.

Ants will pick up the larvae and carry them into their nests, never to be seen again. The ants might ignore the adults, but they stop the next beetle generation from causing even greater harm.

So, the nectar droplets, being actively produced, chemically distinct, and efficient at summoning guardian ants, are very much like the extrafloral nectaries of other plants. The only difference is that they’re not associated with any specific structure—no obvious lump or pit. It’s the “most primitive extrafloral nectary that has been discovered so far and shows how little is needed to make a functioning nectary,” says Martin Heil from CINESTAV in Mexico.

Although such structures are common throughout the plant world, every group with nectary-bearing species also has nectary-less members. “This means that extrafloral nectaries appear and disappear quickly, in evolutionary terms,” says Heil. And Steppuhn’s discovery “helps us understand why and how these nectaries can evolve out of nowhere.”

Perhaps, at first, fluids that passively leak from wounds are visited by ants. Gradually, plants evolve to recruit the ants more effectively by controlling those leaks and tweaking the liquids that emerge, as the nightshade has done. Eventually, they develop specialised structures.

But nectaries are lost so frequently among plant families that they clearly incur some cost, says Pringle. It takes a lot of up-front investment to build the dedicated structures and to keep them constantly brimming with nectar. By contrast, the nightshade’s droplets show that plants can summon ants in a more ad hoc and less effortful way.

Whether plants go for that cheaper option, or head towards full-blown nectaries, probably depends on how badly they’re threatened by plant-eaters, how effective ants are, and how much energy it takes to summon and reward them. Nothing in nature comes for free, and evolution is the ultimate arbiter of costs and benefits.

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Birds on Islands Are Losing the Ability to Fly

Before the arrival of humans—and the rats, cats, and other predators that we brought—New Zealand was an idyllic haven for birds. Without ground-dwelling mammalian hunters to bother them, many of the local species lost the ability to fly. There’s the kakapo, a giant, booming parrot with an owl-like countenance; the takahe, weka, and other flightless relatives of coots and moorhens; a couple of flightless ducks; and, of course, the iconic kiwi.

Kakapo (Strigops habroptilus) at night, Codfish Island, New Zealand. Photograph by Stephen Belcher, Minden Pictures, Corbis
Kakapo (Strigops habroptilus) at night, Codfish Island, New Zealand. Photograph by Stephen Belcher, Minden Pictures, Corbis

These birds are part of a pattern that plays out across the world’s islands. Wherever predators are kept away by expanses of water, birds become flightless—quickly and repeatedly. This process has happened on more than a thousand independent occasions, producing the awkward dodo of Mauritius, the club-winged ibis of Jamaica, and the tatty-winged flightless cormorant of the Galapagos.

The call of the ground is a strong one, and it exists even when the skies are still an option. Natalie Wright from the University of Montana demonstrated this by collecting data on 868 species. She showed that even when island birds can still fly, they’re edging towards flightlessness. Compared to mainland relatives, their flight muscles (the ones we eat when we tuck into chicken breasts) are smaller and their legs are longer.

“Pretty much all island birds are experiencing these pressures to reduce flight, even if some can’t go to the extreme,” Wright says.

Her results show that flying isn’t a binary thing, with a clear boundary between taking to the air and staying on the ground. Instead, there’s a full spectrum of abilities between aeronautical swifts and shuffling kiwis, and island birds exist on all parts of that continuum. “None of the species I looked at were flightless or close to being truly flightless,” says Wright. “There’s no point where, all of a sudden, they have much smaller flight muscles.”

Her study began about 20 years ago, when her undergraduate advisor David Steadman started weighing the flight muscles of birds at the Florida Museum of Natural History. When Wright got her hands on the data set, she noticed that fruit doves had smaller flight muscles on islands that were further from the mainland. She then travelled to five natural history museums herself to examine more skeletons. For each one, she measured the long bones in the lower legs and the size of the breastbone—the latter revealed how heavy the bird’s flight muscles would have been in life.

Across nine major groups of birds, with a wide range of lifestyles, body shapes, and diets, Wright found the same trend. On smaller islands with fewer species, no mammalian predators, and fewer birds of prey, birds have repeatedly reallocated energy from forelimbs to hindlimbs, away from big flight muscles and towards longer legs.

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To her surprise, the trend even applied to hummingbirds, for whom flying is an inextricable part of life. Hummingbirds hover in front of flowers to drink nectar. A flightless hummingbird is a dead hummingbird. And yet, even though “islands hummingbirds look like hummingbirds when they fly, they were still reducing their flight muscles and evolving longer legs on islands without predators,” says Wright.

The same was true for kingfishers, flycatchers, tanagers, honeyeaters, and other groups that are extremely dependent on flight. Wright studied the Todiramphus kingfishers across 27 Pacific islands. “Members on islands with fewer than 20 species of birds, which don’t have any predators that can kill an adult kingfisher, have much smaller flight muscles and much longer legs than any members on larger and more populated islands,” she says. “They sit on perches and fly out to grab prey. Their foraging style requires flight, but they’re edging towards flightlessness.”

Why? It’s easy to see why a diving bird like a cormorant or a ground-dwelling one like a kakapo might lose its ability to fly when predators are absent. But why should a hummingbird or kingfisher, which flies all the time, sacrifice some of its aerial prowess?

Because flight muscles come with a cost. Even at rest, larger ones require more energy to maintain. So if birds can get away with smaller ones, evolution pushes them in that direction. Large flight muscles are especially useful when birds take off. That’s the most energetically demanding part of flying, and the bit that’s most important for escaping from ground predators. If such predators are absent, birds can take off at a more leisurely pace, and they can afford to have smaller (and cheaper) flight muscles. (This might also explain why they developed longer legs: they take off more by jumping than by flapping.)

Wright’s results suggest that island birds might be more vulnerable to introduced predators than anyone appreciated. Even those that can fly aren’t as good at it as their mainland counterparts. They may also help to explain why island birds diversify into such wondrous forms. When they settle in a remote landmass, even the flying ones might quickly lose the power they need to cross oceans and find new homes.

Islands, it seems, create birds that stay on islands.

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Gut Microbes Can Evolve From Foe to Friend—And Do It Fast

 

Bacteria grow quickly, and can evolve quickly.
Bacteria grow quickly, and can evolve quickly.
Photograph By HansN/Flickr

Dangerous microbes can evolve rapidly. When we throw antibiotics at them, new strains can quickly shrug off the drugs and cause untreatable cases of tuberculosis, gonorrhoea, or staph. But most microbes don’t cause disease. Many share our bodies and those of other animals, and these residents—our so-called microbiome—are important parts of our lives.

And they can evolve too.

A microbe can even evolve quickly from a parasite into an allyKayla King from the University of Oxford found an excellent example of this in the guts of nematode worms. She showed that a bacterium called Enterococcus faecalis, which causes mild disease, can suddenly turn into a protector if its host is challenged by another more dangerous threat, Staphylococcus aureus or Staph.

King began by infecting worms with either Enterococcus or Staph. The two microbes behaved very differently. Enterococcus caused mild infections, killing fewer than one in a hundred worms, and only then after a week. By contrast, Staph killed half the worms within a day and all of the after a second. When mixed, Enterococcus protected the worms from its more virulent peer, slashing the death rate from 52 percent to just 18 percent.

To see if this dynamic would change over time, King picked out some infected worms, removed Enterococcus from their bodies, grew the microbes up, and then fed them to another generation of worms. She repeated 15 times. And in each new round she added the Enterococcus to genetically identical worms from the same stock, along with the same strains of Staph.

By the experiment’s end, Enterococcus had become an exceptional guardian, saving all but one percent of its hosts. It had evolved the ability to produce large amounts of superoxides—highly reactive oxygen molecules that are toxic to many microbes, Staph included. Enterococcus, by poisoning its rivals, was saving the worms.

This change depended entirely on the presence of Staph. When King exposed 15 generations of worms to Enterococcus alone, the mildly harmful bacterium became slightly more harmful. “On its own, it’s a little bit of a parasite,” says King. “But when it interacts with this much more virulent organism, it shifts along the continuum to be much more beneficial.”

She was surprised at how quickly the protective powers evolved (within just five of the 15 generations), how total they were (almost all the worms survived), and how broad it was. She challenged the worms with seven different strains of Staph, including the drug-resistant MRSA strains that give us humans so much grief. The protective Enterococcus strains beat them all.

There are many examples of microbes protecting animal hosts from parasites and diseases by producing antibiotics. They can also protect us simply by taking up space or using up resources, leaving no opportunities for more dangerous microbes to invade, and no room for them to grow. “We often consider ways in which the microbiome directly impacts host responses to infections,” says Nichole Broderick from the University of Connecticut. “This  paper [shows] how the community can evolve traits that indirectly benefit the host.”

Note: indirectly. Enterococcus wasn’t evolving to protect the worms. It was suppressing a competing microbe, and benefiting its host almost by accident. This isn’t a story of altruism or good will, but of incidental beneficence. (It’s the mirror of another effect that I’ve written about, where microbes become coincidentally better at harming us when they’re exposed to predators or stressful environments.)

King’s study illustrates two other crucial themes in the world of microbiomes. First, as I’ve stressed before, it’s extremely contextual. The same bacterium can be a harmful pathogen (a microbe that causes disease) in one context but a helpful mutualist when its host is challenged by an even worse enemy. Likewise, the insect bacterium Hamiltonella protects aphids from parasitic wasps and becomes commonplace when such wasps are abundant; but it exacts a cost upon its hosts and is lost when wasps are absent. There are no good bacteria or bad bacteria; they live their own lives, and their impact upon our lives depends on all kinds of circumstances.

Second, microbes evolve quickly. In doing so, they can change the lives of their hosts with equal speed. The worms in King’s experiment didn’t need to evolve their own defences against Staph infections when they had Enterococcus to take up the slack. This all happened in the confines of a laboratory, but you can easily imagine how wild worms that consumed the right strains of bacteria would suddenly become immune to some infections (just like some bugs can become instantly resistant to insecticides by swallowing the right microbes).

“We’ve taken a very reductive approach,” says King. “In the future, we want to understand how these interactions play out in a much more diverse community.” Such as those in our bodies, for example. What happens when thousands of species of native microbes are challenged by Staph and other pathogens? How would they evolve in response?

And could we, perhaps, develop ways of directing that evolution to improve our health? “It’s very speculative, but I’d hope this would get people thinking about the possibility of engineering microbes using their natural evolutionary potential,” says King.

For more about the defensive power of microbes, and their ability to quickly change the lives of their hosts, check out my book I Contain Multitudes, out on August 9.

Paleo Profile: The Dawn Mole

The jaw of Eotalpa anglica. From Hooker, 2016.
The lower jaw of Eotalpa anglica. From Hooker, 2016.

The word “mole” is practically synonymous with an underground lifestyle. The little mammals that bear the name are supposed to be near-blind denizens of the world beneath our feet, tunneling through gardens for tasty worms and other morsels. And, fair enough, some moles live this way. But not all. The desman is a snouty mole that swims, some moles forage above the ground but beneath the cover of leaf litter, and the tiny shrew mole Uropsilus doesn’t seem to show any acumen for digging at all. Thanks to some tiny fossils recently found in England, however, it seems that this variety of moles sprung from ancestors that were skilled at scratching into the soil.

Paleontologist Bernard Sigé and colleagues named the critical mole in 1977 from the basis of molars found on the Isle of Wight. They called it Eotalpa anglica, and at 37 to 33 million years old it has stood as the oldest mole ever since. And now, thanks to tiny fossils sifted out of the Eocene rock, it appears that Eotalpa was already doing what moles are famous for.

Natural History Museum paleontologist Jerry Hooker has described the smattering of new bones. The feet of Eotalpa don’t show the swimming adaptations of the star-nosed moses and desmans, Hooker writes, meaning that moles did not start off as semiaquatic mammals as had once been suggested. And while the mole’s hands weren’t quite as extreme as some of its living relatives, their anatomy is more consistent with moles that are dedicated diggers. Even older moles, which Hooker expects might be found in Asia, may help flesh out how moles switched surfaces, but for now Eotalpa indicates that these beasts were underground before it was cool.

eotalpa-claws
The reconstructed finger of Eotalpa anglica in multiple views. From Hooker, 2016.

Fossil Facts

Name: Eotalpa anglica

Meaning: England’s dawn mole.

Age: Between 37 and 33 million years old.

Where in the world?: The Hampshire Basin, England.

What sort of critter?: A mole.

Size: Not estimated, but within the range of living moles.

How much of the creature’s body is known?: Isolated microfossils consisting of the upper and lower jaws, parts of the hand and arm, ankle, and lower leg.

Reference:

Hooker, J., 2016. Skeletal adaptations and phylogeny of the oldest mole Eotalpa (Talpidae, Lipotyphla, Mammalia) from the UK Eocene: the beginning of fossoriality in moles. Palaeontology. doi: 10.1111/pala.12221

Previous Paleo Profiles:

The Unfortunate Dragon
The Cross Lizard
The South China Lizard
Zhenyuan Sun’s dragon
The Fascinating Scrap
The Sloth Claw
The Hefty Kangaroo
Mathison’s Fox
Scar Face
The Rain-Maker Lizard
“Lightning Claw”
The Ancient Agama
The Hell-Hound
The Cutting Shears of Kimbeto Wash
The False Moose
“Miss Piggy” the Prehistoric Turtle
Mexico’s “Bird Mimic”
The Greatest Auk
Catalonia’s Little Ape
Pakistan’s Butterfly-Faced Beast
The Head of the Devil
Spain’s Megatoothed Croc
The Smoke Hill Bird
The Vereda Hilarco Beast
The North’s Sailback
Amidala’s Strange Horn
The Northern Mantis Shrimp
Spain’s High-Spined Herbviore
Wucaiwan’s Ornamented Horned Face
Alcide d’Orbigny’s Dawn Beast
The Shield Fortress
The Dragon Thief
The Purgatoire River’s Whale Fish
Russia’s Curved Blade

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CDC Recommendations for Pregnant Women Exposed to Zika

An Aedes aegypti mosquito, the chief vector of Zika virus.
An Aedes aegypti mosquito, the chief vector of Zika virus.
Photograph by James Gathany, CDC

(This post has been updated twice.)

The Centers for Disease Control and Prevention has responded to growing alarm over the Zika virus epidemic in Central and South America with quickly published guidelines covering health care and tests for pregnant women who may have been exposed to the virus.

The guidelines come on the heels of the CDC’s recommendation last Friday night that US women who are pregnant, or planning to become pregnant, avoid traveling to the 13 countries where transmission of Zika has occurred, and also to the US territory of Puerto Rico.

Zika, which is transmitted by mosquitoes, arrived in South America in 2014 and ignited a pandemic. Most of the adult cases, which number more than 1 million, have been mild. (It is generally accepted that four out of five people infected with Zika do not develop symptoms; so the true number of those infected is likely more than 5 million.) But in Brazil, there has been an epidemic of a birth defect called microcephaly—smaller than usual brains and heads in newborns— that is associated temporally, and by some lab tests, with Zika infection. So far in Brazil there have been more than 3,500 cases of microcephaly. Zika has come to the United States as well, with local transmission in Puerto Rico and an imported case in the county surrounding Houston, and on Friday, a baby born in Hawaii to a woman who lived in Brazil while she was pregnant was diagnosed with Zika microcephaly. Today, the Illinois Department of Public Health disclosed that it is monitoring two pregnant women who traveled to Zika transmission areas.

(Update, Jan. 20: According to Florida media, that state’s department of health has announced three cases in Florida, all travel-related.)

The CDC’s guidelines today offer advice for pregnant women who traveled to a location where Zika is circulating, whether or not the woman reports symptoms of Zika infection: sudden fever, a rash, conjunctivitis, and joint pain. Broadly, women with a travel history and symptoms should have blood drawn to be tested for Zika infection—the test can be performed only by the CDC and some health departments—and if positive, should have regular ultrasounds to track fetal development and should be seen by one of several specialists. Pregnant women who traveled to a Zika area but did not experience symptoms are recommended to undergo ultrasounds first, and to seek a test to confirm infection if there are abnormalities in the imaging.

The CDC's advice for testing and treating pregnant women exposed to Zika virus, expressed as a flow chart.
The CDC’s advice for testing and treating pregnant women exposed to Zika virus, expressed as a flow chart.
Graphic by the CDC; original here.

Within the text of the recommendations, which were published as an early release from the CDC’s weekly journal Morbidity and Mortality Weekly Report, there are hints of how complex this emerging situation has become. There is no vaccine for Zika, so as prevention the agency can recommend only “wearing long-sleeved shirts and long pants, using U.S. Environmental Protection Agency-registered insect repellents, using permethrin-treated clothing and gear, and staying and sleeping in screened-in or air-conditioned rooms.” There is no specific treatment, so it can recommend only “rest, fluids, and use of analgesics and antipyretics. Fever should be treated with acetaminophen.” (The CDC specifically rules out aspirin, because the mosquito-borne diseases chikungunya and dengue are also circulating in the areas where Zika is, and dengue can lead to hemorrhagic fever—so drugs that can increase bleeding are not recommended.)

The limited options for confirming Zika in a fetus are especially difficult, since amniocentesis—which could yield a sample for testing—also carries a risk of miscarriage. The CDC says:

Zika virus RT-PCR testing can be performed on amniotic fluid. Currently, it is unknown how sensitive or specific this test is for congenital infection. Also, it is unknown if a positive result is predictive of a subsequent fetal abnormality, and if so, what proportion of infants born after infection will have abnormalities. Amniocentesis is associated with an overall 0.1% risk of pregnancy loss when performed at less than 24 weeks of gestation…. early amniocentesis (≤14 weeks of gestation) is not recommended. Health care providers should discuss the risks and benefits of amniocentesis with their patients.

The CDC has also published guidance for health care professionals here, and explanations of how to send samples for testing here.

Update, Jan. 22: The CDC has added Barbados, Bolivia, Ecuador, Guadeloupe, Saint Martin, Guyana, Cape Verde, and Samoa to its “don’t travel if pregnant” list.

Previous posts in this series:

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Last-Ditch Resistance: More Countries, More Dire Results

An E. coli bacterium.
An E. coli bacterium.
Photograph by the Public Health Image Library, CDC.gov.

The frantic international hunt triggered by the discovery of genetically mobile resistance to colistin, a last-resort antibiotic, is producing many more findings this evening. The resistance factor is showing up in more countries, but, much more important, it has combined in some bacterial samples with genes conferring resistance to other potent drugs, creating bacteria that look effectively untreatable.

These disclosures are made in letters from research groups in a number of countries that are being published by the journal Lancet Infectious Diseases at 11:30pm London time, which is 6:30pm East Coast time here in the US. They represent evidence that this drug resistance, which was driven by agricultural use of colistin during the years that human medicine did not make use of it, is an imminently serious issue for human health.

“We’re watching our demise in real time,” Lance Price, PhD, a prominent resistance microbiologist and founder of the Antibiotic Resistance Action Center at George Washington University, who not involved in any of the research, told me. “I guess this is one of the advantages of next-generation DNA sequencing, is we can watch ourselves fall apart.”

Here’s a quick way to think about what follows. It’s natural to imagine that antibiotic resistance proceeds step-wise; that in the leapfrog between bug and drug, bacteria gain resistance to one drug, and then the next toughest drug presented to them, and then a last-resort drug after that. But in the wild, the way bacteria accumulate resistance DNA is more like being dealt cards in a hand of poker: one might have a 3, a 5, and a Jack, while another has a King, a Queen and a 10.

In these papers published tonight, researchers are finding bacteria that already possess colistin resistance— call it the Ace—and are accumulating the rest of a winning hand. Only, what looks like winning would be losing, for us. Here are the details:

Laurent Poirel and colleagues in Switzerland have identified an E. coli strain, recovered from an 83-year-old Swiss man who was hospitalized last month, that possesses both colistin resistance and also VIM resistance to the carbapenems, the family of antibiotics that was considered the last and toughest before colistin. The colistin-resistance gene shared a plasmid with genes conferring resistance to chloramphenicol, flofenicol and co-trimoxazole. The authors warn, “Such accumulation of multidrug resistance traits may correspond to an ultimate step toward pandrug resistance.”

Our data suggest that the advent of untreatable infections has already arrived.

Marisa Haenni and collaborators in France and Switzerland queried the Resapath network in France, which conducts surveillance for antibiotic resistance in animals, found that 21 percent of bacterial samples collected from veal calves on French farms between 2005 and 2014 carried the signal of mobile colistin resistance, the gene mcr-1. There were 106 positive samples (out of 517) and they came from 94 different farm properties. On seven of those isolates, the mcr gene lived alongside ones for ESBL resistance—that’s to penicillins and to the first three generations of cephalosporin drugs—and also genes for resistance to sulfa drugs and tetracycline.

Linda Falgenhauer and collaborators in the Reset consortium in Germany examined the sequences of 577 isolates taken from human patients and livestock and from the environment since 2009. They identified four carrying the mcr-1 gene, three from humans and one from a hog. The three from swine also possessed ESBL resistance; the one from the human was also carbapenem-resistant (KPC-2). One of the swine samples dated back to 2010. They say, somberly: “Our data suggest that the advent of untreatable infections has already arrived, as every colistin-resistant isolate described in this study is also resistant to either third-generation cephalosporins or to carbapenems.”

Surbi Malhotra-Kumar and colleagues at the University of Antwerp examined 105 E. coli strains collected from piglets and calves in 2011 in Belgium that had previously been identified as colistin-resistant. They found mcr-1 in 13 of them, and also found that it is being carried on a different plasmid than those identified in China and in Denmark. They descrcibe this as “a marked presence of mcr-1 in animal pathogenic bacteria in Europe, an indication that this is already a truly global phenomenon”— and also note that the 92 resistant strains that did not contain mcr might indicate other transferable colistin resistance that has not yet been identified.

In a separate letter, the same research group and several Vietnamese collaborators report mcr-1 in nine out of 24 E. coli collected from chickens and pigs in two provinces in Vietnam. One isolate contained resistance to eight additional drug families. They also screened 112 ESBL E. coli from three hospitals in Hanoi, but, they report, did not find any mcr.

Nicole Stoesser and colleagues from England and collaborators in Virginia and Bangkok examined sequences from a database of E. coli and Klebsiella collected in North America, Europe and Southeast Asia between 1967 and 2012, and found only a single isolate carrying mcr. It was taken frmo a child hospitalized in Cambodia in 2012, and also possessed ESBL resistance.

In Japan, Satowa Suzuki and collaborators from several institutions say they scoured the sequences of  1,747 plasmid genomes from Gram-negative bacteria, originally taken from human patients and livestock and from the environment, and found five animal isolates carrying mcr, but no human ones. None carried other resistance genes. They also examined a separate database of E. coli from livestock and, out of 9.308, found only two carrying mcr—but 88 others that were colistin-resistant.

And in the eighth letter, Mauro Petrillo and colleagues of the European Union’s Molecular Biology and Genomics Unit present a hypothesis for how the mcr-1 gene is being acquired.

There are some important leads in these reports: that mcr is in more countries,  is appearing on different plasmid backbones, and, apparently, seems more common in animals than in humans in the locations where it has been found. That may suggest, as the CDC said last month, that molecular analysis allowed this to be identified relatively earlier than other dire resistance factors have been in the past.

But the discovery that colistin resistance is combining in the same plasmids with other resistance genes should especially raise alarm bells. That indicates that using any of those drugs—some of which are very common—could amplify this resistance and and increase its spread. It signals that, as serious as mobile colistin resistance appeared at first, it is even more complex and more urgent.

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Last-Ditch Drug Resistance: China and Europe Respond

A cattle feedlot from the air.
A cattle feedlot from the air.
Photograph by Wongaboo (CC), Flickr.

I have a couple of pieces of news regarding the discovery of resistance to colistin, the last-resort antibiotic that is the only thing that works for some multi-drug resistant infections. Two are positive news, and the third is a corrective to some earlier reporting, and a revelation of how complex the antibiotic traffic between human and animal medicine can be.

The positive news first: Both Europe and China are moving to examine the use of colistin in agriculture. The European Medicines Agency has asked the European Commission to be allowed to examine whether colistin use should be restricted. And in China, the central government is studying whether it should ban the drug from agricultural use altogether.

Timothy Walsh, DSc, a British microbiologist who has been studying antimicrobial resistance in China’s agriculture and who collaborated with Chinese researchers on the blockbuster paper announcing the colistin discovery, told me: “The Chinese government have been very receptive” to concerns being expressed about colistin use. He added, “They are conducting a review now, to look at the impact of removing colistin from animal feed, and it is hoped in the next couple of weeks that they will indeed remove colisitin from animal feed.”

Quick update, if you’re coming to this fresh: Colistin is an old drug, first isolated in 1949, that languished on the shelf for decades but was recently revived. It it the only antibiotic that works against a growing category of serious infections; if widespread resistance to it developed, those infections, known as CREs, would become untreatable. In November, Walsh and his collaborators made the bombshell announcement in Lancet Infectious Diseases that they had found resistance to colistin in China, contained in a mobile genetic element that can reproduce and move freely among bacteria, and that its existence—in pigs, pork meat, and human patients—was due to colistin use in agriculture.

That news set off an international furor and also a hunt. The mcr-1 gene conferring this resistance was swiftly identified in stored bacterial samples in Denmark, and then England; the count is now up to 10 countries. (With more no doubt to come.)

That brings us up to date, and also to the corrective piece of news.

The early days of reporting about mobile colistin resistance gave the impression that it arose through China callously wasting a crucial drug. (This slots into China’s well-documented reputation for dubious food safety.) The message was that, unlike Europe and the United States, which have taken steps to control farm antibiotic use, China is allowing a free-for-all.

Turns out, it’s not that simple. The situation is not that agriculture, in China or elsewhere, is using up a drug that medicine has always needed. It’s more that medicine handed the drug to agriculture in the 1950s, and now wants it back.

Colistin use in agriculture in Europe in 2011 (expressed in a per-animal measure).
Colistin use in agriculture in Europe in 2011 (expressed in a per-animal measure).
Grpahic by the European Medicines Agency, original here.

You can see this most clearly in Europe. The EU has had the word’s strictest control on livestock antibiotics  since 2006, when it banned the routine micro-doses called growth promoters that make animals put on weight more quickly. Yet it is an abundant user of colistin. An eye-opening paper published last September lists colistin (and a related drug; both belong to the polymyxin class) as being used in “rabbits, pigs, broilers, veal and beef cattle, and meat-producing sheep and goats; furthermore, the antibiotic is used also in laying hens and dairy cattle, sheep and goats producing milk.” Of all the classes of antibiotics used in animals in Europe, the polymyxins were the 5th most-sold. That is all prophylaxis, to prevent the occurrence of diseases, which remained legal under the 2006 ban.

“Colistin is a survivor of the ban on antimicrobial growth promoters in Europe,” Boudewijn Catry, DVM, PhD, told me. Catry is the first author on that paper and the head of healthcare-associated infections and antimicrobial resistance at Belgium’s Scientific Institute of Public Health. He said that colistin gets so much use for two reasons: first, because it was so toxic in humans that it seemed medicine would never want it; and second, because other drugs were taken away from agriculture over the years precisely because medicine needed them preserved. Those other drugs include penicillin, the tetracyclines, and vancomycin, the last-resort drug for MRSA (agriculture used a close analog, avoparcin). Catry added: “When many compounds were banned, others were still possible to give in large quantities by the oral route, for prevention of major diseases, and colistin is one.”

Multi-drug resistant CREs began moving across the globe in the mid-2000s. There were different categories—the KPCs in the US, NDM in South Asia, OXA in the Mediterranean—but what they all had in common was resistance to carbapenems, essentially the last reliable, nontoxic drugs for highly resistant organisms. With nothing else left, human medicine was forced to turn back to colistin.

At that point, the European Union began re-evaluating the way that it had allowed agriculture to use the drug. In 2013, the European Medicines Agency recommended disallowing preventive use, and that recommendation has been chugging through the system since, without great urgency because resistance migrating from agriculture did not seem to be a problem. With the discovery of mobile colistin resistance, that has changed.

The MCR story is going to go on for a while, but right now, there are two important things to note. The first is that antibiotic control is porous. Colistin resistance is occurring in Europe because it entered agriculture through allowed preventive use; when the United States finalizes its long-awaited actions against growth promoters in 2016, it will allow preventive use too.

The second is that the progress of resistance is unpredictable. Medicine allowed agriculture to use avoparcin because it never thought vancomycin would be important; it allowed polymyxin use in agriculture because it never though it would need colistin either. It turns out both drugs are crucial. That seems to me a lesson that all antibiotics should be used conservatively. We never know what will arise next.

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Polio Eradication: Is 2016 The Year?

A polio victim crawls on a sidewalk in India.
A polio victim crawls on a sidewalk in India.
Photograph by Wen-Yai King Flickr (CC).

As Yogi Berra (or Niels Bohr or Samuel Goldwyn) is supposed to have said, it’s difficult to make predictions, especially about the future. It’s especially dangerous to try to predict the behavior of infectious diseases, when small unpredictabilities in climate or trade or the behavior of governments can bring a problem that we thought was handled roaring back to life.

But as 2016 opens, it is fair to say that the disease public health experts are pinning their hopes on, the one that might truly be handled this year, is polio. There were fewer cases last year than ever in history: 70 wild-type cases, and 26 cases caused by mutation in the weakened virus that makes up one of the vaccines, compared to 341 wild-type infections and 51 vaccine-derived ones the year before. Moreover, those wild natural infections were in just two countries, Afghanistan and Pakistan, and the vaccine-derived cases were in five. The noose is tightening.

The most that health authorities can hope for this year is to end transmission of polio. The ultimate goal is eradication, which has happened only twice—for one human disease, smallpox, and one animal one, rinderpest. To declare a disease eradicated requires that the entire world go three years without a case being recorded. If there are no polio cases in 2016, eradication might be achieved by the end of 2018.

Which would make for nice round numbers, because the polio eradication campaign began in 1988. It is safe to say that no one expected it would take anywhere near this long; the smallpox eradication campaign, which inspired the polio effort, reached its goal in 15 years.

Smallpox was declared eradicated in 1980, so long ago that most people have no knowledge of how devastating a disease it was, or even what a case of the disease looked like. (There are survivors left, but they are aging; the last person infected in the wild, Ali Maow Maalin of Somalia, died in 2013.) In the same way, we’ve forgotten how difficult it is to conduct an eradication campaign. Smallpox was the first campaign that succeeded, but it was the fifth one that global authorities attempted. In its success, it demonstrated what any future campaign would need: not just a vaccine that civilians could administer, but an easy-to-access lab network, granular surveillance, political support, huge numbers of volunteers, and lots and lots of money.

In its own trudge to the finish, the polio eradication campaign has stumbled over many of those, from local corruption to extremist opposition to the still almost unbelievable interference of the CIA (which I covered here and here), along with the virus’s own protean ability to cross borders (to China) and oceans (to Brazil).

But now, at last, the end does look in sight. I asked Carol Pandak, director of the Polio Plus program at Rotary International — which since 1988 has lent millions of volunteers and more than a billion dollars to the eradication campaign —  how she thinks the next 12 months will go.

“We are getting closer,” she told me. “We have only two endemic countries left. Of the three types of the virus, type 2 was certified eradicated in September, and there have been no type 3 cases globally for three years. And Pakistan and Afghanistan have goals to interrupt transmission internally in May 2016.”

The diminishment of wild polio paradoxically creates greater vulnerability to vaccine-derived polio, which happens when the weakened live virus used in the oral vaccine mutates back to the virulence of the wild type. The only means of defusing that threat is to deploy the killed-virus injectable vaccine, which is widely used in the West but until recently was considered too expensive and complex to deliver in the global south.

To begin the transition, Pandak said, countries that still use the oral vaccine have agreed to give one dose of the injectable as part of routine childhood immunizations for other diseases. That should strengthen children’s’ immune reactions to polio, so that the reversion to wild type — which occurs as the weakened virus replicates in the gut — does not take place.

In the smallpox campaign, when eradicators thought they were almost done, there was a freak weather event—the worst floods that Bangladesh had experienced in 50 years—that triggered an internal migration and redistributed the disease. Polio is just as vulnerable to last-minute disruptions, especially since the two remaining endemic countries are hotspots of unpredictability. Travelers from Pakistan actually carried polio into Afghanistan in August.

“In Pakistan, the army has committed to providing protection for vaccinators in conflict areas,” Pandak told me, “and another strategy that has been successful has been to set up border posts to immunize people as they are fleeing areas of conflict and military operations. I have seen Rotary volunteers staffing 24/7 kiosks in train stations and toll booths, so that we can get people wherever they happen to be.”

There is no question that hurdles remain. By the World Health Organization’s order, polio is still considered a “public health emergency of international concern,” which requires countries where the disease is extant to either ensure its citizens are vaccinated before leaving, or prevent their crossing the border. And polio still lives quiescently in lab freezers all over the world, and those will have to be searched and their contents eliminated lest a lab accident bring the disease alive again (a warning that was recently circulated for rinderpest as well). Plus, up til now, the injectable vaccine has been made by starting with a virus that is not only live but virulent, posing the risk that a lab accident that could release it; British scientists announced on New Year’s Eve that they may have found a way to weaken it while still yielding a potent vaccine.

When it goes, if it does, polio will gift the world not only with its absence, but also with the abundant health infrastructure that was set up to contain and eliminate it, and can be turned to other uses. When I talked to Pandak, she sounded excited at the possibility that countries and volunteers would be able to turn their attention away from a single disease and toward ensuring the overall health of children.

“We have been doing this for 30 years,” she said. “We’ll continue to fundraise, advocate and raise awareness to the last case. We are committed to seeing this to the end.”

 

Filter Feeder Was the First of its Kind on Earth

Fossils and a reconstructed model of Tribrachidium. From Rahman et al., 2015.
Fossils and a reconstructed model of Tribrachidium. From Rahman et al., 2015.

If you like enigmatic blobs, then you would have loved the Ediacaran. Back then, between 575 and 541 million years ago, much of life came in a range of fronds, pancakes, and medallions that have puzzled and inspired paleontologists for decades. Some of them were animals. Others were forms of life that defy categorization. But even though mysteries still abound, paleontologist Imran Rahman and colleagues have solved one aspect of how a particular species of Ediacaran oddball fed and what that meant for the evolution of our seas.

Rahman and coauthors settled on a tiny button of an organism named Tribrachidium heralicum. This circular, triple-ridged species has been found in marine rocks in South Australia, Russie, and Ukraine dating between 555 and 550 million years old. No one knows exactly what the organism is – the species has triradiate symmetry, which no animal possesses today – but, through fluid dynamics experiments, Rahman and colleagues were able to determine that Tribrachidium now holds the title of the oldest filter-feeder yet known.

Water flow over the surface of Tribrachidium. Image: I.A. Rahman
Water flow over the surface of Tribrachidium. Image: I.A. Rahman

Up until now, most Ediacaran critters were thought to be osmotrophs. That means they passively absorbed organic particles that they either shuffled over or that fell upon them. But Rahman and coauthors found that current flow over the surface of Tribrachidium directed water towards the apex of the organism, over small branches called a “tentacular fringe” and into specialized pits. As water carrying little organic tidbits flowed over Tribrachidium, in other words, the organism’s shape directed that water upwards to a spot where the flow lost some of its speed and dropped the tiny organic morsels to a place where they could be consumed.

That food didn’t just fall from above. Tribrachidium lived during a time when expansive organic mats covered much of the seabottom, Rahman and colleagues point out, and when currents shook up all that muck some of the organic particles were thrown back up into the mix. The fact that the shape of Tribrachidium had the same filtering effect regardless of current direction is a sign that it made the most of habitats where water frequently sloshed the organic debris around.

At about 10 million years before the onset of the “Cambrian explosion“, when animal life ran riot for the first time, this new discovery adds a new dimension to how life changed the seas.  Tribrachidium was likely an “ecosystem engineer”, Rahman and coauthors write, removing organic material from the water column that helped more light shine in and oxygenated the water column. This early pop could have been important in setting up one of evolution’s most explosive chapters.

Reference:

Rahman, I., Darroch, S., Racicot, R., Laflamme, M. 2015. Suspension feeding in the enigmatic Ediacaran organisms Tribrachidium demonstrates complexity of Neoproterozoic ecosystems. Science Advances. doi: 10.1126/sciadv.1500800

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More Countries Are Seeing a Last-Ditch Antibiotic Failing

An E. coli bacterium.
An E. coli bacterium.
Photograph by the Public Health Image Library, CDC.gov.

(This post has been updated; read to the end.)

More news is emerging about the dire new antibiotic resistance factor announced last month: MCR-1, a gene that disables the action of colistin, a very last-resort drug in human medicine. (If you’re just coming to this, my past posts are here and here.)

Quick recap: A gene conferring resistance to colistin was found in pigs, retail meat, and human patients in China; then it was spotted in Malaysia; then in Portugal. Then, in the next major development, researchers in Denmark announced they had identified the gene in one human patient and five samples of imported meat.

Here’s the newest news: The Danish researchers tell me that they have identified another patient who was infected with a bacterium bearing that same resistance factor. And Public Health England has announced that it has found the gene in 15 stored bacterial samples in its databases: 10 Salmonella bacteria and three E. coli that came from hospitalized patients, and two Salmonella on a single sample of imported poultry meat.

The news is both alarming—more instances of this gene that creates resistance to last-ditch drugs, and that can transfer easily between bacteria—and also puzzling. The British samples were taken between this year and 2012. The Danish samples announced 10 days ago date back to 2012, and the newly discovered one comes from 2011. So the gene has been circulating for several years, without causing any outbreaks.

Is that a bullet dodged? Perhaps. But researchers studying the new gene say it may be a slow-burning fuse.

In human medicine, colistin is a rarely used drug, a survivor from the earliest decades of antibiotic development that was left on the shelf for decades because it was toxic. But in veterinary medicine, colistin has had wide use, which is probably what caused this resistance factor to emerge. Now, with the loss of other antibiotics to resistance, colistin use in humans is climbing, and that could set the stage for this effectively untreatable resistance to bloom.

“This seems to have been around for five to six years,” Robert Skov, MD of the Statens Serum Institut in Copenhagen, and the senior author in the Danish team’s rapidly produced article on their discoveries, told me by phone. “One thing is for sure: We are using more and more colistin in humans due to the increase in [bacteria resistant to carbapenems, the next-to-last-resort drug], and thus we are probably selecting for this colistin resistance to emerge.”

How the gene—which resides on a plasmid, a mobile piece of DNA that can move between bacteria— is traveling the world is a puzzle. Skov said the Danish government has done an emergency survey of the country’s animal herds and found no trace of the gene. (Which, before now, no one would have been looking for.) The chicken meat in which the gene was found in Denmark was imported from Germany. The two people in whom the MCR gene has been found had not traveled to Asia. In Britain, three out of 10 patients had been to Asia, and the meat on which two MCR-bearing Salmonella strains were found was imported from elsewhere in Europe.

When NDM, the last last-resort resistance threat, began to spread across the world, it did so in the guts of patients who visited India, where it first emerged, and then traveled home to Europe and Britain. It’s possible a similar thing is happening with MCR. “We have five chicken isolates [bacterial samples] and one human isolate, and when we compare the plasmids in the chicken and human isolates and what has been published from China, the greatest resemblance to the Danish human isolate is the isolates from China and not from the German chicken,” Skov said. “This suggests it was brought, not by chicken, but by people coming from Asia to Denmark.”

In the past few days, I asked antibiotic resistance experts in various parts of the world whether they had seen MCR yet, and whether they were looking for it. All of them were looking; outside of Britain, none had discovered it yet in any national collections of bacterial isolates. (Or, given that disclosing a finding might keep them from publishing in major medical journals, were willing to admit to discovering it.)

Lance Price, PhD of the Antibiotic Resistance Action Center at George Washington University, told me that additional analysis of the isolates found in Denmark shows two troubling things. All of the bacteria in which the gene was found were unique—six different strains of E. coli—and the gene has found a home in two different plasmids. Together those suggests that it has no difficulty moving among bacteria and finding a comfortable home in them. “It’s real world, empiric evidence that this thing can spread very widely,” he said. “Its’s almost like it possesses a universal key.”

Price told me that one concern at this point will be which bacterial strains the gene jumps into: indolent ones that cause little disease, or fast-moving virulent ones that cause infections in many body systems and are already resistant to many other drugs. One of the Danish isolates that carries MCR, he said, is an E. coli of a type known as ST131—which in the United States is already multi-drug resistant and causes thousands of serious bladder and bloodstream infections every year. “At this point we don’t know what the denominator is going to be,” he said. “We don’t know how many different strains this is going to get into, and this underscores the possibility it will jump into something really bad.”

Update: On Dec. 17, Dutch authorities announced they too had identified MCR-1 in a bacterial collection in the Netherlands. The Central Veterinary Institute, housed at Wageningen University, said it found three bacterial isolates containing the MCR-1 gene in a collection of 3,274 Salmonella strains from 2014 and 2015. Two similar strains came from chicken meat that originated in the Netherlands, and a different strain from imported turkey. (It does not give the source of the turkey.) They are now undertaking a broader search through other bacterial collections.

There will no doubt be more such discoveries as other health authorities complete searches through whatever national collections they have. But as Lance Price says above, this is further evidence that this gene has great facility for jumping among different bacteria and bacterial species.

Meanwhile, if you’re interested in more on this, Price, Skov and I were on the NPR show On Point on Dec. 16, discussing MCR. Replay and podcast instructions at the link.

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You’re Surrounded by Bacteria That Are Waiting for You to Die

Antibiotic-resistant Staphylococcus aureus bacteria (yellow) killing and escaping from a human white blood cell.
Antibiotic-resistant Staphylococcus aureus bacteria (yellow) killing and escaping from a human white blood cell.
Photograph by NIAID

You are filled with bacteria, and you are covered in them. And a whole lot of them are just waiting for you to drop dead.

As soon as you die, they’ll swoop in. This week, we learned exactly how microbes chow down on us. A brave and strong-stomached team of scientists spent months watching dead bodies decompose, tracking all the bacteria, fungi, and worms, day by day. Forensic scientists can use this timeline, published in Science, to help determine time—and even place—of death. (More on that in a previous Gory Details.)

The microbes in your intestines get first dibs, the scientists found. As soon as you die, they’ll start decomposing you from the inside out. Meanwhile, other bacteria on your skin or in the soil beneath you start mounting an attack from the outside in. As Michael Byrne at Motherboard so nicely summed it up, “Earth is just waiting for you to drop dead.”

That’s a little unsettling, if you think about it. And it begs the question: What keeps all those bacteria from decomposing you alive?

That’s silly, you say. I’m alive. Only dead things decompose.

Yes, but why?

What keeps all those bacteria from decomposing you alive?

As the new study points out, two of our most crucial defenses against being decomposed are toppled as soon as we die. Our immune system shuts down, and our bodies cool off. Bacteria like this; they don’t have an easy time growing in a hot body. (Think about it: When we have an infection our bodies develop a fever to ward it off.)

Basically, a big part of life involves your cells waging a battle to the death with bacterial cells. As long as you’re alive and healthy, your cells are winning. Decomposition is when your cells lose. 

One of the clearest descriptions I’ve read comes from Moheb Costandi’s “This is what happens after you die“:

Most internal organs are devoid of microbes when we are alive. Soon after death, however, the immune system stops working, leaving them to spread throughout the body freely. This usually begins in the gut, at the junction between the small and large intestines. Left unchecked, our gut bacteria begin to digest the intestines—and then the surrounding tissues—from the inside out, using the chemical cocktail that leaks out of damaged cells as a food source. Then they invade the capillaries of the digestive system and lymph nodes, spreading first to the liver and spleen, then into the heart and brain.

As soon as you die, your body essentially gets its first break from a war that it has been fighting every moment of your life.

When the bacteria start to win that war in a living person, we call it an infection, and we try to flush the invaders out of a wound. Or we go in with antibiotics to poison them.

Let’s pause for just a moment to appreciate those antibiotics. We thought we had outwitted bacteria. But now we’ve overused and misused antibiotics, giving the bacteria a chance to figure out our defenses. They’re adapting, becoming resistant to our weapons, and we’re already seeing the failure of some of our last lines of defense, leading to more infections, illness, and death.

Ultimately, we lose our battle with bacteria when we die. But until then, it’s pretty amazing to think of the fine line between life and becoming bacteria food. Imagine the evolutionary arms race that has led to an immune system so vigilant that it can fend off constant attack for decades. 

I’m just grateful not to be decomposing right now.

Paleo Profile: Spain’s Megatoothed Croc

The skull of Lohuecosuchus megadontos. From Narváez et al., 2015.
The skull of Lohuecosuchus megadontos. From Narváez et al., 2015.

Paleontology is still pretty new as sciences go. It’s only been around in any kind of organized form for less than 200 years, and while today’s explorers and researchers can trace their pedigrees through multiple generations, paleo practitioners have really only just begun to literally scratch the surface of what’s out there. This is true even on continents that have been considered well-sampled and studied. Case in point, the Lo Hueco fossil site in central Spain.

The Late Cretaceous boneyard, located in the village of Fuentes, was only discovered in 2007. Since that time paleontologists have found fish, amphibians, turtles, lizards, crocodiles, and various dinosaurs from this one spot, and they’ve just named a new species from the assemblage. Described by Iván Narváez, Christopher Brochu, and colleagues, the large-toothed crocodile has been dubbed Lohuecosuchus megadontos.

Back when Lohuecosuchus was alive, around 72 million years ago, much of Europe was an archipelago. Tongues of ocean separated islands where dinosaurs roamed, and the separation of once-connected landmasses led new species to evolve among the scattered islands. Lohuecosuchus megadontos was one of these evolutionary spinoffs, and even had a close – but distinct – relative in Cretaceous France named Lohuecosuchus mechinorum by Narváez and coauthors. Along with the other European crocs of the time, these two new species show what evolution can do with a little isolation.

 

Two additional skulls of Lohuecosuchus megadontos. From Narváez et al., 2015.
Two additional skulls of Lohuecosuchus megadontos. From Narváez et al., 2015.

Fossil Facts

Name: Lohuecosuchus megadontos

Meaning: Lohuecosuchus means “crocodile from Lo Hueco”, while megadontos is a reference to the reptile’s large teeth.

Age: Around 72 million years old.

Where in the world?: Lo Hueco, central Spain.

What sort of critter?: An ancient crocodile belonging to a group called allodaposuchids.

Size: The skull measures about 15 inches long and 11 inches wide.

How much of the creature’s body is known?: Three skulls – ranging from complete to fragmentary – and three lower jaws.

Reference:

Narváez, I., Brochu, C., Escaso, F., Pérez-García, Ortega, F. 2015. New crocodyliforms from southwestern Europe and Definition of a diverse clade of European Late Cretaceous basal eusuchians. doi: 10.1371/journal.pone.0140679

Previous Paleo Profiles:

The Unfortunate Dragon
The Cross Lizard
The South China Lizard
Zhenyuan Sun’s dragon
The Fascinating Scrap
The Sloth Claw
The Hefty Kangaroo
Mathison’s Fox
Scar Face
The Rain-Maker Lizard
“Lightning Claw”
The Ancient Agama
The Hell-Hound
The Cutting Shears of Kimbeto Wash
The False Moose
“Miss Piggy” the Prehistoric Turtle
Mexico’s “Bird Mimic”
The Greatest Auk
Catalonia’s Little Ape
Pakistan’s Butterfly-Faced Beast
The Head of the Devil

Crocodiles Are Not “Living Fossils”

Crocodiles aren't as unchanged over the millennia as scientists once thought.
Crocodiles aren’t as unchanged over the millennia as scientists once thought.
Frans Lanting, National Geographic Creative

 

Crocodiles look ancient. Maybe it’s something to do with the eyes, the armor, and the teeth that remind us of the Age of Reptiles. Or maybe it’s simply because crocs are often used as window dressing to set Mesozoic scenes that gives us the impression that they’ve always been watching from just beneath the surface of the water. Whatever the reason for these alligator impressions, though, paleontology has undeniably shown that these archosaurs are far from the “living fossils” we love to portray them as.

Paleontologist Julia Molnar and her coauthors set the record straight in the very first line of their latest paper. “The lineage leading to modern Crocodylia has undergone dramatic evolutionary changes in morphology, ecology, and locomotion over the past 200+ Myr.” While it’s true that crocs in the flavor of “semi-aquatic ambush predator” of one lineage or another have been around since the Jurassic, focusing on these amphibious carnivores blinds us to the wider variety of crocodylomorphs that have come and gone over the past 245 million years. There were terrestrial pipsqueaks that ran on their tippy-toes, crocs that spent almost their entire lives at sea, and, of course, the 40-foot monsters that snatched dinosaurs from the water’s edge, among others. And as Molnar and colleagues demonstrate, one way to see this diversity is in the spine.

 

Terrestrisuchus, one of the earliest crocodiles. Art by Jaime Headden, CC BY 3.0.
Terrestrisuchus, one of the earliest crocodiles. Art by Jaime Headden, CC BY 3.0.

Today’s alligators, crocodiles, and gharials get around in a surprising variety of ways. They’re accomplished swimmers, they can drag their bellies along the ground or push up into a “high walk”, and little crocodiles can even gallop. But are these recent specializations, or are some of their capabilities ancient holdovers from the long, long history of their greater family? To investigate this question Molnar and colleagues created virtual models of five extinct crocs to see how their trunk flexibility matched up with their mode of life, checked against a model of a Nile crocodile spine verified by trunk-bending experiments on a carcass from the living species.

The spread of crocs in the new study bridged land and water. Two of the earliest, Terrestrisuchus and Protosuchus, were little terrestrial predators, while Pelagosuchus, Steneosaurus, and Metriorhychus document the change from semi-aquatic crocs to ones that propelled themselves around the seas with paddle-shaped limbs and fluke-tipped tails. From these reconstructed lifestyles Molnar and colleagues predicted that the land-dwelling crocs that moved more like mammals would have had spines that were more flexible up-and-down than from side-to-side and that the marine species would show increasing stiffness of the trunk to cope with moving through the water at speed, but their results yielded some surprises.

Millions and millions of years before the first whales took the plunge, the thalattosuchian crocs transitioned from nearshore life to one out in the open ocean. And, much like the whales, the prehistoric crocodiles went through a similar process of increasing flexibility in the spine in amphibious forms followed by greater trunk stiffness among the species that were full-time swimmers. Compared to Pelagosaurus, Molnar and coauthors found, the increasingly aquatic Steneosaurus and Metriorhychus had spines that were stiffer from side-to-side as their tails took one more of the propulsive work. These crocs swam in a variation of what dolphins do today, keeping the body rigid to plow through the water while all that power comes from swishes of the tail.

 

Estimating trunk flexibility of a Nile crocodile. From Molnar et al., 2015.
Estimating trunk flexibility of a Nile crocodile. From Molnar et al., 2015.

Based on the similar biomechanical lines of logic, Molnar and coauthors predicted that the early, land-dwelling crocs Terrestrisuchus and Protosuchus would have trouble bending side-to-side but would be flexible in the up-and-down plane. This would fit with the way they moved, with vertical movements of the spine as they pumped their legs forward-and-back beneath their bodies. But this isn’t what the researchers found. Terrestrisuchus, which would have more of a mammal-like walk than any of its relatives in the study, had a spine that was more flexible from side-to-side than in the vertical plane, and, in fact, would have been even stiffer along that axis because of a set of osteoderms – bony armor – that ran down the vertebral column. Trackways have confirmed that crocs like Terrestrisuchus really did walk with more upright limbs, but, Molnar and colleagues point out, the way the spine and legs worked together must have been different than we see in mammals.

Paleontologists have found plenty of other prehistoric crocs that could be thrown into the mix. But even from these five, it’s clear that crocs have not been in stasis since they first trotted out onto the evolutionary scene in the Triassic. The species we see around us today are really just a sliver of what once existed, and are specialized creatures in their own right rather than being stagnant holdovers from the depths of the Mesozoic. And given how much they’ve changed since their origin, I can’t help but wonder what might happen in the future. Should today’s crocodylians survive us, might any of them reprise the roles their predecessors took on land and in the seas?

Reference:

Molnar, J., Pierce, S., Bhullar, B., Turner, A., Hutchinson, J. 2015. Morphological and functional changes in the vertebral column with increasing aquatic adaptation in crocodylomorphs. Royal Society Open Science. doi: 10.1098/rsos.150439

Paleo Profile: Catalonia’s Little Ape

A restoration of Pliohates. Art by M. Palmero.
A restoration of Pliobates. Art by M. Palmero.

What did the last common ancestor of living apes look like? That’s a difficult question to answer. Today’s apes – gibbons, orangutans, gorillas, chimpanzees, and ourselves – are varied and specialized primates with relatively sparse fossil records. Depending on which paleoanthropologist you ask, then, the last common ancestor of today’s apes was either small and gibbon-like or more like a great ape, with gibbons hanging from a dwarfed branch of the family tree.

Pliobates might help resolve the debate. Described by David Alba and colleagues, this 11.6 million year old ape was on the evolutionary “stem” leading to the last common ancestor between the gibbons and the great apes. Rather than being a large-bodied primate, though, Pliobates was relatively small and more gibbon-like in form, an adept climber with some ability to swing beneath the branches of the Miocene forest.

Not that Pliobates was one of our direct ancestors. Molecular evidence suggests that the split between gibbons and the rest of the apes occurred between 16 and 17 million years ago, long before this newly-named ape. Instead, Alba and coauthors write, Pliobates is more of a “persistent type” – an archaic remnant of the apes that led up to the major hominoid division. More fossils will help outline how the actual transition occurred, but, for now, Pliobates is an echo of what our forebears might have been like at the dawn of the apes.

A reconstruction of Pliobates. From Alba et al., 2015.
A virtual reconstruction of the Pliobates skull. From Alba et al., 2015.

Fossil Facts

Name: Pliobates cataloniae

Meaning: Pliobates is a reference to the primate’s intermediate place between Pliopithecus and gibbons (Hylobates), while the species name honors where the fossil was found.

Age: About 11.6 million years old.

Where in the world?: Catalonia, southeastern Spain.

What sort of critter?: An Old World monkey – or catarrhine – closely related to the last common ancestor of today’s apes.

Size: About 10 pounds.

How much of the creature’s body is known?: A partial skeleton including elements of the limbs and a skull.

Reference:

Alba, D., Almécija, S., DeMiguel, D., Fortuny, J., Pérez de los Ríos, M., Robles, J., Moyà-Solà, S. 2015. Miocene small-bodied ape from Eurasia sheds light on hominoid evolution. Science. doi: 10.1126/science.aab2625

Previous Paleo Profiles:

The Unfortunate Dragon
The Cross Lizard
The South China Lizard
Zhenyuan Sun’s dragon
The Fascinating Scrap
The Sloth Claw
The Hefty Kangaroo
Mathison’s Fox
Scar Face
The Rain-Maker Lizard
“Lightning Claw”
The Ancient Agama
The Hell-Hound
The Cutting Shears of Kimbeto Wash
The False Moose
“Miss Piggy” the Prehistoric Turtle
Mexico’s “Bird Mimic”
The Greatest Auk