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.

The historical diagnosis of dropsy – which is now obsolete – indicated simply an abnormal accumulation of fluid; the word derives from the Greek hydrops (water). Alternative or supplementary terms included hydrothorax (fluid in the chest cavity), ascites (which still indicates excess free fluid in the abdominal cavity), anasarca (still used to describe generalized edema throughout the body), hydrocephalus (used until the nineteenth century to indicate excess fluid within the skull), and ovarian dropsy (large ovarian cysts filled with fluid). Edema was often a synonym for dropsy, but it now has additional connotations, and pulmonary edema has been differentiated from hydrothorax. Since the mid-nineteenth century, dropsy has been recognized as a sign of underlying disease of the heart, liver, or kidneys, or of malnutrition. Untreated dropsy was, eventually, always fatal.

Etiology and Epidemiology

The major underlying causes of dropsy are congestive heart failure, liver failure, kidney failure, and malnutrition. Because they were not clearly differentiated before the nineteenth century, a historical diagnosis of dropsy cannot be taken to indicate any one of these alone in the absence of unequivocal supporting evidence, as from an autopsy. However, heart failure was probably the most frequent of the four.

The etiologies of dropsy can be explained most conveniently in terms of fluid balance. One principal force in the maintenance of normal fluid balance is the hydrostatic (or hydraulic) pressure within capillaries. The other major force is oncotic pressure, the normal tendency for sodium or large particles (e.g., proteins) in capillary blood to draw water out of tissues, tissues, much as salt draws water to the cut surface of a raw potato.

The “Q” in Q fever stands for “query,” the designation applied by E. H. Derrick to an acute illness with fever and severe headache of unknown cause occurring in abattoir workers and dairy farmers in Queensland, Australia, in 1935. Despite the discovery of the causative agent, a rickettsia-like organism, this unenlightening name has remained current, although an alternative is abattoir fever. Q fever, occurring in epidemics in military personnel stationed in the Balkans and Italy during World War II, was known as Balkan influenza or Balkan grippe.

Q fever is caused by infection with Coxiella burnetii, previously known as Rickettsia burnetii, and is the sole member of the genus Coxiella, family Rickettsiaceae. It was initially confused with viruses, but though C. burnetii is an obligate intracellular parasite, it has a true bacterial cell wall.

Q fever is a zoonosis of worldwide distribution, and many species of animals, birds, ticks, and other biting insects are natural hosts. In animals, naturally acquired infection appears to be asymptomatic so that Q fever is not of any economic significance to farmers. Transmission to humans occurs via inhalation of contaminated dust while infected animals, carcasses, or animal products are being handled; via laboratory accidents; and sometimes via tick bite and the consumption of unpasteurized milk. Asymptomatic infection is common. Illness may take two forms. Acute Q fever is usually a self-limiting febrile flulike illness or atypical pneumonia lasting up to 4 weeks. Untreated, the fatality rate is less than 1 percent. Chronic Q fever may develop months to years later, presenting as endocarditis and/or hepatitis. Endocarditis usually occurs in those with preexisting heart valve disease; untreated, it is usually fatal.

South Asia, also known as the Indian subcontinent, extends from the Himalayas south to form a huge triangle that juts into the Indian Ocean with the Arabian Sea on one side and the Bay of Bengal on the other. India, Bangladesh, Afghanistan, Sri Lanka, the Maldives, and the small Himalayan countries of Nepal and Bhutan are included in this area. South Asia can be divided roughly into three parts, beginning with the triangle-shaped Deccan Plateau, moving north to the fertile plain along the Ganges and Indus rivers, and finally extending to the northernmost section at the foot of the Himalayas.

Background: The Ancient Indian Texts

The Ayurvedic Texts

Ancient Indian Medicine had close ties with philosophy and religion. The basic texts of Hinduism are the four Vedas: Rg, Sam, Yajur, and Atharva. Ayurveda, meaning the “science of life,” is considered to be the fifth of these texts and as important as the other four. All of the first four Vedas have sections that deal with healing and the prevention and cure of sickness. Yet the approach is usually magical or by prayer to the deities of the Vedic pantheon.

The Ayurvedic texts, by contrast, are of later origin and tend to attribute disease to divine causes less frequently. The codification of Ayurveda probably occurred around the sixth century B.C., and the texts presumably took their defined forms, in which they are still available, by the sixth or seventh century A.D. They were compiled in the northwestern part of India and in areas that today include Pakistan and Afghanistan, although, with the spread of the Aryans and their culture, Ayurveda came to be practiced over much of the country.

Poliomyelitis is an acute disease caused by inflammation and destruction of motor neurons after infection by a poliovirus. Sensory functions are not affected. Although frequently asymptomatic, the infection may cause fever and a number of other general symptoms, described as abortive polio or minor illness. Occasionally, however, these prodromal symptoms are followed a few days later by infection of the central nervous system (CNS) and fever, with meningitis, or paresis (weakness) or paralysis of one or more muscles. Many patients recover use of the muscle or some muscles affected in the following months, although some have permanent paralysis or paresis. When the muscles of respiration are affected, death may follow.

Other enteroviruses of the ECHO (Enteric Cytopathic Human Orphan virus) and Coxsackie groups may also cause meningitis and paresis, or temporary paralysis. In the past, cases of abortive polio and those with paralysis who later recovered were often included in statistics as polio cases. Today, only cases with paralysis or paresis after 3 months are recorded as paralytic polio.

Poliomyelitis was known by several names until the 1870s, when it became known as acute anterior poliomyelitis. Among them was Heine–Medin disease (after two early researchers, Jacob von Heine and Karl Oscar Medin) and infantile paralysis because it affected mainly young children. As more adults and older children were affected, poliomyelitis – inflammation of the gray marrow – became the name of choice and is often shortened to polio.

Acute diarrheal illness can be defined as the sudden onset of the passage of a greater number of stools than usual that show a decrease in form. It is generally accompanied by other clinical symptoms such as fecal urgency, tenesmus, abdominal cramps, pain, nausea, and vomiting. In most cases the symptom complex is a result of intestinal infection by a viral, bacterial, or parasitic enteropathogen; occasionally it is secondary to ingestion of a microbial exotoxin.

Distribution and Incidence

Acute diarrhea is often hyperendemic in certain populations: infants and young children in developing tropical countries of Latin America, Africa, and southern Asia; persons traveling from industrialized to developing regions; military populations stationed in or deployed to tropical areas; and toddlers who are not toilet trained and are attending daycare centers. Diarrhea rates in children less than 5 years of age in developing countries range from between three and seven episodes per child each year. The rate of diarrhea for non-toilet-trained infants in day-care centers in urban areas of the United States is comparable to the rate of illness seen in Third World countries. Travelers’ diarrhea occurs in 20 to 40 percent of persons visiting high-risk areas from regions showing low disease endemicity. The rate of diarrhea occurrence in infants and young children under 5 years of age in the United States is approximately 0.8 to 1.0 episode per child each year. In all populations, acute diarrhea occurs less commonly in older children and adults than in infants.

Etiology and Epidemiology

The ultimate source of most of the enteric pathogens is infected humans, although for selected pathogenic organisms (i.e., Salmonella, Giardia), animals may serve as a reservoir.

Sudden unexplained death syndrome (SUDS) occurs when a relatively young healthy person, usually male and Asian, dies unexpectedly while sleeping. The victim has no known antecedent illnesses, and there are no factors that might precipitate cardiac arrest. At autopsy, no cause of death can be identified in the heart, lung, or brain. Postmortem toxicologic screening tests reveal no poisons. A sudden fatality during sleep in a previously healthy member of an ethnic group subject to SUDS, but whose death is not investigated with an autopsy, is defined as a presumptive case of SUDS.

Distribution and Incidence

SUDS has occurred in the 1980s among Southeast Asian refugees and immigrants in the United States, mainly among Laotians, Hmong, Kampucheans, and Filipinos. In Asia, SUDS has been described in the Japanese and Filipino medical literature and is also observed in refugee camps in Thailand. In 1983 the death rate ascribed to SUDS in the 25- to 44-year age group of Laotian and Hmong males in the United States, 87 per 100,000, was comparable to the sum of the four leading causes of natural death among other U.S. males in that age group. The incidence of SUDS has decreased since 1983, and there is evidence that the longer a refugee has been in the United States, the lower the risk.

Epidemiology

The first comprehensive report of SUDS in the United States was published by the Centers for Disease Control (CDC) on December 4, 1981; it described 38 victims, all Southeast Asian refugees. All but one of the cases were males: 25 Hmong, 8 Laotian, 4 Vietnamese, and 1 Kampuchean.