A Blog by Maryn McKenna

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.

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A Blog by Maryn McKenna

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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A Blog by Maryn McKenna

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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A Blog by Maryn McKenna

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.”

 

A Blog by Brian Switek

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

A Blog by Maryn McKenna

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.

A Blog by Erika Engelhaupt

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.

A Blog by Brian Switek

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

A Blog by Brian Switek

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

A Blog by Brian Switek

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

A Blog by Brian Switek

Paleo Profile: The Greatest Auk

Auk body sizes. From Smith, 2015.
Auk body sizes. From Smith, 2015.

At nearly three feet tall and weighing ten pounds, the Great Auk was the bulkiest member of its family of seabirds. But, despite its name, it wasn’t the largest of all time. Between 8.7 and 4.9 million years ago, there was an even bigger auk.

The bird, named Miomancalla howardae by paleontologist N. Adam Smith in 2011, was found in the Pliocene rock of southern California. It didn’t belong to the same group as modern auks and murres – called alcids – but was on just the next branch over, fitting into a wider group called pan-alcids. A sort of proto-auk, in other words. And in a new analysis of how the body sizes of pan-alcids changed over time, Smith found that Miomancalla howardae significantly surpassed the famous Great Auk in size.

Drawing on data from living and fossil birds, Smith estimates that Miomancalla howardae weighed 11.8 pounds. That’s almost a pound and a half heavier than Smith’s estimate for the Great Auk, the next largest bird in the sample. Not all auks and their relatives were huge – Smith estimates that the extinct Miocepphus mergulellus was only about four ounces – but, within this ancient and varied family, Miomancalla howardae was the greatest auk.

A partial skeleton of Miomancalla howardae. From Smith, 2011.
A partial skeleton of Miomancalla howardae. From Smith, 2011.

Fossil Facts

Name: Miomancalla howardae

Meaning: Miomancalla indicates this genus includes relatives of the bird Mancalla that were around during the Miocene, while the species name honors zoologist Hildegarde Howard.

Age: Around 4 million years old.

Where in the world?: The Capistrano Formation of southern California.

What sort of critter?: A bird closely related to alcids, or auks.

Size: About three feet tall and 11.8 pounds.

How much of the creature’s body is known?: A partial skeleton including a skull, elements of the limbs, sternum, hips, and two vertebrae, as well as an isolated humerus.

References:

Smith, N. 2011. Taxonomic revision and phylogenetic analysis of the flightless Mancallinae (Aves, Pan-Alcidae). ZooKeys. doi: 10.3897/zookeys.91.709

Smith, N. 2015. Evolution of body mass in the Pan-Alcidae (Aves, Charadriiformes): the effects of combining neontological and paleontological data. Paleobiology. doi: 10.1017/pab.2015.24

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”

A Blog by Brian Switek

Fossil Fuzz Gives “Ostrich Mimic” Dinosaur a New Look

A feathery Ornithomimus strolls through a forest in Cretaceous Canada. Art by Julius Csotonyi.
A feathery Ornithomimus strolls through a forest in Cretaceous Canada. Art by Julius Csotonyi.

It’s not hard to see why paleontologists call ornithomimosaurs the “ostrich mimic” dinosaurs.

The term is a little backwards. If anything, today’s ostriches are mimics of their distant Mesozoic cousins. But, all the same, Struthiomimus and Gallimimus of Jurassic Park fame had the same toothless, long-necked, burly-legged look exhibited by many of today’s flightless birds, albeit with long, three-clawed hands added on. And thanks to a spate of recent discoveries in Canada, we now know that the ornithomimosaurs shared the same plumage pattern as their living relatives, too.

For almost a century artists envisioned dinosaurs like Struthiomimus as shaved, clawed ostriches. And even as evidence mounted that these dinosaurs were fluffy, the fossil feathers themselves remained elusive. Finally, in 2012, paleontologist Darla Zelenitsky and colleagues announced evidence of dinofuzz on three specimens of Ornithomimus from the 75 million year old rock of Canada. While the juveniles seemed to be mostly fuzzy, the arms of one of the adults seemed to show evidence of large, long feathers that would have been superficially similar to those seen on the arms of modern ostriches.

The new Ornithomimus skeleton, showing the extent of feather and skin preservation. From van der Reest et al., 2015.
The new Ornithomimus skeleton, showing the extent of feather and skin preservation. From van der Reest et al., 2015.

Now Aaron van der Reest, Alexander Wolfe, and Philip Currie have added another fluffy Ornithomimus to the mix, and this one provides a new interpretation of just how feather-covered this dinosaur was.

Discovered in 2009 within Alberta’s Dinosaur Provincial Park, the partial Ornithomimus skeleton preserves soft tissue details never before seen in this species. Simple, wispy feathers run along the neck, chest, back, and tail, and the flexed lower leg is wrapped in fossilized skin.

Ornithomimus wasn’t completely covered with fluff from head to toe, van der Reest and coauthors conclude, but instead had a relatively even covering of simple fuzz over most of the body, with expanded feathers on the arms and naked legs. This distribution of plumage recalls the arrangement on ostriches, emus, and their relatives, the bare-legged look helping the birds dump excess heat to the cooler air. In short, Ornithomimus was an even better ostrich mimic than paleontologists expected.

Reference:

van der Reest, A., Wolfe, A., Currie, P. 2015. A densely feathered ornithomimid (Dinosauria: Theropoda) from the Upper Cretaceous Dinosaur Park Formation, Alberta, Canada. Cretaceous Research. doi: 10.1016/j.cretres.2015.10.004

A Blog by Brian Switek

Paleo Profile: Mexico’s “Bird Mimic”

Struthiomimus - a relative of the newly-named Tototlmimus - at the Oxford Natural History Museum. Photo by Brian Switek.
Struthiomimus – a relative of the newly-named Tototlmimus – at the Oxford Natural History Museum. Photo by Brian Switek.

North America has been a dinosaur hotspot for a century and a half. The Bone Wars of the 19th century, the Second Jurassic Dinosaur Rush of the early 20th, and the continuing profusion of new species and specimens all rely on the fossil riches held in the Mesozoic rocks of Canada and the United States. But the dinosaurs just to the south, in Central America, are only just now starting to stalk into the light. The latest to trot out into view is Tototlmimus, Mexico’s “bird mimic”.

For the moment, at least, the new dinosaur isn’t much to look at. Pieces of the feet and the hands are the only parts yet known. But paleontologist Claudia Inés Serrano-Brañas and colleagues make the case that these 72 million year old fragments really do represent a previously-unknown ornithomimid dinosaur that lived along the southern stretch of the long-lost subcontinent Laramidia. The articulation of the foot bones called metatarsals and the shape of one of the toe claws indicate that this dinosaur was an different from closely-related contemporaries that lived further north.

And Tototlmimus isn’t the only dinosaur of its kind found in Mexico. Martha Carolina Aguillon Martinez documented additional ornithomimids found near Coahuila, to the southeast of Sonora, in her 2010 thesis and hypothesized that the bones belonged to a new species. Theses are among the many mystery dinosaurs coming out of this part of the world, and, along with new finds in the U.S. and Canada, they’re starting to highlight the evolutionary explosion dinosaurs underwent in the Late Cretaceous. The dinosaurs found in this 80 to 70 million year old window vary along the latitudes and from basin to basin – pockets of novelty scattered across Laramidia. Finding and identifying the unexpected number of new dinosaur species is just the first step in figuring out why this span of time was so good for dinosaurian novelty.

Foot bones of Tototlmimus in multiple views. From Serrano-Brañas et al., 2015.
Foot bones of Tototlmimus in multiple views. From Serrano-Brañas et al., 2015.

Fossil Facts

Name: Tototlmimus packardensis

Meaning: “Bird mimic of the Packard Shale”, the word “Tototl” meaning “bird” in Náhuatl and the species name referring to the formation in which the dinosaur was found.

Age: Around 72 million years old.

Where in the world?: Sonora, northwestern Mexico.

What sort of critter?: One of the superficially ostrich-like ornithomimid dinosaurs.

Size: Comparable in size to related dinosaurs like Gallimimus.

How much of the creature’s body is known?: Fragments of the hands and feet.

References:

Inés Serrano-Brañas, C., Torres-Rodríguez, E., Reyes-Luna, P., González-Ramírez, I., González-León, C. 2015. A new ornithomimid dinosaur from the Upper Cretaceous Packard Shale Formation (Cabullona Group) Sonora, Mexico. Cretaceous Research. doi: 10.1016/j.cretres.2015.08.013

Rivera-Sylva, H., Carpenter, K. 2014. “Mexican Saurischian Dinosaurs” in Dinosaurs and Other Reptiles From the Mesozoic of Mexico, Rivera-Sylva, H., Carpenter, K., and Frey, E., eds. Bloomington: Indiana University Press. pp. 143-155

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

A Blog by Brian Switek

New Spiky-Haired Mammal Roamed During Dinosaurs’ Heyday

Spinolestes in its Cretaceous habitat. Art by Oscar Sandirisio.
Spinolestes in its Cretaceous habitat. Art by Oscar Sandirisio.

When I think of mammals from the Age of Dinosaurs, I think of a shrew-like critter snuffling through the nighttime undergrowth. I can’t help it. That’s the meme that museums, books, and documentaries popularized when I was a fossil-crazed kid.

The classic view of the meek mammal eking out a living in a world dominated by dinosaurs is too simplistic, though. Mesozoic mammals are undergoing a renaissance – much like their saurian oppressors got in the 1970s – and have turned out to be far more varied than anyone expected. Mammals of the Triassic, Jurassic, and Cretaceous were small, to be sure, but they counted swimmers, climbers, diggers, gliders, and more in their fuzzy family. They didn’t just live alongside the dinosaurs. They thrived. And the latest wee beastie to be added to their ranks is a spiky mammal uncovered from the 125 million year old rock of Spain.

The skeleton of Spinolestes. Photo courtesy the University of Chicago.
The skeleton of Spinolestes. Photo courtesy the University of Chicago.

Named Spinolestes xenarthrosus by paleontologist Thomas Martin and colleagues, the mammal belonged to an extinct group called eutriconodonts. The skeleton is about what you’d expect for a little shuffling insectivore. But what makes Spinolestes really special is what surrounded the Cretaceous bones. The critter was preserved with a halo of spine-like hairs.

Spinolestes wasn’t as prickly as a hedgehog. It probably looked a little more like a rat with a midline mohawk of bristles that the researchers term “protospines.” Each of them is made of a combination of several hair-like structures, and are associated with little bits of body armor made of keratin (the same stuff your fingernails are composed of). With the rest of the preserved soft tissue remnants, they show that mammals evolved a multi-layered coat of underfur, guard hairs, and spines relatively early in their history.

Think about that the next time you pet your cat or dog. When you run your hand over their soft coats, you’re touching the past.

Reference:

Martin, T., Marugán-Lobón, J., Vullo, R., Martín-Abad, H., Luo, Z., Buscalioni, A. 2015. A Cretaceous eutriconodont and integument evolution in early mammals. Nature. doi: 10.1038/nature/14905

A Blog by Brian Switek

How Giraffes Became Winners by a Neck

Giraffes have taught generations of students how evolution works. Not directly, of course. Communicating through nocturnal humming is a barrier to classroom instruction. But the modern giraffe – Giraffa camelopardalis – is often used as the textbook example of why Darwin and Wallace were right and Lamarck was wrong.

The setup goes something like this. Think of a little protogiraffe gazing hungrily at some tasty leaves high up on a tree. Someone from the Lamarckian school of evolution, the argument goes, might assume that the little giraffoid would stretch its neck to grab the lowest of those high leaves and, through exertion, develop a longer neck that it would then pass on to its offspring. Repeat for best results. A Darwinian, on the other hand, would expect the protogiraffes to vary in neck length and those that just happened to have slightly longer necks would be able to reach more food, survive longer, and mate often enough to pass on that variation to the next generation, who would play out the scenario over again.

While the scenario is a bit of a caricature of what Lamarck actually thought, it’s still useful in getting at the basic evolutionary equation that Darwin and Wallace independently distilled. Yet, despite the thought experiment’s popularity, we’ve known little of how the giraffe actually got its neck. Today’s tall browsers definitely evolved from shorter-necked ancestors, but how? A new study by New York Institute of Technology’s College of Osteopathic Medicine anatomist Melinda Danowitz and colleagues now provides an answer.

Giraffes aren’t the only animals to have evolved impressively-long necks. The sauropod dinosaurs and aquatic plesiosaurs, for example, stretched out to ludicrous lengths both by adding additional vertebrae to the column and elongating those individual bones. But giraffes have the standard number of neck vertebrae shared by most mammals – seven – with the first element in the thoracic part of the spine being modified as a possible eighth “neck” bone. But that’s it. Evolution, constrained by mammalian anatomy, molded giraffes in a different way than the long-necked saurians.

Danowitz and coauthors looked at anatomical landmarks on 71 giraffe vertebrae spanning 11 species from over 16 million years ago to the present, focusing on the second and third vertebrae in the neck. As it turns out, a proportionally-long neck isn’t new for these mammals.

The best candidate for a real protogiraffe, Prodremotherium, and an early giraffe named Canthumeryx already had neck bones that were long compared to their width. “[N]ot only did the giraffid lineage begin with a relatively elongated neck,” Danowitz and coauthors write, “but that this cervical lengthening precedes Giraffidae” – the giraffe subgroup typically thought of as encompassing all the long-necked forms.

The evolution of giraffe neck vertebrae. From Danowitz et al., 2015.
The evolution of giraffe neck vertebrae. From Danowitz et al., 2015.

But even though the earliest giraffes already had slightly-elongated neck bones, there was no “March of Progress” towards towering heights. At least one – and possibly more – giraffe lineages reverted to abbreviated necks hung around stout vertebrae. Giraffokeryx was among the earliest of the short-necked giraffes, browsing low-lying foliage around 12 million years ago, and within the last three million years Sivatherium, Bramatherium, and the okapi followed suit. The short-necks proliferated alongside their lankier relatives, which is why we still have both short- and long-necked giraffes today.

Truly long-necked giraffes didn’t evolve until about 7.5 million years ago. Samotherium, Palaeotragus, Bohlinia, the extinct Giraffa sivalensis and the living Giraffa camelopardalis preserve enough transitional features to let Danowitz and colleagues reconstruct how this stretching occurred. It wasn’t simply a matter of drawing out their vertebrae as if they were in some sort of anatomical taffy pull. The front half of the neck vertebrae became elongated in Samotherium and Palaeotragus, generating forms intermediate between today’s Giraffa and their foreshortened predecessors. Then, within the last two millions years or so, the lineage leading up to the modern Giraffa elongated the back half of their neck vertebrae, giving them even more reach and making them literally at the top of their class.

If you could assemble all these fossil bits and pieces into a short film replaying giraffe evolution, you wouldn’t end up with the smooth transformation of a small-statured herbivore into a towering, checkered browser. There’d be starts and stops and side stories, the ending not being a goal but a happenstance. In short, it’s time again to update those textbooks.

Reference:

Danowitz, M., Vasilyev, A., Kortlandt, V., Solounias, N. 2015. Fossil evidence and stages of elongation of the Giraffa camelopardalis neck. Royal Society Open Science. doi: