Diphtheria is a human disease caused by Corynebacterium diphtheriae, so named for its clubbed shape (Greek: koryne, or “club”) and for the hidelike pseudomembrane (Greek: diphtheria, for “shield” or “membrane”) that forms on the tonsils, palate, or pharynx in severe cases of infection. Although this bacillus may cause no more than an innocent, subclinical infection and can be transmitted via well carriers, during diphtheria epidemics more virulent strains are responsible for case fatality rates ranging from 30 to 50 percent of affected young children. In such circumstances the bacterium itself is infected by a phage virus responsible for the elaboration of a potent exotoxin. Even though the exotoxin can cause rapid fatty degeneration of the heart muscle and peripheral nervous system damage resulting in paralysis, young children often die because the airway is occluded. Both the suddenness of suffocation in children and the capricious emergence of virulent epidemics of diphtheria are important features of historical interest in the disease.

Also called the Klebs-Löffler bacillus in early twentieth-century medical literature, this gram-positive organism is usually spread by respiratory secretions and droplet infection. After a brief incubation period of 2 to 4 days, the bacillus multiplies in the upper respiratory tract, creating a membranous exudate on pharyngeal tissues. The bacillus invades the local tissues and kills cells, causing necrosis and, often, discoloration of the membrane. The foul breath associated with necrosis and the greenish or blackened membrane are hallmarks of the disease to most clinical observers differentiating diphtheria from streptococcal sore throat and from croup.

The Greek historian Thucydides interrupts his history of the Peloponnesian War between Athens and Sparta to describe the following epidemic in 430 B.C.:

Smallpox (variola) no longer is an active infection. Its virus exists only in laboratories. It was an acute viral disease usually transmitted by airborne droplets and entering the body through the upper respiratory tract. It infected as many as 90 percent or more of people at risk. It affected all races, and neither age nor gender seems to have influenced susceptibility directly. There never was a cure, but during its last decades of existence antibiotics were often prescribed to prevent or limit secondary infections. Closely related diseases exist, like cowpox and monkeypox, but smallpox appears to have been an exclusively human infection. Virologists recognized two kinds of smallpox: Variola major, with a mortality rate commonly of 25 to 30 percent; and Variola minor, with mild symptoms and a death rate of 1 percent or less. The characteristics of smallpox viruses varied over the centuries, and strains intermediate in virulence between V. major and V. minor in all probability existed. The worst strains, of course, attracted the most attention, and the recorded history of smallpox is for the most part a history of V. major.

Etiology and Epidemiology

Within the range of recorded history, as far as we know, the source of smallpox was always a human being with the infection. There was no animal reservoir. The virus could survive in scabs for considerable periods, and laundry workers on occasion contracted the disease from clothing and bedding of smallpox patients, but most transmissions were airborne and occurred over distances of no more than a few meters.

Infectious mononucleosis is an acute infectious disease of children, adolescents, and young adults. It is caused by the Epstein–Barr virus (EB virus) and is followed by lifelong immunity.

Distribution and Incidence

On the basis of the populations investigated, it would seem that infectious mononucleosis occurs worldwide but attacks only those persons who have had no EBV antibodies. The virus replicates in the salivary glands, is present in the oropharyngeal secretions of patients ill with the disease, and continues to be shed for months following convalescence. As a lifelong inhabitant of the lymphoid tissues, it is excreted intermittently into the oropharynx.

In the underdeveloped countries it is a disease of childhood, and, since it spreads by contact with oral secretions, crowding and unhygienic surroundings favor its ready transmission. In more developed countries, it strikes especially those of the 15- to 25-year age group and is recognized clinically as infectious mononucleosis. In the United States, on college campuses, the disease is commonly known as the “kissing disease.”

Children of low socioeconomic state almost universally show antibodies to the virus. (In Ghana, 84 percent of infants have acquired antibodies by age 21 months.) In a worldwide prospective study of 5,000 children and young adults without EB virus antibodies, 29 percent developed antibodies within a period of 4 to 8 years. Among susceptible college students the annual incidence of the disease is about 15 percent.

Streptococci are responsible for many common and not so common human and animal diseases. Streptococcal pharyngitis, scarlet fever, impetigo, erysipelas, neonatal meningitis and sepsis, puerperal sepsis, and bacterial endocarditis all follow infection with streptococci. In addition, some streptococci provoke two peculiar postinfectious conditions: acute rheumatic fever and acute glomerulonephritis. Rebecca Lancefield (1933) divided streptococci into distinct serologic groups, labeled A, B, C, D …, each with a number of separate subgroups. In addition to these groups, microbiologists further classify streptococci on whether and how they hemolyze red blood cells (alpha: incomplete or green hemolysis; beta: complete or clear hemolysis). According to this tradition, the streptococcus responsible for pharyngitis is known as a “group A beta-hemolytic streptococcus.” Another member of the genus Streptococcus is the Streptococcus pneumoniae, the bacteria responsible for pneumonia.

The streptococcus has a number of biological peculiarities that alter its ability to infect humans. The genetic insertion of a bacteriophage produces a toxin responsible for the rash of scarlet fever. A group of proteins, known as the M protein, renders the streptococcus impervious to the normal bodily defense of phagocytosis. Hemolysins and enzymes, when present, help the streptococcus to invade the host. One can speculate that this potential biological variability is responsible for the abrupt changes that streptococcal illnesses have made in the past (Gallis 1984).

Streptococcal illness can be extremely common. Few have escaped streptococcal pharyngitis or superficial impetigo of the skin. Alternately, some forms of streptococcal illness are rare. An example is streptococcal endocarditis. Most streptococcal diseases are spread through respiratory droplets.

The knowledge of acquired resistance to disease and the practices connected with it are very old. Ancient medical systems of both East and West offered explanations of why no one got smallpox twice and how one might be protected from getting it at all. But the history of immunology as a science began only 100 years ago with the experiments of Louis Pasteur.

This history falls into two distinct periods, roughly before and after World War II. It begins with a fanfare, with the production of protective vaccines and antisera, probably the earliest example of truly effective medical treatment. The great theoreticians of the period were biochemists, investigating the chemistry of antigen and antibody and the nature of the antigen–antibody reaction. The part played by blood cells in the body’s defenses had been in the foreground of discussions before the turn of the century, but it was pushed into the shade by the discovery of the striking therapeutic effects of immune sera.

After World War II, when it became clear that antibiotics could control infections for which there was no serological treatment, interest in immunological methods of treatment waned and focused instead on the cellular biology of the immune process as a part of general biology. A single theory came to unite all of immunology, making possible the striking expansion of the field that took place in the 1970s.

In the past 15,000 years, epochal social and cultural changes have created fundamentally different relationships between humankind and the environment. One of the most important innovations has been the domestication of plants and animals, a major factor in the gradual establishment of agriculture as the world’s predominant economic base. The development of agriculture brought an increase in sedentism, in which human groups lived in more or less permanent communities.

Associated with farming was the domestication of animals and, in some societies, nomadic pastoralism. By about 6000 B.C., animal husbandry provided a relatively widespread and stable source of high-quality protein in the Near East. Moreover, the protein was typically produced in ways that did not compete directly for agricultural land resources. Domestic herds grazed on agricultural land after the harvest (Bentley 1987) or on land that was fallow, marginal, or inadequate for farming.

The greater control that agriculture and the domestication of animals gave people over food production resulted in food surpluses. Surplus food created the potential for the emergence of specialists such as craftsmen, merchants, and a ruler class, which are essential components of urban society, another major social change. Urbanism began in the Near East during the Chalcolithic Age (c. 4000–3200 B.C.) but had its major efflorescence during the Early Bronze Age (c. 3200–2000 B.C.)

The advent of agriculture, the domestication of animals, and the development of urbanism had a significant impact on human health. Although agriculture dramatically increased the calories that could be produced by a given individual, the emphasis on a few cultigens increased the vulnerability of agricultural societies to famine and malnutrition (Cohen 1984a).

Geography and Demography

The islands of Oceania are divided into three large geographic areas. Polynesia occupies an enormous triangle in the eastern and central Pacific, stretching from Hawaii in the north, to French Polynesia and Easter Island in the east, to New Zealand in the west. Melanesia encompasses the western island chains that lie south of the equator and extend from New Guinea to New Caledonia and Fiji. Micronesia includes the groups of islands that lie west of Polynesia and north of Melanesia. Although Polynesia is spread widely across the Pacific, the physical environments – whether volcanic high islands or coral atolls – are all quite similar in being lushly vegetated and almost all rich in food resources from land and sea. Melanesia has the greatest variety of physical environments: mountain rain forests, grassy plateaus, gorges and valleys, low jungles and alluvial plains, mosquito-ridden riverine and coastal swamps, sandy beaches, volcanic fields, and earthquake-prone rifts. In western Micronesia, weathered volcanic islands are interspersed among small, lush coral atolls. Farther to the east (Marshall Islands and Kiribati), the Micronesian atolls are generally much drier and larger. Except for temperate New Zealand and arid or temperate Australia, the climate of Oceania remains generally hot and humid year-round. It is generally accepted that Oceania and Australia were populated by waves of immigrants initially from Southeast Asia (Oliver 1962; Howe 1984; Marshall 1984). In fact, it was over 30,000 years ago that Southeast Asian hunter-gatherers crossed land bridges and narrow channels into New Guinea, Australia, and Tasmania. Intermigration among these landmasses was curtailed around 8,000 years ago, when New Guinea and Tasmania became separate islands.

Acute rheumatic fever is a noncontagious disease characterized by febrile, nonsuppurative inflammation, primarily of articular and cardiac tissues, less frequently affecting the skin and brain. The cerebral manifestation – Sydenham’s chorea – and the superficial manifestations – subcutaneous nodules and erythema marginatum – are limited to children and young adults.

Etiology and Treatment

The disease is caused by infection, most often of the throat, with type A beta-hemolytic strains of streptococcus. Fever, migratory joint pains and tachycardia, the most frequent symptoms, typically begin 1 to 3 weeks after the onset of untreated streptococcal pharyngitis. However, only 0.1 to 3.0 percent of untreated bouts of this infection result in a first attack of rheumatic fever. Consequently, various largely unidentified permissive factors must participate in initiating the immunologic pathogenesis of the disease.

First attacks of acute rheumatic fever can be prevented by timely treatment of the streptococcal infection with penicillin or another appropriate antibiotic, but such treatment does not influence the course of the disease once it has begun. Rheumatic fever recurs only as a result of a new infection with a pathogenic strain of streptococcus. Prophylactic antibiotic treatment diminishes, but does not eradicate recurrences (Taranta et al. 1964). The shorter the interval since the previous bout of rheumatic fever, the greater is the likelihood that a new attack will be elicited. An infection that occurs within 2 years of an attack has a 20 to 25 percent chance of inducing a recurrence. If the first attack does not affect the heart, a recurrence usually spares it as well, but if the heart has been involved, a second bout it likely to result in greater damage (Spagnuolo, Pasternack, and Taranta 1971).

When Hegel presented his lectures on aesthetics in the 1820s, he probably believed that his system of beauty and the fine arts was the most up-to-date and comprehensive of its time. And perhaps he was right. But Hegel himself would have been the first to admit that only in retrospect would a proper assessment of his theory emerge. As we now look back, Hegel's aesthetic theory stands as the product of mutually influencing currents of inquiry within German intellectual life of the early 1800s, the most salient of which was the philosophical effort to comprehend the universe within the contours of an encyclopedic, organically structured thought-system. Under the spell of this hopeful enterprise, Hegel composed his theory of art and beauty as a movement within his comprehensive metaphysical theory. Following the interpretative conventions of the time, he tacitly assumed that his readers would view his aesthetic theory as part of this greater metaphysical symphony - as a reflection and extension of his conception of a dynamic but essentially rational and harmonious universe. Although systematic, Hegel's aesthetics is not self-contained, and it solidly depends upon the presuppositions of his idealistic outlook.

Fasciolopsiasis is caused by the giant intestinal fluke, Fasciolopsis buski. Discovered in 1843, the organism occurs in China, Korea, Southeast Asia, and parts of India and Indonesia. The adult worm, which has a life-span of only 6 months, attaches itself to the wall of the small intestine of humans. Pigs and dogs can also be infected, and sometimes are important reservoir hosts. Eggs produced by the hermaphroditic adults pass out in the feces and, if they reach fresh water, produce motile larvae that penetrate into the tissues of certain planorbid snails. After two generations of reproduction, another motile form leaves the snail, finds a plant like the water chestnut, water caltrop, or water bamboo, and encysts on it. Humans become infected with cysts by peeling raw fruits of plants with their teeth or eating them uncooked. The disease can become very prevalent in areas where these plants are cultivated with human feces as fertilizer.

Mild infections are often asymptomatic, but flukes can irritate and even ulcerate the intestinal mucosa. Abdominal pain, diarrhea, anemia, and fluid accumulation in the abdomen are common symptoms. Extreme cases can be fatal. Diagnosis is made by discovery of the eggs in the feces. Drug therapy is usually effective. Prevention includes better rural sanitation and control of swine reservoir hosts. Cooking vegetables would also be very beneficial, but drastic changes in long-established culinary habits are unlikely.

Foremost among recorded encephalitis epidemics was the global pandemic of encephalitis lethargica that emerged in and from Europe during the last years of the Great War and occurred in successive waves throughout the world during the following decade. Although the diagnosis of encephalitis lethargica is sometimes applied to sporadically occurring cases of inflammation of the brain having a strong lethargic or stuporous aspect, this discussion focuses upon the encephalitis pandemic that accompanied and followed the 1918 influenza pandemic.

Clinical Manifestations and Pathology

Clinically, encephalitis lethargica was characterized by diffuse involvement of the brain and spinal cord, producing practically the entire range of the signs and symptoms of neurological disease. Sometimes occurring in close conjunction with respiratory-spread influenza, but more often after a long interval, encephalitis patients developed an illness usually characterized by the triad signs of fever, lethargy, and disturbances of eye movement, along with a broad range of other signs and symptoms. These included headache, tremor, weakness, depression, delirium, convulsions, the inability to articulate ideas, coordinate movements, or recognize the importance of sensory stimuli, as well as psychosis and stupor. Oculogyric crisis (eyeballs fixed in one position for a period of time) and other disorders of eye movement, the most frequent sign of localized damage to the nervous system, were present in three-fourths of the cases. Lethargy, another common symptom, in some patients lasted only a few days, but in others it persisted for weeks and months or until death from comatose respiratory failure. Not infrequently, spasmodic twitching and severe psychic and behavior changes persisted long after the acute illness.

The nematode Trichuris trichiura, the whipworm or threadworm, is a very common parasite that occurs worldwide but is most abundant in warm, moist climates. It still exists in the southern United States, but it has declined there and in other developed countries in recent decades with improved sanitation; it is now found mostly in poor tropical countries. Adult worms range up to 2 inches in length, so whipworms were probably seen by ancient observers, but they were first clearly recognized by an early Portuguese writer on tropical medicine, Aleixo de Abreu, in 1623. Several scientists described the species in the mid-eighteenth century. Archaeological evidence shows that the worm infected people in the Americas prior to the voyage of Columbus.

Trichuris attaches itself to the wall of the large intestine and passes its eggs in the host’s feces. Eggs require 10 to 14 days in the soil to mature or “embryonate.” Embryonation is most successful in warm, moist soils in shady places. Like Ascaris, which has a similar range, Trichuris infects people who have swallowed embryonated eggs in soil or in contaminated food or water. Unlke Ascaris, however, the whipworm does not require an elaborate period of larval migration in the host. The eggs hatch in the, small intestine, where the larvae spend some time before moving to their home in the cecum.

Trichuriasis rarely causes much harm unless there is a heavy worm load. Severe infections can cause abdominal discomfort, bloody or mucoid diarrhea, weight loss, weakness, and anemia. Masses of worms can cause appendicitis, and prolapse of the rectum can occur in children harboring large numbers of worms.

The liver fluke Fasciola hepatica is usually a parasite of sheep and cattle. “Liver rot” in sheep was described in a French work in 1379, and the first human case was described in 1760. The fluke’s life cycle was discovered in 1881. Fascioliasis is a significant veterinary problem, but human infection is also fairly common. The fluke’s life cycle is much like that of Fasciolopsis buski (Fasciolopsiasis), with people or herbivores infected by eating raw watercress or other plants contaminated by the cysts of the fluke. Adult worms settle down in the bile ducts after a period of wandering in the liver. Mild infestations may cause little damage, but fever, jaundice, and right upper quadrant abdominal pain radiating to the shoulder blade are common symptoms. Bile ducts may become partially or totally obstructed, and liver destruction can be severe.

F. hepatica is cosmopolitan in distribution, with important foci of human infection in southern France, in Algeria, and in South America. Diagnosis is made by examining the feces of symptomatic patients with a microscope to find the eggs. Treatment is generally effective. Prevention is by treating sheep to keep them from perpetuating the cycle, controlling snail intermediate hosts, and keeping domestic animals away from ponds where watercress is grown.

Varicella (chickenpox) is an acute infection of short duration caused by Varicella-Zoster virus (VZV), which is spread in the early stages of disease by droplets of secretions from the nasopharynx. It is followed by lifetime latency that may be broken in occasional patients by reactivation of virus in sensory ganglia manifested as herpes zoster (shingles).

Epidemiology and Incidence

Chickenpox is endemic worldwide, is highly communicable, and commonly appears as epidemics among children who are usually attacked between 2 and 8 years of age. (Infants are protected by transplacental maternal antibodies.) Few escape infection until adult life, and these usually live in isolated rural communities. Probably most of those who have seemed to escape the disease had subclinical infections. (The annual Report of Morbidity and Mortality in the United States shows, for 1984, 221,983 cases of varicella reported from 33 states, an incidence of 138 cases per 100,000 population. The age was known in 28 percent; 56 percent of these cases appeared in the 5- to 9-year age group, less than 6 percent were 15 years of age or older.)

The sporadic reactivation of the virus as shingles is unrelated to exposure to exogenous infection and, in general, is uncommon even in populations in which practically all have had chickenpox. Its peak incidence is after age 50. Of those who develop shingles, only 1 percent have two attacks. Patients with impaired cellular immunity are at risk, and herpes zoster is not uncommon in those suffering from malignant disease.

There is a story told among the Kiowa Indians of North America’s southern Great Plains about the arrival in their midst, in a time long past, of a stranger in a black suit and a tall hat. This missionary-appearing figure is confronted by Saynday, a mystic hero of the Kiowa.

“Who are you?” asks the stranger.

“I’m Saynday. I’m the Kiowa’s Old Uncle Saynday. I’m the one who’s always coming along. Who are you?”

“I’m smallpox.”

“Where do you come from and what do you do and why are you here?”

“I come from far away, from across the Eastern Ocean. I am one of the white men – they are my people as the Kiowa are yours. Sometimes I travel ahead of them, and sometimes I lurk behind. But I am always their companion and you will find me in their camps and in their houses.”

“What do you do?”

“I bring death. My breath causes children to wither like young plants in the spring snow. I bring destruction. No matter how beautiful a woman is, once she has looked at me she becomes as ugly as death. And to men I bring not death alone but the destruction of their children and the blighting of their wives. The strongest warriors go down before me. No people who have looked at me will ever be the same.” (Crosby 1986)

Stories such as this abound among indigenous peoples throughout the world. Sometimes they are simple sayings, as among the Hawaiians: “Lawe li’ili’i ka make a ka Hawai’i, lawe nui ka make a ka haole” – “Death by Hawaiians takes a few at a time; death by white poeple takes many.”

Chiropractic is a system of healing that holds that disease results from a lack of normal nervous function caused by a disordered relationship between the musculoskeletal and nervous systems. Controversial from its inception, chiropractic has grown into the largest nonallopathic healing profession in the United States, with nearly 35,000 active practitioners. Although considered by many a “marginal” group, chiropractors are licensed in all 50 states, are reimbursed by Medicare, Medicaid, and many thirdparty payers, and in 1984 earned an average yearly net income of $55,000. The recent defeat of the American Medical Association (AMA) by chiropractors in a major lawsuit dramatically emphasizes chiropractic’s current strength. The public image of chiropractic has significantly improved, and opposition from medical organizations has abated. Chiropractic has successfully established itself as an alternative healing profession.

At first glance, it seems an unlikely system to have achieved such success. Chiropractic was founded in 1895, just as medicine was being transformed into a dominant profession. Successfully uniting disparate elements of the medical community, the AMA reorganized in the early 1900s and developed into a powerful force, influencing nearly every aspect of the U.S. health care system. The homeopathic and eclectic sects, important mid-nineteenth-century competitors, virtually disappeared during the first decades of the twentieth century. Physicians actively and effectively suppressed competition from patent medicine vendors with pure food and drug legislation. Yet despite the impressive strength of the medical profession, chiropractic thrived. Whereas nearly every other form of unorthodox healing was being suppressed, banned, or co-opted, this system of healing established itself as an independent profession.

Murine typhus is an acute illness characterized by symptoms similar to those of epidemic typhus but milder in character. Unlike its epidemic relative, it is a natural infection of the rat and transmitted sporadically to humans by the rat flea, Xenopsylla cheopis. Its relation to the rat is reflected in the name murine typhus. The etiologic agent is Rickettsia typhi.

Clinical Manifestations

Symptoms and the course of illness in murine typhus are similar to those in epidemic, louse-borne typhus. For this reason, distinguishing between the two diseases has been difficult. The flea-borne illness, however, is almost never fatal, with about a 2 percent mortality in persons over age 50.

Etiology and Epidemiology

Murine typhus is found worldwide and is infectious for persons of all ages (see previous chapter, Map VIII.151.1). Those living or working in areas where rats are abundant are most susceptible. Like epidemic typhus, murine typhus is transmitted mechanically, through rubbing infected feces of the flea Xenopsylla cheopis into a skin abrasion, through the eye, or through mucous membranes of the respiratory tract. In the years following World War II, active campaigns against rats and their fleas with DDT and rodenticides sharply reduced the incidence of murine typhus in the United States. The causative agent of epidemic typhus is known as R. typhi, although some investigators prefer to call it Rickettsia mooseri in honor of Herman Mooser, a Swiss pathologist who, working in Mexico, differentiated between this organism and Rickettsia prowazekii. In guinea pigs, R. typhi causes a characteristic reaction in scrotal cells useful for distinguishing between murine and epidemic typhus.