Epidemics may be defined as concentrated outbursts of infectious or noninfectious disease, often with unusually high mortality, affecting relatively large numbers of people within fairly narrow limits of time and space. They probably emerged in human populations with the "Neolithic Revolution," roughly eight to ten thousand years ago, as humans began to domesticate animals, practice agriculture, and settle into towns and villages, with a corresponding increase in the density of population. This entry will cover the history of epidemics with particular reference to their implications for bioethics, beginning with a survey of ancient and medieval times, moving on to responses to epidemics before the nineteenth century, then examining in more detail the impact of cholera and the bacteriological revolution. It will conclude with a discussion of the epidemiological transition and its aftermath, the emergence of new epidemics in the late twentieth century, and the ethical implications of the data surveyed. The focus will be mainly but not exclusively on Europe and North America, where historical source material is richest, and scholarly and scientific studies are most numerous.
Ancient and Medieval Times
Hippocratic texts indicate the presence of tuberculosis, malaria, and influenza in the population of ancient Greece, and the historian Thucydides provides the first full description of a major plague, the precise nature of which remains uncertain, in Athens (430–429 b.c.e.), in his history of the Peloponnesian War. The increase in trade brought about by the growth of the Roman Empire facilitated the transmission of disease, and there were massive epidemics in the Mediterranean (165–180 c.e. and 211–266 c.e.). The "plague of Justinian" (542–547 c.e.), which was said to have killed ten thousand people per day in Constantinople, is the first recorded appearance of bubonic plague (McNeill). In Europe and Asia, diseases such as measles and smallpox gradually became endemic, affecting virtually all parts of the population on a regular basis, with occasional epidemic outbursts. Periodic epidemics of bubonic plague continued, most seriously in the fourteenth century, when perhaps as much as one-third of Europe's population perished.
When Europeans arrived in the Americas, from 1492 on, they brought many of these diseases to native American populations for the first time, with devastating effects. The importation of African slaves introduced malaria and yellow fever by the seventeenth century (Kiple, 1984). The merging of the disease pools of the Old and New Worlds was completed by what appeared to be the transmission of syphilis to Europe from the Americas at the end of the fifteenth century, though the subject remains disputed by historians, some arguing that it was a recurrence or mutation of a disease that already existed on the Continent (Crosby).
Responses to Epidemics before the Nineteenth Century
The ancient Greeks and Romans commonly, though not universally, believed that epidemics were brought into human communities from outside. Thucydides, for example, described the plague that struck Athens during the Peloponnesian War as having arrived by sea. This belief was the basis of official reactions to epidemics in medieval Europe. Following the closure of the port at Venice to all shipping for thirty days as the plague threatened in 1346, regulations imposed in Marseilles in 1384, and in other ports thereafter, prescribed the biblical period of isolation for a "quarantine" (forty days) outside the harbor for any ship thought to have called previously at a place infected with the plague. In 1423 the Venetians set up a hospital where plague victims were isolated, and by 1485 the city had a sanitary authority armed with wide-ranging powers during epidemics. In some epidemics, as in the Great Plague of London in 1665, victims were compulsorily isolated in their own houses, which were marked with a red cross to warn the healthy not to enter. Compulsory screening was not an issue before the late nineteenth century, however, because diseases were recognized as such only after the onset of obvious symptoms, and the concept of the asymptomatic carrier did not exist. In addition to these measures, the authorities in many medieval towns, working on the theory that epidemics were spread through the contamination of the atmosphere, ordered the fumigation of the streets to try to clear the air. Doctors and priests were expected to attend to the sick; and those who fled, as many did, are strongly criticized in the chronicles of these events.
Popular reactions to epidemics included not only flight from infected areas and evasion of public health measures, but also attacks on already marginalized and stigmatized minorities. As bubonic plague spread in Europe in 1348–1349, for example, rumors that the Jews were poisoning water supplies led to widespread pogroms. Over nine hundred Jews were massacred in the German city of Erfurt alone (Vasold). Such actions reflected a general feeling, reinforced by the church, that plagues were visited upon humankind by a wrathful Deity angered by immorality, irreligion, and the toleration of infidels. A prominent part in these persecutions was played by the flagellants, lay religious orders whose self-flagellating processions were intended to divert divine retribution from the rest of the population. Jews were scapegoated because they were not part of the Christian community. Drawing upon a lengthy tradition of Christian anti-Semitism, which blamed the Jews for the killing of Christ, the people of medieval Europe regarded Jews at such times as little better than the agents of Satan (Delumeau).
State, popular, religious, and medical responses such as these remained essentially constant well into the nineteenth century. The medical understanding of plague continued throughout this period to draw heavily on humoral theories, so that therapy centered on bloodletting and similar treatments designed to restore the humoral balance in the patient's body. They were of limited effectiveness in combating bubonic plague, which was spread by flea-infested rats. The isolation and hospitalization of victims also therefore did little to prevent the spread of plague. Nevertheless, the disease gradually retreated from western Europe, for reasons that are still imperfectly understood. The introduction of more effective quarantines with the emergence of the strong state in the seventeenth and eighteenth centuries was almost certainly one of these reasons, however, and helped prevent the recurrence of epidemics in the seventeenth and eighteenth centuries (Vasold).
State intervention also played a role in reducing the impact of smallpox, the other major killer disease of the age after bubonic plague. Its spread was first reduced by inoculation, before compulsory programs of cowpox vaccination brought about a dramatic reduction in the impact of the disease in nineteenth-century Europe. Despite the imperfections of these new methods, which sometimes included accidentally spreading the disease, vaccination programs in particular may be regarded as the first major achievement of the "medical policing" favored by eighteenth-century absolutist monarchies such as Prussia. Police methods that paid scant attention to the liberties of the subjects were used to combat the spread of epidemics. They included the use of troops to seal off infected districts, quarantines by land and sea, and the compulsory isolation of individual victims. Most of these measures had little effect, however, either because of lack of medical knowledge or because poor communications and lack of police and military manpower prevented them from being applied comprehensively (Rosen).
The Impact of Cholera
These theories and practices were brought into question above all by the arrival in Europe and North America of Asiatic cholera. The growth of the British Empire, especially in India, improved communications and trade, and facilitated the spread of cholera from its base in the Ganges delta to other parts of Asia and to the Middle East. Reaching Europe by the end of the 1820s, the disease was spread further by unsanitary and overcrowded living conditions in the rapidly growing towns and cities of the new industrial era. At particular moments of political conflict, above all in the European revolutions of 1830 and 1848, the AustroPrussian War of 1866, and the Franco-Prussian War of 1870–1871, it was carried rapidly across the continent by troop movements and the mass flight of affected civilian populations (Evans, 1988).
Cholera epidemics affected the United States in 1832, 1849, and 1866, on each occasion arriving from Europe in the aftermath of a major conflict. State, popular, and medical responses in 1830–1832 were unchanged from earlier reactions to epidemics. Quarantine regulations were imposed, military cordons established, victims isolated, hospitals prepared. In Prussia, the breaching of such regulations was made punishable by death. But the opposition that such measures aroused among increasingly powerful industrial and trading interests, and the feeling among many liberals that the policing of disease involved unwarranted interference with the liberty of the individual, forced the state to retreat from combating cholera by the time of the next epidemic, in the late 1840s. In addition, medical theories of contagion were brought into disrepute by the failure of quarantine and isolation to stop the spread of the disease in Europe. Until the 1880s, many doctors thought that cholera was caused by a "miasma" or vapor rising from the ground under certain climatic circumstances. It could be prevented by cleaning up the cities so as to prevent the source of infection from getting into the soil (Evans, 1987). This was a contributory factor in the spread of sanitary reform in Europe and the United States during this period. But its importance should not be overestimated. Boards of health established in American cities in the midst of the cholera epidemics of 1832 and 1849 were short-lived and of limited effectiveness, and even in 1866 the more determined official responses had less to do with the impact of cholera than with the changed political climate (Rosenberg).
The fact that cholera affected the poorest sectors of society most profoundly was the result above all of structural factors such as unsanitary and overcrowded living conditions, unhygienic water supplies, and ineffective methods of waste disposal. But state and public responses to epidemics in the nineteenth century, at least in the decades after the initial impact of cholera, were primarily voluntaristic. Religious and secular commentators blamed cholera on the alleged immorality, drunkenness, sexual excess, idleness, and lack of moral fiber of the victims. Fast days were held in eleven New England states in 1832, in the belief that piety would divert God's avenging hand. Once again, the socially marginal groups of industrial society, from vagrants and the unemployed to prostitutes and beggars—or, in the United States in 1866, the newly emancipated slaves and the newly arrived Irish immigrants—were blamed (Rosenberg).
The rise of the medical profession, with well-regulated training and a code of ethics, ensured that doctors were more consistently active in treating victims of epidemics in the nineteenth century than they had been in previous times. Partly as a result, there were popular attacks on the medical profession in Europe during the epidemic of 1830–1832. Angry crowds accused doctors of poisoning the poor in order to be able to reduce the burden of support they imposed on the state or, in Britain, in order to provide fresh bodies for the anatomy schools (Durey). As late as 1892, doctors and state officials were being killed in cholera riots in Russia (Frieden). There were also disturbances in the United States, where a hospital was burned down in Pittsburgh and a quarantine hospital on Staten Island, in New York City, was destroyed by rioters fearing the spread of yellow fever. However, in most of Europe, public disturbances caused by epidemics had largely ceased by the middle of the nineteenth century. Fear of disorder was another reason for the state's withdrawal from policing measures (Evans, 1988). In Europe, too, religious responses to epidemics had become less important by the end of the century as religious observance declined. In 1892, however, as cholera once more threatened America's shores, it fed nativist prejudice and led to the introduction of harsh new restrictions on immigration.
The Bacteriological Revolution
Cholera was only the most dramatic of a number of infectious diseases that took advantage of urbanization, poor hygiene, overcrowding, and improved communications in the nineteenth century (Bardet et al.). Typhus, typhoid, diphtheria, yellow fever, tuberculosis, malaria, and syphilis continued to have a major impact, and even smallpox returned on a large scale during the Franco-Prussian War of 1870–1871. Treatment continued to be ineffective. But the rapid development of microscope technology in the last quarter of the century enabled medical science to discover the causative agents of many infectious diseases in humans and animals. Building on the achievements of Louis Pasteur, Robert Koch identified the tubercle bacillus in 1882 and the cholera bacillus in 1884. These discoveries marked the triumph of bacteriology and completed the swing of medical opinion back from belief in "miasmas" as causes of epidemics toward a contagionist point of view.
From the 1880s, states once more imposed quarantine and isolation, backed by preventive disinfection. The greater effectiveness of state controls, compared with the earlier part of the century, was combined with the more precise focus on eliminating bacterial organisms. Once the role of victims' excretions in contaminating water supplies with the cholera bacillus became known, it was possible to take preventive action by ensuring hygienic water supplies and safe waste disposal. By the outbreak of World War I in 1914, the role of the human body louse in spreading typhus, and that of the mosquito in transmitting malaria and yellow fever, had been identified. Mosquito control programs were launched by the U.S. Army in Cuba following the Spanish-American War of 1898, and subsequently in the Panama Canal Zone, in order to reduce the incidence of yellow fever cases to an acceptable level. Regular delousing reduced typhus among armies on the western front in Europe during World War I. The Japanese army prevented casualties from typhoid and smallpox by a campaign of systematic vaccination during the war with Russia in 1904–1905 (McNeill; Cartwright).
The bacteriological revolution thus inaugurated an age of sharply increased state controls over the spread of disease. Laws were introduced in many countries making the reporting of infectious diseases compulsory. The growth of a comprehensive, state-backed system of medical care, working through medical officers, medical insurance plans, and the like, made comprehensive reporting easier. Hospital building programs in the second half of the nineteenth century facilitated the isolation of victims in hygienic conditions where they could be prevented from spreading the disease. The greater prestige of the medical profession in most industrialized countries by the late nineteenth and early twentieth century ensured that doctors were no longer attacked, and that the necessity of compulsory reporting and isolation was widely accepted by the public. However, a bacteriological understanding of disease causation also involved a narrowing of focus, in which increased emphasis was placed on the compulsory reporting of cases, followed by their isolation, at the expense of broader measures of public health and environmental improvement (Porter).
The Epidemiological Transition
Lower death rates from diseases such as cholera, typhoid, and tuberculosis were only partially the consequence of bacteriologically inspired state preventive measures, and the disease burden from acute infectious disease began to decline rapidly. The provision of clean, properly filtered water supplies and effective sewage systems reflected growing municipal pride and the middle-class desire for cleanliness. It made epidemics such as the outbreak of cholera that killed over eight thousand people in Hamburg, Germany, in little over six weeks in the autumn of 1892 increasingly rare. Just as important were improvements in personal hygiene, which again reflected general social trends as well as the growing "medicalization" of society in western Europe and the United States. Such developments reinforced the stigmatization of poor and oppressed minorities as carriers of infection, since they were now blamed for ignoring official exhortations to maintain high standards of cleanliness, even though their living conditions and personal circumstances frequently made it difficult for them to do so. Particular attention was focused on working-class women, who were held responsible by official and medical opinion for any lack of hygiene in the home (Evans, 1987).
The development of tuberculin by Koch in 1890 made possible the compulsory screening of populations even for asymptomatic tuberculosis. This was increasingly implemented after 1900, in conjunction with the forcible removal of carriers to sanatoria, although this was more effective in isolating people than in curing them. Educational measures also helped reduce the spread of the disease. The development and compulsory administration in many countries of a preventive vaccine against tuberculosis from the 1920s aroused resistance among the medical community, not least because by creating a positive tuberculin reaction in noncarriers, it made it impossible to detect those who truly had the disease, except where symptoms were obvious. These measures had some effect in reducing the impact of the disease. However, although the precise causes of the retreat of tuberculosis remain a matter of controversy among historians, the long-term decline of the disease from the middle of the nineteenth century was probably more the result of improvements in housing, hygiene, environmental sanitation, and living standards than of direct medical intervention. The introduction of antibiotics such as streptomycin after World War II proved effective in reducing to insignificant levels mortality from a disease that had been the most frequent cause of death or disability among Americans aged fifteen to forty-five (Dubos and Dubos).
Similarly, official responses to syphilis centered, especially in Europe, on the forcible confinement of prostitutes to state-licensed brothels or locked hospital wards, where they were subjected to compulsory medical examination. Before World War I, New York, California, and other states had introduced compulsory reporting of cases of venereal disease, and official concern for the health of U.S. troops led to the jailing of prostitutes. Measures such as these had no discernible effect on infection rates, which rose sharply during the war. They also represented a serious restriction on the civil liberties of an already stigmatized group of women, while the men who were their customers, and equally active in the sexual transmission of disease, were regarded as irresponsible at worst, and were not subjected to similar measures. The development of Salvarsan (arsphenamine) by Paul Ehrlich in 1910 introduced the possibility of an effective treatment for syphilis. But here again there was resistance, both within the medical community and from outside, from those who considered that an increase in sexual promiscuity would be a result. This view became even more widespread following the use of penicillin on a large scale during World War II (Brandt).
Epidemics of the Late Twentieth Century
In the West, epidemic infectious disease was regarded by the second half of the twentieth century as indicating an uncivilized state of mind, and was ascribed above all to nonwhite populations in parts of the world outside Europe and North America. This reflected structural inequalities in the world economy, as the great infections became increasingly concentrated in the poor countries of the Third World. By the middle of the twentieth century, however, rapidly increasing life expectancy was bringing rapid growth of noninfectious cardiac diseases, cancer, and other chronic conditions that posed new epidemic threats to an aging population in the affluent West. Under increasing pressure from the medical profession, the state responded not only with education initiatives but also with punitive measures directed toward habits, such as cigarette smoking, that were thought to make such conditions more likely. The arsenal of sanctions governments employed included punitive taxation on tobacco and the banning of smoking, under threat of fines and imprisonment, in a growing number of public places. Increasingly, institutions in the private sector also adopted these policies. They raised the question of how far state and nonstate institutions could go in forcing people to abandon pleasures that were demonstrably harmful to their own health. At the same time, they contrasted strongly with the reluctance of many states and companies to admit responsibility for cancer epidemics caused by factors such as nuclear weapons testing, the proximity of nuclear power stations to human populations, or the lack of proper precautions in dealing with radioactivity in industrial production.
In the 1980s, the identification of a new epidemic, known as acquired immune deficiency syndrome (AIDS), once more raised the ethical problems faced by state and society, and by the medical profession, in the past. Lack of medical knowledge of the syndrome and the danger of infection from contact with blood or other body fluids, posed the question of whether the medical profession had a duty to treat AIDS sufferers in the absence of any cure. The evidence of the overwhelming majority of past epidemics, for which there was also no known cure, seems to be, however, that medical treatment, even in the Middle Ages, could alleviate suffering under some circumstances, and was therefore a duty of the practitioner. In a condition that could prove rapidly fatal, the ethics of prolonged tests of a drug such as AZT, in which control groups were given placebos, was contested by AIDS sufferers anxious to try anything that might possibly cure the condition, or at least slow its progress.
If this was a relatively novel ethical problem, then the question of compulsory public-health measures was a very old one. Like the sufferers in many previous epidemics, AIDS victims tended to come from already stigmatized social groups: gays, drug abusers and prostitutes, Haitians and Africans. The ability to screen these high-risk groups for the presence of the causative agent, the HIV retrovirus, even at the asymptomatic stage, raised the possibility of compulsory screening measures, quarantine, and isolation. On the other hand, individuals publicly identified as HIV-positive generally found it difficult or impossible to stay employed, to obtain life or health insurance, or to avoid eviction from their homes. In the absence of adequate supportive measures, public-health intervention reinforces existing discrimination against these groups, as in many past epidemics.
An alternative state response has consisted of neglect, on the assumption that AIDS is unlikely to affect the heterosexual, non-drug-abusing, nonpromiscuous majority of the voting public. It is noticeable that, generally, politicians have invested resources in public education and other preventive measures only when they have believed that the majority population is at risk. These problems have been raised again by the recent resurgence of tuberculosis in Western countries, among the HIV-positive but also among the poor and the homeless. Drug-resistant strains of the disease have become common, and the transient, jobless, and destitute have neither the means nor the stability of lifestyle to complete the lengthy course of drugs that is necessary to effect a cure. The compulsory isolation of victims and their forcible subjection to a course of treatment is not a satisfactory long-term solution to the problem, since reinfection is likely upon release, unless the social and personal circumstances of the affected groups undergo a dramatic improvement.
Conclusion: Ethical Implications
The history of epidemics suggests that society's responses have usually included scapegoating marginal and already stigmatized groups and the restriction of their civil rights. From the Jews massacred during the Black Death in medieval Europe, through the beggars and vagrants blamed for the spread of cholera in the nineteenth century, to the prostitutes arrested for allegedly infecting troops with syphilis during World War I, and the minorities whose life-styles were widely regarded as responsible for the spread of AIDS in the 1980s and 1990s, such groups have frequently been subjected to social ostracism and official hostility in times of epidemic disease. Frequently, though not invariably, they have been the very people who have suffered most severely from the disease they were accused of spreading. Doctors have sometimes been reluctant to treat them; the state has often responded with punitive measures.
At no time have public-health measures to combat epidemics been politically uncontested. Nineteenth-century feminists, for example, campaigned vigorously against the state's restriction of the civil liberties of prostitutes in the name of disease control. The fact that their male customers were left free to spread sexually transmitted diseases unhampered by the attentions of the state implied an official endorsement of different standards of morality for men and for women, and it was this major structural element of the social value system that the feminists were seeking to change. Without such change, not only was medical intervention ethically indefensible, but there would never be any likelihood of effective control of sexually transmitted diseases. Similarly, many nineteenth-century epidemics, such as cholera or tuberculosis, were spread by poor nutrition, overcrowded housing, and inadequate sanitation. Social reformers therefore regarded major improvements in these areas as more important than direct medical intervention through measures such as compulsory hospitalization.
Epidemics are frequently caused by social and political upheavals. In the past, movements of large masses of troops and civilians across Europe, from the Crusades to the Crimean War, brought epidemics in their wake. In the early 1990s, a major cholera epidemic broke out in Peru as the result of the flight of thousands of peasants from their mountain settlements, driven out by the pitiless armed conflict between the army and the "Shining Path" guerrillas, to the narrow coastal strip, where they lived in makeshift shantytowns with no sanitation. Economic crisis and the dismantling of welfare measures for the homeless, the mentally disturbed, and the destitute in many Western countries in the 1980s contributed to a massive increase in the transient population on the streets of the great cities. Discrimination against AIDS sufferers by landlords and employers has added to this problem. By the early 1990s there were an estimated ninety thousand homeless on the streets of New York City, half of whom were HIV-positive and several thousand of whom were suffering from tuberculosis. Any long-term solution to these epidemics must be more than merely medical, as must any explanation of their occurrence. Public-health measures are thus inevitably political in their implications, since they can be considered and administered only with reference to the wider social and cultural context within which the disease they seek to prevent or control has originated.
richard j. evans (1995)
SEE ALSO: AIDS; Bioethics, African-American Perspectives; Bioterrorism; Care; Communitarianism and Bioethics; Human Rights; Literature and Healthcare; Medical Ethics, History of Europe; Narrative; Public Health, History; Public Health, Philosophy; Sexual Behavior, Social Control of
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From the onset of the statistical era (which began around 1840 in Britain and the United States) until the present time, roughly half the world's population were (and are) infants and children under the age of fifteen. This must also have been the situation among all humankind before 1840. In the eighteenth century in the West, in those regions for which some crude figures exist, such as Massachusetts, Britain, the core lands of modern France, Sweden, and the German lands, it can be said with some confidence that life expectancy at birth occasionally touched forty years but even there it was generally less. Given that measles and several other epidemic diseases tended to target people under fifteen–half of the population–it follows that they had a very large clientele to work on.
An endemic disease is one that is continuously present in any given population in nascent form. Its rate of occurrence as an illness–which is to say, its prevalence–may differ according to the season of the year and other variables, but its causal agent is almost always found within the locality. Heading the list of today's endemic, or always present, child killers are the water-borne ailments collectively known as dysentery and the diarrheal diseases. In contrast, an epidemic disease, such as smallpox in its most virulent forms (extinct since 1977 in its free-ranging state) or measles (which still exists), only occasionally attacked any given human population. The disease agents, or pathogens, which had the potential to periodically set this sort of epidemic in motion almost always came in from outside the place in which victims lived.
Unlike a dread disease such as bubonic plague (essentially a disease of rats and other rodents), smallpox had no nonhuman host. Thus, over time it was vital to the perpetuation of the smallpox variola that it not kill off all its child hosts. If it did, the children would not be there in a few years, in their capacity as sexually mature adults, producing children of their own, who in turn could host the variola. Without hosts, the variola would become extinct.
It is essential to understand that the causal agents of infectious disease are living things that have the potential to change their forms over time. These mutations make their presence felt in the altered way the disease makes its presence felt among humankind.
In the case of smallpox as it affected populations in western Europe and the Middle East before around 1650, it was most commonly a benign endemic disease that did not kill its victims. Aside from sickly infants, who in any case could not be expected to live, pre-1650s smallpox neither killed nor scarred nor blinded nor neutered its victims. It was in this benign form that smallpox first entered the medical record.
Writing in Baghdad before 925 c.e., the Persian physician-philosopher Abu-Bakr al-Razi reported that smallpox was a common disease which most Middle Eastern children underwent with no ill effects. Al-Razi noticed that the illness never struck the same person twice. Nearly 700 years later, this was apparently still the situation in the British Isles. William Shakespeare, who died in 1616, in his many sonnets in praise of beautiful young men and women nowhere mentioned the threat of disfigurement or death from the disease. Thus, before 1616, it would appear that rampaging lethal smallpox was still unknown in England.
Opinions are divided about when and where the variola virus of smallpox first changed into its violently nasty forms. On the one hand, many historians argue that the Spanish, Genoese, and other European adventurers who went to the Caribbean Islands in the New World in and after 1518 were responsible. Having acquired smallpox immunity by hosting a benign case of the disease in their infancy at home, they brought forms of smallpox with them that, when let loose, quickly changed into lethal forms that killed millions of non-immune Native Americans who had never before been exposed to smallpox. If these events–so catastrophic from the First Nation point of view–actually happened, it can be suggested that disease mutation may have first occurred in the New World.
Or it may have already happened in parts of sub-Saharan Africa, or in Bengal, in northeastern India. In both regions, sometime before medically aware European observers came on the scene in the late seventeenth century, village curers recognized that some cases of smallpox were now lethal. They also observed that little children who survived a bout of the disease in any of its forms were immune to further attacks. Putting two and two together, they devised the control technique known as inoculation.
In this process, a curer took a bit of a smallpox scab from a moderately sick child, diluted it, and then scratched it into the skin of the child being inoculated. The curer and the parents realized that this process was not risk free, yet they continued to use it. In the 1870s it was found that more than eighty percent of the Bengali men who were imprisoned in government jails in that province had already been inoculated.
The processes of inoculation first described by Western observers in Bengal in the late seventeenth century were also being commonly used at that time in parts of West Africa, from whence they were brought to the New World. In 1706, the slave Onesimus taught his master, the Reverend Cotton Mather of Old North Church, Boston, the mysteries of smallpox prevention through inoculation. In earlier years, between 1620 and 1700, Massachusetts had been blessed by an exceptionally benign disease environment and a low infant mortality rate that had allowed far more babies to survive to adulthood than was the case in the middle colonies and in Europe. However, in the years just before 1706, Old World diseases, including smallpox, had begun to strike youthful New Englanders. For this reason, Mather was atypically willing to listen to what his African dependent said and to put it into practice. He had the children in his immediate circle inoculated and encouraged his friends to follow suit.
Massachusetts-style inoculation against smallpox caught on in the New England colonies and in some of the more smallpox-prone parts of Europe. Thus in authoritarian Sweden, the central government gradually realized that if smallpox were allowed to rage among its infants unchecked the country would be in danger of being depopulated. During bad periods, such as the years between 1779 and 1782, nearly a fifth of all deaths were from smallpox; most of the victims were children under the age of nine. Aware of this, the Swedish government strongly encouraged parents to have their offspring inoculated.
Among western Europeans and European-Americans, inoculation processes may have turned the tide against smallpox, even before the immunization process known as vaccination was devised by Edward Jenner in the late 1790s and put into common use early in the next century.
At the opening of the twenty-first century, twenty-five years after smallpox was abolished in its free-ranging state worldwide, measles–an air-borne virus–continues to kill one million children each year and to make an additional 42 million seriously ill. First tentatively identified as a separate disease by the Persian philosopher-physician al-Razi in the tenth century, measles today is most common among the third of the world's children who are chronically malnourished and who live in the non-West.
In addition to children with an unfavorable nutritional status, young children living in large families are also much more prone to being infected with measles than are children living in families with one or two siblings. Nowadays, when the total population of most western European countries is rapidly shrinking due to the limitation of family size, and at a time when most European and European-American parents have their children immunized against all common infectious diseases, measles has become rare in the West. This means that it has become one of the many infectious diseases most commonly found in the non-West. Its non-Western survivors, their immune systems weakened through a bout with the disease, often fall prey to pneumonia.
From 1348 through 1351, western Europe and Egypt were ravaged by a terrible disease, which killed between a quarter and a third of the population. The first great onslaught was called the Black Death. In Europe visitations of what used to be regarded as the same disease (at the time there were no means for identifying disease agents) recurred until the late seventeenth century. In western Europe, the last major out-break was imported into Marseilles, France, in 1721 by a rogue ship coming from the Orient.
Conventional scholarship once held that humans who survived one attack of the bubonic plague did not develop immunity against a subsequent attack. Conventional scholarship also held that bubonic plague did not necessarily target children. Given that roughly half of the population in any place was under the age of fifteen, one could expect that roughly half the victims of the disease would be non-adults. However, according to Samuel K. Cohn Jr. (2002), the late medieval plagues that repeatedly hit western Europe after 1351 directed their attention primarily against children; children who survived acquired life-time immunity.
Given that these events happened before the advent of modern laboratory medical science and before the statistical age, we have no sure way of knowing just what disease agents were actually at work in Europe between 1347 and 1721. In time, new scholarship may permit the writing of comparative studies based on findings from the non-West. It is already clear, however, that the Bubonic plague that continued to kill people in Egypt until 1844 was the same as, or closely related to, modern laboratory-certified Bubonic plague.
Much more certain is our knowledge of the so-called summer plague, more usually known as poliomyelitis or infantile paralysis. In the summer of 1916, several thousand middle-class children in New York City and the surrounding region were struck with a strange new disease. Although outright death was rare–because hospital care was available–many survivors were left severely crippled in their legs and unable to walk. Other less fortunate survivors suffered impairment of their breathing apparatus and had to be placed in an iron lung.
Caused by viruses (there are three main viral strains), polio spreads from one person to another by a fecal-oral route and in the East Coast of the United States was very often contracted by middle-class young people who had access to public swimming pools. Polio was a high-profile disease–its victims included President Franklin Delano Roosevelt. Accordingly, it attracted the attention of highly qualified American scientists. In the development of a preventive vaccine suitable for mass distribution, the first great breakthrough was by Dr. Jonas Salk in the 1950s. In most areas of the world, Salk's techniques, which were based on the use of an injection, have now been replaced by an orally administered vaccine by Dr. Albert Sabin that was released in 1961.
Thanks to preventive immunization, polio has all but disappeared in the United States and elsewhere in the West. Yet in India, Nigeria, and some other parts of the non-West, young children and infants over the age of six months are still at risk from the disease. As of 1998, more than 18,000 fatalities were reported. Given that the quality of hospital care found in most non-Western countries is far below the standard found even half a century ago in the United States, cases that in the United States might have been successfully treated are left all but unattended and commonly result in death.
Human Immunodeficiency Virus (HIV) and Acquired Immuno-Deficiency Syndrome (AIDS) was first reported in 1981 and has become the world's fourth most common cause of death. As of 2002, 40 million people bore the lethal virus, 70 percent of them in sub-Saharan Africa.
According to the conventional wisdom of leading funding agencies as expressed by the World Health Organization (WHO), "99 percent of the HIV infections found in Africa in 2001 are attributable to unsafe sex." (WHO 2002, p. xv). However, four years earlier, the same organization admitted that half a million victims were under the age of fifteen (WHO 1998, p. 93).
An alternative assessment of the situation was found in the International Journal of STDs and AIDS in October 2002. Here, David Gisselquist and his colleagues found that a sizeable percentage of Africans suffering from HIV had not yet reached the age of puberty. Though none of these children had engaged in sexual activity involving a partner, all of them had been the recipients of clinically administered injections which were intended to prevent communicable diseases, fevers, or other childhood illnesses. On-site study showed that the cash-strapped clinics often reused syringes simply because no other instruments were available; more than half of all HIV and AIDS victims in Africa may have been infected in this way. In many cases, newborn infants may have been infected in utero by infected mothers who had made use of the disease-prevention services of clinics.
The current AIDS epidemic affects infants and young children under the age of fifteen in financially hard-pressed sub-Saharan regions in two ways. First, many of them will die of pneumonia and the other killers that strike down people whose immune systems have been rendered useless. Very often their deaths will be recorded as having been caused by something other than AIDS.
Second, and more difficult to capture statistically, millions of young Africans are becoming orphans through the AIDS deaths of their parents, aunts and uncles, and other potential care-givers. In several countries in southern Africa, where nearly half the adult population is HIV-positive, orphans have little chance of survival. For this reason, many of these who do survive do not acquire the veneer of civilization and instead become teenaged mercenary soldiers, drug-dealers, extortionists, or all-purpose terrorists.
As of 2003, the AIDS epidemic continues, and in the next two or three years is expected to make its presence heavily felt in China and in India, nations which between them are the home of half the world's population. Because many non-Western countries are burdened with debt repayment to financial institutions based in the West and are thus unable to fully fund proper health services, the AIDS epidemic may well become the non-Western world's principal childhood killer. The prognosis is not good.
See also: AIDS; Contagious Diseases; Infant Mortality.
Cohn, Samuel K., Jr. 2002. "The Black Death: End of a Paradigm." American Historical Review 107, no. 2: 703–38.
De Waal, Alex. 2003. "How Will HIV/AIDS Transform African Governance?" African Affairs 102: 1–23.
Gisselquist, David, Richard Rothenberg, John Potterat, et al. 2002. "HIV Infections in Sub-Saharan Africa Not Explained by Sexual or Vertical Transmission." International Journal of STDS and AIDS 13, no. 10: 657–666.
Gisselquist, David, John Potterat, Paul Epstein, et al. 2002. "AIDS in Africa." The Lancet 360, no. 9343L: 1422–1423.
Joralemon, Donald. 1982. "New World Depopulation and the Case of Disease." Journal of Anthropological Research 38, no. 1:108–127.
Lovell, W. George. 1992. "'Heavy Shadow and Black Night': Disease and Depopulation in Colonial Spanish America." Annals ofthe Association of American Geographers 82, no. 3: 426–446.
Mercer, Alex. 1990. Disease, Mortality, and Population in Transition: Epidemiological-Demographic Change in England since the Eighteenth Century as Part of a Global Phenomenon. Leicester, UK: Leicester University Press.
Watts, Sheldon. 1997. Epidemics and History: Disease, Power, and Imperialism. London: Yale University Press.
World Health Organization. 1998. World Health Report 1998. Geneva: World Health Organization.
World Health Organization. 2002. World Health Report 2002. Geneva: World Health Organization.
Epidemic diseases break out, reach a peak, and subside; endemic diseases cause a relatively constant amount of illness and death over time (see Figure 1). Epidemic diseases can be new or normally endemic to a community. They break out on a local level and remain localized, or spread out in diffusion waves to surrounding communities. Very large-scale epidemics that strike several continents or the entire globe are called pandemics. Although relatively infrequent, pandemics are exceptionally disruptive; the economic, social, and demographic damage they do insures that they receive the lion's share of attention from both contemporaries and historians.
The most familiar epidemic diseases are propagated by direct contact between infected and uninfected persons, as is the case with tuberculosis, smallpox, measles, polio, syphilis, and AIDS, among others. But some of the most devastating epidemic diseases were and are transmitted to human beings by insect vectors, such as bubonic plague, malaria, typhus, and yellow fever. Among the epidemic diseases spread by water-borne pathogens are cholera, typhoid, and dysentery. Some epidemic outbreaks do not involve microorganisms at all; these common vehicle epidemics can be caused by food-borne or other toxins (e.g., ergotism). Under certain circumstances, even vitamin deficiency diseases like scurvy (Vitamin C) or night blindness (Vitamin A) can break out suddenly in certain populations. Every epidemic disease has its own distinctive etiology, and its own complex relationship with both natural and social environments.
Epidemiologists identify epidemic outbreaks by observing the statistical behavior of a specific disease over time, based on the number of reported cases and/or deaths the disease causes. In theory, if zero cases of a specific disease are expected in a normal year, then even one observed case can signal an epidemic and call for a public health response. This reasoning was used in 1976 to declare a national public health emergency in the United States, based on a single unexpected death from a type of influenza that seemed similar to the 1918 outbreak.
By using statistical criteria alone, more and more diseases have been perceived as taking epidemic form. Around 1950, several chronic diseases were classified as epidemics, including lung and breast cancer and ischemic heart disease. Some slowly-developing "social" diseases–like alcoholism and drug addiction–and a few mental diseases like depression have also been described as epidemics. But instead of erupting and subsiding in a year or less, chronic-, social-, or mental-disease epidemics rise and fall over several decades. As a consequence, they can only be observed by experts with access to high quality morbidity and/or mortality data.
History of Epidemics
The existence of epidemics has been recorded since the beginning of written history, and in all probability they predate it. Just as epizootics (epidemic animal diseases) have always been part of the demography
of animal populations, epidemics were part of the evolution of human populations. It is widely supposed that during the transition from hunting and gathering to agriculture, when human beings began to live in larger groups and at higher densities, the frequency–and possibly the severity–of epidemics increased. Subsequently, the development of cities made epidemic disease an even greater threat to human life.
But knowledge about epidemics and mortality in history is necessarily limited by the relative absence of reliable quantitative data. Although the Black Death is one of history's most famous and well-researched epidemics, data problems have kept everything about the epidemic controversial, except for the fact that it arrived in Southern Europe in 1347 and spread to Northern Europe by 1352. Historians continue to disagree on whether or not the "plague" was one disease or several. (Before the seventeenth century, plague was still a generic concept used in connection with any sudden outbreak of disease.) Accounts from the time often describe the plague as killing the majority of the living. Most historians, however, believe that about one third of Europeans died in the first outbreak, although estimates range from less than a fifth to more than two thirds. Subsequently, major epidemics seem to have erupted with sufficient frequency and intensity in Europe that the continent's population was cut in half. Demographic recovery took two centuries or more.
It was the continuing social and economic disruption caused by recurrent outbreaks of plague that led city officials in Europe, particularly in Renaissance Italy, to develop novel measures of disease management, including the formal surveillance of mortality. By 1500, several cities in Italy were tracking deaths on a week-by-week basis, and trying to distinguish between those that were and were not caused by plague. These data have been used to estimate that, on average, plague outbreaks in the 1400s and 1500s multiplied the normal number of urban deaths by a factor of four to seven (Del Panta and Livi Bacci 1979, p. 72). In Sienna, when the normal death rate was about 35 per 1,000 per year, mortality increased by a factor of five to ten during a plague year (Livi-Bacci 2001, p. 39). In Florence, it has been estimated that epidemic disease caused 38 percent of the total number of deaths among girls under age 15 in the two centuries after the first outbreak of bubonic plague (Morrison, Kirshner and Molho 1985,p. 531).
The ancient Greek concept of epidemic was revived in connection with increasingly sophisticated disease surveillance systems, and was used by leading physicians to speculate on the natural causes of any sudden outbreak of disease. (Outbreaks of "influenza" received that name because university-educated physicians once thought they were caused by astral influences). Eventually all the other diseases thought to be causes of death were tracked as well.
London followed the example of cities in Italy, and by the early 1600s its officials had institutionalized the continuous surveillance of death and its causes. Thus, when John Graunt (1620–1674) published demography's founding text in 1662 (Natural and Political Observations Made Upon the Bills of Mortality), he could draw on more than a half-century of annual data on about 70 diseases that were thought to be causes of death. The data made it very clear that, while bubonic plague remained the most lethal epidemic disease, smallpox epidemics seemed to be getting worse. In 1665, London, with a population of about 500,000, could still lose some 80,000 lives to plague, while Copenhagen lost 20,000 people out of its total population of 60,000 in 1711.
There were no more major outbreaks of bubonic plague in Europe after the 1720s. Historians still disagree about the relative importance of human agency (particularly in the form of public health measures) versus exogenous natural causes in its disappearance. The evidence is inconclusive for Europe, but it is worth noting that outside Western Europe, in countries such as Russia, Turkey, Egypt, China, and India, bubonic plague continued to erupt on a large scale long after 1720. It ceased to do so only after European-style public health measures were adopted and enforced.
When T. R. Malthus published the first edition of his essay on population in 1798, there was enough mortality data–both urban and rural–to hypothesize about the role played by more ordinary epidemics in the regulation of population growth. To Malthus, sudden outbreaks of disease were just one of a set of four mortality-related positive checks on growth, the others being poverty, war, and famine (which he regarded as the last and most deadly positive check). Subsequent historical research suggests that before the twentieth century most deaths that occurred during wars and famines were caused by epidemic disease, not by battle casualties or starvation. Since the poor are often (but not always) hardest hit by epidemic disease, there seems limited value in distinguishing between poverty, war, famine, and epidemic disease as separate checks on population growth, at least before 1900.
Modern Study of Epidemics
Modern demographic historians tend to study epidemic disease as part of "crisis mortality," those sudden increases in deaths or death rates that were a general feature of pre-modern mortality patterns. In theory, mortality crises can be caused by natural disasters as well as by wars, persecution, genocide, and famine; but in practice most crises were caused by epidemics, at least before the early twentieth century. Using historical data, demographers have attempted to gauge how much death rates must rise above some "normal" or background level of mortality in order to constitute a mortality crisis. No agreement has been reached on how to measure either "normal" or "crisis" mortality–especially in cities, where death rates were exceptionally volatile. Thus the relative importance of crisis mortality, and by implication, epidemic disease, in keeping life expectancy levels low (below 40 years) before the modern era remains a matter of controversy.
In theory, the extent to which epidemics as mortality crises can regulate population growth depends on their frequency, amplitude, and duration. But with respect to amplitude, using a high threshold to identify a mortality crisis (for example, requiring that the crisis death rate must be at least five times the "normal" level) would mean that mortality crises (and, by implication, major epidemics) were too infrequent to check population growth in most places and times. In contrast, if death rates must only exceed normal levels by 10 percent, then frequent mortality crises (caused mostly by epidemics) would clearly have been the major brake on population growth in the past. In general, the importance of mortality crises, or epidemics, cannot be assessed independently of the demographic criteria used to identify them.
The uncertainties connected with crisis mortality stimulated demographic research on all short-term fluctuations in pre-modern populations, including marriages and births as well as deaths. In some localities, harvest failures could cause grain shortages, rising prices, and (with a lag) rising death rates, mostly in connection with epidemic disease. But in other cases, a steep rise of grain prices has been observed to lag behind the sharp rise in death rates associated with an outbreak of epidemic disease. Historical research suggests that up to half of all epidemics in early modern Europe broke out and caused mortality crises for reasons unconnected to harvest failures, high prices, or food shortages. The implication is that some epidemics were Malthusian–meaning that they were related to increasing poverty and malnutrition–while others were not.
From a biological standpoint, this conclusion is not surprising, since those diseases that take epidemic form are differentially, not equally, sensitive to the nutritional status of the individuals exposed. This observation is relevant to the study of economic development, where it is still widely but mistakenly assumed that whenever per capita incomes rise, nutrition will improve and death rates will fall automatically without public health reforms. This overlooks the extent to which economic development stimulated urbanization, and thus the frequency with which density-dependent, air-and water-borne diseases broke out. The empirical evidence is that death rates rose during Europe's development, despite rising income levels, until effective measures were taken to control infectious diseases that often took epidemic form.
During the twentieth century, the same story can be told on a global scale: it is primarily the decline of the infectious and parasitic diseases as leading causes of death that produced the global rise of life expectancy. These diseases were first targeted for control through public health measures because of their close connection to epidemic outbreaks of disease and death. Wherever common epidemics were prevented by effective measures of disease control, death rates declined and remained relatively flat from year to year.
The last traditional mortality crisis in the developed countries occurred in 1918 as part of a worldwide pandemic of influenza. This one outbreak was estimated to have caused more deaths in one year than World War I did in several years. (Estimates range from 20 to 40 million deaths caused by influenza, versus 15 million for war-related losses). Nevertheless, in America and Europe influenza was not particularly lethal; many more people were infected than died. In the United States, although one-third of the population is estimated to have developed the symptoms of influenza, at most less than 3 percent of the infected died (Davies 1999, p. 219). Even so, the influenza epidemic produced at least 500,000 excess deaths; as many as 650,000 if pneumonia cases are included. Had death rates prevailing during the epidemic continued, life expectancy levels in the United States would have dropped by 12 years (Noymer and Garenne 2000, p. 568). Instead, death rates quickly returned to normal levels, and subsequently resumed their decline.
Despite the relative absence of mortality crises in the last half of the twentieth century, new pathogenic diseases (newly discovered, newly reportable, or newly resurgent) have continued to turn up at the rate of six to seven per decade (Karlen 1996, p. 6). Most of these new epidemics caused few cases and fewer deaths. Indeed, in most modern epidemics, even those producing hundreds of thousands of cases, so few die that life expectancy levels are not affected. For example, an epidemic of dengue fever broke out in Brazil in 2002. In the Rio de Janeiro area alone, over 400,000 cases were reported. There were fewer than 20 deaths.
While the twentieth century saw undeniable progress in disease control, the twenty-first century began in the shadow of an unusually deadly epidemic disease. HIV-AIDS was discovered in the United States; based on 31 suspicious deaths, it was declared a new epidemic in 1981. Subsequently hundreds, then thousands, of Americans began to die from the disease. But unlike a classic epidemic disease, AIDS fatalities in the United States took more than a decade to reach their peak. By 1995 AIDS was causing 50,000 deaths a year, but even this carnage was insufficient to appreciably increase the death rate at the national level. With respect to the developed countries (and many developing ones), AIDS has not been sufficiently deadly to prevent the continued rise in life expectancy at birth.
In Sub-Saharan Africa, however, the scale of HIV-AIDS deaths has been compared to that of the bubonic plague. Because the data are often defective or incomplete, it is hard to estimate the impact. Nevertheless demographers have made valuable contributions to the estimation of the impact of AIDS on Africa's future population growth, age-structure, and fertility, as well as on mortality. United Nations estimates for 1995 through 2000 indicate that in 35 highly-affected African countries, life expectancy at birth is about 6.5 years lower than it would have been in the absence of AIDS. In the 11 worst-affected countries, life expectancy at birth may drop to 44 years by 2005–2010, instead of reaching 61 years.
As the tragic social and economic implications of the HIV-AIDS epidemic unfold in the twenty-first century, demographers reflect that epidemic disease has long been a major force in human demographic history. It is possible that research on earlier epidemics may offer valuable insights into the continuing threat posed by both epidemic disease and mortality crises to human welfare.
Epidemics in Europe have received the most historical attention. L. Del Panta (1980) has reconstructed major epidemics in various Italian cities over five centuries. J. Biraben (1975) studied epidemics in early modern France. English epidemics are the subject of C. A. Creighton's classic, mostly descriptive, two volume history (1891). E. A Wrigley and R. Schofield's Population History of England (1981: Part 2, Sections 8 and 9) takes a more quantitative approach, and focuses on smaller-scale outbreaks in England, as do S. Scott and C. Duncan (1998). Recently, more research has been done on epidemics outside Europe: China (C. Benedict, 1996); Japan (A. Janetta, 1987), India and the Near East (S. Watts, 1997). For China, traditional sources have been used to compile a list of hundreds of major epidemics occurring between 243 b.c.e. and 1911 c.e. (W. McNeil, 1976). But the data available are not sufficiently accurate or detailed to permit detailed comparative work until the late nineteenth and early twentieth centuries (P. Cliff, P. Haggett, and M. Smallman-Raynor, 1998).
Biraben, J. 1975. Les hommes et la peste. The Hague: Mouton.
Charbonneau, H., and A. Larose, eds. 1979. The Great Mortalities: Methodological Studies of Demographic Crises in the Past. Liège: Ordina Editions.
Cliff, P., P. Haggett, and M. Smallman-Raynor. 1998. Deciphering Global Epidemics. Cambridge, Eng.: Cambridge University Press.
Creighton, C. 1891. A History of Epidemics in Britain from AD 664 to the Extinction of the Plague, 2 vols. Cambridge, Eng.: Cambridge University Press.
Del Panta, L. 1980. Le epidemie nella storia demografica Italiana (secoli XIV-XIX) Turin.
Easterlin, R. 1999. "How Beneficent is the Market? A Look at the Modern History of Mortality." European Review of Economic History 3: 257–294.
Flinn, M. 1981. The European Demographic System 1500–1820. Baltimore: Johns Hopkins University Press.
Haggett, P. 2000. The Geographical Structure of Epidemics. Oxford, Eng.: Oxford University Press.
Jannetta, A. 1987. Epidemics and Mortality in Early Modern Japan. Princeton, NJ: Princeton University Press.
Johansson, S., and C. Mosk. 1987. "Exposure Resistance and Life Expectancy: Disease and Death during the Economic Development of Japan, 1900–1960." Population Studies 41: 207–235.
Karlen, A. 1996. Plague's Progress: A Social History of Disease. London: Indigo Edition.
Kiple, K. 1993. "The Ecology of Disease." In Companion Encyclopedia of the History of Medicine, Vol. 1. London: Routledge.
Lee, J., and Wang Feng. 1999. One Quarter of Humanity: Malthusian Mythology and Chinese Realities, 1700–2000. Cambridge, Eng.: Harvard University Press.
Livi Bacci, M. 2001. The Population of Europe: A History, 3rd edition. Oxford, Eng.: Blackwell Publishers.
McNeil, W. 1976. Plagues and Peoples. Garden City, NY: Anchor Press.
Mosk, C., and S. Johansson. 1986. "Income and Mortality: Evidence from Modern Japan." Population and Development Review 12: 415–440.
Noymer, A., and M. Garenne. 2000. "The 1918 Infuenza Epidemic's Effects on Sex Differentials in Mortality in the United States." Population and Development Review 26: 565–581.
Omran, A. 1971. "The Epidemiologic Transition: A Theory of the Epidemiology of Population Change." Milbank Memorial Fund Quarterly 49:509–538.
Palloni, A. 1988. "On the Role of Crises in Historical Perspective: An Exchange." Population and Development Review 14: 145–158.
Preston, S. 1976. Mortality Patterns in National Populations. New York: Academic Press.
Riley, J. 2001. Rising Life Expectancy: A Global History. Cambridge, Eng.: University of Cambridge Press.
Scott, S., and C. Duncan. 1998. Human Demography and Disease. Cambridge, Eng.: Cambridge University Press.
Spielman, A., and M. D'Antonio. 2000. A Natural History of Our Most Persistent and Deadly Foe. London: Hyperion.
United Nations (UNAIDS and WHO). 1998. Report on the Global HIV/AIDS Epidemic. Geneva: United Nations.
Wrigley, E. A., and R. Schofield. 1981. The Population History of England 1541–1871: A Reconstruction. Cambridge, MA: Harvard University Press.
S. Ryan Johansson
An epidemic is an occurrence of cases of a disease in excess of usual expectations for a particular population. An outbreak of influenza that affects thousands of people in a month in a nation and a half dozen cases of a rare form of liver cancer affecting industrial workers in a chemical plant over a period of several years are both examples of epidemics. Another kind of epidemic can be seen in the sharp rise in the prevalence of cigarette smoking throughout the twentieth century—first among males and then females—and of smoking-related respiratory system cancers. The surging death rate from coronary heart disease among men in many industrial nations in the middle third of the twentieth century may also be described as an epidemic.
A pandemic is a worldwide epidemic that kills or incapacitates huge numbers in many countries. Outbreaks of influenza in 1919 and HIV/AIDS (human immunodeficiency virus/acquired immunodeficiency syndrome) since the 1980s are both examples of pandemics. Conditions that are constantly present in a community are called "endemic;" examples include malaria in some tropical regions, and goiter due to deficiency of iodine in the soil of certain areas.
A single case of a rare and dangerous contagious disease that has never occurred before or has long been absent from a community represents a potential epidemic, as does a small cluster of cases of a disease such as typhoid in an urban community with good sanitation. Infectious pathogens (bacteria and viruses) cause most epidemics, while some are caused by a toxic industrial process or a toxic substance in food or water. A toxin in cooking oil in Spain in 1981 poisoned several thousand people, damaging their kidneys, liver, lungs, and nervous system and causing many deaths and widespread chronic disability. The precise nature of this contaminant was never established. In 1976, members of the American Legion who had attended a convention in Philadelphia began to fall ill and die of an unusual form of pneumonia, mostly after they returned to their homes elsewhere in the United States. Investigations by the Centers for Disease Control revealed this to be an epidemic of what is now called Legionnaire's disease, which is caused by a previously unknown microorganism that can be disseminated via the moist air in poorly maintained air-conditioning systems.
Charles Mackay, in his classic work Extraordinary Popular Delusions and the Madness of Crowds, described what is known as a behavioral epidemic. This phenomenon can be seen in the reactions of impressionable teenagers at a rock concert—and in a more sinister form in movements such as Nazism, when an entire nation is gripped by destructive fanaticism. The huge increase in traffic-related death and injury rates during the twentieth century, which has continued into the twenty-first century, is a behavioral epidemic associated with addiction to high-speed automobiles (the phenomenon called "road rage" is a psychopathic variation of this epidemic).
Human history has been punctuated frequently by epidemics, and occasionally by pandemics, that have shaped the rise and fall of civilizations and the victories and defeats of warring armies. The outcome of the Peloponnesian War (431–404 b.c.e.) between Athens and Sparta—and the future course of Western civilization—might have been very different had it not been for the epidemic that decimated the Athenians at the beginning of the war. Although the historian Thucydides, who had the disease himself, described its symptoms and signs in detail, modern epidemiologists cannot identify it.
Epidemic sweating sickness recurred several times in medieval Europe, but it has vanished since. The Black Death, or plague, that struck Europe in 1347 killed between one-third and one-half of the people in many cities and towns, arresting the advance of civilization for several generations. Some epidemic diseases, such as the plague, smallpox, typhus, and influenza, have persisted throughout recorded history. Smallpox was eradicated worldwide by 1980. Cholera appeared along the world's major trade routes in several devastating epidemics beginning in the eighteenth century, and it still causes massive epidemics, most recently in South America in early 1990s.
In the final quarter of the twentieth century over thirty new infectious pathogens were identified. Many of these have caused deadly localized epidemics (e.g. Ebola virus, hantavirus, and other viral hemorrhagic fevers), and some have spread worldwide—HIV/AIDS being the foremost among these. Since its first recognition in 1981, HIV has affected almost 40 million people and killed over 10 million, making it the most lethal and dangerous pandemic since the Black Death. Other new and emerging infections that have caused epidemics include Legionnaire's disease, Lyme disease, newly identified hepatitis viruses spread in epidemic form through contaminated blood and blood products used in transfusion services, and several bacterial and viral diseases affecting the gastrointestinal tract.
An epidemic is a public health emergency requiring immediate investigation. The steps in investigating an epidemic are as follows:
- Confirm the diagnosis.
- Verify that the number of cases is outside normal expectations.
- Define features in common among the cases (including inapparent cases).
- Distinguish cases from members of the community who are not affected.
- Compare the exposure history of the cases with a sample of noncases.
- Conduct appropriate laboratory tests for pathogenic organisms.
- Review environment and social conditions.
- Arrange, classify, and analyze the data.
- Plot graphs of time trends and the number of cases; create maps of the distribution of cases.
- Report findings to the public health authorities for action to control the epidemic.
In the investigation it is important to consider the host (the affected individuals), the agent (the cause of the condition), and the environment. Physical, biological, social, behavioral, and cultural factors must also be considered. Investigating an epidemic can be as exciting as detective fiction, and such investigations (both real and fictional) have yielded many best-selling books and movies. The Epidemic Intelligence Service (EIS) of the U.S. Centers for Disease Control and Prevention has an illustrious record of successfully investigating and controlling epidemics, including some great public health importance. The first investigations of HIV/AIDS were done mainly by EIS staff and close collaborators in New York and Los Angeles.
Several kinds of epidemics can be distinguished. A point-source epidemic is one in which a group of people all fall ill as a result of a single exposure, typically to an agent in food they have all consumed. An example would be an outbreak of acute food poisoning due to staphylococcal enterotoxin. A common-vehicle epidemic is due to an agent that is spread on an ongoing basis in a "vehicle" such as food, water, or air. Food-borne common-vehicle epidemics usually cause gastrointestinal disease, and are sometimes perpetuated by a carrier who is a foodhandler. Waterborne epidemics include typhoid, giardia, viral hepatitis A, and many others. The best known airborne common vehicle epidemic is Legionnaire's disease. Notorious blood-borne common-vehicle epidemics have occurred since the 1980s in many countries after the blood supply became infected with HIV or Hepatitis C virus. Vector-borne epidemics are spread by insect vectors and include viruses such as dengue and viral encephalitis, which are transmitted by mosquitoes.
Control and prevention of an epidemic requires elimination of the source, or, if this is not feasible, precautions to prevent transmissions from the source to susceptible human hosts. The same approach applies when the agent causing the epidemic is not an infectious pathogen but a chemical poison or an allergen; and it can even be applied, with suitable adjustments, to control of behavioral epidemics like mass hysteria and schoolyard vandalism.
Viewed from the perspective of evolutionary biology, epidemics will forever be a part of human-kind's experience. The interaction of human hosts with infectious pathogenic organisms is everchanging, in complex ecosystems that are also ever-changing, often as a result of human activity.
John M. Last
(see also: Adherence or Compliance Behavior; Black Death; Blood-Borne Diseases; Centers for Disease Control and Prevention; Classification of Disease; Common Vehicle Spread; Communicable Disease Control; Contagion; Emerging Infectious Diseases; Epidemic Intelligence Service; Epidemiologic Surveillance; Epidemic Theory: Herd Immunity; Epidemiology; Food-Borne Diseases; HIV/AIDS; Notifiable Diseases; Vector-Borne Diseases; Waterborne Diseases; and articles on specified diseases mentioned herein )
Mackay, C. (1841). Extraordinary Popular Delusions and the Madness of Crowds. Reprint. Boston: L. C. Page & Company, 1932.
Roueché, B. (1954). Eleven Blue Men and Other Annals of Medical Detection. Boston: Little, Brown, & Co.
Early pandemicsWhile new infectious diseases emerge from time to time as a result of human contact with normally elusive animal reservoirs of disease (Lassa fever, for example, was discovered in 1973 to have originated among rodents in Nigeria), they require special circumstances of human activity to achieve pandemic status. Human mobility — notably migration and warfare, but also exploration, travel, and trade — has played a key role in past pandemics. It is likely that pandemics have occurred periodically since the establishment of the earliest civilized, urban societies between 3000 and 500 bc, but the surviving historical records do not permit conclusive distinctions between pandemics and epidemics until late in human history. It is clear, however, that epidemic disaster struck the Roman Empire in ad 165–80, and again in ad 251–66, with an unidentifiable infection breaking out in different cities year by year, and sometimes returning. It is possible that one or both of these pandemics were due to smallpox, or even measles.
Smallpox was (the WHO declared it eradicated in 1977) a very ancient scourge related to, and possibly deriving from, one of the various animal poxes. It may have originated in India, where ancient temples still survive to Sitala, the Hindu goddess of smallpox, and where smallpox in recent times retained very much the character of an endemic disease. One attack of smallpox conferred a lifelong immunity, which permitted it eventually to establish itself as an endemic disease in the urban societies of Europe and elsewhere. It was one of the disease which, imported into the Americas by Spaniards in the fifteenth century, caused terrible devastation among the native populations, and facilitated the European conquest.
The best attested pandemics belong to relatively recent history, and to three diseases in particular: bubonic plague, cholera, and influenza. Bubonic plague, which devastated medieval and early modern Europe with successive pandemics between 1346 and the early eighteenth century, caused alarm worldwide with another pandemic between 1894 and 1900. The Black Death of 1346–50 remains the classic pandemic of popular memory.
CholeraSince bubonic plague, cholera in the nineteenth century, and influenza in 1918, have both achieved classic pandemic status, even though their full horror has not remained in popular memory. Cholera, like smallpox, has its natural home in India, in the delta of the Ganges river. The cholera bacillus is extremely sensitive to heat and humidity, but can survive almost indefinitely where the conditions are right. In the early nineteenth century, the activities of British traders and troops in India led to its breaking out of its historic heartland in the Ganges delta, and moving beyond its established epidemic hinterland in India and neighbouring areas. Between 1817 and 1823, travelling both by land and by sea, the disease reached out through south-east Asia, China, and Japan, and through Arabia to Africa, the Persian Gulf, and southern Russia, before being cut short, perhaps by the very severe winter of 1823–4. The rapid development of trade and travel at this period ensured further pandemics of increasing geographical range.
Cholera infection is spread by food and water via the faecal–oral route, and is especially explosive when it enters a widely-distributed water supply. In the great, insanitary cities of newly industrializing Europe and America, opportunities for infection were legion. Six pandemics of cholera swept out of India between 1817 and 1923: 1817–23, 1826–37, 1846–62, 1864–75, 1883–94, and 1899–1923. The second pandemic was perhaps the most severe, with succeeding pandemics having a more variable global impact. Britain, for example, as a result of improved surveillance systems and public health reform, experienced no epidemic after 1866, while the 1866 epidemic was largely centred on London, and in particular in the water field of the East London Water Company, which had distributed contaminated supplies.
Cholera's ability to travel the nineteenth-century world was the result both of military activity and of the human and commercial interests which impelled ever-increasing numbers of people to travel or to migrate long distances. The disease regularly travelled the long-established trade-route across Russia, for example, and the 1893 epidemic at Hamburg was introduced by Russian Jews fleeing from persecution at home to a new life in the US, and who sought to travel on the regular migrant ships that sailed out of Hamburg port.
Both cholera and bubonic plague are example of diseases whose pandemic potential was eventually broken by patient observation and public health responses. Although it is likely that the cessation of plague pandemics was multicausal, the transmission routes of both diseases made them relatively susceptible to public health interventions. Infections which spread by direct contact, or the respiratory route, present a more serious challenge to human societies. The great influenza pandemic of 1918–9 illustrates the potential which such infections still have to devastate human populations.
InfluenzaInfluenza assumes many degrees of severity. It is caused by a notoriously unstable virus, which spreads with great speed and facility, and leaves only a brief immunity. Although it is another old disease, and although the evidence suggests some sixteen pandemics between c.1100 and 1900, on the scale of global epidemic problems it was not highly rated by public health authorities before 1918. The pandemic of 1918–9 was a very different matter: with a death toll of more than 21 million persons worldwide, it was quite simply the worst disease pandemic ever experienced by human populations — a human catastrophe equalled only by the carnage of World War II. The disease strain was a particularly virulent one, and was especially lethal to young adults in the age group 20–40, although no age group was immune. Originating in America in the spring of 1918, the disease was rapidly disseminated through Europe by American troops arriving in support of the Allied armies for the final offensive against Germany, only assuming its extreme lethal character in the autumn of that year. In the climax of local outbreaks, public services broke down entirely, medical services were unable to cope with the numbers of sick and dying, and burial services were overwhelmed by the number of bodies needing interment. Those who survived often acknowledged it as one of the most profound experiences of their lives. The American writer Katharine Anne Porter spoke for many when she said of it that ‘It just simply divided my life, cut across it like that.’
Sexually transmitted diseasesThe airborne nature of influenza gave the 1918 pandemic its peculiarly immediate, universal, and devastating quality. The global pandemic of HIV infection which has spread out of the US since 1980 has less of this character and more in common with the pandemic of syphilis, which spread across Europe in the late fifteenth and sixteenth centuries, and whose initial characteristics were far more florid and alarming than those which it has subsequently manifested as an endemic disease. Both HIV and syphilis are essentially sexually-transmitted diseases, slower in manifestation and spread than airborne influenza. Nevertheless, the relatively rapid global spread of HIV as the result not only of late twentieth-century sexual mores but also of the ease and speed with which humans travel across the globe, taken together with the experience of 1918, affords some indication of the likely devastation should another lethal airborne — or easily transmitted — infectious disease acquire pandemic impetus.
Garrett, L. (1996). The coming plague. Newly emerging diseases in a world out of balance. Penguin Books, London.
McNeill, W. H. (1979). Plagues and peoples. Penguin Books, Harmondsworth.
See also epidemics; infectious diseases.
Epidemic diseases, introduced from both tropical Africa and Western Europe were frequent visitors to the British North American colonies during the late colonial period and to the United States during the early years of the new nation. The two major epidemic diseases that broke out in the period from 1754 to 1829 were smallpox from the British Isles and yellow fever from West Africa via the West Indies. A number of other diseases, including diphtheria, scarlet fever, measles, whooping cough, and mumps also appeared in epidemic form and swept parts of eastern North America. This vulnerability to exotic disease continued through the nineteenth century. Cholera, spreading from an initial outbreak in South Asia, struck the United States of America for the first time in 1831 and 1832.
Epidemics typically broke out among urban populations that had little or no immunological experience with the pathogen. The outbreaks could be spectacularly frightful and impress themselves into cultural memory. Yellow fever and smallpox wreaked concentrated havoc in cities and spread terror and sickening fear both within and outside the immediate zones of infection.
Epidemics of yellow fever, a mosquito-borne viral disease, were spread by the arrival in port cities of ships from the West Indies, where the disease was endemic. The transmission of yellow fever depended upon an infected individual being bit by an Aedes aegypti mosquito that would in turn bite an uninfected individual. The first epidemics in the British North American colonies took place in the late seventeenth century. A succession of epidemics occurred in the mid-eighteenth century. Philadelphia was struck twice in the 1740s, once in 1762, and then three times in the 1790s. The most famous of these was the 1793 epidemic that killed nearly four thousand, sweeping away to death 10 percent of the urban population. In the early nineteenth century, yellow fever epidemics began to strike the southern ports of New Orleans, Mobile, Charleston, and Savannah. The only effective public health policy was the imposition of quarantine upon ships that were known or suspected to carry the disease.
The yellow fever outbreaks rent the fabric of family and community life. The means of transmission was unknown, and the disease was feared to be contagious. As ever, desperate circumstances brought out the worst and the best. Some families abandoned their sick. Others stayed to nurse their loved ones through the moment of death. The wealthy took flight from the cities; the poor were left to the ravages of the disease. The high fevers and characteristic black vomit that signaled the approach of death inspired particular horror and unleashed racial fears and prejudices. In Philadelphia, African Americans volunteered to care for the sick and did so valiantly; after the epidemic had receded, fearful whites blamed them for the outbreak.
Smallpox was also a deadly viral disease, but unlike yellow fever, it was highly contagious and spread directly from human to human. Immigrants from the British Isles, where smallpox infection was endemic and the principal victims were children, introduced it into the British North American colonies. There, the disfiguring pox destroyed both old and young; survivors of smallpox carried their immunities into adulthood, but the disease never became fully endemic and thus new generations reached adulthood without immunity. In the colonies, smallpox leapt beyond the communities of whites and their slaves into the worlds of the Native Americans, where it wreaked disaster. The death rates among Native Americans are thought to have ranged from 25 to 50 percent. During the epidemic of 1775–1782, smallpox ravaged most of the North American continent, killing more than one hundred thousand and disfiguring many more.
Until the late eighteenth century, the only recourse against smallpox infection was a form of inoculation known as variolation that had been in occasional use since the 1720s. Variolation was dangerous; it involved the intentional subcutaneous introduction of smallpox pus and produced immunity in the 95 percent of the initiates who survived the procedure. The first enforced use of this technique took place during the American Revolution, when General George Washington made the decision to inoculate by variolation all of the troops of the Continental Army. At the end of the eighteenth century, a new type of inoculation, known as vaccination, used what is thought to have been either a cowpox or horsepox virus that proved safe and effective. The broad acceptance of vaccination in the United States reduced greatly the threat of smallpox and constituted a major advance in the efficacy of public health interventions.
Duffy, John. Epidemics in Colonial America. Baton Rouge: Louisiana State University Press, 1953.
Fox, Elizabeth A. Pox Americana: The Great Smallpox Epidemic of 1775–82. New York: Hill & Wang, 2001.
Powell, J. H. Bring Out Your Dead. The Great Plague of Yellow Fever in Philadelphia in 1793. Philadelphia: University of Pennsylvania Press, 1949. Reprint: 1993.
James L.A. Webb Jr.