Depending on lung infection, or sanitary conditions, plague can be spread in the air, by direct contact, or by contaminated undercooked food or materials. The symptoms of plague depend on the concentrated areas of infection in each person: bubonic plague in lymph nodes, septicemic plague in blood vessels, pneumonic plague in lungs, and so on. It is treatable if detected early. Plague is still endemic in some parts of the world.
The etymology of the word "plague" is believed to come from the Latin word plāga ("blow, wound") and plangere (“to strike, or to strike down”), cf. German Plage (“infestation”).
In 1898, the 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 recently dead rats, who 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 which had recently died of the plague.http://www.asnom.org/en/423_peste.html
A systematic review by the Cochrane Collaboration found no studies of sufficient quality to make any statement on the efficacy of the vaccine.
When a flea bites a human and contaminates the wound with regurgitated blood, the plague carrying bacteria are passed into the tissue. Y. pestis can reproduce inside cells, so even if phagocytosed, they can still survive. Once in the body, the bacteria can enter the lymphatic system, which drains interstitial fluid. Plague bacteria secrete several , one of which is known to cause dangerous beta-adrenergic blockade.
Y. pestis spreads through the lymphatics of the infected human until it reaches a lymph node, where it stimulates severe haemorrhagic inflammation that causes the lymph nodes to expand. The expansion of lymph nodes is the cause of the characteristic "bubo" associated with the disease.
If diagnosed in time the various forms of plague are usually highly responsive to antibiotic therapy. The antibiotics often used are streptomycin, chloramphenicol and tetracycline. Amongst the newer generation of antibiotics, gentamicin and doxycycline have proven effective in monotherapeutic treatment of plague.
The earliest account describing a possible plague epidemic is found in I Samuel 5:6 of the Hebrew Bible (Tanakh). In this account, the Philistines of Ashdod were stricken with a plague for the crime of stealing the Ark of the Covenant from the Children of Israel. The word "" is used in most English translations to describe the sores that came upon the Philistines. The account indicates that the Philistine city and its political territory were stricken with a "ravaging of mice" and a plague, bringing death to a large segment of the population.
In the second year of the Peloponnesian War (430 BC), Thucydides described an epidemic disease which was said to have begun in Ethiopia, passed through Egypt and Libya, then come to the Greek world. In the Plague of Athens, the city lost possibly one third of its population, including Pericles. Modern historians disagree on whether the plague was a critical factor in the loss of the war. Although this epidemic has long been considered an outbreak of plague, many modern scholars believe that typhus, smallpox, or measles may better fit the surviving descriptions. A recent study of DNA found in the dental pulp of plague victims suggests that typhoid was actually responsible.
In the first century AD, Rufus of Ephesus, a Greek anatomist, refers to an outbreak of plague in Libya, Egypt, and Syria. He records that Alexandrian doctors named Dioscorides and Posidonius described symptoms including acute fever, pain, agitation, and delirium. Buboes—large, hard, and non-suppurating—developed behind the knees, around the elbows, and "in the usual places." The death toll of those infected was very high. Rufus also wrote that similar buboes were reported by a Dionysius Curtus, who may have practiced medicine in Alexandria in the third century BC. If this is correct, the eastern Mediterranean world may have been familiar with bubonic plague at that early date.Simpson, W.J.Patrick, A.
In the second century, the Antonine Plague, named after Marcus Aurelius’ family name of Antoninus and also known as the Plague of Galen, who had first hand knowledge of the disease, may in fact have been smallpox. Galen was in Rome when it struck in 166 AD, and was also present in the winter of 168–69 during an outbreak among troops stationed at Aquileia; he had experience with the epidemic, referring to it as very long lasting, and describes its symptoms and his treatment of it. Unfortunately, his references are scattered and brief. According to Barthold Georg NiebuhrNiebuhr, 1873. Lectures on the history of Rome, p 733. "this pestilence must have raged with incredible fury; it carried off innumerable victims. The ancient world never recovered from the blow inflected upon it by the plague which visited it in the reign of M. Aurelius." The mortality rate of the plague was 7–10 percent; the outbreak in 165–6–168 would have caused approximately 3.5 to 5 million deaths. Otto Seek believes that over half the population of the empire perished. J. F. Gilliam believes that the Antonine plague probably caused more deaths than any other epidemic during the empire before the mid-3rd century.
In AD 588 a second major wave of plague spread through the Mediterranean into what is now France. It is estimated that the Plague of Justinian killed as many as people across the world. The History of the Bubonic Plague Scientists Identify Genes Critical to Transmission of Bubonic Plague It caused Europe's population to drop by around 50% between 541 and 700. It also may have contributed to the success of the Arab conquests. The Great Arab Conquests An outbreak of it in the AD 560s was described in AD 790 as causing "swellings in the glands ... in the manner of a nut or date" in the groin "and in other rather delicate places followed by an unbearable fever". While the swellings in this description have been identified by some as buboes, there is some contention as to whether the pandemic should be attributed to the bubonic plague, Yersinia pestis, known in modern times.
The plague repeatedly returned to haunt Europe and the Mediterranean throughout the 14th to 17th centuries. ξ4 According to Biraben, plague was present somewhere in Europe in every year between 1346 and 1671. ξ5 The 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). ξ6 According to Geoffrey Parker, "France alone lost almost a million people to plague in the epidemic of 1628–31." ξ7
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, The Black Death in Egypt and England: A Comparative Study, Stuart J. Borsch, Austin: University of Texas and a postincident population figure as low as 2 million.Secondary sources such as the Cambridge History of Medieval England often contain discussions of methodology in reaching these figures that are necessary reading for anyone wishing to understand this controversial episode in more detail. By the end of 1350, the Black Death subsided, but it never really died out in England. Over the next few hundred years, further outbreaks occurred in 1361–62, 1369, 1379–83, 1389–93, 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 1479–80 could have been as high as 20%. ξ8 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.
In 1466, perhaps 40,000 people died of plague in Paris. Plague, 1911 Edition of the Encyclopædia Britannica During the 16th and 17th centuries, plague visited Paris for almost one year out of three. ξ9 The Black Death ravaged Europe for three years before it continued on into Russia, where the disease hit somewhere once every five or six years from 1350 to 1490. Plague epidemics ravaged London in 1563, 1593, 1603, 1625, 1636, and 1665, ξ9 reducing its population by 10 to 30% during those years." Plague in London: spatial and temporal aspects of mortality", J. A. I. Champion, Epidemic Disease in London, Centre for Metropolitan History Working Papers Series, No. 1 (1993). Over 10% of Amsterdam's population died in 1623–1625, and again in 1635–1636, 1655, and 1664. Geography, climate, population, economy, society. J.P.Sommerville. There were 22 outbreaks of plague in Venice between 1361 and 1528. ξ10 The plague of 1576–1577 killed 50,000 in Venice, almost a third of the population. ξ11 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 from 1348 to 1350. The last plague outbreak ravaged Oslo in 1654.
In the first half of the 17th century, a plague claimed some 1.7 million victims in Italy, or about 14% of the population.Karl Julius Beloch, Bevölkerungsgeschichte Italiens, volume 3, pp. 359–360. In 1656, the 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 Seventeenth-Century Decline, S. G. Payne, A History of Spain and Portugal 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, ξ12 and 300,000 in Prussia. ξ13 The plague killed two-thirds of the inhabitants of Helsinki, and claimed a third of Stockholm's population. ξ14 Western Europe's last major epidemic occurred in 1720 in Marseilles, in Central Europe the last major outbreaks happened during the plague during the Great Northern War, and in Eastern Europe during the Russian plague of 1770-1772 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. ξ15 Plague repeatedly struck the cities of North Africa. Algiers lost 30,000–50,000 to it in 1620–21, and again in 1654–57, 1665, 1691, and 1740–42. ξ16 Plague remained a major event in Ottoman society until the second quarter of the 19th century. Between 1701 and 1750, 37 larger and smaller epidemics were recorded in Constantinople, and 31 between 1751 and 1800. Baghdad has suffered severely from visitations of the plague, and sometimes two-thirds of its population has been wiped out. ξ17
In the early 20th century, following the identification by Yersin and Kitasato of the plague bacterium that caused the late 19th and early 20th century Asian bubonic plague (the Third Pandemic), most scientists and historians came to believe that the Black Death was an incidence of this plague, with a strong presence of the more contagious pneumonic and septicemic varieties increasing the pace of infection, spreading the disease deep into inland areas of the continents.
Some modern researchers have argued that the disease was more likely to have been viral, pointing to the absence of rats from some parts of Europe that were badly affected and to the conviction of people at the time that the disease was spread by direct human contact. According to the accounts of the time the Black Death was extremely virulent, unlike the 19th and early 20th century bubonic plague. Samuel K. Cohn has made a comprehensive attempt to rebut the bubonic plague theory. ξ18 Researchers have offered a mathematical model based on the changing demography of Europe from AD 1000 to 1800 demonstrating how plague epidemics, 1347 to 1670, could have provided the selection pressure that raised the frequency of a mutation to the level seen today that prevent HIV from entering macrophages and CD4 that carry the mutation (the average frequency of this allele is 10% in European populations). It is suggested that the original single mutation appeared over 2,500 years ago and that persistent epidemics of a haemorrhagic fever struck at the early classical civilizations.
However recent research published in the open-access scientific journal PloS Pathogens in October 2010 presented conclusive evidence that two previously unknown (variant strains) of Y. pestis were responsible for the Black Death. A multinational team conducted new surveys that used both ancient DNA analyses and protein-specific detection to find DNA and protein signatures specific for Y. pestis in human skeletons from widely distributed mass graves in northern, central and southern Europe that were associated archaeologically with the Black Death and subsequent resurgences. The authors concluded that this research, together with prior analyses from the south of France and Germany,
The study also identified two previously unknown but related strains of Y. pestis that were associated with distinct medieval mass graves. These were found to be ancestral to modern isolates of the present-day Y. pestis strains 'Orientalis' and 'Medievalis', suggesting that these variant strains (which are now presumed to be extinct) may have entered Europe in two waves. Surveys of plague pit remains in France and England indicate that the first variant entered Europe through the port of Marseille around November 1347 and spread through France over the next two years, eventually reaching England in the spring of 1349, where it spread through the country in three successive epidemics.
Surveys of plague pit remains from the Netherlands town of Bergen op Zoom showed evidence of a second Y. pestis genotype which differed from that found in Britain and France and this second strain is now thought to have been responsible for the pandemic that spread through the Low Countries from 1350. This discovery implies that Bergen op Zoom (and possibly other parts of the southern Netherlands) was not directly infected from England or France c. AD 1349, and the researchers have suggested that a second wave of plague infection, distinct from that which occurred in Britain and France, may have been carried to the Low Countries from Norway, the Hanseatic cities, or another site.
Plague occurred in Russia in 1877–1889 in rural areas near the Ural Mountains and the Caspian Sea. Efforts in hygiene and patient isolation reduced the spread of the disease, with approximately 420 deaths in the region. Significantly, the region of Vetlianka in this area is near a population of the bobak marmot, a small rodent considered a very dangerous plague reservoir. The last significant Russian outbreak of Plague was in Siberia in 1910 after sudden demand for marmot skins (a substitute for sable) increased the price by 400 percent. The traditional hunters would not hunt a sick Marmot and it was taboo to eat the fat from under the arm (the axillary lymphatic gland that often harboured the plague) so outbreaks tended to be confined to single individuals. The price increase, however, attracted thousands of Chinese hunters from Manchuria who not only caught the sick animals but also ate the fat, which was considered a delicacy. The plague spread from the hunting grounds to the terminus of the Chinese Eastern Railway and then followed the track for 2,700 km. The plague lasted 7 months and killed 60,000 people.
Hong Kong in 1894 had particularly high death rates, 90%. As late as 1897, medical authorities in the European powers organized a conference in Venice, seeking ways to keep the plague out of Europe. Mumbai plague epidemic struck the city of Bombay (Mumbai) in 1896. The disease reached the Territory of Hawaii in December 1899, and the Board of Health's decision to initiate controlled burns of select buildings in Honolulu's Chinatown turned into an uncontrolled fire which led to the inadvertent burning of most of Chinatown on January 20, 1900. Shortly thereafter, plague reached the continental US, initiating the /ref>
Although the outbreak that began in China in 1855 is conventionally known as the Third Pandemic (see above), it is unclear whether there have been fewer, or more, than three major outbreaks of bubonic plague. Most modern outbreaks of bubonic plague amongst humans have been preceded by a striking, high mortality amongst rats, yet this phenomenon is absent from descriptions of some earlier plagues, especially the Black Death. The buboes, or swellings in the groin, that are especially characteristic of bubonic plague, are a feature of other diseases as well.
Research done by a team of biologists from the Institute of Pasteur in Paris and Johannes Gutenberg University Mainz in Germany by analyzing the DNA and proteins from plague pits was published in October 2010, reported beyond doubt that all 'the three major plagues' were due to at least two previously unknown strains of Yersinia pestis and originated from China. A team of medical geneticists led by Mark Achtman of University College Cork in Ireland reconstructed a family tree of the bacterium and concluded in an online issue of Nature Genetics published on 31 October 2010 that all three of the great waves of plague originated from China. Europe’s Plagues Came From China, Study Finds
In 1347, the Genoese possession of Caffa, a great trade emporium on the Crimean peninsula, came under siege by an army of Mongol warriors of the Golden Horde under the command of Janibeg. After a protracted siege during which the Mongol army was reportedly withering from the disease, they decided to use the infected corpses as a biological weapon. The corpses were catapulted over the city walls, infecting the inhabitants. The Genoese traders fled, transferring the plague (Black Death) via their ships into the south of Europe, whence it rapidly spread.
During World War II, the Japanese Army developed weaponised plague, based on the breeding and release of large numbers of fleas. During the Japanese occupation of Manchuria, Unit 731 deliberately infected Chinese, Korean, and Manchurian and prisoners of war with the plague bacterium. These subjects, termed "maruta", or "logs", were then studied by dissection, others by vivisection while still conscious. Members of the unit such as Shiro Ishii were exonerated from the Tokyo tribunal by Douglas MacArthur but 12 of them were prosecuted in the Khabarovsk War Crime Trials in 1949 during which some admitted having spread bubonic plague within a 36-km radius around the city of Changde.Daniel Barenblatt, A plague upon Humanity, HarperCollns, 2004, pp.220-221
Ishii innovated bombs containing live mice and fleas, with very small explosive loads, to deliver the weaponized microbes, overcoming the problem of the explosive killing the infected animal and insect by the use of a ceramic, rather than metal, casing for the warhead. While no records survive of the actual usage of the ceramic shells, prototypes exist and are believed to have been used in experiments during WWII.
After World War II, both the United States and the Soviet Union developed means of weaponising pneumonic plague. Experiments included various delivery methods, vacuum drying, sizing the bacterium, developing strains resistant to antibiotics, combining the bacterium with other diseases (such as diphtheria), and genetic engineering. Scientists who worked in USSR bio-weapons programs have stated that the Soviet effort was formidable and that large stocks of weaponised plague bacteria were produced. Information on many of the Soviet projects is largely unavailable. Aerosolized pneumonic plague remains the most significant threat. The plague can be easily treated with antibiotics, thus a widespread epidemic is highly unlikely in developed countries.
A combination of heavy monsoon rain and clogged sewers led to massive flooding which resulted in unhygienic conditions and a number of uncleared animal carcasses. It is believed that this situation precipitated the epidemic. There was widespread fear that the sudden rush of people from this area might spread the epidemic to other parts of India and the world, but that scenario was averted, probably as a result of effective public health response mounted by the Indian health authorities. Some countries, especially those in the nearby Gulf region, took the step of cancelling some flights and putting a pause on shipments from India.
Much like the Black Death that spread through medieval Europe, some questions still remain unanswered about the 1994 epidemic in Surat.
Initial questions about whether it was an epidemic of plague arose because the Indian health authorities were unable to culture Yersinia pestis, but this could have been due to poor laboratory procedures. Yet, there are several lines of evidence strongly suggesting that it was a plague epidemic: blood tests for Yersinia were positive, a number of individuals showed antibodies against Yersinia and the clinical symptoms displayed by the affected were all consistent with the disease being plague.