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English Mass Grave Sheds New Light on the Horrors of the Black Death

Smithsonian Magazine

The Black Death is among the most traumatic epidemics in recorded history. The disease swept through 14th century Europe, killing hundreds of millions of people. Now, a newly-discovered burial pit at the site of a former abbey in the English countryside could shed new light on how people outside of major cities were devastated by the plague, Haroon Siddique reports for The Guardian.

Historians estimate that nearly half of England’s population was killed by the plague in the mid-14th century, but until now the only cemeteries that researchers knew of with evidence of the Black Death were found inside London. But recently, archaeologists working at the ruins of a medieval abbey in the countryside north of the capital came across a mass grave dating back to 1349, a year after the plague first hit England, writes Siddique.

"The finding of a previously unknown and completely unexpected mass burial dating to this period in a quiet corner of rural Lincolnshire is thus far unique, and sheds light into the real difficulties faced by a small community ill-prepared to face such a devastating threat," Hugh Willmott, a researcher at the University of Sheffield's Department of Archaeology, says in a statement.

The grave contained 48 skeletons, 27 of which were children. After the archaeologists uncovered it, they were able to recover tooth samples from some of the remains, which were then sent off to McMaster University in Canada for DNA analysis. The scans found traces of DNA left from Yersinia pestis, the bacterium responsible for the plague, suggesting that these bodies fell victim to the black death, the BBC reports.

An archaeologist examining the remains of plague victims buried at Thornton Abbey, north of London. (University of Sheffield)

The origins of the pit may be gruesome, but finding a mass burial like this is rare in England. Most people at the time were buried in graves in their local parish, as communities tried to maintain some semblance of normal rites despite the high death rates, Oliver Moody reports for The Times. Even though these bodies were buried all together, they were still found laid out in even rows, suggesting that the mourners still took care with the bodies of the deceased.

“You only get graves like this when the normal system of burial has broken down,” Willmott tells Moody. “Whether the priest [was] dead or the gravediggers had died, we don’t know. This clearly was a community that was hit very hard and had to rely on the monastery for help.”

In addition to the human remains, Willmott and his colleagues uncovered little trinkets and remnants of the things these people may have carried while alive. One intriguing find was a small amulet in the shape of a T, which people at the time may have believed could cure certain diseases, Moody reports.

As the excavation continues, Willmott and his team hope that they can uncover more details about these people’s lives from objects from the mass grave and more genetic clues gathered from the remains. With more insight into how these people lived, historians can finally start to figure out how people in the countryside managed the devastating disease.

A pendant found at the site shaped like a "Tau Cross," which may have been believed to cure sickness. (University of Sheffield)

Playing Pandemic, the Board Game

Smithsonian Magazine

Sunday afternoon, some friends and I sat down to play Pandemic, the board game. It seemed appropriate, since we had just been discussing the swine flu outbreak. Pandemic is a cooperative board game in which 2 to 4 people work together to cure four diseases before it’s too late. There is no winner—either you all win or you all lose (i.e., everyone dies).

Each person takes on a role—such as scientist or medic—and on each turn travels the world, treating people, building research centers and finding cures for the four diseases. Through careful planning, players collaborate to decide where they should go and what actions to take to most effectively and quickly find the cures before the diseases spread out of control. At the end of a turn, new cities are infected, and if they reach a certain level of infection, the disease spreads to neighboring cities. Occasionally an epidemic (card) will occur and make the situation even worse.

One oddity of the game is that it ends when the four cures are found, not when all of the cities are wiped clean of disease. It seemed somewhat mean to leave people still sick. Also, we found that the game was too easy for us. There never seemed to be a time when we were at risk of a true pandemic—we seemed to be controlling the outbreaks well enough and finding cures quickly.

Some of the dissatisfaction may derive from the cooperative nature of the game. Perhaps it would have been more challenging if one player had been selected to work against the others. Or there could have been more roadblocks, such as uncooperative governments, rapidly mutating viruses or treatments/vaccines that lost efficacy. But overall Pandemic seems to have a good basis in actual disease treatment, and it was pretty fun, too.

Real life is, of course, both simpler and more complex than the game. Simpler, because we are unlikely to encounter four diseases spreading so quickly at the same time. And we can see the complexity in each day’s news about swine flu (the H1N1 virus).

This morning brought the report of the first swine flu death in the United States—a child in Texas. Anything more I write is likely to be out of date by the time you read it, so here are some good sources for up-to-date information on swine flu:

CDC’s Swine flu page

WHO Swine influenza page

Flu Wiki

Also, the blogs Effect Measure and Aetiology are keeping a close watch on this.

My advice: Don’t panic.

Human Diseases May Have Doomed the Neanderthals

Smithsonian Magazine

In the last decade, researchers have realized that the interactions between ancient humans and Neanderthals were much more complicated than previously believed. Not only did Homo sapiens compete with Neanderthals for resources, we extensively interbred with our hominid cousins, an inter-species hookup that gave some modern humans one to four percent of Neanderthal DNA. A new study shows that humans likely gave Neanderthals something too: tropical diseases.

The study, published in the American Journal of Physical Anthropology suggests that waves of ancient humans traveling out of Africa and into the Neanderthal’s stronghold in Europe probably passed along bugs like tuberculosis, herpes, tapeworms, and stomach ulcers.

“Humans migrating out of Africa would have been a significant reservoir of tropical diseases,” study author Charlotte Houldcroft of Cambridge University’s Division of Biological Anthropology says in a press release. “For the Neanderthal population of Eurasia, adapted to that geographical infectious disease environment, exposure to new pathogens carried out of Africa may have been catastrophic.”

It was assumed many infectious diseases evolved after the development of agriculture, which allowed humans to crowd together in cities and put them in regular contact with domestic animals. But recent studies of infectious disease genomes reveal that they developed tens of thousands or millions of years earlier. Though the researchers found no direct evidence for transmission of disease between humans and Neanderthals, the paper suggests that these new timelines for diseases means its highly likely humans carried them when they migrated into Neanderthal territory.

Melissa Hogenboom at the BBC points out that researchers thought that Heliobacter pylori, the bug that causes stomach ulcers appeared about 8,000 years ago, soon after the beginning of agriculture. But H. pylori’s genome reveals it is at least 88,000 years old. A study of Herpes Simplex 2, the cause of genital herpes, shows it was transmitted to humans from an unknown hominid 1.2 million years ago.

Unlike disease transfers from Europeans to Native Americans, which led to massive epidemics like smallpox that killed millions of people in a short period of time, it’s more likely the disease transfer between humans and Neanderthals was much more localized, Houldcroft says. Because hunter-gathers lived in small bands of about 15 to 30 people, infectious diseases would have affected one isolated band at a time, weakening their overall health.

“Our hypothesis is basically that each band of Neanderthals had its own personal disaster and over time you lose more and more groups,” she tells Hogenboom. “I don't think we'll ever find a [single] theory of what killed the Neanderthals, but there is increasing evidence that lots of things happened over a period of a few thousand years that cumulatively killed [them] off.”

Children in the U.S. Are Eating Fewer Calories, But Fewer Is Still Too Many

Smithsonian Magazine

Photo: jamieanne

In the U.S., children consumed fewer calories in 2010 than they did a decade ago. But before anyone runs out to get a celebratory muffin, heath experts warn that the decline was pretty incremental, meaning we haven’t beat the obesity epidemic quite yet. The New York Times reports:

For boys, calorie consumption declined by about 7 percent to 2,100 calories a day over the period of the analysis, from 1999 through 2010. For girls, it dropped by 4 percent to 1,755 calories a day.

National obesity rates for children have been flat in recent years, but some cities have reported modest declines. The new evidence of a lower calorie intake for children may also foreshadow a broader national shift, experts said.

The study revealed that a drop in carbohydrate and sugar intake likely explained the calorie decrease. Calories from fat remained stable, while those from protein rose. 

The calorie decline was most pronounced among boys ages 2 to 11, and among teenage girls.

Carbohydrate consumption declined among white and black boys, but not among Hispanic boys. Among girls, whites were the only group that consumed fewer calories from carbohydrates.

According to Yahoo News, the Centers for Disease Control researchers behind the study found their results surprising given that childhood obesity levels in the country as a whole have not declined.

The Chicago Tribune points out that this may be because children get many of their calories from saturated fat, found in butter, coconut oil, animal fat, dark chocolate, cheese, whipped cream and processed meat.

Recommended U.S. guidelines suggest that no more than 10 percent of one’s daily calories should come from such fat, but American youth took in between 11 percent and 12 percent from 2009 to 2010, data from the CDC’s National Center for Health Statistics showed.

America leads the world in calorie consumption and portion sizes: seventeen percent of children—12.5 million—in the U.S. are obese, and another third are overweight.

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Why Warmer Weather Probably Won’t Stop COVID-19

Smithsonian Magazine

COVID-19 is not the flu. But amidst the ongoing pandemic, many people hold out hope that the two diseases have something crucial in common: a seasonality that will loosen the global grip of SARS-CoV-2 as the weather warms.

Many infectious diseases wax and wane with the changing months. Some, like flu, spike when the weather turns cold, while others, like cholera, thrive during warm, rainy summers. Whether such a pattern applies to SARS-CoV-2 is unclear. With spring just barely sprung, scientists haven’t had the time to suss out SARS-CoV-2’s annual schedule—if it sticks to one at all.

Besides, relying on seasonality to curb a pandemic can be a dangerous line of thought, says C. Brandon Ogbunu, a computational epidemiologist at Brown University.

“Seasonality has the potential to decrease the rate of infection,” he says. But this factor alone won’t get the world anywhere close to resolving the outbreak. “If I was a betting person … all [my money] would be on the impact of human behavior and infrastructure” to slow transmission, he adds. “That’s where we need to put our emphasis.”

Why Are Diseases Seasonal, Anyway?

The first time a severe infectious disease tears through a new population, it’s sure to wreak havoc. Without previous exposure, no members of the community are immune, leaving the virus with numerous potential hosts to sustain it for months to come, regardless of the weather forecast.

Columbia University epidemiologist Micaela Martinez compares early outbreaks to a fire igniting in a forest full of kindling. The occasional rainstorm might do a bit to slow the conflagration. But with so many vulnerable trees, a touch of precipitation would be nowhere near enough to snuff out the flames. “For the first wave, the seasonality is not as relevant,” she says. “We can’t expect [the virus] to just go away.”

Peak flu activity in the United States by month for the 1982-1983 through 2017-2018 flu seasons. During this 36-year period, flu activity most often peaked in the winter months. (CDC)

Once the current pandemic subsides, however, future infections would propagate amongst a population with a smaller proportion of immune individuals. These likely tamer outbreaks could reveal a seasonal cycle, which Martinez believes is a quality ubiquitous among infectious diseases. In 2018, she set out to catalog these trends and was surprised to find that all of the nearly 70 infections she studied showed some sort of seasonal rise and fall.

Generally speaking, Martinez says, each season comes with a distinct infectious twist: Winter winds bring bouts of pneumonia, flu and other respiratory diseases before the blooms of spring usher in bursts of chickenpox and herpes. The arrival of summer sees spikes in Lyme disease, polio and syphilis before autumn resets the cycle with blips of yellow fever. Other diseases are generalists, favoring any extended period of dryness or rain, especially in and around the tropics where seasonal boundaries blur.

Disentangling the drivers of these patterns is a complex pursuit. Some factors are obvious: Infections caused by bacteria, parasites or viruses that must be ferried from host to host by an insect vector like a mosquito will inevitably ebb and flow with the natural breeding seasons of their buggy chauffeurs. In other cases, the environment can have a direct effect on the pathogen, Ogbunu says. Some viruses—including influenza and SARS-CoV-2—are packaged in a fragile, fatty outer layer called an envelope that’s both necessary for infection and sensitive to harsh conditions, including heat and the ultraviolet rays found in sunlight. High humidity can weigh down the infectious, airborne droplets needed to ferry the virus from person to person, preventing the microbes from traveling as far.

To further complicate matters, our bodies feel the effects of weather and climate. Studies in mice have shown that low humidity can compromise the germ-trapping mucus in their airways and impair the production of critical immune molecules, leaving the rodents more vulnerable to flu viruses, explains Laura Yockey, a virologist at Massachusetts General Hospital.

And biology doesn’t manifest in a vacuum. Disease-transmitting behavior also shifts with the seasons, triggering outbreaks that can even override a pathogen’s typical itinerary. Children returning to school at the beginning of fall, for example, can prompt an uptick in certain infections like chickenpox. Similarly, people gathering indoors during rainy summer months can spread flu during its “off” season.

These patterns are so pronounced that they “almost form a calendar” of pathogens that humans can track and follow, says Elena Naumova, an epidemiologist at Tufts University. “I honestly believe by nature, life on our planet is seasonal,” she says. “Therefore, infections are seasonal, too.”

What We Can Do Right Now

As a respiratory virus with a delicate envelope, SARS-CoV-2 has several traits that might someday reveal a seasonal pattern. Years from now, if or when the pathogen returns to the human population, COVID-19 cases may peak when the weather is consistently cold and dry, before dipping down in summer months. For now, though, Naumova says that passively waiting for the virus to disappear is “nonsense.” A population’s suceptibility to a given infection trumps all else. And with so many vulnerable individuals around, any warmth-related wanes in disease will do little to rein in its spread.

Seasonality’s influence—or lack thereof—on this coronavirus shouldn’t inspire feelings of helplessness. Quite the opposite, Naumova says. “We cannot control the weather,” she says, but we can control “how we prepare for that specific weather.” The same goes for infectious disease. As such, humans should take charge of the disease driver they know best: their behaviors. As the pandemic continues to evolve, Ogbunu stresses the importance of continuing to drive down risks for transmission. Practicing good hygiene, avoiding crowds and being mindful of our surroundings remain crucial—to protect not only ourselves, but also those around us whose wellbeing depends on the actions of their fellow community members.

“One of the main drivers of epidemics are contact rates,” Martinez says. “It can make a huge impact on disease transmission. Just like it can drive epidemics, it can stop them.”

Ask Smithsonian: Is the World Due for Another Massive Plague Outbreak?

Smithsonian Magazine

The specter of another plague like the one that affected Eurasia in the middle of the 14th century has hung like a ghastly pallor over the intervening centuries. But the likelihood of a naturally occurring outbreak happening on that massive a scale is extremely unlikely in modern times.

The Black Death of the 1300s has been noted as one of the worst pandemics in recorded history, killing 25 to 30 percent of the inhabitants of Europe, North Africa and the Near East and possibly affecting as many in China, India and the Far East as well. Some 50 million people died.

Unsanitary living conditions and a complete ignorance of what caused the disease or how it was transmitted fueled the spread of the plague across continents. As the world has developed, plague has become less of a threat. The World Health Organization estimates that in 2013, for instance, there were just 783 cases of plague across the globe, resulting in 126 deaths.

Modern sanitation and scientific and medical advances have had a big impact. Humans in the 21st century are also a lot different than the ones who walked the Earth 700 years ago; they’re better-nourished and have stronger immunity, says Amesh Adalja, a senior associate at the University of Pittsburgh Medical Center’s Center for Health Security.  “It’s the effect of civilization overall that has made plague less likely,” says Adalja.

Adalja says he “highly doubts that a massive plague outbreak” could occur again—at least on its own. But an epidemic fueled by a plague-based bioterror weapon is another issue.

The Black Death was due to the naturally occurring bubonic form of plague. Rats infested with fleas carrying the Yersinia pestis bacterium were sharing close quarters with humans. Now, as it was then, people bitten by infected fleas will develop flu-like symptoms within days, with a sudden onset of fever, chills, aches, nausea and vomiting.

If left to its own devices, the bacteria quickly replicate in lymph nodes; the nodes spread the agent throughout the bloodstream, leading to hemorrhaging and eventually septicemia (blood poisoning) and death. Often, if the victim lives long enough, the buboes burst, becoming open sores that ooze bacteria. The infection tends to kill within days or a week. Even after death, cadavers can still be infectious.

Fourteenth century humans didn’t understand infectivity, but when the Black Death began ravaging the Crimean peninsula, the Tartars—who had been engaged in a multi-year war in the area—began catapulting the suppurating bodies of plague victims over the walls of Kaffa, today’s Feodosia in Ukraine. The plague likely spread inside the city as people tried to move the mangled, odiferous cadavers. Many researchers cite the attack as the first known episode of biowarfare, says Adalja.

Meanwhile, the bubonic plague spread throughout Eurasia along shipping routes, thanks to rats that stole aboard the vessels. Eventually that outbreak died down, but there have been others throughout the centuries. No one truly understood what caused plague or how it spread until Swiss scientist Alexandre Yersin discovered a bacterium—isolated from buboes­­—while investigating an outbreak in China in 1894. The microbe was later named Yersinia in his honor.

Meanwhile, the plague continues to surface periodically, particularly in Africa, Asia and South America.

The disease did not get to the United States until 1900, arriving in San Francisco, via China, carried by infected rats riding on steamships. More than 100 people died within the decade. The plague then spread south to Los Angeles causing a short epidemic in 1924. Harbored by rats and other small animals, the plague made its way out to the desert east of Los Angeles and then kept going.

Most of the American cases—anywhere from one to 17 a year—occur in northern New Mexico, northern Arizona, southern Colorado, California, southern Oregon and western Nevada.

This year, a Colorado teenager died from the bubonic plague in June, and an adult from the state died in August. A Michigan woman was diagnosed in September, after traveling to Colorado.

Plague isn’t always transmitted by fleas. It can also be spread when someone expels the bacteria through coughing or sneezing. The aerosolized droplets can be inhaled, leading to pneumonic plague.

In May, the U.S. Centers for Disease Control and Prevention reported on a 2014 outbreak in Colorado, in which a dog got plague and then transmitted it to its owner by coughing. Two veterinary employees also were infected by the dog, and another worker may have been infected by the owner. All had the pneumonic form, and all survived, except the dog.

Left untreated, the plague kills 90 percent of those infected. But it can be cured with common antibiotics, and with treatment, only about 16 percent of those infected with any plague will die.

A vaccine, however, has been more elusive. Researchers have tried to improve on a vaccine that was used beginning in the late 1800s to no avail. Even though the U.S. has few cases, a vaccine would be useful in developing countries, says Adalja. And, he adds, “plague is a national security threat, and that has fostered a lot of investment in developing countermeasures.”

The Japanese Imperial Army developed and used plague as a weapon of war, launching at least one attack against the Chinese in 1940, and was preparing to use it in the U.S.

The former Soviet Union had a large bioweapons program, including plague-based weapons, as did Iraq, and both North Korea and Syria are rumored to have bioweapons, Adalja says.

The U.S. had an offensive bioweapons program until 1969, he says. Now, “we have some of these pathogens to develop defensive measures,” including vaccines and treatments, Adalja adds.

The plague—especially the pneumonic form—could be an effective weapon, in part because it might not be immediately diagnosed. And that’s probably about the only way a new Black Death pandemic could occur.

It's your turn to Ask Smithsonian.

What can two 19th century cartoons reveal about disease and hysteria?

National Museum of American History

Every few years, we read the headlines about a new, or resurgent, disease that threatens global health. Fears of transfer erupt and hysteria sets in, at least in the initial months. If someone coughs in public, I'll recoil in concern; who knows if they have this year’s contagious disease? Every stranger becomes suspect. Of course, a more rational version of myself would realize that a cough could be caused by anything.

When it comes to disease, fear of air quality and of strangers has historical roots. One of the first epidemic diseases to excite worldwide hysteria was cholera. According to Dr. Margaret Linley, cholera became "a media disease," through the explosion of widely disseminated writings and images that intensified fear of the disease. Likewise, the historian Christopher Hamlin, explains, "it was the magnitude of the reaction to it that cholera stands out as the signal disease of the 19th century." Despite its extensive media coverage, cholera was far from the greatest killer of the 19th century (compared to malaria and tuberculosis) and rarely visited western nations.

We now know that the Vibrio comma is a marine organism that spreads through infectious vomit and fecal matter (that can contaminate food, water supplies, and even linen), but cholera remained a mysterious disease throughout much of the 19th century. When it first reached Europe and North America in 1832, cholera came as a shock to 19th century sensibilities as fluids streamed uncontrollably from both ends. Dehydration turned skin a deathly blue, made eyes appear sunken, and thickened the blood. Its onset was sudden and it could kill within hours. This initial visit would kill thousands and "King Cholera" returned to western nations four more times during the century.

The Cholera Prevention Man. Wundet, Germany and England, ca., 1830s 

While researching cholera for my advisor at the museum, I found two seemingly humorous cartoons dating to the 1830s in the museum's Medicine and Science collection. These images were first loaned to the museum—when it was still the National Museum of History and Technology—in 1945 as part of a collection of European pharmaceutical artifacts from the 15th to 19th century. Both titled "Cholera Prevention Man," they depict a man covered from head to toe in protective layers in an attempt to safeguard himself from the oncoming cholera epidemic. Germ theory had not been developed, nor was the cause of cholera understood, but bodies were still in danger. Medical writings and images were internationally exchanged, as Western nations tried to find cures and explain the horrifying disease.

The first image illustrates many 19th century remedies and preventatives for cholera. Wrapped around his waist is a grey "cholera belt" (a thermal remedy primarily used by British soldiers in order to keep the body warm), while a mask and container of camphor or vinegar vapors envelope his face in an effort to neutralize any cholera miasmas that tainted the atmosphere. He stands in a doorway made of boxed medicinals (such as calomel, cayenne pepper, and laudanum) as well as other treatments for cholera: a clyster and hot water bottle (to administer enemas) and a commode. The words roughly translate to "a well stocked home to prevent cholera." However, the ghostly apparition of cholera still lurks behind the man. Desperate people stocked their “medicine cabinets” with numerous treatments and remedies from both medical men and quacks alike that ranged from sadly ineffective to wildly dangerous.

The second cartoon (published both in German and English) is a satirical comment on the effectiveness of the overabundance of protective items that were sought out as fear of the approaching cholera pandemic grew. In the English version of this cartoon, the caption warns: "By exactly following these instructions you may be certain that the cholera… will attack you first." Early theory established that cholera was not contagious because filth and overall poor sanitation that produced miasmas in the air were attributed to its cause. 

The Cholera Prevention Man. Moritz Gottlieb Saphir, Germany and England, ca., 1832. Thousands of copies of this image were produced and disseminated. Image from the museum's Medicine and Science collection.

Both cartoons express this miasma theory through their concern with purification and sanitation (the man has both a juniper bush and vapor mask to purify the air). Yet, in mocking the effectiveness of the protective items, the cartoon expresses a widespread uncertainty regarding cholera's contagiousness since it was known to travel along trade routes over land and sea. This uncertainty of the disease's contagiousness is reflected in the ex-mayor of New York's, Philip Hone's, personal writings on September 20, 1832, "It is stated that forty-nine thousand five hundred and sixty-nine emigrants have arrived at Quebec… a large proportion find their way into the United States destitute and friendless. They have brought the cholera this year, and they always bring wretchedness and want."

Cholera became intertwined with the anxieties over the health of the social body. Not surprisingly, poverty and immigrants seemed to attract the disease. Cholera did strike its victims disproportionally from the poor; however, in the 19th century a life of filth and ruined morality was largely seen as a personal choice, instead of a result of poverty, poor infrastructure, and a lack of resources. Both cholera and immigration influenced newly forming cities. While Western nations became increasingly involved in the global world in the 19th century, there were increased global movements of people, especially from non-Protestant and non-white backgrounds. In America, the threat of cholera was one of the biggest concerns proposed by those who supported restricted immigration. Two of the earliest International Sanitary Conferences (the predecessor to the World Health Organization) grappled with the issue of cholera's contagiousness as well as with the attempt to coordinate measures to prevent cholera's spread from India (as it was regarded to be the home of cholera) into Europe.

In Western nations, huge capital investments in water sanitation created cholera-free cities while other measures within cities began under public health movements in order to track the disease and prevent its spread. However, the stigma of filth as a cultural choice is still prevalent as countries in Africa, South Asia, and South America deal with the seventh pandemic that has been raging since the 1960s as a result of a lack of infrastructure and resources.

Kayla Reddecliff is an intern in the Medicine and Science department. One of her favorite areas of study is the history of fashion, so disease prevention costumes were a perfect fit.

Medicine and Science Intern Kayla Reddecliff
OSayCanYouSee?d=qj6IDK7rITs OSayCanYouSee?d=7Q72WNTAKBA OSayCanYouSee?i=IvJ9gmZy6DQ:9XEc_Sy-Vlg:V_sGLiPBpWU OSayCanYouSee?i=IvJ9gmZy6DQ:9XEc_Sy-Vlg:gIN9vFwOqvQ OSayCanYouSee?d=yIl2AUoC8zA

Violence Among Teens Can Spread Like a Disease, Study Finds

Smithsonian Magazine

If you’re a teenager, how do you know whether it’s cool to smoke cigarettes, curse or get a cartilage piercing? Look around: To find out what’s socially acceptable, impressionable adolescents generally turn to their peers. Now, new research finds that this social dynamic also plays out when it comes to more violent behaviors.

A new study, published yesterday in the American Journal of Public Health, draws on surveys of thousands of teens to reveal how the people around you influence your tendency to engage in violence. The authors report that adolescents are far more likely to commit a violent act if a friend has already done so—adding evidence to a mounting theory that violence in communities can spread like a disease.

The study was born of an unusual collaboration between Ohio State University social psychologist Brad Bushman and OSU political scientist Robert Bond. Bushman, who has written and lectured extensively on humans and violence, was interested in exploring the model of violence spreading like a contagious disease that had beens popularized by University of Illinois at Chicago epidemiologist Gary Slutkin. Bond had expertise in analyzing social networks. "We just really hit off and decided that we should to try find a way to merge our research interests," Bond says.

For the study, the two tracked the behavior of more than 90,000 American teenagers at 142 schools, who were surveyed in class starting in the mid-1990s as part of the National Longitudinal Study on Adolescent to Adult Health. By accessing follow-up interviews that were done with nearly 6,000 of the teenagers years later, the researchers were able to see whether they had practiced violent behavior in the past year—namely, getting into a serious fight, pulling a weapon on someone or hurting someone badly enough that they needed medical attention.

The teenagers were then asked to identify five male and five female friends, who were subsequently interviewed by the surveyors about their violent behavior. With this web of data, Bond and Bushman were able to piece together nodes of violence and their effect on the people connected to them.

What they found was a contagious model. Teenagers were 48 percent more likely to have been in a serious fight, 140 percent more likely to have pulled a weapon and 183 percent more likely to have hurt someone badly enough to require medical attention if they knew someone who had done the same. Moreover, the influence of one violent person can spread through up to 4 degrees of separation. In other words, if your friend's friend's friend's friend practices violent behavior, it's more likely you will too.

"People who exhibit these kinds of behaviors tend to be friends with one another," Bond says, adding: "They're teenagers. They're still sort of learning how to navigate their social environment."

For years, social scientists have theorized that violent behavior can spread from person to person like an illness, infecting whole neighborhoods and communities. This contagious theory was pioneered by Slutkin, who spent his early career working to prevent the spread of communicable diseases such as tuberculosis in San Francisco and Somalia, and AIDS in Uganda.

After returning to the U.S., Slutkin was troubled by the amount of violent crime he saw present in American culture. “I saw that these kids were killing each other,” he says. Soon, he started to see parallels between how violence was being viewed and treated by officials and how the AIDS epidemic was mismanaged and underfunded. “[Violence] is the only contagious epidemic that is not being managed by the health sector,” Slutkin says. “It's been fundamentally misdiagnosed.”

In 2000, Slutkin founded the movement Cure Violence to gain support for viewing violence as a contagious disease as opposed to solely a criminal justice issue. Cure Violence uses epidemiological techniques to target the people most at risk of spreading violence, and by working to stop its spread by “interrupting” violence before it starts. Slutkin has given a TED Talk on his approach, which was featured in the 2011 documentary The Interrupters. Cure Violence’s model, however, has faced resistance from law enforcement suspicious of treating violent criminals as victims.

Slutkin says that Bushman and Bond’s study adds to the now “thousands of studies that show the contagion of violence.” It also shows evidence that different forms of violence can be similarly contagious, from physical fights to violence using weapons, he says. This supports what he’s seen in his work. “We all unconsciously copy each other, especially with violence,” Slutkin says.

When it comes to other communicable diseases—say, a virus—the best way to avoid falling ill is to avoid the bug in the first place. Bushman thinks that this avoiding exposure is also the best for prevent violent behavior in teenagers. He also believes that the same contagious model could be used to spread non-violent behavior: By training teenagers to practice more empathy, schools and social workers could unleash positive behavior into social networks that would spread to people who don't receive treatment directly, he says.

Bond pointed to school-based violence prevention programs already in place across America to train students to practice peaceful conflict resolution, and said that their research could lead to better targeting of teenagers who would have the most social influence on their networks. "Those types of programs might be a lot more effective," Bond says, "because they're affecting not only who is directly affected by it, but the other people who see the changes in those people's behavior."

For future research, Bond is considering collecting his own data on how teenagers process and react to violence in some kind of a laboratory setting, while Bushman is interested in studying how violence could spread through other kinds of social networks, such as networks of terrorists on social media or in neighborhoods worldwide.

Slutkin, meanwhile, still hopes that people and governments will someday adopt his model of ending preventable violence. He draws parallels between his model and the new theory of our solar system proposed by astronomer Galileo Galilei, who faced opposition when his observations of the planets and moons didn’t fit with the prevailing theory of an Earth-centered solar system. “The theory was wrong,” Slutkin says. “It required a new theory.”

As the World Faces One of the Worst Flu Outbreaks in Decades, Scientists Eye a Universal Vaccine

Smithsonian Magazine

With the deadly 2017-2018 flu season still fresh in public health officials’ minds, this year’s outbreak is shaping up to be just as severe. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases (NIAID), says this flu season could be one of the worst in decades. “The initial indicators indicate this is not going to be a good season—this is going to be a bad season,” Fauci told CNN earlier this month.

Last week, the Centers for Disease Control and Prevention announced that there have been at least 9.7 million cases of the flu since early October. The CDC has also been tracking flu mortality, reporting at least 4,800 flu-related deaths this season. The young, elderly and immuno-compromised are especially susceptible to the flu—this season, 33 children have died from the virus.

Even in mild cases, the flu virus can cause unpleasant symptoms like high fevers, muscle aches and fatigue. To protect yourself against the annual flu outbreak, public health officials have a simple piece of advice: get your flu shot.

While the flu shot is the best defense currently available against seasonal influenza, it is not 100 percent effective. The CDC reports that the influenza vaccine typically reduces the risk of illness by between 40 and 60 percent, and that’s only if the viruses included in the vaccine match the subtypes of influenza circulating that season.

As an RNA virus, influenza has a high tendency to mutate, Fauci told Smithsonian. Even within subtypes of influenza, the virus’s genetic code is constantly mutating, causing season-to-season changes that scientists call antigenic drift.

“Most of the time, the virus changes just enough from one season to another so that last year's flu isn't exactly the same as what this year's flu is,” Fauci says. “In order to get optimal protection, you recommend vaccinating people every year. That's very unique. There really is no other vaccine that you recommend somebody getting vaccinated every single year.”


To keep up with antigenic drift, scientists are constantly tweaking the flu vaccine, which is designed to respond to a surface protein called hemagglutinin, targeting what Fauci calls the “head” of the protein. “When you make a good response, the good news is you get protected. The problem is, the head is that part of the protein that has a propensity to mutate a lot.”

The other end of the protein—the “stem”—is much more resistant to mutations. A vaccine that targets the hemagglutinin stem has the potential to provide protection against all subtypes of influenza and work regardless of antigenic drift, offering an essentially universal defense against the flu. NIAID, part of the National Institutes of Health (NIH), is currently working to develop a candidate for a universal flu vaccine in a Phase 1 clinical trial, the first time the vaccine candidate has been given to people. Results on the safety and efficacy of the vaccine are due in early 2020.

Along with protecting against the seasonal influenza, a universal vaccine would also arm humanity with a weapon against the next pandemic strain of the flu. Flu pandemics come along occasionally and unpredictably, usually when a subtype of influenza jumps from animals to humans. This phenomenon, called antigenic shift, introduces a flu so novel to humans that our immune systems are caught entirely off guard.

The most severe flu pandemic in recorded history was the 1918 influenza, which infected one-third of the world’s population and claimed at least 50 million lives. The first outbreak of illness occurred at Camp Funston in Fort Riley, Kansas, in March 1918, according to the CDC. Genetic evidence suggests the particular virus came from a bird. The deployment of troops to fight in World War I contributed to the spread of disease, and at the conclusion of the war, the flu’s death toll surpassed the total number of civilian and military casualties due to the fighting. Unlike the seasonal flu, the 1918 pandemic was fatal for many otherwise healthy adults aged 15 to 34, lowering the life expectancy in the United States by more than 12 years.

Kanta Subbarao, director of the World Health Organization Collaborating Centre for Reference and Research on Influenza, says there are three criteria for a strain of influenza to be considered pandemic: novelty, infectiousness and ability to cause disease. “If a novel virus emerges, we need to know two things,” she says. “What is the likelihood that it would infect humans and spread? But also, if it were to do that, how much of an impact would it have on human health?”

The infectiousness and severity of impact can dictate whether a pandemic turns out to be relatively mild, like the 2009 swine flu, or as brutal as the 1918 epidemic.

Sabrina Sholts, curator of the exhibition “Outbreak: Epidemics in a Connected World” at the Smithsonian’s National Museum of Natural History, says the human activities that drive the emergence and spread of disease—like living in close quarters and traveling around the globe—have only intensified since 1918. But while globalization can escalate the transmission of disease, it can also facilitate the worldwide dissemination of knowledge.

“Now, we have a means to monitor and coordinate globally that didn't exist at that time [in 1918],” Sholts says. “I think that that communication is a tremendous tool, and that's an opportunity to respond rather quickly when something like this happens.”

Subbarao points to the WHO’s Global Influenza Surveillance and Response System (GISRS) as one example of global cooperation on flu research. She estimates that there are about 145 national influenza centers in 115 countries monitoring seasonal influenza, as well as any flu viruses that manage to jump from animals to humans.

In a statement in March, WHO Director-General Tedros Adhanom Ghebreyesus announced a Global Influenza Strategy for the upcoming decade. The strategy has two overarching goals: to improve every country’s preparedness to monitor and respond to influenza and to develop better tools to prevent and treat influenza. Research on a universal vaccine could support the second objective of arming the global population with a stronger defense against the flu.

“The threat of pandemic influenza is ever-present,” Ghebreyesus said in the statement. “We must be vigilant and prepared. The cost of a major influenza outbreak will far outweigh the price of prevention.”

Anti-vaccination in America

National Museum of American History

In 1926 seven-year-old Belema Siegfried was turned away from school. The reason? Her parents had refused to submit paperwork proving that she had been vaccinated. Several months after Belema was turned away from school, her father, a Brooklyn chiropractor named Louis Siegfried, was arrested. Siegfried's arrest may have been calculated; just six months before his arrest, he had launched a new journal, The Quest (Against Vaccination and Cruel Vivisection). Like many of his fellow chiropractors, Siegfried advocated a non-interventionist approach to health, seeing vaccination as an "inherent poison" which was introduced into a healthy body.

The Quest was divided into two main themes. The first half discussed vaccination; the second discussed vivisection. (Vivisection is the practice of operation on a living animal.) However, the placement of anti-vaccination articles in the journal—at the front of the journal—as well as the tone of Siegfried's language when discussing vaccination indicate that his first and paramount concern was probably the issue of compulsory vaccination.

Cover of "The Quest," which includes illustrations of a baby and a dog

Siegfried claimed that his journal would conduct a "clean fight" against vaccination. However, in his first issue, he lambasted advocates of vaccination, calling them "unfair, ungenerous, misleading and untruthful." Insisting that pro-vaccinators often demonstrated a "brazen flaunting of false claims" while promoting "tampered statistics," Siegfried provided his readers with a range of arguments, both religious and medical, against compulsory vaccination.

But the centerpiece of the first issue of The Quest was the story of "Little Belema Siegfried," who had been denied admission to school because her parents had refused to allow her to be vaccinated. The Quest was printed anonymously, making it appear that the story of "Little Belema" had no relationship to the editor of the journal. However, Siegfried used the news articles covering his arrest to promote not only his anti-vaccination views, but also his journal.

Photo of article titled "Writ in Child's Case Tests School Vaccination"

The Quest was just one of many journals founded to oppose vaccination. In some ways, the vocal and highly organized nature of anti-vaccination societies during the late 19th and early 20th centuries made it difficult for a small journal such as The Quest to succeed; facing a great deal of competition, many of these journals folded relatively quickly. The Quest, however, was published for six years—between 1926 and 1932. It folded only with the death of its founder in 1932.

Even as vaccination against smallpox became increasingly common in the 19th century, many people viewed this procedure with skepticism. Part of the problem stemmed from the fact that, while the smallpox vaccine worked, scientists and physicians could not explain just why vaccination worked. The development of vaccines against a variety of other disease, including rabies during the mid-19th century, did little to assuage many people's concerns.

In 1879 Americans opposed to vaccination founded the Anti-Vaccination Society of America. Other smaller and more local anti-vaccination groups such as the New England Anti-Compulsory Vaccination League also emerged during this period.

If anti-vaccinators had any doubts about the justice of their cause, two high-profile events in the early 20th century reinforced their concerns. In 1901 contaminated diphtheria antitoxin led to the death of thirteen children in St. Louis. That same year, contaminated smallpox vaccine also caused the death of several children in Camden, New Jersey.

In response, Congress passed the Biologics Control Act in 1902, establishing standards for the development of vaccines and requiring pharmaceutical companies which produced vaccines to possess a license.

In 1905, reassured no doubt by the purity of vaccines that were now used, the Supreme Court upheld the right of states to require compulsory vaccination. Compulsory or mass vaccination can arrest an epidemic, protecting those who are too young to be vaccinated or those who have suppressed immune systems. In early 20th century America, where epidemics of potentially lethal diseases such as smallpox often ran rampant, compulsory vaccination made a great deal of sense as it protected large segments of the population.

Pin that says, "I am vaccinated with Mulford's vaccine, are you?"

But not everyone embraced the idea of compulsory vaccination. From the 19th and well into the 21st century, Americans have debated and rejected vaccination on religious grounds, others have rejected the idea on political grounds, and still others have argued that vaccination not only failed to protect people against any diseases, it actually causes disease.

Alexandra M. Lord, Ph.D., is chair of the History of Medicine and Science division.

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Monday, August 31, 2015 - 08:30
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Can Saving Animals Prevent the Next Deadly Pandemic?

Smithsonian Magazine

In the fall of 2014, the deadly Ebola virus jumped from an unknown animal to a 2-year-old boy in Guinea. The virus quickly spread to others around him and began terrorizing West African nations; by April 2016, more than 11,000 people had died. Researchers now believe that fruit bats were the origin of this zoonotic disease—which refers to any disease that makes the jump from animals to humans (or vice versa), and includes around 75 percent of all emerging infectious diseases. 

Zoonotic diseases are at the root of some the world’s worst pandemics. Bubonic plague, for instance, originated in city rats, and was usually transferred to humans via an infected flea bite. HIV/AIDS started as a virus in Old World monkeys in Africa. The more recent swine flu, while less fatal, has been traced back to pigs raised for food in North America. The Spanish Influenza of 1918 has been traced back to birds and killed around 50 million people, more than twice as many as were killed in World War I. 

Not all of these species-jumping sicknesses are viruses. Bubonic plague stems from a bacterial infection, and malaria, which may have killed as many as half of all humans who have ever lived, is a parasite transmitted by mosquitoes. But there’s a reason viruses are the inspiration behind classic pandemic horror stories like World War Z or Contagion.

“Many of the bacterial or fungal or parasitic diseases that humans get from animals are harder to transmit between people,” says Kali Holder, a wildlife pathologist and Morris Animal Foundation Global Health Fellow at Smithsonian. “Viruses mutate so much faster than anything else, and because many are easily transmitted, what you have is a perfect storm.”

Yet the Ebola outbreak, bad as it was, could have been much worse. In August of that same year, another scare quietly took place in the Équateur Province of the Democratic Republic of the Congo. But in that case,  just 49 people died, and the World Health Organization declared the end of the outbreak within three months. This remarkable success was thanks to fast action by local governments, medical partners and a relatively new global disease surveillance network known as USAID PREDICT.

Now eight years old, USAID PREDICT is a collaborative effort to monitor, predict and prevent emerging diseases, many of them zoonotic, from becoming devastating global pandemics the likes of Ebola. It’s led by Jonna Mazet, an epidemiologist at the University of California at Davis’s One Health Institute and School of Veterinary Medicine, and also partners with the Wildlife Conservation Society, Metabiota, EcoHealth Alliance and the Smithsonian Institution’s Global Health Program.

In the case of Ebola in 2014, PREDICT had done extensive advance work in the DRC, training local researchers in safe sampling techniques and setting up a regional network to respond quickly to zoonotic diseases like Ebola. That work is a big part of why most people never heard of that second Ebola outbreak.

Image by Wikimedia Commons. A physician dressed in the attire to treat the Bubonic plague in the 17th century. (original image)

Image by Wikimedia Commons. Boccaccio's "The Plague of Florence in 1348." The Bubonic plague has killed millions of people around the world. (original image)

Image by Wikimedia Commons. An emergency hospital that popped up during the Spanish Influenza outbreak of 1918, which killed 50 million people. (original image)

In its first five years, PREDICT trained 2,500 government and medical personnel in 20 countries on things like the identification of zoonotic diseases and implementing effective reporting systems. They collected samples from 56,340 wild animals, using innovative techniques like leaving chew ropes for monkeys then collecting saliva afterwards. They also detected 815 novel viruses—more than all the viruses previously recognized in mammals by the International Committee on Taxonomy of Viruses.

Part of the way PREDICT prevents outbreaks is by monitoring diseases in animals, in the hopes of keeping viruses from crossing over to humans. So far the group has provided support during 23 outbreaks and four wildlife epidemics; it also creates vaccines for domestic livestock like poultry. This is all part of the “one health” theory that undergirds the program: When wildlife and ecosystems are healthy, and diseases are diluted, humans are healthier, too.

Which means that the immediate goal of human health comes with a nice side effect: wildlife conservation.

“When you disrupt an ecosystem by removing a species through culling, you have a less healthy ecosystem and higher risk of disease,” says Megan Vodzak, a research specialist for Smithsonian’s Global Health Program. “Sometimes you increase the level of the virus within the population because you eliminate some but not all of the animals, and they’re still circulating it.”

This is known as the dilution effect, which hypothesizes that a higher rate of species richness creates a buffer against zoonotic pathogens.

In her pathology work for Smithsonian’s Global Health Program, Holder has done everything from develop safer protocols for collecting samples from bats—“they’re amazing transmitters of disease, so we [have to find] how much we can detect without putting our grubby little paws on a grubby little bat”—to identifying a pathogen causing oozing skin lesions in rhinos (it turned out to be a nematode worm).

While this work undoubtedly helps the animals suffering from these pathogens, it could also have benefits for humans. “Not only are we responding to save ecosystems and endangered animals, we’re also the first line of defense with regards to identifying potential zoonotic diseases,” Holder says.

Even though the animals at the National Zoo aren’t exposed to most of the diseases wild populations contract, scientists can use the captive species to learn about treatment. One recent example is using long-lasting antibiotics in giant pandas. “Now that we know they can maintain levels for over 10 days, that changes how we would treat an animal in the wild,” says Suzan Murray, director of the Global Health Program. Smithsonian virologists, pathologists, anesthesiologists and wildlife veterinarians who can identify diseases in lions and elephants and rhinos all contribute their knowledge and expertise to the program.

For those who value both conservation and human health, the idea that protecting wildlife can also mean preventing epidemics is a welcome one. But, like most conservation challenges in world shaped by humans, it’s not always that simple. A recent study published in the journal Philosophical Transactions of the Royal Society B found no significant human health benefit from increasing biodiversity. The researchers surveyed biodiversity and infectious diseases around the world for 20 years (they used forestation as a proxy for biodiversity, since there are no reliable counts of species going back 20 years).

Although this study looked at 24 known diseases rather than emerging pandemic threats, the lessons may still be applicable when it comes to conservation. “Results from our analysis indicate as you increase forest, you can exacerbate the number of diseases transmitted,” says Chelsea Wood, one of the study’s authors and a conservation ecologist at the University of Washington. “That’s a message I hesitate to deliver as a conservationist, but it’s what the data show.”

Wood became skeptical of the dilution effect when she did comparative studies of islands being fished versus un-fished. What she found was that certain parasites actually disappeared in the presence of fishing, and flourished in the more “pristine” environment. She found another example in onchocerciasis, a disease transmitted by a parasitic worm in East Africa known more commonly as “river blindness.”

Since a drug was invented to treat river blindness in the 1970s, the disease has declined dramatically. But another reason for the decline, Wood points out, is regional deforestation. River blindness is transmitted by black flies that breed on the backs of crustaceans that live in shadowy freshwater rivers. As shade cover from trees decreased due to deforestation, the prevalence of the disease-transmitting flies lessened as well.

“I know that conservation provides so many benefits to human society beyond infectious disease transmission,” Wood says. “But [with dilution theory] we consistently find a mixed bag, which is not a good outcome for people interested in selling conservation as disease control.”

Again, Wood emphasized that her findings apply to known diseases, not future possible pandemics we have yet to identify. But when researchers do embark on conservation projects, she cautions that they should also consider other possible outcomes besides the protective benefit humans get from healthy wildlife and ecosystems. “We have to recognize that conservation could provide benefits for public health and it could endanger public health," she says.

How the 1918 Flu Pandemic Helped Advance Women’s Rights

Smithsonian Magazine

When disaster strikes, it can change the fabric of a society – often through the sheer loss of human life. The 2004 Indian Ocean tsunami left 35,000 children without one or both parents in Indonesia alone. The Black Death killed more than 75 million people worldwide and more than a third of Europe’s population between 1347 and 1351.

While disasters are by definition devastating, sometimes they can lead to changes that are a small silver lining. The 2004 tsunami ended a civil conflict in Indonesia that had left 15,000 dead. The 14th century’s plague, probably the most deadly disaster in human history, set free many serfs in Europe, forced wages for laborers to rise, and caused a fundamental shift in the economy along with an increased standard of living for survivors.

One hundred years ago, a powerful strain of the flu swept the globe, infecting one third of the world’s population. The aftermath of this disaster, too, led to unexpected social changes, opening up new opportunities for women and in the process irreversibly transforming life in the United States.

The virus disproportionately affected young men, which in combination with World War I, created a shortage of labor. This gap enabled women to play a new and indispensible role in the workforce during the crucial period just before the ratification of the 19th Amendment, which granted women suffrage in the United States two years later.

Why did the flu affect men more than women?

Known as the Spanish flu, the 1918 “great influenza” left more than 50 million people dead, including around 670,000 in the United States.

To put that in perspective, World War I, which concluded just as the flu was at its worst in November 2018, killed around 17 million people – a mere third of the fatalities caused by the fluMore American soldiers died from the flu than were killed in battle, and many of the deaths attributed to World War I were caused by a combination of the war and the flu.

The war provided near perfect conditions for the spread of flu virus via the respiratory droplets exhaled by infected individuals. Military personnel – predominantly young males – spent months at a time in close quarters with thousands of other troops. This proximity, combined with the stress of war and the malnutrition that sometimes accompanied it, created weakened immune systems in soldiers and allowed the virus spread like wildfire.

When soldiers shipped out, influenza virus could be stowing away onboard. (AP Photo)

Overcrowding in training camps, trenches and hospitals created an ideal environment for the 1918 influenza strain to infect high numbers of people. In fact, the conditions of war helped the virus perfect itself through several waves of infection, each more deadly than the last.

Many troops were doomed before they even reached Europe, contracting the flu on the packed troop ships where a single infected soldier could spread the virus throughout. When soldiers returned to the U.S., they scattered to every state, bringing the flu along with them.

It was more than just male conscription in war, however, that led to a greater number of men who were infected and died from the flu. Even at home, among those that were never involved in the war effort, the death rate for men exceeded that of women. Demographic studies show that nearly 175,000 more men died than women in 1918.

In general, epidemics tend to kill more men than women. In disease outbreaks throughout history, as well as almost all of the world’s major famines, women have a longer life expectancy than men and often have greater survival rates.

The exact reason why men tend to be more vulnerable to the flu than women continues to elude researchers. The scoffing modern term “man flu” refers to the perception that men are overly dramatic when they fall ill; But recent research suggests that there may be more to it than just exaggerated symptoms.

The flu’s aftermath furthered a trend started by the war effort. (AP Photo)

Flu brought more women into the workforce

The severity of the epidemic in the U.S. was enough to temporarily shut down parts of the economy in 1918. In New England, coal deliveries were so severely affected that people, unable to keep their homes heated, froze to death at the height of winter. During the 1918 flu outbreak, researchers estimate businesses in Little Rock, Arkansas, saw a decline of 40 to 70 percent.

The worker shortage caused by the flu and World War I opened access to the labor market for women, and in unprecedented numbers they took jobs outside the home. Following the conclusion of the war, the number of women in the workforce was 25 percent higher than it had been previously and by 1920 women made up 21 percent of all gainfully employed individuals in the country. While this gender boost is often ascribed to World War I alone, women’s increased presence in the workforce would have been far less pronounced without the 1918 flu.

Women began to move into employment roles that were previously held exclusively by men, many of which were in manufacturing. They were even able to enter fields from which they had been banned, such as the textile industry. As women filled what had been typically male workplace roles, they also began to demand equal pay for their work. Gaining greater economic power, women began more actively advocating for various women’s rights issues – including, but not limited to, the right to vote.

Once a woman’s the boss, how can you deny her the vote? (AP Photo)

How the flu helped change people’s minds

Increased participation in the workforce allowed many women to obtain social and financial independence. Leadership positions within the workforce could now be occupied by women, especially in the garment industry, but also in the military and police forces. The U.S. even got its first woman governor, when Nellie Taylor Ross took her oath of office, in 1923, in Wyoming. An increased ability to make decisions in their personal and professional lives empowered many women and started to elevate their standing.

With the war over and increased female participation in the labor force, politicians could not ignore the critical role that women played in American society. Even President Woodrow Wilson began to argue in 1918 that women were part of the American war effort and economy more broadly, and as such, should be afforded the right to vote.

Outside of work, women also became more involved in community decision-making. Women’s changing social role increased support for women’s rights. In 1919, the National Federation of Business and Professional Women’s Clubs was founded. The organization focused on eliminating sex discrimination in the workforce, making sure women got equal pay and creating a comprehensive equal rights amendment.

The 1918 influenza pandemic was devastating. But the massive human tragedy had one silver lining: It helped elevate women in American society socially and financially, providing them more freedom, independence and a louder voice in the political arena.

This Pandemic Isn't the First Time the Hajj Has Been Disrupted for Muslims

Smithsonian Magazine

Saudi Arabia has urged Muslims to delay their plans for the hajj, amid speculation that the obligatory pilgrimage may be canceled this year due to the coronavirus.

Earlier this year, Saudi authorities halted travel to holy sites as part of the umrah, the “lesser pilgrimage” that takes place throughout the year.

Canceling the hajj, however, would mean a massive economic hit for the country and many businesses globally, such as the hajj travel industry. Millions of Muslims visit the Saudi kingdom each year, and the pilgrimage has not been canceled since the founding of the Saudi Kingdom in 1932.

But as a scholar of global Islam, I have encountered many instances in the more than 1,400-year history of the pilgrimage when its planning had to be altered due to armed conflicts, disease or just plain politics. Here are just a few.

Armed conflicts

One of the earliest significant interruptions of the hajj took place in A.D. 930, when a sect of Ismailis, a minority Shiite community, known as the Qarmatians raided Mecca because they believed the hajj to be a pagan ritual.

The Qarmatians were said to have killed scores of pilgrims and absconded with the black stone of the Kaaba—which Muslims believed was sent down from heaven. They took the stone to their stronghold in modern-day Bahrain.

Hajj was suspended until the Abbasids, a dynasty that ruled over a vast empire stretching across North Africa, the Middle East to modern-day India from A.D. 750-1258, paid a ransom for its return over 20 years later.

Political disputes

Political disagreements and conflict have often meant that pilgrims from certain places were kept from performing hajj because of lack of protection along overland routes into the Hijaz, the region in the west of Saudi Arabia where both Mecca and Medina are located.

In A.D. 983, the rulers of Baghdad and Egypt were at war. The Fatimid rulers of Egypt claimed to be the true leaders of Islam and opposed the rule of the Abbasid dynasty in Iraq and Syria.

Their political tug-of-war kept various pilgrims from Mecca and Medina for eight years, until A.D. 991.

Then, during the fall of the Fatimids in A.D. 1168, Egyptians could not enter the Hijaz. It is also said that no one from Baghdad performed hajj for years after the city fell to Mongol invasion in A.D. 1258.

Many years later, Napolean’s military incursions aimed at checking British colonial influence in the region prevented many pilgrims from hajj between A.D. 1798 and 1801.

Diseases and hajj

Much like the present, diseases and other natural calamities have also come in the way of the pilgrimage.

There are reports that the first time an epidemic of any kind caused hajj to be canceled was an outbreak of plague in A.D. 967. And drought and famine caused the Fatimid ruler to cancel overland Hajj routes in A.D. 1048.

Cholera outbreaks in multiple years throughout the 19th century claimed thousands of pilgrims’ lives during the hajj. One cholera outbreak in the holy cities of Mecca and Medina in 1858 forced thousands of Egyptians to flee to Egypt’s Red Sea border, where they were quarantined before being allowed back in.

Indeed, for much of the 19th century and the beginning of the 20th century, cholera remained a “perennial threat” and caused frequent disruption to the annual hajj.

So did the plague. An outbreak of bubonic plague in India in 1831 claimed thousands of pilgrims’ lives on their way to perform hajj.

In fact, with so many outbreaks in such quick succession, the hajj was frequently interrupted throughout the mid-19th century.

Recent years

In more recent years, too, the pilgrimage has been disrupted for many similar reasons.

In 2012 and 2013 Saudi authorities encouraged the ill and the elderly not to undertake the pilgrimage amid concerns over Middle East Respiratory Syndrome, or MERS.

Contemporary geopolitics and human rights issues have also played a role in who was able to perform the pilgrimage.

In 2017, the 1.8 million Muslim citizens of Qatar were not able to perform the hajj following the decision by Saudi Arabia and three other Arab nations to sever diplomatic ties with the country over differences of opinion on various geopolitical issues.

The same year, some Shiite governments such as Iran leveled charges alleging that Shiites were not allowed to perform the pilgrimage by Sunni Saudi authorities.

In other cases, faithful Muslims have called for boycotts, citing Saudi Arabia’s human rights record.

While a decision to cancel the hajj will surely disappoint Muslims looking to perform the pilgrimage, many among them have been sharing online a relevant hadith—a tradition reporting the sayings and practice of the prophet Muhammad—that provides guidance about traveling during a time of an epidemic: “If you hear of an outbreak of plague in a land, do not enter it; but if the plague breaks out in a place while you are in it, do not leave that place.”

The Story of a Resurrected Antiviral Could Hold Lessons for Combating Zika

Smithsonian Magazine

In 2009, pharma giant GlaxoSmithKline published an article in Antiviral Research describing a promising new drug its scientists had been investigating. The drug, called GSK983, was a broad-spectrum antiviral—a drug that could fight a variety of different viruses—that seemed to be effective against HPV, mononucleosis and more. The paper described the compound’s synthesis and effects and went on to conclude that it warranted further study. But strangely, according to the study, researchers had little idea how the compound worked.

The pharma giant put a lot of resources into the drug; a corresponding article shows synthesis on the scale of kilograms, and some animal trials were conducted. Then, the company quietly ceased its experiments. GSK983 had been abandoned.

Years passed, but the drug was not forgotten. When no subsequent articles came out, a group of scientists at Stanford decided to tackle the problem themselves. “It was interesting that there was a good antiviral that industry sort of left alone, probably because they could not explain the mode of action of this drug,” says Jan Carette, who runs a virology lab at the Stanford School of Medicine. Carette collaborated with colleagues from the genetics and chemistry departments on a study, published in Nature Chemical Biology in March, which examined GSK983’s mechanism and addressed some of its problems.

Thanks to several new techniques, GSK983 may have a future after all—one that could help doctors combat emerging diseases like Zika without having to go through as much FDA red tape. But GSK983 is just one drug, applicable only to certain classes of viruses. It could be great, or it could merely be one in a line of compounds in the search for broad-spectrum antivirals—and a program of dual genetic screening pioneered in this study could be a potent tool that'll speed up the whole process.

If you have a bacterial infection, you go to the doctor, who prescribes an antibiotic. Some are more effective than others, and some are better suited to particular infections, but in general, if you throw an antibiotic at a bacterium, it’ll clear up the infection. Not so with viruses, most of which require their own targeted drugs or vaccines. The process to develop such treatments can stretch a decade or more, by which time the virus has often evolved and changed.

This is why a broad-spectrum antiviral could be so powerful. Having one drug (or a small number of drugs) that are applicable in emerging epidemics like Zika, as well as rare diseases that don’t attract enough attention to warrant specific drugs, would be hugely important to both pharmaceutical companies and public health organizations, speeding up global epidemic response and saving lives.

But typically, antiviral development a painfully slow process. Unlike bacteria, which are susceptible to general antibiotics, it’s a challenge to make compounds that will target multiple viruses because the way viruses replicate are so varied, and because they’re active within the host’s cells, explains Johan Nyets, a professor of virology at the University of Leuven, Belgium who has been advocating broad-spectrum research for decades.

The pace of drug development can be key in minimizing the scale of an outbreak. “If a new pathogen is emerging, as was the case with Zika, and you have to start developing drugs at the time that this novel pathogen emerges, you’re too late because it takes an average 8-10 years before you have a compound developed in the lab to clinical use,” says Nyets. As Congress debates how (and how much) to fund Zika research, we fall farther and farther behind.

GSK983 targets a class of viruses that hijack a host cell’s RNA and uses that replication mechanism to make more viruses. Disrupting that process (a technique known as host targeting) is one way to attack an infection, but because the enzymes the virus uses to hijack the host cell are important for the host itself, side effects often include killing or stunting the very cells we’re trying to protect.

The Stanford crew suspected that this may be what was holding GSK983 back. In the original paper, the authors mentioned that host cells would sometimes die or cease to multiply when the drug was administered. “The challenge is to separate the antiviral and growth inhibition effects,” wrote the authors. GlaxoSmithKline has confirmed that the drug never progressed to human trials due to toxicity.

“We really have no idea what GSK’s plans were for this drug, what their actual findings are, internally,” says Michael Bassik, an assistant professor whose lab ran genetic screens for the Stanford study. Bassik’s needed to discover exactly what genes the drug targeted, so that they could figure out what was killing the cells. To do this, he employed an entirely new technique—or, really, two techniques in parallel: CRISPR and RNA interference.

CRISPR is the latest gene editing technology du jour, using a protein to splice, or in this case, cut out genetic information. It’s not quite so simple as toggling a switch, but the process effectively turns off the genes one at a time, to see which change the behavior of the drug.

RNA interference, on the other hand, introduces a piece of RNA data which, when transcribed, suppresses gene action, rather than shutting it off completely. Because this modifies the genes’ function, rather than destroying them, they maintain some of their actions. Thus, the technique generates data on essential genes that, were they knocked out completely, would kill the cell.

Each technique finds a different set of genes; by cross-referencing them, the Stanford team was able to isolate probable targets—that is, the genes (and the enzymes they produce) that the drug affects.

“The point of this paper is to say, you do get, by doing these two strategies in parallel, a much more comprehensive picture of the biology of the system, and in this case, the biology of the way this particular drug works,” says Bassik.

What it showed was this: GSK983 works as an interferon—it blocks an enzyme called DHODH that is used in replication. (This was, in fact, GlaxoSmithKline’s guess as well.) Without that enzyme, neither the RNA-based virus nor the DNA-based cell can replicate. This insight gives researchers a better understanding of how to leverage the compound to fight these kinds of viruses without killing the cells they’re trying to save.

This still leaves the problem of toxicity. But by knowing what enzyme was blocked, the Stanford team was able to restore only the DNA replication by adding a compound called deoxycytidine, thus reversing toxicity but not antiviral activity. They demonstrated its efficacy with dengue, says Carette, and next steps include testing it on Zika.

This was only tested in vitro in the study, points out Bassik, and in vivo tests are in progress. It does suggest future potential for GSK983, but perhaps more importantly, it shows that the dual CRISPR/RNA screen could be useful against one of the major drug-discovery stumbling blocks. “You have a series of molecules, you don’t know what their target is,” says Bassik. “[If] we can come in with this technology and identify the actual target, it really should facilitate the development of those drugs.”

GlaxoSmithKline, for its part, is listening. “The renewed interest has motivated us to look again at how we can publish those data and make the information available to the scientific community,” says spokesperson Kathleen Cuca.

Are Fake Drugs The Reason Malaria Sickens Millions a Year?

Smithsonian Magazine

Malaria, a mosquito-borne parasitic infection that affects about 3.2 billion people in 95 countries, has become largely a disease of the young and poor.

Due to effective medications like chloroquine and artemisinins, malaria deaths dropped an estimated 60 percent worldwide between 2000 and 2015. The Americas and Africa saw the greatest improvements.

Still, 216 million new cases of malaria were reported in 2016, the latest data available. Most of them occurred in Nigeria, the Democratic Republic of the Congo, Uganda, Ivory Coast and Mozambique. And of the 445,000 people who died from the infection, about 70 percent were children under the age of 5.

If malaria is a curable disease with effective treatment, why does it still kill so many?


Our research on the pharmaceutical industry has revealed that one reason for malaria’s continued virulence in the developing world is ineffective medicine. In fact, in some poor African countries, many malaria drugs are actually expired, substandard or fake.

Globally, some 200,000 preventable deaths occur each year due to anti-malarial drugs that do not work. Substandard and counterfeit medicines may be responsible for up to 116,000 malaria deaths annually in sub-Saharan Africa alone, according to recent World Health Organization estimates.

Fraudulent pharmaceuticals are on the rise. Reports of counterfeit or falsified anti-malarials rose 90 percent between 2005 and 2010, according to a 2014 article in the Malaria Journal.

In 2012, a research team from the U.S. National Institutes of Health found that about one-third of anti-malarial medicines distributed in southeast Asia and sub-Saharan Africa were of poor quality. A few years prior, fully 44 percent of anti-malarial supplies in Senegal had failed quality control tests.

For as long as effective medicines have existed, people have produced fake versions. That’s because counterfeiting pharmaceutical drugs is profitable business for manufacturers. This illegal activity is most common in places with little government oversight and limited access to safe, affordable and high-quality medicines.

Various reports have found that many fake medicines originate in India, followed by China, Hong Kong and Turkey. Some illicit drug manufacturers appear to have connections with organized crime groups.

It’s a good racket: Public officials in the developing countries where these medicines are distributed typically struggle to detect and investigate the crime – much less prosecute it – due to lack of funding and regulatory restrictions.


Generally, fake malaria drugs imitate one of two types of common antimalarial medicines: quinines and artemisins.

Quinine and its chemical derivatives are derived from the bark of the South American quina-quina tree. Artemisinin is isolated from a variety of wormwood. Both medicines, which cost between $12 and $150 per course, are affordable to rich-world patients but largely inaccessible to people in countries where malaria is most widespread.

Quinine was first used to treat malaria in the 17th century. Synthetic quinine-based drugs became available in the early 20th century. The most common is chloroquine.

Artemisinin came about in the 1970s, though it had been used as a traditional Chinese medicine for hundreds of years. In combination with other anti-malarials, it is now the primary treatment for malaria, largely because it has less severe side effects than quinines.

Mosquitoes are only one problem when it comes to malaria. Fake medicines are another. (Athit Perawongmetha/Reuters)


Poor quality medicines – not just for treating malaria but in general – usually fall into one of three categories.

Medicines may be falsified, meaning that the treatment has been deliberately and fraudulently mislabeled with respect to identity, source or pharmaceutical content. Some fake drugs contain no active ingredients at all or contain them in incorrect amounts. This is generally a scam to earn money illegally.

Anti-malarial drugs distributed in the developing world may also be substandard. Such drugs are produced by legitimate manufacturers but are not compliant with World Health Organization standards. Frequently, they are short on artemisinin, the key active ingredient.

Such medicines, which may be produced deliberately or unintentionally, do not prevent malaria in the individuals who take them. Worse yet, they can lead the malarial parasite to develop drug resistance, a significant danger for everyone who lives in a place affected by malaria.

So far, resistance to drugs derived from artemisinin has only been reported in southeast Asia, but doctors fear resistance will spread.

Finally, medical literature shows that some anti-malarial drugs found in poor countries have either expired by the time they reach consumers or been damaged by exposure to extreme heat.


Ineffective malaria treatments – whether fake, substandard or degraded – are also expensive for consumers and national health care systems.

Patients who unwittingly purchase ineffective anti-malarial drugs are out of pocket for medicines that do nothing. Then, they pay for additional treatments when the first course of medicine fails.

According to the World Health Organization, repeated medical treatments due to ineffective drugs is estimated to cost to sub-Saharan African patients and health care providers as a whole about $38.5 million annually.

The problem of fake and substandard malaria drugs is so widespread that the World Health Organization, Global Fund and the United States Agency for International Developmenthave all developed guidelines regarding the procurement of malaria medicines.

A Guide to What to Know About COVID-19

Smithsonian Magazine

Since Saturday, the United States has reported its first six known COVID-19-related deaths, all in the Seattle area, prompting Washington state Governor Jay Inslee to declare a state of emergency. On Sunday, both Rhode Island and New York announced their first probable cases of coronavirus, making them the second and third states on the east coast (after Massachusetts).

Although the Centers for Disease Control and Prevention (CDC) maintain that the immediate health risk posed by COVID-19 remains low for the general American public, Nancy Messonnier, director of the organization’s National Center for Immunization and Respiratory Diseases, has warned that the disease’s spread throughout the country is “not so much a question of if this will happen anymore, but rather more a question of exactly when this will happen.”

As the coronavirus—now officially named SARS-CoV-2—spreads, so too has misinformation, stymieing efforts to educate and protect the global community. Many questions about the virus and the disease remain unanswered. Thanks in part to a solid understanding of other types of coronaviruses that have plagued us in the past, researchers are quickly homing in on COVID-19’s potential impacts and identifying some of the most important preventative measures people can take. Here’s a quick rundown of what we have learned so far.

Under a microscope, coronaviruses have the appearance of a crown, hence corona. (Image Courtesy of Center for Disease Control and Prevention )

What exactly is COVID-19?

First, let’s get some terms straight. SARS-CoV-2 is the name of the virus that’s spreading; COVID-19 is the disease it causes. Although most media reports have used the term “coronavirus” to describe SARS-CoV-2, the term is, by itself, not very informative.

Ccoronaviruses comprise an entire branch of the virus family tree that includes the disease-causing pathogens behind SARS, MERS and several variants of the common cold. Using “coronavirus” to refer to a potentially dangerous viral strain is a little bit like saying “mammal” when you mean “lion,” technically accurate, but not specific.

The fact that this new virus belongs to the coronavirus group, however, is telling, as humans have encountered plenty of these pathogens before. Named for the spiky, crown-like fringe that shrouds each viral particle—giving them a “coronated” appearance—coronaviruses tend to target the respiratory systems of bats and other mammals, as well as birds. More often than not, the viruses remain restricted to their wild hosts. But occasionally, they make the hop into humans, as occurred with the 2003 SARS and 2012 MERS outbreaks, both of which likely originated in bats.

The animal source of SARS-CoV-2 has yet to be pinpointed definitively. Given the history, bats remain a probable culprit, with some researchers suspecting the pangolin—an endangered mammal prized on the black market for its scales—as a potential intermediary, reports Joel Achenbach for the Washington Post.

What are the symptoms of COVID-19, and how is it transmitted?

Like other coronaviruses, the COVID-19 virus infiltrates the airways of its hosts. At worst, these pathogens can cause severe forms of viral pneumonia, which in some cases leads to death. Though researchers caution that numbers could shift as the outbreak progresses, the new coronavirus’s fatality rate appears to be around 2 percent. That’s a small fraction of the 10 and 35 percent figures reported for SARS and MERS, respectively.

The vast majority of COVID-19 cases—about 80 percent—appear to be mild, causing a spate of cold-like symptoms like coughing, shortness of breath and fever. Many people are suspected to carry the virus without presenting any symptoms. As physicians continue to identify more of these less-severe cases, which are more difficult to detect, the COVID-19 death rate may drop closer to 1 percent or even below it, reports Denise Grady for the New York Times.

That said, in the few months since it was first reported in China’s Hubei province, COVID-19 has killed about 3,000 people. That’s more than SARS (about 770 deaths) and MERS (about 850 deaths) combined. COVID-19’s death rate suggests the virus is more contagious than these predecessors, as well as most strains of the distantly related influenza virus, according to the Times. (According to the CDC, severe cases of the flu lead to at least 140,000 hospitalizations in the United States each year out of a total of more than 9 million cases of influenza documented annually. With an average of 12,000 deaths each year, influenza’s death rate is about 0.1 percent.)

A reported 2,873 deaths have occurred in Hubei province alone. According to the World Health Organization, COVID-19’s death rate increases with age, with the highest mortality rate of 21.9 percent occurring among people over 80 years of age. Those with underlying medical issues including respiratory and heart conditions, as well as smokers, are among those at highest risk, reports Allison Aubrey at NPR. Despite some reports to the contrary, children can be infected, but appear less vulnerable. Importantly, a multitude of factors—including many that scientists don’t yet understand—can affect how a given person tolerates an infection.

The virus is capable of moving directly from person to person through droplets produced by coughs or sneezes that travel through the air to settle directly on skin or frequently touched surfaces, like doorknobs or cell phones. After a person is exposed, symptoms can take weeks to appear, if they do at all. Those who carry the virus without showing signs of illness can still spread the disease.

How can I protect myself and others?

To avoid infection, the CDC recommends the same preventative actions one should follow during flu season. The top tip? Wash your hands thoroughly for at least 20 seconds, especially before eating, after using the bathroom, and after blowing your nose, coughing or sneezing. Though soap doesn’t destroy viruses, it plays a big role in dislodging them from skin. If you cannot wash your hands, the CDC notes that alcohol-based sanitizers are a decent second option as long as the sanitizer contains at least 60 percent alcohol. If your hands are visibly dirty, hand sanitizer will not be effective. (Some sanitizers labeled “anti-bacterial” contain only antibiotics, which will not protect against viruses.)

Based on preliminary estimates of contagiousness, those infected with SARS-CoV-2 are expected to infect two or three more people on average, according to WHO. If someone is already sick, wearing a face mask can reduce the spread of disease. However, most face masks, including loose-fitting surgical masks, are not effective at protecting individuals from respiratory diseases. Even medical-grade N95 masks, named for their ability to filter 95 percent of airborne particles, are difficult to use without training and won’t be airtight unless they are professionally fit-tested, says Timothy Brewer, an epidemiologist at UCLA, to Washington Post. Ultimately, N95 masks should be reserved for health workers and those who suspect they may have fallen ill.

Above all, don’t panic, Brewer tells Washington Post. While many media outlets have framed the current situation as one that does not “yet” warrant panic, at no point will excessive anxiety or rash behavior help contain the pathogen’s spread. Infection is by no means a death sentence, and should not be treated as one. “Don’t let fear and emotion drive the response to this virus,” Brewer says.

What about antiviral treatments or a vaccine?

Vaccines to combat SARS-CoV-2 are being developed, but requisite safety testing is likely to keep any new formulation off the market for months or possibly years. Vaccines also tend to be less effective in older individuals with weaker immune systems—the very people that the virus most strongly affects.

However, a drug to treat patients may be available sooner, reports Matthew Herper and Damien Garde for STAT News. It is important to remember that thousands—approximately 45,000 people in total, according to Johns Hopkins University—around the world have already recovered from the disease—many never knowing they had it in the first place.

What has been the economic and cultural impact of the outbreak?

As of Monday, March 2, SARS-CoV-2 had reached at least 60 countries. But nearly all nations have been affected by the disease’s cultural aftershocks as the global community struggles to contain its spread.

As businesses and cultural institutions continue to close, economists warn of severe stagnation in the global economy. Here in the United States, the government has issued travel alerts for China, South Korea, Italy, Iran and Japan—the five countries with the most cases to date—stressing that all non-essential trips should be canceled or postponed. The American stock market just suffered through its worst week since the 2008 Great Recession.

In Japan, lawmakers have shocked parents and guardians by suspending classes nationwide. China, which celebrated Lunar New Year at the end of January, has struggled to get back on its feet as workers remain homebound, leaving factories empty and international orders for products unmet. In France, where at least two people have died from the disease, indoor gatherings of 5,000 people or more are now prohibited, and the Louvre museum has closed its doors.

Following close on the virus’ heels has also been a wave of prejudice against people of Asian ancestry. Reports of people avoiding Chinese restaurants and shirking packages shipped from China have peppered the news cycle. (To be clear, Chinese food is no riskier than any other cuisine. Receiving packages from China also remains completely safe, according to the World Health Organization. Viruses, which need to enter living cells to replicate and propagate, don’t last long on objects exposed to the elements, especially when they’re being shipped overseas at room temperature.)

A similar display of discrimination followed the spread of SARS in 2003, when media reports began to ubiquitously lead their coverage with images of people of Asian descent wearing face masks. As medical anthropologist Laura Eichelberger told Undark magazine last month, these “innumerable pictures … racialized the epidemic by identifying Asian bodies as the source of contagion, contributing to their stigmatization.”

Locations with confirmed COVID-19 cases (Centers for Disease Control and Prevention)

What’s next?

In anticipation of COVID-19’s continued spread, the United States has ramped up its diagnostic efforts, which will undoubtedly reveal more cases, reports Nell Greenfieldboyce for NPR. These reports aren’t necessarily an indication that the virus is spreading faster, only that health officials are becoming more aware of its movements within American borders.

Like other coronaviruses as well as the flu, SARS-CoV-2 might follow a seasonal pattern, waning as the weather warms before rising to a second peak in the fall. But this ebb and flow is not guaranteed, and most experts hesitate to forecast when the outbreak will come to a close. Before then, thousands more will certainly be sickened, likely reaching the point where COVID-19 becomes a pandemic, or a disease that’s rapidly spread worldwide, according to the WHO. So far, both the CDC and WHO have been hesitant to give this formal designation, hoping to avoid triggering a panic.

Still, semantics don’t change reality. Officials worldwide have stressed the importance of practicality and preparedness for institutions and individuals. As hospitals revamp their protocols to ready themselves for an influx of patients, governments must weather what might be a prolonged period of suspended travel and trade.

Speaking with NPR, the Center for Global Health Science and Security’s Rebecca Katz recommends stocking up on essentials like medications and non-perishable pantry items, in case a local outbreak makes frequent trips to the store imprudent.

Above all, information and transparency remain humankind’s greatest weapons against disease—especially as the epidemic and its repercussions continue to evolve. The virus is unlikely to disappear anytime soon, and the best we can do is take its presence in stride and try to learn from past mistakes.

Tips for preventing the spread of germs, according to the CDC. (Centers for Disease Control and Prevention)

Glossary of COVID-19 terms


  • A medicine that specifically targets and inactivates viruses. Distinct from an antibiotic, which targets bacteria.


  • The simultaneous presence of two or more diseases in a patient. Patients with pre-existing respiratory illnesses, for example, face a higher mortality rate when infected with COVID-19.


  • The name given to the members of a large group of viruses that includes the disease-causing pathogens of COVID-19, SARS, MERS and several variants of the common cold.


  • The disease caused by SARS-CoV-2, first detected in China’s Hubei province in 2019. COVID-19 stands for “coronavirus disease 2019.”

Disease transmission

  • How a disease is transferred from person to person. COVID-19 is transmitted by droplets from the airways—the wet flecks produced by sneezing, coughing or sometimes even talking. If these droplets land on another person’s mouth, nose or eyes (or a hand that touches those parts), it can result in infection.


  • The spray produced by sneezing, coughing or sometimes even talking. When produced by a person infected by a pathogen, droplets can spread disease.


  • A large outbreak that spreads quickly or unexpectedly within a population or restricted geographic region.

Fatality or mortality rate; also called case fatality rate or crude fatality ratio (CFR)

  • In a group of people with a given disease, the proportion who die of the disease.


  • A sudden increase in the number of cases of a disease, above what is expected for a specific place or time.


  • An epidemic that has spread over several countries or continents at a rapid pace, usually affecting a large number of people.


  • Bacteria, viruses or other microorganisms that cause disease


  • The official name of the virus behind COVID-19, named for its genetic similarity to SARS-CoV, which caused an outbreak of SARS in 2003. Often referred to as the “novel” or “new” coronavirus, or simply “coronavirus.”


  • A set of negative and unfair beliefs associated with a specific group of people. The COVID-19 outbreak has triggered extreme stigmatization of people with cold-like symptoms, especially those of Asian descent.


  • A medical formulation that teaches the immune system to recognize and destroy a pathogen without causing disease. This is usually accomplished by introducing the body to a weakened or partial form of the pathogen in question. No vaccine yet exists for SARS-CoV-2.


  • A term used to describe a disease that passes from animals to people. Many coronaviruses, including SARS, MERS, and SARS-CoV-2, are zoonotic in nature.

How Smithsonian Curators Are Rising to the Challenge of COVID-19

Smithsonian Magazine

As families, communities and colleagues around the world grapple in their own ways with the invisible threat of the novel coronavirus, humankind shares an unusually acute sense of traversing a period of deep historical import. Once-bustling downtown areas sit deserted while citizens everywhere sequester themselves for the common good. Social media platforms and teleconferencing services are ablaze with the messages of isolated friends and loved ones. As medical workers risk their lives daily to keep ballooning death tolls in check, musicians and comedians broadcast from their own homes in the hopes of lifting the spirits of a beleaguered nation. It is a time of both ascendant empathy and exposed prejudice, of collective fear for the present and collective hope for a brighter future.

It is, in short, a time that demands to be documented. Stories institutional, communal and personal abound, and it is the difficult mandate of museums everywhere to collect this history as it happens while safeguarding both the public they serve and their own talented team members. This challenge is magnified in the case of the Smithsonian Institution, whose constellation of national museums—19 in all, 11 on the National Mall alone—has been closed to visitors since March 14.

How are Smithsonian curators working to document the COVID-19 pandemic when they are more physically disconnected from one another and their public than ever before? The answer is as multifaceted and nuanced as the circumstances that demand it.

In a statement calling for a Rapid Response Collecting Task Force to address the COVID-19 pandemic, the Smithsonian's National Museum of American History announced it would be "pursuing leads to many kinds of objects and archival materials from medical history and business history to social structures and culture." (Photo illustration by Meilan Solly / Photos via Getty Images)

In recognition of the sociocultural impact of the current situation, the curatorial team at the Smithsonian’s National Museum of American History (NMAH) has assembled a dedicated COVID-19 collection task force even as it has tabled all other collection efforts. Alexandra Lord, chair of the museum’s Medicine and Science Division, explains that the team first recognized the need for a COVID-specific collection campaign as early as January, well before the museum closures and severe lockdown measures took effect nationwide.

They've been working with their partners since before the crisis, she says. “The Public Health Service has a corps of over 6,000 officers who are often deployed to deal with emerging health crises, some of them work at CDC and NIH. We started talking to them during the containment stage and started thinking about objects that would reflect practitioners as well as patients.”

These objects range from personal protection equipment like N95 respirators to empty boxes emblematic of scarcity, from homemade cloth masks to patients’ hand-drawn illustrations. Of course, physically collecting these sorts of items poses both logistical and health concerns—the last thing the museum wants is to facilitate the spread of COVID through its outreach.

“We have asked groups to put objects aside for us,” Lord says. “PHS is already putting objects to the side. We won’t go to collect them—we’ll wait until all of this has hopefully come to an end.”

Image by NMAH. This camphor- and chloroform-laced liniment was first marketed around 1895. Following the deadly influenza pandemic of 1918, the Jones Medicine Company claimed their product contained “germ-destroying ingredients” that would positively prevent an attack of this “frightful disease.” (original image)

Image by Collection of NMAAHC, gift from the family. In the collections of the National Museum of African American History and Culture, a World War I diary belonging to soldier Roy Underwood Plummer chronicles his day-to-day experiences, including the 1914 flu epidemic. (original image)

Image by NMAH. Before the advent of antitoxin and vaccines, diphtheria was an ever-present source of terror. Known as "the strangling angel," the disease causes a thick build up in the throat and nose that makes breathing and swallowing extremely difficult. Intubation was a method used to open the throat to prevent asphyxiation. This intubation kit, 1886-1891, contains tools for inserting and removing the gold-plated tubes, which were used to keep the patient’s airway open. (original image)

Image by NMAH. This vaccine was formulated specifically to combat the H2N2 “Asian strain” of the influenza virus which caused the pandemic of 1957-58. Scientists at Walter Reed Medical Center obtained a sample of the virus in April 1957, and the first vaccines were ready for distribution by September. (original image)

The artifacts collected in this push will feed into Lord’s upcoming “In Sickness and In Health” exhibition, a scholarly look at infectious disease in America across hundreds of years of history. Already deep in development before the COVID crisis, the exhibition—which will include studies of two antebellum epidemics and one pandemic followed by a survey of the refinement of germ theory in the 20th century—will now need a thoughtful COVID chapter in its New Challenges section to tell a complete story.

A complete medical story, that is; the economic ramifications of the coronavirus are the purview of curator Kathleen Franz, chair of the museum’s Division of Work and Industry.

Franz works alongside fellow curator Peter Liebhold to continually update the “American Enterprise” exhibition Liebhold launched in 2015, an expansive overview of American business history that will need to address COVID’s economic impact on companies, workers and the markets they serve. “For me, as a historian of business and technology,” Franz says, “I’m looking at past events to give me context: 1929, 1933, 2008. . . I think the unusual thing here is this sudden constriction of consumer spending.”

Image by NMAAHC. The U.S. Coast Guard used this rescue basket during Hurricane Katrina in 2005. The artifact is now held by the National Museum of African American History and Culture. (original image)

Image by NMAAHC . Also held by NMAAHC, is a door scrawled with rescue markings from the recovery effort following Hurricane Katrina. (original image)

As federal and state governments continue to place limits on the operations of non-essential businesses, it is up to Franz and her colleagues to document the suffering and resilience of a vast, diverse nation. Usually, she says, “We collect everything: correspondence, photos, calendars. . . and we may collect that in digital form. But we’re still working out the process.” Above all, she emphasizes the need for compassion now that Americans everywhere are grieving the loss of family, friends and coworkers.

Museum as Educator

With many busy parents suddenly thrust into de facto teaching jobs with the closures of schools across the country, the museum has placed special emphasis on shoring up its educational outreach. From the beginning, says director Anthea Hartig, the museum “privileged K-12 units, because we knew that’s what parents would be looking for.” Some 10,000 Americans responded to a recent survey offered by the museum, with most pressing for a heightened focus on contemporary events. Now is the perfect time for the museum’s leadership to put that feedback into practice.

Hartig sees in this crisis the opportunity to connect with the public in a more direct and sustained way than ever before. Thousands have already made their voices heard in recent discussions on social media, and fans of the Smithsonian are taking on transcription projects for the museums with fresh zeal. Beyond simply livening up existing modes of engagement, though, Hartig hopes that her museum will be able to seize on the zeitgeist to make real strides with its digital humanities content. “Our digital offerings need to be as rich and vibrant as our physical exhibitions,” she says. “They should be born digital.”

An airplane panel recovered after the 9/11 terrorist attacks became part of the American History Museum's collections. (NMAH)

For inspiration amid all the flux and uncertainty, Hartig is reflecting on the NMAH’s response to the terrorist attacks that rocked the nation nearly 20 years ago. “We learned a lot through 9/11, where the museum was the official collecting authority for Congress,” she says. That moment in history taught her the value of “quietness and respect” when acquiring artifacts in an embattled America—quietness and respect “matched by the thoroughness of being a scholar.”

Hartig appreciates fully the impact of the COVID moment on America’s “cultural seismology,” noting that “every fault line and every tension and every inequity has the capacity to expand under stress, in all our systems: familial, corporate, institutional.” She has observed a proliferation in acts of goodness paralleled by the resurfacing of some ugly racial prejudice. Overall, though, her outlook is positive: “History always gives me hope and solace,” she says, “even when it’s hard history. People have come out through horrors of war and scarcity, disease and death.” History teaches us that little is unprecedented and that all crises, in time, can be overcome.

Inviting Participation

Benjamin Filene, NMAH’s new associate director of curatorial affairs, shares this fundamental optimism. On the job for all of two months having arrived from North Carolina Museum of History, the experienced curator has had to be extremely adaptive from the get-go. His forward-thinking ideas on artifact acquisition, curation and the nature of history are already helping the museum to effectively tackle the COVID crisis.

“For a long time, I’ve been a public historian committed to helping people see contemporary relevance in history,” he says. Against the backdrop of the coronavirus crisis, he hopes to remind Smithsonian’s audience that they are not mere consumers of history, but makers of it. “We [curators] have something to contribute,” he says, “but as a public historian, I’m even more interested in encouraging people to join us in reflecting on what it all means.”

And while hindsight is a historian’s best friend, Filene maintains that historians should feel empowered to leverage their knowledge of the past to enlighten the present as it unfolds. “I personally resist the notion that it has to be X number of years old before it’s history,” he explains. “We’ll never have the definitive answer.”

He views history as an ongoing refinement that begins with contemporaneous reflection and gradually nuances that reflection with the benefit of added time. “Even when you’re talking about something a hundred years ago, we’re continually revisiting it,” he says. “We can ask questions about something that happened five months ago or five days ago. But no doubt we will be revisiting this in five years, in 50 years.”

With that future reconsideration in mind, Filene’s priority now is the collection of ephemeral items that could be lost to history if the Smithsonian fails to act quickly. “Using our established community networks, full range of digital tools, publicity outreach,” and more, Filene hopes the museum can persuade Americans everywhere to “set aside certain items that we can circle back on in a few months.”

Image by Collection of NMAAHC. A button promotes American Red Cross programs to help African victims of HIV and AIDS in the 1980s. (original image)

Image by NMAAHC, gift of Jack Vincent in memory of Marlon Riggs. A poster advertises a 1996 exhibition of the NAMES Project Foundation AIDS Memorial quilt. The artifact was gifted to NMAAHC in memory of filmmaker, poet and gay rights activist Marlon Riggs. (original image)

Image by NMAH. A panel from the famous AIDS Memorial Quilt Panel, 1985-1990, honors Roger Lyon, who died in 1984 shortly after testifying before Congress to appeal for funding to combat the growing epidemic. The quilt was first displayed on the National Mall in Washington, D.C. in 1987. (original image)

Paralleling the efforts of NMAH, the National Museum of African American History and Culture (NMAAHC) is mounting its own campaign to document the impact of COVID-19 across the country. Curator William Pretzer frames the museum’s objective as “collecting as a way of building community.” In the coming days, NMAAHC will be issuing a “plea” to “organizations, community groups, churches” and individuals to pinpoint artifacts emblematic of this time and allow the museum to collect them.

Many of these materials will be digital in nature—diaries, oral histories, photographs, interviews—but Pretzer makes clear that internet access will not be a prerequisite to participation. “We’re going to work with local organizations,” he says, “without violating social distancing, to talk to members of their communities who maybe aren’t online.” Then, at a later date, NMAAHC can employ these same relationships to preserve for posterity “the signs people put up in their stores, the ways they communicated, the works of art they created, the ways they educated their children.”

Since its founding, NMAAHC has committed itself to building relationships with African Americans nationwide and telling emphatically African American stories. Pointing to the heightened tensions of COVID-era America, Pretzer says this collection effort will offer the chance to “analyze topics we often talk about casually—the digital divide, health care, educational gaps, housing problems—under this pressure cooker circumstance, and see how communities and individuals are responding.” He stresses that the museum’s interest in these narratives is far from strictly academic. “People want to have their stories heard,” he says.

A 2015 "Black Lives Matter" T-shirt resides in the collections of the National Museum of African American History and Culture after being donated by Baltimore City Council Member Sharon Green Middleton. (Collection of NMAAHC, gift of Glenard and Sharon Middleton)

Pretzer likens this all-out community push to the one the museum mounted when collecting Black Lives Matter materials in 2014, which told a richly textured story using artifacts from community groups, business owners, activists, photographers and law enforcement personnel. “It took us to Ferguson, it took us to Baltimore,” he recalls. “That’s when we made connections with local churches." Now, as then, Pretzer and the other curators at the museum hope to uncover the “institutional impact” of current events on African Americans, “which will by nature demonstrate inequalities in lived experience.”

The Smithsonian’s curatorial response to COVID-19 extends beyond NMAH and NMAAHC, of course—every Smithsonian knowledge hub, from the Anacostia Community Museum to the National Air and Space Museum to the National Museum of the American Indian, is reckoning with COVID in its own way. But the various teams are also collaborating across museum lines like never before, supporting one another logistically as well as emotionally and sharing strategic advice. Pretzer says that roughly ten Smithsonian museums have put together “a collaborative proposal to conduct a pan-Institutional collection effort” and are currently seeking funding to make it happen. The concept is a 24-hour whirlwind collection period “in which we would try to collect from around the country the experiences of what it’s like to be under quarantine. And from that initial binge, we would create connections that would allow us to continue.”

As far as physical artifacts are concerned, all Smithsonian museums are taking the utmost care to avoid acquiring items that Americans may still need and to thoroughly sanitize what materials do come in to ensure the safety of museum staff.

“What we’re learning is to give ourselves a lot of room,” says Hartig. “We’re trying to be courageous and brave while we’re scared and grieving. But we’re digging deep and playing to our strengths.”

Ultimately, she is proud to be a part of the Smithsonian during this trying time and is excited for the Institution to nurture its relationships with all the communities and individuals it serves in the weeks and months ahead. “We’re very blessed by our partnership with the American people,” she says. “What can we be for those who need us most?”

For Real - Center for Study of Short-lived Phenomena

Smithsonian Institution Archives

1 of 18

Event card - Sudan and Zaire Ebola Fever Epidemic, January 26, 1977

Event card - Sudan and Zaire Ebola Fever Epidemic, January 26, 1977 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Sinkiang Province Nuclear Explosion, November 24, 1976

Event card - Sinkiang Province Nuclear Explosion, November 24, 1976 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - North Pacific Ocean Shark Discovery, November 22, 1976

Event card - North Pacific Ocean Shark Discovery, November 22, 1976 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Asteroid "1976 UA" Sighting, November 15, 1976

Event card - Asteroid "1976 UA" Sighting, November 15, 1976 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Groton Finback Whale Beaching, January 30, 1976

Event card - Groton Finback Whale Beaching, January 30, 1976 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Imminent Kouprey Extinction, August 15, 1975

Event card - Imminent Kouprey Extinction, August 15, 1975 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Cascade Creek Gasoline Spill, August 12, 1975

Event card - Cascade Creek Gasoline Spill, August 12, 1975 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Mariana Islands Submarine Volcanic Activity, May 15, 1975

Event card - Mariana Islands Submarine Volcanic Activity, May 15, 1975 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Florida Love Bug Infestation, May 13, 1975

Event card - Florida Love Bug Infestation, May 13, 1975 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Graceham Bird Roosting, May 9, 1975

Event card - Graceham Bird Roosting, May 9, 1975 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - "Brazilian Bee" Infestation, April 7, 1975

Event card - "Brazilian Bee" Infestation, April 7, 1975 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Volcano Islands Submarine Volcanic Activity, March 28, 1975

Event card - Volcano Islands Submarine Volcanic Activity, March 28, 1975 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - The Plains Fish Kill, March 27, 1975

Event card - The Plains Fish Kill, March 27, 1975 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Massachusetts Ross's Gull Sighting, March 10, 1975

Event card - Massachusetts Ross's Gull Sighting, March 10, 1975 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Maui Mouse Invasion, September 13, 1974

Event card - Maui Mouse Invasion, September 13, 1974 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Sakurazima Volcanic Eruption, November 15, 1972

Event card - Sakurazima Volcanic Eruption, November 15, 1972 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Jarso (Walaga) Meteorite, August 4, 1970

Event card - Jarso (Walaga) Meteorite, August 4, 1970 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

Event card - Ozarks Fireball, October 10, 1969

Event card - Ozarks Fireball, October 10, 1969 - Accession 11-301 - Center for Short-lived Phenomena, Event Cards, 1969-1978, Smithsonian Institution Archives.

The Center for Study of Short-lived Phenomena (CSLP) was established under the direction of Robert A. Citron in order to study rare or infrequent natural phenomena such as volcanic eruptions, earthquakes, meteorite falls, the birth of new islands, and other sudden changes in biological and ecological systems. Located at the Smithsonian Astrophysical Observatory, the Center existed from 1968 to 1975. After some restructuring CSLP became the Scientific Event Alert Network (SEAN) in 1975 with the purpose of alerting scientists as soon as possible to selected geophysical, biological, astronomical, and athropological events taking place anywhere on Earth and to collect and store event information in a central repository for research purposes. SEAN went on to become the Global Volcanism Program, which is based at the National Museum of Natural History.

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Where Did the FDA Come From, And What Does It Do?

Smithsonian Magazine

In the past month, the Trump administration has already started to reshape the alphabet soup of federal agencies that regulate Americans’ food, air and water. Most of the spotlight has been on the Environmental Protection Agency, which underwent a hearing this week titled “Make EPA Great Again” that laid out a controversial bill seeking to limit the scientific data the agency can use to create regulations. But there are plenty of other science-focused agencies that regulate issues critical to Americans’ health and well-being.

As fundamental changes come to some of these agencies, it’s worth looking back at how they originated and what they actually do. We’ll start with the Food and Drug Administration, which exists to ensure the safety of America's food, cosmetics, drugs and medical devices. For most Americans, the phrase “FDA approved” serves a seal of trust: It means that the product in your hands—whether it’s a tube of lipstick, an insulin pump or a condom—has been deemed scientifically, medically and nutritionally sound. But who’s doing all that vetting?

What it does

Overall, the FDA estimates that it regulates roughly $1 trillion worth of products annually. These include consumer products that emit radiation, such as microwaves and sunlamps, and even tobacco products and pet and livestock food and medicines. 

The FDA conducts this regulation through the rules it issues, and employs more than 14,000 people to inspect food and drug production and conduct research into new technologies for inspection. (Meat, poultry and eggs fall under the jurisdiction of the Department of Agriculture, while tap water falls under the purview of the EPA.)

How it came to be

The FDA got its start with the passage of the country’s first major food and drug safety bill, the 1906 Pure Food and Drug Act. That law's origins stem from a decades-long fight for the government to regulate food.

As the Industrial Revolution swept America, the production of food and medicine became a large-scale enterprise. Inventions like canning allowed foods to last long enough to be shipped around the country, and sit on store shelves for extended periods. Meanwhile, "patent medicines" started being sold in catalogs for a variety of ailments. This industrialization put a new veil between consumer and product: Besides artful labels and hyped slogans, there was no way of knowing what a product really contained.

Naturally, manufacturers began to exploit this ambiguity. Using spices or additives, canners could mask the taste of expired meat and other substandard ingredients. Many patent medicines ended up relying on large quantities of morphine or cocaine to give users a high instead of actually healing them.

The federal government largely took a hands-off approach to food and drug safety at this time. It didn't help that manufacturers had a significant influence on Congress through aggressive lobbying. But there was resistance from within: One of the most powerful advocates of food and drug regulation was Harvey Wiley, who served as head of the USDA's Bureau of Chemistry. Wiley’s official role was to support scientific developments to help farmers, but his passion was to make America's foods and medicines safe.

Wiley tapped into a network of powerful support: millions of American women who feared for the safety of themselves and their families. Led by activist Alice Lakey, these women formed an unstoppable crusade of lobbyists. "Historians and Dr. Wiley himself credit the club women of the country for turning the tide of public opinion in favor of the 'pure food' bill," FDA historian Wallace Janssen wrote in 1981.

The crusade for the Pure Food and Drug Act received a final push from the 1906 publication of Upton Sinclair's The Jungle. This powerful exposé, which set out to document the inhumane labor conditions in America's factories, also ended up drawing attention to the horrifically unsanitary production of many processed foods. As Sinclair famously wrote: “I aimed at the nation's heart and by accident hit its the stomach." Around the same time, muckraking journalist Samuel Hopkins Adams published a 12-part expose on the fraudulence and dangers of the patent-medicine industry in the widely read Collier’s magazine. Soon after the book and series’ publication, an outraged President Theodore Roosevelt signed the bill into law on June 30, 1906.

The law was nicknamed the Wiley Act, and regulation power was given to Wiley's Bureau of Chemistry. Later amendments and laws expanded and reorganized the agency, which eventually grew into today’s Food and Drug Administration.

A key accomplishment

The FDA has maintained its watch over the American consumer for a century. One of its most famous accomplishments was its rejection of thalidomide, a widely used drug that was later revealed to cause significant birth defects. The drug was marketed extensively in Europe in the late 1950s as a way to suppress morning sickness in pregnant women. At the time, doctors thought that drugs given to a mother couldn’t affect fetuses. Thus, they didn’t even bother to test its safety for developing babies.

When thalidomide’s manufacturers sought approval from the FDA to sell the drug in the U.S. in 1960, FDA inspector Frances Kelsey put the brakes on the process by requesting the company conduct more safety studies. The following year, reports of thousands of babies being born with severe birth defects started coming out. The FDA’s work on thalidomide earned Kelsey praise from President John Kennedy and helped spur the passage of amendments strengthening the FDA’s drug review process.

“Her exceptional judgment in evaluating a new drug for safety for human use has prevented a major tragedy of birth deformities in the United States,” Kennedy said while awarding her with a medal for distinguished federal service in 1962.

Major criticisms

One of the biggest critiques against the FDA in recent years has been for its continued approval of opioid medicines, despite the increasingly devastating epidemic of opioid abuse nationwide, with overdoses now killing 91 people per day, according to the Centers for Disease Control.

“They’re listening to these patients, and the people who stand to gain a lot financially from opiates, instead of taking notice of the evidence,” University of Washington physician Jane Ballantyne told Roll Call in 2015.

Ballantyne, who also served as president of the Physicians for Responsible Opioid Prescribing, said that the FDA had repeatedly declined to consider the highly addictive nature of opioid drugs when it reviewed the medicines. This left many patients unaware of the dangers of the pain medicines they were prescribed.

Marion Nestle, a food historian and professor of nutrition and food studies at New York University, also worries about the FDA’s rapid approval of many other kinds of drugs. This process, she says, has led to the approval of controversial drugs that she believes should not have been marketed. “The drug industry wants fast approval of the drugs that it’s coming up with, whether they work or not,” she says.

Its leadership

The majority of the FDA's leaders have been medical doctors. This includes the most recent Commissioner of Food and Drugs, cardiologist Robert Califf. Califf, who worked at Duke University for 35 years before being appointed by President Barack Obama to serve as commissioner in 2015. In an exit interview with the Washington Post last month, Califf defended his efforts to speed up the approval of generic drugs to fight the rising cost of medicines while still cracking down on ineffective medicines.

"I think we have pretty clear evidence from the public that they would like to have a system that's giving them some assurance that the treatments they are given work," Califf says.

In response to rumors that the next FDA commissioner may come from the investment world, Nestle says that a non-medical or scientific figure would reshape the agency in potentially negative ways. “To put somebody who doesn't have any science background at all in that job turns it into a very different kind of agency,” says Nestle, who has also served on the FDA’s science advisory board. She also calls for strong future government support for the FDA, despite its shortcomings.

“It's an enormously important agency that needs more funding, not less,” she says.

A ridiculous fact

Maggots are an FDA-approved medical device. In 2004 the agency certified that doctors could use these creepy-crawlies to safely clean dead and infected tissue from open wounds, and help stimulate healing growth. And they aren't the only bug the agency regulates: Leeches and worms are also recognized as medical treatments. Something to think about the next time you see the words "FDA approved."

Editor’s note: This is the first in a series of Smithsonian primers on science-driven government agencies and how they came about.

How American Scientists Are Planning to Thwart a Salamander Apocalypse

Smithsonian Magazine

They didn’t see it coming.

By the time scientists discovered the first outbreak of chytridiomycosis, a disease caused by a fungus called Bd, it was too late; worldwide, the pathogen had already begun tanking populations of some 200 species of frogs that have gone extinct since the 1970s.

That was then. Now, another closely-related fungus called Bsal threatens to release a new wave of chytridiomycosis on amphibians—and this time, salamanders are the target. Though Bsal remains isolated in Asia and Northern Europe, researchers say it’s only a matter of time before it reaches the United States, home to the world’s highest salamander diversity.

But when the new pathogen strikes, scientists won’t be caught off guard.

With the devastating impacts of Bd still fresh in their minds, they’ve mounted a defense against Bsal—a volunteer-led task force, comprised of researchers from academia, government and nonprofits, that’s been preparing for the pathogen’s arrival for years.

“We’re preparing ourselves enough so we can pounce on it when it’s detected—and maybe actually contain it,” says Priya Nanjappa, a program manager at the Association of Fish and Wildlife Agencies, who’s a core part of the response effort. “The potential for impact is immense.”

Whether their efforts will be enough to prevent another amphibian epidemic in the U.S., however, hinges on how quickly they can detect an initial outbreak. And even if they are prepared, Nanjappa says, “it’s definitely going to be an experiment when it gets here.”

A perfect pathogen

The emerging pathogen Bsal is like something out of the Ridley Scott movie Alien. Like its relative Bd, spores ejected into the environment latch onto the skin of a host—in this case, at least a few dozen species of salamanders, research suggests—and then begin to consume the amphibian’s skin to build root-like masses and “mother cells,” which fire off even more spores. The salamander dies in as little as a week as a result, but not before the fungus multiplies and seeks out additional hosts.

A fire salamander covered in Bsal ulcerations (F. Pasmans via Wikimedia Commons)

The potential impact of Bsal was evident when it first arrived in the Netherlands, likely through the pet trade from Asia where it’s believed to be native. There, the pathogen wiped out 96 percent of the resident population of fire salamanders in a few years. And it’s since been discovered in wild populations of other species like the alpine newt in neighboring countries.

The pathogen now appears to be spreading—both in the wild and through the pet trade, experts say.

“We’ve seen several instances of it moving through the pet trade in Europe,” says Katie Richgels, chief of the Applied Wildlife Health Research Branch of the National Wildlife Health Center. “The pet trade is by far the biggest reason why we’re moving amphibians around.”

As a precautionary measure, the U.S. Fish and Wildlife Service placed an import ban on 201 salamander species thought to be potential vectors of the disease in 2016. These species were listed as “injurious” to wildlife under the Lacey Act—rarely used to thwart wildlife diseases—restricting their importation and interstate movement.

But even a ban won’t be enough to block Bsal’s arrive, says Stefano Canessa, a research fellow at Ghent University in Belgium, who’s been involved in mitigating the pathogen’s impact in Europe. It will find a way here, he says, if not through trade, then through an agriculture stow-away or the mud on the bottom of a hiker’s boot.

“Due to the size of the trade and the numbers we’re playing with, introduction is basically a certainty,” he says. “It will come in if it’s not already there.”

Scientists in the U.S. are worried.

In many ways, Bsal is a perfect pathogen, they say. It’s not only highly virulent—its effects are severe and swift—but it can also persist in the environment for days without a host. It can even be carried on the feet of wading birds, research shows, which could further aid its spread.

There’s another reason why Bsal is so nasty: While the pathogen may be lethal to at least 60 species of salamanders in the U.S., scientists believe that other species—like the midwife toad and the alpine newt—can carry Bsal yet remain asymptomatic. In other words, they serve as “reservoirs” for the disease.

“They don’t get sick, but they’re spreading it to those that are susceptible,” Richgels says. “In the disease world, that’s really hard to manage.”

But scientists in the U.S. do have an advantage that offers a glimmer of hope: time and experience.

Preventing a pandemic

When Bd was first described in 1999, it was already at work for nearly two decades, scientists say, lethally infecting frogs in a similar way to how Bsal infects salamanders; the two fungi are in the same genus, Batrachochytrium, and they both produce the disease chytridiomycosis. At the time, researchers knew little about the disease’s pathology and how to prevent it from spreading.

That’s what makes the emergence of Bsal so unique. Scientists in the U.S. not only have time ahead of its arrival to prepare, but they also have a general idea of what to expect.

“We have a huge toolkit now,” says Jake Kerby, a biologist at the University of South Dakota who’s been working on Bd for a decade. And it includes “the ability to very quickly assess the presence of these diseases.”

“That’s a huge advantage,” he adds.

In 2015, a group of scientists, government officials and other researchers seized the opportunity. Motivated in part by fear—many having witnessed the impacts of Bd and other wildlife diseases like white-nose syndrome—they formed the country’s greatest defense against another chytridiomycosis epidemic: The National Bsal Task Force.

Sure, it’s not as sexy as the Avengers, but for the country’s salamanders, which play a critical role in any environment, from transporting nutrients between habitats to feeding other species, they are indeed superheroes.

Their goal is simple: Prevent Bsal from spreading among salamander populations in the U.S.

Central to that mission is a 30-page emergency response plan, published in June. It reads something like a guidebook for a zombie outbreak: “Individual quarantine for all potentially exposed animals until causative agent is determined,” reads one step. “Restricted public access to the exposed area(s).”

“The response plan has an exhaustive list of scenarios,” says Reid Harris, co-lead of the task force, from discovering a confirmed case of Bsal in the wild to hearing about a sick salamander in captivity. Now that the plan is drafted, the next step is helping state wildlife agencies understand and be ready to implement the plan, he says.

The plan isn’t designed to stop the pathogen altogether, Nanjappa says. Rather, it’s meant to minimize the pathogen’s reach and, in doing so, buy the task force time to come up with treatment or a cure.

“Right now we don’t have an answer to Bsal, but that doesn’t mean we won’t,” Richgels says. “If we find it early there are things we can do to slow the spread, which gives us time to find answers—treatments, cures and whether there’s some way to treat the environment.”

Midwife toads, known for carrying their eggs on their back, can carry Bsal without showing symptoms of the disease. (Buiten-Beeld/Alamy)

Indeed, there are still massive gaps in research, Kerby says. Scientists need to better understand which species of salamanders in the U.S. are susceptible to Bsal—and to what extent. Without knowing which kinds of salamanders are most vulnerable to the disease (and which are already at risk from other pressures like habitat loss), he says, it’s difficult to efficiently allocate resources.

Kerby and other researchers are also scrambling to find ways to rid the pathogen permanently. While they’ve already learned that the right combination of temperature and antifungal agents could treat individual salamanders—in part, thanks to previous work on Bd—a treated salamander could simply walk back into the environment and contract the disease again.

But there’s a new line of research that’s showing promise: “probiotics.”

Not all species of salamanders are susceptible to chytridiomycosis, research has shown, and scientists believe that natural immunity is linked to beneficial bacteria found on amphibians’ skin. In other words, some salamanders may have a microbial army, of sorts, ready to fight off Bsal as it starts to invade. If researchers can identify what the soldiers look like—what kind of bacteria they are, that is—they might be able to create a “probiotic bath” for salamanders.

But they’re still far from a cure. Until one’s developed, scientists are on high alert for sick or dead salamanders, especially in the Appalachian Mountains and Pacific Northwest, where their diversity is greatest.

“Any suspicious-appearing amphibians should be investigated,” the plan says. It goes on to describe symptomatic animals as “sick or lethargic individuals, those with black circular or oblong lesions, or inability to right themselves.”

Scientists still worry they won’t discover the disease right away, even with state wildlife agencies on the ready, armed with a response plan. The area over which Bsal could invade is vast and the resources for surveillance are limited, they say.

That’s why it’s so important that everyone, including the general public, assist in the hunt, Canessa says. “There are lots of people out there like hikers that could report Bsal,” he says. “To harness that potential is our best bet.”

To that end, Partners in Amphibian and Reptile Conservation, a network of nonprofits, federal agencies and other institutions dedicated to the conservation of herpetofauna, launched an email-based disease alert system last summer. They encourage everyone to report signs of Bsal.

“We want reports of apparently sick, dying or dead animals with disease signs,” Dede Olson, an ecologist with the U.S. Forest Service, said in a press release. “It would help if the greater community of nature enthusiasts and recreationists would report their observations of disease events, as these can be cryptic and go unnoticed.”

A few recent reports have been unnerving, Nanjappa says, including one about salamanders with lesions on their skin. But tests revealed all of them to be false alarms—still, there’s no sign of Bsal in the United States.

“As far as far as we know, nothing has come back with a Bsal positive,” she says. “That’s great news, absolutely.” But, from here, it’s a question of when—not if—the disease will arrive.

“I’m nervous,” Nanjappa says.

Cuba’s Fascinating Babalú-Ayé Procession Honors African and Catholic Traditions

Smithsonian Magazine

After more than 50 years of economic embargo and political brinksmanship, the announcement one year ago of the renewal of diplomatic relations between Cuba and the United States came as a surprise. Washington, D.C., had been awash in rumors that a change was in the offing, but almost no one guessed at the magnitude of this remarkable development in global geopolitics. For many, particularly Cuban exiles around the world, it was one of those unforgettable historic moments, like the first man on the Moon or the fall of the Berlin Wall.

Some called it a miracle, as it occurred on an auspicious day for Cubans.

“Isn’t it amazing that this occurred on December 17,” exclaimed Cuban-American anthropologist Ruth Behar in a piece she wrote for the Washington Post. “It’s a day of great significance to Cubans, when thousands of them make an annual pilgrimage to the shrine of Rincón to mark the feast day of San Lázaro.”

Many of my Cuban friends and colleagues told me that this momentous event “had” to take place on this day. Since 1992, I have been visiting Cuba as an ethnographer and researcher of a unique Afro-Cuban tradition that honors both the Catholic St. Lazarus and the African-inspired Babalú-Ayé. (Yes, this is the same Babalú that performer Desi Arnaz sang to in “I Love Lucy.”)

In Cuban Catholicism, Lazarus, the patron saint of the poor and sick, is represented as a homeless beggar surrounded by dogs. Some say he was a fourth-century bishop, but most Cubans imagine him as the Biblical Lazarus—the poor man who cannot enter the kingdom of heaven, who Jesus raises from the dead. Cuba’s Lazarus works miracles for the destitute and the infirm, making him one of the country’s most popular saints.

In the African-inspired religious tradition known as Santería or Oricha, Babalú-Ayé is both feared and beloved. Thought to be responsible for bringing epidemics like smallpox, leprosy and AIDS, Babalú-Ayé also cures these diseases. Oricha elders tell of his exile from his homeland with the Lucumí because he spread smallpox among them, and they tell of his journey to the Arará, who were healed by him and ultimately made him their king.

The elders teach that he is an irascible old man and so mysterious that his omnipotence is nearly impossible to comprehend. They also teach that everyone should always pray for health, and Babalú is one of the guarantors of this most important blessing.

Some people push a carretilla, a little cart. Like the modest altar for alms, these improvised carts usually include a statue of St. Lazarus. (Alejandro Ernesto/epa/Corbis)

Cubans know poverty and illness. Before the American occupation of Cuba in 1902, scarlet fever epidemics erupted almost every year, and thousands died. Before the Cuban Revolution, many agricultural workers lived through annual cycles of poverty and hunger as they waited for the sugar harvest to provide work. More recently, the collapse of the Soviet Union in 1989 resulted in an economic contraction of some 50 percent, and again many Cubans went hungry.

On my first research trip in 1992, as a guest of the Academy of Sciences, my single daily meal consisted of one cup of rice and one fried egg each day, along with mangos and coffee.

On December 17, pilgrims flood the streets of Rincón, home to a leprosarium and a church dedicated to Saint Lazarus. Some have flown into Havana from overseas and traveled the 25 miles to the little town. Some have walked from their homes in Santiago, and others from Bejucal, the next town over.

Around dusk, the police shut down the main road to cars in order to accommodate the crowds. So central is walking to this enterprise that people call it the caminata—the special walk, instead of a pilgrimage.

In Cuban Catholicism, Lazarus, the patron saint of the poor and sick, is represented as a homeless beggar surrounded by dogs. (Enrique De La Osa/Reuters/Corbis)

Popular images of Saint Lazarus show him dressed in sackcloth and walking on crutches along a road that leads toward a distant tower. (Stories about Babalú-Ayé also include his walking long distances.) By the end of the day, most everyone in Rincón will make their way to the church.

Some people push a carretilla, a little cart. Like the modest altar for alms, these improvised carts usually include a statue of St. Lazarus. Often the statue is cloaked in burlap and wearing a red cloth—just like the famous "miraculous image" of St. Lazarus found within the sanctuary of the church in Rincón.

Pilgrims often fill their carretillas with the offerings of flowers, candles and coins for alms. Sometimes they blow cigar smoke at the images of the saint—similar to an African-inspired tradition of blowing smoke onto an altar.

Sometimes they blow cigar smoke at the images of the saint—similar to an African-inspired tradition of blowing smoke onto an altar. (Michael Mason)

Many people perform these acts of devotion because of a promise—they are keeping their word to the spirit after he granted their petitions. Still others do these things as solemn acts of prayer—gestures designed to solicit the saint’s attention.

Some people dress in sackcloth and carry crutches. They walk jorobado—hunchbacked—just like Babalú-Ayé did when he was wandering the desolate places of the Earth. At his darkest moment, Babalú-Ayé was completely crippled and could not even walk. So urgent was his journey that he kept moving forward, dragging himself along the road toward his destination, or as the religious elders would say, his destiny. 

And so the devoted grimly lie down on the ground and drag themselves forward. Others turn on their backs and use their legs to propel themselves, scraping their clothes and their flesh on the hard pavement. Often you cannot see them on the dark road, but the experience of hearing the moans of their suffering rising into the night is as eerie and discomfiting as it is difficult to describe.

Whether their journey began in Havana, or in the nearby towns, or at the police barricade at the edge of Rincón: All of them pay homage to the deity by becoming dusty and bloody—reminding us of the precarious and raw quality of human life.

The devoted lie down on the ground and use their legs to propel themselves along the pavement. (Michael Mason)

All are headed to the church. And all of them seek to heal their wounds. Once they arrive, they await the arrival of his feast day, December 17.

At the same time that the streets of Rincón overflow with pilgrims, those not making the journey perform a complex ceremony in their homes.

The African-inspired world of Santería is complex, and different communities who practice the ritual in ways that maintain historical and geographical distinctions from those traditions practiced in Africa. All across the island, Cubans practice their own versions of the awán, a ceremony dedicated to Babalú-Ayé, where a basket is lined with sackcloth and encircled with plates of food. Some religious elders say 13 plates, some say 17 and some even say 77 plates must be present.

At his darkest moment, Babalú-Ayé was completely crippled and could not even walk. (STR/Reuters/Corbis)

After sunset, participants gather round the basket, taking handfuls of food from each plate and rubbing it over their bodies to remove negativity or osobo. Each handful of food is then cast back into the basket, until everyone is cleansed. A speckled rooster, a guinea hen, two eggs and the , the ritual broom of Babalú are used as part of the cleansing ritual. At the end people walk around the basket and sing praises for the deity.

Each religious lineage completed the awán ritual in different ways, but the essential elements remain across the island.

One awán follows the strictures of the Lucumí tradition, the Arará-Dajomé lineage popularized by the Armando Zulueta, who hailed from the small Cuban town of Perico in Matanzas Province. At the bottom of the basket, they layer crumbled charcoal, followed by a piece of bread smeared with palm oil and topped with seven guinea peppers. Each of these objects brings a material presence to some aspect of the Babalú-Ayé’s story.

In contrast, Pedro Abreu, a leading priest of the Arará-Sabalú lineage, begins another awán tradition by tracing a circle of chalk on the ground. Inside the circle a series of complex markings is made to invoke the key moments in the life history of Babalú-Ayé. Called atenas, these signs come from the divination system; each brings the specific aché—spiritual power—of the sign to bear on the awán and the lives of those who participate.

In the face of unprecedented political change on December 17, this day also remains one of ceremony and tradition in Cuba.

The Cuban people continue to honor St. Lazarus in Rincón and to perform the awán in their homes. They commemorate their history as a people, they acknowledge their human vulnerability, and they call out to be made whole.   

Virus Genes in Human DNA May, Surprisingly, Help Us Fight Infections

Smithsonian Magazine

The viruses that plagued our ancestors millions of years ago aren't ancient history—they're still with us. Remnants of viral genes make up a relatively large part of our modern DNA, and scientists have been mostly uncertain what roles, if any, they play.

Now evidence suggests that during human evolution we've co-opted leftover genetic material from some of these "fossil viruses" to turn the tables and help our immune system fight diseases.

Scientists have known that our DNA is peppered with bits of viruses since the human genome was first sequenced some 15 years ago. Still, “it is surprising to many people,” says study co-author Cedric Feschotte, a geneticist at the University of Utah. “It's almost unsettling.”

The extra genetic code comes specifically from retroviruses, which invade host cells in a unique way. “Among all animal viruses, they are the only ones that integrate their own genetic material into the chromosomes of their host,” Feschotte says.

When ancient retroviruses infected our ancestors, they occasionally infiltrated a human sperm or egg cell. If those cells went on to fertilize an embryo, any viral genes incorporated into them had a ticket to ride from one generation to the next.

Along the way, these invaders' DNA sometimes gave rise to new viruses—but only for a while. Over the generations, genetic mutations gradually altered these viruses and eventually shut down their ability to infect new cells or fully replicate themselves. Today, most of the ancient viral oddities left in the human genome have no obvious function.

“It's important to understand that out of this 8 percent—these hundreds of thousands of bits and pieces of DNA scattered throughout the whole genome—most of that material just sits there and decays,” Feschotte explains. “Our job, and really that of our post-doctoral associate Ed Chuong, who did all this work, was to find the needles in the haystack—to identify some of those few elements that may have been co-opted for cellular innovation in the course of evolution.”

As part of their work, the scientists looked at pieces of ancient retroviruses that sit near genes known to function in immunity. They found that the fossil viruses activate when exposed to signaling proteins called interferons, which are released by white blood cells and other cells during a viral infection. Interferons inhibit viral growth and launch the production of anti-viral proteins in other nearby cells.

The team then looked at three different lines of human cells to see if fossil viruses in their genomes could bind with pro-inflammatory signaling proteins that help to fire up the immune system. They identified 20 families that did so, including one dubbed MER41 that entered our evolutionary tree as a virus some 45 to 60 million years ago.

The team then explored how the immune system functioned without some of these viral components. They used a genome editing tool called CRISPR/Cas9 to remove four pieces of the remnant virus DNA. Each time they did so, it crippled our innate immune system—the cells didn't fully respond to interferons as they had before, the team reports this week in Science.

The researchers speculate that such regulatory switches once ensured that the ancient virus would be able to replicate itself ahead of the immune response, a strategy that has been seen in modern retroviruses, including HIV.

“We were not too surprised to see that 50 million years ago a virus out there might have already been using that strategy for its own selfish purpose,” Feschotte says. "It is ironic that the tables have turned, and that these viral-derived elements have been co-opted to regulate genes that control, among other things, viral infections.”

The study is exiting because it adds to the mounting evidence for the ways genetic material from ancient viruses has been repurposed to our advantage, says University of Oxford medical virologist Gkikas Magiorkinis. For example, a protein called syncytin, which is essential for building the placenta in mammals, is derived from an ancient viral gene that once helped the virus to spread in the body.

“It's only rarely that it happens that some of these viral sequences were landed at the right spot at the right time, but clearly there have been many opportunities, and that's the key,” Feschotte says. “This is likely the tip of the iceberg."

Magiorkinis notes, though, that while viral DNA does seem to give our genes a boost under certain circumstances, it's not necessarily something that was indispensable for our survival. Instead, some viral helpers likely became active because they gave ancient humans an advantage under specific circumstances.

“For example,” he speculates, “a boost of the innate immune responses as described in the paper is likely to have provided a way to fight an ancient epidemic caused by the exogenous form of the retrovirus, or maybe even another one.”

Similar processes could also have produced darker results. Such viral remnants have been linked to numerous ailments, including the neurodegenerative disease ALS. The role these genes may play in this and other ailments remains murky, but Feschotte and his team think their work may offer new clues to the reasons viral remnants become active in our genome and what happens when that process goes awry.

“The reactivation of some of these viral-derived switches could suggest a testable hypothesis as to what could happen when these viral sequences become misregulated, for instance in the context of certain cancer and autoimmune diseases,” he says.

Forbidden City and Parts of Great Wall Close Temporarily in China to Limit Spread of Coronavirus

Smithsonian Magazine

On January 24, authorities in China announced the closing of various tourist sites, including a high-traffic section of the Great Wall, the Forbidden City in Bejing and Shanghai Disney Resort. The decision is an effort to limit the spread of the so-called Wuhan coronavirus, Channel News Asia reports.

Public transportation has been stopped in 18 cities in Hubei province, and travel has stopped entirely out of Wuhan, the province’s capital and biggest city, per Asia Times. The disease—also called the 2019 novel coronavirus (2019-nCoV)—was first discovered in the city in December and originally linked to a wet market. However, a new study on the first 41 cases of the disease gives evidence that the virus may have jumped to humans days or weeks before the market, reports Jon Cohen at Science magazine.

The virus spreads through airborne droplets released when an infected person coughs or sneezes, so large crowds would pose a risk. Crowds are especially common this time of year, when people are travelling to see family and celebrate the Lunar New Year.

The Forbidden City is normally packed with tourists during the Lunar New Year festival, per CNA, and Shanghai Disneyland sold out last year, selling around 100,000 tickets during last year’s festivities, Reuter’s Judy Hua and Cate Cadell report. The Juyongguan section of the Great Wall has been closed, and the wall's temple fair was cancelled. Festivals in Wuhan and Beijing that normally attract hundreds of thousands of visitors annually were also cancelled to limit spread of the disease.

But people are still travelling—even to Wuhan—to visit their families. One man who arrived in the outbreak’s epicenter by train told Reuters, “What choice do I have? It’s Chinese New Year. We have to see our family.”

Over 4,400 cases of 2019-nCoV have been identified in China, with more than half of those in Hubei, and 106 deaths have been confirmed, per Time’s Sanya Mansoor. The disease has also been confirmed in more than a dozen countries, with five cases confirmed in the United States.

Other measures taken in China include cancellations of film premieres and the suspension of McDonald’s business in five Hubei cities. China also extended the national New Year holiday to encourage people to stay home. Hong Kong has closed its borders to travel with China, and the World Health Organization is sending a delegation to China to better understand the outbreak. Last week Thursday, the organization said it was “too early” to designate the outbreak an emergency of international concern.

“The mass involuntary quarantine in Wuhan and its neighboring cities is counterproductive,” Georgetown University Law School public health expert Lawrence Gostin tells Reuters. “A lockdown of Wuhan will drive the epidemic underground, provoking fear and panic.”

Gao Fu, head of the Chinese Center for Disease Control and Prevention, has urged the country to forego New Year gatherings, asking them to instead stay home until all is clear, per Asia Times.

“There’s so much news, so much data, every 10 minutes there’s an update,” Lily Jin, who lives in Wuhan, told Reuters by phone. “It’s frightening, especially for people like us in a severely hit area.”

2012 Festival: A Volunteer's Reflections

Smithsonian Center for Folklife and Cultural Heritage

I have volunteered and worked at several Smithsonian Folklife Festivals before, but I did not know what to anticipate when I went down to the Festival grounds on Sunday, July 1. Deadly winds had ripped through the D.C. metro area the previous Friday night, downing power lines, toppling trees, and creating havoc in the District, Maryland and Virginia. Even the Festival itself, which almost never closes unexpectedly, was forced to close down on Saturday, June 30, because of damage to Festival tents and exhibits.

Arriving on the Sunday morning after the Festival closure, I was thrilled to see that the Festival staff and volunteers had worked overtime on Saturday to make the Festival grounds as good as new. Some signs were still blown over, and some piles of tree limbs and debris remained on the periphery. A few display items were still drying out. Yet, as opening time approached, everyone was in good cheer and ready for a fun day on the Mall.

I was slated to volunteer at the Campus and Community program, so I took a few minutes before things opened to view the tall, moving murals at the Citified program and some of the personalized panels on the AIDS Memorial Quilt at the Creativity and Crisis program. The exuberant murals, with flashes of color and both representational and abstract pictures, made the Citified program grounds come alive, even though the steel drums, choral groups, master storytellers, and other performers had not yet appeared. Clusters of excited youngsters preparing to dance, sing, or just watch the performers added to the anticipation as another Festival day was about to begin.

Over at the AIDS Memorial Quilt, the staff and volunteers had created a more somber but equally moving experience. With the sun still behind the Capitol building, rows of quilt panels stretched almost to the horizon. These 3 by 6 foot panels, each roughly the size of a grave, stood as mute reminders of lives cut short by AIDS.

Yet, because they were created by loved ones, each quilt panel was a visual haiku. Photos, favorite clothing items, car keys, and references to favorite musicians memorialized each person as more than a name. Combined into a web of care, the panels brought the tragic cost of the AIDS epidemic down to human scale. Each life, so precious, had left a hole that even this giant quilt could not cover.

The Campus and Community program—which celebrated 150 years of Land-grant colleges and their contributions to the United States—was so varied that there was literally something for everyone. For example, music lovers could enjoy Texas mariachi, a West Virginia steel drum band, and Hawaiian hula. Representatives from some of the nation’s Land-grant universities and colleges demonstrated how to preserve fossil specimens, milk a cow, create robots, and much more.

When I think of Land-grant institutions, I think of big public universities in rural settings, so I was surprised to see that even though the District of Columbia is a city, it has its own land-grant institution: the University of the District of Columbia. Dean Sabine O’Hara of UDC’s College of Agriculture, Urban Sustainability & Environmental Sciences (CAUSES) was at the Festival, speaking on a Transforming Communities panel with Jimar Jimenez of Iowa State University and Brian Boulanger of Texas A&M.

Reaching out to immigrant communities, designing innovative water filtration systems using ceramic pot filters, and creating green spaces on the tops of urban parking garages were some of the innovative solutions discussed by the three panelists. Dean O’Hara also discussed five pillars of sustainable economic development (education, health and wellness, environment and recreation, social and cultural amenities, and technology and transportation) that are applicable far beyond the urban campus of UDC.

In sum, the Smithsonian Folklife Festival continues to expand our horizons—whether seeing the nation’s Capitol building framed in quilting, celebrating D.C. communities east of the Anacostia River, or remembering that even urban D.C. can be a leader in sustainable agriculture. Thanks to all the participants, staff and volunteers for making this another memorable year.

Phil Tajitsu Nash is a Festival volunteer, Asian American Studies faculty at the University of Maryland, and curator of the Asian Pacific American program at the 2010 Smithsonian Folklife Festival.

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