Search This Blog

Friday, March 27, 2020

Black Death

From Wikipedia, the free encyclopedia
Spread of the Black Death in Europe and the Near East (1346–1353)

The Black Death, also known as the Pestilence, Great Bubonic Plague, the Great Plague or the Plague, or less commonly the Great Mortality or the Black Plague, was the most devastating pandemic recorded in human history, resulting in the deaths of an estimated 75 to 200 million people in Eurasia, peaking in Europe from 1347 to 1351. The bacterium Yersinia pestis, which results in several forms of plague (septicemic, pneumonic and, the most common, bubonic), is believed to have been the cause. The Black Death was the first major European outbreak of plague and the second plague pandemic. The plague created a number of religious, social and economic upheavals, with profound effects on the course of European history.

The Black Death probably originated in Central Asia or East Asia, from where it travelled along the Silk Road, reaching Crimea by 1343. From there, it was most likely carried by fleas living on the black rats that traveled on Genoese merchant ships, spreading throughout the Mediterranean Basin, reaching the rest of Europe via the Italian peninsula.

The Black Death is estimated to have killed 30% to 60% of Europe's population. In total, the plague may have reduced the world population from an estimated 475 million to 350–375 million in the 14th century. It took 200 years for Europe's population to recover to its previous level, and some regions (such as Florence) only recovered by the 19th century. Outbreaks of the plague recurred until the early 20th century.

Names

The phrase "black death" (mors nigra) was used in 1350 by Simon de Covino or Couvin, a Belgian astronomer, who wrote the poem "On the Judgment of the Sun at a Feast of Saturn" (De judicio Solis in convivio Saturni), which attributes the plague to a conjunction of Jupiter and Saturn. In 1908, Gasquet claimed that use of the name atra mors for the 14th-century epidemic first appeared in a 1631 book on Danish history by J. I. Pontanus: "Commonly and from its effects, they called it the black death" (Vulgo & ab effectu atram mortem vocitabant). The name spread through Scandinavia and then Germany, gradually becoming attached to the mid 14th-century epidemic as a proper name.

However, atra mors is used to refer to a pestilential fever (febris pestilentialis) already in the 12th-century On the Signs and Symptoms of Diseases (Latin: De signis et sinthomatibus egritudinum) by French physician Gilles de Corbeil. In English, the term was first used in 1755. Writers contemporary with the plague described the event as "great plague" or "great pestilence".

Chronology

Origins

The plague disease, caused by Yersinia pestis, is enzootic (commonly present) in populations of fleas carried by ground rodents, including marmots, in various areas, including Central Asia, Kurdistan, Western Asia, North India, and Uganda. Due to climate change in Asia, rodents began to flee the dried-out grasslands to more populated areas, spreading the disease. In October 2010, medical geneticists suggested that all three of the great waves of the plague originated in China. Research in 2017 concerning Nestorian graves dating to 1338–1339 near Issyk-Kul in Kyrgyzstan that have inscriptions referring to plague, has led many epidemiologists to think they mark the outbreak of the epidemic; from which it could easily have spread to China and India.

Research in 2018 found evidence of Yersinia pestis in an ancient Swedish tomb, which may have been the cause of what has been described as the Neolithic decline around 3000 BC, in which European populations declined significantly. In 2013, researchers confirmed earlier speculation that the cause of the Plague of Justinian (541–542 AD, with recurrences until 750) was Yersinia pestis.

The 13th-century Mongol conquest of China caused a decline in farming and trading. Economic recovery had been observed at the beginning of the fourteenth century. In the 1330s, many natural disasters and plagues led to widespread famine, starting in 1331, with a deadly plague arriving soon after. Epidemics, that may have included the plague, killed an estimated 25 million across Asia during the fifteen years before it reached Constantinople in 1347.

The disease may have traveled along the Silk Road with Mongol armies and traders, or it could have arrived via ship. By the end of 1346, reports of plague had reached the seaports of Europe: "India was depopulated, Tartary, Mesopotamia, Syria, Armenia were covered with dead bodies".

Plague was reportedly first introduced to Europe via Genoese traders from the port city of Kaffa in the Crimea in 1347. During a protracted siege of the city by the Mongol army under Jani Beg, whose army was suffering from the disease, the army catapulted infected corpses over the city walls of Kaffa to infect the inhabitants. The Genoese traders fled, taking the plague by ship into Sicily, then the Italian mainland, whence it spread north. Whether or not this hypothesis is accurate, it is clear that several existing conditions, such as war, famine, and weather, contributed to the severity of the Black Death. Among many other culprits of plague contagiousness, malnutrition, even if distantly, also contributed to such an immense loss in European population, since it weakened immune systems.

European outbreak

The seventh year after it began, it came to England and first began in the towns and ports joining on the seacoasts, in Dorsetshire, where, as in other counties, it made the country quite void of inhabitants so that there were almost none left alive.
... But at length it came to Gloucester, yea even to Oxford and to London, and finally it spread over all England and so wasted the people that scarce the tenth person of any sort was left alive.--Geoffrey the Baker, Chronicon Angliae
There appear to have been several introductions into Europe. The plague reached Sicily in October 1347, carried by twelve Genoese galleys, and rapidly spread all over the island. Galleys from Kaffa reached Genoa and Venice in January 1348, but it was the outbreak in Pisa a few weeks later that was the entry point to northern Italy. Towards the end of January, one of the galleys expelled from Italy arrived in Marseille.

From Italy, the disease spread northwest across Europe, striking France, Spain (which was hit due to the heat – the epidemic raged in the early weeks of July), Portugal and England by June 1348, then spread east and north through Germany, Scotland and Scandinavia from 1348 to 1350. It was introduced into Norway in 1349 when a ship landed at Askøy, then spread to Bjørgvin (modern Bergen) and Iceland. Finally, it spread to northwestern Russia in 1351. The plague was somewhat more uncommon in parts of Europe with less developed trade with their neighbours, including the majority of the Basque Country, isolated parts of Belgium and the Netherlands, and isolated alpine villages throughout the continent.

According to some epidemiologists, periods of unfavorable weather decimated plague-infected rodent populations and forced their fleas onto alternative hosts, inducing plague outbreaks which often peaked in the hot summers of the Mediterranean, as well as during the cool autumn months of the southern Baltic states. However, other researchers do not think that the plague ever became endemic in Europe or its rat population. The disease repeatedly wiped out the rodent carriers, so that the fleas died out until a new outbreak from Central Asia repeated the process. The outbreaks have been shown to occur roughly 15 years after a warmer and wetter period in areas where plague is endemic in other species, such as gerbils.

Middle Eastern outbreak

The plague struck various regions in the Middle East during the pandemic, leading to serious depopulation and permanent change in both economic and social structures. It may have spread from Central Asia with the Mongols to a trading post in Crimea, called Kaffa, controlled by the Republic of Genoa. As infected rodents infected new rodents, the disease spread across the region, including South Africa entering also from southern Russia. By autumn 1347, the plague reached Alexandria in Egypt, through the port's trade with Constantinople, and ports on the Black Sea. During 1347, the disease travelled eastward to Gaza, and north along the eastern coast to cities in modern Lebanon, Syria, Israel and Palestine, including Ashkelon, Acre, Jerusalem, Sidon, Damascus, Homs, and Aleppo. Within two years, the plague had spread throughout the entire Muslim empire from Arabia across North Africa. In 1348–1349, the disease reached Antioch. The city's residents fled to the north, but most of them ended up dying during the journey.

Mecca became infected in 1349. During the same year, records show the city of Mosul suffered a massive epidemic, and the city of Baghdad experienced a second round of the disease. 

Muslim religious scholars taught that the plague was a “martyrdom and mercy” from God, assuring the believer's place in paradise. For non-believers, it was a punishment. Some Muslim doctors cautioned against trying to prevent or treat a disease sent by God. Others adopted many of the same preventive measures and treatments for the plague used by the Europeans. These Muslim doctors also depended on the writings of the ancient Greeks.

Signs and symptoms

A hand showing how acral gangrene of the fingers due to bubonic plague causes the skin and flesh to die and turn black
 
An inguinal bubo on the upper thigh of a person infected with bubonic plague. Swollen lymph nodes (buboes) often occur in the neck, armpit and groin (inguinal) regions of plague victims.

Contemporary accounts of the plague are often varied or imprecise. The most commonly noted symptom was the appearance of buboes (or gavocciolos) in the groin, the neck and armpits, which oozed pus and bled when opened. Boccaccio's description:
In men and women alike it first betrayed itself by the emergence of certain tumours in the groin or armpits, some of which grew as large as a common apple, others as an egg ... From the two said parts of the body this deadly gavocciolo soon began to propagate and spread itself in all directions indifferently; after which the form of the malady began to change, black spots or livid making their appearance in many cases on the arm or the thigh or elsewhere, now few and large, now minute and numerous. As the gavocciolo had been and still was an infallible token of approaching death, such also were these spots on whomsoever they showed themselves.
The only medical detail that is questionable in Boccaccio's description is that the gavocciolo was an "infallible token of approaching death", as, if the bubo discharges, recovery is possible.

This was followed by acute fever and vomiting of blood. Most victims died two to seven days after initial infection. Freckle-like spots and rashes, which could have been caused by flea-bites, were identified as another potential sign of the plague.

Some accounts, like that of Lodewijk Heyligen, whose master the Cardinal Colonna died of the plague in 1348, noted a distinct form of the disease that infected the lungs and led to respiratory problems and is identified with pneumonic plague.
It is said that the plague takes three forms. In the first people suffer an infection of the lungs, which leads to breathing difficulties. Whoever has this corruption or contamination to any extent cannot escape but will die within two days. Another form ... in which boils erupt under the armpits, ... a third form in which people of both sexes are attacked in the groin.

Causes

The Oriental rat flea (Xenopsylla cheopis) engorged with blood. This species of flea is the primary vector for the transmission of Yersinia pestis, the organism responsible for spreading bubonic plague in most plague epidemics. Both male and female fleas feed on blood and can transmit the infection.
 
Oriental rat flea (Xenopsylla cheopis) infected with the Yersinia pestis bacterium which appears as a dark mass in the gut. The foregut (proventriculus) of this flea is blocked by a Y. pestis biofilm; when the flea feeds on an uninfected host Y. pestis is regurgitated into the wound, causing infection.
 
Yersinia pestis (200× magnification), the bacterium which causes bubonic plague
 
Medical knowledge had stagnated during the Middle Ages. The most authoritative account at the time came from the medical faculty in Paris in a report to the king of France that blamed the heavens, in the form of a conjunction of three planets in 1345 that caused a "great pestilence in the air". This report became the first and most widely circulated of a series of plague tracts that sought to give advice to sufferers. That the plague was caused by bad air became the most widely accepted theory at the time, the miasma theory. The word plague did not at first refer to a specific illness, and only the recurrence of outbreaks during the Middle Ages gave it the meaning which persists in modern medicine. 

The importance of hygiene was recognised only in the nineteenth century; until then streets were commonly filthy, with live animals of all sorts around and human parasites abounding, facilitating the spread of transmissible disease. One early medical advance as a result of the Black Death was the establishment of the idea of quarantine in the city-state of Ragusa (modern Dubrovnik, Croatia) in 1377 after continuing outbreaks.

Today, the dominant explanation for the Black Death is the plague theory, which attributes the outbreak to Yersinia pestis, also responsible for an epidemic that began in southern China in 1865, eventually spreading to India. The investigation of the pathogen that caused the 19th-century plague was begun by teams of scientists who visited Hong Kong in 1894, among whom was the French-Swiss bacteriologist Alexandre Yersin, after whom the pathogen was named. The mechanism by which Y. pestis is usually transmitted was established in 1898 by Paul-Louis Simond and was found to involve the bites of fleas whose midguts had become obstructed by replicating Y. pestis several days after feeding on an infected host. This blockage starves the fleas and drives them to aggressive feeding behaviour and attempts to clear the blockage by regurgitation, resulting in thousands of plague bacteria being flushed into the feeding site, infecting the host. The bubonic plague mechanism was also dependent on two populations of rodents: one resistant to the disease, which act as hosts, keeping the disease endemic, and a second that lack resistance. When the second population dies, the fleas move on to other hosts, including people, thus creating a human epidemic.

The historian Francis Aidan Gasquet wrote about the Great Pestilence in 1893 and suggested that "it would appear to be some form of the ordinary Eastern or bubonic plague". He was able to adopt the epidemiology of the bubonic plague for the Black Death for the second edition in 1908, implicating rats and fleas in the process, and his interpretation was widely accepted for other ancient and medieval epidemics, such as the Plague of Justinian that was prevalent in the Eastern Roman Empire from 541 to 700 CE.

An estimate of the case fatality rate for the modern bubonic plague, following the introduction of antibiotics, is 11%, although it may be higher in underdeveloped regions. Symptoms of the disease include fever of 38–41 °C (100–106 °F), headaches, painful aching joints, nausea and vomiting, and a general feeling of malaise. Left untreated, of those that contract the bubonic plague, 80 percent die within eight days. Pneumonic plague has a mortality rate of 90 to 95 percent. Symptoms include fever, cough, and blood-tinged sputum. As the disease progresses, sputum becomes free-flowing and bright red. Septicemic plague is the least common of the three forms, with a mortality rate near 100%. Symptoms are high fevers and purple skin patches (purpura due to disseminated intravascular coagulation). In cases of pneumonic and particularly septicemic plague, the progress of the disease is so rapid that there would often be no time for the development of the enlarged lymph nodes that were noted as buboes.

A number of alternative theories, implicating other diseases in the Black Death pandemic, have also been proposed by some modern scientist.

DNA evidence

Skeletons in a mass grave from 1720–1721 in Martigues, France, yielded molecular evidence of the orientalis strain of Yersinia pestis, the organism responsible for bubonic plague. The second pandemic of bubonic plague was active in Europe from 1347, the beginning of the Black Death, until 1750.

In 1998, Drancourt et al. reported the detection of Y. pestis DNA in human dental pulp from a medieval grave. Another team led by Tom Gilbert cast doubt on this identification and the techniques employed, stating that this method "does not allow us to confirm the identification of Y. pestis as the aetiological agent of the Black Death and subsequent plagues. In addition, the utility of the published tooth-based ancient DNA technique used to diagnose fatal bacteraemias in historical epidemics still awaits independent corroboration".

Definitive confirmation of the role of Y. pestis arrived in 2010 with a publication in PLOS Pathogens by Haensch et al. They assessed the presence of DNA/RNA with polymerase chain reaction (PCR) techniques for Y. pestis from the tooth sockets in human skeletons from mass graves in northern, central and southern Europe that were associated archaeologically with the Black Death and subsequent resurgences. The authors concluded that this new research, together with prior analyses from the south of France and Germany, "ends the debate about the cause of the Black Death, and unambiguously demonstrates that Y. pestis was the causative agent of the epidemic plague that devastated Europe during the Middle Ages". In 2011, these results were further confirmed with genetic evidence derived from Black Death victims in the East Smithfield burial site in England. Schuenemann et al. concluded in 2011 "that the Black Death in medieval Europe was caused by a variant of Y. pestis that may no longer exist."

Later in 2011, Bos et al. reported in Nature the first draft genome of Y. pestis from plague victims from the same East Smithfield cemetery and indicated that the strain that caused the Black Death is ancestral to most modern strains of Y. pestis.

Since this time, further genomic papers have further confirmed the phylogenetic placement of the Y. pestis strain responsible for the Black Death as both the ancestor of later plague epidemics including the third plague pandemic and as the descendant of the strain responsible for the Plague of Justinian. In addition, plague genomes from significantly earlier in prehistory have been recovered.

DNA taken from 25 skeletons from 14th century London have shown the plague is a strain of Y. pestis almost identical to that which hit Madagascar in 2013.

Alternative explanations

The plague theory implicating Y. pestis was first significantly challenged by the work of British bacteriologist J. F. D. Shrewsbury in 1970, who noted that the reported rates of mortality in rural areas during the 14th-century pandemic were inconsistent with the modern bubonic plague, leading him to conclude that contemporary accounts were exaggerations. In 1984, zoologist Graham Twigg produced the first major work to challenge the bubonic plague theory directly, and his doubts about the identity of the Black Death have been taken up by a number of authors, including Samuel K. Cohn, Jr. (2002 and 2013), David Herlihy (1997), and Susan Scott and Christopher Duncan (2001).

It is recognised that an epidemiological account of the plague is as important as an identification of symptoms, but researchers are hampered by the lack of reliable statistics from this period. Most work has been done on the spread of the plague in England, and even estimates of overall population at the start vary by over 100% as no census was undertaken between the time of publication of the Domesday Book and poll tax of the year 1377. Estimates of plague victims are usually extrapolated from figures for the clergy. 

In addition to arguing that the rat population was insufficient to account for a bubonic plague pandemic, sceptics of the bubonic plague theory point out that the symptoms of the Black Death are not unique (and arguably in some accounts may differ from bubonic plague); that transference via fleas in goods was likely to be of marginal significance; and that the DNA results may be flawed and might not have been repeated elsewhere or were not replicable at all, despite extensive samples from other mass graves. Other arguments include the lack of accounts of the death of rats before outbreaks of plague between the 14th and 17th centuries; temperatures that are too cold in northern Europe for the survival of fleas; that, despite primitive transport systems, the spread of the Black Death was much faster than that of modern bubonic plague; that mortality rates of the Black Death appear to be very high; that, while modern bubonic plague is largely endemic as a rural disease, the Black Death indiscriminately struck urban and rural areas; and that the pattern of the Black Death, with major outbreaks in the same areas separated by 5 to 15 years, differs from modern bubonic plague—which often becomes endemic for decades with annual flare-ups.

McCormick has suggested that earlier archaeologists were simply not interested in the "laborious" processes needed to discover rat remains. Walløe complains that all of these authors "take it for granted that Simond's infection model, black rat → rat flea → human, which was developed to explain the spread of plague in India, is the only way an epidemic of Yersinia pestis infection could spread", whilst pointing to several other possibilities. Similarly, Green has argued that greater attention is needed to the range of (especially non-commensal) animals that might be involved in the transmission of plague.

Anthrax skin lesion

A variety of alternatives to Y. pestis have been put forward. Twigg suggested that the cause was a form of anthrax, and Norman Cantor thought it may have been a combination of anthrax and other pandemics. Scott and Duncan have argued that the pandemic was a form of infectious disease that they characterise as hemorrhagic plague similar to Ebola. Archaeologist Barney Sloane has argued that there is insufficient evidence of the extinction of numerous rats in the archaeological record of the medieval waterfront in London and that the plague spread too quickly to support the thesis that Y. pestis was spread from fleas on rats; he argues that transmission must have been person to person. This theory is supported by research in 2018 which suggested transmission was more likely by body lice and human fleas during the second plague pandemic.

However, no single alternative solution has achieved widespread acceptance. Many scholars arguing for Y. pestis as the major agent of the pandemic suggest that its extent and symptoms can be explained by a combination of bubonic plague with other diseases, including typhus, smallpox and respiratory infections. In addition to the bubonic infection, others point to additional septicemic (a type of "blood poisoning") and pneumonic (an airborne plague that attacks the lungs before the rest of the body) forms of the plague, which lengthen the duration of outbreaks throughout the seasons and help account for its high mortality rate and additional recorded symptoms. In 2014, Public Health England announced the results of an examination of 25 bodies exhumed in the Clerkenwell area of London, as well as of wills registered in London during the period, which supported the pneumonic hypothesis.

The historian George Hussman claimed that the plague had not occurred in East Africa until the 1900s. However, other sources suggest that the Second pandemic did indeed reach Sub-Saharan Africa.

Consequences

Death toll

Citizens of Tournai bury plague victims

There are no exact figures for the death toll; the rate varied widely by locality. In urban centres, the greater the population before the outbreak, the longer the duration of the period of abnormal mortality. It killed some 75 to 200 million people in Eurasia. According to medieval historian Philip Daileader in 2007:
The trend of recent research is pointing to a figure more like 45–50% of the European population dying during a four-year period. There is a fair amount of geographic variation. In Mediterranean Europe, areas such as Italy, the south of France and Spain, where plague ran for about four years consecutively, it was probably closer to 75–80% of the population. In Germany and England ... it was probably closer to 20%.
A death rate as high as 60% in Europe has been suggested by Norwegian historian Ole Benedictow:
Detailed study of the mortality data available points to two conspicuous features in relation to the mortality caused by the Black Death: namely the extreme level of mortality caused by the Black Death, and the remarkable similarity or consistency of the level of mortality, from Spain in southern Europe to England in north-western Europe. The data is sufficiently widespread and numerous to make it likely that the Black Death swept away around 60 per cent of Europe's population. It is generally assumed that the size of Europe's population at the time was around 80 million. This implies that around 50 million people died in the Black Death.
Half of Paris's population of 100,000 people died. In Italy, the population of Florence was reduced from 110,000–120,000 inhabitants in 1338 down to 50,000 in 1351. At least 60% of the population of Hamburg and Bremen perished, and a similar percentage of Londoners may have died from the disease as well. In London approximately 62,000 people died between 1346 and 1353. While contemporary reports account of mass burial pits being created in response to the large numbers of dead, recent scientific investigations of a burial pit in Central London found well-preserved individuals to be buried in isolated, evenly spaced graves, suggesting at least some pre-planning and Christian burials at this time. Before 1350, there were about 170,000 settlements in Germany, and this was reduced by nearly 40,000 by 1450. In 1348, the plague spread so rapidly that before any physicians or government authorities had time to reflect upon its origins, about a third of the European population had already perished. In crowded cities, it was not uncommon for as much as 50% of the population to die. The disease bypassed some areas, and the most isolated areas were less vulnerable to contagion. Monks, nuns and priests were especially hard-hit since they cared for victims of the Black Death.

The most widely accepted estimate for the Middle East, including Iraq, Iran and Syria, during this time, is for a death toll of about a third of the population. The Black Death killed about 40% of Egypt's population.

Economic

With such a large population decline from the plague, wages soared in response to a labor shortage. Landowners were also pushed to substitute monetary rents for labour services in an effort to keep tenants.

Environmental

Some historians believe the innumerable deaths brought on by the plague cooled the climate by freeing up land and triggering reforestation. This may have led to the Little Ice Age.

Persecutions

Inspired by the Black Death, The Dance of Death, or Danse Macabre, an allegory on the universality of death, was a common painting motif in the late medieval period.
 
Renewed religious fervour and fanaticism bloomed in the wake of the Black Death. Some Europeans targeted "various groups such as Jews, friars, foreigners, beggars, pilgrims", lepers, and Romani, blaming them for the crisis. Lepers, and others with skin diseases such as acne or psoriasis, were killed throughout Europe.

Because 14th-century healers and governments were at a loss to explain or stop the disease, Europeans turned to astrological forces, earthquakes, and the poisoning of wells by Jews as possible reasons for outbreaks. Many believed the epidemic was a punishment by God for their sins, and could be relieved by winning God's forgiveness.

There were many attacks against Jewish communities. In the Strasbourg massacre of February 1349, about 2,000 Jews were murdered. In August 1349, the Jewish communities in Mainz and Cologne were annihilated. By 1351, 60 major and 150 smaller Jewish communities had been destroyed. During this period many Jews relocated to Poland, where they received a warm welcome from King Casimir the Great.

Second plague pandemic

The Great Plague of London, in 1665, killed up to 100,000 people.

The plague repeatedly returned to haunt Europe and the Mediterranean throughout the 14th to 17th centuries. According to Biraben, the plague was present somewhere in Europe in every year between 1346 and 1671. (Note that some researchers  have cautions about the uncritical use of Biraben's data.) The second pandemic was particularly widespread in the following years: 1360–1363; 1374; 1400; 1438–1439; 1456–1457; 1464–1466; 1481–1485; 1500–1503; 1518–1531; 1544–1548; 1563–1566; 1573–1588; 1596–1599; 1602–1611; 1623–1640; 1644–1654; and 1664–1667. Subsequent outbreaks, though severe, marked the retreat from most of Europe (18th century) and northern Africa (19th century). According to Geoffrey Parker, "France alone lost almost a million people to the plague in the epidemic of 1628–31."

In England, in the absence of census figures, historians propose a range of pre-incident population figures from as high as 7 million to as low as 4 million in 1300, and a post-incident population figure as low as 2 million. By the end of 1350, the Black Death subsided, but further outbreaks occurred in 1361–1362, 1369, 1379–1383, 1389–1393, and throughout the first half of the 15th century. An outbreak in 1471 took as much as 10–15% of the population, while the death rate of the plague of 1479–1480 could have been as high as 20%. The most general outbreaks in Tudor and Stuart England seem to have begun in 1498, 1535, 1543, 1563, 1589, 1603, 1625, and 1636, and ended with the Great Plague of London in 1665.

Contemporary engraving of Marseille during the Great Plague in 1720

In 1466, perhaps 40,000 people died of the plague in Paris. During the 16th and 17th centuries, the plague was present in Paris around 30 percent of the time. The Black Death ravaged Europe for three years before it continued on into Russia, where the disease was present somewhere in the country 25 times between 1350 and 1490. Plague epidemics ravaged London in 1563, 1593, 1603, 1625, 1636, and 1665, reducing its population by 10 to 30% during those years. Over 10% of Amsterdam's population died in 1623–1625, and again in 1635–1636, 1655, and 1664. Plague occurred in Venice 22 times between 1361 and 1528. The plague of 1576–1577 killed 50,000 in Venice, almost a third of the population. Late outbreaks in central Europe included the Italian Plague of 1629–1631, which is associated with troop movements during the Thirty Years' War, and the Great Plague of Vienna in 1679. Over 60% of Norway's population died in 1348–1350. The last plague outbreak ravaged Oslo in 1654.

A plague doctor and his typical apparel during the 17th Century Outbreak.

In the first half of the 17th century, a plague claimed some 1.7 million victims in Italy, or about 14% of the population. In 1656, the Naples Plague killed about half of Naples' 300,000 inhabitants. More than 1.25 million deaths resulted from the extreme incidence of plague in 17th-century Spain. The plague of 1649 probably reduced the population of Seville by half. In 1709–1713, a plague epidemic that followed the Great Northern War (1700–1721, Sweden v. Russia and allies) killed about 100,000 in Sweden, and 300,000 in Prussia. The plague killed two-thirds of the inhabitants of Helsinki, and claimed a third of Stockholm's population. Western Europe's last major epidemic occurred in 1720 in Marseille. The 1770–1772 Russian plague killed up to 100,000 people in Moscow. An estimated 60,000 people died during the Caragea's plague in 1813–1814, 20–30,000 of them in Bucharest.

Contemporary engraving of Naples during the Naples Plague in 1656

The Black Death ravaged much of the Islamic world. Plague was present in at least one location in the Islamic world virtually every year between 1500 and 1850. Plague repeatedly struck the cities of North Africa. Algiers lost 30,000–50,000 inhabitants to it in 1620–1621, and again in 1654–1657, 1665, 1691, and 1740–1742. Plague remained a major event in Ottoman society until the second quarter of the 19th century. Between 1701 and 1750, thirty-seven larger and smaller epidemics were recorded in Constantinople, and an additional thirty-one between 1751 and 1800. Baghdad has suffered severely from visitations of the plague, and sometimes two-thirds of its population has been wiped out.

Social

One theory that has been advanced is that the devastation in Florence caused by the Black Death, which hit Europe between 1348 and 1350, resulted in a shift in the world view of people in 14th-century Italy and led to the Renaissance. Italy was particularly badly hit by the plague, and it has been speculated that the resulting familiarity with death caused thinkers to dwell more on their lives on Earth, rather than on spirituality and the afterlife. It has also been argued that the Black Death prompted a new wave of piety, manifested in the sponsorship of religious works of art. However, this does not fully explain why the Renaissance occurred specifically in Italy in the 14th century. The Black Death was a pandemic that affected all of Europe in the ways described, not only Italy. The Renaissance's emergence in Italy was most likely the result of the complex interaction of the above factors, in combination with an influx of Greek scholars following the fall of the Byzantine Empire.

Pieter Bruegel's The Triumph of Death reflects the social upheaval and terror that followed plague, which devastated medieval Europe.
 
The plague was carried by fleas on sailing vessels returning from the ports of Asia, spreading quickly due to lack of proper sanitation: the population of England, then about 4.2 million, lost 1.4 million people to the bubonic plague. Florence's population was nearly halved in the year 1347. As a result of the decimation in the populace the value of the working class increased, and commoners came to enjoy more freedom. To answer the increased need for labor, workers traveled in search of the most favorable position economically.

The demographic decline due to the plague had economic consequences: the prices of food dropped and land values declined by 30–40% in most parts of Europe between 1350 and 1400. Landholders faced a great loss, but for ordinary men and women it was a windfall. The survivors of the plague found not only that the prices of food were cheaper but also that lands were more abundant, and many of them inherited property from their dead relatives, and this probably destabilized feudalism

The spread of disease was significantly more rampant in areas of poverty. Epidemics ravaged cities, particularly children. Plagues were easily spread by lice, unsanitary drinking water, armies, or by poor sanitation. Children were hit the hardest because many diseases, such as typhus and congenital syphilis, target the immune system, leaving young children without a fighting chance. Children in city dwellings were more affected by the spread of disease than the children of the wealthy.
Italian chronicler Agnolo di Tura recorded his experience from Siena:
Father abandoned child, wife husband, one brother another; for this illness seemed to strike through the breath and sight. And so they died. And none could be found to bury the dead for money or friendship. Members of a household brought their dead to a ditch as best they could, without priest, without divine offices ... great pits were dug and piled deep with the multitude of dead. And they died by the hundreds both day and night ... And as soon as those ditches were filled more were dug ... And I, Agnolo di Tura ... buried my five children with my own hands. And there were also those who were so sparsely covered with earth that the dogs dragged them forth and devoured many bodies throughout the city. There was no one who wept for any death, for all awaited death. And so many died that all believed it was the end of the world.
The Black Death caused greater upheaval to Florence's social and political structure than later epidemics. Despite a significant number of deaths among members of the ruling classes, the government of Florence continued to function during this period. Formal meetings of elected representatives were suspended during the height of the epidemic due to the chaotic conditions in the city, but a small group of officials was appointed to conduct the affairs of the city, which ensured continuity of government.

Third plague pandemic

Worldwide distribution of plague-infected animals, 1998

The third plague pandemic (1855–1859) started in China in the mid-19th century, spreading to all inhabited continents and killing 10 million people in India alone. Twelve plague outbreaks in Australia between 1900 and 1925 resulted in well over 1,000 deaths, chiefly in Sydney. This led to the establishment of a Public Health Department there which undertook some leading-edge research on plague transmission from rat fleas to humans via the bacillus Yersinia pestis.

The first North American plague epidemic was the San Francisco plague of 1900–1904, followed by another outbreak in 1907–1908.

Modern treatment methods include insecticides, the use of antibiotics, and a plague vaccine. It is feared that the plague bacterium could develop drug resistance and again become a major health threat. One case of a drug-resistant form of the bacterium was found in Madagascar in 1995. A further outbreak in Madagascar was reported in November 2014. In October 2017 the deadliest outbreak of the plague in modern times hit Madagascar, killing 170 people and infecting thousands.

Great Plague of London

From Wikipedia, the free encyclopedia
 
Collecting the dead for burial during the Great Plague

The Great Plague, lasting from 1665 to 1666, was the last major epidemic of the bubonic plague to occur in England. It happened within the centuries-long time period of the Second Pandemic, an extended period of intermittent bubonic plague epidemics which originated in China in 1331, the first year of the Black Death, an outbreak which included other forms such as pneumonic plague, and lasted until 1750.

The Great Plague killed an estimated 100,000 people—almost a quarter of London's population—in 18 months. The plague was caused by the Yersinia pestis bacterium, which is usually transmitted through the bite of an infected rat flea.

The 1665–66 epidemic was on a far smaller scale than the earlier Black Death pandemic; it was remembered afterwards as the "great" plague mainly because it was the last widespread outbreak of bubonic plague in England during the 400-year timespan of the Second Pandemic.

London in 1665

Map of London by Wenceslas Hollar, c.1665

As in other European cities of the period, the plague was endemic in 17th century London. The disease periodically erupted into massive epidemics. There were 30,000 deaths due to the plague in 1603, 35,000 in 1625, and 10,000 in 1636, as well as smaller numbers in other years.

During the winter of 1664, a bright comet was to be seen in the sky and the people of London were fearful, wondering what evil event it portended. London at that time consisted of a city of about 448 acres surrounded by a city wall, which had originally been built to keep out raiding bands. There were gates at Ludgate, Newgate, Aldersgate, Cripplegate, Moorgate and Bishopsgate and to the south lay the River Thames and London Bridge. In the poorer parts of the city, hygiene was impossible to maintain in the overcrowded tenements and garrets. There was no sanitation, and open drains flowed along the centre of winding streets. The cobbles were slippery with animal dung, rubbish and the slops thrown out of the houses, muddy and buzzing with flies in summer and awash with sewage in winter. The City Corporation employed "rakers" to remove the worst of the filth and it was transported to mounds outside the walls where it accumulated and continued to decompose. The stench was overwhelming and people walked around with handkerchiefs or nosegays pressed against their nostrils.

Some of the city's necessities such as coal arrived by barge, but most came by road. Carts, carriages, horses and pedestrians were crowded together and the gateways in the wall formed bottlenecks through which it was difficult to progress. The nineteen-arch London Bridge was even more congested. The better-off used hackney carriages and sedan chairs to get to their destinations without getting filthy. The poor walked, and might be splashed by the wheeled vehicles and drenched by slops being thrown out and water falling from the overhanging roofs. Another hazard was the choking black smoke belching forth from factories which made soap, from breweries and iron smelters and from about 15,000 houses burning coal.

Scenes in London during the plague of 1665

Outside the city walls, suburbs had sprung up providing homes for the craftsmen and tradespeople who flocked to the already overcrowded city. These were shanty towns with wooden shacks and no sanitation. The government had tried to control this development but had failed and over a quarter of a million people lived here. Other immigrants had taken over fine town houses, vacated by Royalists who had fled the country during the Commonwealth, converting them into tenements with different families in every room. These properties were soon vandalised and became rat-infested slums.

The administration of the City of London was organised by the Lord Mayor, Aldermen and common councillors, but not all of the inhabited area generally comprising London was legally part of the City. Both inside the City and outside its boundaries there were also Liberties, which were areas of varying sizes which historically had been granted rights to self-government. Many had been associated with religious institutions, and when these were abolished in the Dissolution of the Monasteries, their historic rights were transferred along with their property to new owners. The walled City was surrounded by a ring of Liberties which had come under its authority, contemporarily called 'the City and Liberties', but these were surrounded by further suburbs with varying administrations. Westminster was an independent town with its own liberties, although it was joined to London by urban development. The Tower of London was an independent liberty, as were others. Areas north of the river not part of one of these administrations came under the authority of the county of Middlesex, and south of the river under Surrey.

The "Woodcut" map of London, dating from the 1560s

At that time, bubonic plague was a much feared disease but its cause was not understood. The credulous blamed emanations from the earth, "pestilential effluviums", unusual weather, sickness in livestock, abnormal behaviour of animals or an increase in the numbers of moles, frogs, mice or flies. It was not until 1894 that the identification by Alexandre Yersin of its causal agent Yersinia pestis was made and the transmission of the bacterium by rat fleas became known. Although the Great Plague in London had long been believed to be bubonic plague caused by Yersinia pestis, this was only definitively confirmed by DNA analysis in 2016.

The recording of deaths

In order to judge the severity of an epidemic, it is first necessary to know how big the population was in which it occurred. There was no official census of the population to provide this figure, and the best contemporary count comes from the work of John Graunt (1620–1674), who was one of the earliest Fellows of the Royal Society and one of the first demographers, bringing a scientific approach to the collection of statistics. In 1662, he estimated that 384,000 people lived in the City of London, the Liberties, Westminster and the out-parishes, based on figures in the bills of mortality published each week in the capital. These different districts with different administrations constituted the officially recognized extent of London as a whole. In 1665, he revised his estimate to 'not above 460,000'. Other contemporaries put the figure higher, (the French Ambassador, for example, suggested 600,000) but with no mathematical basis to support their estimates. The next largest city in the kingdom was Norwich, with a population of 30,000.

There was no duty to report a death to anyone in authority. Instead, each parish appointed two or more 'searchers of the dead', whose duty was to inspect a corpse and determine the cause of death. A searcher was entitled to charge a small fee from relatives for each death they reported, and so habitually the parish would appoint someone to the post who would otherwise be destitute and would be receiving support from the parish poor rate. Typically, this meant searchers would be old women who were illiterate, might know little about identifying diseases and who would be open to dishonesty. Searchers would typically learn about a death either from the local sexton who had been asked to dig a grave or from the tolling of a church bell. Anyone who did not report a death to their local church, such as Quakers, Anabaptists, other non-Anglican Christians or Jews, frequently did not get included in the official records. Searchers during times of plague were required to live apart from the community, avoid other people and carry a white stick to warn of their occupation when outdoors, and stay indoors except when performing their duties, to avoid spreading the diseases. Searchers reported to the Parish Clerk, who made a return each week to the Company of Parish Clerks in Brode Lane. Figures were then passed to the Lord Mayor and then to the Minister of State once plague became a matter of national concern. The reported figures were used to compile the Bills of Mortality, which listed total deaths in each parish and whether by the plague. The system of Searchers to report the cause of death continued until 1836.

Graunt recorded the incompetence of the Searchers at identifying true causes of death, remarking on the frequent recording of 'consumption' rather than other diseases which were recognized then by physicians. He suggested a cup of ale and a doubling of their fee to two groats rather than one was sufficient for Searchers to change the cause of death to one more convenient for the householders. No one wished to be known as having had a death by plague in their household, and Parish Clerks, too, connived in covering up cases of plague in their official returns. Analysis of the Bills of Mortality during the months plague took hold shows a rise in deaths other than by plague well above the average death rate, which has been attributed to misrepresentation of the true cause of death. As plague spread, a system of quarantine was introduced, whereby any house where someone had died from plague would be locked up and no one allowed to enter or leave for 40 days. This frequently led to the deaths of the other inhabitants, by neglect if not from the plague, and provided ample incentive not to report the disease. The official returns record 68,596 cases of plague, but a reasonable estimate suggests this figure is 30,000 short of the true total. A plague house was marked with a red cross on the door with the words "Lord have mercy upon us", and a watchman stood guard outside.

Preventive measures

Reports of plague around Europe began to reach England in the 1660s, causing the Privy Council to consider what steps might be taken to prevent it crossing to England. Quarantining of ships had been used during previous outbreaks and was again introduced for ships coming to London in November 1663, following outbreaks in Amsterdam and Hamburg. Two naval ships were assigned to intercept any vessels entering the Thames estuary. Ships from infected ports were required to moor at Hole Haven on Canvey Island for a period of 30 days before being allowed to travel upriver. Ships from ports free of plague or completing their quarantine were given a certificate of health and allowed to travel on. A second inspection line was established between the forts on opposite banks of the Thames at Tilbury and Gravesend with instructions only to pass ships with a certificate.

The quarantine duration was increased to forty days in May 1664 as the continental plague worsened, and the areas subject to quarantine changed with the news of the spread of plague to include all of Holland, Zeeland and Friesland (all regions of the Dutch Republic), although restrictions on Hamburg were removed in November. Quarantine measures against ships coming from the Dutch Republic were put in place in 29 other ports from May, commencing with Great Yarmouth. The Dutch ambassador objected at the constraint of trade with his country, but England responded that it had been one of the last countries introducing such restrictions. Regulations were enforced quite strictly, so that people or houses where voyagers had come ashore without serving their quarantine were also subjected to 40 days of quarantine.

Outbreak

Plague was one of the hazards of life in Britain from its dramatic appearance in 1348 with the Black Death. The Bills of Mortality began to be published regularly in 1603, in which year 33,347 deaths were recorded from plague. Between then and 1665, only four years had no recorded cases. In 1563, a thousand people were reportedly dying in London each week. In 1593, there were 15,003 deaths, 1625 saw 41,313 dead, between 1640 and 1646 came 11,000 deaths, culminating in 3,597 for 1647. The 1625 outbreak was recorded at the time as the 'Great Plague', until deaths from the plague of 1665 surpassed it. These official figures are likely to under-report actual numbers.

Early days

Rattus rattus, the Black Rat. Smaller than the Norwegian rat, which later supplanted it, it is also keener to live near to humankind. Timber houses and overcrowded slums provided great homes. The link between the rat as reservoir of infection and host to fleas which could transfer to man was not understood. Efforts were made to eliminate cats and dogs but not rats. If anything, this encouraged the rats.
 
Although plague was known, it was still sufficiently uncommon that medical practitioners might have had no personal experience of seeing the disease; medical training varied from those who had attended the college of physicians, to apothecaries who also acted as modern doctors, to simple charlatans. Other diseases abounded, such as an outbreak of smallpox the year before, and these uncertainties all added to difficulties identifying the true start of the epidemic. Contemporary accounts suggest cases of plague occurred through the winter of 1664/5, some of which were fatal but a number of which did not display the virulence of the later epidemic. The winter was cold, the ground frozen from December to March, river traffic on the Thames twice blocked by ice, and it may be that the cold weather held back its spread.

This outbreak of bubonic plague in England is thought to have spread from the Netherlands, where the disease had been occurring intermittently since 1599. It is unclear exactly where the disease first struck but the initial contagion may have arrived with Dutch trading ships carrying bales of cotton from Amsterdam, which was ravaged by the disease in 1663–1664, with a mortality given of 50,000. The first areas to be struck are believed to be the dock areas just outside London, and the parish of St Giles. In both of these localities, poor workers were crowded into ill-kept structures. Two suspicious deaths were recorded in St. Giles parish in 1664 and another in February 1665. These did not appear as plague deaths on the Bills of Mortality, so no control measures were taken by the authorities, but the total number of people dying in London during the first four months of 1665 showed a marked increase. By the end of April, only four plague deaths had been recorded, two in the parish of St. Giles, but total deaths per week had risen from around 290 to 398.

Although there had been only three official cases in April, which level of plague in earlier years had not induced any official response, the Privy Council now acted to introduce household quarantine. Justices of the Peace in Middlesex were instructed to investigate any suspected cases and to shut up the house if it was confirmed. Shortly after, a similar order was issued by the King's Bench to the City and Liberties. A riot broke out in St. Giles when the first house was sealed up; the crowd broke down the door and released the inhabitants. Rioters caught were punished severely. Instructions were given to build pest-houses, which were essentially isolation hospitals built away from other people where the sick could be cared for (or stay until they died). This official activity suggests that despite the few recorded cases, the government was already aware that this was a serious outbreak of plague.

With the arrival of warmer weather, the disease began to take a firmer hold. In the week 2–9 May, there were three recorded deaths in the parish of St Giles, four in neighbouring St Clement Danes and one each in St Andrew Holborn and St Mary Woolchurch Haw. Only the last was actually inside the city walls. A Privy Council committee was formed to investigate methods to best prevent the spread of plague, and measures were introduced to close some of the ale houses in affected areas and limit the number of lodgers allowed in a household. In the city, the Lord Mayor issued a proclamation that all householders must diligently clean the streets outside their property, which was a householder's responsibility, not a state one (the city employed scavengers and rakers to remove the worst of the mess). Matters just became worse, and Aldermen were instructed to find and punish those failing their duty. As cases in St. Giles began to rise, an attempt was made to quarantine the area and constables were instructed to inspect everyone wishing to travel and contain inside vagrants or suspect persons.

People began to be alarmed. Samuel Pepys, who had an important position at the Admiralty, stayed in London and provided a contemporary account of the plague through his diary. On 30 April he wrote: "Great fears of the sickness here in the City it being said that two or three houses are already shut up. God preserve us all!" Another source of information on the time is A Journal of the Plague Year, which was written by Daniel Defoe and published in 1722. He had been only six when the plague struck but made use of his family's recollections (his uncle was a saddler in East London and his father a butcher in Cripplegate), interviews with survivors and sight of such official records as were available.

Exodus from the city

By July 1665, plague was rampant in the City of London. The rich ran away, including King Charles II of England, his family and his court, who left the city for Salisbury, moving on to Oxford in September when some cases of plague occurred in Salisbury. The aldermen and most of the other city authorities opted to stay at their posts. The Lord Mayor of London, Sir John Lawrence, also decided to stay in the city. Businesses were closed when merchants and professionals fled. Defoe wrote "Nothing was to be seen but wagons and carts, with goods, women, servants, children, coaches filled with people of the better sort, and horsemen attending them, and all hurrying away". As the plague raged throughout the summer, only a small number of clergymen, physicians and apothecaries remained to cope with an increasingly large number of victims. Edward Cotes, author of London's Dreadful Visitation, expressed the hope that "Neither the Physicians of our Souls or Bodies may hereafter in such great numbers forsake us".

The poorer people were also alarmed by the contagion and some left the city, but it was not easy for them to abandon their accommodation and livelihoods for an uncertain future elsewhere. Before exiting through the city gates, they were required to possess a certificate of good health signed by the Lord Mayor and these became increasingly difficult to obtain. As time went by and the numbers of plague victims rose, people living in the villages outside London began to resent this exodus and were no longer prepared to accept townsfolk from London, with or without a certificate. The refugees were turned back, were not allowed to pass through towns and had to travel across country, and were forced to live rough on what they could steal or scavenge from the fields. Many died in wretched circumstances of starvation and thirst in the hot summer that was to follow.

Height of the epidemic

A bill of mortality for the plague in 1665

In the last week of July, the London Bill of Mortality showed 3,014 deaths, of which 2,020 had died from the plague. The number of deaths as a result of plague may have been underestimated, as deaths in other years in the same period were much lower, at around 300. As the number of victims affected mounted up, burial grounds became overfull, and pits were dug to accommodate the dead. Drivers of dead-carts travelled the streets calling "Bring out your dead" and carted away piles of bodies. The authorities became concerned that the number of deaths might cause public alarm and ordered that body removal and interment should take place only at night. As time went on, there were too many victims, and too few drivers, to remove the bodies which began to be stacked up against the walls of houses. Daytime collection was resumed and the plague pits became mounds of decomposing corpses. In the parish of Aldgate, a great hole was dug near the churchyard, fifty feet long and twenty feet wide. Digging was continued by labourers at one end while the dead-carts tipped in corpses at the other. When there was no room for further extension it was dug deeper until ground water was reached at twenty feet. When finally covered with earth it housed 1,114 corpses.

Plague doctors traversed the streets diagnosing victims, although many of them had no formal medical training. Several public health efforts were attempted. Physicians were hired by city officials and burial details were carefully organized, but panic spread through the city and, out of the fear of contagion, people were hastily buried in overcrowded pits. The means of transmission of the disease were not known but thinking they might be linked to the animals, the City Corporation ordered a cull of dogs and cats. This decision may have affected the length of the epidemic since those animals could have helped keep in check the rat population carrying the fleas which transmitted the disease. Thinking bad air was involved in transmission, the authorities ordered giant bonfires to be burned in the streets and house fires to be kept burning night and day, in hopes that the air would be cleansed. Tobacco was thought to be a prophylactic and it was later said that no London tobacconist had died from the plague during the epidemic.

Trade and business had completely dried up, and the streets were empty of people except for the dead-carts and the desperate dying victims, as witnessed and recorded by Samuel Pepys in his diary: "Lord! How empty the streets are and how melancholy, so many poor sick people in the streets full of sores… in Westminster, there is never a physician and but one apothecary left, all being dead."  That people did not starve was down to the foresight of Sir John Lawrence and the Corporation of London who arranged for a commission of one farthing to be paid above the normal price for every quarter of corn landed in the Port of London. Another food source was the villages around London which, denied of their usual sales in the capital, left vegetables in specified market areas, negotiated their sale by shouting, and collected their payment after the money had been left submerged in a bucket of water to "disinfect" the coins.

Records state that plague deaths in London and the suburbs crept up over the summer from 2,000 people per week to over 7,000 per week in September. These figures are likely to be a considerable underestimate. Many of the sextons and parish clerks who kept the records themselves died. Quakers refused to co-operate and many of the poor were just dumped into mass graves unrecorded. It is not clear how many people caught the disease and made a recovery because only deaths were recorded and many records were destroyed in the Great Fire of London the following year. In the few districts where intact records remain, plague deaths varied between 30% and over 50% of the total population.

Although concentrated in London, the outbreak affected other areas of the country as well. Perhaps the most famous example was the village of Eyam in Derbyshire. The plague allegedly arrived with a merchant carrying a parcel of cloth sent from London, although this is a disputed point. The villagers imposed a quarantine on themselves to stop the further spread of the disease. This prevented the disease from moving into surrounding areas, but around 33% of the village's inhabitants died over a period of fourteen months.

Aftermath

By late autumn, the death toll in London and the suburbs began to slow until, in February 1666, it was considered safe enough for the King and his entourage to come back to the city. With the return of the monarch, others began to return: The gentry returned in their carriages accompanied by carts piled high with their belongings. The judges moved back from Windsor to sit in Westminster Hall, although Parliament, which had been prorogued in April 1665, did not reconvene until September 1666. Trade recommenced and businesses and workshops opened up. London was the goal of a new wave of people who flocked to the city in expectation of making their fortunes. Writing at the end of March 1666, Lord Clarendon, the Lord Chancellor, stated "... the streets were as full, the Exchange as much crowded, the people in all places as numerous as they had ever been seen ...".

Plague cases continued to occur sporadically at a modest rate until the summer of 1666. On the second and third of September that year, the Great Fire of London destroyed much of the City of London, and some people believed that the fire put an end to the epidemic. However, it is now thought that the plague had largely subsided before the fire took place. In fact, most of the later cases of plague were found in the suburbs, and it was the City of London itself that was destroyed by the Fire.

According to the Bills of Mortality, there were in total 68,596 deaths in London from the plague in 1665. Lord Clarendon estimated that the true number of mortalities was probably twice that figure. The next year, 1666, saw further deaths in other cities but on a lesser scale. Dr Thomas Gumble, chaplain to the Duke of Albemarle, both of whom had stayed in London for the whole of the epidemic, estimated that the total death count for the country from plague during 1665 and 1666 was about 200,000.

The Great Plague of 1665/1666 was the last major outbreak of bubonic plague in Great Britain. The last recorded death from plague came in 1679, and it was removed as a specific category in the Bills of Mortality after 1703. It spread to other towns in East Anglia and the southeast of England but fewer than ten percent of parishes outside London had a higher than average death rate during those years. Urban areas were more affected than rural ones; Norwich, Ipswich, Colchester, Southampton and Winchester were badly affected, while the West of England and areas of the Midlands escaped altogether.

The population of England in 1650 was approximately 5.25 million, which declined to about 4.9 million by 1680, recovering to just over 5 million by 1700. Other diseases, such as smallpox, took a high toll on the population even without the contribution by plague. The higher death rate in cities, both generally and specifically from the plague, was made up by continuous immigration, from small towns to larger ones and from the countryside to the town.

There were no contemporary censuses of London's population, but available records suggest that the population returned to its previous level within a couple of years. Burials in 1667 had returned to 1663 levels, Hearth Tax returns had recovered, John Graunt contemporarily analysed baptism records and concluded they represented a recovered population. Part of this could be accounted for by the return of wealthy households, merchants and manufacturing industries, all of which needed to replace losses among their staff and took steps to bring in necessary people. Colchester had suffered more severe depopulation, but manufacturing records for cloth suggested that production had recovered or even increased by 1669, and the total population had nearly returned to pre-plague levels by 1674. Other towns did less well: Ipswich was affected less than Colchester, but in 1674, its population had dropped by 18%, more than could be accounted for by the plague deaths alone.

As a proportion of the population who died, the London death toll was less severe than in a number of other towns. The total of deaths in London was greater than in any previous outbreak for 100 years, though as a proportion of the population, the epidemics in 1563, 1603 and 1625 were comparable or greater. Perhaps around 2.5% of the English population died.

Impact

The plague in London largely affected the poor, as the rich were able to leave the city by either retiring to their country estates or residing with kin in other parts of the country. The subsequent Great Fire of London, however, ruined many city merchants and property owners. As a result of these events, London was largely rebuilt and Parliament enacted the Rebuilding of London Act 1666. Although the street plan of the capital remained relatively unchanged, some improvements were made: streets were widened, pavements were created, open sewers abolished, wooden buildings and overhanging gables forbidden, and the design and construction of buildings controlled. The use of brick or stone was mandatory and many gracious buildings were constructed. Not only was the capital rejuvenated, but it became a healthier environment in which to live. Londoners had a greater sense of community after they had overcome the great adversities of 1665 and 1666.

Rebuilding took over ten years and was supervised by Robert Hooke as Surveyor of London. The architect Sir Christopher Wren was involved in the rebuilding of St Paul's Cathedral and more than fifty London churches. King Charles ll did much to foster the rebuilding work. He was a patron of the arts and sciences and founded the Royal Observatory and supported the Royal Society, a scientific group whose early members included Robert Hooke, Robert Boyle and Sir Isaac Newton. In fact, out of the fire and pestilence flowed a renaissance in the arts and sciences in England.

Plague pits have been archaeologically excavated during underground construction work. Between 2011 and 2015, some 3,500 burials from the 'New Churchyard' or 'Bethlam burial ground' were discovered during the construction of the Crossrail railway at Liverpool Street. Yersinia pestis DNA was found in the teeth of individuals found buried in pits at the site, confirming they had died of bubonic plague.

Yersinia pestis (Black Death)

From Wikipedia, the free encyclopedia
Yersinia pestis
Yersinia pestis.jpg
A scanning electron micrograph depicting a mass of Yersinia pestis bacteria in the foregut of an infected flea
Scientific classification edit
Domain: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Yersiniaceae
Genus: Yersinia
Species:
Y. pestis
Binomial name
Yersinia pestis
(Lehmann & Neumann, 1896)
van Loghem, 1944
Synonyms
Bacillus
  • Bacille de la peste
    Yersin, 1894
  • Bacterium pestis
    Lehmann & Neumann, 1896
  • Pasteurella pestis
    (Lehmann & Neumann, 1896) The Netherlands, 1920

Yersinia pestis (formerly Pasteurella pestis) is a gram-negative, non-motile, rod-shaped, coccobacillus bacterium, with no spores. It is a facultative anaerobic organism that can infect humans via the Oriental rat flea (Xenopsylla cheopis). It causes the disease plague, which takes three main forms: pneumonic, septicemic, and bubonic.

All three forms have been responsible for high-mortality epidemics throughout human history, including the Plague of Justinian in the sixth century; the Black Death, which accounted for the death of at least one-third of the European population between 1347 and 1353; and the Third Pandemic, sometimes referred to as the Modern Plague, which began in the late 19th century in China and spread by rats on steamships, claiming close to 10 million lives.

Those plagues may have originated in Central Asia or China and were transmitted west via trade routes. However, research in 2018 found evidence of the pathogen in an ancient Swedish tomb, which may have been the cause of what has been described as the Neolithic decline around 3000 BC, in which European populations declined significantly. This would suggest that Y. pestis may have originated in Europe in the Cucuteni–Trypillia culture instead of Asia.

Y. pestis was discovered in 1894 by Alexandre Yersin, a Swiss/French physician and bacteriologist from the Pasteur Institute, during an epidemic of the plague in Hong Kong. Yersin was a member of the Pasteur school of thought. Kitasato Shibasaburō, a German-trained Japanese bacteriologist who practised Koch's methodology, was also engaged at the time in finding the causative agent of the plague. However, Yersin actually linked plague with Y. pestis. Formerly named Pasteurella pestis, the organism was renamed Yersinia pestis in 1944.

Every year, thousands of cases of the plague are still reported to the World Health Organization, although with proper treatment, the prognosis for victims is now much better. A five- to six-fold increase in cases occurred in Asia during the time of the Vietnam War, possibly due to the disruption of ecosystems and closer proximity between people and animals. The plague is now commonly found in sub-Saharan Africa and Madagascar, areas that now account for over 95% of reported cases. The plague also has a detrimental effect on nonhuman mammals. In the United States, mammals such as the black-tailed prairie dog and the endangered black-footed ferret are under threat.

General characteristics

Y. pestis is a nonmotile, stick-shaped, facultative anaerobic bacterium with bipolar staining (giving it a safety pin appearance) that produces an antiphagocytic slime layer. Similar to other Yersinia species, it tests negative for urease, lactose fermentation, and indole. Its closest relative is the gastrointestinal pathogen Yersinia pseudotuberculosis, and more distantly Yersinia enterocolitica.

Genome

A complete genomic sequence is available for two of the three subspecies of Y. pestis: strain KIM (of biovar Y. p. medievalis), and strain CO92 (of biovar Y. p. orientalis, obtained from a clinical isolate in the United States). As of 2006, the genomic sequence of a strain of biovar Antiqua has been recently completed. Similar to the other pathogenic strains, signs exist of loss of function mutations. The chromosome of strain KIM is 4,600,755 base pairs long; the chromosome of strain CO92 is 4,653,728 base pairs long. Like Y. pseudotuberculosis and Y. enterocolitica, Y. pestis is host to the plasmid pCD1. It also hosts two other plasmids, pPCP1 (also called pPla or pPst) and pMT1 (also called pFra) that are not carried by the other Yersinia species. pFra codes for a phospholipase D that is important for the ability of Y. pestis to be transmitted by fleas. pPla codes for a protease, Pla, that activates plasmin in human hosts and is a very important virulence factor for pneumonic plague. Together, these plasmids, and a pathogenicity island called HPI, encode several proteins that cause the pathogenesis, for which Y. pestis is famous. Among other things, these virulence factors are required for bacterial adhesion and injection of proteins into the host cell, invasion of bacteria in the host cell (via a type-III secretion system), and acquisition and binding of iron harvested from red blood cells (by siderophores). Y. pestis is thought to be descended from Y. pseudotuberculosis, differing only in the presence of specific virulence plasmids.

A comprehensive and comparative proteomics analysis of Y. pestis strain KIM was performed in 2006. The analysis focused on the transition to a growth condition mimicking growth in host cells.

Small noncoding RNA

Numerous bacterial small noncoding RNAs have been identified to play regulatory functions. Some can regulate the virulence genes. Some 63 novel putative sRNAs were identified through deep sequencing of the Y. pestis sRNA-ome. Among them was Yersinia-specific (also present in Y. pseudotuberculosis and Y. enterocolitica) Ysr141 (Yersinia small RNA 141). Ysr141 sRNA was shown to regulate the synthesis of the type III secretion system (T3SS) effector protein YopJ. The Yop-Ysc T3SS is a critical component of virulence for Yersinia species. Many novel sRNAs were identified from Y. pestis grown in vitro and in the infected lungs of mice suggesting they play role in bacterial physiology or pathogenesis. Among them sR035 predicted to pair with SD region and transcription initiation site of a thermo-sensitive regulator ymoA, and sR084 predicted to pair with fur, ferric uptake regulator.

Pathogenesis and immunity

Oriental rat flea (Xenopsylla cheopis) infected with the Y. pestis bacterium, which appears as a dark mass in the gut: The foregut (proventriculus) of this flea is blocked by a Y. pestis biofilm; when the flea attempts to feed on an uninfected host, Y. pestis is regurgitated into the wound, causing infection.
In the urban and sylvatic (forest) cycles of Y. pestis, most of the spreading occurs between rodents and fleas. In the sylvatic cycle, the rodent is wild, but in the urban cycle, the rodent is primarily the brown rat (Rattus norvegicus). In addition, Y. pestis can spread from the urban environment and back. Transmission to humans is usually through the bite of infected fleas. If the disease has progressed to the pneumonic form, humans can spread the bacterium to others by coughing, vomiting, and possibly sneezing.

In reservoir hosts

Several species of rodents serve as the main reservoir for Y. pestis in the environment. In the steppes, the natural reservoir is believed to be principally the marmot. In the western United States, several species of rodents are thought to maintain Y. pestis. However, the expected disease dynamics have not been found in any rodent. Several species of rodents are known to have a variable resistance, which could lead to an asymptomatic carrier status. Evidence indicates fleas from other mammals have a role in human plague outbreaks.

The lack of knowledge of the dynamics of plague in mammal species is also true among susceptible rodents such as the black-tailed prairie dog (Cynomys ludovicianus), in which plague can cause colony collapse, resulting in a massive effect on prairie food webs. However, the transmission dynamics within prairie dogs do not follow the dynamics of blocked fleas; carcasses, unblocked fleas, or another vector could possibly be important, instead.

In other regions of the world, the reservoir of the infection is not clearly identified, which complicates prevention and early-warning programs. One such example was seen in a 2003 outbreak in Algeria. Domestic house cats are susceptible to plague. Their symptoms are similar to those experienced by humans. Cats infected with plague can infect people through bites, scratches, coughs, or sneezes.

Vector

The transmission of Y. pestis by fleas is well characterized. Initial acquisition of Y. pestis by the vector occurs during feeding on an infected animal. Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage system and Yersinia murine toxin (Ymt). Although Ymt is highly toxic to rodents and was once thought to be produced to ensure reinfection of new hosts, it is important for the survival of Y. pestis in fleas.

The hemin storage system plays an important role in the transmission of Y. pestis back to a mammalian host. While in the insect vector, proteins encoded by hemin storage system genetic loci induce biofilm formation in the proventriculus, a valve connecting the midgut to the esophagus. Aggregation in the biofilm inhibits feeding, as a mass of clotted blood and bacteria forms (referred to as "Bacot's block" after entomologist A.W. Bacot, the first to describe this phenomenon). Transmission of Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges bacteria lodged in the proventriculus, which is regurgitated back into the host circulatory system.

In humans and other susceptible hosts

Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors, including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses a plasmin activator that is an important virulence factor for pneumonic plague and that might degrade on blood clots to facilitate systematic invasion. Many of the bacteria's virulence factors are antiphagocytic in nature. Two important antiphagocytic antigens, named F1 (fraction 1) and V or LcrV, are both important for virulence. These antigens are produced by the bacterium at normal human body temperature. Furthermore, Y. pestis survives and produces F1 and V antigens while it is residing within white blood cells such as monocytes, but not in neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils.

In addition, the type-III secretion system (T3SS) allows Y. pestis to inject proteins into macrophages and other immune cells. These T3SS-injected proteins, called Yersinia outer proteins (Yops), include Yop B/D, which form pores in the host cell membrane and have been linked to cytolysis. The YopO, YopH, YopM, YopT, YopJ, and YopE are injected into the cytoplasm of host cells by T3SS into the pore created in part by YopB and YopD. The injected Yops limit phagocytosis and cell signaling pathways important in the innate immune system, as discussed below. In addition, some Y. pestis strains are capable of interfering with immune signaling (e.g., by preventing the release of some cytokines).

Y. pestis proliferates inside lymph nodes, where it is able to avoid destruction by cells of the immune system such as macrophages. The ability of Y. pestis to inhibit phagocytosis allows it to grow in lymph nodes and cause lymphadenopathy. YopH is a protein tyrosine phosphatase that contributes to the ability of Y. pestis to evade immune system cells. In macrophages, YopH has been shown to dephosphorylate p130Cas, Fyb (Fyn binding protein) SKAP-HOM and Pyk, a tyrosine kinase homologous to FAK. YopH also binds the p85 subunit of phosphoinositide 3-kinase, the Gab1, the Gab2 adapter proteins, and the Vav guanine nucleotide exchange factor.

YopE functions as a GTPase-activating protein for members of the Rho family of GTPases such as RAC1. YopT is a cysteine protease that inhibits RhoA by removing the isoprenyl group, which is important for localizing the protein to the cell membrane. YopE and YopT has been proposed to function to limit YopB/D-induced cytolysis. This might limit the function of YopB/D to create the pores used for Yop insertion into host cells and prevent YopB/D-induced rupture of host cells and release of cell contents that would attract and stimulate immune system responses.

YopJ is an acetyltransferase that binds to a conserved α-helix of MAPK kinases. YopJ acetylates MAPK kinases at serines and threonines that are normally phosphorylated during activation of the MAP kinase cascade. YopJ is activated in eukaryotic cells by interaction with target cell phytic acid (IP6). This disruption of host cell protein kinase activity causes apoptosis of macrophages, and this is proposed to be important for the establishment of infection and for evasion of the host immune response. YopO is a protein kinase also known as Yersinia protein kinase A (YpkA). YopO is a potent inducer of human macrophage apoptosis.

Depending on which form of the plague with which the individual becomes infected, the plague develops a different illness; however, the plague overall affects the host cell’s ability to communicate with the immune system, hindering the body to bring phagocytic cells to the area of infection.

Y. pestis is a versatile killer. In addition to rodents and humans, it is known to have killed dogs, cats, camels, chickens, and pigs.

Immunity

A formalin-inactivated vaccine was in the past available in the United States for adults at high risk of contracting the plague until removal from the market by the Food and Drug Administration. It was of limited effectiveness and could cause severe inflammation. Experiments with genetic engineering of a vaccine based on F1 and V antigens are underway and show promise. However, bacteria lacking antigen F1 are still virulent, and the V antigens are sufficiently variable such that vaccines composed of these antigens may not be fully protective. The United States Army Medical Research Institute of Infectious Diseases has found that an experimental F1/V antigen-based vaccine protects crab-eating macaques, but fails to protect African green monkey species. A systematic review by the Cochrane Collaboration found no studies of sufficient quality to make any statement on the efficacy of the vaccine.

Isolation and identification

In 1894, two bacteriologists, Alexandre Yersin of Switzerland and Kitasato Shibasaburō of Japan, independently isolated in Hong Kong the bacterium responsible for the Third Pandemic. Though both investigators reported their findings, a series of confusing and contradictory statements by Kitasato eventually led to the acceptance of Yersin as the primary discoverer of the organism. Yersin named it Pasteurella pestis in honor of the Pasteur Institute, where he worked. In 1967, it was moved to a new genus and renamed Yersinia pestis in his honor. Yersin also noted that rats were affected by plague not only during plague epidemics, but also often preceding such epidemics in humans and that plague was regarded by many locals as a disease of rats; villagers in China and India asserted that when large numbers of rats were found dead, plague outbreaks soon followed.

In 1898, French scientist Paul-Louis Simond (who had also come to China to battle the Third Pandemic) established the rat–flea vector that drives the disease. He had noted that persons who became ill did not have to be in close contact with each other to acquire the disease. In Yunnan, China, inhabitants would flee from their homes as soon as they saw dead rats, and on the island of Formosa (Taiwan), residents considered the handling of dead rats heightened the risks of developing plague. These observations led him to suspect that the flea might be an intermediary factor in the transmission of plague, since people acquired plague only if they were in contact with rats that had died less than 24 hours before. In a now classic experiment, Simond demonstrated how a healthy rat died of plague after infected fleas had jumped to it from a rat that had recently died of the plague. The outbreak spread to Chinatown, San Francisco, from 1900 to 1904 and then to Oakland and the East Bay from 1907 to 1909. It has been present in the rodents of western North America ever since, as fear of the consequences of the outbreak on trade caused authorities to hide the dead of the Chinatown residents long enough for the disease to be passed to widespread species of native rodents in outlying areas.

Ancient DNA evidence

In 2018, the emergence and spread of the pathogen during the Neolithic decline (as far back as 6,000 years ago) was published. A site in Sweden was the source of the DNA evidence and trade networks were proposed as the likely avenue of spread rather than migrations of populations.

DNA evidence published in 2015 indicates Y. pestis infected humans 5,000 years ago in Bronze Age Eurasia, but genetic changes that made it highly virulent did not occur until about 4,000 years ago. The highly virulent version capable of transmission by fleas through rodents, humans, and other mammals was found in two individuals associated with the Srubnaya culture from the Samara region in Russia from around 3,800 years ago and an Iron Age individual from Kapan, Armenia from around 2,900 years ago. This indicates that at least two lineages of Y. pestis were circulating during the Bronze Age in Eurasia. The Y. pestis bacterium has a relatively large number of nonfunctioning genes and three "ungainly" plasmids, suggesting an origin less than 20,000 years ago.

Three main strains are recognised: Y. p. antiqua, which caused a plague pandemic in the sixth century; Y. p. medievalis, which caused the Black Death and subsequent epidemics during the second pandemic wave; and Y. p. orientalis, which is responsible for current plague outbreaks.

Plague causes a blockage in the proventriculus of the flea by forming a biofilm. The biofilm formation is induced by the ingestion of blood. The presence of a biofilm seems likely to be required for stable infection of the flea. It has been suggested that a bacteriophage – Ypφ – may have been responsible for increasing the virulence of this organism.

Recent events

In 2008, the plague was commonly found in sub-Saharan Africa and Madagascar, areas that accounted for over 95% of the reported cases.

In September 2009, the death of Malcolm Casadaban, a molecular genetics professor at the University of Chicago, was linked to his work on a weakened laboratory strain of Y. pestis. Hemochromatosis was hypothesised to be a predisposing factor in Casadaban's death from this attenuated strain used for research.

In 2010, researchers in Germany definitely established, using PCR evidence from samples obtained from Black Death victims, that Y. pestis was the cause of the medieval Black Death.

In 2011, the first genome of Y. pestis isolated from Black Death victims was published, and concluded that this medieval strain was ancestral to most modern forms of Y. pestis

In 2015, Cell published results from a study of ancient graves. Plasmids of Y. pestis were detected in archaeological samples of the teeth of seven Bronze Age individuals, in the Afanasievo culture in Siberia, the Corded Ware culture in Estonia, the Sintashta culture in Russia, the Unetice culture in Poland, and the Andronovo culture in Siberia.

On September 8, 2016, the Y. pestis bacterium was identified from DNA in teeth found at a Crossrail building site in London. The human remains were found to be victims of the Great Plague of London, which lasted from 1665 to 1666.

On January 15, 2018, researchers at the University of Oslo and the University of Ferrara suggested that humans and their parasites were the biggest carriers of the plague.

Two cases of pneumonic plague were diagnosed at a hospital in Beijing's Chaoyang district on 13 November 2019, prompting fears of an outbreak. Doctors diagnosed a middle-aged man with fever, who had complained of difficulty breathing for some ten days, accompanied by his wife with similar symptoms. Police quarantined the emergency room at the hospital and controls were placed on Chinese news aggregators. On the 18th, a third case was reported in a 55-year-old male from Xilingol League, one of the twelve Mongolic autonomous regions in Northern China. The patient received treatment and 28 symptomless contacts were placed in quarantine. 

Cooperative

From Wikipedia, the free encyclopedia ...