Infectious Disease

As the agricultural revolution progressed, it promoted population growth and a much greater population density - indeed, a density not known since the decline of Rome in the late empire. This density in turn became the new enemy of population growth in the West. The Near East had long been characterized by a relatively high density of population and urban centers, and consequently the peoples of the region had long been developing resistance to the disease generated in such dense populations. Thus, Europeans who came in contact with the old centers of civilization were at serious risk of developing infection.

Nonetheless, travel to these centers increased throughout the Middle Ages. Simple pilgrimages drew Europeans to the Holy Land as early as the fourth century. Wars of Christian reconquest in Sardinia, Spain, and Sicily reopened the Mediterranean Sea in the eleventh century, and from 1096 to 1271 Crusaders struck out for the Holy Land. Contact with the East stimulated a taste for its products, especially textiles, furs, and spices, and led to the establishment of permanent trade routes, with caravans regularly traveling as far as the Mongol Empire.

This trade contributed to the widespread growth of European cities and the birth of new towns. Overcrowding in poorly ventilated dwellings with thatched roofs and dirt floors, and infested with rats and fleas, provided fertile ground for the spread of communicable diseases inevitably brought in, often from afar.

The water supply in these urban areas was usually dependent on a river, which underwent seasonal variation in volume and was subject to contamination from sewage and refuse. Brewers, dyers, tanners, and other trades people dumped waste into waterways, as did butchers and fishmongers; in 1369 London butchers were ordered to stop polluting the Thames (Talbot 1967). Perhaps the greatest pollution was found in the streets: Household waste was thrown from windows, dead animals were left to decay where they fell, and the entire contents of stables were swept outside.

The absence of good personal hygiene also predis posed the populace to contagious disease. Although physicians prescribed steam, cold, or herb baths, and bathing had a role in rituals such as those performed upon induction into knighthood or on certain feast days (Talbot 1967), baths, partly because of limited water supplies, could not have been as common as they are today, even for the well-to-do. Urban dwellers were undoubtedly better served: Public baths were available in many towns, even for the less wealthy. Country people surely bathed less than town dwellers, and had few changes of clothing. Apparel, predominantly woolen in northern Europe, was relatively expensive and difficult to launder. For rich and poor alike, clothing and hair sheltered lice and fleas, according to medical treatises of the time (Talbot 1967). All of these conditions greatly assisted the spread of contagious diseases.

With population density at a critical level, the last few centuries of the Middle Ages saw the unique social, intellectual, economic, and demographic influence of four contagious diseases - plague, influenza, leprosy, and tuberculosis. The dramatic impact of the Black Death in 1347-50 inspired contemporary accounts as well as subsequent studies, now literally in the thousands. Leprosy has also been a favorite subject for historians. The study of influenza, however, has long suffered from problems of correct identification. And the presence and importance of medieval tuberculosis must be largely inferred.


The incidence of tuberculosis, an age-old malady, is believed to have increased greatly during the Middle Ages, although this is difficult to document. Although excavation of medieval graves has disclosed only a few skeletons showing tuberculosis of the bone, this tells us very little since the disease is known today to affect the bone in only 5 to 7 percent of untreated cases (Steinbock 1976; Manchester 1984).

Tuberculosis is a population-density-dependent illness, and the growth of towns may well have been accompanied by an increase in the disease. Relying on the assumption that a high death rate in the years from 20 to 40 is evidence of widespread tuberculosis, (historically it has ravaged this age group the most), investigators examining skeletons dating from the years 1000 to 1348 in Germany and other areas have concluded that an increase in the disease did indeed parallel urbanization (Russell 1985). Evidence for the importance of tuberculosis in the Middle Ages is provided by the ancient custom among French and English kings of attempting to cure vic tims of scrofula (tuberculosis of the cervical lymph nodes) by touching them. Called the king's evil or the royal disease, this form of tuberculosis was sufficiently widespread to have attracted the attention of the court. According to English records of the king's pence given as alms to the sick, Edward I touched 1,736 victims during 1289-90, 983 during 1299-1300, and 1,219 during 1303-4 (Bloch 1973). In part because of the natural remissions of scrofula (if, indeed, these cases were correctly diagnosed), which were thought to be effected by the God-given powered of the monarch, the practice persisted, in some form at least, into the nineteenth century in France.

No doubt, the design of medieval farm homes, in which cattle and humans were housed under the same roof, contributed to the spread of the bovine tuberculosis bacillus to humans, and thus spread of tuberculosis in Europe. Bovine tuberculosis existed in Po Valley dairy cattle before their introduction to northern Europe in the thirteenth century (Manchester 1984). Crowded conditions in the new towns also increased the diffusion of the disease, for it can spread by droplets produced by sneezing, coughing, and the like.

Tuberculosis is caused by Mycobacterium tuberculosis, which is of the same genus as Mycobacterium leprae, the causative agent of Hansen's disease, termed leprosy by commentators in the Middle Ages.

Exposure to tuberculosis confers an immunity to leprosy. Because tuberculosis was often transmitted to small children by human or cow milk, early immunity to both tuberculosis and leprosy might have been acquired by those who survived the first few years of life. One factor in the late medieval decline of leprosy may have been the concurrent increase in tuberculosis in the densely populated urban centers. Unfortunately, leprosy does not confer an immunity to tuberculosis (Manchester 1984).


Leprosy flourished in Europe during the twelfth and thirteenth centuries, afflicting as much as 1 percent of the populace, according to some authorities. Possibly brought to the West from India with the returning army of Alexander in 327-6 B.C., leprosy traveled across Europe with Roman colonization. Skeletons from fifth-, sixth-, and seventh-century England display clear evidence of lepromatous leprosy in the skull or limbs, with loss of phalanges. Anglo-Saxon England apparently did not segregate lepers, because the bones of victims have been found in general cemeteries (Manchester 1984), but a few lazar houses were established as early as the eleventh century. The disease seems to have reached a high point in England during the first half of the thirteenth century, when 53 hospitals were constructed. In all, some 200 such institutions are known to have been established. By the fifteenth century no new ones had been built, and by the sixteenth century the disease had nearly disappeared from England.

The pattern in other European countries was similar. In the twelfth and thirteenth centuries almost every Italian town had a leper house outside its walls. France was said to have had 2,000 leprosaria in the thirteenth century. Medieval Denmark had 31, and in the cemetery of the leprosarium of St. Jorgens in Naestved, Denmark, 650 patients were buried between 1250 and 1550 (M0ller-Christensen 1969).

The Third Lateran Council in 1179 directed that lepers be segregated from the rest of society, and that separate churches and burial places be provided for them. Great differences in the stringency of rules among communities existed, varying from clement care to the burning of live victims. Typically, a ceremony was conducted over a male leper in which he was declared to be "dead unto the world, but alive unto Christ." As the leper stood in a grave, a priest threw earth over him (Brody 1974). He, in fact, lived on, but he was dead in the eyes of the law, and his heirs inherited his possessions, though divorce was usually not permitted. Bishops or abbots endowed leprosaria with income from tithes, rents, and tolls; and in parts of Europe — northern Italy, for example -lepers were under civic control. A leper house usually lodged 6 to 12 people, but might be built for one victim alone. Such community efforts to prevent the spread of the disease were no doubt motivated by terror of the dire symptoms of leprosy, despite widespread ecclesiastical declarations that the illness was caused not by mere exposure to the disease but by divine punishment for lechery and other sins. Though the mechanism of contagion might be unclear, medieval Europe was ready to be empirical. Lepers were provided with cloaks and bells and ordered to keep their distance on penalty of death, and lazar houses were built downwind from towns.

Historians long believed that "leprosy" in the Middle Ages actually included a range of skin disorders, perhaps including syphilis. However, the excavation of medieval leper cemeteries, principally in Naestved, Denmark, has demonstrated that diagnosis by medieval doctors was actually conservative. Approximately 80 percent of the 650 skeletons at Naestved showed evidence of advanced lepromatous leprosy, whereas only a small percentage of modern cases, even untreated, are known to involve bones. Therefore, it can be speculated that only those most severely affected by the disease were confined there (M0ller-Christensen 1969). As John of Gaddesden advised in the fourteenth century, "No man is to be adjudged a leper and isolated from all his fellows until the appearance and shape of his face be destroyed" (as cited by Cholmeley 1912). This was a merciful criterion in view of the grief and penalties of banishment, but one that allowed the population to contract the disease from those with early or less apparent forms.

Medieval physicians had repeatedly observed that the blood of lepers was thick, greasy, or gritty (Bernard of Gordon 1496; Guy de Chauliac 1890; John of Gaddesden, cited in Cholmeley 1912). Recently, laboratory tests have substantiated these descriptions. Blood samples show two or three times normal platelet adhesiveness, among other qualities (Parvez et al. 1979; Ell 1984a). The age-old claims that lepers were unusually sexually active and that leprosy was sexually transmitted have been harder to explain. It has been demonstrated, first, that subclinical leprosy may become overt during pregnancy (Duncan et al. 1981), thereby giving the impression that the disease has sexual origin, and second that remissions of leprosy in men might heighten sensitivity to testosterone. In addition, confinement in a leper house could have released the sexual inhibitions of both sexes (Ell 1984a). Yet because of the similarities of the early stages of leprosy and syphilis, syphilis may in fact have been present in medieval Europe and mislabeled leprosy. Modern lepers show an unusually high incidence of syphilis, suggesting an unknown affinity (Murray 1982; Ell 1984a). V. M0ller-Christensen (1969), however, found no skeletal evidence of syphilis in the 650 leprosy victims at Naestved.

Historians have long believed that the Black Death greatly diminished the incidence of leprosy during the second half of the fourteenth century, attacking the weakened victims in their leper houses, which were found virtually empty at the end of the plague. However, it has recently been recognized that leprosy was already in decline when the plague began. The immune defect in the lepromatous patient is specific; it is not a generalized immune deficiency until the disease becomes advanced. In many ways, leprosy represents a hyperimmune state (Ell 1987). Leprosaria were probably found empty because members of the religious orders serving as keepers suffered a high death rate (Biraben 1975; Russell 1985), and the lepers fled to find food, escape the plague, or run from persecution as scapegoats. Alternatively, leprosy has been claimed to confer an immunity to plague, because leper houses consistently served meals very sparse in meat, whereas the plague bacillus requires a high serum iron level (Richards 1977; Ell 1984b, 1987). For all these reasons some medieval scourge other than plague may have hastened the end of leprosy. Tuberculosis, as noted earlier, confers an immunity to leprosy (only one leper with tuberculosis was found among the victims at Naestved; M0ller-Christensen 1969), though leprosy does not confer immunity to tuberculosis (Manchester 1984). Thus, tuberculosis itself may have promoted the end of the leprosy epidemic in the late thirteenth and fourteenth centuries as tuberculosis increased among the new urban population.


Believed in the Middle Ages to be a singularly English disease, "sweating sickness" (now widely accepted as influenza) first appeared in the very month in 1485 in which Richard III was defeated at Bos-worth Field. Four other outbreaks - in 1508, 1517, 1528, and 1551 - occurred in the first half of the sixteenth century, before, according to the theory that prevailed until recent times, the disease vanished forever. After the eminent Tudor physician John Caius had treated victims in 1551, he described the disease as a sweat and fever with pains in the back, extremities, head, with "grief in the liver and the nigh stomacke," killing "some in one hour, many in two," but lasting only 24 hours if the patient survived (Caius 1912).

Even though an epidemic of fever and sweats was known to have devastated much of northern Europe in 1529 at approximately the same time as an English outbreak of the sweating sickness, no relationship between the two phenomena was seen at the time. In keeping with the prevailing doctrine of humoral pathology, which accounted for all disease as an imbalance of the four natural humors - blood, phlegm, black bile, and yellow bile-the English sweating sickness was believed to be drawn to a constitution predisposed by an excess of one of the humors and possibly by an immoderate life-style. The immediate cause was believed to be, in the words of Caius, "evel mists and exhalations drawn out of the grounde by the sune in the heate of the yeare." Explanations of the causation and character of the disease remained localist and miasmatic into the nineteenth century, when in 1844 German historian J. F. C. Hecker (1844) called it a "spirit of the mist" and said that epidemics were inevitable if

"rain be excessive ... so that the ground is completely saturated, and the mists attract baneful exhalations out of the earth."

Even August Hirsch (1883) accepted the unique nature of the English sweating sickness, and not until the twentieth century were the five British epidemics recognized to be influenza, an illness known to be caused by an unstable microorganism having variable disease patterns.

Traditionally, the first influenza epidemic, as identified by Hirsch (1883), occurred in 1173 in Italy, Germany, and England, during which the monk Godefridus described an intolerable cough as a symptom. There were major bouts of influenza in France and Italy in 1323, when nearly all of the citizens of Florence fell ill with chills and fever, and again in 1387, when the disease was described as ex influentia coelesti, giving rise to the use in Italy of the term una influenza. When the disease struck Paris in 1411, one of the symptoms was a cough so severe that it caused women to abort. Influenza returned in 1414 to Italy and to Paris, where some 100,000 cases were claimed, and again in 1427. Following this, Hirsch (1883) described no more epidemics until the great 1510 outbreak, with general diffusion all over Europe, starting in Sicily in July and reaching northern Italy in August, France in September, and the Netherlands and Spain in October. But even as the visitations of influenza in Europe were increasing and the incidence of leprosy diminishing, a greater scourge than either was about to strike.

Bubonic Plague

Bubonic plague (Black Death or the Black Plague) was commonly known as the Great Mortality or the Great Pestilence. Probably in the majority of cases, certain symptoms were characterized as "black." In the words of Giovanni Boccaccio (1978), an eyewitness: "There appeared . .. certain swellings, either on the groin or under the armpits ... of the bigness of a common apple . . . [or] an egg. From these . . . after awhile . . . the contagion began to change into black or livid blotches ... in some large and sparse and in others small and thick-sown." Other sources describe small black blisters spread widely over the body, swollen glands and boils surrounded by black streaks, or the throat and tongue black and swollen with blood. But many victims experienced no "black" symptoms. As a consequence, many believe that the black in the name of the disease derives from a too-literal translation in sixteenth-century Scandinavia of a common fourteenth-century Latin phrase, atra mors meaning "terrible death," as "black death."

In 542, during the reign of Justinian, bubonic plague was reported to have taken the lives of 25 percent of the population of the Roman Empire, in what has been called the first European epidemic. Though the exact nature of this outbreak has been debated, plague is now believed, on the basis of literary and cemetery evidence, to have spread across Europe, reaching the British Isles in 544 and returning there in 664 (when, significantly, the Venerable Bede described St. Cuthbert as having a tumor [or bubo] on the thigh) and again in 682 (Russell 1976). Probably, episodes of plague attacked Rome in 1167 and 1230, Florence in 1244, and Spain and southern France in 1320 and 1333. It was during the last outbreak that Roch of Languedoc, who was on a pilgrimage to Rome, contracted the disease, was cured, began to nurse plague victims, and subsequently became the patron saint of plague.

In 1331 civil war and plague struck Hopei, China, and both soon raged throughout that nation; chronicles report that two-thirds of the population perished. The disease moved west along the caravan routes through Tashkent, Astrakhan, and other cities of southern Russia, transmitted by rats and fleas perhaps lodged in the grain supplies of the caravans (for a discussion of caravan transportation, see McNeill 1976). It reached the Crimea in 1346, where Genoese merchants were being attacked in their fortified trading post of Caffa by a Mongol army. The attackers were suffering from plague, and before they withdrew they transmitted their affliction to the besieged town by catapulting corpses of victims over the walls.

Fleeing Caffa, the ships of the now-diseased Genoese were driven away from Messina, Sicily, and the disease was carried to North Africa and the western Mediterranean. Soon Corsica and Sardinia, Spain and southern Italy were affected, then all of Italy, Austria, Hungary, Yugoslavia, and Bavaria. Marseilles was the destination of one of the ships, and the disease quickly spread up the Rhone and then throughout France. By 1348 most of France and Switzerland were under siege by the plague, which soon reached the southern coast of England, Germany, Sweden, and Poland. The plague's assault on Russia was delayed until 1351, good evidence that the disease traveled by the international trade routes and not by river transport, or it might have reached Russia from the Crimea several years earlier.

Plague was transported by armies and ships, merchants, pilgrims, fair goers, transient laborers, and other human travelers. Traders hauling grain, fodder, forage, hides, furs, and bolts of cloth also transported rats, fleas, and other vermin. Pilgrimage routes and trade routes to fairs were natural paths of the disease, which first broke out in London at the time of the Bartholomew Fair. When Edward III began the construction of Windsor Castle in 1359, plague attacked the workforce (Shrewsbury 1970).

Plague is a millennia-old disease of wild rodents. In a cycle widely believed to be the method of transmission of the Black Death, rat fleas (Xenopsylla cheopis) carry the Yersinia pestis bacillus to the black or house rat, Rattus rattus. When the host rat dies, its fleas leave to find another living rat, but failing that, they may jump temporarily to less favored hosts, human beings, and by biting them transmit the disease.

In humans, plague has three major forms: bubonic, septicemic, and pneumonic. The first form results from an insect bite, with the bacillus moving through the lymphatic system to the nearest lymph node, frequently in the groin, where it forms a palpable swelling, the characteristic "bubo," from the Greek word for groin. Other possible sites for buboes are the armpits and the neck, depending on the location of the bite. In the septicemic form, the insect injects the bacillus directly into the bloodstream of the victim, where it multiplies quickly. Blood seeps from the mouth and the nose, and death results in a few hours. Septicemic plague is virtually always fatal. Nevertheless, the most menacing form is pneumonic plague. A modern outbreak in Manchuria in 1921, for example, was 100 percent lethal (McNeill 1976). Because the pneumonic form is a lung infection, it can be transferred directly from human to human by airborne sputum or by fomites (clothing and other articles contaminated by victims).

All three forms of the disease were found in the fourteenth-century pandemic, and judging by a study of 300 contemporary literary sources, the relative importance of the three types may have been 77 percent bubonic, 19 percent septicemic with secondary pneumonia, and 4 percent pneumonic (Ell 1980).

Because of the entrenched medieval belief in the humoral pathology inherited from the Greeks, which had not been seriously challenged in more than a thousand years, therapeutic measures were based on correction of the imbalance of humors. The imbalance might be precipitated by an immoderate intake of food or drink or by meteorological or astronomical phenomena. Because plague was of a short incubation period and therefore could readily be seen to be transferred from person to person, the best etiologic explanation consistent with the traditional, pathology was that corrupt air emanated from the ill person or a corpse, or even from someone still not ill but coming from a place of sickness. Standing only a few feet away from such a source might be enough to contract the disease. Belief in the vital role of air was so strong that the clergy of Avignon imagined that mountain dwellers had been immunized against the plague by their own pure air and so imported them as gravediggers in 1348. Unfortunately, they died of the infection as soon as they arrived (Biraben 1975).

Medieval physician and surgeon Guy de Chauliac (1890) wrote the most accurate and complete medical account of the 1348 plague epidemic of any contemporary observer. In it he described both the pneumonic and bubonic types of the disease, and may also have recognized the septicemic type with a reference of blood spitting. His first counsel was the traditional injunction "Fuge cito, vade longe, rede tarde" - "Flee quickly, go far, and come back slowly." But he also advised such surgical and medical measures as reducing blood volume by phlebotomy, purifying the air by fire and incense, and opening or cauterizing buboes. Most of the medical texts of the time echo the treatments Guy de Chauliac advocated. Surgical intervention, baths, and apothecary cures were recommended. Physicians visiting the sick were accompanied by boys carrying incense burners to purify the air, and all held before their noses a sponge soaked in vinegar and spices. When Philip VI of France ordered the Paris medical faculty to ascertain the cause of the disease, a confident report came back that the pestilence was caused by the conjunction of Saturn, Jupiter, and Mars, which had occurred at 1 P.M. on March 20, 1345 (Campbell 1931).

Those who could afford to, including physicians, fled the infected towns. Orvieto, for example, had to offer a doctor 100 livres per year to stay and treat the poor. The Catalonian Cortés fled Barcelona, and all the inhabitants of Agrigento, Sicily, ran away in 1347. Citizens of Marseilles burned the La Rousselle quarter to contain the plague (Biraben 1975). Perhaps because both cities forbade entry by travelers, Milan and Parma remained largely free of the disease during its first outbreak in 1347-50. In Milan early victims were also heartlessly walled up in their houses (Ziegler 1970; Ell 1984b). At Ragusa (now Dubrovnik, Yugoslavia), ships were isolated for 40 (quaranta) days, in a first effort at quarantine.

The first great outbreak of the Black Death was followed by three waves in the same century, in 1360,

1369, and 1375. It has been estimated that the death rate in Britain decreased with each successive wave, starting with 25 percent in 1348 and becoming 22.7 percent in 1360, 13.1 percent in 1369, and 12.7 percent in 1375. It is assumed that the disease lost its virulence at the same time that people's immunity increased (Russell 1948; Carpentier 1978).

Persistent questions about the Black Death perplex modern historians. Was bubonic plague the sole disease, or where there others? Why was no unusual black rat mortality mentioned by contemporary writers? Why is the black rat unknown today in Europe except in a few port cities? Was a sylvatic, or wild, home for the plague ever created in Europe - either at the time of the sixth-century eruption or in the fourteenth century? If so, what eradicated it? Modern sylvatic foci, in the southwestern United States and Russia, are almost impossible to eradicate (McNeill 1976).

It has been suggested that more than one disease was active during the fourteenth-century epidemics, with typhus, smallpox, and anthrax as candidates. Scholars have been puzzled by records of high infection rates during the winter months, since plague is a warm-weather disease. This and other contradictory factors support the case for anthrax, which is caused by a much hardier organism, is characterized by pustules with a jet-black center, often precipitates the voiding of black blood, and also has a pulmonary form (Twigg 1984).

Doubts about the classical explanation of plague transmission derive partly from the present-day absence of R. rattus in northern Europe, except in a few port cities. Moreover, no medieval record exists of the explosive black rat mortality that would have been expected. Finally, R. rattus is timid and not normally migratory (Shrewsbury 1970; Ell 1980).

As already mentioned, spring and summer are the seasons of ratborne plague in cities (infection occurs most commonly when both Fahrenheit temperature and humidity are between 68 and 80; Russell 1976), yet the Black Death occurred throughout the year. The explanation may lie in two possible forms of interhuman transmission: Respiratory infection, which produces pneumonic plague, would explain the winter occurrences, and transmission by the human flea, Pulex irritans, would account for the undoubted majority of bubonic cases (Ell 1980). P. irritans, which can transmit plague, would have needed no rat host and could have lodged in long, loose clothing, traveling from person to person. Lice, ticks, and bedbugs, which can also transmit plague, may have been vectors as well (Biraben 1975; Ell 1980).

As for the sylvatic foci in rodents, an alternative explanation would be that multiple human and animal reservoirs, based on complete and partial immunities, perhaps constantly shifting, propagated the plague bacillus without a sylvatic home. Plague immunity is known or suspected to be conferred by salmonella infections, Yersinia enterocolitica, tularemia, and typhus, as well as leprosy (Ell 1984b).

Explanations for the final disappearance of plague from Europe in the eighteenth century included speculations that the bacillus mutated to a less virulent form, that R. rattus was replaced by Rattus norvegicus, and that new practices of housing construction, shipping, personal hygiene, nutrition, and public health finally brought the disease to an end (for reviews of theories see Appleby 1980; Ell 1984b). In addition, the rats themselves may have become immune. Communities of immune rats are known to have existed in India in the twentieth century. The reason the rats did not become immune in northern Europe until the seventeenth century (and a few decades later in the south) may be that a certain high density of population would have been required for all remaining susceptible rats to be infected and finally killed (Appleby 1980).

Historians have long accepted a type of Malthu-sian theory to account for the appearance of plague in 1348. According to this theory, a too rapid population expansion led to the clearing of all arable land and crowding into already overpopulated cities. The populace then suffered a series of crop failures and famines when the weather turned unusually cold early in the fourteenth century. As rats fled empty granaries to find food in human dwellings, the human population, weakened by starvation, fell victim to a chance epidemic. Critics of this Malthusian position have objected that the weakest members of society were not eliminated by the plague; men between 20 and 40 died in larger proportion than women, children, the aged, or even lepers. The Y. pestis organism requires exogenous iron for growth and replication, and young men were the least iron-deficient group in the medieval population (Ell 1984b, 1987).

Believed to have left in its wake some 20 million dead in Europe in the four years from 1346 to 1350, the Black Death brought about critical social and ideological changes. Considering the medical world alone, we find that the public health tradition, inherited from the care of lepers, was strengthened - even though social efforts to clean streets, collect garbage, empty sewers, remove bodies, regulate the sale of food, and enforce quarantines of ships did little to stop the spread of plague. A new charitable impulse, encouraged by the religious revival after the plague, led to the building of hospitals, both religious and civic. New religious orders were devoted to the care of the sick. Owing to the heavy loss among scholars, physicians, and other educated men, Latin ceased to be the sole language of important texts, and medical as well as other books began to be written in the vernacular (Campbell 1931).

A widespread interest in disease prevention became current, and many works on diet, hygiene, proper clothing, and other topics of health care were published. Because surgeons had made heroic efforts to lance or cauterize buboes during the plague, the status of this profession was considerably enhanced, rising relative to that of physicians, too many of whom had fled. The growth of surgery as a discipline and desire to ascertain the causes of the pandemic led to an increased sanctioning of postmortem examinations, a practice that was to contribute directly to the growth of academic anatomic dissections in the following century.

Finally, humoral pathology suffered a serious blow - from which it would ultimately expire in centuries to come - because of its complete failure to palliate suffering and effect cures, not only for plague but for the other contagious illnesses of leprosy, tuberculosis, and influenza that ravaged the late Middle Ages.

Y nez Violé O'Neill

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