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Why It’s Crucial the New Superbug Was in a Urinary Tract Infection

Escherichia coli bacteria live in the intestines of humans and are a common cause of urinary tract infections.
Escherichia coli bacteria live in the intestines of humans and are a common cause of urinary tract infections.
Janice Haney Carr, Centers for Disease Control and Prevention

The alarm over the arrival of a grave new superbug in the United States is obscuring part of the story that is crucial to understanding what might happen next. Here it is: The woman who was carrying an E. coli containing resistance to the last-resort antibiotic colistin went for medical care because she had what felt like a routine urinary tract infection, a UTI for short.

The discovery of colistin-resistant bacteria is worrisome: Researchers have been watching for the arrival of this new superbug  for several months. But that it was found in  urine sample puts the discovery into a larger context. Highly drug resistant urinary tract infections happen potentially hundreds of thousands of times a year just in the United States. A small, dedicated corps of researchers has been trying for years to emphasize that these infections represent a serious danger, an unexamined conduit of bacterial resistance from agriculture and meat into the human population, and have mostly been dismissed.

Now that the new-new superbug has thrown light on the problem, will someone listen?

The Centers for Disease Control and Prevention weighed in Tuesday with a statement and a press briefing with health officials from Pennsylvania, where, last week, military researchers said they found the mcr-1 gene in an E. coli bacterium carried by a woman living there.

There are up to 8 million urinary-tract infections in the U.S. each year, and probably at least 10 percent, or 800,000, are antibiotic-resistant.

The MCR gene is important because it represents a breach in the last line of antibiotic defense: It confers protection against colistin, one of the oldest antibiotics out there, and one of the few that continues to work even against bacteria that resist multiple other drugs. Colistin was seldom used in people until recently because it is toxic, but agriculture has been using it enthusiastically for decades, which has seeded resistance through the bacterial world.

And those highly drug-resistant bacteria are turning up in urinary-tract infections. Why UTIs? Because E. coli bacteria are carried in feces, which can easily spread to the urethra and cause urinary-tract infections, especially in women. I’ve written about this several times; the long version in MORE magazine, and, even longer, in a collaborative investigation between the Food and Environment Reporting Network, the Atlantic, and ABC News.

The short version is this: Up to 8 million urinary-tract infections occur in the United States each year, and each year, a growing and significant proportion—hard to measure, but probably at least 10 percent, or 800,000—are antibiotic-resistant.

This has been happening with such frequency that it has actually changed medical practice. Medical specialty societies have been advising doctors for several years now that they should always do a test to determine which antibiotic will work for a UTI, rather than prescribing based on a standard checklist.

But only a few researchers have investigated why that tide of resistance is rising. What they have found is that these resistant UTIs infections are not random and singular, but instead constitute a focused epidemic, caused by particular sets of E. coli that bear the same resistance signatures as ones found in meat animals given antibiotics.

This idea has had difficulty gaining traction, because UTIs are usually dismissed as a minor problem, something that causes a few days of annoyance and requires a few days of antibiotics to fix. (And, not coincidentally, because they overwhelmingly happen to women.) But when UTIs go untreated—which is effectively what happens when the antibiotic administered for them doesn’t work —they climb up the urinary system from the bladder, into the kidneys, and thence into the bloodstream.

At that point, the minor problem becomes literally life-threatening. And resistant UTIs are not only a problem for the individual sufferer: They also pose the possibility of infecting others, if the original victim goes into a hospital for treatment and carries the resistant organism unrecognized in their system.

One reason it has taken so long to recognize this problem is that there is no single surveillance network that could capture all the resistance patterns in all those UTI sufferers, and compare them. There is also the problem of belief: It’s just difficult to imagine that something as minor as a UTI could be the signal of something as grave as a widespread epidemic.

Because of that, the MCR finding in Pennsylvania could end up being fortunate—no only for detecting a grave development early, but also for shining a light on a danger that has been growing, unrecognized, for a while.

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Africa’s Yellow Fever Outbreak is a Glimpse of Our Connected Future

Zika virus has been earning all the headlines, because it is already affecting Americans—including 300 pregnant women, according to a new CDC estimate—and is expected to move into U.S. mosquitoes as the summer bug season starts.

But outside the United States, another mosquito-borne disease is attracting the world’s attention, and it may predict more than Zika does about how epidemics will move around the world in the future. The disease is yellow fever, the epicenter of the outbreak is Angola, and the force that could push it around the globe is Chinese investment in the developing world.

A member of the Angolan military administers a yellow fever vaccine to a child at 'Quilometro 30' market, Luanda, Angola, in February.
A member of the Angolan military administers a yellow fever vaccine to a child at ‘Quilometro 30’ market, Luanda, Angola, in February.

The Angolan outbreak began in December and is large: more than 2,400 cases and 298 deaths, according to the latest report from the World Health Organization. It was originally centered on the capital, Luanda, and has spread through the western half of the country. It has also hopped borders: There are 42 cases in the neighboring Democratic Republic of the Congo and two cases in Kenya (along with an an unrelated outbreak in Uganda, between Kenya and the DRC).

But what has some researchers unusually alarmed is that there are 11 cases in China: workers or families who returned from Angola into an area where yellow fever does not now exist—but the mosquitoes that spread it do.

“Approximately two billion people live in Aedes aegypti-infested countries in Asia,” Sean Wasserman, Paul Anantharajah Tambyah, and Poh Lian Lim, researchers from South Africa and Singapore, say in a paper published online in May in the International Journal of Infectious Diseases. “The prospect of a yellow fever introduction into this unvaccinated population poses a major global health threat,” they write.

Maps of Angola showing month-to-month spread of yellow fever.
Maps of Angola showing month-to-month spread of yellow fever.
Courtesy the World Health Organization.

Yellow fever is a persistent problem in West Africa, where the virus cycles between monkeys and mosquitoes and spills over to humans. That happens first in villages at forest edges, and then in cities as infected people carry the virus to urban mosquitoes. (These happen to be the same kinds of mosquitoes that transmit Zika, and also chikungunya and dengue: voracious day-biters that breed in pools of water as small as a bottle cap, and attack people not only outdoors but inside houses.)

A vaccine prevents yellow fever, but only about 70 percent of Angolans receive it, not enough to create the herd immunity that would prevent an outbreak from taking hold.

That is a serious gap, because unlike the other diseases carried by Aedes mosquitoes—which except for the birth defects of Zika mostly cause mild illnesses—yellow fever can kill. As many as one in four of those who develop symptoms go on to have liver and kidney failure, jaundice (which gives the disease its name) and bleeding, and one in four of those victims die.

Fumigating a Texas town infected with yellow fever, 1873.
Fumigating a Texas town infected with yellow fever, 1873.
Photograph by North Wind Picture Archives, Alamy

Yellow fever has never taken hold in Asia. Lack of familiarity with the disease may explain why the 11 infected people who returned to China were not vaccinated, despite Chinese regulations saying they should have been.

They probably have a lot of company: Angola is one of China’s biggest investment targets in Africa, for cropland and for energy. In 2009, according to the Centre for Chinese Studies in South Africa, China bought almost one-third of Angola’s crude oil. The Chinese expatriate community in Africa is estimated to be 20,000 people, who include not just semi-permanent residents but temporary construction workers who are shipped from job to job.

Because the continents harbor the same mosquito species—Singapore, where Tambyah and Lim work, wages a constant battle against dengue—the researchers suggest that just one unknowing traveler carrying yellow fever virus in their blood could spark a chain of transmission. That could trigger what The Economist warned in an editorial earlier this month would be “a preventable tragedy,” an epidemic as explosive as chikungunya after it arrived in India in 2005, or Zika in the Americas this year.

The authors of the new paper say: “The current scenario of a yellow fever outbreak in Angola, where there is a large community of non-immune foreign nationals, coupled with high volumes of air travel to an environment conducive to transmission in Asia, is unprecedented in history… The growing number of imported cases in China shows how critical it is to recognize this risk now in order to take adequate preventive action so that a global catastrophe can be averted.”

The action that is most needed is vaccination. Monday marked the start of the World Health Assembly, the annual conclave of member states of the World Health Organization. In the opening meeting, director general Dr. Margaret Chan delivered what she called a “stern warning” on failures to vaccinate adequately. (Chan’s term ends in June 2017, so she may have felt safe being blunt—though she did not name names.)

A Rockefeller scientist administers yellow-fever vaccine in Santiago de Guayaquil, Ecuador, in the 1920s.
A Rockefeller scientist administers yellow-fever vaccine in Santiago de Guayaquil, Ecuador, in the 1920s.
Photograph Courtesy of Rockefeller Foundation

“The world failed to use an excellent preventive tool to its full strategic advantage. For more than a decade, WHO has been warning that changes in demography and land use patterns in Africa have created ideal conditions for explosive outbreaks of urban yellow fever,” she said. “Yellow fever vaccines should be and must be used more widely to protect people living in endemic countries.”

Because of the Angolan outbreak, yellow fever vaccines are in short supply worldwide, as Kai Kupferschmidt reported in Science in April. Only four factories, in Russia, Brazil, France and Senegal, make the compounds, and one is about to close. But in May, a WHO emergency committee declined to rank yellow fever as a “public health emergency of international concern.” As global health-law scholars Daniel Lucey and Lawrence Gostin wrote in JAMA two weeks ago, that designation could have given the agency increased leverage to negotiate with vaccine manufacturers. (Following the decision, the committee advised “rapid evaluation” of dividing vaccine doses so that more people can be protected.)

But that may not be enough. In its editorial, The Economist did the vaccine math:

Should yellow fever come to Asia, some experts reckon that over 100m people living in large, well-connected cities would need to be vaccinated. That would rapidly exhaust the world’s supply of vaccine, even if only a fifth of a dose (thought to be enough to confer immunity to adults) were administered to each person who needed it. In the long term, if the disease establishes itself in Asia’s jungles, over 1 billion more people could be at risk…

The world has already failed to thwart yellow fever effectively in Africa. That threatens to put millions more lives at risk.

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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.

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Can We Keep Zika Out of the US Blood Supply?

A doctor draw blood from Luana, who was born with microcephaly, at the Oswaldo Cruz Hospital in Recife, Brazil, Thursday, Jan. 28, 2016. Photograph by Felipe Dana, AP
A doctor draw blood from Luana, who was born with microcephaly, at the Oswaldo Cruz Hospital in Recife, Brazil, Thursday, Jan. 28, 2016. Photograph by Felipe Dana, AP

If Zika virus comes to the United States, will the US blood supply be at risk?

Because the disease has demonstrated that it can pass via blood from mother to fetus, and via other bodily fluids between sexual partners, the question lurks in the back of most discussions of Zika’s likely arrival on the US mainland. And because there is not now a test for donated blood, keeping the virus out of the blood supply relies on people adhering to restrictions published by the Food and Drug Administration that ask travelers to defer donating for a period of time—an imprecise deterrent, but currently as good as it gets.

The concern for the blood supply is reasonable. In 2002, when West Nile virus was newly arrived in the United States, transfusions given to a teenage accident victim—who died of her injuries, and became an organ donor—caused that disease to pass to all four recipients of her organs. Dengue, another mosquito-borne illness that is burgeoning in Central and South America and has become established in south Florida, has also passed between blood donors and recipients, though there are only a few cases on record. And Zika virus was identified in 3 percent of donated blood in French Polynesia in late 2013 and early 2014, when the virus first landed in that area.

(See: Pictures Capture Daily Battle Against Zika Mosquitoes)

The concern has been sharpened by a new analysis, published Wednesday in the journal PLoS Currents Outbreaks, that plots the range of the mosquito species known to carry Zika against the numbers of travelers who arrive from the Zika zone. The researchers—from several US government agencies, North Carolina State University and University of Arizona, and Durham University in England—predicted that cities within the mosquito’s range are at highest risk of local transmission of Zika if they have international airports, or airports receiving connecting flights from those hubs. Other cities receiving large numbers of travelers from the Zika transmission zone were at moderate or lower risk if they fell near the edge of the mosquito’s range. So, for instance, Miami, Orlando, Jacksonville, Tallahassee, and New Orleans were at high risk of receiving the disease; New York, Atlanta and Houston were at moderate risk, and Dallas, Denver and Los Angeles at low risk.

A map of cities most at risk for arrival and local transmission of Zika virus.
A map of cities most at risk for arrival and local transmission of Zika virus.
Graphic from Monaghan et al., PLoS Current Outbreaks, March 16, 2016.

What was jaw-dropping in the study, though, were the sheer numbers of people who arrive in US cities from the Zika transmission zone: up to 1 million per month in Miami and New York, 500,000 per month in Atlanta, Houston, New York and Dallas, and millions per month through the ground border crossings of San Diego, El Paso and Laredo.

To prevent Zika contaminating the blood supply, the FDA issued guidelines last month addressing blood donation and this month regarding donated cells and tissues. For blood donation, the agency recommended that blood agencies ask people to defer donation for four weeks after experiencing Zika symptoms, traveling in the Zika transmission zone,  or having sex with a man who either had the symptoms or traveled in the Zika zone. For tissues such as ligaments and corneas, and cells (which include sperm and eggs), the agency extended the deferral to six months. The FDA has not placed any restrictions on donation of solid organs, arguing that because they are both life-saving and in short supply, the benefit outweighs the risk.

Blood donations.
Blood donations.
Photograph by MikeHT, Flickr (CC).

Dr. Matthew Kuehnert, who is director of the office of blood, organ and other tissue safety at the Centers for Disease Control and Prevention, and is serving as the lead for the blood safety team in the CDC’S Zika response, said knowing how far to go to protect the blood supply is challenging because data is so sparse.

“There is little that we know about transfusion transmission of Zika, although I think we should assume it can happen,” he said by phone. “From the data that has been collected on Zika, about 80 percent of people don’t know they are infected. There is a period of viremia”—when virus circulates in the blood—”but we don’t know how long that viremia is. It is thought to be 7-10 days, but as we start to collect more data we may find it is longer than that.”

“It is possible we could get a transfusion or transplant transmission case before we even know local transmission of Zika is occurring.”

A problem, Kuehnert pointed out, is that because symptoms are the signal of an infection, only people who show signs of Zika infection—mostly fever, headache, rash and red eyes—are being interviewed and tested to add to knowledge about the disease. People who do not experience symptoms are not visible to investigators. They also become viremic; but since they are not interviewed or tested, the duration of their viremia, when the virus in their blood could pass into a blood donation, is not being uncovered. And there are early signals that, even after it passes out of the blood, the virus can take shelter in other tissues and fluids. “Zika can be sexually transmitted long after viremia is thought to be gone, so there are likely protected sites where it can hide,” he said. “Thus there might be blips of viremia occurring after symptoms have resolved. So there is a lot of potential for transfusion transmission.”

Those considerations apply in areas where Zika is not yet locally established. Where it is—which in the United States is Puerto Rico (160 cases as of March 9), American Samoa (13 cases) and the Virgin Islands (1 case)—blood is assumed to be a risk, and workarounds are being urgently sought. Because there is no test for Zika in donated blood—an approved test is “weeks to months away,” Kuehnert said—the only alternative is to use what are called “pathogen reduction” treatments, which inactivate viruses. Currently, pathogen reduction can only be used on platelets and plasma; red blood cells can be altered by pathogen reduction, and authorities are urgently searching for better techniques..

In a sign of how quickly an epidemic can upset the balance of blood supplies, Puerto Rico is now receiving outsourced blood from the US mainland, via a joint effort of three blood-collection agencies—the  American Red Cross, Blood Centers of America, and America’s Blood Centers—and the Department of Health and Human Services. The CDC estimates the current need for clean blood and blood products in Puerto Rico is 2,500 units of red blood cells, and an additional 1,000 units of other blood products, every week.

Despite the protections put in place by the FDA, public health authorities are braced for the possibility that transfusion-associated Zika could begin occurring in the United States. “This could happen at any time,” Kuehnert acknowledged.

He added: “It is possible we could get a transfusion or transplant transmission case before we even know local transmission of Zika is occurring,” because the illness that necessitates a transfusion—or the immunosuppressive drugs that transplants recipients take—make them more vulnerable to disease. “We are doing a lot of work to be prepared.”


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For Fear of Zika, CDC Recommends Pregnant Women Not Travel

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

(This post has been updated with news of the first Zika birth defects case found in the United States.)

In an extraordinary statement likely to launch international controversy, the US Centers for Disease Control and Prevention recommended Friday evening that pregnant women not travel to 14 countries and territories—the commonwealth of Puerto Rico, and Brazil, Colombia, El Salvador, French Guiana, Guatemala, Haiti, Honduras, Martinique, Mexico, Panama, Paraguay, Suriname, and Venezuela—for fear of birth defects associated with infection by mosquito-borne Zika virus.

The recommendation comes in the form of a “Level 2 travel alert,” which in the agency’s lingo represents a warning to “practice enhanced precautions.” In the Zika announcement, the CDC says that pregnant women “should consider postponing travel,” adding, “pregnant women who must travel to one of these areas should talk to their doctor or other healthcare provider first and strictly follow steps to avoid mosquito bites.” Women planning to become pregnant, it says, “should consult with their healthcare provider before traveling to these areas.”

Zika virus has been exploding in South and Central America. In Brazil, where the virus arrived just seven months ago, there have been more than 1 million cases of infection, and more than 3,500 cases of a rare birth defect called microcephaly, babies born with smaller than normal skulls and brains.

The warning follows the CDC’s own analysis of samples from two stillborn children and two who died after birth who suffered microcephaly. The agency said:

“For the two full-term infants, tests showed that Zika virus was present in the brain. Genetic sequence analysis showed that the virus in the four cases was the same as the Zika virus strain currently circulating in Brazil.  All four mothers reported having experienced a fever and rash illness consistent with Zika virus disease during their pregnancies.”

The countries and territories named by the CDC Friday are jurisdictions where Zika virus transmission has been confirmed. (On Friday, one other country not mentioned in the CDC’s list, Guyana, also reported cases, according to Caribbean media.)

The warning not to travel—made, the CDC said, “out of an abundance of caution”— is likely to be controversial. It warns women away from the site of the Olympics, which take place in Rio de Janeiro in August, as well as from most of the beach and tourist economies of Central and South America. In what may be a first, it warns citizens of the United States from entering a part of the United States, the unincorporated territory of Puerto Rico.

Puerto Rico is part of the advisory because Zika infections have occurred there. Zika has also landed in Texas, via a local resident who was infected in Latin America and returned there, but has not been transmitted locally.

How far the risk of imported Zika might be spread by local mosquitoes.
How far the risk of imported Zika might be spread by local mosquitoes.
Graphic from Bogoch et al., The Lancet.

But researchers from several countries said in The Lancet Thursday that infected travelers should also be considered a risk to their home countries, because virus levels in their blood could be high enough to pass Zika back to local mosquitoes when they return.

As a result, they said, some among the 9.9 million travelers who leave from Brazilian airports every year could bring the disease with them and establish it at their destinations. The US receives 2.7 million travelers yearly from Brazil; Italy, 419,000; France, 404,000; and China, 84,000.

The main mosquito species responsible for spreading Zika, Aedes aegypti, flourishes in the far Southern US, and a second species that may transmit the virus, Aedes albopictus, ranges as far north as New York. Thus, the researchers said, if Zika virus came to the United States, 22.7 million people — primarily in Southern California, South Texas and Florida — would be at risk of contracting the disease year-round, and possibly 60 million seasonally if both mosquito species were involved.

Update: Late Friday evening, the CDC also sent out a HAN, a Health Alert Network advisory to health care workers to help them recognize possible cases of Zika. It’s here.

Update 2: Also late Friday, the Hawaii State Department of Health announced that it has identified the first case of Zika-related birth defects in the US, in a baby born on Oahu to a woman who became pregnant while living in Brazil last summer.

“This case further emphasizes the importance of the CDC travel recommendations released today,” state epidemiologist Dr. Sarah Park said in the announcement. “An astute Hawaii physician recognized the possible role of Zika virus infection, immediately notified the Department of Health, and worked with us to confirm the suspected diagnosis.”

So far six Hawaii residents have been found infected with Zika, the announcement said, but all caught the disease outside the state. Hawaii has made Zika a reportable disease, which means physicians who recognize a case are obliged to inform the state department.

Previous posts in this series:

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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.”


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Bloodletting Is Still Happening, Despite Centuries of Harm

An illustration of a bloodletting, circa 1675.
An illustration of a bloodletting, circa 1675.

In the shadow of India’s largest mosque, the gutters run red with blood.

It’s a bizarre scene, if you’ve never seen a modern-day bloodletting. First, men wrap patients’ arms and legs with straps as tourniquets, to control the blood flow. Then they use razor blades to make tiny pricks in the hands and feet, and blood trickles into a concrete trough stained red with the day’s work.

The bleeding people look pretty happy, though. After all, they’ve paid for the service. They come to be cured of everything from arthritis to cancer.

(Video: Meet the bloodletters of Delhi and their patients.) 

But why? How has the bloodletting business, which many doctors today would rank along with reading bumps on the head as olde timey quackery, managed not to dry up?

The appeal seems to be in its simple logic.

Muhammad Gayas runs his bloodletting business in the garden of the Jama Masjid mosque in Old Delhi. He says pain and illness happen “when the blood goes bad,” which is pretty much the same basic premise that bloodletters have sold the public since Hippocrates advocated balancing the four humors—blood, black bile, yellow bile, and phlegm—more than 2,000 years ago. 

Bloodletting has been practiced around the world even longer than that, tracing at least 3,000 years ago to the Egyptians. It remained an obsession among many Western doctors through the 19th century, and was still a recommended treatment for pneumonia in a 1942 medical textbook—lest you think it went out after the Middle Ages along with the laying on of leeches. (Oh, and leeches still get some play, too, mainly for drawing down pockets of blood after plastic surgery or vascular microsurgery.)

So Does Bloodletting Ever Work?

It may be helpful for people with a few particular blood abnormalities. Doctors still use bloodletting, for instance, in cases of polycythemia—an abnormally high red blood cell count—and in a hereditary disease called hemochromatosis, which leaves too much iron in the blood.

I also came across a preliminary study suggesting vascular benefits in some diabetics with high iron levels, but this is far from a general treatment for the disease. Another small study in BMC Medicine got a lot of press in 2012 for showing that 33 people who gave up to a pint of blood had improved cholesterol ratios and blood pressure six weeks later compared with people who didn’t give blood, which the doctors also attributed to a reduction of iron levels. (Note that the amount of blood removed in the study was fairly low—a pint is about as much as you’d give when donating blood, which for the record is  a great thing for healthy people to do and is not the same thing as bloodletting.) 

When George Washington developed a swollen sore throat in 1799, doctors drained nearly half his blood and created blisters in his throat. Within a day, he died.
When George Washington developed a swollen sore throat in 1799, doctors drained nearly half his blood and created blisters in his throat. Within a day, he died.
Life of George Washington, Junius Brutus Stearns, 1851

But the design of that study doesn’t rule out a placebo effect—which has certainly contributed to bloodletting’s popularity in the past. What’s more, other studies suggest that too little iron is bad for cardiovascular health, so again, the potential benefit of removing blood is unclear.

Meanwhile, depleting the body’s blood supply can be risky. Not only is there the risk of losing too much blood, causing a dangerous drop in blood pressure and even cardiac arrest, but people who are already sick take their chances with infection or anemia. Not to mention that in most cases, bloodletting doesn’t cure what ails you.  

So no, we don’t need to revive the tradition of the neighborhood bloodletter. In a sense, though, their legacy is still around: Red-and-white barber poles represent blood, bandages, and the stick that patients would grip during barbers’ days as bloodletters.

How Bloodletting Bled Out

It took the great bloodletting wars of the 1800s to begin turning the tide against the practice. The prominent doctor Benjamin Rush (a signer of the Declaration of Independence) set off a fury when he began bleeding people dry during the 1793 yellow fever epidemic in Philadelphia. By all accounts, Rush was a bloodletting fanatic and in general a real piece of work: “unshakable in his convictions, as well as self-righteous, caustic, satirical, humorless, and polemical,” writes doctor Robert North in a biography.

Rush recommended that up to 80 percent of his patients’ blood be removed, and during the yellow fever outbreak, North recounts that “so much blood was spilled in the front yard that the site became malodorous and buzzed with flies.”

Bloodletting’s detractors grew in numbers after that, and eventually Pierre Louis, the founder of medical statistics, began convincing doctors to rely on statistical evidence over anecdotal “recoveries” of patients who had been bled. A particularly impressive analysis showed that bloodletting did not help pneumonia victims in Europe, and after bitter disputes among doctors in the 1850s, the practice began dying out.

In fact, one history of bloodletting refers to the stamping out of the practice—over the objections of the medical establishment, no less—as a triumph of reason and “one of the greatest stories of medical progress.”

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Leaky Vaccines Enhance Spread of Deadlier Chicken Viruses

Over the past fifty years, Marek’s disease—an illness of fowl—has become fouler. Marek’s is caused by a highly contagious virus, related to those that cause herpes in humans. It spreads through the dust of contaminated chicken coops, and caused both paralysis and cancer. In the 1970s, new vaccines brought the disease the under control. But Marek’s didn’t go gently into that good night. Within ten years, it started evolving into more virulent strains, which now trigger more severe cancers and afflict chickens at earlier ages.

Andrew Read from Pennsylvania State University thinks that the vaccines were responsible. The Marek’s vaccine is “imperfect” or “leaky.” That is, it protects chickens from developing disease, but doesn’t stop them from becoming infected or from spreading the virus. Inadvertently, this made it easier for the most virulent strains to survive. Such strains would normally kill their hosts so quickly that they’d die out. But in an immunised flock, they can persist because their lethal nature has been neutered. That’s not a problem for vaccinated individuals. But unvaccinated birds are now in serious trouble.

This problem, where vaccination fosters the evolution of more virulent disease, does not apply to most human vaccines. Those against mumps, measles, rubella, and smallpox are “perfect:” They protect against disease and stop people from transmitting the respective viruses. “You don’t get onward evolution,” says Read. “These vaccines are very successful, highly effective, and very safe. They have been a tremendous success story and will continue to be so.”

He is more concerned about the next generation of vaccines that are being developed against diseases like HIV and malaria. People don’t naturally develop life-long immunity to these conditions after being infected, as they would against, say, mumps or measles. This makes vaccine development a tricky business, and it means that the resulting vaccines will probably leak to some extent. “This isn’t an argument against developing those vaccines, but it is an argument for ensuring that we carefully check for transmission,” says Read.

“The candidate Ebola vaccines are also foremost in my mind,” he adds. “Some of the monkey trials suggest that they may be perfect, but we need to be very confident that they don’t leak. If they do, and some vaccinated individuals are capable of passing on Ebola, that might lead to the evolution of very dangerous pathogens.”

He is also concerned about animal vaccines, which are often leaky. These include vaccines against Newcastle disease in poultry, Brucella in livestock, and especially bird flu. When bird flu outbreaks hit American and European farms, the birds are culled. But in Southeast Asia, they’re often vaccinated, “and those vaccines are leaky,” says Read. “It creates an analogous situation to Marek’s.” The birds might survive more lethal forms of the virus, which they could then spread to each other—and potentially to people.

Read first proposed the “imperfect vaccine hypothesis” back in 2001, on purely theoretical grounds. It proved controversial, not least because he had neither experimental evidence nor case studies to support the idea. Then, a colleague told him that the hypothesis might explain the increasing virulence of Marek’s disease. “I wrote the name down, misspelled it, and couldn’t find anything in the literature!” Read says. He only heard about the condition again when he was asked to speak at a Marek’s conference. There, someone put him in touch with Marek’s expert Venugopal Nair from the Pirbright Institute.

The duo infected vaccinated and unvaccinated chicks with five different strains of Marek’s virus, of varying virulence. They found that when unvaccinated birds are infected with mild strains, they shed plenty of viruses into their surroundings. If they contract the most lethal strains, they die before this can happen, and their infections stop with them. In the vaccinated chicks, this pattern flips. The milder strains are suppressed but the lethal ones, which the birds can now withstand, flood into the environment at a thousand times their usual numbers.

Read and Nair also found that the “lethal” strains could spread from one vaccinated individual to another, and that unvaccinated chickens were at greatest risk of disease and death if they were housed with vaccinated ones.

All of this is consistent with the imperfect vaccine hypothesis. It doesn’t prove that imperfect vaccines drove the evolution of today’s extra-virulent strains, “and we may never know for sure why those evolved in the first place,” Read writes. Other factors, like the fact that modern chickens are genetically similar or raised in dense, crowded conditions, may have also played a role. Still, it’s at least clear that vaccines can keep virulent strains in circulation. “For the chicken industry, these results are actually an argument for getting the vaccine,” says Read. “Any chicken that doesn’t get it is at even greater risk than it would be in the 1950s.”

“This work may drive change in the way that vaccines are developed and tested, so that there is much greater emphasis on their ability to prevent infection and transmission, rather than only on their ability to prevent clinical disease,” says Joanne Devlin from the University of Melbourne.  “I think that would be a positive step.”

Katherine Atkins from the London School of Hygiene and Tropical Medicine agrees. “While more theoretical work is now being conducted prior to vaccine roll-outs,” she says, researchers need to look beyond how vaccines curb epidemics. They must also consider “the long-term evolutionary consequences of new vaccine introduction.”

But Vincent Racaniello from Columbia University says, “We still do not have any proof that allowing a virus to replicate in a vaccinated individual will select for more virulent viruses.” The new results simply show that leaky vaccines allow virulent viruses to spread—not that they allow those viruses to evolve in the first place. The only way of doing that is to infect vaccinated chickens with mild strains and see if more virulent ones arise after many rounds of transmission.

Racaniello is also unconvinced that the effect would generalise to other vaccines. For example, the Salk polio vaccine—one of two that are used—is a little leaky. “People who are immunized can be infected with poliovirus and the virus can replicate in their guts, be shed, and transmitted to others,” says Racaniello. “This behaviour has been well documented in human populations, yet the virulence of poliovirus has not increased for the 50+ years during which this vaccine has been used.”

That is no reason to rest on our laurels, says Read. It’s important to at least check for the emergence of deadlier viruses if vaccines are imperfect—and perhaps to take preventative measures. For example, a leaky malaria vaccine could be paired with bed nets that would stop mosquitoes from spreading more virulent strains of malarial parasites to unvaccinated people. “If someone developed [such a vaccine] and it worked, we should go ahead and use it, but not think of it as a magic bullet,” says Read. “I’d say that anyone who is vaccinated against malaria should be under a bed net too.”

Reference: Read, Baigent, Powers, Kgosana, Blackwell, Smith, Kennedy, Walkden-Brown & Nair. 2015.  Imperfect Vaccination Can Enhance the Transmission of Highly Virulent Pathogens. PLoS Biol http://dx.doi.org/10.1371/journal.pbio.1002198

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How Giant Prawns Could Fight Tropical Disease and Poverty

In 1986, after almost five years of construction, the Diama Dam was finally completed along the mouth of the Senegal River. The dam stopped saltwater from intruding upstream, thus creating a stable reservoir of freshwater for farmers and for Senegal’s capital city of Dakar.

But it also had unintended consequences. By restraining the saltwater, the dam favoured the growth of freshwater algae and plants, which in turn fed large numbers of snails. The snails are hosts for parasitic flatworms that cause schistosomiasis—a horrible water-borne disease that damages the kidneys, bladder, intestines, and liver. As the snail population boomed, they triggered a huge outbreak of schistosomiasis, which spread with unprecedented speed and still persists today. In some places, more than 90 percent of villagers are infected. In damming the river, Senegal also damned the people along it.

But help is at hand. A team of scientists led by Susanne Sokolow from Stanford University has been working on a way of stopping the outbreak by bringing the snails—and their parasites—under control. Their plan? Add prawns.

The lower Senegal River used to be home to a hand-sized, long-clawed prawn called Macrobrachium vollenhovenii, that would devour the parasite-carrying snails. Every year, the female prawns would walk downstream to the estuary to lay their eggs; later, the larvae would swim back upstream. The Diama Dam cut off both routes and exterminated the prawns. By reintroducing them, Sokolow hopes to control the rampant snails and bring schistosomiasis to heel.

“It’s not a new idea,” she says. In 1999, a team of scientists successfully used crayfish to reduce both snail populations and schistosomiasis infections in a couple of Kenyan villages. Unfortunately, they used an American crayfish that had been introduced to Africa several decades before, and was considered an invasive species. “There was a strong backlash from the environmental community, so nothing ever came of it,” says Sokolow.

To avoid a similar backlash, her team—known as The Upstream Alliance—used M.vollenhovenii, an indigenous West African species, rather than the foreign crayfish. Working with parasitologists Armand Kuris and Kevin Lafferty, Sokolow ran several lab tests to confirm that the prawn would actually eat the infected snails. (It did, and voraciously so.)

Buoyed by that success, the team staged a pilot experiment in June 2011. At a village called Lampsar, they netted off a part of the river that villagers frequent, and stocked it with prawns. At a nearby village, slightly upstream but otherwise as similar to Lampsar as possible, they did nothing.

Before the prawns arrived, the Lampsar villagers were five times more likely to carry schistosomiasis parasites than their upstream peers. After they added the prawns, Sokolow’s team treated anyone who was infected with drugs. Eighteen months later, they checked for re-infections. This time, they found the opposite ratio: the upstream village had four times as much schistosomiasis as Lampsar, whose waters contained half as many snails and a fifth as many parasite-shedding ones. The village, which had been written about since World War II as a hotspot for schistosomiasis, had become almost free of disease.

In other words: the prawns had worked.

Sokolow would be the first to admit that with just two villages, it is impossible to draw any broader conclusions about how effective the prawns might be. “We know that it was just a demonstration,” she says. The promising results are consistent with ecological theory, the lab experiments, and the Kenyan trial, but “we need to do a wide-scale replicated study and really nail the proof of concept.”

Sokolow’s colleague Giulio de Leo created a mathematical model to predict what would happen. He found that at a certain density—0.3 prawns per square metre—the prawns will completely eliminate schistosomiasis by eating any newly infected snails before they can release their own parasites. This will take at least 20 years, but not if infected villagers are also treated with the drug praziquantel.  Then, schistosomiasis ought to decline and disappear within just five years.

De Leo says that this combined approach has many advantages over praziquantel alone, effective though the latter is. “After praziquantel administration, villagers in rural areas of Senegal have no other option than go back to river and step into schistosome-contaminated waters for their daily chores, thus getting re-infected over and over again,” says de Leo. In other words, the villagers might briefly shake off the disease, but the river will never let them forget it.

By contrast, the prawns should prevent infections in the first place, by decimating the snails that harbour and transmit the parasites. Others have tried to do this by attacking the snails with toxic “molluscicides”. Like praziquantel, that was just a temporary measure, and one heavy in collateral damage: the chemicals killed off many fish and crustaceans, too. “Re-introduction of native prawns may offer an ecologically friendly and much more lasting solution to snail control,” says de Leo. “We believe that, when coupled with praziquantel administration, it may be the game changer in the fight against schistosomiasis.”

“We have too long been enamored of the idea that pills alone could solve the problem,” says Eric Loker from the University of New Mexico, who led the Kenyan study in 1999. “I commend the authors for putting a needed spotlight back on what happens in the water. The snails are abundant, often resilient, and impart stability to the transmission cycle. We don’t have a bed-net like option for snail control like we do for the mosquitoes that transmit malaria.”

But “a dose of reality is also in order,” he says. The snails often live in “complex, heavily vegetated, small bodies of water”, many of which were created by the construction of the Diama dam. Whether the prawns can even reach their pre-dam levels, let alone penetrate these new habitats, is unclear.

Meanwhile, the dam still prevents the prawns from travelling to and from their breeding grounds. If the team wants a new population to establish itself in the river, they’ll have to create some kind of bypass around the dam—a “prawn passage”—that will allow the animals to traverse their old migration routes.

Even that might not be enough. De Leo’s model shows that to eradicate schistosomiasis entirely, the team will need densities of prawns 2.5 times higher than what they actually managed in their small pilot study. That’s not unachievable, but it might be higher than what artificial prawn corridors can maintain. So, in areas where schistosomiasis is especially common, the team might have to regularly supplement the waters with prawns raised in aquaculture.

This isn’t a problem, though. It might even be a good thing, because the prawns have two important benefits beyond their hunger for snails: they are tasty, and valuable. They can sell for three to five times the price of local fish. The Upstream Alliance team believes villagers should be able to rear them in small aquaculture facilities to get both food and money. This idea is especially feasible because it’s the small, fast-growing prawns that kill the most snails, leaving villagers to harvest the larger and more valuable individuals with impunity. (It’s also okay to eat prawns that have dined on infected snails because their digestive systems kill the parasites.)

These economic benefits are crucial. Schistosomiasis affects more than 260 million people around the world, including some 114 million children. These huge numbers make it unfeasibly expensive to treat people with even a really cheap drug. But if countermeasures can actually return money to a community, they stand an even greater chance of succeeding. It’s a rare win-win-win scenario, where conserving a displaced animal can benefit human health and alleviate poverty. “We’re now working with geographers, ecologists, economists, and government ministries to find out how we can optimise a sustainable, long-term strategy,” says Sokolow.


Reference: Sokolow, Huttinger, Jouanard, Hsieh, Lafferty, Kuris, Riveau, Senghor, Thiam, N’Diaye, Faye & de Leo. 2015. Reduced transmission of human schistosomiasis after restoration of a native river prawn that preys on the snail intermediate host. PNAS http://dx.doi.org/10.1073/pnas.1502651112

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Surgeon Reveals Head Transplant Plan, But Patient Steals the Show

ANNAPOLIS, Md.—Valery Spiridonov looks impossibly small. He is dressed in all white, from his white button-down shirt to the white socks on his feet, which dangle at the ends of white pants and a white blanket. Breaking up the look is a black strap, which holds him to a motorized wheelchair.

He uses his left hand, which he can still move, a little bit, to steer the wheelchair into a hotel meeting room. There, he confirms that he would like to be the first person ever to have his head transplanted onto a new body.

Spiridonov flew from Russia to be at this conference, the American Academy of Neurological and Orthopaedic Surgeons (AANOS). He joined the surgeon proposing to do the transplant, Sergio Canavero of Turin, Italy. Canavero had built up his talk, a keynote address, for months, promising a big reveal of his plans to transplant Spiridonov’s head onto a donor body. (For background, see my earlier blog post and a good overview at New Scientist.)

The meeting is small, maybe 100 or fewer surgeons, and held in a very normal-looking Westin hotel in Annapolis, Md. Conference organizer Maggie Kearney spent much of the day turning away reporters in anticipation of a packed room. She says that in 15 years, she can’t remember a reporter ever attending the surgical conference before.

By the end of Canavero’s three-hour-long presentation (it was supposed to be an hour and a half, Maggie tells me), most of the reporters in the room seem worn out, and a bit confused about what the fuss was all about.

Sergio Canaveros
Sergio Canaveros, right.
Erika Engelhaupt

Canavero reviewed, at length, the scientific literature on spinal cord injury and recovery, regrowth of various parts of the central nervous system, and why some of the basic assumptions of neurosurgery are wrong. Throughout the lecture, he would occasionally point to Valery Spiridonov, his wheelchair parked near the stage, and make a declaration (“Propriospinal tract neurons are the key that will make him walk again!”).

Answering detractors’ comments that the transplant could be “worse than death” or could drive Spiridonov insane, Canavero asked Spiridonov directly, “Don’t you agree that your [current] condition could drive you to madness?”

Spiridonov answered quietly in the affirmative.

His condition is grave: a degenerative motor neuron disease that is slowly killing him. “I am sure that one day gene therapy and stem cells will fulfill their future,” Canavero said, “but for this man it will come too late.”

Finally, near the end of the talk, Canavero roughly outlined the surgery. He plans to sever the spinal cord very cleanly, using a special scalpel honed nano-sharp. (I could not see Spiridonov’s reaction to the special scalpel, but wondered.)

To minimize any die-off of cells at the severed ends during the transfer, Canavero says he will cut Spiridonov’s spinal cord a bit lower on the spine than needed, and the body’s a bit higher, and then at the last minute slice them again for a fresh cut. Then, add some polyethylene glycol (shown to stimulate nerve regrowth in animals), join the two ends together with a special connector, and voila. Electrical stimulation would then be applied to further encourage regrowth.

Of course, there’s a bit more to it, like reconnecting all the blood vessels and so forth, but Canavero is a neurosurgeon and the spinal cord was his focus.

Other neurosurgeons at the meeting responded cautiously to the proposal. The surgery might be possible “someday, but it is really a delicate situation,” said Kazem Fathie, a former chair of the board of AANOS.

Craig Clark, a general neurosurgeon in Greenwood, Mississippi, calls Canavero’s idea “very provocative.”

“There have been many papers over the years that have shown regeneration, but for one reason or another they didn’t pan out when applied clinically,” he said.

“There’s a lot of ethical questions about it,” said neurosurgeon Quirico Torres of Abilene, Texas. But Torres thinks it could be ethical to allow volunteers to do the surgery, and one day we might consider it normal. “Remember, years ago people were questioning Bill Gates: why do you need a computer? And now we can’t live without it.”

What’s Next?

Apart from the rundown of previous work on spinal cord injury, much of what Canavero said about the surgery was pretty much what he has said before. He supported his arguments for individual elements of a head transplant (or body transplant, if you prefer) but did not reveal any new demonstration of the entire procedure working in a person or an animal.

But Canavero has no shortage of confidence. He says he wants to do the surgery in America (implying Italy doesn’t have its act together enough to host a cutting-edge project like this).

“I have a detailed plan to do it,” he said, adding that he is asking Bill Gates and other billionaires to donate. He invited surgeons at the meeting to join his team, which could be enormous—more than 100 surgeons, he has said—and he wants team leaders in orthopedics, vascular surgery, and so on. These surgeons should work on the project full time for the next two years, he said, “and you will be paid through the nose, because I think doctors involved in this should be paid more than football players.”

Valery Spiridonov entering the conference room. Photo: Erika Engelhaupt

After the talk, Spiridonov disappeared into a room to rest. When he came back out, he answered questions for the TV crews that had descended, sounding a bit weary of answering the same questions he’s been asked before. “What will happen to you if you don’t get this surgery?” a reporter called out. “My life will be pretty dark,” he said. “My muscles are growing weaker. It’s pretty scary.”

He looked tired.

During his interviews, I stepped aside to talk with his hosts in Annapolis, who are friends of a friend of the Spiridonov family. “He’s brilliant, he’s happy, he’s funny,” said Briana Alessi. “If this surgery were to go through and if it works, it’s going to give him a life. It’s life-changing. He’ll be able to do the things he could only dream of.”

And if not? “He’s taking a chance either way,” she said.

The final question he takes from the press: What do you say to people who say this surgery should not be done?

Spiridonov’s reply: “Maybe they should imagine themselves in my place.”

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Easter Chicks: Cute, Fluffy, and Probably Bad For You

In the United States—and for that matter in much of the world—the foodborne disease Salmonella is a major public health problem. Here, it causes an estimated 1 million cases every year. We tend to think of those cases, and most foodborne illness, as minor episodes of needing to stay close to the bathroom—but every year, 19,000 of them end up in the hospital and almost 400 people die. And even if they survive, people aren’t necessarily out of danger; after decades of dismissing foodborne illness as unimportant and self-limited, researchers are beginning to understand that it can have lifelong consequences.

So it’s important, as much as possible, to identify the sources of Salmonella infection, and to alert people to the ways in which they can protect themselves.

And that’s why the Centers for Disease Control and Prevention, the CDC, is worried about those fluffball Easter chicks that might be appearing in households this weekend, as well as the juvenile poultry that backyard farmers and urban locavores may begin buying as the weather warms.

As I mentioned in my intro post yesterday, I also am writing for National Geographic‘s food site, The Plate, and I have a new post up there about the under-appreciated danger posed by live baby poultry. Whether you are buying them for immediate adorableness on top of an Easter basket, or eventual eggs or meat in a small-scale coop, most of us find baby chicks irresistible, in the hard-wired way that makes us melt before kittens and babies too. So we cradle them, and cuddle them, and smooch them on top of the head. But we forget that, just like babies of every other species, they are poop machines. And Salmonella travels in poop.

There are millions of baby chicks and other poultry sold every year: several millions pounds’ worth, according to the US Post Office, which ships most of them. In the past several years, they have caused significant outbreaks: 363 people in 43 states in 2014; 158 people ill, in 30 states in 2013; 195 people sick in 27 states in 2012; and 316 people sick in 43 states in the years before that.

This isn’t an argument against buying baby poultry, especially not if you’re doing it for small-scale egg or meat production. (Animal welfare organizations urge not buying baby animals just for Easter, because of the likelihood they will be dumped.)

But it is a plea on behalf of something I’m probably going to be saying a lot as we go forward: Don’t forget to wash your hands.

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Introducing Germination: Diseases, Drugs, Farms, and Food

When I was a kid, my favorite part of school wasn’t class — even though I loved studying, and liked showing off what I knew. It wasn’t the uniforms, though my boarding school’s dresses and blazers, and shoes for indoor and outdoor games, were a puzzle that came together differently every time. And it certainly wasn’t the food: School dinner in England was a mystery of boiled sprouts and stewed rhubarb, even if the Texas high school lunches that came after taught me how to make Frito pie.

What I loved most about school, with a fierceness that bordered on devotion, were school supplies. The incense of a just-sharpened pencil. The order in a fresh box of pen cartridges. And more than anything, the promise in a new notebook, and the anticipation of filling its empty, perfect pages with everything I would discover and learn.

I’m feeling a similar thrill now, viewing this new space at Phenomena. Welcome to Germination, a blog that will explore public health, global health, and food production and policy—and ancient diseases, emerging infections, antibiotic resistance, agricultural planning, foodborne illness, and how we’ll feed and care for an increasingly crowded world.

If you followed me here from my previous blog Superbug at Wired, thanks, and get comfortable. If I’m a new discovery for you, here’s a capsule bio. I’m a freelance journalist working mostly for magazines (Wired,  Scientific American, Nature, Slate, the Atlantic, the Guardian and Modern Farmer, along with an array of women’s magazines). I’ve written two books so far—Superbug, about the global rise of antibiotic resistance, and Beating Back the Devil, about the Epidemic Intelligence Service, the disease-detective corps of the US Centers for Disease Control and Prevention—and am working on a third, about how we came to use antibiotics in agriculture, and what a mistake that turned out to be.

Before I was a magazine writer, I was a newspaper reporter, doing mostly investigative work: on the causes of cancer clusters, the social effects of drug trafficking, and a mysterious illness in reservists that turned out to be the first cases of Gulf War Syndrome. In my last newspaper job, I covered the CDC, under orders from the editor who hired me to “get in there and tell us these people’s stories.” I spent a lot of time talking my way into investigations and onto planes in the middle of the night. It was enormous fun.

Me, at TED, on March 18, 2015. Original here/a>.
Me, at TED, on March 18, 2015. Original here.
Maryn McKenna speaks at TED2015 - Truth and Dare, Session 6, March 16-20, 2015, Vancouver Convention Center, Vancouver, Canada. Photo: Bret Hartman/TED

I’m also a Senior Fellow of the Schuster Institute for Investigative Journalism at Brandeis University, and just finished a fellowship at MIT. I do some video. And I just gave a TED talk, on imagining what the world will be like after we’ve used up antibiotics. (The video has not gone up yet, but I’ll let you know when it does.)

As a journalist, my interest is complexity, inadvertence, and unintended consequences. (My Phenomena colleague Ed Yong jokes that he covers the “Wow” beat; I think of what I do as the “Oops” beat.) We got to widespread resistance because we wanted to cure infections quickly; we got to factory farming because we wanted to ensure affordable food. There isn’t (much) malfeasance in either of those endeavors,  but there is a ton of good intentions—and good intentions gone bad are a rich, rewarding subject. We might be here a while.

Here’s what you can expect at Germination: reports on new scientific findings; inquiries into policy initiatives; profiles and interviews with researchers doing cool things; history; and, occasionally, whimsy. I have been writing for a year for National Geographic‘s food platform The Plate, and some posts that deal more purely with food will be loaned or cross-posted there. (About which: You make Frito pie by opening a serving-size bag of Fritos along the back seam and plopping in a ladle of chili and some shredded yellow cheese. It tastes best when served by a lunch lady in a hairnet and a Texas Longhorns jersey.) If you’d like to hear more about my plans, head over to The Loom, where my new colleague Carl Zimmer has kindly conducted a Q&A with me.

When I think back to being a kid at the start of a school year, the initial thrill might have been those pristine new notebooks—but the bigger thrill was filling them. Phenomena is the most exclusive science-writing club on the internet, and I’m excited to join it. Please come along.

(Much gratitude to Jonathan Eisen, PhD, for suggesting Germination as a blog name.)


UCLA Superbugs Reveal Stubborn Resistance Problem

Guest Post by Maryn McKenna

The UCLA Health System announced earlier this week that seven patients—two of whom died—became infected by highly drug-resistant bacteria that remained on pieces of medical equipment after disinfection, and 179 more were exposed to the bacteria and are at risk of developing infections.

The outbreak is one of several that have occurred in the United States in connection with duodenoscopes, complex flexible tubes that are used to treat problems in narrow ducts in the liver and pancreas. In each outbreak, despite the devices being cleaned, patients have been infected with superbugs known as CRE, short for carbapenem-resistant Enterobacteriaceae: a group of bacteria that reside benignly in the gut but have acquired an array of genetic defenses against antibiotics, including to the last-resort drugs carbapenems. CREs remain vulnerable to only one or two antibiotics, and CRE infections can kill two in five patients.

On Thursday, the Food and Drug Administration issued a warning about the difficulty of cleaning the devices, which it said are used at least 500,000 times per year in the US. The agency said it has been notified of 135 patient infected with CRE by duodenoscopes since January 2013 and added, “It is possible not all cases have been reported.”

The UCLA episode follows a large outbreak at a Seattle hospital and a separate one in Illinois along with smaller ones in other states. It is causing alarm because the superbugs transmitted by the scopes are a growing problem in the US, and because there can be such a long lag time—weeks or months—between when patients are exposed and when they develop symptoms of infection.

For a better understanding of the problem, I talked to Dr. Alexander J. Kallen, a medical epidemiologist in the division of the Centers for Disease Control and Prevention that handles infections transmitted in healthcare.

Maryn McKenna: Are all these outbreaks similar?

Alexander Kallen: They’re related in that they all involve a small number of scopes—duodenoscopes, which are specialized endoscopes—with persistent contamination, which ended up in each case with 100 to 200 people exposed. Most people did not develop infections; they ended up colonized with the bacteria, but that is still a problem from a community standpoint (because they may be able to pass the bacteria along).

MM: Is there any other relationship among them?

AK: All three large outbreaks that we’re aware of, while they were CRE, were all different types of CRE—and all types that are unusual in the United States. In Illinois, which we at the CDC investigated, it was a type called NDM, in Los Angeles it is a type known as OXA, and in Seattle it was a type known as Amp-C. These are very unusual organisms, so to have a cluster of them definitely prompts an investigation. And they may turn out to be a canary in the coal mine for the difficulty of cleaning these scopes. If what had been passed between these patients because of the scopes was regular old E. coli, we would never have noticed, because it is not an unusual bug.

MM: Do you have any sense of where the infections originated?

AK: They were likely imported originally by people who got healthcare outside the United States. But we looked hard in Illinois for instance to try to identify the original person and were not able to.

MM: Surely this isn’t the first time there have been outbreaks of illness, even of resistant bacteria, from endoscopes?

AK: No. But the outbreak we investigated in Illinois in 2013, which we reported in the Journal of the American Medical Association, is the first time that we know of where there was transmission of a highly resistant pathogen, from a scope, unrelated to an infection-control breach. You almost always see that someone forgot this step or that step. But in these last three outbreaks, there was persistent contamination despite not identifying a breach, and that is fundamentally different. It starts to raise the suspicion this is more a fundamental issue with these types of scopes, rather than just failures to adhere to recommendations for cleaning.

MM: These scopes are obviously complicated. It is possible that they just can’t be sterilized?

AK: Technically they’re not sterilized, because they aren’t intended for use in sterile spaces in the body the way surgical instruments are. They undergo high-level disinfection, a step below sterilization. All these devices are required to have instructions for cleaning that are validated by the FDA, but it is possible that what is validated via tests in a lab under certain circumstances is one thing, and performing the steps in practice is something different. That may also be true for a scope that is brand new versus one that has been used for a year or two, that it acquires persistent contamination that once established can be very difficult to eradicate. In our investigation in Illinois, the scope that was sent to us had been out of use for weeks or months and we were still able to recover bacteria from it.

MM: At the CDC, you’ve been watching the CRE problem build for 15 years. What do these outbreaks mean for that larger epidemic?

AK: It’s important to say that the spread from duodenoscopes is a tiny portion of the CRE problem. But it highlights that the central issue with CRE is person to person spread between people in medical facilities. The people who are at risk, and who get CRE, tend to be people who have complex medical problems and spend a lot of time in hospitals, nursing homes, long-term acute care facilities. In the Illinois investigation, people were infected in the hospital and then were sent out to long-term care and transmitted CRE to their roommates.

MM: Do you see any hope for controlling further spread?

AK: CRE is still rare in most places in the US, but we have not previously been able to identify outbreaks early enough to intervene. There is a movement in the CDC and in some parts of healthcare to change the approach to preventing the transmission of multi-drug resistant organisms by collecting very granular data and sharing it regionally among institutions. I personally think that has a great chance of success.

Maryn McKenna blogs for National Geographic’s the Plate and is writing a book about antibiotic use in agriculture for National Geographic Books.

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The Power of a Press Release

In 2011, Petroc Sumner of Cardiff University and his colleagues published a brain imaging study with a provocative result: Healthy men who have low levels of a certain chemical in a specific area of their brains tend to get high scores on tests of impulsivity.

When the paper came out, thousands of people across England were rioting because a policeman had shot a young black man. “We never saw the connection, but of course the press immediately saw the connection,” Sumner recalls. Brain chemical lack ‘spurs rioting’, blared one headline. Rioters have ‘lower levels’ of brain chemical that keeps impulsive behaviour under control, said another.

“At the time, like most scientists, we kind of instinctively blamed the journalists for this,” Sumner says. His team called out these (shameful, really) exaggerations in The Guardian, and started engaging in debates about science and the media. “We quickly began to realize that everyone was arguing on the basis of anecdote and personal experience, but not evidence. So we decided to back off, stop arguing, and start collecting data.”

And the data, published today in BMJ, surprised Sumner. His team found that more than one-third of academic press releases contain exaggerated claims. What’s more, when a study is accompanied by an exaggerated press release, it’s more likely to be hyped in the press.

Because press releases are almost always approved by a study’s leaders before being distributed, Sumner’s findings suggest that scientists and their institutions play a bigger role in media hype than they might like to acknowledge.

“We’re all under pressure as scientists to have our work exposed,” Sumner says. “Certainly I think a lot of us would be quite happy not to take responsibility for that — just to say, ‘Well, we can’t do anything about it, if they’re going to misinterpret that’s up to them but it’s not our fault’. And I guess we’d like to say, it is really important and we have to do something more about it.”

Sumner and his colleagues looked at 462 health or medicine-related press releases about issued by 20 British universities in 2011. For each press release, the researchers also analyzed the scientific study it was based on, and news articles that described the same findings.

The researchers limited the analysis to health and medicine partly because (as I’ve written about before) these stories tend to influence people’s behavior more than, say, stories about dinosaurs or space. They focused on three specific ways that press releases can distort or exaggerate: by implying that a study in animals is applicable to people; by making causal claims from observational data; and by advising readers to change their behaviors (“these results suggest that aspirin is safe and effective for children,” say, or, “it’s dangerous to drink caffeine during pregnancy”).

More than one-third of the press releases did each of these things, and the misinformation showed up in the media, too. For example, among press releases that gave exaggerated health advice, 58 percent of subsequent news articles also contained exaggerated health advice. In contrast, among press releases that didn’t make exaggerated recommendations, only 17 percent of news articles did so. The researchers found similar trends for causal claims and for inferring that animal work applies to people.

“We certainly don’t want to be blaming press officers for this,” Sumner says. “They’re part of the system. The academics probably don’t engage as much as they should.”

I called Matt Shipman, a science writer and press information officer at North Carolina State University, to ask what he thought of the findings. Shipman has been a press officer for seven years, and before that he was a journalist. “The numbers are very powerful,” he said, and they underscore the importance of press releases at a time when reporters often don’t have the time or resources for thorough reporting. (Shipman has just signed on with Health News Review to rigorously evaluate the quality of health-related press releases.)

Shipman also brought up an important caveat. Because this study is observational, it doesn’t prove that press releases are themselves the cause of hype. “If a researcher is prone to exaggeration, which leads to exaggerated claims in a news release, the researcher is likely to also be prone to exaggeration when conducting interviews with reporters,” Shipman says. “The news release may be a symptom of the problem, rather than the problem itself.”

When he writes press releases, Shipman says he almost always begins by meeting with the researcher in person and asking him or her to explain not only the findings, but what work led to them, why they’re interesting, and what other experiments they might lead to. Then Shipman writes a draft of the release and sends it back to the researcher for approval. He asks the scientist to check not only for factual inaccuracies, but for problems in emphasis, context, or tone. Different press officers at other institutions, however, write press releases using far less rigorous methods, as I have learned by swapping stories with them over the years. And some press officers are judged by the quantity of stories that come out in big outlets, which naturally creates an incentive to make research seems newsworthy, even when it might not be.

“What I think is probably the case is that all of the variables at play here — the researchers, the press officers, and the journalists — are all humans,” Shipman says. “And all of them are capable of making mistakes, intentionally or unintentionally.”

So. Is there any concrete way to reduce those mistakes?

In an editorial accompanying the BMJ study, author and doctor Ben Goldacre makes two suggestions. First, the authors of press releases and the researchers who approved them should put their names on the releases, he writes. “This would create professional reputational consequences for misrepresenting scientific findings in a press release, which would parallel the risks around misrepresenting science in an academic paper.” That seems reasonable to me.

Second, to boost transparency, press releases shouldn’t only be sent to a closed group of journalists, Goldacre writes. “Instead, press releases should be treated as a part of the scientific publication, linked to the paper, referenced directly from the academic paper being promoted, and presented through existing infrastructure as online data appendices, in full view of peers.”

That sounds good, but “would require a significant shift in the culture,” according to Shipman. Press officers would have to be brought into the process much earlier than they are now, he says. And scientists would have to be far more invested in press releases than many of them are now.

I think we journalists need to own our portion of the blame in this mess, too. Let’s go back to Sumner’s 2011 brain-imaging study, for example. His university’s press release didn’t have any wild exaggerations, and it certainly didn’t make a connection between the research and the riots. That came from the journalists (and/or their editors).

But that actually doesn’t happen very often, it turns out,” Sumner says. “Most of the time, the media stories stay pretty close to what’s in the press release.”

Which isn’t exactly great news, either.

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Category Fail

I’ve written a lot of stories about autism research, and I’d say one of the biggest scientific developments in the past few years was the creation of ‘autistic’ mice. Researchers first found many, many genes associated with autism in people, and then created dozens of mouse models that carry one or more of those same genetic glitches.

In the fall of 2011, for example, one team debuted mice with extra copies of a gene called UBE3A. Approximately 1 to 3 percent of children with autism carry extra copies of the same gene. These mutant mice show little interest in social interactions, compared with controls. They also emit fewer vocalizations and repetitively groom themselves. This was heralded as something of an autism trifecta, as the animals mimicked the three ‘core’ symptoms of people with the disorder: deficits in social behaviors and in communication, as well as repetitive behaviors.

The same goes for mouse models based on environmental, rather than genetic triggers. Mice whose mothers got an infection while pregnant end up with abnormal social interactions and vocalizations, and they repetitively bury marbles. Once again, the animals show all three “core” deficits, and are thus considered to be a valid model of autism.

There’s a nice and tidy logic to this approach, understandably appealing to neuroscientists. If a mouse model mimics the three behaviors used to define autism, then studying the cells and circuits of those mice could lead us to a better understanding of the human disorder. But there’s a big hole in that logic, according to a provocative commentary published by Eric London in this month’s issue of Trends in Neurosciences. The problem is that the symptoms of autism — like those of all psychiatric disorders — vary widely from one person to the next. So using the fuzzy diagnostic category of ‘autism’ to guide research, he writes, “is fraught with so many problems that the validity of research conclusions is suspect.”

London begins with a short history of the Diagnostic and Statistical Manual of Mental Disorders, or DSM, the book that since 1980 has dictated what collections of symptoms define one disorder or another. There’s nothing wrong with a categorical diagnosis, per se. It can have enormous explanatory power. If a doctor diagnoses you with strep throat, for example, you have a good idea of what that is (a bacterial infection) and how you might treat it (antibiotics). “A psychiatric diagnosis, by contrast, is rarely as informative,” London writes.

People diagnosed with schizophrenia, bipolar disorder, depression, or autism often don’t know what caused the trouble, and they struggle with unpredictable symptoms, ineffective treatments, and unpredictable responses to those treatments.

What’s more, most people who fall into the bucket of one psychiatric disorder also meet criteria for others. London cites some fascinating numbers: Some 90 percent of people with schizophrenia, for example, have another diagnosis as well. More than 60 percent of people with autism have another diagnosis, and one-quarter have two or more. “Autism is comorbidly present in over 50 specific diagnoses comprising other genetic and medical conditions,” London writes.

The three supposedly core behaviors of autism don’t correlate well with each other, he adds. In other words, many kids just have one or two of the three. Francesca Happé has conducted many studies suggesting that each of these symptoms is inherited independently, suggesting that each has its own, separate biological cause.

The danger of focusing on these three behaviors is that it might cause clinicians and researchers to overlook other symptoms that are common in people with autism. Many kids with autism have gastrointestinal issues, for example, and many show a range of motor problems, such as head lag, trouble sitting up, or a wobbly gait. And more than 80 percent of people with autism have anxiety, London notes. Mouse models of the disorder may have some of these problems, too, but researchers don’t usually test for them.

The DSM has tried to address some of these problems. Its latest version, released last year, defines autism with two criteria: social and communication deficits, and repetitive behaviors. But London doesn’t think that goes nearly far enough, for all the reasons outlined above. He proposes an even broader category of “neurodevelopmental disorder,” which would include more than 20 different DSM categories, including autism and schizophrenia. Just as they do today, clinicians could still focus on specific symptoms — whether sensory sensitivities, anxiety, psychosis, attentional problems, etc. — when deciding how to treat each person.

London’s commentary is only the latest in an old debate about diagnoses: Is it better to lump, or to split? Some scientists agree with him, others don’t, and I see merit in the scientific arguments on both sides. One point I think sometimes doesn’t get enough attention, though, is the social power of a diagnosis.

These labels carry meaning, for better or worse. For people with mysterious illness, such as chronic fatigue syndrome, a label can make them feel acknowledged and validated, or completely marginalized. Diagnoses for brain disorders, such as Asperger’s syndrome, can unite people under a common identity, or create dangerous societal stigma. Rational diagnostic categories are crucial for scientific progress, as London argues. But scientists would do well to remember that their labels also have lasting consequences outside of the lab.