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Why It Took So Long to Eliminate Measles

Why It Took So Long to Eliminate Measles

It took more than a decade for scientists to develop a single-shot vaccine that worked to fend off the measles without causing high fevers and rashes.

Then health officials had to convince people to use it.

Until the vaccine’s debut in 1963, many considered measles, which still killed 500 Americans a year and hospitalized 48,000, an inevitable childhood disease that everyone had to suffer through.

“Measles was such a common disease and its mortality was comparatively low,” says Graham Mooney, an associate professor at the Johns Hopkins Institute of the History of Medicine. “People had more problems than measles.”

One of the earliest accounts of measles comes from a Persian doctor named Rhazes in the 9th century, but it wasn’t until 1757 that Scottish doctor Francis Home discovered it was caused by a pathogen and first attempted to make a vaccine. By then, measles was a worldwide killer.

“It’s an ancient disease, but it really became globally important with increased global explorations from the 16th century on,” says Mooney. As the most contagious disease humans had ever faced, measles was virtually guaranteed after exposure.

Deaths were greatest in populations with no immunity, such as island nations. An 1875 outbreak in Fiji wiped out up to a third of the population in four months, and Hawaii’s first outbreak in 1848 similarly killed up to a third of the population, just two decades later the king and queen contracted it and died on a trip to England.

READ MORE: How Measles Helped Destroy the Hawaiian Monarchy

Though mortality rates eventually began falling, epidemics could still be devastating. In 1916, 12,000 people died of measles, and three out of four deaths were children under 5 years old. But that same year, a pair of French doctors found measles antibodies in patients’ blood. They showed how the antibodies could protect others from developing the disease, laying the groundwork for developing a vaccine.

By the 1950s, measles deaths had dropped to only 400 to 500 a year, thanks to the availability of antibiotics and improvements in sanitation, medical supportive care and nutrition, says Paul Offit, chief of division of infectious diseases at Children's Hospital of Philadelphia and director of their Vaccine Education Center. (Though antibiotics couldn’t treat a viral illness, bacterial pneumonia was one of measles’ deadliest complications.)

Nearly Everyone Once Got the Measles

Still, nearly everyone got it. The disease led to an estimated 48,000 hospitalizations a year from complications such as ear infections, croup, diarrhea and pneumonia. About 1,000 children a year developed encephalitis, brain swelling that could cause intellectual disability or death.

Among those parents left reeling from the death of their children from the disease was children’s author Roald Dahl, who watched his daughter die from measles encephalitis in 1962. He would later dedicate his book, The BFG, to his daughter’s memory.

Even surviving a measles infection didn’t end your risk of death: a very rare, fatal complication called subacute sclerosing panencephalitis (SSPE) could develop one to two decades later, causing gradual deterioration until the person entered a coma and eventually died.

A measles vaccine would lighten a huge public health burden, and scientist John Enders at Boston Children’s Hospital was determined to make one.

When a measles outbreak hit a boys’ boarding school about 45 minutes outside Boston in January 1954, Enders sent one of his researchers, Thomas Peebles, to collect blood samples. Peebles drew blood from infected boys, telling each one, “Young man, you are standing on the frontiers of science. We are trying to grow this virus for the first time. If we do, your name will go into our scientific report of the discovery. Now this will hurt a little. Are you game?”

First Measles Vaccine Was 'Toxic as Hell'

Within a month, Peebles had isolated the virus from the blood of 13-year-old David Edmonston. By 1958, the Boston Children’s team had a live virus measles vaccine to test in disabled children institutionalized at Fernald School and Willowbrook State School, where close living quarters increased infection risk during outbreaks.

But the virus in the vaccine wasn’t weak enough: Most children developed high fevers and rashes similar to mild measles. Enders then shared the strain with other scientists, including Maurice Hilleman, the top Merck scientist responsible for developing more vaccines than any other person in history.

“It was toxic as hell,” Hilleman told Offit, a protege of Hilleman, who recounted the conversation in his biography of Hilleman. “Some children had fevers so high that they had seizures.”

After turning to other experts, researchers came up with a way to grow the vaccine safely in eggs and give the vaccine with a simultaneous shot of measles antibodies to reduce side effects. By March 21, 1963, the FDA licensed the first live virus measles vaccine, Merck’s Rubeovax.

Other measles vaccines were soon approved, including an inactivated (non-live) one that same month with fewer side effects but less protection. It was pulled from the market in 1968, the same year Hilleman refined the vaccine into the one used today—one without the severe side effects and which didn’t require the extra shot of measles antibodies.

By then, measles cases had dropped by 90 percent, and the CDC had already declared a plan to eliminate measles two years earlier. The next step was persuading parents to immunize their children.

School Vaccine Rules Lead to Measles Elimination

“Public apathy in the face of infectious disease has always been a problem for public health,” Mooney says. The problem wasn’t the hesitancy seen today so much as complacency.

“It was a case of parents prioritizing getting food in their kids mouths than vaccinating them against measles,” particularly among poorer Americans, Mooney says. It cost parents about $10 ($82 today) to vaccinate one child against measles. The Vaccination Assistance Act in 1965 provided funds for measles immunization, but the money ran out in the 1970s, contributing to an upsurge in cases.

“Many mothers simply have not been educated about the benefits of and need for immunization,” noted the New York State Department of Health in 1971. That same year, Hilleman combined measles, mumps and rubella vaccines into the single MMR shot to cut down kids’ total jabs.

But it wasn’t until widespread school vaccination requirements and permanent federal funding that the country began inching toward measles elimination, finally achieved in 2000. (While cases of measles still crop up, the Centers for Disease Control defines elimination of a disease as the absence of continuous disease transmission for 12 months or more in a specific geographic area.)

“Relatively few people are alive now who witnessed epidemics of those diseases and their effects,” says Stanley Plotkin, the scientist who developed the rubella vaccine used in today’s MMR.

“As somebody who practiced university pediatrics in the 1950s and 60s, I don’t take those diseases lightly at all.”


Measles is a highly contagious, serious disease caused by a virus. Before the introduction of measles vaccine in 1963 and widespread vaccination, major epidemics occurred approximately every 2&ndash3 years and measles caused an estimated 2.6 million deaths each year.

More than 140 000 people died from measles in 2018 &ndash mostly children under the age of 5 years, despite the availability of a safe and effective vaccine.

Measles is caused by a virus in the paramyxovirus family and it is normally passed through direct contact and through the air. The virus infects the respiratory tract, then spreads throughout the body. Measles is a human disease and is not known to occur in animals.

Accelerated immunization activities have had a major impact on reducing measles deaths. During 2000&ndash 2018, measles vaccination prevented an estimated 23.2 million deaths. Global measles deaths have decreased by 73% from an estimated 536 000 in 2000* to 142,000 in 2018.

Deleting browsing history taking a very long time

I have IE 8, letely I have had some issues with IE. It used to be that when IE was running slow I would delete browsing history and that would usually fix the problem. Now when I choose to delete browsing history the delete browsing history window comes up and just keeps going one time I left it running to see how long it would go went for hours. When I tried closing the delet browsing history window IE freezes and stops responding. I have run antivirus recently and have not found any spyware or virus. Can you assist?

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Method 1: Open Internet Explorer (IE) in no add-ons mode and check if that fixes the issue.

To start Internet Explorer without add-ons,

a. Click the Start button, and select All Programs.

b. Click Accessories, and select System Tools.

c. Click Internet Explorer (No Add-ons).

If disabling all add-ons solves the problem, you might want to use Add-on Manager to disable all add-ons and then turn on add-ons only as you need them. This will allow you to figure out which add-on is causing the problem.

See the section “Disable add-ons in Internet Explorer 8" in the following article for further instructions:

Method 2: Reset Internet Explorer and see if that fixes the issue.

Run the “Fix it” from the following article:

Disclaimer: Please note that resetting Internet Explorer settings will reset all user-defined settings including those set by installed extensions, toolbars and other add-ons to IE Defaults. This includes all Security, Privacy and Zone settings. Also this will clear browsing history, delete all temporary Internet Files, cookies, form data and especially all stored passwords.

Method 3: Internet Explorer does not start or stops responding


Hookworms are among a group of parasitic worms that cause a type of infection known as helminthiasis.

Hookworms are found in many parts of the world, typically those with poor access to clean water and sanitation.

Infection occurs when the larvae, known as filariform, come in contact with and penetrate the skin.

Hookworm infection occurs in the intestines and typically starts with a localized rash. This is soon followed by other symptoms, including abdominal pain, diarrhea, loss of appetite, weight loss, and anemia-induced fatigue.

Today, an estimated 500 million people around the world are affected by hookworms, resulting in over 65,000 deaths each year. Even so, improvements in community sanitation and hygiene have reduced the global incidence of hookworms from its peak of 740 million in 2009.

In the early part of the 20th century, an estimated 40% of people living in the southern United States had hookworms. Indoor plumbing and improved sanitation halted its spread, and today helminthiasis is no longer the endemic disease it once was.

What are the benefits of eradicating diseases?

The immediate benefit of eradicating a disease is obvious — preventing suffering and saving people’s lives.

But eradicating a disease can also have significant economic benefits. Disease eradication takes years to achieve and requires a lot of financial investment: smallpox eradication had an estimated cost of $300 million over a 10-year period polio eradication efforts to date amounted to $4.5 billion. 14 But, as the chart here illustrates, while the initial costs of disease eradication efforts are high, in the long-term these costs pay-off. Simply controlling a disease can be more expensive because of the continued burden a disease poses on a healthcare system and the lost productivity of a sick population. 

How much we should spend on eradicating a disease? There will always be other good causes we can spend money on. These include non-health causes, health causes with greater burden, eradication of different diseases, and even research into more cost effective treatments instead of eradication. The scenario or intervention which brings the highest benefit needs to be assessed for each disease separately.  

As a classical paper by Walter R. Dowdle’s classical paper on disease eradication states: 𠇎limination and eradication are the ultimate goals of public health. The only question is whether these goals are to be achieved in the present or [by] some future generation”. 15

Following the eradication of smallpox, scientists and public health officials determined there was still a need to perform research using the variola virus. They agreed to reduce the number of laboratories holding stocks of variola virus to only four locations. In 1981, the four countries that either served as a WHO collaborating center or were actively working with variola virus were the United States, England, Russia, and South Africa. By 1984, England and South Africa had either destroyed their stocks or transferred them to other approved labs. There are now only two locations that officially store and handle variola virus under WHO supervision: the Centers for Disease Control and Prevention in Atlanta, Georgia, and the State Research Center of Virology and Biotechnology (VECTOR Institute) in Koltsovo, Russia.

Three-year-old Rahima Banu with her mother in Bangladesh. Rahima was the last known person to have had naturally acquired smallpox in the world. An 8-year-old girl named Bilkisunnessa reported the case to the local Smallpox Eradication Program team and received a 250 Taka reward. Source: CDC/World Health Organization Stanley O. Foster M.D., M.P.H.

WHO poster commemorating the eradication of smallpox in October 1979, which was officially endorsed by the 33rd World Health Assembly on May 8, 1980. Courtesy of WHO.

Disease Eradication

When a disease stops circulating in a region, it’s considered eliminated in that region. Polio, for example, was eliminated in the United States by 1979 after widespread vaccination efforts.

If a particular disease is eliminated worldwide, it’s considered eradicated. To date, only one infectious disease that affects humans has been eradicated.* In 1980, after decades of efforts by the World Health Organization, the World Health Assembly endorsed a statement declaring smallpox eradicated. Coordinated efforts rid the world of a disease that had once killed up to 35% of its victims and left others scarred or blind.

Smallpox eradication was accomplished with a combination of focused surveillance—quickly identifying new smallpox cases—and ring vaccination. “Ring vaccination” meant that anyone who could have been exposed to a smallpox patient was tracked down and vaccinated as quickly as possible, effectively corralling the disease and preventing its further spread. The last case of wild smallpox occurred in Somalia in 1977.

Smallpox was a good candidate for eradication for several reasons. First, the disease is highly visible: smallpox patients develop a rash that is easily recognized. In addition, the time from exposure to the initial appearance of symptoms is fairly short, so that the disease usually can’t spread very far before it’s noticed. Workers from the World Health Organization found smallpox patients in outlying areas by displaying pictures of people with the smallpox rash and asking if anyone nearby had a similar rash.

Second, only humans can transmit and catch smallpox. Some diseases have an animal reservoir, meaning they can infect other species besides humans. Yellow fever, for example, infects humans, but can also infect monkeys. If a mosquito capable of spreading yellow fever bites an infected monkey, the mosquito can then give the disease to humans. So even if the entire population of the planet could somehow be vaccinated against yellow fever, its eradication could not be guaranteed. The disease could still be circulating among monkeys, and it could re-emerge if human immunity ever waned. (The discovery of an animal reservoir for yellow fever was in fact what derailed a yellow fever eradication effort in the early 1900s.) Smallpox, however, can infect only humans. In effect, aside from the human population, it has nowhere to hide.

Equally important is the ability to protect individuals against infection. People who survived smallpox naturally developed lifelong immunity against future infection. For everyone else, vaccination was highly effective. WHO trained vaccinators quickly, and they could immunize large groups of people in a short time.

The eradication of smallpox raised hopes that the same could be accomplished for other diseases, with many named as possibilities: polio, mumps, and dracunculiasis (Guinea worm disease), among others. Malaria has also been considered, and its incidence has been reduced drastically in many countries. It presents a challenge to the traditional idea of eradication, however, in that having malaria does not result in lifelong immunity against it (as smallpox and many other diseases do). It is possible to fall ill with malaria many times, although individuals may develop partial immunity after multiple attacks. In addition, although promising steps have been made, no effective malaria vaccine yet exists.

Other diseases present additional challenges. Polio, though it has been reduced or eliminated in most countries through widespread vaccination, still circulates in some areas because (among other reasons) many cases do not present easily recognizable symptoms. As a result, an infected person can remain unnoticed, yet still spread the virus to others. Measles is problematic in a similar way: although the disease results in a highly visible rash, a significant period of time elapses between exposure to the virus and the development of the rash. Patients become contagious before the rash appears, and can spread the virus before anyone realizes they have the disease.

Guinea worm disease is likely on the verge of eradication. Only 30 cases were reported in 2017, from just 2 countries (Chad [15 cases], Ethiopia [15 cases]). [1] Though the case count increased from 2016, experts are still hopeful about the possibility of eradication. The Carter Center International Task Force for Disease Eradication has declared six additional diseases as potentially eradicable: lymphatic filariasis (Elephantiasis), polio, measles, mumps, rubella, and pork tapeworm. [2]

*Rinderpest, a disease that affected livestock, has also been eradicated, largely due to vaccination.

I question the narratives about vaccines saving us

A rapid coronavirus rebound would require at least 2 things to be true:

  1. The vaccines are capable of eliminating the coronavirus.
  2. Vaccines will be rapidly adopted at high rates.

Historical experience has demonstrated that #2 rarely occurs and that the process takes years. As far as #1 goes, there are many scientists who don’t believe that the coronavirus will be eliminated in developed countries. A Nature article published in February 2021 states that 52% of scientists polled believe that it is unlikely that some regions of the world will succeed in eliminating the coronavirus. I am of that opinion. Of course, there isn’t solid science to support either opinion.

Here’s what I think that the most likely scenario will look like. Transmission will be lower due to vaccines and other advances (e.g. health authorities slowly recognizing aerosol transmission). This will lead to a lot of the onerous social restrictions coming down because less needs to be done to keep infections flat. (Like it or not, all societies are keeping infections flat. Citizens will impose social restrictions on themselves when cases surge too much.) However, the remaining restrictions will mean that some areas of the economy will not fully recover.

Natural selection will lead to many different variants. The antibodies and immune defenses that work well against one variant won’t be fully effective against some other variants. This will likely be countered with multiple vaccines, which is how the agricultural industry fights IBV and how we vaccinate against the flu. A yearly vaccination with multiple vaccines seems likely. An ongoing coronavirus problem means that society will use lots of vaccines (from MRNA and PFE) and therapeutics like monoclonal antibody treatments (LLY, REGN), Remdesivir (GILD), and other treatments like Actemra (RHHBY).

*Disclosure: Long REGN and GILD via call options. Short AMC, LYV and DIS via put options. I don’t own MRNA, but may do so in the future.

The 60-Year-Old Scientific Screwup That Helped Covid Kill

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Early one morning, Linsey Marr tiptoed to her dining room table, slipped on a headset, and fired up Zoom. On her computer screen, dozens of familiar faces began to appear. She also saw a few people she didn’t know, including Maria Van Kerkhove, the World Health Organization’s technical lead for Covid-19, and other expert advisers to the WHO. It was just past 1 pm Geneva time on April 3, 2020, but in Blacksburg, Virginia, where Marr lives with her husband and two children, dawn was just beginning to break.

Marr is an aerosol scientist at Virginia Tech and one of the few in the world who also studies infectious diseases. To her, the new coronavirus looked as if it could hang in the air, infecting anyone who breathed in enough of it. For people indoors, that posed a considerable risk. But the WHO didn’t seem to have caught on. Just days before, the organization had tweeted “FACT: #COVID19 is NOT airborne.” That’s why Marr was skipping her usual morning workout to join 35 other aerosol scientists. They were trying to warn the WHO it was making a big mistake.

Over Zoom, they laid out the case. They ticked through a growing list of superspreading events in restaurants, call centers, cruise ships, and a choir rehearsal, instances where people got sick even when they were across the room from a contagious person. The incidents contradicted the WHO’s main safety guidelines of keeping 3 to 6 feet of distance between people and frequent handwashing. If SARS-CoV-2 traveled only in large droplets that immediately fell to the ground, as the WHO was saying, then wouldn’t the distancing and the handwashing have prevented such outbreaks? Infectious air was the more likely culprit, they argued. But the WHO’s experts appeared to be unmoved. If they were going to call Covid-19 airborne, they wanted more direct evidence—proof, which could take months to gather, that the virus was abundant in the air. Meanwhile, thousands of people were falling ill every day.

On the video call, tensions rose. At one point, Lidia Morawska, a revered atmospheric physicist who had arranged the meeting, tried to explain how far infectious particles of different sizes could potentially travel. One of the WHO experts abruptly cut her off, telling her she was wrong, Marr recalls. His rudeness shocked her. “You just don’t argue with Lidia about physics,” she says.

Morawska had spent more than two decades advising a different branch of the WHO on the impacts of air pollution. When it came to flecks of soot and ash belched out by smokestacks and tailpipes, the organization readily accepted the physics she was describing—that particles of many sizes can hang aloft, travel far, and be inhaled. Now, though, the WHO’s advisers seemed to be saying those same laws didn’t apply to virus-laced respiratory particles. To them, the word airborne only applied to particles smaller than 5 microns. Trapped in their group-specific jargon, the two camps on Zoom literally couldn’t understand one another.

When the call ended, Marr sat back heavily, feeling an old frustration coiling tighter in her body. She itched to go for a run, to pound it out footfall by footfall into the pavement. “It felt like they had already made up their minds and they were just entertaining us,” she recalls. Marr was no stranger to being ignored by members of the medical establishment. Often seen as an epistemic trespasser, she was used to persevering through skepticism and outright rejection. This time, however, so much more than her ego was at stake. The beginning of a global pandemic was a terrible time to get into a fight over words. But she had an inkling that the verbal sparring was a symptom of a bigger problem—that outdated science was underpinning public health policy. She had to get through to them. But first, she had to crack the mystery of why their communication was failing so badly.

Marr spent the first many years of her career studying air pollution, just as Morawska had. But her priorities began to change in the late 2000s, when Marr sent her oldest child off to day care. That winter, she noticed how waves of runny noses, chest colds, and flu swept through the classrooms, despite the staff’s rigorous disinfection routines. “Could these common infections actually be in the air?” she wondered. Marr picked up a few introductory medical textbooks to satisfy her curiosity.

According to the medical canon, nearly all respiratory infections transmit through coughs or sneezes: Whenever a sick person hacks, bacteria and viruses spray out like bullets from a gun, quickly falling and sticking to any surface within a blast radius of 3 to 6 feet. If these droplets alight on a nose or mouth (or on a hand that then touches the face), they can cause an infection. Only a few diseases were thought to break this droplet rule. Measles and tuberculosis transmit a different way they’re described as “airborne.” Those pathogens travel inside aerosols, microscopic particles that can stay suspended for hours and travel longer distances. They can spread when contagious people simply breathe.

The distinction between droplet and airborne transmission has enormous consequences. To combat droplets, a leading precaution is to wash hands frequently with soap and water. To fight infectious aerosols, the air itself is the enemy. In hospitals, that means expensive isolation wards and N95 masks for all medical staff.

The books Marr flipped through drew the line between droplets and aerosols at 5 microns. A micron is a unit of measurement equal to one-millionth of a meter. By this definition, any infectious particle smaller than 5 microns in diameter is an aerosol anything bigger is a droplet. The more she looked, the more she found that number. The WHO and the US Centers for Disease Control and Prevention also listed 5 microns as the fulcrum on which the droplet-aerosol dichotomy toggled.

There was just one literally tiny problem: “The physics of it is all wrong,” Marr says. That much seemed obvious to her from everything she knew about how things move through air. Reality is far messier, with particles much larger than 5 microns staying afloat and behaving like aerosols, depending on heat, humidity, and airspeed. “I’d see the wrong number over and over again, and I just found that disturbing,” she says. The error meant that the medical community had a distorted picture of how people might get sick.

Linsey Marr stands in front of a smog chamber in her laboratory at Virginia Tech. For years, she says, the medical establishment treated her as an outsider.

Epidemiologists have long observed that most respiratory bugs require close contact to spread. Yet in that small space, a lot can happen. A sick person might cough droplets onto your face, emit small aerosols that you inhale, or shake your hand, which you then use to rub your nose. Any one of those mechanisms might transmit the virus. “Technically, it’s very hard to separate them and see which one is causing the infection,” Marr says. For long-distance infections, only the smallest particles could be to blame. Up close, though, particles of all sizes were in play. Yet, for decades, droplets were seen as the main culprit.

Marr decided to collect some data of her own. Installing air samplers in places such as day cares and airplanes, she frequently found the flu virus where the textbooks said it shouldn’t be—hiding in the air, most often in particles small enough to stay aloft for hours. And there was enough of it to make people sick.

In 2011, this should have been major news. Instead, the major medical journals rejected her manuscript. Even as she ran new experiments that added evidence to the idea that influenza was infecting people via aerosols, only one niche publisher, The Journal of the Royal Society Interface, was consistently receptive to her work. In the siloed world of academia, aerosols had always been the domain of engineers and physicists, and pathogens purely a medical concern Marr was one of the rare people who tried to straddle the divide. “I was definitely fringe,” she says.

Thinking it might help her overcome this resistance, she’d try from time to time to figure out where the flawed 5-micron figure had come from. But she always got stuck. The medical textbooks simply stated it as fact, without a citation, as if it were pulled from the air itself. Eventually she got tired of trying, her research and life moved on, and the 5-micron mystery faded into the background. Until, that is, December 2019, when a paper crossed her desk from the lab of Yuguo Li.

An indoor-air researcher at the University of Hong Kong, Li had made a name for himself during the first SARS outbreak, in 2003. His investigation of an outbreak at the Amoy Gardens apartment complex provided the strongest evidence that a coronavirus could be airborne. But in the intervening decades, he’d also struggled to convince the public health community that their risk calculus was off. Eventually, he decided to work out the math. Li’s elegant simulations showed that when a person coughed or sneezed, the heavy droplets were too few and the targets—an open mouth, nostrils, eyes—too small to account for much infection. Li’s team had concluded, therefore, that the public health establishment had it backward and that most colds, flu, and other respiratory illnesses must spread through aerosols instead.

Their findings, they argued, exposed the fallacy of the 5-micron boundary. And they’d gone a step further, tracing the number back to a decades-old document the CDC had published for hospitals. Marr couldn’t help but feel a surge of excitement. A journal had asked her to review Li’s paper, and she didn’t mask her feelings as she sketched out her reply. On January 22, 2020, she wrote, “This work is hugely important in challenging the existing dogma about how infectious disease is transmitted in droplets and aerosols.”

Even as she composed her note, the implications of Li’s work were far from theoretical. Hours later, Chinese government officials cut off any travel in and out of the city of Wuhan, in a desperate attempt to contain an as-yet-unnamed respiratory disease burning through the 11-million-person megalopolis. As the pandemic shut down country after country, the WHO and the CDC told people to wash their hands, scrub surfaces, and maintain social distance. They didn’t say anything about masks or the dangers of being indoors.

A few days after the April Zoom meeting with the WHO, Marr got an email from another aerosol scientist who had been on the call, an atmospheric chemist at the University of Colorado Boulder named Jose-Luis Jimenez. He’d become fixated on the WHO recommendation that people stay 3 to 6 feet apart from one another. As far as he could tell, that social distancing guideline seemed to be based on a few studies from the 1930s and ’40s. But the authors of those experiments actually argued for the possibility of airborne transmission, which by definition would involve distances over 6 feet. None of it seemed to add up.

Scientists use a rotating drum to aerosolize viruses and study how well they survive under different conditions.

Marr told him about her concerns with the 5-micron boundary and suggested that their two issues might be linked. If the 6-foot guideline was built off of an incorrect definition of droplets, the 5-micron error wasn’t just some arcane detail. It seemed to sit at the heart of the WHO’s and the CDC’s flawed guidance. Finding its origin suddenly became a priority. But to hunt it down, Marr, Jimenez, and their collaborators needed help. They needed a historian.

Luckily, Marr knew one, a Virginia Tech scholar named Tom Ewing who specialized in the history of tuberculosis and influenza. They talked. He suggested they bring on board a graduate student he happened to know who was good at this particular form of forensics. The team agreed. “This will be very interesting,” Marr wrote in an email to Jimenez on April 13. “I think we’re going to find a house of cards.”

The graduate student in question was Katie Randall. Covid had just dealt her dissertation a big blow—she could no longer conduct in-person research, so she’d promised her adviser she would devote the spring to sorting out her dissertation and nothing else. But then an email from Ewing arrived in her inbox describing Marr’s quest and the clues her team had so far unearthed, which were “layered like an archaeology site, with shards that might make up a pot,” he wrote. That did it. She was in.

Randall had studied citation tracking, a type of scholastic detective work where the clues aren’t blood sprays and stray fibers but buried references to long-ago studies, reports, and other records. She started digging where Li and the others had left off—with various WHO and CDC papers. But she didn’t find any more clues than they had. Dead end.

She tried another tack. Everyone agreed that tuberculosis was airborne. So she plugged “5 microns” and “tuberculosis” into a search of the CDC’s archives. She scrolled and scrolled until she reached the earliest document on tuberculosis prevention that mentioned aerosol size. It cited an out-of-print book written by a Harvard engineer named William Firth Wells. Published in 1955, it was called Airborne Contagion and Air Hygiene. A lead!

In the Before Times, she would have acquired the book through interlibrary loan. With the pandemic shutting down universities, that was no longer an option. On the wilds of the open internet, Randall tracked down a first edition from a rare book seller for $500—a hefty expense for a side project with essentially no funding. But then one of the university’s librarians came through and located a digital copy in Michigan. Randall began to dig in.

In the words of Wells’ manuscript, she found a man at the end of his career, rushing to contextualize more than 23 years of research. She started reading his early work, including one of the studies Jimenez had mentioned. In 1934, Wells and his wife, Mildred Weeks Wells, a physician, analyzed air samples and plotted a curve showing how the opposing forces of gravity and evaporation acted on respiratory particles. The couple’s calculations made it possible to predict the time it would take a particle of a given size to travel from someone’s mouth to the ground. According to them, particles bigger than 100 microns sank within seconds. Smaller particles stayed in the air. Randall paused at the curve they’d drawn. To her, it seemed to foreshadow the idea of a droplet-aerosol dichotomy, but one that should have pivoted around 100 microns, not 5.

The book was long, more than 400 pages, and Randall was still on the hook for her dissertation. She was also helping her restless 6-year-old daughter navigate remote kindergarten, now that Covid had closed her school. So it was often not until late at night, after everyone had gone to bed, that she could return to it, taking detailed notes about each day’s progress.

One night she read about experiments Wells did in the 1940s in which he installed air-disinfecting ultraviolet lights inside schools. In the classrooms with UV lamps installed, fewer kids came down with the measles. He concluded that the measles virus must have been in the air. Randall was struck by this. She knew that measles didn’t get recognized as an airborne disease until decades later. What had happened?

Part of medical rhetoric is understanding why certain ideas take hold and others don’t. So as spring turned to summer, Randall started to investigate how Wells’ contemporaries perceived him. That’s how she found the writings of Alexander Langmuir, the influential chief epidemiologist of the newly established CDC. Like his peers, Langmuir had been brought up in the Gospel of Personal Cleanliness, an obsession that made handwashing the bedrock of US public health policy. He seemed to view Wells’ ideas about airborne transmission as retrograde, seeing in them a slide back toward an ancient, irrational terror of bad air—the “miasma theory” that had prevailed for centuries. Langmuir dismissed them as little more than “interesting theoretical points.”

But at the same time, Langmuir was growing increasingly preoccupied by the threat of biological warfare. He worried about enemies carpeting US cities in airborne pathogens. In March 1951, just months after the start of the Korean War, Langmuir published a report in which he simultaneously disparaged Wells’ belief in airborne infection and credited his work as being foundational to understanding the physics of airborne infection.

How curious, Randall thought. She kept reading.

In the report, Langmuir cited a few studies from the 1940s looking at the health hazards of working in mines and factories, which showed the mucus of the nose and throat to be exceptionally good at filtering out particles bigger than 5 microns. The smaller ones, however, could slip deep into the lungs and cause irreversible damage. If someone wanted to turn a rare and nasty pathogen into a potent agent of mass infection, Langmuir wrote, the thing to do would be to formulate it into a liquid that could be aerosolized into particles smaller than 5 microns, small enough to bypass the body’s main defenses. Curious indeed. Randall made a note.

When she returned to Wells’ book a few days later, she noticed he too had written about those industrial hygiene studies. They had inspired Wells to investigate what role particle size played in the likelihood of natural respiratory infections. He designed a study using tuberculosis-causing bacteria. The bug was hardy and could be aerosolized, and if it landed in the lungs, it grew into a small lesion. He exposed rabbits to similar doses of the bacteria, pumped into their chambers either as a fine (smaller than 5 microns) or coarse (bigger than 5 microns) mist. The animals that got the fine treatment fell ill, and upon autopsy it was clear their lungs bulged with lesions. The bunnies that received the coarse blast appeared no worse for the wear.

For days, Randall worked like this—going back and forth between Wells and Langmuir, moving forward and backward in time. As she got into Langmuir’s later writings, she observed a shift in his tone. In articles he wrote up until the 1980s, toward the end of his career, he admitted he had been wrong about airborne infection. It was possible.

A big part of what changed Langmuir’s mind was one of Wells’ final studies. Working at a VA hospital in Baltimore, Wells and his collaborators had pumped exhaust air from a tuberculosis ward into the cages of about 150 guinea pigs on the building’s top floor. Month after month, a few guinea pigs came down with tuberculosis. Still, public health authorities were skeptical. They complained that the experiment lacked controls. So Wells’ team added another 150 animals, but this time they included UV lights to kill any germs in the air. Those guinea pigs stayed healthy. That was it, the first incontrovertible evidence that a human disease—tuberculosis—could be airborne, and not even the public health big hats could ignore it.

The groundbreaking results were published in 1962. Wells died in September of the following year. A month later, Langmuir mentioned the late engineer in a speech to public health workers. It was Wells, he said, that they had to thank for illuminating their inadequate response to a growing epidemic of tuberculosis. He emphasized that the problematic particles—the ones they had to worry about—were smaller than 5 microns.

Inside Randall’s head, something snapped into place. She shot forward in time, to that first tuberculosis guidance document where she had started her investigation. She had learned from it that tuberculosis is a curious critter it can only invade a subset of human cells in the deepest reaches of the lungs. Most bugs are more promiscuous. They can embed in particles of any size and infect cells all along the respiratory tract.

What must have happened, she thought, was that after Wells died, scientists inside the CDC conflated his observations. They plucked the size of the particle that transmits tuberculosis out of context, making 5 microns stand in for a general definition of airborne spread. Wells’ 100-micron threshold got left behind. “You can see that the idea of what is respirable, what stays airborne, and what is infectious are all being flattened into this 5-micron phenomenon,” Randall says. Over time, through blind repetition, the error sank deeper into the medical canon. The CDC did not respond to multiple requests for comment.

In June, she Zoomed into a meeting with the rest of the team to share what she had found. Marr almost couldn’t believe someone had cracked it. “It was like, ‘Oh my gosh, this is where the 5 microns came from?!’” After all these years, she finally had an answer. But getting to the bottom of the 5-micron myth was only the first step. Dislodging it from decades of public health doctrine would mean convincing two of the world’s most powerful health authorities not only that they were wrong but that the error was incredibly—and urgently—consequential.

Measles virus classification

When someone who is not immune gets measles, wild-type measles virus causes the infection. Scientists divide wild-type measles viruses into genetic groups called genotypes. Of 24 known genotypes, the World Health Organization (WHO) lists 5 genotypes that are known to currently circulate and are most commonly seen: B3, D4, D8, D9, and H1. MMR vaccine protects you against all types of measles.

Scientists identify the genotype in a laboratory using a method called nucleic acid sequencing. The genotype is based on the RNA (ribonucleic acid) sequence of the measles virus that caused the disease in an infected person. Learn about Genetic Analysis of Measles Viruses.

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