The Black Death in London (33 page)

Our modern knowledge of the bionomics [of the rat flea] explains why in medieval England epidemics usually erupted towards the end of spring, rose rapidly to a peak of intensity in late summer or early autumn, collapsed or declined sharply with the arrival of autumn frosts, and were extinguished in or remained dormant throughout the winter months.
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Indeed, his whole thesis comprised a sustained attack on the documentary evidence for high mortality and winter spread precisely because it did not fit the bionomics of rat and flea populations and the aetiology of bubonic plague. He argued for a range of coterminous diseases being responsible for the mortality seen in the fourteenth-century outbreaks.

Despite the inherent contradictions that this kind of situation gives rise to, it was to be another decade before a cautionary note was sounded. In 1979 Stephen Ell, undertaking an examination of more than 300 medieval plague accounts, concluded that the human flea, and thus human-to-human transmission, more closely fitted the bill.
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Three years later, the risks associated with extrapolating modern plague experience backwards to the 1348–9 outbreak were raised by medical historian N.G. Siraisi,
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and in 1984 the first co-ordinated confrontation of the bubonic model was mounted by zoologist Graham Twigg. In it he argued that the specific problems of the reproductive capacity of fleas in cold winters and cold climates, and the presence of appropriate rodents (i.e. the black rat) in appropriate numbers for them to prey on, were too great to be surmounted. He expressed doubts about whether the speed of transmission was consonant with the requirements of bubonic plague. The bubos and other symptoms described in the contemporary literature he thought were potentially associated with other diseases as readily as with bubonic plague. He also brought into play references to chroniclers who mentioned the death of larger animals as well as men, and concluded that the answer was more likely some form of disease of animals that also affected humans, and made a tentative case for anthrax, spread person-to-person.

Detractors from this view raised the issue of our ability to compare like with like, the dangers of using sources selectively, and the lack of any real evidence for widespread larger animal deaths in the plagues of the later sixteenth and seventeenth centuries. It was in one case also noted that the physicians of the day knew the difference between pestilence buboes and anthrax carbuncles.
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Bean rejoined the debate in 1982. Accepting bubonic plague as the agent, he reasserted that since there was undoubtedly a rapid spread of the disease during winter months, ‘it was reasonable to assume … there was pneumonic plague’. However, he recognised that if the plague had indeed assumed different seasonal characteristics (bubonic in summer, pneumonic in winter), we should expect to see different mortality rates – much higher in the areas affected in winter. The fact that this was not borne out in studies of summer mortality in Orvieto, Siena and San Gimignano (with mortality rates of 50 per cent or more) he sought to explain away by arguing that cities were at far greater risk.
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In 1986 the issue of the black rat itself came under scrutiny by David E. Davis, a zoologist at North Carolina State University. Following a survey of archaeological and documentary indications of rats and a consideration of the ecological requirements of
Rattus rattus,
he concluded that ‘the accumulated evidence, interpreted by ecological and epidemiological methods, does not support the traditional view that black rats were responsible for the Black Death’. Subsequent studies concluded that the archaeological evidence for
Rattus
in the medieval period was more considerable than Davis had allowed for, but one French study raised the issue of the viability of the flea carrier itself:

the rat population had gradually grown from a fairly restricted one in the early Middle Ages to a significant one in the 11th and 13th centuries. The rodents spread along the major highways explaining the very different geographical impact of the various plague epidemics of the early and late medieval periods. However, the mystery of the exact mechanisms by which plague spread has still not been entirely elucidated, since the Asian rat flea,
Xenopsylla cheopis,
whose role as vector was demonstrated by P.L. Simond [an early twentieth-century bubonic plague researcher], could not have survived in the temperate European climate.
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The role of rats came under increased pressure, this time from Iceland in 1996. This related to two plague outbreaks argued to be of the Black Death type, in 1402–3 and 1494–5, which may have resulted in more than 50 per cent mortality rates, and which were able to attack the human population even in winter. The researcher, Gunnar Karlsson, argues that there were no rats in Iceland at the time, and that in winter the plague spread rapidly into areas of the country which enjoy a mean temperature of 0°C at that time of year. He supported the view of an earlier scholar, Jon Steffensen, who had proposed that pneumonic plague, not bubonic plague, was the cause.
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A further alternative was proposed by Susan Scott and Christopher Duncan in 2001.
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They had taken the very detailed documentary evidence from the outbreak of plague in Penrith, Cumbria, in 1597 and used analysis of this, in conjunction with wider epidemiological and environmental concerns over the identification of bubonic plague as the killer, to argue that whatever it was, the pestilence was transmitted person to person, had a long incubation period (around thirty-two days, allowing it to be spread widely before a plague event was obvious), and was haemorrhagic in nature. They adopted the term ‘haemorrhagic plague’. They were also able to develop a simulated model of what should happen in terms of death rates and compare this with real late sixteenth-and seventeenth-century examples of plague outbreaks (assuming that these were the same as the Black Death itself, of course). The argument against bubonic plague as the culprit was based around the low speed of transmission of this disease, the impact of climate on rat and flea vectors, and the low mortality rate of modern bubonic plague in comparison with reported and inferred death rates during the medieval pestilence. As with Twigg, critics of this approach cited selective use of documentation.
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The most sustained published attack on the bubonic model, drawing on many of the specific concerns raised previously, has come from historian Sam Cohn.
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His approach was essentially to deconstruct the century-old assumptions regarding the relationship between modern bubonic plague and the documentary evidence for the spread not only of the 1348–9 outbreak of pestilence, but the subsequent fourteenth-century outbreaks across Europe. In it he uses important new evidence for contemporary description and understanding of the plague from plague tractates, as well as assembling a formidable array of primary documentary evidence from wills and other quantifiable sources. He does not pretend to know what the disease was, but, like the pre-Yersin historians, he is certain that it was not the bubonic plague. His arguments against that diagnosis are well worth reading, but can be summarised as:

– The symptoms do not satisfactorily tie the disease down as bubonic plague.

– There is no contemporary report of elevated rat mortality (although there are chronicles reporting birds and sheep and other kinds of animals dying during the plague period).

– The mortality rates far exceed anything like modern bubonic plague.

– The seasonality of the outbreaks defy standard bubonic plague progression.

– The evidence for reducing mortality rates in successive outbreaks, combined with increasing proportions of child mortality, suggest increasing acquired immunity, something not possible for modern bubonic plague.

– In some well-documented Italian cities, epicentres of plague outbreaks were not associated with granaries as modern bubonic plague has been, but were associated with poor, artisan parishes.

– The pestilence struck regions where the rat/flea vectors could not have been present.

Also using documentary evidence, but bringing statistical analysis to bear on them, historical anthropologist James Woods, and colleagues from Pennsylvania State Universities and Georgetown University, re-examined the use of bishops’ registers (recording the replacement dates of parish priests who had died) in the diocese of Coventry and Lichfield.
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They discovered that the standard one-month estimate for the replacement used by most researchers actually varied considerably between a few days and several months, hiding the true dates of the plague’s arrival at any given parish, and thus potentially underestimating the speed of transmission. They also found that hidden within the overall blanket of nine months (March to November 1349), in which the pestilence raged in the diocese, individual archdeaconries suffered in shorter bursts of four to six months, and noted that if this were true at archdeaconry level, the speed of transmission from parish to parish would almost certainly be faster again. This they saw as profoundly different from anything presented by the nineteenth/twentieth-century evidence, and as an argument against bubonic plague.

An unusual explanation for the plague has been presented by Mike Baillie, a palaeoecologist specialising in events dated in palaeoenvironmental sequences such as tree rings and ice-cores.
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In 2006 he presented his idea that the Justinian and Black Death plague outbreaks were associated with very significant environmental and climatic changes, possibly as a result of comet strikes; what the plague was actually caused by he remains cautious about, but he believes it was air-borne (and not bubonic) and raises the possibility of biological pathogens being introduced into earth’s atmosphere by the comets. Such a proposal, he recognises, will be seen as far-fetched by many, but the environmental markers he establishes for the fourteenth century are convincing and important for the study of this period.

One final twist to this swirl of debate and research has been the report that bubonic plague may actually be transmissible faster than previously thought. Researchers at the Division of Vector-Borne Infectious Diseases at the National Center for Infectious Diseases in Colorado conducted a study of an American carrier of bubonic plague (O. montana). In their words:

in contrast to the classical blocked flea model, O. montana is immediately infectious, transmits efficiently for at least 4 days post-infection … and may remain infectious for a long time because the fleas do not suffer block-induced mortality. These factors match the criteria required to drive plague epizootics as defined by recently published mathematical models.
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While this still requires a rodent or similar vector to produce the plague reservoir, the long incubation period and short infection window described in the existing bubonic model could be dismissed. If the disease was bubonic plague, the impact this research might have on, for example, Benedictow’s carefully plotted chronology of spread and infection could be considerable. In any event, their acceptance that the characteristics of modern bubonic plague do not match at all well with the documentary evidence of past epidemics is important.

This short summary demonstrates the difficulties in getting a definitive identification. The capacity for pathogens to evolve, the variability of the primary documentary sources, and the complexities surrounding the science of the epidemiology and DNA character of the plague agent all present formidable challenges. However, further research into the evidence from specific cities, towns, villages and manors remains of the greatest importance in helping to solve this mystery.

A Consideration of the Evidence – The Plague’s Arrival

The other great unknown about the plague, contingent of course on what caused it, is the definite timing of its arrival and the speed and manner of its spread across the country. Again, as a prelude to a consideration of London’s contribution, it is necessary to look at current evidence. The most frequently deployed evidence comes from a range of medieval chroniclers. The advantage of this kind of source is that many had lived through, or were near contemporaries of, one or more of the outbreaks; some were eye-witnesses. The disadvantage is that there were differing concepts of truth within chronicles, used to impart separate messages to the reader,
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and that the sources for such chronicles might rely on second-or third-hand information. The evidence is, therefore, not straightforward.
Table 5
shows the range of dates in a selection of chronicles broadly contemporary with the time of the epidemic. Considerable variation exists bracketing a three-month period from late June to the end of September. There is also a disagreement over a south or west coast entry point. On this uncertain basis, scholars have ascribed different levels of dependability to the chronicles, from overall caution to confident assertion that a date in late June or early July must be accepted.
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Most agree that the south coast, specifically Weymouth (Melcome), was the first port affected.