Georg Wilhelm Friedrich Hegel was born in Stuttgart on 27 August 1770. He was the eldest son of a senior financial official in the administration of the duchy of Wiirttemberg; the family belonged to the “notables” of the duchy. He was a serious and clever child. His mother (who gave him Latin lessons before he went to school) may have hoped he was destined for the Church; his father probably hoped for a successor in the civil service.

By the time his mother died in September 1783, Hegel was keeping a diary full of academic matters in which he practiced his Latin. He was first in his class every year at the Stuttgart Gymnasium. At about the time that he passed to the upper school (autumn 1784), Hegel began to organize his own private studies “encyclopaedically.” He copied out long excerpts from the books that he read under headings and subheadings, which indicate a Baconian ambition to organize all knowledge under its proper “science. ” He continued this habit until after he entered the Theological Institute at Tubingen in October 1788. He never lost the habit of reading with pen in hand, and we have “excerpts ” from all periods of his life; but at Tubingen he stopped writing his classificatory headings at the top of the page. Since he kept his schoolboy collection all his life, his biographer, Rosenkranz, was able to describe it in some detail. A small part of it survived and was printed by Gustav Thaulow in 1854 (see Dok . . ., pp. 54-166).

Strongyloidiasis, or Cochin-China diarrhea, is caused by a minute nematode, the threadworm Strongyloides stercoralis. The organism was first discovered in 1876 in French troops who had suffered severe diarrhea in the Cochin-China region of Vietnam. Strongyloides occurs around the world, with a range similar to that of the hookworms. Millions of people harbor the organism. Because poor sanitation and going without shoes favor transmission, it is especially prevalent in poor tropical countries. Like hookworm disease, strongyloidiasis prevalence has declined greatly in the southern United States since the early twentieth century, but it still exists in foci in Kentucky and other states.

The worm has a complex life cycle. Parasitic males may not exist, but if they do, they are eliminated from the body shortly after infection. The females burrow in the mucosa of the intestine, where they feed and lay their eggs, apparently by parthenogenesis. The eggs pass into the lumen of the intestine, where they hatch into a rhabditiform larval stage. In most cases these larvae are voided in the feces to the soil and either transform themselves directly into an infective filariform larval stage, or, if conditions are favorable, undergo one or more generations of sexual reproduction before filariform larvae appear. Like the hookworms, the filariform Strongyloides larvae penetrate human skin, often on an unshod foot, enter the venous circulation, and are carried through the heart to the lungs. Here they burrow through the walls of the air sacs, ascend to the throat, and are swallowed. The adult females bore into the walls of the small intestine and sometimes into the wall of the large intestine as well.

Brucellosis, or undulant fever, is a zoonotic infection caused in humans by organisms of three main species of the genus Brucella: Brucella melitensis, whose natural host is the goat; Brucella abortus, transmitted largely from cattle; and Brucella suis, transmitted from pigs. Clinically; all three types cause similar infections in humans characterized by intermittent waves of fever that may persist for weeks, often with subsequent relapses and prolonged periods of ill health. The causal relationship between organism and disease was first recorded by David Bruce in Malta in 1887; the name Malta fever, which reflects its prevalence among civilians and British troops in that island in the nineteenth century, has been in general use for most of the present century. More recently, other Brucella species have been found to be implicated in the human disease, which has been shown to be widespread around the globe. The terms “Malta fever” and “Mediterranean fever” have been gradually replaced by undulant fever, or brucellosis.

Etiology and Epidemiology

The type of brucellosis originally studied in Malta and described by Bruce in 1887 is caused by B. melitensis. It is transmitted to human beings by consumption of milk from infected goats; occasional cases due to contamination of skin with infective material have also been observed. The mode of transmission became established only during the first decade of the twentieth century. In Malta and elsewhere around the Mediterranean littoral, the disease was endemic rather than epidemic during the nineteenth century, its highest incidence occurring during the summer months.

Sickness and death are individual- and population level phenomena. At the individual level, they are best understood in terms of their causes. In illness the best prognosis derives from what is known about the cause and about the individual. At the population level, sickness and death can also be understood in terms of incidence. Future rates of sickness and death can be forecast from experience, taking into account the trend and likely variations from it. Population-level statements about sickness and death – morbidity and mortality rates – can be considered statements of comparison. As such, they underlie many judgments about health and health care.

Morbidity and mortality are also structural phenomena, which is to say that, considered for a sizable number of people, they display certain regularities. The most important of these relate to age and appear as curves or schedules when morbidity and mortality data are arranged by age. Age-specific sickness and death rates should not be expected to be identical in any two populations, but their structure – their distribution by age – should be similar. This makes it possible to make estimates for missing data and to compare individual- and population-level experience with sickness and death over time. This essay summarizes the basic method of analysis, which employs a life table, and suggests some ways in which the problem of incomplete information can be overcome with various estimation procedures.

Between 1860 and 1864, August Hirsch published his monumental Handbuch der historisch-geographischen Pathologie in two volumes. In 1881 he finished an introduction to an updated edition, which Charles Creighton translated from German into English. This opus, published by the New Sydenham Society in three volumes, appeared during the years 1883 to 1886 and was entitled Handbook of Geographical and Historical Pathology. The Handbook represented a Herculean effort to detail the distribution of diseases of historical and geographic interest in time and in place.

Our work represents a similar undertaking, but with a major difference. In the second half of the nineteenth century, the dawn of germ theory, it was still possible (as Hirsch proved) for an individual working alone to produce a compilation of this sort. Today even the contemplation of such an attempt boggles the mind. The Cambridge World History of Human Disease project was launched in 1985 as a collective effort of some 160 social and medical scientists to provide at the close of this century something of what the Hirsch volumes provided at the end of the preceding century. We hope that, like the Hirsch volumes, our own effort will aid future students of health and disease in grasping our present-day understanding of diseases in their historical, spatial, and social dimensions.

Another important purpose of the project is to make available an understandable and accessible history of disease to social scientists and humanists in their many varieties. As historians, geographers, anthropologists, and other researchers have become increasingly aware of the importance of adding a biological dimension to their work, they have found the usual medical tomes, with their unfamiliar terminology and concepts, daunting indeed. We do not, however, ignore the needs of specialists in the many fields our work encompasses.

Throughout most of the past, ideas about the means and necessity of providing for the health of the general community were based on notions of what ensured an individual’s well-being. At this personal level, measures that we might consider motivated by aesthetic choices (rather than fully developed ideals of cleanliness and the health necessities of personal hygiene) were interwoven with practices designed to minimize exposure to disease and injury. In a narrow sense, public health practices refer only to the organization of care for the sick of a community and the implementation of epidemic controls. Public sanitation includes all collective measures taken to protect the healthy from disease. Yet even today many believe that what ensures the health of an individual should be reflected in the rules for maintaining the public’s health.

Through much of the past and present, the view of “public” health has involved a compromise between available community resources and the ideals of health maintenance at the individual level. Thus, in order to examine the history of public health and sanitation before the 1700s, it is necessary to include some discussion of the ideas and ideals of personal hygiene along with the development of concepts that led to genuine public health practices. “Basic” sanitary organization largely comprised rudimentary sanitation and sanitary law, care of the sick poor, provision for public physicians, and epidemic controls.

Sanitation

Archaeological records testify to the antiquity of communal efforts to provide clean water and dispose of human and animal wastes. The engineering achievements of some peoples, such as the ancient Peruvians in the Western Hemisphere and the Etruscans in Europe, were most impressive.

Influenza, also known as flu, grip, and grippe, is a disease of humans, pigs, horses, and several other mammals, as well as of a number of species of domesticated and wild birds. Among humans it is a very contagious respiratory disease characterized by sudden onset and symptoms of sore throat, cough, often a runny nose, and (belying the apparent restriction of the infection to the respiratory tract) fever, chills, headache, weakness, generalized pain in muscles and joints, and prostration. It is difficult to differentiate between single cases of influenza and of feverish colds, but when there is a sudden outbreak of symptoms among a number of people, the correct diagnosis is almost always influenza.

There is at present no specific cure that is effective against this viral disease. In mild cases the acute symptoms disappear in 7 to 10 days, although general physical and mental depression may occasionally persist. Influenzal pneumonia is rare, but often fatal. Bronchitis, sinusitis, and bacterial pneumonia are among the more common complications, and the last can be fatal, but seldom is if properly treated. Influenza is generally benign, and even in pandemic years, the mortality rate is usually low – 1 percent or less–the disease being a real threat to life for only the very young, the immunosuppressed, and the elderly. However, this infection is so contagious that in most years multitudes contract it, and thus the number of deaths in absolute terms is usually quite high. Influenza, combined with pneumonia, is one of the 10 leading causes of death in the United States in the 1980s.

Derived from Greek roots meaning “difficult digestion,” dyspepsia has long served as a synonym for indigestion, one of the most common – and etiologically varied – of human miseries. It has thus been as regularly employed to label the symptoms of diverse organic disorders as to identify a distinct disease, with the result that some gastroenterologists find the word uselessly elastic: “This is really a meaningless term because it has so many meanings.” The majority of practitioners, however, have reached a consensus to use dyspepsia to denote either the ailment of functional indigestion or the symptoms of peptic ulcer.

Distribution and Incidence

Peptic ulcer dyspepsia is rare in people under the age of 20, but by age 30, 2 percent of the males and 0.5 percent of the females in a population have developed the condition. For men, the incidence increases steadily with age, reaching a peak of around 20 percent in the sixth decade of life. The incidence for women remains low, about 1 percent, until menopause, after which it climbs as rapidly as in men. A morbidity rate of nearly 14 percent has been reported in women in the age group 70 to 79. Death from peptic ulcer occurs three times as often in men as women.

The prevalence of functional dyspepsia, by contrast, is uncertain. Having no distinct pathology, being neither communicable nor reportable, and only occasionally motivating its victims to seek medical help, it does not generate statistics. The widely shared clinical impression is that women are affected more than men, and people under the age of 40 more than those over age 40.

In its broadest sense, ophthalmia is an inflammation of the eye, especially of the conjunctiva of the eye. The term derives from the Greek word ophthalmos (the eye). Hence, almost any disease that attacked the eye was called ophthalmia in many Greco- Roman and later European sources until the beginning of the twentieth century. As medical knowledge was refined, defining terms were attached, such as “purulent ophthalmia,” “neonatorum ophthalmia,” or “Egyptian ophthalmia.” The problem for historians attempting to define eye diseases in the past is that the term “ophthalmia” meant many diseases that attack the eyes or that manifest symptoms in the eye, and that blindness due to “ophthalmia” had many causes. Two important causes of ophthalmia were trachoma and conjunctivitis; this essay is limited to these.

Trachoma (also called granular conjunctivitis and Egyptian ophthalmia) has been defined as a contagious keratonconjunctivitis caused by Chlamydia trachomatis (serotypes A, B, Ba, and C). It is characterized by the formation of inflammatory granulations on the inner eyelid, severe scarring of the eye in the fourth stage, and blindness (but not in all cases). It was one of the leading causes of blindness in the past, and still blinds millions in Asia, the Middle East, and Africa (Bietti and Werner 1967; Rodger 1981; Insler 1987).

Conjunctivitis (purulent ophthalmia) may appear with trachoma and may complicate the progression of the disease so that blindness rather than healing occurs. Although conjunctivitis may denote any inflammation of the conjunctiva (“the mucous membrane lining the inner surface of the eyelids and covering the frontpart of the eyeball”), bacteria often infect the conjunctiva at the same time as does trachoma, thus causing an acute bacterial conjunctivitis.

Textbooks on tropical diseases in Africa are well out of date. With the recognition of new and deadly viral infections – Lassa, Marburg, Ebola, Congo–Crimean Hemorrhagic Fever, Rift Valley Fever, and AIDS – the classical descriptions of major diseases such as malaria and yellow fever must be thoroughly revised, and to the roster of more minor ailments can be added dengue, Chikungunya, O’Nyong Nyong, West Nile fever, and others. One must be ready to challenge earlier descriptions of African fevers in general. Malaria in particular has been an “umbrella” diagnosis, which obscured and still obscures the diagnosis of other, sometimes dangerous concomitant illnesses in regions where malaria itself is endemic to hyperendemic. The absolute need for laboratory confirmation to support the clinical impression is slowly being recognized. This must extend beyond the simple demonstration of presence of malaria parasites in the blood. Malaria parasites in the blood certainly prove that the individual in question harbors the parasite. But it is not necessarily proof that the actual immediate infection from which the individual is suffering is related to the existing chronic malarial position. Treatment of the malarial infection is indicated, and is followed almost universally in tropical Africa, with or without confirmation of the presence of malaria parasites. The first diagnosis entertained for all of the viral infections listed above is almost always “malaria.”

It is when the patient does not respond to the antimalarial therapy exhibited that other possible diagnoses are considered. In addition to the viral possibilities, the list should also include influenza, typhoid fever, various rickettsioses, leptospiral infections, bacterial and viral enteropathogenic agents – indeed the range of infections capable of inducing a febrile response.

Sexual “deviance” is technically any deviation from the sexual norm. Sexual disease, a new diagnostic category in the eighteenth century, was classed as a syndrome and seems in retrospect to have been an iatrogenic one based more on philosophical and moral grounds than on any medical ones. The disease entity, however, was fitted into some of the medical theories of the time, and as these theories were challenged and undermined, modifications were made in order to justify maintaining certain forms of sex behavior in the category of disease.

In recent decades much of the sexual behavior previously classed as disease has been removed from that category. This redefinition has been based on a better understanding of sexual behavior. It has also been a result of the protests of some groups who reject being classed as ill or sick and having their behavior categorized as pathological, emphasizing the iatrogenic component of the disease. Nonetheless, efforts are being made to maintain other kinds of sexual activity under the rubric of disease. Generally, these are activities that are regarded as unacceptable by society or viewed as compulsive behavior maintain the classification as a way of justifying their intervention or of promising a cure.

Medical Background

Though physicians throughout recorded history have been interested in diseases and infirmities that affect sexual performance, the concept that certain forms of sexual behavior constitute a disease in and of themselves is a modern phenomenon. It also seems to be restricted to western Europe and people and cultures descended from or influenced by western European culture.

Trichinosis, also known as trichinellosis, trichiniasis, or trichinelliasis, is a disease of humans and of other mammals infected with the nematode worm Trichinella spiralis. The pathological changes and the symptomatology of Trichinella infection are manifestations of three successive stages in the life history of the worm: (1) penetration of adult female worms into the intestinal mucosa, (2) migration of juvenile worms, and (3) penetration of juvenile worms and subsequent encystment in muscle cells.

Distribution and Incidence

Although trichinosis occurs worldwide, in humans it is found principally in the United States, Canada, and eastern Europe. It is also well known in Mexico, parts of South America, Africa, southern Asia, and the Middle East. People acquire trichinae by ingesting uncooked or poorly cooked meat, especially pork. Home-made sausages have caused many recent outbreaks in the United States. Hence, the prevalence of trichinosis is less in the tropics and subtropics, where less meat is consumed. Trichinosis does not occur among Hindus, Jews, and Moslems, for whom there are religious bans on eating pork.

Although the prevalence of trichinosis in human populations is low (probably 2.2 percent or less in the United States, based on autopsy surveys), epidemic outbreaks are not infrequent. Incidence of infection is likely to be higher than suspected because of the vagueness of symptoms, which usually suggest other conditions.

Syphilis or, more properly, venereal syphilis is a chronic communicable disease, which, until the acquired immunodeficiency syndrome emerged in the early 1980s, was the most serious and dreaded of the so-called sexually transmitted diseases (STD) – formerly, venereal diseases (VD). Caused by Treponema pallidum subspecies pallidum, a spirochetal bacterium, the only known natural host of which is the human being, venereal syphilis is thus one of the human treponematoses – along with pinta, yaws, and endemic syphilis. Although predominantly transferred by sexual contact, T. pallidum is also capable of being transmitted from an infected mother to her fetus across the placenta at any stage of pregnancy (congential syphilis).

Syphilis develops naturally through three clinical stages (primary, secondary, and tertiary or late), each separated by a subclinical period. Of the subclinical periods, the one between the secondary and tertiary stages (latent syphilis) is the most pronounced. Clinical manifestations of syphilis are extremely protean, and capable, at the tertiary stage, of affecting any system of the human body.

Syphilis took its name from Girolamo Fracastoro’s well-known poem, Syphilis, sive morbus gallicus (1530), in which the Italian humanist-physician invented this phrase to name the disease then known all over Europe as morbus gallicus. However, the term syphilis did not become widely used until the late eighteenth century, and that usage was vague and applied to many other symptoms besides those of venereal syphilis until the development of the germ theory in the late nineteenth and early twentieth centuries.

The agent of this disease, the sporozoan protozoan Toxoplasma gondii, is a common parasite of many species of birds and mammals. The organism was first seen in 1908 in the tissues of a Tunisian rodent, the gundi, and fully described in 1909. Human disease was first described in 1923 and congenital neonatal disease was reported in 1939, but the complex life cycle of the parasite was not elucidated until 1970. Serologic tests show that humans around the world harbor T. gondii, but because almost all infections are asymptomatic, very few have the disease. The protozoan is an intracellular parasite of a variety of tissues in warm-blooded vertebrates. It multiplies by binary fission in a host cell, eventually rupturing the cell and releasing parasites to attack other cells. Sexual reproduction can take place only in cats and other felines. These definitive hosts release oocysts, the stage infective for herbivores, in their feces. Asexual intracellular replication takes place in the herbivore, and, if the tissues containing T. gondii are eaten by a carnivore, asexual reproduction may also occur in their tissues. Humans can become infected by eating poorly cooked or raw meat or poultry, by ingesting oöcytes from the feces of cats, or congenitally.

Clinical Manifestations

Human infections are usually inapparent, although they sometimes can lie dormant for years and flare up in weakened or immunodeficient hosts. Most cases in otherwise healthy people are mild and cause vague symptoms like fever and weakness. The disease often mimics infectious mononucleosis. Chronic cases can cause diarrhea, headache, and eye damage.

Goiter is an ancient disease that has always been more common in some places than in others. Chinese writings show that goiter was known at least by the third century B.C. (Lee 1941) and possibly earlier (Needham et al. 1970). When Juvenal (Decimus Junius Juvenalis), the Roman satirist, wrote, about A.D. 127, “Who is amazed at a swollen neck in the Alps?” he knew that goiter was so much more common there than elsewhere that it should be no surprise.

Terminology

The word “goiter” (or goitre in Europe) derives from the Latin gutter, but the meaning has shifted from “throat” or “neck” to mean specifically an enlarged thyroid gland. An ancient Greek synonym was bronchocele, a term actually used to describe any enlargement in the neck, although it meant literally a swelling or an outpouching of the trachea. Over time this term also came to mean an enlarged thyroid (e.g., the English “bronchocele” of the eighteenth and nineteenth centuries). Modern synonyms are the Spanish bocio (from Latin, botium), the Italian gozzo, and the German Kropf. The ancient Latin word struma was probably originally used to describe inflamed lymph nodes in the neck, most likely tuberculous, but was later used to denote the normal thyroid gland, and is still so used although it is almost obsolete.

Confusion over names is understandable, as the thyroid gland itself was unknown until the sixteenth century. Leonardo da Vinci may have drawn the thyroid about the year 1500, but the drawing was not published until much later. Andreas Vesalius did note “laryngeal glands” in 1543, but not in humans.

America north of the Rio Grande, that life zone sometimes referred to as the Nearctic region, presents the scholar of history and geography of disease with numerous challenges. These include such questions as the following: What potential disease-causing agents existed in the hemisphere before the comparatively recent arrival of human beings? How effective was the “cold screen” (Stewart 1960) in ensuring the health of the migrants crossing the link from Eurasia to the New World? Given the isolation of this population, how varied was it in a genetic sense, and how well adapted did it become to North American ecologies? Were native North Americans indeed “far more healthy than any others of whom we know” (Ashburn 1980)? Just what was the impact of the “Columbian exchange” (Crosby 1972)? Did these invaders receive the country “from the hands of nature pure and healthy” (Rush 1786)? What relative contribution to ill health and disease did the European group provide compared to that of the enslaved African populations? What were the dimensions and timing of the “epidemiologic transition” in North America (Omran 1977)? How real have urban and rural differences in health experience been through time? How serious is the threat today of “life-style” diseases?

Clearly all of these and other equally intriguing questions arise. This brief discussion can only hope to touch on some of them and to review a portion of the work by persons from biochemists to medical historians, from archaeologists to medical geographers, who have applied their learning to the fascinating question of human well-being through the ages in North America.

Legionnaires’ disease is an acute infection of humans, principally manifested by pneumonia, that occurs in a distinctive pattern in epidemics and is caused by bacteria of the genus Legionella. Typically the incubation period – the interval between exposure to the bacterium and the onset of illness – is 2 to 10 days, with an average of 5 to 6 days, and the attack rate – the proportion of people exposed to the bacterium who become ill – is less than 5 percent. Without specific antibiotic treatment, 15 percent or more of the cases are fatal, although the percentage of fatal cases rises sharply in immunosuppressed patients.

Legionnaires’ disease is one form of presentation of Legionella infections, which are generally referred to by the umbrella term legionellosis. Another distinctive clinicoepidemiological pattern of legionellosis is Pontiac fever. Pontiac fever affects 45 to 100 percent of those exposed and has an incubation period of 1 to 2 days. Pneumonia does not occur, and all patients recover. More than 20 species of Legionella have been identified, 10 of which are proven causes of legionellosis in humans. The most common agents of human infection are Legionella pneumophila, Legionella micdadei, Legionella bozemanii, Legionella dumoffii, and Legionella longbeachae.

Legionellae are distinguished from other bacteria in being weakly staining, gram-negative, aerobic rods that do not grow on blood agar or metabolize carbohydrates, and have large proportions of branched-chain fatty acids in their cell walls and major amounts of ubiquinones with more than 10 isoprene units on the side chain.

The term “filariasis” refers to several diseases of both humans and animals caused by infection with a specific group of parasitic nematodes called filarial worms (named for the hairlike appearance of the adult form). Those worms that affect humans belong to the Order Filarioidea, Family Dipetalonematidae. They include (1) Wuchereria bancrofti and Brugia malayi, which are common causes of elephantiasis (extreme swelling and skin thickening of the legs, scrotum, labia, or arms) and chyluria (lymph and emulsified fat globules in the urine); (2) Loa loa, the “eye worm”; and (3) Onchocerca volvulus, the cause of onchocerciasis. Depending upon their species, adult filarial worms of both sexes reside in the lymphatic system, subcutaneous tissues, or peritoneal and pleural cavities. Sexual reproduction results in embryos (microfilariae) that enter blood or skin, where they are ingested by a particular intermediate host (certain species of mosquitoes, horse fly, black fly, or other arthropods). The microfilariae develop into larvae in their intermediate hosts and then reenter vertebrate hosts (humans or animals) through bites in the skin made by the intermediate host arthropods. Loa Loa is endemic in West and central Africa, whereas onchocerciasis is found in Mexico, Central America, and West Africa. Discussion of human lymphatic filariasis in the remainder of this entry will be limited to the most prevalent form (90 percent of infections), that caused by W. bancrofti (Sasa 1976; Beaver, Jung, and Cupp 1984; Mak 1987; Manson-Bahr and Bell 1987).

Southeast Asia can be visualized as the part of Asia that spills into the sea, comprised of long coasts, tidal plains, peninsulas, and islands. There are high mountains, inland plains, plateaus, and upland valleys; nonetheless, to a very large degree, human culture has developed with an acute awareness of water, from the sea, the rivers, and the monsoon rains. It is therefore not surprising that many of the endemic health problems in the region are related to water; indeed, since prehistoric times, nearly all major areas of habitation have been exposed to global contact by water transport.

Maritime routes linking the littoral civilizations of the Eurasian landmass have passed through Southeast Asia for more than two millennia. We can accordingly assume that from early times the region experienced all of the epidemic diseases familiar to the ancient world. What inhibits discussion of diseases in the earlier historical periods of Southeast Asia is the lack of data. Because of the prevailing tropical-equatorial climate, the preservation of written records has, until recently, required greater effort than most human societies were prepared to make. Our first information comes from the observations of Chinese annalists, whose works survived in the temperate climate of northern China. As the Chinese moved southward into what is today northern Vietnam, they recorded perceptions of disease associated with what for them were southern lands.

Most prominent among the health problems encountered by ancient Chinese armies in Vietnam were malaria and other “fevers” associated with the monsoon rain season. Chinese generals timed their expeditions into Vietnam to coincide with the dry season, from November to May.