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BLACK DEATH OR REVENGE OF THE?UNKNOWN

Posted on August 18, 2010 by chepeyja<!-- .entry-meta -->
BLACK DEATH
Though Nobel Laureate Albert Camus immortalized it as a metaphor of the evil that lies dormant everywhere, in the fiction, The Plague, and Robert Downey, Meg Ryan and Hugh Grant made more than a passing reference to it in the movie, Restoration, Black Death or Black Plague seems to have slipped down from people's memory of past horrors. This pandemic of the 14th century surpassed the loss of life in a catastrophe for all time to come. It is generally thought to be caused by the bacteria Yersinia Pestis (Bubonic plague) but recent findings point to other diseases as well. It is believed to have started first in Central Asia, from where it spread to Europe around 1340. Decimating a total of about 75 million people in the contemporary world, it brought about a loss of 50 million lives (or nearly 60 percent of population) in Europe. Changing medieval demography, it is thought to have reduced world population from an estimated 450 million to 375 million in 1400.
The plague continued with its visits to Europe till the end of the 18th century but its spread and death toll varied. There were about 100 plague outbreaks during this period, among which the London plague of 1603 finished 38,000. Other killer epidemics were Italian (1629-31), Seville (1647-52), London (1665-66), Vienna (1679), Marseille (1720) and Moscow (1771). The origins of such virulent forms of the disease are debated but from the 19th century on it seemed to have been absent in Europe. The looming threat of death at all times affected the society and the Roman Catholic faith to a great extent and gave rise to intolerance of minorities like Jews, foreigners, beggars and lepers. In 1833, the term black death was first used, derived from the symptoms like blackening of skin and gangrene of limb extremities. There was also the bubonic type, in which glands swelled in armpits and other parts of the body leading to formation of buboes. The buboes filled with pus and burst open subsequently. Patients usually died within 3-5 days after the appearance of the buboes and disease spread through flies sitting on the dead. It was believed earlier that the epidemic was spread by black rats and flies, but recent research suggests that it is always present and is only lying dormant.
BEGINNING AND SPREAD
Though populations of ground rodents in Central Asia are common carriers of the disease, it is not clear how the 14th century outbreak started. The popular belief is that it began in the steppes of Central Asia while some think that North India was the place of origin. Yet another view is that considering the historical evidence of Mediterranean epidemics (plague of Justinian and so on) it probably began in Africa and found among the rodents of Central Asia a suitable vector and then travelled to Mongolia via the Silk Route. The trading city of Caffa in Crimea was besieged by the Mongols under Janibeg in 1347. When his soldiers died of the disease, the Mongol chief catapulted dead bodies over the city walls in order to infect the citizens. Genoese traders living in the city fled by ships and brought the disease to Sicily, from where it spread to Europe. Though it is merely a hypothesis, it points to several factors like war, weather and famine as contributing to the spread. Mongol invasion of China in the !4th century severely affected agriculture and trade, brought famines and reduced the Chinese population by nearly 60 million. Then came the plague killing a further 20 million.
Europe had unusually warm periods intermittently throughout the !4th century, at the end of which there were harsh winters leading to reduced harvests. Before that time, in the centuries preceding, European population had been increasing steadily, and a stage was reached when the agricultural output was barely sufficient. When a famine started in North Western Europe in 1315, it quickly assumed catastrophic dimensions. Innovative farming practices like heavy plows and three-field system introduced in the mediterranean for bringing in virgin lands under cultivation were not successful in North Europe because of the clayey soil there. Consequently, high prices were prevailing even a century before the plague, everything was scarce and hunger and malnutrition was rampant. People became vulnerable to diseases due to feeble immune systems. Compounding the situation further, the ruling classes of England and France, afraid that their lifestyles would go down, raised taxes. With diets getting limited by the day, the poor suffered terribly, and their health conditions became increasingly bad. Then it began to rain heavily in late 1314, several years of bitingly cold winters followed, the already reduced harvests went down further and the seven-year famine began killing about 10 percent of the population. Such was the economic and social condition when portends of the calamity in waiting appeared. The first was a typhoid outbreak in which many thousands perished in congested urban areas like Ypres. The second was a disease of unknown origin (presumably anthrax) killing in 1318 a large number of animals in Europe and affecting food source and income of people.
IN ASIA
Probable conditions which had caused the plague to break out in Central Asia were similar to those recorded during the first reports of the disease in the Chinese province of Hubei in 1334. Thereafter, following the catastrophe in Europe, the plague appeared in Jiangxi, Shanxi, Hunan, Guangdong and Suiyuan in China in 1353-54. There are extensive records of the pestilence and social disruption of the times in Chinese, but no one seems to have studied them properly. In 1347, the plague struck the trading cities of Constantinople and Trebizond and then spread among the soldiers of Mongol chief Janibeg laying a siege on the Genoese commercial enclave of Caffa in Crimea. Probably the first in history to wage a biological warfare, Janibeg catapulted the dead bodies of his soldiers over the city walls to infect the citizens. The strategy worked and Genoese traders left the city. The ships sailed into the Sicilian port of Messina in October 1347 carrying infected crews and rats, some were ghost ships with everyone on board dead from the disease, while some more ran aground to be looted by people living by the shores. There was thus no dearth of carriers or vectors of the disease, which spread to Genoa, then Venice and next to most of Italy. Onto France, Spain, Portugal and England by June 1348, when it turned and ravaged Germany and Scandinavia between 1348 and 50. Skipping Poland and some remote areas of Belgium and Holland, the vectors finally travelled to North Western Russia in 1351. As regards the horrors experienced by people, a resident of Siena in Tuscany, Italy wrote:
"They died by the hundreds, both day and night, and all were thrown in … ditches and covered with earth. 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 so many died that all believed it was the end of the world."
IN THE MIDDLE EAST
The plague spread in the countries in the Middle East after reaching the port city of Alexandria in Egypt in the autumn of 1347 presumably through trading connections of the city with Constantinople and ports on the Black Sea. Next year, it travelled to Gaza in east and then to north to eastern coastal cities of Lebanon, Ashkelon, Acre, Israel, Jerusalem, Sidon, Damascus and Aleppo. Antioch came under its attack in 1348-49, when most of the residents deserted the city to go to north and died during the journey. The spread of infection, however, did not stop and struck the people of Asia Minor. Makkah fell to the disease in 1349 and so did Mawsil (modern Mosul) where records show a large number of deaths due to the pandemic. In Baghdad, it struck twice. King Mujahid of Yemen released from imprisonment in Cairo returned to his kingdom in 1351 and apparently brought the disease with his party.
RETURN VISITS
Without any census figures to depend on, historians usually estimate the population of England between 4 to 7 million in 1300 and as low as 2 million after the plague. It was absent from 1350 but never really extinct in England. In the next few centuries, it returned time and again, notably at Norwich (1579) and Newcastle (1636) killing nearly 40 percent of people there. Actually, 8 major outbreaks in Tudor and Stuart England coincided with those in Germany, Belgium and Holland in the years 1498 to 1636. Europe and the Mediterranean were under its attack repeatedly from the 14th to 17th century, and there are isolated instances of bubonic plague even today. The Great Plague of London (1665-66) is regarded as one of the last major outbreaks, others being Italian Plague (due to army movements in war, 1629-31), Vienna (1679), Moscow (2 lakkhs dead, 1654-56), Oslo (1654), Naples (1.5 lakh, 1656), Amsterdam (1665) and Helsinki & Stockholm (1710).
HOW BUBONIC INFECTION STARTS
Michel Drancourt prepared models of sporadic, limited and large plague outbreaks by reviewing the ecology of Yersinia pestis in soil and in rodents along with a study camiseta de futbol baratas of human ectoparasites. It is found that plague among prairie dogs are more due to occasional reservoirs of infection like an infectious carcass than the conventional "blocked fleas" theory. It was also observed that epidemiology, appearance, spread and eventual disappearance of plague from Europe was due to the succession by another species of the flea-bearing rodent reservoir of disease. Originally introduced by trade from Asia to Europe, the black rat was subsequently displaced by the bigger brown rat in Europe. That specis was not as prone to transmit germ-bearing fleas to humans as the black rat in large die-offs due to a different rat ecology. The dynamic complexities of rat ecology, herd immunity of the specis in that particular reservoir, interaction with human ecology, secondary transmission routes between humans with or without fleas, human herd immunity and changes in each of the above are possible causes of the eruption, dissemination and recurrence of the plague for centuries in Europe. It probably also holds true for the plague's so far unexplained disappearance from the continent.
INDICATIONS
Actually, there are two more forms of plague besides the bubonic, each with its different signs and symptoms. Blood poisoning is the consequence of septicaemic plague while pneumonic type attacks the lungs first through aspirated air and then other parts of the body. Bubonic causes buboes, resulting from internal bleeding, to appear in the neck, groin and armpits. The damages to the skin and tissue beneath turn the body black, pus and blood ooze out from the swellings and the patient dies within seven days of the infection. Black Death in Europe came in the bubonic form mostly, first in the port cities and then to countrysides. Its mortality rate was over 80 percent and symptoms included fever, aching joints, nausea and vomitting. The pneumonic form was second most common witha mortality rate of about 90 percent. The
signs were fever, cough and bloody sputum, which became more and more red as the disease took hold. Septicaemic plague was not quite common. It came with high fever and purple patches on the body and had a hundred percent mortality. According to David Herlihy, a further symptom of the disease was freckle like spots and rashes in the body. Unlike buboes, these were darkish points or pustules covering large parts of the body.
OTHER THEORIES
The long-held belief that the Black Death was an epidemic of bubonic plague has been challenged by recent historic and scientific findings. Gunnar Karlsson in 2000 pointed out that the Black Death killed between half and two-thirds of the population of Iceland, although there were no rats in Iceland at that time. Rats were accidentally Introduced accidentally only in the nineteenth century, rats have never spread beyond a small number of urban areas attached to seaports. In the fourteenth century there were no urban settlements in Iceland had no urban settlements the 14th century, and was unaffected by the later plagues known to have been spread by rats. Nonetheless, in the absence of a rodent reservoir, it is possible for pneumonic plague to spread from human to human by respiratory transmission, and likewise bubonic plague by human-biting fleas. Although a study carried out on tooth pulp tissue from a 14th century plague cemetery in Montpellier showed molecules associated with Y pestis, other similar studies yielded different results. A team of researchers from Oxford University conducted tests on 121 teeth from 66 skeletons from a 14th century mass grave in 2003, and did not find any genetic trace of Y. pestis.
Samuel K. Cohn in a controversial article, "The Black Death: End of the Paradigm" (2002) says that the medieval and modern plagues are two distinct diseases having different signs, symptoms and epidemiologies. He argues that the agent causing the bubonic plague, Yersinia pestis, "was first cultured at Hong Kong in 1894." So, the medieval European plague was not the bubonic plague carried by fleas on rats as conventionally held by both scientists and historians. Supporting his argument that medieval plague was not rat-based, Cohn further states that the modern and medieval plagues hit in different seasons, had unparalleled cycles of recurrence, and varied in the manner in which immunity was acquired. As fleas on rats thrive in temperatures below 26 degrees C with high humidity, modern plague reaches its peak in seasons with that kind of weather. As opposed to this, Black Death is recorded as breaking out in periods when rats' fleas could not survive, seasons having weather conditions similar to hot Mediterranean summers with temperatures above 26 degrees C. As regards return period, the Black Death generally did not come back in an area 5 to 15 years after the event, while modern plagues often hit an affected area after an interval of eight to forty years. Cohn also presents evidence that individuals acquired immunity against the Black Death during the 14th century, unlike the modern plague. It seems that in 1348 two-thirds of those suffering from plague died as compared to one-twentieth in 1382. Current statistical figures also support the notion that immunity to the modern plague has not been acquired so far.
Arguing further, Cohn points out that in the latter part of the nineteenth century buboes appeared mostly on an infected person's groin, while medieval primary sources indicate that the Black Death caused buboes to appear on necks, armpits, and groins. According to Cohn, this difference corresponds to the fact that fleas caused the modern plague and not the Black Death. As fleas do not usually bite in the areas covered by the dress (down pantalon futbol baratos to a person's ankles in colder climes), in modern period the groin is the nearest lymph node that could be infected. Considering that the neck and the armpit were often infected during the medieval plague, those infections did not appear to have been caused by fleas on rats.
About two decades before (1984) Cohn, Graham Twigg published The Black Death: A Biological Reappraisal, and stated that the climate and ecology of Europe and specially England are such that its very difficult if not impossible for fleas and rats to spread the bubonic plague. Studying the biology of black and brown rats as also of common fleas he cross checked the details with modern findings of plague epidemiology, particularly in India, where the black rat is a native species and conditions are always favourable for plague to be spread. His conclusion is that it would have been nearly impossible for Yersinia pestis to start the plague, and propagating its explosive spread across Europe is out of question. According to him, the common theory of entirely pneumonic plague is not quite correct. He puts forward, after a re-examination of the evidence and symptoms, the theory that the Black Death may actually have been an epidemic of pulmonary anthrax.
A pantalones futbol DIFFERENT VIRUS
Susan Scott and Christopher Duncan of Liverpool University in 2001 suggested that the outbreak of Black Death is probably due to an Ebola-like virus and not a bacterium. In support of their theory, they pointed out that this plague spread much faster and the incubation period was much longer than other confirmed Y.Pestis-caused plagues.Viruses with a longer period of incubation would allow vectors to travel farther and infect more people than did one with a shorter period. As the primary vectors are humans, and not birds, this aspect becomes significant. This is corroborated in English church records showing an unusually long incubation period in excess of thirty days, which accounted for the rapid spread, reaching a speed of 5 km/day. In places in Europe, such as Iceland, where rats are not common, the plague struck as well. It would appear from epidemiological studies that the disease was transferred between humans-an extremely rare happening with Yersinia pestis and yet more unusual for anthrax bacilli. Also, there are some genes found widely in Europe, which contribute significantly to the development of immunity to anthrax bacilli. Such genes are not so common in other parts of the world. Publishing their research and findings in Biology of Plagues, the researchers recently brought out computer models showing how the Black Death immunised about 10 percent Europeans against HIV.
ANTHRAX
Likewise, historian Norman Cantor in his book In the Wake of the Plague, says that the Black Death could be a combination of pandemics along with a form of anthrax known as cattle murrain. His evidences include reported disease symptoms unlike the known effects of either bubonic or pneumonic plague, the discovery of anthrax spores in a plague pit in Scotland, and the reported sale of meat from infected cattle in many rural English areas prior to the onset of the plague. The point to note is that the means of infection varied widely, from human-to-human contact as in Iceland (rare for plague and skin-related anthrax bacilli) to infection in the absence of living or recently-dead humans, as was seen in Sicily. Actually, the Sicilian example is generally against most viruses. Then, diseases with similar symptoms were generally not differentiated in that period because disease identification, at least in the Christian world, was not that detailed. It is possible that Chinese and Muslim medical records of the period may give better information pertaining to the specific diseases, which affected those areas.
POINTS AGAINST
Supporters of bubonic plague based theory of Black Death argue that the very rapid spread of the plague could be due to respiratory droplet transmission coupled with low levels of immunity in the European population at that time. In populations without previous exposure, historical examples (like transmission of smallpox and tuberculosis by aerosols amongst indigenous people of the Americas) show that the first instance of an epidemic spreads faster and is far more virulent than later instances among the descendants of survivors, for whom natural selection by then has produced characteristics protective against the disease.