The major forms of urolithiasis consist of either upper tract stones within the kidneys or ureters (renal stones) or lower tract stones formed within the bladder. These two forms of urolithiasis have distinct differences in etiology, chemical composition, and epidemiological features, and should therefore be considered two separate diseases.

Historical evidence has shown a striking increase in incidence of renal stone disease in more developed countries over the past 100 years. There has been a simultaneous decrease in bladder stone incidence, demonstrating an inverse relationship between the two disorders. Changes in the environment have a profound effect on the epidemiology of human diseases. An unusual example of this interplay is the role of dietary change in the shifting epidemiological pattern from bladder stone to renal stone disease.

Etiology

The large majority of bladder stones occur in young boys from rural or impoverished areas. In these regions, the disorder is known as endemic bladder stone disease. Information from both historical and experimental sources points to a nutritional deficiency during infancy or possibly in utero as the major factor in endemic bladder stone formation. Other less common causes of bladder stone are schistosomiasis (producing bladder wall thickening, stricture, and outlet obstruction) as well as obstruction in elderly males from benign prostatic hypertrophy.

Although deficiencies of vitamin A, vitamin B6, or magnesium have been suggested in endemic bladder stone disease, low intake of animal protein in combination with high intake of grain carbohydrate is more important. Indeed, it seems that whereas low animal protein intake in infancy may cause bladder stone, a high animal protein diet provokes renal stones (Robertson 1978).

This disease is generally associated with ergotism, a disease resulting from the ingestion of the ergot fungus that grows on rye. Most authorities assume that the name St. Anthony’s fire refers to St. Anthony the Great, a third-century A.D. hermit and founder of Christian ascetic monasticism. This saint renounced the world for the deserts of Egypt and, according to hagiographers, there combatted the devil numerous times. His visions of the devil took the form of worldly pleasures, seductive women, dragons, banquet tables, and the like. However, St. Anthony of Padua, born in the late twelfth century, may also be connected to the name of the disease. This saint was a noted preacher, popular for his ability to exorcise demons. He was also known for restoring the insane to health, and was credited with miraculously healing an individual whose limb had been amputated.

Supposedly the “fire” part of the name refers to the painful skin infections, gangrene, and neurological disturbances that occur with ergot poisoning. Thus, in France north of the Loire where rye was a traditional staple grain, attributing most cases of mal des ardents to ergotism has seemed reasonable to historians. Sufferers there reportedly lost limbs, attributable to the gangrenous form of ergotism, if they survived both the initial inflammatory process and the generalized famine that accompanied epidemics of the disease. On the other hand, it is also quite possible that erysipelas and other bacterial skin infections were at the root of the symptoms mentioned, for these diseases also flourish under conditions of famine.

Hegel has two books that are called Science of Logic, but neither of them resembles what normally serves as a logic text. Instead of beginning with symbols and rules, they start by talking about “being,” “nothing,” and “becoming.”And the structures of formal inference appear only well into the third and final part, called the “Doctrine of Conceiving.”

Because of this discrepancy between expectation and actuality, many interpreters discount the term “logic” in the title of the two works and discuss their content in terms of metaphysics or, if they are of a Kantian frame of mind, in terms of a transcendental system of categories. Yet Hegel seemed to be serious when he placed them under the rubric of the traditional discipline. The smaller of the two versions, the first part of his Encyclopedia of the Philosophical Sciences (1817), continued to develop through the two subsequent editions of that work in 1827 and 1830. And the larger version was being extensively revised when Hegel died in 1831. The question to be asked, then, is: What did Hegel mean by “logic”?

Arterial hypertension is a condition characterized by abnormally high systolic and/or diastolic blood pressure levels. Systolic and diastolic blood pressure levels are usually estimated indirectly by use of an inflatable rubber bladder to compress the artery in the upper arm. The pressure exerted on the artery by the bladder is registered by a device called a manometer. The level of the blood pressure is a measure of the force exerted against the walls of the artery during each heart beat or pulse. The peak of the pressure wave occurs when the heart beats or contracts (systole) and is called the systolic pressure. The valley of the pressure wave occurs when the heart relaxes (diastole) and is termed the diastolic pressure. Blood pressure is recorded as systolic over diastolic.

Although longitudinal research studies such as the one in Framingham, Massachusetts, and the life insurance industry have noted that even slight elevations of blood pressure are associated with increased risk of premature death, the World Health Organization has recommended that the following blood pressure levels be used to classify adults (blood pressure levels defining juvenile hypertension are under review):

Hypertensive: Greater than or equal to 160 millimeters of mercury (mmHg) systolic and/or greater than or equal to 95 mmHg diastolic.

Normotensive: Less than or equal to 140 mmHg systolic and less than or equal to 90 mmHg diastolic.

Borderline Hypertensive: Between hypertensive and normotensive. The condition is also divided etiologically into two types: secondary and primary or essential hypertension. Secondary hypertension, resulting from some known cause (including diseases of the kidney or the adrenal glands), represents less than 10 percent of all the cases of the disease.

The kind of leptospirosis manifested by severe jaundice was first described as a human disease in 1886 by A. Weil. Named Weil’s disease the following year, the term was meant to designate a distinctive infectious jaundice, and it would not be known until much later that leptospirosis was caused by numerous leptospires that triggered various clinical syndromes. The first of the causative pathogens were independently discovered in 1915 by R. Inada among Japanese mine workers and by P. Uhlenhut and W. Fromme among German soldiers. Leptospira, a genus of the family Treponemataceae, order Spirochaetales, is a fine threadlike organism with hooked ends (see Figure VIII.81.1) that is pathogenic for humans and other mammals, producing meningitis, hepatitis, and nephritis both separately and together. In the past, the disease killed between 15 and 40 percent of those infected. Modern treatment has reduced mortality to about 5 percent. As a zoonosis, the disease is generally maintained in rodent reservoirs.

Etiology and Epidemiology

Leptospires are obligate aerobes and classified serologically as a bacterium, subdivided into two species. One is Leptospira biflexa, which includes the various water spirochetes, whereas the other, Leptospira interrogans, embraces the parasitic strains. The species interrogans (so named because of an appearance like a question mark) is now subdivided by the main antigen into 187 serotypes or serovars. Human leptospirosis generally results from direct or indirect exposure to the urine of infected animals, although it can also be transmitted by handling infected animal tissue, by animal bites, and by the ingestion of contaminated food and water.

Plague has often been used as a synonym for pestilence, which refers nonspecifically to any acute epidemic accompanied by high mortality. But the term also refers to the recurrent waves of bubonic plague punctuating European history from 1348 to 1720. Bubonic plague epidemics occurred when Yersinia pestis, a rodent disease, was communicated to humans through the bite of infected fleas. Humans have exceedingly poor immune defenses to this organism, and within 6 days of infection most victims develop a grossly swollen lymph node, a bubo, signifying the body’s attempt to contain and arrest multiplication of Y. pestis. On the average, around 60 percent of those infected died within a week after the appearance of the bubo. Thus bubonic plague brought high and dramatic rates of mortality when it extended into human communities.

Distribution and Incidence

With the historically ironic exception of western Europe, Y. pestis today occurs naturally throughout the world among the wide variety of rodents and lagomorphs (i.e., rabbits and related species). Some of the more than 300 rodent species affected are relatively resistant to disease from Y. pestis and can survive and reproduce while technically infected by the organism. Y. pestis infects new animals either because fleas transmit it or because the microbe is shed and survives in the protective microclimate of warm rodent burrows. Some literature refers to this part of the plague cycle as “sylvatic” plague, or “enzootic” plague.

Typhoid fever is a systemic infection caused by the bacterium Salmonella typhi, usually manifested by the slow onset of a sustained fever and a variety of other symptoms including headache, cough, digestive disturbances, abdominal pain, and profound weakness. In a minority of sufferers, findings more specific for typhoid fever may be present, such as enlargement of the spleen or liver, or a characteristic “rose spot” rash. Untreated, the illness lasts 3 to 4 weeks; it claims the lives of about 10 percent of those affected and leaves about 2 percent as permanent carriers of the organism. Three-quarters of the world’s population live in areas where typhoid is endemic, and 1 out of every 300 of the world’s population contracts the disease each year. One million persons die of it annually, mostly children.

A variant illness, called paratyphoid fever, has many of the same features as typhoid fever, but is caused by members of the Salmonella bacterial family other than S. typhi. Typhoid and paratyphoid fevers are sometimes lumped together under the term enteric fever.

Etiology

The microorganism responsible for typhoid fever is a member of one of the largest and most widespread families of bacteria on Earth with over 1,700 serotypes recognized. The salmonellae are rod-shaped bacteria that have a cell wall and flagella, which give the bacterium motility.

Salmonellae can colonize the gastrointestinal tract of a broad range of animal hosts including mammals, birds, reptiles, amphibians, fish, and insects. Some types of salmonellae are highly adapted to specific animals; others have a wide range of hosts. Because of this versatility and the enormous consequent animal reservoir, the eradication of all salmonellosis would be essentially impossible.

Beriberi is a disease caused by a deficiency of thiamine, or vitamin B1, that is expressed in three major clusters of symptoms, which vary from person to person. It involves edema, or swelling, of the legs, arms, and face. The nerves may be affected, causing, first, a loss of sensation in the peripheral nerves and, later, paralysis. The cardiovascular system may be involved, evidenced by enlargement of the heart and extremely low diastolic blood pressure. Beriberi may be chronic and so low-grade that it cannot be detected by clinical examination; in its chronic form, it may alternatively result in disability for months or years; or it may be acute and result in death in a few weeks. Until major tissue damage occurs, it is curable and reversible by consumption of thiamine.

The name “beriberi” derives from a Sinhalese word, meaning weakness. As kakke, it has been known in Japan since antiquity and is described in the earliest Chinese medical treatises. The several forms of beriberi have often been considered as separate diseases. In “wet” beriberi, swelling and heart complications occurred, although often with loss of the sense of touch, pain, or temperature. In “dry” beriberi, there was little swelling, but instead a progressive loss of those senses and then of motor control followed by atrophy of the muscles of the paralyzed limbs and a general wasting syndrome. Today it is thought that dry beriberi was partly due to a deficiency of vitamin B2. Shoshin beriberi was a term used to denote a fulminating, or acute form with severe heart complications.

Down syndrome, previously called “mongolism,” is a relatively common condition resulting from the presence of an extra chromosome, number 21, in all the cells of the body. In each human cell, there are 23 chromosome pairs containing basic genetic material that organizes the body’s development and physiological functioning. Each pair has a distinctive size and conformation and can be readily identified on microscopic examination. Chromosome pair number 21 is one of the smaller chromosomes. In Down syndrome there are usually three (trisomy) rather than two number 21 chromosomes (trisomy 21: found in 95 to 98 percent of all cases). In a small number of children with Down syndrome, the extra number 21 chromosome is attached to a chromosome of a larger pair (numbers 13 to 15; translocation Down syndrome–about 2 percent of all cases). In some children with the features of Down syndrome, the extra chromosome is present in less than 90 percent of the cells (mosaic Down syndrome–about 2 to 4 percent of all cases). Down syndrome is the most frequently occurring chromosome abnormality in live-born humans, and is also among the most frequently identified chromosomal abnormalities, representing about 4 percent of all aborted fetuses (Lilienfeld 1969). Down syndrome is usually recognizable at birth as a cluster of physical and neurological abnormalities (see Clinical Manifestations), which develop in a characteristic fashion during the life cycle.

The term tobaccosis in this essay denotes, collectively, all diseases resulting from the smoking, chewing, and snuffing of tobacco and from the breathing of tobacco smoke. They include cancers of the mouth, nasopharynx, larynx, trachea, bronchi, lungs, esophagus, stomach, liver, pancreas, kidney, bladder, prostate, and cervix, as well as leukemia. They also include atherosclerosis of the cardiovascular system – coronary heart disease (with ischemia and infarction), cardiomyopathy, aortic and other aneurysms, cerebrovascular hemorrhages and blockages; renal failure and peripheral vascular disease; emphysema and chronic obstructive pulmonary diseases; peptic ulcer disease and regional ileitis; cirrhosis of the liver; immunological deficiencies and failures of endocrine and metabolic functions; and fetal diseases and perinatal disabilities.

Tobaccosis is the foremost plague of the twentieth century and thus joins the most fearsome plagues that devastated humanity during this millennium such as the Black Death, smallpox, malaria, yellow fever, Asiatic cholera, and tuberculosis. But unlike microparasitic plagues, whose victims experienced pathognomonic disease manifestations within days or weeks of exposure, tobaccosis is an extraordinarily insidious disease entity of long latency resulting from exposure to tobacco for many years or decades and manifested by increased occurrence of any of a broad spectrum of neoplastic and degenerative diseases ordinarily associated with advanced age. Thus, the powerfully malignant nature and magnitude of the tobaccosis pandemic went largely undetected during the first four centuries of its global march; and it is only late in the fifth century of the post-Columbian world’s exposure to tobacco that the extent of tobacco’s depredations is being fully revealed.

Gangrene is the term used by the clinician to describe local death of tissue (necrosis) occurring in the living body. Gangrene implies a fairly rapid process (developing in days) extending over a large visible area (a few to many centimeters) with an obvious inability of the tissues to repair or replace the gangrenous part. Although gangrene can occur in internal organs (e.g., large intestine), it generally refers to a process occurring on the surface of the body. It may involve only the skin, or it may extend into deeper tissues such as muscle or nerves.

Gangrene may be either dry or moist. Dry gangrene describes necrosis of the tissues of the extremities resulting from vascular occlusion, such as occurs in severe arteriosclerosis of the legs. Wet or moist gangrene occurs when bacteria invades dead tissue, producing putrefaction. When the gas-forming group of bacteria is involved, gas gangrene occurs. A gangrene may be dry at first, and be converted to the moist type by invading bacteria.

Clinical Manifestations

In dry gangrene, the arterial supply is gradually cut off and a drying or mummification of the tissues results. There is frequently an absence of inflammation, but pain of varying degree may precede the color changes. The soft tissue slowly and progressively shrinks and the color gradually deepens until the whole area is coal black. Constitutional symptoms may occur but are less severe than in moist gangrene.

The giant intestinal roundworm, Ascaris lumbricoides, is a very common parasite with a worldwide distribution. The adult worms are 15 to 35 cm (6 to 14 inches) long and reside in the lumen of the small intestine. Sometimes, however, they are passed in the feces and, if vomited into the oral cavity, may exit from the host’s mouth or nostrils; thus they have been known to medical observers for millennia. Female worms produce up to 200,000 fertilized eggs daily, which are passed in the feces. Eggs incubate in the soil for at least 2 to 3 weeks to produce an infective larval stage within them. The eggs are very resistant to chemicals, desiccation, and extreme temperatures, but they mature or “embryonate” most rapidly in warm, moist, shady conditions in clay soils. People become infected by eating embryonated eggs in food or water contaminated with feces; or, in the case of toddlers, infection occurs by direct ingestion of eggs with dirt. Poor rural sanitation and the use of human feces for fertilizer obviously favor transmission. Mature eggs hatch in the small intestine, and the larvae then undergo a remarkable series of migrations in the host. They penetrate the intestinal wall and are carried in blood or lymph vessels to the liver and heart, and then the lungs. Here they break out into the air sacs, develop, and molt for about 3 weeks, and then climb up the trachea to the throat, where they are subsequently swallowed to establish themselves as adults in the small intestine.

Tay-Sachs disease (TSD) is the best known of the sphingolipidoses, a group of genetic disorders that includes Niemann-Pick disease, Gaucher’s disease, and others. Specifically, TSD is GM2 (beta) gangliosidosis, an autosomal recessive disease with complete penetrance. Affected individuals (recessive homozygotes) produce virtually no functional hexosaminidase A (hex A), an enzyme necessary for normal neurological development and function. TSD is very rare in most populations, but is, overall, about 100 times more prevalent among Ashkenazi Jews. This indicates that the TSD gene frequency is about 10 times higher in the Ashkenazi Jewish population. Persons with the disease usually show clinical symptoms of neurological degeneration by 6 months of age. Their condition steadily deteriorates, and they seldom live beyond the age of 4 years. There is no cure, but heterozygous “carriers” of the defective gene can be identified by clinical test, and amniocentesis can detect an affected fetus.

History

The British ophthalmologist Warren Tay (1881) first reported some of the early clinical signs of TSD. In the United States, Bernard Sachs (1887) further documented the clinical course and pathology of the disease he later called “amaurotic family idiocy” (Sachs 1896). 1896). It was Sachs who first noted the familial nature of the disease, and its seemingly exclusive occurrence in Jewish families. However, reports were soon made of non-Jewish cases. D. Slome (1933) was the first to survey the literature on the population characteristics of TSD and confirmed the disease’s autosomal recessive mode of transmission as well as the TSD gene’s higher frequency among Jews.

Schistosomiasis (bilharzia), known also by many local names such as “red-water fever,” “snail fever,” “big-belly,”and “Katayama disease,”is an “mmunologic disease”induced by eggs of blood-vesselinhabiting worms of the class Trematoda, genus Schistosoma. These eggs induce an immunologic response after they become trapped in the body organs, especially the liver, gut wall, and urogenital tract.

There are three major human schistosome species: Schistosoma haematobium, which inhabit the veins of the bladder area and whose eggs are discharged in the urine; and Schistosoma mansoni and Schistosoma japonicum, which inhabit the mesenteric veins supplying the intestines and whose eggs are discharged in the feces. In every case, however, the worms may also be found in the liver and portal system. There are also a few other species that can parasitize humans. These include the japonicum-like Schistosoma mekongi from the lower Mekong River basin, and some African schistosomes, such as Schistosoma intercalatum, that normally parasitize cattle and wild animals.

Terminology

The terminology of this disease is very confusing. Theodor Bilharz, the discoverer of the trematode worm responsible for the disease, placed it in the genus Distoma, a broad genus that was soon abandoned as more trematode species were discovered. Numerous generic names were thereafter invented to label the worm, including Schistosoma in 1858 (the name that must stand according to the rules of zoological nomenclature), Gynaecophorus in 1858 Bilharzia in 1859, and Thecosoma in 1860. Before World War II, however, in an understandable desire to honor the name of Bilharz, the disease was commonly called bilharziasis.

Old Diseases

It is very difficult to trace precisely the historical development of particular epidemic diseases in China. First, traditional Chinese medical terminology is based on a system hardly translatable into modern Western terms. Second, not only the concepts of disease, but the diseases themselves have changed, so much so that it is impossible to determine whether an ancient classical term meant the same thing when used in premodern texts, or to find the exact modern counterpart of a disease discussed in old texts.

Only during the second half of the nineteenth century did diseases in China begin to be scrutinized by Western medical practitioners, and as late as the early twentieth century, it was difficult to construct a complete picture because “there were classes of disease that were rarely brought for treatment to modern doctors” (Polunin 1976).

One principal feature of the traditional Chinese medical system (a system that achieved classical form by the second century) that makes it difficult to identify individual epidemic diseases in premodern China is the ancient categorization of both epidemic and endemic diseases along with other afflictions into a large group labeled shanghan (“affection by cold,” although today it is the modern term for typhoid fever). Ge Hong, one of China’s most important early medical thinkers, specified in the early fourth century A.D. that the Shanghan diseases included not only those caused by winter cold but also those caused by spring warmth and by seasonal liqi (epidemic “breath”). However, he conceded that differences among the origins of the three types of diseases were slight and they should therefore be grouped into a single category.

In recent years, occupational diseases have become an area of intense interest to medicine, public health, industry, and labor. Whole new areas of medical and public health specialization have developed since the end of World War II, partly in response to the detection of carcinogens in the workplace, dust in the air that workers breathe, and human-made chemicals that workers touch, taste, or inhale. Black lung (coal workers’ pneumoconiosis), brown lung (byssinosis), and white lung (asbestosis) are three industry-specific diseases that have gained international attention and highlighted the role of occupation in the creation of illness. Laborers as well as physicians have become acutely aware of the dangers posed by substances and materials at work in a host of industries from steel to petrochemicals.

The growing attention to the hazards of the industrial workplace has alerted workers even in “clean” worksites to occupational disease. Physical dangers are posed to office workers by video display terminals, poorly designed furniture, noise, and vibrations. Stress at the workplace is now seen as important in the creation of the modern epidemics of high blood pressure, heart disease, and stroke. The very definition of disease has been altered by a rising popular and professional consciousness of the importance of occupation as a source of illness.

The subject of early (for our purposes, pre–World War II) data on mortality is a vast one, and thus this treatment is quite broad. The emphasis is on identifying classes of data, sources of ambiguity, and general approaches to problems of interpretation. Wherever possible, citations are made to critical surveys of the literature, rather than to the literature itself. Some of the points discussed here can be extended, with appropriate caution and revision, to the equally important, but much less tractable area of early morbidity data.

Protostatistical Populations

There are rich opportunities for studying death and disease in populations for which vital statistics in the modern sense are nonexistent. Primary data sources include faunal evidence obtained by archaeological excavation, epigraphic evidence from funerary monuments, and information contained in parish records and family genealogies. In most cases, however, although these data allow inferences to be made regarding overall mortality among specific and highly localized populations, they contain little information on national-level populations and, with the exception of some faunal evidence, on causes of death. We can address the first shortcoming merely by assuming that the population studied accurately represents the total population, an assumption that is probably robust in very high mortality populations. The second difficulty – the lack of information on causes of death – is irremediable in the main. Furthermore, these data are rarely complemented by accurate population statistics, which are essential for computing rates and probabilities. Because of the dearth of early census data, genealogies and parish records, which provide a link between birth and death records, are especially important for estimating life expectancy (e.g., Henry 1956; Hollingsworth 1964; Wrigley 1968).

The pinworm Enterobius vermicularis (formerly Oxyuris) is a common parasite around the world and is the most prevalent parasitic helminth in developed countries today. Enterobiasis has afflicted and annoyed humans from ancient times; it was known to ancient Chinese, classical, and Islamic writers and was present in pre-Columbian America. Humans are the only hosts. Mature worms, ranging from 2 to 13 millimeters in length, inhabit the cecum and adjacent regions of the large and small intestines. Gravid females migrate out the host’s anus and deposit thousands of eggs on the skin of the perianal region. The eggs mature quickly and are infectious in several hours. Infection by ingestion of eggs from the hands is common, as the worms induce itching and scratching. Eggs are frequently eaten with contaminated food, and, because they are light, they are easily inhaled in household dust. Eggs hatch in the small intestine and develop into mature adults in as short a time as 4 weeks. Retroinfection, when the eggs hatch on the perianal skin and the larvae crawl back into the rectum, is possible but rare. Pinworms are especially prevalent among small children and often become a family affair.

Enterobiasis is rarely a serious disease. Intestinal disturbances, if any, are minor, but pinworms can cause great discomfort, and scratching can lead to secondary infections. Migrating worms occasionally reach the vagina or appendix, but rarely cause serious harm. Rectal itching and consequently insomnia, especially in children, are suggestive of pinworm infection.

The rickettsial diseases are a group of related maladies with common characteristics such as arthropod vectors, obligate intracellular etiologic agents, and similar symptoms, including skin rashes, high fever, and headache. The prototype is classic, epidemic, louse-borne typhus fever. Most other rickettsial diseases were originally described as “typhus-like” and were differentiated from the classic disease during the twentieth century.

Those whose etiologic agents share the Rickettsia genus with the historic disease are murine, or fleaborne typhus, Rocky Mountain spotted fever and other members of the spotted fever group of diseases, and scrub typhus or tsutsugamushi. Two other diseases, Q fever and trench fever, are also known as rickettsial diseases. In recent decades, however, key differences in the clinical manifestations, in mode of transmission, and in the physiology of the etiologic agents of these two diseases have caused them to be placed in separate genera.

Pathological rickettsiae were discovered early in the twentieth century and named after Howard Taylor Ricketts, a University of Chicago investigator, who lost his life in research on typhus in Mexico after several years of fruitful research on Rocky Mountain spotted fever. Although smaller than most bacteria, rickettsiae are visible under the light microscope. Unlike common bacteria, they are obligate intracellular parasites – that is, they metabolize and multiply only inside living cells, a characteristic shared with the viruses. This peculiar combination of traits caused the rickettsiae to be classified for several decades as organisms midway between bacteria and viruses. By the late 1960s, however, research revealed that they were true, if highly fastidious, bacteria.