This disease is a pathological condition resulting from infection with the parasite Dracunculus medinensis. In most instances, the adult worms, which are about 1 meter long, are quite evident as they emerge slowly through the skin of their victims.

Distribution and Incidence

In the 1980s and 1990s, Dracunculiasis is found mainly in India, in Pakistan, and in a band of 19 African countries between the Sahara Desert and the equator, from Senegal in the west to Ethiopia in the east (see Map VIII.38.1). Formerly this disease was much more widespread in the Middle East and Africa, and it occurred for some years in the Americas after it was introduced there by infected Africans during the slave trade.

In general, the incidence of dracunculiasis is significantly higher in endemic rural Africa communities than in endemic Asian villages. In West Africa especially, for example, rates of infection in affected areas often reach 20 to 40 percent, and sometimes exceed 50 percent, whereas in Asia, the rates usually are below 20 percent. In rural areas, the disease occurs sporadically, with adjacent villages sometimes differing greatly in the percentage of those infected. Susan Watts (1987), a medical geographer, has estimated that the number of persons at risk of this infection in Africa is about 120 million, with Map VIII.38.1. Areas in which dracunculiasis is reported or probably exists. another 20 million at risk in India and Pakistan, based on the assumption that everyone is at risk ho is living in a rural district where a minimum of one case of dracunculiasis has occurred.

The semantic and logical quagmires that await anyone audacious enough to safari through the changing concepts of disease, illness, and health are portended by a cursory analysis of the definition formulated by the World Health Organization. “Health,” we are informed, “is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity” (Caplan, Engelhardt, and McCartney 1981). Aside from the fact that this seems more realistic for a bovine than a human state of existence, problems abound in what appears to be a fairly straightforward statement. The word “complete” immediately removes the definition from the realm of human reality. What is complete mental well-being, or physical for that matter? Worse still, the phrase “complete social wellbeing” is so freighted with individual interpretations that it alone renders the definition useless, if not pernicious.

This essay concentrates on ideas of physical health and disease, which is not to minimize the importance of psychiatric disease, but rather to admit that concepts of mental health and illness, although sharing most of the definitional difficulties of physical health and disease, are even more difficult to handle. In large part this is because with mental illness we lack the kinds of objective tools to measure brain function that have helped, though not resolved, questions of what constitutes health and disease in the physical realm. This is not, however, to deny the interconnectedness of the psychic and the physical, which is assumed in all of what follows.

Perhaps no one sentence captures the history of changing notions about disease better than a paraphrase of Humpty Dumpty’s haughty admonition: “When I use the word disease, it means just what I choose it to mean – neither more nor less.” mean - neither more nor less. A number of important considerations lead to this generalization. Among these are the following: (1) The definition of disease has varied with time and place in history; (2) the names assigned to diseases are ultimately abstractions, although it is useful at times to act as though they are real; (3) what we mean by diagnostic terms, as with words in general, can be discerned more accurately by what we do with them than what we say about them.

Ergotism is a disease condition acquired by eating cereal grains infected with ergot fungus. Known since the time of Galen, it was prevalent in medieval Europe, particularly among the poor who, during famine, consumed bread made from spoiled rye. Ergot (secale cornutum, spur of the corn, horned rye, womb grain), the dried sclerotium of Claviceps purpurea, develops on the ovary of common rye, or on corn, where it was previously known as corn smut. The actual cause of ergot in grasses was hotly debated by early naturalists, some of whom thought it occurred in rainy weather and was attributable to fog or impure atmosphere. Others believed it to be the work of worms or butterflies, whereas still others regarded it as the product of improper fecundation or perhaps the cooking of the sexual parts of the plants.

Classification

Ergotism has two forms: (1) convulsive, or spasmodic, also known as creeping, which affects the central nervous system; and (2) gangrenous, which affects the blood vessels and blood supply to the extremities. Common names for the gangrenous form are St. Anthony’s fire (after the patron saint of the disease), hidden fire, saint’s fire, evil fire, devil’s fire, and holy fire. As a result of early imprecision in disease specificity and diagnosis, physicians confused ergotism with the plague and a variety of other diseases including leprosy, anthrax, typhus, smallpox, and scurvy.

Malaria is the disease resulting from infection by one or more of four species of protozoan parasites of the genus Plasmodium. These parasites are normally transmitted from one human host to the next by the bite of an infected female mosquito of the genus Anopheles. Although malaria has receded from many temperate regions in this century, the disease continues to be a major cause of morbidity and mortality in many tropical and subtropical countries. Three of the species – Plasmodium viuax, Plasmodium falciparum, and Plasmodium malariae – are widely distributed; the fourth, Plasmodium ovale, is principally a parasite of tropical Africa. P. vivax (the agent of benign tertian malaria) and P. falciparum (causing malignant tertian malaria) are responsible for the great majority of cases and deaths attributed to malaria throughout the world.

Malaria is characteristically paroxysmal, and often periodic. The classical clinical episode begins with chills, extends through a bout of fever, and ends with sweating, subsiding fever, a sense of relief, and, often, sleep. Between the early paroxysms the infected person may feel quite well; as the disease progresses, however, the patient may be increasingly burdened by symptoms, even in the periods between febrile paroxysms. Although infection by any species may have serious, even fatal, consequences, P. falciparum infection is particularly dangerous because of complications associated with this parasite.

The term malaria, from the Italian mala and aria (“bad air”), was certainly in use in Italy by the seventeenth century to refer to the cause of intermittent fevers thought to result from exposure to marsh air or miasma. Horace Walpole wrote home from Italy in 1740 about “[a] horrid thing called mal’aria, that comes to Rome every summer and kills one.”

There are good reasons for believing that diseases and complaints of various kinds and degrees of severity were as much a part of everyday life in classical antiquity as were the assorted battle wounds and injuries so dramatically portrayed from Homer onward. This is indicated not only by the surviving Greek and Latin medical texts and the fragments preserved in Greco-Egyptian papyri, but also by the large corpus of nonmedical Greek and Latin texts, some of which are still being read today. In poetry, tragedy, and comedy, in history and annals, in philosophy and theology, as well as in botanical, agricultural, and pharmacological texts, illness and health and life and death constitute distinctive motifs.

To be certain, the evidence, both written and nonwritten, has survived in different states of preservation. It permits us, nonetheless, to reconstruct in part the intellectual and technological achievements of our past. Large gaps, however, exist in our knowledge of that past, and the absence of crucial details has led to hypotheses and inferences that cannot be tested directly.

Our knowledge of the diseases of classical antiquity stands somewhere between demonstrative certainty and complete ignorance. There is, after all, a sizable body of Greek and Latin medical texts, and it, in turn, has generated an even larger body of secondary literature. But for all that, our knowledge of the diseases of classical antiquity is far from complete. There are several reasons for its incompleteness, but it is important to keep in mind the enormous differences between the conceptual bases of the modern medical sciences and those of antiquity.

Only because of a great movement in China that has been going on for about 70 years have we been able to review the records of diseases in ancient China and publish them in a Western language. This movement has been closely allied with a revaluation of the practice of traditional Chinese medicine by those who have taken a special training in it. Many valuable works have been written in Chinese on the history of Chinese medical art and science. So far, however, all this material has remained practically unassimilated by sinologists and other Western students of Chinese culture. Thus, for example, most of the dictionary definitions in common use are quite out of date. Among the works that we have used in preparing the present contribution is the brilliant monograph of Yü Yün-hsiu on ancient nosology, or what might be called pathognostics – the recognition and classification of individual disease entities. Western historians of medicine should be aware that the treatise of Wu Lien-te and Wang Chi-min (K. C. Wong and Wu Lien-teh 1932) on Chinese medicine (nearly always the only one they know) may be described as the very small exposed piece of an iceberg, 90 percent of which is “below the surface” (i.e., in the Chinese language and therefore inaccessible to most historians of medicine). Since about the mid-1950s, the study of Chinese medicine has been revitalized; a great number of rare medical books from ancient and medieval times have been republished in photographic form, and some ancient texts have been reproduced in the modern colloquial (pai-hua) style, “translated” as it were from the ancient (ku-wen) style, either abridged or complete.

Parkinson’s disease, or parkinsonism, is a syndrome (i.e., a constellation of clinical signs and symptoms) consisting of four cardinal features: resting tremor, bradykinesia (physical and mental sluggishness), rigidity, and impaired postural reflexes. The diagnosis is made on the basis of finding any three of the four cardinal features.

Distribution and Incidence

This disease occurs throughout the world, with no population protected against the condition. Most surveys have investigated Caucasian populations of northern European or of Anglo-Saxon descent, and few studies have been done on the occurrence of Parkinson’s disease in other populations. In Caucasians the prevalence is 84 to 187 per 100,000 of population, with no geographic patterns and no clusters of increased incidence. Two studies seem to indicate a lower prevalence in blacks; this has been the clinical experience as well, probably indicating a decreased risk of Parkinson’s disease for blacks. The annual incidence varies from 5 to 24 per 100,000 of the white population. These figures, of course, depend on the methods of ascertainment, the population studied, the length of time that data have been collected, and many other factors. If the prevalence is divided by the annual incidence, the average duration of the illness is approximately 10 years.

Epidemiology

Parkinson’s disease usually occurs in late middle life or beyond. The mean age of onset is 58 to 62. Onset before age 30 is rare but is not unknown, and there is a juvenile form of Parkinson’s disease. The greatest incidence is in the decade age 70 to 79 years, with an incidence of 1 to 2 per 1,000 population per year.

Pinta (meaning “spotted”) is also called mal de pinto and carate. It is the least destructive of the treponematoses that are pathogenic for humans. Although the taxonomy of these treponemes is by no means resolved, pinta is sufficiently distinctive to argue for a separate causal species, Treponema carateum. As a specific treponemal variety, it was not described until 1938. The disease is chronic, predominantly affects the skin, and is now found only among isolated rural groups in Central and South America and Mexico, where it is endemic. Local names for the illness are tiña, empeines, and vitiligo.

Distribution and Incidence

According to one historian of treponemal diseases, pinta may have had a considerable world distribution at the end of the Paleolithic period, some 10,000 years ago. However, its past geographic distribution is in some doubt, and an alternative view suggests that it may have evolved purely in Amerindian communities of the New World, as a final level of micro-evolutionary change in the treponematoses there. Because it is not a very destructive condition, and may remain untreated in many individuals of the Third World countries of Latin America, it has been estimated that as many as a million individuals may have the disease.

Epidemiology and Etiology

Pinta is caused by T. carateum, which cannot be distinguished from Treponema pallidum (the causative agent of endemic and venereal syphilis). These treponemes are found mainly in the lower Malpighian layers of the epidermis, and may be present for years before the skin lesions eventually become inactive and depigmented. Large areas may be infected, and the disease may remain infectious for a long period.

Although today, some 200 fungi are established as pathogenic for humans, causing a wide range of diverse mycoses (with an incidence measured in millions and a worldwide distribution), through the mid-nineteenth century, only two human diseases (or rather disease complexes) caused by fungi were generally recognized. These were ringworm and thrush, known since Roman times. Two important additions came at the end of the century: mycetoma of the foot (Carter 1874) and aspergillosis (Lucet 1897; Rénon 1897).

Fungi were the first pathogenic microorganisms to be recognized. Toward the end of the eighteenth century and the opening years of the nineteenth, they had been shown experimentally to cause disease in plants and insects, and during the 1840s both ringworm and thrush were shown to be mycotic in origin. For a short period, fungi were blamed for causing many diseases. Cholera, for example, was attributed to fungi. But with the recognition of the major role played by bacteria (and later, viruses) in the etiology of human disease, fungi were neglected and medical mycology became very confused. It has been only since the 1930s, with the deployment of trained mycologists to work in conjunction with clinicians, that the identity of the pathogenic fungi has been clarified, and studies on their ecology have done much to elucidate epidemiological problems. In general, the geographic distribution of mycoses (which at first tended to coincide with that of medical mycologists) has been established, and the relation of mycoses to other human diseases has been brought into perspective.

Cytomegalic inclusion disease (CID) usually occurs as a subclinical infection followed by periodic reactivation revealed by shedding of the virus. It may be serious in the neonate when infection is transmitted to the fetus in utero.

Clinical Manifestations and Pathology

Cytomegalic infection is characterized histologically by the presence of large cells containing inclusion bodies in the midst of an infiltration of mononuclear cells that may be present in any of the body organs.

In prenatal infections most infants are born without clinical evidence of disease, although some 10 to 15 percent may show microcephaly, retardation of growth or mental development, hepatosplenomegaly, jaundice, and calcifications in the brain. There may be abnormalities in liver function tests and in hematopoiesis. Some 10 to 30 percent of infants with symptomatic disease die in early life. Evidence of involvement of the central nervous system can develop in the early years of life, even though the child may appear normal. The evidence is manifested as impaired intellect, neuromuscular abnormalities, chorioretinitis, optic atrophy, or hearing loss.

Neonatal infection acquired at birth from an infected cervix or later from the mother’s milk usually goes unnoticed but can be identified by the development of antibodies. In addition, respiratory symptoms including pneumonia, as well as petechial rash and enlargement of the liver and the spleen, may occur. In these cases, however, acute involvement of the central nervous system is rare. Infection in children is generally asymptomatic and is evidenced only by the development of antibodies and the shedding of virus. Occasionally hepatosplenomegaly and abnormal liver function are found. There is no proof that pharyngitis occurs at the presumed portal of entry.

Addiction has remained a vague concept in spite of efforts to define it with physiological and psychological precision. The word’s Latin root refers to a legal judgment whereby a person is given over to the control of another. In recent centuries the meaning has ranged from a simple inclination toward an activity or interest to an uncontrollable desire to take opium, which historically was viewed as the most addictive of drugs. Opiate addiction is characterized chiefly by the repeated use of the drug to prevent withdrawal symptoms, which include muscle and joint pains, sweating, and nausea. The extreme discomfort of withdrawal passes away after one to three days, although a yearning for the drug may last for a very long time. Some attempts to define addiction in medical terms (e.g., restricting it to opiate withdrawal phenomena) have led to confusion among members of the public because cocaine, according to that restricted definition, would be considered nonaddictive and, by implication, safer than the Opiates.

For the sake of brevity, this essay considers chiefly opium and coca and their constituents and derivatives. The chemicals that could be discussed range from the barbiturates to lysergic acid diethylamide (LSD), but the models of control and therapy commonly applied to these other substances evolved in the past two centuries from experience with the coca bush, opium poppies, and their powerful alkaloids.

Greece and Rome

Before the fifth century B.C., ancient Greece had physician-seers (iatromantis) who combined magical procedures and drug treatments, and wound healers deft at caring for battlefield trauma. Another group of practitioners were engaged in medical dietetics, a tradition that developed primarily in response to the needs of athletes. Ultimately, it encompassed not only questions regarding exercise, bathing, and relaxation, but the regulation of food and drink for all citizens. All of these traditions eventually merged around 500 B.C. into a techne iatriche, or healing science, that sought to define its own intellectual approach and methodology. For this purpose, the new medicine adopted a theoretical framework capable of explaining the phenomena of health and illness. The new techne was also heavily dependent on clinical observations from which careful inferences and generalizations were derived.

The foremost representative of classical Greek medicine was Hippocrates, a prominent practitioner and teacher who came to personify the ideal Western physician. Within a century of his death in 370 B.C., several unknown disciples wrote nearly 60 treatises, come clinical and some theoretical, on medical subjects differing widely in content and style. This collection of writings, which comprised a comprehensive and rational healing system usually known as “Hippocratic” medicine, emphasized the individual patient. Its practitioners focused exclusively on physical factors related to health and disease, including the immediate environment. Indeed, among the most famous works of the Hippocratic corpus was the treatise Airs, Waters, and Places, an early primer on environmental medicine. Another was Epidemics, a day-to-day account of certain patients, and a third was Regimen, a prescription of diet and life-style conducive to health.

Herpes simplex is caused by Herpes virus hominis, of which there are two distinct serologic types designated as HSV-1 and HSV-2. The first mainly causes disease above the waist, such as cold sores; the second most commonly causes disease below the waist, especially genital herpes. Exceptions to this generalization occur especially among the newborn. The initial active phase is followed by prolonged latency. But the virus can be reactivated by another infection, stress, exposure to sunshine, or any number of other bodily changes.

Etiology and Epidemiology

The herpes viruses are visible in infected cells by electron microscopy and may be grown in the chick embryo, in tissue cultures, and in laboratory animals that react differently to types HSV-1 and HSV-2.

HSV-1 is shed from cells in the lacrimal and salivary glands, and both types are shed from the primary and recurrent lesions of the mucous membranes and skin. Samples of infected adults show that 2 to 4 percent are excreting the virus at a given time.

Infection with the herpes simplex virus results from person-to-person contact. HSV-1 infections commonly are transmitted by oral secretions through kissing or the sharing of eating utensils, and thus herpetic infection can easily be spread within a family. Normally HSV-1 infections are painful and bothersome but have no serious consequences. An exception can be when the virus invades the cornea of the eye. Conjunctival or corneal herpes may produce scars that impair vision. It may occur among wrestlers from skin-to-skin contact. Another form of HSV-1 infection, called herpetic paronychia, may occur in dentists and in hospital personnel.

Africa was long characterized as the “dark continent,” impenetrable, disease-ridden, and dangerous. To many Europeans, Africans personified degeneracy and suffering, and their environment seemed a hothouse of fever and affliction. Europeans had good reason to connect sub-Saharan Africa with disease. For centuries, their attempts to penetrate the coastal fringes of the continent had been effectively frustrated by diseases against which they had little or no resistance (Carlson 1984). In the early nineteenth century, Europeans arriving in West Africa suffered appalling mortality from disease (most often yellow fever and hyperendemic malaria) at rates of between 350 and 800 per 1,000 per annum (Curtin 1968), and the West African coast became known as the “white man’s grave.” With such mortality rates, it is no surprise that Europeans believed that Africa was more disease-ridden than other parts of the world.

In fact, many continue to believe that tropical Africa has a well-deserved reputation as a vast breeding ground and dispersal center for dozens of diseases and thus would subscribe to the recent assertion that “Africa is a sick continent, full of sick and – starving people” (Prins 1989). This view has been reinforced by scientific speculation concerning the appearance of so-called exotic new diseases like Ebola, Marburg, and Lassa fevers in the 1960s and 1970s (Westwood 1980; Vella 1985). The HIV viruses that cause the acquired immune deficiency syndrome (AIDS) are the most recent additions to this list. Recent technological advances, especially in electron microscopy, coupled with the rapidly expanding specialties of molecular biology, genetics, and immunology, have given rise to an equally rapid expansion of virology

Typhomalarial fever as a specific disease is not recognized by medical authorities today, but for the last half of the nineteenth century it was a frequently useful diagnostic category of diverse and often imprecise meaning. Joseph J. Woodward, a U.S. Army surgeon, defined the term during the American Civil War for those camp diseases “in which the malarial and typhoid elements are variously combined with each other and with the scorbutic taint.” Woodward considered the disease “a new hybrid of old and well known pathological conditions,” but one that was distinct, both clinically and at postmortem, from malarial and typhoid fevers.

Distribution and Incidence

William Osier once wrote that typhomalarial fever existed “in the minds of doctors but not in the bodies of patients.” If so, it existed in the minds of many American doctors in the South, Midwest, and western regions of the country as well as in the minds of military and other European physicians practicing in the unsanitary, malarious regions of the globe, particularly the Mediterranean, British India, and some areas of China. It was primarily an Anglo-American phenomenon, although there are a few reports from southern Europe, which indicate that the possibility of the diagnosis was at least considered.

Etiology and Epidemiology

Typhomalarial fever was generally regarded as a noncontagious, infectious disease that resulted from exposure to the atmospheric or environmental infections or toxins that caused malarial fevers and typhoid fevers. Most commonly, patients were previously debilitated, or their vital powers were depressed in some way.

Lactose malabsorption describes a physiological situation. It is the basis for lactose intolerance. The inability to digest lactose is a quantitative phenomenon related to the enzyme lactase and its amount and activity in the intestine. Lactose intolerance, then, is a clinical definition. It involves the concept that the individual is unable to tolerate physiologically the lactose present in milk and other dietary products because of an inability to digest the carbohydrate, due to insufficient activity of the lactase enzyme. Intolerance to lactose as a clinical entity has been recognized for some time. Early in this century, Abraham Jacoby hinted at the existence of lactose intolerance in speeches to the American Pediatric Society; later, in 1926, John Howland, in his presidential address to that same organization, was somewhat more explicit when he indicated that many of the infantile diarrheas were the result of a lack of “ferments” necessary for the digestion of carbohydrate (Flatz 1989).

More recently, interest of physicians and nutritionists in the digestion of lactose stimulated reports during the late 1950s. One by A. Holzel and colleagues (1959) reported on a severe diarrhea associated with the ingestion of lactose in two young siblings who, as a consequence, were “failing to thrive.” Another report, by P. Durand (1958), diagnosed two patients with lactose malabsorption and lactosuria. Since then, innumerable articles and reviews have appeared in the world’s literature (Scrimshaw and Murray 1988). Evaluations of that literature may be obtained by consulting G. Semenza and S. Auricchio (1989), G. Flatz (1989), and N. Kretchmer (1971).