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Smallpox Before Edward Jenner Chapter Title: Smallpox before Edward Jenner Book Title: Epidemics and Society Book Subtitle: From the Black Death to the Present Book Author(s): FRANK M. SNOWDEN Published by: Yale University Press Stable URL: https://www.jstor.org/stable/j.ctvqc6gg5.11 JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact [email protected]. Your use of the JSTOR archive indicates your acceptance of the Terms & Conditions of Use, available at https://about.jstor.org/terms Yale University Press is collaborating with JSTOR to digitize, preserve and extend access to Epidemics and Society This content downloaded from 134.84.192.102 on Sat, 28 Nov 2020 03:18:37 UTC All use subject to https://about.jstor.org/terms chapter 6 Smallpox before Edward Jenner Comparing Epidemics It is now time to look for comparative purposes at a second high-impact epi- demic disease—smallpox. Why smallpox? And why cover it at this stage in our study? The answer to this second question is that smallpox followed plague as the most dreaded disease of eighteenth-century Europe. The answer to the first is that smallpox is a very different disease from plague, and one goal of this book is to examine the influence of different types of infectious diseases. Each is a distinctive and special case with its own mechanisms and its own historical impact; therefore, it is important to think comparatively. It is crucial, however, to approach the issue of comparison in a system- atic and explicit manner. For readers for whom the study of epidemic dis- eases is new, the aim is to specify the chief variables that govern the nature and extent of the effect that a particular infectious disease has on society. To that end, it is useful to pose a set of questions to guide the student of history. Let us be clear from the outset that this list of questions is not canoni- cal, and I do not suggest that these are the only questions that need to be asked. It is simply a starting point for orientation as we encounter each new disease, and it is hoped that a cascade of further issues will arise. 1. What is the causative pathogen of the disease? Bubonic plague, as we know, was caused by the bacterium Yersinia pestis. As we move forward we will encounter three 83 This content downloaded from 134.84.192.102 on Sat, 28 Nov 2020 03:18:37 UTC All use subject to https://about.jstor.org/terms 84 Smallpox before Edward Jenner different categories of microbial pathogens: bacteria, viruses, and plasmodia. In a medical course on infectious diseases we would also have to consider prions, which cause such diseases as “mad cow disease” and kuru; but here, the diseases we con- sider are all bacterial, viral, or plasmodial. 2. What is the total mortality and morbidity of the epidemic? “Mortality” indicates the total number of deaths, and “morbid- ity” the total number of cases, both fatal and nonfatal. Clearly, the numbers of deaths and cases are one of the measures of the impact of an epidemic. These statistics, for example, provide some support for the argument that Spanish influenza, which caused perhaps 50 million deaths in 1918–1919, was a more sig- nificant event than the 1995 outbreak of Ebola at Kikwit in the Democratic Republic of the Congo. For all of its international high drama at the time, the Ebola epidemic caused “only” 250 deaths and 315 cases, and it has left a slender legacy. On the other hand, mortality and morbidity figures are no more than a first and coarse assessment of historical signifi- cance, which can be established only by detailed case-by-case analysis that is as much qualitative as quantitative. It would be morally desensitizing and historically wrong-headed, for in- stance, to conclude a priori that by the measure of total mor- tality only major catastrophes such as those created by bubonic plague and Spanish influenza are important events. Indeed, one can argue forcefully that epidemics on a far smaller scale, such as outbreaks of Asiatic cholera in which “only” a few thousand perished, were decisive occurrences that cast a long historical shadow. There is no simple “quick fix” to the prob- lem of weighing historical influence. But morbidity and mor- tality count in the scale and need to be considered. 3. What is the case fatality rate (CFR) of the disease? This question addresses the virulence of the pathogen. CFR is determined by mortality as a proportion of morbidity—or, to put it another way, the percentage of cases that end in death. CFR is therefore the “kill rate” of a disease. One of the reasons that bubonic plague caused such terror and disrup- tion was its exceptionally high CFR, which varied from 50 to 80 percent. At the other extreme, the great Spanish influenza that accompanied the end of the First World War gave rise This content downloaded from 134.84.192.102 on Sat, 28 Nov 2020 03:18:37 UTC All use subject to https://about.jstor.org/terms Smallpox before Edward Jenner 85 to an unparalleled morbidity, but it had a low CFR. This dif- ference is important in assessing the variation in the popu- lar responses to the two diseases. 4. What is the nature of the symptoms of the disease? Symptoms that are particularly painful or degrading in terms of the norms of the society that experiences the affliction— such as those associated with plague, smallpox, and cholera, for instance—can contribute to how the disease is experi- enced and assessed. Smallpox, for example, when it did not kill, maimed, disfigured, and frequently blinded its sufferers. Tuberculosis, by contrast, was agonizing, but it was held by society to make its victims more intelligent, more romantic, and sexually more alluring. This is an important factor in helping to explain the paradox that pulmonary tuberculosis, the chief killer in nineteenth-century Europe, caused so lit- tle terror, while cholera, which had a limited demographic ef- fect, was the most feared disease of the century. 5. Is the disease new, or is it familiar to a population? Familiar diseases tend to be less terrifying than the sudden arrival of an unknown invader. Furthermore, a population is likely to have some degree of immunity against a recurring affliction, and the disease may have adapted itself to its -hu man host by mutating and becoming less deadly. As examples, one can think of the so-called childhood diseases such as mumps and measles. Relatively mild afflic- tions in European society, where they were endemic, these diseases gave rise to devastating catastrophes when they were first introduced to new populations. This is the phenom- enon of “virgin soil epidemics” such as the terrifying die-offs of native peoples in the Americas and Maoris in New Zea- land when they first encountered measles and smallpox. For these reasons “emerging diseases” such as cholera and HIV/ AIDS have tended to unleash more terror than the familiar afflictions of malaria and influenza. 6. What is the age profile of the victims—does it affect the young and the elderly or people in the prime of life? This variable helps determine whether an epidemic is re- garded as “natural” in its passage through a population or whether it seems particularly menacing because it magnifies This content downloaded from 134.84.192.102 on Sat, 28 Nov 2020 03:18:37 UTC All use subject to https://about.jstor.org/terms 86 Smallpox before Edward Jenner its effect by multiplying the numbers of orphans and widows it leaves in its wake. Cholera was especially terrifying because it seemed to target the people who were the economic mainstays of families and communities. 7. What is the class profile of the sufferers, that is, is it a disease of the impoverished and the marginal, or is it a “democratic” affliction? We have seen that a feature of the second pandemic of bu- bonic plague was that it was a universal affliction—a factor that helped to make its social history very distinct from that of cholera, which was clearly marked as a disease of poverty. Such associations generate class and social tensions that a more universal ailment such as influenza fails to unleash. Similarly, the early history of AIDS in the United States re- flected its apparent predilection for male homosexuals rather than the general population. 8. What is the mode of transmission of the disease—through person-to-person contact? contaminated food and water? vec- tors? sexual contact? droplets in the air? The salience of this question is clearly demonstrated by the examples of syphilis and AIDS. As everyone knows, their im- pact and societal ramifications are intelligible only on the ba- sis of the fact that they are sexually transmitted. Scapegoating and stigmatizing are much less likely to occur with regard to an epidemic transmitted through the air, such as influenza. 9. How rapidly does the disease normally progress in its course through the human body—that is, is its course slow and wast- ing or fulminant (coming on quickly and strongly)? Tuberculosis, syphilis, and AIDS are normally afflictions that endure, whereas plague, cholera, and influenza lead to rapid resolutions, whether by death or through recovery. Alterna- tively, malaria can assume either course. Again, the simple measurement of time is no magic key to unlocking the secret of historical significance, but it has a place and its weight on the scales.
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