Meningitis is an acute inflammation of the meninges, the membranes covering the brain and spinal cord. The disease is usually the result of bacterial infection, but a number of viruses, fungi, and other microbial agents can also cause it. Meningitis can develop as well from noninfectious conditions such as tumors, lead poisoning, and reactions to vaccines. Meningococcal meningitis, caused by a bacterium, Neisseria meningitidis, is the only form that occurs in major epidemics. Also called cerebrospinal meningitis (CSM), it has been known in the past as “spotted fever,” cerebrospinal fever, typhus cerebralis, and meningitis epidemica. Aseptic meningitis refers to inflammations of the meninges without detectable bacterial involvement. The most common causes are any of a number of viruses.

Etiology and Epidemiology

Many species of bacteria can cause meningitis, but over 80 percent of all cases in developed countries in recent years have been due to only three: N. meningitidis, Hemophilus influenzae, and Streptococcus (Diplococcus) pneumoniae. Other common members of the human bacterial flora such as Escherichia coli and various streptococci and staphylococci can also produce meningitis under special circumstances, as can members of the genera Listeria, Pseudomonas, and Proteus. Meningitis sometimes develops as a complication of tuberculosis.

Aseptic meningitis is usually the result of viral infection. Among the many types of viruses that can be involved are mumps, echovirus, poliovirus, coxsackievirus, herpes simplex, herpes zoster, hepatitis, measles, rubella, and several mosquito-borne agents of encephalitis. Fungi, most commonly Cryptococcus, are other possible agents.

During the Middle Ages (roughly A.D. 500-1500), Europe changed from an agrarian society composed of relatively small and isolated communities to an increasingly commercial and urban world, though still predominantly agricultural. After centuries of static or declining growth in late antiquity, the population of Europe increased approximately threefold between 800 and 1300. Generally, the history of medieval diseases reflects these demographic and economic facts. While the ancient diseases of pneumonia, tuberculosis, and smallpox, and others including typhoid, diphtheria, cholera, malaria, typhus, anthrax, scarlet fever, measles, epilepsy, trachoma, gonorrehea, and amebiasis persisted throughout our period, many diseases of Europeans during the early Middle Ages were related to deficient diet.

Improved nutrition in the later Middle Ages led to a relatively larger population. As Fernand Braudel (1979) has emphasized, an increase in population alters all aspects of life, bringing advantages but at the same time threatening the existing standard of living and hope of improving that standard. In addition, it can bring disease. Ironically, the improved nutrition that made possible the growth of population, towns, and trade in the Middle Ages in turn created fertile opportunities for the contagious diseases that ultimately changed the face of Europe.

Nutrition and Disease

A revolution in agricultural techniques in northern Europe has been credited with this remarkable population growth (e.g., White, Jr. 1962). Agrarian methods inherited from the Roman Empire were suitable for the warm, dry lands of the Mediterranean and Near East, but proved inadequate on the broad, fertile plains of northern Europe.

Epidemic typhus fever is an acute rickettsial disease transmitted among victims by the human body louse, Pediculus humanus corporis. Its characteristic symptoms include high fever, prostration, headache and body aches, and a widespread rash that covers the trunk and limbs of the body. Mortality rates in untreated cases vary widely. Broad-spectrum antibiotics provide an effective therapy for the disease.

Because of its association with conditions of human misery, typhus has been known by many names. Jail distemper and its variations – morbus carcerum, gaol fever, and jayl fever – indicate the prevalence of typhus in detention facilities. Ship fever, camp fever, and famine fever reflect the poor hygiene characteristic of travel, of military expeditions, and of refugee populations. The characteristic rash of typhus has elicited other descriptive names, including spotted fever in English, Fleckfieber and typhus exanthematicus in German, typhus exanthématique in French, tifo exantemático and tabardillo in Spanish (the latter meaning “red cloak”), and typhus-esantematico in Italian. Although Hippocrates applied the word typhus, from the Greek word meaning smoky or hazy, to confused or stuporous states of mind frequently associated with high fevers, the word was not associated with the disease as it is currently known until the eighteenth century. After murine typhus was identified, the appellation typhus historique was sometimes applied to the classic, epidemic disease.

Etiology and Epidemiology

Occurring as a natural infection only in humans, epidemic typhus is caused by Rickettsia prowazekii. It is spread from host to host by the human body louse, P. humanus corporis, and less often by the human head louse, Pediculus humanus capitis.

The diseases of early modern Japan (the Tokugawa period) are of particular interest to the history and geography of disease. The Japanese Islands, situated as they are at the far eastern periphery of East Asia, had relatively little contact with the people of other world regions until the late nineteenth century. Historically Japan’s isolation afforded the people some measure of protection from exposure to certain of the world’s diseases, and in the early seventeenth century, the Tokugawa shoguns reinforced this natural protection when they imposed severe restrictions on foreign contacts. They limited official foreign trade to the port of Nagasaki, restricted the number and the nationality of ships that could enter that port, denied mobility beyond the port to the crews of foreign ships, and prohibited the Japanese from going abroad and returning to Japan. These policies were a response, in part, to the unwelcome activities of Westerners who had begun to reach the islands in the second half of the sixteenth century. They remained in effect until a U.S. fleet forced Japan to open its ports to international commerce in the 1850s.

Elsewhere explorers, adventurers, traders, and settlers were circumnavigating the globe, carrying new diseases to previously unexposed peoples, and causing waves of high mortality among the populations of many world regions. By 1850 the increasing volume of international contacts had produced a worldwide system of disease dissemination, but Japan, remaining aloof from world affairs, had also remained largely unaffected by the epidemiological events of the early modern world.

Two categories of fungus poisoning may be distinguished: (1) mycetism, the result of eating poisonous fungi mistaken for the edible variety (which has a long history and a worldwide incidence), and (2) mycotoxicoses, the result of inadvertent ingestion of food containing toxins produced by fungi. The latter, although also of worldwide incidence, has (with the exception of ergotism) been generally recognized only during the twentieth century.

Mycetism

Calamities tend to impress, and the first reference to fungi in the Greek classics is an epigram by Euripides writing about 450 B.C. He was commemorating the death of a woman and her two children, in one day, after eating poisonous fungi. During Roman times, edible fungi were a delicacy, and diverse advice regarding them was offered by several authors such as Horace, Celsus, Dioscorides, Galen, and Pliny. The advice consisted of how to avoid poisonous species, how to render poisonous forms harmless, and how to treat fungus poisoning.

Much of this ancient folklore on precautions to ensure edibility was compiled by the authors of the first printed herbals in the fourteenth and fifteenth centuries, and some has even survived to the present day. It is, however, invariably unreliable because the distribution of poisonous and edible species seems to be random. For example, the esteemed esculents Amanita caesarea (“Caesar’s mushroom,” a Roman favorite) and Amanita rubescens (“the blusher”) are congeneric with Amanita phalloides (“death cap”) and several related species (Amanita pantherina, Amanita verna, Amanita virosa) that have been, and still are, responsible for most fatalities from fungus poisoning in north temperate regions.

Sickle-cell disease is an inherited disorder resulting from an abnormality in the structure of a protein in the red blood cell called hemoglobin. It represents a spectrum of disorders ranging from the full-blown form, sickle-cell anemia, to the carrier state called sickle-cell trait. Also included in this spectrum are several other variant hemoglobin disorders, which all have the sickle hemoglobin. Sickle-cell anemia is the prototype for most molecular diseases and was the first disease to have its cause isolated to a single molecular change in the human genetic structure. This single change is responsible for all of the dramatic physiological changes and clinical events that occur in this disease.

Sickle-cell trait occurs when the individual is heterozygous for the sickle-cell gene and results in red blood cell concentrations of the abnormal hemoglobin (hemoglobin S) of less than 50 percent. It generally does not result in serious illness although this generalization has recently been disputed. In addition to sickle-cell trait, several sickle-cell syndromes occur when hemoglobin S is present in a heterozygous state with other hemoglobin variants – some with similar properties. Common examples of these include hemoglobin C and hemoglobin E.

Distribution and Incidence

Sickle-cell anemia is found in as many as 4 percent of Africans and in 1 percent of black Americans (1 per 500). Upward of 40 percent of Africans carry the sickle-cell trait as compared to 9 percent of black Americans. In some Mediterranean cultures the trait is also present. It is now generally believed that the sickle-cell gene mutation occurred independently in several areas of Africa.

To date, seven immunologically distinct forms of botulinum toxins, labeled A through G, have been identified. Botulism in humans has generally been associated with A, B, E, or F toxins, whereas the C and D toxins have been identified in botulism outbreaks among various animal species, as shown in Table VIII.19.1.

Clinical Manifestation and Pathology

The onset of disease usually occurs within 12 to 36 hours of ingestion of food contaminated with botulinum toxin. Botulism typically presents with an array of distressing signs of motor nerve dysfunction, including double or blurred vision and difficulty with speech and swallowing. The unabated disease progresses to generalized paralysis and death from respiratory muscle involvement.

Diagnosis is confirmed by detecting botulinum toxin in the blood, feces, or wound site of the patient. Depending on the dose of toxin, untreated botulism carries a high fatality rate. Early treatment with antitoxin accompanied by respiratory assistance and other supportive intensive care may be life-saving.

The pathophysiology involves inhibition of release of the neurotransmitter substance acetylcholine at the neuromuscular junction, thus preventing the initiation of the electrical impulse needed for muscle contraction. Electromyography shows a characteristic decrease in amplitude of the evoked muscle action potential in response to an electrical stimulus.

Infant botulism, a condition confined to babies between 2 weeks and 9 months of age, typically presents with listlessness and generalized weakness (“floppy baby”) and has been shown to cause some cases of sudden infant death syndrome (SIDS). It has been associated with ingestion of various processed infant foods–honey in particular–that contain botulinum spores.

Paget’s disease of bone was described as “osteitis deformans,” a “chronic inflammation of bone” by Sir James Paget in an address to the Royal Medical Chirurgical Society of London in 1876.

His original description was masterful and thus has withstood the test of time. Paget’s disease of bone describes an abnormal osseous (bony) structure whereby isolated and sometimes contiguous areas of the skeleton undergo changes leading to clinical deformity for some of those affected. Clinically affected people may have the appearance of enlarged bone, bowed extremities, shortened stature, and simian posturing because the body’s usual system for maintaining strong and healthy bone malfunctions. Normal bone turnover is altered in the affected areas. The resorption process accelerates, and the repair process responds by building a heavy, thickened, and enlarged bone. Although the new bone contains normal or increased amounts of calcium, the material of the bone is disorganized, and the bone is structurally weak. The result may be pain, deformity, fracture, and arthritis.

Distribution and Incidence

The disease appears to have its greatest prevalence in Europe and in regions inhabited by European emigrants such as Australia, New Zealand, and areas of South America. For no apparent reason, the disease is distinctly uncommon in African blacks, Orientals, and inhabitants of India and Scandinavia. Where studied, the incidence ranges between 3.5 and 4.5 percent of the population in high prevalence regions of the world, with a high of 8.3 percent in a part of Lancashire, England, to a low of 0.4 percent in Sweden.

Although the antiquity of the earliest colonists in the Americas remains a controversial subject, human presence is well established by the close of the Pleistocene, approximately 10,000 B.P. (before the present) (Bryan 1978, 1986; Shutler 1983; Fagan 1987). Kill sites and habitation areas, in conjunction with lithic tools and a few human remains, provide convincing evidence for the presence of highly mobile, small groups whose subsistence was based on hunting and gathering of naturally available “wild” resources.

The health of these most ancient American populations, poorly documented owing to a paucity of human remains (Hrdlicka 1907, 1912; Stewart 1946, 1973; Young 1988), can best be inferred by analogy with recent hunting and gathering peoples. In making inferences we must keep in mind that such groups today tend to occupy marginal environments, unlike the often resource-rich ecosystems that attracted early human populations. If we use contemporary hunter-gatherers for our model, then parasitic infections, infections for which insects and animals serve as the primary vectors or intermediate hosts, and traumatic episodes would have been among the primary sources of ill health among the earliest Americans (Dunn 1968; Truswell and Hansen 1976; Howell 1979; Lee 1979; Cohen 1989). Degenerative diseases, neoplasms, and epidemic diseases would have been extremely rare, as would have been chronic undernutrition. Seasonal periods of nutritional stress would, however, have been expected. Thus, health status would have reflec ted the exceptionally close relationship between hunter-gatherers and their environment.

Histoplasmosis is an infection caused by Histoplasma capsulatum, a soil fungus. Exposure occurs by inhalation, and the primary infection is in the lung. The disease is usually benign and self-limited, despite a strong tendency for invasion of the bloodstream during the primary infection. This fungemia seeds reticuloendothelial organs throughout the body. Under favorable conditions, the organism can cause progressive disease in one or in multiple sites, resulting in a wide variety of clinical manifestations.

Distribution and Incidence

H. capsulatum has been isolated from soil of more than 50 countries. It is most common in temperate climates along river valleys and has been found in North, Central, and South America; India; Southeast Asia; and rarely Europe.

By far the most heavily endemic area in the world is the east central United States, particularly the Mississippi and Ohio River valleys. It is most prevalent in the states of Ohio, Kentucky, Indiana, Illinois, Kentucky, Tennessee, and Arkansas. Surrounding states also have many infections.

Infection is almost universal in the most heavily endemic areas. Skin test surveys reveal that over 90 percent of persons living in some counties in the central United States have had histoplasmosis before age 20 (Edwards et al. 1969). Based on skin test surveys, there are probably 40 to 50 million people in the central United States who have had histoplasmosis, and there are several hundred thousand new cases each year. The number of serious infections requiring diagnosis and treatment is very small, perhaps 1 or 2 percent of the total.

The term erysipelas (erythros = red, pella = skin) was used in Hippocratic times (often but not always) to describe classic cellulitis. For the past century or so, however, erysipelas has commonly referred to infection of the derma with a streptococcal organism, usually Streptococcus pyogenes. Infection with a group A, beta-hemolytic streptococcus can produce a painful, red, edematous indurated skin lesion called peau d’orange for its resemblance to the texture of an orange skin. Sharp borders of the infection extend rapidly, dissecting the underlying dermis from the epidermis. Erysipelas usually appears on the face, producing a butterfly rash over the cheeks and nose. The same streptococci that cause erysipelas can also cause scarlet fever, giving both diseases a fairly distinctive age pattern: Erysipelas is much more common among adults who generally escape scarlet fever, which normally attacks the young. The prognosis for untreated erysipelas is especially serious when this infection is secondary to some other insult such as laryngeal infection, or puerperal sepsis. Indeed distinctions are still made among gangrenous erysipelas, erysipelas grave internum (a form of puerperal fever), surgical erysipelas (which occurs after a surgical procedure), and traumatic erysipelas (which begins in a wound).

History

Antiquity Through the Eighteenth Century

Early accounts of erysipelas are often confusing because they lumped purulent and gangrenous afflictions under this rubric. Thus Hippocrates distinguished between “traumatic” erysipelas, which accompanied wounds, and a myriad of other skin lesions that had no known external cause. Galen in turn distinguished between “phlegmon,” including suppurative ulcers and gangrene, and nonnecrotic cellulitis – but viewed both as forms of erysipelas.

Neonatal tetanus is a form of tetanus, an acute toxic illness confined to the newborn. It is characterized as a neurological disease resulting in severe muscle spasms, which can persist for at least a week and commonly results in death. The agent is Clostridium tetani, which usually enters the bloodstream or motor nerves through an infected umbilicus. C. tetani produces two toxins, including tetanospasmin, the extremely potent neurotoxic component causing spasms. This toxin reaches the nervous system and eventually becomes fixed in the ganglion cells of the spinal cord or cranial nerves. Neonatal tetanus differs from numerous other bacterial diseases in that it is not transferred from person to person; instead, C. tetani is found in soil and is introduced into the body through an exposed area. The disease has been known by various names, including tetani neonatoria, trismus nascentium, lockjaw, and the “9-day illness” or “fits” because it normally occurs during the first 9 days of life. Its association with filth and rural conditions means that neonatal tetanus is still common in Third World nations and is one of their greatest public health problems. Mortality rates are high, even with modern treatment, and preventive measures are essential to avoid the disease.

Distribution and Incidence

Neonatal tetanus today is a problem confined primarily to Africa, Asia, and the West Indies, although before the twentieth century, it was global in occurrence. The bacillus, found in soil, water, intestines, and the feces of animals and humans (where it can survive for years if not exposed to sunlight) is ubiquitous.

In conventional terms the standard of living has become practically synonymous with a material standard, and consequently the concept has most often been equated with and measured by per capita income. Yet it can be interpreted much more broadly to encompass the psychological and biological dimensions of human existence (i.e., the quality of life in all of its manifestations). Distinguishing among these components of well-being would not add much that is conceptually meaningful to our understanding of the past if they all correlated positively and perfectly with one another. But recent empirical evidence has tended to show the importance of not conflating them into one concept.

Historians have begun to explore ways to illuminate this issue from another perspective, namely by considering the biological standard of living as an equally valid measurement of human well-being (Komlos 1989). One approach has been to study the health of historical populations, though this avenue is obviously limited by the scanty systematic evidence at our disposal (Riley and Alter 1986). Another approach has been to consider mortality an integral component of welfare and, in fact, to incorporate mortality into the conventional index of the material standard of living (Williamson 1981, 1982; Davin 1988). Yet this attempt to collapse the biological and material standards of living into a single index is vexed by the inherent difficulty of gauging the monetary value of human life.

Still another promising approach, and one with an abundant evidential basis from the seventeenth century onward, is anthropometric history, meaning the analysis of secular changes in human height, weight, and weight for height (Tanner 1981; Fogel 1987; Komlos 1987; Ward 1987; Riggs 1988; Cuff 1989; Floud and Wachter 1989).

Gout is a chronic, intermittently symptomatic disease. It is manifested primarily by small numbers of acutely painful swollen joints that result from an inflammatory reaction to the precipitation of crystals of monosodium urate.

Etiology

The predisposing metabolic factor for primary gout is an abnormally high or rapidly changing concentration of uric acid in the blood. Hyperuricemia may result from an accelerated synthesis of uric acid, or decreased excretory capacity for uric acid in otherwise normal kidneys as a result of unidentified but probably heritable causes. Hyperuricemia leading to secondary gout occurs particularly (1) in diseases of the blood-forming tissues that increase the availability of precursors of uric acid; (2) in kidney failure, which limits the excretion of uric acid; or (3) as a result of medications that either accelerate the breakdown of purine-rich cells (e.g., antineoplastic drugs) or interfere with the renal excretory mechanism (e.g., some diuretics). Dissolved in the serum, uric acid is harmless. However, because of unidentified local circumstances it may leak from capillaries and crystallize. The crystals of monosodium urate elicit the inflammatory reaction, which is the gouty attack, and the microscopic identification of the crystals in synovial fluid confirms the diagnosis. Why this inflammation occurs predominantly in joints, and why much more commonly in some joints (such as those of the feet or in the knee) than in others (such as the hip or those of the vertebral column) are unexplained characteristics.

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.

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.