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Although contemporaries occasionally called their plague inguinal, not a single medieval source pointed explicitly to the groin as the bubo's principal site. However, plague signs and symptoms, even with bubonic plague in various parts of the world since , have been neither so regular nor so consistent as many textbooks on infectious diseases sometimes describe them or as historians often presume.

But this form of bubonic plague rarely noticed or at least commented upon by others working in the US, the Soviet Union, India, and China where plague has been endemic in the twentieth century 90 , nonetheless differs in two crucial respects from medieval and early modern plague with their own variety of pustules and boils. Chroniclers and doctors from to the very end of the so-called second pandemic in the eighteenth century saw multiple pustules and carbuncles as an integral part of their plague and as its most deadly sign, more so than the bubo.

From at least the beginning of the twentieth century, scientists have noted discrepancies dividing the characteristics of the so-called second and third pandemics. Biraben has instead tried to convince us of the supposed tremendous mortality of rats during plague by pointing to less than a handful of examples such as that at Uelzen in , when one man alone was paid 6 schillings to poison rats in the town. In the instance above, what was the explanation for killing still more if so many already littered streets and houses?

By contrast, peasants in subtropical regions even going back to the Middle Ages have left traces in records and folklore of rat epizootics when their rat-based disease gave rise to boils and quick death. The appearance of dead and dying rats was the sure sign that they should abandon their dwellings and camp out nearby until the end of the plague season.

Why should Europeans alone have been so blind, not only during the horrific events of —51 but with successive and less deadly attacks of this plague to the end of the eighteenth century? At this point, I have no explanations, but such differences certainly do not accord with the narrow temperature and humidity bands found with the fertility cycles of rat fleas or incidents of Yersinia pestis. For the mixture of skin disorders—buboes in the lymph glands, migrating buboes, and a host of other pustules that covered plague bodies—microbiologists and medievalists have claimed that the bubonic plague activated a penumbra of disease, possibly typhus and smallpox—and that these diseases account for those other skin disorders not generally seen with twentieth-century plague.

They fail to explain, however, why this penumbra of disease suddenly appeared with such ferocity and became even more deadly than the new virgin-soil bubonic disease of medieval plague. Nor do they explain why Yersinia pestis in modern times has never displayed this synergy, suddenly causing an explosion of a wide host of other diseases, much less ones with skin disorders similar to typhus or smallpox but which were more contagious and deadly than these diseases are today.

Perhaps most vexing for those who wish to label the Black Death Yersinia pestis has been the drastic difference between the transmission of the two diseases: one travelling with astonishing speed and efficiency; the other discovered early on by plague commissioners to have been hardly contagious at all, especially in bubonic form. To resolve this riddle, historians and doctors first turned to pneumonic plague to explain the seeming absence of rats with the Black Death along with its contagion and rapid dissemination.

Yet the late medieval plagues especially in the Mediterranean recurred consistently during the hottest months of the year, not the usual time for respiratory diseases and for pneumonic plague in particular to reach their peaks. The head of the Manchurian plague commissions in and , Wu Lien-Teh, observed that pneumonic plague, as in its other forms, remains a rodent disease and must begin with an epizootic of rodents. In Manchuria it was the tarabagan, whose furs soared in price in the early twentieth century, leading to an influx of inexperienced trappers into the region.

Pneumonic plague can spread person-to-person, especially in the extraordinary conditions in which the tarabagan trappers found themselves, forty or more crammed into unventilated underground huts measuring 15 by 12 feet in sub-freezing temperatures. He noted that in tightly packed train cars travelling across Manchuria those infected with pneumonic plague rarely passed it on to fellow passengers.

As a consequence, the worst-known epidemic of pneumonic plague, that of Manchuria in , infected and killed less than 0. As Wu concluded, it did not spread with anything like the speed or efficiency of influenza or the Black Death although later in life and further removed from the events of and , he thought that the Black Death may have been Yersinia pestis. Historians and now many from the scientific community speculate that the human flea, Pulex irritans , was the vector—a proposition first raised cautiously by C J Martin in If present in great abundance, they argue, this flea might explain the absence of rodents as carriers at least after an initial outbreak and the wide differences in epidemiology between the second and third pandemics, that is, the lightning speeds of late medieval plagues, their high contagion, household clustering of cases, and high mortality.

As far as I am aware, the most detailed study of a plague transmitted person-to-person and perhaps by the human flea was that of the outbreak in the mountain village of Nawra, Nepal. It resulted in six cases of tonsillar plague, one of primary pneumonic plague and seventeen of the bubonic variety. Unlike bubonic plague in India, Sydney, China, and most other places, plague here clustered tightly in households and could be shown to have been transmitted person-to-person.

Finally, in the bubonic cases, again unlike classic plague in India and most other places, the buboes did not concentrate in the femoral regions and groin but formed on shoulders, calves, facial and cervical regions. To date, no one has shown that this vector has ever caused an epidemic on any noticeable scale or explained how a flea that is far less efficient in transmitting Yersinia pestis than Xenopsylla cheopis can account for the medieval mortalities that were at least an order of magnitude higher than anything ever scored by Yersinia pestis since its discovery in and that spread more widely over space in a given period of time by two orders of magnitude and without twentieth-century modes of transportation.

The plague commissioner Fabian Hirst in the s showed the difficulty in grasping this straw to solve the riddle. He then went further, maintaining that the reverse transmission of plague from humans to rats, other mammals, or other humans was highly unlikely: the concentration of the bacillus in humans is far too low to transmit the plague effectively to other animals or humans. Other entomologists, rat specialists, and plague scientists such as Atilio Macchiavello, and even C J Martin, have repeated Hirst's first doubts about this flea transmitting plague in the twentieth century and have connected the severity of plague since with the prevalence of the most efficient vector, Xenopsyllus cheopis.

Secondly, while plague transmitted by Pulex irritans might spread rapidly through a single village as it may have done in Nepal in , it can extend beyond the village only with great difficulty. This failure, moreover, cannot be attributed to efficient medical intervention. In the cases of plague in the mountains of Iran and Nepal, health workers from the Institut Pasteur at Tehran arrived on the scene only after these epidemics had almost completed their course.

Even the most vigorous supporter of human ectoparasites as the vectors of the late medieval, early modern, and twentieth-century plagues, Georges Blanc, recognized these difficulties:. Inter-human contagion is strictly limited to those who enter the mortuaries of plague victims, or who change or wear their clothes.

For the most part, they are family members, or of the same farm or hamlet. The transport of infected ectoparasites at any distance is thus nil, the opposite of what happens with typhus.

The Black Death: The Greatest Catastrophe Ever

He then went on, however, to speculate that in urban areas such restrictions on the mobility of the disease would not pertain. But, in addition to failing to explain the rapid and devastating spread of the Black Death or other plagues such as those of —30 through isolated rural districts, such an urban transmission has yet to happen even on a minuscule scale in urban areas since , even in cities such as Dakar and St Louis Senegal where both plague and human fleas have been plentiful.

Instead, the suspected examples of outbreaks of inter-human plague transmitted by human ectoparasites have come solely from nomadic tribesmen in cold climates or those in desert circumstances such as on the steppes of Russia, where herdsmen have been accustomed to wearing thick layers of clothing for protection.

These characteristics of plague transmitted by Pulex irritans do not, moreover, tally well with the epidemiology of the Black Death and its subsequent strikes through the early modern period or with the habits and conditions of its people.

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First, these late medieval and early modern plagues were capable of spreading rapidly from village to village and from one rural region to another even in isolated and sparsely populated mountainous territories such as Snowdonia, the Apennines of Italy, and the cantons of Switzerland.

Such clothing habits in summer time are not seen among Florentines or Romans in the Middle Ages or today. As early as the late thirteenth century, Italians had developed spinning technology to weave light summer cloth for their Mediterranean climates. David Herlihy and John Munro have shown that these new fabrics spread to the peasantry and may well have constituted the first mass- market goods in the west. Thirdly, the spread of plague by Pulex irritans makes certain assumptions about medieval life across social classes—that they were all equally dirty, insanitary, and rarely washed themselves, their bedding or clothing.

In various places chroniclers even commented that the rich fell to the disease in greater numbers than the poor. Fourthly, from the plague legislation at Pistoia in to the eighteenth century, communities made strenuous efforts to restrict the movement of goods as well as persons by imposing quarantines; governors and health magistrates were particularly suspicious of clothing, bedding, and textiles as prime culprits in the transmission of plague. More than any other articles, these were subjected to careful scrutiny and, by the eighteenth century, even experimentation in the transmission of plague.

Albertus Magnus, for instance, described various characteristics of fleas pulices —their eggs, biting mechanisms, how they drew blood, their leap, and seasonality. He saw them, however, exclusively as an insect that drew blood from animals, not man. Finally, with early industrialization to the late nineteenth century or even later, overcrowding, public hygiene and sanitation worsened, infectious diseases rose in intensity, and life expectancies often dipped dramatically below levels of the late Middle Ages and early modern period.

For instance, Pulex irritans became the principal rat flea in Dakar and St Louis Senegal by the s. The two trends, moreover, may be related. Geneticists and archaeologists such as Mike Prentice, Alan Cooper, Thomas Gilbert, Carsten Pusch, and others have cast doubts on these claims on several fronts—laboratory contamination, misused methods, and the absence of such results in well-preserved plague pits in Britain, Denmark, France, and Italy.

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Or would such a result instead open new problems and questions for microbiologists, geneticists, others in the scientific community, and historians? How in the space of a century but perhaps even less given the evidence from nineteenth-century Russia would a disease that once spread quickly and efficiently, person-to-person without the complexities of a rodent carrier or an insect vector, have suddenly become transformed into the inefficient, barely contagious bubonic plague, whose agent was first cultured in ?

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Why would this pathogen have suddenly withdrawn from its previous pathways toward symbiosis with its human host? Why would humans, who once possessed natural immunity to this pathogen and could acquire it over the long term, suddenly have lost these characteristics? What biological event in the nineteenth century led to such a quick and radical genetic mutation in both humans and bacteria at precisely the same moment and not just in one or two locales but across the globe?

These are questions the historian cannot answer, but which multidisciplinary research and cooperation as seen at the Oslo conference in November might help to unravel. Both camps—those who believe the Black Death was Yersinia pestis and those who doubt it—must now be open to new possibilities. See discussion below. Come gli orribili effetti della peste conuengono con quelli delli peccati mortali; et il securissimo porto da saluarsi da tali flagelli , Venice, n. Some of these plagues may have been Yersinia pestis of the rat—rat-flea variety, others appear to have been more of the contagious and inter-human Black Death sort.

Studies of plague in the nineteenth century before Yersin are needed.

Chronicle of the Black Death

For now, see Daniel Panzac, La peste dans l'empire ottoman — , Leuven, Peeters, , where, despite his conclusions, his descriptions provide testimony of epidemics that spread rapidly throughout vast regions, killing up to 44 per cent of populations, without any evidence of prior or simultaneous epizootics of rodents. O M Dalton, 2 vols, Oxford, Clarendon, , vol. Procopius, ibid. Hygiene , , 7 : Sallares, op. The comparison, however, is forced: a failure to see and understand insects as the vectors of a disease is hardly the same as observing what would have been the sudden death of thousands, even millions, of rats falling from rafters, littering buildings, streets and lanes, not only in , but in numerous other plagues until the nineteenth century.

In India and Africa, native villagers could see them and took them as the sign to leave their villages during the plague season: why would Europeans alone have been so blind or ignorant? For other examples, see Morony, op. Enrico Musacchio, Bologna, Capelli, , p. Luigi Belloni, Milan, n. Arturo Castiglioni, Bologna, in Archeografo Triestino , , ser. The authors admit that the descriptions of chroniclers do not match the long incubation period of 32 days and a day infectious period argued by Susan Scott and Christopher Duncan, Biology of plagues: evidence from historical populations , Cambridge University Press, , pp.

Scott and Duncan's conclusions are based on an unexplained sample of nine households in their first book and three taken from the previous nine in the second. These have been selected from plague-stricken households reconstructed at Penrith, Cumbria, with a similarly small sample taken from parish burial records during the plague at Eyam.

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For the Milanese plagues to and at Nonantola Modena during the plague of , using over a thousand reconstructed households, as much as a quarter of plague deaths within households occurred within twenty-four hours of one another. This interval zero days was the mode of plague deaths within households.

These definitions and descriptions will be further developed in a book on plague literature in the sixteenth-century that I am now writing: Evolutions of plague: disease and thought in sixteenth-century Italy. Elina Bellondi, R.

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Vittore Branca, Milan, Rusconi, , p. Hygiene , , 45 : — Greek was largely forgotten, and with it much of the learned texts of antiquity. There was a limited edition vinyl with different cover artwork that was released in by Northern Heritage. From Wikipedia, the free encyclopedia. Dark Ages. The Metal Archives. Retrieved July 22, Retrieved February 9, Archived from the original on July 16, Historians believed that the Black Death was caused by the dirt and squalor that people lived in which was easily spread in crowded highly populated areas. The city of London was a particularly dirty and highly populated place, it is believed that rats thrived in these conditions and that the black death was spread by fleas that lived on the rats and carried the bubonic plague and transferred the disease to humans when they bit them.

A medieval doctor would wear a herb mask to protect against the Black death. The symptoms of the Black death or bubonic plague were particularly gruesome, within minutes of being bitten by a rat flea the victim would break out in black blotches and large painful lumps would appear all over their bodies.

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The victims would be in excruciating pain for days shaking and vomiting, parts of their body such as their fingers and toes would turn black and completely fall off until they finally succumbed to the disease and died. The Black death quickly spread through the towns, villages and cities of medieval times, the bigger more populated areas suffered the most. People were even afraid to leave their homes for fear of catching the bubonic plague and they would rather starve to death than risk catching the Black death.