Lessons From Past Outbreaks Could Help Fight The Coronavirus Pandemic

Emergency flu hospital, staffed by U.S. Navy hospital corpsmen, that was set up in San Francisco to help care for those stricken by the influenza outbreak in 1918. Image: Getty
The 1918 influenza pandemic and 2002–2003 SARS outbreak suggest social distancing measures, communication and international cooperation are the most effective methods to slow COVID-19

On March 11 the World Health Organization officially designated the novel coronavirus outbreak a pandemic. Defined as the worldwide spread of a new disease, such a declaration is the first to be made since the 2009 H1N1 swine flu. As of this writing, there have been approximately 336,000 confirmed cases of the new disease, called COVID-19, resulting in more than 14,600 deaths worldwide.

Although a coronavirus—a family of viruses that cause illnesses ranging from the common cold to severe acute respiratory syndrome (SARS)—had not previously triggered a pandemic, this is not the first time we have seen the global transmission of a serious disease. Studying past outbreaks can help scientists better estimate the trajectory of COVID-19 and identify the best measures to slow its spread.

“Historically, we could look at everything back to the 1918 influenza pandemic. But in more contemporary times, we’d be looking at the 2015–2016 Zika outbreak in Central and South America, the global SARS outbreak from 2002 to 2003 and the Ebola outbreak in West Africa from 2014 to 2016,” says Jeremy Youde, dean of the College of Liberal Arts at the University of Minnesota Duluth and an expert on global health politics.

Whereas COVID-19 is caused by a coronavirus and not an influenza virus, the 1918 flu pandemic—which caused at least 50 million deaths worldwide, according to the Centers for Disease Control and Prevention—might be the best model to understand this novel pathogen’s behavior. It is also an outbreak for which massive social interventions were undertaken.

“Past influenza pandemics give some sense of what the overall [trajectory] of a virus like this would be because the reproductive number of this virus”—defined as how many people each infectious person transmits the disease to in a completely susceptible population—“is pretty similar to that of a pandemic flu,” says Marc Lipsitch, a professor of epidemiology and director of the Center for Communicable Disease Dynamics at Harvard University. Although it is difficult to determine exact figures for an emerging disease, reports put the reproductive number of COVID-19 between 2 and 2.5. The median reproductive number for the 1918 flu pandemic was around 1.8. Lipsitch estimates that between about 20 and 60 percent of the global population will ultimately become infected with the novel coronavirus, or SARS-CoV-2.

Although every virus and resulting disease is different, a look at epidemic dynamics of both COVID-19 and the 1918 flu points to similar successful containment procedures. In a 2007 study published in JAMA, Howard Markel of the Center for the History of Medicine at the University of Michigan Medical School and his co-authors analyzed the excess deaths from pneumonia and influenza (meaning how many more there were than usual during nonpandemic years) in 43 U.S. cities from September 8, 1918 through February 22, 1919. Despite the fact that all of the cities implemented nonpharmaceutical interventions, it was the timing of activation, the duration and the combination of measures that determined their success. The researchers found “a strong association between early, sustained, and layered application of [such] interventions and mitigating the consequences of the 1918–1919 influenza pandemic in the United States.”

The most effective class of nonpharmaceutical control measures were those related to social distancing: canceling public gatherings, closing places of worship, schools, bars and restaurants, isolating the sick and quarantining those they came in contact with. (Many cities around the world have adopted such measures in the current outbreak.) “In my opinion, that is probably the most important single class of things to do, as quickly as possible, to slow the spread” of a pandemic, Lipsitch says. “Waiting until you can see that you have a problem is waiting too long, because there’s a delay in seeing the fruits of the measures.”

By undertaking these steps early, populations can also prevent peak demands on their health care systems and flatten the pandemic curve—that is, have a gradual increase in cases over time rather than many all at once. This slowdown is especially important because it can take two or three weeks before those infected with SARS-CoV-2 are sick enough to require intensive care, so demand could spike quickly. In a 2007 Proceedings of the National Academy of Sciences USA paper, Lipsitch and two other researchers showed that during the 1918 influenza pandemic, cities that intervened early and intensively to slow transmission through social distancing, such as such as St. Louis, Mo., had slower epidemics with smaller peaks, compared with those that waited longer to act, such as Philadelphia.

Similarly, in a preprint report, Lipsitch and his colleagues analyzed the timing of control measures and of community spread of COVID-19 in the Chinese cities of Wuhan and Guangzhou from January 10 to February 29, 2020. Wuhan implemented measures such as strict social distancing and quarantining contacts of infected individuals six weeks after sustained local transmission was observed, whereas Guangzhou implemented these measures within one week. The researchers found that early intervention, relative to the course of the disease in the population, resulted in Guangzhou having “lower epidemic sizes and peaks” than Wuhan in the first wave of the outbreak.

Intense public measures are also one reason SARS, which resulted in around 8,000 cases with a global case fatality rate of 11 percent, was eliminated from the population. One difference, however, is that with SARS, those who were infected were likely quite sick before they became very infectious, whereas with COVID-19, people appear to be fairly infectious when they first start developing symptoms—or even before then—according to Lipsitch. In fact, in a paper published last week in Science, researchers note that with the novel coronavirus, “undocumented infections often experience mild, limited or no symptoms and hence go unrecognized, and, depending on their contagiousness and numbers, can expose a far greater portion of the population to virus than would otherwise occur.” So despite the lower fatality rate, COVID-19 has resulted in more deaths than SARS and Middle East respiratory syndrome (MERS)—which has a 34 percent case fatality rate—combined.

Other disease countermeasures include making buildings less favorable to viral transmission by humidifying and ventilating them and implementing ongoing communication with the public so it can understand and react appropriately. One issue during the SARS outbreak was that, for a number of months, the government in China actively denied the existence of the disease. Instead people relied on text messages and rumors about a new killer flu.

“Because the government wasn’t proving itself to be reliable, it became that much harder to actually address the outbreak. And it allowed the disease to really take more of a hold than it might otherwise have,” Duluth’s Youde says.

In order to slow down epidemics and pandemics, either the conditions for transmission need to become unfavorable over a long period of time or enough people have to become immune so that transmission cannot pick up again if the virus is reintroduced. The latter scenario, of course, means the fraction of the population that is immune has to be high enough so that each contact and infected case creates fewer than a single new one.

Regular flu and cold viruses have a strongly seasonal pattern of infectiousness in temperate regions such as the continental U.S. This seasonality is partly related to changing weather conditions and how easily the pathogens are transmitted, but it is also because of the number of susceptible hosts as people are made immune by past exposure. The same is not true of new viruses, such as the one that causes COVID-19, however.

“Pandemics happen out of season. And pandemic viruses have the whole world before them,” says Lipsitch, who explains that the advantage for novel viruses is that almost no one is immune to them. Seasonal viruses, on the other hand, operate on a thinner margin—meaning the majority of people have some immunity. So those pathogens are most successful when conditions for transmission are most favorable, which is usually winter. With COVID-19, Lipsitch adds, “I think [it’s] more likely seasonal changes will modestly reduce the rate of transmission and maybe slow things down—but probably not to the point of making the number of cases [decrease but rather] go up more slowly.”

For now, a coordinated global effort among researchers, countries, and nongovernmental and international organizations is necessary to address the current pandemic itself while learning basic information about the virus and its spread dynamics. “In terms of having some sort of international response, we’re trying to build the airplane as we’re flying it,” Youde says.