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Friday, March 27, 2020

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. 

Bubonic plague

From Wikipedia, the free encyclopedia

Bubonic plague
Plague -buboes.jpg
A bubo on the upper thigh of a person infected with bubonic plague.
SpecialtyInfectious disease
SymptomsFever, headaches, vomiting, swollen lymph nodes
Usual onset1–7 days after exposure
CausesYersinia pestis spread by fleas
Diagnostic methodFinding the bacteria in the blood, sputum, or lymph nodes
TreatmentAntibiotics such as streptomycin, gentamicin, or doxycycline
Frequency650 cases reported a year
Deaths10% mortality with treatment
30-90% if untreated

Bubonic plague is one of three types of plague caused by bacterium Yersinia pestis. One to seven days after exposure to the bacteria, flu-like symptoms develop. These symptoms include fever, headaches, and vomiting. Swollen and painful lymph nodes occur in the area closest to where the bacteria entered the skin. Occasionally, the swollen lymph nodes may break open.

The three types of plague are the result of the route of infection: bubonic plague, septicemic plague, and pneumonic plague. Bubonic plague is mainly spread by infected fleas from small animals. It may also result from exposure to the body fluids from a dead plague-infected animal. In the bubonic form of plague, the bacteria enter through the skin through a flea bite and travel via the lymphatic vessels to a lymph node, causing it to swell. Diagnosis is made by finding the bacteria in the blood, sputum, or fluid from lymph nodes.

Prevention is through public health measures such as not handling dead animals in areas where plague is common. Vaccines have not been found to be very useful for plague prevention. Several antibiotics are effective for treatment, including streptomycin, gentamicin, and doxycycline.Without treatment, plague results in the death of 30% to 90% of those infected. Death, if it occurs, is typically within ten days. With treatment the risk of death is around 10%. Globally between 2010 and 2015 there were 3248 documented cases, which resulted in 584 deaths. The countries with the greatest number of cases are the Democratic Republic of the Congo, Madagascar, and Peru.

The plague was the cause of the Black Death that swept through Asia, Europe, and Africa in the 14th century and killed an estimated 50 million people. This was about 25% to 60% of the European population. Because the plague killed so many of the working population, wages rose due to the demand for labor. Some historians see this as a turning point in European economic development. The disease was also responsible for the Justinian plague originating in the Eastern Roman Empire in the 6th century CE, as well as the third epidemic affecting China, Mongolia, and India originating in the Yunnan Province in 1855. The term bubonic is derived from the Greek word βουβών, meaning "groin". The term "buboes" is also used to refer to the swollen lymph nodes.

Signs and symptoms

Necrosis of the nose, the lips, and the fingers and residual bruising over both forearms in a person recovering from bubonic plague that disseminated to the blood and the lungs. At one time, the person's entire body was bruised.

The best-known symptom of bubonic plague is one or more infected, enlarged, and painful lymph nodes, known as buboes. After being transmitted via the bite of an infected flea, the Y. pestis bacteria become localized in an inflamed lymph node, where they begin to colonize and reproduce. Buboes associated with the bubonic plague are commonly found in the armpits, upper femoral, groin and neck region. Bubonic plague symptoms appear suddenly a few days after exposure to the bacterium. Symptoms include:
  • Chills
  • General ill feeling (malaise)
  • High fever >39 °C (102.2 °F)
  • Muscle cramps
  • Seizures
  • Smooth, painful lymph gland swelling called a bubo, commonly found in the groin, but may occur in the armpits or neck, most often near the site of the initial infection (bite or scratch)
  • Pain may occur in the area before the swelling appears
  • Gangrene of the extremities such as toes, fingers, lips and tip of the nose.
Other symptoms include heavy breathing, continuous vomiting of blood (hematemesis), aching limbs, coughing, and extreme pain caused by the decay or decomposition of the skin while the person is still alive. Additional symptoms include extreme fatigue, gastrointestinal problems, lenticulae (black dots scattered throughout the body), delirium, coma, and death. Other forms of the disease include septicemic plague and pneumonic plague in which the bacterium reproduces in the persons blood and lungs respectively.

Cause

Oriental rat flea (Xenopsylla cheopis) infected with the Yersinia pestis bacterium which appears as a dark mass in the gut. The foregut of this flea is blocked by a Y. pestis biofilm; when the flea attempts to feed on an uninfected host, Y. pestis from the foregut is regurgitated into the wound, causing infection.

Bubonic plague is an infection of the lymphatic system, usually resulting from the bite of an infected flea, Xenopsylla cheopis (the rat flea). In very rare circumstances, as in the septicemic plague, the disease can be transmitted by direct contact with infected tissue or exposure to the cough of another human. The flea is parasitic on house and field rats, and seeks out other prey when its rodent hosts die. The bacteria remain harmless to the flea, allowing the new host to spread the bacteria. The bacteria form aggregates in the gut of infected fleas and this results in the flea regurgitating ingested blood, which is now infected, into the bite site of a rodent or human host. Once established, bacteria rapidly spread to the lymph nodes and multiply.

Y. pestis bacilli can resist phagocytosis and even reproduce inside phagocytes and kill them. As the disease progresses, the lymph nodes can hemorrhage and become swollen and necrotic. Bubonic plague can progress to lethal septicemic plague in some cases. The plague is also known to spread to the lungs and become the disease known as the pneumonic plague.

Diagnosis

Laboratory testing is required in order to diagnose and confirm plague. Ideally, confirmation is through the identification of Y. pestis culture from a patient sample. Confirmation of infection can be done by examining serum taken during the early and late stages of infection. To quickly screen for the Y. pestis antigen in patients, rapid dipstick tests have been developed for field use.

 Samples taken for testing include:
  • Buboes: Swollen lymph nodes (buboes) characteristic of bubonic plague, a fluid sample can be taken from them with a needle.
  • Blood
  • Lungs

Treatment

Several classes of antibiotics are effective in treating bubonic plague. These include aminoglycosides such as streptomycin and gentamicin, tetracyclines (especially doxycycline), and the fluoroquinolone ciprofloxacin. Mortality associated with treated cases of bubonic plague is about 1–15%, compared to a mortality of 40–60% in untreated cases.

People potentially infected with the plague need immediate treatment and should be given antibiotics within 24 hours of the first symptoms to prevent death. Other treatments include oxygen, intravenous fluids, and respiratory support. People who have had contact with anyone infected by pneumonic plague are given prophylactic antibiotics. Using the broad-based antibiotic streptomycin has proven to be dramatically successful against the bubonic plague within 12 hours of infection.

Epidemiology

Distribution of plague infected animals 1998

Globally between 2010 and 2015 there were 3248 documented cases, which resulted in 584 deaths. The countries with the greatest number of cases are the Democratic Republic of the Congo, Madagascar, and Peru.

For over a decade since 2001, Zambia, India, Malawi, Algeria, China, Peru, and the Democratic Republic of the Congo had the most plague cases with over 1,100 cases in the Democratic Republic of the Congo alone. From 1,000 to 2,000 cases are conservatively reported per year to the WHO. From 2012 to 2017, reflecting political unrest and poor hygienic conditions, Madagascar began to host regular epidemics.

Between 1900 and 2015, the United States had 1,036 human plague cases with an average of 9 cases per year. In 2015, 16 people in the Western United States developed plague, including 2 cases in Yosemite National Park. These US cases usually occur in rural northern New Mexico, northern Arizona, southern Colorado, California, southern Oregon, and far western Nevada.

In November 2017, the Madagascar Ministry of Health reported an outbreak to WHO (World Health Organization) with more cases and deaths than any recent outbreak in the country. Unusually most of the cases were pneumonic rather than bubonic.

In June 2018, a child was confirmed to be the first person in Idaho to be infected by bubonic plague in nearly 30 years.

A couple died in May 2019, in Mongolia, while hunting marmots. Another two people in the province of Inner Mongolia, China were treated in November 2019 for the disease.

History

Yersinia pestis was discovered in archaeological finds from the Late Bronze Age (~3800 BP).

First pandemic

The first recorded epidemic affected the Eastern Roman Empire (Byzantine Empire) and was named the Plague of Justinian after emperor Justinian I, who was infected but survived through extensive treatment. The pandemic resulted in the deaths of an estimated 25 million (6th century outbreak) to 50 million people (two centuries of recurrence). The historian Procopius wrote, in Volume II of History of the Wars, of his personal encounter with the plague and the effect it had on the rising empire. In the spring of 542, the plague arrived in Constantinople, working its way from port city to port city and spreading around the Mediterranean Sea, later migrating inland eastward into Asia Minor and west into Greece and Italy. Because the infectious disease spread inland by the transferring of merchandise through Justinian's efforts in acquiring luxurious goods of the time and exporting supplies, his capital became the leading exporter of the bubonic plague. Procopius, in his work Secret History, declared that Justinian was a demon of an emperor who either created the plague himself or was being punished for his sinfulness.

Second pandemic

Citizens of Tournai bury plague victims. Miniature from The Chronicles of Gilles Li Muisis (1272–1352). Bibliothèque royale de Belgique, MS 13076-77, f. 24v.
 
People who died of bubonic plague in a mass grave from 1720 to 1721 in Martigues, France
 
In the Late Middle Ages Europe experienced the most deadly disease outbreak in history when the Black Death, the infamous pandemic of bubonic plague, hit in 1347, killing a third of the European human population. Some historians believe that society subsequently became more violent as the mass mortality rate cheapened life and thus increased warfare, crime, popular revolt, waves of flagellants, and persecution. The Black Death originated in Central Asia and spread from Italy and then throughout other European countries. Arab historians Ibn Al-Wardni and Almaqrizi believed the Black Death originated in Mongolia. Chinese records also showed a huge outbreak in Mongolia in the early 1330s. Research published in 2002 suggests that it began in early 1346 in the steppe region, where a plague reservoir stretches from the northwestern shore of the Caspian Sea into southern Russia. The Mongols had cut off the trade route, the Silk Road, between China and Europe which halted the spread of the Black Death from eastern Russia to Western Europe. The epidemic began with an attack that Mongols launched on the Italian merchants' last trading station in the region, Caffa in the Crimea. In late 1346, plague broke out among the besiegers and from them penetrated into the town. When spring arrived, the Italian merchants fled on their ships, unknowingly carrying the Black Death. Carried by the fleas on rats, the plague initially spread to humans near the Black Sea and then outwards to the rest of Europe as a result of people fleeing from one area to another.

Third pandemic

The plague resurfaced for a third time in the mid-19th century. Like the two previous outbreaks, this one also originated in Eastern Asia, most likely in Yunnan Province of China, where there are several natural plague foci. The initial outbreaks occurred in the second half of the eighteenth century. The disease remained localized in Southwest China for several years before spreading. In the city of Canton, beginning in January 1894, the disease killed 80,000 people by June. Daily water-traffic with the nearby city of Hong Kong rapidly spread the plague there, killing over 2,400 within two months.

Also known as the modern pandemic, the third pandemic spread the disease to port cities throughout the world in the second half of the 19th century and early 20th century via shipping routes. The plague infected people in Chinatown in San Francisco from 1900 to 1904, and in the nearby locales of Oakland and the East Bay again from 1907 to 1909. During the outbreak from 1900 to 1904 in San Francisco is when authorities made permanent the Chinese Exclusion Act. This law was originally signed into existence by President Chester A. Arthur in 1882. The Chinese Exclusion Act was supposed to last for ten years but was renewed in 1892 with the Geary Act and subsequently made permanent in 1902 during the outbreak of plague in Chinatown, San Francisco. The last major outbreak in the United States occurred in Los Angeles in 1924, though the disease is still present in wild rodents, and can be passed to humans that come in contact with them. According to the World Health Organization, the pandemic was considered active until 1959, when worldwide casualties dropped to 200 per year. In 1994, a plague outbreak in five Indian states caused an estimated 700 infections (including 52 deaths) and triggered a large migration of Indians within India as they tried to avoid the plague.

A boy in Kyrgyzstan died in August 2013 from the disease.

Society and culture

Contemporary engraving of Marseille during the Great Plague in 1720

The scale of death and social upheaval associated with plague outbreaks has made the topic prominent in a number of historical and fictional accounts since the disease was first recognized. The Black Death in particular is described and referenced in numerous contemporary sources, some of which, including works by Chaucer, Boccaccio, and Petrarch, are considered part of the Western canon. The Decameron, by Boccaccio, is notable for its use of a frame story involving individuals who have fled Florence for a secluded villa to escape the Black Death. First-person, sometimes sensationalized or fictionalized, accounts of living through plague years have also been popular across centuries and cultures. For example, Samuel Pepys' diary makes a number of references to his first-hand experiences of the Great Plague of London in 1665–6.

Later works, such as Albert Camus's novel The Plague or Ingmar Bergman's film The Seventh Seal have used bubonic plague in settings, such as quarantined cities in either medieval or modern times, as a backdrop to explore a variety of concepts. Common themes include the breakdown of society, institutions, and individuals during the plague, the cultural and psychological existential confrontation with mortality, and the allegorical use of the plague in reference to contemporary moral or spiritual questions.

Biological warfare

Some of the earliest instances of biological warfare were said to have been products of the plague, as armies of the 14th century were recorded catapulting diseased corpses over the walls of towns and villages to spread the pestilence.

Later, plague was used during the Second Sino-Japanese War as a bacteriological weapon by the Imperial Japanese Army. These weapons were provided by Shirō Ishii's units and used in experiments on humans before being used on the field. For example, in 1940, the Imperial Japanese Army Air Service bombed Ningbo with fleas carrying the bubonic plague. During the Khabarovsk War Crime Trials, the accused, such as Major General Kiyoshi Kawashima, testified that, in 1941, 40 members of Unit 731 air-dropped plague-contaminated fleas on Changde. These operations caused epidemic plague outbreaks.

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