/ Maggie Koerth-Baker / 8 am Mon, Apr 8 2013
  • Submit
  • About Us
  • Contact Us
  • Advertise here
  • Forums
  • Shedding light on the Black Death

    Shedding light on the Black Death

    Seven hundred years ago, millions of Europeans were wiped out by a disease we still don’t entirely understand. The Black Death might seem like a pretty open-and-shut case at this point: It was caused by plague-bearing fleas that hitched rides on the rats that infested a grim and grimy medieval world. The End.

    But that simplified version only makes sense if you overlook some important facts about how the plague (which still exists) operates today. “The Black Death killed between 30 and 50 percent of the affected population,” says Sharon DeWitte, assistant professor of anthropology and biology at The University of South Carolina. “Modern plague, at most, kills between 2 and 3 percent, and that’s even in areas without access to modern medicine.”

    What’s more, DeWitte says, recorded symptoms from the Black Death don’t entirely match up with those of modern plague. And the Black Death seems to have spread through populations faster and killed much faster than its modern cousin. The differences are striking enough that some scientists, including DeWitte at one point, have suspected that the Black Death might not have been caused by plague at all. But genomic reconstructions of ancient DNA suggest the two are one. So what changed? Ultimately, that’s the question that makes last month’s discovery of a new Black Death cemetery in London so important.

    Given the vast numbers of people who died in the Black Death, there are relatively few burials that can be absolutely confirmed as containing Black Death victims, and only Black Death victims. DeWitte could only think of three when I spoke to her. But it makes sense. To put it simply, in the midst of a horrific catastrophe nobody was really thinking about how to makes sure the data would be nice and tidy for scientists to find hundreds of years later. Medieval writers didn't necessarily record information that would have helped archaeologists identify a Black Death cemetery. What's more, it wasn't even totally normal to bury nothing but Black Death victims together in one place. "A lot of them were just incorporated into existing cemeteries," DeWitte said.

    That's made it difficult to know whether Yersinia pestis — the bacteria that causes the plague — really is present in Black Death victims. This work is already hampered by the degradation of DNA over the centuries. Finding tiny Y. pestis is hard enough, even in people who were killed by it. Mixed burials add the extra complexity of not knowing whether the body you're working on actually died from Black Death, to begin with.

    Because of that, the best work in this field comes from England, where we have good documentation of a few places that were set aside specifically for victims of the Black Death. The newly uncovered cemetery might be one of those places — at any rate, there was definitely a recorded Black Death cemetery that would have been in about the same location.

    If that turns out to be the case, then the bones of the people buried there could help scientists fill in the gaps on the Black Death.

    In 2011, a team led by McMaster University paleogeneticist Hendrik Poinar became the first to reconstruct a full genome for Black Death era Yersinia pestis.

    This was not a full and complete genome drawn from a single bacterium inhabiting the body of a single victim. Instead, the genome was patched together from bits and pieces of DNA in remains taken from London's East Smithfield cemetery. The small chunks were lined up to create a whole, similar to the way you make a panoramic photo by combining a series of different shots. Hendrik Poinar calls it a "draft" of the genome, rather than a smooth, polished work of biology.

    The draft tells us a couple of things. First, the Y. pestis of the Black Death era is related to modern Y. pestis. In fact, it's probably the ancestor of all the strains of Y. pestis that exist today. Second — and this is the weird part — there is really not much difference between the old Y. pestis and the new. It boils down to about 100 genetic changes, few of which seem to have given the bacteria enough of an evolutionary advantage that they spread widely through the population.

    Genetically, Y. pestis has barely changed. Its infection profile in the real world, though, has changed massively. That suggests that at least some of those small alterations in the genome must have been extremely important. But which ones? And why? To answer those questions, you could reverse-engineer the evolution of Y. pestis in the lab. "We'd have an opportunity to test those changes, one at a time, and find out," Poinar said. "... If we could do it in a form or fashion that wouldn't terrify people."

    But, you know, good luck with that.

    Instead, what would be really helpful is some burials from later outbreaks of the Black Death. Poinar's draft genome comes from bodies that date to the 14th and early 15th centuries. And his draft of the Y. pestis genome suggests that this bacterium might have a relatively slow rate of evolutionary change. During outbreaks, though, when there are more bacteria multiplying and they have more hosts to multiply in, change can happen faster.

    "Now, if the new burial dates to the Great Plague of London, around 1665, I'd really like to see that," Poinar said. That outbreak was less deadly than earlier ones, killing "only" about 20 to 30 percent of the people who contracted it. If you could compare the DNA of Y. pestis of the 14th century with that of Y. pestis of the 17th, you might begin to see which changes ultimately made the bacteria less of a killer.

    That, however, remains to be seen. So far, 13 bodies have been found at the new cemetery site. Those, unfortunately, are of the same vintage as the ones in East Smithfield. But, if the new cemetery is the recorded Black Death cemetery that experts think it is, then we know it was in use all the way up through the 1500s. Find the right bodies, and you might be able to get a peek at how Y. pestis was tamed.

    / / COMMENTS

    / /


    1. How have scientists ruled out the possibility that it’s not the bacteria that has changed, but Humans.  As a population, it sounds like we underwent a fairly serious selection – specifically for susceptibility to black death.

      1. That wouldn’t have been inherited uniformly by all humans though – is there any data on survival rates for people with ancestors outside of Eurasia at the time of the plagues?

        1. Apparently plague (like a lot of things) really only pops up in the developing world these days.  In particular I’ve always heard the only place you were at risk for catching it was in South Pacific islands.


          So I’d assume a good chunk of the modern data we have covers the “not exposed during the middle ages” bases. 

          1. Actually, you can catch it in the Jemez Mountains in New Mexico, USA. It’s endemic in the ground squirrels. You don’t walk there without making certain that your pants are closed at the ankles and sleeves at the wrists. Animals need excellent flea treatments if they go or are outside. Classic signs of an outbreak are dead ground squirrels in plain sight. Arrived there about a century ago.

        2. No guarantee that resistance to the black death is exclusive to the black death. In general, as population density increased, plagues like this happened. We could be seeing a more generic “increased resistance to communicable diseases” than a “resistance to disease X” that many populations were selected for as they hit certain population milestones.

          1. That could hypothetically be the case but only if there is a plausible mechanism by which it could be accomplished.  And that seems incredibly implausible to me.  Evolution doesn’t operate on abstract concepts like “resistance to communicable diseases”, it operates on particular sequences of DNA bases.  And in context it’s going to look like any other optimization problem: if you make the immune system robust to one particular type of threat (let’s say it gets better at dissolving the protein coats of viri) then it will become less effective against some other type of threat (perhaps it’s now less effective against bacterial infections).  Plus the immune system is fighting a moving target — check out some of the “clever” strategies “used” by viri to get past the immune system.  If your immune system gets really good at recognizing the protein coat of a virus then only viri that effectively disguise their protein coats get through to the next generation and now you have shape-changing viri for which your immune system is not optimized.

            TL;DR: “Universal optimization” is pretty much an oxymoron so it seems unlikely to me that one could develop a blanket “resistance to communicable diseases”.

            1. I was thinking more like folks with more active immune systems would have a higher rate of survival in a density populated area than those with less active systems, but would have a higher rate of autoimmune illness.

            2. I have every confidence that your biology is spotless, but for god’s sake man, promise me, right now, to never, ever, EVER write (or say) “viri” ever again! The proper plural of “virus” is “viruses”, not anything else. 

              The whole “pluralize by swapping -us with an -i” comes from Latin, specifically Latin second declension nouns where the nominative singular ending is -us (like “fungus”, for instance), which is pluralized with an -i ending (like “fungi”).

              The word “virus” is indeed Latin, but in Latin it is a mass noun meaning something like “venom”, and thus it does not pluralize. It’s like saying “homeworks” in English, it makes no sense. Even if it did pluralize, it is not at all certain that it would pluralize as “virii” (like “radius/radii”, and by the way, you really should be saying “radiuses” even though “radii” is technically not incorrect).

              More importantly, we’re writing in English right now, and in English, we have our own rules for making plurals. “Virus” is just as much an English word as it is a Latin one by now, so just write “viruses”. It has the advantage of both actually being accurate and not making you look like a buffoon. 

              Also, to forestall any future mishaps: “octopus”, “platypus” and “cactus” all derive from Greek, not Latin, so writing “octopi”, “platypi” and “cacti” is even more silly than writing “viri” (though that one is hard to beat). “Octopuses”, “platypuses” and “cactuses” are the proper plurals.  

            3. I’ll give you octopuses when you pry octopodes from my cold, dead lips!

              That said, both platypus and cactus entered the English language from Latin, despite their Greek roots, which is why they are commonly – and correctly so –  associated with Latin rather than Greek plurals.

        3. The great plague has been endemic in parts of Eurasia and Africa since at least the mid 6th century, and parts of North America since the early 20th century. But I think the estimated survival rates rely on a few cities which kept records through the 14th century epidemics.

      2. So there’s a couple of things going on here. They can’t rule that out completely, but I chose not to focus on it because there’s some good evidence that the bacteria, itself, is the larger issue. 

        Humans, as a whole, weren’t selected on by the Black Death. Europeans were. And the genetic evidence suggests that all the plague that exists today descended from the strain involved in the Black Death. So if this is about human adaptation, then only Europeans and their descendants should have low death rates from plague. But that’s not the case. If I recall correctly (notes aren’t currently in front of me) the single digit kill rate percentages cited in this story actually come from Malaysia. 

        I should have clarified this. Thanks for pointing it out. 

        1. “Humans, as a whole, weren’t selected on by the Black Death. Europeans were.”

          I think this is a bit misleading. First, the Black Death was only one outbreak of the Great Plague. In Africa and Eurasia, there have been several known outbreaks since the Sixth Century, with wild reservoirs in Africa and Eurasia. In the Americas, at least since the Nineteenth Century, although it’s possible that some parts of the Americas were affected by some of the Seventeenth Century outbreaks. Second, the Black Death itself hit China and India at least as hard as it hit Europe.

    2. For anyone who has not read it, The Doomsday Book by Connie Willis is an amazing sci-fi account of the plague.

      1.  I enjoyed the book (Willis writes very well) but would not recommend it as a basis for understanding the historical Black Death.

      2.  Yuk, what a horrible read. It takes a character three quarters of the book to utter a simple sentence, and all the other characters are bumbling idiots. I’ve rarely been so annoyed by a book. To say nothing of the fact that it is basically the same story as her other book “To say nothing of the dog”. I was actually rooting for the black death.

    3. I was surprised not to see any mention of the historian Samuel Cohn, who’s been arguing for years now that the Death wasn’t Y. Pestis; see his _The Black Death Transformed: Disease and Culture in Early Renaissance Europe_ (London: Arnold, 2002). I’m not sure is he’s backed down from that stance at all with all the recent DNA testing, but his arguments are compelling.

    4. I recommend Philip Ziegler’s purple-jacketed book if you want a comprehensive overview of the historical Black Death.

      Keep in mind there were three forms of Black Death identified – the pneumonic, bubonic and septicemic plague.  The pneumonic variant both spreads and kills extremely rapidly, with a near 100% mortality rate.

      1. You’re right; once the pneumonic form got going, it was game over.  I suspect that later plagues, like in 1665, weren’t as bad as the Black Death because living conditions, while still squalid, were improved enough that the pneumonic form couldn’t get a foothold.

    5. is not just that we are the offspring of those people who , for whatever reason, had immunity to the bubonic plague. We have by definition more immunity that the 80% of medieval people who didnt have immunity and so didnt pass on any offspring. 

    6. It seems obvious there is a huge selective advantage for bacteria in becoming slower in their lethality, and eventually less deadly altogether.  For those who’ve never thought about it before: intuitively, the longer an infected person lives, the more chance their bacteria have to infect others; thus you’d expect that mutated bacteria which are 50% less deadly (or take twice as long to kill) will spread about twice as widely. 

      Perhaps one could consider the jump from one infected human to another is close – analogically – to the jump of an organism from one ecosystem to a new one, in terms of the accelerated evolutionary pressure it exerts.

      It’s worth considering, as a point of comparison, the history of syphilis in Europe.  During the first known outbreak (without getting into the disputes about its origin) the disease was so deadly that it often killed within a few months – not years, months.  Within less than a century it had become a much slower killer, but was still considered universally deadly through the 1700s.  By the 1800s, it was something one could survive to old age.  The current form of the disease is now considered to be fatal only somewhere between 10-50% if completely untreated.

      1. That’s an interesting assertion, but how do you determine whether it was the organism self selecting for more efficient distribution, or simply that the infected people were becoming more resistant, and selecting for more efficient survival strategies?  It wouldn’t take very long to weed out the populations that were most susceptible, and to favor those who were more resistant ( in this case,  died slowest ) – not more than a few generations… so close to your century.  ( As I mentioned above, resistance and immunity are two different things, and should not be confused ).  

        I suspect the truth is probably some combination of the two.  A degree of herd resistance ( in the form of increased survival and delayed onset of deficits ), combined with deselection of overly agressive forms of the disease. 

        1. One reason to suppose that the selection for less lethal bacteria will have had a larger effect than selection for less killable humans is that it has been occurring over enormously many more generations over the same amount of calendar time.  Human generations are rarely less than 14 years, whereas the relevant “generation” time for plague would be the length of time it takes to pass from one host to another.

          1. Exactly.  I should have spelled that out explicitly as part of my reasoning. 

            If we take a single human generation to be 20 years, and the reproductive generation for bacteria to be a few hours, and taking the average course of the disease in humans to be ~4 days from infection to death, one generation for humans might correspond to about 50,000 reproductive generations for the bacterium and 1800 “generations” in terms of points of transmission.

    7. I’d suggest reading New light on the Black Death: the cosmic connection by M. G. L. Baillie.
      There is a definite cosmic connection aka comets which makes much more sense to understand how a plague could travel so fast and kill so many people. FYI.

      1. Scientists: “Well, we’re not entirely sure.  We have some good ideas but the data is a little sketchy and there’s a lot more work to be done.”

        Crackpots:  “There is a Definite Cosmic Connection!  Definite!  No more questions!”

        And somehow it’s the scientists who get written off as closed-minded bores.

        (Yes, I know Mike Baillie is a scientist too.  He’s a dendrochronologist and his work on comet impacts and the environment looks very interesting.  However he is not an expert on the black death and this book seems to follow the crackpot formula: Write a popular book (to avoid peer review) about how your work explains everything to do with unrelated fields in which you are not an expert.)

      2. Comets can kill lots of people just by travelling fast into the ground. They don’t need to be carrying highly improbable space bacteria. :)

        I say highly improbable because  *Y pestis* seems to have a common ancestor with everything else down here and is well adapted to living on fleas and small mammals, not so much in a cold irradiated vacuum. So the question of how it would get up onto a comet in the first place places quite the explanatory burden on that “cosmic connection”.

    8. If the Black Death killed from 30%-50% of the European population, then it had a severe evolutionary effect. I remember that during the AIDS crisis one resistance mechanism associated with Europeans was also effective against Y. pestis, so human evolution may be one reason the plague was less deadly in the 17th century.

      For a really good account of the 17th century plague, read Defoe’s Journal of the Plague Year. It’s a very good account. DeFoe was born after the plague, but there were obviously a lot of survivors and survivor stories. In addition to the individual stories, he describes the societal effects and reactions to the plague. London suffered from pestilence, but not famine. Despite the risks and the evacuation, farmers continued to bring food to the city.

      There was no CDC back then. Most who could flee did, but there wasn’t a total breakdown in societal function. There was food. There was nursing care. The bodies were buried. I wonder how different the societal response was in the 13th century when populations were smaller and institutions less developed. (Chaucer’s The Pardoner’s Tale may have been set during the 13th century plague, but its focus was on morality, not survival.)

    9. I was curious to know why human evolution wasn’t mentioned in the article?  Even in today’s third world countries, there has been medical advancement.  Just because Y. Pestis was virulent then doesn’t mean that the human immune system hasn’t adapted since; 500 years is a lot of time!  Perhaps our ancestors, ones that were survivors(?), conceived children that had a stronger immune system?

    10. Must-read on the Black Plague: William H. McNeill’s Plagues and Peoples. I’m surprised no one has mentioned it. He makes a strong case that Plague outbreaks led to the demise of feudalism.

    11. We can rule out humanity as a whole evolving to resist plague better.  I
      wonder,  though, if just Europeans of the time were especially
      vulnerable.  A gene variant that confers some other advantage but interferes with immune response to one genus of bacteria could
      spread widely in a region, before being selected out again.  In the
      aftermath we would be mystified until we sequence enough victims to
      notice the variant that has disappeared.  Maybe it’s worth getting that
      variant back again, for whatever advantage it conferred, now that Y. p.
      is treatable — although there’s little reason to think that it would be
      similarly advantageous in today’s environment: it might have helped
      populations living under religious dictatorship, or malnourishment, or
      not bathing.

    12. Fascinating! Thanks for the thoughtful, deep research. It puts me in mind of the scene in Herzog’s NOSFERATU where the ship lands at the dock and the rats scurry off – equating the fantastic horror of the vampyr with the real life threat of The Plague. 

      1.  Why would that matter?  The fleas were only the means of spreading the disease.  They didn’t affect survival rates once you were infected.

    13. Actually, bubonic plague is endemic in the ground squirrels which live in the Jemez Mountains of New Mexico.  I know because I used to live near that area, and still live in that state. If you live there, you spread flea powder around their burrow entrances, protect any animal who goes outside, and are very carefull to protect yourself. Still, there are periodic die offs of the squirels and human cases. Last deaths I have heard of were in the 1990s. It seems to flare up when the ground squirrel population explodes and dies down when the squirrels die off. Perhaps there was a large increase of the rats and mice during that period due to favorable conditions for their breeding which helped the plague spread.

    14. Great article! Has anyone read “the years of rice and salt”? The novel explores how subsequent world history may have been different if the Black Death plague had killed 99% of Europe’s population, instead of a third.A great “what if” ! Thanks again!!!

    15. Michael Crichton observed, in The Andromeda Strain, that diseases and their hosts evolve accomodations: four hundred years ago, syphilis was a deadly killer;  since then, virulence has declined, and while dangerous if left untreated, syph is not the fast-burning horror that it used to be.

    16. I am going to have to spend far more time at BoingBoing. I seriously long for this type of quasi-scholarly (read: love of knowledge) debate/discussion. This feels like home. I mean I read Cory’s pieces now and again, but honestly I had not realized how far this site has evolved from its days as a simple link aggregation/curation site, or how it seems to be the epicenter of highly-literate and relentlessly curious individuals like those commenting on the Black Plague herein..

      If anyone here is on G+, I would like to add you to my circles, and more importantly, I think a 10 person hangout–where the erudite and esoteric intersect, would be immensely enjoyable. There are just too many cat gifs and squabbling over partisan politics currently occupying my stream.

      Please drop me a note through disqus. I am starving for this type of discussion…

    Comments are closed.