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Shortly after one of us (Jared Diamond) boarded a flight from Hong Kong back to Los Angeles, the passenger in the next seat sneezed. She sneezed again—and again—and then she began coughing. Finally she gagged, pulled out the vomit bag from the seat back in front of her, threw up into the bag, stood up, squeezed past, and lurched to the toilet at the front of the plane. The woman was obviously miserable, but sympathy for her pain was not what I felt. Instead I was frightened and asked the flight attendant to move me to a seat as far from her as possible.
All I could think of was another sick person, a man from Guangdong province in southern China, who spent the night of February 21, 2003, at the Metropole Hotel in Hong Kong, an upscale establishment with a swimming pool, fitness center, restaurants, a bar, and all kinds of areas where visitors could socialize and connect. The man stayed a single night in room 911. Unfortunately for him and for many other people, he had picked up severe acute respiratory syndrome, or SARS—perhaps directly from an infected bat or from a small, arboreal mammal called a civet, common in one of Guangdong’s famous “wet markets” that sell wild animals for food, or else from a person or chain of people ultimately infected from one of those animal sources.
In the course of his brief stay, the man initiated a SARS “super spreader” event that led to at least 16 more SARS cases among the hotel’s guests and visitors and then to hundreds of other cases throughout Asia, Europe, and North America as those guests and visitors continued on their travels—just as my neighbor was now traveling to L.A. The infectiousness of room 911’s guest can be gauged from the fact that three months later, the carpet right outside the door and near the hotel elevator yielded genetic evidence of the SARS virus, presumably spewed out in his own sneezing, coughing, or vomiting.
I didn’t end up with SARS, but my experience drives home the terrifying prospect of a novel, unstoppable infectious disease. Globalization, changing climate, and the threat of drug resistance have conspired to set the stage for that perfect microbial storm: a situation in which an emerging pathogen—another HIV or smallpox, perhaps—might burst on the scene and kill millions before we can respond.
Pathogen Paradox
To grasp the risk, we first must understand why any microbe would evolve to sicken or kill us. In evolutionary terms, how does destroying its host help a microbe to survive?
Think of your body as a potential “habitat” for tiny microbes, just as a forest provides a habitat for bigger creatures like birds and squirrels. The species living in the forests of our bodies include lice, worms, bacteria, viruses, and amoebas. Many of those denizens are benign and cause us no harm. But some microbes seem to go out of their way to make us sick—either mildly sick, as in the case of the common cold, or else sick to the point of killing us, as in the case of smallpox.
Killer microbes have long posed a paradox for evolutionary biologists. Why would a microbe evolve to devastate the very habitat on which it depends? By analogy, you might reason that there should be no squirrels that destroy the forest they live in, because such a species would quickly go extinct.
The answer stems from the fact that in order to survive over the long haul, any microbe restricted to humans must be able to spread from one victim to the next. There is a simple mathematical requirement here: On average, the germ must infect at least one new victim for every old one who either dies or recovers and purges himself of the microbe. If the average number of new victims per old drops to fewer than one, then the spread of the microbe is doomed.
A microbe can’t walk or fly from one host to the next. Instead it must resort to a range of nefarious tricks. What from our point of view is simply a disease symptom can, from the bug’s perspective, be an all-important means of enlisting our help to move around. Common microbe tricks are to make us cough or sneeze, suffer from diarrhea, or develop open sores on our skin. Respectively, these symptoms spread the microbe into our exhaled breath, into the local water supply via our feces, and onto the skin of those who touch us, explaining why a microbe might want to induce unpleasant symptoms in its victims.
Evolutionary biologists reason that keeping us alive and pumping out new microbes would be an excellent strategy for such a bug, which might therefore evolve to be less, not more, virulent over time. An example comes from the history of syphilis. When it first appeared in Europe in 1495, it caused severe and painful symptoms within a few months, but by 1546 it had begun evolving into the slowly progressing disease that we know today.
Yet if keeping us alive is strategically sound, why do some pathogens go so far as to actually kill us?
Sometimes a microbe’s deadly rampage through a human population stems from an accident of nature. For instance, the microbe could be comfortably adapted to some animal host that it routinely inhabits without deadly consequences, but it could be maladapted to the human environment. The microbe may rarely infect people, but when it does, it may kill the human host, who becomes a literal dead end for the virus as well.
But what of those killer microbes that target humans, making us their primary host? Their survival strategy, evolutionary biologists now realize, differs from that of a disease like syphilis but works just as well. Take the cholera bacterium that gives us diarrhea or the smallpox virus that makes us develop skin sores; both of these can kill us in days to weeks. Such virulence may be evolutionarily favored if, in the brief time between our becoming infected and dying, the fatal symptoms spread trillions of microbes to potential new victims. The fact that we may die is unfortunate for us but an acceptable cost for the microbe. In the world of evolution and natural selection, anything that the microbe does to us is fair—just as long as at least one new victim gets infected for each old one.
Hence the recipe for a killer disease is for the microbe to achieve a balance between two things: the probability of its killing us quickly once we become infected and its efficiency in leading our bodies to transmit the microbe to new victims.
