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The sweating sickness, or sudor anglicus, is one of the great puzzles of historical epidemiology because no modern disease corresponds very well to its principal epidemiological and clinical features. Thus it is a topic that has generated much speculation and debate in the understanding of what caused the five English epidemics attributed to the “Sweat.”
The first description was written in 1486, which indicated that the earliest epidemic occurred (northern England) during June of 1485, where strictly contemporary accounts use the words “plague” and “pestilence” to describe the local mortality crisis (Wylie and Collier 1981). However, Charles Creighton (1891), whom most authors follow, claims that the initial outbreak began later, in London, on September 19, 1485, brought back with Henry VII’s mercenaries from France and Flanders.
Once in London the epidemic displayed some of its most characteristic and consistent features: higher mortality among men than women, peaking during middle adulthood among the economically advantaged, and a sudden, acute fever accompanied by profuse sweating. Its victims generally lapsed into coma and died within 24 to 48 hours. Similar outbreaks have been identified: in 1508, 1517, 1528, and 1551. Oddly, the disease favored Englishmen at home and abroad. In the British Isles, Scots, Welsh, and Irish were spared.
The “Sweat” had no important demographic repercussions, as the numbers affected were always small in comparison to the poxes and plagues of this period. Nonetheless, each recurrence of the disease produced widespread fear (Gottfried 1977; Slack 1979). In 1528-9, the Sweat uncharacteristically extended to Calais and to many German regions, but was clearly associated with severe famine, as well as an epidemic of typhus (petechial fever) and plague.
Arbovirus is a truncated term for arthropod-borne viruses, all of which require multiplication in their vectors for transmission. Arboviruses diseases may be simpler to understand when viewed solely from the position of the end product, which is disease in humans or other vertebrates. The diseases fall into a few recognizable sets: (1) encephalitides; (2) diseases with fever and rash, often fairly benign; (3) diseases with hemorrhagic manifestations, often fatal; and (4) mild fevers, quite undiagnosable except through laboratory study. A common feature of all of these is periodic outbreaks, with dozens, hundreds, or thousands of cases. A second common feature is lack of specific treatment. In addition, only for very few of the diseases do vaccines exist. Possibility of disease control is real, however, and is based on a knowledge of the epidemiology of arbovirus infections in general, the role that vectors play, and the particular features in regard to the transmission of the specific disease in question.
Etiology
Arboviruses, numbering at latest count 512 separate and identifiable agents, are placed in 11 families, with a few as yet unclassified agents. Table VIII. 10.1 presents a listing of family and subfamily groupings, limited to those viruses of major importance in human and veterinary diseases.
It is evident from the table that there is no simple delimiting definition of an arbovirus on a taxonomic basis, or even on a biochemical basis. There are 511 RNA viruses, and then there is African swine fever virus (ASF), a DNA virus. ASF belongs to the Iridoviridae and is the only Iridovirus (so far as is yet known) with an arthropod vector and a vertebrate host.
The name ainhum is derived from a word in the Nagos language of East Africa meaning “to saw.” It describes the development of constricting bands about digits, almost always the fifth, or smallest, toe, which ultimately undergoes self-amputation. Typically the disease is bilateral (i.e., affecting both small toes).
Ainhum is ordinarily a disease of middle-aged black Africans of both sexes accustomed to going barefoot. The disease is common in Nigeria and East Africa, and has been reported less frequently in other tropical areas, including India, Burma, Panama, the Antilles, and Brazil (Burgdorf and Goltz 1987).
Ainhum was noticed frequently among slaves in Brazil and was first described in detail in 1867 by Brazilian doctor J. F. da Silva Lima who also named the disease. Silva Lima’s description is outstandingly accurate, and has not been bettered. In one case he wrote that the toe had taken the shape of a small oval potato; the covering skin had become coarse and scabrous, and very tender to touch. As the disease progressed, wrote Silva Lima, a strong constriction appeared at the base of the toe, and, as the blood flow to the toe was impeded, the bones ceased to exist. In time, spontaneous amputation of the toe occurred (Cole 1965; Silva Lima 1867).
The cause of ainhum is unknown. According to Walter Burgdorf and Robert Boltz, chronic trauma, infection, hyperkeratosis, decreased vascular supply, and impaired sensation may alone or in combination produce excessive fibroplasia, and lead to ainhum. It is an acquired condition, although a hereditary pre-disposition has not been ruled out (Curban and Moura 1965).
Except for the addition of cholera, the diseases of Korea of the nineteenth century and the first half of the twentieth century differed little from the ones prevailing in earlier times. In fact, Westerners who came to Korea in the 1880s and 1890s thought that the illnesses found in Korea were generally the same as those in North America. George W. Woods, for example, a surgeon aboard the U.S.S. Juniata of America’s Asiatic Squadron, reported that he knew of no diseases peculiar to Korea, but he was struck by the almost universal presence of smallpox and malaria. Woods, who spent almost 3 months of 1884 in Korea, was one of the first Americans to visit the peninsula (Bohm and Swartout, Jr. 1984).
Medical missionaries, upon whose observations we rely for much of this essay, tended to believe that Korean medical knowledge was entirely borrowed from China and that the history of real medical work in Korea began in September 1884, when Horace N. Allen of the Presbyterian Mission came to Seoul. Medical missionaries soon realized that foreign doctors could best establish a claim to medical superiority through surgery. Among the operations Allen performed were excision of the ankle, knee, shoulder, and wrist; amputation of fingers, arms, legs, cancers, and tumors; dissection of scrofulous glands; enucleation of the eyeball; treatment of cataract and pterygium; and closure of harelip. One of the most frequently performed minor surgical operations was for fistula. One Western physician, Oliver R. Avison, blamed this apparently common condition on the Korean custom of sitting on the floor instead of on chairs (Avison 1897).
The Arenaviridae are a small group of viruses, containing several of considerable importance as human disease agents. They are listed in the Catalogue of Arthropod-Borne Viruses, not because they are arboviruses but because they have been discovered in large part by arbovirologists, working on details of arthropod-transmitted viruses. Most of the 14 members of the group have rodents as reservoir hosts, but they occasionally infect humans who imbibe or ingest the virus when accidentally consuming rodent-contaminated food and drink, or are otherwise in contact with an environment contaminated by rodent excreta. At least one of the viruses, however, Lassa virus, can pass directly from person to person. This happens particularly in hospital settings. Other Arenaviruses important in human disease are Junin (Argentine hemorrhagic fever), Machupo (Bolivian hemorrhagic fever) from South America, and the virus causing lymphocytic choriomeningitis (LCM). Six of the viruses - Junin, Machupo, Pichinde, Tacaribe, Lassa, and LCMs have infected laboratory workers. (Because Lassa fever is covered elsewhere in this work, it will not be treated here in any detail.)
Virus Morphology, Size, and Structure
Electron micrographic studies of infected cells reveal round, oval, or pleomorphic budding particles with mean diameters of 110 to 130 nanometers. The envelopes, which have spikes, are derived from the plasma membranes of the host cell by budding. The interior contains variable numbers of electron-dense granules measuring 20 to 25 nanometers and resembling ribosomes. These sandy grains gave rise to the name Arenavirus because arena means “sand” (Rowe et al. 1970). The exact composition of this core material and its derivation are as yet uncertain. The virions are enveloped RNA-containing nucleocapsids. The genome consists of two single-stranded RNA molecules (Lehmann-Grube 1988).
Milk sickness, usually called milksick by early nineteenth-century American pioneers, denotes what we now know to be poisoning by milk from cows that have eaten either the white snakeroot or the rayless goldenrod plants. The white snakeroot, common in the Midwest and upper South, is a member of the Compositae called Eupatorium urticaefolium. It is also known as white sanicle, squaw weed, snake weed, pool wort, and deer wort. A shade-loving plant, it is frequently seen growing on roadsides, in damp open areas of the woods, or on the shaded north side of ridges. The rayless goldenrod, Haplopappus heterophyllus, is the cause of the disease in southwestern states, such as Arizona and New Mexico.
Milk sickness has been called variously alkali poisoning, puking disease, sick stomach, the slows or sloes, stiff joints, swamp sickness, tires, and trembles (when it occurs in animals). It is now known as tremetol poisoning after an identified toxic ingredient of the white snakeroot and rayless goldenrod. Tremetol, obtained from the leaves and stems of these plants by extraction with ether, is an unsaturated alcohol with the empirical formula C16H22O3. In consistency and odor, it resembles turpentine.
Distribution and Incidence
Milk sickness was unknown in Europe or in any other region of the world except North America. It appeared in North Carolina as early as the American Revolution near a mountain ridge named Milk Sick. Its highest incidence was in dry years when cows wandered from their brown pastures into the woods in search of forage. As more forests were cleared so that cattle had more adequate pasture, and as fences were built, the incidence of milk sickness decreased rapidly.
Protein-energy malnutrition (PEM) or, as it is still sometimes called, protein-calorie malnutrition (PCM), is a term of convenience that refers to a range of syndromes among infants and children of preschool age in whom manifestations of growth failure occur because of protein and energy deficiencies. In most instances this condition besets those in the less developed world of Asia, Africa, and Latin America, where dietary factors are thought to be a crucial part of the etiology. PEM thereby tends to exclude what is conventionally known as “failure to thrive” in Europe and North America, in which the vast majority of cases result from organic disorders such as cystic fibrosis or congenital heart disease problems and are not so directly associated with diet as such.
PEM is best described in its two clinical versions of kwashiorkor and marasmus. In the former, edema is always present, whereas extreme wasting (commonly defined as below 60 percent that of normal weight for height) identifies the latter. Much of the research in the 1950s and 1960s focused on differentiating between the symptoms and etiologies of kwashiorkor and marasmus, but since then it has become evident that cases purely of one or the other are the exception rather than the rule. The majority display both edema and extreme wasting, plus a variable mix of other symptoms, that have earned them the rather inelegant designation of marasmic kwashiorkor. In addition, far more common than all of the three put together are numerous subclinical syndromes, usually referred to as mild-to-moderate PEM.
In 1628 William Harvey, physician to St. Bartholomew’s Hospital, London, used quantitative, experimental methods to show that the blood must move in a circle, rather than being continuously regenerated as earlier theories had proposed. In addition, Harvey showed that the heart supplies the power to send the blood on its circuit around the body. Harvey’s revolutionary ideas reflected ancient thought about the perfectibility of circular motion as much as they did new ideas about the value of experimental evidence. Nonetheless, in many ways and by most accounts, the year 1628 marks the beginning of current Western ways of looking at the heart and its diseases. However, although Harvey’s demonstration of cardiac physiology in animals seemed logically applicable to human beings, it failed to lead immediately to any dramatic changes in the diagnosis or treatment of human heart disease. Over the next few centuries many people tried to discover what was going on within the thoraxes of patients who showed the debilitating signs of cardiac disease. Their notions about heart disease were reflected in the diagnostic techniques they thought appropriate.
Diagnosing Heart Disease
Physical Diagnosis
During the mid-eighteenth century, Leopold Auenbrugger, working in Vienna, described a new diagnostic technique. By percussing the chest – that is, by striking the chest and both listening to and feeling the reverberation – he was able to tell, to some extent, what lay within. His method enabled him to ascertain the size of the heart and to determine the presence of fluid in the chest, a common manifestation of heart failure.
The dialectical method is pervasive in Hegel's mature philosophy. It governs all three parts of his system proper: the Logic, the Philosophy of Nature, and the Philosophy of Spirit. And it also governs the discipline that he developed as an introduction to this system, the Phenomenology of Spirit (expounded in the book of that name).
Few aspects of Hegel's thought have exerted as much influence or occasioned as much controversy as this method. Yet, paradoxically, it remains one of his least well understood philosophical contributions. The aim of this essay is to cast a little light where there remains much darkness.
It seems to me that three main shortcomings in the secondary literature have hindered a clear understanding of the method. First, most interpreters, if not actually denying that there is such a thing as the dialectical method, have at least characterized it in terms that remain too vague. Second, interpreters have generally made too little effort to explain the method's philosophical motivation. Third, many critics have been too hasty in dismissing the method as guilty of one or more of a variety of original sins that would render it useless in principle, such as violating the law of contradiction.
Japanese B encephalitis is a relatively uncommon disease, even in areas where the infection is endemic. The disease is one of several caused by arthropod-borne viruses (arboviruses); carried by mosquitoes of the genus Culex, this one is a member of the family Togaviridae and genus Flavivirus and thus is an RNA virus. The species of Culex that is the most common insect vector for Japanese B encephalitis is Culex tritaeniorhyncus. The disease was first recognized and described in 1871, and the virus was first isolated in 1935. The infection may appear in epidemic or in sporadic outbreaks, and is carried particularly in swine, but also has been isolated from a variety of birds and from equine animals. The virus is distributed principally in East and Southeast Asia.
Epidemic outbreaks of Japanese B encephalitis, like those of arboviruses in general, tend to occur in regions that are usually dry and arid and, therefore, relatively free of viral activity; such areas may accumulate a large number of individuals who, because of lack of previous exposure, are relatively susceptible. Then with rain and the appearance of conditions favorable to the proliferation of the insect vector, epidemic outbreaks may occur, particularly where there are relatively high population densities of the human host and of the amplifying hosts such as equine or porcine animal species. In addition, there is evidence that for some arboviruses a change occurs in the relative virulence of the infecting strain, which may also account for an epidemic outbreak.
In 1392 Yi Songgye assumed the throne as King T’aejo and the Yi Dynasty (1392–1910) began. His supporters initiated a sweeping land reform program that began with a cadastral survey of landholding throughout the country and the destruction of previous registers of public and private landholdings. New developments in agriculture as well as in science, technology, and medicine followed, stimulating inventions and publications. For example, the agricultural manual called The Art of Farming, compiled in 1430, was based on the reasonable but novel premise that because Korean climate and soil differed from those of China, agricultural methods should be designed to meet the specific conditions found in the peninsula. Improvements in agricultural techniques produced increased yields, and the spread of cotton cultivation provided improved clothing for the common people.
Important developments in medical knowledge took place in the early years of the Yi dynasty, as the government encouraged its study and created two specialized institutions for medical care. One served the royal family and elite officials, and the other was to serve the general population. Candidates who scored well on the “Miscellaneous Examinations” could be employed in the Palace Medical Office, which trained regional medical officials.
The concept that indigenous conditions must be considered was increasingly incorporated into medical as well as agricultural writings. China’s influence on medical philosophy remained strong, but interest in the study and exploitation of Korea’s own traditional folk remedies stimulated the development of independent medical scholarship as may be seen in the Hyang-yak kugup pang (Emergency Remedies of Folk Medicine 1236).
Trematodes or flukes are flatworms of the class Trematoda of the phylum Platyhelminthes. They have complex life cycles that usually involve a snail as an intermediate host. The definitive host that harbors the adult worms, generally a mammal, acquires the parasite by ingesting an encysted form in a second intermediate host or on vegetation. Many species can infect human beings, but most of these are normally resident in other mammals, and humans are just accidental hosts.
Disease ecology refers to the intricate human and environmental relationships that form the context of one or a group of diseases. Diseases are not simply biomedical entities; rather, they have their physical, environmental, sociocultural, psychological, and even political parameters. Distinctive human and biophysical environmental webs form the context of distinctive groups of human diseases. Major changes in this web, whether brought about by human intervention, environmental catastrophes, or a combination thereof, can result in a new context and possibly a new group of diseases. In developing countries, human control of the environment is limited, basic needs of a healthful life are not met, and, therefore, infectious and communicable diseases are the major cause of death. Improvements in health conditions will no doubt reduce the incidence of mortality resulting from infectious diseases and, in turn, bring about the prominence of chronic diseases more closely related to life-styles and life stages than to environmental parameters. South Asia as a geographic region still remains a region of poverty within which there is a marked contrast between the rural and urban genre de vie. Morbidity and mortality patterns in the rural and urban areas are, therefore, likely to be somewhat different, although paucity and quality of data make generalizations hazardous.
Ecologically, South Asia is one of the most distinctive regions of the world. Physiographically well demarcated, and climatically distinguished by the monsoonal rainfall regime, South Asian life has a rhythm marked by seasonality. Although agriculture is still the dominant occupation, rapidly swelling cities create air pollution, overcrowding, social stress, and the immense problem of waste disposal.
Cirrhosis is a chronic hepatic disorder, anatomically characterized by diffuse liver fibrosis and nodule formation. These pathological changes produce the clinical features of portal hypertension and hepatocellular failure. Cirrhosis is the end product of progressive liver injury resulting from many diverse causes including toxins, drugs, viruses, and parasites. The clinical manifestations of cirrhosis vary according to the severity and duration of the underlying disease. In the West, cirrhosis is a major cause of disability and death among middle-aged alcoholic males. In the East and Africa, cirrhosis is predominantly an intermediate lesion in the evolution from chronic hepatitis B infection to primary hepatocellular carcinoma.
Classification
Cirrhosis is classified on the basis of morphology and etiology. The morphological classification recognizes three types based on the size of the nodules:
1. Macronodular cirrhosis. The liver is firm, large or small in size, with bulging irregular nodules greater than 3 millimeters in diameter.
2. Micronodular cirrhosis. The liver is usually enlarged, and very firm or hard in consistency. The nodules on cut sections appear small and uniform, less than 3 millimeters wide.
3. Mixed micro/macronodular cirrhosis. The liver shows groups of small nodules interspersed with fields of large nodules.
The terms “micronodular” and “macronodular” cirrhosis replace the older terminology, Laennec’s and postnecrotic cirrhosis.
Neither the gross nor the microscopic appearance of the liver can alone differentiate among the many causes (see Table VIII.28.1). In individual cases, the etiology is often unknown. Alcohol injury is most frequently associated with the pattern of micronodular cirrhosis, and other causes in this category include primary biliary cirrhosis, primary hemochromatosis, and chronic right heart failure.
A concern with illness has been documented in China for three millennia; the earliest written evidence extant today on the theoretical and practical consequences of this concern dates from approximately the eleventh century B.C. At that time, and for centuries to come, it was assumed that the well-being of the living – be it related to success on the battlefield, to an abundant harvest, or to physical health – depended to a considerable extent on their interactions with the nonliving members of the community (i.e., with their ancestors). An adherence to specific norms was thought to guarantee social and individual health; transgressions were known to cause the wrath of the dead, who then had to be propitiated with sacrifices. The communication between the living and the nonliving that was necessary to establish the cause of an affliction and to identify an appropriate remedy was recorded on bones and turtle shells, many of which were found in the soil, especially in the province of Henan, earlier this century. Whether the belief in ancestral intervention was supplemented by a pragmatic application of drugs or other empirically valuable means of therapy was not documented in written form at this early time.
Political changes during the first millennium B.C., when the Chou dynasty fell into a period of turmoil with several centuries of civil war, may have been responsible for the rise of a new worldview. Even though a belief in the effect of ancestral curses or blessings on the health of the living has survived in Chinese culture well into the twentieth century, especially among some rural strata of the population, Chou sources indicate a change in emphasis.
Chagas’ disease (American; trypanosomiasis, trypanosomiasis cruzi) is an illness of the Americas which can take the form of either an acute, febrile, generalized infection or a chronic process. The cause is a protozoan, Trypanosoma cruzi, which is harbored by both domesticated and wild animals. When it is transmitted to humans by insects, this essentially untreatable disease is associated with fever, edemas, and enlargement of the lymph nodes and can cause dilation of parts of the digestive tract leading to megacolon and megaesophagus as well as cardiac enlargement and failure. In fact, Chagas’ disease is the leading cause of cardiac death of young adults in parts of South America.
Distribution and Incidence
The disease, which probably had its origins in Brazil, is limited to the Western Hemisphere, with heavy concentrations in Brazil, Argentina, Chile, and Venezuela. Cases are also reported in Peru, Mexico, and most other Central and South American countries along with the Caribbean islands and the United States.
Epidemiology and Etiology
T. cruzi, a member of the class Mastigophora, family Trypanisomidae, has over 100 vertebrate hosts including dogs, cats, armadillos, opossums, monkeys, and humans. Unlike other trypanosomes it does not multiply in the bloodstream, but rather lives within various tissues of the host and multiplies by binary fission. It is transmitted by reduvid bugs that ingest the trypanosome during a blood meal from a vertebrate host. The trypanosomes in turn develop in the intestines of the bug, and, while they neither enter its saliva nor are injected when the bug bites, they do pass out in its feces.
Ancylostomiasis, or hookworm disease, is caused by hookworm infection and is characterized by progressive anemia. In 1989, it was estimated that perhaps as many as one billion people, most of them living in tropical and subtropical regions, are afflicted to some extent with hookworm infection, although it is not known how many thus infected can be said to be victims of hookworm disease. It is difficult to define the difference between hookworm infection and hookworm disease because a host whose diet contains adequate amounts of iron may sustain a worm burden without debilitating consequences that would render a malnourished person anemic. A person exhibiting signs of the anemia associated with hookworm infestation, therefore, may be said to have hookworm disease regardless of the number of parasites present. Hookworm disease does not appear on the short list of major causes of death in developing countries, but it should be regarded as an important contributing factor in millions of deaths annually and as a source in its own right of widespread human suffering.
Two species of intestinal nematode, Ancylostoma duodenale and Necator americanus, are the parasites that cause ancylostomiasis. Although they apparently cause the same disease, there are important differences between the two species. A. duodenale is slightly larger, sickle-shaped, with hooks or teeth; N. americanus is smaller, “S” shaped, with shell-like semilunar cutting plates instead of teeth. Despite being named the “American killer,” N. americanus is less pathogenic than A. duodenale, as measured by comparative blood loss. A. duodenale has a higher reproductive rate and a shorter life-span. It is also able to infect the host in more ways than can N. americanus.