Black Death

The Black Death was one of the most destructive pandemics in human history. It was caused by the bacterium bacterium Yersinia pestis and spread across Eurasia in the mid-14th century, peaking in Europe between 1347 and 1351. Its estimated death toll, roughly 30 to 50 percent of Europe's population, made it the first major European outbreak of plague and the opening episode of the second plague pandemic. The term "Black Death" came into use only later; contemporaries called it "the pestilence." The disease is an important case in infectious disease history, epidemiology and public health, because it combined rapid spread, very high mortality and long-lasting social change.

The article first explains the pathogen and the forms of the disease, then traces the pandemic's origins in central Eurasia and its routes into Europe, the mechanisms of transmission and the difficulties of estimating mortality. It then turns to the economic, religious, medical and political responses and consequences, the recurrences that followed, and the scientific methods, especially ancient DNA research, that have resolved the question of the pathogen's identity. Its scope covers the historical event itself, not the general history of plague, which is treated elsewhere.

Name, dating and scope

Naming the epidemic

Contemporaries did not use the name that now dominates. In English the epidemic was usually called the pestilence, the great pestilence, the plague or the great death, and after the pandemic, "the first pestilence" was used to distinguish it from later epidemics of plague. Vernacular writers across Europe mostly reached for phrases that translate roughly as "the great dying" or simply "the plague," according to the etymological record.

The label "Black Death" is a later creation. The Oxford English Dictionary's earliest evidence for the English noun is a 1755 translation, and it notes that the epithet "black" is not attested in fourteenth- or fifteenth-century sources in any European language for the 1347 epidemics. The specific sense first surfaces in Scandinavian chronicles of the sixteenth and early seventeenth centuries, and the English compound is probably modelled on the Danish den sorte død. The Latin phrase atra mors had earlier been used for plague in general, but the link to this epidemic is unclear. A Danish historian, J. I. Pontanus, recorded in 1631 that people commonly called it the black death, a statement written nearly three centuries after the event. Sources differ on when the modern English usage became standard: Etymonline gives 1823 as the date when the term was introduced in English history writing.

Explanations for the epithet vary. One view links it to the Latin atra, which could mean "terrible" and was read as "black." Another connects it to the haemorrhages and gangrene that sometimes followed septicaemia. A third points to the dark skin discolouration seen in severe cases.

Dating and geographic scope

The core period of the pandemic in Europe is usually given as 1347-1351, although it is often placed within a wider window of 1346 to 1353. The pandemic is generally described as striking Europe, Asia, the Middle East, and North Africa between 1347 and 1353. Its entry into Europe is tied to sea traffic from the Black Sea: Genoese galleys carried plague from Caffa to Messina, Sicily, in October 1347.

The Black Death is the first major episode of the second plague pandemic, not the whole of it. That wider pandemic reached medieval Europe in 1346 and killed up to half of the population of Eurasia in the next four years, and it was followed by recurrences that became endemic and recurred regularly after 1353. The second plague pandemic is usually dated from 1346 to the eighteenth century.

The earlier Plague of Justinian is a separate episode. Its first wave is generally dated to circa 541 to 544 CE, and it recurred over the following two centuries. Genetic work shows that the Justinianic strain lies on a distinct branch: it is distant from strains associated with the second and third pandemics. The scale of the sixth-century epidemic is also contested. A PNAS study argues that the demographic damage traditionally attributed to it does not fit the surviving evidence.

Death toll and estimates

Global estimates are wide. One common summary puts the toll across Eurasia and North Africa at about 75 million to 200 million people. For Europe, the usual range is 30–60% of the population, although published figures vary with region and method. Europe's population is often put at about 75 million before the plague, falling to roughly 50 million in the years 1347 to 1351.

These numbers are reconstructions, not counts. No reliable population counts exist for the 14th century, so historians work backward from tax records, manorial rolls, church records, and burial evidence, and even where the historical record is considered reliable, only rough estimates of the total number of deaths from the plague are possible. The contemporary chronicler Jean Froissart gave a one-third figure, which modern scholars read as an allusion to the Book of Revelation rather than a measurement. The older consensus of 25 to 33 percent for Western Europe has been questioned: historian James Belich notes that research since 2004, into such things as manorial records of tenant turnover, strongly suggests that the Black Death toll was 50%, not 30%.

The pathogen and forms of the disease

The Black Death was caused by a bacterium named Yersinia pestis, a Gram-negative organism that also produces the bubonic, pneumonic and septicemic forms of plague. It was the cause of the Black Death in Europe during the middle ages. Genetic studies also support a single bacterial cause for the Justinian, medieval and third pandemics. All three suspected plague pandemics were caused by this bacterium.

Evolutionary relationship to Y. pseudotuberculosis

Y. pestis is a very young lineage that descends from a gut pathogen. Molecular clock estimates place its divergence from Y. pseudotuberculosis at 1,500–20,000 years ago, shortly before the first known pandemics of human plague. The ancestor is a relatively mild organism: Y. pseudotuberculosis is a soil- and water-borne enteropathogen, while Y. pestis is far more dangerous. Its virulence did not arise mainly from acquiring new genes. Research on genome rearrangements has found that insertion sequence-mediated genome rearrangements and reductive evolution through massive gene loss mattered more than gene acquisition. One key change is the loss of the O-antigen layer of the cell envelope. Where the ancestor keeps it, Y. pestis has lost the O-antigen during evolution and therefore exposes its core LPS. That exposed surface lets the bacterium engage immune cells and spread to lymph nodes, spleen and liver, and the initiation of a systemic infection.

A second change concerns the insect vector. The ancestral rcsA gene, which suppresses biofilm formation, has become a pseudogene in Y. pestis. Experiments showed that restoring the functional gene strongly represses biofilm formation and essentially abolishes flea biofilms. This links the genetic history of the bacterium directly to its transmission by fleas.

Bubonic, pneumonic and septicemic forms

The three clinical forms differ mainly by the tissue the bacteria invade first. In bubonic plague, Y. pestis bacteria enter the body through the bite of an infected flea or through a cut or break in the skin, the bacteria multiply near where they entered the body. The lymph node that drains that site swells into a bubo. Symptoms onset 2-8 days after exposure. Typical features include fever and chills, headache, muscle pain, general weakness, and painful swelling in the groin, armpits, neck, or site of the insect bite or scratch.

In septicemic plague, Y. pestis bacteria accumulate in the bloodstream, septic shock occurs. Symptoms can include bleeding (blood may not be able to clot), shock, and skin and other tissues may turn black and die, especially on fingers, toes, and the nose. This tissue death and hemorrhage is the feature most associated with the dark appearance that gave the disease its popular name.

Pneumonic plague affects the lungs. It occurs when Y. pestis bacteria are inhaled, they infect the lungs, or when bacteria spreads to the lungs of a patient with untreated bubonic or septicemic plague. It progresses quickly, with symptoms typically start within 1-3 days. The chest findings are a bloody or watery cough due to infection of the lungs (pneumonia), and without early treatment the pneumonia rapidly becomes worse and it can be fatal.

Why bubonic and pneumonic plague differed

The distinction between flea-borne and person-to-person spread comes from where the bacterium is deposited. Bubonic plague is confined to the lymphatic system near the bite until it spreads, whereas the pneumonic form can move between people. Pneumonic plague is of particular concern because it can be spread from person to person. It spreads through respiratory droplets, which is why pneumonic plague is treated as the more alarming form from a public health standpoint. Modern outcomes also differ: bubonic plague is the most survivable form, while without treatment, septicemic plague and pneumonic plague are both fatal. Quick antibiotic treatment makes it less deadly now. These outcomes describe the disease under modern conditions; medieval mortality is treated in a later section.

Plasmids and mammalian virulence

Y. pestis carries three virulence plasmids: typical strains of Y. pestis harbor three virulence plasmids (pCD1, pMT1, and pPCP1), which encode various virulence determinants. Of these, pCD1 is an inherited feature. The plasmid pCD1 is commonly shared in all three pathogenic species of Yersiniae. It encodes a type III secretion system, which is responsible for injecting into host cells a number of cytotoxins and effectors that interfere with immune defenses. Studies of the hemorrhagic features of plague point to this plasmid, which is responsible for the powerful tissue invasiveness capacity of the plague bacillus and the hemorrhagic features of plague.

The other two plasmids are specific to Y. pestis. The other two plasmids (pPCP1 and pMT1) are laterally acquired by Y. pestis. pMT1 carries genes for the F1 capsule: the genes (caf) for the F1 capsule are encoded by pMT1. pPCP1 carries plasminogen activator and coagulase activity that is encoded on the same gene (pla) and the toxin pesticin. Researchers have suggested that these two plasmids promote deep tissue penetration by Y. pestis and contribute to the acute infection associated with this species. Their exact contribution remains uncertain, since the precise role in virulence for pMT1 and pPCP1 is still unknown. The plasmid story therefore explains much of the pathogen's invasiveness, but the full route by which these elements enabled the bacterium to infect mammals is still under study.

Origins in central Eurasia

For roughly two centuries, scholars debated whether the Black Death began in China or in Central Asia, and without ancient DNA there was no way to prove either theory. The question was settled in part by archaeological and genetic work on a small group of cemeteries.

The most discussed evidence comes from two cemeteries, Kara-Djigach and Burana, in the Chüy Valley near Lake Issyk-Kul in what is now Kyrgyzstan. Excavations of these cemeteries between 1885 and 1892 revealed an unusual assemblage that may be linked to a fourteenth-century epidemic. Tombstone inscriptions show a disproportionately high number of burials dated 1338 and 1339, and some give "pestilence" as the cause of death. Syriac-language stones of this kind had long been disputed as evidence for the European pandemic. In 2022, a team led by Maria Spyrou extracted ancient DNA from seven individuals at these sites. Three were found to carry Yersinia pestis, and the team reconstructed a genome from them. The reconstructed strain sits at the base of a major phylogenetic branching event, and that branching is dated to the first half of the fourteenth century. Comparison with present-day bacteria from the wider Tian Shan region supports a local emergence of the recovered ancient strain.

The region sat on the Silk Road, and its trading communities were in regular contact with the wider world. Both sites lay at the heart of the international trade route known as the Silk Road. By the fourteenth century, the Golden Horde, a successor khanate of the Mongol empire, controlled the steppe corridors linking Central Asia with the northern Black Sea. This political order made long-distance movement of goods and people possible, and it also allowed pathogens to travel along the same routes. The reported arrival of the disease in the Mediterranean followed this path: plague first entered the Mediterranean on trade ships carrying goods from Golden Horde territories on the Black Sea, less than a decade after the Issyk-Kul epidemic. The Mongol-era networks are therefore best understood as the channel that connected an outbreak in Central Asia with the ports of Europe, rather than as the source of the bacterium itself.

The siege of Caffa is the most dramatic episode in this chain, but it is also the most contested. In 1346, Golden Horde forces besieged Caffa, a Genoese trading center on the Crimean Peninsula. While Janibeg, the Golden Horde's ruler, waited for the city to surrender, his fighters began to succumb to an unidentified illness. The main literary source is the memoir of the Genoese notary Gabriele de' Mussi, which claims that the attackers ordered corpses to be placed in catapults and lobbed into the city, and that fleeing residents then carried the disease to the Mediterranean. Historians disagree about how much weight to give this account. One scholar argues that the biological-attack claim is plausible and provides the best explanation of the entry of plague into the city. Others point out that the notary was not in Caffa during the siege, and a critical study concludes that the Mongol catapulting of plague-infected bodies at Kaffa is a historically unsubstantiated narrative. A widely cited assessment accepts that plague may have been introduced into the city during the siege, but considers the idea that Caffa then seeded plague across the Mediterranean to be incorrect. Modern authorities believe that the description may indicate that plague was successfully introduced into Kaffa by the Tartars, but that the belief that events at Caffa spread the disease further is not supported.

The original reservoir of the bacterium in animal populations is a separate question, and it remains open. Slavin has argued that the 1338–1339 strain very plausibly originated and evolved in local marmot plague reservoirs of the Tian Shan region, rather than in a faraway region. The study's authors suggest the bacterium spilled over to humans, perhaps from a marmot, which are abundant in the Tian Shan mountain region. The strain from the cemeteries was closely related to ones found in rodents near Issyk Kul today. These findings narrow the origin to a specific region and a specific lineage, but they do not establish the full ecology of the rodent hosts or the route by which the bacterium moved from them into human populations.

Spread through Europe, 1347–1353

Arrival in Sicily and the Mediterranean

The pandemic entered Europe by sea. One chronicle records that a fleet of Genoese galleys reached Messina in October 1347, and plague broke out within days of the ships' arrival. Sources disagree on the order of the first landfalls. A chronology of 1347 places the disease at Marseille on September 1, before the October arrival at Messina, and other accounts describe ships that were refused at Genoa and then docked at Marseille. From Sicily, the disease reached Tunis, Corsica, Sardinia, the Balearics, the Iberian peninsula and southern Italy, arriving in Genoa and Venice around January 1348. By mid-1348 it had reached Paris, which the Plague Atlas dates to June 1348, with mortality at 800/day at the peak.

Northward and westward: England, Scandinavia and the German lands

England was reached through a port rather than overland. The first recorded case is a seaman who arrived at Weymouth, Dorset, from Gascony in June 1348. From the coast the disease moved inland: it spread through the south-west to Bristol and then eastwards to Oxford and London, which it had reached by the end of October or the beginning of November. Within a year the plague had covered the entire country by summer 1349, before dying down by December. Local records in Dorset suggest the same pattern of coastal entry followed by movement up river valleys.

Scandinavia and the German lands were reached later. A timeline of the pandemic places Norway, Sweden, northern Germany, then Moscow in 1349–1351, and another source notes that in the summer of 1349, the plague reached Scotland, Ireland and Scandinavia. Maps of the pandemic show it advancing in ever-expanding concentric circles each year through 1351, and they also show that some inland areas, such as the regions around Milan, Warsaw, Magdeburg and Bruges, had only minor outbreaks.

Eastward into the Near East and Egypt

Plague reached the Middle East in the same period. In Egypt, the disease was present in autumn 1347 when a ship carrying the plague came to Alexandria, and it moved through northern Egypt in the spring of 1348 with its peak between October 1348 and January 1349. Cairo, then the largest city in the region, was struck in September 1348; the sultan left the city and remained outside it while the epidemic lasted. Estimates of Cairo's losses, around 200,000 deaths, a third of the population of the city, are widely repeated, although the figures are approximate. Overland routes carried the disease into Syria and Palestine during 1347 and 1348, and by 1349 it had reached Anatolia and southeast into Mosul and Baghdad.

Recurrent outbreaks and the early 1350s

The European epidemic did not end in a single wave. By 1351 the disease had reached Russia, and the broader European phase is often dated to 1353, after which the disease returned in later outbreaks. Renewed waves are commonly listed for 1361 and 1369, and England experienced recurrent epidemics for centuries, with very few years without some plague deaths recorded between 1348 and 1665.

Regional variation in timing and severity

Timing and severity varied sharply. Ports were struck first and often most severely, because ships brought the disease directly to them. In Sicily, frightened Messinese fled into the countryside carrying the disease with them, which shows how flight could spread infection from cities into rural areas. Catania tried to limit the danger by controlling movement: officials in Catania instituted strict control over the movement of people. In Egypt, the pattern was reversed in parts of the population: the peasantry fled to the cities to escape the plague, while in parallel the city people fled to the countryside, and the south of the country was hit in early 1349, after the north. Mortality therefore reflected both the arrival date and the movement of people during the epidemic.

Transmission mechanisms and debates

The traditional account of the Black Death rests on a rodent cycle. In this model, Yersinia pestis circulated among rats and their fleas, and when the rodents died, the fleas sought new hosts and carried the pathogen to people. The bacterium cycled between rats and their fleas in a deadly loop. When infected rats died, their fleas jumped to new hosts, including humans, carrying the pathogen with them. The flea most associated with this loop is the Oriental rat flea (Xenopsylla cheopis). It prefers rats, but it will not pass up a human meal if one is closer. Infection through such a bite produces the bubonic form, whereas inhaled droplets produce the pneumonic form.

Alternative vectors came into view in the later twentieth and twenty-first centuries. The human flea (Pulex irritans) and the body louse (Pediculus humanus) were proposed as direct carriers between people. Previous studies had suggested that either rodents or direct human-to-human transmission through ectoparasites such as human fleas and body lice may have played a role. Critics of the rat model stress several points. Rats would have needed to carry the disease through an extra step, and that step would slow the epidemic. Stenseth, a co-author of a 2018 study, put it this way: it would be unlikely to spread as fast as it did if it were transmitted by rats, because it would have to go through an extra loop of rats rather than passing from person to person. The archaeological record also gives limited support to a rat-driven epidemic. There is a scarcity of rats in the archaeological record, and no masses of dead, infected rats were found as they were during the Third Pandemic. European black rat fleas, moreover, do not like to bite people much.

The 2018 study by Stenseth and colleagues tested this alternative directly. The researchers used publicly available mortality data for nine plague outbreaks spanning the duration and geographic spread of the Second Pandemic to develop models for the pneumonic, rat-borne, and human ectoparasite transmission routes. In 7 of the 9 regions studied, the bubonic plague model with a human ectoparasite vector better reflected mortality patterns than the other two models. The seasonal pattern of later plague points the other way in one respect. Plagues of the third pandemic have closely followed the fertility cycles of rat fleas, rising with relatively humid conditions and within a temperature band between 10°C and 25°C. Some scholars have also asked whether climate shaped transmission. One 2015 study suggests that warmer, wetter climate conditions influenced its transmission.

Person-to-person transmission has its own difficulties. Pneumonic plague does pass from human to human through infectious droplets. McCormick states that this does not spread as easily as previous historians have imagined. Dense living conditions nevertheless offered abundant opportunity for lice and fleas. Human fleas and lice were very common in people during the period under study because of infrequent bathing. Laboratory evidence also exists for louse-borne plague. Body louse–borne plague had been demonstrated experimentally in rabbits before the 2010 studies. Yet the evidence for a louse or human-flea route to people remains incomplete, since the transmission from body lice and human fleas to humans had not yet been documented. The microbiological basis of the identification is also disputed. A 2007 study found the bacterium in 5 of 36 teeth of "plague" victims, none of which were dated to the Black Death era (1347–1351). All three locations in that study were port cities.

Trade and ports are central to the spread debate. Black rats lived close to people, and they moved along trade routes; the black rat was introduced from Asia to Europe by trade, but was later displaced throughout Europe by the larger brown rat. Ships and warehouses were part of this environment, and the same routes that carried goods also carried rodents, fleas and, potentially, infected people. Crowded ports and urban quarters would have multiplied contact among hosts, which may explain why cities often suffered sharp early losses. Whether rats, human parasites or direct airborne contact drove the spread of the pandemic remains unresolved, and most current explanations combine several of these routes.

Mortality estimates and demographic effects

Estimates of the Black Death's European death toll cluster in a broad band, and the disagreement is large. The epidemic killed 30 to 50 percent of the entire population of Europe, a range that appears often in popular and scholarly summaries. At the upper end, the historians John Aberth and Ole Benedictow have proposed 51–58 percent or upwards of 60 percent, respectively. At the lower end, economists Jedwab, Johnson and Koyama estimated in 2019 that 38.75 percent of Western Europe's population had died on average, using a dataset of more than a hundred cities.

These figures are reconstructions rather than counts. There are no census figures, no national mortality statistics, no systematic surveys conducted during or immediately after the pandemic. Historians instead work from fragments: tax and rent registers, parish records, court documents, guild records, and archaeological remains from many localities. Direct evidence is uneven, since direct records of mortality are sparse and mostly relate to deaths among the nobility, and clergy and wealthy landowners are far better documented than peasants or townspeople. The urban evidence is especially indirect and tied to individual towns. A tax comparison from Canterbury, for example, shows that about two-thirds of the taxpaying population disappeared between 1346/7 and 1351/2, while monastic rolls at Rochester and Durham record very high losses among their tenants and residents. Such local cases must then be extrapolated to whole regions and countries, a step that is methodologically complex and contested. Belich adds that medieval population statistics are notoriously dodgy, often amounting to a guess based on other guesses. Research since 2004 on manorial records of tenant turnover has pushed some scholars toward a figure near 50 percent for the overall toll (research since 2004, into such things as manorial records of tenant turnover, strongly suggests that the Black Death toll was 50%, not 30%).

Mortality also differed sharply from place to place. In France and Italy, regional rates ran from forty to fifty percent in Languedoc to sixty to eighty percent in Tuscany. Cities often recorded the highest losses; for the English town of Nottingham, a historian's estimate is that approximately 60 per cent of the townspeople died during the Black Death of 1349. The urban-rural question is contested. One leading historian of plague maintains that rural regions suffered greater mortality than towns, but most historians argue the reverse. A study using the Jedwab team's city data found that marginal rural areas suffered relatively greater population losses following the Black Death. Scholars also caution that the sources themselves are skewed: many of the quantitative sources that have been used to construct Black Death case studies come from urban areas, and a pollen-based study of nineteen modern countries found that the Black Death's mortality in Europe was not as universal or as widespread as long thought.

Recovery was slow and uneven. Studies of cities find that cities recovered their pre-plague population within two centuries on average, but the averages conceal wide differences: some cities did not recover their pre-Black Death populations until the 19th century. Coastal cities on the Atlantic, North Sea and Baltic generally rebounded faster than inland cities or those near the Mediterranean. Rural recovery lagged urban recovery; in one analysis, rural areas near the hardest-hit cities recovered their populations around a century after the recovery in urban populations. Migration, rather than higher birth rates, appears to have driven much of the local recovery. Taken as a whole, Europe regained its pre-Plague population by 1600. England shows the scale of the collapse: the first strike alone reduced the English from 4.8 million in 1348 to 2.6 million in 1351, a decline of 46%. Later plague outbreaks kept the population down, and recovery did not begin until after 1500 in England, according to Belich. Other sources date the start of growth somewhat differently. A historical overview of the economy notes that population growth recommenced at different times in different places but rarely earlier than the second half of the fifteenth century and in many places not until c. 1550.

Demographic recovery was thus neither a single event nor a fixed timetable. The uncertainty in the death toll, the thin and urban-biased sources, and the variation in migration and local economic conditions all limit what can be said with confidence about how many people died in each region and how quickly each one recovered.

Economic and labor consequences

The most immediate economic effect of the Black Death was a sharp fall in the number of people available to work the land. Before 1347, demographic growth had kept pay low and rents and prices high, which suited lords who could bind peasants to insecure dependent tenures Before the plague, rising population had kept wages low and rents and prices high. Once that surplus of labor disappeared, the balance moved toward workers. Pay levels in England climbed by roughly 12 to 28 percent over the 1350s compared with the 1340s, and by 20 to 40 percent over the following decade Wages in England rose from twelve to twenty—eight percent from the 1340s to the 1350s and twenty to forty percent from the 1340s to the 1360s. Local cases could be sharper. At Fornham All Saints in Suffolk, part of the hired reaping that had cost the pre-plague rate in 1348–49 was paid at a considerably higher rate During the plague year (1348—49) at Fornham All Saints (Suffolk), the lord paid the pre—plague rate of 3d. per acre for more half of the hired reaping but the rest cost 5d.

Landlords responded by changing how they secured labor. Lords who feared losing tenants substituted wages or money rents in place of labor services in an effort to keep their tenants. Estate finances suffered in the process, and a more lasting and serious consequence was the drastic reduction of the amount of land under cultivation, due to the deaths of so many laborers. This proved to be the ruin of many landowners.

Outcomes varied by region. Historians distinguish western Europe from the lands east of the Elbe. In most of western Europe, widespread efforts by rulers and parliaments to maintain the old order failed: serfdom ended, real wages tripled, and landowning elites were weakened. East of the Elbe, by contrast, elites used coercion to keep wages low and land rents high. A comparative study of later European pandemics also suggests that these labor-market effects emerged mainly where economies were already relatively free Plague-induced labor shortages, however, have these effects only in economies that already are, or are forced to become, relatively free.

Governments first tried to hold wages down by law. An earlier measure, the Ordinance of Labourers of 1349, was followed by the Statute of Labourers, which the English Parliament passed in February 1351 at its first meeting after the plague It was further refined as the Statute of Labourers at the first post-plague meeting of Parliament in February 1351. The statute forbade pay above pre-plague standards and restricted movement in search of better terms aimed at regulating the labour force by prohibiting requesting or offering a wage higher than pre-Plague standards and limiting movement in search of better conditions. Its compulsory-service provisions covered able-bodied people under sixty who had no trade or independent livelihood, obliging them to work at customary rates the statute mandates that able-bodied individuals below the age of sixty, not engaged in trade or possessing their means of sustenance, must serve others at customary wages. Workers who left a contract early faced imprisonment if a reaper or mower, or other workman or servant... do depart from the said service before the end of the term agreed, without permission or reasonable cause, he shall undergo the penalty of imprisonment.

Historians disagree about how far the statute succeeded. One long-standing view holds that it was poorly enforced and did not stop the rise in real wages. Others note that immediately after the Black Death, real wages did not rise, despite the labour shortage. Resentment of such controls was among the factors behind the English Peasants' Revolt of 1381, though the source places it among others.

Rural unrest also erupted in France. The Jacquerie of 1358 emerged in a country still feeling the effects of plague and war; the revolt occurred in the wake of the Black Death and during the Hundred Years War, and it was closely connected to a rebellion in Paris against the French crown. It began in May 1358 near Compiègne and spread quickly throughout the countryside. The peasants destroyed numerous castles and slaughtered their inhabitants. Peasant bands then joined forces with Parisian rebels under Étienne Marcel. Noble forces defeated the rebels in June, and a massacre of the insurgents followed their defeat. Recent scholarship treats the movement less as a single program than as a constellation of many events that evolved over time. Much of the surviving narrative comes from aristocratic writers; Froissart's account, for instance, emphasized the destruction of noble property and the perceived breakdown of hierarchical authority.

Beyond wages and labor relations, the crisis reshaped production and commerce. Trade and warfare paused at first, but a sudden slump in trade immediately followed but were only of short duration. Urban crafts shared in the gains: there was also a general rise in wages for artisans and peasants. These changes brought a new fluidity to the hitherto rigid stratification of society. Some Italian centers suffered more lasting damage; the economy of Siena received a decisive check. Contemporary observers noticed the labor market's new terms. One chronicler complained that scarcity was so acute that the humble turned up their noses at unemployment, and could scarcely be persuaded to serve the eminent unless for triple wages.

Religious, medical and public-health responses

Medical explanations

Medical learning in 1348 had no concept of bacteria, and the most authoritative explanation came from the Paris medical faculty. Its report, issued in October 1348 at the request of Philip VI, attributed the epidemic to a planetary conjunction of 1345 (Their verdict: the plague was caused by a cosmic event. Specifically, a conjunction of three planets in the constellation Aquarius on March 20, 1345.). Its explanation also depended on miasma theory, the belief that corrupted air carried disease. Physicians pointed to specific sources of this bad air: southern winds, fumes rising from swamps, rotting plants and animal carcasses, cesspools, sewers, and dung heaps. Because the framework was Galenic, the advice was largely about the body's humoral balance. Diet, exercise, sleep and bathing were all regulated, and the Paris text warned that going out at night, and even until three o'clock in the morning, is dangerous on account of the dew. Remedies followed the same logic. People burned juniper, oak, and other aromatic woods in their homes and in the streets, hoping the smoke would overpower or neutralize the poisonous atmosphere. Physicians were not uniformly convinced of the Paris line. A Montpellier doctor wrote in 1349 that the epidemic was airborne, and could kill in high numbers.

Quarantine and containment

Some port cities adopted measures that did not depend on the miasma model. The Venetian authorities are said to have begun detaining ships in 1348: a council in the republic of Venice gained power to detain ships in the Venetian lagoon for up to 30 days and turn others away. The best-documented early measure is from Ragusa (Dubrovnik). In 1377 the city's council required that those who come from plague-infested areas shall not enter [Ragusa] or its district unless they spend a month on the islet of Mrkan or in the town of Cavtat, for the purpose of disinfection. The chief physician of Ragusa also proposed a site outside the walls for treating the sick (the chief physician of Ragusa, Jacob of Padua, also advised establishing a place outside the city walls for the treatment of sick (or suspected to be infected) citizens.). The 30-day period later grew to 40 days, the root of the word "quarantine" (In the following decades, the practice spread to other cities and was extended from 30 to 40 days (quarantino).). Venice opened a permanent isolation island in 1423, the Lazzaretto Vecchio. Other cities also used travel restrictions; Milan, for example, imposed bans on goods and people from plague-affected cities (From the Duchy of Milan to the west it adopted the use of travel bans on goods and people from plague-affected cities.).

Penitential processions and flagellants

Public prayer and penance were the main religious responses. Pope Clement VI had permitted a procession in Avignon in 1348 (As early as 1348, Pope Clement VI had permitted a similar procession in Avignon in entreaty against the plague.). The flagellant movement grew from that penitential culture but moved beyond Church control. It seems to have started in late 1348 in the areas of Austria and Hungary. By the spring of 1349, the flagellant movement had reached central Germany. Participants believed the plague was a divine punishment and sought mercy by punishing their own bodies (punished by God for its sins through the destruction of the plague, and their solution was to "punish" themselves in hopes of receiving God's mercy.). Their marches, often lasting weeks, drew large crowds. The movement also challenged clerical authority. These bands posed a great threat to the authority of the Church and exposed its weakened hold over the Christian laity. In late 1349 Clement VI condemned the movement in a papal bull, criticizing their "shedding the blood of Jews".

Persecution of Jewish communities, 1348–1349

Rumours that Jews had poisoned wells spread rapidly. As a result of this theory of infected water and air as the source of the plague the Jews were suddenly and violently charged with infecting wells and water and corrupting the air. The violence began in 1348: pogroms against Jews had occurred in European cities, starting in Toulon. By November of that year, they spread via Savoy to German-speaking territories. Flagellant processions often intensified the attacks (They sought scapegoats to blame for the evil and accused Jews of poisoning the water wells.). Some local bishops encouraged the massacres, although the papacy, under Clement VI and his successor Innocent VI, opposed them (Although these beliefs, and the accompanying massacres, were frequently encouraged by local bishops or itinerant Flagellants, the Catholic Church, including Pope Clement VI under whom the Flagellants and the Black Death began, and his successor, Innocent VI, were firmly against it.). In some cities, authorities who tried to protect Jews were overthrown by mobs (In this city the authorities, who attempted to save the Jews, were overthrown by a fear-stricken mob). The largest single atrocity occurred at Strasbourg, where the entire Jewish community of 2,000 Jews was publicly burnt to death on 14 February 1349.

Burial, charity and institutional strain

The scale of death overwhelmed ordinary funerary practice. In Venice, for example, bodies piled in streets, trade collapsed during the epidemic. Churchyards filled quickly, and many towns resorted to mass burial in large pits, often outside the walls. The clergy, who ministered to the dying, suffered heavy losses, and the Church struggled to replace them (succumbed to the pestilence, and the individuals whom the Church recruited to take their place could not adequately perform their duties.). Charitable responses were largely local and institutional: confraternities, hospitals and, later, dedicated plague hospitals such as the Lazzaretto Vecchio.

Social, political and cultural legacies

Historians still disagree about how far the pandemic reshaped medieval society. Its effect on the manorial order is the most debated case. Feudalism and serfdom had been weakening for several generations before the Plague struck, driven by expanding markets, and the Plague acted as a catalyst that hastened a process that might otherwise have taken much longer. In the longer run, manorialism never recovered. With land plentiful, wages high, and fewer limits on social and geographical mobility, serfdom all but disappeared. Recent scholarship has qualified the older account. Mark Bailey, for example, argues that manorial lordship is presented as less of a constraining force on English economic development compared to a previous view in the historiography, and he places the decisive change in the period immediately after the epidemic rather than later in the century.

The Church's standing is a second contested question. The disease killed people of every rank, which tested their faith in the feudal system: God had struck down people of all classes with the pestilence. Clerical losses and falling congregations also weakened ecclesiastical institutions in many places. Whether this produced a lasting decline in clerical authority, or only a short crisis of confidence, remains a matter of interpretation, and the evidence varies by region.

The pandemic's imprint on culture is easier to document. The effects of such a large-scale shared experience on the population of Europe influenced poetry, prose, stage works, music and artwork throughout the period. Boccaccio's Decameron, whose frame story depicts a group of Florentines sheltering from plague, is the best-known literary example. Its imagery of mortality also shaped visual art. The artistic movement that was fascinated with death and what happens after you die produced works such as the danse macabre, in which skeletal figures lead people of every station to the grave. Most surviving examples of this motif date from the fifteenth century, so the link to 1347–1353 is an inference from the timing and subject rather than a documented direct commission. Architectural change is similarly debated: in England, a shift from the Decorated to the Perpendicular style can be attributed to the Black Death, although the same source notes that economic causes, such as reduced capital for decoration, may have been more important.

The relationship between the plague and the Renaissance is the most disputed of these legacies. The older interpretation saw the crisis as a catalyst for secularism, individualism and humanist learning, and it linked the questioning of Church authority to later intellectual energy. A more recent reading argues that a fresh reading of the late medieval sources across intellectual strata from merchant chronicles to the plague tracts of university-trained doctors shows another trajectory, an about-face in the reactions to the plague after its initial onslaught. On this view, Italian political violence declined in the decades after the epidemic, and a new emphasis on fame and civic status emerged. Critics of direct causation stress that the Renaissance had many roots, and that the plague's role cannot be separated from economic and intellectual developments already underway.

Governance and taxation changed unevenly. In England, the crown's need for money was constrained by the requirement for parliamentary consent: the king could not tax his people without the permission of Parliament and so this body had to be called each time a monarch required more cash. The labor shortage also reduced the revenue base, since less available labour also meant less profit, and therefore less tax. Labor legislation was an administrative response in its own right. England's Ordinance of Laborers (1349) and Statute of Laborers (1351) called for a return to the wages and terms of employment of 1346. Similar measures appeared in the Córtes of Aragon and Castile, the French crown, and cities such as Siena, Orvieto, Pisa, Florence, and Ragusa. Their limited success is evident: the French crown revised its 1349 enactment in 1351 to permit a wage increase of one third.

In France, the strengthening of royal finance is usually attributed mainly to the Hundred Years' War rather than to the plague. Taxes levied at will by the king and the new apparatus needed to collect them required a whole new state apparatus of tax collectors, keepers of public records, and assessors for payment disputes. High wartime taxation, rather than the epidemic alone, is cited as a major source of the popular discontent that produced the Jacquerie of 1358.

Recurrences and the second plague pandemic

The Black Death of 1346–1353 was not the last wave. Historians usually treat it as the opening phase of a longer second plague pandemic, which recurred regularly until the 19th century. Other accounts place its end in the mid-18th century, describing intermittent bubonic plague epidemics that lasted until about 1750. The difference reflects how the pandemic's end is defined, not a dispute over the outbreaks themselves. In London, for example, plague deaths were recorded in the early 17th century on a large scale, with 30,000 deaths due to the plague in 1603, 35,000 in 1625, and 10,000 in 1636, and the city was affected by plague in most decades in between.

The Great Plague of London, 1665–1666

The last and most severe English epidemic was the Great Plague of London. It began in London's suburb of St. Giles-in-the-Fields, and its worst effects fell on densely crowded poor districts such as Stepney, Shoreditch and Clerkenwell. The court left the city in the summer of 1665, and the weekly toll peaked in September, when London mortality bills recorded 7,165 deaths from plague in a single week. The official count was 68,596 people, but the actual number is suspected to have exceeded 100,000 out of a total population estimated at 460,000. Deaths fell sharply in December 1665. From 1667 on there was no epidemic of plague in any part of England, although sporadic cases continued to appear in the bills of mortality until 1679. The Great Fire of September 1666 is often cited as a cause of the decline, but it also subsided in other cities without such cause, and scholars generally agree that the cessation of plague in England was spontaneous.

The third plague pandemic

The third plague pandemic began in the 1850s. It began in Yunnan, China, in 1855, and it was named as the third of the major pandemics caused by Yersinia pestis. Genetic studies have placed its origin in Yunnan Province; a 2026 study linked its emergence to a severe drought on the southeastern Tibetan Plateau during the 1850s–1880s, when troop movements, refugees, and opium trade sped its spread through Hong Kong. Its scale was far larger than any earlier wave in the modern era, with more than 12 million deaths in India and China, and by the beginning of the 20th century, infected rats traveling on steamships had carried it to all six inhabited continents. Unlike the Black Death, it manifested almost exclusively as bubonic plague. Its activity is usually dated to the middle of the 20th century, with one source noting that it would eventually claim some 15 million lives before petering out in the 1950s, while another gives 1960 as the year worldwide casualties fell to about 200 per year.

The third pandemic also shaped modern understanding of the disease. Its outbreak in Hong Kong in 1894 allowed Alexandre Yersin and Kitasato Shibasaburō to identify the bacterium independently, and the bacterium is named after Yersin. Paul-Louis Simond's work around 1898 supported the link between rat fleas and transmission, which became the basis for later control measures.

Plague today

Plague has not disappeared. Plague has been absent from Europe for over half a century now, but is still widespread in the Americas, Africa and Asia, and a few thousands of cases are reported worldwide each year. The disease persists in natural foci, where the presence of Y. pestis along with a compatible animal reservoir (rodents) and vector (fleas) allows it to circulate, and the wild rodents involved normally undergo a subclinical course of infection. Madagascar reported 80.5% of all human cases in the world between 2015 and 2018, making it the most affected country in that period.

Surveillance now combines human, rodent, flea and carnivore monitoring. Public-health authorities watch for early warning signs such as sudden decreases in rodent density and higher than normal numbers of dead rats. Treatment has changed the outcome for patients: streptomycin, gentamicin or tetracyclines (doxycycline) are the most appropriate antibiotics, and common antibiotics for enterobacteria can effectively cure the disease if they are delivered early. There is no approved vaccine, so prevention relies on reducing contact with wild rodents and their fleas.

Research history, sources and methods

Early written sources

Most of what historians know about the pandemic comes from written records. Chroniclers such as Henry Knighton, along with Petrarch and Boccaccio, documented the Great Death from secular and religious institutional viewpoints, and tax records, court rolls and property inheritance lists also survive. Boccaccio's introduction to the Decameron is the best-known of these accounts. Boccaccio survived the 1348 outbreak in Florence, and the Decameron frames its stories around young Florentines who flee the disease. Among medieval historians and literary critics, his account is probably the most familiar portrayal of the plague in Florence. Its mix of fiction and observation has made it a source that scholars must read with care.

Other chroniclers wrote from different vantage points. Knighton, a canon at Leicester, wrote his chronicle toward the end of the fourteenth century and recorded the post-plague years largely from memory, describing how labor shortages left fields and animals unattended and pushed landowners to pay higher wages. Early modern scholarship also shaped the field. In 1832 the Berlin medical historian Justus Friedrich Carl Hecker published an account in German that drew on chronicles and earlier records to explain the disease's origin and its spread across Europe. Modern historians still note that most knowledge of the symptoms comes from medieval chroniclers, many of them eyewitnesses, and from plague treatises written years and often decades after the first outbreak. Because of this gap, some historians, such as Samuel Cohn, have argued from the same medieval sources that the Black Death was not modern bubonic plague.

Ancient DNA and the 2011 London genome

For much of the twentieth century, the identity of the pathogen was inferred rather than proven. Ancient DNA has since confirmed that Yersinia pestis was involved in both the medieval and the later historical pandemics. Beginning in 2010, researchers extracted DNA from the pulp of teeth from victims in London's Black Death cemeteries and from medieval Barcelona and other European sites.

In 2011 a team led by Kirsten Bos and Johannes Krause reported a draft genome from the East Smithfield burial ground in London. The plague pits there lay beneath what is now the Royal Mint. The researchers sequenced the bacterium to 30-fold average coverage, using victims securely dated to 1348–1350. Their phylogenetic analysis placed it close to the ancestral node of the Y. pestis lineage that infects humans. They also argued that the 1347–1351 pandemic was the main event that spread the ancestor of today's human-pathogenic strains. To guard against contamination, the work was carried out in a laboratory that had never handled Y. pestis, the results were replicated independently, and a medieval cemetery that predated the pandemic yielded no Y. pestis DNA. The ancient genome differs from a modern reference by only 97 DNA letters out of around 4.6 million. One tooth carried a version that was three letters closer to modern strains than the others, which shows the bacterium was already changing during the pandemic.

Evidence for multiple lineages

The genomic record shows that the second pandemic involved more than one bacterial lineage. A 2016 study reported no detectable differences between a Black Death strain from Barcelona and three London strains from 1348–1350. The same study identified a lineage that originates from Black Death strains represented by the London and Barcelona isolates. Such results indicate that closely related variants circulated across Europe, although the precise number of variants and their routes remain under study.

The 2022 central Eurasian study and open questions

In June 2022 a team led by Maria Spyrou published findings in Nature that drew on ancient DNA from seven people exhumed at the Burana and Kara-Djigach cemeteries near Lake Issyk-Kul. Two reconstructed genomes represent a single strain, which is the most recent common ancestor of a major diversification linked to the pandemic's emergence, dated to the first half of the fourteenth century. Comparisons with present-day strains found that closely related lineages occur in eastern Kazakhstan, eastern Kyrgyzstan and Xinjiang, which the authors interpreted as consistent with local emergence in the Tian Shan region. The study's model links this early diversification to human movement during the territorial expansion of the Mongol Empire in the early thirteenth century. The lead author has said the source strain can be dated to 1338.

Several questions remain open. The sampling is too narrow to show how far the strain spread. Earlier work also shows that Y. pestis can spread quickly without accumulating much genetic variation, so identical sequences may occur across wide areas. The authors themselves concluded that earlier attributions of outbreaks to the 14th century require further investigation. Commentators have described the origin of the Black Death as one of the biggest unsolved mysteries in the history of medicine, and some have framed the 2022 study as a new beginning rather than a closed case.

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