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.
At least that was the understanding of DIC’s role in Ebola virus disease at the time Karesh alerted me to it. More recently, Karl Johnson and others have begun questioning whether the immune-shutdown effect that the virus somehow achieves, and the consequent blossoms of bacteria, might better explain some of the damage formerly blamed on DIC. “When it was first discovered, DIC, da da da, was the key to everything in hemorrhagic fever,” Johnson told me, again cheerily dismissive of conventional wisdom. Now, he said, he was reading a hell of a lot