Mental disease refers, at present, to disorders of perception, cognition, emotion, and behavior. The disorder may be mild or severe, acute or chronic, and may be attributed to a defect of mind or body or of some unknown combination of the two. A diagnosis of mental illness is the judgment that an individual is impaired in his or her capacity to think, feel, or relate to others. In mild cases, the impairment may intrude on a person’s ability to gain satisfaction from meeting the challenges of everyday life. In severe instances, an individual may be thought so dangerous or incompetent that sequestration within a psychiatric facility is necessary, with a resulting loss of rights normally granted to citizens.

The Problem of Mental Illness

The simple title of this section belies the extraordinary scope, complexity, and controversial state of contemporary psychiatric thought. Some have argued that if the myriad types of disorders bedeviling humankind were ranked by the net misery and incapacitation they caused, we would discover that psychiatry captures a larger share of human morbidity than does any other medical specialty. It seems ironic - if not tragic - that a clinical field of such magnitude is at the same time distinguished among its peers by a conspicuous lack of therapeutic and philosophical consensus. That the discipline lacks a set of internal standards by which to differentiate unequivocally the correct theory from the false, or the efficacious therapy from the useless, is an open secret.

African trypanosomiasis, or sleeping sickness, is a fatal disease caused by a protozoan hemoflagellate parasite, the trypanosome. It is transmitted through the bite of a tsetse fly, a member of the genus Glossina. Sleeping sickness is endemic, sometimes epidemic, across a wide band of sub-Saharan Africa, the so-called tsetse belt that covers some 11 million square kilometers. Although the disease was not scientifically understood until the first decade of the twentieth century, it had been recognized in West Africa from the fourteenth century.

The chemotherapy to combat trypanosomiasis has remained archaic, with no significant advances made and, indeed, very little research done between the 1930s and the 1980s. Most of the victims are poor, rural Africans, which has meant that there is little or no economic incentive for pharmaceutical firms to devote research resources to the disease (Goodwin 1987). However, in the mid-1980s field trials of a promising new drug, D1-alpha-difluoromethylornithine (DFMO), demonstrated the drug’s efficacy in late-stage disease when there is central nervous system involvement. In addition, there have been exciting recent developments in the field of tsetse eradication with the combined use of fly traps and odor attractants (Hall et al. 1984). And, the World Health Organization’s Special Program on Tropical Disease is trying to overcome the research problem resulting from the reluctance of pharmaceutical firms to get involved.

In current nosology, diseases are categorized as degenerative, malignant, genetic, endocrine, and so on. For purposes of the history of diseases we must add a category that we might term ephemeral. This requires a bit of literary license, because many conditions that fall in the class of ephemeral diseases had a longer existence than that word usually implies. Ephemeral diseases comprise a large number of entities that carried working diagnostic names for earlier physicians (see, e.g., typhomalarial fever), but that are no longer recognized, at least by their previous names (Straus 1970; Hudson 1977a; Jarcho 1980).

Clinical Manifestations

A historical example of a disease that died only to leave behind a host of sprightly ghosts is the “green sickness” or chlorosis. Although noted in two Hippocratic treatises, Prorrhetic and The Diseases of Girls, the condition received its now classic description by Johann Lange in 1554 (Hippocrates 1853, 1861). He called the condition morbus virgineus. His description contains many of the elements found in the Hippocratic texts, as does the account by Ambroise Pare in 1561. Also reflecting the Hippocratic corpus is the work of Jean Varandal who is credited with first using the word “chlorosis” in 1615 (Starobinski 1981). For Varandal, chlorosis was a class of syndromes.

Reflecting a different approach, Thomas Sydenham’s description in 1683 embodied many of the clinical features relied upon at least two centuries later:

Yellow fever is an acute group B virus disease of short duration transmitted to humans by different genera of mosquitoes, but especially by the Aedes aegypti (known previously as the Stegomyia fasciata). It remains endemic in the tropical regions of Africa and the Americas in a sylvan or jungle form, but historically its greatest impact on humans has been in an epidemic or urban form. The disease can appear with symptoms ranging from extremely mild to malignant; in classic cases it is characterized by fever, headache, jaundice, albuminuria (high-protein content in the urine), and hemorrhage into the stomach and intestinal tract. High mortality rates were frequently recorded during epidemics (20 to 70 percent), although today we know that yellow fever mortality is actually relatively low, suggesting of course that the majority of the cases were mild and went undiagnosed. The jaundice has prompted the appellation yellow fever, and other designations such as the mal de Siam, fièvre jaune, gelbfieber, and virus amaril, whereas the hemorrhaging of black blood led to the name “black vomit” or vomito negro.

Known early in the New World as the “Barbados distemper,” “bleeding fever,” the “maladie de Siam,” “el peste,” vomito negro, and later yellow jack (because of the yellow quarantine flag flown by ships), the disease has been called by some 150 names. It was first termed “yellow fever” apparently by Griffin Hughes in his Natural History of Barbados (1750).

Pellagra is a recurring nutritional disease associated with a severe deficiency of niacin, a vitamin of the B-complex group that includes both nicotinic acid and nicotinamide. Because the body can convert the essential amino acid tryptophan into niacin, inclusion of enough tryptophan in the diet is as effective as niacin in preventing the disease. Pellagra is usually associated with signs of deficiencies of other B complex vitamins and nearly always is linked with poverty and a diet composed substantially of maize. In recent years, pellagra in India and Egypt has been tied to consumption of another grain, jowar, a type of millet or sorghum.

Pellagra is characterized by dermatitis, diarrhea, and dementia, and thus is known as the disease of the “3 D’s.” If untreated, a fourth “D,” death, may ensue. Before the cause of the disease was known, mortality was as high as 70 percent. As knowledge about the disease increased, however, and many mild cases, previously undiagnosed, were recognized, the mortality rate was reduced substantially.

Dermatitis is the characteristic symptom of pellagra and the one on which diagnosis is based. Symmetrical lesions appear on the hands and arms, on the tops of the feet and around the ankles, on the back of the neck, and across the face in a butterflyshaped design. Weakness, a sense of malaise, and a reddened skin, sometimes confused with sunburn, are the first indications of the disease. Later the skin crusts and peels, revealing a smooth glossy skin underneath. In Spain, where the disease was first described in the eighteenth century, it was called mal de la rosa; in France, peasants named it mal de la misère.

Epilepsy is characterized by the repeated occurrence of seizures that result from recurrent, abnormal, excessive, synchronous discharges of populations of cerebral neurons (Epilepsy Foundation of America 1981). It has a worldwide distribution and probably has been in existence since the dawn of human history. The condition is chronic but rarely fatal, and most types of epilepsy do not disturb the affected individual’s desire or ability to lead a normal life. Modern antiepileptic medications most often control seizures, and the limitations imposed by the disorder may be negligible. Unfortunately, epileptics are all too frequently stigmatized and excluded from many activities of daily life. Outdated beliefs and misconceptions about epilepsy have only recently shown signs of lessening in the United States and other industrialized societies.

It is misleading to think of epilepsy as one disease. There are many causes of this symptom cluster, just as there are for the symptom cluster of nausea and vomiting. A better term would be “the epilepsies.” The epilepsies do, however, share certain physiological characteristics. Clusters of neurons in some parts of the brain begin to discharge impulses in a disorganized fashion. The parts of the body controlled by the affected neurons respond with disorganized activity such as convulsions or tremors, or by loss of normal function such as loss of consciousness, paralysis of a limb, or localized numbness. The condition is also chronic, marked by the recurrence of seizures. By monitoring the brain with electrodes, an electroencephalographer can often detect abnormal brain waves, either localized in one part of the brain or coming from all parts at once.

The idea that diet is an important factor in health is a very old one and, if anything, had greater prominence in the time of Hippocrates than it does now. However, the development of a workable system or science of nutrition had to await the development of modern chemistry with its significant advances at the end of the eighteenth century. Before that time, the purpose of nutrition in adults was assumed to be the replacement of abraded (or worn-out) tissues. Meat, the tissues of other animals, seemed an effective food for this purpose, because it provided essentially like-for-like, but vegetable foods seemed to be made of quite different “stuff.” Animal tissues allowed to decompose became putrid and alkaline, whereas most vegetables became acid and did not become putrid. When heated and dried, animal tissues became hornlike, whereas vegetables became powdery. However, Iacopo Bartolomeo Beccari of the University of Bologna pointed out in 1728 that, when sieved (i.e., debranned) wheat flour was wetted and pummeled into a dough and then kept under running water until the floury starch had been washed out, the residual gluten had all the properties of animal tissues. Similar fractions were found in other plant foods. It was thought that these were the essential nutrients, and it was the job of the digestive system to winnow away the unwanted starch, fiber, and so forth and leave the glutenlike material to be circulated in the blood, for patching and filling.

Protein

With the discovery of nitrogen as an element toward the end of the eighteenth century, and the development in France of methods for analyzing the amount of nitrogen in different materials, came the discovery that both animal tissues and the “animal-like” fractions in vegetables contained nitrogen, whereas starch, sugar, fats, and vegetable fibers contained only carbon, hydrogen, and oxygen.

The Chinese liver fluke is a small worm that parasitizes the bile ducts and livers of humans, dogs, cats, pigs, and several wild animals in China, Japan, Korea, and Indochina. It was discovered in 1875, and recently, it was estimated that 20 million individuals in China alone are infected. Eggs are laid in the bile ducts, pass in the feces, and if they reach the proper freshwater snail, undergo a series of stages in this intermediate host. Eventually, free-swimming larvae are formed, which penetrate and encyst the skin or muscles of fish, expecially those of the carp family. Human beings and other definitive hosts become infected by eating the cysts (metacercaria) in raw or poorly cooked fish. Raw fish are a delicacy in many Asian countries, and fish are sometimes raised in ponds fertilized with human feces. Encysted metacercaria larvae are resistant to smoking, pickling, salting, and drying. Imported fish have caused human cases in Hawaii, and the popularity of Asian cuisine poses a potential danger to gourmets far beyond Asia.

Light infections are often asymptomatic. Heavy infections may produce diarrhea, fever, jaundice, and abdominal pain. Bile duct blockage and liver abscesses occur in chronic cases, and Clonorchis sinensis has been tentatively linked to liver cancer. Diagnosis is made by microscopic examination of the feces to discover the characteristic eggs. Drug therapy is sometimes successful. Preventive measures include rural sanitation, regulation of fish-farming methods, and cooking fish thoroughly. It is unlikely, however, that long-established culinary practices can be changed.

In past centuries people feared epidemic diseases with their sudden onset, ghastly symptoms, agonizing death for many, and sometimes disfigurement or physical impairment for survivors. Today, especially in the developed world (with a few notable exceptions), the dread of epidemic contagion seems almost as anachronistic as the burning of witches. It has been replaced by the dread of cancer. As with the epidemics of yesterday, the basic causes of cancer remain shrouded in mystery, while its effects in terms of human suffering are all too well known.

Cancer is a process whereby a loss of control of normal cell division and multiplication produces a tumor that can invade adjacent tissues and metastasize, that is, implant cancerous cells at a site that is noncontiguous to their origin, where abnormal multiplication continues. When cancer originates in connective tissues (mainly bone or muscle), it is called sarcoma; when it originates in epithelial tissues (lining tissues and organs such as the breast, lungs, or stomach), it is called carcinoma. The latter is by far more common. Invasive tumors occur in all complex species and probably antedate the advent of vertebrates. The oldest paleopathological evidence is limited to lesions that affected bones, such as those found in dinosaurs. Tumors have been found in Egyptian mummies dating from 2000 to 3000 b.c., and physicians of that ancient land knew of and treated patients for cancers of several sites.

The muscular dystrophies are a group of genetically determined, almost exclusively pediatric diseases. Generally, the earlier the age at which symptoms begin, the poorer is the prognosis. Because of a considerable overlap of manifestations and rates of progression and, until recently, the lack of any biochemical test, their classification is still unsettled. As a group, the principal differential diagnosis of the muscular dystrophies is from the muscular atrophies. In the former, the primary defect is in the voluntary muscle fibers; in the latter, it is in the innervation of muscles.

Classification

The most common of the dystrophies and the first to be described was that delineated by Guillaume B. A. Duchenne, a French neurologist, in 1868. Duchenne muscular dystrophy (DMD) is a sex-linked recessive disorder. Consequently, it clinically affects only males and is inherited through female carriers of the gene. Although affected boys have abnormally elevated concentrations of muscle cell enzymes such as creatine phosphokinase in their blood, this abnormality is also found in about three-fourths of the asymptomatic female carriers. DMD appears to have a rather uniform incidence worldwide, with a mean incidence estimated to be about 1 case per 4,000 live male births, or 15 to 33 cases per 100,000. Most surveys have been of predominantly Caucasian populations, but the results of a study in Japan were consistent with the others. A family history of DMD can be obtained in only about one-third of cases. The others are attributed to either a previously unexpressed carrier state or to a new mutation.

Historically the terms puerperal fever and childbed fever referred to any acute fever occurring in puerperae during the first few days after delivery. Less frequently, the terms were also applied to symptomatically similar diseases that occurred during pregnancy or even among the newborn. From a modern point of view, what was formerly called puerperal fever includes a range of disorders most of which would now be referred to as puerperal sepsis. Typically, puerperal sepsis involves postpartum infection in the pelvic region, but it can refer to disorders focused in other areas, such as mastitis. In modern usage, the term puerperal fever occurs mainly in discussions of the great fever epidemics that afflicted maternity clinics in earlier centuries.

Etiology and Epidemiology

A wide range of aerobic and anaerobic microorganisms have been associated with acute pelvic inflammation and with other postpartum inflammations that could be identified as puerperal fever. Group A streptococci (pyogenes) were probably the leading causal agent in most puerperal fever epidemics in earlier centuries. However, since the 1970s, group B streptococci (agalactiae) have become the most prevalent causal agent.

Clinical Manifestations and Pathology

Among puerperae the clinical manifestations of puerperal sepsis include acute fever, profuse lochial flow, and an enlarged and tender uterus. Onset is generally between 2 and 5 days after delivery. Normally there is inflammation of the endometrium and surrounding structures as well as of the lymphatic and vascular systems. One also finds pelvic cellulitis, septic pelvic thrombophlebitis, peritonitis, and pelvic abscesses. Among neonates, infection usually becomes apparent in the first 5 days after birth, but onset is sometimes delayed by several weeks. Symptoms include lethargy, poor feeding, and abnormal temperature. Infection by group B streptococci is often clinically indistinguishable from other bacterial infections.

Tularemia is primarily a specific, infectious disease of rodents and lagomorphs. The causative organism, however, has been isolated from over 100 species of mammals, 9 species of domestic animals, 25 species of birds, 70 species of insects, and several species of fish and amphibians. Humans can become infected by being bitten by infected blood-sucking insects, by handling infected animal carcasses, and by ingesting contaminated water or poorly cooked meat. In humankind, tularemia is an acute, infectious, moderately severe, febrile disease, which has a mortality rate of approximately 7 percent in untreated cases. The causative agent, Francisella (Pasteurella) tularensis, is a tiny gram-negative, pleomorphic coccobacillus requiring special media for isolation and growth. Tularemia is also know as deer-fly fever, Pahvant Valley plague, rabbit fever, Ohara’s disease, yatobyo, and lemming fever.

Etiology and Epidemiology

Two variants (biovars) of the causative organism are recognized. F. tularensis biovar tularensis (type A) has been isolated in nature only in North America and is the most virulent in human beings. The second is designated F. tularensis biovar palaearctica (type B) and is found in all areas where tularemia is endemic in the Northern Hemisphere.

Tularemia is unique in the number of ways in which humans can become infected, and the clinical picture of the disease depends upon the infection route. The most common route is via the skin, either by insect bite or by direct passage through intact skin by contact with infected carcasses or a scratch from an infected animal. Of the numerous insects that transmit the disease, the tick is the most important.

Rabies is an acute viral encephalomyelitis or inflammation of the brain and spinal cord of humans and other mammals, especially carnivores. The disease, known since antiquity, is almost always transmitted to human beings in the saliva of biting animals and is almost invariably fatal. The name hydrophobia, “fear of water, ” and the French term la rage illustrate two common symptoms.

Distribution and Incidence

Rabies occurs in most of the world, including Africa, Asia, the Americas, and most of Europe. It has never occurred in, or has been eliminated from, Britain, Ireland, Sweden, Norway, Japan, Australia, New Zealand, Hawaii, and many other islands in the Pacific and the Caribbean. Rabies is primarily a disease of wild carnivores, particularly canids such as the fox, wolf, jackal, and coyote. Skunks and raccoons are also common hosts, as are many species of bats. Virtually any species of mammal can contract the disease when bitten by an infected animal. Domestic dogs are the major threat to humans; cats are a growing danger in North America. Cattle, horses, sheep, and other livestock may also be affected. Outbreaks among farm animals may cause considerable economic loss, but bovine or equine rabies usually poses little danger for humans.

Rabies is a relatively uncommon disease in humans, occurring sporadically as isolated cases or in small clusters. Epizootics develop at irregular intervals in wild carnivores, and may infect humans mainly through dogs or rarely directly. Persons working alone in remote areas, such as hunters, trappers, or shepherds, are vulnerable to attack by infected animals.

The word “pyorrhea” comes from the Greek pyon (“pus”) and rhoia (“to flow”). Thus the definition is a graphic description of the disease in which there is an outflowing of pus from the gingival (gum) tissues of the oral cavity. The term “pyorrhea” has been used in Europe since the mid-1500s and in America since the late 1800s. However, it was not until 1937 that the American Academy of Periodontology abandoned the term in favor of “periodontal disease.”

The term “periodontal disease” is used in reference to any disease of the supporting structures of the teeth. These structures include the gingiva, periodontal ligament, and alveolar bone. In simplest terms, periodontal disease can be divided into two distinct, but not mutually exclusive, disease processes. The first involves inflammation of the gingival tissues, called “gingivitis,” and the second, a destructive loss of bone and connective tissue attachment termed “periodontitis.”

Distribution, Incidence, and Epidemiology

Epidemiological research during the past 25 years indicates that periodontal disease is one of the most common diseases affecting humankind. There is a direct cause-and-effect relationship between the bacterial colonization on the surface of the tooth and the inflammation (and often consequential destruction) of the tooth’s supporting structures. The rate of destruction varies, and is dependent on the individual’s response to the bacterial irritation.

Periodontal disease is a widespread chronic disease and remains as the primary reason for the loss of teeth in the adult population throughout the world. In fact, virtually all individuals in any population exhibit manifestations of the disease.

In ancient times physicians wrote primarily on the care of infants, and only incidentally about children’s diseases, because their concept of medicine stressed the maintenance of health rather than the diagnosis of specific disease entities (for medical perspectives on children during antiquity, see Etienne 1973). The earliest of these “pediatric” texts known to us was that of Soranus of Ephesus (active around A.D. 100), On Gynecology, which included 23 chapters on infant care (see Soranus 1956; also Ruhräh 1925; Still 1931; Garrison 1965; Peiper 1966). First, Soranus gave instructions on sectioning the umbilical cord, feeding, swaddling, choosing a wet nurse (if necessary), bathing the baby, and other activities essential to infant care. Then he discussed the treatment of common disorders of infancy, including teething, rashes, and “flux of the belly,” or diarrhea.

Soranus was a leader of the Methodist sect at a time when Greek medicine was enlivened by various contending schools of thought. Methodism taught that disease was due to excessive relaxation or contraction of internal pores of the body, leading to immoderate secretion and moisture in the first instance and to diminished secretion and dryness in the second. The cause of disease was considered unimportant, stress being laid instead on treatment that, crudely put, consisted of inducing the contrary state, drying the moist or humidifying the dry. In his section on infant management, Soranus concentrated on the practicalities of care and treatment without slavish adherence to the tenets of Methodism. The result was a pragmatic guide uncomplicated by theoretical or speculative overtones.

Infection with the small flagellate Giardia lamblia is found around the world. This protozoan inhabits the small intestine of humans and is especially common in children. Other mammals, including beavers and muskrats, also harbor Giardia and are important reservoir hosts. The parasite was first seen by Anton van Leeuwenhoek in 1681 and described scientifically in 1859.

Adult parasites, the trophozoites, attach to the intestinal wall with sucking disks. As trophozoites detach and pass down the intestinal tract, they transform themselves into cysts that are able to resist many environmental pressures, including water filtration and chlorination. Humans almost always acquire infection by swallowing fecally contaminated food or water. In developed countries, many cases of giardiasis have been traced to campers who have drunk from what appeared to be pure wilderness streams, but that had been contaminated by animals. Because the cysts are surprisingly resistant to normal water purification methods, public water supplies can become infected by faulty sewer lines, as happened in two fashionable Colorado ski resorts in 1964 and 1978. Giardiasis is a frequent cause of “traveler’s diarrhea,” and tourist groups in Leningrad have suffered well-publicized outbreaks. In 1983, 22 of New York City’s 55 police and fire department scuba divers had Giardia, presumably from the heavily polluted waters of the harbor. Four percent of 1 million stool samples submitted to state laboratories in the United States from 1977 to 1981 were positive for Giardia. Prevalence rates in developing countries range from 8 to 20 percent and higher.

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.