In that year one other parish, St Mary Somerset on the Thames, began to show increased burials at the end of April. The second feature of interest, seen in both and , is that in the same way that outer parishes were the first to show increasing mortality so, in general, the central rich parishes were the last to begin the epidemic, there being a progression in the onset of higher deaths from the outer parishes to the inner ones.
This is a simple observation of events in a time sequence; it does not necessarily mean that a specific disease was beginning peripherally and spreading inwards. It may have been but other evidence is needed before we can be sure. The third point is the time interval between first and last parishes to show increased mortality. In the first parish began in the week beginning 1 July and the last in the week beginning 27 August. With the early start of the epidemic there was a much wider time span; St Botolph started in the week beginning 15 April and the last parishes, three in the west central part of the city, did not show increased deaths until the week beginning 6 August, almost four months later.
Once again there was a broad movement from peripheral to central parishes in commencement times with parishes north of a line running roughly north-west to south-east across the city being affected before early July and those south of the line after that date. This pattern was repeated in St Botolph was again the first parish to show increased burials in the first week of June.
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Again, those parishes north of a line running from the west end of St Olave in Hart Street in a north-westerly direction to Aldersgate had begun by 7 July, the parishes to the south starting between then and 17 September. During that week the last parish showed an increase in deaths; this was St Mary Somerset which, it will be remembered, had begun during late April in St Botolph was again the first parish to show signs of increasing mortality in but this was even earlier than before, during the week beginning 11 March.
St Katharine by the Tower had increased burials at the end of April but it was not until the week beginning 13 August that deaths began to increase in St Stephen Walbrook in the city centre. This was the last parish to start in that epidemic. The pattern in again showed that parishes in the north and east all had increased burials by the end of June.
Thereafter there was a progressive series of starts towards the south-west part of the city. Unfortunately, no registers have survived after June for St Botolph. There was a less orderly pattern to the beginning of high mortality in ; during the week beginning 3 June burials increased in St James Clerkenwell and St Benet, Paul's Wharf, two parishes a long way apart.
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A month later, in the week beginning 1 July, deaths increased in three parishes in the southern half of the city, two of them, St Mary Somerset and St Dunstan in the East being on the river although well apart. Four of these were close together in the west of the city but the rest were scattered.
There is, then, little evidence of maritime introductions during the five major plague years and much to suggest that the high mortality was due to disease organisms that were already in place, in and around the city. There are many puzzling aspects of the great epidemics but the outstanding one must be the long period between the time when first and last parishes began to show an increase in deaths.
If bubonic plague was present throughout the city and was the main disease responsible for the high mor tality, then as the temperature reached the point where flea breeding was initiated there should have been an increase in burials more or less simultaneously. That there was this wide degree of variation is a strong argument against plague being the sole cause of the high mortality.
The long period of time from first to last parish to show increased deaths may be explained when deaths are plotted weekly in each parish from the beginning to the end of the epidemic. It can then be seen that significantly different mortality patterns existed amongst the parishes during plague years and at least three types of mortality curves can be identified Fig. Typical of bubonic plague or any other disease with a steady incremental build up to the peak of deaths is a from All Hallows London Wall in In this instance the increase phase was less steep than the decline and although this was often a featu re of modern plague between and , 7 it can be seen in other disease mortality curves also.
The second pattern b shows a long drawn out epidemic lacking the regularity of the plague curve. Most usually, there is in this type an early increase above normal burial levels and then, with small peaks and troughs, this elevated level may last for several months. In this extended type in St Katharine during a minor plague year in , the increase began in mid April and deaths were still higher than normal at the end of December. Mortality patterns. In the third type c the onset is abrupt and the curve form owes its shape to the fact that as the temperature rises the organisms in, for example, drinking water divide rapidly so that within a few hours the source is heavily contaminated.
If this is a public supply then all those using it will become infected almost simultaneously and become ill and die within a very short space of time. Many deaths occurring within the first few days give rise to the steep form of the mortality graph. From modern experience a pattern such as this resembles cholera or typhoid fever where drinking water or a food source has been contaminated. In c there was an abrupt rise at the end of August when deaths increased from thirteen to fifty-four in one week. In this type of epidemic the decline phase is always less steep than the increase and the epidemic may smoulder on for several weeks, especially when the source of the disease is not understood.
The mortality patterns of plague type a and enteric type c were both seen in All Hallows London Wall in and respectively. However, all three mortality types, the plague, the extended and the enteric can be seen during the same epidemic year in different parishes in the city. Distribution of mortality patterns in plague years: , , , , In Fig. Ten years later in Fig. On some occasions a parish could show two types of mortality pattern during the epidemic period, implying that more than one disease was at work. Examples of this are present in all the epidemic years but it has to be admitted that on some occasions the mortality patterns are even more complex and defy analysis.
Support for a dual disease epidemic can be found in the registers on a few occasions; in St Mary Aldermary in Fig. A more striking example can be seen in St Mary Somerset in Fig. Plague deaths in the parish register accounted for only a very small proportion of those dying and were recorded between the last week in May and the first week of July. Most of the total deaths took place later and the epidemic came to an end in September. If there were at least three different organisms acting on the population of the city and its surroundings it would help to explain the discrepancies between the parishes in the onset of high mortality.
In addition it might also be relevant to the long lists of plague 'diagnosticks' which, whilst mentioning buboes, also include a wide variety of other symptoms that would not be considered characteristic of true plague. Support for the view that those factors that favoured plague might also increase deaths from other environmental organisms can be found in the Bills of Mortality for As just one example, 'feaver' deaths in the city rose as follows:.
Deaths from 'spotted feaver' increased twenty-fold in some of the summer months of compared with previous years and deaths from 'wormes' also increased. This might be the result of more favourable environmental conditions for the organisms concerned but it is less easy to explain why deaths from 'consumption' should show a marked increase, viz:.
It is equally difficult to see why deaths from such causes as 'aged', 'dropsie', 'childbed', 'convulsions', 'rickets', 'rising of the lights', 'surfet' and 'teeth' should also be markedly higher in than in previous years for these are not the resu lt of temperature-dependent organisms.
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This whole question needs more study and it is essential that, amongst other things, climatic information be collected and added to the story of the London epidemic scene. The events taking place in the great epidemic years tend to obscure the fact that in some parishes, notably St Botolph Bishopsgate, St James Clerkenwell and St Katharine by the Tower, there occurred regularly a series of epidemics whose features have been largely ignored. In St Botolph these were both frequent and quite severe and in many ways resemble the outbreaks of the plague years.
As an example, in and in St Botolph there were typical summer epidemics, the monthly distribution of deaths being as follows:. Not only were deaths high in the same months as in plague years but in addition the mortality patterns in St Botolph in these lesser epidemics were frequently identical to a typical plague curve.
In some years the extended pattern was seen and on some occasions the pattern resembled the enteric form. The year produced a mortality pattern indistinguishable, save in number dying, from a plague year Fig. This took place during a plague-endemic period and, if it was bubonic plague, the question arises as to why in that year it failed to spread and what factors would be needed to convert such a year into a city-wide plague year. The difficult biological logistics of repeated introductions of plague for each major outbreak are not supported by the manner in which each of the epidemics developed.
If we consider plague to have been the sole disease organism, then it appears to have been in place by the time of each outbreak and the pattern of development in each of the five years was not dissimilar. If plague began first in the poor, crowded out parishes such as St Botolph this would not accord well with what we know of the biology of the rat, for in modern times it has selected the well to do parts of the city where warmth was greater and food more plentiful.
There seems no reason why the same features should not have controlled its distribution in sixteenth- and seventeenth-century London. It is interesting to note here that the effects of the great epidemics of , , , and were more severe in the large, outer parishes than the inner ones.
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This was in contrast to , when the position was reversed with the suburbs and riverside parishes being less affected than the central parishes. There does not appear to be any good evidence that plague died out from time to time through loss of virulence, for small numbers of plague deaths occurred between the great epidemics and the same parishes regularly functioned as permanent plague foci Fig.
The fact that there were years without plague deaths may merely reflect aspects of the climate rather than a complete loss of the disease but at the moment there is little evidence on this. Permanent plague foci in inter-plague years Numbers refer to the number of years when plague deaths occurred. It can be seen that parishes with between The overwhelming part that plague has been believed to play in the London epidemics is curious, for at no time, even during the plague of Canton, has it produced such high death rates. For example, in India plague killed only 0. In London, though, plague in is thought to have killed almost twenty per cent of the population whilst in other years even higher rates were reco rded in individual parishes.
The dominance of bubonic plague would be reduced considerably by the recognition of at least two other disease patterns, the enteric and the extended forms and whilst it may not be easy to define their origins it is clear that they were different from the plague-type mortality pattern. The latter, it should be noted, is not diagnostic of plague alone and is a common mortality pattern in other diseases.
It was, for example, seen in the severe outbreaks of epidemic diarrhoea in early twentieth-century London. It would not be unreasonable to suggest that the part played by such organisms was important, for the conditions that favoured plague would almost certainly enhance the role of all other temperature-dependent organisms. It may be countered, though, that the Bills of Mortality, the parish registers and contemporary accounts all speak of 'plague'. Perhaps, after all, this has been translated too literally as bubonic plague, for not long after the last great outbreak a different view prevailed in some quarters.
It is unlikely that he had seen plague, at least not in his professional career, but writing in Dr George Pye expressed his opinion that plague.
If this was so then the difficulty of explaining the presence of bubonic plague at unseasonable times of year, or its movements and behaviour in totally atypical ways, would be removed and we could consider plague as a generic term more appropriate to what was undoubtedly a complex epidemic pool in a large city with regular influxes of immigrants. To accept a diminished role for bubonic plague in the London plagues and an enhanced position for other diseases would not only help to explain the 'measure of diversity' seen in those epidemics but enable true plague to comprise a proportion of total deaths more in keeping with its complex biology.
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