Just how long does the Ebola virus linger in semen?

The 2013-2016 West African Ebola virus outbreak altered our perception of just what an Ebola outbreak could look like.

While none of the three primary affected countries–Liberia, Sierra Leone, and Guinea-have had a case since April 2016, the outbreak resulted in a total of over 28,000 cases of Ebola virus disease (EVD)–65 times higher than the previous largest EVD outbreak, and more than 15 times the total number of cases of all prior EVD outbreaks combined, from the virus’s discovery in 1976 to a concurrent (but unrelated) outbreak in the Democratic Republic of Congo in 2014.

In March 2016, cases were identified once again in both Liberia and Guinea, just after the outbreak had been declared over. Both countries were declared Ebola-free in June 2016; Guinea for the second time and Liberia for the fourth time. The last series of cases in these countries demonstrated just how different this epidemic was from prior ones, changing what we thought we knew about the virus:

Previous research suggested Ebola could persist in the semen for 40 to 90 days. But that window has been eclipsed in this epidemic by a considerable amount. A probable case of sexual transmission occurred approximately six months after the patient’s initial infection last year in Liberia. Another study found evidence of Ebola in the semen of 25% of surviving men tested seven to nine months after infection. And it takes only a single transmission to kick off a fresh recurrence of the disease.

A recent paper extended this window of virus persistence in the semen even longer–over 500 days. It also explains how the outbreaks began in both countries after being declared Ebola-free–so where did the virus come from?

In a convergence of old-fashioned, “shoe leather” epidemiology/tracing of cases and viral genomics, two converging lines of evidence led to the identification of the same individual: a man who had been confirmed as an EVD case in 2014, and had sexual contact with one of the new cases. Author Nick Loman discussed via email:

The epidemiologists told us independently that they had identified a survivor and we were amazed when we decoded the metadata to find that case was indeed the same person. The sequencing and epidemiology is tightly coordinated via Guinea’s Ministry of Health who ran National Coordination for the Ebola outbreak and the World Health Organisation.

It shows that the genomics and epidemiology works best when working hand-in-hand. If we’d just had the genomics or the epidemiology we’d still have an element of doubt.

The sequencing results also suggested that it was likely that the new viral outbreak was caused by this survivor, and unlikely that the outbreak was due to another “spillover” of the virus from the local animal population, according to author Andrew Rambaut:

If the virus was present in bats and jumped to humans again in 2016, it might be genetically similar to the viruses in the human outbreak but not have any of the mutations that uniquely arose in the human outbreak (it would have its own unique mutations that had arisen in the bat population since the virus that caused human epidemic).

It might be possible that the virus jumped from humans to some animal reservoir in the region and then back to humans in 2016 but because we have the virus sequence from the patients acute disease 15 months earlier we can see that it essentially exactly the same virus. So this makes it certain the virus was persisting in this individual for the period.

So the virus–persisting in the survivor’s semen for at least 531 days–sparked a new wave of cases. Ebola researcher Daniel Bausch noted elsewhere that “The virus does seem to persist longer than we’ve ever recognized before. Sexual transmission still seems to be rare, but the sample size of survivors now is so much larger than we’ve ever had before (maybe 3,000-5,000 sexually active males versus 50-100 for the largest previous outbreak) that we’re picking up rare events.”

And we’re now actively looking for those rare events, too. The Liberia Men’s Health Screening Program already reports detection of Ebola virus in the semen at 565 days following symptoms, suggesting we will need to remain vigilant about survivors in both this and any future EVD epidemics. The challenges are clear–we need to investigate EVD survivors as patients, research participants, and possible viral reservoirs–each of which comes with unique difficulties. By continuing to learn as much as we can from this outbreak, perhaps we can contain future outbreaks more quickly–and prevent others from igniting.

Mike Adams and NY Post promote more hysteria over Ebola

I’ve been asked several times about this NY Post article on the CDC’s “admission” that a sneeze could spread Ebola. The Post (which, I should note, is the least credible newspaper in New York City, for those not familiar with the paper) suggests that the CDC has changed their tune regarding the spread of Ebola.

Except, they haven’t, and this is a ridiculous, trumped-up non-story, passed along not only by the Post but by others of the typical suspects like conspiracy theorist extraordinaire Mike Adams, aka “The Health Ranger” of Natural News.

Here’s what the NY Post claims:

“Droplet spread happens when germs traveling inside droplets that are coughed or sneezed from a sick person enter the eyes, nose or mouth of another person,” the poster states.

Nass slammed the contradiction.

“The CDC said it doesn’t spread at all by air, then Friday they came out with this poster,” she said. “They admit that these particles or droplets may land on objects such as doorknobs and that Ebola can be transmitted that way.”

Of course, no poster is linked in their article, so I feel like I’m playing a game of telephone, trying to figure out just what has been added.

The NY Post article is basically messing up the definition of “airborne,” as I and others have discussed ad nauseum. The kind of contact the NY Post describes above isn’t “airborne,” as measles or chickenpox are, where one can come into a space that had been occupied by an infected person, breathe in the suspended virus, and get ill. With Ebola, you have to have *direct contact* with a person’s secretions. So their entire story (not surprisingly, due to their tabloid-y nature) is based on either a purposeful or accidental incorrect definition of just what it means to be “airborne.”

Adams takes it one step further, suggesting that CDC not only misinformed, but revised history; that a poster was  “scrubbed” from CDC’s site because it supported “airborne” transmission.

From what I can tell, Adams claims this poster (which he saved) was removed from the CDC site, and replaced by this file. Adams claims that the latter is “entirely empty,” so he may have tried the link before it went live? I have no idea. In any case, the two documents are almost identical in content. Both note that droplet spread can happen, when “germs traveling inside droplets that are coughed or sneezed from a sick person enter the eyes, nose, or mouth of another person” in the first poster, and “droplets that are coughed or sneezed from a sick person splash the eyes, nose, or mouth of another person” in the second poster.

Wow, that’s a sinister difference there.

You can see that both documents still show a picture of doorknobs as possible fomites for transmission (possible in theory, but they’d have to be heavily contaminated by a person late in the disease). It appears that CDC just did a minor redesign of the poster, with the first having an emphasis just on Ebola and the second version trying to be more of an explainer on “air vs. droplet spread,” with Ebola as the example. The content is almost exactly the same: the first portion defines “airborne” spread; the second “droplet” spread; the third focuses on how one protects oneself from getting sick; and the final one clarifies that Ebola is not spread by air, but it could be by droplets. There are minor wording changes as I noted above, but that’s it.

This is nothing new. There’s never been a conspiracy to suggest that droplet transmission can’t happen–but the CDC and others have tried to emphasize that droplet transmission is still direct contact. That’s what people like Adams don’t want to accept. They assume because those droplets travel via air, it’s “airborne,” taking a layman term instead of one accepted and used by the scientific community. Now, given, I understand this can be a source of confusion as scientific terms frequently are. Virologist Ian Mackay has even solicited ideas for other terms to describe such transmission, and make it more clear to the general public what the difference is. But either way, the usage has been clear from the beginning and I guarantee Adams understands the difference. He just doesn’t care.

And now I just spent a half hour of my life to uncover that vast governmental conspiracy-that-wasn’t. Not that it will stop Adams or the NY Post from misinforming and driving fear of the virus and distrust of the government, because *that’s what they do.* Adams is making a pretty penny, I’m sure, off of his absurd Pandemic Prevention kits (only $99 or $199! Bargain!). Perhaps I should get into a different and more lucrative business, because if you believe shtick from Adams or the Post over the CDC or, hey, a trained epidemiologist like myself, I just may have a shiny bridge to sell you.

Granny’s mean pot of bushmeat stew

Left to right, Granny Beck, my Grandma June, and Great-Great Grandma Bertha, circa 1961. Who knows what was on the menu that day.

My Great-Grandpa and Granny Beck were, in some ways, ahead of their time. My Grandpa’s mom and step-dad, they both went through scandalous divorces and then switched partners with another couple, Granny Orpha marrying Wade and my Grandpa’s dad Lee marrying Wade’s ex-wife, Edna. Orpha and Wade raised 5 of Orpha’s boys together, and had a daughter after the divorce/remarriage.

By the time I was born, my Granny Beck was in her 80s, and I have only vague recollections of going over to visit her at her home. But I remember hearing about her cooking. I was a picky eater anyway, and my mom once told me she was always afraid to eat Granny Beck’s stew, because it could be rabbit, it could be ‘possum, it could be squirrel, it could be groundhog…you just never knew. I never ate anything over there.

Grandpa Beck used to have coon dogs, and would bring home anything that the dogs would catch. My great-aunt affirmed my mom’s recollection of Granny Beck’s cooking (and Grandpa Beck’s eating):

My mom did cook some pretty weird things. We always had wild game such as rabbit and pheasant, but I do remember when she cooked a raccoon (I didn’t try it!). My dad was the one that would eat anything, and I do mean anything! We used to bring him such things as chocolate covered ants, pickled pigs feet, and pickled rooster combs. He loved them!

Over the weekend, my neighbor sent along some meat packages for us. He had recently gotten back from another hunt and bagged his third deer of the season (you’re allowed four per year in my county). He was grilling when my partner stopped over on the way home, and sent some ground deer (I think–I’ve not opened the package yet), deer steaks, and a still-warm hunk of a deer heart, well done.

Deer assortment
Various deer parts brought over by my neighbor this weekend.


All of this is to say that we can eat some really weird things here in the “civilized,” first-world, developed United States.

Why bring this up now? The current Ebola outbreak has brought out all kinds of biased to outright racist views of Africa and disease. Because it’s postulated that the outbreak started with the consumption of or contact with an infected animal—possibly a fruit bat, which the index family noted they do hunt—people have come out of the woodwork to pontificate on how those in Guinea and other countries “brought this on themselves” because of their consumption of “bushmeat,” and that they’re so uneducated and backwards to eat that in the first place–because really, how could people eat that stuff, especially when it could be diseased?

Prominent magazines run pictures of butchered meat and primates with headlines that are intended to scare and “other.”

People judge harshly, partly because of bush meat consumption:

“Is it time that we drag ignorant, superstitious third world Africans kicking and screaming into the 21st century or should we stop giving aid to Africa and let them fend for themselves? Would the later propel the former?”

Even though we do the same. damn. thing. in the United States.

“Bushmeat” is the name given to pretty much any kind of wild game hunted in Africa–bats (obviously a concern given their possible role in Ebola spread and maintenance of the virus); primates; birds, duikers, lizards, crocodile, various rodents, even elephant, and more.

What do we call “bushmeat” in the US? Or just about everywhere else?

Just “wild game,” or some variation thereof.

In the U.S., we hunt thousands of deer, elk, pheasant, turkey, rabbit, and other animals every year. There are even wild game restaurants that cater to those tastes (though many “wild game” species are actually farmed to some degree). Yet even the bushmeat page at United States’ Fish and Wildlife Service ignores the hunting that goes on in the United States, noting that:

Here in the United States, we have laws that control the preparation, consumption, and trade of meat, ensuring that animals are treated appropriately, kept healthy, and sold legally. This is not the case in some countries in Africa and other parts of the world.

This seems to refer mostly to domestically-raised meats, as it’s much harder to police the treatment, health, and sale of hunted animals. Though one needs a license to hunt many animals and generally to fish, laws vary from state to state. Here in Ohio, though a hunting license or permit needs to be obtained for most types of hunting or trapping, and there may be limits on the number of animals of certain species one can kill per season (such as deer and turkey), for most animals, there’s merely a daily limit (6 squirrels, 4 rabbits, etc. per day). For other animals, including fox, raccoon, skunk, opossum, weasel, crow, groundhog, and coyote, there is no daily bag limit. So one could, conceivably, feed themselves fairly well on just a diet of wild game if they had the time and inclination to do so.

Of course, most people in the U.S. don’t get our food this way. We look at Daryl Dixon of the Walking Dead and his squirrel-hunting prowess as something that could carry one through the zombie apocalypse, but not school lunches for a family of 4. We think it’s awesome when he finds an opossum in a cupboard and proclaims, “Dinner!” I’m sure many readers have plans for their own apocalypse survival plan, which likely involve some kind of wild source for food.

But in modern-day Africa, such hunting is somehow “barbaric” and “backward,” regardless of whether it is for sustenance or trade.

Though Ebola has not been identified in wild animals in the US, our animals are far from disease-free. No wild (or domesticated) animal is. We certainly can find Tularemia and Pasturella in rabbits; deer can carry tuberculosis, Brucella, Hepatitis E, and maintain transmission of Lyme disease and potentially Erlichia. Other zoonotic pathogens that could be acquired from a variety of wild animals include Campylobacter, E. coli, plague (mainly in the Southwestern United States); Cryptosporidia, Giardia, avian influenza from waterfowl, rabies (more likely from handling than ingestion); hantavirus, Trichinella, Leptospira, Salmonella, Histoplasma, and I’m sure many more from handling or consumption of wild animals.

Finally, while people malign “bushmeat” hunters in Africa, let’s not forget that almost any source of food can be contaminated with potential pathogens. Even in the United States, 1 in 6 Americans (48 million people) get sick, 128,000 are hospitalized, and 3,000 die of foodborne diseases. Every year. And that’s with our “high standards” for animal husbandry and processing.

So perhaps rather than looking to countries in Africa and judging their food consumption habits as they relate to infection, we should turn a mirror to our own. If we don’t judge Granny Beck for her wild game consumption, neither should we judge those a continent away.

Additional readings

The long and ugly tradition of treating Africa as a dirty, diseased place

If you can’t be a good example, be a warning. How EcoInternet’s #Scicomm #Fail can make you a more culturally aware science communicator

 American Bushmeat

“The Hot Zone” and the mythos of Ebola

The Hot Zone was first released in 1994, the year I graduated high school. Like many readers, that book and Laurie Garrett’s The Coming Plague* really sparked my interest in infectious diseases. In some sense, I have those books to thank (or blame?) for my career.

But I’m still going to criticize The Hot Zone, because as a mature infectious disease epidemiologist and a science communicator in the midst of the biggest Ebola outbreak in history, The Hot Zone is now one of the banes of my existence. A recent article noted that the book is back on the bestseller list, going as high as #7 on the New York Times list recently, and #23 on Amazon. It’s sold over 3.5 million copies, and it’s reported as “a terrifying true story.” Many people have gotten almost all of their Ebola education from just The Hot Zone (as they’ve told me over, and over, and over in the comments to this blog and other sites).

Here’s why The Hot Zone is infuriating to so many of us in epidemiology and  infectious diseases.

First–the description of symptoms.Preston himself admits that these were exaggerated. Over and over, he uses words like “dissolving,” “liquefy,” “bleeding out” to describe patient pathology. (If I had been playing a drinking game while reading and did a shot every time Preston uses “liquefy” in the book, I’d be dead right now).

Of a Marburg patient, pseudonymously named Charles Monet, he describes him as

“…holding an airsickness bag over his mouth. He coughs a deep cough and regurgitates something into the bag. The bag swells up….you see that his lips are smeared with something slippery and red, mixed with black specks, as if he has been chewing coffee grounds. His eyes are the color of rubies, and his face is an expressionless mask of bruises. The red spots…have expanded and merged into huge, spontaneous purple shadows; his whole head is turning black-and-blue…The connective tissue of his face is dissolving, and his face appears to hang from the underlying bone, as if the face is detaching itself from the skull…The airsickness bag fills up to the brim with a substance known as the vomito negro, or black vomit. The black vomit is not really black; it is a speckled liquid of two colors, black and red, a stew of tarry granules mixed with fresh red arterial blood. It is hemorrhage, and smells like a slaughterhouse….It is highly infective, lethally hot, a liquid that would scare the daylights out of a military biohazard specialist…The airsickness bag is brimming with black vomit, so Monet closes the bag and rolls up the top. The bag is bulging and softening, threatening to leak, and he hands it to a flight attendant.

“…the body is partly transformed into virus particles…The transformation is not entirely successful, however, and the end result is a great deal of liquefying flesh mixed with virus…The intestinal muscles are beginning to die, and the intestines are starting to go slack…His personality is being wiped away by brain damage…He is becoming an automaton. Tiny spots in his brain are liquefying…Monet has been transformed into a human virus bomb.

“…The human virus bomb explodes…The victim has “crashed and bled out.”…He becomes dizzy and utterly weak, and his spine goes limp and nerveless and he loses all sense of balance….He leans over, head on his knees, and brings up an incredible quantity of blood from his stomach and spills it onto the floor with a gasping groan. He loses consciousness and pitches forward onto the floor. The only sound is a choking in his throat as he continues to vomit while unconscious. Then comes a sound like a bedsheet being torn in half, which is the sound of his bowels opening and venting blood from the anus. The blood is mixed with intestinal lining. He has sloughed his gut. The linings of his intestines have come off and are being expelled along with huge amounts of blood. Monet has crashed and is bleeding out.”

And later, at autopsy:

“His liver…was yellow, and parts of it had liquefied–it looked like the liver of a three-day-old cadaver. It was as if Monet had become a corpse before his death…Everything had gone wrong inside this man, absolutely everything, any one of which could have been fatal: the clotting, the massive hemorrhages, the liver turned into pudding, the intestines full of blood.”

And I didn’t even get to what Preston says about Ebola and testicles. Or pregnant women. Seriously, there’s pages upon pages upon pages of this stuff.

Throughout the book, Preston presents these types of symptoms as typical of Ebola. Not “in worst case, this is what Ebola could do,” but simply, “here’s what happens to you when you get Ebola.” It’s even beyond a worst case scenario, as he notes in part: “In the original ‘Hot Zone,’ I have a description of a nurse weeping tears of blood. That almost certainly didn’t happen.”

Compare that to just about any blog post by actual workers with Médecins Sans Frontières, healthcare workers on the front lines of this and many previous Ebola outbreaks. Stories are scary enough when the reality of the virus is exposed, and with it the dual affliction of poverty and the terrible health system conditions of affected countries. I interviewed MSF’s Armand Sprecher a few years back during a different Ebola outbreak, and he noted this about symptoms–quite different from the picture Preston paints:

The patients mostly look sick and weak. If there is blood, it is not a lot, usually in the vomit or diarrhea, occasionally from the gums or nose.

The clinical picture of Ebola that people take away from The Hot Zone just isn’t accurate, and with 3.5 million copies sold, is certainly driving some (much? most?) of the fear about this virus.

Second, airborne Ebola. Though this trope is often traced back to “Outbreak,” Preston clearly suggests that both Zaire Ebolavirus and Reston Ebolavirus can be airborne. What he never discusses nor clarifies is that the “evidence” for this potential airborne spread is really thin, and not even indicative of animal-to-animal or animal-to-person transmission.

Rather, it’s much more likely that if airborne spread was involved, it was aerosols generated by husbandry (such as spraying while cleaning cages), rather than ones which would have been generated by infected primate lungs (a necessary step for primate-to-primate transmission via a respiratory route). Indeed, this is the paper that Nancy Jaax et al. published on the findings Preston talks to Jaax about, 13 years after the fact (the experiment is marked as 1986 in The Hot Zone), and noting that transmission due to husbandry practices could not be completely ruled out. It’s unclear also that the Reston strain moved through the primate facility via air, rather than via spread due to caretakers, equipment, or husbandry. Nevertheless,  it’s frequently cited as fact and without any qualification that Reston is an airborne type of Ebola.

Instead, here is what Preston says about it:

“If a healthy person were placed on the other side of a room from a person who was sick with AIDS, the AIDS virus would not be able to drift across the room through the air and infect the healthy person. But Ebola had drifted across a room. It had moved quickly, decisively, and by an unknown route. Most likely the control monkeys inhaled it into their lungs. ‘It got there somehow,’ Nancy Jaax would say to me as she told me the story some years later. ‘Monkeys spit and throw stuff. An when the caretakers wash the cages down with water hoses, that can create an aerosol of droplets. It probably traveled through the air in aerosolized secretions. That was when I knew that Ebola can travel through the air.'”

He then comes back to “airborne Ebola” several times, based in part on this idea.

But here’s the thing. Just about any virus or bacterium could be aerosolized this way–via high pressure washing of cages, for example. If it can bind to lung cells and replicate there, as we already know Ebola can, it can cause an active infection.

But that’s not the same as saying “Ebola can drift across the room” from one sick person to a healthy person and cause an active infection, as Preston tries to parallel with HIV in the above paragraph. Even in Jaax’s experiment and others like it, there’s zero evidence that primates are expelling Ebola from their lungs in a high enough concentration to actively infect someone else. And that is the key to effective airborne transmission. Think of anthrax–if it’s released into the air, we can inhale it into our lungs. It can replicate and cause a deadly pneumonia. But anthrax isn’t spread person-to-person because we don’t exhale the bacteria–we’re dead ends when we breathe it in. This is what happens with primates as well who are experimentally infected with Ebola in a respiratory route, but Preston implies the opposite.

Third, if it wasn’t for points one and two, The Hot Zone really could be read as a “damn, Ebola really isn’t that dangerous or contagious so I have little to worry about” narrative. Preston describes many “near misses”–people who were exposed to huge amounts of “lethally hot” Ebola-laden body fluids, but never get sick–but doesn’t really bother to expose them as such. All 35 or so people on the little commuter plane Monet flies on between his plantation in western Kenya and Nairobi, deathly ill, vomiting his coffee grounds and dripping nasal blood into the airsickness bag he handed to a flight attendant–none of them come down with the disease.

The single secondary infection Monet causes is in a physician at the hospital where he’s treated, after his bowels “ripped open” like a bedsheet. That physician, Shem Musoke, not only swept out Monet’s mouth until “his hands became greasy with black curd” but also was “showered” with black vomit, striking him in the eyes and mouth. Monet’s blood covered Musoke’s “hands, wrists, and forearms,” because “he was not wearing rubber gloves.” Musoke developed Marburg virus disease, but survived–one of the few secondary cases of infection described in the book.

Another “close call” was that of Nurse Mayinga N. She had been caring for one of the Ebola-infected nuns at Ngaliema Hospital in Kinshasa during the 1976 outbreak in Zaire, the first detected entry of Zaire Ebolavirus into the human population. Beginning to feel ill herself, she ditched her job and disappeared into the city for two days. She took a taxi to a different, larger, hospital in the city, but was sent away with a malaria shot. She’s examined at a third hospital and sent away. Finally she returns to Ngaliema hospital and is admitted, but by that time, had caused a panic. Preston says:

“When the story reached the offices of the World Health Organization in Geneva, the place went into full-scale alert…Nurse Mayinga seemed to be a vector for an explosive chain of lethal transmission in a crowded third-world city with a population of two million people. Officials at WHO began to fear that Nurse Mayinga would become the vector for a world-wide plague. European governments contemplated blocking flights from Kinshasa. The fact that one infected person had wandered around the city for two days when she should have been isolated in a hospital room began to look like a species-threatening event.”

How many secondary cases were the result of Mayinga N’s wanderings? That possibly “species-threatening” event? Preston again devotes several paragraphs to Mayinga’s gruesome illness and death, and notes that 37 people were identified as contacts of hers during her time wandering Kinshasa. He tells us they were quarantined “for a couple of weeks.”

The fact that exactly zero people were infected because of Mayinga’s time in Kinshasa merits half a paragraph, and not dramatic or memorable. “She had shared a bottle of soda pop with someone, and not even that person became ill. The crisis passed.” <–Yes, that is a direct quote and the end of the chapter on Mayinga. Contrast that to Preston’s language above.

Finally, beyond the science and the fear-mongering about Ebola, beyond everything and everyone in the story “liquefying” and “dissolving” and “bleeding out,” reading this book again as an adult, as a woman in a science career with a partner and kids, I was also left annoyed at the portrayal of the scientists. All of the major characters except one, Nancy Jaax, are men of course, ranging in age from late 20s to 50s-60sish. Understandable since this is in a mostly-male military institution and in a BLS4 setting to boot, but the one Preston focuses on for much of the narrative is Jaax.

While Preston may have been trying to portray Jaax as the having-it-all, tough-as-nails woman scientist, the fact that she’s the only one with any kind of home life is telling–mostly because he devotes more paragraphs to how she neglects both her children and her dying father than any success she has in her life outside of work. She is told early on by one of her colonels that “This work is not for a married female. You are either going to neglect your work or neglect your family.” This thought comes up repeatedly for Jaax, and in the end, while she was accepted and even honored by her colleagues and bosses, we hear over and over again how her children are left on their own to microwave meals and tend to their homework. How they desperately wait up for her to get home after work, often eventually falling asleep in her bed before she arrives. How she tells her father, dying of cancer back in Kansas and both knowing he only has a few hours to days to live, good-bye and “I’ll see you at Christmas” over the phone. How she barely arrives on time for his funeral after he passes.

We hear one paragraph about how another colleague, Thomas Geisbert, had a crumbling marriage with two small children, and how he left the children at his parents’ house for a weekend. Other than that, the personal lives of any other characters are practically absent, save for Jerry Jaax, Nancy’s husband. Even with him, much of the character development revolves around his fears of his wife working in a BSL4 lab.

The Hot Zone, for me, is unfortunately one of those books that you read as a young person and think is amazing, only to revisit years later and see it as much more shallow and contrived, the characters one-dimensional and the plot predictable. The problem is that The Hot Zone is not just a young adult novel–it’s still presented and defended as an absolutely true story, especially by huge Preston fans who seem to populate comment threads everywhere. And now it looks like there will be a sequel. At least it should be good for a drinking game.


*I’ll note that The Coming Plague is much more measured when it comes to Ebola–the two were grouped together because temporally, they were released close together, not because they display the same type of hype regarding the virus.

Ebola fears at Kent State

Though I haven’t had a chance to write about this here, I have an article at Mic.com on Kent’s experience with Ebola exposure in our area. Amber Vinson, the second Ebola-infected nurse in Texas, is a Kent State alumna and has relatives that work here. Our experience on campus so far is described here in this article.

Deadly distrust

Gregg Mitman’s article in the September 17th New England Journal of Medicine, “Ebola in a Stew of Fear,” is unfortunately all too prescient. Dr. Mitman highlighted “the ecology of fear” in Western Africa. Fear is present on both the part of Westerners (scared of Africa’s yellow fever, malaria, Ebola, its mere “different-ness”), and by native Africans (of whites’ history of colonization and slavery, of medical exploitation dating back well over a century). Fear of each other.

This history of fear, the cultural legacy of decades of mistrust of both Western people and their medical science, played a role in the murders of 8 people working on the Ebola outbreak in Guinea–journalists, medical officers, local administrators, and a preacher who were just trying to educate locals about the virus. The hostile crowd first threw stones at the team, and ended in their brutal deaths. The steps in-between have not been reported.

This is the extreme end of the science and medical denial continuum. We can scoff in America and attribute such horrors to the “brutal, savage Africans,” who cut their daughters and rape virgins to cure AIDS, as I’ve unfortunately already seen in some Twitter comments–some of our notions of “them” not so dissimilar from American colonists of centuries past regarding the slaves they once owned.

We can accept this scape-goating and ignore the West’s own modern-day culpability, with our fake vaccination campaigns that have left others dead in the aftermath; with our movies and popular culture depicting Africans as the West’s guinea pigs, and our shady pharmaceutical dealings that make that characterization all too believable.

No, it isn’t always a battle of Africans against Westerners. In South Africa, former President Thabo Mbeki was deceived by false claims about the relationship between HIV and AIDS that he had read on the internet, suggesting that HIV was not the cause of AIDS, and that  Western science should be distrusted in favor of traditional herbal remedies recommended by his health minister, such as garlic and beetroot. Because of his suspension of Western medical treatments, an estimated 330,000 South Africans died prematurely from HIV/AIDS between 2000 and 2005 , and at least 35,000 babies were born with HIV infections that could have been prevented.

Denialism kills. Distrust kills. Fear kills.

Here in the U.S., Natural News, a site run by the self-dubbed “Health Ranger,” Mike Adams, ran a piece this past summer suggesting that journalists and scientists who defended genetically-modified organisms (GMOs) were similar to Nazis, accelerating “heinous crimes being committed against humanity” and collaborating with an “with an anti-human regime,” and that such individuals should be named as such for future crimes:

“Just as history needed to record the names and deeds of Nazi war criminals, so too must all those collaborators who are promoting the death and destruction caused by GMOs be named for the historical record. The true extent of their collaboration with an anti-human regime will all become readily apparent once the GMO delusion collapses and mass global starvation becomes an inescapable reality.

I’m hoping someone will create a website listing all the publishers, scientists and journalists who are now Monsanto propaganda collaborators. I have no doubt such a website would be wildly popular and receive a huge influx of visitors, and it would help preserve the historical record of exactly which people contributed to the mass starvation and death which will inevitably be unleashed by GMO agriculture (which is already causing mass suicides in India and crop failures worldwide).”

Adams is similarly anti-vaccine, and currently is featuring on his website “11 horrible truths about Ebola the government doesn’t want you to know.” These “truths” include suggesting that infected individuals should avoid hospitals, and that citizens everywhere should prepare for the inevitable quarantine at gunpoint.

The worst part of Adams’ misinformation of this type is that it doesn’t stay within the borders of the U.S.–misinformation on Ebola epidemiology and quack cures like those Adams promotes are also being spread in African nations via Facebook pages and other types of social media

Denialism kills. Distrust kills. Fear kills.

Because of distrust of Western medicine, a recent article noted that parts of Africa have better vaccination rates than many wealthy neighborhoods in Los Angeles–and as a result, 10 babies died in a 2010 outbreak of whooping cough in California.

The deaths of the workers in Guinea show this fear and denial writ large; the purposeful killing of those only wanting to help their local and global neighbors in the face of a terrible epidemic. Those murdered are the latest victims of the most malignant form of distrust. They will not be the last.

Are we *sure* Ebola isn’t airborne?

Since yesterday’s post, several people have asked me on various social media outlets about the airborne nature of Ebola. Didn’t I know about this paper (“Transmission of Ebola virus from pigs to non-human primates“), which clearly showed that Ebola could go airborne?

Indeed I do–I wrote about that paper two years ago, and it in no way changes my assertion that Ebola doesn’t spread between people in an airborne manner.

Let me back up. The paper in question was an experimental study done in the wake of the 2008 finding of the Reston Ebola virus in pigs and a previous study looking at the Zaire virus in pigs. In the air transmission study, they inoculated pigs with Ebola and examined transmission to macaques (who were not in direct contact with the infected pigs). They did find aerosolized Ebola in air samples, and some of the macaques did come down with symptoms of Ebola. So, it looked like pigs could spread Ebola through the air, which is something that had already been suggested by the epidemiology of the 2008 pig Ebola outbreak. It’s always nice when experimental data matches up with that observed during a real-life occurrence of the virus.

*However*, the kicker was not that Ebola is transmitted by air in human outbreaks, but rather that there may be something unique about pig physiology that allows them to generate more infectious aerosols as a general rule–so though aerosols aren’t a transmission route between primates (including humans, as well as non-human primates used experimentally), pigs may be a bigger threat as far as aerosols. Thus, this may be important for transmission of swine influenza and other viruses as well as Ebola.

So unless you’re sitting next to an Ebola-infected pig, seriously, airborne transmission of Ebola viruses isn’t a big concern. (Perhaps this corollary should be added to this handy diagram examining your risk of Ebola).


Find more of my writing on Twitter or Facebook

Pig-to-monkey Ebola: is there something in the air?

Ebola has long been known to be a zoonotic virus–one which jumps between species. Though it took several decades to find evidence of Ebola virus in bats, these animals had previously been associated with human index cases of Ebola disease have worked in bat-infested warehouses or traveled to caves where bats roost. Non-human primates have also become infected with the virus, sometimes transmitting the virus to humans when killed primates are butchered for food. Ebola has also been suggested to infect dogs and other wild animals. However, livestock are a newer angle to Ebola virus ecology.

Ebola was first found in pigs in 2008 in the Philippines. This was the Reston virus, named after its discovery in imported Filipino monkeys in a facility in Reston, Virginia, in 1989. Though this virus spread among the captive monkeys, no humans came down with symptoms. However, follow-up studies showed that some humans did develop an immune response to the Reston virus–suggesting they had been infected, even if they didn’t realize it. At the time, there was suggestion that perhaps Reston might be spread via aerosol, as the virus appeared to spread amongst monkeys in two different rooms who did not come into physical contact with one another. However, this was not proven at the time and alternative explanations were possible.

When Reston resurfaced in swine and swine farmers in 2008, a similar phenomenon was observed. Though it was not known how the pigs initially became infected with the virus, they did appear to be able to spread it to humans working amongst them, even if those farmers didn’t have contact with blood or other secretions (the most efficient way to transmit Ebola viruses). Suggestive of possible transmission from pigs to people via air, but far from conclusive. Since then, two experimental studies have examined airborne transmission of Ebola via pigs.

The first study examined transmission of the Zaire strain of Ebola–the nastiest one, which can kill up to 90% of those infected–within laboratory pigs. Pigs were inoculated with the Zaire virus and housed with uninfected pigs, who were later tested and found to have acquired the virus. Interestingly, when the pigs got sick with Ebola Zaire, the symptoms were mainly respiratory and the virus replicated in the lungs. This was quite unlike what Zaire does in humans and our other primate cousins, where it’s a systemic disease and we can find virus in the blood. This suggests that pigs could be infected with even nasty types of Ebola, and we wouldn’t realize it.

Last week, Ed Yong reported on a new paper examining transmission of Zaire virus from experimentally-infected pigs to co-housed macaques. Like the previous paper, they observed that Ebola in pigs was a respiratory disease, and that it could spread to other animals (in this case, non-human primates). The macaques they tested developed the symptoms of Ebola that were expected–a systemic disease, with virus isolated from the blood. In this study, they also added in an air sampling component, and were able to detect evidence of virus (via PCR) in the air. However, the authors do note that this could have been aerosolized in other manners than directly from the exhaling pigs (such as during the floor-cleaning process). Finally, even if it does become aerosolized and spread in this manner, as noted in Ed’s article, Ebola is not “suddenly an airborne virus, like influenza.” Certainly more efficient transmission takes place via close contact with infected secretions during hospital procedures and funeral rites.

Interestingly, the authors note that other experimental studies that have looked specifically at airborne, primate-to-primate transmission of Ebola have come up negative, and that swine are known to generate “infectious short range large aerosol droplets more efficiently then other species.” Is there something specific about pig physiology that may make them better respiratory virus shedders? We know that pigs can be intermediate hosts for other viral pathogens as well, such as Nipah virus and of course influenza.  Are pigs playing any role in Ebola ecology, either in Asia or Africa? Might Ebola have more airborne potential than we previously thought? According to Ed, the authors of the second study are currently working on field studies in Africa to examine the pig question outside of the laboratory. The timing may be good for them, as Uganda is currently experiencing another Ebola outbreak;–the country’s third Filovirus outbreak in five months.


Weingartl, H., Embury-Hyatt, C., Nfon, C., Leung, A., Smith, G., & Kobinger, G. (2012). Transmission of Ebola virus from pigs to non-human primates Scientific Reports, 2 DOI: 10.1038/srep00811