A Blog by

Peek Into Tiny Crime Scenes Hand-Built by an Obsessed Millionaire

At first glance, the miniatures in the Maryland medical examiner’s office look like ordinary dollhouses. But look inside, and each is a carefully crafted crime scene, right down to the tiny murder weapons and minuscule clues.

And it’s all based on true crimes. Frances Glessner Lee, heir to International Harvester’s tractor and farm equipment fortune, was transfixed by criminal investigations. Much to her family’s dismay, she spent much of her life—and a small fortune—building dioramas depicting the scenes of real crimes in New England, incorporating evidence that’s still used to train investigators in crime scene analysis. Even today, the clues woven into her dioramas are closely guarded secrets.

Glessner Lee called the scenes Nutshell Studies of Unexplained Death, and she built them with a grand purpose: to elevate gumshoe cops into an elite squad of homicide detectives. She founded a department of legal medicine at Harvard and a weeklong seminar, still held annually in Baltimore, using the dioramas to teach the art of observation and the science of crime scene analysis.

(To see more of the dioramas, click through the gallery at the top of this story, with photos by National Geographic photographer Max Aguilera-Hellweg.)

Not only are the Nutshell dioramas still used to train investigators, but Glessner Lee overcame her outsider status to become a well-regarded criminalist of her day. Today she’s often called the “mother of forensic science.”  

She built the deathly dioramas in the 1940s and ‘50s on a scale of one inch to one foot, shrinking down details that she pulled from autopsy reports, police records, and witnesses—tempered with a dose of obfuscation. Sometimes she changed names and dates in her scene descriptions, and she took liberties with details that weren’t essential as evidence, such as wallpaper and decor. She spent as much on some of the miniatures as a full-size house cost at the time, says Bruce Goldfarb, executive assistant to the chief medical examiner of Maryland and de facto curator of the dioramas.

Glessner Lee built the dioramas from her home in New Hampshire, and mostly depicted crimes in New England. Here, a teenager was stabbed in a parsonage.
Glessner Lee built the dioramas from her home in New Hampshire, and mostly depicted crimes in New England. Here, a teenager was stabbed in a parsonage.
Photograph by Max Aguilera-Hellweg

“It couldn’t be toylike at all. They had to be as gritty and realistic as possible,” Goldfarb says.

In one, a woman lies dead in a bathtub, plastic water frozen in time as it streams across her face. Her home is shabby. The linoleum in front of the wooden commode is rubbed bare as if from years of use.

“What blows my mind is the boards under the sink are water-stained. It has no significance at all, but nothing escaped her observation,” says Goldfarb.

Glessner Lee’s attention to detail is legendary. Sometimes entire rooms were constructed that couldn’t even be seen without taking the diorama apart, and she once insisted, Goldfarb says, that a tiny rocking chair should rock the same number of times after being pushed as its full-size counterpart. “There was real plaster and lath; those walls have studs, and the doors are framed,” he says.

The dioramas speak not just to a macabre obsession, but to Glessner Lee’s passion for and fascination with the victims she depicted, many of which were women, in her 19 known dioramas (she’s thought to have made at least 20).

“This was a society woman, a millionairess, and it’s striking who’s portrayed,” says Goldfarb. “Most are marginalized, alcoholics or prostitutes—poor people living quite desperate lives. She chose to document the lives of people who were far removed from her social circles.”

Max Aguilera-Hellweg is the photographer who shot the images above for National Geographic’s July feature story on forensic science. His eerie photos spotlight the victims in the dioramas as well.

“I look at photography as mathematics, and this was using light and subtraction to reveal what’s important to me,” he says. No one is allowed to touch the fragile dioramas, so the photographer spent hours setting up each shot using tiny flashlights and positioning the camera to put the viewer inside the crime scenes.

As a former medical doctor who had declared death, Aguilera-Hellweg thought he had seen it all. He has photographed autopsies, surgeries, and dead bodies, but says he was shocked to learn of the Nutshell dioramas for the first time. “I didn’t know they existed,” he says.

After three days of staring at the scenes, Aguilera-Hellweg says he thinks he may have picked up on a few important clues. “What can the crime scene tell you by looking at what’s there? That what Frances Glessner Lee wanted to teach,” he says. “It’s all about the art of observation.”

Read more about the state of forensic science today in “How Science Is Putting a New Face on Crime Solving” and a companion quiz feature, “Can You Rule Out Suspects Using Faces Drawn From DNA?”

A Blog by

To Slow Down Antibiotic Resistance, Focus on the Basics

Washing hands.
Washing hands.
Photograph by Arlington County, Flickr (CC).

A project chartered by the British government, which has been examining everything that can be done to stem the tide of antibiotic resistance, in its next-to-last report has focused on the basics: municipal sanitation and hospital hygiene.

It’s something of a change in tone for the Review on Antimicrobial Resistance, a two-year effort created by Prime Minister David Cameron, supported by the Wellcome Trust and chaired by Lord Jim O’Neill, the former chief economist of Goldman Sachs (who now also serves in an unpaid post in Cameron’s government). The Review’s previous reports have examined what could be changed or created to solve problems that contribute to the rise of resistance: funding drug development, supporting vaccine research, detecting counterfeit drugs, innovating rapid-diagnosis devices and improving vaccine use.

In its new analysis, the group backs away from technological optimism to address seemingly intractable problems: how hospitals continue to cause antibiotic-resistant infections in their most vulnerable patients, and how the lack of clean water and sanitation both create diseases that demand antibiotic use, and also spread antibiotic-resistant bacteria.

Obviously neither of those concerns are new: Ignaz Semelweis  linked unwashed hands to fatal childbed fever in 1847, and John Snow made the connection between contaminated water and a cholera outbreak in 1854. Yet today, just in the United States, more than 1.7 million people contract healthcare-associated infections each year, and worldwide, more than 2 million people die from waterborne diarrheal disease.

So the problems are not solved. “We felt it would be of value to point out that just doing the basics can make a huge amount of difference,” Lord O’Neill said by phone. “It is concerning that not enough has happened, and that’s a reason for a new, independent voice to highlight that.”


The Review commissioned an analysis from postgraduate students at the London School of Economics which found that, just in four countries with emerging economies (India, Indonesia, Nigeria and Brazil), 494 million cases of diarrhea each year are treated with antibiotics, a number that could rise to 622 million cases by 2030. If infrastructure were improved, 60 percent of those courses of antibiotics could be foregone. The report says that contaminated water also allows bacteria to cycle between humans and the environment, spinning up the dissemination of resistance genes. (In fact, in 2011, the team who discovered the resistance supergene NDM identified municipal water supplies and puddles as a major contributor to the spread of that almost untreatable bug.)

If sanitation seems a simple goal, so does hygiene—yet the Review finds that persistent neglect of simple tasks such as washing hands is fueling the spread of resistance. As few as 30 to 40 percent of hospital staff wash their hands as often as they should, it says, and doctors perform worse than nurses or staff who are lower in the hierarchy. Though it is crucial those rates be improved, there group finds there is nowhere near enough research into what actually motivates healthcare workers to change their behavior, and recommends funding studies that could pick apart what works. (Dismayingly, that does not now happen. A few years ago, infection-prevention specialist Dr. Eli Perencevich and several colleagues analyzed funding awarded by the National Institutes of Health to study AIDS, versus funding for research into hospital infections. For every US death from AIDS, they found, the NIH awarded the equivalent of $69,000; for every US death from MRSA, drug-resistant staph, $570.)

In its final comments, the Review calls for something that, for years, researchers deep in the trenches of antibiotic resistance research have been begging for: the creation of a comprehensive, global, rapid surveillance system that could alert the world when something new emerges. Two examples of where that would have made a difference: NDM was first identified in Sweden in 2008, but was subsequently found to have been diagnosed in India, its place of origin, as early as 2006. And MCR-1, the most recent dismaying superbug—which is resistant to the utterly last-resort drug colistin—was found last fall to have spread to more than a dozen countries, but was first identified in China in 2013.

“Even in some of the world’s most developed health systems, AMR surveillance data is often patchy and retrospective—virtually none is ‘real time’,” the Review says. “Without effective monitoring, we will lack early warning of emerging patterns of drug resistance, and lack the insights needed to guide and evaluate our response.”

The Review will conclude its two years of research with a final presentation of big-picture recommendations for health agencies and governments this summer, with presentations to the World Health Assembly and the United Nations.

A Blog by

Some US Hospital Infections Dropping, But Superbug Risks Are High

Handwashing after exposure to bacteria at a petting zoo.
Handwashing after exposure to bacteria at a petting zoo.
Photograph by Blue Yonder, Flickr (CC)

Fifteen years after a national report exposed how many Americans were being made sick and dying because of medical errors, some infections caused by hospitals are decreasing, according to the Centers for Disease Control and Prevention. But in a report published Thursday, the agency warns that the incidence of other infections remains stubbornly high, despite fixes that are simple in some cases—and the proportion of them that are antibiotic-resistant is, in its director’s words, “chilling.”

Drawing on data from its National Healthcare Safety Network, which compiles reports from 4,000  hospitals, 1,135 rehab facilities and 501 long-term acute care hospitals (which house severely ill patients who need ICU-level care for a long time), the agency reported that in 2011, 722,000 “healthcare-associated infections” occurred, and approximately 75,000 patients died. Between 2011 and 2014, it said:

  • for central line-associated bloodstream infection, which start from a tube threaded near the heart to deliver medications: a 50 percent reduction in hospitals and 9 percent in  long-term acute care hospitals;
  • forurinary-tract infections caused by catheters inserted into the bladder: no change in hospitals, an 11 percent reduction in long-term acute care hospitals, and a 14 percent reduction in inpatient rehab facilities;
  • for infections in surgical incisions, a 17 percent reduction in hospitals;
  • and for Clostridium difficile infections—the devastating antibiotic-associated diarrhea that is a signal for high antibiotic use and insufficient hygiene—an 8 percent reduction in hospitals.
Changes in four healthcare-associated infections in US healthcare facilities.
Changes in four healthcare-associated infections in US healthcare facilities.
Graphic by the CDC; original here.

But while those reductions are good news, the troubling aspect of the report is the percentages of hospital-caused infections that are antibiotic-resistant. In 2014, the CDC said, 14.9 percent of those infections were resistant. Breaking those down:

  • in hospitals, 18 percent of central line-associated bloodstream infections, 15 percent of surgical-site infections and 10 percent of catheter-associated urinary tract infections were resistant;
  • in rehab facilities, 12 percent of urinary-tract infections were resistant;
  • and in long-term acute care hospitals, 28 percent of central line-associated bloodstream infections and 29 percent of cather-associated urinary tract infections were resistant.

In a phone briefing with reporters, Dr. Thomas Frieden, the CDC’s director, called the high levels of resistance in infections in long-term care facilities—more than one in four of each infection— “chilling.” Asked how he would describe the rate in regular hospitals, which exceeds one in seven, he replied: “deeply concerning.”

According to the CDC’s data, 4 percent of patients develop an infection as a result of a hospital stay. Many of those, Frieden said, are the responsibility of healthcare personnel who fail to follow simple, known procedures, from washing hands to neglecting rules for installing catheters to continuing antibiotics beyond when they are needed. “Doctors are the key to stamping out superbugs,” he said. “No one should get sick when they are trying to get well.”

But, Frieden said, forcing down rates of healthcare infections and resistance in hospitals will also require investment in new diagnostics and patient records, beyond what hospitals can currently afford—especially since resistant bacteria can be carried into hospitals from longterm care facilities, which may have fewer staff and less resources for infection control.

Dr. Peter Pronovost, director of the Armstrong Institute for Patient Safety and Quality at Johns Hopkins—an early champion of cockpit-style checklists to prevent healthcare infections, who was also on the call to reporters—added: “We need things to better identify organisms faster, so we could implement appropriate checklists. We  need to better understand when surfaces are clean very much earlier, so we know if our cleaning efforts are effective. And we need to have better regional and networked information systems, so we know what resistance patterns are in community hospitals and longterm care facilities, and be able to link them when patients come to acute-care hospitals and then go back again.”

At the same time as it released its report, the CDC launched an Antibiotic Resistance Patient Safety Atlas, a web-based interactive that creates data visualizations of hotspots of resistant infections, nationally and by state, by drawing from the National Healthcare Safety Network database. Using the atlas, here is what MRSA, drug-resistant staph, looks like in hospital infections from 2011 to 2014:

MRSA (multi-drug resistant staph) in all hospital infections from 2011 to 2014.
MRSA (multi-drug resistant staph) in all hospital infections from 2011 to 2014.

And here is the occurrence of CRE—carbapenem-resistant Enterobacteriaceae—the “nightmare bacteria” that respond to only one or two antibiotic families:

CRE (carbapenem-resistant Enterobacteriaceae), which are resistant to almost all antibiotics, in hospitals between 2011 and 2014.
CRE (carbapenem-resistant Enterobacteriaceae), which are resistant to almost all antibiotics, in hospitals between 2011 and 2014.

The CDC’s report was released Thursday in many pieces: in addition to the atlas, a press release, a scientific paper, a simpler factsheet, and a state-by-state report assessing progress against national benchmarks.

A Blog by

An Epidemic 14 Years Ago Shows How Zika Could Unfold in the US

An Aedes albopictus mosquito, which health authorities worry may begin to spread Zika.
An Aedes albopictus mosquito, which health authorities worry may begin to spread Zika.
Photograph by James Gathany, CDC.

If the Zika virus comes to the United States, we could face the threat of the same sort of virgin soil epidemic—an infection arriving in a population that has never been exposed to it before—that has caused more than 1 million known infections, and probably several million asymptomatic ones, in Central and South America. It’s nerve-wracking to wonder what that would be like: How many people would fall ill, how serious the effects would be in adults or in babies, and most important, how good a job we would do of protecting ourselves.

But, in fact, we can guess what it would be like. Because we have a good example, not that long ago, of a novel mosquito-borne threat that caused very serious illness arriving in the United States. And the data since its arrival shows that, despite catching on fairly quickly to what was happening, the U.S. didn’t do that good a job.

This possibility became more real Monday when the Pan American Health Organization released a statement that predicts Zika virus, the mosquito-borne disease that is exploding in South and Central America and seems likely to be causing an epidemic of birth defects especially in Brazil, will spread throughout the Americas. PAHO, which is a regional office of the World Health Organization, said:

There are two main reasons for the virus’s rapid spread (to 21 countries and territories): (1) the population of the Americas had not previously been exposed to Zika and therefore lacks immunity, and (2) Aedes mosquitoes—the main vector for Zika transmission—are present in all the region’s countries except Canada and continental Chile.

PAHO anticipates that Zika virus will continue to spread and will likely reach all countries and territories of the region where Aedes mosquitoes are found.

Those “countries and territories where Aedes mosquitoes are found” include a good portion of the United States, as these maps from the Centers for Disease Control and Prevention demonstrate:

CDC maps of the ranges of two mosquito species that could transmit Zika virus.
CDC maps of the ranges of two mosquito species that could transmit Zika virus.
Graphic from CDC.gov, original here.


The recent history is this: In the summer of 1999, the New York City health department put together reports that had come in from several doctors in the city and realized that an outbreak of encephalitis was moving through the area. Eight people who lived in one neighborhood were ill, four of them so seriously that they had to be put on respirators; five had what their doctors described as “profound muscle weakness.”

Within a month, 37 people had been identified with the perplexing syndrome, which seemed be caused by a virus, and four had died. At the same time, veterinarians at the Bronx Zoo discovered an unusual numbers of dead birds: exotics, like flamingos, and city birds, primarily crows. Their alertness provided the crucial piece for the CDC to realize that a novel disease had landed in the United States: West Nile virus, which was well-known in Europe, but had never been seen in this country before.

West Nile is transmitted by mosquitoes in a complex interplay with birds. It began moving with both birds and bugs down the East Coast and then across the Gulf Coast. As it went, the CDC realized that the neurologic illness that marked the disease’s first arrival had not been a one-time event, but its own looming epidemic within the larger one. “Neuroinvasive” West Nile, which in its worst manifestations caused not transient encephalitis but long-lasting floppy paralysis that resembled polio — and sometimes killed — bloomed in the summer of 2002 east of the Mississippi, and then moved west in the years afterward as the disease exhausted the pool of the vulnerable.

The CDC’s maps showing the emergence of “neuroinvasive” West Nile virus disease from 2001 to 2004; areas in black had the highest incidence.
Graphic by Maryn McKenna using maps by the CDC; originals available here.

So far, so normal, for a newly arrived disease. But here’s where the story gets complicated. By the beginning of this decade, West Nile had become endemic in the lower 48 states. It is not a mysterious new arrival; it is a known, life-altering threat. Its risk waxes and wanes with weather and insect populations, but it has one simple preventative: not allowing yourself to be bitten by a mosquito.

And yet: Here are the CDC’s most recent maps of neuroinvasive West Nile—showing that people are still falling to its most dire complication, 14 years after it was identified.

The CDC's maps for 2011-2014 showing the incidence of "neuroinvasive" West Nile virus disease; areas in black had the highest incidence.
The CDC’s maps for 2011-2014 showing the incidence of “neuroinvasive” West Nile virus disease; areas in black had the highest incidence.
Graphic by Maryn McKenna using maps by the CDC; originals available here.

The point here is not that people are careless or unthinking; in the early years of West Nile, two of the victims were the husband of the CDC’s then director, and the chief of its mosquito-borne diseases division, who would have been well aware of the risks. (Both recovered fully.) The point is that always behaving in a manner that protects you from a mosquito bite—conscientiously, persistently, faultlessly emptying pots and puddles, putting on long sleeves and repellent, choosing when not to go outdoors—is very difficult to maintain.

Zika is not West Nile. Among other things, Zika is spread by many fewer species of mosquitoes — one or possibly two, compared to 65 for West Nile. And West Nile’s non-human hosts, birds, live in closer proximity to more of us than Zika’s, which appear to be non-human primates. But though the rare, deadly complications of West Nile virus infection are different from those of Zika, they are just as serious and life-altering — and yet we failed to protect ourselves from them. As Zika spreads, we can hope that is a lesson we learn in time.

Previous posts in this series:

A Blog by

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:

A Blog by

Zika Virus: A New Threat and a New Kind of Pandemic

An Aedes aegypti mosquito, the chief vector of Zika virus.
An Aedes aegypti mosquito, the chief vector of Zika virus.

The leader of infectious disease research in the U.S. government says that the pandemic of Zika virus spreading across the global south, which may be causing an epidemic of birth defects in South America, heralds a new kind of infectious disease threat. It is exploding at the same time and in the same areas as other diseases carried by the same vector, mosquitoes—and thus demonstrates that it is no longer enough to be prepared to counter one disease at a time.

Dr. Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, writes in a study released Wednesday in the New England Journal of Medicine with Dr. David Morens of NIAID that Zika arrives in the Americas on the heels of three other mosquito-borne diseases: West Nile virus, in the United States since 1999 and still causing cases; chikungunya, which has invaded the Caribbean and Central America; and dengue, which moved north from the tropics to become re-established in Florida.

“Zika virus forces us to confront a potential new disease-emergence phenomenon: pandemic expansion of multiple, heretofore relatively unimportant arboviruses previously restricted to remote ecologic niches,” they write. “To respond, we urgently need research on these viruses and the ecologic, entomologic, and host determinants of viral maintenance and emergence. Also needed are better public health strategies to control arboviral spread.”

As I reported a month ago, Zika—which is often a mild disease of fever, aches and rash—has spiked extraordinary alarm in Brazil because it is overlaid with, and may be causing, an epidemic of babies being born with unusually small brains and heads. The microcephaly, as it is called, has not been proven to be caused by Zika, but people are so alarmed that, as one commenter here wrote, “People here are very worried about Zika virus, especially pregnant women and the ones trying to get pregnant… In the timespan of two weeks my city has gone from ‘never heard of this virus’ to thousands of infecteds, inclunding myself, my husband, and several relatives and friends of mine.”

At that point, Zika had spread from the shoulder of South America up through Central America and into Mexico. Since then, it has also been found in Puerto Rico, in a person who had not traveled outside the country—putting it on U.S. soil though not in the continental United States—and on Monday, in the vicinity of Houston, though that person was probably infected while traveling.

Zika, dengue and chikungunya are spread by the same mosquito species, A. aegypti, which has adapted to live near humans: It flourishes in small pools and containers of water, like a flower pot or the puddle in a tire. There are limited tests for the diseases—none for Zika, and sparsely distributed ones for the other two —and no treatments for them other than supportive care. Their initial symptoms are similar, but because they have different serious complications—birth defects for Zika, hemorrhagic fever for dengue, reactive arthritis for chikungunya—it is possible to make mistakes in the early stages that can make the late consequences worse.

The researchers argue that all of this adds up to a new responsibility to both prevent diseases, and also confront that prevention is a broader task than has previously been understood. In the case of these mosquito-borne diseases, a “one bug one drug” approach is inadequate, they say. What is needed: broad-spectrum drugs that can address whole classes of viruses, and vaccine “platforms” that can be adjusted as needed to prevent infection with whatever virus arrives on the scene. But more broadly, these diseases provide a lesson, of how rapidly and lethally emerging threats—possibly, multiple threats— will take us by surprise if we do not prepare.

“In our human-dominated world, urban crowding, constant international travel, and other human behaviors combined with human-caused microperturbations in ecologic balance can cause innumerable slumbering infectious agents to emerge unexpectedly,” they write. “We clearly need to up our game with broad and integrated research that expands understanding of the complex ecosystems in which agents of future pandemics are aggressively evolving.”


Previously on Phenomena:

Dec. 2, 2015: Mosquitoes Bring Disease, Maybe Birth Defects, to US Border.





A Blog by

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

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

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

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

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

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

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

Yes, but why?

What keeps all those bacteria from decomposing you alive?

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

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

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

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

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

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

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

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

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

A Blog by

Look Up! There’s an Invisible Zombie Highway Right Above You

Step outside on a clear day this summer and look up.

What do you see? Blue. Nothing more. Or so you think.

But surprise! In July and August, an enormous herd of animals is passing directly over our heads. There are so many creatures up there, creatures that are so busy, so athletic, so tiny, so invisible. I’m talking about three to six billion of them every month soaring through the air directly above us. You should meet them. They are insects. High-flying insects. When I read about them in a science paper five years ago (I was at NPR at the time), I made this video, which provides a short introduction:

And now for the update.

It turns out, as you just saw, that the highest flying insect made it to 19,000 feet above sea level. That’s almost the height of Mount McKinley in Alaska. But more recently scientists have found another, even higher zone that’s also home to live critters that soar way, way up—miles higher, to the upper edge of the Earth’s atmosphere.

They are Earthlings that spend days, even weeks, practically in outer space.

What Are They?

According to David J. Smith and his team at the University of Washington and Kostas Konstantinidis and his team at Georgia Tech, there are thousands of species of very small, simple Earth life—bacteria, fungi, viruses—that get swept up by storms and make it to where there’s hardly any oxygen, where the temperatures are fiercely cold, and where they’re no longer protected from solar radiation by the Earth’s ozone layer.

And yet, write Peter Ward and Joe Kirschvink in their new book A New History of Life, most of these microbes will eventually come back down to Earth no worse for wear. They’re teeny. You can’t see them without a microscope. Typically, it would take almost 40,000 of them laid end to end to make it around your thumb.

Drawing by Robert Krulwich
Drawing by Robert Krulwich
Drawing by Robert Krulwich

But there are lots of them up there, so many that Ward and Kirschvink say this zone is becoming “the most newly discovered ecosystem on Earth,” a vast territory (many, many times greater than our oceans) where microbes routinely spend time dancing in the air.

Drawing by Robert Krulwich
Drawing by Robert Krulwich
Drawing by Robert Krulwich

Some bacteria have been in this high zone so regularly or for so long that they’ve adapted to life in the sky. Some species develop pigments that mimic sunscreen; some, says the New York Times, feed only on cloud water; and some can reproduce within clouds.

Drawing by Robert Krulwich
Drawing by Robert Krulwich
Drawing by Robert Krulwich

Scientists call this new family of creatures-in-the-sky “high life,” and it is a biological zone with its own rules. Up there is not like down here.

How Do They Survive Up There?

For one thing, scientists differ about how microbes at the upper end of the zone stay alive. When deoxygenated and freezing, do they slow way, way down like a hibernating bear? Or do they go dormant and essentially suspend their lives until they return? Or, as Ward and Kirschvink suggest, do they spend a brief period being dead?


This is one of the most provocative passages in Ward and Kirschvink’s book. “Most of us would agree,” they write, “that for mammals, and perhaps all animals, dead is dead.” You don’t come back from “dead.” But then they go on:

“… in simpler life, such is not the case. It turns out that there is a vast new place to be explored between our traditional understanding of what is alive and what is not.”

What if, in this new airy realm high above the planet, there could be “a place in between,” where bacteria might take wing, arrive in that freezing, irradiated zone, lose their life-giving machinery, and then, somehow, on the trip back down, build it back again?

Ward and Kirschvink are both well-respected senior scientists. Ward studies mass extinctions, Kirschvink magnetofossils. Neither is given to overstatement, which is why when I hit this line in their book, I put down my copy, stared out the window and thought, What?

How can anything be undead?

In the chapter I was reading, Ward and Kirschvink explore how life came to be four billion years ago. They suggest that instead of a single Genesis-like event (a bag of inert chemicals suddenly sparks into living chemistry), maybe “in the beginning,” chemistry switched back and forth, sometimes alive (on), sometimes not (off), and maybe, just maybe, in the simplest creatures, this may still be a habit—in fact, it may be happening to this day. Very simple creatures high in the sky, they say, might be alive, then not, then alive again, or as they put it:

“Life, simple life at least, is not always alive.”

Woah! This is a new idea to me. I tried to talk more with Peter Ward, but he’s in Papua New Guinea doing ocean research in a dugout canoe and doesn’t have a good internet connection, and Kirschvink is not answering email at Caltech, where he teaches. But I’m curious: Have any of you readers bumped into this notion? Life de-animating, then reanimating? It seems wonderfully preposterous—and very intriguing.

Let me know …

Peter Ward and Joe Kirschvinck’s new book “A New History of Life: The Radical New Discoveries About the Origins and Evolution of Life on Earth” goes after the hardest questions in life’s history, how did we begin, how simple life grew more complex, the origin of sex; they attack these puzzles carefully, feasting on the latest and especially the wildest research, so if you want an up-to-date primer guaranteed to keep your inner-college-sophomore up all night arguing, binging on ideas, going “no way”—this is a pretty good book. I also relied on David Montgomery and Anne Bikle’s “The Hidden Half of Nature, The Microbial Roots of Life and Health,” to get my head around itty bitty bits of life, the fungi, the bacteria, the archaea, the viruses, the protists. Their book took me into intestines, soil, and, yes, to the sky. It comes out in November. Also, my artist for the video, Benjamin Arthur, is about the most elegant, sly, multi-talented illustrator around; give him a tale, he’ll give you a perfect look to tell it with. Each of our ventures has a completely different visual style. Check out Why Can’t We Walk Straight? Last year he even turned in a piece (not with me, alas) on microbes. You can find it here.

Editor’s Note: This post has been updated to correctly reflect the spelling of Anne Bikle’s name.

A Blog by

People Sometimes Like Stinky Things—Here’s Why

Updated September 30, 2015

A corpse flower smells like a heady mix of rotten fish, sewage, and dead bodies. It’s a stench meant to draw flies, but just as surely, it draws tourists. Braving a blustery Chicago night, thousands of people lined up Tuesday for a whiff of a corpse flower named Alice at the Chicago Botanic Garden.

This woman shows a classic "disgusted" face in a video about the 2013 blooming of a corpse flower (see video, top).
This woman shows a classic “disgusted” face in a video about the 2013 blooming of a corpse flower (see video, top).

In fact, the demand to see and smell a corpse flower is so great that botanical gardens now vie to own one. Gardeners lavish them with care, hoping to force more stinky blooms from a plant whose scent is so rare (up to a decade between flowerings) and so fleeting (eight to 12 hours) that visitors are often disappointed to miss peak stench.

But why do people want to smell the thing? The reaction is usually the same: the anticipation, the tentative sniff, then the classic scrunched-up face of disgust. And yet everyone seems happy to be there.

It turns out there’s a name for this: benign masochism.

Psychologist Paul Rozin described the effect in 2013 in a paper titled “Glad to be sad, and other examples of benign masochism.” His team found 29 examples of activities that some people enjoyed even though, by all logic, they shouldn’t. Many were common pleasures: the fear of a scary movie, the burn of chili pepper, the pain of a firm massage. And some were disgusting, like popping pimples or looking at a gross medical exhibit.

The key is for the experience to be a “safe threat.”

“A roller coaster is the best example,” Rozin told me. “You are in fact fine and you know it, but your body doesn’t, and that’s the pleasure.” Smelling a corpse flower is exactly the same kind of thrill, he says.

It’s a bit like kids playing war games, says disgust researcher Valerie Curtis of the London School of Hygiene and Tropical Medicine. “The ‘play’ motive leads humans (and most mammals, especially young ones) to try out experiences in relative safety, so as to be better equipped to deal with them when they meet them for real,” she says.

People around the world make the same face when disgusted, with a downturned mouth and sometimes a protruding tongue.
People around the world make the same face when disgusted, with a downturned mouth and sometimes a protruding tongue.

So by smelling a corpse flower, she says, we’re taking our emotions for a test ride. “We are motivated to find out what a corpse smells like and see how we’d react if we met one.”

Our sense of disgust, after all, serves a purpose. According Curtis’ theory of disgust, outlined in her insightful book “Don’t Look, Don’t Touch, Don’t Eat,” the things most universally found disgusting are those that can make us sick. You know, things like a rotting corpse.

Yet our sense of disgust can be particular. People, it seems, are basically fine with the smell of their own farts (but not someone else’s). Disgust tends to protect us from the threat of others, while we feel fine about our own grossness.

Then there are variations in how we perceive odors. Some smells are good only in small doses, as perfumers know. Musk, for instance, is the base note of many perfumes but is considered foul in high concentrations. Likewise for indole, a molecule that adds lovely floral notes to perfumes but is described as “somewhat fecal and repulsive to people at higher concentrations.”

University of California Botanical Garden
University of California Botanical Garden

No one has yet, to my knowledge, tried out a low dose of corpse flower in a perfume (though you can try on an indole brew in “Charogne,” which translates to “Carrion,” by Etat Libre d’Orange). But someone could. There’s an entire field of perfumery—called headspace technology, it was pioneered by fragrance chemist Roman Kaiser in the 1970s—that’s dedicated to capturing a flower’s fragrance in a glass vial and then re-creating the molecular mix chemically. I would love to see someone give eau de corpse flower a whirl, if only they can find a headspace vial large enough.

The stench of a corpse flower, after all, is a mix of compounds, including indole and sweet-smelling benzyl alcohol in addition to nasties like trimethylamine, found in rotting fish. So I’d be very curious to know if a small amount of corpse flower would be a smell we would hate, or maybe love to hate.

I’ll leave you with my favorite example of a “love to hate” smell, from my childhood in the 1980s. At a time when I loved Strawberry Shortcake dolls and scratch-and-sniff stickers, the boys in my class were playing with He-Man dolls. Excuse me, action figures. And among the coolest, and grossest, of them was Stinkor. He was black and white like a skunk, and his sole superpower was to reek so badly that his enemies would flee, gagging.

To give Stinkor his signature stink, Mattel added patchouli oil to the plastic he was molded from. (This confirms the feelings of patchouli-haters everywhere.) It meant that you couldn’t wash Stinkor’s smell away, and it wouldn’t fade like my Strawberry Shortcakes did. The smell was one with Stinkor. And of course, children loved him.

Writer Liz Upton describes the Stinkor figure that she and her brother adored (their mother did not). The kids would pull Stinkor out and scratch at his chest, smelling him again and again. “Something odd was going on here,” Upton writes. “Stinkor smelled dreadful, but his musky tang was strangely addictive.”

If you’re the kind of benign masochist who wants to smell Stinkor for yourself, you can pay $125 or more for a re-released collector’s edition Stinkor—or you can just find an old one on eBay. The amazing thing: 30 years later, the original Stinkor dolls still stink. And people still buy them.

A Blog by

The Week’s Most Eerily Fascinating Stories

I can’t look away.

That’s the mark of an eerily fascinating story, and this week served up a pile of them. Whether it’s the clown who scaled a cemetery fence in Chicago and then stood waving very, very slowly to passersby, or the discovery of a snake with four little grasping “hands,” it just seemed like a creepier-than-average week. So here’s a little roundup of spooky science that had me riveted.

(OK, the scary clown has nothing to do with science, but I made you look.)

Art + Science

Artist Kate Clark does taxidermy with a twist: she molds human faces from clay and shapes an animal’s skin over the face to create surreal hybrid creatures.

“This is not in an effort to create a creature from fantasy or nightmares,” writes Kathryn Carlson on National Geographic’s photo blog PROOF.

VIDEO: Human-Looking Faces on Animal Bodies—Taxidermy as Art

Instead, the artist hopes to “confront the viewer with mankind’s innate connection with the animal kingdom by evoking empathy, curiosity, and, sometimes, discomfort,” she says.

It is uncomfortable. To be honest, the first word that popped into my head when I saw the kudu with a human face was “abomination.” But then I watched the video and looked more closely at the creatures, and I was entranced by their eerie beauty. Consider this: Clark uses recycled pelts—ones rejected for normal taxidermy—and turns them into art with a conservation message.

People are, in some sense, wired to seek out human faces (hence pareidolia, seeing faces in inanimate objects like the moon, or toast). And we relate to them. So maybe seeing a reflection of our own faces in animal form does evoke a stronger sense of empathy for animals. Try it yourself and see.

Creepy Animals

Behold Tetrapodophis in its leggy glory.
Credit: Julius Cstonyi.

The four-legged snake takes the prize this week. The strange fossil was discovered lurking in a drawer in a German museum and inspired many colorful exhortations from the scientist who found it (“Bloody hell!”), much to the delight of science journalists.

As our own Ed Yong described, if the animal is indeed a four-legged snake, it is the only one ever found. Its discover calls it the Archaeopteryx of the snake world, linking snakes and their lizard ancestors as Archaeopteryx linked birds with dinosaurs.

But is it even a snake? As Yong and others note, some scientists are not convinced. Maybe it’s an offshoot in one of many experiments in leglessness that reptiles have played out over the millenia. Either way, it’s an important find. “This is the single most extraordinary fossil that I’ve ever seen,” vertebrate paleontologist Bhart-Anjan Bhullar told Sid Perkins in Science. And the idea of a constrictor holding its prey with tiny feet is also pretty creep-tastic.

Also of note on the nightmare-animals beat: the plant that covers itself in insect corpses to attract bodyguards. It’s a “beneficial coating of death.”

Spooky Trick

The skeleton flower turns from white to clear when wet. As the flowers transform, pieces of petal appear to almost melt away, revealing white “bones” before the whole petal disappears.

Super cool, but how does it work?

I had trouble finding a satisfying explanation in short blog posts and videos, but here’s a paper that tells more. Jiale Yong and colleagues used the flowers as inspiration for new materials that turn clear underwater. “The color does not come from a natural white pigment; rather it results from the highly loose cell structure of the plant petals,” they write.

Here’s how it works. On a sunny day, light reflects off the interface between plant cells and air pockets between them, creating the white color. When it rains, water floods the spaces between cells and because light passes similarly through both the rainwater and the fluid in the plant cells (technically, they have about the same refractive index), the whole petal turns transparent!

Oh No, Not Dolls
Oh yes. Linda Rodriguez McRobbie has a long story on Smithsonian.com about the history of creepy dolls. It’s currently listed as the most popular story on the website, which says a lot about the concept of morbid curiosity.


The story traces some well-worn turf about the uncanny valley and movies featuring murderous playthings, but also points out some interesting research on whether the uncanny valley is real and on what creepiness really is: possibly a state of hyper-vigilance when faced with ambiguity. Or as McRobbie puts it, “If someone is acting outside of accepted social norms—standing too close, or staring, say—we become suspicious of their intentions. But in the absence of real evidence of a threat, we wait and in the meantime, call them creepy.”

Bonus: the story links to an article on the history and psychology of scary clowns. Heaven help us.

A Blog by

Should You Put a Baby Bird Back in the Nest? Depends If It’s Cute

Ah, the first days of summer—the smell of cut grass, kids on vacation… and baby birds falling out of trees.

Every year, I see a new flock of people rescuing fallen birds, and then arguing on Twitter and Facebook about whether it’s OK to put them back in the nest.

Some are adamant that if you handle a baby bird, its mother will reject it. Others say it’s fine; just put the bird back.

A lot of people face this dilemma at the beginning of summer, when many baby birds are taking their first flight from the nest—in bird-nerd speak, they’re fledging. I was in Mississippi in early June, and it seemed like it was raining dead baby birds there. One fell from its nest onto my car, and another mysteriously turned up on the porch steps. It was too late for those birds, but what do you do when faced with a little peeper like this?

First, you should ask yourself how cute the bird is.

Okay, that sounds cruel and judgmental. But it’s basically true. The Cornell Lab of Ornithology gives excellent advice: The first thing you need to know is whether the baby is a nestling or a fledgling. Most of the birds people find are fledglings. Fledglings have feathers, can hop, and are “generally adorable and fluffy, with a tiny stub of a tail.”

“When fledglings leave their nest they rarely return, so even if you see the nest it’s not a good idea to put the bird back in—it will hop right back out. Usually there is no reason to intervene at all beyond putting the bird on a nearby perch out of harm’s way and keeping pets indoors.”

And if you’ve got an ugly little unfeathered friend?

“If the baby bird is sparsely feathered and not capable of hopping, walking, flitting, or gripping tightly to your finger, it’s a nestling.

If you can find the nest (it may be well hidden), put the bird back as quickly as possible. Don’t worry—parent birds do not recognize their young by smell. They will not abandon a baby if it has been touched by humans.”

So leave the cute ones alone, and put the little ratty-looking ones back in the nest.

And if you don’t stumble across any fledglings this year, the Cornell Lab of Ornithology has a website where you can watch live video of baby birds on Birds Cams.

There are plenty of adorable Bird Cam moments, like this fledgling hawk returning to the nest and checking out the camera.

But it wasn’t all pretty. “This has been probably our toughest year on record,” says Charles Eldermire, who runs the Bird Cams program. The ospreys were hit by dime-sized hail a week before their eggs were to hatch, cracking all the eggs. A baby owl died, and the parents fed it to its siblings. Eldermire even had to put up warnings that viewers had to click on before watching particularly bad things happening.

“We started this project in part to help people learn about what happens in nature,” Eldermire says. “We’re aware that many have never had an unfiltered view of what happens in nature.”

The Bird Cam folks make a point of not interfering. “We can learn by letting it play out. Any intervention could have a negative impact; if we feed that baby owlet to save it, maybe it’s sick, or maybe the environment won’t support another barn owl.”

I love what Eldermire said next. Think about this as you watch the ospreys in the video above hunker over their eggs in a hailstorm: “The struggles that we go through as people in our own lives aren’t all that different from the animals on the screen.”

“The truth is we can’t control everything in our lives. One thing we can all learn from watching wild things and how they survive is that sense of resilience that is really at the core of any wild thing.”