Found 380 Resources containing: Epidemic
Prior to my first trip to Ecuador in 2010, I spent my teenage summers combing through stacks of CDs sold by Otavalan merchants at venues like the Great New York State Fair. When I traveled to Otavalo during the Hatun Puncha-Inti Raymi summer solstice festival, I expected to hear groups of musicians playing sanjuanitos on panpipes (zampoñas, Spanish), notched end-blown flutes (quenas, Sp.), violins, and guitars. Upon my arrival at the Maldonado household, however, I was introduced to transverse cane flutes (called flautas or gaitas, Sp.), which sounded nothing like what I had listened to on my recordings of well-known Otavalan groups like Runakuna, Sisa Pacari, or Ñanda Mañachi. When I asked Patricio Maldonado (one of my host brothers and manager of Hatun Kotama) about the flutes, he modestly told me, “It’s just a little tradition we have here.”
The music that Hatun Kotama will perform during the 2013 Smithsonian Folklife Festival is – for the most part – ritualistic and played by men. Throughout Hatun Puncha-Inti Raymi, musicians perform facing each other, turning in a small, tight circle while dancers form a large spiral around them. The repetitive characteristic of the music places the participants in a trance-like state, allowing for them to connect with each other, spirits, Mother Earth, and our cosmos through song and dance. The songs are in a two-part form and do not have a standard ending or closure to the music because flutists repeat the same tune until the next duo or trio of musicians interrupts with another song.
Flauta music still maintains its own unique tuning system, or musical language, that does not correspond to the Western twelve-tone organization of pitches. Songs, or tunus, are polyphonic, short, and repetitive. To someone not familiar with this music, it may sound melancholic, spooky, or urgent, though to the Runakuna, it is spirited and enlivening. One may also assume that the music is simple because the instruments are rustic in appearance, but as I became more acquainted with this tradition, I began to realize how difficult it is to master even one song. Flute masters’ performance technique includes ornamentations, such as trills and vibrato, and an impeccable embouchure, which creates a strong sound capable of cutting through ambient noise of festival onlookers, dancers, and competing groups of musicians.
By far, one of the most challenging aspects of playing the Otavalan transverse flute is being able to maintain one’s endurance throughout Hatun Puncha-Inti Raymi, performing day and night over a week’s time with little rest. A competent flutist must adhere to strict performance standards and memorize the melodies without error, or else they risk being ejected from the player’s circle.
Hatun Kotama is at the forefront of the flauta grassroots revival movement. Whereas other Otavalan villages have traditionally been known for their flute makers, Kotama has been regarded as a home of outstanding flutists. The founders of Hatun Kotama, several of whom you will meet at this year’s Folklife Festival, recognized that the tradition was disappearing and at risk of becoming obsolete due to religious conversion, migration, economic changes, the adaptation of new instruments, and the 1990s cholera epidemic. They are also aware of the important role flauta music holds in Runa culture. At their cultural center, the flute teachers do not only intend to pass on flauta techniques and repertoire; rather, they hold themselves responsible for transmitting other types of cultural knowledge, such as the Kichwa language (all classes are run completely in Kichwa), and how to live together (convivir, Sp.). Their recording project with Smithsonian Folkways, ¡Así Kotama!: The Flutes of Otavalo, Ecuador, is an example of Hatun Kotama’s mission to preserve their tradition while redefining it in today’s world.
During my field research in Ecuador, one of the phrases I was most often told by the Maldonado family and flute masters was “kashnami kawsanchik,” or “this is how we live!” It has been an honor for me to learn from them, and I look forward to being able to reciprocate by sharing my life and culture with them during their residency at the festival. If you will be in the D.C. area for the second week of the Folklife Festival, stop by the One World, Many Voices: Endangered Languages and Cultural Heritage exhibit to meet the flute players. This week is also a great opportunity for you to convivir by not only observing, but also dancing with the flutists and sharing with them how you live, too.
Hatun Kotama will be in the “tree plot” area of the One World, Many Voices program starting July 3. They perform an evening concert on the Voices of the World Stage on Saturday, July 6, 6:00 p.m.
Click on images to enlarge and view captions. All photos courtesy of Jessie M. Vallejo. <
Jessie M. Vallejo is a Ph.D. candidate at the University of California, Los Angeles. Her dissertation focuses on the Otavalan transverse flute tradition (called flauta or gaita). She began working with flutists from the Hatun Kotama Cultural Center and other nearby Kichwa communities in 2010. Apart from her research activities, Jessie has performed violin with indigenous ensembles and mariachi groups in northern Ecuador. At UCLA, she is co-director of Mariachi de Uclatlán and member of the Chinese Silk and Bamboo ensemble.
In 1854, in response to a devastating cholera epidemic that was sweeping through London, British doctor John Snow introduced an idea that would revolutionize the field of public health: the epidemiological map. By recording instances of cholera in different neighborhoods of the city and plotting them on a map based on patients’ residences, he discovered that a single contaminated water pump was responsible for a great deal of the infections.
The map persuaded him—and, eventually, the public authorities—that the miasma theory of disease (which claimed that diseases spread via noxious gases) was false, and that the germ theory (which correctly claimed that microorganisms were to blame) was true. They put a lock on the handle of the pump responsible for the outbreak, signaling a paradigm shift that permanently changed how we deal with infectious diseases and thus sanitation.
The mapping technology is quite different, as is the disease, but there’s a certain similarity between Snow’s map and a new project conducted by a group of researchers led by Henry Kautz of the University of Rochester. By creating algorithms that can spot flu trends and make predictions based on keywords in publicly available geotagged tweets, they’re taking a new approach to studying the transmission of disease—one that could change the way we study and track the movement of diseases in society.
“We can think of people as sensors that are looking at the world around them and then reporting what they are seeing and experiencing on social media,” Kautz explains. “This allows us to do detailed measurements on a population scale, and doesn’t require active user participation.”
In other words, when we tweet that we’ve just been laid low by a painful cough and a fever, we’re unwittingly providing rich data for an enormous public health experiment, information that researchers can use to track the movement of diseases like flu in high resolution and real time.
Kautz’ project, called SocialHealth, has made use of tweets and other sorts of social media to track a range of public health issues—recently, they began using tweets to monitor instances of food poisoning at New York City restaurants by logging everyone who had posted geotagged tweets from a restaurant, then following their tweets for the next 72 hours, checking for mentions of vomiting, diarrhea, abdominal pain, fever or chills. In doing so, they detected 480 likely instances of food poisoning.
But as the season changes, it’s their work tracking the influenza virus that’s most eye-opening. Google Flu Trends has similarly sought to use Google searchers to track the movement of flu, but the model greatly overestimated last year’s outbreak, perhaps because media coverage of flu prompted people to start making flu-related queries. Twitter analysis represents a new dataset with a few qualities—a higher geographic resolution and the ability to capture the movement of a user over time—that could yield better predictions.
To start their flu-tracking project , the SocialHealth researchers looked specifically at New York, collecting around 16 million geotagged public tweets per month from 600,000 users for three months’ time. Below is a time-lapse of one New York Twitter day, with different colors representing different frequencies of tweets at that location (blue and green mean fewer tweets, orange and red mean more):
To make use of all this data, his team developed an algorithm that determines if each tweet represents a report of flu-like symptoms. Previously, other researchers had simply done this by searching for keywords in tweets (“sick,” for example), but his team found that the approach leads to false positives: Many more users tweet that they’re sick of homework than they’re feeling sick.
To account for this, his team’s algorithm looks for three words in a row (instead of one), and considers how often the particular sequence is indicative of an illness, based on a set of tweets they’d manually labelled. The phrase “sick of flu,” for instance, is strongly correlated with illness, whereas “sick and tired” is less so. Some particular words—headache, fever, coughing—are strongly linked with illness no matter what three-word sequence they’re part of.
Once these millions of tweets were coded, the researchers could do a few intriguing things with them. For starters, they looked at changes in flu-related tweets over time, and compared them with levels of flu as reported by the CDC, confirming that the tweets accurately captured the overall trend in flu rates. However, unlike CDC data, it’s available in nearly real-time, rather than a week or two after the fact.
But they also went deeper, looking at the interactions between different users—as represented by two users tweeting from the same location (the GPS resolution is about half a city block) within the same hour—to model how likely it is that a healthy person would become sick after coming into contact with someone with the flu. Obviously, two people tweeting from the same block 40 minutes apart didn’t necessarily meet in person, but the odds of them having met are slightly higher than two random users.
As a result, when you look at a large enough dataset of interactions, a picture of transmission emerges. They found that if a healthy user encounters 40 other users who report themselves as sick with flu symptoms, his or her odds of getting flu symptoms the next day increases from less than one percent to 20 percent. With 60 interactions, that number rises to 50 percent.
The team also looked at interactions on Twitter itself, isolating pairs of users who follow each other and calling them “friendships.” Even though many Twitter relationships exist only on the Web, some correspond to real-life interactions, and they found that a user who has ten friends who report themselves as sick are 28 percent more likely to become sick the next day. In total, using both of these types of interactions, their algorithm was able to predict whether a healthy person would get sick (and tweet about it) with 90 percent accuracy.
We’re still in the early stages of this research, and there are plenty of limitations: Most people still don’t use Twitter (yes, really) and even if they do, they might not tweet about getting sick.
But if this sort of system could be developed further, it’s easy to imagine all sorts of applications. Your smartphone could automatically warn you, for instance, if you’d spent too much time in the places occupied by people with the flu, prompting you to go home to stop putting yourself in the path of infection. An entire city’s residents could even be warned if it were on the verge of an outbreak.
Despite the 150 years we’re removed from John Snow’s disease-mapping breakthrough, it’s clear that there are still aspects of disease information we don’t fully understand. Now, as then, mapping the data could help yield the answers.
With nearly 40 percent of the world’s population now classified as obese, and increasing evidence pointing to sugar as the culprit, people are turning to foods that contain low-calorie sweeteners to give them the sweet taste they enjoy, without the risk of gaining weight. However, new research from George Washington University in the U.S. suggests that artificial sweeteners may actually increase a person’s risk of becoming obese.
The obesity epidemic is caused by an increase in fat and sugar in people’s diets. Fat accumulation in obesity increases the chances of getting type 2 diabetes, heart conditions and cancer. As such, new guidelines from Public Health England encourage the public to buy lower calorie and lower sugar products.
So changing our diet to include low-calorie sweeteners, such as sucralose and aspartame, should be a good way to get all the sweet taste without any of the guilt. Instead, the new study suggests that eating these sweeteners could do the opposite and increase the chance of us accumulating fat in our bodies, in a “dose-dependent” fashion. In other words, the more artificial sweetener you consume, the more fat your body creates and stores.
For many years, we have known that sweet substances (sugars or artificial sweeteners) bind to sensors in our mouth called “sweet-taste receptors.” These receptors send a message to our brain to tell us that we are eating something sweet.
In the last decade, these sensors have been found in other parts of our body, such as the bladder, the lungs and even in bones. This has raised questions about what effect sweeteners, and these sweet taste receptors, could be having inside our bodies.
The new research, results of which were presented recently at the 100th annual meeting of the Endocrine Society in Chicago, looks at the effect that artificial sweeteners have on the cells that make up our fat stores. These cells have a glucose transporter (a protein that helps glucose get into a cell) called GLUT4 on their surface and, when we eat more sugar, the cells take up more glucose, accumulate more fat and become larger.
The researchers in this latest study found that the artificial sweetener, sucralose, commonly found in diet foods and drinks, increases GLUT4 in these cells and promotes the accumulation of fat. These changes are associated with an increased risk of becoming obese.
Indeed, the research studied a small number of obese people who consume artificial sweeteners and found that they had more of these fat cells and increased expression of genes associated with fat production.
When consumed in low quantities, artificial sweeteners have been shown to aid weight loss, improve metabolic conditions and even protect against injury during infection. However, this new study suggests that, rather than keeping us healthy, artificial sweeteners, especially when consumed in larger doses, could be contributing to the obesity epidemic.
Given the limited number of studies on the subject–and that few studies compare low-calorie sweeteners with sugar–we do not yet have clear answers. However, with a supply of new, natural sweeteners on the market, such as stevia and monk fruit, we have plenty of them to choose from. These are based on fruit extracts and are aimed at providing a more natural approach to improving the tastiness of food and drink compared with their artificial counterparts.
However, it’s too early to say whether these natural products are a safer option than artificial sweeteners or whether they, too, have the potential to increase the risk of obesity.
Cataloging supported by Smithsonian Institution Women's Committee
Edited film documenting an American expedition into the Amazon Basin of Venezuela to perform various medical studies on the Yanomamo. Geneticists are seen taking height and weight measurements, various samples, and administering vaccinations in order to stop a measles epidemic. Project from which the film was made was funded by U.S. Atomic Energy Commission, Division of Biology and Medicine; National Institutes of Health; and National Science Foundation.
Mosquitoes are coming. The Unicode Consortium has just announced that alongside your smiling face – or perhaps crying face – emoji you’ll soon be able to add a mosquito.
The mosquito emoji will join the rabble of emoji wildlife including butterflies, bees, whales and rabbits.
We see a strong case that the addition of the much maligned mosquito to your emoji toolbox could help health authorities battle the health risks associated with these bloodsucking pests.It may be small but it could make all the difference in battling mosquito-borne disease outbreaks. (https://emojipedia.org/mosquito/)
Given it is the most dangerous animal on the planet, the mosquito is more than deserving of an emoji. But will it make a difference to the way the science behind mosquito research is communicated? Could it influence how the community engages with public health messages of local authorities? Will more people wear insect repellent because of the mosquito emoji?
We won’t know for sure until the mosquito is released.
Where did the mosquito emoji idea come from?
A staggering sixty million emoji are shared on Facebook each day!
We’ve needed a mosquito emoji for a while now (although the blood filled syringe has been a useful substitute). While heavily promoted last year by the Johns Hopkins Center for Communication Programs and the Bill & Melinda Gates Foundation, it was one of us, an Australian virologist, who played a critical role in the emoji’s development by submitting the original proposal in June 2016.
The idea arose during the Zika virus epidemic in South America, when the mosquito-borne infection was triggering many questions and few answers. While the emoji doesn’t represent a specific mosquito species, it captures the distinctive shape of a mosquito.Time spent outdoors may be the perfect opportunity to employ the mozzie emoji. (jiulliano)
How might a mosquito emoji make a difference?
The mosquito emoji will give health professionals and academics a more relatable way to communicate health risks and new research using social media.
Surveillance programs across the world routinely monitor mosquitoes. Local health authorities could simply tweet a string of mosquito emoji to indicate the relative mosquito risk or identify that there is a risk. Adding in the new microbe emoji (currently in the form of a generic green microscopic shape) could even indicate the presence of mosquito-borne viruses such as dengue virus, West Nile virus or Ross River virus.
Emoji could remind us to tip out, drain or cover backyard water-holding containers that may be a source of mosquitoes following rain. Weather monitoring services or health authorities could simply add the mosquito emoji in alerts featuring a string of storm clouds and water droplets.
More than likely, it’ll be used by the public to punctuate those summer tweets complaining of bites and bumps following backyard BBQs.
Social media is changing public health
Social media will continue to play a role in public health campaigns. Whether promoting better nutrition, encouraging exercise or addressing concerns over vaccine coverage, Twitter, Facebook, Instagram, and whatever platform comes next will remain important for the communication tool kits of local health authorities.
Smartphones have already been identified as tools for surveillance of mosquito-borne disease outbreaks.
The addition of a mosquito emoji, together with concise public health messaging, may increase the chances a message hits home, maybe even changing behaviour and reducing the risk of bites.
Simple communication works
The usefulness of emoji as a communication tool has been shown in several fields of research. Emoji can accurately express emotional associations with commercial products, reflect state of mind in cancer patients and aid communication with sick young patients.
Applying these examples to the mosquito emoji, we predict it may aid citizen science – for example, if the community can signal how bad nuisance-biting mosquitoes are in their area. Perhaps this mobile surveillance network could help pick up the introduction of exotic mosquitoes such as the Asian Tiger Mosquito, a species often first detected because of reports by the community. Measuring a rise in mosquito emoji use may identify regions under attack by mosquitoes.
Big corporations have already identified the usefulness of emoji, and fork out serious cash for hashtag-customized emoji. If branded emoji work for commercial enterprises, why not for public health and why not a mosquito? A simple image may provide a critical reminder to put on insect repellent, sleep under a bed net or get appropriately vaccinated for mosquito-borne diseases such as Japanese encephalitis or Yellow Fever.
It is increasingly difficult to escape our social media streams, and emoji use shows no sign of waning. Health authorities should embrace these tiny visual prompts to better engage the community with key health messages.
The mosquito emoji may pave the way for more medically important arthropods: perhaps the tick, flea, lice and bed bug emoji will be on their way soon. Perhaps even viruses and bacteria.
From the middle of 2018, we look forward to watching the creative ways researchers, health workers and the general public incorporate the mosquito emoji into their communications.
Is autism cool?
It is in literature, as novels featuring characters on the autism spectrum become so frequent that they’ve spawned a new genre: “autism lit,” or “aut lit.”
Many of the works put a positive spin on autism. These autistic characters have abilities as well as disabilities; they exist not only as mirrors or catalysts to help others solve their problems, but as active agents with inner lives.
The Curious Incident of the Dog in the Night-Time, first published in 2003, did more than any other book to give life to this genre. Christopher Boone, the narrator, is a 15-year-old autistic savant; that is, he can perform computer-like math in his head. He also has trouble with language and social interactions, the two primary symptoms of autism. Still, he’s shown to have an inner life that includes many opinions, as well as hopes for the future. Perhaps of greatest importance is that he has the ability to pursue his goal of solving the mystery of who killed his neighbor’s dog.
A successful book that breaks new ground will breed many imitations. Back in the late 1970s, Robin Cook’s Coma introduced the medical thriller to the world. And so Curious Incident has been followed by a wide range of novels, including the pseudo-science fiction novel, The Speed of Dark (2005); fiction-that-reads-as-memoir, such as Daniel Isn’t Talking (2006) and Tilt: Every Family Spins On Its Own Axis (2003); young adult novels such as Mindblind (2010); and the light-hearted The Rosie Project (2013) and its sequel, The Rosie Effect (2014).
Of particular interest is M is for Autism (2015), the moving result of a collaboration of young students at Limpsfield Grange, a school for autistic girls. Boys are diagnosed with autism four times more often than girls, and the face of autism is almost always that of a young boy. This novella looks at some of the special issues that young women face, and by doing so it’s an exception in the genre.
Back to our young men, though: Somewhere on the journey from Curious to Rosie a transformation occurred. The smart, but anti-social and clueless Christopher Boone morphed into the smart and somewhat clueless but also charming husband and father Don Tillman. Don is a professor of genetics in The Rosie Project and an equally successful professor in New York in the sequel.
On this same literary journey, the perceived limitations of these autistic characters have been turned either into strengths, or into obstacles that, once overcome, become strengths. For example, many of these fictional beings “miss social cues” (a stereotype, but like all stereotypes based in some reality), and therefore don’t dissemble or manipulate the way that neurotypical people do.
Lou Arrendale, the hero of The Speed of Dark, is a thoughtful young man with a superior moral sense. He lives in a not-too-distant future when autism can be cured in infancy. Lou was born just a little too late for that, but now science has invented a way to “fix” autism in adulthood, and Lou has to decide whether he wants to give up the advantages of his condition for the sake of fitting into society’s mold. It’s difficult to imagine a character debating this question 20 years ago, let alone 50.
Mindblind is a contemporary young adult novel; no scientific advances here. But Nathaniel Clark, the hero and narrator, not only drives the action, he ends up being a rock star, at least in his own social circle.
Perhaps the most powerful statement, though, is uttered by the heroine’s therapist in M is for Autism: “You are a wonderful teenage girl. And you have autism. The truth is, you will need some support and guidance with life’s inevitable ups and downs but you can have a glorious, fulfilled life, M, and this is the truth, too.” In other words, even without medical intervention or a touch of wishful thinking, there’s no reason for people on the spectrum to give up on their future.
This positive prediction wouldn’t be made about to Boo Radley, the recluse from To Kill a Mockingbird. Rumors surround Boo: he eats raw squirrels; he drools most of the time. Though these are indeed rumors, from what we do learn about Boo, he may well be autistic. Regarded as a shadowy, sinister figure, Boo ends up saving Scout’s and Jem’s lives, but his “reward” is to have his brave act go unrecognized. We last see him as Scout leads him by the hand back to his lonely existence.
Autism lit is not without controversy: Many readers object to the prevalence of the autistic savant. And in fact, most of these protagonists are gifted: Christopher Boone, for example, is about to sit for his A levels in math, a heady accomplishment in England, where the book takes place. Nathaniel Clark is graduating college (with a double major, he reminds us more than once) at the age of 14.
In reality, savant skills are as rare in the autism spectrum community as they are in the neurotypical one. Those who dislike the novels for this reason cite the 1988 film Rain Man in which Dustin Hoffman plays Raymond Babbit, who can memorize a thick phone book in one night. As novelist and cultural observer Greg Olear wrote, “Thirty years later, the belief persists that autistics can reliably count a pile of toothpicks at a glance. This is a powerful negative stereotype that autistic children (and their parents) must overcome.”
But there doesn’t seem to be any stopping “autism lit,” exploitative or not. In fact, the fascination with the autism spectrum and fiction has launched yet another literary trend: the “retroactive diagnosis.” Some readers now believe that Mr. Darcy of Pride and Prejudice is on the spectrum; that’s the explanation for his reserve. Some readers suspect that the narrator of Hermann Hesse’s Steppenwolf falls into this category as well. The word “autism” didn’t exist, the theory goes, before World War II, and that’s the explanation for why Austen and Hesse didn’t label their characters themselves.
I’m not ready to jump onto this bandwagon. Calling Mr. Darcy autistic is a way of granting stature to people truly on the spectrum who don’t need your literary charity, thank you very much. But there are worse alternatives. (The retroactive diagnoses might apply to Boo Radley.)
In the world outside victimhood, we remain in the midst of an unexplained epidemic of autism spectrum disorders; some sources say that as many as 1 in 68 children are being diagnosed with the condition. And even with the onslaught of fictional characters on the spectrum, much of the story of autism remains untold.
There’s a saying that has been variously attributed to Temple Grandin, the autistic professor of animal science and advocate for the humane treatment of livestock, as well as to the autism advocate and author Stephen Shore, which has become one of those aphorisms that belong to the world: “If you’ve met one person with autism, you’ve met one person with autism.”
Since each story is different, we can expect the category of autism lit to swell, ideally with more portrayals of people on the spectrum who have jobs, partners, and most of all, purpose.
Donna Levin’s latest novel, There’s More Than One Way Home, was published in May of this year by Chickadee Prince Books. Her papers are part of the Howard Gotlieb Archival Research Center at Boston University and her novels are part of the “California novels” collection in the California State Library.
Even as Zika dominates headlines, another mosquito-transmitted disease has been marching steadily across Africa: yellow fever. With over 900 confirmed cases and thousands more suspected in Angola and the Democratic Republic of Congo, health officials are scrambling to vaccinate populations in these areas in time to halt the virus’ spread. The problem: there isn’t enough of the vaccine to go around.
The yellow fever vaccine stockpile, which usually stands at 6 million doses, has already been depleted twice this year. Producing more takes nearly six months—time Africa doesn’t have. Last week, the dire situation led the World Health Organization to approve the use of a mini-dose—just 20 percent of the full vaccination—to help struggling populations make it through this latest epidemic.
According to WHO, the fractional dosing measure likely protects against the disease for at least 12 months, compared to the lifetime protection that regular vaccination usually affords. “We don't have any data on long-term durability,” says Anna Durbin, a researcher specializing in vaccines at John Hopkins Bloomberg School of Public Health. In fact, the vaccination decision illustrates a broken system when it comes to vaccine supply and demand.
Around 1 billion people in 46 countries are at risk for yellow fever, a mosquito-transmitted disease primarily found in South America and Africa that belongs to the same genus as Zika, Dengue and West Nile. About 15 percent of those who are infected fully develop the disease, whose symptoms include fever, chills, body aches, nausea, weakness and jaundice—the yellowing of the skin and eyes that inspired the virus’ name. Up to 50 percent die.
Once you have it, yellow fever is incurable; doctors can only treat the symptoms. But it can easily be prevented. A single dose of the highly-effective yellow fever vaccine can impart lifetime immunity. The yellow fever vaccine is a live attenuated vaccine, which means it contains a form of the live virus that has been altered to prevent it from causing disease. Injecting this hobbled virus stimulates the body to produce antibodies that guard against yellow fever infection.
This latest outbreak has proved to be unexpectedly virulent. “It is the largest outbreak [of yellow fever] that we've seen in a very, very long time,” says Durbin. The WHO and its partners have so far delivered an estimated 18 million vaccine doses to Angola, Democratic Republic of the Congo and Uganda. But it hasn’t been enough to quell the spread—hence the mini-doses.
In the past, fractional dosing has successfully been used for rabies and is currently being used for Polio, according to Sarah Cumberland, a spokesperson for WHO. Clinical trials have shown it elicits a similar antibody response as the full injection. In fact, some trials suggest that the dose can be reduced to as little as ten percent.
But no research has yet tested fractional dosing on children, notes Cumberland. It is still unclear how children respond to the vaccine, but some suggest they have a weaker response than adults, so the lower doses may not impart full immunity.Aedes aegypti, the species of mosquito that transmits Zika and yellow fever, enjoying a blood meal. (Wikimedia Commons)
The latest recommendation for yellow fever is not a permanent mandate. Once vaccines become available again, WHO notes that doctors should return to full potency vaccines—and routine, preventative vaccinations—for all. “Vaccine shipments are being reprogrammed to prioritize the emergency response, but at the same time we are rescheduling vaccine supplies for routine vaccination,” says Cumberland.
Yet at the root of this outbreak and the repeated vaccine shortages lurks a cyclical problem. As vaccine shortages grow, fewer people are routinely vaccinated and the population as a whole becomes more susceptible to the virus. This, in turn, could provoke more outbreaks that place even greater strain on the limited stores. “With the regular shortage of the vaccine, what we are seeing is less vaccine being given…as part of the routine immunization programs,” says Durbin. This lack of routine vaccination adds to the "vicious cycle" of perpetual shortage.
Increasing production of the vaccine is no small task. Current methods rely on growing the weakened virus in an in a chicken egg, a nearly 80-year-old method that takes up to six months and requires pathogen-free chicken eggs, which are hard to come by. Advancements in modern cell-culture technology may ultimately speed up yellow fever vaccine production. But making such a large change in production will take time and research to ensure the new products are safe.
The problem is, vaccines aren’t particularly profitable. They cost millions or billions of dollars to develop, and the resulting product is sold at low prices to impoverished regions. Plus, people only need one or two shots in a lifetime.
“In the past, a lot of companies dropped out of making vaccines,” says Art Reingold, an epidemiologist at Berkeley School of Public Health who serves on the Advisory Committee on Immunization Practices. Ultimately, these companies realized that “they could make more profit by producing a drug that old people in the United States have to take every day of their life—to lower their cholesterol or their blood pressure or to give them an erection—than they could by making a vaccine to give to poor children that, when you give them one or two doses, they are protected for life,” he says.
As a result, today there are only six manufacturers worldwide producing yellow fever vaccines, and stores fall short nearly every year.
Fear and anti-vaccine sentiment further perpetuate these troubles, Reingold adds. Along with the cost of vaccination, fear also likely drives the black-market trade of fake yellow fever vaccination certificates, placing even more people at risk of contracting the disease.
But if we want vaccines, which have prevented millions of deaths and illnesses throughout history, then “somebody has to do the research, somebody needs to do the development, and somebody needs to invest the money in it,” says Reingold. If not, then these kinds of perpetual vaccine shortages will swiftly become the new normal.
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.”
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.”
On a summer day on the island of Kaua`i, a Hawaiian monk seal hauls his 500-pound body out of the surf and galumphs toward a nursing female and her newborn pup. When he gets a few feet away from the mother, she arches her back and faces him, head high. He does the same. She barks. He barks. Snot and saliva fly.
It’s typical—if awkward—monk seal courtship behavior, more posturing than physical. But scientists are concerned that this kind of scene could swiftly turn into a deadly disease outbreak for one of the most endangered marine mammals in the world. The Hawaiian monk seal has been listed under the Endangered Species Act since 1976, after its numbers were devastated by decades of hunting and other forms of human contact.
About a decade ago, researchers grew worried that a strain of morbillivirus, the genus of viruses that includes measles and canine distemper, could wipe out the last of these rare seals. In response, they’ve launched the first-ever effort to vaccinate a species of wild marine mammals—an effort that has come with a host of first-ever challenges.
The 1,200 or so monk seals that survive in the wild are spread over vast swaths of ocean, coming ashore for only brief periods of time to rest, molt and give birth on islands that stretch across the Central Pacific. Morbillivirus, which is spread by respiratory secretions, could kill off a significant chunk of them without anyone knowing. Thankfully, a growing population of monk seals in the main Hawaiian Islands is making it easier for researchers and their dedicated volunteer network to find—and immunize—them.
For the endangered monk seal, disease has always been the “monster lurking over the horizon,” says Charles Littnan, lead scientist for the National Oceanic and Atmospheric Administration’s Hawaiian Monk Seal Research Program (HMSRP). But it wasn’t until the past decade that research revealed that the species had precariously low genetic diversity. At that point, that infectious diseases “rocketed to an immediate concern,” Littnan says.
In fact, disease may have contributed to the demise of the only other species of Neomonachus, the genus that includes the Hawaiian monk seal: the extinct Caribbean monk seal. Disease “can wipe out seal populations all over the world, and we know that there are disease concerns for the living monk seals,” Kris Helgen, a zoologist at the National Museum of Natural History who studies the extinct monk seal’s evolutionary history, told Smithsonian.com in 2014.
“Simply put, morbillivirus outbreaks in pinnipeds and cetaceans are the things that marine mammal stranding responders have nightmares about,” says Dr. Michelle Barbieri, the lead veterinarian with HMSRP who is supervising rollout of the vaccine program. “The disease could spread easily, infecting many animals out in the ocean before we are able to detect what's going on.”Two monk seals tussle on a beach on Kaua`i in 2015. (Kim Rogers)
Littnan and his team had already started developing a plan to respond to the event of a morbillivirus outbreak when, in 2010, their fears were validated. That was when researchers identified the first known case of morbillivirus in the Central Pacific, in a Longman’s beaked whale that stranded on Maui.
Littnan knew that the disease had already killed tens of thousands of seals and dolphins in the Atlantic, Mediterranean, Arctic and North Pacific oceans. Soon after, a northern fur seal, whose native habitat is the west coast of the United States, turned up on an O‘ahu beach near where monk seals are known to haul out and rest. While the fur seal wasn’t infected, its species is known to carry the disease.
Fortunately, there have been no known cases of morbillivirus in Hawaiian monk seals—yet. Blood tests indicate no prior population exposure, probably because the seals are buffered by the archipelago’s isolation in the middle of the Pacific Ocean. While that’s good, it also means there is no natural immunity. And that leaves this already-vulnerable species quite exposed.
If morbillivirus does break out, Hawaiian monk seals won’t stand a chance. An invasive disease, like an exotic species, can quickly wipe out a vulnerable population. In seals, morbillivirus targets the lungs and brain. Pneumonia may develop, skin lesions may erupt, and the animal may exhibit abnormal behavior, resulting in death in as little as five days.
Littnan and Barbieri knew the only hope for these seals was total vaccination. But 85 percent of the species live in the remote Northwestern Hawaiian Islands, among atolls and islets, elusive even to field biologists who study them. Finding monk seals to vaccinate, especially if the vaccine required a follow-up booster, would be a challenge.
Another challenge was finding the right vaccine. The most effective vaccines generally contain a live virus, which runs a chance of infecting the vaccinated animal. There was no way that the National Marine Fisheries Service, the regulatory agency overseeing the seal’s recovery, would risk introducing the live virus into the population. That left vaccines with dead viruses. But the immune responses in those are short-lived and require frequent boosters—hardly an option when dealing with a wild marine species that spends two-thirds of its life at sea.
The best choice turned out to be recombinant vaccine, which takes advantage of the way viruses inject their genetic material into cells. Researchers create recombinant vaccines by inserting harmless viruses with genetic material that stimulate an immune response in the host subject. The vaccine the researchers chose was one made for ferrets. It isn’t as strange as it sounds: Because all morbilliviruses are antigenically similar, meaning that vaccines made for one can cross-protect against another. However, there can always be adverse reactions.A juvenile and weaner monk seal greet each other on a Kauai beach in 2014. (Kim Rogers)
Meanwhile, across the Pacific in California, researchers were conducting trials using the ferret vaccine in five captive harbor seals. It worked: Tests found that the initial vaccination, followed by a booster one month later, produced persistent antibodies to the virus. The seals had no noticeable side effects.
The project hit a snag when, in 2013, after nearly a decade of work into a vaccination program, the manufacturer, Merial, put the vaccine on indefinite backorder. “That took us totally by surprise,” Littnan says. “It was unfortunate timing because this vaccine has been strong production for a long time and used quite broadly not only for ferrets in the wild but very broadly in the zoo and aquaria industry to vaccinate marine mammals and other mammals.”
Littnan kept moving forward, modeling potential spatial and temporal progress of the disease, and planning his team’s response in the advent of an outbreak.
This form of aggressive intervention to save the species wasn’t new to HMSRP. In the past, Littnan’s team had stepped in to disentangle seals trapped in marine debris and de-hook seals caught on fishing lines. They translocated young seals from areas of low survival to high. And with The Marine Mammal Center of Sausalito, California, they started rehabilitating underweight and malnourished seals.
Littnan reports that more than 30 percent of monk seals alive today are due to these interventionist efforts. The annual decline of the population has slowed, from 8 percent in the 1980s to 2.8 percent now.
In late 2015, the manufacturer made a limited quantity of the ferret vaccine available. Littnan didn’t waste any time in procuring enough vaccines for 58 animals. Because the vaccines had about a year before they expired, he decided to inoculate the population immediately to—hopefully—prevent an outbreak rather than respond to one.
Barbieri started with seven monk seals at Ke Kai Ola, the rehabilitation center run by The Marine Mammal Center on Hawai‘i Island. Now, they’re targeting seals in the wild around O‘ahu and Kaua‘i, where 40 to 50 seals regularly show up on each island.
The inoculation itself is a simple process, utilizing a pole syringe to inject one millimeter of vaccine through a 10 millimeter syringe and topping that off with a booster three to five weeks later. As of this writing, at least 43 animals have received vaccinations. Because seals often go on multi-day foraging trips at sea and circumnavigate an island at will, you never know when or where they’ll turn up. Thus, finding a seal during the window its booster is required may be the trickiest part of the inoculation process.
While 58 portions certainly isn’t enough to vaccinate every animal in the population, it is enough to create herd immunity among the growing pocket populations of seals around the Main Hawaiian Islands. The idea is that, if the disease does enter the population, it won’t spread to epidemic proportions.
“We’re using this project as an opportunity to learn about how long the antibodies are detectable in the blood of vaccinated monk seals,” Barbieri says, “And we will be able to compare those data to previous studies.” In the future, such a program could lay the groundwork for protecting seals against other diseases like West Nile.
Littnan hopes to roll out the vaccination program to the remote Northwestern Hawaiian Islands, a stretch of uninhabited islands, islets, and atolls that make up the recently expanded Papahānaumokuākea Marine National Monument where Littnan’s field crews stay for five months every summer. But that all depends on vaccine availability.
“There’s hope,” Littnan says. “We’ve been reaching out to the company. Hopefully, they understand the need and will stick with the product.”
Even with an unlimited supply of vaccines, however, the success of the program hinges on all vaccinated seals achieving what Barbieri calls “perfect immunity.” “Antibodies to morbillivirus do not exactly predict protection in the face of exposure,” says Barbieri. “We will never expose vaccinated monk seals to the virus to find out if they acquire disease or not, so there will remain several unknowns surrounding this question.”
That is, unless a monk seal finds itself naturally infected. But that is a scenario scientists would rather not ponder.
Does it ever seem like you’re invited to an awful lot of summer birthday gatherings? For good reason. In the United States, most births occur between June and early November. Count back nine months, and you’ll see that places most conceptions in the fall and winter.
What’s going on? Is the crisp autumn air, or the joy (or anxiety) of the holiday season, triggering more unprotected sexual intercourse? Or is it something else entirely?
It turns out reproduction is seasonal across all living organisms, from plants, to insects, to reptiles, to birds and mammals – including human beings. The ultimate explanation for this phenomenon is an evolutionary one.
Earth’s environment is seasonal. Above or below the equator, the year is structured by the winter, spring, summer and fall. In equatorial regions, the wet and dry seasons punctuate the year. Organisms have evolved strategies to reproduce at the time of year that will maximize their lifetime reproductive success.
Humans are no exception and maintain this evolutionary outcome: birth seasonality. Researchers, including us, have recently been working to understand more about why births are seasonal because these patterns can have a big impact on childhood disease outbreaks.
Tracking birth peaks across the globe
In some countries, local customs can explain birth seasonality. For example, in the 1990s, researchers showed that the traditional July-August wedding season in Catholic communities in Poland resulted in lots of births in the spring. But wedding season does not drive birth seasonality everywhere, and there is only a small correlation between weddings and births 9 to 15 months later in most locations. Thus, nuptial beds are not the full story.
There is a clear pattern of births across latitude. Here in the U.S., states in the North have a birth peak in early summer (June-July), while states in the South experience a birth peak a few months later (October-November).
Globally, popular birthdays follow a similar pattern with peaks occurring earlier in the year the further north you get from the equator – for instance, Finland’s is in late April, while Jamaica’s is in November. And in the U.S., states further south, like Texas and Florida, experience birth peaks that are not only later in the year, but also more pronounced than those seen in the North.
So what influences conception?
Research shows that the seasonality of births correlates with changes in local temperature and day length. And regions with extreme temperatures typically have two peaks in births every year. For example, data from the early 1900s showed two pronounced birth peaks per year in West Greenland and Eastern Europe.
Rural populations tend to have a more dramatic seasonal birth pulse than urban populations, probably because country dwellers may be more subject to environmental conditions, including changes in temperature and day length. Environmental factors like these could influence human sexual behavior.
Additionally, as in other animals, these environmental changes could drive seasonal changes in fertility. This means that, rather than just an increase in frequency of sexual intercourse, female and/or male fertility may change throughout the year, as an endogenous biological phenomenon, making people more likely to conceive at certain times – with the prerequisite of sexual intercourse, of course.
Biologists know that the fertility of non-human mammals is influenced by day length, which may act like a reproductive calendar. For example, deer use the shortening days of autumn as a signal for timing reproduction. Females get pregnant in the fall and carry their pregnancy through winter. The goal is to give birth at a time when plenty of resources are available for newborns – being born in springtime is evolutionarily beneficial.Evolution ensures that babies come when resources are abundant, to give newborns the best chance at survival. (Mary Terriberry / Shutterstock.com)
So animals with long pregnancies tend to be short-day breeders, meaning they only breed in the short days of autumn and winter; they’re pregnant through the winter and give birth in spring. Whereas animals with short gestation periods are long-day breeders; they conceive in the long days of spring or summer and, because their pregnancy is short, have their young that same spring or summer. Many species only mate and are only capable of getting pregnant during a specific time of year – those long or short days, for instance – and the length of day itself directs their hormones and ability to conceive.
Humans may not be so different from other mammals. Day-length has the potential to influence human fertility and it does seem to explain the patterns of birth seasonality in some places, but not others. In addition to the length of day, researchers have shown that social status and changes in the standard of living also affect birth seasonality. There seems to be no single driver for birth seasonality in people, with an array of social, environmental and cultural factors all playing a role.
What does birth season have to do with disease?
Forest fires require fuel to burn. After a big fire, kindling must be replenished before another fire can spread.
Disease epidemics are no different. Childhood infectious diseases require susceptible children for a pathogen to spread through a population. Once children are infected and recover from diseases like polio, measles and chickenpox, they are immune for life. So for new epidemics to take off, there must be a new group of susceptible infants and children in the population. In the absence of vaccination, the birth rate in a population is a major determinant of how often childhood disease epidemics can occur.
Babies are born with maternal immunity: antibodies from mom that help guard against infectious diseases like measles, rubella and chickenpox. This immunity is usually effective for the first 3 to 6 months of life. Many infectious diseases that strike infants in the U.S. tend to peak in the winter and spring months. That leaves infants born in the U.S. birth season of summer and autumn becoming susceptible as their maternal immunity wears off three to six months later, just when many infectious diseases are striking in winter and spring.
In humans, the average birth rate is extremely important for understanding disease dynamics, with changes in birth rate influencing whether an epidemic will occur every year, or every few years, and how big an epidemic can be. For instance, polio epidemics in the first half of the 20th century resulted in many thousands of children paralyzed by polio each summer in the U.S. The size of polio outbreaks was dictated by the birth rate. Because of this, polio outbreaks became more extreme after the World War II baby boom, when the birth rate increased.During the polio epidemic of summer 1955, a hospital in Boston helps patients breathe with iron lungs. (AP Photo)
Similarly, the timing and strength of birth peaks also affects the length of time between epidemics. Importantly, regardless of how often an epidemic occurs – like births – it is always seasonal. And births have been shown to directly alter the seasonal timing of viral outbreaks in children.
Does the number of children born in summer drive seasonally occurring childhood diseases? Does disrupting patterns in births alter seasonal outbreak patterns? We know that the change in the average birth rate can modify the size of childhood disease epidemics, as was seen for polio during the baby boom. Theoretical models suggest changes in birth seasonality can alter the size and frequency of childhood disease outbreaks. But it remains an open question if the changes in birth seasonality that have been occurring over the past 50-plus years have in fact altered childhood diseases; more research is needed in this area.
Losing our seasonal connection
There is one thing all researchers in this field agree on: People are starting to lose birth seasonality throughout the Northern Hemisphere. (Due to a lack of data, it is currently unknown what is happening in countries south of the equator, such as those in Latin America and Africa.)
There are two pieces of evidence to support this. First, the strength of the birth pulse – from June to November in the U.S. – has been decreasing for decades; and second, locations that had two birth peaks per year now only have one.
This loss of birth seasonality may be partially due to social factors, such as pregnancy planning and the increasing disconnect humans have with the natural environment and, therefore, the seasons. The root of this change is likely tied to industrialization and its downstream societal effects, including indoor work, fewer seasonal jobs, access to family planning, and modern housing and artificial light that obscures the natural day length that could influence fertility.
Whatever the cause of birth seasonality, one thing remains clear, at least here in the U.S. – right now remains the prime time for conception.
Some time around 1920, a person carried a virus down the Sangha River, from Cameroon toward the capital of the Democratic Republic of the Congo. The virus was a strain of HIV, and the city—then called Léopoldville and, now, Kinshasa—gave it the perfect soup of conditions to ignite the AIDS epidemic. Since then, HIV has infected nearly 75 million people worldwide.
A new study, published in Science, looks at how HIV, an infection that had previously affected people only in the immediate region of its origins could bloom into one that crossed international boarders.
Researchers already knew that chimpanzees in southern Cameroon harbor viruses most closely resembling HIV-1, group M, the strain that went global. By comparing the genetic changes between different strains, researchers had figured out that HIV-1’s lineage made the leap from chimp to human some time in the early 1900s. In fact, HIV likely jumped several times to people handling bushmeat, but only one strain created the pandemic we grapple with today.
The researchers combed through the genetics of hundreds of tissue samples from people infected with HIV from the last 50 years. By creating a kind of virus family tree, they traced back and discovered a common ancestor from about 1920 in Kinshasa.
Contrary to some theories, the new study suggests that there wasn’t any thing special about that group M strain. “Perhaps the [new study’s] most contentious suggestion is that the spread of the M-group viruses had more to do with the conditions being right than it had to do with these viruses being better adapted for transmission and growth in humans,” scientist Jonathan Ball of the University of Nottingham told the BBC.
At that time, Kinshasa’s population was booming. The Congo river connected the growing city to Kisangani, and rail lines carried hundreds of thousands of passengers to major mining locations Lubumbashi and Katanga. With the influx of largely male laborers came many sex workers. Contaminated needles may have also played a role.
“There were lots of different factors,” lead author Oliver Pybus, an infectious disease researchers from the University of Oxford in the United Kingdom, told Science Magazine. “Basically this one was at the right time and the right place—and it hit the jackpot.”
The U.S. military is launching a massive effort to counter the Ebola outbreak coursing through western Africa. More than 3,000 troops will be sent to the region to set up a command-and-control center, coordinate efforts, build hospitals, train health workers and bolster the flow of supplies, says the Washington Post.
As President Obama noted yesterday, Ebola is spreading exponentially, with the rate of infection growing faster and faster. “Since the virus was discovered, no Ebola outbreak’s toll has risen above several hundred cases,” says health reporter Maryn McKenna at Wired. “This now truly is a type of epidemic that the world has never seen before.” A much larger effort is needed to wrest control over the epidemic, says Policy Mic.
It's not immediately clear why the U.S. military should be part of that effort. The scope and scale of this mission, after all, “is unprecedented as a public-health operation led by the U.S. military,” says policy analyst Stephen Morrison to the Wall Street Journal.
Despite the seemingly odd fit, the U.S. military may actually be the right people for the job, says the Journal:
The operation will require the military to fuse its experience in responding to natural disasters with its training in biowarfare to minimize the risks of Americans contracting the disease. Personnel will bring medical assistance and training, logistical expertise and engineering experience to set up 17 field hospitals with 100 beds each, more than tripling current capacity.
"The U.S. military, with its enormous logistical capability, extensive air operations, and highly skilled medical corps, could address gaps in the response quickly," says the Washington Post.
Having troops on the ground could also be useful given that Nigeria, one of the countries affected by the ongoing Ebola epidemic, is also facing pressure from the Boko Haram terrorist organization.
The military might even be able to provide a special set of skills that would be foreign to most healthcare workers.
One of the problems plaguing efforts to fight the Ebola outbreak has been a lack information. Not all cases are reported, and the disease can spread outside of the watchful eye of emergency managers. According to Fast Company, data assimilation techniques that have been previously used by the military to track terrorists could be turned on the epidemic.
The mission is expected to cost $750 million over the next six months, an even bigger effort than the one the World Health Organization called for in August, though smaller than the $987 million figure the U.N. cited this week.
Avoid close contact with sick patients. Stay home if you’re feeling unwell. Scrub your hands with soap and water for at least 20 seconds and for goodness’ sake, stop touching your face.
By now, you’ve probably heard or seen the advice from the Centers for Disease Control and Prevention (CDC) for staving off COVID-19, the viral epidemic ricocheting across the globe. Most cases of the disease are mild, triggering cold-like symptoms including fever, fatigue, dry cough and shortness of breath. The death rate appears to be low—about two or three percent, perhaps much less. But the virus responsible, called SARS-CoV-2, is a fearsomely fast spreader, hopping from person to person through the droplets produced by sneezes and coughs. Since COVID-19 was first detected in China’s Hubei province in December 2019, nearly 100,000 confirmed cases have been reported worldwide, with many more to come.
To curb the virus’ spread, experts stress the importance of hand hygiene: keeping your hands clean by regularly lathering up with soap and water, or, as a solid second choice, thoroughly rubbing them down with an alcohol-based sanitizer. That might sound like simple, even inconsequential advice. But such commonplace practices can be surprisingly powerful weapons in the war against infectious disease.
“[Washing your hands] is one of the most important ways to interrupt transmission of viruses or other pathogens,” says Sallie Permar, a physician and infectious disease researcher at Duke University. “It can have a major impact on an outbreak.”
How to Destroy a Virus
In the strictest sense of the word, viruses aren’t technically alive. Unlike most other microbes, which can grow and reproduce on their own, viruses must invade a host such as a human cell to manufacture more of themselves. Without a living organism to hijack, viruses can’t cause illness. Yet viral particles are hardy enough to remain active for a while outside of the host, with some staying infectious for hours, days or weeks. For this reason, viruses can easily spread unnoticed, especially when infected individuals don’t always exhibit symptoms—as appears to be the case with COVID-19.
Researchers are still nailing down the details of exactly how SARS-CoV-2 is transmitted and how resilient it is outside the body. Because the virus seems to hang out in mucus and other airway fluids, it almost certainly spreads when infected individuals cough or sneeze. Released into the air, infectious droplets can land on another person or a frequently touched surface like a doorknob, shopping cart or subway seat. The virus can also transfer through handshakes after someone carrying the virus sneezes or coughs into their hand.
After that, it’s a short trip for the virus from hand to head. Researchers estimate that, on average, humans touch their faces upwards of 20 times an hour, with about 44 percent of these encounters involving eyes, mouths and noses—some of the quickest entry points into the body’s interior.
Breaking this chain of transmission can help stem the spread of disease, says Chidiebere Akusobi, an infectious disease researcher at Harvard’s School of Public Health. Sneezing or coughing into your elbow can keep mucus off your mitts; noticing when your hand drifts towards your face can help you reduce the habit.
All this public-health-minded advice boils down to a game of keep away. To actually infect a person, viruses must first get inside the body, where they can infect living cells—so if one lands on your hands, the best next move is to remove or destroy it.
The Science Behind Hand-Washing
The most important step to curbing infection may be hand-washing, especially before eating food, after using the bathroom and after caring for someone with symptoms. “It’s simply the best method to limit transmission,” says Kellie Jurado, a virologist at the University of Pennsylvania’s Perelman School of Medicine. “You can prevent yourself from being infected as well as transmitting to others.”
According to the CDC, you should wet your hands—front and back—with clean, running water; lather up with soap, paying mind to the easily-forgotten spaces between your fingers and beneath your nails; scrub for at least 20 seconds; then rinse and dry. (Pro tip: If counting bores you or you’re sick of the birthday song, try the chorus of these popular songs to keep track.)
Done properly, this process accomplishes several virus-taming tasks. First, the potent trifecta of lathering, scrubbing and rinsing “physically removes pathogens from your skin,” says Shirlee Wohl, a virologist and epidemiologist at Johns Hopkins University.
In many ways, soap molecules are ideal for the task at hand. Soap can incapacitate SARS-CoV-2 and other viruses that have an outer coating called an envelope, which helps the pathogens latch onto and invade new cells. Viral envelopes and soap molecules both contain fatty substances that tend to interact with each other when placed in close proximity, breaking up the envelopes and incapacitating the pathogen. “Basically, the viruses become unable to infect a human cell,” Permar says.
Alcohol-based hand sanitizers also target these vulnerable viral envelopes, but in a slightly different way. While soap physically dismantles the envelope using brute force, alcohol changes the envelope’s chemical properties, making it less stable and more permeable to the outside world, says Benhur Lee, a microbiologist at the Icahn School of Medicine at Mount Sinai. (Note that “alcohol” here means a chemical like ethanol or isopropyl alcohol—not a beverage like vodka, which contains only some ethanol.)
Alcohol also can penetrate deep into the pathogen’s interior, wreaking havoc on proteins throughout the virus. (Importantly, not all viruses come with outer envelopes. Those that don’t, like the viruses that cause HPV and polio, won’t be susceptible to soap, and to some extent alcohol, in the same way.)A schematic of an enveloped virus (left) and a non-enveloped virus (right). SARS-CoV-2 and other coronaviruses are enveloped, meaning they have a fatty outer coating that can be targeted by soap and alcohol. (Modified from Nossedotti / Wikimedia Commons (CC BY-SA 3.0))
Hand sanitizers made without alcohol—like some marketed as “baby-safe” or “natural”—won’t have the same effect. The CDC recommends searching for a product with at least 60 percent alcohol content—the minimum concentration found to be effective in past studies. (Some water is necessary to unravel the pathogen’s proteins, so 100 percent alcohol isn’t a good option.)
As with hand-washing, timing matters with sanitizers. After squirting a dollop onto your palm, rub it all over your hands, front and back, until they’re completely dry—without wiping them off on a towel, which could keep the sanitizer from finishing its job, Jurado says.,
But hand sanitizers come with drawbacks. For most people, using these products is less intuitive than hand-washing, and the CDC notes that many people don’t follow the instructions for proper application. Hand sanitizers also don’t jettison microbes off skin like soap, which is formulated to lift oily schmutz off surfaces, Akusobi says.
“Soap emulsifies things like dirt really well,” he says. “When you have a dirty plate, you don’t want to use alcohol—that would help sterilize it, but not clean it.”
Similarly, anytime the grit is visible on your hands, don’t grab the hand sanitizer; only a full 20 seconds (or more) of scrubbing with soapy water will do. All told, hand sanitizer “should not be considered a replacement for soap and water,” Lee says. “If I have access to soap and water, I will use it.”
Too Much of a Good Thing?
Technically, it is possible to overdo it with both hand-washing and hand sanitizing, Akusobi says. “If your skin is chronically dry and cracking, that’s no good. You could be exposing yourself to other infections,” he says. But “it would take a lot to get to that point.”
In recent weeks, hand sanitizers have been flying off the shelves, leading to shortages and even prompting some retailers to ration their supplies. Some people have begun brewing up hand sanitizers at home based on online recipes.
Many caution against this DIY approach, as the end products can’t be quality controlled for effectiveness, uniformity or safety, says Eric Rubin, an infectious disease researcher at Harvard’s School of Public Health. “On average, one would imagine that [a homemade sanitizer] would not work as well, so it would be a mistake to rely on it,” he says.
As more information on SARS-CoV-2 and COVID-19 emerges, experts stress the importance of awareness. Even as the news changes and evolves, people’s vigilance shouldn’t.
“Do the small things you need to do to physically and mentally prepare for what’s next,” Wohl says. “But don’t panic. That never helps anybody.”
In 2008, Google announced an intriguing new service called Google Flu Trends. Engineers at the company had observed that certain search queries (such as those including the words "fever" or cough") seemed to spike every flu season. Their idea was to use the frequency of these searches to calculate nationwide flu rates faster than could be done with conventional data (which generally takes a few weeks to collect and analyze), letting people know when to take extra precautions to avoid getting the virus.
The service has consistently overestimated flu rates, when compared to conventional data collected afterward by the CDC, estimating the incidence of flu to be higher than it actually was for 100 out of 108 weeks between August 2011 and September 2013. In January 2013, when national flu rates peaked but Google Flu Trends estimates were twice as high as the real data, its inaccuracy finally started garnering press coverage.
The most common explanation for the discrepancy has been that Google hasn't taken into account the uptick in flu-related queries that occur as a result of the media-driven flu hysteria that occurs every winter. But this week in Science, a group of social scientists led by David Lazer propose an alternate explanation: that Google's own tweaks to its search algorithm are to blame.
It's admittedly hard for outsiders to analyze Google Flu Trends, because the company doesn't make public the specific search terms it uses as raw data, or the particular algorithm it uses to convert the frequency of these terms into flu assessments. But the researchers did their best to infer the terms by using Google Correlate, a service that allows you to look at the rates of particular search terms over time.
When the researchers did this for a variety of flu-related queries over the past few years, they found that a couple key searches (those for flu treatments, and those asking how to differentiate the flu from the cold) tracked more closely with Google Flu Trends' estimates than with actual flu rates, especially when Google overestimated the prevalence of the ailment. These particular searches, it seems, could be a huge part of the inaccuracy problem.
There's another good reason to suspect this might be the case. In 2011, as part of one of its regular search algorithm tweaks, Google began recommending related search terms for many queries (including listing a search for flu treatments after someone Googled many flu-related terms) and in 2012, the company began providing potential diagnoses in response to symptoms in searches (including listing both "flu" and "cold" after a search that included the phrase "sore throat," for instance, perhaps prompting a user to search for how to distinguish between the two). These tweaks, the researchers argue, likely artificially drove up the rates of the searches they identified as responsible for Google's overestimates.
Of course, if this hypothesis were true, it wouldn't mean Google Flu Trends is inevitably doomed to inaccuracy, just that it needs to be updated to take into account the search engine's constant changes. But Lazer and the other reserachers argue that tracking the flu from big data is a particularly difficult problem.
A huge proportion of the search terms that correlate with CDC data on flu rates, it turns out, are caused not by people getting the flu, but by a third factor that affects both searching patterns and flu transmission: winter. In fact, the developers of Google Flu Trends reported coming across particular terms—those related to high school basketball, for instance—that were correlated with flu rates over time but clearly had nothing to do with the virus.
Over time, Google engineers manually removed many terms that correlate with flu searches but have nothing to do with flu, but their model was clearly still too dependent on non-flu seasonal search trends—part of the reason why Google Flu Trends failed to reflect the 2009 epidemic of H1N1, which happened during summer. Especially in its earlier versions, Google Flu Trends was "part flu detector, part winter detector," the authors of the Science paper write.
But all of this can be a lesson for the use of big data in projects like Google Flu Trends, rather than a blanket indictment of it, the researchers say. If properly updated to take into account tweaks to Google's own algorithm, and rigorously analyzed to remove purely seasonal factors, it could be useful in documenting nationwide flu rates—especially when combined with conventional data.
As a test, the researchers created a model that combined Google Flu Trends data (which is essentially real-time, but potentially inaccurate) with two-week old CDC data (which is dated, because it takes time to collect, but could still be somewhat indicative of current flu rates). Their hybrid matched the actual and current flu data much more closely than Google Flu Trends alone, and presented a way of getting this information much faster than waiting two weeks for the conventional data.
"Our analysis of Google Flu demonstrates that the best results come from combining information and techniques from both sources," Ryan Kennedy, a University of Houston political science professor and co-author, said in a press statement. "Instead of talking about a 'big data revolution,' we should be discussing an 'all data revolution.'"
Last month, alarming numbers of dead bottlenose dolphins started turning up on the beaches of Virginia and other states in the Mid-Atlantic region. In an average July, the Virginia Aquarium & Marine Science Center—which operates a Stranding Response Team to collect and analyze beached animals—encounters seven dolphins washed ashore. In July 2013, the team picked up 44 animals.
Overall, the East Coast has seen at least 124 dolphin deaths since July—a rate that authorities say is seven times higher than normal. All of this led the National Marine Fisheries Service, a branch of the NOAA, to officially designate the deaths as an “unusual mortality event” last week, which means that increased federal funds will be allotted to help researchers investigate what’s going on.
Currently, dozens of marine biologists along the Atlantic are examining stranded dolphin carcasses for clues. Last week, Charles Potter, a marine mammal expert with the Smithsonian Natural History Museum, traveled to Virginia Beach to assist with the Virginia Aquarium & Marine Science Center’s investigation.
“We basically perform necropsies of the carcasses that come in,” Potter says. “We’re assuming nothing, and looking at the entire animal for the cause of death, and any abnormal tissues. We also harvest a whole suite of specimens from each carcass, and these are sent out to labs for analysis.” During his time in Virginia Beach, he conducted five in-depth necropsies—animal autopsies—in total.
The investigation is still in its earliest stages, but researchers have a few potential suspects in mind. In 1987—when the last major die-off of Atlantic dolphins occurred, resulting in the deaths of 740 animals—morbilivirus was found to be the main culprit. At least one dolphin found this year has tested positive for the same virus, which produces lesions in the lungs and central nervous system tissue, and Potter speculates that the time that’s passed since the previous epidemic has allowed for a generation of dolphins never exposed to the pathogen.
But establishing a potential cause of the die-off as a whole is much harder than diagnosing a particular cause of death for any one individual. With humans, if you ask someone in the hospital what a specific patient died from, you may be told that the person had pneumonia, explains Potter, who also participated in the 1987 investigation. “But that’s only because we become so debilitated by other factors that, at some point, we can’t clear our airways, and we develop these pneumonia infections,” he says. In much the same way, it’s possible that a susceptibility to morbilivirus or other pathogens found in the dolphins could be caused by a separate, underlying factor.
That underlying factor might be a particularly disconcerting one: humans. Disproportionate numbers of males and calves are among the dolphins turning up dead, which makes Potter and other suspicious that environmental contaminants—such as heavy metals, pesticides and hydrocarbons—might play a role.
“Males don’t have a mechanism for shedding contaminants,” he says. “The females shed significant amounts of their lipid-soluble contaminants through lactation, so the calf gets a hell of a dose early on in life, and some of the most outrageous levels of contaminants we’ve seen have been in calves.” It’s possible that the overall buildup of contaminants in these animals—along with other stresses attributable to human activity, such as increased noise and competition for space and food with humans—is making them more susceptible to infectious pathogens.
Potter says that he and other investigators will continue testing the dolphins for the virus, contaminants and other factors so they can try to find further clues to solve the mystery. Getting the animals in a fresh condition is crucial to collecting as much useful information as possible. “All too often, the response team will go out and pick up a carcass and will hear that it was first seen the night before, so by 9 o’clock in the morning, it’s been lying out there since sunup, and we’ve lost a tremendous amount of data,” he says. “As soon as someone sees a dolphin, whether dead on the beach or in distress, they need to call it in to the authorities immediately.”
The NOAA operates a Stranding and Entanglement Hotline for all marine life. If you find a dolphin, they recommend staying away from it and calling the hotline at 1-866-755-6622.
Sometimes a saint may be all too human.
Junipero Serra, the missionary who brought Catholicism to California, is set to be canonized this week on the occasion of Pope Francis’ visit to the United States in a Spanish-language ceremony expected to draw tens of thousands of worshippers. But some Native American groups think the event is cause for outcry, not celebration.
Serra’s story is the West Coast incarnation of some of the founding myths of the United States. Just as the stories of Columbus, Pocahontas and the Puritans are incomplete without including the fate of displaced and mistreated native populations, so too is that of the settlement of the Pacific Coast.
The mission system lasted over 60 years and was integral to Spain’s colonization of the recently conquered California land mass. Serra’s canonization, meanwhile, is stirring up controversy about whether the system he founded was holy or horrible. Between 1769 and 1784, Serra formed nine Spanish missions. Many were massive in size; Mission San Luis Rey had 60,000 head of cattle at one point. Each mission was a closed Catholic community that offered native nations, like the Kumeyaay, Chumash and Cahuilla, Spanish citizenship and education in exchange for their conversion, labor and permanent residency.
The mission system lasted long after Serra’s death—21 missions were formed before newly independent Mexico abandoned the project in 1833. The missionaries’ promises to entrust mission lands to the native people who built and turned them into self-sustaining communities were broken: Most of the land was “secularized” and distributed to non-native owners. Though many mission lands were eventually regained by the Catholic church, they were never returned to the people who built them.
To Serra’s supporters, the missions were forces for good, spreading Catholicism, settling the state and building beautiful sanctuaries. But for many others, Serra’s legacy is much darker than the whitewashed plaster of California’s iconic missions.
Jeffrey M. Burns, a Serra scholar who directs the University of San Diego’s Frances G. Harpst Center for Catholic Thought and Culture, says that Serra and his fellow missionaries measured success in terms of souls saved. “Serra offered the native people membership in the missions in exchange for eternal life,” says Burns. “He would have seen everything at the mission as the native people’s property, something he was holding in trust for them. It may not have worked out that way, but that’s how he understood it.”
Though native peoples could hypothetically decide whether to enter the missions, some were lured in when the missions needed more manual labor. Others felt they had no choice—as animals imported from Europe changed the ecosystem and diseases threatened the native populations, missions became a more attractive (but by no means ideal) option.
Mission life exacted a high cost from native peoples, Serra biographer and University of Riverside history professor Steven W. Hackel says. As they farmed, labored and went to church, “Indians were expected to give up most of the important aspects of their culture in return for what the missionaries promised them was salvation,” says Hackel. Confined inside the missions among a diverse group of mission-bound Native Americans, says Hackel, indigenous people were encouraged to abandon both their cultural practices and traditional farming techniques.
“Indians who challenged the mission’s authority were flogged,” says Hackel. The Indians’ “spiritual fathers,” he continues, “punished them as children even when they were adults.” Those who tried to escape were hunted down by Spanish soldiers and forced to return. Crowded missions were also hot spots for diseases like pneumonia and diphtheria. One missionary wrote that an epidemic of measles “has cleaned out the missions and filled the cemeteries.” According to the Huntington Library’s Early California Population Project, 71,000 burials were performed in California’s missions between 1769 and 1850. And the University of California’s Calisphere notes that though there were an estimated 300,000 native people living in the area before Spanish colonization, only 30,000 remained by 1860.
“There were no easy answers” for Native Californians, says Burns, who notes that converts had to weigh their survival against a mission system that “didn’t have cultural sensitivity.” And according to some tribal leaders, modern-day conversations about Serra are no better.
Though Pope Francis has asked forgiveness for mission-era crimes against native peoples in July, some see the canonization of the system’s figurehead as a slap in the face. The Pope is “evidently unaware of the deadly toll and devastating effect that the Catholic Mission system had on our nations and peoples here in California,” wrote Robert Smith, chairman of Pala Band of Mission Indians and the Southern California Tribal Chairmen’s Association, in a letter of protest.
“Neither the missions nor Serra’s methods are worthy of secular or state pride,” wrote Valentin Lopez, chairman of the Amah Mutsun Tribal Band in an open letter urging California governor Jerry Brown to protest the canonization. Nonetheless, missions still have plenty of visibility in California: Serra’s name can be found on everything from high schools to highways. A fourth-grade project on the missions has been part of the state curriculum for decades, and the mission system’s legacy is present in California’s architecture, statuary and even sports teams—San Diego Padres, anyone?
“The missions were an unmitigated disaster for the Indians of California,” says Andrew Galvan, museum curator at Mission Dolores in San Francisco. “There’s no denying that.” But Galvan, whose Ohlone ancestors were forcibly baptized and brought to live in the missions, also sees a silver lining in Serra’s canonization. “This negativity is an opportunity for transformation,” he says.
Galvan, who served Serra’s canonization cause, doesn’t see a contradiction between admiring the man who brought Catholicism to California and condemning the system that he helped found. Instead, he is alarmed at church and museum officials’ furthering of what he calls “the mission myth”—a romanticized version of mission life that erases the struggles and contributions of Native Californians.
“There’s an opportunity to tell the true story now,” says Galvan—the story of a man “on fire” with missionary zeal and at the helm of a system that had fatal consequences for Native Californians. He calls on the Catholic Church to go beyond canonizing Serra and begin to reweave native contributions and stories into the story of the missions. “They’re Indian missions,” he insists. “They’re our places. Indian people are still here.”
Visitors to the United States’ Pacific coast over the last six years may have noticed that something is missing. A massive number of sea stars that used to dot the coastline are gone. And it’s not just tidepools and coastal inlets that are missing their sea stars either—they've vanished from the deeper ocean as well, new research shows.
Research shows that one species in particular, the huge sunflower sea star, has been hit especially hard, leading to dire consequences for kelp forests where it is a top predator, according to a new study in the journal Science Advances.
In the fall of 2013, ecologists and divers began to see something terrifying along the west coast of North America, from Alaska to Mexico. The seafloor was littered with severed sea star arms, and sea stars of every species clinging to coastal rocks were covered in sores and disintegrating into white mush, reports Ed Yong at The Atlantic.
The apocalyptic scenario has continued off and on to this day, with sea stars disappearing from entire swathes of coastline. While researchers have determined some of the 20 or so species impacted by the die-off were infected with a virus that causes sea star wasting disease, SSWD, not all species were susceptible to the disease, meaning there are likely other broader, overlapping causes.
Researchers sought to quantify the impact of the disease and understand the cause of the die-off in Pycnopodia helianthoides, or sunflower sea star. These predators can grow up to roughly three feet in diameter, munch on sea urchins and mussels, and, until recently, could be commonly found all the way from Alaskan waters to the coasts of Mexico.
Since SSWD first appeared, sunflower stars have more or less completely disappeared from their 2,000-mile range and are gone from the California coast. Some ecologists thought that the stars may have migrated into deeper water to avoid the factors leading to the sea star apocalypse. But according to the new study, that's not the case.
Deep water trawls and surveys by recreational divers confirm that the sea sunflowers have vanished down to about 3,000 feet. Trawls by NOAA in California and Oregon between 2013 and 2015 found that 100 percent of the stars were gone from deep water, and in Washington state they had declined by 99.2 percent. Yong reports that in 2016, over 700 trawls NOAA not find a single star, and last summer they found just one.
“This thing was as common as a robin,” study author Drew Harvell of Cornell University tells Yong. “You would go on a dive and always see sunflower stars.”
The revelation that the stars are dead and not sitting in deep water, waiting out the epidemic is a bad omen for many marine scientists.
“This is shocking,” Mark Carr, a University of California, Santa Cruz marine ecologist who was not involved in the study, tells Alex Fox at Science. “This is not just a population reduction, this is virtually the loss of a key species over thousands of miles. We’ve never seen anything like this before.”
The loss of the sunflower star is already having major effects on coastal ecosystems. The manhole-sized, 24-armed star is a highly-tuned keystone predator and kept kelp-munching urchins and coast-clogging mussels in check. Fox reports that without the sunflower star doing its job, northern California has already lost 90 percent of its kelp forests, which are one of the most biodiverse and important coastal ecosystems.
That, in turn has led to a ban on red abalone fishing, since the mollusk relies on kelp and are now dying off at a high rate. Whales, sea otters, seals and many species of birds rely on the kelp forests for food and protection from the elements too, but many former kelp forests have already been transformed into urchin barrens, with nothing but the spiny black creatures covering the seafloor.
So why have the sunflower stars been hit so hard? The researchers believe that the sunflower is particularly susceptible to whatever pathogen is causing the wasting disease, and that other creatures more tolerant of the virus keep transmitting it to the vulnerable stars.
But the severity of the die-off is likely caused by a one-two punch. There have been smaller-scale die-off in the past, but the researchers believe large increases in ocean temperatures caused by strong El Nino years in the past decade and climate change are likely stressing the stars, making them more susceptible to the pathogens and causing a much broader pandemic.
“The heat wave in the oceans—a product of increasing atmospheric temperatures—is exacerbating the sea star wasting disease,” Harvell says in a press release. “It’s a lethal disease, and when you add a higher temperature to that, it kills faster, causing a bigger impact.”
Research published last summer showed that one species hit by the wasting disease, the ochre sea star, seems to be recovering and its genome has even changed as a result of the disease. It’s yet to be seen whether the sunflower star will also have the genetic resources to weather the storm. As Yong at The Atlantic points out, these types of disease outbreaks compounded by high temperatures are becoming more common and have impacted other marine species as well and have even begun to take toll on land mammals as well.
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.
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.
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.
Midway through a marathon hockey game, in the midst of what is still regarded as one of the most intense championship series in the history of the sport, Joe Hall skated off the ice, exhausted and feverish. It was March 29, 1919, and Hall, a 37-year-old defenseman, was one of the stars of the National Hockey League’s Montreal Canadiens, who were in Seattle to play the Metropolitans of the Pacific Coast Hockey Association on their home ice for the Stanley Cup. The teams had already labored through four grueling contests of the best-of-five series; Game 4 had ended three days earlier with both teams literally collapsing onto the ice following three periods and a pair of overtimes, after no one on either side could muster a single goal.
As Hall retreated to the locker room, Game 5 took a dramatic turn. Montreal, trailing 3-0, tied the game at 3-3, and then pushed one last goal past a drained Seattle squad to win 4-3. The series was tied 2-2-1, and the local newspapers began looking toward a deciding game. “Players Are in Poor Condition for Game 6” read a headline in the March 31 edition of the Seattle Post-Intelligencer. And yet even as it listed Hall and another of his teammates as struck by “high fever,” there was no mention, nor even any speculation, about the underlying cause of that fever: A deadly strain of influenza, known as the “Spanish flu,” that had already struck millions of Americans of all ages, and would end up killing roughly 675,000 Americans.
In a way, this was understandable. The flu’s second and deadliest wave--which followed a less severe outbreak in the spring of 1918--had peaked the previous fall, as World War I neared its end. In the midst of the panic, a number of sporting events were canceled, and the college football season was largely abandoned. On January 28, 1919, Seattle’s health commissioner announced that the epidemic was over, though isolated cases would remain. By the time of the Stanley Cup Finals, the concern over the flu had largely faded from the public consciousness, and the front pages.
“By March, it wasn’t really in the headlines anymore, and part of that is because people were really anxious to get back to their normal lives.” says Nancy Bristow, history professor at the University of Puget Sound and author of American Pandemic: The Lost Worlds of the 1918 Influenza Epidemic. “But people were continuing to die, even though the emergency was off.”
The presumption of prominent sportswriters like the Post-Intelligencer’s Royal Brougham (a key character in The Boys in the Boat, Daniel James Brown’s best-seller about a crew team competing in the 1936 Olympics) was that both teams had simply worn each other out. But it soon became clear that this was a late and high-profile resurgence of the flu in the United States—and it would claim the life of a prominent figure who was cut down in the prime of his life. It would also result in the only unfinished Stanley Cup Final in history, one that’s still memorialized on the trophy’s face with both teams’ names and three engraved words: SERIES NOT COMPLETED.
The Stanley Cup was commissioned in 1892, and in its earliest years it was awarded via “challenges” between rival leagues. In 1907, the Kenora Thistles, based in tiny Kenora, Ontario, defeated the Montreal Wanderers in a two-game, total-goals challenge series (the Thistles would cede it back to Montreal in a rematch two months later). Among the players on the Kenora roster: Joe Hall, who was born in Britain, raised in Canada, and took up hockey at the age of 19.
Hall quickly developed a reputation as a hard-hitter, as one of hockey’s first “enforcers,” and while he was well-liked off the ice, his playing style earned him the nickname “Bad Joe.” He bounced from one team to another as leagues and clubs came and went in those early days; when the National Hockey Association dissolved and gave way to the National Hockey League in 1917, Hall found a place with the Canadiens, where he led the league in penalty minutes for two seasons in a row. By then, the NHA (and eventually the NHL) had formed a gentleman’s agreement with the PCHA: The champions of each league would face each other for the Stanley Cup. The NHL’s ranks, wrecked both by the war and the presence of rival leagues like the PCHA, had dwindled to just two teams—Montreal and Ottawa—after the Toronto Arenas ceased operations, and the Canadiens beat the Senators in a best-of-seven series four games to one.
The Seattle Metropolitans had already defeated the Canadiens in 1917 to become the first American team to ever win the Cup. They upset regular-season champ Vancouver to win the three-team PCHA once again in 1919. But as the Stanley Cup Final opened, Seattle had a pronounced disadvantage—not because of the flu, but because of the lingering shadow of World War I. The Metropolitans’ star player, Bernie Morris, was arrested and charged with draft evasion.
Morris insisted it was a simple mistake. He pleaded his case to the authorities, stating that the notice had been sent to his home in Seattle while he was in Vancouver during the offseason. But after the military learned that Morris had testified to living the past three years in Seattle, Morris was detained and prosecuted during divorce proceedings against his wife earlier in 1919. The Army apparently sought to make an example out of him, according to Kevin Ticen, author of a book about the Metropolitans. (Morris was sentenced to two years of hard labor at Alcatraz, though he was eventually transferred to an Army unit and granted an honorable discharge.)The Seattle Ice Arena, where the last game of the 1919 Finals was played. (David Eskenazi Collection)
So Seattle entered the series short-handed, but that didn’t dampen the fans’ enthusiasm. Standing-room crowds jammed into the Seattle Ice Arena (capacity 2,500) to watch those Stanley Cup games, seemingly oblivious to any fears about the last vestiges of the flu spreading to them. What they witnessed was a war of attrition that climaxed in Game 5, when Seattle, on the verge of clinching the Cup and battling exhaustion brought on by its lack of depth, couldn’t hold that 3-0 lead.
Two days later, on the morning of April 1, the news began to leak: Game 6 would not be played at all. By then, five Canadiens players had been hospitalized, along with coach George Kennedy (who never fully got over his symptoms and died a couple of years later); the flu had also hit at least Seattle players, as well. But Hall—who would be voted into the Hockey Hall of Fame in 1961—was the hardest hit of them all. Five days later, on the morning of April 6, the Post-Intelligencer ran a banner headline: “JOE HALL, FRENCH HOCKEY PLAYER, IS DEAD.”
The paper called those Stanley Cup Finals “the most unusual world’s series in history” and “the hardest fought series since the Stanley cup was put up for competition.” Wrote the Seattle Times: “Not in the history of the Stanley cup series has the world’s hockey championship been beset with hard luck as has this one.”
By the following year—when the Ottawa Senators defeated the Metropolitans for the Stanley Cup—the NHL had grown to four teams, and it would continue to mature in the post-war era. The Metropolitans would fail to compete for another Stanley Cup after 1920; in 1924, after their arena was knocked down to build a parking garage for an adjacent hotel, the franchise disbanded.
More than a century later—as Seattle grapples with its place as the epicenter of the COVID-19 outbreak and prepares to launch its own NHL franchise in 2021, and as the NHL itself suspended its season to "flatten the curve"—those Finals remain utterly unique, their forever-unfinished status a reminder that the ramifications of the Spanish flu epidemic extended beyond the natural chronological boundaries that it’s typically associated with. “There were thousands of orphans, and thousands of people who suffered a complete breakdown of family,” Bristow says. “It was a complete social change, even after the rest of the community had moved on.”
In fact, Hall’s final days coincided with perhaps the most consequential flu case of all: Just two days before the hockey star’s death, president Woodrow Wilson, travelling to the Paris Peace Conference, fell ill with symptoms believed to be caused by influenza. A number of historians and advisers believe that it impacted Wilson’s ability to negotiate a proper treaty, and that the president was never quite the same again.
Earlier this month, a gun rights activist made national headlines when her four-year-old son shot her in the back with her handgun while she was driving. Her story, unsurprisingly, drew intense scrutiny. A Facebook page she operated featured posts such as, “My right to protect my child with a gun trumps your fear of my gun,” which in turn lead to many online commenters to take a seemingly perverse, outsized pleasure in her suffering. One Slate reader commented on a story about the case, “While it’s good she didn’t die, she got what she deserved.” (Meanwhile, her county Sheriff’s office is pursuing misdemeanor charges for the unsafe storage of a firearm and, according to The Gainsville Sun, the state has opened a child protective investigation.)
Though the story has a distinctly 21st-century feel to it, at its core, it’s a story older than our country, and that it reached a wide and vociferous audience is, actually, nothing new either. Accidental gun deaths and injuries, especially those inflicted on family members, are as American as apple pie – at least according to American religious history scholar Peter Manseau.
In 2012, while at work on his previous book, One Nation Under Gods, Manseau discovered a genre of newspaper reports dating back to colonial America called “melancholy accidents.” As he explains in the introduction to his new book, Melancholy Accidents: Three Centuries of Stray Bullets and Bad Luck, “Though these accident reports also took note of drownings, horse tramplings, and steamship explosions, guns provided their assemblers with the most pathos per column inch.” Over four years, Manseau read and collected hundreds of these reports, ultimately gathering more than 100 of them into his book, which contains reports spanning nearly two centuries of American history.
Melancholy accidents “bridge a gap not of geography or politics, but of time,” Manseau writes about the reports. In America, the news media continues to write news stories about accidental gun deaths, and it seems unlikely the feed will ever stop. As one report from 1872 reads, “We thought a good strong frost would put an end to shot-gun accidents, but people still blaze away at themselves.”
And, as Manseau discovered in his research, the accidents themselves are not the only constant. The way we react to them has remained surprisingly similar, too. From the time when we called these deaths and injuries “melancholy accidents” through to today, the age of the hashtag #gunfail, history has shown us to be a people who can’t live with their guns, but won’t live without them.
Manseau spoke to Smithsonian.com about his research, the book, and what he calls the “alternate history of guns in America” that he discovered in the melancholy accident reports.
You mention in the introduction that you stumbled upon the phenomenon of “melancholy accidents” while doing historical research. What were you researching when you discovered melancholy accidents and when did you realize you wanted to collect these accidents and publish them?
My last book, One Nation Under Gods, told the story of religion in America from the point of view of religious minorities, going back into the early 18th century. I was reading a lot of newspaper accounts looking for evidence of religious minorities, and while I was doing that research, I kept coming across this phrase “melancholy accidents.”
This was a genre of newspaper reporting that seems to have started in England and was brought to colonial America very early on. It would often refer to people drowning in rivers or being blown up by steam ships and that sort of thing, but what seemed most common for “melancholy accidents” was that they were gun accidents. They were reports of musket exploding or misfiring, killing the person who was using it or someone who happened to be unfortunate enough to be nearby.
It began to seem to me that the genre of gun accident reports has been part of American journalism from the very beginning. The stories spoke to each other across the centuries as this genre of journalism, this type of American storytelling that endured no matter what changes were going on politically or within the population as it changed. That struck me as a fascinating thing, that here was something that remained unchanging in American culture throughout the centuries.
Had you heard of “melancholy accidents” before?
Other scholars have noted them, but not specifically having to do with guns so, after I discovered them for myself, I began to research them.
This is my sixth or seventh book, and it was a great relief as a writer to write with other people's words, to compile these reports and let them speak for themselves. I found that they had a power that is difficult to bring in your own writing.
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
Image by Melville House. (original image)
How systematic were you in looking for them? Is the book a small representative slice of all of the melancholy accidents reported from 1739 to 1916 or is this the grand total of melancholy accidents on public record?
I really could have included, without exaggeration, hundreds more. These were published in dozens of newspapers for centuries. I continue to find new ones, in fact, and often I'll find a new one and think, “I wish I had included that in the book.” They are really such a fascinating window on lives lived long ago.
Many of them are just so haunting. The style of early American newspaper writing is, in some ways, very spare and yet, in other ways, is very florid in its language. There’s something about them. They’re so different from the way we write stories now, or different from the way we often read stories now. It gives them this haunting quality. They linger and you can really feel the anguish felt by the people on the page.
Why did you stop at 1916?
I could have continued well past 1916, all the way up to today, certainly. I chose 1916 because it is 100 years before today exactly, but also because something seems to happen with the arrival of the First World War to the way violence is spoken about in the American press. It also seems the be the end of this phrase “melancholy accidents.” It doesn't turn up in the press at all as far as I can remember after that. In the 20th century, it began to seem archaic in a way it wasn’t before and so it seemed to me a natural stopping point.
Can you talk about some of the things you realized about America’s relationship with guns through history?
One of the things that I kept running into was this idea of divine indifference. We think of colonial America and the young United States as being a very religious place, and yet when you read these gun accident reports, they give this sense of feeling that if you come in contact with guns, you're ruled suddenly, entirely by fate, that God takes no interest in how people are interacting with guns, and there's no question or lament about this: How did this happen? How do bad things happen to good people? It's just a feeling that if we choose to make guns a part of our lives, this is bound to be part of our experience, and we are bound to experience this again and again.
How has gun culture in our country evolved over time?
Guns play a very different role in American society today than they used to. Once upon a time, they were, for many people, tools that you would use for sustenance. You might feel you needed to have them for protection if you are living in remote places and need to defend yourself against wolves and bears and whatnot. They were very practical tools for early Americans.
For Americans today, they seem to be far more often tools of enjoyment and tools of hobbyists, and that very fact makes them entirely different objects as far as what they mean to Americans. That, to me, makes them far less necessary. And yet, as they have become less necessary, they have also become a symbol of the clash between those who use them for enjoyment and those who fear those who use them for enjoyment. They've become a symbol of this clash within the culture in a way that they were not in early American history.
Have the ways that we’ve struggled to come to terms with accidental gun deaths changed?
I guess we've come to terms with them in the sense that they keep happening, and we all just throw up our hands about it and say, “Well, that's what happens when you have guns in your life, that's what happens when you have so many guns in your country, when you have as many guns in the United States as there are people.” They're bound to intersect in these fatal ways very often, and so there's a sense of resignation, this helplessness that this is bound to continue to happen.
And that’s very similar to what I found in these early accident reports, this feeling that if you have objects in your life that are designed to kill, you have to assume that they will do so very often, even when you don't want them to. The feeling of helplessness in the face of guns endures.
The reason I collected these stories and chose to retell them the way I did, was that I hoped to provide a kind of corrective to the stories that we usually tell about guns. Guns within American culture, the way we think and talk about them, there's so much determined by the mythology of the frontier or the mythology of the western. We think of guns as being these heroic machines that allow for the preservation or protection of freedom. And yet I started to wonder as I collected these stories, what if that is not the most enduring meaning of guns? What if the most enduring meaning is not heroism, but tragedy? What if accidents are really what happens far more often with guns than them being used as they are intended? I wanted to propose another, an alternate history of guns in America, through these primary sources to let them speak for themselves.
I really didn't write the book with any kind of political agenda, though. I have no problem with hunting culture or responsible gun use, people who choose to own and use guns for recreation. I have no problem with any of that, and I don't expect that anyone's going to read this book and suddenly say, "I had no idea how dangerous guns could be!"
Gun owners know that best of all. They know far better than people who never get close to them how dangerous they can be. But I did want to open up this view of the past that shows how these accidents are far from a modern phenomenon. These small-scale tragedies have shaped our experience with guns entirely from the beginning. I am, first of all, a person interested in the stories and to me, that’s how these accidents reports resonate.
Some of these are stunningly tragic; others have a note of dark humor. Were there any melancholy accidents that stayed with you or affected you most?
The ones that stay with me for their tragedy are usually the parents who accidentally take the lives of their children. The telling of those stories, with just a sentence or a detail, make it so easy to imagine yourself into that situation and know the pain they must have felt. For me those are the most haunting.
But again and again I would find these accident reports that you just couldn’t help laughing at. One I'm thinking about right now is a woman who was doing her ironing, she's ironing handkerchiefs, and she's accidentally shot in the leg. The accident report is careful to note that she finished her ironing before she called a physician. It's a very funny situation to read on the page. It's also suggestive of the way the accidents, all told, are taken in stride.
Every day there's a new gun accident in the news. When we read about them, we either find them absurd and funny or terribly tragic, and yet we take them in stride, we go about our business, because this is what life with guns is, it's what it means. We hear the gunshot and we go on with our ironing.
How long did the project take?
The book actually began as a little piece I wrote for the New Yorker three years ago this month. But they just lingered with me, the idea of them. And so I kept looking for them. I began finding them accidentally, but then I began looking for them, and that's when I couldn't stop. It became this obsession for a little while, finding these and wanting to show them to world. All told, off and on it was probably a matter of four years I spent wondering about melancholy accidents.
Was it difficult to do so much research on private and personal tragedies?
I didn’t find it ultimately depressing. The interesting thing about the melancholy accidents is that they are ultimately not about death. They are ultimately about the living, about the people who survive and how they deal with this tragedy. That's true of any stories of tragedy, I think. It's ultimately about what comes next and what we can learn from it. I think they raise questions that anyone living asks about what it means to be alive and how we endure in the face of such tragedies.
One that topic, some of the reports talk about the grief that the shooters feel afterwards, how they dealt with it for the rest of their lives. Has that changed over time?
The accident reports go into such detail of the grief these people felt, whether it was a brother who accidentally killed his sister and then they had to try to stop him from taking his own life after seeing what he had done, or the father who accidentally killed his child and then the report notes that he himself died of a broken heart weeks later… I imagine that the feelings of grief have changed very little, no matter how much the technology of the weapons has changed or the way we think about weapons as a culture has changed. That part seems, to me, to endure.
A difficult part of being involved in a tragedy like this today is that you probably can't escape it in the way that you could then. The digital trail of having your name associated with one of these things is going to follow you for the rest of your life. With the book coming out, I've been doing more research on gun accidents more recently, and I happened to come across an article from sometime in the early 90s. It showed a picture of a little boy with his mother, and it noted that the little boy had accidentally killed his baby sister with gun. I thought, “That little boy in the early 90s is now a grown man. No doubt he still lives with that.” And his story, his pain, is there to be found by anyone who happens to stumble across it online. It's a way that the tragedy continues to echo.An example of a "melancholy accident" (Courtesy of Peter Manseau)
In a little village called Kalachi, tucked away in the northern region of Kazakhstan, over 120 residents have been hit by a strange malady that has doctors and scientists baffled.
Without warning a person will inexplicably fall into a coma-like sleep they often won’t wake from for days. When they do come to, they’re often left with “debilitating symptoms – dizziness, nausea, blinding headaches and memory loss,” Joanna Lillis reports for the Guardian.
The mystery illness was first officially recorded in the spring of 2013 and has affected about a fourth of the village’s population with some experiencing repeat attacks. The two most recent cases emerged in early March, bringing the total number of incidences, according to Lillis, to 152.
Scientists, along with the government of Kazakhstan, have been scrambling to find a cause for the strange ailment. But despite some strong leads, they have yet to nail one down. Two likely culprits are radon and carbon monoxide poisoning. The symptoms of these problems closely resemble those experienced by Kalachi’s residents. Testing showed unusually high levels of both in some village homes, but still, local officials have ruled them out as a cause.
The scientists involved are determined to find an explanation, however. Thanks to a research coordination commission set up by the Kazakhstan prime minister “by the end of last year over 20,000 laboratory and clinical test had been conducted – on the air, soil, water, food, animals, building materials, and on the residents themselves,” writes Lillis.
Many residents and one Russian scientist interviewed by Newsweek think the cause of the illness may not be coming from Kalachi, however, but rather a site just outside the village. That’s where an old Soviet-era uranium mine lies abandoned since the 1990s.
“In my opinion, a gas factor is at work here,” professor Leonid Rikhvanov from the Tomsk Polytechnic University in Russia told Newsweek. “Radon could be operating as a narcotic substance or an anesthetic. Currently, the underground space of the mine is flooded and gases are being squeezed to the surface.”
The theory is as yet unproven, however—and in the meantime, authorities have chosen to take drastic measures against the sleeping sickness by offering to relocate locals to villages outside the perceived danger zone. Over 100 citizens have reportedly embraced the “voluntary relocation” already, which officials hope to be complete by May.
There are many in Kalachi who don’t want to move and who have no plan to effectively abandon their lives, despite warnings from Rikhvanov and others that more cases are likely to present themselves. But, as one resident told Lillis of the worrisome illness, “They say it affects the brain; they say it gives people headaches, but our headache now is where we’re being resettled.”