Tetanus is an acute disease caused by the production of a neurotoxin, tetanospasmin, by a bacterium, Clostridium tetani, when the spores of the organism enter a wound, and develop into the toxin-producing vegetative form. The case-fatality rate averages 50 percent in adults and is higher in neonates (especially those in developing nations) and in patients over 60 years of age.

Etiology and Epidemiology

C. tetani is an obligate anerobe, a spore-forming, gram-positive motile rod. The terminal spore caused the organism to be called the “drumstick” rod. The protein toxin, tetanospasmin, blocks acetylcholine release at the motor end-plates. The toxin travels up the nerve trunks, as well as fixing directly on nerve cells. The spinal cord is the primary target organ, with chromatolysis of the motor neurons and inhibition inhibition of antagonists accounting for the spasm and rigidity that characterize the disease. Toxin fixation to central nervous system neurons may lead to seizures; involvement of the sympathetic nervous system may evoke vascular irregularities.

Humans may be considered accidental interveners in the life cycle of the organism, which is a soil saprophyte and a harmless inhabitant of the intestines of many herbivores. The organism requires a wound to invade mammals. Traumatic, surgical, dental, umbilical, burn, and cosmetic wounds are the most common causes of infection in humans. “Skin popping” of addictive drugs, insect bites, and nonmedical abortions are less common causes of infection. As an obligate anaerobe, the organism can reproduce and produce toxin only when local oxidation-reduction processes reduce tissue oxygen to near zero; deep, infected wounds are thus ideal culture media.

Infections of the middle ear and mastoid encompass a spectrum of potentially serious medical conditions and sequelae. Decreased hearing from ear infections may have a lifelong impact on speech, learning, and social and vocational development, causing these conditions to remain a major health concern. Because of the anatomic relationship of the middle ear and mastoid to the middle and posterior cranial compartments, life-threatening complications may occur.

Classification

Inflammatory diseases of the middle ear and mastoid are categorized according to the underlying disease process and location:

1. Acute suppurative otitis media (AOM) is characterized by obstruction of the eustachian tube, allowing the retention and suppuration of retained secretions. AOM is the medical term associated with, most commonly, the acute ear infection of childhood. Generally the course of this infection is self-limited, with or without medical treatment, and the retained infected secretions are discharged through either the eustachian tube or a ruptured tympanic membrane.

Acute coalescent mastoiditis can result from failure of these processes to evacuate the abscess. Coalescence of disease within the mastoid leads to pus under pressure and ultimately dissolution of surrounding bone. This condition may require urgent surgical evacuation because the infection is capable of spreading to local and regional structures.

3. Otitis media with effusion (OME) is an inflammatory condition of the middle ear in which serous or mucoid fluid accumulates. Both AOM and OME are precursor conditions to tympanic membrane retractions and perforations. Ongoing eustachian tube dysfunction predisposes to persistent retained secretions in the ear and recurrent acute attacks of otitis media. A small percentage of these patients develop a chronic tympanic membrane perforation which, in most cases, allows eventual aeration of the middle ear and mastoid air-cell spaces and resolution of the underlying disease process.

4. …

Anemia, an insufficiency of red blood cells (RBC) and hemoglobin for oxygen-carrying needs, results from a variety of disease processes, some of which must have existed since ancient times. It was defined in quantitative terms in the mid-nineteenth century, but before that the evidence of anemia is found in the descriptions of pallor or in the occurrence of diseases that we now know cause anemia. For example, lead poisoning decreases RBC production and was apparently widespread in Rome. Intestinal parasites cause iron deficiency anemia and were known to exist in ancient times. Parasites found in paleopathological specimens include Ascaris lumbricoides, Trichiuris trichiuria, and various species of Taenia (ovis, globosa, solium, and saginata), all of which can cause intestinal blood loss and anemia. Diphyllobothrium latum, which leads to malabsorption of vitamin B12 and a megaloblastic anemia, has been found in mummies in Prussia and Peru.

Congenital abnormalities in RBC metabolism, including glucose 6-phosphate dehydrogenase (G6PD) deficiency and various forms of thalassemia and sickle-cell disease, were probably present also in ancient times. Thalassemia protects against malaria, and the incidence of the relatively mild, heterozygotic form of thalassemia (thalassemia minor) probably increased in the Mediterranean region after the appearance of falciparum malaria, the most fatal form of the disease.

The history of disease in modern South Asia has been dominated by epidemic diseases. Smallpox, cholera, and malaria, along with plague and influenza, figured prominently among the leading causes of sickness and mortality in the region for much of the period from the eighteenth to the mid-twentieth centuries. The recent decline or disappearance of several of these diseases has correspondingly resulted in a marked fall in overall levels of mortality.

Although the statistics are unreliable in detail (with perhaps a quarter or more of all deaths passing unrecorded), the broad trend is clear. From a peak mortality of nearly 50 deaths per 1,000 inhabitants in British India in the late nineteenth and early twentieth centuries, mortality rates were roughly halved by the 1950s, declining from 42.6 per 1,000 in 1901–10 and 48.6 in 1911–20, to 36.3 in 1921–30, 31.2 in 1931–40, and 27.4 in 1941–50 and 22.8 in 1951–60. In 1966–70, the figure was 15.3 per 1,000. The fall in infant mortality over the same period further confirms this trend. From an annual average of 212 deaths per 1,000 live births between 1911 and 1920, infant mortality in India fell to 176 in 1921–30, 168 in 1931–40, 148 in 1941–50, and 113 in 1966–70 (Davis 1951; Chandrasekhar 1972).

Mortality Levels

The reasons underlying this fall in mortality (and the earlier high levels of mortality) have been much debated. Kingsley Davis (1951) argued that India became “the home of great epidemics” only during the period of British rule (1757–1947), when it was “exposed to foreign contact for the first time on such a great scale.“

Anorexia nervosa is a psychophysiological disorder especially prevalent among young women and is characterized by prolonged refusal to eat or to maintain normal body weight, an intense fear of becoming obese, a disturbed body image in which the emaciated patient feels overweight, and the absence of any physical illness that would account for extreme weight loss. The term anorexia is actually a misnomer, because genuine loss of appetite is rare, and usually does not occur until late in the illness. In reality, most anorectics are obsessed with food and constantly struggle to deny natural hunger.

Clinical Manifestations and Pathology

In anorexia nervosa, normal dieting escalates into a preoccupation with being thin, profound changes in eating patterns, and a weight loss of at least 25 percent of the original body weight. Weight loss is usually accomplished by a severe restriction of caloric intake, with patients subsisting on fewer than 600 calories per day. Contemporary anorectics may couple fasting with self-induced vomiting, use of laxatives and diuretics, and strenuous exercise.

The most consistent medical consequences of anorexia nervosa are amenorrhea (ceasing or irregularity of menstruation) and estrogen deficiency. In most cases amenorrhea follows weight loss, but it is not unusual for amenorrhea to appear before noticeable weight loss has occurred. The decrease in estrogens causes many anorectics to develop osteoporosis, a loss of bone density that is usually seen only in postmenopausal women (Garfinkel and Garner 1982).

Glomerulonephritis, an immunologic disease of the kidneys, affects the glomerulus. This structure, a cluster of capillaries, is the filter in the functioning unit of the kidney, the nephron. Inflammation, initiated by immune complexes (defined below), injures the glomerulus. Often the disease is acute, but it may be silent and completely undetected until signs and symptoms of chronic kidney failure prompt a biopsy, leading to diagnosis. Alternatively, this silent disease may prove fatal, and the diagnosis is made at autopsy.

The urine-secreting structure (nephron) (Figure VIII.60.1) consists of the glomerulus and its tubular system. Each glomerulus consists of a tangle of interconnecting capillaries branching between two tiny arteries (arterioles). A glomerular cross section shows these capillary loops (Figure VIII.60.2). The glomerulus is a blood filter that controls passage of molecules through the basement membrane, depending on their size and charge. Normally red blood cells and albumin are not permitted to pass through the membrane. The tubules reabsorb, secrete, synthesize, and excrete solutes and metabolites, thereby maintaining physiological equilibrium.

This article will deal only with poststreptococcal glomerulonephritis. This disease, described by Richard Bright in the early part of the nineteenth century, still bears his name. Other forms of glomerulonephritis, which he also described, and the glomerular diseases termed glomerulopathies, seen in diabetes or amyloidosis, are not discussed.

Distribution and Incidence

Glomerulonephritis occurs worldwide. The disease was seen frequently in Europe during the eighteenth and nineteenth centuries as a complication of scarlet fever during epidemics. Today glomerulonephritis occurs sporadically. Several epidemics have occurred since the 1950s in the United States, Trinidad, and Venezuela.

Osteoporosis is defined as a proportional decrease of both bone mineral and bone matrix, leading to fracture after minimal trauma. It differs from osteomalacia in which there is a normal amount of bone matrix (osteoid) but decreased mineralization. There are two clinical syndromes of osteoporosis. Type I, or postmenopausal osteoporosis, occurs in women aged 51 to 75; it involves primarily trabecular bone loss, and presents as vertebral crush fractures or fracture of the distal radius. Type II, or senile osteoporosis, occurs in both men and women, particularly after the age of 60; it involves trabecular and cortical bone loss, and more commonly presents with hip and vertebral wedge fractures. Postmenopausal osteoporosis is associated with decreased serum levels of parathyroid hormone and a secondary decrease in activation of vitamin D, whereas senile osteoporosis is associated with a primary decrease in activation of vitamin D and increased parathyroid hormone.

Osteoporosis is an enormous public health problem, responsible for at least 1.2 million fractures in the United States each year. Fractures of the vertebral bodies and hip comprise the majority, and the complications of hip fracture are fatal in 12 to 20 percent of cases. Nearly 30 percent require long-term nursing home care. The direct and indirect costs of osteoporosis in the United States are estimated at over 8 billion in 1989 dollars annually.

The existence of a hereditary tendency to excessive bleeding was recognized in the second century A.D. by Rabbi Judah, who exempted from circumcision the son of a woman whose earlier sons had bled to death after this rite. But only in this century has expanding knowledge of the physiology of hemostasis – the arrest of bleeding – made evident the diverse nature of inherited bleeding disorders. In addition, only recently has it been recognized that a tendency to thrombosis might likewise be due to an inherited hemostatic defect.

Physiology of Hemostasis

The mechanisms by which blood loss in mammals is stopped after vascular disruption are complex. Small vascular injuries are sealed by platelets that adhere to the site of damage, where they attract other circulating platelets, so as to form an occlusive aggregate or plug that can close small gaps. Larger defects in vessel walls are occluded by coagulation of blood – that is, by its transformation from a fluid to a gel-like state. Uncontrolled bleeding and its antithesis, thrombosis (the formation of a clot within a blood vessel), are important pathogenetic factors for human disease, including a large variety of hereditary disorders.

The basic structure of both the occlusive clots that halt blood loss and pathological intravascular clots (or thrombi). is a meshwork of fibrous protein (fibrin) that entraps blood cells. Plato and Aristotle both described the fibers found in shed blood. When the blood vessel wall is disrupted, whether by trauma or disease, a soluble plasma protein, fibrinogen (factor I), is transformed into the insoluble strand of fibrin.

Relapsing fever is a disease characterized by the occurrence of one or more relapses after the primary febrile paroxysm has subsided. Various types of relapsing fever are caused by blood parasites of the Borrelia group. There are two chief forms of the disease: the endemic, transmitted to humans by various ticks of the genus Ornithodoros, and maintained among a variety of rodents; and the epidemic, caused by a parasitic spirochete, Borrelia recurrentis, which is transmitted by human head and body lice. B. recurrentis is less virulent than the tick-borne forms. Under favorable conditions, mortality is about 5 percent, but in times of distress, as in war or famine, it can reach 60 to 70 percent.

It is also known as famine fever and tick fever, and in the past as yellow fever, because of associated jaundice. The term “relapsing fever” was first used by David Craigie of Edinburgh in 1843. The disease was often, and frequently is still, confused with malaria and typhus, whose symptoms are similar.

Etiology and Epidemiology

Tick-borne relapsing fever is normally contained within the relationship between tick and rodent host; human beings become affected only when they accidentally become involved in that relationship. For example, if human shelters such as log cabins attract rodents, they may in turn become tick habitats. Transmission of relapsing fever is through the infected saliva or coxal fluid of the tick, making it essentially a disease of locality. In the case of louse-borne relapsing fever, the only reservoir of B. recurrentis is human beings, despite the fact that the disease is spread by lice, either in the bite, or by contact with the body fluids of the louse through scratching.

Rubella (German measles; 3-day measles) is a common, acute, viral infectious disease, principally of children and young adults, with worldwide distribution frequently characterized clinically as a mild rash illness. Inapparent infection is common and may occur in as many as half of infections. Rubella has special significance when a pregnant woman contracts the disease in early pregnancy because fetal infection can ensue and result in developmental abnormalities known as the congenital rubella syndrome (CRS). Rubella is a vaccine-preventable disease, but the vaccine is not yet widely used on a global basis.

Etiology and Epidemiology

Rubella is caused by the rubella virus, which is in he genus Rubivirus of the family Togaviridae. Rubella virus is 50 to 60 nanometers in diameter and contains a single-stranded RNA genome.

Rubella is a highly contagious disease transmitted by contact of susceptible individuals with the nose and throat secretions of infected persons, primarily by droplet spread. Infection also occurs by direct contact, by indirect contact through freshly soiled articles, and by airborne transmission. There is no reservoir for rubella other than human beings, which means that a continuous chain of susceptible contacts is necessary to sustain transmission. The period of communicability is from about 1 week before rash onset to at least 4 days after. There is no carrier state except for infants with congenital rubella, who may shed virus for many months after birth. Rubella’s incubation period from time of exposure to onset of rash is 16 to 18 days, with a range of 14 to 23 days.

In the inscriptions that record the divinations of Shang dynasty China (eighteenth to eleventh centuries B.C.), we find a number of diagnostic queries like this: “Divining this tooth affliction. Should we hold a festival for Fuyi?” Fuyi refers to a Shang ancestor, and the concern about a propitiatory festival reflects the belief, frequently voiced in the oracles, that sickness arises from the anger and envy of ancestors toward their descendants (Hu 1944; Miyashita 1959). If the welfare of the dead depended on the rituals of the living, the resentments of the dead were something to which the living remained ceaselessly vulnerable.

Disease thus first appears in China embodied in dangerous others, as a menace from without. After the Shang dynasty, the focus of concern would broaden and shift from disgruntled ancestors to parasites and poisons, demons and witchcraft spells. But whomever or whatever the Chinese accused of inspiring sickness, the defining feature of the earliest conceptions of disease was their independence from a conception of the body. In other words, the peculiarities of an individual’s somatic condition were no more relevant to understanding a fever or a toothache than they were for explaining why one’s crops were destroyed in a storm. The fact that an affliction happened to attack the body was incidental. The vengeful spirits that brought sickness could just as easily have inflicted drought and famine.

This accounts in part for why a collection of cures such as the Wushier bing fang (Recipes for fifty-two ailments) of the late third century B.C. tells us so much, on the one hand, about noxious demons and the techniques for exorcizing them and teaches us so little, on the other hand, about the afflicted body itself (Harper 1982).

This form of pneumonia is caused by Pneumocystis carinii, a protozoan of uncertain taxonomic status in the class Sporozoa. An extracellular parasite of the lungs of humans, dogs, rodents, and other mammals, the organism occurs worldwide. It appears to be of low virulence and almost never causes disease except in weak or immunosuppressed individuals. P. carinii was discovered in guinea pigs in 1909, but human disease was first recognized in the 1940s in malnourished and premature infants. Patients suffering from leukemia, Hodgkin’s disease, and other immunosuppressive diseases, or organ transplant recipients and other patients whose treatment requires suppression of the immune system, are also vulnerable to infection. In the early 1980s, pneumocystis pneumonia achieved prominence as the most common opportunistic infection afflicting patients with acquired immune deficiency syndrome (AIDS). Over half of all AIDS victims suffer from this form of pneumonia, and it frequently is the proximate cause of death.

Transmission is usually by airborne droplets, although transplacental passage resulting in fetal death has been reported. Latent infection may be common, with clinical disease and droplet transmission developing only in weakened hosts. The parasite damages the alveolar walls and induces an abundant foamy exudate and fibrosis. Death results from asphyxiation due to the exudate. Although initial response to chemical therapy is common, treatment is difficult because of side effects of the drugs and the debilitated state of the patients.

We can consider the ecology of disease to be the sum total of all the influences on pathogens and their hosts and, because of the interdependence of the two for disease expression, the internal structures and systems of both that bear upon a disease question. Thus we are clearly considering a structure of relations whose complexity surpasses all comprehension. Such may also be said of a single disease. No one has yet fully defined all that constitutes the expression of even one disease, and such an explanation would be its ecology. To describe the disease ecology of Europe is a task at first so daunting as to admit no possibility. Still, there are a few aspects of the ecology of disease in Europe that can be described, if without claim to completeness or ultimate value, at least with an eye to creating a target for more detailed studies and criticism.

With such cautions in mind, I should like to offer a few general comments on human disease and its expression, and then set forth a very limited number of aspects of the totality of my subject, which I feel can be discussed. For most of the sojourn of humankind on Earth, we have only skeletal remains upon which to build any concept of disease in the past. Even after the advent of agriculture and the earliest civilizations, we have little upon which to develop a coherent view. General trends are perceptible in classical times, and very sketchy numbers can be offered for population in the late medieval period.

World War II reduced the Southeast Asian economies, already weakened by the Great Depression, to their lowest levels in modern times. Warfare itself accounted for much of the destruction, particularly in Burma and the Philippines, where the Allied forces resisted longest and returned soonest. When the British retreated from Burma they blew up railways and refineries as they withdrew, and the American liberation of the Philippines employed massive concentrations of naval and aerial firepower; these operations probably accounted for most of the physical destruction in those two countries. By the end of the war Burma had lost all its oil refineries, 90 per cent of its boats, and 85 per cent of its locomotives (along with most of its rolling stock and bridges), while 70 per cent of its roads and most of its docks and factories were severely damaged. As one scholar put it, ‘both in internal transport and external trade, Burma was thrown back a century, without warning or previous preparation’. The Philippines was scarcely better off; much of the damage occurred during the 1945 liberation of Manila, in which the country’s industrial and modern services sectors—factories, ware houses, power plants, radio stations, telephone exchanges, newspapers, hospitals and universities—had been concentrated. By the end of the battle, the city was 80 per cent destroyed.

Seagoing trade made Southeast Asia a fertile meeting ground from early history, and at the close of World War II Landon aptly characterized the region as a ‘crossroad of religion’. He emphasized that up to then imported religions had been subordinated to ancestral spirit cults which were grounded in relatively autonomous villages, and noted that even the Westernized élites had adapted modern ideas with in a world-view shaped by local traditions. In the same breath he suggested that the middle of this century marked a turning point because the closing years of colonial rule and the disruptions of the war had definitively shaken the foundations of local life. Despite the range of changes since then, the region remains a site of encounter between deeply held and widely divergent world-views. A rich tapestry of ancient local traditions is still sustained with remarkable force, and significant communities derive their practices from all of the major world faiths in many of their forms. The diversity, vitality and depth of religious commitments with in the region combine so that it remains an especially rich laboratory for the exploration of religion.

The region is filled with vibrant ritual enactments, such as those in Hindu Bali, and many people routinely enter altered states through ritualized trance, as in Malaysia’s annual Thaipusam festival, touching realms of consciousness which are remote for most people in industrialized societies. Meditation practices of Javanese syncretic mystics and the Theravāda forest monastries counterpoint orthodox Islam and ritual Buddhism. Vigorous communities of new Christians exist alongside animists and some, mainly in urban contexts, who live without knowing religious meanings.

This part of the work deals with Southeast Asia between the late eighteenth century of the Christian era and World War II. The opening chapter, which is in a sense complementary to the closing chapter of the previous volume, describes and endeavours to account for the incorporation of most of the region within the frontiers of European empires. Subsequent chapters describe the political structures, the economic and social life, and the religions and popular culture of the region. A final chapter includes a discussion of nationalism and nationalist movements.

In the previous phase, Spanish and Dutch realms had been established in maritime Southeast Asia. By the end of the nineteenth century, only Siam (Thailand) stood outside the formal empires of external powers. Those powers sought to avoid conflict among themselves by settling the frontiers of their territories. In so doing they took more or less notice of the previous history and present condition of the lands and peoples over which they claimed authority. Yet the frontiers had a degree of rigidity unusual in Southeast Asia.

Chapter 1 describes this outcome. It also endeavours to describe the process by which it was reached, and in particular to take account of the role within it of the rulers and peoples of Southeast Asia as well as the Europeans. Within the emerging framework, there was further interaction in many fields of human endeavour. This is in a sense the subject of the subsequent chapters in this part, which also pursue lines of investigation that parallel chapters in the first volume. Chapter 5, too, deals with the emergence of nationalism within the colonial framework. The statecraft of the imperial period came under challenge.

Writing about recent history can be an incautious exercise. The closer the past gets to the present, the more insecure it is for the historian. The natural instinct is to withdraw from the present, which is precariously perched on the edge leading to the future, and find that comfortable distance between the writer and the brink. The aim is to gain the security that is often professionally called ‘perspective’. From the historian’s point of view, the trouble with the contemporary past is that it is still happening and there are no reliable records (‘primary sources’) to cite. Equally problematic is the possibility that the people described in the narrative may still be alive, and writing about living personalities can be notoriously insecure for the historian. Another dilemma is the fact that readers— fellow historians and others—bring to bear on that same narrative their own experiences and interpretations.

Couple these built-in disabilities in writing contemporary history to a description of the political structure of the independent states of Southeast Asia and there will emerge a veritable nightmare. So much needs to be discussed. So many themes can be presented. It is like a Balinese painter at work. He tries to depict as much as possible so that the canvas is completely covered, including the corners. The viewer then faces the task of relating the numerous features to each other. Very often, especially to the uninitiated, the end product merely registers as a patchwork of colours and shapes with no discernible message.