HIST 234: Epidemics in Western Society Since 1600
|Transcript||Audio||Low Bandwidth Video||High Bandwidth Video|
Epidemics in Western Society Since 1600
HIST 234 - Lecture 6 - Smallpox (I): "The Speckled Monster"
Chapter 1. Smallpox [00:00:00]
Professor Frank Snowden: I want to turn to the next topic, which marks a new unit in our course. That is to say, until now we’ve dealt with bubonic plague, in a series of talks and in your first section meeting. Now I’d like to look, for comparative purposes, at a very different high-impact disease; and this time and next we’ll be dealing with smallpox. So, I think you deserve an answer to the obvious questions: why smallpox, and why at this stage in the course? So, I want to give you a little bit of explanation, to see where we’re going. The first has to do with I might call a varied intellectual diet, and I want us to deal with diseases of very different types, and so we’ll have to examine the impact of different kinds of infectious diseases.
Plague was a bacterial disease. Smallpox instead is viral. Plague was transmitted by vectors. You know the drill now, the role of rats and fleas. Smallpox instead is spread by contact and airborne inhalation of droplets. Plague is a classic epidemic disease, in the sense that it’s an outside invader that ravages a locality for a season and then departs. Smallpox is different in that it can be both endemic and epidemic. So, we’ll see a different dynamic. It’s also true that the social responses to smallpox were quite different.
Plague was associated with terror and social disruption, and in the New World we’ll see that it had an even more dramatic impact on the Native — smallpox did — on the Native American population. But in European conditions it was a familiar endemic disease with a less dramatic — as a cause — was less dramatic as a cause of social tensions and disruption. We’ll see too that in terms of impact, for chronology it makes sense to look at smallpox at this stage in our class. It had long been present in human history, but there was an upsurge in smallpox in the seventeenth and eighteenth centuries that accompanied the surge in the demography of Europe. And it also reflected the transformation of social and economic conditions associated with the commercialization of agriculture, the onset of industrial development, and rapid, unplanned urbanization, with those associated pathologies such as overcrowding, both at home and in the workplace.
In those conditions, smallpox was a great killer, and it succeeded plague as the most dreaded disease of the late-seventeenth and the eighteenth century. In a sense, we’re moving from bubonic plague, the most dreaded disease of its era, to — in a sense, in terms of fear — to smallpox as the next most dreaded disease of the next period in the eighteenth century. But there’s more to it that that. Smallpox, as you’ll see in our reading and in our lecture next time, was also extraordinarily important in terms of its impact in the New World. It led to a demographic catastrophe for the Native American population, largely spontaneously, but there were also intentional acts of genocide involved.
So, we’re going to see, in terms of one of the themes of our course, that disease, and particularly smallpox, played an important role in the big picture of history; in conditioning or creating factors that were important in European settlement in the New World, and that led to the introduction of African slavery, as the Native American population had no immunity and perished from smallpox, and therefore could not be enslaved; whereas Africans, possessing immunity, were imported to replace them.
Another major feature and reason for dealing with smallpox has to do with another theme of our course, and that is public health. We’ve already dealt with plague measures of public health. You know what they are, the plague measures: boards of health, quarantine, lazarettos, sanitary cordons, emergency burial regulations. Smallpox, by contrast, was to lead to a very different but highly effective style of public health; that is, first inoculation and then vaccination, associated with Edward Jenner. Even more spectacularly than plague measures, vaccination ultimately promoted a victory over smallpox, leading in 1980 to its total global eradication, at least naturally occurring smallpox; the first, and still as we speak, the only human disease to be so intentionally eradicated.
Unlike plague measures, vaccination was a powerful tool of public health. Successful vaccines have subsequently been developed against other diseases: measles, rubella, whooping cough, tetanus, diphtheria, rabies, polio. But again, like plague measures, vaccines have been controversial — and we’ll be talking about when vaccines form an appropriate strategy — and eradication has been ever more elusive for diseases other than smallpox. It may be that smallpox is a special case, rather than, as many hoped, a model for the eradication of diseases sequentially, one after another.
We’ll be looking also at smallpox because of its demographic and economic effects. We talked, in terms of plague, of a mortality revolution, in terms of demography, and also of its impact on industrialization. Smallpox and the successful containment of smallpox through inoculation and vaccination also had a major impact on that mortality revolution, and therefore also on economic development. We’ll be looking also at cultural impact, and we’ll see that smallpox also produced the cult of certain new saints; that it too became a theme in the arts and literature.
More speculatively, we talked last time about the possible relationship of the successful conquest of plague on the coming of the Enlightenment. Well, smallpox provides us with a second instance of the successful deployment of human means to control a major cause of death and anguish, making life more secure and longer. It’s suggested that a number of leading philosophes were avid proponents of inoculation, including Voltaire and Condorcet. So, we’ll be dealing with those issues. But this morning what I’d like to do is to concentrate on something more narrow, which is — but forms the basis for our understanding of the impact of this disease — its nature as a disease. How it affects the individual human body, and what were the treatments in the seventeenth, eighteenth centuries.
Chapter 2. Etiology [00:09:13]
Let’s begin with smallpox as a disease. Smallpox, often nicknamed, for reasons we’ll soon see, “the speckled monster.” It’s a virus belonging to the family of orthopox viruses that includes Variola major, Variola minor and cowpox. We’ll talk about cowpox next time, because of its influence in the development of vaccination. But our theme will concern Variola major and Variola minor; especially Variola major, which is the causative agent, primarily, of smallpox. This is a picture of Variola major, the largest of all viruses, first seen by the microscope in 1905. This causes classical smallpox. There’sVariola minor as well, that first appeared in the twentieth century; and for our purposes we can afford to ignore it. It was of minor impact and now, like Variola major, it’s extinct as well.
Now, one question is, what’s a virus? We talked about the term microbe; microbe being a generic term for microscopic organisms, including bacteria, like our friend Yersinia pestis, the causative agent of bubonic plague, and viruses likeVariola major and Variola minor, the pathogens that cause smallpox. Plague was caused by bacteria, and those, as you know — and will be studying more on Science Hill — are unicellular organisms that are definitely and unequivocally alive. They reproduce by dividing. They contain DNA, plus all the cellular machinery necessary to read it, and to produce the many proteins that enable it to live and reproduce. Viruses are something different. And here there’s a possible confusion lurking for the historian.
The word “virus” itself is ancient. In the humoral system, in fact, when diseases were seen to arise from assaults on the body on the outside, one of the major environmental insults that was thought to lead to disease was the corrupted air or miasma, and this was influenced by a poison, that might be called a virus. So, if you do research on medical history, you’ll see the term “virus” used in an old sense for many centuries. But “virus” in present medical discourse is a term that dates its modern usage from the early twentieth century, and it refers to parasitic particles, perhaps 500 times smaller than bacteria. Their existence was established by elegant scientific experiments in the first years of the century, completed by about 1903. But they couldn’t actually be seen until the invention of electron microscope in the 1930s, and their functioning wasn’t understood until the DNA revolution of the 1950s.
So, viruses, we now know, consist of some of the elements of life, stripped to their most basic. A virus really is nothing more than a piece of genetic material wrapped in a protein case. They’re particles that are inert on their own. Viruses lack the machinery to read DNA, or to make proteins, or carry out metabolic processes. They can do nothing on their own, and they cannot reproduce by themselves. Their survival depends instead on invading living cells. Once inside, they highjack the cell and its machinery. The genetic code of the virus — and the virus, after all, is almost nothing else — gives the cell the message it needs to reproduce more virus, thus transforming cells into virus producing factories, and in the process they destroy the host cell. As they produce more and more viruses, and destroy more and more cells, the effect on the human body can be severe, even catastrophic, depending on the capacity of the immune system to contain or destroy the invasion.
Here we have, in a sense, the opposite of a Hippocratic idea of disease; the body assaulted, not from the outside, but rather from a parasitic pathogen deep within. There is an exotic debate, of course — are viruses alive? Those who argue that they are alive, note that they’re capable of transmitting genetic material, one of the key indications of life. Those who claim they’re not alive, note that on their own they’re inert, that they can’t carry on metabolic processes, or produce proteins. Viruses, they note, are the ultimate parasites. Virologists often say that whether you decide that viruses are alive or not is ultimately a matter or disciplinary perspective, or perhaps even personal preference. The reassuring point for us is that, perhaps excepting theology, the answer doesn’t really matter.
In any case, what we need to know is that smallpox was caused by a virus, and a virus that has no animal reservoir. The disease was restricted entirely to human beings, and that will prove to be important in making it eventually a good candidate for eradication. The name for the virus, Variola, derives from the Latin varius, meaning spotted. And in England the disease, in fact, was popularly called, as I’ve said, “the speckled monster.” So, here’s a picture of the smallpox virus — oops, it’s gone out; there it is. And that’s a schematic image of a smallpox virus. And as I said, there is a mutation that occurred in the twentieth century, causing the rise of Variola minor, as well as Variola major. But we’ll be concerned exclusively here with Variola major; the main cause of smallpox historically.
Chapter 3. Transmission and Epidemiology [00:16:49]
Well, how was it transmitted? Here we need to remember that smallpox is an exceedingly contagious disease. A smallpox patient sheds millions of infective viruses into his or her immediate surroundings, from the rash and from the open sores in the sufferer’s throat. The patient is infective from just before the onset of the rash until the very last scab falls off weeks later. Not everyone, of course, who is exposed is infected. Living along with people with immunity — and leaving that aside — it has been estimated that the chances are about 50:50 that a susceptible member of a household would contract smallpox from an ill patient in the home.
The dominant manner to spread smallpox was by contact infection, droplets breathed out in face-to-face contact with a susceptible person and inhaled by that person. Normally the spread was in the context of intense contact over a period of time; that is, a family member, or someone on a hospital ward, in an enclosed workplace — an office, a factory, a mine — a school classroom, an army barrack, a refugee camp. And it’s most easily transmitted in dry, cool seasons. That’s the primary mode of transmission. There are two more, however, that are more relatively secondary.
A second mode of transmission is by what are called — another bit of jargon here — fomites. A fomite is simply an inanimate object, capable of carrying infectious material from one person to another. Examples might be bed linen, clothing; the shroud from an infected person that transmits viruses from one body — that is, of the sufferer — to the next person. Other examples are simply doorknobs, eating utensils, and so on. So, that’s a second mode of transmission. There’s a third too, that smallpox can be vertically transmitted; that is, from mother to infant. It’s possible for an infant to be born with congenital smallpox.
Well, that’s the mode of transmission. What about its epidemiology? Well, some favoring factors include large urban populations. It’s not coincidental that smallpox raged in Western Europe in the eighteenth century. The crowded living conditions and workplaces were ideal for its transmission. Trade and the movement of people, displaced people, warfare. People who assembled and reassembled in crowds were ideal for transmitting smallpox. The disease is known to have afflicted Ancient Egypt. Mummies are known to have been victims of smallpox. But the important point is that it became endemic in Europe, that became the world reservoir of infection, from which it spread by trade, colonization, warfare. And in European cities it became, above all, a disease of childhood. But about a third of the deaths of children in the seventeenth century were due to smallpox.
So, a reason then for dealing with smallpox now, in our course, is that it was on a major upsurge in the seventeenth and eighteenth centuries. How was it named? Why is it called smallpox? A small point. But we need to know that it’s from a comparative description of its characteristic lesions. The “great pox” is a disease which we’ll be dealing with pretty soon, which was syphilis, that creates large lesions and affects adults. The smallpox had small lesions and primarily affected children; at least in countries in which it was endemic.
Another point we should know about smallpox is that after infection, a person enjoys a lifelong immunity. We need to know that because it’s a major factor in the public health measures that the disease eventually generated. Well, what about its symptoms? How does it affect the individual human body? After inhaling the virus, there’s an incubation period, which normally lasts something like twelve days. This is important in its epidemiology because it allowed the spread of the disease; because an infected person had ample time to travel before falling ill, and therefore time to take the disease with him or her and to spread it.
Chapter 4. Symptomatology [00:22:32]
Now, I’m going to give some attention — perhaps more than you might like when you see the images — to the symptoms of smallpox. And there’s a reason for that. Part is that smallpox is tremendously, terribly, terrifyingly painful. Plus it leads — and this is important too, in the way that it impacted society — it often produces lifelong scarring, disfiguring and blindness, and these in turn spread fear of it and terror. And, so, the very word smallpox has a particular resonance in popular imagination, associated with dread.
People sometimes ask, in a course like this, which of the diseases we encounter was really the worst? The question doesn’t permit empirical verification, because no one has ever suffered, mercifully, all the afflictions we study and had the opportunity to compare. But it is meaningful to note the impression of those who lived through the times when smallpox claimed its legions of victims. They thought — and the physicians who treated them — that smallpox was the worst of human maladies; that was a term that was said at the time. And this, in fact, was the view, closer to home, of the Illinois State Board of Health in 1902, where Dr. Donald Hopkins wrote this: “In the suddenness and unpredictability of its attack, in the grotesque torture of its victims, in the brutality of its lethal or disfiguring outcome, and in the dread that it inspired, smallpox is the worst. It’s unique among human diseases.” To the extent that that’s true, it’s also one of the reasons that smallpox appeals to the malevolent as a possible instrument of bioterror.
It’s well-known that a major outbreak of smallpox would spread death, maximize suffering, and lead to widespread fear, flight and social disruption. The symptoms are important to examine as an integral part of this disease. And more generally, unless we appreciate the distinctive symptoms of each of the diseases we examine, there’s a distorting temptation to allow them to run together, the diseases, as so many interchangeable causes of death; a point of view that prevents us from understanding that each of these epidemic diseases had a distinctive and different imprint.
Smallpox was the disease that it was, in part because of the dread that it generated; fear not only of death, but also of exquisite suffering, maiming, disfiguring and blindness. Only with that in mind, can we understand why it’s also so widely thought to be a candidate for bioterror. So, we’ll look at images of the disease. And I apologize to those of you who’ve just finished breakfast or just about to have lunch. In any case, first after the incubation period, there’s the pre-eruptive stage. The virus multiplies in the system for twelve days after incubation, and symptoms of disease begin with a viral shower, as the pathogen is released into the bloodstream and spreads systemically throughout the body, localizing eventually in the blood vessels of the skin, just below the superficial layers. The viral load released, and the efficiency of the body’s immune response, determine the severity and type of the disease. Onset is sudden, with fever of 100 to 102 degrees, and a general malaise.
This, then, is the beginning of perhaps a month of excruciating suffering and the danger of spreading contagion. The early symptoms are fever, vomiting, severe backache, splitting frontal headache, and in children sometimes convulsions. Sometimes the disease is so overwhelming that it leads to what’s called fulminating smallpox, which causes death within thirty-six hours, with no outward manifestations at all; although post-mortem exams reveal hemorrhages in the respiratory tract, the alimentary tract or the heart muscles.
Let me give you a description of a hyper-acute case of that kind. Physicians wrote: “After three to four days, the patient has the general aspect of someone who’s passed through a long and exhausting struggle. His face has lost all expression, is mask-like, and there’s a wont of tone in all muscles. When he speaks, this condition becomes more apparent, speaking as with evident effort, and the voice is low and monotonous. The patient is listless and indifferent to surroundings. The mental attitude is similar. There’s a loss of tension, a lengthening of reaction time, and defective control. In the most fulminant cases, the aspect of the patient resembles that of someone suffering from severe shock and loss of blood. The face is drawn and pallid. Respiration is sighing or gasping. The patient tosses about continually, and cries out. His attention is fixed with difficulty, and he complains only of agonizing pain; now in the chest, now in the back, the head or the abdomen.”
But normally smallpox wasn’t fulminant quite like that, and the patient passed on to the next phase, which was the eruptive one, exhibiting the classical symptoms of smallpox that led to its diagnosis. On the third day after onset, the patient usually felt a little better, and in mild cases he or she could return to normal activities, with the unfortunate effect that this spread the disease further. But concurrently a rash appeared; a small round or oval, rose-colored lesion, known as a macule, that’s up to a quarter-of-an-inch in diameter. The macules appeared first on the tongue and palate, and then, within twenty-four hours, it spread to cover the body, down to the palms of the hands and soles of the feet. On the cheek and forehead, the appearance is of severe sunburn, and indeed the sensation felt by the patient is of scalding pain or intense burning. There’s a characteristic pattern, called centrifugal distribution; that is, that the rash is least spread on the trunk of the body and most densely apparent on the face and the extremities.
Let me show you a slide of a very ill little boy, and you can see this centrifugal pattern in which the rash is most apparent on the extremities, rather than the trunk. On day two of the rash, a little further into the infection, the lesions alter. At this time the macule becomes harder, and generally rises above the surface into structures known as papules, with a flattened apex. To the touch, they were said, by physicians, to feel like buckshot embodied in the skin. And there we can see the picture of a face, at that stage of the disease. The disease then moves on, by the fifth day of the rash, when fluid begins to accumulate in pockmarks, which are then raised and firm to the touch — so we’ll pass on — now called vesicles. They’ve grown in size. They’ve changed in color from red to bluish or purple. And they’ve transformed from solid to blister-like fluid. It’s umbilicated as well.
The process of what’s called vesiculation, the rise of this stage of the rash, takes about three days and lasts a further three. It’s at this stage that the physical diagnosis of smallpox becomes reliable, with the disease presenting its most distinctive appearance. The patient experiences increasing difficulty in swallowing and in talking, due to extensive lesions in the mucous membranes in the palate and the throat. And there’s a child at this stage of the disease. Then by the sixth day of the rash, pus begins to form in the pockmarks. The patient feels much worse. Septicemia can set in. The pustules, as they’re now called, begin to fill with yellow fluid, and the lesions become globular in shape; a process that takes about two days, and they’re fully matured on the eighth day of the eruptive phase.
The patient feels dreadful at this point. Fever has risen in proportion to the severity of the attack. The eyelids, lips, nose and tongue are tremendously swollen. And we can see a picture of an adult at that phase of the infection. At this point, the patient is almost totally unable to swallow or talk, and deteriorates slowly, being drowsy most of the time and restless at night. Often he or she is in a condition of delirium, and thrashes about; may even try to escape. The psychological effects weren’t simply a sign of high fever. They resulted also from the involvement of the central nervous system in the infection, and the neurological effects and sequelae could often be lasting and result in long-term impairment.
Then, by the ninth day of the rash, the pustules were firm and embedded in the skin, and for this reason were likely — and this was important in the impact of the disease — to leave permanent scars and deep pits on the face, or wherever they appeared on the body; if you can imagine by at this stage. Another unpleasant aspect at this stage was that a terrible sickly smell developed, the fetor of smallpox, that physicians claimed that it was impossible to describe but was found to be overpowering. It’s now nearly impossible for the patient to drink, and even milk caused intense burning sensations in the throat. The patient experiences great loss in weight — as much as thirty to forty pounds in an adult — and may suffer from frank starvation. In addition, there’s a complete loss of muscle tone, while the face, in severe cases, takes on the appearance of a cadaver, making the patient almost unrecognizable, even to his or her closest relatives. The scalp may be one large lesion, and tangled with hair. And lesions, as you can imagine, under the nails of fingers and toes were exquisitely painful.
I want to show another disturbing image — this was important, but you can look away if you like — which was the lesions of the eyes. Because smallpox was a major cause of blindness, as well as death and disfigurement, in this period. Well, after about ten to fourteen days of rash, scabs appear, and these contain live smallpox virus as well, and are highly infective and important in the spread of the disease by fomites. At this point, the fluid portion of the pustule is absorbed, leaving behind the solid part. Large areas of the skin may begin to peel off, leaving deeper tissues raw and exposed. These areas are all painful, and contribute to the frightening appearance and the misery of the patient. Fatal cases often occurred from about the eighth day, and an important reason was toxemia, because these lesions were susceptible to infection. So, attentive nursing, good hygiene and sound nutrition reduced the likelihood of that sort of complication. And, to that degree at least, the prosperous, the well-nursed and well-cared for were more likely to survive.
The appearance of the patient was often described by physicians as mortification; the still living patient taking on the appearance of being mummified, and the skin of the face fixed in a grotesque mask, with the mouth permanently open. The appearance of scabs and crusting though was a favorable sign in terms of prognosis for the patient. But they did lead to one final torment of the disease, which was an intolerable itching that accompanied that period; indeed, a large portion of the scarring that resulted from smallpox was undoubtedly due to patients scratching and tearing at their lesions.
Well, the appearance and distribution of the pustules was of major importance for diagnosis, and it could be what was called “discrete smallpox,” where the rash was — each lesion was distinct and separated from the next. And this meant that you had a case fatality rate of as low as about nine percent; you had a ninety percent chance of survival. If instead the lesions were much closer together — semi-confluent it was called — the case fatality rate rose to something like thirty-seven percent. Or in cases of what was called “confluent smallpox,” in which the lesions touched one another and formed a network surrounded by islands of unaffected skin, the case fatality rate was about sixty-five percent. So, the appearance of the lesions was very important in your prognosis.
The rarest form was hemorrhagic smallpox, which had a hundred percent mortality, so-called because the natural clotting mechanisms of the blood were impaired, and the victim died of massive internal hemorrhaging. Overall, the case fatality rate for smallpox was estimated to be about thirty to forty percent. The virus then attacked not only the skin and the throat, but also the lungs, the heart, the liver and other internal organs, and could result in hemorrhaging and death. A major danger was also secondary bacterial infection of the lesions; a very common cause of mortality. Meanwhile, the lesions of the mouth and throat were of great epidemiological importance, because they’re the source of the viruses that commonly form droplets in the air and infect others. Also, the tongue became swollen and misshapen. There was difficulty breathing. The patient became hoarse, swallowing was difficult. And all of that was important.
There were other sources of anguish and suffering: blindness, scarring and disfigurement, respiratory complications. But after the drying up of the rash, the patient began to recover. And among the population that survived, the symptoms declined and the patient regained strength and possessed a lifelong immunity from a second exposure. All of this led, of course, as you can imagine, to tremendous fear of the disease — as in this picture — of Variola.
Chapter 5. Remedies [00:41:14]
Well, how did physicians deal with this disease? Smallpox no longer occurs naturally anywhere on the planet. But it’s worth remembering that there is still no specific remedy or cure for the disease. Treatment, should a case appear today, would be largely supportive, depending above all on intensive nursing, to keep the lesions scrupulously clean, to prevent bedsores and to minimize the breakdown of the skin. In addition, modern medicine would replace lost fluids and nutrients, and would administer antibiotics, not to deal with the virus, but with the bacterial infections that are its complications.
What were traditional remedies? Some of them were surprising. One was a great vogue in the color red. There was a vogue to hang red curtains around the bed of a patient. Red furniture was brought into the sickroom, and patients, including Queen Elizabeth I of England, were wrapped in red blankets. Later on, the discovery of ultraviolet rays in fact gave new impetus to this traditional mania for red, and red glass went up on windows. In the late nineteenth century, medical journals published studies suggesting also that red light could be soothing to the eyes of the sufferer, and that perhaps it prevented scarring of the skin. So, that was one factor.
Another idea that was very common was to open the pustule with a golden needle, to drain the fluid, and then sometimes the lesions were cauterized in an attempt to prevent scarring; procedures that were exceedingly painful. The next idea was what was called “the hot regimen,” to pile the sufferer with blankets, to induce him or her to sweat profusely, to rid the body of the over-abundant humor. Or the patient could be immersed in a hot bath. Light and fresh air, according to this therapeutic fashion, were deemed to be harmful, and the patient was kept in the dark, if possible, with minimal ventilation.
Sunlight was said to aggravate the disease and increase scarring. And sometimes patients were given internal medications, sudorifics, to help the evacuation of the excess humor. The opposite was also tried, the so-called “cold regimen,” to keep the room cool, and frequently to sponge down the patient with cold water, to place-ice bags on the face. Then there was purging and bloodletting. There was also the administration of opiates, in the nineteenth century, and especially morphine, to calm the patient in delirium. Astringent eye drops were resorted to.
A particularly perverse theory, with no empirical basis, was the idea that scarring on the face could be reduced or prevented by causing more intense irritation of the skin elsewhere; so that mustard plasters, mercury and corrosives were applied on the back, in order to save the face. There were also all kinds of local applications to the face, to try to prevent scarring. Nitrate of silver, mercury, iodine, mild acids, a lotion of sulfur; all of those had their vogues. There were ointments and compresses of virtually every substance known to man. Some physicians held the theory that their preparations would soften the lesion and mitigate scarring. So, indeed, ingenious doctors applied lint, boric acid or glycerin; or they covered the face with a mask, leaving holes for the eyes, nose and mouth. Or they wrapped the face and hands in oiled silk.
Alcoholic beverages were administered to deteriorating patients to revive their energy. And sometimes delirious patients were actually tied to their beds. Some doctors recommended restraints, such as splints, in later stages, to prevent patients from scarring their faces by scratching. After hearing of all of these treatments for smallpox, perhaps you’ll appreciate the work of Thomas Sydenham, in the seventeenth century, the so-called English Hippocrates, who decided that the wealthy and noble who received extensive attention and treatment for smallpox perished of the disease more frequently than the poor, who had no access to treatment. And his advice was that the best physician was the one who did the least. He was an advocate of therapeutic minimalism. He advised instead a simple cool regimen, giving his patients fresh air and light bed coverings.
Well, that’s how the disease afflicted the human body. What I want to do next time, now that we understand this terrible disease and the suffering it caused, is to deal with its impact historically, its effect on society, and to look at the development of a public health strategy, which was to be vaccination.
[end of transcript]Back to Top
|mp3||mov [100MB]||mov [500MB]|