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Biology of Plagues:
Evidence from Historical
Populations
CAMBRIDGE UNIVERSITY PRESS
SUSAN SCOTT AND
CHRISTOPHER J. DUNCAN

Biology of Plagues:
Evidence from Historical Populations
The threat of unstoppable plagues, such as AIDS and Ebola, is always with
us. In Europe, the most devastating plagues were those from the Black
Death pandemic in the 1300s to the Great Plague of London in 1665. For
the last 100 years, it has been accepted thatYersinia pestis, the infective
agent of bubonic plague, was responsible for these epidemics. This book
combines modern concepts of epidemiology and molecular biology with
computer modelling. Applying these to the analysis of historical epidemics,
the authors show that they were not, in fact, outbreaks of bubonic plague.
Biology of Plaguesoﬀers a completely new interdisciplinary interpretation
of the plagues of Europe and establishes them within a geographical,
historical and demographic framework. This fascinatingdetective work
will be of interest to readers in the biological and social sciences, and
lessons learnt will underline the implications of historical plagues for
modern-day epidemiology.
 is a research worker in historical demography in the School
of Biological Sciences at the University of Liverpool.
 .is Emeritus Professor of Zoology also in the
School of Biological Sciences at the University of Liverpool.
They previously co-authoredHuman Demography and Disease(1998)
and have published many papers on population dynamics and historical
epidemiology.

This Page Intentionally Left Blank

Biology of Plagues:
Evidence from Historical Populations
SUSAN SCOTT AND CHRISTOPHER J. DUNCAN
School of Biological Sciences
University ofLiverpool

PUBLISHED BY CAMBRIDGE UNIVERSI TY PRESS (VIRTUAL PUBLISHING)
FOR AND ON BEHALF OF THE PRESS SYNDICATE OF THE UNIVERSITY OF
CAMBRIDGE
The Pitt Building, Trumpington Street, Cambridge CB2 IRP
40 West 20th Street, New York, NY 10011-4211, USA
477 Williamstown Road, Port Melbourne, VIC 3207, Australia

http://www.cambridge.org

© Cambridge University Press 2001
This edition © Cambridge University Press (Virtual Publishing) 2003

First published in printed format 2001

A catalogue record for the original printed book is available
from the British Library and from the Library of Congress
Original ISBN 0 521 80150 8 hardback

ISBN 0 511 01599 2 virtual (netLibrary Edition)

Contents
Preface page xiii
Conversion table for imperial to metric units xiv
1 Introduction 1
1.1 What is a plague? 2
1.2 Four ages of plague 2
1.2.1 Plague at Athens, 430—427 BC 2
1.2.2 The plague of Justinian 5
1.2.3 The Great Age of plagues: the Black Death and
thereafter 6
1.2.4 Bubonic plague in the 20th century 7
1.3 The dangers of emerging plagues 8
1.4 Populations and metapopulations 12
1.5 A cautionary note 14
1.6 Pioneers in the study of plagues 15
1.7 Objectives 18
2 Epidemiological concepts 21
2.1 Transmission probability 23
2.2 Secondary attack rate 23
2.3 Basic reproductive number,R
ﬀ
25
2.4 Virulence,R
ﬀ
and the case fatality ratio 27
2.5 Serial generation time: the Reed and Frost model 28
2.6 Contact rates 30
2.7 Decaying and driven epidemics 38
2.8 Time-series analysis of data 39
v

2.9 Lethal smallpox epidemics in London, 1650—1900:
a case study 39
2.10 Mixing patterns 41
2.11 Open versus closed population dynamics 43
2.12 Spatial components of epidemic spread 44
3 The biology of bubonic plague 47
3.1 History and geographical distribution of bubonic plague 47
3.2Yersinia pestis 51
3.3 The rodent host 53
3.4 Murine versus sylvatic phases 54
3.5 Black and brown rats 55
3.6 The role of the ﬂea 57
3.7 Flea survival 58
3.8 Flea reproduction 59
3.9 Population dynamics of bubonic plague 61
3.10 Evolution of bubonic plague virulence 63
3.11 Spread of bubonic plague to humans 65
3.12 Clinical manifestations of bubonic plague inhumans 66
3.13 The signiﬁcance of pneumonic plague 68
3.14 Pathology 70
3.15 Case studies of the dynamics and epidemiology of
bubonic plague in India in the 20th century 72
3.15.1 Mixed epizootics in Bombay City, 1905—672
3.15.2 Epidemiology of bubonic plague in India in the
20th century 74
3.15.3 Eﬀects of population size 77
3.16 Conclusions: key points about the biology of bubonic
plague 78
4 The Great Pestilence 81
4.1 Arrival of the Black Death in Europe 82
4.2 The plague in Sicily 82
4.3 Spread of the Black Death in continental Europe: a
metapopulation pandemic 86
4.4 The pestilence arrives in England 88
4.5 The Great Pestilence moves through the Midlands to the
north of England 91
4.6 Spread of the epidemic in northeast England 94
vi Contents

4.7 The consequences of the Black Death in England 96
4.8 The Black Death: conclusions 98
4.8.1 Reservations expressed by Shrewsbury 98
4.8.2 The death toll of the Black Death in England 101
4.8.3 Epidemiological notes on the Black Death 103
4.8.4 Eﬀects of malnutrition 105
4.9 Seasonality of the outbreaks of the Great Pestilencein
diﬀerent localities in England 105
4.10 Was the Black Death an outbreak of bubonic plague? 107
4.11 Plagues in England following the Great Pestilence: the
14th century 109
4.12 Age-speciﬁc mortality of four epidemics in the 14th
century 111
4.13 Plagues in the 15th century 112
5 Case study: the plague at Penrith in 1597—98 115
5.1 Traditional account of events in the plague 116
5.2 Size of the population at Penrith 118
5.3 The three phases of the epidemic: the serial generation
time and contact rate 119
5.4 Spread of the epidemic at Penrith 126
5.5 The epidemic during the ﬁrst two phases: elucidation
of the epidemiological characteristics of plague 126
5.6 Explosion of the epidemic in phase three 135
5.7 Age- and sex-speciﬁc mortality in the plague at Penrith 137
5.8 Wills and testaments of those who died in the plague at
Penrith 140
5.9 Response of the population at Penrith after the plague 146
5.10 Classiﬁcation of the epidemics of haemorrhagic plague 148
6 Pestilence and plague in the 16th century in England 149
6.1 The Sweating Sickness 149
6.2 Plagues in London in the 16th century 152
6.2.1 The ﬁrst half of the century 152
6.2.2 Did plague become endemic in London during
the second half of the 16th century? 154
6.2.3 Epidemics in London, 1542—1600 155
6.3 Plagues in central and southern England during the
16th century 165
viiContents

6.4 Case study of the plague at Stratford-upon-Avon, 1564 170
6.5 Conclusions 173
7 Plagues in the 16th century in northern England:
a metapopulation study 175
7.1 The ﬁrst half of the 16th century 176
7.2 Plague and pestilence in the Northern Province, 1550—95 178
7.3 The plague of 1597—98 in northern England 181
7.4 Durham 182
7.5 The plague at Richmond 183
7.6 Plague arrives to the west of the Pennines 184
7.7 Carlisle 185
7.8 Minor outbreaks of the plague in the Eden Valley 186
7.9 Symptoms of the 1597—98 plague 189
7.10 Conclusions 190
8 Plagues in London in the 17th century 192
8.1 The outbreak in London in 1603 193
8.2 Plague in London after the epidemic of 1603 198
8.3 Plague in London in 1625 199
8.4 Recovery of the population of London after 1625 205
8.5 Plague in London in 1636 206
8.6 The Great Plague in London in 1665—66 211
8.6.1 Origins and spread of the epidemic 211
8.6.2 Seasonality and mortality 215
8.6.3 Signs and symptoms 217
8.6.4 Changes in virulence 220
8.6.5 Animals, clothing and wigs 221
8.6.6 Eﬀect of the Great Fire of London 222
8.6.7 Identity of the ﬁrst victim in households in plague
epidemics in London 222
8.7 Dynamics of plague in London 223
9 Plagues in the provinces in the 17th century 225
9.1 The years 1603—5 226
9.1.1 Spread of the plague in the northeast 226
9.1.2 Chester as a focus 228
9.1.3 Plague at Manchester 234
viii Contents

9.1.4 The Midlands and East Anglia 237
9.1.5 Southern England, 1603—5 239
9.2 The years 1609—11 239
9.3 The plague of 1625—26 240
9.4 The years 1630—37 243
9.5 Widespread plague in 1644—46 248
9.5.1 The northeast corridor 248
9.5.2 The West Country 249
9.5.3 East Anglia and the Midlands 250
9.6 The mid-17th century 250
9.6.1 Chester as a focus 251
9.6.2 Spread of the plague of 1665—66 through the
metapopulation 255
9.7 Overview of plagues in England 258
10 Plague at Eyam in 1665—66: a case study 261
10.1 The traditional story of bubonic plague at Eyam 261
10.2 Origins of the plague at Eyam 263
10.3 The ﬁrst phase of the epidemic 265
10.4 The second phase: maintenance of the epidemic
through the winter 269
10.5 The third phase: explosion of the epidemic in summer
1666 275
10.6 Percentage mortality of the population during the
epidemic 279
10.7 Public health measures during the plague at Eyam 280
10.8 The nature of the infectious agent 282
11 Continental Europe during the third age of plagues:
a study of large-scale metapopulation dynamics 284
11.1 Frequency of epidemics in the metapopulation of Europe 284
11.2 Plagues in France: the endemic situation 286
11.2.1 Oscillations in the frequency of the occurrence of
epidemics 286
11.2.2 The 17th century in France 292
11.2.3 Regional diﬀerences within the metapopulation
of France 293
11.2.4 Plague centroids in France 295
11.2.5 Localities with a high frequency of epidemics 297
ixContents

11.3 Italy 303
11.3.1 Occurrence and frequency of the epidemics in
Italy 304
11.3.2 Signs and symptoms 305
11.3.3 Analysis of the spread of epidemics 306
11.3.4 Plague epidemics in Italy 308
11.3.5 Conclusions 315
11.4 The Iberian peninsula 318
11.4.1 The major epidemics 318
11.4.2 Epidemics at Barcelona 324
11.5 Germany, Austria, Bohemia and Switzerland 328
11.6 The Benelux countries 331
11.7 Spread of the plague across Europe 331
12 The plague at Marseilles, 1720—22: an outbreak of bubonic
plague? 338
12.1 Spread of the plague from Marseilles to the countryside 344
12.2 Spread of the plague at Aix and Apt 350
12.3 Spread of the plague at Mende and Marve´jols 350
13 Conclusions 352
13.1 The receptor for the entry of HIV 352
13.2 Was the same causative agent responsible for all
the plagues in England from 1348 to 1666? 354
13.3 WasYersinia pestisthe infectious agent in the plagues? 356
13.4 Classiﬁcation of the plague epidemics in the provinces in
England 362
13.5 Seasonality of the epidemics 364
13.6 Density dependence of plague epidemics 366
13.7 Endemic versus epidemic plague 367
13.8 How were plagues initiated? 370
13.9 Spread of the plague through the metapopulation 371
13.10 Resistance, immunity and virulence 376
13.11 Medium-wavelength oscillation in the spread of the
plague 378
13.12 Symptoms 379
13.13 Public health measures and the signiﬁcance of the
period of quarantine 381
13.14 Why did the plague disappear? 383
x Contents

13.15 What was the causative agent of haemorrhagic plague? 384
13.16 Co-existence of two plagues 389
13.17 Population recovery after the mortality crisis of a
plague epidemic 389
13.18 Postscript 393
References 396
Index 410
xiContents

This Page Intentionally Left Blank

Preface
When studying the population dynamics of northwest England for our
earlier bookHuman Demography and Disease(also published by Cam-
bridge University Press) we became interested in the biology of the plagues
that beset Europe after the Black Death. A plague struck this part of
England and spread rapidly in 1597—98 and it was obvious from a basic
training in zoology that this was not an outbreak of bubonic plague. By
making a full family reconstitution study of the community at Penrith in
Cumbria (where some 40% of the population died) it was possible to trace
the spread of the disease between named individuals in the same family and
between households. From this starting-point, we have made an interdisci-
plinary study of the epidemiology and biology of the plagues that have
aﬄicted western Europe, concentrating on the outbreaks from the Black
Death, which began in 1347, to the Great Plague of London. We have
combined modern epidemiological concepts, computer modelling of epi-
demics, recent molecular biology studies, spatial analysis techniques, time-
series analysis of the epidemics and the careful analysis of the sequence of
infections in selected epidemics. We hope that our monograph will be of
interest to a wide variety of readers who will come to look at historical
plagues with diﬀerent eyes.
Once again we thank Dr S. R. Duncan, of the University of Oxford, for
introducing us to the intricacies of time-series analysis and for developing
the mathematical models that we have used.
We are grateful to members of the Cheshire Parish Register Transcrip-
tion project, in particular Mr and Mrs C. D. Leeming and Mr and Mrs J. R.
Fothergill, for providing unpublished data. Mrs J. J. Duncan also provided
invaluable assistance in reading documents in Secretary Hand and in
translating original articles.
We salute the pioneering work of Dr G. Twigg and gratefully acknowl-
edge his generous help in the early stages of this project.
S.S.
C.J.D.
xiii

Conversion table for imperial to metric units
Imperial unit Metric equivalent
1 inch 25.4 millimetres
1 foot 0.3048 metre
1 yard 0.9144 metre
1 mile 1.609 kilometres
1 acre 0.405 hectare
1 square mile 259 hectares
xiv

1
Introduction
We ﬁrst became interestedin plagues when studying the demography of
northwest England (Duncanet al., 1992; Scott & Duncan, 1998), where an
epidemic in the town of Penrith in 1597—98 killed some 40% of the
population and initiated endogenous oscillations in the annual numbers of
births and deaths. In this way, its eﬀects persisted for 150 years. The
outbreak spread rapidly, travelling 20 to 30 milesin 2 or 3 days and it was
obvious that it was a biological impossibility that this was an outbreak of
bubonic plague. We initially thought that this must have been an isolated
outbreak of an unknown and unique infectious disease (Scottet al., 1996)
but further study convinced us that this regional epidemic had many points
in common with other outbreaks in England that were believed to be
bubonic plague.
In this book, we have attempted an objective (though not exhaustive)
study of the plagues that have ravaged humankind for hundreds of years,
giving the biological, demographic and epidemiological viewpoints of the
available historical evidence. Obviously, the diﬃculties faced are vastly
greater than those of a modern epidemiologist investigating a new out-
break of an unknown disease today. He or she has an array of techniques
available from microbiology and molecular biology, can take biopsy and
autopsy samples with the back-up of a pathology laboratory, can make
on-site investigations of the ecology and epidemiology of the disease, and
can discover the clinical features and mode of transmission of the infection.
Even so, some features of present-day outbreaks of Ebola, such as the
elucidation of the reservoir host, are not yet established with certainty.
Where the disease has a complex biology, as in bubonic plague, it took
years of painstaking study before all the details were elucidated.
1

1.1 What is a plague?
The Bible uses the word ‘plague’ to describe an aﬄiction that was regarded
as a sign of divine displeasure or as an aﬄiction of humankind such as the
plague of locusts. Nowadays, it is a term used to describe a deadly epidemic
or pestilence andTheWordsworth Encyclopedia of Plague and Pestilence
(Kohn, 1995) lists a seemingly endless catalogue of historical epidemics
from all over the world, including smallpox, cholera, typhus and malaria.
They were all infectious and potentially lethal, caused high mortality and
were serious historic events. The inﬂuenza pandemic of 1917—19, with a
ﬁnal death toll worldwide estimated at more than 20 million, is a good
example. The incubation period was often less than 2 days so that its
worldwide spread was dependent on 20th century means of rapid travel
that could move people in bulk, namely steamtrains and steamships of
which the troop ships of the First World War are a good example.
However, the basic etiology of these diseases is now usually well under-
stood and, in spite of the terrible death toll, the percentage mortality of the
aﬀected populations was not relatively high (Langmuiret al., 1985). In this
book, we are mainly, but not exclusively, concerned with the Black Death,
arguably the most awful epidemic ever to have struck, which raged in
Europe from 1347 to 1350, and the unremitting succession of plagues that
followed it for 300 years. These reached their peak in continental Europe
during 1625—31 and in England in 1665—66, but they then disappeared
completely after about 1670. When these plagues struck a naive popula-
tion, where we have reasonably accurate data available in Italy and Eng-
land, mortality could reach about 50%; we do not know what was the
causative agent in these terrible epidemics.
1.2 Four ages of plague
From whence did the Black Death come? The probable answer to this
question is that it originated in the Levant, but Europe had suﬀered from a
series of mysterious plagues for many years before 1347 and it is possible to
identify tentatively and arbitrarily four historic ages of plague.
1.2.1 Plague at Athens, 430–427 BC
The epidemic that struck Athens in 430 BC remains one of the great
medical mysteries of antiquity and has been discussed by a number of
scholars (Morens & Littman, 1972, 1994; Poole & Holladay, 1979;
2 Introduction

Longrigg, 1980; Langmuiret al., 1985; Kohn, 1995; Olsonet al., 1996;
Retief & Cilliers, 1998), but the ﬁrst vivid description was given by Thucyd-
ides, himself a victim who survived the outbreak (see Page, 1953). It is
sometimes termed the Thucydides syndrome because of his evocative
narrative.
People were stricken suddenly with severe headaches, inﬂamed eyes, and
bleeding in their mouths and throats. The next symptoms were coughing,
sneezing, and chest pains followed by stomach cramps, intensive vomiting
and diarrhoea, and unquenchable thirst. The skin was ﬂushed, livid and
broken with small blisters and open sores. The patients burned with fever
so extreme that they could not tolerate being covered,choosing rather to
go naked. Their desire was to cast themselves into cold water, and many of
those who were unsupervised did throw themselves into public cisterns,
consumed as they were by unceasing thirst. Manybecame delirious and
death usually came on the seventh or eighth day of the illness, although
those who survived the ﬁrst phase often died from the weakness brought on
by constant diarrhoea. Many who recovered had lost their eyesight, their
memory, or the use of their extremities.
This plague is believed to have originated in Ethiopia and travelled
through Egypt and the eastern Mediterranean before reaching Athens. The
ﬁrst cases appeared in Piraeus, the Athenian port and base for many
travellers and merchants who probably contracted the disease in their
journeys abroad. It spread rapidly to the upper city and whole households
were left empty. Mortality among doctors, as among other attendants of
the sick, was especially high. Fearful of an attack by the Spartans, the
Athenian leader Pericles ordered the inhabitants of the surrounding coun-
tryside to move inside the city, where they could be protected by the army
and the fortiﬁed walls. Many country dwellers, coming to an already
overpopulated city, had no place to live except in poorly ventilated shacks
and tents. This mass of people, crowded together in the hot summer,
created a situation that was ideal for the rapid transmission of the disease.
Though there were many dead bodies lying unburied, there was said to be a
complete disappearance of birds of prey and dogs. Apparently it was rare
to catch the disease twice, or if someone did, the second attack was never
fatal. A peak case rate was reached during the Spartan siege, which lasted
40 days, after which the crowded refugees dispersed. The disease remained
at a low level through 429 BC (when Pericles died of it) and returnedin
force in the summer of 428 BC at the time of another Spartan siege. The
disease was quiescent, or even absent, from the winter of 428 BC until the
summer of 427 BC, but broke out again in the autumn or early winter of
31.2 Four ages of plague

427 BC. This epidemic lasted no less than a year, but there is no further
mention of the disease. The total number of Athenians who died is not
recorded but, over the 3-year period, of 13 000 enrolled hoplites (soldiers
4400 died—a mortality rate of 33%. Hagnon took the ﬂeet and sailed to
Potidaea carrying the plague there also and this made dreadful havoc
among the Athenian troops. Even those who had been there previously and
had been in good health caught the infection and so 1050 men out of 4000
were lost in about 40 days.
There have been several identiﬁcations of the causative agent of the
plague at Athens, including smallpox (Littman & Littman, 1969), scarlet
fever, measles and typhus (Shrewsbury, 1950; Page, 1953) but these are all
now discredited. Langmuiret al. (1985
tions clearly indicated the involvement of speciﬁc organ systems and that
there was an obvious inﬂammatory condition of the eyes and respiratory
tract; this acute respiratory infection was severe and probably necrotising;
the initiation with vomiting followed by empty retching and later by
‘watery diarrhoea’ strongly suggested a gastroenteropathy mediated by
the central nervous system rather than a local inﬂammatory process.
Langmuiret al. (1985
bullous impetigo. They did not suggest that the Thucydides syndrome was
identical with the modern toxic shock syndrome but believed that the
same basic pathogenic mechanisms were involved, in that there was infec-
tion in predisposed hosts by a possibly non-invasiveStaphylococcussp.
that was capable of producing an exotoxin similar to toxin-1 of the toxic
shock syndrome (Rasheedet al., 1985). This toxin may have diﬀered from
toxin-1 in that it produced predominantly enterotoxic eﬀects and less
profound circulatory collapse, and hadonly moderate or no erythrogenic
potential.
Morens & Littman (1992, 1994) have approached the plague at Athens
from a diﬀerent viewpoint and have arrived at a conclusion that is strongly
opposed to that of Langmuiret al. (1985
brieﬂy because they use mathematical modelling techniques that we shall
also employ to elucidate the epidemiological parameters of later plagues.
They have reduced the reliance on clinical symptoms in favour of the
epidemiology of the disease because pre-modern descriptions, which lack
detailed information on serology and accurate accounts of rashes and
other clinical features, always retain a high degree of uncertainty.Use of
the Reed and Frost mathematical model (section 2.5) led them to conclude
that, under any conditions of crowding that probably prevailed in Athens
in 430 BC, an epidemic of inﬂuenza would have died out rapidly in a few
4 Introduction

weeks. They excluded all common diseases and most respiratory diseases
and concluded that the cause of the Athenian epidemic could be limited to
either a reservoir disease (zoonotic or vector-borne) or one of the few
respiratory diseases that are associated with an unusual means of persist-
ence: either environmental/fomite persistence, or adaptation to indolent
transmission among dispersed rural populations. They suggested that the
diseases in the ﬁrst category include typhus, arboviral diseases and bubonic
plague and, in the second category, smallpox. Retief & Cilliers (1998
reviewed the epidemiological evidence and agreed that the only possibili-
ties are epidemic typhus, bubonic plague, arboviral disease and smallpox.
Other workers have suggested that the plague atAthens was an early
manifestation of Ebola (sections 1.3 and 13.15). Olsonet al. (1996
that a modern case deﬁnition of Ebola virus infection records sudden onset,
fever, headache, pharyngitis followed by cough,vomiting, diarrhoea,
maculopapular rash, and haemorrhagic diathesis, with a case fatality rate
of 50% to 90%, death typically occurring in the second week of the disease.
In a review of the 1995 Ebola outbreak in Zaire, the Centre for Disease
Control and Prevention reported that the most frequent initial symptoms
were fever (94%
phagia and clinical signs of bleeding also frequently present. Symptomatic
hiccups were also reported in 15% of patients. Olsonet al. (1996
cluded that the proﬁle of the plague at Athens was remarkably similar to
that of the recent outbreaks of Ebola in Sudan and Zaire. Certainly, as we
shall see, this devastating epidemic had features in common with later
plagues in Europe (section 1.3).
1.2.2 The plague of Justinian
Procopius, the Greek historian, believedthat this epidemic (like the plague
of Athens) originated near Ethiopia. The pandemic began in Egypt in AD
541 and it then moved through Asia Minor, Africa and Europe, arriving in
Constantinople, the capital of the Byzantine Empire, in the late spring and
summer of AD 542. Merchant ships and troops then carried it through the
known western world and it ﬂared up repeatedly over the next 50 years,
causing an enormous mortality, perhaps aided by wars, famines, ﬂoods and
earthquakes. The plague raged in Constantinople for 4 months in AD 542,
with the death toll rising from 5000 to 10 000 per day and even higher
during the three most virulent months. The Byzantine emperor Justinian
fell ill and recovered, but 300 000 people were said to have died in Constan-
tinople alone in the ﬁrst year, although Russell (1968
51.2 Four ages of plague

(1984
completely overwhelmed by the task of disposing of the dead bodies
(Kohn, 1995).
Procopius recorded that people (understandably
ing that they could be struck without warning. The ﬁrst symptoms were a
mild fever which did not seem to be alarming, but bubonic swellings
followed within the next few days. Once the swellings appeared, most
suﬀerers either went into a deep coma or became violently delirious,
sometimes paranoid and suicidal. It was diﬃcult to feed and care for them
properly, although mere contact with the sick did not seem to increase the
chances of contracting the disease. Most victimsdied within a few days, but
recovery seemed certain for those whose buboes ﬁlled with pus. Black
blisters were a sure sign of immediate death; otherwise, doctors often could
not predict the course of the disease or the successof various treatments.
Autopsies revealed unusual carbuncles inside the swellings and these clini-
cal features led to the conclusion that the Justinian plague was a pandemic
of bubonic plague (Kohn, 1995). Shrewsbury (1970
that other serious diseases, such as smallpox, diphtheria, cholera and
epidemic inﬂuenza were also present. It is not possible to be certain from
the evidence available, but the rapid spread over great distances, the heavy
mortality and other biological features of the pandemic suggest that bu-
bonic plague was not the major component, but that some other infectious
disease, spread person-to-person, was responsible.
1.2.3 The Great Age of plagues: the Black Death and thereafter
The Black Death erupted in Sicily in 1347 and the pandemic spread
through Europe during the next 3 years, reaching Norway (where two-
thirds of the population died; Carmichael, 1997) and Sweden and crossing
to England (and thence to mainland Scotland, the Hebrides, Orkney and
the Shetland Islands) and to Ireland (Biraben, 1975) and, possibly, to
Iceland and Greenland (Kohn, 1995). Its arrival presaged a continuous
succession of epidemics in Europe for the next 300 years before it disap-
peared completely around 1670. The enormous mortality of the Black
Death had a major impact on the demography of Europe, and the popula-
tion of England did not fully recover for 150 years. Events during 1347—50
are described in Chapter 4 and the demographic consequences of a major
mortality crisis on a population are discussed further in section 13.17. Were
the multiplicity of plagues throughout Europe from 1350 to 1670 all the
result of the same causative agent as that responsible for the Black Death,
6 Introduction

albeit with some minor mutations during that time? It is not possible to
answer this question with certainty, but we believe that the most probable
explanation of the etiological and epidemiological details is that it was so.
During the second half of the 14th century, the epidemics in England and
continental Europe were less virulent but the infection gradually regained
its ferocity, reaching its peak around 1630 in France and 1665—66 in
England.
1.2.4 Bubonic plague in the 20th century
The details of the complex biology of bubonic plague were ﬁnally unravel-
led around 1900: it is a bacterial disease of rodents depending on the rat ﬂea
for its spread and on a reservoir of resistant rodent species for the mainte-
nance of the disease. Only occasionally does the infection spread to hu-
mans when one is bitten by a rat ﬂea but, in the days before antibiotics and
modern medicine, this was usually fatal and serious epidemics could be
established.
Unfortunately, historians of Europe in the 20th century, almost univer-
sally, have concluded that all plagues in the Middle Ages were bubonic, in
spite of the fact that the people at that time sawclearly that it spread
person-to-person and, even in the 14th century, had already instituted
speciﬁc quarantine periods. A major objective of this book is to examine
the historical facts dispassionately, eschewing any preconceived notions
about the behaviour of rats and ﬂeas and to determine the nature of the
epidemics of the Middle Ages in Europe. Normally, we refer to these as
plagues, but where there is possible confusion with bubonic plague, we
designate the former as haemorrhagic plague. To distinguish between
haemorrhagic and bubonic plagues we begin in Chapter 3 with a detailed
account of the complex biology, etiology and epidemiology of bubonic
plague and explain how, in consequence, the spread and maintenance of
the disease in rodents and humans is strictly constrained.
Although we have described bubonic plague from 1900 to the present
day as the fourth age of plague, the disease has been identiﬁed (presumably
correctly) and recorded in detail from China since AD 37 (Wu, 1926; Wuet
al., 1936) and it is likely that it has been present in India and in a gigantic
swathe across central Asia for hundreds of years. It probably extended
westwards to the Levant and the north African coast and may have erupted
sporadically in the warm Mediterranean coastal regions in the 6th century
AD (Twigg, 1984) and it was certainly present there in the Middle Ages and
continued with occasional epidemics in the 18th century (see Chapter 12).
71.2 Four ages of plague

Where climatic conditions were suitable and reservoir rodent species were
present locally, endemic bubonic plague could be established. Where only
the climate was suitable, as in the coasts of France, Spain and Italy,
epidemics of bubonic plague could potentially break out, having been
brought into the ports by sea, but these terminated once the local rats had
died. During the third age of plagues, 1347—1670, therefore, Europe prob-
ably experienced minor outbreaks of bubonic plague along the Mediterra-
nean coasts of Italy, Spain and France in addition to the major epidemics
of haemorrhagic plague.
Finally, endemic bubonic plague erupted in a series of epidemics in India
at the very end of the 19th century and spread across southeast Asia, and so
began the fourth age of plagues. As we show in Chapter 3, the arrival of
steamships then allowed rats and their ﬂeas carrying bubonic plague to be
rapidly transported from the grain stores on the docks of China to sub-
tropical regions wherever suitable indigenous rodents occurred.
1.3 The dangers of emerging plagues
From whence did the plague of Athens, the Justinian plague and the Black
Death come? How did they emerge with such sudden ferocity? We have
seen in the 20th century the emergence of a number of new deadly diseases
that are largely resistant to medical science: scientists have identiﬁed more
than 28 new disease-causing microbes in 1973 (Olshanskyet al., 1997).
Indeed, it has been suggested that the history of our time will be marked by
recurrent eruptions of newly discovered diseases (e.g. Hantavirus in the
American West), epidemics of diseases migrating to new areas (e.g. cholera
in Latin America), diseases that become important through human tech-
nologies (water cooling towers provided an opportunity for legionnaires’
disease) and diseases that spring from insects and animals because of
human-engendered disruptions in local habitats. Two of the terrors that
haunt are the fears that new, unstoppable infectious diseases will emerge
and that antibiotics will be rendered powerless. To some extent, these
processes have been occurring throughout history. What is new, however,
is the increased potential that at least some of these diseases will generate
large-scale pandemics, such as a resurgence of the 1918 inﬂuenza pan-
demic; the global epidemic of human immunodeﬁciency virus (HIV
most powerful and recent example. Yet the acquired immune deﬁciency
syndrome (AIDS
modern, large-scale epidemics of infectious diseases. The world has rapidly
become much more vulnerable to the eruption and, most critically, to the
8 Introduction

widespread and even global spread of both new and old infectious diseases.
This new and heightened vulnerability is not mysterious; the dramatic
increases in the worldwide movement of people, goods, and ideas is the
driving force behind the globalisation of disease because not only do
people travel increasingly, they also travel much more rapidly, and go to
many more places than ever before. The lesson is clear: a health problem in
any part of the world can rapidly become a widespread health threat
(Mann, 1995).
Most emergent viruses are zoonotic, with natural animal reservoirs a
more usual source of new viruses than is the spontaneous evolution of a
new entity. Human behaviour increases the probabilityof the transfer of
viruses from their endogenous animal hosts to humans. The original source
of the AIDS pandemic has been traced back to a subspecies of chimpanzee
that has been used for food in West Central Africa,the hunters being
exposed to infected blood during the killing and dressing. The virus has
probably been living harmlessly in chimpanzees for hundreds of years and
may have been transferred to humans throughout history, but the socio-
economic changes in Africa provided the particular circumstances leading
to the spread of HIV and AIDS.
An outbreak of encephalitis in Malaysia in 1999, which killed 76 people
may have been caused by a more deadly version of the Hendra virus, which
was ﬁrst identiﬁed in Australia 5 years previously. The diﬀerence is that,
whereas the virus in the earlier outbreak did not spread easily between
animals, the Malaysian version apparently did: all the Malaysian victims
were connected with pig rearing. Health oﬃcials in Asia now fear that a
dangerous new human pathogen has emerged that has spread from fruit
bats via pigs and consequently more than 300 000 pigs were slaughtered in
southern Malaysia as an initial precautionary measure. The spinal ﬂuid
taken from ﬁve patients contained a paramyovirus (named ‘Nipah’) and
analysis of the amino acid and RNA sequences conﬁrmed that it is related
to the deadly Hendra virus. Why has the virus suddenly begun to kill pigs
and people when the bats may have harboured it safety for centuries?
The Ebola virus, a member of the Filoviridae, burst from obscurity with
outbreaks of severe haemorrhagic fever. It was ﬁrst associated with an
outbreak of 318 cases and a case fatality rate of 90% in Zaire and caused
150 deaths among 250 cases in Sudan. Smaller outbreaks continue to
appear periodically, particularly in East, Central and southern Africa.In
1989, a haemorrhagic disease was recognised among cynomolgus
macaques imported into the USA from the Philippines; strains of Ebola
virus were isolated and serologic studies indicated that the virus is a
91.3The dangers of emerging plagues

prevalent cause of infection among macaques. Epidemics have resulted
from person-to-person transmission, nosocomial spread and laboratory
infections but it must be emphasised that the mode of primary infection
and the natural ecology of these viruses are unknown. The possible role of
the Ebola virus as the causative agent in haemorrhagic plague is discussed
in section 13.15.
A mysterious epidemic of Marburg virus (related to Ebola virus) broke
out in a remote area of the Democratic Republic of Congo, Central Africa,
in December 1998. At least 72 miners suﬀered from fever, pain, rash and
bleeding and 52 had died by May 1999. The victims had spent time in caves
and bats are considered to be the leading contender for an animal reservoir
of the virus; monkeys die too quickly from the virus for them to be
considered for this role.
A virulent inﬂuenza pandemic struck from 1917 to1919, with a ﬁnal
worldwide estimated death toll of more than 20 million lives (Kohn, 1995).
It has been termed Spanish inﬂuenza (dryly known as ‘the Spanish Lady’)
because this was believed to be the ﬁrst serious point of attack, with 8
million Spaniards falling ill in 1917—18. It then struck at military bases
throughout Europe and death rates mounted ominously in 1918. At the
same time (beginning in March 1918) acute respiratory infections were
reported at military installations in the USA and by October some US
army camps were reporting a death every hour; Britain was then counting
2000 deaths per week, with London at about 300 deaths per week. Country
after country felt the ravages of the disease. The weak, the young and the
old usually suﬀer worst in epidemics, but the age group 21 to 29 years
proved to be the most vulnerable in this outbreak of Spanish inﬂuenza.
While manifesting the ordinary symptoms of inﬂuenza (headache, severe
cold, fever, chills, aching bones and muscles), the Spanish form also gener-
ated complications such as severe pneumonia (with purplish lips and ears
and a pallid face), purulent bronchitis, mastoid abscess and heart problems.
The frightening disease subsided after the end of the First World War and
later vanished completely but, by then, it had attacked every country in the
world, particularly China, India, Persia, South Africa, Britain, France,
Spain, Germany, Mexico, Canada, the USA and Australia.
A radical genetic mutation, called antigenic shift, accounts for the ap-
pearance of new viral subtypes capable of engendering inﬂuenza pan-
demics. New viral types originate in ducks, chickens, pigs and otherani-
mals, in which reservoirs of inﬂuenza viruses change genetically and are
then passed into the environment, and to human beings. The strain that
caused the 1918 epidemic, H1N1, was found inside pigs and there is always
10 Introduction

the fear that this strain may resurface, perhaps in as virulent a form as in
1918. Many pandemics originate in Asia, notably China, where enormous
numbers of ducks, pigs, and other virus-producing animals live in close
proximity to human beings (Kohn, 1995). Avian inﬂuenza A (H5N1
has recently been shown to be transmitted from patients to healthcare
workers in Hong Kong and this ﬁnding may portend ‘a novel inﬂuenza
virus with pandemic potential’ (Bridgeset al., 2000).
Fragments of the virus responsible for Spanish inﬂuenza were found in
1998 in the lungs of a woman who died in the 1918 epidemic and whose
body was preserved by huge layers of fat and the frost of Alaska and it is
hoped that it will be possible soon to map the RNA of the virus to identify
the gene that made it so deadly. Preliminary work has produced the
complete sequence of one key gene and the existing strain to which the 1918
sequences are most closely related is A/Sw/Iowa/30, the oldest classical
swine inﬂuenza strain. More recently, inﬂuenza 1918 RNA has been found
in respiratory tissue and the brains of Spitzbergen coal miners who died in
the epidemic and Oxford (2000
jigsaw linking pandemic inﬂuenza to the ensuing outbreak of the sleeping
disease encephalitis lethargica.
A virulent and drug-resistant form of typhoid caused by the pathogen
Salmonella typhi, which kills 600 000 people a year, has now emerged in
Vietnam. The study of its genome is now almost complete: the nucleus
contains three separate pieces of DNA, a massive coil some 4.5 million
bases long and two plasmids, smaller loops of genetic data. One of the
plasmids contains an array of oﬀensive and defensive genes, which prob-
ably explain the potency of this strain of typhoid. It came as a great surprise
when it was discovered that the other plasmid contained a sequence of
50—60 genes that are found inYersinia pestis, the bacterium of bubonic
plague and thus the Vietnamese microbe appears to be fortiﬁed with the
genes of other pathogens (Farrar, 2000).
There is a seemingly endless catalogue of lethal infectious diseases that
have emerged. Some of these have been described in a very lively manner
by Garrett (1995
virus, the Brazilian meningitis epidemic and the Hantaviruses. Health
oﬃcials in New York City reported, in August 1999, an outbreak of what
appeared to be St Louis encephalitis, a disease that can spread to humans
from birds via mosquitoes. However, it has now been discovered that the
infectious agent is West Nile virus, which is normally found in Africa and
Asia and is also transmitted by mosquitoes. Helicopters sprayed entire
neighbourhoods in Queens, New York, after the disease killed horses,
111.3The dangers of emerging plagues

thousands of birds and several people; there has been a fresh outbreak in
New York City in summer 2000 and what really alarms American health
oﬃcials is the danger of the disease establishing itself permanently in the
country. It remains an open question as to how the virus reached the USA
(Boyce, 1999). So, it should not surprise us that the classical pandemics of
historical times emerged and it is probable that they originated as viral
zoonoses. Viruses have a great capacity for mutating and are opportunistic
parasites; the worrying thought is (as suggested above) where and when
will they next strike?
1.4 Populations and metapopulations
The study of how disease aﬀects groups, or populations, of people is known
as epidemiology; the discipline began when doctors wanted to study out-
breaks of infectious diseases such as cholera and bubonic plague. Epi-
demiological studies today gather such data as age, race, sex and even
social class, together with the incidence of the disease (the number of new
cases appearing in a given time period) and its prevalence (the number of
suﬀerers at any one time). The information can then be used to establish
patterns in the disease and thus pinpoint aggravatingfactors.
Epidemiology can be deﬁned in a number of diﬀerent ways as, for
example, ‘the science of the infective diseases—their prime causes, propaga-
tion and prevention. More especially it deals with their epidemic manifes-
tations’ (LeRiche & Milner, 1971). This deﬁnition can then be extended
because, if a communicable disease conforms to biological laws, epi-
demiological processes could be interpreted in terms of medical ecology
(Gordon & LeRiche, 1950). Thus what we are studying in this book are the
health and diseases of populations and groups and, in contrast to clinical
medicine, the unit of study in epidemiology is the population and not the
individual (Morris, 1957).
We investigate ﬁrstly the epidemiology of plagues in towns, large and
small, treating them as circumscribed populations that have an identity
but, of course, are not completely closed—infectives will have come into the
population and a proportion of the inhabitants may have ﬂed when an
epidemic has been recognised. The temporal and spatial spread of the
plague within the community (or unit) is governed by the household
infection rate and by the ways in which it can spread to other households
and thence to other streets and the results may then be compared with
other populations. If the spread of the plague is density dependent, the
pattern of the epidemic would be expected to be diﬀerent in communities of
12 Introduction

diﬀerent sizes. The city of London, as we shall see, was a complex popula-
tion; a very large number of individuals crammed together but with subsets
delineated by class and parish, with partial intercourse. The population
was freely open, with many immigrants, travellers and merchants arriving
daily by land and sea.
The spread of an outbreak of plague may also be studied at a higher
population level, i.e. throughout a geographically deﬁned area that might
be the size of a country or even part of a continent. Examples are island
Britain, and the Iberian peninsula, which was eﬀectively separated from
continental Europe by the Pyrenees and, in both, plague epidemics had to
enter from the sea via the ports. These may be called metapopulations, a
term used by ecologists to describe a population of populations. The study
of metapopulation dynamics in biology is normally concerned with the
behaviour of a single species over time; there are no static populations and
likewise there is no such thing as a static metapopulation. The metapopula-
tion concept in ecology is closely linked with the processes of population
turnover, extinction and the establishment of new populations. Ecological
metapopulation theory, with one important exception, has not been ap-
plied to human populations; indeed, as originally deﬁned, it is not strictly
applicable because it deals with extinctions and recolonisations and makes
the simplifying assumption that each ecological site is regarded as being in
one of two alternative states, either empty or ﬁlled at their local carrying
capacity, characteristics that were rarely found in England during the age
of plagues. The exception concerns studies of spatial heterogeneity and the
epidemic spread of infectious diseases through a human metapopulation
where individuals can be either infected or uninfected, an example of the
interaction between demography and disease.
The spread of epidemics is an important part of modern Geography and
we have used such techniques as disease centroids to trace the spatial
movements of the plague in a metapopulation where it was endemic (see
section 2.12). It becomes evident that the Black Death had a diﬀerent
pattern of spread from subsequent plague epidemics which, in turn, ex-
hibited a range of sharply diﬀering characteristics. The Black Death recog-
nised no boundaries, either natural or human engendered, and spread in a
wave-like movement all across Europe and to oﬀ-shore islands in about 3
years before disappearing. We can regard its territory for this brief period
as a ‘supermetapopulation’. Bubonic plague as a disease of rodents,and
secondarily of humans, was certainly established as endemic across a huge
subtropical area by 1900, from the Levant across to China and Southeast
Asia. It has persisted for many years and we can regard this also as a
131.4 Populations and metapopulations

‘supermetapopulation’. Haemorrhagic plague slowly established itself in
Europe after the Black Death, with France as its endemic centre. England,
Spain and Italy experienced epidemics of diﬀering frequency, being separ-
ated from France by various geographical features, but France expanded
from a metapopulation into a ‘supermetapopulation’ in the Middle Ages,
which was composed of present-day Germany, the Benelux Countries and
France. Here, plague was maintained as endemic, there being a handful of
widespread epidemics somewhere maintained by long-distance travelling
infectives.
1.5 A cautionary note
It is sometimes diﬃcult to determine whether a marked increase in deaths
in a year (a mortality crisis) was really the consequence of a plague
epidemic. The health authorities in the city states of northern Italy in the
14th century went to great lengths to distinguish between minor (which
they disregarded) and major (which were very serious) ‘pests’ (as they were
called) by examining the victims personally, but historians rarely have such
direct evidence on which to base their conclusions. Livi-Bacci (1977
on the size of the crisis and wrote
For several parts of Tuscany between 1340 and 1400 I have calculated that on
average a serious mortality crisis—deﬁned as an increase in deaths at least three
times the normal—occurred every 11 years; the average increase in deaths was at
least sevenfold. In the period 1400—50 these crises occurred on average every 13
years and deaths increased ﬁvefold. In the following half century (1450—1500) the
average frequency declined to 37 years and the average increase to fourfold.
Shrewsbury (1970
annual burials occurs in the three months of July to September inclusive,
the record is almost certainly indicative of an outbreak of bubonic plague’
and this led him to conclude, for example, that there were multiple plague
epidemics in northwest England in 1623. However, this area was living on
the margins of subsistence at this time and mortality was sensitive to a 5- to
6-year cycle in grain prices (Scott & Duncan, 1998) and the constituent
communities suﬀered major mortalities not only in 1623, but in 1587—88
and 1596—97 also. We have shown that in these years the peak of wheat
prices coincided with a low in the 12-year cycle of wool prices (Scott &
Duncan, 1997, 1998). Those populations that depended on both commodi-
ties suﬀered severely whereas those that depended on only one for their
livelihood escaped unscathed. They did not suﬀer from plague in 1623. It is
evident that by the end of the 16th century all towns could recognise plague
14 Introduction

when it struck their community and, if an outbreak is not recorded in the
parish registers, a rise in mortality should be assumed to be the conse-
quence of a plague epidemic only with extreme caution.
1.6 Pioneers in the study of plagues
We all owe a debt of gratitude to Yersin and his co-workers, to Wu and to
the Plague Commission of India for the way in which they slowly and
meticulously unravelled the complex biology and epidemiologyof bubonic
plague. A splendid piece of detective work. However, in this book we also
wish to acknowledge the work and writings of a number of people who
have inﬂuenced us and on whom we have relied heavily:
(i —1927, is the doyen of epidemiologists
whoseHistory of Epidemics in Britainwas published in two volumes in
1891 and 1894. He graduated from Aberdeen University MA in 1867
having studied Latin, Greek, Mathematics, English, Logic, Moral
Philosophy, Natural Philosophy and Natural History, and as Bach-
elor of Medicine and Master of Surgery in 1871. His approach in his
classic work, which was to provide a chronicle of death and disease in
the life and people of England, was that of a professional historian and
he worked with great care on his sources (Eversley, 1965). We have
relied heavily on his data series in our earlier work on lethal infectious
diseases (Duncanet al., 1993a,b, 1994a,b, 1996a,b; Scott & Duncan,
1998). He probably knew something about the biology of bubonic
plague when he was writing in 1891 because this was being elucidated
at the time but he does not seem to assume that this was necessarily
related to the plagues in England that he was describing and, conse-
quently, his descriptions are not modiﬁed to ﬁt within the life histories
of the rat and ﬂea. In later life, he spent 3 months in India at the end of
1904 and reported about rats living in the mud walls of houses and of
dead rats being found in a house where the inmates had died of
bubonic plague (Underwood, 1965).
(ii Infectious Diseases:
Epidemiology and Clinical Practice, published in 1969, A. B. Christie
wrote ‘A good book, it has been said, should be opened with expecta-
tion and closed with proﬁt . . .’. His treatise not only lives up to these
high standards, but it is read with pleasure: he makes even dull topics
interesting, spicing his account with classical allusions, gentle humour
and personal anecdotes. He writes authoritatively and clearly on every
151.6 Pioneers in the study of plagues

infectious disease and this is particularly apparent when he deals with
bubonic plague. His clinical experience across continents is revealed
when he says that he believes that he had patients in Libya with
bubonic plague who were infected by contact with a camel that had
been ailing before slaughter and had a swelling in its neck.
(iii
work of scholarship in hisA History of Bubonic Plague in the British
Isles, published in 1970, in which ‘He has ransacked virtually all
published local histories and parish records and he has read very
widely in contemporary chronicles and memoirs’ (Morris, 1977). Al-
though we have relied heavily on his studies as a data source, we have
not attempted to repeat the details of his ﬁndings and we suggest that
readers who require more information about plagues in England
should refer to this basic source book. It is a little dull and confusing in
places but is occasionally illuminated by his dry humour:
‘John Toy ascribed the visitation to God’s punitive anger, because He had
already twice warned the people of Worcester of their sins by inﬂicting slighter
outbreaks of the disease upon the city; but it apparentlynever occurred to him
that the Almighty would not thus degrade the Inﬁnite to single Worcester out
for such irrational punishment, for Worcester was certainly no more sinful
than Lincoln, Salisbury, Canterbury, or any other English episcopal centre. It
certainly never drew part of its revenue from brothels like the see of Winches-
ter . . .’
‘[T]he parish of St Giles, Cripplegate, where a parishioner was summoned in
April to appear at the next sessions to answer ‘‘for receivinge people into his
house sick of the plague brought from other parts to the prejudice of the
parish’’ and for having ‘‘at the same tyme another sick of the French pockes
[who] liveth incontynently with one Fayth Langley’’. Was he running the
seventeenth-century equivalent of a nursing home?’
‘In 1610 the churchwardens of St Margaret’s, Westminster, paid 6d. to ‘‘Good-
wife Wells for salt to destroy the ﬂeas in the churchwardens’ pew’’. Evidently
the Anglican worshippers of the seventeenth century were as tormented by this
ectoparasite as the monks had been in Salimbene’s day. Most of the ﬂeas,
which undoubtedly were equally devout and attentive in most English par-
ishes, were the human ﬂea . . .’
As his title suggests, Shrewsbury believed whole-heartedly that bu-
bonic plague was responsible for the majority of the plague epidemics
in England and Scotland and yet, as a trained medical microbiologist,
he saw that the facts on many occasions, made this a biological
impossibility. He was therefore frequently forced to adapt his con-
clusions. When plague was reported in the months December to
February he stated that it must have been a mild winter. When other
16 Introduction

facts about an epidemic did not ﬁt bubonic plague he frequently
declared it to be an outbreak of typhus, even when plague is recorded
in the registers. He invented what he called ‘trailer epidemics’ to
circumvent other diﬃcult events. He was well aware that the mortality
levels in many of the epidemics were much higher than would be
expected in bubonic plague, particularly in the Black Death, and he
reluctantly concluded that the sources from which he had quoted had
overestimated the death toll.
Nevertheless, Shrewsbury steadfastly maintained that bubonic
plague was the cause of most of the plague epidemics in the British
Isles and it is most unfair that he should have twice been attacked,
apparently for daring to suggest that there might be weaknesses in the
story.
Gottfried (1978
‘Herein lies one of the book’s major shortcomings—Shrewsbury’s failure to
investigate any but printed and easily accessible chronicles and letters. No
eﬀort is made to search more obscure printed and manuscript sources: and
even when original data are searched, it is done in an extremely uncritical
manner. Often, the validity of the records is denied on the basis of uncor-
roborated value judgements and twentieth century medical information . . .
One of his major premises is that epidemic bubonic plague has not changed in
character ‘‘during the period of recorded history’’. This is contrary to what
other epidemiologists have written. Shrewsbury diminishes the signiﬁcance of
the eﬀects of pneumonic plague in ﬁfteenth century England, saying that it
cannot ‘‘occur in the absence of the bubonic form’’. This too seems to run
contrary to the evidence . . . Also, interregional travel was far more common in
the Middle Ages than Shrewsbury indicates, and was by no means restricted
solely to merchants. Thus, both bubonicand pneumonic plague could survive
in sparsely populated regions.’
Morris (1977
because Shrewsbury, who was a medical microbiologist, refused to
allow the pneumonic form of bubonic plague to have a role in the
epidemics:
‘for some reason he has chosen to turn a blind eye to any evidence of
pneumonic plague. He does not noticehow often the victims are said to have
succumbed in three days and if he meets with any reference to plague in cold
weather he jumps to the conclusion that the disease must have been something
else, preferably typhus . . . But there is much evidence, all of it ignored by
Shrewsbury, that the Great Pestilence of 1348—50 contained a high percentage
of pneumonic cases and indeed that in many places the plague ﬁrst appeared in
its pneumonic form. This would easily account for the high mortality which
Shrewsbury is anxious to whittle down.’
171.6 Pioneers in the study of plagues

Morris also attacks because of Shrewsbury’s statement that bubonic
plague has an unvarying relationship with rodent enzootics:
‘Shrewsbury’s main contention is that the country would have had to be
constantly re-infected by fresh importations of plague-bearing rats. He has not
thought of the possibility that England might well have become an enzootic
area in which some rats at any given time are diseased. This is odd since he
knows very well that in other parts of the world plague has taken permanent
root and produced notorious enzootic or endemic centres. Indeed he argues,
mistakenly as it happens, that India has always been one such centre from
which Europe has drawn its periodic re-infections . . . Besides, if England
became, as obviously it did, a permanently enzootic area in the seventeenth
century, why should it not have done so two centuries earlier? That plague was
endemic, or at least enzootic in London, needing no imported re-infections, for
more than half a century before 1665 is abundantly clear from the annual
mortality bills.’
(iv Les hommes et la peste en
France et dans les pays europe´ens et mediterrane´enshas assembled an
impressive set of data on plague epidemics in Europe after the Black
Death. He has combed the literature extensively and his bibliography
runs to over 225 pages. We have used these data-sets for analysis in
Chapters 11 and 12.
(v
rodents and who has discussed with Dr D. E. Davis the status of rats in
the Middle Ages. In 1984 he wroteThe Black Death:A Biological
Reappraisal, in which he carefully develops the evidence that shows
that bubonic plague was not the cause of this great pandemic. He
summarised his seminal work in the conclusion ‘The logistics of the
epidemic in England support the hypothesis of an air-borne organism
of high infectivity and virulence, having a short incubation period and
being spread by respiratory means’ (Twigg, 1989). All students of
plague should read his work.
1.7 Objectives
An epidemiologist must, by deﬁnition, be an historian, even if only in the
short term. We present a new analysis of the plagues that scourged Europe
from the 14th to the 17th centuries, approaching from biological, ecologi-
cal and epidemiological viewpoints. We analyse the historical data (hope-
fully objectively) using modern techniques of theoretical epidemiology,
clinical molecular biology, computer-based modelling and the spatial
models of epidemic spread that have been developed by geographers.
18 Introduction

There is a substantial literature on the Black Death and the Great
Plague of London in 1665 but, during the intervening 300 years, Europe
suﬀered from repeated outbreaks of the pestilence and these epidemics
have received less attention. Were these epidemics all the result of the same
infectious agent? What were its epidemiological characteristics? Were all,
some or none the result of bubonic plague? What determines the dynamics
of plague epidemics?
To answer these questions we begin by deﬁning epidemiological con-
cepts, such as transmission probability and basic reproductive number,
and then explain how the epidemics of some infectious diseases can be
modelled with the aid of computer-driven simulations.Once the basic
parameters of a disease in historic times have been determined or estimated
it is possible to construct models of the epidemics from which the underly-
ing etiology can be suggested.
We have also tried to include the human story of the epidemics in
England, showing how each population responded to the outbreak, how
the disease spread through the community, how the members responded
and how they made their wills. We give detailed case studies of the
epidemics at Penrith (Chapter 5) and Eyam (Chapter 10) and have devised
a new method of analysing and displaying the spread of the infection in
each family group using family reconstitution techniques; this is the only
means by which the epidemiological characteristics (e.g. incubation, latent
and infectious periods, contact rates and transmission probability) can be
determined.
We begin the story of the age of plagues in Chapter 3 with an account of
the Black Death and the subsequent outbreaks in the 14th and 15th
centuries, but it is not until the 16th century, when parish registers started
in England, that ﬁrm and detailed information becomes available. The
epidemiological characteristics of plague can be deduced therefrom and,
the key feature that emerges is the lengthy incubation period of this
infectious disease. When one is armed with this information, the reasons for
the spread and behaviour of haemorrhagic plague in continental Europe
over a period of 300 years (described in Chapter 11) become clear: the key
to understanding its epidemiology is the endemic status of the pestilence in
France.
Chambers (1972
have often been caused, not by Malthusian ﬂuctuations in the balance
between population levels and food supplies, but by independent biological
changes in the virulence of disease and by the rise and fall of the great
epidemic scourges, which were not economic in origin. Slack (1977a
191.7 Objectives

therefore concluded that the epidemiology of plague is a subject that bears
on some of the central issues of demographic and social history. Historians
have long been puzzled by the paradoxical rapid recovery of the popula-
tion of England after the undoubted heavy mortality of the Black Death
and in section 13.17 we examine some of the demographic consequences of
a major mortality crisis in a single population, using the techniques of
time-series analysis and computer modelling. We show that, although a
population can apparently recover remarkably quickly, subtle demo-
graphic consequences could still be detected for over 100 years after the
plague had disappeared.
20 Introduction

2
Epidemiological concepts
Any serious attempt to elucidate the identities of the infectious agents in
the plagues that struck at Europe over several centuries must begin with a
scientiﬁc study of their biology and characteristics so far as we can discover
them—every disease leaves its ﬁngerprints on which the epidemiologist
may work. Infectious agents may be viral, bacterial or protozoan, as well as
larger animals such as nematodes or helminths, butthey all have one
feature in common, namely that humans are their ecological niche wherein
they have shelter and food and can reproduce prodigiously. However,
transmission from one host to another is fundamental to the survival
strategy of all infectious diseases because a host will eventually clear the
infection or die and hence the arrival of a disease in an individual depends
crucially on the occurrence of that disease in other members of the popula-
tion (Halloran, 1998). Transmission may be direct, person-to-person (as in
measles or smallpox) or indirect, involving an intermediate host (e.g., the
anopheline mosquito, which transmits the protozoan parasitePlasmodium
of malaria). However, zoonoses are primarily diseases of animal hosts that
are occasionally transmitted to humans. Examples are Lyme disease and
bubonic plague; it is important to note that events arenotcritically
dependent on the human population in these diseases.
We found the review by Halloran (1998
this brief overview of modern epidemiological concepts; the works by
Gisecke (1994
mended. The sequence of events during a simple, directly transmitted
disease (such as inﬂuenza or chicken pox) is shown in Fig. 2.1; the infection
of a susceptible person is followed by an incubation period—the interval
between the entry of the agent and the appearance of the symptoms (Fig.
2.1A); it is not a ﬁxed number of days and the actual period is often
dependent on the infectious dose. It is generally thought of as the time
21

Time of
infection
Incubation period Symptoms
Time
(A)
(B)
Latent
period
Infectious period
Recovered
or dead
Fig. 2.1. The sequence of events during a simple, directly transmitted disease. The
dynamics of the disease are shown in A and the dynamics of infectiousness in B. The
victim may cease to be infectious before the end of the symptomatic period.
required for the multiplication of the microorganism within the host up to
a threshold point where the pathogen population is large enough to
produce symptoms in the host (Lilienfeld & Stolley, 1994). Thus each
infectious disease has a characteristic incubation period that is largely
dependent on the rate of growth of the organism in the host (Benenson,
1990) but, in addition to the eﬀect of the dose, this is modulated by the
immune response of the host, so that the incubation period varies among
individuals. The disease eventually runs its course and for the infectious
agent to persist it must have infected at least one other human. There are
diﬀerent outcomes for the host, who may have died (as usually happened in
plagues) or recovered, when he or she may have an immunity of variable
duration that protects from future exposure to the disease. Part B in Fig.
2.1 correlates the infectious period with the time-course of the disease; there
is a latent period after infection before the host becomes infectious. Finally,
the host passes to the non-infectious stage, often before the symptoms
disappear, and transmission then becomes impossible.
The time-courses of parts A and B (Fig. 2.1) and their relationship to one
another are speciﬁc for each infectious agent (Halloran, 1998); the relation-
ship between the incubation and latent periods are of critical importance.
In chickenpox (Varicella zoster), the latent period is shorter than the
incubation period so that patients become infectious before the develop-
ment of symptoms. Indeed, for many childhood diseases the period of
greatest infectivity is just towards the end of the incubation period; these
diseases are particularly diﬃcult to control because an apparently healthy
person will establish many contacts in everyday life and, consequently,
isolation in quarantine when the symptoms have appeared is of limited
value. The latent period of HIV is of the order of days to weeks whereasthe
median incubation period, before symptoms appear, is greater than 10
22 Epidemiological concepts

years, during which time a great many people may be infected (Halloran,
1998). We show in Chapter 5 that people in England infected with plague
were infectious for some 22 days before the symptoms appeared, a critically
important factor that ensured the establishment of an epidemic in spite of
some of the public health measures that were enforced.
2.1 Transmission probability
The probability that the successful transfer of a parasite from an infective
source to a susceptible host is deﬁned as the transmission probability and
its estimation is important for understanding the dynamics of the infection.
It depends on the characteristics of the infectivesource, the parasite, the
susceptible host and the type of contact. Considering the possible infec-
tions for the plagues, the infectious source could be another person (as in
inﬂuenza), an insect vector (as in the rat ﬂea in bubonic plague) or bacter-
ially contaminated drinking water (as in cholera). The epidemiologist
dealing with present-day epidemics has a battery of techniques to hand to
determine the characteristics and biology of a disease but it must be
remembered that, in spite of this, the remorseless spread of HIV still
continues in sub-Saharan Africa. It is much more diﬃcult to derive an
estimate of the transmission probability of the plagues that occurred 400
years ago.
Halloran (1998
mission probability. In the ﬁrst, infectious individuals are identiﬁed and the
proportion of contacts that they make with susceptibles that result in
transmission is determined (secondary attack rate). In the second method
(the binomial model), susceptibles are identiﬁed and data are gathered on
the number of contacts they make and their infection outcomes but this
technique is less suitable for our purposes.
2.2 Secondary attack rate
In this case-contact approach to the estimation of transmission probabil-
ity, infectious persons (primary or index cases) are identiﬁed and then the
susceptibles who come in contact with them are determined. The conven-
tional secondary attack rate (SAR
contagiousness. It is deﬁned as the probability of the occurrence of the
disease among susceptibles following contact with a primary case as
follows:
232.2 Secondary attack rate

SARﬄ
number of persons exposed who develop the disease
total number of susceptibles
Using the data available for the plagues that we describe in detail in
subsequent chapters, estimations can be made of the household SAR,
which is concerned solely with infections within the house, although, even
with a full family reconstitution, the exact number of resident susceptibles
cannot be known; for example, some of the children may have left home.
There is another caveat to bear in mind; the record of a burial in the
registers is the only indication of an infection andwe have no means of
identifying individuals who contracted the plague and recovered. However,
we have been encouraged by the consistency with which the pattern of the
spread is replicated in each parish that we have analysed.The technique
that we have used is shown diagrammatically in Fig. 2.2, where the point of
infection of the index (primary
ﬃ
); this indicates the start of
the infection in the household. The latent period of P
ﬃ
(see Fig. 2.1) follows
this starting point and anyone else infected during this time is designated as
a co-primary (P

) because they cannot have been infected by P
ﬃ
. Anyone
infected during the infectious period of P
ﬃ
(Fig. 2.2) is designated a second-
ary (S
ﬃ
) or co-secondary (S

,S

etc.).
Tertiary and higher cases are those occurring after the maximum allow-
able time interval for the secondary cases. We assume that the infectious
period is terminated in haemorrhagic plague by the death of the victim,
who was probably displaying symptoms, on average, for the last 5 days of
his life. The picture is complicated when co-primaries are identiﬁed because
their infectious periods extend beyond the death of P
ﬃ
. By working through
the data for a large number of households derived by family reconstitution
from the parish registers, it is possible to derive estimates of the latent,
infectious and incubation periods for haemorrhagic plague, as shown in
Fig. 2.2.
Thus, in assessing the household SAR, it is necessary to determine
whether each case in each household is a co-primary, secondary, tertiary,
or higher generation case. The estimated household SAR is the total
number of secondary cases in all households divided by the total number of
at-risk susceptibles in all households. Co-primary cases are excluded from
the denominator; tertiary or higher cases are excluded from the numerator
but included in the denominator. As we shall see, there was wide variation
in the household SAR of the plague, apparently dependent on such factors
as the season and the progress of an epidemic.
24 Epidemiological concepts

LP
LP
LP
LP
LP
Maximum
infectious
period
of P 1
1
(I)
P
2
(I)
P
1
(I)
S
2
(I)
S
1
(I)
T
Fig. 2.2. Diagram to illustrate the time-course of the spread of an infectious disease
such as haemorrhagic plague. The time between the point of infection (I
end of the infectious period (which may coincide with the death of the victim) is
shown as a scaled horizontal line which is subdivided into latent (LP
periods. In this example, two primary cases (P
ﬃ
and P

) are shown and the time
limits when P
ﬃ
can infect secondary cases (P
ﬃ
’s infectious period) are shown by
the vertical dashed lines. Two secondary cases (S
ﬃ
and S

) are shown; they could
have been infected by either P
ﬃ
or P

. One tertiary case (T
ﬃ
) is shown; I occurred
after the end of the infectious periods of both P
ﬃ
and P

and so this could not be a
secondary case.
2.3 Basic reproductive number,R
o
A second important parameter in the epidemiology of infectious diseases is
the basic reproductive number,R
ﬀ
. For diseases caused by viruses and
bacteria,R
ﬀ
is the average number of persons directly infected by an
infectious case during his or her entire infectious period when the infective
enters a totally susceptible population.R
ﬀ
does not include the new cases
produced by the secondary cases, or further down the chain (Halloran,
1998).R
ﬀ
is a dimensionless number. IfR
ﬀ
equals 8 for a disease in a given
population, then the introduction of one infective would be expected, on
average, to produce 8 secondary infectious persons.
For microparasitic infections,R
ﬀ
is a composite of three important
aspects of infectious diseases: the rate of contacts (c), the duration of
infectiousness (d), and the transmission probability per potentially infective
contact (p). The average number of contacts made by an infective during
the infectious period is the product of the contact rate and the duration of
infectiousness,cd(Halloran, 1998). The number of new infections produced
252.3 Basic reproductive number,R
o

by one infective during the infectious period is the product of the number of
contacts in that time interval and the transmission probability per contact:
number of transmission
duration of
R
ﬀ
ﬄcontacts perﬀprobabilityﬀ
infectiousness
ﬄcpd
unit time per contact
An infectious disease does not have a speciﬁc value forR
ﬀ
that diﬀers
within particular host populations at particular times. For example, con-
tact rates in rural areas will be lower than contact rates in urban areas, i.e.
R
ﬀ
of smallpox would have been lower in rural England than in London
(Scott & Duncan, 1998). As we shall see,R
ﬀ
for the plague in one locality
apparently diﬀered markedly at diﬀerent seasons.
R
ﬀ
ofYersinia pestis, the bacterium of bubonic plague of rodents (see
Chapter 3), in infections in a rat population may be high during the season
of high ﬂea density but low when the ﬂeas are not active. This is an example
of an indirectly transmitted disease, where the bacterium is transmitted
between two diﬀerent host populations, the rat and the ﬂea; it is clearly a
more complex situation than in person-to-person infection, as is illustrated
in Fig. 2.3.R
ﬀ
for indirectly transmitted diseases depends on the product of
the two components of transmission.
R
ﬀ
assumes that all contacts are with susceptibles and that none are
already immune, unlike the situation with the regular lethal smallpox
epidemics in rural towns in 17th century England where virtually the only
susceptibles were those born since the last epidemic (Duncanet al., 1993a;
Scott & Duncan, 1993). The plague at Penrith in 1597—98 is described in
detail in Chapter 5 and it was foundthat the mortality in the diﬀerent age
groups was indiscriminate. Some 45% of the population died but it seems
certain that some individuals were exposed to the infection but survived;
they may have contracted the disease but not have died of it, or they may
have been resistant. We begin by assuming that all individuals in the plague
at Penrith and certainly in the Black Death (but not necessarily in London
in the 17th century) were potentially susceptible.
The parameterR
ﬀ
allows the comparison of diseases from the viewpoint
of population biology—the aim of this book. When a disease is endemic (i.e.
the disease lingers at about the same incidence for a long time) an infectious
case produces, on average, one new infectious case, i.e.R
ﬀ
ﬄ1. IfR
ﬀ
ﬄ1,
the disease will disappear, whereas ifR
ﬀ
ﬃ1 an epidemic will be initiated.
As an epidemic proceeds the number of susceptibles will inevitably fall and
whenR
ﬀ
ﬄ1, the epidemic will die out.
26 Epidemiological concepts

Fig. 2.3. Diagram to illustrate direct and indirect transmission. The quantitiesT
ﬃ
andT

represent a summation of the transmission parameters for the ﬂow of the
infectious agent. In direct, person-to-person transmission, as in measles (A
R
ﬀ
ﬄT
ﬃ
. In indirect transmission, as in bubonic plague whereYersinia pestiscycles
between rodents and ﬂeas (BR
ﬀ
ﬄT
ﬃ
ﬀT

.
2.4 Virulence,R
o
and the case fatality ratio
Virulence is a measure of the speed with which a parasite kills an infected
host (Halloran, 1998). SinceR
ﬀ
is a function of the time spent in the infective
state,R
ﬀ
could decrease as virulence increases. If the parasite is so highly
virulent that it kills its host quickly, thenR
ﬀ
could beﬄ1 and the parasite
will die out. This is an important point because, except in a few very large
populations where it may have been endemic, plague epidemics in individ-
ual localities in Europe inevitably died out after 1 or 2 years, as we describe
in section 13.7. However, plague was pseudo-endemic in France for some
250 years, i.e. the disease was always present somewhere in this vast
metapopulation and it continued to cycle round the major towns, in each
of which it usually persisted for only 1—2 years (see section 11.2). Viewed in
this way, there is evolutionary pressure on parasites to become less virulent
and to develop a more benign relationship with the host and it must be
remembered that haemorrhagic plague, a particularly malignant disease,
disappeared after about 1670.
The case fatality ratio is the probability of dying from a disease before
recovering or dying of something else; as virulence increases, the case
fatality ratio increases (Halloran, 1998). It is impossible to estimate accu-
rately the case fatality ratio of the plague because of the inadequacy of the
272.4Virulence,R
o
and the case fatality ratio

data but it was certainly very high indeed, although there is evidence that it
may have decreased in the later stages of some epidemics.
2.5 Serial generation time: the Reed and Frost model
The unpublished mathematical model of epidemics developed by Reed and
Frost has been described by Maia (1952 N
within which people intermingle fairly uniformly, it is assumed that, in a
certain period of timet, every individual will have about the same number
of contacts with other individuals. If the degree of intimacy of the contact is
postulated to be suﬃcient for a patient with a certain contagious disease to
transmit the disease to a susceptible person, this number of contacts,K, will
be the average number of contacts for transmission of the disease per
individual per timet.Iftis made equal to the serial generation time, the
individuals infected during one period will then be infectious during the
next.
The serial generation time has been deﬁned as the period between the
appearance of symptoms in successive cases in a chain of infection that is
spread person-to-person and, in present-day infections, is readily deter-
mined by observation of patients. However, where the latent and infectious
periods for historical plagues can be determined (see section 2.2 and Figs.
2.1 and 2.2), the mean serial generation time can be estimated as the time
between two successive infections as follows:
Lis the duration of latent period (days
Iis the duration of infectious period, pre-symptoms (days
Sis the duration of period showing symptoms and presumably infectious
(days).
Total infectious periodﬄIS
Mean time of transmitting the disease from the primary to the secondary
case is assumed to be the mid-point of the infectious periodﬄ(IS)/2.
Therefore, the mean time at which the primary case infects a secondary
caseﬄL[(IS)/2] days after the point of infectionﬄthe serial gener-
ation time,t.
IfKis the average number of adequate contacts per individual per serial
generation time,t, and the population size isN, then the probability of an
adequate contact between any two given individuals during timetwill be
pﬄ
K
Nﬀ1
(2.1)
28 Epidemiological concepts

and
qﬄ1ﬀp (2.2)
will be the probability of any given individual avoiding adequate contact
with any other given individual during timet.
Thus the population is at any time,t, composed of cases,C
ﬀ
, susceptibles,
S
ﬀ
, and immunes,I
ﬀ
, and the probability of any given individual avoiding
contact with any of the cases will beqand, with all theC
ﬀ
cases, will be
Q
ﬀ
ﬄqﬄﬀ (2.3)
and the probability of any given individual having at least one adequate
contact with any of the cases will be
P
ﬀ
ﬄ1ﬀQ
ﬀ
ﬄ1ﬀqﬄﬀ (2.4)
In the transmission of disease we are interested only in the contacts
between cases and susceptibles. Thus, in the next time period (t1), we
shall have
C
ﬀﬃﬃ
ﬄS
ﬀ
(1ﬀqﬄﬀ) (2.5
The theory presented by Reed and Frost rests on certain assumptions.
(i
epidemic, i.e.pis constant. (ii
ptomatic or subclinical infections does not take place. (iiiqis
considered a constant as applied to a particular epidemic, the theory does
not postulate thatqis constant for a certain disease; it may change from
one occasion to another in the same community and it may be diﬀerent in
diﬀerent communities at the same time.
Consequently, the theory assumes that the rise and fall of epidemics, at
least when evolving in a short period of time, will be dependent upon the
numbers of susceptibles available and their depletion through infection
and (usually in haemorrhagic plague) death, to a subliminal level or com-
plete exhaustion.
However, the theory cannot explain diseases such as bubonic plague (see
Chapter 3) and typhus with multiple hosts, such as insect vectors and
animal reservoirs, where the situation is too complex for measurement of
all the factors and the disease in humans does not follow Reed and Frost
dynamics.
292.5 Serial generation time

The results of modelling Equation 2.5 are shown in Figs. 2.4 and 2.5,
using a population of 1200 and thereby replicating a rural town in Tudor
times. The overallshapesof the graphs are similar, usually rising to a peak
of cases more slowly than they decay, but changing the parameters makes a
major diﬀerence to thetime-courseof an epidemic. It can be seen that in
most epidemic proﬁles at least 90% of the susceptible population become
infected.
Figure 2.4 illustrates the time-courses of the epidemics of diﬀerent infec-
tions in which the mean number of contacts is standardised at 12 (i.e.
pﬄ0.01). Serial generation times are as follows: Aﬄ3 days (inﬂuenza
Bﬄ10 days (measlesﬄ15 days (chickenpoxﬄ22 days (haemor-
rhagic plague). All the epidemics, withpﬄ0.01, were completed in 5 serial
generation times and hence lasted from 15 days in inﬂuenza (A
in plague (D
Figure 2.5 illustrates the eﬀects of changing the average number of
contacts when the serial generation time is maintained constant at 22 days,
i.e. equivalent to haemorrhagic plague. When the number of contacts was
set at the low value of 3 (Fig. 2.5A) the epidemic lasted over 200 days (9
generation times) and there was a slow build-up to the peak of cases.
Increasing the number of contacts (Fig. 2.5B and C) markedly reduced the
duration of the epidemics until, with an average of 40 contacts, the epi-
demic exploded dramatically and was ﬁnished in 4 generation times (Fig.
2.5D).
Clearly, Equation 2.5 depends on the random mixing of infectives and
susceptibles, which is not the case in some circumstances. Nevertheless, the
modelling shows how each disease leaves its ﬁngerprints on the epidemic,
dependent on the serial generation timethrough which it can be identiﬁed
by the epidemiologist. It also reveals how the time-course and pattern of an
epidemic is modiﬁed by local factors such as the probability of an adequate
contact between two individuals, which, in turn, is dependent on such
factors as the density and social customs of the population, i.e.pwill be
much higher (i
snow-bound in the depths of winter and (ii
isolation and quarantine practices were not in force. We shall see that this
is an important point because there were marked seasonal diﬀerences in the
dynamics of plague, both in England and continental Europe.
2.6 Contact rates
Thus the contact patterns in a population play an important part in
30 Epidemiological concepts

determining exposure and transmission. The rate of contact is governed by
population density; people come into contact with an infective in an urban
environment more frequently, even if infection was by air-borne trans-
mission over many yards, than if they were less densely distributed, as in a
rural environment. Population density therefore plays a role in determin-
ing the value ofR
ﬀ
in diseases that are spread by casual contact.
The theory of regular epidemics of infectious diseases that are spread
person-to-person has been widely studied (for detailed accounts, see An-
derson & May, 1982a,b, 1985, 1991; Olsen & Schaﬀer, 1990; Tiddet al.,
1993; Bolker & Grenfell, 1993, 1995) and basic models have been presented
that cover the spread of a virus in a population, a proportion of which is
made up of non-immune, and hence susceptible, individuals who may be
exposed to the disease and become infected. Of these, a proportion will die
but some (depending on the nature of the disease) will recover and will then
be immune. Studies of measles in the 20th century (Bolker & Grenfell, 1993;
Fine, 1993) or smallpox in the 17th and 18th centuries (Duncanet al.,
1993a,b, 1994a,b) are good examples. These are termed SEIR (susceptibles-
exposed-infectives-recovered) models and can be summarised as follows.
The population,N, is assumed to remain constant where the net input of
susceptibles (new births) equals the net mortality,N(whereis the overall
death rate of the population, and hence the life expectancy of the popula-
tionﬄ1/). The population is divided into susceptibles (X), latents (infec-
ted, not yet infectious,H), infectious (Y) and recovered (and hence immune,
Z); see Fig. 2.1. ThusNﬄXHYZ. It is assumed that the net rate
at which infections occur is proportional to the number of encounters
between susceptibles and infectives,XY(whereis a transmission coeﬃ-
cient). Individuals move from latentto infectious at a per capita rate,, and
recover, so becoming immune, at rate. The dynamics of the infection as it
spreads through these classes are then described (see Anderson & May,
1982b) by the following equations:
dX/dtﬄNﬀXﬀXY (2.6)
dH/dtﬄXYﬀ()H (2.7)
dY/dtﬄHﬀ()Y (2.8)
dZ/dtﬄYﬀZ (2.9)
The mathematical theory of epidemics is essentially concerned with the
introduction of a ‘seed’ of infection into a largely susceptible population
312.6 Contact rates

Fig. 2.4. Results of Reed and Frost modelling for a population whereNﬄ1200
(representing a Tudor rural town) and the mean number of eﬀective contactsﬄ12.
Serial generation times (daysﬄ3, Bﬄ10, Cﬄ15 and Dﬄ22. The duration of
the epidemic is dependent on the serial generation time. Note the diﬀerent scales.
32 Epidemiological concepts

332.6 Contact rates

Fig. 2.5. Results of Reed and Frost modelling for a population whereNﬄ1200 and
the serial generation timeﬄ22 days (replicating haemorrhagic plague). Mean
number of eﬀective contacts: Aﬄ3, Bﬄ6, Cﬄ20 and Dﬄ40.
34 Epidemiological concepts

352.6 Contact rates

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Dodo got out of her chair, and plucked a couple of roses from a bush
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Dodo fastened the roses in the front of her dress, and laughed
again.
"I laugh for pure happiness," she continued. "I laughed when I saw
the cliff of Dover to-day, not because I was sea-sick—I never am
sea-sick—but simply because I was coming home again. Jack parted
from me at Dover. I am very happy about Jack. I believe in him
thoroughly."
Dodo was getting serious again in spite of herself. Lady Grantham
was watching her curiously, and without any feeling of
disappointment. She did not wear spectacles, she was, at least, as
tall as herself, and she dressed, if anything, rather better. She was
still wearing half-mourning, but half-mourning suited Dodo very well.
"Decidedly it's a pity to analyse one's feelings," Dodo went on, "they
do resolve themselves into such very small factors. I am well, I am
in England, where you can eat your dinner without suspicion of
frogs, or caterpillars in your cauliflower. I had two caterpillars in my
cauliflower at Zermatt one night. I shall sleep in a clean white bed,
and I shall not have to use Keating. I can talk as ridiculously as I
like, without thinking of the French for anything. Oh, I'm entirely
happy."
Dodo was aware of more reasons for happiness than she mentioned.
She was particularly conscious of the relief she felt in getting away
from the Prince. For some days past she had been unpleasantly
aware of his presence. She could not manage to think of him quite
as lightly as she thought of anyone else. It was a continual effort to
her to appear quite herself in his presence, and she was constantly

rushing into extremes in order to seem at her ease. He was stronger,
she felt, than she was, and she did not like it. The immense relief
which his absence brought more than compensated for the slight
blankness that his absence left. In a way she felt dependent on him,
which chafed and irritated her, for she had never come under such a
yoke before. She had had several moments of sudden anger against
herself on her way home. She found herself always thinking about
him when she was not thinking about anything else; and though she
was quite capable of sending her thoughts off to other subjects,
when they had done their work they always fluttered back again to
the same resting-place, and Dodo was conscious of an effort, slight
indeed, but still an effort, in frightening them off. Her curious
insistence on her own happiness had struck Edith. She felt it
unnatural that Dodo should mention it, and she drew one of two
conclusions from it; either that Dodo had had a rather trying time,
for some reason or other, or that she wished to convince herself, by
constant repetition, of something that she was not quite sure about;
and both of these conclusions were in a measure correct.
"Who was out at Zermatt when you were there?" inquired Miss
Grantham.
"Oh, there was mother there, and Maud and her husband, and a
Russian princess, Waldenech's sister, and Jack, of course," said
Dodo.
"Wasn't Prince Waldenech there himself?" she asked.
"The Prince? Oh yes, he was there; didn't I say so?" said Dodo.
"He's rather amusing, isn't he?" said Miss Grantham. "I don't know
him at all."
"Oh, yes," said Dodo; "a little ponderous, you know, but very
presentable, and good company."
Edith looked up suddenly at Dodo. There was an elaborate
carelessness, she thought, in her voice. It was just a little overdone.
The night was descending fast, and she could only just see the lines
of her face above the misty folds of her grey dress. But even in that

half light she thought that her careless voice did not quite seem a
true interpretation of her expression. It might have been only the
dimness of the shadow, but she thought she looked anxious and
rather depressed.
Lady Grantham drew her shawl more closely round her shoulders,
and remarked that it was getting cold. Edith got up and prepared to
go in, and Miss Grantham nestled in her chair. Only Dodo stood quite
motionless, and Edith noticed that her hands were tearing one of the
roses to pieces, and scattering the petals on the grass.
"Are you going in, Dodo?" she asked; "or would you rather stop out
a little longer?"
"I think I won't come in just yet," said Dodo; "it's so delightful to
have a breath of cool air, after being in a stuffy carriage all day. But
don't any of you stop out if you'd rather go in. I shall just smoke one
more cigarette."
"I'll stop with you, Dodo," said Miss Grantham. "I don't want to go in
at all. Edith, if you're going in, throw the windows in the drawing-
room open, and play to us."
Lady Grantham and Edith went towards the house.
"I didn't expect her to be a bit like that," said Lady Grantham. "I
always heard she was so lively, and talked more nonsense in half an
hour than we can get through in a year. She's very beautiful."
"I think Dodo must be tired or something," said Edith. "I never saw
her like that before. She was horribly serious. I hope nothing has
happened."
The piano in the drawing-room was close to a large French window
opening on to the lawn. Edith threw it open, and stood for a
moment looking out into the darkness. She could just see Dodo and
Nora sitting where they had left them, though they were no more
than two pale spots against the dark background. She was conscious
of a strange feeling that there was an undercurrent at work in Dodo,

which showed itself by a few chance bubbles and little sudden
eddies on the surface, which she thought required explanation.
Dodo certainly was not quite like herself. There was no edge to her
vivacity: her attempts not to be serious had been distinctly forced,
and she was unable to keep it up. Edith felt a vague sense of coming
disaster; slight but certain. However, she drew her chair to the piano
and began to play.
Miss Grantham was conscious of the same sort of feeling. Since the
others had gone in, Dodo had sat quite silent, and she had not taken
her cigarette.
"You had a nice time then, abroad?" she remarked at length.
"Oh, yes," said Dodo, rousing herself. "I enjoyed it a good deal. The
hotel was full of the hotel class, you know. A little trying at times,
but not to matter. We had a charming party there. Algernon is
getting quite worldly. However, he is ridiculously fond of Maud, and
she'll keep him straight. Do you know the Prince?"
"Hardly at all," said Miss Grantham.
"What do you think of him, as far as you've seen?" asked Dodo.
"I think he is rather impressive," said Miss Grantham. "I felt I should
do as he told me."
"Ah, you think that, do you?" asked Dodo, with the most careful
carelessness. "He struck me that way, too, a little."
"I should think he was an instance of what Edith meant when she
said that to be intimate with anyone was to be under their
influence."
"Edith's awfully wrong, I think, about the whole idea," said Dodo,
hastily. "I should hate to be under anyone's influence; yet, I think,
the only pleasure of knowing people is to be intimate. I would
sooner have one real friend than fifty acquaintances."
"Did you see much of him?" asked Miss Grantham.

"Yes, a good deal," she said, "a great deal, in fact. I think Edith's
right about intimacy as regards him, though he's an exception. In
general, I think, she's wrong. What's that she's playing?"
"Anyhow, it's Wagner," said Miss Grantham.
"I know it," said Dodo. "It's the 'Tannhauser' overture. Listen, there's
the Venus motif crossing the Pilgrim's march. Ah, that's simply
wicked. The worst of it is, the Venus part is so much more attractive
than the other. It's horrible."
"You're dreadfully serious to-night, Dodo," said Miss Grantham.
"I'm a little tired, I think," she said. "I was travelling all last night,
you know. Come, let's go in."
Dodo went to bed soon afterwards. She said she was tired, and a
little overdone. Edith looked at her rather closely as she said good-
night.
"You're sure it's nothing more?" she asked. "There's nothing wrong
with you, is there?"
"I shall be all right in the morning," said Dodo, rather wearily. "Don't
let them call me till nine."
Dodo went upstairs and found that her maid had unpacked for her. A
heap of books was lying on the table, and from among these she
drew out a large envelope with a photograph inside. It was signed
"Waldenech."
Dodo looked at it a moment, then placed it back in its envelope, and
went to the window. She felt the necessity of air. The room seemed
close and hot, and she threw it wide open.
She stood there for ten minutes or more quite still, looking out into
the night. Then she went back to the table and took up the envelope
again. With a sudden passionate gesture she tore it in half, then
across again, and threw the pieces into the grate.

CHAPTER NINETEEN
Dodo slept long and dreamlessly that night; the deep, dreamless
sleep which an evenly-balanced fatigue of body and mind so often
produces, though we get into bed feeling that our brain is too deep
in some tangle of unsolved thought to be able to extricate itself, and
fall into the dim immensity of sleep. The waking from such a sleep is
not so pleasant. The first moment of conscious thought sometimes
throws the whole burden again on to our brain with a sudden start
of pain that is almost physical. There is no transition. We were
asleep and we are awake, and we find that sleep has brought us
only a doubtful gift, for with our renewed strength of body has come
the capability of keener suffering. When we are tired, mental
distress is only a dull ache, but in the hard, convincing morning it
strikes a deadlier and deeper pain. But sometimes Nature is more
merciful. She opens the sluices of our brain quietly, and, though the
water still rushes in turbidly and roughly, yet the fact that our brain
fills by degrees makes us more able to bear the full weight, than
when it comes suddenly with a wrenching and, perhaps, a rending of
our mental machinery.
It was in this way that Dodo woke. The trouble of the day came to
her gradually during the moments of waking. She dreamed she was
waiting for Jack in the garden where she had been sitting the night
before. It was perfectly dark, and she could not see him coming, but
she heard a step along the gravel path, and started up with a vague
alarm, for it did not sound like his. Then a greyness, as of dawn,
began to steal over the night, and she saw the outline of the trees
against the sky, and the outline of a man's figure near her, and it
was a figure she knew well, but it was not Jack. On this dream the
sense of waking was pure relief; it was broad day, and her maid was
standing by her and saying that it was a quarter past nine.
Dodo lay still a few moments longer, feeling a vague joy that her
dream was not true, that the helplessness of that grey moment,
when she saw that it was not Jack, was passed, that she was awake
again, and unfettered, save by thoughts which could be consciously

checked and stifled. It was with a vast sense of satisfaction that she
remembered her last act on the evening before, of which the
scattered fragments in the grate afforded ocular proof. She felt as if
she had broken a visible, tangible fetter—one strand, at any rate, of
the cord that hound her was lying broken before her eyes. If she
had been quite securely tied she could not have done that..—
The sense of successful effort, with a visible result, gave her a
sudden feeling of power to do more; the absence of bodily fatigue,
and the presence of superfluous physical health, all seemed part of a
different order of things to that of the night before. She got up and
dressed quickly, feeling more like her own self than she had done for
several days. The destruction of his photograph was really a great
achievement. She had no idea how far things had gone till she felt
the full effect of conscious effort and its result. She could see now
exactly where she had stood on the evening before, very
unpleasantly close to the edge of a nasty place, slippery and steep.
Anyhow, she was one step nearer that pleasant, green-looking spot
at the top of the slope—a quiet, pretty place, not particularly
extensive, but very pleasing, and very safe.
The three others were half-way through breakfast when Dodo came
down. Lady Grantham was feeling a little bored. Dodo flung open
the door and came marching in, whistling "See the Conquering Hero
comes."
"That's by Handel, you know, Edith," she said. "Handel is very
healthy, and he never bothers you with abstruse questions in the
scandalous way that Wagner does. I'm going to have a barrel-organ
made with twelve tunes by Handel, you only have to turn the handle
and out he comes. I don't mean that for a pun. Your blood be on
your own head if you notice it. I shall have my barrel-organ put on
the box of my victoria, and the footman shall play tunes all the time
I'm driving, and I shall hold out my hat and ask for pennies. Some of
Jack's tenants in Ireland have refused to pay their rents this year,
and he says we'll have to cut off coffee after dinner if it goes on. But
we shall be able to have coffee after all with the pennies I collect. I

talked so much sense last night that I don't mean to make another
coherent remark this week."
Dodo went to the sideboard and cut a large slice of ham, which she
carried back to her place on the end of her fork.
"I'm going for a ride this morning, Edith, if you've got a horse for
me," she said. "I haven't ridden for weeks. I suppose you can give
me something with four legs. Oh, I want to take a big fence again."
Dodo waved her fork triumphantly, and the slice of ham flew into the
milk-jug. She became suddenly serious, and fished for it with the
empty fork.
"The deep waters have drowned it," she remarked, "and it will be
totally uneatable for evermore. Make it into ham-sandwiches and
send it to the workhouse, Edith. Jambon au lait. I'm sure it would be
very supporting."
"It's unlucky to spill things, isn't it?" Dodo went on. "I suppose it
means I shall die, and shall go, we hope, to heaven, at the age of
twenty-seven. I'm twenty-nine really. I don't look it, do I, Lady
Grantham? How old are you, Edith? You're twenty-nine too, aren't
you? We're two twin dewdrops, you and I; you can be the dewdrops,
and I'll be the twin. I suppose if two babies are twins, each of them
is a twin. Twin sounds like a sort of calico. Two yards of twin, please,
miss. There was a horrid fat man in the carriage across France, who
called me miss. Jack behaved abominably. He called me miss, too,
and wore the broadest grin on his silly face all the time. He really is
a perfect baby, and I'm another, and how we shall keep house
together I can't think. It'll be like a sort of game."
Dodo was eating her breakfast with an immense appetite and
alarming rapidity, and she had finished as soon as the others.
"I want to smoke this instant minute," she said, going to the door as
soon as she had eaten all she wanted. "Where do you keep your
cigarettes, Edith? Oh, how you startled me!"

As she opened the door two large collies came bouncing in, panting
from sheer excitement.
"Oh, you sweet animals," said Dodo, sitting down on the floor and
going off at another tangent. "Come here and talk at once. Edith,
may I give them the milky ham? Here you are; drink the milk first,
and then eat the ham, and then say grace, and then you may get
down."
Dodo poured the milk into two clean saucers, and set them on the
floor. There were a few drops left at the bottom of the jug, and she
made a neat little pool on the head of each of the dogs.
"What are their names?" she asked. "They ought to be Tweedledum
and Tweedledee, or Huz and Buz, or Ananias and Sapphira, or Darby
and Joan, or Harris and Ainsworth. It ought to be Harris and
Ainsworth. I'm sure, no one man could have written all that rot
himself. Little Spencer is very fond of Harrison Ainsworth; he said it
was instructive as well as palatable. I don't want to be instructed,
and it isn't palatable. I hate having little bits of information wrapped
up and given to me to swallow, like a powder in jam. Did you have
to take powders when you were little, Lady Grantham?"
Dodo's questions were purely rhetorical; they required no answer,
and she did not expect one.
"It is much nicer being completely ignorant and foolish like me," she
said. "Nobody ever expects me to know anything, or to be
instructive on any subject under the sun. Jack and I are going to be
a simple little couple, who are very nice and not at all wise. Nobody
dislikes one if one never pretends to be wise. But I like people to
have a large number of theories on every subject. Everyone is bound
to form conclusions, but what I dislike are people who have got
good grounds for their conclusions, who knock you slap down with
statistics, if you try to argue with them. It's impossible to argue with
anyone who has reasons for what he says, because you get to know
sooner or later, and then the argument is over. Arguments ought to
be like Epic poems, they leave off, they don't come to an end."

Dodo delivered herself of these surprising statements with great
rapidity, and left the room to get her cigarettes. She left the door
wide open, and in a minute or two her voice was heard from the
drawing-room, screaming to Edith.
"Edith, here's the 'Dodo Symphony'; come and play it to me this
moment."
"There's not much wrong with her this morning," thought Edith, as
she went to the drawing-room, where Dodo was playing snatches of
dance music.
"Play the scherzo, Edith," commanded Dodo. "Here you are. Now,
quicker, quicker, rattle it out; make it buzz."
"Oh, I remember your playing that so well," said Dodo, as Edith
finished. "It was that morning at Winston when you insisted on
going shooting. You shot rather well, too, if I remember right."
Lady Grantham had followed Edith, and sat down, with her
atmosphere of impenetrable leisure, near the piano.
Dodo made her feel uncomfortably old. She felt Dodo's extravagantly
high spirits were a sort of milestone to show, how far she herself
had travelled from youth. It was impossible to conceive of Dodo ever
getting middle-aged or elderly. She had racked her brains in vain to
try to think of any woman of her own age who could possibly ever
have been as insolently young as Dodo. She had the habit, as I have
mentioned before, of making strangely direct remarks, and she
turned to Dodo and said:—
"I should so like to see you ten years hence. I wonder if people like
you ever grow old."
"I shall never grow old," declared Dodo confidently. "Something, I
feel sure, will happen to prevent that. I shall stop young till I go out
like a candle, or am carried off in a whirlwind or something. I
couldn't be old; it isn't in me. I shall go on talking nonsense till the
end of my life, and I can't talk nonsense if I have to sit by the fire
and keep a shawl over my mouth, which I shall have to do if I get

old. Wherefore I never shall. It's a great relief to be certain of that. I
used to bother my head about it at one time! and it suddenly flashed
upon me, about ten days ago, that I needn't bother about it any
more, as I never should be old."
"Would you dislike having to be serious very much?" asked Edith.
"It isn't that I should dislike it," said Dodo; "I simply am incapable of
it. I was serious last night for at least an hour, and a feverish
reaction has set in. I couldn't be serious for a week together, if I was
going to be beheaded the next moment, all the time. I daresay it
would be very nice to be serious, just as I'm sure it would be very
nice to live at the bottom of the sea and pull the fishes' tails, but it
isn't possible."
Dodo had quite forgotten that she had intended to go for a ride, and
she went into the garden with Nora, and played ducks and drakes on
the pond, and punted herself about, and gathered water-lilies. Then
she was seized with an irresistible desire to fish, and caught a large
pike, which refused to be killed, and Dodo had to fetch the gardener
to slay it. She then talked an astonishing amount of perfect
nonsense, and thought that it must be lunch-time. Accordingly, she
went back to the house, and was found by Edith, a quarter of an
hour later, playing hide-and-seek with the coachman's children,
whom she had lured in from the stable-yard as she went by. The
rules were that the searchers were to catch the hiders, and Dodo
had entrenched herself behind the piano, and erected an
impregnable barricade, consisting of a revolving bookcase and the
music-stool. The two seekers entirely declined to consider that she
had won, and Dodo, with a show of reason, was telling them that
they hadn't caught her yet at any rate. The situation seemed to
admit of no compromise and no solution, unless, as Dodo suggested,
they got a pound or two of blasting powder and destroyed her
defences. However, a deus ex machina appeared in the person of
the coachman himself, who had come in for orders, and hinted
darkly that maternal vengeance was brewing if certain persons did
not wash their hands in time for dinner, which was imminent.

"There's a telegram for you somewhere," said Edith to Dodo, as she
emerged hot and victorious. "I sent a man out into the garden with
it. The messenger is waiting for an answer."
Dodo became suddenly grave.
"I suppose he's gone to the pond," she said; "that's where I was
seen last. I'll go and get it."
She met the man walking back to the house, having looked for her
in vain. She took the telegram and opened it. It had been forwarded
from her London house. It was very short.
"I arrive in London to-day. May I call?
—"WALDENECH."
Dodo experienced, in epitome at that moment, all she had gone
through the night before. She went to a garden-seat, and remained
there in silence so long that the footman asked her: "Will there be
an answer, my lady? The messenger is waiting."
Dodo held out her hand for the telegraph form. She addressed it to
the caretaker at her London house. It also was very short:
"Address uncertain; I leave here to-day. Forward nothing."
She handed it to the man, and gave orders that it should go at once.
Dodo did not move. She sat still with her hands clasped in front of
her, unconscious of active thought, only knowing that a stream of
pictures seemed to pass before her eyes. She saw the Prince
standing on her doorstep, learning with surprise that Lady
Chesterford was not at home, and that her address was not known.
She saw him turn away, baffled but not beaten; she saw him
remaining in London day after day, waiting for the house in Eaton
Square to show some signs of life. She saw—ah, she dismissed that
picture quickly.
She had one sudden impulse to call back the footman and ask for
another telegraph form; but she felt if she could only keep a firm
hand on herself for a few moments, the worst would be passed; and

it was with a sense of overwhelming relief that she saw the
telegraph boy walk off down the drive with the reply in his hand.
Then it suddenly struck her that the Prince was waiting for the
answer at Dover Station.
"How savage he will be," thought Dodo. "There will be murder at the
telegraph office if he waits for his answer there. Well, somebody
must suffer, and it will be the telegraph boys."
The idea of the Prince waiting at Dover was distinctly amusing, and
Dodo found a broad smile to bestow on the thought before she
continued examining the state of her feelings and position. The
Prince's influence over her she felt was local and personal, so to
speak, and now she had made her decision, she was surprised at the
ease with which it had been made. Had he been there in person,
with his courtly presence and his serene remoteness from anything
ordinary, and had said, in that smooth, well-modulated, voice, "May
I hope to find you in to-morrow?" Dodo felt that she would have said
"Come." Her pride was in frantic rebellion at these admissions; even
the telegram she had sent was a confession of weakness. She would
not see him, because she was afraid. Was there any other reason?
she asked herself. Yes; she could not see him because she longed to
see him.
"Has it come to that?" she thought, as she crumpled up the telegram
which had fluttered down from her lap on to the grass. Dodo felt she
was quite unnecessarily honest with herself in making this
admission. But what followed? Nothing followed. She was going to
marry Jack, and be remarkably happy, and Prince Waldenech should
come and stay with them because she liked him very much, and she
would be delightfully kind to him, and Jack should like him too. Dear
old Jack, she would write him a line this minute, saying when she
would be back in London.
Dodo felt a sudden spasm of anger against the Prince. What right
had he to behave like this? He was making it very hard for her, and
he would get nothing by it. Her decision was irrevocable; she would

not see him again, for some time at any rate. She would get over
this ridiculous fear of him. What was he that other men were not?
What was the position, after all? He had wanted to marry her; she
had refused him because she was engaged to Jack. If there had
been no Jack—well, there was a Jack, so it was unnecessary to
pursue that any further. He had given her his photograph, and had
said several things that he should not have said. Dodo thought of
that scene with regret. She had had an opportunity which she had
missed; she might easily have made it plain to him that his
murmured speeches went beyond mere courtesy. Instead of that she
had said she would always regard him as a great friend, and hoped
he would see her often. She tapped the ground impatiently as she
thought of missed opportunities. It was stupid, inconceivably stupid
of her. Then he had followed her to England, and sent this telegram.
She did not feel safe. She longed, and dreaded to see him again. It
was too absurd that she should have to play this gigantic game of
hide-and-seek. "I shall have to put on a blue veil and green goggles
when I go back to London," thought Dodo. "Well, the seekers have
to catch the hiders, and he hasn't caught me yet."

Meanwhile the Prince was smoking a cigar at Dover Station. The
telegram had not come, though he had waited an hour, and he had
settled to give it another half-hour and then go on to London. He
was not at all angry; it was as good as a game of chess. The Prince
was very fond of chess. He enjoyed exercising a calculating long-
sightedness, and he felt that the Marchioness of Chesterford elect
was a problem that enabled him to exercise this faculty, of which he
had plenty, to the full.
He had a sublime sense of certainty as to what he was going to do.
He fully intended to marry Dodo, and he admitted no obstacles. She
was engaged to Jack, was she? So much the worse for Jack. She
wished to marry Jack, did she? So much the worse for her, and none
the worse, possibly the better, for him. As it was quite certain that
he himself was going to marry Dodo, these little hitches were
entertaining than otherwise. It is more fun to catch your salmon
after a quarter of an hour's rather exciting fight with him than to net
him. Half the joy of a possession lies in the act of acquisition, and
the pleasure of acquisition consists, at least in half of the excitement
attendant on it. To say that the Prince ever regarded anyone's
feelings would be understating the truth. The fact that his will
worked its way in opposition to, and at the expense of others,
afforded him a distinct and appreciable pleasure. If he wanted
anything he went straight for it, and regarded neither man, nor
devil, nor angel; and he wanted Dodo.
His mind, then, was thoroughly made up. She seemed to him
immensely original and very complete. He read her, he thought, like
a book, and the book was very interesting reading. His sending of
the telegram with "Reply paid," was a positive stroke of genius.
Dodo had told him that she was going straight to London, but, as we
have seen, she did not stop the night there, but went straight on to
Edith's home in Berkshire. There were two courses open to her;
either to reply "Yes" or "No" to the telegram, or to leave it
unanswered. If she left it "unanswered" it would delight him above
measure, and it seemed that his wishes were to be realised. Not

answering the telegram would imply that she did not think good to
see him, and he judged that this decision was probably prompted by
something deeper than mere indifference to his company. It must be
dictated by a strong motive. His calculations were a little at fault,
because Dodo had not stopped in London, but this made no
difference, as events had turned out, to the correctness of his
deductions.
He very much wished Dodo to be influenced by strong motives in
her dealings with him. He would not have accepted, even as a gift,
the real, quiet liking she had for Jack. Real, quiet likings seemed to
him to be as dull as total indifference. He would not have objected
to her regarding him with violent loathing, that would be something
to correct; and his experience in such affairs was that strong
sympathies and antipathies were more akin to each other than quiet
affection or an apathetic indifference were to either. He walked up
and down the platform with the smile of a man who is waiting for an
interesting situation in a theatrical representation to develop itself.
He had no wish to hurry it. The by-play seemed to him to be very
suitable, and he bought a morning paper. He glanced through the
leaders, and turned to the small society paragraphs. The first that
struck his eye was this: "The Marchioness of Chesterford arrived in
London yesterday afternoon from the Continent."
He felt it was the most orthodox way of bringing the scene to its
climax. Enter a newsboy, who hands paper to Prince, and exit. Prince
unfolds paper and reads the news of—well, of what he is expecting.
He snipped the paragraph neatly out from the paper, and put it in his
card-case. His valet was standing by the telegraph office, waiting for
the message. The Prince beckoned to him.
"There will be no telegram," he said. "We leave by the next train."
The Prince had a carriage reserved for him, and he stepped in with a
sense of great satisfaction. He even went so far as to touch his hat
in response to the obeisances of the obsequious guard, and told his
valet to see that the man got something. He soon determined on his

next move—a decided "check," and rather an awkward one; and for
the rest of his journey he amused himself by looking out of the
window, and admiring the efficient English farming. All the
arrangements seemed to him to be very solid and adequate. The
hedges were charming. The cart horses were models of sturdy
strength, and the hop harvest promised to be very fine. He was
surprised when they drew near London. The journey had been
shorter than he expected.
He gave a few directions to his valet about luggage, and drove off to
Eaton Square.
The door was opened by an impenetrable caretaker.
"Is Lady Chesterford in?" asked the Prince.
"Her ladyship is not in London, sir," replied the man.
The Prince smiled. Dodo was evidently acting up to her refusal to
answer his telegram.
"Ah, just so," he remarked. "Please take this to her, and say I am
waiting."
He drew from his pocket a card, and the cutting from the Morning
Post.
"Her ladyship is not in London," the man repeated.
"Perhaps you would let me have her address," said the Prince,
feeling in his pockets.
"A telegram has come to-day, saying that her ladyship's address is
uncertain," replied the caretaker.
"Would you be so good as to let me see the telegram?"
Certainly, he would fetch it.
The Prince waited serenely. Everything was going admirably.
The telegram was fetched. It had been handed in at Wokingham
station at a quarter to one. "After she had received my telegram,"
reflected the Prince.

"Do you know with whom she has been staying?" he asked blandly.
"With Miss Staines."
The Prince was very much obliged. He left a large gratuity in the
man's hand, and wished him good afternoon.
He drove straight to his house, and sent for his valet, whom he
could trust implicitly, and who had often been employed on
somewhat delicate affairs.
"Take the first train for Wokingham to-morrow morning," he said.
"Find out where a Miss Staines lives. Inquire whether Lady
Chesterford left the house to-day."
"Yes, your Highness."
"And hold your tongue about the whole business," said the Prince
negligently, turning away and lighting a cigar. "And send me a
telegram from Wokingham: 'Left yesterday,' or 'Still here.'"
The Prince was sitting over a late breakfast on the following
morning, when a telegram was brought in. He read it, and his eyes
twinkled with genuine amusement.
"I think," he said to himself, "I think that's rather neat."
CHAPTER TWENTY
If Dodo had felt some excusable pride in having torn up the Prince's
photograph, her refusal to let him know where she was gave her a
still more vivid sense of something approaching heroism. She did not
blame anyone but herself for the position into which she had drifted
during those weeks in Switzerland. She was quite conscious that she
might have stopped any intimacy of this sort arising, and
consequently the establishment of this power over her. But she felt
she was regaining her lost position. Each sensible refusal to admit

his influence over her was the sensible tearing asunder of the fibres
which enveloped her. It was hard work, she admitted, but she was
quite surprised to find how comfortable she was becoming. Jack
really made a very satisfactory background to her thoughts. She was
very fond of him, and she looked forward to their marriage with an
eager expectancy, which, was partly, however, the result of another
fear.
She was sitting in the drawing-room next day with Miss Grantham,
talking about nothing particular very rapidly.
"Of course, one must be good to begin with," she was saying; "one
takes that for granted. The idea of being wicked never comes into
my reckoning at all. I should do lots of things if I didn't care what I
did, that I shouldn't think of doing at all now. I've got an admirable
conscience. It is quite good, without being at all priggish. It isn't
exactly what you might call in holy orders, but it is an ecclesiastical
layman, and has great sympathy with the Church. A sort of lay-
reader, you know."
"I haven't got any conscience at all," said Miss Grantham. "I believe
I am fastidious in a way, though, which prevents me doing
conspicuously beastly things."
"Oh, get a conscience, Grantie," said Dodo fervently, "it is such a
convenience. It's like having someone to make up your mind for you.
I like making up other people's minds, but I cannot make up my
own; however, my conscience does that for me. It isn't me a bit. I
just give it a handful of questions which I want an answer upon, and
it gives me them back, neatly docketed, with 'Yes' or 'No' upon
them."
"That's no use," said Miss Grantham. "I know the obvious 'Yeses'
and 'Noes' myself. What I don't know are the host of things that
don't matter much in themselves, which you can't put down either
right or wrong."
"Oh, I do all those," said Dodo serenely, "if I want to, and if I don't,
I have an excellent reason for not doing them, because I am not

sure whether they are right. When I set up my general advice office,
which I shall do before I die, I shall make a special point of that for
other people. I shall give decided answers in most cases, but I shall
reserve a class of things indifferent, which are simply to be settled
by inclination."
"What do you call indifferent things?" asked Miss Grantham,
pursuing the Socratic method.
"Oh, whether you are to play lawn tennis on Sunday afternoon," said
Dodo, "or wear mourning for second cousins, or sing alto in church
for the sake of the choir; all that sort of thing."
"Your conscience evidently hasn't taken orders," remarked Miss
Grantham.
"That's got nothing to do with my conscience," said Dodo. "My
conscience doesn't touch those things at all. It only concerns itself
with right and wrong."
"You're very moral this morning," said Miss Grantham. "Edith," she
went on, as Miss Staines entered in a howling wilderness of dogs,
"Dodo has discovered a conscience."
"Whose?" asked Edith.
"Why, my own, of course," said Dodo; "but it's no discovery. I always
knew I had one."
"There's someone waiting to see you," said Edith. "I brought his card
in."
She handed Dodo a card.
"Prince Waldenech," she said quietly to herself, "let him come in
here, Edith. You need not go away."
Dodo got up and stood by the mantelpiece, and displayed an
elaborate attention to one of Edith's dogs. She was angry with
herself for needing this minute of preparation, but she certainly used
it to the best advantage; and when the Prince entered she greeted
him with an entirely natural smile of welcome.

"Ah, this is charming," she said, advancing to him. "How clever of
you to find out my address."
"I am staying at a house down here," said the Prince, lying with
conscious satisfaction as he could not be contradicted, "and I could
not resist the pleasure."
Dodo introduced him to Edith and Miss Grantham, and sat down
again.
"I sent no address, as I really did not know where I might be going,"
she said, following the Prince's lead. "That I was not in London was
all my message meant. I did not know you would be down here."
"Lord Chesterford is in England?" asked the Prince.
"Oh, yes, Jack came with me as far as Dover, and then he left me for
the superior attractions of partridge-shooting. Wasn't it rude of
him?"
"He deserves not to be forgiven," said the Prince.
"I think I shall send you to call him out for insulting me," said Dodo
lightly; "and you can kill each other comfortably while I look on.
Dear old Jack."
"I should feel great pleasure in fighting Lord Chesterford if you told
me to," said the Prince, "or if you told him to, I'm sure he would feel
equal pleasure in killing me."
Dodo laughed.
"Duelling has quite gone out," she said. "I sha'n't require you ever to
do anything of that kind."
"I am at your service," he said.
"I wish you'd open that window then," said Dodo; "it is dreadfully
stuffy. Edith, you really have too many flowers in the room."
"Why do you say that duelling has done out?" he asked. "You might
as well say that devotion has gone out."

"No one fights duels now," said Dodo; "except in Prance, and no
one, even there, is ever hurt, unless they catch cold in the morning
air, like Mark Twain."
"Certainly no one goes out with a pistol-case, and a second, and a
doctor," said the Prince; "that was an absurd way of duelling. It is no
satisfaction to know that you are a better shot than your
antagonist."
"Still less to know that he is a better shot than you," remarked Miss
Grantham.
"Charming," said the Prince; "that is worthy of Lady Chesterford.
And higher praise—"
"Go on about duelling," said Dodo, unceremoniously.
"The old system was no satisfaction, because the quarrel was not
about who was the better shot. Duelling is now strictly decided by
merit. Two men quarrel about a woman. They both make love to
her; in other words, they both try to cut each other's throats, and
one succeeds. It is far more sensible. Pistols are stupid bull-headed
weapons. Words are much finer. They are exquisite sharp daggers.
There is no unnecessary noise or smoke, and they are quite orderly."
"Are those the weapons you would fight Lord Chesterford with, if
Dodo told you to?" asked Edith, who was growing uneasy.
The Prince, as Dodo once said, never made a fool of himself. It was
a position in which it was extremely easy for a stupid man to say
something very awkward. Lady Grantham, with all her talent for
asking inconvenient questions, could not have formed a more
unpleasant one. He looked across at Dodo a moment, and said,
without a perceptible pause,—
"If I ever was the challenger of Lady Chesterford's husband, the
receiver of the challenge has the right to choose the weapons."
The words startled Dodo somehow. She looked up and met his eye.

"Your system is no better than the old one," she said. "Words
become the weapons instead of pistols, and the man who is most
skilful with words has the same advantage as the good shot. You are
not quarrelling about words, but about a woman."
"But words are the expression of what a man is," said the Prince.
"You are pitting merit against merit."
Dodo rose and began to laugh.
"Don't quarrel with Jack, then," she said. "He would tell the footman
to show you the door. You would have to fight the footman. Jack
would not speak to you."
Dodo felt strongly the necessity of putting an end to this
conversation, which was effectually done by this somewhat
uncourteous speech. The fencing had become rather too serious to
please her, and she did not wish to be serious. But she felt
oppressively conscious of this man's personality, and saw that he
was stronger than she was herself. She decided to retreat, and made
a desperate effort to be entirely flippant.
"I hope the Princess has profited by the advice I gave her," she said.
"I told her how to be happy though married, and how not to be
bored though a Russian. But she's a very bad case."
"She said to me dreamily as I left," said the Prince, "'You'll hear of
my death on the Matterhorn. Tell Lady Chesterford it was her fault.'"
Dodo laughed.
"Poor dear thing," she said, "I really am sorry for her. It's a great
pity she didn't marry a day labourer and have to cook the dinner and
slap the children. It would have been the making of her."
"It would have been a different sort of making," remarked the
Prince.
"I believe you can even get blasé of being bored," said Miss
Grantham, "and then, of course, you don't get bored any longer,
because you are bored with it."

This remarkable statement was instantly contradicted by Edith.
"Being bored is a bottomless pit," she remarked. "You never get to
the end, and the deeper you go the longer it takes to get out. I was
never bored in my life. I like listening to what the dullest people
say."
"Oh, but it's when they don't say anything that they're so trying,"
said Miss Grantham.
"I don't mind that a bit," remarked Dodo. "I simply think aloud to
them. The less a person says the more I talk, and then suddenly I
see that they're shocked at me, or that they don't understand. The
Prince is often shocked at me, only he's too polite to say so. I don't
mean that you're a dull person, you know, but he always
understands. You know he's quite intelligent," Dodo went on,
introducing him with a wave of her hand, like a showman with a
performing animal. "He knows several languages. He will talk on
almost any subject you wish. He was thirty-five years of age last
May, and will be thirty-six next May."
"He has an admirable temper," said the Prince, "and is devoted to his
keeper."
"Oh, I'm not your keeper," said Dodo. "I wouldn't accept the
responsibility. I'm only reading extracts from the advertisement
about you."
"I was only reading extracts as well," observed the Prince. "Surely
the intelligent animal, who knows several languages, may read its
own advertisement?"
"I'm not so sure about your temper," said Dodo, reflectively: "I shall
alter it to 'is believed to have an admirable temper.'"
"Never shows fight," said the Prince.
"But is willing to fight if told to," said she. "He said so himself."
"Oh, but I only bark when I bite," said the Prince, alluding to his
modern system of duelling.

"Then your bite is as bad as your bark," remarked Dodo, "which is a
sign of bad temper. And now, my dear Prince, if we talk any more
about you, you will get intolerably conceited, and that won't do at
all. I can't bear conceited men. They always seem to me to be like
people on stilts. They are probably not taller than oneself really, and
they're out of all proportion, all legs, and no body or head. I don't
want anyone to bring themselves down to my level when they talk to
me. Conceited people always do that. They get off their stilts. If
there's one thing that amuses me more than another, it is getting
hold of their stilts and sawing them half through. Then, when they
get up again they come down 'Bang,' and you say: 'Oh, I hope you
haven't hurt yourself. I didn't know you went about on stilts. They
are very unsafe, aren't they?'"
Dodo was conscious of talking rather wildly and incoherently. She
felt like a swimmer being dragged down by a deep undercurrent. All
she could do was to make a splash on the surface. She could not
swim quietly or strongly out of its reach. She stood by the window
playing with the blind cord, wishing that the Prince would not look at
her. He had a sort of deep, lazy strength about him that made Dodo
distrust herself—the indolent consciousness of power that a tiger has
when he plays contemptuously with his prey before hitting it with
one deadly blow of that soft cushioned paw.
"Why can't I treat him like anyone else?" she said to herself
impatiently. "Surely I am not afraid of him. I am only afraid of being
afraid. He is handsome, and clever, and charming, and amiable, and
here am I watching every movement and listening to every word he
says. It's all nonsense. Here goes."
Dodo plunged back into the room, and sat down in the chair next
him.
"What a charming time we had at Zermatt," she said. "That sort of
place is so nice if you simply go there in order to amuse yourself
without the bore of entertaining people. Half the people who go
there treat it as their great social effort of the year. As if one didn't
make enough social efforts at home!"

"Ah, Zermatt," said the Prince, meditatively. "It was the most
delightful month I ever spent."
"Did you like it?" said Dodo negligently. "I should have thought that
sort of place would have bored you. There was nothing to do. I
expected you would rush off as soon as you got there, and go to
shoot or something."
"Like Lord Chesterford and the partridges," suggested Edith.
"Oh, that's different," said Dodo. "Jack thinks it's the duty of every
English landlord to shoot partridges. He's got great ideas of his
duty."
"Even when it interferes with what must have been his pleasure,
apparently," said the Prince.
"Oh; Jack and I will see plenty of each other in course of time. I'm
not afraid he will go and play about without me."
"You are too merciful," said the Prince.
"Oh, I sha'n't be hard on Jack. I shall make every allowance for his
shortcomings, and I shall expect that he will make allowance for
mine."
"He will have the best of the bargain;" said the Prince.
"You mean that he won't have to make much allowance for me?"
asked Dodo. "My dear Prince, that shows how little you really know
about me. I can be abominable. Ask Miss Staines if I can't. I can
make a man angry quicker than any woman I know. I could make
you angry in a minute and a quarter, but I am amiable this morning,
and I will spare you."
"Please make me angry," said the Prince.
Dodo laughed, and held out her hand to him.
"Then you will excuse my leaving you?" she said. "I've got a letter to
write before the midday post. That ought to make you angry. Are
you stopping to lunch? No? Au revoir, then. We shall meet again

sometime soon, I suppose. One is always running up against
people."
"Dodo shook hands with elaborate carelessness and went towards
the door, which the Prince opened for her.
"You have made me angry," he murmured, as she passed out, "but
you will pacify me again, I know."
Dodo went upstairs into her bedroom. She was half frightened at her
own resolution, and the effort of appearing quite unconcerned had
given her a queer, tired feeling. She heard a door shut in the
drawing-room below, and steps in the hall. A faint flush came over
her face, and she got up quickly from her chair and rah downstairs.
The Prince was in the hall, and he did not look the least surprised to
see Dodo again.
"Ah, you are just off?" she asked.
Then she stopped dead, and he waited as if expecting more. Dodo's
eyes wandered round the walls and came back to his face again.
"Come and see me in London any time," she said in a low voice. "I
shall go back at the end of the week."
The Prince bowed.
"I knew you would pacify me again," he said.
CHAPTER TWENTY-ONE
Dodo was up again in London at the end of the week, as she had
told the Prince. Jack was also staying in town, and they often spent
most of the day together; riding occasionally in the deserted Row, or
sitting, as they were now, in Dodo's room in the Eaton Square
house. They were both leaving for the country in a few days' time,
where they had arranged to come across one another at various

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Biology Of Plagues 1st Edition Susan Scott Christopher J Duncan

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Biology Of Plagues 1st Edition Susan Scott Christopher J Duncan

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