Smallpox and the Modern Rise of Population

Smallpox was long recognized as a contagious dis­ease with a pustular rash. Distinctive clinical fea­tures, such as the simultaneous maturation of pus­tules (this distinguishes it from chickenpox) and the centripetal distribution of pustules over the body, were not noted.

Even if many cases were missed because the vic­tim was severely infected, or was very young, and died before the rash appeared, mortality records from England, Italy, Sweden, and elsewhere testify to the accelerating intensity of smallpox over the course of the seventeenth and eighteenth centuries. Epidemic years of smallpox in Italian cities of the eighteenth century could account for up to 30 per­cent of the annual mortality, and recurrences swept urban areas at least once a decade (Panta 1980). In London, the largest city of Europe by the eighteenth century, there were no gaps between major out­breaks of smallpox. Annual mortality in the metropo­lis averaged 10 percent of all deaths. Thus, there is much agreement that smallpox was one of the princi­pal causes of morbidity and mortality after plague disappeared. The residual questions are: Why was smallpox increasing in incidence and prevalence, and what effect on population and other diseases did inoculation and vaccination against smallpox have? Finally, can the stepwise retreat of smallpox with the introduction of innovative therapies explain any part of the modern rise of population, which began in the eighteenth century?

The answers to these questions depend in part on the assumptions demographers and epidemiologists make about the principal causes of death in early modern cities.

William H. McNeill (1976) portrays cities as the frontlines of the human battle against microbes that entered these cities through commerce and mi­gration. City residents were usually the first group to be hard hit by a novel infection, but over the long run city populations were, on the whole, immunized earlier in life to viral diseases, which produced life­long immunity. Young adults migrating into the city from the countryside might add to the pool of individuals susceptible to common infections. Un­healthy-appearing, impoverished urban dwellers would better survive an epidemic of measles than a comparable group of strapping young adults from the provinces.

McNeill’s view would make smallpox an excellent example of the long-term advantages, largely immu­nological, to city dwellers, and John Landers and Anastasia Mouzas (1988) have found robust empiri­cal support for this view in the records of London mortality. Moreover, Landers (1987) has found the beginning of a decline in the summer peaks of deaths from gastrointestinal infections by the late seventeenth century.

In addition, A. J. Mercer (1985) argues that small­pox may have been uniquely important in a demo­graphic sense not only because it killed a large num­ber of young children, but because its survivors often succumbed to other infections, once “weakened” by smallpox. Although general crisis mortality, in city or countryside, cannot be linked to famine or to weather conditions, statistically it can, in the eigh­teenth century, be linked to epidemic waves of small­pox. Mercer is not willing to ascribe a determinant role to smallpox among the diseases of the eigh­teenth century, but he is convinced that vaccination, where adopted even halfway, contributed signifi­cantly to the survival of children to adulthood, accel­erating population growth in the early nineteenth century.

Other scholars consider typhus and tuberculosis to have been as important as smallpox. There is once again an artifactual aspect to the high preva­lence of typhus, for it was only during the eigh­teenth century that physicians first described its clinical and epidemiological features well and differ­entiated typhus from a miscellany of other fevers - nervous, biliary, inflammatory, continuous, hectic, and intermittent.

Most have accepted Hans Zinsser’s (1935) argu­ment in his celebrated Rats, Lice and History that epidemic typhus fever was a new disease in the late fifteenth century, brought to Spain and Italy during the battles against Turkish expansion in the Medi­terranean. The dramatic urbanization of northern Europe (London grew from c. 400,000 in 1650 to more than 1 million by the early nineteenth cen­tury) accelerated crowding and poverty, optimal so­cial conditions for the spread of typhus by body lice.

It was during this era of earliest industrialization that population began to swell, and thus the model of the city as a death dispensary or as a provider of immunity may not be especially relevant. Indeed, Thomas McKeown (1976) has been the principal spokesperson for a view that credits improving nutri­tion rather than declining disease with that growth. According to McKeown, whether an individual sur­vives a disease, be it an acute viral infection such as measles or a chronic infection such as tuberculosis, depends on the individual’s state of nutrition. Yet this argument is based more on experiential data generated by physicians treating well-nourished and undernourished mothers and children than on laboratory studies of human nutrition and specific infectious diseases. With many diseases, there is little direct relationship between the outcome of in­fection and the prior nutritional state of the host. Yet the ability to outlast several serious infections does depend on steady access to food and, obviously, to protection from further health insults. In a few diseases, such as measles and tuberculosis, there is, moreover, a positive association between poor nutri­tion and severity of infection. Insofar as these two were among the most common diseases of the early modern period, nutritional security and the gener­ally improved standards of living this implies may have permitted the survival of more children to re­productive age. When smallpox, the last great killer of little children, came under control, population growth was dramatic, even though exposure to multi­ple infections and specific medical measures did not change the features of disease experience for nineteenth-century Europeans.

At just the time McKeown finds general improve­ments in human nutrition, the appearance of wide­spread deficiency diseases marked further change in the Etuopean disease experience. The prevalence of scurvy increased, including that of “land scurvy” suf­fered by the most impoverished city dwellers. Pella­gra was described first in the eighteenth century among the desperately poor farmers of northern Italy and Spain, who became dependent on American maize. Potato and squash cultivation eased the lives of many northern Europeans, helping them to avoid famine crises that had been common before the eigh­teenth century, but well into the nineteenth century the dependence on single crops or foodstuffs often gave the poor no relief from a miserable nutritional regimen. Thus, in many instances, the benefits of improvements in nutrition may have largely accrued to upper- and middle-class urban dwellers. It would seem that the disappearance first of plague - a relent­less killer of young adults - and then smallpox per­mitted the survival of a greater number of reproduc­tive adults, well nourished or not.