One of the things that I've always thought that it was not the Bubonic Plague (Y. Pestis) as we see it today.
Specifically, the spread of the Plague was blisteringly fast (5-8 km a day) for the transportation systems of the day, which mitigates against the modern plague.
There are variants of the disease that are more likely to move at this speed, most notably the marmot variant that are far more likely to infect lung tissue.
Because they allow for direct human to human (HtH) transmission, the spread is accelerated.
Now an analysis of the disease in Eyam in Derbyshire indicates that the spread of the disease was largely HtH:
Without a doubt, the bubonic plague has been one of the deadliest and most devastating infectious diseases in all of human history. The bacterial infection—caused by Yersinia pestis—has sparked dozens of outbreaks and three massive pandemics, killing hundreds of millions of people. The Justinian Plague from 541 to 767 is estimated to have killed up to 50 percent of the population at the time and spurred the demise of the Roman Empire. Likewise, the fourteenth century Black Death, which circumnavigated Europe in just a few years, ended up slaughtering as much as 60 percent of the continent’s population.I would expect more results to support the differences between the current and historical versions will become clearer as more genetic data is collected from graves and more epidemiological studies like this one are conducted..
But despite the indelible mark the dark disease has left on humanity, researchers still aren’t certain how exactly Yersinia sweeps through cities and countries. The highly infectious disease has historically been linked to rodents, in which the bacteria can fester, and rat fleas, which take in and then vomit out the bacteria in subsequent bites. Thus, booming vermin populations have long been assumed to spark and sustain outbreaks. But a fresh analysis of a tiny village in England—made famous for its handling of a plague outbreak from 1665 to 1666—stands to challenge the view.
The Derbyshire village of Eyam, estimated to have a population of around 700 at the time of the outbreak, took the remarkable step of imposing a quarantine on itself—a move almost unheard of at the time. While the villagers aimed to spare neighboring parishes—which they did—the quarantine and the villagers’ detailed death records also provided a perfect opportunity for studying plague transmission dynamics.
In a new analysis of the outbreak, researchers estimate that rodent-to-human transmission accounted for only a quarter of all infections, while human-to-human transmission made up the rest. The finding, published Wednesday in Proceedings of the Royal Society B, adds fuel to a hot debate among academics about how plague spreads. And more importantly, it has the potential to inform public health responses to modern-day plague outbreaks, which still occur around the world, particularly in Africa and South America (albeit on much smaller scales than historical outbreaks).
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They arrived at the point by first digging into historic population and death records of Eyam—now known as “plague village.” The researchers looked at factors such as age, wealth, household structure, and gender of the 257 people who died of plague. The deaths, which began after the delivery of flea-infested cloth from London, lasted from September 1665 to October 1666.
Next, the researchers used a stochastic compartmental model and Bayesian analytical methods to recreate the pattern of deaths and trajectory of the outbreak revealed by the records. The model included rodent-to-human transmission and human-to-human transmission, which was estimated to occur within a fixed window of 11 days between exposure, infection, and death. (While there were oral reports that three villagers recovered from the plague, those weren’t recorded in documents so the researchers tossed them out of their main analysis. However, when they did try including them, it didn’t alter their overall findings.)
The researchers found that human-to-human transmission accounted for 75 percent of all infections, with age, wealth, and household structure playing big roles in who got sick. Kids and family members of victims were the groups most affected by the plague. The village’s wealthy were less likely to get the plague, possibly due to less contact with general village folk and vermin.
1 comments :
Note the "May upend" in the title.
Couple of caveats
This isn't a new theory, I have seen arguments about the relative roles for years.
Human to Human could be by vermine, just as Rat to Human, and indeed that is what the underlying article argues.
The village is from the 1665-66 plague outbreak, so the question of how it would apply to the 14th C out break nature is complicated.
I have personally wondered if the high mortality of that plague, and the following Children's plague were due to selection in the human population.
This may in fact explain the relative virulence of the 1665-66 plague, as the disease hasn't been seen in England since Shakespeare's day.
There could be selection on the Y Pestis side too: the last couple of studies I have seen seem to say it was Y Pestis in Justine's, the 14th C, and the 1665-66 plague. Getting the degree of genetic variation between is hard (they are having trouble with analyzing the 1919 Flu, and the DNA is no where near as degraded. Though I am not clear how much being a virus makes it harder).
However, all this is consistent with rodents as initial vector.
The most modern plague outbreak started in Manchuria, and is attributed to newly active Chinese -- as opposed to Manch -- marmot hunters.
BTW, the plague of Justian, according to contemporary sources -- which are not reliable -- came to Constantinople without either humans or rats carrying: it was ships with entirely dead crews and not a living thing on them that washed up. That begs the questions of what the fleas lived on, but it make a Hell of a good story.
For gigles, Fred Hoyle thought it was a space bug, and Cantor thought it was antrax.
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