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).

Anthrax is an acute zoonotic disease, primarily of herbivorous animals, which is transmissible to human beings. The causative organism is Bacillus anthracis, often referred to in earlier, and especially in French, texts as bactéridie, the name first bestowed on it by Casimir Davaine in 1863. Humans are infected only secondarily through contact with animals or animal products, and thus the disease in human beings must be considered in relation to anthrax in animals.

The species of domestic animals most commonly affected are cattle, sheep, and goats; pigs, dogs, and cats are less susceptible. Since an enlarged spleen is a classic observation in animals with anthrax, the disease has also been known as splenic fever or splenic apoplexy. In humans the cutaneous form is known as malignant pustule, and the pulmonary or intestinal, industrial type, as woolsorters disease or industrial anthrax. In French the equivalent of splenic fever is sang de rate, in German Milzbrand; other French synonyms include charbon and pustule maligne.

Etiology and Epidemiology

Because B. anthracis produces resistant spores in suitable soils, the disease has long been endemic in many areas throughout the world, with a majority of the outbreaks occurring in Europe and Asia. The Americas, Africa, and Australasia are less affected. Once contaminated with anthrax spores, an area can be extremely difficult to clear, as has been demonstrated on the island of Gruinard off the west coast of Scotland, which was experimentally contaminated during World War II. This is of prime importance for the eipdemiology of the disease because it is rarely spread directly from animal to animal, but almost always through ingestion of contaminated food, either by grazing or, in cooler climates, through imported winter foodstuffs.

Lupus erythematosus (LE) is a clinical syndrome that has multiple, but largely unknown causes. It exhibits an extremely broad spectrum of symptoms, and it can range in severity from being potentially fatal within a few weeks to eliciting minor indolent symptoms which, prior to immunologic testing, are virtually undiagnosable. When limited to the skin, it is called discoid lupus erythematosus (DLE); when the viscera are symptomatically affected, it is termed systemic lupus erythematosus (SLE). The inciting causes activate immunologic mechanisms that mediate the pathological, predominantly inflammatory, tissue responses.

History

Medical use of the term lupus has been traced to the fifteenth century, when it designated a variety of cancer. The term was reintroduced by London physician Robert Willan in 1808 to designate cutaneous tuberculosis, particularly when it affected the face. Cutaneous tuberculosis eventually received the synonym lupus vulgaris. In 1851 P. L. Alphée Cazenave of Paris used the term lupus erythemateaux to describe the condition that came to be called discoid lupus erythematosus (DLE) by Vienna’s Moriz Kaposi in 1872 (Jarcho 1957). During 1866–70, Kaposi diagnosed this disease in 22 patients and concluded that it was more common and more severe in women. All 3 deaths occurred among his 15 female patients. Although one of these had pulmonary tuberculosis, and cutaneous tuberculosis was common, Kaposi believed that DLE is not related to tuberculosis. Such a causal relationship, however, came to be advocated, particularly by French dermatologists, and remained under discussion until the 1930s. During the 5 years in which Kaposi saw 22 cases of DLE, 279 cases of lupus vulgaris were seen in the same department (Kaposi 1872).

This disease has suffered from variable and confusing descriptions. It is now generally called yaws, although the term framboesia is also still in common use. Although primary, secondary, and tertiary stages of the condition are recognized, further subdivisions have been made that are associated with various alternative terminology.

Yaws is generally considered to be a highly contagious disease in tropical areas of the world, and in populations with limited hygiene. It is characterized in the early stages by variable cutaneous changes, and eventually affects joints and bones. The causal organism is considered to be Treponema pertenue, although the taxonomy of the pathogenic treponemes is in some doubt, and some reclassification may well take place in the near future. An incubation period of up to 28 days is followed by the appearance of the primary lesion, 2 to 5 centimeters in diameter, which develops into granular excrescences at times with lymph node enlargement. Further eruptions take place, which can be characterized by a “waxing and waning” of successive lesions. Single or multiple lesions can eventually develop on the feet (“crab yaws,” “ulcerative plantar papules”) and are some of the most painful and disabling lesions of all. Eventually, in what some would see as a tertiary stage, there can be patchy depigmentation, deep destruction and remodeling of bones, and gangosa (changes to nasopharyngeal structures). The internal organs are not normally involved, and in this respect it contrasts markedly with the sister treponematosis venereal syphilis.

Acquired immune deficiency syndrome (AIDS), first identified in 1981, is an infectious disease characterized by a failure of the body’s immunologic system. As a result, affected individuals become increasingly vulnerable to many normally harmless microorganisms, eventually leading to severe morbidity and high mortality. The infection, spread sexually and through blood, has a high fatality rate, approaching 100 percent. Caused by a human retrovirus known as HIV-1, AIDS can now be found throughout the world – in both Western industrialized countries and also the developing nations of Africa and Latin America.

Although precise epidemiological data remain unknown, public health officials throughout the world have focused attention on this pandemic and its potentially catastrophic impact on health, resources, and social structure. Treatments for the disease have been developed, but there is currently no cure or vaccine.

Etiology and Epidemiology

Beginning in the late 1970s, physicians in New York and California reported the increasing occurrence of a rare type of cancer, Kaposi’s sarcoma, and a variety of infections including pneumocystis pneumonia among previously healthy young homosexual men. Because of the unusual character of these diseases, which are typically associated with a failure of the immune system, epidemiologists began to search for characteristics that might link these cases. AIDS was first formally described in 1981, although it now appears that the virus that causes the disease must have been silently spreading in a number of populations during the previous decade. Early epidemiological studies suggested that homosexual men, recipients of blood transfusions and blood products (especially hemophiliacs), and intravenous drug users were at greatest risk for the disease.

Disease Patterns Before A.D. 1000

The prevalence and distribution of diseases in sub- Saharan Africa have been determined by the natural environment, indigenous living patterns, and the interrelationships between African peoples and newcomers from other continents. The spread of agriculture since about 3000 B.C.; the extensive commercial contacts with the Moslem world from about A.D. 1000, and with Europe since the fifteenth century; and the establishment of colonial rule in the late nineteenth century - all have had important consequences for health conditions in Africa.

There is little evidence about the disease environment confronting Africans until fairly recent times. Literacy dates back to only about A.D. 1000, and then only in Ethiopia and some areas of the savanna zone just south of the Sahara desert. Written accounts of conditions on parts of the western and eastern coasts begin with the Portuguese voyages of the fifteenth and sixteenth centuries, but literary information on most of the vast interior is not available until well into the nineteenth century. Serious medical data collection really began with the colonial period, but even today knowledge of disease incidence and prevalence is far from adequate.

Africa south of the Sahara is a vast area with many different ecological zones. Besides the Sahara itself, there are extensive desert regions in the Horn of northeastern Africa, and the Kalahari in Namibia and Botswana in the southwestern part of the continent. Tropical rain forest prevails along most of the west coast, in the Zambezi valley of Mozambique, and in large areas of western equatorial Africa, including much of Gabon, Congo-Brazzaville, and northern Zaire. Forest, however, covers only about 10 percent of the land area.

The inflammatory bowel diseases (IBD) – ulcerative colitis and Crohn’s disease – constitute a group of disorders of the small and large intestine whose causes and interrelationships remain obscure (Kirsner and Shorter 1988). Their course is acute and chronic, with unpredictable remissions and exacerbations, and numerous local and systemic complications. Treatment is symptomatic and supportive. The economic drain imposed by these diseases in terms of direct medical, surgical, and hospitalization expenses, loss of work, and interrupted career development is enormous. The emotional impact upon the patient and upon the family is equally substantial. In these contexts, the inflammatory bowel diseases today are one of the major worldwide challenges in medicine.

Ulcerative Colitis

Clinical Manifestations, Pathology, and Diagnosis

The principal symptoms of ulcerative colitis are rectal bleeding, constipation early (in ulcerative proctitis), diarrhea usually, abdominal cramping pain, rectal urgency, fever, anorexia, fatigue, and weight loss. The physical findings depend upon the severity of the colitis, ranging from normal in mild disease, to fever, pallor from loss of blood, dehydration and malnutrition, and the signs of associated complications. X-ray and endoscopic examinations demonstrate diffuse inflammation and ulceration of the rectum and colon in 50 percent of patients, and the adjoining terminal ileum. Ulcerative colitis begins in the mucosa and submucosa of the colon (the inner bowel surface); in severe colitis the entire bowel wall may be involved. The principal histological features are the following: vascular congestion, diffuse cellular infiltration with polymorphonuclear cells, lymphocytes, plasma cells, mast cells, eosinophils, and macrophages; multiple crypt abscesses; and shallow ulcerations. Chronic ulcerative proctits is the same disease as ulcerative colitis, except for its restriction to the rectum and its milder course.

East Asian scholars have begun only recently to examine Chinese, Korean, and Japanese sources for evidence of the history of disease in East Asia. Research is at a very early stage: There is much that we do not know, and some of what we think we know may turn out to be wrong. At present, scholars disagree about basic facts as well as about how to interpret them. It is possible, however, to discuss how disease ecologies changed as East Asian civilization developed, and this essay will consider how long-term historical change in East Asia altered the disease ecologies of this major world region.

East Asia is a large ecological niche bounded on all sides by less hospitable terrain. To the north and northwest lie the vast steppe lands of Central Asia and the virtually impossible Takla Makan Desert. To the west lie the high Tibetan Plateau and the Himalayan Range with the world’s highest mountains. To the south is the mountainous terrain of southwest China and the jungles of Southeast Asia. And to the east lies the Pacific Ocean. These formidable barriers and the great distances between eastern and western Eurasia long separated East Asia from the ancient civilizations of the West, and permitted a distinctive culture to develop and to spread throughout the region with relatively little influence from the outside.

East Asia can be divided into two major ecological zones. The northern zone encompasses the steppe and forest lands that lie north of China’s Great Wall and today includes the modern regions of Inner Mongolia and Manchuria.

Rickets and osteomalacia are diseases with multiple etiologies primarily related to abnormal metabolism of vitamin D and secondarily to calcium and phosphate metabolism. Of the many causes, by far the most important relate to dietary vitamin D deficiency and the activation of vitamin D precursors by the kidney and sunlight. Rickets and osteomalacia are characterized pathophysiologically by a failure of normal mineralization of bone and epiphyseal cartilage and clinically by skeletal deformity. Rickets occurs in growing infants and children, and both bone and epiphyseal cartilage are affected. Osteomalacia occurs in adults after closure of the epiphyses, and its manifestations are often much less prominent.

History

Historically, rickets was among the earliest diseases to be described. As early as 300 B.C., Lu-pu-wei described crooked legs and hunchback; however, these can occur with other disorders. More specifc references are found in the separate writings of three Chinese physicians of the seventh and eighth centuries A.D., including enlarged head, body wasting, pigeon breast, and delayed walking. By the tenth century, Chien-i, the Father of Chinese pediatrics, described many cases of rickets (Lee 1940).

In the second century A.D., Soranus of Ephesus mentioned characteristic deformities of the legs and spine in young children and remarked on the higher frequency in urban Rome compared to Greece. Slightly later, Galen’s work included a description of skeletal deformities in infants and young children, particularly the knock-knee, bow leg, and funnel-shaped chest, and pigeon breast seen in rickets. Sporadic and somewhat ambiguous references to the disease were made until the mid-seventeenth century, when the classic descriptions of Daniel Whistler and Francis Glisson appeared.

Onchocerciasis is caused by a filarial nematode, the roundworm Onchocerca volvulus. Humans are infected by larval microfilariae transmitted by bloodfeeding female flies of the genus Simulium. Symptoms include skin damage, extreme itching, and ocular lesions, which can lead to permanent blindness. Synonyms include river blindness in West Africa, sowda in Yemen, and enfermedad de Robles in Latin America.

Distribution and Incidence

Onchocerciasis is widely distributed in Africa south of the Sahara, especially in the savanna grasslands from Senegal to Sudan. Its range extends southward into Kenya, Zaire, and Malawi. The region encompassing the headwaters of the Volta River system in northern Ghana, northeastern Ivory Coast, southern Burkina Faso (Upper Volta), and adjacent territories has been a major center for the disease. Onchocerciasis was almost certainly indigenous to Africa, but it has been transmitted by the slave trade to the Arabian Peninsula (Saudi Arabia and Yemen) and to the Caribbean basin, where scattered foci exist in Mexico, Guatemala, Colombia, Venezuela, Ecuador, and Brazil. The disease has a patchy distribution within its range; infection rates in particular villages may range from zero to virtually 100 percent. In the 700,000 square-kilometers of the Volta Basin region alone, the World Health Organization estimated that in the early 1970s, about 1 million of the 10 million inhabitants were infected, with about 70,000 classified as “economically blind.” In northern Ghana alone, surveys in the early 1950s determined that about 30,000 people, roughly 3 percent of the population, were totally blind because of onchocerciasis. In some West African villages, adult blindness rates of from 10 to 30 percent have been observed. Conversely, dermatologic symptoms predominate in Arabia, and ocular involvement is rare.

During the first 200 years of European exploration and settlement of the Americas, native populations experienced catastrophic die-offs from the introduction of acute infectious diseases. Pinpointing which parasites were responsible for this decimation is not a simple matter. European knowledge of the infectious disease process was primitive in the sixteenth and seventeenth centuries, with the result that conquerors, settlers, and clergy were ill-prepared to describe the illnesses they witnessed. Statements that simply describe the death experience of native peoples are the most common. In the Roanoke documents of 1588, for instance, T. Hariot described native death from disease, but he attributed the outbreaks to witchcraft:

Multiple sclerosis is a disease of the central nervous system characterized clinically by recurring episodes of neurological disturbance which, especially early in the course of the disease, tend to remit spontaneously, although as time goes by there is often a gradual accumulation of disability. The course of the disease is quite variable, at one extreme lasting for 50 years without the development of significant disability, and at the other terminating fatally in a matter of months. Overall, about one quarter of patients remain able to work for up to 15 years after the first recognized clinical manifestation, and the mean duration of life is approximately 25 years from that time. Nevertheless, because the disease commonly affects young adults and produces disability in the prime of life, the economic burden is heavy, in the United States averaging $15,000 per annum per family with a member afflicted (Inman 1983 data, cited in McDonald and Silberberg, eds. 1986, 180).

Overview

Multiple sclerosis is a remarkable disease. It was first clearly described more than 120 years ago in a way which we would recognize as a modern, pathologically based account that discusses the clinical features of the illness and their possible pathophysiology (Charcot 1868). It is only since the early 1970s, however, that real progress has been made in understanding its nature, course, and pathogenesis. It was discussed in treatises on pathology by R. Carswell (1838) and J. Cruveilhier (1835–42), and more knowledge was added by E. Rindfleisch (1873), but the French school did most to delineate the disease.