Yves here. Here we have what is taken as a well-established fact, that rats were the big perps in the propagation of the Black Death, shown as likely to be false. Among other reasons, it spread far too rapidly….suggesting human and human-borne insects like fleas are more likely prime suspects.
By Samuel Cohn, Professor of History, University of Glasgow, and Philip Slavin, Associate Professor of History, University of Stirling. Originally published at The Conversation
The Black Death ravaged Europe between 1347 and 1353, killing millions. Plague outbreaks in Europe then continued until the 19th century.
One of the most commonly recited facts about plague in Europe was that it was spread by rats. In some parts of the world, the bacterium that causes plague, Yersinia pestis, maintains a long-term presence in wild rodents and their fleas. This is called an animal “reservoir”.
While plague begins in rodents, it sometimes spills over to humans. Europe may have once hosted animal reservoirs that sparked plague pandemics. But plague could have also been repeatedly reintroduced from Asia. Which of these scenarios was present remains a topic of scientific controversy.
Our recent research, published in the Proceedings of the National Academy of Sciences (PNAS), has shown that environmental conditions in Europe would have prevented plague from surviving in persistent, long-term animal reservoirs. How, then, did plague persevere in Europe for so long?
Our study offers two possibilities. One, the plague was being reintroduced from Asian reservoirs. Second, there could have been short- or medium-term temporary reservoirs in Europe. In addition, the two scenarios might have been mutually supportive.
However, the rapid spread of the Black Death and subsequent outbreaks of the next few centuries also suggest slow-moving rats may not have played the critical role in transmitting the disease that is often portrayed.
European Climate
To work out whether plague could survive in long-term animal reservoirs in Europe, we examined factors such as soil characteristics, climatic conditions, terrain types and rodent varieties. These all seem to affect whether plague can hold on in reservoirs.
For example, high concentrations of some elements in soil, including copper, iron, magnesium, as well as a high soil pH (whether it is acidic or alkaline), cooler temperatures, higher altitudes and lower rainfall appear to favour the development of persistent reservoirs, though it is not entirely clear why, at this stage.
Based on our comparative analysis, centuries-long wild rodent plague reservoirs were even less likely to have existed from the Black Death of 1348 to the early 19th century than today, when comprehensive research rules out any such reservoirs within Europe.
This contrasts sharply with regions across China and the western US, where all the above conditions for persistent Yersinia pestisreservoirs in wild rodents are found.
In central Asia, long-term and persistent rodent reservoirs may have existed for millennia. As ancient DNA and textual evidence hints, once plague crossed into Europe from central Asia, it appears to have seeded a short- or medium-term reservoir or reservoirs in European wild rodents. The most likely place for this to have been was in central Europe.
However, as local soil and climatic conditions did not favour long-term and persistent reservoirs, the disease had to be re-imported, at least in some instances. Importantly, the two scenarios are not mutually exclusive.
Radical Difference
To go deeper into the role of rats in spreading plague in Europe, we can compare different outbreaks of the disease.
The first plague pandemic began in the early sixth century and lasted until the later eighth century. The second pandemic (which included the Black Death) began in the 1330s and lasted five centuries. A third pandemic began in 1894 and remains with us today in places such as Madagascar and California.
These pandemics overwhelmingly involved the bubonic form of plague, where the bacteria infect the human lymphatic system (which is part of the body’s immune defences). In pneumonic plague, the bacteria infect the lungs.
The plagues of the second pandemic differed radically in their character and transmission from more recent outbreaks. First, there were strikingly different levels of mortality, with some second pandemic outbreaks reaching 50%, while those of the third pandemic rarely exceeded 1%. In Europe, figures for the third pandemic were even lower.
Second, there were different rates and patterns of transmission between these two plague epochs. There were massive differences in the frequency and speed of transporting goods, animals, and people between the late middle ages and today (or the late 19th century). Yet the Black Death and many of its subsequent waves spread with astonishing speed. Over land, it raced almost as fast each day as the modern outbreaks do over a year.
As described by contemporary chroniclers, physicians, and others – and as reconstructed quantitatively from archival documents – the plagues of the second pandemic spread faster and more widely than any other disease during the middle ages.Indeed they were faster than in any period until the cholera outbreaks from 1830 or the great influenza of 1918-20.
Regardless of how the various European waves of the second pandemic began, both wild and non-wild rodents – rats, first and foremost – move much slower than the pace of transmission around the continent.
Third, the seasonality of plague also shows wide discrepancies. Plagues of the third pandemic (except for the rare ones, principally of pneumonic plague) have closely followed the fertility cycles of rat fleas. These rise with relatively humid conditions (although lower rainfall is important for plague reservoirs to first become established) and within a temperature band between 10°C and 25°C.
By contrast, plagues of the second pandemic could cross winter months in bubonic form, as seen across the Baltic regions from 1709-13. But in Mediterranean climes, plague from 1348 through the 15th century was a summer contagion that peaked in June or July – during the hottest and driest months.
This deviates strikingly from plague seasons in these regions in the 20th century. Because of the low relative humidity and high temperatures, these months were then the least likely times for plague to break out among rats or humans.
These differences raise a crucial question about whether the bubonic form of the plague depended on slow-moving rodents for its transmission when instead it could spread much more efficiently directly, from person to person. Scientists have speculated that this could have occurred because of ectoparasites (fleas and possibly lice), or through people’s respiratory systems and through touch.
Questions such as the precise roles played by humans and rats in past plague pandemics need further work to resolve. But as shown by this study, and others, major steps forward can be made when scientists and historians work together.
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I think its long been recognised that the rat flea hypothesis has never matched up with the actual spread of the plague. The flea is also mostly associated with the black rat, not the brown rat, and the former has never had a foothold in colder climates, but the plague still spread in Scandinavia and Ireland.
I think what is striking about the bubonic plague is that it seems to have been pretty indiscriminate – unlike most infectious diseases it didn’t seem to strike stronger on any one cohort, housing type or geographical location (except that dense cities got hit harder than rural areas). So that strongly suggests that it had several vectors.
Variations would have to play a major role too and we have seen during this Pandemic how these variants bang into each other and come up with new variants in surprisingly short spans of time. Years ago I was reading contemporary sources from northern Italy describe how some people were infected by touching infected people and what they had come into contact with while others were infected by aerosols. That shouts different variants at work here. Also, another indication of variants would be how some people would take several days to die while others died within 24 hours after being infected. Maybe they need to do a major DNA analysis program on any and all death pits found from this era to try to sort out what was happening – if that is possible anymore.
But what if there was human to human flea transmission? Fleas can spread really rapidly. I don’t know since current human flea might not be there in the middle ages as it is thought it comes from South America. It could be the case the pathogen, Yersinia pestis changed the behaviour of fleas as it has been described or suggested for ticks and Lyme disease. We underestimate Borrelia as well as Yersinia.
I think its always been assumed that the fleas are highly species specific in their behaviour – they only live on a specific number of rodents. Of course, it may be that they could survive or hop along some kinds of natural fibre clothes (I once saw a hat made of fifty mouse skins in a Chinese antique shop, I wondered at the time if that could be a vector for some unusual pathogens).
From contemporary sources, I think that people at the time were confused by what seemed to be a random spread – it wasn’t running in households or families, but was spreading in distinct waves. It seemed to have an ability to ‘hop’ geographical areas in a way that seemed terrifying to people at the time. I think its this which convinced early researchers that a rodent vector was the probable cause.
The spread in Ireland was interesting as Ireland was semi-isolated for long periods. In the 14th Century the plague was recorded as having hit the English harder than the Gaelic peoples – most probably because they were mostly living in port cities. But a later wave did hit the mountain peoples harder than before – possibly because of a new vector, or maybe they lacked immunity? While chronicles tend to say it hit the towns harder, studies indicate afforestation in the period which is usually an indicator of a major reversal in population. But it certainly was noted by contemporaries that different waves impacted differently on populations.
Just to show i wasn’t writing on thin air:
Pathogens Manipulating Tick Behavior-Through a Glass, Darkly
Interplay between Yersinia pestis and its flea vector in lipoate metabolism
Vector-pathogen interactions could be relevant on the outcome.
Fleas would still need human hosts to travel between towns and villages.
Come to think of it, Finland and the Baltics lacked two things the rest of the medieval Europe had: monasteries and the Black Death. Coincidence?
Polar Socialist:
There were plenty of monasteries, both Catholic and Orthodox, in Finland and the Baltic States. And still are, especially in Lithuania.
Here’s Finland:
https://en.wikipedia.org/wiki/List_of_Christian_monasteries_in_Finland
So there is no association, plague/monks
Finland had 5 medieval monasteries, of which only one was operational at the time of the Black Death. I don’t consider that plenty. In most of the Europe there were monasteries within days travel of each other. Comparable Sweden at the time had around 80 monasteries.
Lithuania turned to Christianity from paganism 30 years after the Black Death so I doubt there were even that many priests around, and certainly no monasteries at the time.
And no, I’m not saying there’s an association of plague with monks. I just find it a peculiar coincidence that the least ecclesiastical/monastic places in Europe apparently evaded The Plague.
The traditional explanation for the relatively light impact in northern climes is that the main vector, the black rat, does not breed very well in colder countries. It seems to have spread widely during the time of the Romans (it originated in India) into non-optimal habitats where it was later displaced by the more robust brown rat.
This is interesting though of course very speculative. As usual, we tend to underestimate the microorganisms and their properties/capabilities at our own risk while focusing on rats and humans. In the middle age, given the ease and speed of spread, person to person transmission would have almost certainly play a role whether through fleas, droplets, airborne (oh, no!), direct contact etc. I miss in this article some more considerations on the biology of fleas and Y. pestis. High mortality rates might be associated with unidentified virulence factors in Yersinia pestis medievalis even if we have full genome sequences. Some have been identified indeed but we may have missed a few. If spread was as fast as suggested by the article one has to take airborne transmission in consideration though this is conductive of pneumonic pest rather than bubonic. The seasonal pattern in the Mediterranean region, provided correct, suggests the involvement of vectors in human to human and/or rodent to human transmission.
An interesting read indeed.
So about third wave mortality, Y. Pestis is one of the last pathogens that is still susceptible to first generation antibiotics. Good ole OG Penicillin will cure it in a couple days. So third wave mortality probably should be broken up into pre/post 1950(?) western world, pre/post 1970(?) developing world.
Also would like to point out that in 16th century England they had a plague protocol to deal with outbreaks. One of the things they would do is (warning sad fact ahead) kill all the dogs from the neighborhood where the out break was. This was before germ theory of course, but I’d like to make the unsupported claim that the reason for them to do this was because they were doing contact tracing and noticed a few times no human contact between afflicted houses, but perhaps a dog in common. Dogs and people probably share fleas more then rats and people, and I totally forgot the point I was gonna make. So there, random plague lore for your Friday morning.
Pneumonic spread by humans in periods of high humidity/rainfall? Bubonic spread by fleas in periods of low humidity/drought? Probably breaking out from isolated rat populations in Asia via the Silk Road and imported along with the goods, and once shipwrecked far from their preferred host population, what was a hungry flea to do but mingle, sample the locals, and reproduce?
My favorite part of that theory has been ‘The Mummy’* twist. That the locals knew there were parts of the desert it was unwise to park your caravan for the night because death often followed. The equivalent of marking the poisonous watering hole lest it kill your thirsty horse and somehow the message got lost in translation or was ignored. Did it have anything to do with the ‘gifts’ the Europeans introduced in their travels to the local populations? Did disease in its many forms travel both West and East? Unlike Latin America were the Asians populations immune? There’s a story I haven’t read. The plague is always described as moving in one direction, toward poor unsuspecting Europe.
* It’s poo-pooed as a silly superstition of the stupid heathen locals, but may have a basis in (unproven) fact with unfortunate consequences for the heedless.
It appears that the Black Death variant of the plague had more of a tendency to go pneumonic than do the current variants, except for the Marmot variant, so that the clade of the plague might have had a different reservoir is not a surprise.
It should also be noted that the Plague moved blisteringly fast during the Black Death, on the order of 5 km/day, which might also suggest something much faster moving than rats.
The History I recall was the 1300 version of the Death was death flea born, and animal could be a carrier.
I don’t recall that it was only carried by fleas.
If only flea born than one has a difficult time explaining how the fleas jumped from village to village and parish to parish, as peoples travel was very limited in the 1300 England. Traveling out of one’s parish without permission was a punishing offense – flogging or hanging..
IMO, the Medeival Black Death was actually an influenza virus…..
https://www.canterbury.ac.nz/engage/cup/catalogue/books/black-november-the-1918-influenza-pandemic-in-new-zealand.html
“How would you feel if you woke one morning to find your partner lying dead beside you, not just still and cold, but their skin turned purple-black? Or if your neighbour’s children came to ask for food because their parents had been ‘asleep’ for two days?
Too horrible to think about? Yet such things happened all over New Zealand in November 1918 when the country was swept by the so-called ‘Spanish’ influenza pandemic….”
Also, in NZ Samoa
https://www.rnz.co.nz/international/pacific-news/375404/how-nz-took-influenza-to-samoa-killing-a-fifth-of-its-population
“As the Talune’s (ship from NZ carrying flu) passengers fanned out, so did the disease. People went into Apia town. Others rode goods wagons up into rugged interior. A Christian missionary walked from village to village along the coast, taking a hacking cough with him.
Within days, people were dying. Within weeks, entire villages had died. Within two months, about 8,500 people were dead – a fifth of Samoa’s entire population….”
The death rate of the European NZ population was much less than that of Maori and Samoan people, who died in vast numbers.
I think that European, and Asian people had inherited some natural resistance, because all of their ancestors had survived the Medeival Black Death, and passed on some natural resistence.
The 1918 flu devastated the set-apart indiginous population, like the American Indians, Pacific Islanders… Who had never been infected by the 14th century scourge.
Entire indiginous villages in Alaska……
everyone dead….
The rats, fleas and Bubonic bacterium was a “theory” that was presented, publicized, defended….
But, imo, it is an other stupid theory that is actually another ” logical sounding” delusion.
FI, remember how the Indian Populations of North and South America by measles.. They had never encountered that bug before, and died in vast numbers…..
Whilst I don’t think it was a flu, you’ve certainly identified what is the (still IIRC) unresolved issue of “how can a bacterial infection prime 10% of Northern Europeans to select for a genetic mutation that confers immunity from HIV – A VIRUS”?
I first became aware of this issue quite early on when it was observed that nobody got HIV in a part of the UK Midlands near me. It is now fairly well established (with SOME uncertainty remaining) what the gene mutation conferring HIV immunity is (get it from one parent and your transition to full blown AIDS may be so late in life that you die of something else, get two copies, one from each parent, and you’re immune). Smallpox has also been suggested as the “HIV defence” but that doesn’t quite add up either.
A prime example of correlation doesn’t imply causation should be noted here. Communities noted in historical records as having horrifically high rates of the black death have, via low rates of emigration (parts of the Midlands) and/or genetic panels linking people to those communities, illustrated the low incidence of HIV.
This led to the gene hunt identifying the suspected main mutation that conferred HIV immunity (though other routes to HIV immunity have since been found). I do “the stats” but rely on clinicians and lab scientists to propose hypotheses. I’m perfectly willing to accept that some bacterial infection carried by rats/air etc also had effects on immune system that had beneficial effects against viruses……. Just thought I’d say that before someone else did and encourage the cleverer people on here familiar with immunogenetics to pipe up!
A prime example of correlation doesn’t imply causation should be noted here. Communities noted in historical records as having horrifically high rates of the black death have, via low rates of emigration (parts of the Midlands) and/or genetic panels linking people to those communities, illustrated the low incidence of HIV.
This led to the gene hunt identifying the suspected main mutation that conferred HIV immunity (though other routes to HIV immunity have since been found). I do “the stats” but rely on clinicians and lab scientists to propose hypotheses. I’m perfectly willing to accept that some bacterial infection carried by rats/air etc also had effects on immune system that had beneficial effects against viruses……. Just thought I’d say that before someone else did and encourage the cleverer people on here familiar with immunogenetics to pipe up!
There is an article that argues the black death was possibly caused by a filovirus IIRC. Thus it is better thought of as a viral haemorragic fever. Interestingly this is linked to resistance to HIV-1, which is found in approximately ten percent of populations with historical exposure to the medieval/early modern Black Death.
The title is ‘What caused the Black Death?’ by C J Duncan, S Scott.
That link between plague and HIV is what I was curious about. I knew of the theory that plague was actually some viral haemorrhagic fever but I (as biostats PhD NOT clinician) struggled to reconcile the typically differing symptoms…..I had got as far as knowing that talk of THE plague is misleading since symptoms described in the “old plagues” don’t match modern plague but I’d have to locate and read the source material you mention to get further.
I do have enough medical Dr friends who could spot red flags if the theory is out and out wrong. Thanks.
Hi actually paddlingwithoutboats linked the article I mentioned in this comment:
https://www.nakedcapitalism.com/2023/01/the-black-death-may-not-have-been-spread-by-rats-after-all.html#comment-3839517
This possibility of an ebola or marburg relative explaining these pandemics is fascinating.
Epidemiology of the Black Death and Successive Waves of Plague by Samuel K Cohn JR presented a large body of evidence, it’s linked in the above article. The footnotes alone were illuminating.
Plague without rats: The case of fifteenth-century Iceland
Gunnar Karlsson
Pages 263-284 | Published online: 03 Jan 2012
https://www.tandfonline.com/doi/abs/10.1016/S0304-4181%2896%2900017-6?journalCode=rmed20#:~:text=The%20case%20of%20Iceland%20seems,any%20kind%20of%20rodent%20fleas.
In the fifteenth century, Iceland was ravaged by two epidemics which usually have been identified as plague. It is shown here that these epidemics were no less lethal than the Black Death in Europe. The first one probably killed half the population or more and persisted in the country for at least a year and a half. Since, for several reasons, it can safely be assumed that Iceland was not populated by rats at this time, this may offer the strongest available proof that an epidemic like the Black Death was not dependent on rats for its dissemination.”
Years ago, I had full access to this article through my University. If anyone is interested in The Plague, it is worth getting your library or University to get it for you.
There are good records from Icelandic diary writers of this time of the plague. It was a nightmare…..
Interesting link on potential that the “black” death was not plague, probably from NC sometime ago:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1743272/pdf/v081p00315.pdf