The Black Death in London (32 page)

The plague brought a shortage of priests and in 1370 six chantries were vacant at St Paul’s, a situation resolved only by a major amalgamation of chantries in 1391. The impact was therefore two-fold: a drop in foundation rate and a reduction in the number of existing chantries.
⁵¹⁷
This is not, however, to say that chantry foundation as a whole decreased. A study of the bequests to chantries in the Husting wills shows that from 1259 to 1348, a total of 450 wills made mention of chantries (perpetual and temporary), an average of five wills per year. From 1349 to 1370, 383 wills made mention of chantries – an average of seventeen per year. This increase is partly skewed by the inclusion from 1341 of pecuniary bequests in Husting wills, but the trend is undoubtedly genuine.

More people left money to a greater number of temporary chantries, rather than providing larger grants to single long-term institutions. A related phenomenon appears after 1349 of large numbers of Masses being requested. To the 10,000 Masses of William de Thorneye (see
Chapter 2
) can be added the example of Johanna Cros, who left bequests to both plague chapels, to ‘chantries’ for the souls of her and her family, and for 11,000 Ave Marias and 11,000 paternosters to be said. In effect, the temporal dimension of a chantry foundation was being eschewed in favour of the quantity of intercession.
⁵¹⁸
Overall, therefore, the pattern of chantry support shifted significantly in response to the plague, tending away from perpetual foundations towards more immediate and more intense approaches to intercession and commemoration: faith in long-term stability appears to have been weakened.

Burial practice itself may have changed in the wake of the 1348 outbreak, probably reflecting another stratagem for ensuring intercession for the soul. The use of papal bullae as amulets or charms to accompany the dead has been described elsewhere (see Fig. 16),
⁵¹⁹
but the importance of the rite here is that the majority of known examples date to the period 1350–70. The link between the discovery of these lead seals in graves, the rise of Chaucer’s despised pardoners in the later fourteenth century, and good evidence in the same period for the counterfeiting and import of such seals, suggests a lively market in the purchase of talismans to reduce the pain of Purgatory or to ward off sudden death.

These observations on the social impacts of the plague are only part of the story. The impact on London’s economy and its relationship with its markets and its hinterland, and the longer-term changes wrought in demographic structure and population movement, have not been the subject of this study, but the potential must surely be there. The examples of social change suggest that it is reasonable to assert that the plague triggered a fundamental shift in charity and good works, linked to strategies for securing the salvation of the soul, but also, clearly, linked to simple empathy and sympathy for those less fortunate than the benefactors themselves. It is dangerous to generalise, but there is a sense that while better-off Londoners were perhaps more choosy about what they gave and to whom, they gave more than they had before the plagues, and they placed an increasing value on family, friends and neighbours through their ties with the parish, the fraternities, and through their choices for the hereafter. And this pattern developed in the face of disasters which saw whole families extinguished and neighbourhoods transformed. If there is a single word which captures the character of the city through this extraordinary trial, it is resilience.

Appendix

LONDON’S CONTRIBUTION
TO UNDERSTANDING
THE BLACK DEATH

The Nature of the Pestilence: Current Debates

T
HIS BOOK does not set out to prove whether the great mortality or pestilence, as it was known to those who suffered it, was bubonic plague, anthrax, typhus, haemorrhagic fever or some other disease. However, the London evidence can contribute to the debate in this contested arena, since it would appear to point away from the argument for bubonic plague and towards something else. It is impossible for this author in this volume to attempt a full critical survey of all published theories on the Black Death and its character, but in order to provide the basis for any such argument, a summary of the different approaches and theories is necessary; it is hoped that the key elements of the various arguments have been acceptably precised here.
⁵²⁰

The pestilence was, for the vast majority of schoolchildren and researchers alike, bubonic plague. This has been the accepted identification of the Black Death for most of the twentieth century, since the outbreak of a plague in Hong Kong in 1894 by a team including Alexandre Yersin: the bacterium was eventually called
Yersinia pestis
after him. In the early 1900s, the link between the bacillus, fleas and rats was made, and in 1914 the mechanism which caused rat fleas to attack humans.
⁵²¹
Yersin himself made the first connection between the nineteenth-and early twentieth-century outbreak of bubonic plague and the medieval scourge, linking it also to the even earlier outbreak in
c.
ad 540 known as the Justinian plague.
⁵²²

The main arguments in favour of this being the medieval pestilence are based around its observed characteristics – the common presence of bubos in most of the chronicles and many medical observations, and the similarities of other symptoms and of the progress of the disease. Variants in description (such as the spitting of blood, or of victims dying within hours almost unmarked) are explained through the presence of three varieties of plague caused by
Yersinia
: bubonic, where the infection passes from the bite site into the lymphatic system causing bubos; pneumonic, where the bacteria are transported from the bite site to the lungs causing secondary pneumonia; and septicaemic, where the infection is directly into a vein effectively allowing rampant bacterial reproduction and assault before the body can mount any effective defence. Interpersonal infection risk in all cases is low. The disease can be moved effectively around urban and rural areas by the presence of rats and the capacity for people to transport infected fleas in grain or clothing.
⁵²³
Death rates for nineteenth and twentieth-century outbreaks can be as high as 35 per cent in particular localised settlements, but at a regional level seldom exceed 3 per cent.
⁵²⁴

The requirements for a bubonic plague outbreak are a suitable rodent vector (the black rat is the usual suspect) and a flea population that is active (most of the year except winter).
⁵²⁵
A forceful supporter of the bubonic plague argument is Professor Ole Benedictow, who has attempted a detailed reconstruction of the spread of the first plague outbreak across Europe in terms of a sequence of epizootics (where first the rat population in a given area contracts and perishes from the disease, and then, as the infected fleas seek new food, creates epidemics within the associated human population), spread and established by human transport of rat and flea vectors. His assertion that modern bubonic plague and experiences of its outbreaks are directly comparable with those of medieval pestilence has, however, been questioned, and his particular use of chronicle sources to support an epidemiological analysis of spread is considered by some to be rather too risky.
⁵²⁶

Support for the bubonic model has been offered on the basis of the reported extraction of ancient
Yersinia
DNA (aDNA) from the dental pulp of skeletons recovered from cemeteries argued to be from plague outbreaks, with the interpretation that this evidence concludes the debate. However, questions have been raised about the basic assumptions underlying the samples used for the aDNA research, and some scientists have questioned the possibility of contamination of some samples. A test to obtain aDNA from skeletons from the London East Smithfield plague cemetery (among others) proved negative, although many other kinds of aDNA were recovered; but a more recent study of the mid-fourteenth-century mass burials excavated at Hereford Cathedral (and other European sites) has again identified the bacillus.

Correspondence among researchers demonstrates the difficulties in using such approaches to obtain a definitive answer.
⁵²⁷
There are two principal issues with claims, for example by Haensch et al., that aDNA discovery ‘ends the debate about the etiology of the Black Death’. The first is the assumption during sample selection for testing that mass burial equates to plague (‘mass’ has been as few as two burials in a single grave in one study). This is unsupportable, since outbreaks of infectious disease other than plague must have been extremely common in the medieval period, and we know that severe famine caused mass deaths on at least two occasions (in the midthirteenth century and in the early fourteenth century). The second is that the discovery of
Y. pestis
aDNA simply tells us that the plague bacillus was present; to offer categorical assertion that it was the agent of the 1348 disaster requires us to prove both its prevalence in skeletal material firmly tied to the outbreak, and in addition its absence in skeletons dating before this date. One thing that all researchers seem to agree on is the need for suitable independent and blind testing in order to solve the issue.

The fit of modern bubonic plague to the documented evidence for the pestilence has always been problematic to a degree. As early as 1893 (and thus a year before Yersin started his work in Hong Kong), Gasquet noted of the 1348 outbreak that ‘together … with the usual characteristics of the common [meaning bubonic] plague, there were certain peculiar and very marked symptoms, which although not universal, are recorded very generally in European countries’. These were, he said, ‘gangrenous inflammation of the throat and lungs, violent pains in the region of the chest, the vomiting and spitting of blood, and the pestilential odour coming from the bodies and breath of the sick’. He concurred with Charles Anglada, a Parisian physician, who in his study of extinct and new diseases published in 1869 expressed a ‘profound conviction that the Black Death stands apart from all those which preceded or followed it’.
⁵²⁸
This recognition of the highly unusual nature of the 1348 pestilence was set aside as the post-Yersin bubonic model became firmly established. Nonetheless, subsequent researchers into the impact and effects of the pestilence, while content to accept bubonic plague as the culprit, continued to have some problems with making the evidence fit the diagnosis. In 1963 historian J.M.W. Bean noted that the Black Death must have:

contained a very considerable pneumonic element, a fact which is suggested by three of its features: first, the exceptionally high death rate; second, the descriptions by contemporary observers of the symptons which are nowadays met in pneumonic plague; and third, the fact that the Black Death raged in winter as well as summer, so that many bubonic victims are likely to have contracted pneumonia and ‘triggered off’ pneumonic outbreaks.
⁵²⁹

The inherent problem with this analysis was recognised just a few years later, in 1970, by the bacteriologist J.F.D. Shrewsbury, who noted that ‘the pneumonic plague cannot occur in the absence of the bubonic form and it cannot persist as an independent form of plague’. He went further: