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The Black Death was so extreme that it’s surprising even to scientists who are familiar with the general details. The epidemic killed 30 to 50 percent of the entire population of Europe. Between 75 and 200 million people died in a few years’ time, starting in 1348 when the plague reached London. The pandemic moved fast: It often killed a host within days of their first developing the high fever, the telltale rash, and the repellent buboes or swellings in the armpits and groin, which turned black and burst, expelling pus and bacteria. The disease spread through families, houses, villages, towns, and cities with terrifying speed and staggering mortality. This tragedy launched a socioeconomic and evolutionary transformation in Europe that changed the course of history. So many were struck down and so rapidly, that it was long thought that the Black Death killed indiscriminately. Certainly the disease took men, women, and children, rich and poor. But was it a selective form of death? Anthropologist Sharon DeWitte, who is currently at University of South Carolina, felt the answer could be obtained by studying skeletal remains of plague victims and comparing them to other medieval skeletons buried in normal, nonplague cemeteries, and she tackled that question for her dissertation work at Pennsylvania State University. (Disclosure: I was at Penn State at the time, but I did not serve on DeWitte’s PhD committee.) Because of its severity and the existence of documentary as well as biological evidence, the Black Plague looked like a perfect case to investigate the influence of pandemic disease on human populations. When the plague hit in the mid-1300s, no one knew what caused this dreadful pestilence. Some took it as divine punishment for the world’s wicked ways, possibly the end of the world. Others blamed Jews, foreigners, travelers, and lepers, who were shunned and turned away where once they had been welcomed or at least accepted. Some towns barricaded themselves in, afraid to let anyone in who was not already there and equally afraid to let anyone out. Mothers abandoned husbands and children—and vice versa—for fear of catching the contagion. Few other than those in religious orders dared to nurse the sick. Sometimes houses were burned to the ground with the inhabitants inside if they were known to be ill. Ordinary parish burial grounds were insufficient to hold the massive numbers of dead, and new plague cemeteries were opened. The social and economic havoc created by the plague was almost beyond imagining, yet it is now being paralleled in many ways by the impact of the Ebola virus epidemic. Whole villages die within a few weeks, and fear spreads even faster than the infectious agent. With hindsight, the pandemic can be traced to the Mongol Empire, which in addition to conquering with its vast army enormous areas of Asia, opened and ensured the safety of the Silk Road for trade. This Pax Mongolica facilitated relatively rapid, long-distance transport, both of people and diseases, as airplanes and railroads do today with sufferers of the Ebola virus. Where travel is highly restricted and populations are small, deadly diseases tend to burn themselves out fairly quickly. But where the disease can be spread easily to new areas, with a new supply of victims, efforts to contain such pandemics are far more difficult.  In medieval times, where the Mongol army went, so went the plague; where the sailing ships carried trade and traders, the pestilence arrived in new regions. According to a contemporary account by Gabriel de’ Mussi, a turning point came when the Mongols besieged the trading city of Kaffa in Crimea between 1346 and 1349. Because the army remained in one place for so long, the Black Death had time to spread from man to man or from rat-carried fleas to humans. In the end, the army deliberately hurled the rotting corpses of the dead over the city walls, infecting those inside, poisoning wells, and causing a sickening stench. This strategy has been cited as the first biological warfare. Those that escaped Kaffa fled by ship to Sicily, Genoa, and Venice in 1347 and 1348, carrying the disease with them. Plague ships soon reached busy ports in France, Spain, and Norway, off-loading their deadly cargo at each stop. The plague arrived in England on or about May 8, 1348, at Melcombe Regis, traveling on a ship that had left Bordeaux a few weeks earlier. The epidemic is mentioned in historical documents shortly before June 24 of that year. The disease reached London in August 1348 and reached epidemic proportions by the end of September. From there, it spread into the countryside. By 1351, the pandemic had died down, but whole villages and their fields were empty of inhabitants; cottages and houses sat vacant; many crops had rotted in the field for lack of labor to harvest them; stock animals died, unfed and unwatered, for lack of human care. There were simply not enough serfs and peasants left in England to do the work. The aristocrats also died in droves. The medieval economic system broke down because of the rapid drop in population. Plague struck in three forms, which made its identification problematic until recent times. All three have been traced to the bacterium Yersinia pestis by extracting genetic material from bones and dental pulp of victims buried in plague cemeteries and then comparing it to the genotype of modern samples of the bacterium. Although bubonic plague may be carried by black rats and their infected fleas to new areas, it also was transmitted from human to human as a respiratory form and from humans to other humans who handled infectious tissues. Without modern antibiotic treatment, the plague kills 72 to 100 percent of those who contract it. Today, the tragedy of the Black Death offers a unique opportunity to study past human health and the social and genetic consequences of pandemics. DeWitte explains, “I got started on plague because I knew I wanted to study health in the past using skeletal material, but I wanted to do it in the most rigorous way possible, which requires large sample sizes. The Black Death provided the best possible case study because of the existence of exclusive Black Death cemeteries—large samples of people who died within a short period of time from a single known cause of death.” For her PhD thesis, DeWitte studied 490 skeletons from a plague burial in England, the East Smithfield Black Death cemetery, and compared the results with those from a study of 291 skeletons from two medieval but normal and nonepidemic cemeteries of Viborg and Odense in Denmark. For each individual, DeWitte established age at death from skeletal indicators of maturity and sex. She also documented the location and frequency of various bony or dental lesions that indicated poor health, malnutrition, or other causes of “frailty.” She found that older individuals and those with significant signs of frailty were at higher risk of dying of the plague than their peers. “By targeting frail people of all ages, and killing them by the hundreds of thousands within an extremely short period of time, the Black Death might have represented a strong force of natural selection,” DeWitte observes. The disease apparently removed the weakest individuals on a very broad scale over much of Europe, whether their frailty was due to poor immune systems, prior disease, or malnutrition. “We know the Black Death marked the beginning or, at the very least, an acceleration of a huge economic and sociological shift in Europe,” says DeWitte. It took 200 years for population levels to recover. In the meantime, the medieval system of serfdom collapsed, because labor was more valuable when there were fewer laborers. Despite the dearth of workers, there was more land, more food, and more money for ordinary people. “You might see this as a benefit to the laboring classes,” she says. DeWitte’s more recent studies explore the long-lasting biological impact. When the plague returned in 1361—and again in 1368, 1375, 1382, and 1390—DeWitte looked for signs that the population might have been healthier and better fed: Were they taller with fewer signs of lesions? She looked at 464 skeletons from cemeteries used before the Black Death and 133 skeletons from another that was in use from just after the plague hit until 1538, gathering comparable data to her previous work. Looking simply at age at death, DeWitte found that a higher proportion of people lived to older ages after the Black Death. That is, if you or your parents or grandparents lived through the first plague epidemic, you were more likely to survive until you reached age 50 or above. Descendants of plague survivors were more likely to live through their reproductive years, thus passing on whatever genetic advantages enabled their ancestors to survive the plague. DeWitte’s results do not agree with several documentary studies of population well-being during this time, such as one based on wills by Jens Röhrkasten of University of Birmingham in England. These documents showed spikes in mortality associated with plague epidemics in 1361, 1368, 1375, 1382, and 1390. However, wills and other documents tend to provide evidence only on well-to-do men, excluding married or unmarried women, children, servants, apprentices, laborers, and paupers. The sheer number of wills recorded in various counties amply demonstrates the appalling wave of death, but Röhrkasten’s data give only part of the story of the aftermath of the plague. DeWitte argues that her bioarchaeological data provide information about a much broader sweep of medieval society. Despite repeated plague outbreaks and other episodes of crisis mortality, such as famines or volcanic eruptions, her study indicates that the general population enjoyed a period of at least 200 years during which mortality and survival overall improved compared to conditions before and during the Black Death. Did such a strong selective event produce changes that can be seen today? The first suggestion, made in 1998, was that plague survivors had stronger immune systems, which might be expressed as a relatively higher incidence among Europeans of a genetic allele known as CCR5-Δ32. It has been identified as conveying resistance to the modern pandemic HIV/AIDS. However, the link between CCR5-Δ32 and the plague is more tenuous than it at first seemed. The areas that suffered most profoundly from the Black Death correspond only loosely with the modern distribution of the CCR5-Δ32 gene. Other scientists suggest that smallpox epidemics are a better candidate for the causal agent behind the CCR5-Δ32 distribution. A recent study has pointed to another possibility. A team led by Jaume Bertranpetit and Mihai G. Netea decided to investigate genetic differences between Romanian Europeans and people who lived in the same area of Romania but were of Rroma ancestry (traditionally identified as Gypsies). Linguistic and genetic documentation indicates that the Rroma migrated from northwest India between the 5th and 11th centuries, when they began to settle in Romania. Over the centuries, the Rroma remained largely isolated from Romanians of European descent, although they lived in the same region. Thus the infectious agents that potentially shaped the Rroma genomes during the last millennium—including the plague—were shared with the European Romanians, but their initial genetic backgrounds were different. Because India did not suffer from the Black Death, the immune-related genes put under positive selection by exposure to the disease should be similar among European Romanians and Rroma but different from those among Indians in Gujarati, home of the populations ancestral to the Rroma. Because Netea is himself Romanian, he realized that these two genetically distinct but adjacent populations offered a rare opportunity to document the plague’s evolutionary effects. The team took DNA samples from 100 European Romanians, 100 Rroma, and 500 individuals from northwest India. The team assayed almost 200,000 small genetic changes known as single nucleotide polymorphisms (SNPs), which are often used as a proxy for genomic differences among cohorts of people. Then they analyzed the results looking for genes under positive selective pressure among the Rroma and European Romanians but not shared by the northwest Indians. Four genes on chromosome 4 met these criteria. Three of the four genes in this cluster are so-called TLR genes involved in recognizing pathogens such as bacteria and initiating an immune, anti-inflammatory response. Of course, the Rroma and European Romanians were subjected to other infectious agents during the last millennium, including smallpox, leprosy, and tuberculosis. Netea finds that the plague was “very likely” to have caused the genetic differences he found. “These other infections are also possible causes,” he explains, “but in my opinion somewhat less likely than plague: The geographic distributions of these diseases are more general than plague.” He also observes that the role of TLR genes in mounting an immune response to a virus, such as that which causes smallpox, is not as well established as their role in combating bacterial infections. His team is currently obtaining complete genotypes for the Indian, Romanian, and Rroma samples and conducting a parallel study focusing on adjacent but distinct African populations. By synthesizing information from documentary sources, bioarchaeological studies, and genomic studies, researchers are slowly but surely figuring out the awful mysteries of the Black Death. As we meet with new and as-yet-untreatable diseases, like Ebola, insights from the past may help ease the future.
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What was the Black plague Where did it come from why did it spread so easily in Europe?
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