Danse Macabre: The Black Death Part 3
“Death is Coming”
As regular readers will know, just before Christmas I started an amateur investigation into the so-called “Black Death”, the deadly plague of unparalleled ferocity and virulence that spread across Europe, Britain and beyond in the late 14th century. It may have killed up to 50% of the population of Britain and Europe, with estimates of up to twenty million or more dead, and it was to hang around in sporadic outbreaks for the next 300 years or so. I have been surprised, intrigued and not a little moved by the results.
To recap, the consensus in the history books has always been that “The Black Death” was Bubonic Plague, which was first properly diagnosed in the late 19th Century. In the previous posts I tried to explain why that explanation is almost certainly wrong; how the disease was spread by human to human contact, and how it was not only hugely more contagious but also considerably nastier than “mere” Bubonic Plague, exhibiting a pathology which is much closer to a modern form of haemorrhagic fever, such as Ebola. I therefore reached the conclusion that although the Black Death may have been biologically related to Bubonic Plague, it was certainly not the same.
It turns out I was partly right, and partly way off the mark.
It is time for some science. Recently, I have had the opportunity to travel to the United States to discuss the topic with some veterinary surgeons in the United States. They have good reason to be aware of Bubonic Plague, by the way, because in parts of the United States (California and Arizona for example, and also and Colorado, where a 12 year old girl was infected after a recent camping trip, but happily survived) it remains an issue, and vets have to be aware of the effects and, indeed, the possibility of infection.
In particular I had the benefit of a long interview with a hugely able and very experienced veterinary doctor who, remarkably, has been a long term follower of the blog and got in touch to put me right. I shall refer to my source by the pseudonym Dr Firenze Pesta. It is a name which she found both amusing and highly ironic.
I had it in mind to do a jokey, rather jovial little piece as a result of this discussion, but on reflection I have decided not approach the matter in that way. After all, what I am about to describe is a phenomenon which carried away the lives of millions, loved ones of all ages, and was an immense human tragedy. And frankly it was a pretty nasty end, and not really a laughing matter.
Dr Pesta is an animated figure who married a very highly trained scientific mind, a no nonsense manner and a hugely warm personality. However, as we discussed the issue in a New England coffee shop the first thing she did was give me a singular telling off for sloppy research and bad science!
Dr Pesta was not too concerned with my discussion of the epidemiology of the Black Death. That is to say, she was reasonably content with my discussion of the rate of spread and the ability to infect. Indeed, she too thought the Bubonic Plague theory was highly unconvincing. The only thing that troubled her was possible research which suggests that DNA of Bubonic Plague had been found in victims of the “Black Death”. However, as I have briefly mentioned, there are some real issues about the veracity of that research, not least because of the age of the samples, and because it is not clear whether samples could have been cross contaminated, or even taken from the “wrong” victims. And our discussion made me more convinced than ever that “scientists” and historians who confused the Black Death with Bubonic Plague were making a number of very serious scientific errors.
Dr Pesta began by pointing out the crucial and fundamental error of confusing bacterial infection with viruses. This in itself proved an interesting insight as Dr Pesta explained the crucial and profound differences.
Bacteria (or “bacilli”) are relatively big unicellular microorganisms. They are typically a few micrometers long and have many shapes including curved rods, spheres, rods, and spirals. They are in “our” terms biologically complete organisms. All bacteria are surrounded by a cell wall. They can reproduce independently, and inhabit virtually every environment on earth, including soil, water, hot springs, ice packs, and the bodies of plants and animals – as well as left-over food.
Salmonella and E-coli are bacterial infections. So are Legionnaire’s disease and, critically, the Bubonic Plague itself. To be specific, Bubonic Plague is caused by the Y-Pestis bacillus. Bacteria can be very contagious and even spread from person to person by direct contact (unwashed hands) in specific circumstances, but often (and perhaps usually) require some form of medium of transmission. In the case of Legionnaire’s disease, for example, that mechanism is the micro droplets of water produced as a by-product of an air conditioning system or a water tower, which carry the bacillus into the lungs. In the case of Bubonic Plague, it is usually, but not always, the bite of fleas which have been consuming the blood of infected rats. It has, therefore, a relatively cumbersome and inefficient mechanism of transmission.
A virus, however, is totally different. Viruses (from the Latin noun virus, meaning toxin or poison) are sub-microscopic particles. They can only reproduce inside a living cell. They are not complete in themselves but require a host in order to multiply. Compared to bacteria, viruses are tiny. They range in size from 20 to 250 nanometers (one nanometer is one billionth of a meter).
In some ways viruses are more similar to mechanized bits of information, computer programmes or robots than fully functioning self reproducing organisms. Outside of a living cell, a virus is dormant, but once inside it takes over the resources of the host cell and begins the production of more virus particles.
Dr Pesta helpfully drew me a picture of a common form of virus on her napkin. It looked like a singularly evil looking “moon landing craft”, with what she described a kind of “spring” mechanism by which it launched part of itself into the cytoplasm of the host cell like an injection, and then takes over the cell.
Some viruses only have a single strand of genetic code – RNA (Ribonucleic acid) rather than DNA (Deoxyribonucleic acid). I asked Dr Pesta if this meant that a virus was a more primitive organism than bacteria. Her reply surprised me. She did not think so at all. If anything, she said, it was cleverer than bacteria, more sophisticated in its reproduction. They do not simply breed, like bacteria; viruses engage in bio re-engineering.
She also had an interesting and sympathetic word to say for the nasty old virus. Whilst a virus may in certain circumstances become lethal, that is not at all the virus’ “intention”. The virus aims to live in some degree of harmony with its host. This is logical, because if it were to do otherwise it would kill the very organism that it needs to let it breed. Viruses therefore aim to adapt to their hosts and form some sort of symbiosis with them. If the virus becomes too aggressive and causes severe illness and death, something has gone very wrong, and the virus is in an environment it was never meant to inhabit. It is for this reason that an animal such as a monkey may be stuffed full of a very “nasty” virus such as Ebola, without any obvious signs ill effects. However, it would be a most unwise human who decided to eat a monkey stew, particularly if it is undercooked…
A virus which has been in the news lately is the winter vomiting virus, or norovirus. The virus is capable of being transmitted by fecally-contaminated food or water, by person-to-person contact, and via aerosolization of the virus and subsequent contamination of surfaces. Influenza is a virus, and so is the common cold. As experience shows, therefore, viruses like this are highly infectious and are capable of spreading very quickly without any external agency to assist them.
This is in fact critical for understanding of the Black Death, because the speed of transmission of the infection is really only consistent with a viral infection, transmitted person to person – just like influenza. To take a prosaic example, if you put someone suffering from salmonella poisoning on a plane, they would have to have contact with the food supply (and nasty contact at that) to infect anyone else. I might say that provided the victim was not suffering from the pneumonic version, the same could be said of a person suffering from Bubonic Plague. However, if a person carrying influenza gets on a plane and starts sneezing, then the infection will spread amongst the passengers like wildfire, and by the time the plane has landed and the passengers have dispersed onto other flights, it will be spreading across the planet with them.
Indeed when I outlined the bare facts of the speed of transmission and the spread of the Black Death to three highly able and experienced veterinary surgeons, each of them quite independently had exactly the same reaction; I quote: “That does not sound like a bacteria; that sounds like a virus.”
Dr Pesta then set about giving a singular and equally telling insight into pathology – the effect on the body – of the “Black Death”, based on the descriptions of the symptoms of the disease and the autopsies I had set out. She was pretty clear what that pathology was, even though she could not define the actual virus, which may now be extinct or merely dormant (!).
To Dr Pesta it was quite clear that what the historical sources were describing is a phenomenon which is perfectly well known to veterinary surgeons, and ought to be known to doctors generally. It is has the technical name of “Disseminated Intravascular Coagulation”, but it is more colloquially referred to within her profession simply as “DIC”. Over another latte Dr Pesta explained to me in laymen’s terms what “DIC” is, and how and why it kills.
Dr Pesta explained that the human body is in a constant state of repair. In particular at the microscopic level the capillaries are full of tiny cuts and tears, and the body has its own hugely sophisticated internal puncture repair kit. Whilst you may not realise it, it is at work within you 24/7, 365 days a year.
Now, imagine that you have suffered a small cut, perhaps whilst shaving or pruning the roses. Blood leaks out. The body needs to stem the tide before you bleed to death. To my surprise Dr Pesta explained that even a small cut can be fatal if not repaired.
In order to do this, the body’s first response is to send emergency aid. This is in the form of “platelets”. Platelets are bits of cells (they do not have a nucleus) which do something akin to the job of sandbags attempting to hold off flood waters although in reverse, in an attempt to stop the flood going out, rather than the flood coming in. These platelets have a life of about 24 hours before they die off and collapse. In order to make the repair permanent, the blood needs to coagulate. It is the coagulation process that actually finally prevents bleeding and allows the wound to heal. The coagulation process is very complex as the body’s repair system moves through a long series of biological transitions and phases. My learned friend Dr Pesta called this process “the coagulation cascade”, and each phase has to be completed properly or the process breaks down and the bleeding continues.
This explains haemophilia. Haemophiliacs lack just one essential protein in their blood called a ‘clotting factor’. There are normally 12 clotting factors circulating in the blood at any one time, and all play an important part in the rather complex process that helps blood to clot. People with haemophilia A are deficient in the essential clotting factor, Factor 8. People with haemophilia B are deficient in the essential clotting factor, Factor 9. The absence of either causes the clotting to fail. So if any stage of the coagulation process is missing or reduced sufficiently, blood clotting will be affected, leaving an individual at risk of extensive internal or external bleeding.
But, and here is the catch, at the same time the body has to control this process. If the process runs out of control the results are also potentially fatal, just as cancer is often caused by the uncontrolled multiplication of ordinarily beneficial cells. As Dr Pesta explained this is one of the reasons why research into cancer and virology have a cross fertilization – both are dealing with a distortion in the correct cellular process. But I digress…
Now bear with me as I set out parts of Dr Pesta’s textbook on “DIC”. It is a bit hard to follow, but I wanted to give a bit of medical gravitas, if only to show I am not making this up:
“DIC – PATHOPHYSIOLOGY
- • DIC begins with a hypocoagulate state leading to microthrombi in many small vessels…
- • Damaged endoththelium promotes thrombin generation which provides feedback activation of the intrinsic coagulation pathway and converts fibrinogen to fibrin. Vascular occlusion follows
- • Platelets and leukocytes contribute to these to mechanism…Mononuclear phagocytes express large quantities of tissue factor and produce proinflammatory TNF that activates endothelium. Neutrophils and platelets release cytokines that activate endothelium and cause aggregation contributing to vascular occlusion and promoting inflammation..
- • Widespread deposition of fibrin…consumes clotting factors and platelets while initiating uncontrolled fibronolysys…Haemorrhage at various sites follows.”
The text then concludes with a chilling simplicity:
- • Uncontrolled progression leads to widespread tissue hypoxia, multiorgan dysfunction, and death.
Goodness me! I asked Dr Pesta to explain this to me in layman’s language. As I understand it, this is basically what happens. Blood contains a soluble protein called fibrinogen. If the platelets are the emergency sandbags, fibrinogen forms the bricks which are the building blocks of final repair of “the dam”. To be a little more precise, when a distress signal is received the fibrinogen is joined by a protease called thrombin to create fibrin (also called Factor Ia), an insoluble fibrous, non-globular protein, which is then polymerised to form a “mesh” that forms a haemostatic plug or clot (in conjunction with platelets) over a wound site, allowing for the repair to take case.
However, when some unnamed toxin or other agent infects the blood, the coagulation system can be disrupted.
Unfortunately, whatever was at work when the Black Death struck affected the blood so badly that the body’s normal system of coagulation started to run out of control and “hypercoagulation” occurred. This process begins with the formation of microthrombi, small blood clots, created by an aggregation of the platelets and clotting materials. This is a bad thing.
When there are tears in the lining of the blood vessels (endothelium) the blood vessels and white blood cells send out a distress call via signalling molecules (cytokines) for the coagulation to come to their aid.
But instead of coagulants going to the damaged areas of tissue, the process goes wrong and the miniature blood clots start to grow like snowballs. There is a massive amount of coagulation in the blood, but now in the form of huge blood clots, not going to the affected areas but blocking up the blood vessels with a soupy mix. This is a very bad thing indeed. Elsewhere the breakdowns in the capillaries continue unabated.
Imagine a bottle of milk in a fridge. It has a uniform, milky colour throughout. Now imagine that you have left the bottle of milk for one, two, or three months. You will now probably have a bottle with a thick nasty viscous semi liquid gloop at the bottom, and a thin, watery, anaemic looking liquid at the top. At a very simple level this is the analogous to the effect of DIC. Part of the blood becomes thick, as the coagulation system goes into hyper drive, using up all the supplies of coagulant and clogging up the blood vessels with goo, or as Dr Pesta called it “jello” (American for jelly, I believe). The rest of the blood is deprived of the necessary coagulation to repair the tissue damage – all the supplies of coagulant have been used up. There is then a fatal paradox. The thick gooey clotted blood interferes with proper blood supply, and the organs are starved of the proper supplies of oxygen and the arteries, veins and capillaries are blocked. This creates a vicious cycle. Oxygen is no longer carried to the organs with the result that the organs produce more toxins and an increase in blood pressure. This increases the internal bleeding from the tears or holes in the capillary system….
It is for this reason that the autopsies from 17th Italy described parts of the internal organs and being filled up with thick, blackish blood (ultra heavy clotting) whilst other organs appear to have melted away (unrepaired).
What of the visible signs? On the surface the visible results are bleeding from the body cavities such as the nasal passage and spontaneous ecchymosis. An “ecchymosis” is the technical term for “a subcutaneous purpura larger than 1 centimeter or a haematoma” – commonly called a bruise, caused by the escape of blood into the tissues from ruptured blood vessels. In short there is bleeding under the surface of the skin giving rise to a widespread bruising effect. This is exactly what is described in many contemporaneous descriptions of the Black Death….
Within the body, the effect is all the more deadly. Dr Pesta gave me this example. Typically one quarter of the circulating blood stream will pass through the kidneys. If there is a tear in blood vessels supplying the kidneys which is unrepaired, each heartbeat will pump a significant amount of blood out of the contained blood vessels and into the abdominal cavity. Similarly, if there even a tiny unrepaired tear in the stomach wall or lungs, the blood will flow in and the victim will start to vomit or cough up blood. Dr Pesta stressed to me that these do not have to be visible tears; a microscopic tear is all that is needed. As Dr Pesta put it, “You’ve got to remember, we are talking about damage at the cellular level.” Nevertheless, without the body’s auto repair system, the bleeding will be extensive.
I put this question to Dr Pesta: what would be the ultimate cause of death? I suggested a heart attack as the body’s system collapsed under the stress. Dr Pesta considered this issue with a professional demeanour as she sipped her latte. She explained that she thought this technically unlikely. She considered that the initial fever would probably fade away (fever being an interesting and problematical phenomenon, by the way) and the victim would more than likely become quite cold as blood pressure collapses. The external extremities (hands, feet) would go cold as the body concentrated its remaining resources to preserve the temperature of the vital internal organs; heart, lungs, liver, kidneys and brain. Dr Pesta thought there would probably be two immediate causes of death. First, a blood clot on the brain causing a massive embolism or stroke. Secondly, “hypo vascular shock” or, as Dr Pesta thought it more accurate to put it, “haemorrhagic shock”. I pressed for an explanation of this which would allow me to understand a little more clearly what that that meant. Dr Pesta sipped her latte and frowned. She put it this way:
“Well,” she said “On the one hand the blood has stopped circulating properly within the body, and on the other you bleed to death inside yourself.”
She sipped her latte again, and picked at a skinny blueberry muffin.
Right…
So, to recap. The almost certain cause of The Black Death was a highly infectious virus, not a less infectious bacillus. Historians who (like me) may have assumed that it was genetically related to albeit a more virulent version of a Bubonic Plague bacillus are getting it completely wrong. They are confusing chalk and cheese.
The pathology of the Black Death is simply not typical of Bubonic Plague. Bubonic Plague does cause swelling of the lymph glands and nasty stuff, but the symptoms described are all much more consistent with the “Disseminated Intravascular Coagulation” or DIC. Just to be clear, DIC simply describes the end game – what happens to the body when there is something extremely nasty going on in or to the blood. It can have many causes; snake or spider bite, a gangrenous infection, an internal cancer such as of the liver, septicaemia, an uncontrolled infection, or even a common cold given the right (or wrong) circumstances. But the pathology is broadly a-typical of Bubonic Plague bacillus, and highly typical and consistent with the viral haemorrhagic fevers such as Ebola, Lassa Fever or Marburg. Equating “The Black Death” with a bacillus like Y-Pestis is like thinking a dangerous dog is a form of nerve gas. It is simply biologically ignorant, even absurd, and completely underestimates the danger.
All very technical stuff. However, as we parted after our coffees, Dr Pesta had one little amusing trick to play on me, and it had a particularly dark but effective resonance.
“By the way,” asked Dr Pesta, “Do you know the nickname we have in our job for “Disseminated Intravascular Coagulation?”
“Well, yes,” I said, earnestly studying my notes. “You call it “DIC” for short.”
Dr Pest laughed merrily with more than a trace of mischief.
“Well yes,” She said. “That is the shorthand. But do you know what we say “DIC” stands for?”
I was perplexed. It seemed we were going round in circles. I consulted my notes again.
“Disseminated Intravascular ….thingy?” I ventured.
She laughed again.
“No dear. That is the technical name. But we simply call it “Death Is Coming”.
And on that merry note we finished our coffee, and headed into the frosty New England evening. Behind us, someone sneezed.
Gildas the Monk
-
January 8, 2013 at 13:06
-
Fascinating, well thought-out, well researched using a textbook scientific
approach and a refreshing willingness to alter your view when your
preconceptions are shown to be erroneous. Ever though of getting a job as a
climate scientist?
Oh as an aside: scientists have always liked to used real-world
descriptions to describe medical phenomena (re. Dr. Pesto’s dubbing of the
gloop as “Jello”). I suffer from Atherosclerosis, the lining of the cardiac
arteries by cholesterol and fatty deposits, which has caused a heart attack in
the past and is now (hopefully!) under control. I found out recently that the
Greek root “Atheros” means “Porridge”….
-
January 7, 2013 at 18:45
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Dear Gildas
A wonderful article.
I have just read your second article
on the Spartans. The seem to have been even more unpleasent than I
thought!
In passing I rememember reading somewhere that in the battle
line-up every third man was the (homosexual) friend of the appropriate number,
on the principal “if you will fight like hell for the state, think how you
will fight for your boyfriend”.
I dont know if it’s true, but it certainly
seems consistent
concerning “will leave interesting topics such as the
renowned beauty and athleticism of Spartan women, their rights and somewhat
liberated attitude to sex for another day” may that day be soon!
I dont
know if you are intrested in ancient egypt, but if interested in the status of
ordinary women the book “Daughters of Isis” by Joyce Tyldsley is well worth
reading.
Please keep up the good – sorry Exellent work
regards Stan
- January
7, 2013 at 02:08
-
Too knackered for a detailed response but generally agree. It was more
likely a virus than a bacterium. Which would lead me to reveal the best
possible bioweapon on the planet if I wasn’t sober enough to be concerned
about arrest… but then I gave away the idea in a short story many years
ago.
Then again, if they came at dawn tomorrow, I’d already have left for work
anyway. Scottish police dawn raids are more leisurely than down south.
A bit of pedantry. E-coli and Y-pestis are Escherichia coli and Yersinia
pestis, and should be abbreviated as E. coli and Y. pestis and italicised.
Sorry, I was a lecturer in this stuff for 13 years
Trivia time: Yersinia pestis used to be Pasteurella pestis in honour of
Pasteur but then someone decided it wasn’t much of an honour really. Nobody
wants to be remembered as a horrible disease.
Pay no attention, it’s just the lecturer in me breaking out again. I’ll be
back with a more reasoned and less pedantic response.
-
January 6, 2013 at 23:08
-
Thanks John G, I have read that article now. I’m still unconvinced, I have
to say. While there are some good points which seem to make sense of the
conflicting spread and symptoms of the three great pandemic waves, I still
think it’s more than possible that the bubonic plague studied in the 19th
century and since is simply a mutated form of the earlier ones.
I agree
with some of the bubonic plague proponents that it’s impossible to actually
clear the question up using those accounts alone, the only thing that could
really do it is some form of testing of known past victims.
This is an
interesting article which explains the plague/no-plague argument and comes
down firmly on the side of plague http://hnn.us/articles/10949.html
- January 7, 2013 at 04:29
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Then you may remain firmly within the bosum of the flock having
successfully evaded the heresy of Gildas the Monk. Although I’m sure when
the Spanish Inquisition had denounced him as an apostate of satan for his
crimes against orthodoxy I heard him say in broken italian “Eppur si
muove”.
“Long is the road, and hard, that leads out of the darkness and up
to the light.”
- January 7, 2013 at 04:29
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January 6, 2013 at 22:26
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Thanks Span
And thanks to to the many comments and observations. I am
certainly not claiming any novelty in the research, because there are many
academics who have done the work; but nobody had told me! I found the whole
story fascinating, like a detective novel. So I hope my little investigation
has been interesting. It is also informative, perhaps, on historical method,
and how we (and I) can make mistakes, and how orthodox thinking is often very
wrong. And one again I never fail to be amazed by the wealth of knowledge of
the readers.
G the M
- January 6, 2013 at 22:14
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The Black Death was a highly infectious virus, not a less infectious
bacillus.
Gildas, don’t beat yourself up about being wrong: you may not be wrong: any
virus is likely to result in secondary effects including bacterial infections.
These days this isn’t a huge problem but hundreds of years ago the secondary
infections would have been just as deadly.
-
January 6, 2013 at 20:29
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It’s very interesting but contemporary accounts are absolutely clear about
the buboes.
How would your theory account for that?
And also the
geographical route, which is pretty well plotted, shows the outbreak spreading
from areas that are known to have endemic bubonic plague.
My understanding
has always been that there was more than one type of infection raging, because
accounts of the symptoms and the speed of spread DO differ, quite markedly.
This was in fact noted by people at the time and they also wondered, if time
granted them the chance, what exactly they were dealing with.
But I think
it would be extraordinary to conclude that there was no bubonic plague at all
in England in the period of the ‘Black Death’.
- January 6, 2013 at 20:58
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While I’m sure Gildas would love to claim this as his theory, he is
merely providing us with an enlightening insight into the work of others,
including some of the worlds experts and at least one Nobel prize-winner
(Mac Burnet). I mention this not as “an appeal to authority”, but rather
that various leading experts have looked at the discrepancies between the
Justinian, Medieval and Modern diseases and acknowledged that there are
fundamental problems.
Although the presence of buboes is mentioned in the historical texts,
they are not in the same positions as the modern disease (around the lymph
nodes) and with the historical outbreaks there are other distinguishing
features that are not present or extremely rare in modern outbreaks.
As mentioned earlier, for more details on the assertion made by Gildas, I
recommend the following summary by Glasgow University’s Professor Samuel K
Cohn on the “Epidemiology of the Black Death and Successive Waves of
Plague”. This is available on the US Government’s National Institute of
Health – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2630035/
I believe the BBC even did a Horizon programme about this a few years
back…
- January 6, 2013 at 21:21
-
Sorry, it was BBC’s Timewatch (not Horizon)
VIDEO:
http://watchdocumentary.org/watch/the-mystery-of-the-black-death-video_9500261f6.html
- January 6, 2013 at 20:58
- January 6,
2013 at 17:59
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Another enthralling and thought-provoking article, Brother Gildas! You are
right up there with Richard Preston (author of ‘The Hot Zone’ and others) in
my estimation!
- January 6, 2013 at 17:49
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Like the good John Galt, I kept my mouth shut as long as possible, because
Gildas’ story has been fascinating.
Some time in the 1970s, I read a long piece (no idea where or by whom after
all this time) which clearly distinguished between the Plague and the Black
Death. I don’t remember the details now – assuming I understood them at the
time – but the distinction was clear, and the respective transmission vectors.
I was surprised it had to be made again.
If there is to be more from Gildas I look forward to it, especially as I
have long been aware that the Death could return.
- January 6, 2013 at 18:46
-
The idea that Gildas has outlined in his postings is not new and has been
challenging the prevailing orthodoxy since at least the mid-1950′s.
Certainly, the majority of UK adults were taught the prevailing orthodoxy
that bubonic plague was the cause and the fleas of rats were the
carriers.
Overturning prevailing orthodoxy is always difficult, but with the Black
Death it is even harder as the disease itself has either died out or we are
no longer in contact with its host. The reason why we have got to the
situation we have is that the epidemiology of the Black Death IS so
different from bubonic plague.
Personally, I think the hosts were the dodos of Mauritius!
- January 6, 2013 at 19:16
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Jeff – I think you may be referring to the book “A History of the Bubonic
Plague in the British Isles” by eminent bacteriologist Dr. J. F. D.
Shrewsbury, which was published in 1970.
-
January 6, 2013 at 20:15
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Many thanks, John. I am not sure that with my lack of medical
education, I would have read Dr Shrewsbury’s book; but it may well be that
I had the benefit of a magazine discussion.
I am intrigued by your positing that we may no longer be in contact
with the host of the Black Death. Perhaps, somewhere along the line, there
has been a beneficial extinction. Better not tell the Greens.
-
- January 6, 2013 at 18:46
- January 6, 2013 at 16:08
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I’ve been looking forward to Part Three, and you don’t disappoint, Gildas.
Now I’m on tenterhooks for Part Four….(please allow it, landlady – it’s
fascinating stuff!)
As an object lesson in how incorrect assumptions can take solid root, this
is a first class example. Your researches and reporting have certainly
expanded my knowledge of the Plague immensely, for which – many thanks!
One does wonder if similar misconceptions concerning science are still
happening. The working of the climate, and the politicisation of some
assumptions or theories relating to the study of climate, is one possible
example; though only time and much more honest research will tell if my
assumption is correct!
- January 6, 2013 at 15:24
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Excellent piece again. I have no medical knowledge (until now), but the
viral conclusion seems to make sense.
Also damned generous of Mme Raccoon to pay the expenses for a research trip
to New England, I say. That’s a real blogger.
- January 6, 2013 at 13:25
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Excellent follow on. As per John Galt I was wondering what protected those
who survived or were not infected in the first place. Thank you.
- January 6, 2013 at 19:49
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Natural selection.
Some folks had natural immunity, or more likely, some variant gene which
prevented the virus from infecting the host. Precolumbian native Americans
were largely wiped out from things like measles because they had no immunity
– Eurasians ancestors had survived it. Similarly I have heard that Syphilis
was imported from North America, and that “salt retention” in modern African
Americans is disproportionately high because their ancestors were more
likely to survive the poor conditions aboard slaving vessels.
Either that or a good hotline to a skypixie …..
- January 6, 2013 at 19:49
- January 6, 2013 at 11:52
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Well that’s another bit of the gardening that’s not been done this
morning.
Thanks for Episode 3, Gildas.
- January 6, 2013 at 11:28
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Well done. Fascinating material as always, Gildas. Nowhere mentioned…but I
detect the implication of a diet low in saturated fats, high in fibre with
much fresh fruit and vegetables + wholesome water + 75mg aspirin/day +
moderate exercise. My God, Death is still coming!
- January 6, 2013 at 18:13
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Fats are vital in controlling inflammation & repair of cells. Without
adequate consumption of fats, and the correct types of fat, the human body
cannot respond correctly to infection & repair itself.
The body needs the correct ratio of omega-3 to omega-6 fatty acids to
control inflammation. Typically most diets are too low in omega-3, and far
to high in omega-6 compromising the body’s natural inflammation response.
Fatty fish are the typical source of omega-3, nuts & seed oils (rape,
corn, soy etc) are a common source of omega-6 in a modern diet. Pasture
raised ruminants (cows, sheep, goats) have both omega-3 & omega-6 in the
correct ratio. Grain feed ruminants have very low levels of omega-3 (which
is bad).
Hormone levels are critical for regulating repair & maintenance of
the body. Most hormones are made in the body by converting saturated fats.
Without saturated fats the body has great difficultly producing normal
levels of many vital hormones.
High fibre is bad for digestive health. Fibre irritates the gut, making
stools looser than normal. Long term consumption of a high fibre diet
compromises the gut/blood barrier allowing substances into the blood stream
which should not be there. This creates a cascade of problems with the
immune system, most auto-immune diseases are the result of a compromised
gut/blood barrier.
Fruit is only healthy in relatively small amounts. Most fruits contain
high levels of fructose which gets converted by the liver into fat (aka
fatty liver).
75mg of aspirin is too high and causes more problems that it solves. 15mg
is indicated in clinical studies, and then only if you have a reason.
The body _must_ have adequate amounts of protein, which is missing from
your list. Typically most people require approx 1g of protein per 1kg of
body weight. Not all proteins are created equal. Animal proteins are vastly
superior to vegetable based proteins.
Unfortunately the diet you suggest promotes many modern diseases –
arteriosclerosis, auto-immune diseases, reproductive problems (PCOS in
woman, erectile dysfunction & poor sperm quality in men) and many, many
other health issues. And if that doesn’t kill, the dysfunctional immune
response allows infective agents to cause heath problems which would not
normally do so.
A diet high in fresh vegetables, meat (including offal) & fish with
appropriate exercise & sun exposure is ideal for health. Animal fats
should always be consumed in preference to seed oils. Carbohydrate intake
should be restricted and consumed relative to the amount of (anaerobic)
exercise.
- January 6, 2013 at 19:49
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A proficient copier but never give up your day job to practise
medicine, Alan.
- January 6, 2013 at 19:49
- January 6, 2013 at 18:13
- January 6, 2013 at 11:18
-
Thank you for a fascinating follow-on. I can see why people become
virologists; it’s the study of something which is almost non-existent until it
decides to exist . . .or something.
-
January 6, 2013 at 09:15
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Another excellent, interesting and well researched posting from Gildas.
Well done old boy.
I had similar concerns to “Dr. Pesta” with regard to your earlier posting
on genetic differentiation between modern and recovered “Yersinia pestis”, but
since this is primarily a Libertarian blog rather than a scientific journal
felt that such criticism would have been uncalled for. I think your overall
conclusions are correct and certainly concur with the reliable information we
have from that time (vanishingly small in my appreciation).
One aspect of this that might be worth a final posting from your good self
Gildas is to look at the question of what (if any) environmental or genetic
components protected the survivors, especially their close relatives or those
having regular close contacts with the dead such as priests, parish officials,
etc. We have seen with other viruses that certain genetic markers (e.g. CCR5
in HIV) can provide protection against viruses although the underlying
mechanisms are not fully understood.
P.S. I think you need to double-check your Wiki links as some of them
appear to be pointed incorrectly.
-
January 6, 2013 at 13:49
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Thank you on both counts John. “Dr Pesta” gave me a real bollocking (in
the nicest possible way!). This little project seems to have taken over a
lot of my attention (and possibly bored many readers to tears) but I have
found it the most fascinating detective and human story. Yes, one more post
dealing with CCR5 and potential immunity ifour learned editor permits; and
also the legacy, human and social which really shaped the modern world just
as much as the industrial revolution.
G the M.
- January 6, 2013 at 14:46
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For readers of Gildas who would like to step into the details of his
assertion, I strongly recommend reading the article by Glasgow
University’s Professor Samuel K Cohn on the “Epidemiology of the Black
Death and Successive Waves of Plague”.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2630035/
- January 6, 2013 at 14:46
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- January 6, 2013 at 09:06
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22 Anna Raccoon January 3, 2013 at 16:54 Previously said:
Yep. Everything that appears as ‘by Anna Raccoon’ is written by me…
Waves at the landlady to get her attention, “Errr,,,,landlady your
petticoat is showing”.
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