Spillover: Animal Infections and the Next Human Pandemic (11 page)

“We have a lot to learn from these people,” Barry Hewlett told me, one day in Gabon, “as to how they’ve responded to these epidemics over time.” Modern society has lost that sort of ancient, painfully acquired accumulation of cultural knowledge, he said. Instead we depend on the disease scientists. Molecular biology and epidemiology are useful, but other traditions of knowledge are useful too. “Let’s listen to what people are saying here. Let’s find out what’s going on. They’ve been living with epidemics for a long time.”

Hewlett is a gentle-spirited man with a professorship at Washington State University and two decades of field experience in Central Africa. By the time I met him, at an international ebolavirus conference in Libreville, we had each visited one other village famed for suffering the disease—a place called Mbomo, in the Republic of the Congo, along the western edge of Odzala National Park. Mbomo lies not far from the Mambili River and the Moba Bai complex, where I had watched Billy Karesh trying to dart gorillas. The outbreak around Mbomo began in December 2002, probably among hunters who handled infected gorillas or duikers, and spread throughout an area that encompassed at least two other villages. A large difference between Hewlett’s experience in Mbomo and mine was that he arrived during the outbreak. The grease was still flaming in the pan when he made his inquiries.

One early patient, Hewlett learned, was pulled out of the village clinic because his family disbelieved the Ebola diagnosis and preferred relying on a traditional healer. After that patient died at home, unattended by medical personnel and uncured by the healer, things got testy. The healer pronounced that this man had been poisoned by sorcery and that the perpetrator was his older brother, a successful man working in a nearby village. The older brother was a teacher who had “risen” to become a school inspector and didn’t share the good fortune with his family. So again, as with ezanga
among the Bakola people in northeastern Gabon, there were jealous animosities underlying the accusations of sorcery. Then another brother died, and a nephew, at which point family members burned the older brother’s Mbomo house and sent a posse to kill him. They were stopped by the police. The older brother, though now taken for an evil magus, escaped vengeance. Then community relations deteriorated generally as more victims died from the invisible terror, with no cure available, no satisfactory explanation, to a point where anyone who looked out of the ordinary or above the crowd became suspect.

Another element of the dangerous brew in and around Mbomo was a mystic secret society,
La Rose Croix
, more familiar (if barely) to you and me as Rosicrucianism. It’s an international organization that has existed for centuries, mostly devoted to esoteric study, but in this part of the Congo it had a bad reputation, akin to sorcery. Four teachers within one nearby village were members, or were thought to be members—and these teachers had been telling children about Ebola virus before the outbreak occurred. That led some traditional healers to suspect that the teachers had advance knowledge—supernatural knowledge—of the outbreak. Something had to be done, yes? On the day before Barry Hewlett and his wife arrived in Mbomo, the four teachers were murdered with machetes while they worked in their crop fields.

Soon afterward, the disease outbreak expanded to include so many community members that sorcery no longer seemed a plausible explanation to local people. The alternative was
opepe
, an epidemic, Mbomo’s equivalent (in Kota, one of the local languages) to what Barry Hewlett had heard about, from the Acholi, as gemo. “
This illness is killing everyone
,” one local man told the Hewletts, and therefore it couldn’t be sorcery, which targets individual victims or their families. By early June 2003, there had been 143 cases in Mbomo and the surrounding area, with 128 deaths. That’s a case fatality rate of 90 percent, at the top of the range even for Ebola virus.

With their deep interest in local explanations and their patient listening methods, the Hewletts heard things that wouldn’t fit within the multiple-choice categories of an epidemiological questionnaire. Another of their informants, an Mbomo woman, declared: “
Sorcery does not kill without reason
, does not kill everybody, and does not kill gorillas or other animals.” Oh, yes, again gorillas. That was another aspect of the Mbomo brew—everyone knew there were dead apes in the forest all roundabout. They had died at the Lossi sanctuary. They had died, so far as Billy Karesh could tell, at Moba Bai. Carcasses had been seen in the environs of Mbomo itself. And, as the woman said, sorcery didn’t apply to gorillas.

16

W
hen a silverback gorilla dies of Ebola, he does it beyond the eyes of science and medicine. No one is there in the forest to observe the course of his agony, with the possible exception of other gorillas. No one takes his temperature or peers down his throat. When a female gorilla succumbs to Ebola, no one measures the rate of her breathing or checks for a telltale rash. Thousands of gorillas may have been killed by the virus but no human has ever attended one of those deaths—not even Billy Karesh, not even Alain Ondzie. A small number of carcasses have been found, some of which have tested positive for Ebola antibodies. A larger number of carcasses have been seen and reported by casual witnesses, in Ebola territory at Ebola times, but because the forest is a hungry place, most of those carcasses could never be inspected and sampled by scientific researchers. The rest of what we know about Ebola’s effect on gorillas is inferential: Many of them—major portions of some regional populations, such as the ones at Lossi, Odzala, and Minkébé—have disappeared. But nobody knows just how Ebola virus affects the gorilla body.

With humans it’s different. The numbers I’ve mentioned above offer one gauge of that difference: 245 fatal cases during the outbreak at Kikwit, another 224 at Gulu, 128 in and around Mbomo, et cetera. The total of human fatalities from Ebola virus disease, since its discovery in 1976, is about fifteen hundred—not many compared to such widespread and relentless global afflictions as malaria and tuberculosis, or to the great waves of death brought by the various influenzas, but enough to generate a significant body of data. Furthermore, doctors and nurses saw many of those fifteen hundred people die. So the medical profession knows a good bit about the range of symptoms and the pathological effects produced on a human body during death by ebolavirus infection. It’s not quite like you might think.

If you devoured
The Hot Zone
when it was published, as I did, or if you have been secondarily exposed to its far-reaching influence on public impressions about ebolaviruses, you may carry some wildly gruesome notions. Richard Preston is a vivid writer, a skillful writer, an industrious researcher, and it was his purpose to make a truly horrible disease seem almost preternaturally horrific. You may recall his depiction of a Sudanese hospital in which the virus “
jumped from bed to bed, killing patients left and right
,” creating dementia and chaos, and not only killing patients but causing them to bleed profusely as they died, liquefying their organs, until “people were dissolving in their beds.” You may have shuddered at Preston’s statement that Ebola virus in particular “
transforms virtually every part of the body
into a digested slime of virus particles.” You may have paused before turning the page when he told you that, after death, an Ebola-infected cadaver “
suddenly deteriorates,
” its internal organs deliquescing in “a sort of shock-related meltdown.” You may not have noticed that meltdown was a metaphor, meaning dysfunction, not actual melting. Or maybe it wasn’t. At a later point, bringing another filovirus into the story, Preston mentioned a French expatriate, living in Africa, who “
essentially melts down with Marburg
virus while traveling on an airplane.” You may remember one phrase in particular, as Preston described victims in a darkened Sudanese hut:
comatose, motionless, and
“bleeding out.” That seemed to be so different from just “bleeding.” It suggested a human body draining away in a gush. There was also the statement that Ebola causes a victim’s eyeballs to fill up with blood, bringing blindness and more. “
Droplets of blood stand out on the eyelids
: You may weep blood. The blood runs from your eyes down your cheeks and refuses to coagulate.” The mask of red death—where medical reporting meets Edgar Allan Poe.

It’s my duty to advise that you need not take these descriptions quite literally—at least, not as the typical course of a fatal case of Ebola virus disease. Expert testimony, some published and some spoken, tempers Preston on several of these more lurid points, without minimizing the terribleness of Ebola in terms of real suffering and death. Pierre Rollin, for instance, deputy chief of the Special Pathogens Branch of the CDC, is one of the world’s most experienced ebolavirus hands. He worked at the Pasteur Institute in Paris before moving to Atlanta, and has been a member of response teams to many Ebola and Marburg outbreaks over the past fifteen years, including those at Kikwit and Gulu. When I asked him, during an interview in his office, about the public perception that this disease is extraordinarily bloody, Rollin interrupted me genially to say:
“—which is bullshit.” When I mentioned the descriptions in Preston’s book, Rollin mockingly said, “They melt, splash on the wall,” and gave a frustrated shrug. Mr. Preston could write what he pleased, Rollin added, so long as the product was labeled fiction. “But if you say it’s a true story, you have to speak to the true story, and he didn’t. Because it was much more exciting to have blood everywhere and scaring everywhere.” A few patients do bleed to death, Rollin said, but “they don’t explode, and they don’t melt.” In fact, he said, the often-used term “Ebola hemorrhagic fever” is itself a misnomer for Ebola virus disease, because more than half the patients don’t bleed at all. They die of other causes, such as respiratory distress and shutdown (but not dissolution) of internal organs.

Karl Johnson, one of the pioneers of Ebola outbreak response, whose credentials I’ve already sketched, offered a similar but even more pointed reaction, expressed with his usual candor. We were talking—in my own office, this time—during one of his periodic trips to Montana for fly-fishing. We had become friends and he had coached me a bit, informally, on how to think about zoonotic viruses. Finally I got him to sit for an interview, and
The Hot Zone
inescapably came up. Waxing serious, Karl said: “Bloody tears is bullshit. Nobody has ever had bloody tears.” Furthermore, Karl noted, “People who die are not formless bags of slime.” Johnson also concurred with Pierre Rollin that the bloodiness angle has been oversold. If you want a really bloody disease, he said, look at Crimean-Congo hemorrhagic fever. Ebola is bad and lethal, sure, but not bad and lethal precisely that way.

In the real world, as described in the scientific literature, the list of major symptoms of Ebola virus disease goes like this: abdominal pain, fever, headache, sore throat, nausea and vomiting, loss of appetite, arthralgia (joint pain), myalgia (muscle pain), asthenia (weakness), tachypnea (rapid breathing), conjunctival injection, and diarrhea. Conjunctival injection means pink eye, not bloody tears. All these symptoms tend to show up in many or most fatal cases. Additional symptoms including chest pain, hematemesis (vomiting of blood), bleeding from the gums, bloody stools, bleeding from needle-puncture sites, anuria (inability to pee), rash, hiccups, and ringing in the ears have appeared in a smaller fraction of cases. During the Kikwit outbreak, 59 percent of all patients didn’t bleed noticeably at all, and bleeding in general was no indicator of who would or wouldn’t survive. Rapid breathing, urine retention, and hiccups, on the other hand, were ominous signals that death would probably come soon. Among those patients who did bleed, blood loss never seemed massive, except among pregnant women who spontaneously aborted their fetuses. Most of the nonsurvivors died stuporous and in shock. Which is to say: Ebola virus generally killed with a whimper, not with a bang or a splash.

Despite all these data, gathered amid woeful and dangerous conditions while the primary mission was not science but saving lives, even the experts aren’t sure exactly
how
the virus typically causes death. “We don’t know the mechanism,” Pierre Rollin told me. He could point to liver failure, to kidney failure, to breathing difficulties, to diarrhea, and in the end it often seemed that multiple causes were converging in an unstoppable cascade. Karl Johnson voiced similar uncertainty, but mentioned that the virus “really goes after the immune system,” shutting down production of interferon, a class of proteins essential to immune response, so that “nothing stops the continued replication of the virus.”

This idea of immune suppression by ebolaviruses has also appeared lately in the literature, along with speculation that it might allow catastrophic overgrowth of a patient’s natural populations of bacteria, normally resident in the gut and elsewhere, as well as unhindered replication of the virus itself. Runaway bacterial growth might in turn put blood into the urine and feces, and even lead to “intestinal destruction,” according to one source. Maybe that’s what Preston had in mind when he wrote about liquefied organs and people dissolving in their beds. If so, he was blurring the distinction between what Ebola virus does and what garden-variety bacteria can do in the absence of a healthy immune system keeping them cropped. But, hey, don’t we all like a dramatic story better than a complicated one?

Still another aspect of the pathology of Ebola virus disease is a phenomenon called disseminated intravascular coagulation, familiar to the medical community as DIC. It’s also known as consumptive coagulopathy (if that helps you), because it involves consumption of too much of the blood’s coagulating capacity in a misdirected way. Billy Karesh had told me about DIC as we boated down the Mambili River after our gorilla stakeout. Disseminated intravascular coagulation, he explained, is a form of pathological blood sludge, in which the normal clotting factors (coagulation proteins and platelets) are pulled out to form tiny clots along the insides of blood vessels throughout the victim’s body, leaving little or no coagulation capacity to prevent leakage elsewhere. As a result, blood may seep from capillaries into a person’s skin, forming bruiselike purple marks (hematomas); it may dribble from a needle puncture that seems never to heal, or it may leak into the gastrointestinal tract or the urine. Still worse, the mass aggregation of small clots in the vessels may block blood flow to the kidneys or the liver, causing organ failure as often seen with Ebola.