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Nature’s Most Perfect Killing Machine

Ebola is nightmare fuel: a biological doomsday device conspiring with our bodies to murder us in uniquely gruesome fashion. It’s also killed fewer than 2,000 people. How has a virus with such a modest body count so fiercely captured the darkest corners of our imagination?

Nature’s Most Perfect Killing Machine

|| Image by Julia Dickens
 

Editor’s note: This story originally appeared in Hazlitt No. 2, and is reprinted here as it appears in that issue. Certain facts related to the scope and size of the current Ebola outbreak have changed since publication. The author, Leigh Cowart, is working on a follow-up story more directly related to the current outbreak, which will appear on Hazlitt in the coming weeks.

On October 13, 1976, Frederick A. Murphy, DVM, Ph.D., saw something that would terrify the masses for decades to come. A few days prior, a box containing a specimen from a patient in Zaire had arrived at the Centers for Disease Control in Atlanta in poor condition, the glass tubes broken in transit. Rather than send it straight to the autoclave for sterilization, his colleague Dr. Patricia Webb scavenged some fluid-soaked cotton from the damaged delivery. After the virus spent a few days in tissue culture—monkey kidney cells, to be specific—Murphy prepared a sample for examination with an electron microscope. When he saw it, the filamentous hook-and-loop formation now so recognizable, he immediately shut down the device. He had to return to where he prepared the sample. He had to bleach the area, to autoclave his equipment and his protective coverings. It was urgent.

He returned his attention to the sample, though. He thought he’d seen Marburg, a lethal filovirus capable of causing a viral hemorrhagic fever, and shot a cassette’s worth of pictures—not realizing he had, in fact, just become the first human to ever photograph the slender, looping tell of the Ebola virus.

Ebola. The name itself has become a synonym for horror. That a strand of 280 or so amino acids carrying little more than simple instructions and lucky keys for vertebrate locks can kill in such a fantastically gruesome manner is a testament to the ferocity of nature at the molecular core. It’s one thing to fear life forms at the macro level—to dread the shark in the water, to gawk at lacerations rimmed by skin flapping around like party streamers, to see the stump and hear the story and be filled with awe at the efficiency of an ancient apex predator. It’s quite another to contemplate your own body liquefying inside you, spilling through all of your available holes as you cling to life—to consider that something so deadly could have such stealth, present only in the bodily destruction it leaves in its wake.

Ebolaviruses and toothy leviathans of the deep do have something in common, though: they are both highly unlikely ways to die.

*

Ebola announced itself in 1976 with two simultaneous epidemics, though they were, in fact, different strains of the virus:Sudan ebolavirus (Sudan virus) and Zaire ebolavirus (Ebola virus). In Sudan, there were 284 cases and 151 deaths, for a fatality rate of 53 percent; in Zaire, that rate was 88 percent, with the virus killing 280 of the 318 people diagnosed.

In the almost four decades since, Ebola has done little to reveal its secrets. There is no predictable pattern to when outbreaks occur, no standard treatment, and no vaccine. We aren’t even certain where it hides between outbreaks, though some clues suggest fruit bats may be the reservoir. What we do know is that of the six known ebolaviruses, five can cause disease in humans. We know that the disease is transmitted by con- tact with the blood or bodily fluids of an infected animal. We know that the semen from a survivor can stay infectious for nearly two months. Oh, and my favourite fact: we know that you can kill it with soap.

You can’t deny mortality when death is on display in this way: bodies disintegrating, the sounds and smells of hot, sick blood and shit and bile erupting and oozing from a not-yet corpse. There will be no one to cradle the deceased, no comments about how they “look so peaceful,” like they’re “just sleeping.” There will not be a burial; there will be a disposal.

But no matter how much we know now, it is still an unpredictable and terrible visitor. In February of this year, an outbreak of Ebola began in Guinea; it has now spread to Liberia and, for the first time, Sierra Leone, infecting 297 people and killing 191. Initially thought to be the strain first seen in Zaire, it now appears to be a distinct species. It’s also the first time Ebola has been found in the Guinean capital of Conakry, a port city with a population of approximately 2 million. The World Health Organization has called this outbreak among their “most challenging” ever—even North America held its breath when a patient was quarantined in Saskatchewan under suspicion of having contracted the virus. Thankfully, authorities managed the risk well, and it turned out the patient, who had just returned from Liberia, didn’t actually have Ebola or any of its relatives. Still, that we heard of the quarantine at all—that it seemed perfectly plausible that it would be tied to the African outbreak—speaks to how deeply Ebola is embedded in our nightmares.

There is perhaps no other disease that captivates the imagination quite like Ebola. It’s served up as pure pop culture nightmare fuel, from Richard Preston’s The Hot Zone, the 1994 non-fiction thriller that chronicled the early days of Ebola, to the fictionalized monkey-hosted virus in 1995’s Outbreak. Even The Walking Dead’s zombies are of the infectious variety, bleeding from their dead eyes in between bites of human flesh. It’s hard to imagine something worse than a virus that leaves people to die in the decaying wreckage of their own cytokine storm, bodies that leak with blood and death, commandeered and turned into Ebola replication machines.

No disrespect, of course, to death by starvation. Or cancer. Or measles.

Part of the horror of Ebola is that it shatters the idea of a “good death.” You can’t deny mortality when death is on display in this way: bodies disintegrating, the sounds and smells of hot, sick blood and shit and bile erupting and oozing from a not-yet corpse. There will be no one to cradle the deceased, no comments about how they “look so peaceful,” like they’re “just sleeping.” There will not be a burial; there will be a disposal.

But dead is dead is dead. And Ebola, for all its evils—implied and whispered or seen and smelled—could actually be a whole lot worse.

*

On August 26th, 1976, a 44-year-old teacher appeared at Yambuku Mission Hospital in Zaire with a fever and what he thought was malaria, and received an injection of the antimalarial drug chloroquine. At the time, the hospital had 120 beds and a medical staff of 17, and ran an outpatient clinic that treated 6,000- 12,000 people monthly. Each morning, administrators issued five syringes and needles to the nursing staff, to be used in the outpatient department, the prenatal clinic, and the inpatient wards. According to a report from the World Health Organization, “[t]hese syringes and needles were apparently not sterilized between their use on different patients but rinsed in a pan of warm water. At the end of the day they were sometimes boiled.”

After the injection, the man’s fever resolved quickly. On September 1, it came back. He was admitted to YMH four days later with gastrointestinal bleeding and died three days after that. By the end of September, when the hospital closed, 11 of its 17 staff members were dead.

Your body contains everything Ebola needs to make more of itself: by providing the blueprint for more virons, the virus uses your own cellular machinery to replicate. And when the cell is packed full of copies of Ebola, the virons bud off in a little envelope of your own cell membrane. Which means that, at least on the outside, the Ebola virons in your body look like you.

The needle that slipped into the schoolteacher’s vein emerged with a stowaway, of which other veins, in other patients, would be the macabre recipients. Bloodborne pathogens such as HIV and Hepatitis B and C spread the same way. What’s interesting about ebolavirons, though, is that when they gain entry into a human host, rather than build slowly like measles or rubella, they waste no time getting to work. They can’t, if they want to replicate. But first, the virus must use your own cellular equipment to make itself infectious. And ultimately, that’s how it kills you.

Monsters that live in the dark are often far more terrifying than those subjected to the bright lights of inquiry and context. Reducing them to something we can catalogue turns their unimaginable horror into something more familiar. There’s a reason H.P. Lovecraft left his horrors undefined: your brain, left to its own devices, can and will conjure fear on a grand scale. And so it is with Ebola: we know the horrors of “average” deaths. There’s at least a general idea of how cancers kill, or heart attacks, or strokes. But Ebola, far away and ripe for the imagination, has grown legendary—and, like most legends, the truth is not quite as awesome as the tale. But before we wake ourselves up from this nightmare, let’s bask in the mechanics of this notorious killer.

An Ebola viron consists of seven structural proteins and some instructions. That’s pretty much it. The instructions are encoded in a single strand of negative- sense RNA, which is to say, they are written backwards: the host cell cannot make copies of it as-is. So, upon gaining entry to the cell, Ebola translates itself into something the host can read: positive-strand antigenomes, which are the literal opposite of Ebola’s RNA. Think of it like holding text up to a mirror—it appears backwards; if you want to read the text in the mirror, you have to flip it. The Ebola viron brings along a bit of equipment for this purpose, the result of which is a bunch of material that can be read in the mirror, so to speak. And so, the host cell, inundated with a deluge of single- stranded RNA—the kind it’s used to seeing—transcribes them, turning all of that “opposite day” Ebola into plain, straight murderbus Ebola.

What this means is that your body contains everything Ebola needs to make more of itself: by providing the blueprint for more virons, the virus uses your own cellular machinery to replicate. And when the cell is packed full of copies of Ebola, the virons bud off in a little envelope of your own cell membrane. Which means that, at least on the outside, the Ebola virons in your body look like you. Through this borrowed lipid membrane goes a spiky glycoprotein, the key Ebola uses to unlock the next cell and begin the process anew.

Of course, this is all for naught if Ebola gets caught. After all, while your body contains all the ingredients necessary to replicate the virus’s RNA, it also contains everything you need to kill the virus before it takes hold. In order to survive, Ebola secretes a glycoprotein that, to hastily butcher the science, allows it to evade detection by messing with the ability of your immune system to sound the alarm. Neutrophils, a type of white blood cell, are like your body’s first responders. Appearing within minutes of trauma, these phagocytes show up to protect you by eating bad shit. (Also, fun fact: they’re the main ingredient in pus, and the reason it’s kind of yellowish.) So, if you think of neutrophils as ambulances, Ebola comes in and shuts down all communication with dispatch.

To Ebola, we are nothing but machinery. And it is our own machinery that conspires to kill us.

An effective response to an outbreak is surprisingly simple. Modest containment efforts, such as gowns and gloves and dilutions of bleach, tend to be successful. People who are infected with Ebola, after all, aren’t out running around spreading the disease for long before they’re too sick to leave the bed.

The presence of viral particles and cell damage unleashes a riot in the body. Infected cells pump out cytokines, small molecules that signal inflammation and fever. This cytokine storm is toxic—a crucial step in the march to liver failure and hemorrhage. Meanwhile, Ebola virons tear through the body, reproducing quickly and killing tissues, leaving little dead zones in their wake. The body can only attempt to compensate for this for so long; soon, tiny blood clots start to form, sticking to the sides of blood vessels. These clots recruit other clots, which leads to blockages, which leads to tissues dying due to lack of oxygen. The body is losing the fight. With clotting factors used up, for about half of those infected, the hemorrhaging begins.

*

From the detached perch of a dis- passionate scientist, it’s easy to see how one might find the Ebolaviruses beautiful: so efficient, so skilled in their purpose, so fascinating in their impressive ability to replicate within a host. And to us on the outside, those glued to the news with a sick pit of dread that collects with the knowledge that these viruses exist in the same world as international air travel, Ebola has become the platonic ideal of a doomsday slate-wiper.

But what of those who see its scourge up close—healthcare workers who risk their lives tending its victims, the medical establishment’s answer to firefighters who rush into a four-alarm blaze?

Craig Manning is a member of the CDC’s Viral Special Pathogens branch. He’s a communications specialist who’s been deployed on missions such as the 2008 outbreak of Rift Valley Fever in Madagascar and 2007’s outbreak of Ebola in Uganda. When I spoke with him recently, he’d just returned from the site of the current Ebola outbreak in Guinea. “If you ask me if I’d rather be in a room with influenza patients or I’d rather been in a room with Ebola patients,” Manning says, “I would tell you I’d rather been in a room with Ebola patients.”

“Because I know what to do to protect myself. Whereas with influenza, which is airborne, any protective measures in that confined space are probably not going to be effective. Ebola is not that easy to transmit person to person, but influenza very easily transmits from person to person.”

Manning has a certain rhythm to his speech that is immediately soothing—which, I imagine, is an excellent trait in his line of work, handling health communication and education in the midst of outbreaks of viral hemorrhagic fevers. His first experience with an Ebola outbreak was in 2007 in Uganda, where 39 of the 116 patients succumbed to the disease. Was he scared?

“I was, actually.” He chuckles slightly as he says this. “I think what happens over time, especially if you work with virologists that study Ebola and epidemiologists that study Ebola, and people whose careers have been built around the study of dangerous viruses, you become not accustomed or habituated, but you become better informed. You know where the real risk lies.”

Apparently, it’s not with Ebola: since its emergence in 1976, there have been 2,586 cases of Ebola virus disease in humans and 1,717 deaths. While that’s a fatality rate of 66.4 percent, or roughly two out of every three patients, influenza kills approximately 500,000 people every year. In 38 years, Ebola has killed a little less than 2,000 people. The flu? Nineteen million.

*

I first read Richard Preston’s The Hot Zone when I was 11 years old or so, and have since been in the habit of weighing every potential catastrophe against “death by Ebola virus disease.” The book is lurid and dramatic; the iconography of a dying patient crying blood and shitting out their intestines is, I admit, compelling. Terror-inducing as it may be, though, it’s perhaps not the most accurate portrait of the threat this particular monster poses.

“People ask, what’s the real risk of it coming to the US?” Manning says. In response, he talks about the sophistication of the United States’ public health preparedness. “There are systems in place whereby patients can be isolated quickly, health staff are wearing some amount of protective equipment, and the diagnostic laboratory testing tools are there quickly, on hand.” There is the additional security of pathogen awareness. If a person returned from Africa with fever and other compatible symptoms, it wouldn’t be long before that person was isolated. “So the prospect of further, onward transmission is pretty darn small.

“I think some people imagine it’s a short leap on an airplane, and I suppose in one sense it is. But a number of other things would have to occur such that there would be successful transmission and sub sequent infection in even one more person.”

Fearing Ebola is morbid escapism, a way to flirt with the inevitability of our own demise, to ponder the frailty of our own ineffectual meat sacks. Ebola is our macabre fantasy not because it’s likely, but because it isn’t. To many in the West, Ebola matters not because of what it does and how it kills; it matters because of what it represents.

An effective response to an outbreak is surprisingly simple. Modest containment efforts, such as gowns and gloves and dilutions of bleach, tend to be successful. People who are infected with Ebola, after all, aren’t out running around spreading the disease for long before they’re too sick to leave the bed.

The virus is too hot—choke the supply of new hosts and it smothers itself.

Yet, in this current outbreak, the Guinean capital of Conakry saw its first formal cases of Ebola ever. And this is no rural town or remote area: this is Ebola in a port city roughly the size of Montreal. What do you do when Ebola hits a port city the size of Montreal?

“The first thing you do when you get on the ground,” Manning says, “is establish who’s here, who’s in charge, and how is it that we are going to be working together and where, and how will we communicate with each other.” This means acquiring local cell phones and SIM cards, as well as getting in touch with all the potential players, such as the WHO and the relevant Ministries of Health. In the case of a city outbreak, rather than a more rural one, that also means alerting the media. When the CDC reached out to the US Embassy in Conakry regarding this outbreak, the embassy supplied them with a comprehensive list of media contacts. “So rather than us having to go out and figure out who are the major newspapers, which are the major radio stations, and so on and so forth, all of that was basically established and presented to us beforehand, so that we could basically leverage our time very efficiently while being in the city.”

The mission for Manning and the rest of the response team from the CDC was to use these platforms to not only educate a population of approximately 2 million, but to assuage panic. Driving around the city, they’d listen to the radio for mentions of the virus, to gauge how well their message was spreading. Manning noted the importance of always driving with the windows down in the van, no matter the heat index; you don’t want people thinking you’re trying to deliberately separate yourself from the population. When the radio mentions of Ebola persisted beyond the first week and into the second, he took this as a good sign: the message was getting out.

“People came round to the idea that unless they were in contact with infectious bushmeat,” he says, “or unless they were involved in the care and treatment of an Ebola patient at home, or unless they were involved in a clinical setting where gloves were not used—perhaps in a remote, rural clinic—anybody who was not one of those three groups basically had very, very little risk.”

To hear Manning discuss these efforts paints a much different picture of what it takes to manage and contain an outbreak. Sometimes it means going village to village and answering individual questions. (“If my wife has Ebola and vomits on the floor, and a chicken eats the vomit, can I eat the chicken?” Answer: chickens make bad hosts for Ebola, but if the preparer comes into contact with vomit or blood remaining on the chicken during preparation, or the chicken still has Ebola inside it and is not cooked properly, it can be infectious. But a properly cleaned and cooked chicken? Safe to eat.) Sometimes it means orchestrating a tour of a Médecins Sans Frontières clinical management centre for the leaders of the communities, letting people see the real scope of the threat, and showing them the risk is not so high as to threaten those in the immediate vicinity. And sometimes it means launching a campaign to correct a rumour, like the one about how Ebola spreads because of infected money.

Maybe our obsession with the horrors of Ebola says more about us than anything else. That it kills so rarely, and, for many of us, so far away makes it more nightmarish to contemplate. Absolutely horrific, sure, and yet, could you really argue that stage IV metastatic cancer is any less gruesome? Fearing Ebola is morbid escapism, a way to flirt with the inevitability of our own demise, to ponder the frailty of our own ineffectual meat sacks. Ebola is our macabre fantasy not because it’s likely, but because it isn’t. To many in the West, Ebola matters not because of what it does and how it kills; it matters because of what it represents.

Fitting, then, that Ebola is often described as looking like a shepherd’s hook. A reminder that we, too, are animals in nature’s flock, merely biding our time until the shepherd culls the herd— however that may be. Those initial Ebola outbreaks occurred in 1976, the same year smallpox was eradicated from the planet—one plague taking the place of another. Since then, we’ve seen our antibiotics start to fail, and vaccine- preventable ills of yore come surging back with a vengeance. We’ve seen SARS, and MERS, and tuberculosis resistant to everything in our arsenal. What’s next is anyone’s guess. The future of infectious disease is impossible to predict, save for one certainty: in the arms race between humanity and nature, never bet against the house.