certified that the monkey house had been nuked, returned to the possession of Hazleton Resrach Products. Hazleton began buying more monkeys from the Philippines, from the same monkey house near Manila, and restocked the building with crab-eating monkeys that had been trapped in the rain forests of Mindanao. Less than a month later, in the middle of January, some of the monkeys in Room C began dying with bloody noses. Dan Dalgard called Peter Jahrling. “Looks like we’re affected again,” he said.
The virus was Ebola. It had come from the Philippines. This time, since there had been no human casualties during the first outbreak, the Army, the C.D.C., and Hazleton jointly decided to isolate the monkeys—leave them alone and let the virus burn. Dan Dalgard hoped to save at least some of the monkeys, and his company did not want the Army to come back with space suits.
What happened in that building was a kind of experiment. Now they would see what Ebola could do naturally in a population of monkeys living in a confined air space, in a kind of city, as it were. The Ebola Reston virus jumped quickly from room to room, and as it blossomed in the monkeys, it seemed to mutate spontaneously into something that looked quite a lot like the common cold. But it was an Ebola cold. The monkeys died with great quantities of clear mucus and green mucus running from their nose, mixed with blood that would not clot. Their lungs were destroyed, rotten and swimming with Ebloa virus. They had pneumonia. When a single animal with a nosebleed showed up in a room, generally 80 percent of the animals died in that room shortly afterward. The virus was extraordinarily infective in monkeys. The Institute scientists suspected that they were seeing a mutant strain of Ebola, something new and a little different from what they had seen just a month before, in December, when the Army had nuked the monkey house. It was frightening—it was as if Ebola could change its character fast. As if a different strain could appear in a month’s time. The clinical symptoms of the disease served as a reminder of the fact that Ebola is related to certain kind of colds seen in human children. It seemed that the virus could adapt quickly to new host, and that it could change its character rapidly as it entered a new population.
bola apparently drifted through the building’s air-handling ducts. By January 24, it had entered Room B, and monkeys in that room started going into shock and dying with runny noses, red eyes, and masklike expressions on their faces. In the following weeks, the infection entered Room I,F,E, and D, and the animals in these rooms virtually all died. Then, in mid-February, a Hazleton animal caretaker who will be called John Coleus was performing a necropsy on a dead monkey when he cut his thumb with a scalpel. He had been slicing apart the liver, one of the favorite nesting sites of Ebola. The scalpel blade, smeared with liver cells and blood, went deep into this thumb. He had had a major exposure to Ebola.
The liver that he had been cutting was rushed to USAMRIID for analysis. Tom Geisbert looked at a piece of it under his microscope and, to his dismay, found that it was “incredibly hot—I mean, wall to wall with virus.” Everyone at the Institute thought John Coleus was going to die. “Around her,” Peter Jahrling told me, “we were frankly fearful that this guy had bought the farm.” The C.D.C. decided not to put him into isolation. So Coleus visited bars and drank beer with his friends.
“Here at the Institute,” Peter Jahrling said, “we were absolutely appalled when that guy went out to bars, drinking. Clearly the C.D.C. should not have let that happen. This was a serious virus and a serious situation. We don’t know a whole lot about the virus. It could be like the common cold—it could have a latency period when you are shedding virus before you develop symptoms—and by the time you know you are sick, you might have infected sixteen people. There’s an awful lot we don’t know about this virus. We don’t know where it came from, and we don’t know what form it will take when it appears next time.”
John Coleus had a minor medical condition that required surgery. Doctors performed the operation while he was in the incubation period after his exposure to Ebola. There is no record indicating that he bled excessively during the surgery. He came through fine, and he is alive today, with no ill effects from his exposure.
As for the monkey house, the entire building died. The Army didn’t have to nuke it. It was nuked by the Ebola Reston virus. Once again, there were no human casualties. However, something eerie and perhaps sinister occurred. A total of four men had worked as caretakers in the monkey house: Jarvis Purdy, who had a heart; Milton Frantig, who had thrown up on the lawn; John Coleus, who had cut his thumb; and a fourth man. All four men eventually tested positive for Ebola Reston virus. They had all been infected with the agent. The virus had entered their bloodstreams and multiplied in their cells. Ebola proliferated in their bodies. It cycled in them. It carried on its life inside the monkey workers. But it did not make them sick, even while it multiplied inside them. If they had headaches or felt ill, none of them could recall it. Eventually the virus cleared from their systems naturally, disappeared from the blood, and as of this writing none of the men was affected by it. The are among the very, very few human survivors of Ebola virus. John Coleus certainly caught the virus when he cut himself with a bloody scalpel, no question about that. What is more worrisome is that the others had not cut themselves, yet the virus entered their bloodstreams. It got there somehow. Most likely it entered their blood thought contact with the lungs. It infected them through the air. When it became apparent to the Army researchers that three of the four men who became infected had not cut themselves, just about everyone at USAMRIID concluded that Ebola can spread through the air.
Dr. Philip Russell—the general who made the decision to send in the Army to stop the virus—recently said to me that although he had been “scared to death” about Ebola at the time, it wasn’t until afterward, when he understood that the virus was spreading in the air among the monkeys, that the true potential for disaster sank in for him. “I was more frightened in retrospect,” he said. “When I saw the respiratory evidence coming from those monkeys, I said to myself, My God, with certain kinds of small changes, this virus could become one that travels in rapid respiratory transmission through humans. I’m talking about the Black Death. Imagine a virus with the infectiousness of influenza and the mortality rate of black plague in the Middle Ages—that’s what we’re talking about.”
The workers at Reston had symptomless Ebola virus. Why didn’t it kill them? To this day, no one knows the answer to that question. Symptomless Ebola—the men had been infected with something like an Ebola cold. A tiny difference in the virus’s genetic code, probably resulting in a small structural change in the shape of one of the seven mysterious proteins in the virus particle, had apparently changed its effect tremendously in humans, rendering it mild or harmless even though it had destroyed the monkeys. This strain of Ebola knew the difference between a monkey and a person. And if it should mutate in some other direction…
ONE DAY IN spring, I went to visit Colonel Nancy Jaax, to interview her about her work during the Reston event. We talked in her office. She wore a black military sweater with silver eagles on the shoulder boards—she had recently made full colonel. A baby parrot slept in a box in the corner. The parrot woke up and squeaked.
“Are you hungry?” she asked it. “Yeah, yeah, I know.” She pulled a turkey baster out of a bag and loaded it with parrot mush. She stuck the baster into the parrot’s beak and squeezed the baster bulb, and the parrot closed it eyes with satisfaction.
She waved her hand at some filing cabinets. “Want to look at some Ebola? Take your pick.”
“You show me.”
She searched through a cabinet and removed a handful of glass slides, and carried them into another room, where a microscope sat on a table. It had two sets of eyepieces so that two people could look into it at the same time.
I sat down and stared in the microscope, into white nothingness.
“Okay, here’s a good one,” she said, and placed a slide under the lens.
I saw a field of cells. Here and there, pockets of cells had burst and liquefied.
“That’s male reproductive tissue,” she said. “It’s heavily infected. This is Ebola Zaire in a monkey that we exposed through the lungs in 1986, in the study that Gene Johnson and I did.”
Looking at the slice of monkey testicle, I got an unpleasant sensation. “You mean, it got into the monkey’s lungs and moved to its—?”
“Yeah. it’s pretty yucky,” she said. “Now I’m going to make you dizzy. I’m going to show you the lung.”
The scene shifted, and we were looking at rotted pink Belgian lace.
“This is a slice of lung tissue. A monkey that was exposed through the lungs. See how the virus bubbles up in the lung? It’s Ebola Zaire.”
I could see individual cells, and some of them were swollen with dark specks.
“We’ll go to higher magnification.”
The cells got bigger. The dark specks became angular, shadowy blobs. The blobs were bursting out of the cells, like something hatching.
