Disease about which we know nothing and against which we have no defense is terrifying, and the plague was one such. In medieval times, its cause was unknown, treatment was nonexistent and its impact was devastating. Death rates are estimated to have ranged from a third to two-thirds for “regular” bubonic plague, and close to 100 percent for the pneumonic form that attacked the lungs. Mortality rates like that make the coronavirus seem practically benign.
Today we know more. Antibiotics were invented in the early 1940s, which is helpful because plague is caused by a bacterium, Yersinia pestis. The plague is still dangerous, especially in the pneumonic form: treatment must begin quickly if it’s to succeed. At least we aren’t reduced to thoughts and prayers.
We also know today that we don’t get plague for our sins. We get the bacteria from being bitten by a Yersinia-carrying rat flea – or from droplets in the air emitted by the sick. Yes, just like the coronavirus.
Given the unknowns of the coronavirus, it’s interesting to know exactly how the plague was transmitted in medieval and Renaissance times, but the truth is we don’t know. Nor are we sure about the precise toll of the disease because of spotty (if any) record-keeping, let alone reliable diagnoses. In London, for instance, the earliest published records of death were in 1538.
However, researchers at Canada’s McMaster University thought of a potential proxy for death records. Their study estimates the manner of the plague’s spread based on thousands of last wills and testaments archived in London from the 14th to the 17th century, parish records and the London “Bills of Mortality.”
“At that time, people typically wrote wills because they were dying or they feared they might die imminently, so we hypothesized that the dates of wills would be a good proxy for the spread of fear, and of death itself,” explains lead author Prof. David Earn of the mathematics and statistics department at McMaster.
These days, documents written on the deathbed might be eyed askance on the grounds that the angel of death’s presence in the room renders one mentally incapacitated. Apparently that wasn’t so back then. It’s true that at least some wills were surely written well in advance of the unhappy day. But when epidemics were raging, will dates were likely to have been correlated with the fear of infection and hence with disease incidence, the researchers postulate. Really? Note that “internet searches for influenza symptoms can predict 21st-century epidemic patterns,” they write.
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While noting the possibility that records were better in the 17th century than in the 14th, the team estimates that the plague spread four times faster during the Great Plague of 1665 than it had 300 years earlier, during the Black Death of 1348. Their study appears in the Proceedings of the National Academy of Sciences.
In the 14th century, the number of people infected during an outbreak doubled approximately every 43 days. By the 17th century, the number was doubling every 11 days, the researcher#s estimate.
By the way, in the year 1348, Pope Clement VI announced that Jews weren’t behind the Black Death, on the reasonable grounds that they were dying of it too. Anybody thinking they were had been “seduced by that liar, the devil,” the pontiff explained.
When the cold comes
What might that fourfold acceleration in the 17th century versus the 14th century indicate? Not evolution of the bacteria, it seems. The team qualifies that the Yersinia bacterial strains behind the medieval and Renaissance plagues are the same one lurking in rat fleas today, based on genetic evidence. While mentioning it, the team also doesn't think it likely that we humans underwent change rendering us more susceptible to the bug.
It may speak of how the epidemic was transmitted in London, the researchers explain. The slow dissemination in the 14th century is inconsistent with direct transmission by direct infection, i.e., spraying droplets on one another. It argues in favor of environmental, ecological and/or demographic factors. The 14th-century Londoners were likely catching the disease after getting bitten by rat fleas.
But plague can reach the lungs. The acceleration in the 17th-century epidemic could argue for more pneumonic transmission, human-to-human, by coughing droplets into the air. Pneumonic plague is generally assumed to spread faster at the level of the population than parasite-borne disease.
Crowding of people and/or rats could have been a factor too. London’s population grew greatly from the 14th to the 17th centuries – and when people fell ill, they and their contacts were isolated in pest houses. Human population density would pertain to pneumonic dissemination, but rat population density could have been a factor too.
Cold may have been a factor in the plague’s acceleration too. The team also notes that the 17th century had become a lot colder than the 14th century.
This is a good place to enter a caveat, which is that records can be misleading. Israeli archaeologists have postulated that another famed epidemic, the “Plague of Justinian” – which supposedly wreaked havoc in Eurasia and Africa from about the year 540 to 745 – may have done no such thing. That epidemic began in Egypt, this is true, and spread throughout Europe and to Western Asia. But after that, the situation turns muddy. Supposedly it killed a quarter to half the population around the Mediterranean and triggered the Dark Ages. The snag is that a calamity of that magnitude, killing as many as 100 million people, should have left behind a great deal of grisly evidence, such as mass graves. And the evidence isn’t there, a separate study found in 2019.
So why did we gain the impression that the Justinianic Plague happened? Because of bad history and the human tendency to cherry-pick horror stories. Even if a given city did experience horrors and a scribe therein described them faithfully, that doesn’t mean other cities did too.
That caveat in place – that the history remains obscure – the parallels with our current situation are eerie.
Today we can cure bacterial diseases, or try to, using antibiotics. There are almost no cures for viruses, on the other hand. Treatment is generally confined to beefing up our immune systems and alleviating the symptoms before they kill us. But when we catch the coronavirus, we have something in common with the plague patients of yore: We don’t know how to make it go away. Moreover, many fear that the onset of winter in the northern hemisphere will drive new spikes in infection rates as people crowd inside closed spaces, though it bears pointing out that, so far, hot countries were not spared and cold ones didn’t necessarily get it worse.
At least we have advantages over the medieval vassal with plague, because their ideas of shoring up the immune system – for instance, bleeding the hapless patient using leeches – were wrong. Which doesn’t mean all our ideas of shoring up the immune system have merit. Note that despite enthusiasm in some quarters, the jury’s still out on the value of injecting coronavirus patients with Remdesivir. But the more we know about how the disease can be disseminated, the better we can protect ourselves and the less we shall have to resort to thoughts and prayers.