Viruses hide among all living things—some are harmless, and some have the potential to wipe out huge swaths of people.
The Ebola virus’s sister virus, Marburg, first appeared in the 1960s. Marburg and Ebola have only emerged a handful of times since, but most of the victims and communities hit with Marburg or Ebola have been devastated by the viruses’ brutal physical attacks, high infectiveness, and astronomical kill rates.
We’ll discuss the known outbreaks of Ebola and Marburg, as well as the potential for future outbreaks. But first, let’s talk about what the virus is and does.
Ebola belongs to a family of viruses named filoviruses, meaning “thread viruses,” because they look like threads or ropes under a microscope.
There are four viruses in the filovirus family:
(Shortform note: Since the book’s publication, three more filoviruses have been identified, all of which are strains of Ebola: Bundibugyo, Taï Forest, and Bombali.)
Viruses are parasites. They lie dormant until they can latch onto another cell, at which point they use the cell’s materials to replicate ceaselessly, until the cell either bursts or is exhausted and destroyed.
The Ebola virus targets its host’s immune system, preventing the host’s body from fighting off the disease. But viruses need a living host to survive, so when a victim dies, the virus must jump hosts. Ebola is transmitted through exposure to the blood or bodily fluids of an infected victim or corpse.
With the exception of Ebola Reston, filoviruses don’t appear to discriminate between people and animals, and they can jump easily from one to the other.
Scientists still don’t know what the filoviruses’ hosts are—whether insects or animals—but the viruses can be transmitted to primates or duikers, a type of antelope. Nor do scientists know where the hosts live, but most cases originated in the region around Mount Elgon, on the border of Kenya and Uganda, not far from Sudan. Specifically, a few cases trace back to Kitum Cave, on the eastern slope of Mount Elgon.
(Shortform note: Scientists still don’t know the hosts of filoviruses, but evidence points to fruit- and insect-eating bats as major carriers—though that doesn’t rule out the possibility that an insect or rat is the original host and simply infected the bats through a bite. Scientists also suspect there could be multiple hosts.)
Marburg virus attacks organs, intestines, skin, and connective tissue through the body. Its symptoms include:
(Shortform note: Besides the kill rate, there are no major identifiable differences between Marburg and Ebola. Scientists don’t know why Ebola is deadlier than Marburg.)
Marburg first appeared in several Ugandan villages around Mount Elgon in the early 1960s, but the “microbreaks” went relatively unnoticed. Then, in 1967, the virus killed 31 people in Marburg, Germany.
The virus arrived through a shipment of Ugandan monkeys to a vaccine factory in Marburg. There could have been as few as two or three sick monkeys among several hundred—and they may have been in the incubation period, during which they wouldn’t have had any visible symptoms.
The first known case of Ebola was in 1976 in southern Sudan, about 500 miles from Mount Elgon. The first victim unknowingly spread the virus to coworkers, who then spread it to friends, families, and a nearby hospital. The hospital’s practice of reusing dirty needles caused the number of cases to explode.
With a 50 percent kill rate, Ebola Sudan killed hundreds of people in central Africa.
Just two months after the Ebola Sudan outbreak, Ebola Zaire appeared 500 miles away, at a rural hospital in northern Zaire.
Ebola Zaire is the most aggressive of the filoviruses. The virus digests victims’ organs and tissues until they liquefy into a slime of replicated virus particles.
Ebola Zaire’s effects include:
As in Sudan, the Zairean hospital’s reuse of dirty needles spread the virus like wildfire, igniting simultaneous outbreaks in 55 surrounding villages.
When one member of the hospital staff contracted the virus, she went to a hospital in the country’s capital, Kinshasa. Doctors at that hospital recognized that her symptoms were similar to Marburg, so they sent samples of her blood and liver to national laboratories in Belgium and England.
The head of the Special Pathogens Branch at the American Centers for Disease Control also got his hands on a sample and realized the virus wasn’t Marburg—it was something new. He named it Ebola, after Zaire’s Ebola River.
In 1989, monkeys in a facility in Reston, Virginia began dying mysteriously. The facility held imported monkeys before sending them elsewhere in the U.S., and it belonged to Hazleton Research Products, a company that imported and sold lab animals.
All the dying monkeys arrived in a shipment from a facility in the Philippines. Infected monkeys developed glazed facial expressions, lost their appetites, and died soon after. Within a month, 29 of the 100 monkeys were dead.
When the company’s veterinarian, Dan Dalgard, dissected the corpses, he found the monkeys’ spleens were swollen and there was blood in their intestines. Seeking a second opinion, Dalgard sent samples from the monkeys to a virologist at the United States Army Medical Research Institute of Infectious Diseases (USAMRIID), which developed vaccines and studied how to contain outbreaks from weaponized or naturally occurring biological threats.
When researchers at USAMRIID viewed the infected monkey samples under a microscope, they saw the signature rope-like shape of the filovirus family. News quickly spread up the chain of command.
The Army officials had to be extremely cautious to contain the threat of an outbreak while also avoiding a public panic. They worked with CDC officials to develop a plan.
There are only three ways to stop a virus:
With permission from Dalgard and Hazleton, the Army would euthanize every monkey in the monkey house and sterilize the entire facility.
The Army assembled a biohazard SWAT team to tackle the monkey house mission. With the virus on the loose inside the monkey house, they considered the facility a Biosafety Level 4 hot zone—an area contaminated with the most dangerous category of viruses, which have no vaccines or cures.
The team had to wear biosafety space suits that encased their entire bodies and take every safety precaution to prevent the virus from getting out of the building. They dealt with the monkeys in five steps:
It took a few days for the biohazard SWAT team to euthanize all 450 monkeys. Then the decontamination team scrubbed every surface of the facility with bleach and gassed the building with formaldehyde.
After the Army was confident that the building was sterile, they returned it to Hazleton. The company resumed importing monkeys from the same supplier in the Philippines, and, within a month, the Reston facility had another outbreak.
During the second outbreak, an employee at the monkey house cut himself while performing a necropsy on an infected monkey. The scalpel was covered in virus-laden monkey blood, and it cut into his thumb and mixed with his own blood. He was surely infected.
But, as time passed, the employee appeared to be fine.
In fact, all four animal caretakers from the Reston facility tested positive for the virus, but none ever broke with symptoms.
Since the virus didn’t appear to affect people, the Army, CDC, and Hazleton agreed to isolate the monkeys inside the building and let the virus work through them—instead of bringing the Army back in for another sterilization mission.
Based on how the virus was moving through the monkey house and affecting the monkeys, the virus seemed to have mutated since the month prior, indicating it could to quickly adapt to new hosts and survive significant changes in its environment.
USAMRIID researchers determined that this virus was a new form of Ebola. They named it Reston.
This virus was so similar to Ebola Zaire that it was hard to distinguish them in microscopic images. But two things were significantly different about Ebola Reston.
First, Ebola Reston appeared to be airborne. While the virus spread through the monkey house, it infected monkeys in different rooms that never interacted. Additionally, two of the Reston employees who tested positive hadn’t been exposed through any cuts or blood contact, so they must have contracted the virus through the air.
Second, unlike the other filoviruses, Ebola Reston didn’t appear to affect people.
Still, researchers remained cautious. Considering how quickly the virus appeared to adapt, they couldn’t eliminate the possibility that one small mutation could make Ebola Reston lethal to humans—and its airborne transmission would make the threat even deadlier.
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Did researchers fear a large-scale outbreak? On one hand, the close contact required for transmission and the relatively successful containment of filoviruses relieved some fear of a major epidemic or pandemic. On the other hand, all the questions that still remained about the filoviruses—including their hosts, where they originate, and how and why they emerge—amplified the fear of future outbreaks.
(Shortform note: Since the book’s publication in 1995, there have been Ebola outbreaks every few years, the majority of which have been Ebola Zaire. Most have been fairly small (less than 100 cases) and centered in Western Africa, but one was a far outlier: From 2013-2016, Ebola Zaire spread across 10 countries, infecting more than 28,000 people and killing more than 11,000.)
In the 1960s, the export of primates for medical research became a big business in Africa. Inevitably, some of the monkeys were sick when they were caught from the wild. As different monkey species were held in close quarters and shipped to industrialized countries around the world, it created prime conditions for viruses to jump species and then cross borders.
Some experts believe the monkey export business led to the international spread of AIDS and other viruses, including the deadly Ebola virus and its sister virus, Marburg.
Scientists still don’t know what the filoviruses’ hosts are—whether insects or animals—but the viruses can be transmitted to primates or duikers, a type of antelope.
(Shortform note: To this day, scientists don’t know the hosts of filoviruses, but evidence points to fruit- and insect-eating bats as major carriers—though that doesn’t rule out the possibility that an insect or rat is the original host and simply infected the bats through a bite. Scientists also suspect there could be multiple hosts.)
Scientists don’t know where the viruses’ unknown hosts live, but most cases of Ebola trace back to the region around Mount Elgon, an extinct volcano on the border of Kenya and Uganda, not far from Sudan. The mountain is an ecological rarity: It houses a rainforest amid arid African savannas.
Specifically, a few cases have traced back to Kitum Cave, a massive cave 8,000 feet up the eastern side of the mountain. Kitum Cave is a perfect environment for Ebola to develop for a few reasons.
First, Kitum Cave is unusually dry and dusty, which are ideal conditions for viruses. Viruses generally don’t last long in sunny or moist environments, but in dry, dark places they can lie dormant for long periods of time, waiting to find a host.
Most caves are carved by water, and they would be too damp for viruses to thrive. But scientists believe the elephants who visit the cave in search of salt carved Kitum Cave through thousands of years of incessant scratching at the rocks with their tusks.
Second, myriad animals, big and small—including monkeys, leopards, rats, and shrews—frequent the cave. The inter-species traffic and the enclosed space create prime conditions for a virus to jump species.
Most of the time, Ebola and its related viruses remain in hiding. But when the viruses have emerged, they’ve devastated local villages and, occasionally, distant cities in other countries and continents. In this summary, we’ll talk about what happened during these outbreaks and the potential for future outbreaks.
But first, let’s discuss what the virus is and how it affects humans.
Ebola belongs to a family of viruses named filoviruses, meaning “thread viruses,” because they look like threads or ropes under a microscope.
There are four viruses in the filovirus family:
(Shortform note: Since the book’s publication, three more filoviruses have been identified, all of which are strains of Ebola: Bundibugyo, Taï Forest, and Bombali.)
With the exception of Ebola Reston, filoviruses don’t appear to discriminate between people and animals, and can jump from one to the other.
Marburg’s kill rate among patients treated in hospitals is about 1 in 4, which makes Marburg an extremely lethal virus. By comparison, yellow fever’s kill rate is about 1 in 20, and it is considered highly lethal.
Marburg virus attacks organs, intestines, skin, and connective tissue throughout the body. Its symptoms include:
The virus is extremely virulent and highly infective, and it can live in corpses’ eyeballs for months after death.
(Shortform note: Besides the kill rate, there are no major identifiable differences between Marburg and Ebola. Scientists don’t know why Ebola is deadlier than Marburg.)
Ebola virus particles are composed of seven different proteins—each of which scientists know little to nothing about—and a strand of RNA, which contains the virus’s genetic information and instructions for the virus’s replication.
Viruses are parasites. They lie dormant until they can use their sticky surface to latch onto another cell. The cell envelopes the virus, at which point the virus uses the cell’s materials to create copies of itself. The virus continues replicating until the cell either bursts or is exhausted and destroyed.
The Ebola virus targets the immune system, preventing victims’ bodies from fighting off the disease. However, Ebola’s lethality doesn’t benefit the virus: When a virus’s host dies, it must jump to another host, or else it will also die. The only two “jobs” of a virus are to survive and replicate.
Scientists believe Ebola is transmitted through the blood and bodily fluids of infected victims and corpses. But if the virus mutated to become airborne, it would have the potential to snowball into a pandemic—and with a 50-90% kill rate, the effects would be devastating.
Although Ebola belongs to the filovirus family, it’s distantly related to other diseases, including:
Ebola’s connections to these diseases are evident in certain symptoms, including rashes (like measles) and psychosis (like rabies).
Ebola Zaire shares many symptoms with other filoviruses, but Ebola Zaire is the most aggressive of the filoviruses, digesting all the organs and tissues in victims’ bodies until they liquefy into a slime of replicated virus particles.
This is how Ebola Zaire affects different parts of victims’ bodies:
Blood
Skin
Organs
Brain
After death, the body continues to liquefy, oozing fluids that are packed with virus particles.
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Now that we’ve introduced the filoviruses, we’ll explore the outbreaks of each and how local, national, and global organizations have attempted to stop their spread.
The first recorded outbreaks of the filoviruses occurred in a 15-year stretch in the 1960s and ‘70s. Distinct symptoms like victims’ red eyes helped doctors draw connections among the diseases.
Between 1962 and 1965, several Ugandan villages around Mount Elgon—not far from Kitum Cave—were hit with outbreaks of an unusual disease that killed not only villagers but also monkeys. The symptoms included a strange skin rash and bleeding.
The village microbreaks went relatively unnoticed, but in 1967 a vaccine factory in the German city of Marburg experienced an outbreak that infected 31 people and killed seven.
The German factory imported African green monkeys in order to harvest their kidney cells to make vaccines. The virus came in with a shipment of several hundred monkeys from a monkey trader in Uganda who exported thousands of monkeys to Europe each year.
The monkey trader’s standard practice was to perform only a visual inspection of the monkeys before they were exported, and to remove any that looked sick or injured. The sick monkeys were then released on a small nearby island in Lake Victoria, making the island a potential hotbed of viruses.
Worse yet, when the trader was short on monkeys for an export, he would get some from the island. It’s possible that Marburg virus was present on the island, and that the trader included some monkeys from the island in his shipment to Germany, setting off the outbreak there.
Only two or three of the monkeys may have had the virus, and they likely didn’t show any symptoms when they arrived. But in the monkeys’ close quarters, the virus quickly spread and several monkeys died.
The virus soon made the jump to humans, first infecting a factory employee tasked with feeding the monkeys and cleaning their cages. He died within weeks.
After the Marburg outbreak, global health officials were eager to find the source of the virus so that they could contain it and avoid future outbreaks. Although the virus arrived in Marburg via monkeys, the virus killed the monkeys too quickly to make them viable hosts—so it had to have been another animal or insect to which the monkeys were exposed.
The World Health Organization sent a team of investigators to Uganda, where the monkeys had been imported from, but they couldn’t identify the source.
The first known case of Ebola was in a man known as Yu. G., in the summer of 1976. Yu. G. lived in a southern Sudan, about 500 miles from Mount Elgon.
Yu. G. never went to the hospital—he died in a cot at home—nor was he well known outside his family and coworkers. Nevertheless, he set off an outbreak of the virus that was later named Ebola Sudan.
No one knows where or how Yu. G. contracted the virus, but it soon spread to a few of his coworkers, from whom it spread to friends, families, and a nearby hospital. From the hospital, the virus took off through the reuse of dirty needles.
Ebola Sudan killed hundreds of people in central Africa. The virus’s 50 percent kill rate was comparable to the bubonic plague of the Middle Ages.
And then, suddenly, it stopped. It’s unclear why the outbreak ended, but two possible reasons are:
Just two months after the Ebola Sudan outbreak ignited, Ebola Zaire appeared 500 miles away, in the mostly rural Bumba Zone of northern Zaire. Ebola Zaire was even deadlier, with almost double the kill rate of Ebola Sudan.
The virus appeared at the rural Yambuku Mission Hospital, which was run by Belgian nuns. No one knows who the first human was to contract Ebola Zaire, or from what—whether animal meat, insect blood, a spider bite, or something else. The hospital’s practice of reusing dirty needles made it impossible to know which patient first brought the virus into the hospital.
Just a drop of infected blood is enough to transmit Ebola, so the virus quickly spread among the hospital’s nurses, injection patients, and their families, hitting 55 surrounding villages at once.
When one nun at the hospital, known as Sister M. E., became infected, a priest and another nun flew her to Kinshasa, the country’s capital. They reasoned that she would receive better treatment there, at Ngaliema Hospital. Sister M. E. survived the trip and then died at Ngaliema Hospital.
The doctors at Ngaliema Hospital recognized the nun’s symptoms as similar to Marburg, so they sent samples of her liver and blood to national laboratories in Belgium and England.
The American Centers for Disease Control (CDC) was eager to get a sample of the nun’s blood as well. Karl Johnson, the head of the CDC’s Special Pathogens Branch—which investigated new and unknown viruses—called a friend at the English lab to ask for a small sample of the blood.
The English researcher agreed and sent a tiny amount of black, tarry blood in glass vials. Through electron-microscope photos, CDC researchers saw that the virus resembled Marburg, but it tested negative for Marburg and other known viruses. They were facing something entirely new. Johnson named the virus Ebola, because the outbreak happened around Zaire’s Ebola River.
Johnson and several other CDC doctors flew to Geneva to tell the World Health Organization what they had found. Then the doctors continued on to Zaire and Sudan to try to stop the outbreaks.
When the doctors arrived in Africa, they discovered that villages had taken their own measures to limit the virus’s spread, including:
Presumably, these measures played a major role in preventing the virus from spreading further and sparking a major epidemic.
Meanwhile, in Kinshasa, a nurse from Ngaliema Hospital who helped care for Sister M. E. became sick.
Despite her symptoms, the nurse, named Mayinga, spent two days walking through Kinshasa. During those two days, she waited in line at the Zairean foreign ministry, took taxis, visited two hospitals, and sat in crowded waiting rooms.
Most likely, Mayinga knew she’d contracted the virus but was in denial. She visited the foreign ministry in hopes of getting a travel permit before she became visibly sick. Mayinga’s denial also explains why she didn’t initially seek treatment at her hospital, where the staff knew her and would have recognized her symptoms.
Finally, after receiving no helpful treatment or advice from the two hospitals, she returned to Ngaliema Hospital for treatment.
News spread among local residents and officials that a nurse who was infected with the same virus that had devastated parts of the Bumba Zone had spent two days traveling around a city of two million people.
Officials at the World Health Organization went into high alert. The Zairean President ordered soldiers to enforce quarantine at Ngaliema Hospital and to isolate Bumba Zone, where the virus originated.
Mayinga died at Ngaliema Hospital. Some of Mayinga’s blood still sits in vials in scientific laboratories as a sample of Ebola Zaire.
Officials tracked down Mayinga’s whereabouts during those two days in Kinshasa and identified 37 people who had close contact with her. None of the 37 people contracted the virus—not even the person with whom she’d shared a bottle of soda. This suggested the virus was neither airborne nor easily transmissible.
In 1980, Charles Monet, a French expatriate living in Western Kenya, spent New Year’s Day exploring Kitum Cave with a friend. A week later, he began getting sick.
The cave holds a petrified rainforest from a volcanic eruption seven million years ago, and the petrified rocks are surrounded by sharp crystals made of minerals. Additionally, the cave’s surfaces are coated with elephant dung and the excrement of both fruit- and insect-eating bats. Monet could’ve easily scratched himself on a sharp rock or crystal, exposing him to viruses in the animal dung.
First, Monet got a throbbing headache. In the following few days, he developed other symptoms, including:
After several days, Monet’s coworker took him to a nearby hospital. The doctors didn’t recognize the illness, nor did they know how to treat it. When antibiotics didn’t help, they suggested he go to the best private hospital in East Africa, Nairobi Hospital. Sick as he was, Monet was still lucid and mobile, so he got in a taxi and headed to the airport.
As soon as Monet boarded the flight, he unknowingly exposed the world to the virus: He was in a cramped, probably full plane with people from anywhere in the world, traveling to anywhere in the world. Modern air travel routes make it possible for a disease to spread anywhere in the world within 24 hours.
During the flight, Monet’s symptoms worsened. They included:
The black vomit was a sign that Monet was experiencing extreme amplification, meaning the virus had multiplied so extensively that it inhabited every part of the body, from skin to brain. The virus was literally taking over its host. By this point, even a drop of Monet’s blood may have had a hundred million particles of the virus, and the black vomit itself was heavily laden with the virus.
Still able to walk, Monet got off the plane, into a taxi, and headed to Nairobi Hospital. As he sat in the waiting room, he entered the final phase—what military biohazard specialists call “crashing and bleeding out.” This entailed:
Monet laid sprawled on the floor of the waiting room in a pool of blood. The virus had nearly killed its host, and now it had to find a new host in order to survive.
The nurses wheeled Monet—barely alive—into the intensive care unit, where a young doctor named Shem Musoke inspected him.
Musoke had no idea what kind of illness this was, but his first priority was to help Monet breathe, which was becoming increasingly difficult as he hemorrhaged and his airways filled with blood and mucus. Without wearing gloves, Musoke put his finger in Monet’s mouth to clear the blood and mucus so he could insert the laryngoscope.
As Musoke leaned close to Monet’s face, peering down his throat, Monet spewed black vomit all over Musoke, the gurney, and the floor around them. Bits of vomit landed in Musoke’s eyes and mouth.
Musoke got Monet breathing again, but Monet was losing so much blood that his blood pressure was plummeting. Musoke attempted to give him a blood transfusion, but each time he tried inserting the needle, Monet’s vein gave way and blood came pouring out, unable to clot. At the same time, Monet continued to hemorrhage from his bowels.
Monet fell deeper into a coma and died hours later. As doctors performed the autopsy, Monet’s body looked like it had been dead for days, not hours. Monet’s liver was yellow and partially liquefied, and his intestinal lining had shed—both of which are common in days-old corpses.
Nine days after treating Monet, Musoke got a backache and his eyes became red. Musoke suspected he had malaria. He took malaria pills and had an antimalarial injection, but neither helped.
Then, Musoke developed a fever, aches throughout his body, and abdominal pain. He began to think he had typhoid fever, but the antibiotics he took for it did nothing.
Musoke continued to work at the hospital, and he kept getting worse. Soon, he developed jaundice.
Finally, Musoke turned to another doctor at his hospital, Antonia Bagshawe, for treatment. Bagshawe suspected gallstones or a liver abscess, which would explain the fever, abdominal pain, and jaundice. However, an ultrasound showed nothing more than an enlarged liver.
Bagshawe suggested exploratory surgery, but the operation provided no answers—in fact, it only raised questions. There were no gallstones, but Musoke’s liver was swollen and red, and no matter what the surgeons did, they couldn’t stop the bleeding. Musoke’s blood wouldn’t coagulate, and even a surgical gel foam that helps stop bleeding had no effect.
After surgery, Musoke’s kidneys started failing and he was quickly getting worse.
Another doctor suspected that a virus was behind Musoke’s strange symptoms. He collected a blood sample for testing and sent it to South Africa’s National Institute of Virology and to the Centers for Disease Control in the United States.
Musoke ultimately recovered completely, and none of the other medical staff at the hospital became infected. However, the microbreak at Nairobi Hospital was a warning of what could happen on a much larger scale if the virus spread further.
Soon afterward, the doctor who’d sent Musoke’s blood sample got a call that the South African laboratory had found Marburg virus in Musoke’s blood.
In 1983, a U.S. Army civilian scientist and Ebola expert named Eugene Johnson led research on the Ebola and Marburg viruses. Johnson and his team infected monkeys with Ebola Zaire, then gave them various drugs in hope of finding one that either treated or cured the virus.
Johnson conducted his experiments at the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) at Fort Detrick, Maryland. The work at USAMRIID focused on fighting viruses and bacteria—whether weaponized or naturally occurring—by developing vaccines and studying how to contain outbreaks.
USAMRIID researchers studied Biosafety Levels 0, 2, 3, and 4 agents (there is no Level 1). Ebola was a Level 4 hot agent, which are lethal viruses that have no vaccines or cures.
Before entering a Level 4 hot zone, researchers went through a multistep safety process, including:
Any researchers whose suits had been breached and who were exposed to a Level 4 hot agent had to be quarantined in the USAMRIID’s biocontainment hospital, called the Slammer. Those who died were buried in a Level 4 biocontainment morgue, called the Submarine.
No risk could be overlooked when dealing with such deadly and highly infective agents.
One researcher in Johnson’s Ebola experiments was Major Nancy Jaax, an army veterinarian who was training in veterinary pathology. When monkeys died in the experiment, Jaax’s job was to find out what had killed them—essentially confirming that Ebola was the cause of death.
One day, Jaax entered the monkey room to find and inspect two monkeys that had crashed and bled out. While working on one of the dead monkeys, Jaax noticed a hole in her glove. She panicked. Jaax’s glove had been covered in the infected monkey’s blood—and worse, she had a deep cut in the palm of that hand from a kitchen accident the night before.
Jaax rushed to the decontamination shower, then tore off her suit and carefully inspected the first of her three layers of hand protection, the latex glove that directly covered her skin. She saw blood under the glove, but couldn’t yet tell if it was the monkey’s or her own.
Jaax filled the glove with water and watched for any leaks, but the glove held. She was safe.
Throughout Johnson’s experiments, none of the drugs worked. Every infected monkey died of the disease.
Eventually, even the two control monkeys who researchers hadn’t infected also caught the virus and died. They’d been kept in their cages, away from all the other monkeys, which should have kept them healthy because researchers believed the virus only traveled via direct contact with bodily fluids.
However, somehow the monkeys had been infected. Jaax believed that when the monkeys’ cages were cleaned, the moisture mixed with the sick monkeys’ spit and other fluids on the cages’ surfaces and created an aerosol of droplets. Jaax theorized that the aerosol allowed the virus to become airborne.
In September 1987, a 10-year-old Danish boy died at Nairobi Hospital after traveling around Kenya with his parents and sister. The boy, known as Peter Cardinal, had symptoms that included:
Johnson, who ran the Ebola experiments at the USAMRIID, infected monkey cells with a sample of the boy’s blood. The monkey cells quickly exploded and were destroyed. The same thing happened to guinea pig cells, which meant the virus was adaptable to different species.
Through more tests, Johnson confirmed what he suspected: Cardinal’s blood contained Marburg virus.
Johnson had to find out:
Johnson found out that Cardinal had visited Kitum Cave with his family shortly before getting sick. Johnson considered two ways Cardinal could’ve become infected:
Johnson led an expedition into Kitum Cave with 35 American and Kenyan doctors and scientists, as well as guinea pigs, baboons, and several types of monkeys. Since there were no virus detection tools, he put animals in cages at different locations to act as canaries in the coal mine—if one got sick, researchers narrowed their search to the location of that animal’s cage and tried to pinpoint how the animal was infected.
However, all the animals in Johnson’s expedition remained healthy.
Additionally, the team caught and dissected small animals and thousands of bugs from the cave, hoping to find a sign of Marburg. But they found nothing.
Johnson’s expedition neither confirmed nor ruled out Kitum Cave as the source of the virus. The only thing he knew definitively was what he knew before the expedition: that Marburg lived somewhere on or near Mount Elgon.
The mysteries surrounding filoviruses’ source and transmission intensified when Ebola appeared in the U.S. two years later.
In October of 1989, 100 wild monkeys were shipped from the Philippines to the Reston Primate Quarantine Unit in Reston, Virginia. The facility was an arm of Hazleton Research Products, a company that imported and sold lab animals. When imported wild monkeys arrive in the United States—typically for laboratory testing—they must be held in quarantine for a month before they’re sent anywhere else in the country.
When this shipment of monkeys arrived, two were already dead. A few dead monkeys wasn’t unusual, but in less than a month, 29 of the 100 monkeys had died.
The monkey colony manager, Bill Volt, considered the fact that the building’s air system was broken, and the heat was running high. The relentless heat could have put a strain on the monkeys and caused the deaths—but that didn’t explain why most of the deaths had been in just one room, Room F. Volt called Hazleton’s consulting veterinarian, Dan Dalgard, to take a look at the monkeys.
When Dalgard inspected the remaining monkeys in Room F, he found two that were sick and feverish. Both died that night, and when Volt and Dalgard dissected the monkey corpses the next day, they found that the monkeys’ spleens were swollen and there was blood in their intestines.
More monkeys in Room F died and Dalgard continued to investigate. None of the monkeys seemed terribly ill, besides having enlarged, tough spleens. However, Dalgard didn’t recognize that their spleens weren’t simply swollen—they had actually become solid blood clots.
Dalgard removed a piece of spleen and collected a throat swab from one of the dead monkeys, and he sent it to Peter Jahrling, a civilian virologist at USAMRIID. Dalgard believed the disease killing these monkeys was simian hemorrhagic fever (SHF), which was fatal for monkeys but didn’t affect humans. After some testing, Jahrling tentatively agreed.
When Dalgard got the verdict from USAMRIID, he killed the rest of the monkeys in Room F, in order to stop the disease from spreading to monkeys in other rooms.
A few days later, Dalgard returned to the Reston facility to find that five monkeys had died in a room two doors down from Room F. This was alarming: Not only was the disease spreading, but it could skip rooms, suggesting it could be airborne.
Thomas Geisbert, an intern at USAMRIID, grew curious about the cultures that Jahrling was growing from the Reston monkey sample. Despite being just an intern, Geisbert specialized in taking high-powered electron-microscope photos and identifying the viruses he saw. He had studied the distinct shapes of various viruses and committed many to memory.
Under a standard light microscope, the Reston cultures looked like they’d been contaminated by outside bacteria. When bacteria destroy cultures, they create a smell—and when Geisbert and Jahrling opened the flask and took a few whiffs, they didn’t smell anything. However, they decided to put it under the electron microscope for a closer look anyway. It was the Friday before Thanksgiving, and they wouldn’t be back at the lab until a week-and-a-half later.
After the holiday, Geisbert inspected the supposedly contaminated cells under his electron microscope. He recognized what he saw: The cells were bulging with rope-like viruses, just like he’d seen in pictures of samples from Cardinal’s blood. It was a filovirus, but the threads were less curled than Marburg virus particles.
Geisbert printed the images and showed Jahrling. Jahrling recognized the signature thread-like shapes. Although there were some differences between the cells in Geisbert’s photos and the images of Marburg in the textbook they consulted, it was close enough to be concerning.
Geisbert and Jahrling thought of how they’d sniffed the flask with the cell cultures, and they worried about their exposure. It had been 10 days, and neither had developed any symptoms—but they were in the middle of the incubation period, so they weren’t in the clear yet. They decided to take the wait-and-see approach, meanwhile testing their blood to check for signs of infection.
Jahrling alerted Colonel Clarence Peters, the chief of USAMRIID’s disease-assessment division. Peters, Jahrling, and Geisbert considered the possibilities:
Peters was alarmed but cautious. Announcing that Marburg or Ebola had appeared in a Virginia suburb outside Washington, DC would cause panic, so they had to be 100 percent positive. Geisberg collected more samples from the monkey liver, and he captured electron-microscope photos that convinced Peters that it was, indeed, a filovirus.
Now they needed to determine whether the virus was Marburg or Ebola. While they waited for the test results, Jahrling called Dalgard to warn him to be careful, though he didn’t reveal many details. Dalgard had dissected 50 potentially infected monkeys 11 days prior, and he still showed no symptoms—but he worried about the other employees in the monkey house.
Jahrling’s tests showed that the monkey samples reacted to Ebola Zaire, meaning that the blood sample of an Ebola Zaire victim glowed under ultraviolet light when it mixed with virus cultures made from the monkeys. The glow signaled that the virus in the culture was the same or similar to the virus in the victim’s blood sample.
The tests weren’t proof positive that the virus was Ebola Zaire. This virus could be something closely related—something new and unknown.
The prospect of a new filovirus was even more terrifying than Ebola Zaire because that would mean they knew nothing about how deadly it was or how it was transmitted. If this virus was anything like the other filoviruses, they’d be facing a potent killer without knowing how to protect themselves or prevent an outbreak.
The news quickly spread up the chain of command:
When Russell, Peters, Huxsoll, Jahrling, and Jaax met, they tried to get a grasp of what they were dealing with and what they were going to do about it. Russell was alarmed at the possibility of an Ebola outbreak in a suburb of Washington, DC.
Worse yet, Jaax told him about two incidents that suggested the virus could be airborne:
The group considered the options. There are three ways to stop a virus:
One way to achieve biocontainment would be to cut off the Reston facility from the world, allow the virus to spread and kill the monkeys, and potentially quarantine all the employees who’d been exposed. But Option 1 would mean allowing the monkeys to suffer as they died off, and it wouldn’t give the researchers an opportunity to collect samples to study.
Option 2 was to enter the facility—a Level 4 hot zone. They would kill, collect samples from, and incinerate the monkeys, and then sterilize the entire building with chemicals.
Peters called Hazleton veterinarian Dalgard to let him know what they were dealing with. Dalgard was relieved to find out the virus wasn’t Marburg, which is well known and feared among professionals who work with monkeys. Dalgard had never heard of Ebola, but when Peters told him Ebola’s kill rate, he understood he was dealing with something even worse than Marburg.
Dalgard needed to loop in his superiors at Hazleton, who were unaware that a monkey-killing virus was spreading through the Reston facility. Dalgard worried that he’d made a mistake by involving the Army in the first place, who now wanted to visit the monkey house and view samples from the dead monkeys—he didn’t want his decision to anger company leaders or hurt business. Dalgard hesitated to give them permission, and instead he suggested they talk again in the morning.
As Dalgard considered the situation, he was more concerned by the prospect of the Army muscling its way into Reston than by the threat of Ebola. He knew Ebola’s kill rate, but he’d been exposed to the infected monkeys’ blood and still felt fine.
The next morning, Dalgard spoke to Peters and agreed to let Johnson, Jaax, and Peters inspect the tissues of the monkey carcasses—but Dalgard was still hesitant to let them into the monkey house.
Then Dalgard called Volt, the monkey colony manager, to tell him about the Army’s findings. Volt told Dalgard that one of the animal caretakers in the monkey house—who is identified as Jarvis Purdy—had suffered a heart attack. Purdy was at the hospital, and he might be dying. Suddenly, the threat became real to Dalgard: Purdy could be infected with Ebola, and the virus could infect and kill others, as well.
Dalgard instructed Volt to suspend all activity in the monkey rooms besides feeding, cleaning, and observation—and those tasks had to be done in full biohazard gear.
Soon after, Johnson, Jaax, and Peters arrived at Dalgard’s office. Jaax viewed a sample from one of the dead monkeys under a microscope, and she saw that the cells looked like bricks that were bursting with replicated virus particles, a signature sign of Ebola.
The Army officials wanted more samples, so Dalgard had Volt give them the carcasses of several monkeys that had died the night before.
Jaax, Johnson, and Peters transported the infected carcasses to USAMRIID, where Jaax took them into the Level 4 hot zone to dissect. When she cut into the first one, she found:
Some of the characteristics looked like Ebola, but it was far from a dead ringer—the organs hadn’t liquified and there was little to no hemorrhaging. Jaax couldn’t confirm that they were dealing with Ebola based on this carcass. She’d need more samples.
While the Army researchers and leaders were forming their plan, they came upon the issue of politics. Congress charged the Centers for Disease Control (CDC)—not the Army—with protecting the country from disease. However, while the CDC had the authority to respond to this threat, the Army had the manpower.
The group felt that they had to move forward with their plan to contain this virus, regardless of the repercussions. They would assemble a biohazard SWAT team and sterilize the Reston monkey house.
The following day, General Russell met with members of the USAMRIID team and a couple CDC officials, including Joe McCormick, the chief of the CDC’s Special Pathogens Branch. Dalgard, Virginia Department of Health officials, and officials from Fairfax County (where Reston is located) also attended.
McCormick had a history of tension with the Army, having publicly criticized Eugene Johnson for neglecting to publish the results of his Kitum Cave expedition after Peter Cardinal’s death. McCormick also had more field experience with Ebola than anyone in the room, and he was the only person there who’d worked with infected people.
McCormick had worked for days in a quarantine hut full of Ebola victims in Sudan, and—despite a close call—he hadn’t caught the virus. As a result, McCormick felt sure that Ebola was difficult to transmit and most likely not airborne, despite what Army officials were suggesting.
As the meeting went on, tensions rose. Russell finally proposed a compromise: The CDC would be in charge of human-related concerns, and the Army would be in charge of the monkeys and the Reston facility. Everyone agreed.
Dalgard decided to allow the Army into the monkey house to clear out one of the rooms.
Peters tapped Nancy Jaax’s husband, Colonel Jerry Jaax, to lead the mission into the Reston facility. Jerry Jaax was the chief of USAMRIID’s veterinary division. Although he had no experience with extreme biohazard agents, he and his team knew well how to handle monkeys.
Jerry Jaax conferred with Johnson about how to approach the mission. They’d have to be extremely careful while sterilizing Reston to prevent the virus from escaping and spreading.
The priorities of the mission were threefold:
Within a few days, the media had caught wind of the viral outbreak at Reston. On the morning of the Army’s first sterilization operation at Reston, the front-page story in The Washington Post was about the discovery of Ebola in the monkey house.
Peters had given the reporter a quote for the story, speaking carefully to avoid raising panic and to assure the public that everything was under control. The Army had to act as cautiously and inconspicuously as possible during its mission to avoid making a scene at the Reston facility.
As Jerry Jaax and his team prepared to enter the monkey house that morning, no one wore uniforms, and they wouldn’t change into their biohazard space suits until they were in a designated staging area inside the building. To onlookers, it appeared to be a benign operation—rather than the serious biohazard mission it was.
Even Dalgard was surprised by the Army’s space suits—he’d been handling infected monkey corpses for weeks with much less protection, and he felt fine. Wearing only a respirator, Dalgard led several Army officials into the monkey room, and he picked out the four sickest-looking monkeys to be studied.
The monkeys were euthanized and then Nancy Jaax took them back to USAMRIID for dissection. This time, she found clear signs of Ebola, including:
As the day went on, Jerry Jaax and his team euthanized the remaining 65 monkeys in the room, collecting samples of each monkey’s blood, liver, and spleen.
Three days after the monkey room sterilization, a second worker at the monkey house got sick. The monkey caretaker, identified as Milton Frantig, vomited, had a fever of 101 degrees, and became weak.
With two of the facility’s four employees sick, Dalgard grew more worried about the seriousness of the situation. He immediately drove to his company’s headquarters to make the case for evacuating and shutting down the Reston facility, and then turning the building over to officials at USAMRIID. The general manager agreed.
Dalgard told Peters and Russell that Hazleton would let the Army take over the monkey house for full sterilization. They drew up an agreement, and the Reston facility was officially under the Army’s charge.
Jerry Jaax and his team would need to go back into the monkey house to deal with the hundreds of animals that were still in the remaining rooms. He made sure that everyone on his team was willing to participate in the mission, and he instructed team members to say nothing to anyone about the operation. Taking on the entire facility would be the first major biohazard mission in the world.
Johnson and Jaax planned the logistics of the operation. The biohazard SWAT team would systematically work through one monkey room at a time, dealing with each monkey in five steps:
The group was split into subteams to perform the various tasks.
They set up the different areas they’d need to carry out the mission safely, including:
As Jerry Jaax and his team worked through the monkey house, he noticed that many of the sick monkeys were coughing, sneezing, and had running noses. It appeared that the virus was a mutated form of the Ebola virus that was airborne and flu-like.
After a few long, exhausting days, the Army finished euthanizing all 450 monkeys in the Reston facility. They had collected 3,500 samples for research.
Now it was time for the decontamination team to sterilize the building. The decon team scrubbed every inch of every surface with bleach, and they finished by gassing the building with formaldehyde. As standard practice, they placed swatches throughout the building that contained the spores of a harmless bacteria that are very difficult to kill; if the bacteria was dead by the end of the gassing, it’d indicate that the virus was also dead.
By the end of three days of gassing, the bacteria spores were dead. The decon team assumed the facility was clean and safe—but, as with any decontamination mission, there was no way to know for sure.
While Jerry Jaax’s team worked through the monkey house, an Army scientist managed to create a rapid test to detect Ebola virus in blood and tissue, called a rapid Elisa test. But when he tested samples from Frantig—the monkey caretaker who vomited and had the high fever—they came up clean.
Frantig was recovering in the hospital and feeling much better. It seemed now that he simply had the flu, so the CDC allowed him to return home.
When Frantig and Purdy—the monkey house worker who’d had a heart attack—each got sick without having had any cuts or blood exposure, it terrified the Army and CDC because it indicated that the virus had gone airborne. However, now both Frantig and Purdy appeared to be fine.
Meanwhile, Jahrling continued testing his and Geisbert’s blood for the virus, and they still tested negative for Ebola. It had been nearly three weeks since they’d sniffed the vial with the virus, and neither had shown any symptoms.
Either Jahrling, Geisbert, and the monkey house workers had dodged infection, or they were dealing with a new filovirus.
As the CDC tried to track down the origin of this virus, their investigation led back to the monkey storage facility in the Philippines that had sent Hazleton the shipment of monkeys. CDC researchers discovered that monkeys in that facility had also been dying, but the monkey workers were all fine.
This virus—which was later named Reston—appeared to be so similar to Ebola Zaire that it was hard to distinguish them in microscopic images. But two things were significantly different about Ebola Reston:
Researchers and officials at USAMRIID and CDC were stuck on several critical questions:
With still so much unknown about Ebola Reston, it remained classified as a Level 4 hot agent, despite the fact that it had yet to make any humans sick.
After the Army was confident that the Reston facility was sterilized, it returned the monkey house to Hazleton’s custody. Hazleton resumed importing monkeys from the same supplier in the Philippines, and, within a month, the Reston facility had another outbreak.
As a result, the CDC imposed serious restrictions on companies that imported monkeys to mandate stricter testing and quarantine practices. The CDC also temporarily revoked Hazleton’s license for quarantine violations—though officials still praised Hazleton for making the responsible decision to turn over the Reston facility to the Army during the first outbreak.
Because Ebola Reston didn’t appear to harm humans, the Army, CDC, and Hazleton agreed to isolate the monkeys inside the facility and let the virus work through them, instead of bringing the Army back in for another round of sterilization.
The virus traveled to every room, eventually killing the entire monkey population. Infected monkeys had flu-like symptoms, including:
Based on how the virus was moving through the monkey house and affecting the monkeys, the virus seemed to have mutated since the month prior, indicating it could quickly adapt to new hosts and survive significant changes in its environment.
As Ebola Reston ran through the facility, one of Hazleton’s animal caretakers—referred to as John Coleus—cut his thumb as he was performing a necropsy on one of the monkeys. The blade was covered in blood from the monkey’s liver, where Ebola virus particles tend to concentrate. There was no question he’d be infected.
However, Coleus appeared to be fine. Another health issue forced him to have a minor surgery shortly after he’d been exposed, but, unlike typical Ebola patients, his blood coagulated normally.
All four caretakers from the Reston facility—Coleus, Purdy, Frantig, and another worker—ultimately tested positive for Ebola Reston. But none of them ever broke with symptoms. Of the four, only Coleus was exposed through a cut, meaning Purdy and Frantig must have contracted the virus through the air.
When USAMRIID researchers viewed samples of infected monkeys’ lungs, they saw that the virus had gotten into the lungs, taken over the cells, and multiplied until the cells were bursting with virus particles. The virus was present in the lungs’ air spaces, so when the infected monkey coughed, the virus shot out with the sputum. The same would be true in infected humans.
Although the virus was harmless to people at that point, researchers worried that it could easily mutate to become just as deadly to people as the other filoviruses—and its airborne transmission would make the effects far deadlier.
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On one hand, the close contact required for transmission and the successful containment at Hazleton relieved some fear of a major epidemic or pandemic. On the other hand, all the questions that still remained about the filoviruses—including their hosts, where they originate, and how and why they emerge—amplified the fear of future outbreaks.
(Shortform note: Since the book’s publication in 1995, there have been Ebola outbreaks every few years, the majority of which have been Ebola Zaire. Most have been fairly small (less than 100 cases) and centered in Western Africa, but one was a far outlier: From 2013-2016, Ebola Zaire spread across 10 countries, infecting more than 28,000 people and killing more than 11,000.)
Four years after Ebola Reston hit the monkey house, the author, Richard Preston, took his own journey to Kitum Cave. Preston wanted to look around the cave, where the subject of all his research presumably originated.
When he arrived near Kitum Cave, he set up camp in the same area where Charles Monet had camped on New Year’s Eve, 13 years earlier.
The author knew all too well the risks the cave held. In an abundance of caution, he brought all the pieces of a Level 4 biological space suit for fieldwork, including a mask with air filters. He even brought bleach to decontaminate his suit after exiting the cave.
As the author approached and explored the cave, he was acutely aware of every possible virus host and exposure risk that he encountered, including:
In Preston’s route to Mount Elgon, he had to travel a stretch of the Kinshasa Highway, which stretched across Africa east-to-west, passing through Kenya, Uganda, and the Democratic Republic of Congo. When sections of Kinshasa Highway were paved in the 1970s (several sections still remain unpaved), the amount of traffic along the route boomed, ultimately leading to the spread of AIDS.
The origin of AIDS was just as murky as the origin of Ebola, but most experts agreed the viruses probably jumped to humans from primates in the same region around Mount Elgon.
When Ebola emerged, infections erupted like wildfire, quickly spreading and rapidly killing its victims. By contrast, HIV’s outbreak was a slow burn, because it incubated for years before its victims finally died.
Scientists have struggled to develop a vaccine for AIDS because the virus mutated so quickly. In fact, an infected person could die with multiple strains present in her body—all of which mutated from the single strain that originally infected her. The virus’s rapid adaptability also made it extremely resilient in the face of changes.
Preston mused that viruses like Ebola and AIDS could be the planet’s natural method of defending against the boom of human population and development. These and other emerging viruses originated in ecosystems under duress, and the strain was often due to human encroachment.
Rainforests—like the one on Mount Elgon—were fertile grounds for viruses because viruses lived in insects and animals, and the majority of the earth’s living things resided in rainforests. But rainforests around the world were also threatened by factors like deforestation and water degradation.
It was as if deadly viruses were like the earth’s immune system response against a harmful parasite: people.
Viruses lurk in all kinds of places—and they can emerge when you least expect it. Remain vigilant, cautious, and prepared.
What do you do regularly to keep yourself safe from microscopic threats, like viruses and bacteria?
How has learning about Ebola impacted the way you view the threat of viruses and potential epidemics?
What additional precautions will you take, if any, to protect yourself from viral and bacterial infections?
What’s your biggest takeaway about how communities and federal agencies can effectively handle outbreak threats?