The grip of the novel coronavirus on the collective consciousness is, in itself, pandemic. But whether this disease will become fixed in the historical record of our species like smallpox, or an accepted part of life like influenza, remains to be seen. Though many of us are preoccupied with the question, we do not know how this situation will end.
Scientists across the globe are racing to find the drug or vaccine that might eradicate Covid-19. But disease endings are rarely so neat — the only infectious disease humans have ever managed to eradicate through medicine is smallpox.
Before coronavirus, the word “pandemic” tended to conjure a very different disease. The Black Death, which first raged through the world from 1346 to 1353, is described by scholars as the “greatest pandemic in recorded history,” killing some 30 to 60 percent of all Europeans. Driven by bubonic plague, the Black Death is typically presented as something horrible that happened once, long ago.
In a new study, researchers show how a wave of plague pandemics hit Europe over the course of 300 years, starting in the 1300s and continuing through to the 17th century. But while the disease itself remained rampant, the havoc it wreaked changed.
Among their key findings: As the years passed, more people got the plague. In the 14th century, during the Black Death, the number of people infected doubled every 43 days. In the 17th century, the number doubled every 11 days.
The findings were published in a study released Monday in the journal Proceedings of the National Academy of Sciences.
This study provides a clear-eyed look at how a pandemic can change, worsen, then dissipate — and give some guesses as to why. But there is only so much we can draw from the history books.
Lessons for coronavirus — Considering Covid-19, the study’s lead author David Earn, a mathematics professor at McMaster University, tells Inverse that this new research doesn’t tell us anything about herd immunity — sometimes touted as a strategy for ending this pandemic.
Plague outbreaks, he explains, “were sometimes separated by decades during which much of the population was replaced with people who had never been exposed.” Plague is also not associated with earned immunity, unlike other coronaviruses. The last plague outbreak in London occurred in 1665, lasting about a year. It grew the fastest of the epidemics that the team studied, yet the reasons for its decline are, at this point, not well understood.
Co-author Bob Bolker, a professor of mathematics and biology at McMaster University, tells Inverse that while the analytical methods for estimating the initial rate of spread they’ve developed aren’t “immediately useful” for Covid-19 application, they could be helpful in comparing the intrinsic rate of spread prior to control measures in different countries.
In the study, Earn’s team of statisticians, biologists, and evolutionary geneticists took a look at the sequence of plague epidemics that affected London from the 14th through to the 17th centuries. They estimated death rates by using data extracted from personal wills and testaments, parish registers, and the London Bills of Mortality.
“I’ve spent a lot of time collecting and digitizing archival records so that epidemic patterns can be revealed,” Earn says. “We wanted to understand whether there are any clear differences in the patterns of plague epidemics over the centuries.”
They found the disease spread faster by the end of the 300-year span. Why the later plague epidemics were faster is unclear, the team notes. But considering the estimated growth rate observed, the primary mode of transmission was not likely a direct transmission classified as pneumonic plague, they say. But they also can’t say confidently if it was one of the other two forms of plague, bubonic and septicemic.
Earn says this finding is especially interesting considering scientists now accept that the same pathogen caused all of the recorded plague epidemics in London. Plague is caused by the Yersinia pestis bacteria, and it’s generally spread via bites from body lice and fleas.
While the team emphasizes the cause of the acceleration in infection rates over time is unclear, they do hypothesize four possible reasons:
- Pathogen/host evolution
- Shifts in transmission mode
- Ecological and demographic changes
- Environmental changes
The “ecological and demographic changes” refer to the swelling population and density of London through the centuries. Bubonic plague is the most likely culprit behind the plagues examined here, so it is unlikely the number of humans directly drove the increase in infection rate — rather, it would be driven by the rising number of rats and fleas that accompanied population growth.
“Environmental changes” refer to the climatic changes in Northern Europe during the period, with the coldest time occurring in the 17th century. Still, the authors write, “it is challenging to make reliable inferences due to the lack of consensus about climate and weather variations.”
In our current quest to understand Covid-19’s future, scientists are considering a plethora of theories, including the possibility of mutated strains, changing modes of encountering and catching it, how being around other people alters odds of infection, and whether or not temperature and humidity have anything to do with spread.
By observing how these patterns in historical pandemics emerged, researchers may find clues to interpreting the present situation. That’s what this study team is working toward, with the aim of better understanding of how infectious diseases have spread, and stopped, over time. Perhaps, soon, we may have a clear idea of how — and why — coronavirus managed to run rampant across the globe.
Abstract: Historical records reveal the temporal patterns of a sequence of plague epidemics in London, United Kingdom, from the 14th to 17th centuries. Analysis of these records shows that later epidemics spread significantly faster (“accelerated”). Between the Black Death of 1348 and the later epidemics that culminated with the Great Plague of 1665, we estimate that the epidemic growth rate increased fourfold. Currently available data do not provide enough information to infer the mode of plague transmission in any given epidemic; nevertheless, order-of-magnitude estimates of epidemic parameters suggest that the observed slow growth rates in the 14th century are inconsistent with direct (pneumonic) transmission. We discuss the potential roles of demographic and ecological factors, such as climate change or human or rat population density, in driving the observed acceleration.