by Anna Raccoon
Note: I’m not convinced by the claim that plague and bubonic plague are not the same. Differences in symptoms and mortality rates may not mean very much. The 14th century Black Death and the 17th century plagues wiped out virtually everyone who had no resistance. We are the descendants of the survivors, and have probably inherited some resistance to the infection. It’s the same with the rats. That in itself would explain slower transmission rates, and lower rates of infection and mortality.
Syphilis was much more virulent on its first appearance at the end of the 15th century. Infections comparatively harmless to Europeans and Asians appear to have wiped out over 90 per cent of the native populations in South America during the 16th century.
Of course, infections also change over time. A bacterium is unlikely to survive for very long when it kills its host before it can spread to another. Therefore, changes in the nature of the bacterium and growing resistance of its victims will, over time, transform catastrophic pandemics into endemic problems. SIG
In mid September 1597 a wandering beggar called Andrew Hodgson came to the Cumbrian town of Penrith. As an itinerant of that time we can imagine him as an undernourished, crushed looking individual. On about the 17th or 18th September 1597 Andrew Hodgson would probably have noted a sweet smell on the air. Soon he would have developed a headache, and then a fever. Soon he was dead. He was buried on 22nd September 1597 he was buried. The Penrith parish register records his burial and the cause of death: (P) – Plague.
11 days later, the first victims died simultaneously in both Carlisle and Kendal, quite some distance apart.
In Penrith, nothing else seemed to happen. Nobody died. And then, 22 days later, the deaths began. The first was Elizabeth Railton. There was a slight pause again, and the next week it really began to let rip. Although the actual figures are a bit unclear, by the time it was over probably certainly more than 600 died in Penrith, at a rough guess around 40% of the population. About par for the course for the well satisfied Reaper of Souls.
Nearly seventy years later, in September 1665 Plague came to the sleepy and peaceful Derbyshire village of Eyam. The first person to die was George Viccars, sometimes a tailor but importantly a known itinerant. I do not know where he had been, but I will again surmise that George Viccars smelt an unusual and aromatic evening air. And then the fever began. Soon it was raging and he was coughing blood and bleeding from the nose. On 7th September 1665 he, too, died of Plague.
Once again, there was a pause. The villagers waited anxiously to see whether the Plague would spread.
At first there was nothing. Then, 15 days later George Viccars’ neighbour on one side of his house died. The next day, the neighbour on the other side died. Then the Thorpe family in a house on the other side of the street began to die. To illustrate how the Plague began to sweep through the village and “snowball”, and to remind us that these were real people just like you and me, here is a short extract of the record of the dead, and their dates of passing on:
- • George Viccars 7 Sept 1665
- • Edward Cooper 22 Sept 1665
- • Peter Hawkesworth 23 Sept 1665
- • Thomas Thorpe 26 Sept 1665
- • Sarah Sydall 30 Sept 1665
- • Mary Thorpe 30 Sept 1665
- • Mathew Hands 1 Oct 1665
- • Elizabeth Thorpe 1 Oct 1665
- • Margaret Bands 3 Oct 1665
- • Mary Thorpe 3 Oct 1665
- • Sythe Torre 6 Oct 1665
- • William Thorpe 7 Oct 1665
- • Richard Sydall 11 Oct 1665
- • William Torre 13 Oct 1665
- • Annie Torre 13 Oct 1665
- • John Sydall 14 Oct 1665
- • Ellen Sydall 15 Oct 1665
- • Humphrey Hawkesworth 17 Oct 1665
- • Martha Bands 17 Oct 1665
- • Jonathan Ragge 18 Oct 1665
- • Humphry Torre 19 Oct 1665
- • Thomas Thorpe 19 Oct 1665
- • Mary Bands 20 Oct 1665
- • Elisabeth Sydall 22 Oct 1665
- • Alice Ragge 23 Oct 1665
- • Alice Sydall 24 Oct 1665
- • George Ragge 26 Oct 1665
- • Jonathan Cooper 28 Oct 1665
- • Humphry Torre 30 Oct 1665
- • Hugh Stubbs 1 Nov 1665
- • Alice Teylour 3 Nov 1665
- • Hannah Rowland 5 Nov 1665…
And on and on it went…
The readers of this blog are pretty switched on. Some are already ahead of me in research. They will spot patterns of itinerancy, a two week period between the initial death and the subsequent wider outbreak. And, looking at the names in the list above, they will gain the impression that this killer was being transmitted within families.
Modern medical science has had it for the past century that the plague was caused by fleas spread by rats. But the consensus at the time was that it was spread by human contact. Believing this, and under the leadership of the local vicar William Mompesson, the villagers took a dramatic and incredibly brave stance. Instead of abandoning the village – and thus probably spreading the disease – they decided to stay, and put the village into quarantine. In so doing they must have assumed that they were in all probabilities handing themselves a death sentence, or at least entering the Lotto of Death with a pretty good chance of “winning”. In fact, it seems that Mompesson’s wife Katherin (sic) did insist on their children being taken away, but she returned to be at his side. It would prove a brave but fatal choice.
With the cooperation of the local magnate the Earl of Devonshire, supplies of food were left to be picked up at a stone on the highway outside the village. But for more than 15 months no one entered the village, and nobody left. Eventually, when it was deemed safe, a party did enter the village. They expected to find almost everyone dead. The destruction was indeed terrible. Some 260 souls had died. But some survived. How many is controversial, but it may have been as low as 80 or more likely as high as 450. Once again the mortality was probably between 30 – 40% .
Mompesson survived but his loyal wife Katherin did not. It is recorded that Mompesson insisted in going about the parish and visiting his flock, and that Katherin Mompesson went with him. One evening, whilst driving home in their carriage Katherine exclaimed how extraordinarily sweet the air was that evening. Mompesson himself could smell nothing remarkable. He knew in that instant that his wife was infected, and almost certain to die. Smelling a “sweet” air was a well known symptom of the onset of plague. For the reasons I shall try to explain below, it was probably caused by olfactory nerves detecting the beginnings of the collapse of internal organs. She was detecting the initial stages of her body beginning to rot under the onset of the Plague. She died in his arms, a few days later.
On the edge of the village Elizabeth Hancock and her family were unscathed for some months. And then August 1666 the Plague struck, and within a week (not a month, as I previously wrote) Elizabeth Hancock buried her husband and all six of her children. Their graves can still be visited today. But the disease did not touch her at all. According to varying accounts, either it did not touch Marshall Howe, the man who took on the role of carting away and burying the dead (and helped himself to a few of their belongings along the way), or he contracted the disease and survived it, and then carried on apparently immune. However, it took his wife and son.
Another villager, Margaret Blackwell, contracted the pestilence and was left for dead. But her fever broke and she rushed downstairs to quench her thirst and famously downed a jug full of bacon fat. Why did she and others contract the disease and still survive?
In line with modern science, the local legend has it that George Viccars contracted the Plague by being bitten by a flea which had been attached to a piece of wool ordered from London. But did he?
In my previous piece on this topic I had explained how in the late 19th Century the Black Death came to be associated with the newly diagnosed and understood Bubonic Plague, and as conventional history teaches, was spread by rat fleas. I hinted that this may be a fundamental error. And I mentioned the odd phenomenon of how one person in a household otherwise totally wiped out might survive unscathed. How could that be explained?
In fact there are several good reasons for reaching the conclusion that whatever it was, the Black Death was not Bubonic Plague – at least not in the form that now still survives – and that that rats had nothing at all to do with. This is why.
First of all, the Black Death moved far, far too quickly. In the mid to late 19th Century when Bubonic Plague spread through South East Asia and into India, it moved slowly, trundling from village to village. Its movement took years, decades, moving at the pace of the migrating (and dying) rats.
The Black Death was quite different. It swept across Europe truly like some horseman of the apocalypse. It engulfed almost all of southern and central Europe in less than a year.
In fact it moved through England, on to Scotland and beyond into the Baltic States at an astonishing rate of about five miles a day. It erupted in multiple towns, cities and villages at once. It moved like wildfire. Rats cannot spread that fast, even if hiding in ships and carts on the main trade routes. Neither is it convincing to have this speed and level of contagions plague being passed on by rat flees in wool and so forth.
Indeed a fundamental problem number for the Bubonic Plague theory is that there are not enough rats anyway. Professor Sam Kohn has teaches history at Glasgow University, He has spent years researching the Black Death, and the contemporary descriptions. But there is no record of sick rats dying just before or at the time of any outbreaks, as was the case in the modern epidemics of Bubonic Plague in India and South Asia.
Further, the only rat in England at the time was the Black Rat (rattus rattus – a great name). The Black Rat is originally a native of Asia, but had spread to Britain by Roman times. It seems a rather sweeter and more timid creature than the nastier and more aggressive cousin the Brown Rat (rattus norvegicus – there is a story in that too) which is now prevalent, but did not arrive in England until the 18th Century. The Black Rat likes warm cosy places. It would not enjoy or be capable of moving across open ground and large parts of Britain are wholly alien to the species. It could not have flourished in Baltic states – and the Plague did.
What is more, natural historians can now work out from bio analysis of stuff such as owl pellets what the predators were eating; they were eating mice and voles, but not rats. And, if rats had been a problem, then barns, farm buildings, dovecots and the like would have been constructed differently. In most of England, there were probably no rats at all when the Black Death raged.
Next is the problem of mortality rates. Bubonic Plague is a killer, but not in the same league as the Black Death. In the Indian pandemic of the late 19th Century, when the association with the Black Death was first made, there was a mortality rate of about 2% of the population. The Black Death wiped out whole towns. Commonly, anywhere between 30 to 70% of the population died.
And then there is a problem with the poor. If it was infection spread by rats, you would expect the brunt of the assault to be borne, as ever, by the poor who would be living in the most squalid conditions and in closest proximity to the rats – unless there were rats running about everywhere. But the Black Death was an astonishingly egalitarian killer. High and low, Cardinals and paupers alike died. Statistical analysis of the dead in London by cross referencing databases of tax and death records shows that there was no particular statistical variation between rich and poor.
Finally, there is a problem with the description of the disease. I gave two or three accounts in the first piece, but bear with you if I take you back again. One of the most famous is that given by the 14th Century philosopher and writer Giovanni Boccaccio. He was to go on to write a book of morality tales based on the pestilence called “The Decamaron”:
“The first signs of the plague were swelling in the groin or armpits. These bulges ranged between the size of an apple and an egg. They were called gavoccioli. Soon after contracting the plague the gavoccioli would spread over the whole body. The next stage of the disease was black or livid spots on the arms and thighs, spreading over the rest of the body in a short time. Nothing could be done, most died within three days, only a few were ever cured. The pestilence passed from the sick to the healthy, being around a sick person in any way including touching their clothing could make you sick. I (the narrator) saw it with my own eyes. Animals even died from the pestilence.”
This all seems consistent with Bubonic Plague, and it is probably the most famous contemporary description because his book was widely circulated. But there is reason to suspect that Boccaccio had fled the city. So the description may not be the best. In any event, the boils he describes cover the while body. Now look again at the first description when the Plague makes its landing in Europe at the Sicilian Port of Messina:
“At the beginning of October, in the year of the incarnation of the Son of God 1347, twelve Genoese galleys . . . entered the harbor of Messina. In their bones they bore so virulent a disease that anyone who only spoke to them was seized by a mortal illness and in no manner could evade death. The infection spread to everyone who had any contact with the diseased. Those infected felt themselves penetrated by a pain throughout their whole bodies and, so to say, undermined. Then there developed on the thighs or upper arms a boil about the size of a lentil which the people called “burn boil”. This infected the whole body, and penetrated it so that the patient violently vomited blood. This vomiting of blood continued without intermission for three days, there being no means of healing it, and then the patient expired.” [My emphasis]
So yes there were boils, but not quite in the same way, and more importantly, there is the tell tale vomiting blood. That is not generally associated with Bubonic Plague except in its rarer form of Pneumonic Plague. But that requires a secondary infection after the lungs of the victim and is rare. And even that produces bloody sputum, but the victim does not “vomit blood”. And it would not spread at the necessary rate.
Once again, Professor Sam Cohn of Glasgow University has collated many hundreds os contemporary accounts of the disease. Most of the accounts talk not of “buboes”, but instead of dark blotches spreading across the skin, the dark pustules erupting, and the vomiting of blood. If you vomited blood that was it. You were dead.
This is not Bubonic Plague. What was it? And how was it spread?
The case of the Derbyshire village of Eyam is very important for a number of reasons. First, because the records are so good. Second, because the community is relatively isolated, it provides a gene pool which allows us too peer back in time and uncover clues about what might have allowed for resistance to the disease.
In their excellent and readable “The Return of the Black Death”, Professor Christopher Duncan, Emeritus Professor of Zoology at Liverpool University and Susan Scott, Social Historian (Wiley Press, available on Amazon) set out the results of their meticulous research into the patterns infection at both Eyam and in the Cumbrian outbreak of 1598. From the available records they establish what is to my mind a really pretty clear picture of how the disease spread. Their research makes perfect sense. In respect of Eyam in particular, by mapping the various families and relationships within the village and cross referencing dates of death you can do two things.
First, you can work out links between the infected victims and follow the spread of the disease by human contact. Second, you can make a reasonable guess from the dates about how long the victim had the disease and crucially remained infectious without showing the symptoms.
I should say that I have spent quite a bit of time looking at modern forensic archeological attempt to work out what the Black Death was. I have indeed been helpfully referred to some results by readers of the Blog last weekend. The gist of these involve taking samples from what are known or believed to be the skeletons of victims of the plague. This process involves taking samples from the bones and particularly teeth of skeletons and searching for signs of the DNA of the Y Pestis bacteria DNA; that being the bacillus that causes modern Bubonic Plague.
Very briefly, from what I can ascertain the position is patchy. It seems that there are strong indications that there are traces of a DNA which matches the DNA of Y Pestis. But, and it is a big but, the match is not 100%. According to my understanding, some scientists think there is a perfect match; some think there is not enough evidence because of the age of the samples: and some that there is a roughly 93% match with the DNA of Bubonic Plague but you have to be careful, because bits of DNA are being patched together. However, the DNA strongly suggested that whatever these people died of, it was closely related to, and maybe the grandparent of, Bubonic Plague.
These, then, are my conclusions.
The Black Death was not Bubonic Plague in its modern incarnation, although it may be closely related to it and have similar DNA. Or in certain there may have been Bubonic Plague around as well; a double whammy for our Medieval ancestors.
The disease would arrive in an area within the body of one or more humans. In the case of the Penrith outbreak, in the body of a travelling stranger called Andrew Hodgson. All infectious diseases have a basic common pathology. There is a period of time when the disease will be present but latent and passive. Then it begins to spread and multiply in the host, and in most cases the bacillus becomes contagious by whatever means – touch, or breath, or more intimate matters depending on the pathology of the individual disease, but without the victim displaying any symptoms. What this infectious period is also varies from disease to disease. In the case of the very highly infectious chicken pox, for example, the infectious period is 10-11 days. In the case of standard influenza which from time to time sweeps the land it is a mere 2-3 days. Then the first visible symptoms arrive, although the victim will usually remain capable of infection. From an evolutionary point of way, it is a very clever way of spreading yourself about, and indeed necessary if you were virus which was so potent as to probably kill the host.
I am convinced that Professor Duncan and Susan Scott are broadly correct in their conclusions that analysis of patterns of death in the Cumbrian outbreak, and that one can make a pretty good calculation of the pathology of this thing. It is as follows:
- • A probable latent period of infection of 10 to 12 days;
- • And infectious period without symptoms appearing of 20 to 22 days;
- • An average period of 3-5 days between onset of symptoms and probable death during which the victim remained infectious.
That is an astonishing infectious period of around 27 days, and for the great bulk of this the victim was free from obvious symptoms. It is, as far as I can tell, unlike nothing on God’s earth today. This is why there was a gap between the deaths of Andrew Hodgson and George Viccars and the outbreak in the wider community. And it is this which explains why the disease spread like wildfire, as its innocent hosts travelled around, meeting with friends and family, or gathering in the local tavern or market. Duncan and Scott even point to a particular wedding party as being one of the key moments of the spread of the Plague in Eyam.
Next, the disease was even worse and more virulent than Bubonic Plague. The fever was horrific and agonizing. A common feature was vomiting blood. Bleeding from the nose and other orifices was often noted. Something like boils or pustules would break out over the whole body, not just the area on the lymph nodes. My research tells me that the depiction above is taken from a 15th Century Bible; I am ashamed to say I have not been able to track down which one. However, whoever created that image was neither a fool, nor had any need to exaggerate. It plainly indicates the pustules – or something – raging over the whole body.
This is an account of autopsies undertaken in Rome and Naples in the mid 17th Century. “Petechiae”, by the way, are in modern parlance livid black and purple blotches caused by failure of the blood vessels beneath the skin:
“The exterior part of the body was found to be covered by black petechiae…the omentum rotten, the gust all black, the peritoneum cyanotic, the stomach very thin, the spleen rotten, the liver doubled in size but of a bad colour and consistency, the gallbladder full of black bile….the pleurae were rotten…the heart livid with its tip black, both ventricles full of very dark blood. The lungs, of bad consistency and colour, were all covered with black petechiae…
It was noticed that all the organs – namely the heart, lungs, liver, stomach and guts – were covered with black spots. Moreover, the gall bladder was found full of black bile, which was very thick and fattish…Especially, however, the major vessels of the heart were full of blood, which was clotted and black.”
I think these symptoms go way beyond what would be expected of Bubonic Plague. As Professor Duncan, Scott and Professor Cohn all argue, they are much closer to what would be expected of what is now known as Haemorragic Fever, such as Ebola and Marburg Fever. Today, these are amongst the most feared killers on earth. Death is almost certain, and it is a very nasty way to go. In brief, the major organs and blood vessels simply start to melt under attack from the virus. Another version is Crimea-Congo haemorragic fever, a disease now occurs sporadically throughout much of Africa, Asia, and Europe and results in an approximately 30% fatality rate. It is spread by ticks. I have taken this description from a scientific journal. After a short incubation period, CCHF is characterized by a sudden onset of high fever, chills, severe headache, dizziness, back and abdominal pains. Additional symptoms can include nausea, vomiting, diarrhea, neuropsychiatric, and cardiovascular changes. In severe cases, hemorrhagic manifestations, ranging from petechiae to large areas of livid bruising appear. Sound familiar?
In “The Return of the Black Death”, Scott and Duncan put sum up the results of their research about the effect with this dramatic conclusion:
“Once the dreaded symptoms appeared, the agonizing end seemed inevitable: when “Gods Tokens” – haemorragic spots caused by blood seeping from damaged blood vessels beneath the skin – were found on the body, this was the death certificate and four of five days of agony, frenzy and delirium followed. The victim’s thirst was unquenchable and some of them ran naked through the streets, screaming, and plunged into water cisterns. Others went completely mad with pain and threw themselves out of windows. There was internal bleeding and in the final days the vital organs began to liquefy.”
Very, very nasty.
But why did some people survive unscathed even though in close proximity to many who died? In the third and final part of this series, I shall try to set out the probably reason, namely the inbuilt immunity of a proportion of the European population probably caused by a slight genetic mutation called the CCR5 – Delta32 mutation, and the and how this is now throwing light on the battle against Aids, and conclude with some reflections on the legacy of the Plague
Many thanks to Odin’s raven for directing me to “The Return of the Black Death”.
And a postscript. The Reverend William Mompesson remarried. He married Elizabeth, the widow of Charles Newby, and she bore him four more children. He did rather well in the Church and prospered, and died age 70. He lies buried at Eakring. I think he deserves his rest.
©Gildas the Monk
Editor’s Note: We have a new tab at the top of the page; a huge technological achievement on Anna’s part, please note!
If you click on ‘Monk’s Ramblings’ you will find all Gildas’ erudite past posts under one heading – no need to wander through Anna’s meanderings to find what you really want any longer…..sniff, sniff. We might even issue a book of them…