This article is adapted from David Quammen's new book, Spillover, available now. You can purchase it here.
In June 2008, a Dutch woman named Astrid Joosten left the Netherlands with her husband for an adventure vacation in Uganda. It wasn’t their first trip to Africa, but it would be more consequential than the others.
At home in Noord-Brabant, Joosten, 41, worked as a business analyst for an electrical company. Both she and her spouse, a financial manager, enjoyed escaping Europe on annual getaways. In 2002, they had flown to Johannesburg and, stepping off the airplane, felt love for Africa at first sight. On later trips they visited Mozambique, Zambia, and Mali. The journey to Uganda in 2008, booked through an adventure-travel outfitter, would allow them to see mountain gorillas in the southwestern highlands of the country as well as some other wildlife and cultures. They worked their way south toward Bwindi Impenetrable Forest, where the gorillas reside. On one day, the operators offered a side trip, an option, to a place called the Maramagambo Forest, where the chief attraction was a site known as Python Cave. African rock pythons lived there, languid and content, grown large on a diet of bats.
Joosten’s husband, later her widower, is a fair-skinned man named Jaap Taal, a calm fellow with a shaved head and dark, roundish glasses. Most of the other travelers didn’t fancy this Python Cave offering, he told me later. “But Astrid and I always said, ‘Maybe you come here only once in your life, and you have to do everything you can.’ ” They rode to Maramagambo Forest and then walked a mile or so, gradually ascending, to a small pond. Nearby, half-concealed by moss and other greenery, like a crocodile’s eye barely surfaced, was a low, dark opening. Joosten and Taal, with their guide and one other client, climbed down into the cave.
The footing was bad: rocky, uneven, and slick. The smell was bad too: fruity and sour. Think of a dreary barroom, closed and empty, with beer on the floor at three a.m. The cave seemed to have been carved by a creek, or at least to have channeled its waters, and part of the overhead rock had collapsed, leaving a floor of boulders and coarse rubble, a moonscape, coated with guano like a heavy layer of vanilla icing. It served as a major roosting site for the Egyptian fruit bat (Rousettus aegyptiacus), a crow-size chiropteran that’s widespread and relatively abundant in Africa and the Middle East. The cave’s ceiling was thick with them—many thousands, agitated and chittering at the presence of human intruders, shifting position, some dropping free to fly and then settling again. Joosten and Taal kept their heads low and watched their step, trying not to slip, ready to put a hand down if needed. “I think that’s how Astrid got infected,” Taal told me. “I think she put her hand on a piece of rock, which contained droppings of a bat, which are infected. And so she had it on her hand.” Maybe she touched her face an hour later, or put a piece of candy in her mouth, “and that’s how I think the infection got in her.”
No one had warned Joosten and Taal about the potential hazards of an African bat cave. They knew nothing of a virus called Marburg (though they had heard of Ebola). They only stayed in the cave about 10 minutes. They saw a python, large and torpid. Then they left, continued their Uganda vacation, visited the mountain gorillas, took a boat trip, and flew back to Amsterdam. Thirteen days after the cave visit, home in Noord-Brabant, Joosten fell sick.
At first it seemed no worse than the flu. Then her temperature climbed higher and higher. After a few days, she began suffering organ failure. Her doctors, knowing of her recent time in Africa, suspected Lassa virus or maybe Marburg. “Marburg,” said Taal, “what’s that?” Joosten’s brother looked it up on Wikipedia and told him: “Marburg virus: It kills, could be big trouble.” In fact, it’s a filovirus, the closest relative to the ebolaviruses (of which there are five species, including the most infamous, Ebola). Marburg was first discovered in 1967, when a group of African monkeys, imported to Marburg an der Lahn, in western Germany, for medical research uses, passed a nasty new virus to laboratory workers. Five people died. In the decades since, it has also struck hundreds of Africans, with a case fatality rate of up to 90 percent.
The doctors moved Joosten to a hospital in Leiden, where she could get better care and be isolated from other patients. There, she developed a rash and conjunctivitis; she hemorrhaged. She was put into an induced coma, a move dictated by the need to dose her more aggressively with antiviral medicine. Before she lost consciousness, though not long before, Taal went back into the isolation room, kissed his wife, and said to her, “Well, we’ll see you in a few days.” Blood samples, sent to a lab in Hamburg, confirmed the diagnosis: Marburg. She worsened. As her organs shut down, she lacked for oxygen to the brain, she suffered cerebral edema, and before long Joosten was declared brain-dead. “They kept her alive for a few more hours, until the family arrived,” Taal told me. “Then they pulled the plug out, and she died within a few minutes.”
A horse dies mysteriously in Australia, and people around it fall sick. A chimpanzee carcass in Central Africa passes Ebola to the villagers who scavenge and eat it. A palm civet, served at a Wild Flavors restaurant in southern China, infects one diner with a new ailment, which spreads to Hong Kong, Toronto, Hanoi, and Singapore, eventually to be known as SARS. These cases and others, equally spooky, represent not isolated events but a pattern, a trend: the emergence of new human diseases from wildlife.
The experts call such diseases zoonoses, meaning animal infections that spill into people. About 60 percent of human infectious diseases are zoonoses. For the most part, they result from infection by one of six types of pathogen: viruses, bacteria, fungi, protists, prions, and worms. The most troublesome are viruses. They are abundant, adaptable, not subject to antibiotics, and only sometimes deterred by antiviral drugs. Within the viral category is one particularly worrisome subgroup, RNA viruses. AIDS is caused by a zoonotic RNA virus.
So was the 1918 influenza, which killed 50 million people. Ebola is an RNA virus, which emerged in Uganda this summer after four years of relative quiescence. Marburg, Lassa, West Nile, Nipah, dengue, rabies, yellow fever virus, and the SARS bug are too.
Over the last half dozen years, I have asked eminent disease scientists and public-health officials, including some of the world’s experts on Ebola, on SARS, on bat-borne viruses, on HIV-1 and HIV-2, and on viral evolution, the same two-part question: 1) Will a new disease emerge, in the near future, sufficiently virulent and transmissible to cause a pandemic capable of killing tens of millions of people? and 2) If so, what does it look like and from where does it come? Their answers to the first part have ranged from maybe to probably. Their answers to the second have focused on zoonoses, particularly RNA viruses. The prospect of a new viral pandemic, for these sober professionals, looms large. They talk about it; they think about it; they make contingency plans against it: the Next Big One. They say it might happen anytime.
To understand what killed Astrid Joosten, and to see her case within the context of the Next Big One, you need to understand how viruses evolve. Edward C. Holmes is one of the world’s leading experts in viral evolution. He sits in a bare office at the Center for Infectious Disease Dynamics, which is part of Pennsylvania State University, and discerns patterns of viral change by scrutinizing sequences of genetic code. That is, he looks at long runs of the five letters (A, C, T, G, and U) that represent nucleotide bases in a DNA or RNA molecule, strung out in unpronounceable streaks as though typed by a manic chimpanzee. Holmes’s office is tidy and comfortable, furnished with a desk, a table, and several chairs. There are few bookshelves, few books, few files or papers. A thinker’s room. On the desk is a computer with a large monitor. That’s how it all looked when I visited, anyway.
Above the computer was a poster celebrating “the Virosphere,” meaning the totality of viral diversity on Earth. Beside that was another poster, showing Homer Simpson as a character in Edward Hopper’s famous painting Nighthawks. Homer is seated at the diner counter with a plate of doughnuts before him.
Holmes is an Englishman, transplanted to central Pennsylvania from London and Cambridge. His eyes bug out slightly when he discusses a crucial fact or an edgy idea, because good facts and ideas impassion him. His head is round and, where not already bald, shaved austerely. He wears wiry glasses with a thick metal brow, and while he looks a bit severe, Holmes is anything but. He’s lively and humorous, a generous soul who loves conversation about what matters: viruses. Everyone calls him Eddie.
“Most emerging pathogens are RNA viruses,” he told me, as we sat beneath the two posters. RNA as opposed to DNA viruses, he meant, or to bacteria or to any other type of pathogen. To say that Eddie Holmes wrote the book on this subject wouldn’t be metaphorical. It’s titled The Evolution and Emergence of RNA Viruses, published by Oxford in 2009, and that’s what had brought me to his door. Now he was summarizing some of the highlights.
There are an awful lot of RNA viruses, he said, which might seem to raise the odds that many would come after humans. RNA viruses in the oceans, in the soil, in the forests, and in the cities; RNA viruses infecting bacteria, fungi, plants, and animals. It’s possible that every cellular species of life on the planet supports at least one RNA virus, though we don’t know for sure because we’ve just begun looking. A glance at his virosphere poster, which portrayed the universe of known viruses as a brightly colored pizza, was enough to support that point. It showed RNA viruses accounting for at least half the slices. But they’re not merely common, Eddie said. They’re also highly evolvable. They’re protean. They adapt quickly.single page
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