If germs hung a recruiting sign for their hosts, it would probably be a version of the World War I poster of Uncle Sam pointing: We want YOU to help us reproduce. All hosts were equally eligible for service, infectious-disease researchers thought. Assuming the recruits weren’t immune due to a prior infection or vaccination, anyone should have roughly the same potential to spread a disease’s pathogens. But then came severe acute respiratory syndrome, or SARS.
This pandemic started as just another strange pneumonia from southern China, but in 2003 it turned into a global outbreak that infected 8,098 people and killed 774. Key to the disease’s spread, researchers found, was a small but crucial portion of the population that became known as “superspreaders,” people who transmitted the infection to a much greater than expected number of new hosts. The more scientists learn about superspreaders, the more they are beginning to realize that this tiny segment of the population is the driving force behind the emergence and spread of infectious diseases.
Perhaps the most infamous superspreader in history was Mary Mallon, aka Typhoid Mary. An Irish cook in New York City in the 1900s, she was chronically infected with Salmonella typhi. Although the infection didn’t cause any symptoms for Mallon, she did excrete large numbers of typhoid bacteria in her feces. Her career as a cook made it easy to transmit fecal bacteria to customers through the food she prepared. She infected about 50 people and killed several (official counts vary) before she was arrested and jailed for refusing to give up her career as a cook.
To epidemiologists, people like Typhoid Mary were seen as an anomaly and not the main drivers of infectious disease spread. Instead, epidemiologists focused on a number they called R0, the average number of people a single person could infect. The value of R0 depends on three main factors: the number of susceptible individuals in the population, the number currently infected, and those resistant to infection. If the value of R0 is less than one, it means that each individual infects less than one other person, and the outbreak will ultimately die out. However, if the value of R0 is greater than one, the disease has the potential to spread.
When you look across a large population, R0 is a good estimate of whether and how a particular infection might spread. At an individual level, it turns out, R0 is less accurate. Most people won’t spread the disease at all, but a very few people will spread the infection to tens or even hundreds of others.
As computer models of infectious disease grew more powerful and precise, scientists began to realize that a lot of infectious disease spread is due to superspreaders. Researchers call it the 80/20 rule: Twenty percent of the population is responsible for 80 percent of disease spread. The key to understanding and stopping outbreaks of infectious disease means homing in on this small portion of the population that drives the majority of transmission.
Accounting for the presence of superspreaders also means accounting for their much more common counterparts: people who don’t spread the disease to anyone. Their R0 is zero. Taken together, that means a disease is much more likely to be introduced into new areas by superspreaders, but it is also more likely to fizzle out in those places due to nonspreaders. Only occasionally, as with SARS, can the pathogen be introduced to somewhere new and then, like a spark on dry kindling, ignite a massive blaze of infection.
On Feb. 21, 2003, a 64-year-old doctor checked into Room 911 at the Hotel Metropole in Hong Kong. He was already sick with SARS but felt well enough to travel. Public health officials documented a total of seven people directly infected by the doctor, making him a superspreader. Several of the people he infected were also superspreaders. One young man infected every doctor, nurse, and medical student who examined him in a Hong Kong hospital—more than 100 health care workers in total. A flight attendant from Singapore went on to infect at least 160 others. These travelers then brought the SARS virus home with them as a very unwelcome souvenir. One of these infected individuals arrived in Toronto. Several days after she returned home, she developed symptoms consistent with SARS and ultimately died. Nine other SARS cases and three deaths were directly linked to her, and the outbreak ultimately spread to 257 others. This chain of contagion accounted for more than 70 percent of Toronto’s total SARS cases. Although Toronto was besieged by SARS in 2003, Vancouver (with a similar population) saw only a handful of cases. The reason? No superspreaders were infected in Vancouver, said infectious disease expert James Lloyd-Smith of the University of California, Los Angeles. “SARS made the superspreader phenomenon so obvious we could no longer ignore it,” he said. But “SARS is just one point along a continuum—all infectious show this [pattern] to some degree.”
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