Excerpt – many people have heard about R0—the basic reproductive number of a pathogen, a measure of its contagiousness on average. But unless you’ve been reading scientific journals, you’re less likely to have encountered k, the measure of its dispersion. The definition of k is a mouthful, but it’s simply a way of asking whether a virus spreads in a steady manner or in big bursts, whereby one person infects many, all at once. After nine months of collecting epidemiological data, we know that this is an overdispersed pathogen, meaning that it tends to spread in clusters, but this knowledge has not yet fully entered our way of thinking about the pandemic—or our preventive practices.
[..] Unsurprisingly, SARS-CoV, the previous incarnation of SARS-CoV-2 that caused the 2003 SARS outbreak, was also overdispersed in this way: The majority of infected people did not transmit it, but a few super-spreading events caused most of the outbreaks. MERS, another coronavirus cousin of SARS, also appears overdispersed, but luckily, it does not—yet—transmit well among humans.
This kind of behavior, alternating between being super infectious and fairly noninfectious, is exactly what k captures, and what focusing solely on R hides. Samuel Scarpino, an assistant professor of epidemiology and complex systems at Northeastern, told me that this has been a huge challenge, especially for health authorities in Western societies, where the pandemic playbook was geared toward the flu—and not without reason, because pandemic flu is a genuine threat. However, influenza does not have the same level of clustering behavior.
We can think of disease patterns as leaning deterministic or stochastic: In the former, an outbreak’s distribution is more linear and predictable; in the latter, randomness plays a much larger role and predictions are hard, if not impossible, to make. In deterministic trajectories, we expect what happened yesterday to give us a good sense of what to expect tomorrow. Stochastic phenomena, however, don’t operate like that—the same inputs don’t always produce the same outputs, and things can tip over quickly from one state to the other. As Scarpino told me, “Diseases like the flu are pretty nearly deterministic and R0 (while flawed) paints about the right picture (nearly impossible to stop until there’s a vaccine).” That’s not necessarily the case with super-spreading diseases.
[..] In study after study, we see that super-spreading clusters of COVID-19 almost overwhelmingly occur in poorly ventilated, indoor environments where many people congregate over time—weddings, churches, choirs, gyms, funerals, restaurants, and such—especially when there is loud talking or singing without masks. For super-spreading events to occur, multiple things have to be happening at the same time, and the risk is not equal in every setting and activity, Muge Cevik, a clinical lecturer in infectious diseases and medical virology at the University of St. Andrews and a co-author of a recent extensive review of transmission conditions for COVID-19, told me.
[..] Given that some people infect others before they show symptoms, or when they have very mild or even no symptoms, it’s not always possible to know if we are highly infectious ourselves. We don’t even know if there are more factors yet to be discovered that influence super-spreading. But we don’t need to know all the sufficient factors that go into a super-spreading event to avoid what seems to be a necessary condition most of the time: many people, especially in a poorly ventilated indoor setting, and especially not wearing masks. As Natalie Dean, a biostatistician at the University of Florida, told me, given the huge numbers associated with these clusters, targeting them would be very effective in getting our transmission numbers down.
[..] Right now, many states and nations engage in what is called forward or prospective contact tracing. Once an infected person is identified, we try to find out with whom they interacted afterward so that we can warn, test, isolate, and quarantine these potential exposures. But that’s not the only way to trace contacts. And, because of overdispersion, it’s not necessarily where the most bang for the buck lies. Instead, in many cases, we should try to work backwards to see who first infected the subject.
Because of overdispersion, most people will have been infected by someone who also infected other people, because only a small percentage of people infect many at a time, whereas most infect zero or maybe one person. As Adam Kucharski, an epidemiologist and the author of the book The Rules of Contagion, explained to me, if we can use retrospective contact tracing to find the person who infected our patient, and then trace the forward contacts of the infecting person, we are generally going to find a lot more cases compared with forward-tracing contacts of the infected patient, which will merely identify potential exposures, many of which will not happen anyway, because most transmission chains die out on their own.
[..] In an overdispersed regime, identifying transmission events (someone infected someone else) is more important than identifying infected individuals. Consider an infected person and their 20 forward contacts—people they met since they got infected. Let’s say we test 10 of them with a cheap, rapid test and get our results back in an hour or two. This isn’t a great way to determine exactly who is sick out of that 10, because our test will miss some positives, but that’s fine for our purposes. If everyone is negative, we can act as if nobody is infected, because the test is pretty good at finding negatives. However, the moment we find a few transmissions, we know we may have a super-spreader event, and we can tell all 20 people to assume they are positive and to self-isolate—if there are one or two transmissions, there are likely more, exactly because of the clustering behavior. Depending on age and other factors, we can test those people individually using PCR tests, which can pinpoint who is infected, or ask them all to wait it out.
[..] Why haven’t our usual analytic tools—case studies, multi-country comparisons—given us better answers? It’s not intellectually satisfying, but because of the overdispersion and its stochasticity, there may not be an explanation beyond that the worst-hit regions, at least initially, simply had a few unlucky early super-spreading events. It wasn’t just pure luck: Dense populations, older citizens, and congregate living, for example, made cities around the world more susceptible to outbreaks compared with rural, less dense places and those with younger populations, less mass transit, or healthier citizenry.
[..] Europe’s achieving a measure of success this summer and relaxing, including opening up indoor events with larger numbers, is instructive in another important aspect of managing an overdispersed pathogen: Compared with a steadier regime, success in a stochastic scenario can be more fragile than it looks.
Once a country has too many outbreaks, it’s almost as if the pandemic switches into “flu mode,” as Scarpino put it, meaning high, sustained levels of community spread even though a majority of infected people may not be transmitting onward. Scarpino explained that barring truly drastic measures, once in that widespread and elevated mode, COVID-19 can keep spreading because of the sheer number of chains already out there. Plus, the overwhelming numbers may eventually spark more clusters, further worsening the situation.
[..] [professor at Tohoku University and member of the National COVID-19 Cluster Taskforce at Japan’s Ministry of Health, Labour and Welfare Hitoshi] Oshitani told me that in Japan, they had noticed the overdispersion characteristics of COVID-19 as early as February, and thus created a strategy focusing mostly on cluster-busting, which tries to prevent one cluster from igniting another. Oshitani said he believes that “the chain of transmission cannot be sustained without a chain of clusters or a megacluster.” Japan thus carried out a cluster-busting approach, including undertaking aggressive backward tracing to uncover clusters. Japan also focused on ventilation, counseling its population to avoid places where the three C’s come together—crowds in closed spaces in close contact, especially if there’s talking or singing—bringing together the science of overdispersion with the recognition of airborne aerosol transmission, as well as presymptomatic and asymptomatic transmission.
[..] It’s not always the restrictiveness of the rules, but whether they target the right dangers. As [Princeton doctoral candidate in ecology and evolutionary biology Dylan] Morris put it, “Japan’s commitment to ‘cluster-busting’ allowed it to achieve impressive mitigation with judiciously chosen restrictions. Countries that have ignored super-spreading have risked getting the worst of both worlds: burdensome restrictions that fail to achieve substantial mitigation. The U.K.’s recent decision to limit outdoor gatherings to six people while allowing pubs and bars to remain open is just one of many such examples.”
Full article, Tufekci Z. Atlantic 2020.9.30