Disease and History:

From Ancient Times to Covid-19

By

Frederick F. Cartwright & Michael Biddiss

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 First published by Rupert Hart-Davis, 1972

Second Edition, 2000

Third Edition, 2014

Copyright © Frederick F. Cartwright & Michael Biddiss

This Fourth Edition published in 2020 by Lume Books

30 Great Guildford Street,
Borough, SE1 0HS

The right of Frederick F. Cartwright & Michael Biddiss to be identified

as the authors of this work has been asserted by them in accordance with
the Copyright, Design and Patents Act, 1988.

All rights reserved. No part of this publication may be reproduced, stored

in a retrieval system, or transmitted in photocopying, recording or
otherwise, without the prior permission of the copyright owner.

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 CONTENTS

Preface

Introduction: Disease and History

1 Disease in the Ancient World

2 The Black Death

3 The Mystery of Syphilis

4 Smallpox, or the Conqueror Conquered

5 General Napoleon and General Typhus

6 Cholera and Sanitary Reform

7 Gin, Flu, and Tuberculosis

8 Mosquitoes, Flies, Travel, and Exploration

9 Queen Victoria and the Fall of the Russian Monarchy

10 Mob Hysteria and Mass Suggestion

11 Current Problems of Survival

Epilogue: The Covid-19 Pandemic

Further Reading

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 PREFACE

This book had its origins in debate and collaboration between a doctor
and a historian, each concerned to provide the general reader with an
accessible account of some of the principal ways in which disease has
often made a dramatic mark upon history.
The first edition was published in 1972, after which it received
various reprintings and was also translated into French and Japanese. An
enlarged and fully revised second edition then appeared in 2000, and
subsequently became the object of a still wider range of foreign
translations. By the time that I undertook some further updating for a
paperback version issued four years later, my co-author Frederick
Cartwright had died at the end of a very long and distinguished career
not only as a consultant anaesthetist but also as a pioneering writer and
teacher on topics related to the development of medical ideas and
practice. A further edition of the book appeared in 2014, ending with my
substantially enlarged treatment of topics that flow from the past into
major issues of current and future concern. I am grateful to Andrew
Lownie for having now encouraged me to prepare a fourth edition,
reinforcing such analysis with a new and particularly topical Epilogue.
This assesses, as far as is currently possible in the midst of swiftly
changing circumstances, the nature and historical significance of the
Covid-19 pandemic which began to develop so rapidly in the course of
2020.
In preparing the present edition I have again enjoyed the benefit of
dialogue with Dr James Willis. His medical knowledge and wisdom stem
from extensive experience in general practice, and I am most
appreciative of the helpful comments that he has continued to make in

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precisely the same spirit of inter-disciplinary collaboration as originally
inspired Disease and History. Further warm thanks for assistance in
preparing this updated version are due to Louise Dilloway and Lesley
Willis, as well as to James Faktor and his colleagues at Lume Books.
MICHAEL BIDDISS
November 2020

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 INTRODUCTION

DISEASE AND HISTORY

Historians and doctors have much in common, sharing particularly an

interest in the influences which condition human existence. The object of
this book is to study the area in which those interests most directly
converge, that of the impact of disease upon history. In medical diagnosis
a single cause for disease will often be found; in historical investigation
the causes are likely to be more complex. Nothing could be more
ridiculous than to contend that disease is always the primary cause of a
great historical change but, particularly at a time when the sociological
aspects of history are being increasingly emphasized, it is worth
examining episodes in which the influence of disease may have been of
real importance, especially when that significance has been neglected or
misconstrued.
Our aim in studying some of the many maladies which have
afflicted the world will be to illustrate their effect not only upon
historically important individuals but also upon peoples. Thus the study
is relevant to History, whether conceived as a saga of great figures or as
the story of social conditions and broader human development. The ills
that have plagued civilized societies are as much a part of civilization as
are their prevention and cure. If disease itself is historically important,
then the conquest of disease is no less so. And, as we shall see, this
conquest, though still only partial, has itself raised problems that are no
less daunting and equally relevant to our subject.
The picture of primitive human beings isolated in their caves is
misleading. The family unit developed into the tribe living a communal

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life. These small communities, a few of which still exist in remote jungle
areas today, dwelt in man-made clearings with little or no contact
between individual settlements. Each group was self-supporting,
dependent upon naturally occurring food sources. In Central Africa, for
instance, bananas and manioc formed a staple diet, varied by small
quantities of palm oil and only rarely by human or animal flesh. The few
enemies of these tribal communities were snakes, carnivorous beasts and
pygmy humans who shot at them with strophanthin-poisoned arrows.
Puerperal fever in childbirth, a high infant mortality and endemic
disease, such as sleeping sickness and yaws, prevented rapid increase in
population. Life span was short, partly because no reliable cure for
illness existed, partly because a high carbohydrate diet led to early
obesity with fatty infiltration of the vital organs. So tribal growth
remained almost static, increasing in a healthy season when live births
outnumbered deaths, decreasing when infant mortality was high. Such is
the natural process of slow increase in a primitive community which is
adequately fed and protected from major disaster but cannot cope with
the hazards of childbirth and sickness.
Disaster in the form of famine, war or epidemic disease could
strike only from outside. A plague of insects might descend upon the
crops and cause famine. Arab slavers, pushing down from the north and
east of Africa, might chance upon one of these villages, engage the
inhabitants in battle and carry off the survivors into captivity. In later
years Europeans would come, bringing with them new diseases relatively
harmless to themselves but lethal to a community lacking any inbred or
acquired resistance.
When thousands of years ago the peoples that would eventually
create the great civilizations of Egypt, Mesopotamia, India and China
began to emerge from self-contained communities the chances of major
disaster multiplied. A greater degree of civilization brought benefits,
including a higher standard of living and a fuller intellectual life, but it

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also produced hazards. As mobility increased so too did the likelihood of
contact with unknown diseases. Tracks became roads that made for
easier and faster travel. New diseases could be carried along such routes,
striking down unaccustomed populations before resistance to the
invading organisms could develop. Cities were built and, as city-dwellers
necessarily rely upon an extraneous food supply, famine became
inevitable whenever that supply failed, for there were no natural
resources to take its place. Hunger, the desire for more and better living
space, or the simple lust of a chieftain for power, would then set one
grouping to fight against another. So mankind’s three great enemies,
Pestilence, Famine and War – the three Horsemen of the Apocalypse
who bring in their train Death upon his Pale Horse – developed on an
ever-increasing scale.
Pestilence, famine and war interact and produce a sequence. War
drives the farmer from his fields and destroys his crops; destruction of
the crop spells famine; the starved and weakened people fall easy victims
to the onslaught of pestilence. All three are diseases. Pestilence is a
disorder of the human. Famine results from disorders of plants and of
animal food sources, caused by inclement weather or more directly by
insect or bacterial invasion. And even war may be regarded, though
perhaps more arguably, as a form of mass psychotic disorder. In the
subsequent chapters, although the diseases of famine and war must
necessarily have their place, our primary concern will be with those
physical ills that have directly affected humanity.

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 CHAPTER ONE
DISEASE IN THE ANCIENT WORLD

Disease associated with civilization is older than written history, for

civilization of a kind existed before the first records were kept. While
archaeologists working on skeletal remains have provided us with an
increasing amount of evidence about disease during the earlier stages of
human development, the oldest textual survivals of any substance date
back only to the epoch around 1500 BC. Most notable is the papyrus
from that period which was found in a tomb at Thebes by Professor
Georg Ebers in 1862. We can readily surmise that its particularly
extensive cataloguing of a wide range of Egyptian remedial practices is
in some ways typical even of more fragmentary ancient medical records,
in the sense that it surely includes some repetition of older texts now lost
and discusses ailments and attempted cures which, even at the time of
writing, would often have been already centuries-old.
In the biblical Book of Exodus there is an account of the plague
which smote Egypt around 1500 BC, killing all the firstborn in the land
from the firstborn of Pharaoh on his throne to the firstborn of the captive
in his dungeon and all firstborn of cattle. This is one example of the
effect of disease upon history, for the last terrible visitation upon the
Egyptians persuaded Pharaoh to allow his Israelite slaves to depart. After
forty years of wanderings and tribulations in the wilderness they at last
reached what they regarded as their promised land. The war-pestilence
sequence is well described in the Book of Samuel. We are told that
around 1140 BC the Israelites went out against the Philistines in battle
and were defeated. The Israelites brought out their sacred Ark of the
Covenant and re-engaged the Philistines, but again suffered defeat. The

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Philistines captured the Ark and bore it off to Ashdod, where plague at
once broke out. The Ark was then removed – by public request – to Gath
and then to Ekron, both places being immediately smitten by plague.
After seven months of suffering, the Philistines decided that the only
hope was to return the Ark to Israel. It was delivered to the field of
Joshua the Bethshemite, the return being greeted with sacrifices. But the
inquisitive Bethshemites looked into the Ark and were punished by a
great pestilence. It seems that the disease then spread throughout Israel,
bringing death to about fifty thousand people.
The plague of Athens in 430 BC provides a particularly striking
example of the effect of disease upon history. At the beginning of the
fifth century the Athenian Empire was at the height of its power. This
tiny Greek nation had defeated mighty Darius the Persian in the land
battles of Marathon and Plataea and in the great naval engagement of
Salamis. The enlightened reign of Pericles opened in 462 BC. Under him
the temples of Athens and Eleusis, destroyed by the Persians, were
restored through the genius of the architect Ictinus and the artist Phidias.
But this golden age of Greece was all too brief. In 431 BC the
Peloponnesian War broke out, an internecine struggle between the two
main Hellenic powers of Athens and Sparta. Sparta had a good army but
no fleet, while Athens was a maritime power with a strong navy but a
weaker army. Since her land defences were almost impregnable and
ample supplies could be imported by sea, Athens could neither be
brought to battle by land nor starved into submission. Fighting a
defensive battle by land and an offensive war at sea, she should have
been able to defeat Sparta without great difficulty. During the first year
of the war the outcome seemed inevitable, for Athens was successful
both on land and sea, but her defensive policy on land necessarily led to
the Athenians being crowded and besieged within their city walls.
Disaster struck in 430 BC. The pestilence is supposed to have
started in Ethiopia, whence it travelled to Egypt and was carried across

10
the Mediterranean by ship to Piraeus and Athens. It raged for only a
short time but caused enormous mortality. Perhaps at least a third and
possibly two-thirds of the population died. More disastrous still was the
breakdown of morale, an unsurprising phenomenon which we shall meet
again in times of pandemic sickness. Thucydides, who left an account of
this horrible time, wrote of the Athenians: ‘Fear of gods or law of men
there was none to restrain them. As for the first, they judged it to be just
the same whether they worshipped them or not, as they saw all alike
perishing. As for the latter, no one expected to live to be brought to trial
for his offences.’ Thucydides added that even the most staid and
respectable citizens devoted themselves to nothing but gluttony,
drunkenness and licentiousness.
When it seemed that the plague had subsided, Pericles sent a
powerful fleet to capture the Spartan-led stronghold of Potidaea. But
hardly had the navy departed when plague broke out in the ships with
such violence that the fleet was forced to return to Athens. A similar
disaster occurred when Pericles himself led his fleet to Epidaurus for ‘the
pestilence not only carried off his own men but all that had intercourse
with them’. Pericles may have caught the infection at this time, for he is
supposed to have died of plague in 429 BC.
The precise nature of the visitation is unknown. No account of it
occurs in the writings attributed to the master physician Hippocrates.
Thucydides described a very rapid onset, raging fever, extreme thirst,
tongue and throat ‘bloody’, the skin of the body red and livid, finally
breaking out into pustules and ulcers. The disease attacked all classes,
rich and poor. Physicians were helpless and themselves succumbed in
large numbers. Recent majority opinion has tended towards proposing
typhus as the cause, but other possibilities that have been speculatively
cited include scarlet fever, smallpox and measles, or even some disease
long since disappeared. Whatever its nature, the infection is likely to
have come from another centre of population which had developed its

11
own disease pattern or pool. The pestilence would then have assumed an
explosive character because the Athenians had had no chance of
acquiring previous immunity. The survivors would gradually develop
increasing resistance as epidemics of the infection recurred and so the
disease became less fatal.
The plague of 430 BC undoubtedly contributed to the downfall of
the Athenian empire. By killing so many, by demoralizing the capital
and, above all, by destroying the fighting power of the navy, the outbreak
prevented Athens from striking a decisive blow against Sparta. The war
dragged on for twenty-seven years and ended with the defeat of Athens
in 404 BC. She was deprived of her navy and her foreign possessions,
while her landward defences were razed to the ground. Fortunately for
posterity, the city and its culture were left intact.

One of the most stupendous historical events, measured in both the

extent and the longevity of its effects, is the downfall of the Roman
Empire. The causes and consequences of its collapse have been long
debated by historians. Here we shall examine only such factors as are
connected to disease and its prevention.
Under the Romans public health and sanitation were more
advanced around the year AD 300 than they were to be again until the
middle of the nineteenth century. Rome’s great drainage system, the
Cloaca Maxima, was started in the sixth century BC and assumed the
function of a modern sewer, the plan being then repeated in many places
elsewhere. For example, the ruins of Pompeii and Herculaneum,
destroyed by an eruption of Vesuvius in AD 79, have revealed an
elaborate system of waterworks connected with flushing closets; and
under the rule of the Emperor Vespasian, about AD 70, a building with
marble urinals was erected in Rome, with a small charge made for
admission. In contrast, London had to wait until the Great Exhibition of
1851 before any public lavatories were provided. For that event ‘public

12
waiting rooms’, available to ladies in Bedford Street and to gentlemen in
Fleet Street, were set up by way of experiment: the charge was two
pence for ‘lavatory privileges’ and fourpence for a hot towel. The cost of
constructing them came to £680 and, despite their distance from the
Exhibition in Hyde Park, admission fees raised £2,470 in five months.
Cleanliness depends upon an adequate water supply. The first
aqueduct brought pure water into Rome as early as 312 BC. At the
beginning of the Christian era there were six, but a hundred years later
ten aqueducts supplied 250 million gallons daily. The public baths
required half this enormous supply but there remained more than 50
gallons a head for the two million inhabitants, about the same amount as
is used by a citizen of London or New York today. In 1954 four of these
aqueducts had been renovated and sufficed for the needs of modern
Rome. The baths of Caracalla, dating from about AD 200, could
accommodate 1,600 bathers at a time. Those of Diocletian built eighty
years later had no fewer than 3,000 rooms. The bath, much like the
modern sauna, accompanied Roman civilization wherever it penetrated
and some places became famed for the curative powers of their warm or
mineral-impregnated waters. A few, such as Bath in England and
Wiesbaden in Germany, retain a modest reputation as medicinal spas
today.
The huge city-state of Rome had long grown haphazardly, with
crooked narrow streets and squalid houses. Almost two-thirds of this was
destroyed in AD 64 by the great fire in the reign of Nero. More fortunate
than London after the blaze of 1666, Rome was rebuilt to a master plan,
a city of broad streets and wide squares. Cleaning of the public roads was
supervised by the aediles, a body of officials who also controlled food
supply, introducing regulations to ensure the freshness and quality of
perishable goods. Among the public health measure was the prohibition
of burials within the city walls, causing the much more hygienic method
of cremation to become common. Cremation was not entirely replaced

13
by burial until general acceptance of Christianity implanted belief in
physical resurrection.
In its cleanliness, sanitation and water supply, Rome was much
more akin to twentieth-century London or New York than to medieval
Paris or eighteenth-century Vienna. The Romans were the first urban-
dwelling people on the grand scale. They must have quickly recognized,
probably as a result of painful experience, that a large body of people
cannot live closely together without a pure water supply, clean streets
and efficient sewers. A seventeenth-century Londoner existed in
conditions that would hardly have been tolerated by a first-century
Roman. But they met on one common ground, for neither knew the cause
of disease. If the seemingly clear water that flowed along the Roman
aqueduct happened to come from a contaminated source, then the Roman
was as much at risk as the Londoners who drew their supply from the
muddy Thames. This lack of essential knowledge rendered the
magnificent health measures of Imperial Rome entirely useless during
the long years of her plague-ridden decadence.
Imagine Rome as a bloated spider sitting in the centre of its web.
At the height of Roman expansion, this web stretched from the Sahara in
the south to the borders of Scotland in the north, from the Caspian Sea
and the Persian Gulf in the east to the western shores of Spain and
Portugal. To north and west lay the oceans, to south and east wide
unknown continents in which dwelt less civilized peoples. Farther
beyond, in the dim shadows, lay the ancient civilizations of India and
China. The long land frontiers were manned by garrisons at strategic
points. From these stretched back the filaments of the spider’s web, the
sea routes from Africa and Egypt, the straight legionary-made roads, all
of which led to Rome.
Herein lay the makings of disaster: a wide hinterland hiding
unknown secrets, among them the micro-organisms of unaccustomed
disease, troops who penetrated into that hinterland and were attacked by

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its inhabitants, easy transit by ship or along the roads specially built for
swift travel, a densely packed population living a highly civilized
existence but lacking the most rudimentary means of combating
infection. Given this conjunction of circumstances, it is little wonder that
the story of the last centuries of Roman power is a long tale of
pestilence.
In the first century BC an unusually severe type of malaria seems
to have infected the marshy districts around Rome, and then remained a
long-term problem. It produced a great epidemic around AD 79, shortly
after the eruption of Vesuvius. The infection seems to have been
confined to Italy, but there it raged destructively in the cities and caused
so many deaths in the Campagna, the market garden of Rome, that the
whole area went out of cultivation and remained a notoriously malarial
district until the end of the nineteenth century.
It was primarily due to malaria, though there were other reasons as
well, that the live-birth rate of the Italo-Romans fell steeply at a time
when the birth rate throughout the conquered regions was rising. Further,
the chronic ill-health and weakness caused by untreated malaria
decreased life expectancy and enervated the nation. By the fourth
century AD the mighty fighting power of the legions was no longer
Italian, with officers as well as common soldiers being drawn
increasingly from Germanic tribes. Possibly malaria, rather than the
alleged decadent luxury imported from the East, accounts for the
slackness of spirit which characterized the latter years of Roman
authority.
Malaria may have originated in Africa but another danger came
from the remote East. Towards the end of the first century AD warrior
forces emerged from the region of Mongolia, riding over the steppes into
south-eastern Europe. Their exodus was probably dictated by disease or
famine or a combination of both in the lands north of China. These
mounted invaders were the Huns who, by pressing on the Germanic

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tribes of Alans, Ostrogoths and Visigoths inhabiting the central Euro-
Asian land mass, instigated a relentless western movement which in the
end submerged Rome and broke the empire into a rabble of warring
states. The Huns brought with them new infections which produced a
series of epidemics generally labelled by historians as ‘plagues’. An
interesting point is that, conversely, the Huns probably encountered a
European disease unknown to them: during the years AD 451-4, under
Attila, they reached as far west as Gaul and northern Italy but were
turned back before invading Rome itself, apparently more by epidemic
sickness than by defensive warfare.
The Plague of Antoninus, sometimes known as the Plague of the
physician Galen, started in AD 164 among troops of the co-Emperor
Lucius Verus stationed on the eastern border of the empire. The sickness
was confined to the east for two years, causing havoc among an army
under the command of Avidius Cassius sent to repress a revolt in Syria.
The infection accompanied the legions homeward, spreading throughout
the countryside and reaching Rome in the year 166. It rapidly extended
to all parts of the known world, causing so many deaths that cartloads of
corpses were removed from Rome and other cities.
The visitation is notable because it caused the first crack in the
Roman defence lines. Until 161 the empire continually expanded and
maintained its frontiers. In that year a Germanic horde forced the north-
east barrier of Italy. Fear and disorganization prevented retaliation for
eight years. In 169 the full weight of Roman arms was thrown against the
invaders. They were driven back but it seems that sickness carried by the
legions played its part, for many Germans were found lying dead on the
battlefield without any sign of wounding. The pestilence raged until 180,
one of the last victims being the noblest of Roman Emperors, Marcus
Aurelius. He died on the seventh day of his illness, having refused to see
his son in case he should also fall a victim. After a short respite, the
pestilence returned again in 189. This second epidemic was less

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widespread but severely affected the city of Rome, causing more than
two thousand deaths a day at its height.
The name of the physician Galen is attached to the plague of 164-
89 not only because he fled from it but because he left a description.
Initial symptoms were high fever, inflammation of the mouth and throat,
parching thirst and diarrhoea. Galen described a skin eruption appearing
about the ninth day, sometimes dry and sometimes pustular. He implies
that many patients died before the eruption appeared. There is here some
resemblance to the Athenian plague, but the undoubted Eastern origin
and the mention of pustules have led many historians to assert that this is
the first record of a smallpox epidemic.
One theory holds that the westward movement of the Huns started
because of a virulent smallpox epidemic in Mongolia, which they
transmitted to German tribes who in turn infected the Romans. Against
this theory must be set the fact that the development of the Roman
outbreak in no way resembles the later history of European smallpox in
the sixteenth to nineteenth centuries. But, as we shall see in some of the
following chapters, the first appearance of an infection often takes a form
and course quite different from that of the established disease.
After the year 189 there is no mention of serious ‘plague’ until
250. Then appeared the great Plague of Cyprian which indisputably
changed the course of history in western Europe. The nature of the
infection is, however, unknown. Cyprian, the Christian bishop of
Carthage, described the symptoms as violent diarrhoea and vomiting, an
ulcerated sore throat, burning fever, and putrefaction or gangrene of the
hands and feet. Another account tells of a very rapid spread of disease all
over the body and of an unassuageable thirst. In neither account is there
any mention of a rash or skin eruption, unless the phrase ‘rapid spread all
over the frame’ implies a visible manifestation. Like the Athenian
plague, the place of origin is said to have been Ethiopia, from where it
passed to Egypt and the Roman colonies in North Africa, which was the

17
granary of Rome. In this respect the Plague of Cyprian resembles the
Plague of Orosius in the year 125, an example of the famine-pestilence
sequence, preceded by an invasion of locusts that destroyed the north
African cornfields. Cyprian’s mention of gangrenous hands and feet
tempts one to think of ergotism as the cause. Epidemic ergotism,
produced by eating bread made from rye infected with the Claviceps
fungus, has certainly occurred quite frequently but there is little evidence
that rye, a crop of the north rather than of the south, was a staple bread
corn in Rome. The very broad spread and longevity of the Plague of
Cyprian are also arguments against the theory.
The Plague of Cyprian resembled the ‘Spanish flu’ of 1918-19 in
producing a pandemic – at least in the sense of affecting all regions of
the world then known to the West. It advanced with great speed, not only
by human-to-human contact but by means of clothing or any article used
by the sick. The first devastating appearance was followed by a
remission which ended with a renewed epidemic of equal violence.
There was a seasonal incidence, outbreaks starting in the autumn, lasting
through winter and spring, and fading out with the coming of hot
weather in summer: a cycle suggestive of typhus fever. Mortality is said
to have been higher than in any previously recorded pestilence, the
deaths of infected persons outnumbering those who survived an attack.
The acute phase of the Plague of Cyprian lasted for sixteen years, during
which time a general panic developed. Thousands fled from the
countryside to overcrowd the towns and so caused fresh outbreaks, and
wide areas of farmland reverted to waste; some thought the human race
could not possibly survive. Despite war in Mesopotamia, on the eastern
frontier and in Gaul, the Roman Empire managed to surmount the
catastrophe. However, by the year 275 the legions had fallen back from
Transylvania and the Black Forest to the Danube and the Rhine, and the
situation appeared so dangerous that the Emperor Aurelian decided to
fortify the city of Rome itself.

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 It is likely that after the acute phase the infection persisted as a
slightly less virulent illness. Throughout the next three centuries, while
Rome slowly collapsed under pressure from Goth and Vandal, there were
recurrent outbreaks of similar pestilence. Gradually the evidence
becomes more blurred, degenerating into a story of generalized war,
famine and sickness, as the darkness descended over Rome and her
mighty empire disintegrated. The Germanic peoples crowded into Italy
and Gaul, crossing the Pyrenees into Spain, and even into North Africa
where an epidemic so weakened the Vandals themselves in 480 that they
were unable to resist a later invasion by Moors. There are rumours of
great mortality in Vienna around 455 and in Rome itself in 467.
Major sickness also afflicted Britain in the year 444. According to
Bede, mortality was so great that barely enough healthy men survived to
bury the dead, while the pestilence depleted the forces of the Romano-
British chieftain Vortigern to such an extent that he was unable to cope
with the incursions of the Picts and Scots. Legend relates that, after
consulting with his fellow-chieftains, Vortigern decided to seek help
from the Saxons who arrived in 449 as mercenaries under Hengist and
Horsa. Thus epidemic disease may well have made a major contribution
to the eventual success of a broader infiltration that created an Anglo-
Saxon society and culture.
Meanwhile a new Roman Empire had arisen in the East. Asia
Minor had been annexed by Rome in the first century BC. In AD 330
Constantine the Great founded an eastern capital at Byzantium
(Constantinople, now Istanbul). The combined Eastern and Western
Empires lasted about a hundred and fifty years. Then the Western portion
disintegrated, even while the Byzantine one survived in the East until its
overthrow in 1204 by the Latin forces of the Fourth Crusade. During the
sixth century Justinian, perhaps the greatest of the Byzantine rulers, had
almost succeeded in implementing the aspiration to resurrect Rome and
to reunite the two halves of the old empire. He launched an attack to the

19
west in the year 532. He recaptured Carthage and much of the north
coast of Africa, retook Sicily and crossed to the mainland of Italy. Naples
fell to his general Belisarius while undefended Rome and most of central
and southern Italy were captured by the imperial armies. By 540 it
seemed that Germanic resistance had been broken. Justinian, having also
recovered part of Spain, formed a bold plan to carry his conquests into
Gaul and even into Britain.
His victories brought no lasting gain. The Moors drove the
Byzantines from most of the newly won African seaboard and in 541 a
brilliant young Goth leader, Totila, recaptured the greater part of Italy.
Totila was willing to make terms with Justinian but the emperor had
determined upon total reconquest. There followed eleven years of bitter
warfare in which Rome underwent siege five times. During one of these
sieges the Goths cut the aqueducts in an attempt to force surrender.
Subsequent medieval squalor and uncleanliness partly derive from this
action because Rome, with its magnificent architecture and historical
prestige, never wholly lost its influence upon European lifestyle. If the
city had still possessed a functioning and plentiful supply of clean water,
other European cities might well have followed its example.
The reign of Justinian should have been a time of imperial
splendour. He girdled his domains with a defensive chain of castles and
forts, and erected many fine buildings, including the cathedral of St
Sophia. His code of laws, embodying those of ancient Rome, formed the
basis of European justice for centuries to come. He recruited well-trained
armies commanded by successful generals such as Belisarius and Narses.
Yet during his long reign the Huns very nearly succeeded in taking his
capital, the Slavs captured Adrianople and the Persians sacked Antioch.
His government, which had begun in a blaze of glory, steadily declined.
When Justinian died in 565 at the age of eighty-three, he left his empire
considerably poorer and weaker than when he had mounted the throne in

20
527. For in 540, the year of his greatest success, an enemy more terrible
than Goth or Vandal had been about to strike.
The Plague of Justinian is one of the most lethal to have ever
emerged. We learn something of it from the account written by
Procopius, the secretary or archivist of Justinian’s reign. The first known
cases were reported in 540 at Pelusium in Lower Egypt from where the
infection spread throughout Egypt and also into Palestine, which then
seems to have been the focus of diffusion to the rest of the known world.
Constantinople was first infected in the spring of 542. The mortality was
not initially great but rapidly increased as the summer advanced until
some ten thousand people were dying each day. Graves could not be dug
quickly enough, so roofs were taken off the towers of forts, the towers
filled with bodies and the roofs replaced. Ships were also loaded with the
dead, rowed out to sea and abandoned.
This is also the first time that we can correctly use the term
‘plague’, for the sickness was undoubtedly a manifestation of its bubonic
form. Victims were seized with sudden high fever. On the first or second
day the typical buboes – swollen glands – appeared in the groin or
armpit. Many patients became quickly comatose, others developed a
violent delirium in which they saw phantoms and heard voices
prophesying death. Sometimes the buboes broke down into gangrenous
sores and the sufferer died in terrible pain. Death usually occurred on the
fifth day of illness or even more quickly, but it was sometimes delayed
for a week or two. Physicians could not prognosticate which cases would
be light and which fatal. They were quite useless for there was no known
remedy, and by the end of the epidemic some 40 percent of the
population of Constantinople were dead. Procopius makes two
particularly interesting points. First, the plague always started on the
coast, and spread inland. Second, contrary to expectation, doctors or
attendants who nursed the sick and laid out the dead seemed not to fall
victim any more frequently than others.

21
 The plague returned repeatedly, lasting until the year 590. It spared
no town or village, ravaging the most remote settlements. If a region
congratulated itself on having escaped, the plague would surely appear in
due time. As in the Plague of Cyprian, there was a seasonal rise and fall
in intensity, but whereas the first reached its height in winter, that of
Justinian caused the greatest number of deaths in the late summer
months. Gibbon states that entire countries never regained their previous
density of population. Procopius makes the observation, found in many
plague chronicles, that the depravity and licentiousness during and after
a visitation suggested that only the most wicked survived.
The extent to which disease contributed to the downfall of Rome
and to the wreck of Justinian’s ambitions must remain an open question.
Incurable infectious illness is no respecter of persons but impartially
attacks the highly civilized and the less civilized. The city-dweller is at
higher risk than the countryman and, in a mortal epidemic, a closely-knit
organization will disintegrate more swiftly than a looser association. Of
supreme importance is the fact that failure of morale is more likely to
occur among those who have lived softly than among people who have
known hardship throughout their lives. Thus, although pestilence may
have seriously affected the fighting spirit of savage tribes, its impact
upon Roman and Byzantine life was likely to have been very much
greater. When we consider the frightful sequence of pestilences that
smote the empire during the time of its decadence we need hardly search
for a more potent contribution to disaster.
Besides undermining the Roman state, the pestilences of the first
three centuries AD produced two far-reaching and long-lasting effects
which are less widely recognized. First, Christianity would hardly have
succeeded in establishing itself as a world force and would certainly not
have taken the form that it eventually did if the Roman Empire had not
been ravaged by incurable disease during the years which followed the
life of Christ. Second, the thousand-year development of medicine from

22
the fourth to the fourteenth century would have been very different had
its practice not fallen under the domination of the Christian Church. To
understand what happened we must go back to the beginning of
European civilization, when priest and doctor were one and the same.
In the early days of Greek legend the god Apollo killed a
venomous snake, a symbol of disease. By this act he became regarded
not only as the god of health but also as the bringer of pestilence which
he visited on mortals by his arrows. He must therefore be both
worshipped and placated. Apollo passed the secrets of his healing
powers to the centaur Chiron who in turn instructed Asklepios or
Aesculapius. The latter, possibly confused with a human healer living
around 1250 BC, also became honoured as a god and was worshipped in
temples scattered throughout Hellas.
The cult of Aesculapius grew and developed into the ritual of
incubation or temple-sleep. Patients made a sacrifice to the healing god
and purified themselves by bathing (lustration). Then they lay down to
sleep in a long open corridor where Aesculapius himself might appear in
a dream and give advice, or the god’s sacred serpents might effect a cure
by licking sores. In later years the magical temple-sleep was reinforced
by physical therapy consisting of exercise, diet, massage and bathing.
Many patients stayed for weeks or months in the temple, which
developed into something closely akin to the nineteenth-century
‘hydropathic’. Treatment was no doubt equally successful in both.
The Greeks initiated the ‘scientific approach’. Pythagoras (c.530
BC) is the father of mathematics but he also founded a system of
medicine. His pupils enunciated the doctrine of the four elements – earth,
air, fire and water – and produced theories of respiration, sight, hearing
and brain function. Their teaching was elaborated in a collection of
writings attributed to the physicians of Cos, or ‘Coan school’, of which
Hippocrates (c.460-377 BC), often regarded as the Father of Medicine, is
by legend the founder. This ‘Hippocratic Corpus’ developed the theory

23
of humours from the theory of elements and tended to deny that disease
was a punishment sent by the gods.
By the mid-fourth century BC Greek medicine had ceased to be
mere magic and had acquired a rational basis, but how far this ‘scientific
approach’ affected actual practice must remain problematical. The Coans
cannot have been only theorists for they described recognizable diseases
and the results of logical treatment. But the cult of Aesculapius certainly
survived the age of Hippocrates and it is noticeable that the latter was
reputed to be a direct descendant of the former. The so-called ‘Coan
school’ was more probably an association of physicians than a teaching
unit and it is unlikely that their theories spread widely or exerted much
immediate influence.
That last point is important in the story of Roman medicine.
According to Pliny the Elder, writing in the mid-first century AD,
Romans got on very well without doctors for six hundred years. Yet there
was medicine of a kind. The head of a household treated his family with
folk remedies and sacrifices to the appropriate gods. Both Apollo and
Aesculapius had their votaries, for Rome borrowed from all countries,
but citizens also recognized a number of native demigods, many of
whom were associated with sickness or bodily functions. So many were
there that it has been said that Romans possessed an appropriate deity for
every part of the body and for every kind of illness, and that each god
must be placated by his or her particular and exact ritual. This made the
doctor’s problem rather simpler than it is today: if the cure did not occur,
the wrong god had been invoked or the incorrect rite performed.
Practice of medicine was beneath the dignity of Roman citizens.
Their early physicians were slaves of Greek extraction. About 220 BC
Archagathus, the first of those identifiable by us, appeared in Rome. He
was followed by many others who seem to have been more interested in
money than in their patients’ welfare. In the first century BC Julius
Caesar granted these slave-physicians their freedom. Their standing

24
improved under Augustus but, so far as is known, medical practice
tended to remain in the hands of foreigners. When the great epidemics
struck Rome, its citizens could call only on their ancient gods or Greek
physicians. Neither were outstandingly successful, so it is not surprising
that the Romans sought help elsewhere.
Because of her contacts with foreign nations and because the
empire embraced so many peoples, Rome sheltered and tolerated a great
variety of religions. Not only did it have its own domestic gods but it
honoured others from Greece and the East. For instance, Mithra, the
most popular deity among the legionaries, originated in India or Persia.
Among the conquered peoples whose religion exerted influence were the
Jews. Small Jewish communities settled throughout the length of the
Mediterranean seaboard and the number greatly increased after the
Diaspora following the Roman destruction of the Temple at Jerusalem in
AD 70.
These Jewish communities were renowned for their moral code,
their upright dealing, their charity and their care of the sick and poor.
Many Gentiles found themselves attracted to their way of living but
disliked certain practices such as circumcision and the refusal to eat meat
that had been offered in sacrifice. The more liberal Jewish communities
accepted Gentiles without insisting that they followed these customs.
They were allowed to attach themselves to the synagogue and form an
outer circle known as ‘God-fearers’. The earliest Christian missionaries,
among them the apostle Paul, found their first converts among these
‘God-fearers’ and it was in such para-Jewish congregations that the
Christians of the Roman Empire established themselves. This is why,
when the emperors insisted on their own unique divinity, the
monotheistic Jew and Christian were regarded as one and the same for
the purposes of persecution.
During much of the first century AD the apostles, the immediate
followers of Christ, were still living and his story was passed by word of

25
mouth. Eventually the basic pattern of Christian doctrine began to be
summarized in creeds and the text of the New Testament. The gospels
contain accounts of a number of ‘miracles’. Twenty of these are
described by St Luke, and only three are not of a medical nature. In four
cases unclean spirits are cast out; in two the dead are restored to life; and
in eleven sickness or disability is cured. In addition, Luke states: ‘He
called the twelve [apostles] together and gave them power and authority
over all devils, and to cure diseases.’ This authority was later extended to
the seventy disciples. The miraculous and divine healing power
attributed to Christ was thereby transferred to his main followers.
As we have seen, the second century AD was a time of epidemic
sickness. To the terror-stricken victims Christianity offered new hope.
There was the promise of physical resurrection after death, coupled with
the surety of everlasting bliss for the sinner who truly repented. Perhaps
above all, the miracles credited to Christ and the healing powers claimed
by his followers were an earnest of divine intervention that might cure
sickness and even defeat death itself. Thus the growth of the Christian
Church was aided by its specific medical mission in a series of
pestilences. By the middle years of the third century the small and
scattered Christian communities had coalesced into an established
Church, through a process greatly accelerated by the Plague of Cyprian
and Cyprian’s teaching. Conversions were more numerous during times
of famine, earthquake or pestilence. At the height of the Plague of
Cyprian he and his fellow-priests in North Africa baptized as many as
two or three hundred persons a day.
So was formed the cult of Christ the Healer. The late-third-century
persecutions of Diocletian failed to stamp out Christianity, and it
received imperial sanction from Constantine the Great in 313. At the end
of the fourth century it became the official religion of the empire after
Theodosius enacted his laws against paganism. Practice of medicine
passed into the hands of the Church, with priest and doctor again

26
becoming one under the Byzantine emperors. The Christian followed the
Jew in medical caring. Sick-nursing formed one of the seven duties of
Christians and, as communities dedicated to the purpose appeared, the
infirmary formed an essential part of their lives. Early churches and early
hospitals were designed on the same plan: a central altar with two or four
long naves or wards leading from it with a number of smaller side-wards
or chapels, each under the patronage of a saint. Treatment in these
hospitals was undertaken by priests, assisted by lay brothers and sisters,
all of whom combated disease almost wholly by appeal to supernatural
agency.
The approach of the Byzantine and medieval ‘doctor’ was
essentially the same as that of the modern Christian Scientist. Disease
was a punishment incurred by sin, a lapse from the purity of Christian
life. The cure, if God decided to effect one, could only be by miraculous
intervention. But such cure did not necessarily come from God alone.
Just as the pagan gods of early Rome had intervened to cure disease, so
the demigods or saints of the Christian Church could be invoked to
perform the miracle. In fact many of the Roman gods and the early
Christian saints were one and the same, a few with almost unchanged
names. Thus Febris, the Roman goddess of fever, became the Christian
St Febronia. Others enshrined the Christian concept of death,
resurrection and a second death. Notable in this particular context are the
two ‘medical’ saints Cosmas and Damian. They might be regarded as the
patrons of transplant surgery, since they are recorded as having
succeeded in grafting a new leg to replace an injured one. It is claimed
that, accused of sorcery, they were stoned to death but miraculously
restored to life, only to suffer a second death by decapitation.
The legend of St Sebastian is of special interest, although his story
is now regarded as mythical. He is supposed to have commanded a
company of the Emperor Diocletian’s Praetorian Guard but secretly
became a Christian. He converted others, including two noble youths.

27
Marcus and Marcellinus. The two youngsters were accused and
confessed under torture their new religious allegiance. They were
condemned to death and their parents implored them to recant but
Sebastian dissuaded them. Impressed by such steadfastness, their guards
and their judges were all converted to Christianity and suffered death in
the year 288. Diocletian himself urged Sebastian to recant, but he refused
and was condemned to be shot to death by arrows. Left for dead, he was
found by Irene, the mother of the two boys, who nursed him back to
health. Despite being begged to leave Rome, Sebastian stationed himself
at the city gate and pleaded with Diocletian for the lives of his fellow-
Christians. Diocletian ordered him to be flogged to death. His body was
flung into the Cloaca Maxima, but it was found and buried in the
catacombs. The church of St Sebastiano marks the site.
The cult of St Sebastian as the patron of epidemic sickness started
about the year 680. The earliest representations depict him as an elderly
bearded man, fully clothed, turning aside an arrow with a fold of his
cloak. Later pictures show him as a youth of great physical beauty, naked
except for a loin cloth. Often an arrow pierces his groin, suggesting an
allusion to bubonic plague. The inference is that Sebastian has become
identified with the beauteous Apollo. There is also the symbolism of the
arrow. Those fired by Apollo conveyed disease. By miraculously
surviving, Sebastian became empowered to protect and restore those who
had been so attacked. His legend is indicative of the ways in which
Christian treatment of disease borrowed from Graeco-Roman practice.
The sacrificial offering to the god became the votive offering to the saint.
The temple-sleep or incubation remained unchanged, but in their dreams
the devotees looked for the appearance of saintly healers. Ritual
purification formed an essential part of Christian treatment but in time
became degraded from beneficial cleansing of the body into a ceremonial
sprinkling with ‘holy water’.

28
 So the cult of Christ the Healer became essential to the work and
faith of the early Church, and to the development of a new system of
medicine. In effect, its practitioners were psychiatrists and faith healers
rather than physicians. For a thousand years they depended primarily
upon supernatural intervention and only secondarily upon mundane
treatment. Most of that treatment itself was plain magic: swallowing of
written prayers or fragments of saintly bone, penitence, fasting and
votive offerings. But there did also exist a more solid foundation of
psychological medicine and some rational basis of medical theory, of
anatomy, and of herbal remedies. During the second century AD it was
Galen who became the principal authority and unchallenged teacher
within this Christian tradition of medicine. Though he did not directly
profess the faith, he seems to have defended Christianity and preferred
monotheism to the Roman welter of demigods. Born in 129 at Pergamos
in Asia Minor, Galen was appointed surgeon to the gladiators of that
town and later moved to Rome. Here he practised and taught medicine,
conducted scientific experiments and produced a huge quantity of
treatises. He is reported to have fled the city during the plague that bears
his name, but he was recalled by Marcus Aurelius and died at Rome in
216. A forceful and dogmatic teacher, he achieved a great and lasting
reputation, not least as a means by which Hippocratic medical thinking
was transmitted to future generations. He made many advances in
anatomy and physiology but he fouled earlier and simpler methods of
herbal treatment with a huge collection of noisome and useless remedies.
Hence came the vile mixtures, often containing as many as fifty
ingredients, that survived into the medieval period.

29
 For more than a thousand years the lamp of Greek medicine
flickered on in scattered monasteries and in those other islands of culture
that successfully withstood the general decline which followed the end of
Imperial Rome. On the other side of the Mediterranean, in Alexandria,
the school of the so-called Arabian physicians, many of them Jews and
Christians, also added to the art of medicine. They, too, had learned from
the followers of Christ, deriving knowledge from the congregation of
Nestorius, Christian Patriarch of Jerusalem, who had been banished as a
heretic in 431. The Arabs revered Galen but, more liberal than the
Christians, they questioned, tested and recast his theories. In the end the
two schools merged into one, but this was not to happen fully until a
change in habits of thought ushered in the Renaissance around the
beginning of the fifteenth century. By that time Church domination of
medicine had become oppressive and the influence of Galen had waxed
so great that to challenge his authority was no less than heresy.

30
 C T
THE BLACK DEATH

The most destructive pandemic in the history of Europe occurred in the

years 1348–61. This was a visitation of bubonic plague which much later
became generally known as the Black Death. We shall continue to apply
this familiar label to the fourteenth-century outbreak, while reserving the
word ‘plague’ to cover later epidemics such as that which afflicted
London in 1665.
The word ‘bubonic’ refers to the characteristic bubo or enlarged
lymphatic gland. Bubonic plague is primarily a disease of rodents and is
passed from rat to rat by the fleas which commonly infest them. The flea
bites an infected rat and ingurgitates plague bacilli with the blood. These
bacilli can remain in the flea’s intestinal canal for as long as three weeks
and are regurgitated when the flea bites another rat or a human. In true
bubonic plague the human will become infected only if fleas migrate
from rodents to humans or from an already infected human to another.
Bubonic plague is not carried by human breath or direct contact.
The common source of infection is the black rat (Rattus rattus),
sometimes known as the Old English Rat. This animal is companionable
with man. It is rather a handsome beast with silky black fur and, unlike
the brown rat, tends to live in houses or ships rather than in farmyards or
sewers. This companionship with man assists migration of fleas from
rats to humans and so permits spread of bubonic plague. The disease,
whether of rat or man, carries a very high mortality among those
infected, a figure of 90 per cent having been recorded in some epidemics
and 60 per cent being regarded as ‘normal’. The causative bacterium,
Pasteurella pestis, now known as Yersinia, rapidly multiplies in the

31
bloodstream, causing a high temperature and death from septicaemia
(blood poisoning). But only relatively few human cases will occur in
epidemics of true bubonic plague because transmission requires heavy
infestation with fleas.
So far the story suggests a very dangerous illness, not common,
occurring in isolated cases or small sporadic epidemics. But in certain
circumstances, the nature of which is unknown, the infection will assume
a pneumonic form which does not require the bite of a flea to infect the
human but can be transmitted directly from one person to another by
breath or by contact. Both forms existed together in the great pandemics,
but it is the pneumonic type which produces a very rapid and wide
spread, a higher incidence of cases and, since the pneumonia is usually
fatal, a larger mortality.

Bubonic plague was rarely, if ever, absent from Europe during

the period 1348–1666, but even over a longer time span only four world-
wide pandemics are known. These are the Plague of Justinian, AD 540–
90, which may possibly have extended as far as England; the Black
Death of 1346–61, reaching England in 1348; ‘the Great Plague’ of the
1660s; and a pandemic starting in Asia in 1855 which caused high
mortalities in Canton, Hong Kong and Russia, reaching England in 1900
where a few deaths occurred in Glasgow, Cardiff and Liverpool. During
this last pandemic the Japanese physician Ogata Masanori noted such a
huge mortality of rats that he gave bubonic plague the name of ‘rat-pest’.
The pneumonic type developed in China and probably Russia, but the
rat-flea-man form dominated in Europe.
In the Plague of Justinian and the Great Plague the pandemic
started as a rat-flea-man infection. The spread was inland from the coast
and those who attended the sick were at little greater risk than those who
did not. In sixth-century Constantinople the number of cases was small at
the beginning but very rapidly rose until the number of deaths was too

32
great for proper burial. A similar pattern is seen in the 1665 Plague of
London. Samuel Pepys noted two or three houses in Drury Lane marked
with a red cross on 7 June. From the end of the first week in June until 1
July the deaths from plague recorded in the Bills of Mortality are 100,
300, 450. Thereafter the rise became increasingly steep, reaching 2,000
in the last week of July, 6,500 at the end of August, and over 7,000 at its
peak, the third week in September. The estimated population of London
in 1665 was 460,000 and plague was rarely entirely absent from the city.
A rise in the death rate from 200 to 300 a week can be attributed to an
increase in the number of infected rats but a mortality of thousands
indicates a direct human-to-human infection. Thus at some point in the
Plague of Justinian and the Plague of London the type of illness must
have changed from true bubonic plague to pneumonic. The same must be
true of the Black Death.
The Black Death almost certainly started in Mongolia. An
infected Tartar horde carried it to the Crimean isthmus, where the Tartars
besieged a small company of Italian merchants in the trading post of
Caffa, now known as Theodosia. According to one account, plague
broke out in Caffa itself, no doubt carried by rats, in the winter of 1346–
7. A second story relates that it was deliberately introduced by the
Tartars throwing infected corpses over the walls. Both sides suffered so
many deaths that the Tartars raised the siege. The horde dispersed,
carrying plague to the lands around the Caspian Sea from where it spread
north to Russia and east to India and China, which was first infected in
1352. The surviving Italian merchants escaped by ship to Genoa. The
chronicler Gabriel de Mussis declared that no case of plague occurred on
the voyage but that it broke out in a deadly form a day or two after the
ship docked. His statement suggests a rat-flea-man infection.
From the European focus in Genoa, plague travelled in a great west and
north half-circle through Italy, France, Germany and Scandinavia,
reaching Moscow in 1352. The devastation was terrible. Historians have

33
reckoned that some twenty-four million people died: about a quarter of
the European and West Asian population. It should be mentioned here
that the havoc wrought in the Scandinavian countries may ultimately
have had a greater effect on world history than almost any other event.
Ships carried the infection to the Greenland settlements originally
founded by Eric the Red in AD 936. These colonies were so weakened
by the plague and by failure of supplies from enfeebled Norway that they
were wiped out by Inuit attacks. The last Viking settlers disappeared in
the late fourteenth century and Greenland became unknown country until
it was rediscovered by John Davis in 1585. It is thought that the Viking
settlements maintained sporadic contact with ‘Vinland’, part of the coast
of Canada or Newfoundland, so the Black Death may have entirely
altered the history of North America.
The Black Death arrived in England about 24 June 1348,
probably carried by a ship from Gascony which docked at the small port
of Melcombe, now part of Weymouth in Dorset. Infection seems to have
remained local and in the bubonic form until early August. From
Melcombe the plague travelled by land and sea, coastal vessels bringing
infection to ports on the south-west coast and along the Bristol Channel.
It moved overland through Dorset and Somerset with increasing speed,
reaching the great port of Bristol, either by sea or by land, on 15 August.
The citizens of Gloucester, learning of Bristol’s plight, tried to prevent
infection by cutting off all communication, but their efforts were in vain.
From Gloucester the plague passed to Oxford and on to London,
reaching the city about 1 November. Westward spread through the
sparsely inhabited counties of Devon and Cornwall was slower, for the
plague did not reach Bodmin in central Cornwall before Christmas. By
then the whole diocese of Bath and Wells, covering the counties of
Dorset and Somerset, had been infected, for on 4 January 1349 the
Bishop wrote of a great mortality and of many parishes left without a
priest to administer the sacraments.

34
 There now came a short respite during the winter months when
rats, fleas and fourteenth-century humans all tended to be less active.
Oxford, infected before November 1348, did not experience its highest
mortality until May 1349. London suffered only a few deaths during the
winter but the number increased rapidly in March, rose to a peak in April
and May, then gradually declined. From London the main route led
through the highly populated eastern counties, Norwich being infected in
March and York towards the end of May 1349. By now the whole of the
south, east and midlands of England had been attacked and the rate of
spread slowed in the more thinly populated north and extreme west.
Ireland received infection by sea in 1349 but Wales and Scotland were
not attacked until 1350. Scotland might possibly have escaped altogether,
had the Scots not decided to take advantage of England’s difficulties by
invading in the autumn of 1349 when mortality was at its greatest in the
northern counties. Plague broke out in the Scottish army encamped near
Selkirk and was dispersed over the country as the soldiers returned to
their homes.
No one knows how many died in the terrible year of 1348–49.
There were no Bills of Mortality as in the Plague of 1665. no Domesday
Book, no census. No one in the fourteenth century was able to estimate
large numbers, to strike a gross figure from investigation of a random
sample. The situation is further complicated by the fact that the Black
Death did not occur as a single visitation. There were recurrent
epidemics on four or five occasions before the end of the fourteenth
century. The worst of these, in 1361. infected England, France and
Poland, among other countries. The name Pestis puerorum, given to this
outbreak, may provide a first clue, for it suggests the presence of an
abnormally high percentage of children in 1361, as would be the case if
all age groups had suffered an unusually high mortality thirteen years
before.

35
 Another clue is provided by the Poll Tax levied across England in
1377. The evidence surrounding this suggests a population in the range
of 2.5 to 3 million. Since the best estimates of the population in 1347
range from 4.5 to 6 million, the number seems to have dropped by 2
million or more in thirty years. The population had risen steadily
between the Norman Conquest and 1300. There was also a fairly
continuous increase from the end of the fourteenth century until a figure
of 3 million or so for England and Wales was again reached in the
middle of the sixteenth century. In both cases the rise can only have
occurred because the live-birth rate outstripped the death rate. Ordinary
disease, including outbreaks of epidemic illness, caused deaths
throughout the whole period from 1066 to 1550 and, as the normal
process of death continued, so did the normal process of birth. Thus a
shrinkage of at least 2 million during roughly thirty years between the
Black Death and the Poll Tax can only have been due to an abnormally
large mortality. Since a great diminution of fecund adults would prevent
a rising birth rate, it is safe to assume that maximum mortality occurred
at the beginning of the period.
It is necessary to emphasize these rather dull facts because of a
recent tendency to dismiss the Black Death as ‘just another epidemic’,
causing at most the death of one in ten of the population. Far more
probable is a mortality that exceeded one-third of the English people.
This in itself is certainly high enough to dictate a social change, but it is
the particular pattern of mortality as well as the total number of deaths
that caused the major social upheaval of the late fourteenth century.
Statistical evidence is scanty but a few monasteries recorded figures.
Christchurch, Canterbury, experienced only four deaths out of eighty
inmates, almost certainly from causes other than plague. The great
Abbey of Crowland is another which seems to have entirely escaped,
although its estates suffered badly. At the other end of the scale are
Luffield Priory which lost all its monks and novices, St Mary Magdalen

36
at Sandon where all perished, and a nunnery at Wolthorpe with only one
surviving sister. Between the two extremes are eleven houses, the largest
group in the series, which lost over 75 per cent, nine with mortalities of
between 50 and 75 per cent and only three which record a death toll from
plague of less than 50 per cent. Although this evidence is slight, it is a
fair assumption that there was some resemblance between the varying
mortalities of monasteries and those of town and village communities.
This pattern accords with the known behaviour of the pneumonic
form of plague. There was considerable variation in the incidence of
infection, and so of mortality, throughout England and Europe. The
crowded walled towns would obviously have been at high risk. Density
of population and ease of communication determined both incidence and
rate of spread. In the thickly populated eastern counties of England,
where villages lay close together and roads had been maintained for
wagon traffic, the death toll must have been large. Inland waterways and
coastal shipping would both have favoured rapid dissemination. In the
more thinly populated north and west of Britain, and to a lesser extent in
some southern counties, there must have been wide areas which escaped
entirely, simply because of bad communications. But in 1348 the riches
and the greater part of the English people were concentrated in the
eastern and midland counties. A high mortality here would have exerted
so profound an effect that the relative freedom from disease of large
tracts, partly composed of forest and waste, can be almost discounted.
We must bear in mind this variation in the pattern of death when
we consider the effect of the appalling mortality on English history. The
impact upon England was greater than it was upon any other European
country. The reason is that the English social system was already
showing signs of strain and the Black Death greatly accelerated collapse.
In Europe the system was more rigidly enforced and survived for many
years. At the beginning of the fourteenth century England was still
governed by the feudal system, of which it has been said that everything

37
ultimately belonged to someone else. The great lord held his lands from
the king, the knight held his manor from the lord, the village landowner
from the knight, and the peasant or villein from the village landowner.
Rental was paid by service. Thus the baron owed so many knights to the
crown, the knight so many men-at-arms to his lord, while the peasant
was forced to work so many days on his lord’s land before he might
cultivate his own. This, of course, is an oversimplification, for the
system was far more complex and less complete in practice. One
complication was the existence of money. So long as money was in very
short supply and confined to the ruling class, the basic principle could be
fairly widely applied. But, when coin entered into more general
circulation, there developed a tendency to commute service for cash. The
lord stayed at home instead of leading his knights, the knight found it
more profitable to leave his farmers to till his land and pay a small force
of professional soldiers, even the peasant sometimes managed to
commute his service for a money rental or to demand a wage for
additional labour. A growing population brought into being a quite large
class of landless workers and these had to be paid in coin for their work.
Thus an increasing flow of money weakened feudalism. The
thirteenth century saw a great agricultural boom and this led to an excess
of crops above the level necessary for national subsistence. The upper
classes and especially the Church, now the largest landowner in the
country, devoted themselves with energy and intelligence to the business
of farming. Trade and industry had both developed since the days of
Norman invasion, but agriculture remained the predominant and most
gainful occupation in England.
By the end of the thirteenth century more land in England had been
brought under the plough than ever before and possibly than ever since.
England had become a grain-exporting country, sending a steady supply
of bread-corn – wheat from the south, barley and oats from the north – to
the Continent in the small ships of her merchant fleet. This corn had to

38
be collected in centres, the market towns and manorial barns, before
being carried by wagon to the ports. The heavy wagons demanded well-
maintained roads, and it is for this reason that the road system of
England, largely Roman in origin, was in better condition in 1300 than at
any time until almost the end of the eighteenth century. The agricultural
boom allowed a good standard of living and this, in turn, affected the
live-birth rate and expectation of life. Population, which had fallen since
the end of Roman occupation, steadily increased from the Norman
Conquest until the last years of the thirteenth century.
Corn exports allowed not only luxury imports but an increase in
coin. Because of a flourishing agriculture and a wider distribution of
money, there was considerable buying and selling of land by free
peasants and exchange or leasing by the unfree as early as the thirteenth
century. But the fact that a peasant possessed money did not necessarily
mean that he could become a free man. His chances of freedom
depended upon local conditions. Generally speaking, it was easier in the
north, which was more remote from the Continental market and where
there was less arable land requiring a large labour force.
Already by the late thirteenth century the basically simple
structure of the feudal state had been complicated by a number of
variants. The greatest weakness and the greatest danger to stability lay in
the anomaly that the poorer peasants of the less highly cultivated areas
had the better chance of freedom, while the relatively wealthy peasants
of the predominantly arable counties found their bondage increased. A
further danger lay in the very fact of prosperity. A glut of labour and a
shortage of arable land developed in the cultivated area around
increasingly highly populated settlements with the result that arable
gradually extended on to marginal ground unsuitable for corn. Then,
about the year 1290 something happened, though opinion is divided as to
what that something was. Perhaps a long period of continental weather,
hot summers and cold winters, gave place to a wetter and less extreme

39
Atlantic system. Perhaps continual arable farming on marginal land,
without adequate manuring or proper rotation, so exhausted the soil as to
make corn-growing uneconomic. Sheep, which assumed the first place in
agricultural economy during the fifteenth and sixteenth centuries, had
already become a quite important branch at the end of the thirteenth, at a
time when shortage of manpower had not yet dictated a type of farming
requiring only a small labour force. Whatever the underlying reason may
be, recession had begun in the early years of the fourteenth century,
followed by a fall in the standard of living and of population growth.
Failure of a harvest resulted in widespread starvation. Only the
able-bodied could hope to live through a long period of extreme scarcity
until the new harvest brought fresh supplies. The very young and the
elderly died of frank malnutrition or of intercurrent disease against which
their enfeebled bodies could offer little resistance. The ills of damp and
cold, particularly lung infections, must have carried off many older
people and young children at these times, symptomatic of a general
diminution of resistance which rendered the whole community more
liable to attack by infectious disease. There is only one record, in 1257–
9, of major famine sickness (possibly typhus fever) during the
agricultural prosperity of the thirteenth century, but there seems to have
been a series of poor harvests from about 1295 onwards culminating in
the great famine of 1315–16.
A change to dairy farming and meat production was impossible
because of the difficulty of keeping beasts through the winter. The
standard of living of the peasantry therefore generally declined with a
resultant fall in the live-birth rate. The peasant’s economic position was
further weakened by the war against the Scots in 1296 and by the
Hundred Years War against the French, which began in 1337. The
continental campaigns of Edward III, especially, could not be sustained
by feudal levy and demanded paid or ‘indentured’ troops whose cost
ultimately fell upon the man who tilled the soil.

40
 Thus in the year 1347 the outwardly stable structure of the feudal
system had developed a number of cracks, the economy of the realm was
shaky and the subsistence of the peasantry lay at the mercy of the
harvest. A network of fairly good roads linked inland communities to the
Channel and North Sea ports. A stream of fighting men passed
backwards and forwards across a short sea route to the battlefields of
France. Given the sequence of a bad harvest, a famine-stricken people
and a pestilence on the European continent, spread of disease throughout
England was inevitable.
Men generally look back on world-shaking events and remember
that they were preceded by signs and wonders in the heavens. There are
reports of earthquakes, volcanic eruptions and even tidal waves in the
years immediately preceding the Black Death but these, if they occurred,
are coincidental. The one recorded antecedent that did affect the course
of the pestilence is a quite appalling weather pattern which seems to have
been general throughout Europe during the years 1346–8. The series of
three abnormally wet and cold summers culminating in that of 1348,
when it is related that rain fell unceasingly from midsummer until
Christmas, imply a period of prolonged dearth with consequent
malnutrition, illness and a reduced resistance to infectious disease.
So there can be little wonder that the immediate effect of the
Black Death in England was a general paralysis. Trade largely ceased
and the war with France was halted by a truce on 2 May 1349 which
lasted until September 1355. In 1350 the death of so many able-bodied
men put the realm in danger, and coastal towns were required to supply
men-at-arms, ships and sailors from their already depleted resources. The
cornfields had been sown or were being sown while the plague gathered
momentum and a much smaller labour force reaped the harvest in 1349.
Those who survived encountered unwonted prosperity: there was more
money per head, more livestock, more grain. Prices fell steeply because
it was a buyer’s market. A good horse which had been worth forty

41
shillings now fetched only sixteen, a fat ox could be bought for four
shillings, a cow for one shilling, a sheep for fourpence. Wheat, which
had been as cheap as sixteen pence a quarter in some of the boom years
and as dear as twenty-six shillings in the famine of 1315–16, now sold at
a shilling a quarter.
The urgent need to reap the harvest in the autumn of 1349
induced landowners to offer high wages. In the eastern, midland, and
southern counties reapers and mowers are said to have received at least
double their accustomed wage. The diet of the surviving labourers
became unusually good as a result of all this plenty. These are the days
of which William Langland wrote that Hunger was no longer Master,
when beggars refused bread made from beans and demanded milk loaves
or fine white wheaten bread and the best brown ale. Day labourers, who
had once been content to eat stale vegetables and a hunk of cold bacon
washed down with small beer, now turned up their noses at anything
except fresh meat and fried or baked fish, served hot lest they catch a
chill on their stomachs.
Initially the landlord suffered. He depended on agricultural
products for his income and prices had fallen steeply. He used more
imported and manufactured goods than the peasant and now had to pay
more for them. But the labourers’ time of gross plenty did not last, for
only a limited number of cattle could be tended and only a limited
acreage be cultivated by the reduced labour force. The continuing rise in
population had outstripped the land available for cultivation in the years
before 1348. The Black Death reversed the situation. Whereas there had
been a glut of labour and a shortage of land in 1347, there was a shortage
of labour and a glut of land in 1350.
Had the plague inflicted a uniform pattern of death throughout
the country, the difficulty would have resolved itself within a short time.
A smaller population would have tilled and fed off a smaller area. But
the death pattern was not uniform and this is the reason for the trouble

42
that followed. In 1350 a labour glut and a land shortage still existed on
those manors which had escaped the Black Death and, only a few miles
away, there would be unploughed acres and insufficient workers on
badly affected estates. We know what happened in a group of three
Norfolk manors belonging to Crowland Abbey. Eighty-eight peasant
holdings were vacant in the autumn of 1349. So numerous were the
Abbey estates that it proved possible to fill seventy-nine of these almost
immediately by transferring landless peasants from manors that had not
been affected. But these moves exhausted the available labour force and
the remaining nine holdings continued vacant and unworked until 1352.
Even then the Abbey had to increase the size of holdings on several
estates so as to find tenants for the empty farms.
It is for reasons such as this that the English peasant became
mobile for the first time in his history. In the autumn of 1349 the need to
get in the harvest dictated the purposeful mobilization of the available
labour force. This movement was at first local but became more
extended as redundant labourers on unaffected manors found that they
could receive wages and land on badly affected estates. The majority of
landlords found it more convenient to hire labour by offering an
attractive wage and the labourer soon found that he could ask a higher
payment. Thus rumours of higher wages tempted peasants to travel
further afield and seek new masters. The masters, though more than
willing to enforce feudal tenure, found themselves so short of labour that
they were obliged to hire the vagabonds without questioning their origin.
The central government took swift action. The 1349 Ordinance
and the Statute of Labourers in 1351 aimed at preventing all kinds of
worker from transferring their services from one employer to another, the
primary target of course being the peasant. But the Statute also sought to
peg prices at the 1347 level and here the law affected employer equally
with employed. The Statute not only forbade the worker to ask higher
wages but the employer to offer them. It is unlikely that these laws

43
would have solved the problem in the long term but they did succeed in
restoring some measure of stability by preventing wages and prices
getting entirely out of control. They bore heavily upon the smaller
employers of labour. The masters were not always great landlords. Many
villeins had become substantial small farmers cultivating forty or fifty
acres. They were not free men, in that they held their land by service to
their lords or had commuted that service for a payment in cash or kind,
but they were masters in that they employed hired labour, drawn from
the landless or almost landless class of ‘cottars and bordars’ which had
greatly increased in numbers during the thirteenth century.
The laws made necessary by this changed situation gave rise to
hardship and a great deal of resentment, but the national economy started
to recover, and it even became possible in 1355 to resume the war with
France. Wages and prices never fell to the 1347 level but at least they
ceased to rise. The labour shortage continued because, since all age
groups had been affected in 1348–50, the normal death rate exceeded the
number of children reaching working age. Population rose slowly as the
number of live births outstripped the number of deaths. A statesman able
to survey the national scene in 1360 might have thought the worst to be
over.
There are no records of serious epidemics between 1350 and
1361. That of 1361 received the name Pestis puerorum because the death
rate among children was especially high, suggesting that an attack of
plague conferred some resistance but maternal or inherited resistance
was lacking. Another theory proposes that the disease was not bubonic
plague but the first visitation of some illness of childhood such as
diphtheria or meningitis. Whatever the truth, a great number of children
in the under-thirteen age group died. Since a boy of fourteen was
regarded as of working age, the supply of labourers again fell in the next
years. The landlord now found himself faced with a virtually insoluble
dilemma. Many of his service tenants had died and their holdings were

44
back on his hands. If he wished to farm the land himself, he needed
labourers. If he did not farm it, the only profitable alternative was to let
the land at a rent. The only person willing to rent the land was the
surviving villein, whose duty it had been to cultivate the landlord’s
fields. The landowning government attempted to solve the dilemma by
enforcing feudal service without mercy. Not only did commutation by
payment cease entirely but service was demanded from those who had
already commuted.
Obviously this attempted solution created increasing hardship as
the available labour declined and, equally obviously, it evoked intense
hostility among that section of the labouring community which had
already tasted comparative freedom. Hostility increased through twenty
troubled years and crystallized in the Peasants’ Revolt of 1381.
Precipitated by the unpopular Poll Tax of 1380 (the third in four years),
this was predominantly an agricultural rising, having as its chief
objective commutation of all servile dues for ‘a fair rent’ of fourpence an
acre. The revolt failed in its immediate purpose and was followed by
harsh repression but, in the end, the landlord at last understood that his
only feasible course was to make the best possible bargain with his
villeins. He retained ownership of the land but ceased to farm it through
his bailiff or reeve. The reeve, who had overseen the labourers on his
lord’s fields, became the estate steward who received the rents from his
lord’s tenants. The service-labourer or villein developed into the tenant-
farmer.
Thus the Black Death struck such a blow to the already weakened
feudal system of tenure that it lost much of its meaning within two
generations and had entirely disappeared within a hundred and fifty
years. But the tenant-farmer himself needed hired labour and he recruited
this from the less able villein and from the landless class of cottar and
bordar. The new pattern had become evident by the early years of the
fifteenth century and was complete in the sixteenth. England had become

45
a country of tenant-farmers, their fields worked by a landless agricultural
proletariat. In the majority of European countries the feudal system of
landlord and peasant lingered on for four or five centuries. In England
the peasant ceased to exist. Farmer and landworker took his place.
The old aristocratic landlord knew of only one source of wealth –
land. Finding himself impoverished, he could visualize only one remedy:
to obtain more land. The new tenant-farmer lived closer to the soil and
understood that an excessive acreage can only be economically farmed
by methods requiring a small labour force. Thus he quickly decreased his
arable and increased his pasture. Even in the strong corn-growing lands
of East Anglia sheep became the farm staple, while in the north and west
sheep virtually ousted all other crops. Tudor prosperity depended upon
wool. So rapid was the change that shortage of labour again turned to
glut in the fifteenth century and by the time of Henry VIII the complaint
was heard that the sheep were eating up the men. We catch a glimpse of
the starving, out-of-work ploughman and labourer in the often-misquoted
nursery rhyme:

Baa, baa, black sheep, have you any wool?

Yes sir. no sir, three bags full.
Two for my master and one for his dame
But none for the little boy who cries down the lane.

So, within little over a century, the villein-farmer developed into

the wool baron. He was helped by the ever-increasing strain imposed
upon the landed class by nearly a hundred and fifty years of almost
continuous warfare. The climax came with the dynastic struggle of
1455–85 known as the Wars of the Roses. The feudal aristocracy turned
the war into a great landgrabbing operation and, in doing so, committed
mass suicide. The tenant-farmer took advantage of the anarchy by
buying up the estate of his ruined lord, emerging as the landowner. The
large majority of older English ‘county families’ arose during this time

46
and by this means, their origins lying in a Saxon and villein ancestry
rather than Norman blood. These ‘new men’ rose to power under the
Tudors. Unlike the Norman barons, they came of the same stock as their
inferiors. Though sometimes harsh and arrogant and often bitterly
resented, they never developed into a closed, aloof caste as did so much
of the continental aristocracy. The strength of the English social structure
lies in the fact that continuing shifts have prevented a rigid
differentiation between classes.
Looking beyond the shores of England, we find widespread
social changes although of shorter duration. The Black Death must have
seemed to the ordinary man to be of supernatural origin, a punishment
inflicted by a higher power upon unknown sinners for unknown crimes.
Culprits were sought: nobles, cripples and Jews in turn came under
suspicion. The Jews in particular were suspected of purposely spreading
plague by contaminating wells or ‘anointing’ houses and persons with an
imagined poison. Their persecution started at Chillon on Lake Geneva in
1348 and spread rapidly to Basel, Freiburg and Strassburg. At Freiburg
all known Jews were herded into a large wooden building and burned to
death. At Strassburg over two thousand are said to have been hanged on
a scaffold set up in the Jewish burial ground. So bitter did the
persecution become that the liberal Pope Clement VI issued two Bulls
declaring Jews to be innocent. Numbers fled from western Europe into
east Germany and Poland. Here they were tolerated and founded
communities which rapidly grew in numbers, a fact which partly
accounts for the very large Jewish population in west Russia, eastern
Germany, Poland and north-east Austria in the nineteenth and early-
twentieth centuries. Thus the Black Death intensified the medieval
Christian tradition of the scapegoat-Jew and, by causing the migration of
so large a number to the east and north of Europe, is linked to the
pogroms of imperial Russia and the gas-chambers of Auschwitz.

47
 The attempt to find culprits was accompanied by a general
relaxation of moral values and a cynical, unhappy pursuit of pleasure, a
natural reaction which was also observed in the 1920s after the horrors of
the First World War. There also developed a masochistic urge to accept
the divine punishment and to divert it from others. The most dramatic
expression of this urge was the mania for organized mass flagellation.
The flagellants were not a product of the Black Death alone, for they
achieved some notoriety in Italy and Germany during a severe famine-
pestilence of 1258–9. In 1348 the movement spread all over Europe and
enlisted tens of thousands. The flagellants organized themselves in
companies each under a master, wore a special uniform, lived under
discipline, and conducted their public and private flagellation according
to a set ritual. To our modern way of thinking, the flagellants are likely to
be sexual deviants, but the reason for their strange behaviour is perfectly
logical. The Black Death was a divine chastisement so the flagellant
attempted to divert it by chastising himself. Thus it was the rumour
rather than the appearance of plague which induced the exhibition. The
flagellant tried to forestall punishment of his fellows by inflicting
punishment on his own body.
The movement was at first welcomed by the Church as a mass
penance. Pope Clement himself ordered public flagellation at Avignon in
an attempt to stay the plague. But the flagellants rapidly got out of
control and assumed the character of a revolutionary movement directed
against Jews, the richer classes and the Church itself. In October 1349
the Pope issued a Bull condemning them. Many were beheaded, hanged
or burned, and all further processions were forbidden. A curious quirk of
clerical psychology condemned a number of flagellants to be flogged by
priests before the high altar of St Peter’s in Rome.
The Christian Church had risen to be a dominant power partly as
a result of the earlier pestilences. It would be strange if so great a
catastrophe as the Black Death did not exert some influence upon the

48
authority of a religion which had now been established for over a
thousand years. Its remarkable grasp upon Europe enabled Christianity to
weather the storm but the authority of the Church did not survive the
Black Death unscathed.
Up to a point, the Church’s influence had been for the public
good. It preserved a limited peace in times of strife, tried to impose a
code of decent human behaviour and acted as schoolmaster. The Church
harnessed and nourished intellect, provided and tutored administrators,
lawyers and physicians, encouraged and preserved literature, architecture
and art. But, although creative work might be encouraged, creative
thought was more often sternly repressed. The doctrine of persecution
formed an integral part of medieval Christianity and those whose written
or spoken thoughts did not follow the rigid line permitted by the Church
stood in danger of persecution as heretics.
In material matters the Church suffered badly from the Black
Death. A great loss of manpower and consequent impoverishment
through inability to cultivate its widespread estates rendered it a less
dominant power in 1350 than it had been in 1346. But greater harm
resulted from the Church’s helplessness in this time of disaster, from the
large loss of priests and monks, and from its failure to control their
successors. Parish priests, the best-loved and most useful of church
workers, died by the hundred and according to William Langland their
benefices were all too often hurriedly filled by ‘numbers of youths that
had only devoted themselves for clerks by being shaven’. If Langland is
to be believed, the friars, who had previously been renowned for holiness
and charity, gave themselves up to ‘gayness and gluttony’ while country
parsons and parish priests spent their time in London, touting for high
places instead of ministering to their parishioners. Langland specifically
states in both instances that these abuses had multiplied ‘sithen the
pestilence time’.

49
 Further, the very fact that the Church possessed the seeming
advantage of being international or supra-national imposed a threat to her
power. In some countries, Germany and England for example, People
and Church had been falling out of sympathy for many years. The
national branches of the Church cried out for reform, but had no power
to reform themselves because they lacked autonomy. In fact they were
outlying parts of a foreign organization of immense power and prestige.
For all these reasons, open opposition to the Church developed in
the years following the Black Death. Popular reaction can be measured
by contrasting the murders of two Archbishops of Canterbury. In 1170
Thomas à Becket was done to death as the result of some hasty words
spoken by King Henry II. Although Becket’s policy was not generally
approved, public horror at this sacrilege forced the king to submit
himself to humiliating penance. In 1381 a band of rebels seized the mild
Simon Sudbury and struck off his head on Tower Hill in London amid
the ferocious applause of a large crowd. ‘The relation of Church and
people had undergone a profound change since the ancestors of these
same men had knelt beside their ploughs to pray for the Holy Martyr,
Thomas à Becket,’ wrote G.M. Trevelyan.
The change was more profound than is suggested by the murder
of Sudbury, Langland’s disapproval or the deviant behaviour of
flagellants. John Wycliffe (c. 1330–84) was a notable theologian and
Master of Balliol College, Oxford. He questioned the Church’s hitherto
unchallenged power, which he considered to be derived from the Caesars
rather than from a divine source. As well as demanding a vernacular
Order of Service and translating part of the Bible into English, he
attacked the worship of images and relics, the sale of pardons and masses
for the dead. Wycliffe gained an immense following who became known
as Lollards. They were drawn not only from the common people but also
from the nobility, friars and some of the lesser clergy who had reason to
dislike wealthy monks and bishops.

50
 As the Church re-established its shaken authority, the Lollards
were subjected to persecution and driven underground, to reappear in the
reigns of Henry VII and VIII. Persecuted again, they re-emerged to
combine with the Protestants of Martin Luther. Luther owed something
to the teaching of the earlier reformer John Huss of Bohemia, who
acknowledged himself a pupil of Wycliffe. Thus it is not too much to
claim that the Protestant Reformation, the sailing of the Brownist Pilgrim
Fathers in the Mayflower from Plymouth on 6 September 1620 and the
foundation of Pennsylvania by the Quaker William Penn in 1681, can all
be linked with the deviation from established religion that followed the
disaster of the Black Death.

One might think that so great a pestilence, in which physicians

and priests alike proved useless, must have profoundly affected the
development of the theocratic medical art. This is not so. The only
medical advance attributable to the Black Death is in the field of public
health. In 1374 the Venetian Republic appointed three officials with the
duty of inspecting and excluding all infected vessels from the ports. In
1377 Ragusa detained travellers from infected places for thirty days
(trentini giorni). When this proved ineffective the period of detention
was lengthened to forty days (quaranti giorni) from which comes our
word ‘quarantine’.
The Black Death also added another saint to the calendar. St
Roch is the special patron of bubonic plague. A native of Montpellier, he
nursed the sick during the Black Death in north Italy and himself fell a
victim. Left to die, Roch was succoured by a dog and recovered. In
Lombardy he became suspected of being a foreign spy and was thrown
into prison where he died. Here again is the sequence of mortal hurt,
miraculous recovery, and ultimate death.
We may credit the Church for its unremitting care of the sick, but
acknowledge that its influence upon medical and scientific advance was

51
almost wholly negative. In Europe the thousand-year repression of
creative thought between the fall of Rome and the Renaissance provides
a miserable picture of sterile plagiarism. Great schools of medicine were
founded – Salerno and Bologna in Italy, Paris and Montpellier in France
– but the teaching in those schools was an uncritical reiteration of ancient
theories, and research took the form of disputations upon the exact
meaning of a text. The huge medical literature of this long period
contains many original observations but hardly any original thought. It is
little better than a series of compilations, the substance derived from
Latin texts of first-century authors and their Islamic commentators.
There are, of course, occasional flashes of the divine fire, for no weight
of repression will ever stifle originality entirely. Thus Mundinus of
Bologna defied the ban on human dissection and did something to
restore the science of anatomy to the standard reached by Greek scholars
about 300 BC. Another flame in the darkness is Roger Bacon of Oxford
and Paris (c. 1214–94), a philosopher rather than a physician and
certainly an original thinker, but his originality earned him imprisonment
for the last thirteen years of his life.
The habit of thought engendered by theocratic intolerance stifled
medical advance until the end of the fifteenth century. Galen remained
the unquestioned authority. This dominance of one man would have been
bad enough in itself, but the texts of Galen had been so debased as to be
almost worthless. The true teachings of Galen were not restored until too
late when, at the end of the fifteenth century, a new way of thinking
opened up wide vistas of learning and beauty. The wonderful
phenomenon of the Renaissance was not merely a revival of classical
culture but a change in the whole outlook of thinking people, who
demanded escape from the tyranny of dogmatism, from the limitations of
thought imposed by the Church. Although the ghost of Galen was not
finally laid until William Harvey disproved his doctrine of the ebb-and-

52
flow movement of blood in the seventeenth century, it was the
Renaissance that finally broke the Church’s stranglehold on medicine.

Bubonic plague remained one of the more lethal European

diseases for three centuries after the Black Death. It disappeared from the
greater part of Europe during the early years of the eighteenth century,
but remained endemic on the southern and eastern shores of the
Mediterranean, in Asia, in Africa and in South America where epidemics
have reached the proportion of national pandemics at times. Prevention
and treatment of bubonic plague are now reasonably successful. The
causative organism was discovered almost simultaneously in 1884 by a
Japanese worker, Sharamiro Kitasato, and a Swiss, Alexander Yersin.
The latter’s name is now attached to the bacillus. Prevention was found
to be possible by inoculation with a killed vaccine prepared from the
organism or by injection of a live but avirulent preparation of Yersinia.
Antibiotic drugs, streptomycin or tetracyclin, have proved successful in
the developed illness. Rats and fleas can be dealt with by pesticides. But
plague, especially in the pneumonic form, is still so dangerous that sick
attendants must wear masks, protective gowns and gloves, just as they
did or were advised to do in the Black Death or the Great Plague of
1665.
None of this explains why plague quite suddenly disappeared
from Europe towards the end of the seventeenth century. There are a
number of suggestions, of which the ‘rat theory’ is the most widely held.
This supposes that the companionable black rat of houses and ships was
killed out by the more ferocious brown or Norwegian rat, said to have
first appeared in Europe in the 1720s, which inhabits sewers and is more
commonly infested with a different flea that rarely transfers to humans.
The theory is attractive but not really tenable. First, the theory that the
brown rat killed out the black is a mere assumption. The two species do
not appear to compete for living space or food. In the many places where

53
they live in proximity, each stays within its own environment and keeps
out of the way of the other. They may even live side by side in apparent
amity when the quarters are sufficiently spacious to provide each with its
preferred conditions. Secondly, the black rat, if it ever disappeared which
is non-proven, has returned. Since 1910 it has steadily increased in
Europe. This fact has been made plain by EE. Loosjes who commented,
‘If epidemics of plague have really vanished with the black rat, it is
imperative that careful study be made of the present increase in the
species and if possible an end made to it.’
There is a type of animal plague known as ‘campestral’ or
‘sylvatic’ which affects wild rodents such as rats, rabbits, hares and
squirrels. Rodent-flea-rodent transmission could carry infection to the
urban or companionable species, black rats, hamsters and guinea pigs.
There is a possibility that this is the type of plague which was once
human and which transferred to the rodent. Our forefathers were quite as
observant as we are, and they appear not to have noticed any unusual
mortality of rats, which has been a marked feature of later outbreaks in
India, China and Mongolia. Perhaps the epidemiology is correct but
operated in reverse. The great plagues may have originated in the human
but been transmitted by fleas to the rat.
Whatever the answer may be, and the above is supposition only,
the three-hundred-year reign of plague in Europe ended by some natural
process and not by any active measures on the part of men. There was no
medical or scientific discovery, no advance in social hygiene, no
improved standard of life, that can possibly account for its
disappearance. Plague ended – or went into hiding. For we must always
remember that three plague-free centuries separate us from 1665, and
eight plague-free centuries separated the Plague of Justinian from the
Black Death.
And if any who read these words believe that accounts of the
Black Death are exaggerated and do not accord with modern medical

54
knowledge, let them consider the evidence of Petrarch. The great poet
was in a position to know, for he lived through the Black Death in Italy.
Laura, his mysterious platonic love, died of plague at Avignon on 6 April
1348. He wrote of the empty houses, abandoned towns, squalid
countryside, fields covered with the dead, a vast and dreadful silence
over the whole world. He told of historians who remained silent when
asked to describe similar disasters, of physicians at their wits’ end, of
philosophers who shrugged their shoulders, wrinkled their brows, laid a
finger on the lip. Petrarch ended his account with these words: ‘Is it
possible that posterity can believe these things? For we, who have seen
them, can hardly believe them.’

55
 C T
THE MYSTERY OF SYPHILIS

One of the most controversial problems in medical history is how and

why the bacterial infection soon known as syphilis suddenly emerged in
Europe at the end of the fifteenth century Syphilis is now primarily a
venereal disease, spreading from one participant to the other during
sexual intercourse. But it can also be acquired in other ways, for example
by the transplacental route, by a person with an open lesion in the mouth
sharing a drinking vessel with a syphilitic, by the use of hypodermic
needles in common, by tending an affected person without wearing
protective gloves, or by a pathologist’s carelessness when performing an
autopsy. After the initial infection an incubation period follows which
can be ten to ninety days but commonly two to four weeks, before the
first sign of disease appears. This takes the form of an ulcer, known as a
chancre, which is a local tissue reaction at the site of contact. Obviously
the chancre will generally develop on or near the genital organs, but will
occur at the site of infection, lip or finger for instance, when the disease
has been acquired by means other than sexual intercourse. The chancre,
even if untreated, will disappear spontaneously within three to eight
weeks, leaving a very thin and inconspicuous scar. Sometimes the
chancre is quite large but often little more than a rather hard pimple. This
is why the primary stage of syphilis is so dangerous. The syphilitic is
capable of infecting other people but the small initial ulcer and the
consequent scar may be so trivial as to escape notice. About a quarter of
all patients seen in the clinics say they have not noticed the primary
lesion.
Six to eight weeks after the appearance of the chancre, the patient
will usually enter the secondary stage but the symptoms may be delayed

56
for a year or even more. The secondary stage is a general tissue reaction
to infection, much like any reaction to bacterial invasion. There is a
feeling of discomfort, headache, perhaps a sore throat, a mild fever and,
in about 75 per cent of cases, a skin rash. The rash is important because
it can take a number of different forms. Syphilis has been called ‘the
great mimic’ because it can be mistaken for so many other diseases. This
is particularly true of the rash which sometimes bears a resemblance to
measles, or to smallpox or to any skin eruption. As a rule the secondary
stage does not last for long and the patient then enters the early latent
stage, in which he or she appears entirely free of all signs and symptoms,
although sometimes the rash will reappear for a week or so and then
disappear again. During both the secondary and early latent stages the
patient is highly infectious. The most dangerous time is during the early
latent stage for the patient can infect others but appears quite free from
disease.
After about two years the late latent stage develops. There are no signs or
symptoms and the patient is often not able to pass on the infection. It
cannot be said that he or she is cured, because blood tests will reveal the
presence of syphilis in the body tissues, but the disease is quiescent and
may remain so for the rest of the patient’s life span, death occurring from
some unrelated cause.
The latent stage may last for years without any incident while the
syphilitic lives in a fool’s paradise, believing that there is no longer any
danger. In reality the disease has only settled into a very prolonged
chronic phase. From three to ten or even twenty years after the primary
infection, the signs of tertiary syphilis may appear. There are many
manifestations, for syphilis can attack almost every system in the body.
The typical lesion of tertiary syphilis, the gumma, can appear anywhere:
in the bones, the heart, the throat, the skin. Some people believe that the
swelling on the side of Henry VIII’s nose, in the portrait by Holbein, is a
gumma.

57
 Due to the development of antibiotic therapy, tertiary syphilis as
distinct from the primary and secondary stages, had become a rarity in
the Western world by the late twentieth century. In the past it had shown
itself by changes in the blood vessels, resulting in weakening and
ballooning of the walls, which led to death by rupture of the aorta or one
of the vessels in the brain. The nervous system could be affected, causing
the illness known as tabes dorsalis when the sufferer gradually became
paralysed and incontinent. Or the brain itself might be damaged, giving
rise to horrible personality changes and sometimes ending in general
paralysis and insanity (GPI) in which the victim was converted into a
helpless maniac. This terminal stage was often preceded by a phase in
which the sufferer conceived ideas or schemes which were superficially
rational but bizarre or grandiose. Conan Doyle tells the story of a young
farmer who surprised his neighbours by taking a very rosy view of his
prospects at a time when his farm was rapidly running downhill owing to
an agricultural depression. He proposed to give up orthodox cropping
and plant the whole area with rhododendrons to corner the market. His
scheme would have been quite sensible had there been any market to
corner. Most untreated patients died within five years of showing the first
signs of GPI but a number never became frankly insane or helpless. The
disease process in their brains changed their pattern of behaviour but
they were able to carry on more or less normal lives and died from some
other illness, perhaps having ruined themselves by foolish speculation or
terrorized their families by violence.
One of the more terrible attributes of syphilis is that it can be
transmitted from parent to child via the placental blood supply. If the
mother is in the active or early latent stages, her child will probably die
while still unborn but death does not usually occur until the fourth month
of pregnancy at the earliest. Thus it can be stated that a history of
repeated miscarriages before the fourth month of pregnancy does not
suggest syphilis but that repeated miscarriages after the fourth month are

58
strongly suggestive. As the mother passes through the later stages, the
child will have a better chance of being born alive and, when and if the
disease has spontaneously cured itself or been cured, normal healthy
children may be born. But syphilis rarely produces a ‘typical pattern’ and
healthy children may alternate with diseased children at any time in a
syphilitic family.
The diseased children pass through the same stages as the parent.
But because the disease process is affecting a growing individual some
special signs are often, though not always, present. These include bone
defects, impaired sight and hearing, and deformed teeth. The well-known
‘Hutchinson’s Triad’, first described by Jonathan Hutchinson of the
London Hospital in 1861, consists of deafness, impaired vision, and
notched peg-shaped teeth. The deafness is caused by damage to the
auditory nerve and persists or worsens throughout life. The particular
defect of vision is known as interstitial keratitis, first appearing as a
diffuse haziness near the centre of one cornea, occurring most commonly
between the ages of five and fifteen. The haziness spreads over the
cornea and the other eye is attacked two or three months later. The child
goes blind, or almost blind, but a surprising improvement occurs within a
year or eighteen months. Patches of haze often remain for life, so vision
may never be entirely normal. For some reason unknown, almost twice
as many male children are affected as female. They suffer eye pain in
strong light and often develop a habit of lowering the eyelids and
eyebrows as though frowning.
Most of what has been said above concerns syphilis as it might have
appeared, if untreated, in recent times. It does not necessarily follow that
exactly the same clinical picture was observed by physicians when the
infection first made its appearance in Europe at the end of the fifteenth
century.
According to contemporary writers, from 1495 onwards
something which seemed to be a new disease swept over Europe. Thence

59
it spread to India, China, Japan and eventually to the rest of the world.
Early medical historians accepted the theory that the disease originated
in the army of Charles VIII of France who, having launched an invasion
of Italy in the autumn of 1494, attacked Naples in February 1495, or that
the disease started in Naples and was transmitted to the French army.
This army of about thirty thousand men was not, in fact, composed of
Frenchmen only, but also of mercenaries from Germany, Switzerland,
England, Hungary, Poland and Spain. The great number of sick forced
Charles to withdraw and abandon his attempted conquest of northern
Italy. This, at least, is fact and provides an example of how disease can
affect the course of history. The classical story, or perhaps legend,
continues that the remnant of his army dispersed to their homelands, thus
spreading the infection to the many parts of Europe from which they
came. Shortly afterwards the disease became known by names which
varied according to the supposed country of origin. We hear of the
‘French’, ‘Neapolitan’ and ‘Polish’ disease. Some years later it became
known in China as ‘Canton disease’ and in Japan as the ‘Chinese
disease’. Englishmen knew it as ‘the French pox’ or ‘the great pox’. In
France it was commonly known as ‘la grosse vérole’. The French also
named it ‘the Spanish disease’ and this brings us to the earliest theory of
the origin of syphilis.
Christopher Columbus first saw the New World, probably one of
the Bahama Islands, on 12 October 1492. Between October and January
he visited Cuba and Haiti. In the latter month he set sail for Europe,
landing at Palos, the port from which he had set out, on 15 March 1493.
He brought with him ten natives of the West Indies, of whom one died
soon after landing, and a crew of forty-four men. The crew were
disbanded and some are said to have joined the troops of Gonzalo de
Cordoba who marched with Charles VIII to Naples. Columbus travelled
with his nine natives to Seville, left three there, and took the remaining
six on to Barcelona. At the end of April the six natives, all males, were

60
shown naked to the Spanish Court. They are described as brown and
comely, resembling Asians more than Africans. There is no mention of
any visible disease.
Twenty-five years later, in 1518, a book printed in Venice first
mentioned the theory that ‘a Spanish disease’ had been imported from
America (or the West Indies) by seamen in the 1492–3 expedition led by
Columbus. This theory was supported and popularized by Gonzalo
Fernandez de Oviedo y Valdes, who had been a page at the Spanish
Court and claimed to have seen the ‘Indians’ shown by Columbus.
Oviedo made several voyages to the West Indies and reported that he had
found evidence of the new disease among the natives. In 1539 Rodrigo
Ruiz Diaz de Isla, a physician, published a description of ‘the West
Indian disease’ or bubas, and claimed to have treated at least one, if not
more, of Columbus’s crew at Barcelona. We are justified in presuming
that men of his crew accompanied Columbus when he showed the
Indians to the court in that city.
The first theory therefore supposes that syphilis was introduced
into Europe from the West Indies by ship in 1493. Many medical
historians support this opinion. The evidence in favour is that a new
disease of great virulence undoubtedly did appear in Europe at about the
time that Columbus returned. Another fact sometimes cited is that one of
the earliest and more popular treatments was by holy wood or guaiacum,
a resin obtained from two evergreen trees, Guaiacum officinale and
Guaiacum sanctum, which are indigenous to South America and the
West Indies. Guaiacum was introduced as a treatment in 1508, that is ten
years before the first known mention of West Indian origin. This is, of
course, a point in favour of the theory. But opponents of the theory
maintain that the useless guaiacum was imported not because it was a
traditional native remedy, but deliberately to support the West Indian
origin. Also against the theory must be set the fact that there is no
evidence whatever of disease in the imported Amerindians or among the

61
forty-four seamen who returned with Columbus. It may, too, be of some
significance that the Columban or American theory did not achieve
credence until over a quarter of a century after his return and the
supposed first appearance of the disease. There is, of course, always the
possibility that new facts may have come to light in later expeditions to
the West Indies.
The second theory maintains that syphilis originated in Africa
and was introduced into Spain and Portugal by the importation of slaves.
In 1442 a Portuguese expedition led by Prince Henry the Navigator
explored the Atlantic coast of Africa and anchored in the Bight of Benin.
One of the captains, Autam Goncalves, captured a few Moors and took
them as prisoners on board his ship. Prince Henry ordered Goncalves to
return them. He did so and was rewarded with gold dust and ten native
Africans. These fetched a large price in Portugal, which led to a quite
extensive trade in black slaves from Africa to Portugal and Spain. The
descendants of many of these slaves became Christians. In 1502 King
Ferdinand ordered that Christian slaves be shipped to the West Indies. So
many were sent that the governor of Haiti became alarmed by the
increasing number of Africans on the island and in the following year
asked that the trade should cease.
This second theory depends upon the existence of an African
disease known as yaws, the bacteriological appearance of which is
virtually indistinguishable from syphilis. Unlike syphilis, it is chiefly
transmitted by non-venereal contact, being particularly common among
children who play together naked. For this reason true yaws is only
found in hot climates, where it appears as a most unpleasant skin
eruption. There is a good deal of argument on the question of whether
yaws and syphilis are or are not different manifestations of the same
disease. Some people believe that if the tropical yaws is introduced into a
cold climate, where the inhabitants are normally fully clothed, the
infection will take the form of ordinary syphilis carried mainly by

62
venereal contact. This theory is attractive because it could explain the
behaviour of syphilis during the first years of its European existence. But
obvious skin disease was undoubtedly sometimes confused with true
leprosy, which aroused particular horror among all humans, partly
because of the terrible destruction of tissues and partly because of the
widely held belief that a leper had been visited with divine punishment
for unforgivable sin. It has been sensibly argued that the six Amerindians
brought back by Columbus and shown naked to the Court cannot have
been diseased, for someone must surely have noticed a gross skin lesion.
The same objection can be applied to the African slave theory. In view of
the general fear of skin disease, traders would not have shipped slaves
suffering from yaws.
An extension of the African theory of origin places the
introduction of syphilis to Europe at a much earlier date. Equatorial
Africans found their way to Egypt, Arabia, Greece and Rome and they
may have brought yaws with them. This implies that syphilis is a very
old European disease and that something unknown caused a great
increase in virulence and infectivity at the end of the fifteenth century.
Some historians hold that leprosy, often said to have been brought back
from the Levant by crusaders, was in fact syphilis. It is undoubtedly true
that leprosy disappeared from Europe (or from European medical
literature) before syphilis became rampant. It is also true that both
infections can produce horrible skin eruptions, which contemporary
doctors might find difficulty in differentiating.
The objection to any theory of an ancient origin depends on the
fact that syphilis often causes permanent and visible changes in the
bones which are now recognizable by pathologists. No skeletal remains
that have been radiocarbon dated to before the beginning of the sixteenth
century have ever been found in Europe with reliable evidence of
syphilitic damage. Such is not the case with bones, particularly skulls,
unearthed in Europe after sixteenth-century or later burial. The evidence

63
regarding South American and West Indian burials is controversial and,
although pre-Columban bones with apparently syphilitic lesions have
been found, the number is too small to postulate with any certainty that
the disease is of American origin.

So we had better leave the argument as to origin unanswered. We

can be sure that contemporary physicians believed that a new disease of
great virulence spread rapidly over Europe in the 1490s. They possessed
none of our modern aids to diagnosis and their descriptions are not
always as clear as we could wish, but they were capable of honest
observation. It is also possible that a modern doctor might not have
recognized this mysterious disease as syphilis had he made only a
superficial examination without blood tests or the help of a
bacteriologist.
In 1519 Ulrich von Hutten published an account of the disease in
Germany. According to him, it first appeared there in 1497, spread
widely, and produced ‘disgusting sores’. After about seven years the
disease underwent a change which was not caused by any kind of
treatment. He said that the acute, obvious skin lesions became less
common and, because the person no longer appeared revolting, the risk
of infection became greater. Von Hutten made the important observation
that, at the time of writing in 1519, transmission seemed to be only by
venereal contact. Diaz de Isla in his description of 1539 described the
stages as they are known today but added a terminal illness of fever,
emaciation, persistent diarrhoea, jaundice, abdominal distension,
delirium, coma and death.
The most important early work on syphilis is that of Girolamo
Fracastoro in 1546. In 1530 he published at Verona a long poem entitled
Syphilis sive Morbus Gallicus (Syphilis or the French Disease) in which
he gave the disease its modern name, derived from an imaginary
shepherd Syphilus, although the term did not come into common use

64
until the end of the eighteenth century. In his book of 1546 published at
Venice and entitled De Contagione et Contagiosis Morbis, by which he
really means About Infection and Infectious Diseases, he described
syphilis as commencing with small ulcers on the genital organs followed
by a pustular skin rash which usually began on the scalp. These pustules
ulcerated to such a depth that bone might be exposed. The patient also
suffered from a ‘pernicious catarrh’ which eroded the palate, uvula and
pharynx. Sometimes the lips or the eyes were entirely eaten away. Later
swellings or ‘gummata’ appeared, accompanied by violent pains in the
muscles, lassitude and emaciation. Fracastoro thought that the infection
had changed its character in the last twenty years (i.e. since 1526) for it
seemed to him that many sufferers showed fewer pustules and more
gummata than before.
This new disease did not spread with the same speed as bubonic
plague. Even if we take 1493 as the date of first appearance of a syphilis-
like disease in Europe, there was a lapse of three years before its
invasion of England in 1496. Poland was infected in 1499, Russia and
Scandinavia in 1500 and Canton in 1505. Some countries escaped
infection until much later: Japan in 1569 and Iceland in 1753, while the
Faroe Islands were free until 1845. An interesting puzzle is the infection
of India in 1498. At first sight this would be an impossibly early date but,
in fact, it provides proof that, wherever the origin of European syphilis
may have been, Europe itself played a role in infecting much of the
world. An expedition of four ships and 160 men led by Vasco da Gama
left Lisbon in July 1497. rounded the Cape of Good Hope and sailed
north and east, landing at Calicut on the Malabar River on 20 May 1498.
The crews carried syphilis with them.
The disease was far more contagious in the opening phase of its
European history than it is today. Figures are unreliable but about a third
of the citizens of Paris are said to have been infected by the opening
years of the sixteenth century. The scholar Erasmus wrote in 1519 that

65
any nobleman who had not contracted syphilis was considered ignobilis
et rusticans, i.e. ‘a country bumpkin’. Very interesting confirmation of
the early virulence and later recession is supplied by Sir Thomas More,
surely a reliable witness. In 1529 he wrote the tract Supplication of Souls
in Purgatory in answer to a demand for the suppression of monastic
hospitals. This contains the sentence: ‘And then of the french pockes
thirty years ago went there about five against one that beggeth with them
now.’ That is, five patients attended the hospitals on account of syphilis
in 1499 for every one attending in 1529.
But why was syphilis so contagious in the sixteenth century? If
the disease was indeed imported from the New World, then it would have
had the impact of any infection introduced to a completely unaccustomed
community. There can have been no immunity, absolute or relative,
maternal or acquired by a previous attack. Thus the illness would tend to
be more severe and the chances of infection higher at its first appearance.
But we must also recognize the possibility that European syphilis derived
from yaws. This would account for the gross skin lesions and also for an
added risk of contagion, infection by direct contact, by means other than
sexual intercourse. One such simple means of contact has been
unaccountably overlooked by historians of syphilis. The common
method of greeting in Tudor times was not the handshake but the kiss.
The kiss was used by both sexes and by all classes, more usually than not
from mouth to mouth.
So the more common method of transmission may have been
innocent, that is non-venereal. Infection was passed from one individual
to another by mouth-to-mouth contact or by drinking from a shared
vessel. In such cases the primary chancre would have appeared upon the
lips or tongue and, in those days of neglected personal hygiene, must
often have passed unnoticed or have been mistaken for the ‘cold sore’ of
impetigo. For instance, Cardinal Wolsey was accused of infecting Henry
VIII by ‘breathing and rowning in his ear’. He may have done so, but

66
equally the Cardinal may have been suffering from a cold sore on his lip.
There must, of course, have been many cases of venereal infection, but
we need not search for immoral relationships or juicy scandals when
investigating the syphilis of the early sixteenth century. There is an equal
or even greater chance that transmission was by innocent contact.
Another reason for the wide spread of syphilis is that the tertiary
stage of nervous or arterial involvement was not yet recognized as being
associated with the earlier phases. Gross cutaneous manifestations were
not always present and the minor lesions of the early stages – the
primary chancre and the secondary rash – could be mistaken for trivial
disorders and, in any case, soon disappeared without treatment. There is
some confirmation for this supposition in the dates at which certain
terms were first used. The Oxford English Dictionary gives the
following: Pox 1476, Great Pox 1503, Small Pox 1518. ‘The Pox’,
preceding the introduction of syphilis, is another name for any kind of
skin eruption. ‘Great Pox’, introduced seven years after England was
first infected, is definitely the common name for the cutaneous signs of
syphilis. ‘Small Pox’, 1518, cannot be a specific name for the infectious
disease known as ‘smallpox’ because that was known long before 1518
and was no doubt lumped with other rashes under the old nurse’s
diagnosis ‘the poor child’s got the pox and fever’. In fact ‘Small Pox’
almost certainly meant what the name implies, a lesser form of the
‘Great Pox’, applied to the secondary rash which often resembled any
other kind of ‘small pox’, for instance measles. Thus it is reasonable to
suppose that many infected people went through life untreated and
without even realizing that they suffered from syphilis.

As for the historical effects of this disease, they have been

devastating. The tale of suffering and misery is multi-faceted.
Magnificent specimens of mankind such as the South Pacific islanders
have been destroyed en masse. Brilliant statesmen in positions of power

67
have become drooling idiots; artists, painters and poets have been ruined.
Francis I of France, Pope Alexander Borgia, Benvenuto Cellini and
Toulouse-Lautrec, Winston’s father Randolph Churchill, these are just a
few names drawn at random from hundreds of victims. Millions of lesser
men and women have suffered equally. Millions more have suffered
indirectly, as we can well see in the case of Ivan the Terrible. There is no
doubt that he was a syphilitic, for during the period of Soviet rule his
remains were exhumed from their resting place in the Moscow Kremlin
and found to show typical lesions in the bones.
Ivan, Grand Duke of Muscovy and first Tsar of All the Russians,
was born on 25 August 1530, and ascended the Grand-Ducal throne
when he was three years old, on the death of his father Vassili III in
December 1533. Outwardly Ivan was a typical Russian prince of his
time, spending his youth in hunting, womanizing, drinking, robbing
merchants and terrorizing the unfortunate peasantry. But there was a
little more to him, for beneath the surface lay a serious scholar who
preferred the company of lower-born but educated clerks to that of
illiterate nobles. He chose one of the former, Alexei Ardatchev, as his
most intimate friend and adviser. On 16 January 1547 Ivan was crowned
Tsar, the first Muscovite ruler to be so styled formally, basing the claim
on his descent from Vladimir, grandson of the Byzantine Caesar,
Constantine Monomakh. Two weeks later he married a pious and
humane woman, Anastasia Zakharina Koshkina.
In the same year a fire destroyed the greater part of Moscow. The
Metropolitan, Archbishop Makary, took this catastrophe as an
opportunity of impressing on Ivan the sinful follies of his youth, urging
him to reform. Now opened a reign which promised to be one of the
most enlightened in the history of Russia. Ivan established some kind of
legal code, banished the most oppressive nobles, partially reformed the
all-powerful Church and founded schools in Moscow and the larger
cities. Although neither a brave man nor a good general, Ivan inspired

68
his troops with a crusading spirit, captured Kazan from the infidel Tartar
horde, and extended his empire down the Volga to Astrakhan. In 1558 he
turned westward against the Teutonic Knights and by the summer of
1560 had reached Riga on the border of Prussia.
By our standards Ivan was no doubt a cruel despot even during
those early years. By contemporary Russian and, indeed, European
standards he ruled wisely and humanely from 1551 to 1560. He played a
vigorous part in the deliberations of his council, but allowed freedom of
speech and opinion. He received petitions from all classes of his
subjects. Legend has it that, for the first and the last time in Russian
history, the poorest man in the country could gain access to his
sovereign.
In October 1552 Anastasia gave birth to a son, Dmitri, who died
when six months old. Nine months later she bore another son, Ivan, and a
third, Fedor, in 1558. Probably Tsar Ivan had been infected with syphilis
during his womanizing years before marriage. We surmise – it is only
surmise – that the infant Dmitri died of congenital syphilis. Giles
Fletcher in his The Russe Commonwealth described Fedor, who survived
Ivan the Terrible as ‘Of mean stature, somewhat low and gross, of a
sallow complexion, and inclining to the dropsy, hawk nosed, unsteady in
his pace by reason of some weakness in his limbs, heavy and inactive,
yet commonly smiling almost to laughter. For quality otherwise simple
and slow witted.’ Although no certain diagnosis can be made on such
slight evidence, the above suggests that Fedor may also have suffered
from congenital syphilis.
Anastasia died in July 1560. Ivan was genuinely broken-hearted
and drowned his grief in a prolonged drunken debauch which started
immediately after her funeral. His brain conceived the fantasy that his
friend Alexei Ardatchev and his wise adviser, the monk Sylvester, had
contrived Anastasia’s death by witchcraft. He spared their lives but
dismissed and imprisoned them both. He then put to death Ardatchev’s

69
brother, a successful soldier, together with his twelve-year-old son. Next,
he condemned to death his friend Maria Magdalena and her five
children. On 21 August 1561 Ivan married a rich Circassian princess, but
this did not stop him making a proposal of marriage to Queen Elizabeth I
of England in 1563. In the same year he led a large army to invade
Lithuania. He captured the important trading city of Polotsk and seemed
to have the whole country at his mercy. Then his martial mood passed
and he returned to his debauch in Moscow, where his new Tsaritsa had
given birth to a son, Vassili, who lived for five weeks.
Towards the end of 1564 there occurred the first ludicrous
incident which clearly shows that Ivan now suffered from cerebral
syphilis (GPI). Early in the morning of 3 December a number of sleighs
gathered in the Kremlin Square. Servants loaded them with gold, silver
and jewels from the palace. The Tsar, the Tsaritsa and their two sons
boarded one of the sleighs. Then the cavalcade drove off, leaving no
forwarding address. Later in the day Ivan sent a message back home:
‘Unable to brook the treachery by which I was surrounded, I have
forsaken the state and taken my way whither God shall direct.’ His
bewildered nobles and bishops set out in search. They found him in the
small village of Alexandrov. a hundred miles north-west of Moscow, and
besought him to return. Ivan consented, making conditions that he was
free to execute any ‘traitors’ he so desired, to live in a house outside the
Kremlin, and to have a personal guard of a thousand men, the
‘oprichniki’. He returned to Moscow on 2 February 1565 and the
executions started two days later. The oprichniki were enlarged to
number over six thousand bandits and the new house outside the Kremlin
became a strange monastery with Ivan as abbot. Three hundred of the
oprichniki served as monks, clad in black cassocks over their sables and
cloth of gold. The day started with early matins at four in the morning
and ended at eight in the evening with vespers, Ivan praying with such
fervour that his forehead was permanently bruised by his prostrations.

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These bouts of prayer were relieved by visits to the torture chamber,
conveniently situated in the cellars.
The remainder of Ivan’s reign is a sickening tale of tortures and
floggings, of burnings and boilings, of all manner of hideous deaths. The
dreadful vengeance that he exacted on the city of Novgorod for an
alleged conspiracy, where for five weeks thousands were flogged to
death, roasted over slow fires, or pushed under the ice, or the executions
at Moscow on 25 July 1570 when Ivan and his son Ivan themselves
helped in the ghastly work, when Prince Viskavati was hanged from a
gallows and sliced to death with knives while Ivan raped the widow and
his son raped the eldest daughter – these are but two of the recorded
episodes in a reign of terror which lasted from 1565 until 1584. Ivan’s
madness culminated in the slaughter of his own son and heir, the
Tsarevitch Ivan, whom he stabbed to death with his steel-pointed staff in
a fit of murderous rage on 19 November 1581.
Disappointed in his hope of marrying Elizabeth of England, Ivan
made overtures to her cousin Lady Mary Hastings and, when she
declined the offer, announced his willingness to marry any kinswoman of
the Queen. Despite the fact that he was already married, Ivan seems to
have been obsessed with the fantasy of a royal union with England.
Elizabeth, probably bearing in mind the fortunes of the Russian
Company which had been founded under the patronage of Ivan in 1553,
caused the envoy to assure him that any one of a dozen of her
kinswomen would be happy to marry him. Fortunately for some
unknown girl, Ivan died on 15 March 1584 before the project went any
further. His last days were horrible, a time of sleeplessness, terror and
insanity, surrounded by soothsayers, his only relaxation the fondling of
his jewels and discoursing on their curative powers. The immediate
cause of death was an apoplectic fit while setting the board for a game of
chess.

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 Thousands of his subjects perished because Ivan suffered from
syphilis but, in the long term, the effect of his disease may have been
even greater. It is debatable whether the whole pattern of Russian
Tsardom would have developed in a different fashion, but there might
have been, in this first of the Tsars, an exemplar of enlightened rule
rather than of cruel despotism. Ivan’s murder of his son probably saved
the country from a no less bloody reign, for Ivan the Terrible had trained
him in cruelty and lust. But the murder left the throne to inheritance by a
congenital idiot, Fedor. Incapable of ruling, he was first under the
tutelage of Boris Godunov and then displaced by him. Chaos descended
on Russia after the death of Boris in April 1605 and no semblance of
unity was achieved until the election of the first Romanov in 1613.

That Ivan was syphilitic is certain but the case of his near
contemporary Henry VIII of England is controversial. Many writers have
emphatically denied that Henry suffered from syphilis. That he suffered
from something is agreed but the various authorities differ on the nature
of the illness. Gout, varicose veins, osteomyelitis of the femur, one or
more injuries suffered in tournaments, scurvy – all these have been
suggested as possible causes for the character change which became
evident in Henry’s forties. In view of all these differing opinions it seems
reasonable to re-examine the evidence for, whatever the nature of the
illness, there is no doubt that its effect upon the king profoundly
influenced the future history of the English nation.
First, let it be said that there is no reason why Henry should not
have suffered from all the disabilities so far mentioned. A sixteenth-
century man who lived to the age of fifty-six must have counted himself
lucky if he suffered from only one chronic illness, for most were
untreatable in those days. Henry took part in the rough sports of the time,
in which he is known to have had two accidents and suffered concussion.
He ate and drank enormously, becoming monstrously obese in his later

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years, so it would not be surprising if he developed varicose veins. Gout
and scurvy, both disorders associated with diet, were common and
Henry’s mode of life would certainly have encouraged the former. But
none of this can be adduced as proof that he did not also suffer from
syphilis.
Henry was born in 1491, at least two years before syphilis
erupted in Europe. While that fact makes it pointless to examine his
ancestry, the question of his progeny is altogether relevant. The first of
his six wives, Katherine of Aragon, mother of Queen Mary, gave birth to
a male infant who died within a few days, and had at least three stillborn
children all in the seventh or eighth month of pregnancy. Anne Boleyn,
mother of Queen Elizabeth I, miscarried at six months, at three-and-a-
half months, and of a foetus of unknown age. Jane Seymour had one son,
King Edward VI, born in 1537, and is unlikely to have had another
pregnancy in her seventeen months of wedded life. The fourth marriage,
with Anne of Cleves, was never consummated. There is no history of any
pregnancy in the cases of Catherine Howard, wedded to Henry from
1540 to 1542, or Catherine Parr who was left his widow in 1547, after
four years of marriage.
Henry had at least four children. The one known illegitimate boy,
Henry Fitzroy, Earl of Richmond, died at age seventeen from a lung
infection, possibly tuberculosis. Nothing else is known of his health.
Elizabeth I died at the great age of sixty-nine. She is reported to have
been short-sighted and may have had reason to believe she could not
bear children. ‘The Queen of Scots is lighter of a fair son and I am but a
barren stock’ was her remark on hearing of the birth of a Stuart heir
north of the Border. Mary Tudor died aged forty-two. She was very
short-sighted, spoke with the kind of loud voice used by a deaf person,
and is reported to have had ‘a nose rather low and wide’ which
discharged foul-smelling pus, of which her husband Philip II
complained. The one legitimate son, Edward VI, died in 1553 aged

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fifteen. He was never a healthy child and the cause of death remains
rather mysterious. Just over a year before, in April 1552, he fell ill of
‘mesels and smallpockes which breaking kindly from him was thought
would prove a means to cleanse his body from such unhealthful humours
as occasion long sickness and death’. There is little or no doubt that from
the beginning of 1553 he became increasingly ill with pulmonary
tuberculosis (consumption) but a skin eruption developed in the last
fortnight of his life, his nails fell off and the top joints of his fingers and
toes became necrotic. There was a widely held opinion that he had been
poisoned.
Every single incident in the above history can be fitted to an
illness other than syphilis. But the evidence is cumulative. Katherine of
Aragon’s three stillborn children, all dying later than the fourth month of
pregnancy, Anne Boleyn’s miscarriage at six months, Edward’s skin rash
in 1552 followed in little over a year by death from something sounding
like a combination of tuberculosis and congenital syphilis producing
syphilitic dactylitis, all are suggestive. Then we have Elizabeth’s and
Mary’s short sight, Mary’s presumed deafness, the flattened bridge of her
nose and a foul, purulent discharge – any of these could result from
congenital syphilis. Finally we have the evidence of Henry’s last two
marriages. If, as historians hold, his marriage policy was dictated by the
desire to found a strong Tudor line, then the inference is that Henry
became sterile or impotent in his late forties. This is a very strong
argument in favour of syphilis.
As for Henry himself, he was described in his youth by the
Venetian Pasquiligo as being: ‘The handsomest potentate I ever set eyes
on, above the usual height with an extremely fine calf to his leg, his
complexion fair and bright, with auburn hair combed straight and short
in the French fashion, and a round face so very beautiful that it would
become a pretty woman, his throat being rather long and thick.’ The
nineteen-year-old boy had everything: physical beauty, a magnificent

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presence, charm, a good brain. He was perhaps the finest specimen of
manhood ever to wear a crown. He revelled in all sports, in dancing and
music, but his chancellor Wolsey makes it plain that Henry also attended
to his business of ruling, held strong opinions, and was not easily
overborne.
In February 1514, when he was twenty-three years old, he fell
sick of the smallpox but he developed no pustules and made a seemingly
uneventful and complete recovery. Perhaps we are justified in
questioning the diagnosis, just as we questioned the nature of his son’s
skin rash in 1552. In 1521 Henry had his first attack of malaria, a
common enough disease in sixteenth-century England, from which he
suffered intermittently for the rest of his life. Three years later, in March
1524, he met with an accident while jousting with the Duke of Suffolk,
but seems not to have sustained a severe injury. Henry started to suffer
from headaches in 1527 and in 1527–8 he developed the notorious ulcer
on his thigh (or thighs) which plagued him for the rest of his days.
In 1527, the crucial year, Henry was aged thirty-six. Until then he
ruled wisely and with moderation. More than one dangerous riot, for
instance the ‘Evil May Day’ of 1517, was suppressed firmly, but without
cruelty by the standards of the time. During these years Henry laid the
foundations of English naval administration, built ships, founded Trinity
House, improved harbours, established shipyards and storehouses. In
1521, aided by ‘all the learned men of England’, he wrote the scholarly
counterblast to Martin Luther which earned him from Pope Leo X the
title Defender of the Faith, used by his successors on the throne to this
day. Henry encouraged Thomas More in his largely unavailing efforts to
provide a clean water supply and sewerage. Since the Black Death
medicine had ceased to be the Church’s prerogative with the result that
quacks and illiterate practitioners flourished. An Act of 1512 sought to
regulate medical practice by requiring examination for proficiency,
conducted by the bishop of the diocese and such experts as he might

75
appoint. The Act led to the institution of the College of Physicians in
1518. Henry, himself a skilled amateur physician, played his part in these
reforms.
From 1527 his character started to change, until the brilliant
young man gave place to a morose and bitter tyrant. Part of the change is
undoubtedly due to the worries of his divorce from Katherine, for the
arguments lasted no less than six years. The first definite sign of
imbalance comes in 1531, when Henry permitted enactment of the new
and frightful punishment of boiling to death. At least three people were
executed by this means. The Act was repealed within a few months of
Henry’s death by the advisers of Edward VI. In 1533 came the first
‘Treason Act’ by which any person who cast a slander on Henry’s
marriage with Anne Boleyn or who tried to prejudice the succession of
its issue was guilty of treason and faced with death by the barbaric
method of hanging and quartering while still alive.
Henry’s reign of terror began in 1534 with an indiscriminate slaughter of
Lollards, Lutherans, Anabaptists and Catholics. This was followed in
1535 by the cruel execution of the prior of the Charterhouse and all his
monks, and the beheading of the saintly Thomas More and Bishop John
Fisher. On 17 January 1536 Henry suffered a severe injury while jousting
and lay unconscious for over two hours, not fully recovering until 4
February. This accident forms the basis for the contention that Henry was
essentially ‘punch drunk’, but it occurred nine years after the character
change became evident. Concussion of the brain could certainly have
exacerbated his trouble and, from now on, we must regard Henry’s
behaviour as definitely abnormal. His treatment of Anne Boleyn was
savage. Head of the Church in England, he could easily have divorced
her but he preferred to put her to death and to declare her daughter a
bastard. The suppression of the abbeys in 1538–40 was marked by the
hanging of any abbot or monk who dared to resist or delay his
submission. The unnecessary vandalism, in which so much of the

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medieval art of England was wantonly destroyed, would surely not have
been countenanced by the brilliant, cultured young scholar who mounted
the throne in 1509.
During these repressive years, Henry suffered from continual
headaches and insomnia, from sore throats, and from the ulcer or fistula
in his leg. In May 1538, at the age of forty-seven, he is reported to have
been ‘sometime without speaking, black in the face and in great danger’.
The French ambassador Castillon, who recorded the incident, associated
the attack with closure of the fistula in the leg. For this reason it has been
suggested that Henry suffered a pulmonary embolism, blockage of the
pulmonary artery by a blood clot from a varicose vein. The loss of
speech is more in favour of an apoplectic fit.
In 1539 came the Statute of Six Articles, a remarkable piece of
legislation directed against any who challenged Henry’s position as
‘Head of the Church in England’, rendering a Protestant liable to be
burned as a heretic and a Roman Catholic to be hanged as a traitor.
Henry’s vacillating policy as to the extent of religious reform was
probably influenced by the changing opinions of his wives and their
‘parties’. There is no doubt that Henry’s chagrin over the ugliness of
Anne of Cleves, introduced to him by the reforming party, led directly to
the fall of Thomas Cromwell, endangered Henry’s firm friend and
supporter Archbishop Cranmer, and resulted in a renewed persecution of
Protestants. The impression given is that Henry started out with the
intention of reforming what was now his own Church and then took
fright at the possible consequences to his soul on the Day of Judgement.
There is here the suggestion of a split mind, one part trying to present
itself as a loyal son of Holy Mother Church, the other part intent on
bending that Church to his own will.
Henry never lost his grip on affairs of state. In fact, after the fall
and death of Wolsey in 1529, he tended towards an absolute rather than a
constitutional monarchy. Only three years before his death he led his

77
army in person during the war with France and actively superintended
measures to combat the threatened invasion of England. Although
prematurely aged, white-haired, monstrously obese, he never decayed
into a mental and physical wreck. Nor did Henry die as Ivan died,
terrified and gibbering. The accounts of his death vary and the actual
cause is obscure, but he died peacefully holding the hand of Archbishop
Cranmer, the only friend who remained devoted to the last.
There is nothing indisputably diagnostic of syphilis in Henry’s
case history, but much that is suspicious, as has been detailed above. A
modern medical student is taught to look for the simple things before
turning to the ‘small print’. If examining a fifteen-year-old child
suffering from a temperature, abdominal pain, and tenderness in the right
flank with some degree of muscular rigidity, he or she should exclude
acute appendicitis before considering a rarer type of illness. Further, the
student should always try to fit the signs and symptoms into one clinical
entity before deciding that the patient must be suffering from two or
more separate complaints. The history of Henry VIII should be
considered in a similar manner. The king undoubtedly suffered from
several minor complaints but his medical history, the obstetric history of
his queens, the suspicious death of his son Edward, the disabilities of his
daughter Mary, even the short-sightedness of Elizabeth, all these must be
balanced in the diagnosis. All can be separately explained by invoking a
number of different ailments but, if taken together, the evidence is more
than just suggestive. Syphilis was a very common infection in the early
sixteenth century and there is no good reason to believe that Henry
escaped it.
Whatever the nature of Henry’s ailment, or combination of
ailments, it exerted a profound effect upon the future of England. His
failure to produce a healthy male line was the beginning of the end of the
strong Tudor dynasty. There were no grandchildren, legitimate or
illegitimate. The firm, efficient rule of the Tudors gave way to the

78
attempted absolutism of the weaker Stuarts and plunged the country into
a civil war.
After Henry’s death the nine-year-old Edward came to the throne
under the guardianship of his mother’s family, the Seymours. With
Seymour patronage, Edward became the champion of Protestants.
Henry’s despoliation of monastic property was continued even more
ruthlessly, the bulk of monastic lands, treasure and revenues being
grabbed by greedy nobles. There was still considerable affection for the
Old Faith. The fanatical iconoclasm of Edward’s reign did not endear
Protestantism to the ordinary Englishman. Had Edward’s successor and
half-sister Mary behaved with moderation she might well have
succeeded in restoring the Roman Catholic Church, perhaps not to its
former power, but lastingly as the official English religion. There is no
doubt that Mary persisted in her persecution despite warnings from her
Catholic husband Philip II of Spain. Had she quietly burned half a dozen
rabid Protestants a year, she might have been honoured as a defender of
the pure faith against heresy. But Mary, almost certainly mentally
abnormal, would not listen to reason. She caused over three hundred
simple men and women to die at the stake in a little over three years and
thereby ensured that the great majority of her subjects would regard
Roman Catholicism as more evil than paganism. The settlement under
Elizabeth I came too late and religious toleration was unthinkable for
many years to come.
The effect of Mary’s persecution is evident even today. It is still
difficult to unravel the truth of many events in the sixteenth and
seventeenth centuries because the account given by a Protestant writer
will often differ materially from that of a Catholic. Nowhere have those
distant fires smouldered on longer than in Northern Ireland. The Marian
persecution also altered the attitude of the English to suffering. Like their
North American cousins they have always honoured valour but, unlike
some other peoples, have never taken kindly to the idea that there is

79
anything particularly noble in the voluntary bearing of pain. Might this
be one of the reasons why the merciful science of anaesthesia found its
first practitioners in America and Britain? The agony of the sixteenth-
century martyrs aroused not only anger and pity but also disgust. These
tortures were borne voluntarily, for the sufferer would have been spared
by a simple recantation, in most cases involving nothing more than a
reversion to doctrines accepted in earlier life. For the great majority of
English people, the medieval concept of a glorious martyrdom perished
in the fires of Smithfield.

In conclusion let us turn to the efforts made towards preventing

and curing syphilis. The earliest known treatment was by purgatives and
semi-magic antidotes to poisoning. The specific drug guaiacum remained
a popular remedy until the end of the sixteenth century, although it was
attacked by Paracelsus, one of the more revolutionary physicians. These
treatments must have been quite ineffective. A more efficient, though
more dangerous, medicament was found in mercury.
Mercury, in the form of the ore cinnabar, had been used for the
treatment of skin diseases by the Arabian school of doctors and an
ointment containing metallic mercury was prescribed by Theodoric of
Lucca in the thirteenth century. This early use of mercury has been
adduced as evidence that syphilis is an ancient disease in Europe, while
the lack of any mention of mercury treatment (which is difficult to hide)
has suggested to some historians that Henry VIII cannot have suffered
from syphilis. Neither argument is particularly convincing. Mercury
seems to have been tried in any severe and intractable skin disease. In
Henry’s case mercury would not have been used unless there was
manifest skin involvement, of which there is no evidence.
It is probably because of evident skin lesions that Giorgio
Sommariva of Verona tried mercury for the treatment of syphilis in 1496.
He was not a doctor but some years later the physician Jacopo

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Berengario da Carpi achieved fame in Italy for his success with mercury.
Benvenuto Cellini was one of his patients. The method became known as
‘salivation’ because near-poisoning with metallic mercury and its salts
produced immense amounts of saliva. This form of treatment by oral
administration, ointments and vapour baths remained a fairly effective
but extremely unpleasant and dangerous medication for over three
centuries. Many attempts were made to find other specifics but the only
one of any lasting value was potassium iodide, introduced in the 1840s
and effective in the later stages of the disease. So much harm resulted
from quacks who claimed success with secret remedies that in 1917
treatment of syphilis by unqualified persons was made a criminal offence
in Britain.
Rational treatment of a disease is impossible unless the cause is
known. The cause of syphilis was not fully understood until the twentieth
century. In 1905 F.R. Schaudinn and P.E. Hoffmann discovered the
causative organism to which they gave the name Spirochaeta pallida.
The name has since been changed to Treponema pallidum, the various
sub-species of which are now known to be the cause not only of the
venereal and non-venereal types of syphilis but of the related yaws, pinta
and bejel. Hideyo Noguchi isolated the bacterium from brains of patients
suffering from the late manifestation, general paralysis of the insane, and
so proved the link, half suspected for a century. In 1906–7 the
Wassermann test was developed which showed the presence of syphilis
even when latent. In 1909 Paul Ehrlich of Frankfurt succeeded, after
many experiments, in producing the first ‘systemic antiseptic’, one
which could be injected into the bloodstream and kill bacteria without
harming the body tissues. This, the famous ‘606’, was an organic arsenic
compound which Erhlich called his ‘magic bullet’ in the belief that it
would prove lethal to a wide range of bacteria. In fact he was wrong for
it was only effective against the important group of spirochaetes or
treponemes. Prescribed under the name ‘salvarsan’ this drug became

81
widely used in the treatment of syphilis but produced quite serious side-
effects and was replaced by neosalvarsan shortly before the First World
War. These arsenical preparations proved their worth when venereal
disease became rampant in the special conditions of warfare. The Second
World War saw the introduction of penicillin, the first of the antibiotic
group of drugs, which was successfully used by John Mahoney in 1943
to treat not only syphilis but the second of the ancient venereal
infections, gonorrhoea.
Prevention is far more important than treatment in a disease of
this nature. The enemy of prevention is secrecy. By the early years of the
twentieth century the Scandinavian countries had been actively and
sensibly tackling the problem for nearly a hundred years. But in
Victorian Britain, and many other countries, prostitution and venereal
disease were taboo subjects, having no official existence. On 1
November 1913 the British government set up a Royal Commission to
explore and recommend action. The Commission reported in February
1916 at a time when venereal disease had enormously increased. Briefly
they recommended that local authorities be empowered to provide free
diagnosis and treatment. One of their recommendations permitted
residents outside the authority’s area to seek advice and treatment, a
sensible means of preserving anonymity. They could devise no way of
combining notification with anonymity and decided the latter to be
essential. The most important part of the report dealt with proper
education in place of secrecy.
Action soon followed the report. Clinics, attached to voluntary
and municipal hospitals, came into operation in 1917. Many local
authorities posted the address of the nearest clinic in public lavatories, a
common-sense method of advertisement. The most notable reform came
in 1925 when local authorities were empowered to undertake a
programme of education. Since education of this kind can be achieved
only by public discussion and open acceptance that there is something to

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be discussed, the social taboo which overlaid the whole subject had at
last been removed. Frank recognition of the public danger combined
with anonymity of the individual removed much both of fear and of
stigma and helped to transform the patient from a sinner into an
unfortunate.
The Second World War saw a world-wide increase in the number
of cases and the British government took firm action. Social workers not
only made people aware of treatment facilities but traced contacts and
persuaded them to be Wassermann tested. At the same time notification
and compulsory treatment of syphilitics found to have infected three or
more contacts was introduced. These measures, combined with effective
penicillin treatment, greatly reduced the number of cases. The
regulations ended in 1947 but social work continued so efficiently that
syphilis had apparently been defeated by 1956 and many clinics closed
for lack of patients. Similar measures, and treatment with penicillin in
particular, achieved excellent results on almost a global scale.
Within ten years the greater part of this good work had been
rendered nugatory. The number of cases of primary and secondary
syphilis had again risen in accordance with a pattern that applied to
Britain and the United States among other countries. This tragedy was
caused partly by the emergence of a penicillin-resistant strain of
organism, partly by introduction of a more virulent type, but chiefly by
the laxer moral code and sheer carelessness of young people in the
‘permissive’ 1960s. Over recent decades the growth of syphilis has been
most evident in the developing world, and has often served to increase its
victims’ susceptibility to the human immunodeficiency virus (HIV)
whose spread we shall consider in the Conclusion.

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 C F
SMALLPOX, OR
THE CONQUEROR CONQUERED

We must now consider a little more deeply those infections which have
developed in the early centres of civilization and have been transferred
from one centre to another, sometimes with devastating results. These
diseases have become tamed in their original habitat by acquired
resistance of the human to the infecting organism but have returned to
their ancient virulence when accidentally transmitted to unaccustomed
communities by immigrants such as explorers, missionaries or traders.
Much of this chapter will be devoted to the history of smallpox
and its prevention. Smallpox, caused by a virus, is one of a group of
infections once known as ‘childish diseases’ of which measles was
another leading example. They are diseases of the crowd and cannot
have persisted in a society of small, scattered settlements. Their origin as
pathogens causing disease in humans must lie in the earliest large
concentrations of population, because the causative organism can only
produce the disease by direct transfer from one actively infected person
to another who has not been infected. In this respect they differ from
diseases such as typhus and bubonic plague, infections of the louse and
of the rat or flea respectively, which can be transferred to the human, but
do not depend on the human host for their existence.
An attack of an acute infection, such as are smallpox and
measles, will confer resistance or actual immunity to a second attack for
a period of time or perhaps for life. A person who is immune can neither
acquire the infection nor transmit it to a person who is not immune,

84
because the disease can only be transmitted or acquired when active.
Such an infection is never totally absent from the community but will be
preserved by sporadic cases and small outbreaks. When in this state the
particular disease is spoken of as ‘endemic’ in the community.
Continuance of the disease always requires a reservoir of uninfected and
non-immune people and they will always be at risk. A single ‘endemic’
case may then infect a number of unprotected individuals until there is an
‘epidemic’ of varying numerical severity. At the end of the epidemic, the
number of totally immune or partially protected people will be at a
maximum, and the disease will retreat into the endemic state. Then the
number of susceptible people will increase and the process repeats itself.
This will determine the age group most susceptible to infection. For
instance, if a major epidemic has not occurred for twenty years, then
children and adolescents will be at greatest risk.
Measles commonly confers a life-long immunity but is so easily
transmitted that in the early part of the twentieth century doctors
expected a severe epidemic about every five years, the great majority of
patients being young children. Thus the larger part of the European adult
population had already suffered from measles in childhood and so were
immune. Many more adults were partially protected by a degree of
resistance inherited from immune parents and so were unlikely to
experience the full severity of the infection. The latter ‘maternal
resistance’ also applied to susceptible children. This is why measles
tended to be regarded as the typical ‘childish disease’ in Europe and why
measles behaved in so unusual a manner when accidentally introduced to
a totally unprotected community in the South Pacific Islands.
In 1872 epidemic measles appeared among a largely unprotected
community in South Africa, spreading to Mauritius in 1873–4 and
Australia in 1874. On 10 October 1874 the British government formally
annexed the Fiji Group of islands. Later that year King Cakobau of Fiji
with his family and royal suite visited Australia to experience the

85
delights of civilization. Measles was one of the civilized delights they
experienced. The party left Sydney for Fiji on the cruiser HMS Dido.
arriving home on 15 January 1875. One or two of the party landed while
still seriously ill with something resembling a very severe attack of
measles. Within a little over three months at least one-fifth and probably
more nearly a quarter of the Fijian population had died. The total number
of deaths in the Fiji Group alone is estimated at over forty thousand. The
illness spread throughout the South Pacific causing similar mortalities
and creating panic wherever it appeared. A contemporary writer, William
Squire, recorded that many died from sheer terror, others from seeking to
relieve the burning skin rash by immersing their bodies in the sea. He
believed that ‘the epidemic only ceased when every person had been
attacked’. In other words all ages, and not children only, had been at risk.
No one really knows how many died of measles, because Europeans
introduced other unaccustomed and lethal infections, tuberculosis and
syphilis among them. It is widely believed that the magnificent physique
of the natives has been ruined and their number reduced to about one-
tenth of the population living in the South Pacific Islands less than a
hundred and fifty years ago.
The story of measles in North America is also instructive. In this
land of wide open spaces and scattered communities, repeatedly
refreshed by immigrants from Britain and France, introduction from the
European centre of infection produced a pattern quite different from the
rapid, explosive pandemic in the South Pacific. The first recorded
outbreaks of measles were in Canada in 1635 and 1687. Boston was
attacked in 1657 and again in 1687, the latter outbreak being probably
derived from the Canadian epidemic rather than from Europe. Further
epidemics occurred in Boston in 1713, 1729, 1739 and, more severely, in
1740. The long sea voyage of the eighteenth-century sailing ships
militated against transmission from Europe. If the report that South
Carolina, Pennsylvania, New York and Connecticut were not attacked

86
until 1747 is correct, it would seem that ‘American’ measles was now
developing. Boston appears as the main centre of a severe epidemic in
1772, in which some hundreds of children are reported to have died in
the district of Charlestown, Massachusetts. Six years later a similar lethal
epidemic ravaged New York and Philadelphia, which suggests that the
infection was now settling into the class of ‘childish diseases’ but
producing an illness of greater severity than in Europe at the same date.
From the East Coast measles rode in the covered wagons to the
Mississippi Valley, Kentucky and Ohio.
Although some of the above statements may be regarded as
questionable, because differentiation between measles and other rash-
producing diseases was not exact, the broad pattern is of great
importance in the history of infection. It well illustrates, first, how a pool
of infection is formed and, second, what happens when one pool
converges on another pool which does not contain the particular
infection. The American pattern can be little different from those which
developed in the earliest centres of civilization. The course taken by
measles in North America was not dictated by any change in the
infecting virus but by growth and cohesion of the population. In the
beginning scattered communities were separately infected, and the small
community might develop a resistance sufficient to prevent persistence
of the causative virus so that no fresh epidemic could develop until a
new invasion came from outside. If the new invasion came within a few
years, then the illness would appear only among children. If invasion
was delayed for twenty or more years, then adults, too, would be at risk.
As the distance between communities decreased and intercommunication
became quicker, so the chance of infection increased and the age of the
susceptible group fell. Thus measles became a nationally rather than a
locally endemic illness. There can be little doubt that a similar merging
of any disease from an exotic pool will produce exceptional virulence
initially, followed by reversion to its previous state.

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 When we turn to the highly controversial history of smallpox, we
must remember not only that an unaccustomed introduction can produce
a more lethal type of illness in a new community, but that an old
infection can be refreshed by introduction of a new strain of causative
organism. Some historians believe that smallpox was a member of the
Mediterranean pool of diseases as early as the fifth century BC. The
illness commonly leaves scars known as pock-marks and no depiction of
a pock-mark has been found on any Greek or Roman representation of
the human features. Such absence may be artistic licence rather than
proof of non-existence. A second school of thought proposes that India is
the original pool of infection and argues that the Indian goddess Shitala
has been invoked as protection against smallpox since time immemorial.
There is a suggestion that the Indian disease and a method of prevention
were exported to China. The earliest definite and recognizable
description is that of Ko Hung, a Chinese physician who lived from AD
265 to 313. Whether of Indian or Chinese origin, smallpox could have
travelled the ancient Silk Road from the East, reaching Europe before
AD 581 when Gregory of Tours described an undoubted -epidemic in
France. By then it had almost certainly been introduced into Japan by
Buddhist missionaries travelling from Korea. Smallpox and measles
were a central feature of the Japanese ‘age of plagues’ covering the
period from 750 to 1000. About 980 there is a mention from Japan of
special buildings to isolate smallpox patients and an interesting form of
treatment with hangings of red cloth. An Englishman, John of
Gaddesden, recommended red drapes for the same purpose in 1314. This
‘red treatment’ persisted in folk medicine for many centuries and
achieved a semi-scientific status in 1893 when the Danish pioneer of
light therapy, Niels Ryberg Finsen, used red light produced by a screen
which excluded ultra-violet rays. In no case was ‘red treatment’ of any
value but it is of interest as an example of the Doctrine of Signatures or

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‘like cures like’, since smallpox produces a confluent rash of crimson
colour.
The most authoritative early account of smallpox is by the
Persian physician commonly known as Rhazes, about AD 900. Part of
his achievement was to differentiate more clearly between this disease
and measles. Smallpox certainly existed in Europe, Asia and Africa from
the tenth century onwards but the severity of the European disease
varied. It seems to have been neither so widely spread nor so lethal as it
was to become in the seventeenth and eighteenth centuries. Some
contemporary writers regarded measles as the more dangerous infection
and it is quite possible that the term ‘smallpox’ was used for a number of
illnesses, measles included, which are characterized by a rash. Smallpox
itself existed in three forms: Variola major or true virulent smallpox:
Variola minor, a mild form known as alastrim; and Variola vaccinae, the
disease primarily of cattle known as Cowpox. As all three are caused by
variants of the same virus, an attack of one will protect against attack by
either of the other two, although the immunity may not be life-long. The
balance of evidence suggests that the mild form alastrim was the more
common in Europe until the seventeenth century.
The true or virulent form of smallpox played a large part in the
Spanish conquest of Mexico and it seems certain that the existence of the
mild alastrim in Europe was also responsible for the comparative ease
with which a very small Spanish force defeated an entire nation. On 18
November 1518 Hernando Cortez sailed from the Spanish colony of
Cuba with an army of eight hundred mixed Spaniards and Amerindians.
He landed on the coast of Yucatan to receive friendly messages and
presents from the Aztec Emperor Montezuma (or Moctezuma) of
Mexico. Continuing his voyage, Cortez founded the city of Vera Cruz,
ensured the loyalty of his hesitant troops by burning the ships so that
they had no means of returning to Cuba, and marched inland to Tlascala.
Here he encountered a hostile force but, after a hard-fought battle,

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concluded a treaty with the Tlascalans and set out for the Aztec capital
Tenochtitlan (Mexico City) with a reinforcement of about a thousand
Tlascalan ‘friendlies’.
The city, a large community of some three hundred thousand
inhabitants, stood isolated in a great lake and was approached by three
stone-built causeways, one of them six miles long. Cortez maintained
friendly relations with Montezuma for some time but they deteriorated
after an attack on Vera Cruz apparently instigated by the Emperor. Cortez
imprisoned him, fined him a large amount of gold and forced him to
acknowledge the overlordship of Spain. Six months later, in May 1520,
Cortez learned that a second Spanish-Amerindian army under Panfilo de
Narvaez was striking inland from the coast with the intention of restoring
Montezuma to power. Leaving one of his officers, Pedro de Alvarado, in
charge of the capital, Cortez intercepted Narvaez and defeated him in a
surprise night attack. Then came news that Alvarado was fighting off an
insurrection in the city. Cortez hastened back, arriving on 24 June 1520
to find Montezuma dead, Alvarado besieged with a tiny remnant of the
army, and the Aztec people in general revolt. Cortez fought his way out
of the city with great difficulty after a heroic struggle in which he lost
almost half his remaining men, and took refuge with the more or less
friendly Tlascalans. By the end of 1520 Cortez had received a few
Spanish reinforcements, recruited an army of ten thousand Tlascalans,
and built a flotilla of small ships. He ordered a canal to be dug and
succeeded in bringing his boats to the lake surrounding the capital, to
which he laid siege in April 1521. Cortez himself commanded his task
force of boats carrying three hundred men. He defeated a superior force
in canoes and made landings on the causeways but suffered a reverse
with many casualties in his first attempt on the city. However, the city
fell to him, after a stubborn defence, on 13 August 1521. When the
Spaniards entered, they found houses filled with dead. The inhabitants
had not died from wounds or starvation but from disease.

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 When Panfilo de Narvaez left Cuba in May 1520 on his voyage
to Mexico, he took with him a number of Africans, probably the same
Christian slaves (or their children) who had been shipped to the West
Indies by order of King Ferdinand. Some of them fell ill and at least one
was landed on the American mainland while still sick. He infected others
and the disease spread very rapidly among the Amerindian population
who called it ‘the great leprosy’. The description bears no resemblance to
leprosy and the very rapid spread with an immediate skin rash does not
favour yaws or syphilis. From the subsequent story, there can be little
doubt that the infection was a lethal form of smallpox.
The illness was certainly more fatal than the smallpox known in
sixteenth-century Europe. It must have assumed an epidemic form
among the native Tlascalans and been carried by them to the capital in
the first abortive attempt at capture during the early summer of 1521.
When Cortez entered the city in August he found that approximately half
the inhabitants had died. Within six months hardly a single village in the
known regions of New Spain remained uninfected. It has been estimated
that almost half the Aztec population perished in this first epidemic.
A second epidemic, known to have been a fresh introduction by
Spanish ships, carried on the devastation in 1531. Three further
visitations in 1545, 1564 and 1576 reduced the native population of New
Spain from a much-disputed ten to twenty-five million before the
conquest to perhaps fewer than two million by the early seventeenth
century. Dreadful as this mortality sounds, another area of Spanish
conquest seems to have suffered even worse. Over much the same period
the Inca population of Peru diminished from some seven million to
approximately half a million. Smallpox is undoubtedly the chief culprit
but the Spaniards also introduced mumps and measles which caused
many deaths. There is no evidence at all that any of these infections
existed in the area before the coming of the Spanish Conquistadores. But
the appalling mortality had another effect. The Amerindians in general

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came to regard resistance as hopeless. Invaders who were able to cause
death on this scale could not be mere mortals but vengeful gods. The
natives of South America were not alone. The aboriginal tribes of south-
eastern Australia may well have felt similarly when, in the last years of
the eighteenth century, they too were more than decimated by sudden
exposure to the smallpox accompanying the first stage of British
colonization.
The reason for the supposed divinity of the Conquistadores is not
that they wore armour capable of turning an Aztec weapon or that they
used gunpowder to outshoot a native arrow. The overriding reason for
regarding them as superhuman is that they themselves appeared immune
to the terrible punishment they inflicted upon the Amerindians. The
initial epidemic among the Aztecs in the summer of 1521 may have been
caused by a chance case of the lethal Variola major introduced by an
African slave or it may be that the milder form Variola minor or alastrim
underwent a change to the major type when introduced to an entirely
unaccustomed and unprotected people. In either case, the Spaniards
came from a far continent in which the milder form was a common
disease and therefore they had at the very least some resistance to
infection. Whatever the explanation may be, there is no doubt that
smallpox, and the relative immunity of the Spaniards to smallpox, played
as great a part, if not a greater part, in the destruction of the Aztec race as
did the superiority of Spanish arms. Thereafter Mexico remained one of
the reservoirs of virulent smallpox. As late as 1947 a traveller from
Mexico introduced a limited epidemic into New York.
Smallpox produced only a comparatively mild illness in Europe
during the whole of the sixteenth century. In the seventeenth century it
started to change to a more lethal type. The reason for the change is not
known, but may well have been refreshment of the virus by re-
introduction from Spanish America. In 1629 the first Bills of Mortality
for London listed smallpox under its name, the number of deaths

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averaging not more than a thousand a year in a population of between
three and four hundred thousand. The figure started to rise steeply in the
last years of the century. From being a relatively innocuous but common
disease of childhood smallpox gradually became the most lethal illness
of the young. At the beginning of the eighteenth century smallpox
destroyed more European children than any other infection except,
perhaps, infantile diarrhoea. In one English provincial town of fewer
than 5,000 inhabitants, 589 children died of smallpox between 1769 and
1774. Of these 466 were under three years and only one over ten. During
a similar period in Berlin, 98 per cent of deaths from smallpox were
children under twelve and in London 85 per cent were under five. Deaths
of young people on this kind of scale must have produced a check on the
increase of population but numerical evidence is unreliable in the
absence of census figures.
Efforts first to control then to defeat such a killer as this must be
as important in world history as the effects of the disease itself, so let us
examine how they came about. Even the most ignorant of witch-doctors
must have observed that some diseases are by nature chronic and some
acute, that a person may fall victim to one disease quite frequently, that
another disease may attack him only once in his lifetime, but not kill
him. Thus the phenomenon of acquired immunity, though not expressed
in that term, has been common knowledge for centuries. Reason would
suggest that, if a dangerous disease does not strike an individual more
than once, a mild attack of that disease is highly desirable. Since it was
also known that such a disease somehow passed from one person to
another, it would also be reasonable (but not invariably correct) to expect
that an uninfected individual would benefit if placed in contact with the
mildest possible case available. An example is found in the diary kept by
John Evelyn. On 13 September 1685 Evelyn travelled to Portsmouth
with his friend Samuel Pepys, stopping at Bagshot on the way. Evelyn
recorded:

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 I went and made a visit to Mrs Graham, wife of James Graham
Esq. Her eldest son was now sick there of the small pox, but in a likely
way to recovery, and other of her children ran about and among the
infected, which she said she let them do on purpose that they might
whilst still young pass that fatal disease she fancied they were to
undergo one time or other, and that this would be for the best, the
severity of this cruell disease so lately in my poor family confirming
much of what she affirmed.

This practice was combined with the Doctrine of Signatures or

‘like cures like’ to produce the method of protection known as
variolation: implantation of tissue or secretion from an infected person
into the subject to be protected. The Chinese are believed to have learned
the first method from India and practised a form of variolation from the
tenth century AD onwards. They removed scales from the drying
pustules on a patient suffering from mild smallpox, ground them to
powder, and blew a few grains into the nostrils of persons who had not
developed the illness. There is no definite evidence of any such method
being practised in Europe.
It is possible, though by no means certain, that variolation, using
matter from a smallpox pustule, had been practised in Asia Minor for a
long time. The first certain attempt was about 1710 when a Greek or
Italian physician, Giacomo Pylarini of Smyrna in the Ottoman Empire,
removed some of the thick liquid from a pustule and rubbed it into a cut
which he had made on the arm of a person he wished to protect. So far as
is known this is the first occasion on which the method of ‘inoculation’
was used. In 1713 another physician, Emanuel Timoni of
Constantinople, performed a small series with apparent success and
wrote an account to Dr John Woodward in London. Woodward published
his findings in Philosophical Transactions, the Journal of the Royal
Society. His paper aroused some interest but little practical experiment.

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In 1717 Lady Mary Wortley Montagu, wife of the British Ambassador in
Constantinople, had her infant sons inoculated. She returned to England
shortly before one of many epidemics caused a number of deaths in
1721, and had her five-year-old daughter inoculated in the presence of
several London physicians who were impressed by the mildness of the
subsequent illness. This success and the status of Lady Mary stimulated
interest. King George I decided to have his grandchildren inoculated but
took precautions. Six prisoners under sentence of death in Newgate
Prison volunteered to be ‘guinea pigs’ on promise of reprieve. A trial
was next made on eleven charity school children of varying ages. So
mild were the following attacks that two royal grandchildren received
treatment.
Royal approval made inoculation fashionable in Europe and a
number of leading physicians commended the practice. But a good deal
of opposition developed when it became clear that the method was by no
means always successful. The ensuing protecting attack of smallpox did
not always take a mild form, two or three deaths occurring in every
hundred inoculations. Further, many intelligent people rightly suspected
that variolation, even though it might protect the individual, spread the
disease more widely by multiplying the foci of infection. For these
reasons inoculation fell into disrepute and was rarely used in Europe
after 1728.
The story took a different turn in the North American colonies,
first infected with smallpox by British settlers in Maryland during the
mid-seventeenth century. The disease slowly spread to Virginia, Carolina
and New England. It never became so prevalent as in Europe because of
the lesser density of population, but was one of the major killers and
aroused proportional fear. The sixth American epidemic, possibly
connected with that in England, developed at Boston, Massachusetts, in
April 1721. The famous minister Cotton Mather, a Fellow of the Royal
Society, had read of Timoni’s experiments and suggested that a trial of

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inoculation be made by the medical profession. Initially only one doctor,
Zabdiel Boylston, showed any interest. He first inoculated his six-year-
old son and two Negro slaves on 26 June 1721. The experiment was
successful and, in the course of the summer, he inoculated 244 people in
all. Unfortunately six of his subjects died and the report that he had used
actual smallpox matter aroused hostility. In September Boylston was
accused of spreading infection and narrowly escaped lynching. Although
forced by public opinion to desist, Boylston lived to see general
acceptance of variolation in America before he died in 1766.
General acceptance depended upon a much lowered death rate. In
1738 a severe epidemic ravaged the town of Charleston, South Carolina.
Using an ‘improved method’ Dr James Kilpatrick carried out a
programme of mass variolation and claimed that a high mortality had
thereby been prevented. In 1736 Benjamin Franklin had lost his only
legitimate son from smallpox and he subsequently became one of
Kilpatrick’s most fervent supporters. Probably Franklin influenced
George Washington who urged inoculation on his troops and set up
special hospitals for the purpose.
Dr Kilpatrick came from Charleston to London in 1743 where he
wrote an account of the 1738 epidemic and emphasized the success of
his new method. Earlier practitioners believed inoculation would be
successful only if the pustular exudate ‘lymph’ was implanted deeply
into the fatty layer underlying the skin. Kilpatrick used a shallow scratch
in the skin itself. The lymph, taken from the mildest available case, was
then rubbed into the scratch. This method tended to produce a local
rather than a general infection and was therefore safer although perhaps
not as certain. Kilpatrick’s enthusiasm combined with an increase in the
severity and incidence of smallpox to bring back the popularity of
variolation in Europe during the 1750s.
Inoculators were specialists in their art and often not medically
qualified. Some of the better-known are Robert Sutton and his son

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Daniel, Jan IngenHousz and Thomas Dimsdale. The Suttons developed
the important advance of ‘removes’ or ‘passaging’. They inoculated
lymph from the mildest possible case into a number of recipients,
selected the mildest of those showing signs of local infection (reaction),
inoculated lymph from this subject into another group, selected the
mildest and so on. IngenHousz, called to inoculate the Royal Court of
Vienna in 1768, used two hundred subjects before the Royal recipients,
probably ten or more removes. In the same year Thomas Dimsdale
inoculated Catherine the Great, Empress of Russia, after passaging the
lymph through several hundred servants. He received a truly imperial fee
and there is still a descendant bearing the title of Baron Dimsdale to
commemorate his success. The Suttons were probably also the first to
use ‘Airing Houses’, premises where inoculated persons stayed under
supervision until danger of spreading infection had passed. These houses
were obviously essential to avoid the accusation that variolation
increased the risk of transmitting smallpox to the community.
Such precautions added to the expense of variolation and for this reason
many medical historians believe that only the more wealthy classes could
afford protection. The evidence provided by England shows this view to
be partly incorrect. Records suggest that, although variolation was very
rarely used for the protection of the poorer classes in towns and
especially in London, it was frequently used in country districts, the fees
being charged to the parish. Here is an extract from the churchwardens’
accounts of a tiny village named Fitzhead in Somerset:

May ye 21st 1769. It is this day agreed upon by the

churchwardens and overseers and the other inhabitants of the said
Parish of Fitzhead that all poor children that have been chargeable to
the said parish, at a parish meeting held this day or a Vestry for that
purpose held, shall be inoculated by the parish expence, as witness our
hands John Comer, John Arscott, Jno Holcombe, William Toogood.

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1769 Paid for inoculating of the parish 01.15.00
1789 Paid Dr Comer his bill for inoculating 27 poor people 05.08.00
1796 Paid Mr Sully for inocklating 34 children 08.10.00
1798 Towards Inocklating Stook and Stone’s children 00.15.00
1798 Paid for inocklating Wm Crewse three children 00.07.06

Another village, Swallowfield in Berkshire, was a little larger.

Many of the village women acted as wet nurses for the Foundling
Hospital in London. In 1767–8 there was much smallpox in the district
and prospective employers demanded that the children, now aged seven
or a little more, should be inoculated before apprenticeship. Mrs Juliana
Dodd, an Inspector of Wet Nurses for the Foundling Hospital, wrote: ‘I
have now but eighteen children under my inspection but mention’d
twenty to the surgeons for inoculation, intending to make up that number
by having two that are already apprenticed inoculated at my expence,
having promised it to their masters at the time of their being
apprenticed.’ Mrs Dodd enclosed two letters from practitioners giving
their terms. The first wrote: ‘The lowest price for servants as indoor
patients is three guineas each. Yet in consideration of the number
proposed, and being children of the poor, he is ready to receive them
under his care at his house near Reading and to find all necessaries,
washing excepted, at two guineas each.’ The second practitioner was
somewhat cheaper: ‘The lowest terms to inoculate twenty poor children
and find them in every thing necessary will be twenty guineas, if
charitably bestowed. All must be taken at once and the children sent
decently clean. If any be afflicted with any complaint or disorder, that
complaint will be cured before they are inoculated.’ Mrs Dodd added
that there would be some additional expense to have the children ‘aired’,
which means that they must be kept in quarantine. If inoculation of the
poor was practised to this extent throughout the country and was

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successful, smallpox must have been a dying disease in the last quarter
of the eighteenth century.
Edward Jenner’s introduction of vaccination in 1798 has tended
to overshadow the value of variolation as a means of protection. For
centuries there had been a folk tradition that cowhands and dairymaids
never contracted smallpox. Cowpox is not common but, if introduced
into a herd, may infect a number of beasts. It usually takes the form of a
local ulcer on the udder and will affect the cow’s general health and milk
production if untreated. The lesion is very contagious. A person who
milks the cow is liable to develop a cowpox pustule or ulcer on the hand
or wrist but the risk of human-to-human spread is slight. Only very
rarely is the local skin lesion followed by a generalized illness, although
there is sometimes a low fever and malaise. Transmission is by direct
contact, that is matter from the ulcer must impinge on a scratch or wound
in the skin before the human can acquire the disease.
There are probably many unknown instances of farm workers
deliberately allowing themselves to be infected with cowpox but only
two have entered the literature. In 1774 a farmer named Benjamin Jesty
of Yetminster in Dorset took matter from a cowpox lesion and rubbed it
into scratches made with a darning needle on the arms of his wife and
two sons. None of them acquired smallpox although there was a
considerable epidemic in the district. The sons are said to have been
inoculated with smallpox fifteen years later with no effect, local or
general. In 1791 a German named Plett performed a very similar
experiment.
As for Jenner, born at Berkeley in Gloucestershire on 17 May
1749, he was a house pupil of the great surgeon John Hunter at St
George’s Hospital in London. There is little doubt that Hunter fired his
pupil with enthusiasm for ‘the experimental approach’. The cowpox
story first came to Jenner’s notice in the 1770s when he was serving his
apprenticeship with a surgeon at Sodbury. Jenner returned to practise in

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Berkeley and, contrary to the popular story, investigated the effect of
cowpox for nearly twenty years before making his first human
experiment. On 14 May 1796 he took lymph from a cowpox pustule on
the wrist of a dairymaid named Sarah Nelmes and inserted it into two
superficial incisions, each about three-quarters of an inch long, made in
the arms of a boy, James Phipps. Jenner thus described his progress:

On the 7th day he complained of uneasiness in the Axilla, and

on the 9th he became a little chilly, lost his appetite and had a slight
headache. During the whole of this day he was perceptibly indisposed
and had rather a restless night, but, on the day following, he was
perfectly well. The appearance and progress of the incisions to a state
of maturation were pretty much the same as when produced in a similar
manner by variolous matter.
On the first of July following, this boy was inoculated with
matter immediately taken from a smallpox pustule. Several punctures
and slight incisions were made in both his arms, and the matter was
well rubb’d into them, but no disease followed.

Jenner was not satisfied with one success but decided to defer
publication until he had a series. Unfortunately cowpox disappeared
from the neighbourhood of Berkeley and did not return for two years. He
then ‘vaccinated’ twenty-three subjects, before proceeding to inoculate
them with smallpox after a lapse of some weeks. In every case
variolation produced nothing more than a slight local reaction. Not until
then, in 1798, did Jenner publish his great classic, a seventy-five page
pamphlet entitled An Inquiry into the Causes and Effects of the Variolae
Vaccinae, a Disease, Discovered in some of the Western Counties of
England, particularly Gloucestershire, and known by the Name of Cow
Pox. Jenner had carefully thought out his subject and had conducted
experiments as opportunity offered over a number of years. He did not
put his theory to the crucial test of human experiment until he believed

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that no harm would result. He did not rush into print. Even with a
volume of evidence, an assured result, and although frustrated by
absence of cowpox for two years, he resisted the temptation to publish
his findings until the results were proved beyond question. Edward
Jenner was a true scientist.
Within five years translations of Jenner’s pamphlet had appeared
in all the major European languages, but despite his careful preparation,
his Inquiry had a mixed reception and aroused prolonged opposition. The
‘inoculators’ obviously attacked Jenner’s ‘vaccination’ because its
general adoption would end their lucrative trade. His method became a
favoured subject for cartoonists. Clergy thundered from their pulpits
against the iniquity of transferring an animal disease to Man. The
protests of those who objected that other and worse infections might be
transmitted from cattle to the human were more rational. This last
criticism, combined with a rather natural distaste for inoculation with
matter from a sick cow, induced early vaccinators to adopt an arm-to-arm
technique whenever possible. It became customary to perform one
inoculation with cowpox from the animal and then to set up a chain by
vaccinating from one human to another, just as the inoculators had used
the system of ‘removes’. The method proved successful and disposed of
the objection to ‘animal matter’ but added considerably to the danger of
transmitting other human infections such as syphilis. Arm-to-arm
inoculation also caused the great vaccination controversy.
By the end of 1801 about a hundred thousand vaccinations had
been performed in England and the method was coming into world-wide
use. It now became difficult to supply sufficient cowpox lymph and to
ensure its activity when sent over long distances. Many different
methods were tried. In 1803 the King of Spain decided to introduce
vaccination into his American colonies. Twenty-two children who had
never suffered from smallpox were enlisted and two of them were
vaccinated. On the voyage, two fresh children were vaccinated from the

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preceding pair every ten days and so the active vaccine arrived at the
port of Caracas in Venezuela. Here the expedition split into two, one
party going to South America where over fifty thousand people were
vaccinated in Peru alone. A second ship picked up twenty-six fresh
children and carried the chain round the Horn to the Philippines, Macao
and Canton. From there British and American missionaries took vaccine
into the Chinese interior.
The highly infected Indian sub-continent received vaccine in
1802 after several abortive attempts. The lymph originally came from
Jenner in Berkeley but travelled via London, Vienna, Turkey, Baghdad
and the port of Bussora on the Persian Gulf. The lymph lost potency and
only one vaccination ‘took’ on its arrival in Bombay. This single case
provided enough for a new series distributed to Madras and Ceylon.
Thus the original ‘Jenner Strain’ travelled to Asia but a second
strain became more widely distributed. Dr William Woodville of the
London Smallpox and Inoculation Hospital found two cows suffering
from cowpox at a dairy in Gray’s Inn Lane on 20 January 1799. He
immediately vaccinated seven subjects at the Smallpox Hospital and then
inoculated all seven with matter from a smallpox pustule, three of them
after an interval of only five days. From the original seven he
‘vaccinated’ a first series of two hundred and then from the latter a
second series of three hundred persons. Woodville reported: ‘In several
instances the cowpox has proved a very severe disease. In three or four
cases out of five hundred, the patient has been in considerable danger
and one child actually died.’
Jenner was furious. He had purposely delayed test smallpox
inoculation of vaccinated subjects for over a month in his own trials. He
believed that Woodville’s strain of vaccine had become contaminated
with smallpox virus, so producing a dangerous illness. But Jenner
practised in a rural area, while Woodville not only worked in the
metropolis, the chief centre of British smallpox, but in a hospital founded

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for the purpose of inoculation and segregation. The demand for vaccine
was such that few questions were asked. Woodville’s strain became
disseminated world-wide and is reckoned to have been passaged through
at least two thousand removes before 1836. The North American strain
probably derives from Woodville because he supplied the Vaccination
Hospital in Bath from which Dr Haygarth sent lymph to Professor
Benjamin Waterhouse of Boston in 1800.
All vaccinations were performed by the arm-to-arm method until 1881.
Continued passage through the human resulted in over-attenuation of the
virus and increased the risk of transmitting such human infections as
erysipelas, tuberculosis and syphilis. In England the government
instituted an Animal Vaccination Establishment in which calves were
deliberately infected with cowpox and lymph distributed. This lymph
proved very uncertain but the quality improved after it was found that
glycerin prolonged preservation. The first ‘glycerinated calf’s lymph’
was sent out in 1895, provision being made to supply ‘humanized
lymph’ to those who objected to inoculation with animal matter.
Opposition to vaccination persisted throughout the nineteenth and
early twentieth centuries. In Britain it came chiefly from the uneducated
class and largely centred on threatened compulsion. But, curiously, the
lower strata of society favoured variolation. An epidemic in 1837–40
caused about thirty-five thousand deaths, almost entirely among infants
and young children of the urban working class. Thomas Wakley MP,
editor of The Lancet, laid the blame squarely upon variolation, arguing
that the epidemic would not have occurred had the practice been
prohibited. The British Parliament accepted his view and passed an Act
making inoculation with smallpox a felony.
Vaccination therefore became the only method of protection and
was made compulsory for infants at the ratepayers’ expense in 1853.
Unfortunately no machinery to enforce the law existed and there was
much evasion. About half the children born in British towns were

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vaccinated, the number being considerably smaller in most rural districts.
The critical period is 1870–3, the most important years in the history of
vaccination. Compulsory vaccination had been introduced by the more
authoritarian European states, one of the first being Bavaria in 1807.
Compulsion became general throughout Germany and army conscripts
were always revaccinated. France did not introduce compulsory
vaccination for either civilians or the armed forces. A general European
pandemic of smallpox started in 1869. The Franco-Prussian War broke
out in 1870. During the war 4,835 cases of smallpox occurred in the
German armies with 278 deaths. Among French prisoners of war held by
Germany, there were 14,178 cases with 1,963 deaths. The total of French
prisoners seems to have been lost but they must have been many fewer in
number than the whole German army.
French refugees are blamed for introducing infection to England
though any human communication between Britain and the Continent
could have done so. The resultant epidemic caused 44,079 deaths, nearly
a quarter occurring in the London slum areas. Average mortality was 148
per 100,000 of the population compared with an estimated 400-500 per
100,000 before the days of vaccination. This epidemic greatly increased
demand for infant vaccination. In the peak year 1871, 821,856 children
were born in England and Wales of whom 93 per cent were vaccinated.
Special Officers were now appointed to ensure that all children received
treatment. Compulsion aroused opposition with the result that about 20
per cent of children escaped between 1871 and 1888, the figure rising to
nearly 30 per cent in 1897. The government then introduced a
‘conscience clause’ which permitted exemption after satisfying two
Justices of the Peace or one Stipendiary Magistrate. Probably because
such exemption involved considerable trouble the number of infants
vaccinated rose in the next ten years. Compulsion ended on 5 July 1948.
Accurate figures for the incidence of non-fatal smallpox in
Britain are not available until 1899 when compulsory notification of

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cases was introduced. By then incidence had greatly decreased and the
fall continued. From 1911 until 1921 annual notifications varied from a
high of 315 to a low of 7, deaths ranging between 30 and 2. Then came
an extraordinary incident. Notifications greatly increased in the years
1922–32 with a peak of 14,767 in 1927. But deaths were not on the same
scale, for only 47 people died in the peak year. In April 1928, while this
mild form was still prevalent, a ship from India brought true virulent
smallpox to Liverpool, causing 35 cases with 11 deaths. This epidemic of
the major type was easily contained by vaccination of all contacts and
rigid segregation. No new cases occurred after the end of May. The
epidemic of the minor form could not be contained because many people
suffered so slight an illness that they did not even call in a doctor.
Incidence must have been much higher than recorded in the notifications
and the epidemic did not die out until the end of 1934. This is obviously
an example of the Variola minor or alastrim prevalent in the sixteenth
century, but whether it developed because of partial protection by
vaccination or was imported from America is an open question.
The widespread success of vaccination first suggested an attempt
to defeat disease on a global scale. In 1851 an international conference in
Paris undertook the standardization of quarantine regulations which had
varied from country to country. This resulted in the first organization for
World Health, the Office International d’Hygiène Publique, established
in Paris in 1907. The League of Nations carried on and enlarged the
scope of the work in 1923. In 1946 an International Health Conference,
held in New York, absorbed the Paris Office and the League to form the
World Health Organization (WHO) on 7 April 1948. This body attacked
a multitude of problems, including tuberculosis, malaria and venereal
disease, and embarked on a massive programme of vaccination. The
programme has been immensely successful, the last countries to be
declared free of infection being Bangladesh, Somalia and Ethiopia. By
1979 the WHO was able to declare that, except for certain laboratory

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specimens, the whole world was now free from the smallpox virus.
Provided strict surveillance is maintained, this terrible killer should never
imperil humanity again.
But who defeated smallpox, Edward Jenner or William
Woodville? What were the twentieth-century vaccinators really using in
their worldwide battle, cowpox or an attenuated strain of smallpox virus?
These issues have been much discussed. One attack of virulent smallpox
seems to have conferred life-long protection from another. Judging by
the relative freedom of the Spaniards in the lethal Aztec epidemics, the
milder alastrim of the sixteenth century must have conferred a
considerable resistance if not actual immunity. Jenner claimed that his
vaccination with cowpox gave life-long immunity from smallpox but
experience must have shown that he was incorrect, for the Germans
made revaccination compulsory every seven years and vaccinated all
conscripts to the armed services whether they had already been
vaccinated or not. Most doctors advised renewal every five or seven
years and insisted on revaccination if a person came in contact with a
case of smallpox. Until very recently, any traveller to a known smallpox
area was advised to undergo revaccination. All this can be put in one
sentence – no one was sure that cowpox gave life-long protection against
smallpox.
Why, then, did vaccination succeed in defeating smallpox? A
very distinguished epidemiologist, Dr Arthur Gale, has probably given
us the correct answer in a small book published shortly after his
tragically early death in 1956. Having given full credit to Jenner, he
discussed Woodville’s work, as described above, and continued:

It is impossible to trace all the ramifications of the early history

of vaccine lymph and it is difficult to interpret even so good an account
of experiments as that of Woodville. One can only make a guess at
what happened in London after 1799. The most plausible guess seems

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to me to be that the bringing together of cowpox and smallpox virus did
in some way produce a modified smallpox virus which by an empirical
process of selection on the part of the vaccinators gradually became
safer and safer. The virus was kept going by arm to arm vaccination
right up to 1881 when glycerinated calf lymph began to be substituted
for it. Arm to arm vaccination was not finally prohibited until 1898.
Modern work on viruses lends some support to this theory, in that, in
the laboratory, the vaccinia virus resembles the smallpox virus rather
more than the cowpox virus, though the cowpox has a similar antigenic
structure.

Gale does not state the origin of the cowpox lymph used to
vaccinate calves and so provide fresh supplies after 1881. As cowpox is
uncommon and supplies of humanized lymph would have been freely
available, it seems probable that the chain continued and the attenuated
strain of mixed cowpox-smallpox virus remained in use until the end of
the story, but that is only supposition.
Nothing of this takes away from the enormous debt that the world
owes to Edward Jenner. He did not know the cause of disease but his
work must be recognized as the starting point of all attempts to combat
infection by immunization. In 1880, after he discovered the existence of
the disease-producing micro-organisms which he named Germs, Louis
Pasteur resumed where Jenner had been forced by lack of knowledge to
leave off. Pasteur’s successful production of a rabies vaccine (that word
itself commemorates Jenner’s work with cowpox) focused attention on
the methods by which the body naturally protects itself against infection.
From Pasteur’s work developed not only the protective vaccines, but also
the antitoxins used successfully in treating developed disease. Diphtheria
antitoxin serum, first used in 1891, reduced the death rate from that
infection in London isolation hospitals from 63 per cent of diagnosed
cases in 1894 to 12 per cent in 1910.

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 Jenner’s work and the train of events which he initiated have
changed the pattern of infectious disease. He also, although quite
unwittingly, effected a social revolution. Vaccination induced official
action in a number of countries, where for the first time in history
governments became actively involved in sustained attempts to eradicate
disease on a national scale. Individual freedom of choice yielded to the
interests of the community. National attempts combined into a great
international campaign. There has been much opposition, sometimes for
reasons that must command respect, but there can now be no doubt that
large-scale compulsory vaccination somehow displaced smallpox from
its position as a common endemic disease to the status of an increasingly
rare exotic infection and finally ensured its extinction. Nor can the most
widely divergent opinions on the merit or demerit of vaccination affect
the indisputable fact that its compulsory application was the first massive
endeavour to vanquish disease. As such, the prevention and eventual
conquest of smallpox is a landmark in social history.

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 C F
GENERAL NAPOLEON AND
GENERAL TYPHUS

Napoleon Bonaparte is a towering personality. But the Napoleonic

adventure is as much the story of his armies as of the man himself. These
armies, born of a nation devastated by revolution, emerged as the
greatest fighting force since the Roman Army and subjugated the whole
of Europe except Britain. The fate of Napoleon cannot be divorced from
that of his soldiers, nor can the fate of his soldiers be divorced from that
of Napoleon. The emperor’s victorious career was ended by the
destruction of his Grand Army, which had itself become the victim of his
own vaulting ambition. Having known almost unbroken success for
nearly twenty years, the army was brought to ruin in the late summer of
1812, partly through Napoleon’s failing judgement and partly by
sickness. A number of diseases attacked his army during the 1812
campaign, the primary and most destructive of them being an epidemic
of the campaign disease known as typhus or gaol fever.
Typhus fever is a disease of dirt. The causative organism,
Rickettsia prowazekii, belongs to a class lying midway between the
relatively large bacteria, which produce diseases such as syphilis and
tuberculosis and can be seen under an ordinary laboratory microscope,
and the viruses which produce infections such as smallpox and measles
and are so minute that they can be identified only with an electron
microscope. The organism is carried by lice. Lice are often found on
animals, in the cracks and crannies of old buildings, or infesting
unwashed human bodies and the seams of their dirty clothing. It is not

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the bite but the excrement and crushed body of the louse which transfers
the organism.
Typhus acquired the name gaol fever because of its association with
poverty and dirt. Since fevers were supposed to be caused by bad smells,
this is the reason why judges ceremonially bear small nosegays of sweet-
scented flowers. The infection originated in the filthy prisons and spread
from the felon in the dock to the judge upon the bench. Three notable
‘assize epidemics’ occurred in the sixteenth century but these epidemics
may have been late incidents in the history of typhus. The origin of the
disease remains obscure. One theory holds that it originated in the East
as an infection of lice and rats but subsequently became an infection of
lice and men. Cyprus and the Levant have been suggested as the first
focus of spread to Europe, the earliest certain outbreak being in the
Spanish armies of Ferdinand and Isabella in 1489–90. Another theory
maintains that typhus is a much older European disease, referred to as
‘famine sickness’ in the records.
There is no doubt that typhus has been associated with the special
conditions of warfare for centuries. Campaign conditions entail that a
number of people are herded closely together, wearing the same clothes
for long periods and lacking means of ensuring bodily cleanliness. Lice
will multiply rapidly in those circumstances and, since typhus is a lethal
disease, the sickness and death rate may have a profound effect on the
fortunes of war. A remarkable example is the relatively small and
localized epidemic which inflicted a mortality of no less than 50 per cent
on a French army besieging Naples in July 1528, thus making a decisive
contribution to the final submission of Pope Clement VII to Charles V of
Spain. Typhus also forced the armies of Maximilian II to break off the
campaign against the Turks in 1566. Soldiers carried typhus across
Europe during the Thirty Years War of 1618–48 and it seems that the
infection became firmly established during this period.

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 Typhus fever remained endemic in the whole of Europe from the
seventeenth to the early twentieth century but it was only in conditions of
warfare, famine or extreme poverty that major outbreaks occurred. The
United States was not infected until early in the nineteenth century,
causing a great epidemic at Philadelphia in 1837, But the story of typhus
is complicated by the existence of more than one form of the disease.
‘True’ typhus fever, characterized by high fever, delirium, a crisis and a
blotchy rash, is very dangerous. Other less serious variants are Rocky
Mountain Spotted Fever, Brill’s Disease (now proved to be a
recrudescence of epidemic typhus and renamed Brill-Zinsser Disease)
and (questionably) Trench Fever. This last variant, the prevalent illness
of the First World War, is carried by lice but caused by an organism,
which in 1961 was removed from the genus Rickettsia and given the
name Rochelima. All armies engaged in the European trenches became
lousy, living in conditions of filth and deprivation unknown since the
Middle Ages, yet the non-fatal trench fever seems to have replaced true
typhus on the Western Front, infecting both German and Allied troops.
True typhus did not occur among them although it wrought havoc among
the Serbian, Austrian and Russian armies of the Balkan and Eastern
Fronts. The Russians were particularly badly affected. After the
revolution of 1917 and the Civil War that followed, famine and disease
devastated the whole country. Approximately twenty million cases of
true typhus occurred in European Russia alone between 1917 and 1921,
causing from 2.5 to 3 million deaths.
The mode of transmission of typhus by an infected body louse
was first described in 1911. The Brazilian H. da Roche Lima isolated the
causative organism in 1916 and named it after the American Howard
Taylor Ricketts and the Pole S.J.M. von Prowazek, both of whom had
died while investigating the disease. In the Second World War
improvements in hygiene, the use of persistent insecticides, the much-
maligned DDT in particular, and a vaccine first prepared by Herald Cox

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in 1937 reduced the danger of typhus to such an extent that only 104
cases occurred in the US armed services with not a single death. Since
the late 1940s broad spectrum antibiotics have also become available as
an even more important means of combating the disease. None the less a
certain mystery still surrounds the infection, for it seems that very special
conditions are necessary before it will flourish in a virulent form even
when there is gross infestation with lice. Typhus seems to require
concomitant malnutrition and sordid living before it will produce a lethal
epidemic. But the disease still exists and causes deaths in areas such as
the Andes, the Himalayas and parts of Africa, so we must hope that a
world-wide standard sufficiently high to deter infection can be instituted
and maintained.

The fall of Napoleon was not inevitable. Given time, patience and
a certain measure of luck, he could have extended his empire to the East,
consolidated his administration of the conquered lands, and forced
Britain into impotent isolation, impregnable upon the seas but helpless to
intervene on the Euro-Asian land mass. Ill-luck and impatience were
chiefly responsible for the defeat of Napoleon’s army.
Napoleon had reached the height of his power and his glory in the
spring of 1812. His empire spread from the frontiers of Russia and
Austria to the coasts of the North Sea, the Atlantic and the
Mediterranean. Three of his brothers wore crowns, Joseph as King of
Spain, Louis as King of Holland and Jerome as King of Westphalia. One
sister was Grand Duchess of Tuscany, another was the Princess
Borghese, while a third had married his marshal Joachim Murat who
now sat on the throne of Naples. Eugène, son of Napoleon’s first wife,
Josephine de Beauharnais, acted as Viceroy of Italy. Napoleon himself,
having divorced Josephine in 1809, had contracted a brilliant marriage
with the Archduchess Marie Louise, great-niece of Marie Antoinette and
daughter of Francis, last Holy Roman Emperor and first Emperor of

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Austria. To this union had been born on 20 March 1811 his first
legitimate child and heir, who had immediately been accorded the title
King of Rome.
All this family splendour and imperial prestige ended at the sea coasts.
No means had been found to cross the narrow Channel, only twenty
miles wide – less than a day’s land march – which separates France from
England. The Royal Navy barred the way. Further, the insolent British
had recently managed to establish a base in Portugal and, having
entrenched themselves behind the strongly fortified lines of Torres
Vedras, demonstrated the possibility of maintaining and supplying an
army by sea. But Britain was still vulnerable by land. A large part of her
trade and the bulk of her wealth derived from India, then administered by
the Honourable East India Company. Britain needed Indian money to
carry on the war. The French navy could not intercept and capture the
armed merchant ships of ‘John Company’ which bore the riches of India
to Britain. But the taking of India itself would not only deny her that
wealth but also immeasurably harm her prestige. The overland route to
India would be long and hard, but the prize which lay at the end of the
road would be worth almost any sacrifice.
Napoleon had already tried the southern route across the
Mediterranean, through Egypt and Arabia to the Indian Ocean. That
adventure ended at Aboukir Bay on 1 August 1798, when Horatio
Nelson inflicted a heavy defeat on the French Navy, transforming the
Mediterranean into a British lake. The French army, cut off in Egypt and
Palestine, was ravaged by sickness and only succeeded in returning to
Europe with great difficulty. Aboukir proved that seaborne invasion was
too dangerous to be practical. The conquest of India and the East could
be attained only with the help of Russia or after her defeat and
submission.
On 25 June 1807, ten days after winning a military victory over
the Russians, Napoleon met Tsar Alexander I at Tilsit and early in July

113
concluded a treaty of everlasting friendship. Six months later Napoleon
outlined his plan for a combined Franco-Russian invasion of India
through Turkey and Persia. The moment was propitious. Napoleon had
beaten every enemy by land and at that time the British had not yet
secured a base in Portugal. He had sufficient forces at command. Backed
by supplies and some military aid from Russia, the campaign might
prove no worse than a long and difficult route march.
The abnormal psychological make-up engendered by absolutism is
seldom conducive to easy negotiation. Given a cooperative France,
Alexander had everything to gain by helping Napoleon and
simultaneously extending his realms to the Dardanelles, the Balkans and
the China Sea. Given a cooperative Russia, Napoleon could have
stabilized his European conquests, fed his peoples from the wide
cornfields of eastern Europe, tapped the wealth of India, fortified his
coasts and contemptuously resigned the empty dominion of the seas to
the British Navy. The scheme held a fair chance of success and, if
successful, must have resulted in an impregnable Franco-Russian
domination of the whole of the Euro-Asian continent. But the essential
trust and cooperation were lacking. The potential victors fell out over
division of the spoils even before the spoils had been won. Alexander
demanded Constantinople and the Dardanelles as a minimum payment
for Russia’s help. Napoleon, looking forward to the reconquest of the
Mediterranean and the Straits of Gibraltar, refused to envisage a solid
Russian entrenchment on his eastern flank. The all too short propitious
moment was wasted in sterile argument. In May 1808 Napoleon found
himself faced with a Spanish insurrection. In August a British
expeditionary force defeated Marshal Jean Junot at Vimiero in Portugal
and the opening shots of the Peninsular War had been fired. Napoleon,
forced to acknowledge that he had a full-scale war in Europe on his
hands, transferred the bulk of his Grand Army to Spain. Meanwhile
Russia became entangled in a war with the Ottoman Empire which

114
engaged her for the next four years. The projected Grand Alliance was
tacitly abandoned.
The two emperors concluded their conference of September–
October 1808 at Erfurt in Germany, outwardly in an amicable fashion.
But one major problem remained unresolved. In 1807 Napoleon had
created the Grand Duchy of Warsaw, which Alexander saw as a
preliminary to detaching Poland from Russia and restoring an
independent Polish state. At Erfurt Alexander promised Napoleon his
support in the event of war with Austria, but he did nothing to prevent
the war and made no move when it broke out in April 1809. His primary
interest had now become the foiling of French ambitions in Poland. The
question became acute in February 1810 when Alexander formally
insisted that ‘the kingdom of Poland shall never be restored’. Napoleon
wrote in the margin of the dispatch ‘Divinity alone can speak as Russia
proposes’.
Another and more intimate disagreement had caused friction
between the emperors. Napoleon’s first marriage to Josephine was
childless, yet she had borne children by her previous marriage with
Beauharnais. Napoleon suspected that he could not father children, a
suspicion widely shared in France. His doubts were resolved in 1807
when his mistress Eléonore Denuelle bore him a son, and another
illegitimate child from Maria Walewska followed. Napoleon now asked
Tsar Alexander for the hand of Anna, his fifteen-year-old sister, but was
implacably resisted by the powerful Dowager Empress of Russia, who
not only hated the French alliance but had heard and believed the rumour
of his impotence. In 1810 Napoleon abruptly ended this negotiation by
making a formal offer of marriage with Archduchess Marie Louise
Habsburg of Austria. The offer was immediately accepted.
This dramatic volte-face was a symptom rather than the cause of
the breach between Russia and France. Ever since the agreement at
Tilsit, Alexander had faced the hostility of his nobles who derived a large

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part of their wealth from the sale of timber to maritime countries,
especially Britain. Napoleon’s Continental System of trade, reinforced by
the British blockade of Europe, cut off that source of income. In
December 1810 Alexander, who until now had acquiesced in the System,
issued an Imperial ukase imposing a high tariff on French goods and
opening Russian ports to neutral shipping. As Britain controlled the seas,
this was equivalent to permitting unrestricted trade with the principal
enemy of France. Russia had opted out of the Continental System and
out of the French alliance.
It now seems obvious that in 1810–11 Napoleon should have
consolidated his empire by clearing his threatened western flank. The
British, though strongly entrenched within their fortified lines, could not
muster a force of more than thirty thousand men. There can be little
doubt that Napoleon, by attacking with overwhelming numbers, could
have driven the British from Europe. But such a campaign would have
been long, costly and inglorious. A military dictator, if he is to survive,
must repay his people’s sacrifices with dramatic successes. To the east
there lay the possibility of a brilliant series of dashing battles and, at the
end, the gilded cupolas and barbaric splendours of Moscow.
Beyond Moscow the road led to the gorgeous East. Napoleon was
a narcissist and something of an exhibitionist – even the simple uniform
he wore as Emperor was in contrast to the gold-bedizened and
multicoloured uniforms of his staff officers. He commissioned the Italian
artist Antonio Canova to sculpt a statue of his body, naked except for the
classical figleaf. He designed his own gem-encrusted coronation robes.
When in Egypt he considered conversion to the Muslim faith and donned
the flowing garb of an Arab chief. Perhaps it was the jewelled turbans,
the diamond aigrettes and the opportunity of wearing exotic ceremonial
robes which drew Napoleon towards India, as much or even more than
the chance of dealing a humiliating blow to England.

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 So Napoleon committed the grievous mistake of sacrificing
reality for a dream. In January 1812 he denuded Spain of many seasoned
troops to reinforce his eastern armies. He commonly spoke of his
proposed campaign as ‘the Polish War’. France was to appear as the
saviour of a Poland enslaved by Russia. He proclaimed to his troops: ‘the
peace which we shall conclude will terminate the fatal influence which
Russia for fifty years has exercised in Europe’. He told his Ambassador
to Russia, Armand de Caulaincourt, ‘I have come to finish once and for
all with the colossus of the barbarian North’. But early in 1812 he
privately revealed his true ambition to the Comte de Narbonne in the
words: ‘Alexander [the Great] was as far as I am from Moscow when he
marched to the Ganges.’ Narbonne thought the scheme to be half-way
between Bedlam and the Pantheon.
From August 1811 onwards Napoleon was fully engaged in
making preparations on an enormous scale for the invasion of Russia. In
March 1812 he induced Prussia and Austria to sign agreements providing
troops for his adventure. In April he made the obvious move of offering
a peace treaty with Britain but met with no success. On the other side,
Tsar Alexander wisely secured his southern and northern flanks by
ending the Turkish war and by inducing the Prince Royal of Sweden to
bring his country over to Russia’s side in return for promised aid against
Norway.
Napoleon’s armies began to assemble in cantonments
strategically sited on a line stretching from northern Germany to Italy,
and in June 1812 started their concentration in East Prussia. The
immense force numbered in all 368,000 infantry, 80,000 cavalry, 1,100
guns and a reserve of 100,000 men. During the campaign reinforcements
brought the total number of troops engaged to well over 600,000. The
Russian armies numbered slightly less than a quarter of a million which
meant that Napoleon had an overwhelming majority for the first time in
his career.

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 Legend has it that almost the whole of Napoleon’s enormous
army was destroyed on the retreat from Moscow. The legend is incorrect.
A much larger number of men perished on the outward march through
Poland and west Russia than on the retreat. Excluding the flanking
forces, mainly German and Austrian, Napoleon’s central or task army
numbered about 265,000 men. Only 90,000 of these reached Moscow.
At first all went well. The summer of 1812 was unusually hot and
dry so the men could march quickly over easy roads and the slower-
moving supply columns, sent on ahead, could maintain their position.
Food was therefore abundant and close at hand. The health of the troops
remained uniformly good. Military hospitals had already been
established at Magdeburg, Erfurt, Posen and Berlin but there was little
demand for their services. On 24 June 1812 the army encamped on the
west bank of the River Niemen, the boundary between Prussia and
Poland. Here Napoleon inspected his army in dazzling review. Then the
troops marched down to the river and crossed over by narrow pontoons
erected by the bridge-building engineers. Four days later the army
reached Vilna where Napoleon slept in the room vacated by the
retreating Alexander a week earlier.
Napoleon had thought of almost everything but had forgotten that
Poland was filthily dirty. The miserable peasants were unwashed, with
foul matted hair, lousy and flea-ridden. Their insanitary hovels abounded
with insects of all kinds. The abnormally hot, dry weather had affected
the wells, water was scarce and polluted by organic matter. The enemy
now menaced the front lines, so the supply trains had to move back to
the rear of the fighting regiments. Poland’s rudimentary roads were
either soft with loose dust or rutted and hardened after the spring rains
and hot sun, causing the wagons to lag behind and food to be scarce in
the leading columns. The huge army – much too large for coherent
command – lacked efficient discipline. Only the best units were
accustomed to long, ordered marches and moved in a compact military

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formation but the greater part of the army dissolved into straggling
undisciplined bands. Despite stringent orders and harsh punishments, this
multitude of stragglers was forced by hunger to pillage the cottages,
livestock and fields of the Polish peasants, their nominal allies. The
Poles can hardly be blamed if they did not greet the French as their
liberators from the Russian tyrant. The supplies, the auxiliary troops, the
guerrilla fighters, upon which Napoleon had counted, failed to
materialize. Instead, the eternal pillaging by his half-starved armies
aroused a sullen fury which was to recoil upon his soldiers during the
retreat.
If the war of liberation had already been lost, so had the chance
of an easy victory over Russia. Nearly twenty thousand horses, twice the
number that might be expected to fall in a single major battle, died from
lack of water and forage on the road to Vilna. Men also suffered. Hunger
and polluted water produced the common campaign diseases of
dysentery and enteric fevers. New hospitals were hastily established at
Danzig, Konigsberg and Thorn but they were unable to cope with the
mob of returning sick. Then, just after the successful crossing of the
Niemen, a few cases of a new and disastrous malady appeared. Men
developed a high temperature and a blotchy pink rash and their faces
assumed a bluish tinge. Many died quickly. Typhus fever now held the
army in its unrelenting grip.
Typhus had been endemic in Poland and Russia for many years.
There is no real evidence that the Napoleonic armies had encountered it
before 1812 and they had certainly never suffered a major epidemic.
Their medical and sanitary arrangements, brilliantly organized under the
great military surgeon Baron D.J. Larrey, were the finest in the world but
could not possibly cope with disease on the scale which now developed.
Any preventive method proved useless because the cause of infection
was unknown. Lack of water and insufficient changes of clothing made
bodily cleanliness impossible. Fear of Russian attacks and Polish

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reprisals caused men to sleep together in large groups. The lice of
infested hovels clung to the seams of clothing, deposited their excrement,
were crushed and released the organisms of typhus fever which entered
the slightest wound, even those made by scratching the site of irritation.
By the time of the battle of Ostrovna in the third week of July, over
eighty thousand men had perished from sickness or were too ill for duty.
Disease alone had robbed Napoleon’s central force of nearly a fifth of its
effective strength within a month. His army was about a hundred and
fifty miles from the Prussian frontier and Moscow was three hundred
miles away.
There had, of course, been wastage from battle casualties as well
as from disease, though not upon the same scale. The Russians had no
overall strategic plan and their two armies, one led by Barclay de Tolly
and the other by Prince Bagration, acted independently. De Tolly just
succeeded in eluding Napoleon at Vilna, while Jerome Bonaparte and
Marshal Davout failed to entrap Bagration. Fierce battles were fought by
Murat at Ostrovna and by Davout at Moghilev but the Russians still
managed to disengage with most of their forces intact. Napoleon
believed that the two armies would join to make a stand at Vitebsk and
this, in fact, had been their original plan. On 27 July Napoleon
established contact with de Tolly’s army but, on the same day, de Tolly
learned that Bagration had decided to retreat to Smolensk. During the
night de Tolly succeeded in slipping away while Napoleon was still
preparing for battle.
De Tolly’s successful withdrawal had the effect of alarming the
more cautious of the French generals. On 28 July Louis Berthier,
Joachim Murat and Eugène de Beauharnais sought a conference with
Napoleon. They sensed that the failure of the Russians to stand and fight
was drawing the French army into a most dangerous situation. They told
Napoleon that wastage of troops through sickness and desertion from
less reliable units had reduced the effective fighting strength to little

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more than half and that the difficulty of provisioning even this depleted
number in a hostile countryside had become formidable. They implored
Napoleon to halt the advance. Having listened to their arguments he
agreed to announce the end of the campaign of 1812. Then the urgent
need for a spectacular victory caused him to change his mind. Two days
later Napoleon reversed his decision and told the generals: ‘The very
danger pushes us on to Moscow. The die is cast. Victory will justify and
save us.’
So the sick, half-starved army struggled on. Just over two weeks
later, on 17 August, they came in sight of Smolensk and the River
Dnieper where the two Russian armies had joined and it seemed that they
would at last make a stand. Napoleon, determined to destroy his elusive
enemy, did not hurry to press the attack. He ordered a frontal
bombardment of Smolensk and a feigned assault, while sending Junot
across the Dnieper to outflank the city and cut the Russian line of retreat.
De Tolly learned of the danger in time, fired the city and hastily
withdrew. On 19 August Junot brought the Russians to battle at Valutino,
ten miles north-east of Smolensk, but he failed to encircle the army and
lost over six thousand men.
At Smolensk, two hundred miles from Moscow, a decisive choice
had to be made, either to turn back or go forward. The option of turning
back would have meant acknowledging humiliating defeat. That of
driving on, whatever the cost, may well have seemed the only way to
realize Napoleon’s eastern dream. However, it has been suggested that he
could have settled for a third and more prudent course of action, by
simply halting at Smolensk and giving his army time to recover.
Napoleon had acquired a considerable knowledge of public
health measures and understood their importance. He showed great
interest in Edward Jenner’s discovery of vaccination. He had his own son
vaccinated when eight weeks old and encouraged a campaign for
vaccination of children and army recruits. No one as yet appreciated the

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relationship between lice and typhus fever but lousiness had been
regarded as a sign of dirty habits for centuries. Samuel Pepys cannot be
accounted the most cleanly of men, but lousiness was unusual enough to
be recorded in his diary on 23 January 1669: ‘when all comes to all she
[his wife] finds that I am lousy having found in my head and body above
twenty lice little and great, which I wonder at, being more than I have
had I believe these twenty years.’ Pepys changed all his clothes and cut
his hair short ‘so shall be rid of them’. This simple treatment was as well
known to Napoleon and his doctors as to Pepys.
Smolensk had been partially destroyed by fire but Napoleon’s
efficient engineers could have improvised shelter. The supply line to
Germany and France was open and could be kept open. A winter of rest,
good rations, ample water, medical care and sanitary control might have
restored the broken army, allowed time for reinforcement of men and
commissariat, and enabled Napoleon to consolidate his position in
Poland and launch an overwhelming attack on Russia in the summer of
1813. Such was the opinion of J.R. de Kerckhove, one of the army
surgeons, who later wrote that if Napoleon had been content to play this
waiting game, his campaign might have been successful and his
domination of central and eastern Europe permanently established.
Apart from Napoleon’s character, there are still two reasons why
this sensible third course did not appeal to him. First, his army had
encountered formidable difficulties in the Peninsular War. In July
Wellington had gained a resounding victory over General Marmont at
Salamanca and had entered Madrid in August. Napoleon could not
foresee that these successes would end, if only temporarily, in
Wellington’s costly and dispiriting winter retreat to Ciudad Rodrigo. The
second and more potent reason is that Napoleon had convinced himself
that the capture of Moscow must force Alexander to capitulate. He
decided to make Smolensk an advanced base for concentration of reserve
troops and supplies, and establish similar bases at Minsk and Vilna.

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Having thus secured the road back to the frontier, he felt free to push on
as quickly as possible to Moscow. He resumed the march on 25 August.
His striking force had now been reduced to 160,000 men; by 5
September 30,000 more fell victims of typhus.
On 30 August Alexander appointed the veteran Prince Michael
Kutusov commander-in-chief of the Russian armies. Kutusov had led the
Russian division at Austerlitz in 1805 where he acquired a healthy
respect for Napoleon as an opponent and gained some knowledge of his
strategical methods. He continued the policy of giving ground, slowly
withdrawing as the French advanced. On 5 September the Russians came
to the banks of the Moscow River, fifty miles to the south-west of the
city. Kutusov would have preferred to continue a planned slow retreat,
relying on the wide barren spaces of Russia and the imminent bitter cold
of winter to destroy the French, but realized that national pride
demanded at least a token defence of the ancient capital. Karl von
Clausewitz, the eminent Prussian strategist and military historian,
summed up the position thus: ‘Kutusov, it is certain, would not have
fought at Borodino where he obviously did not expect to win. But the
voice of the Court, the Army, all of Russia, forced his hand.’
Kutusov did not risk the whole of his command. The Russian forces
engaged at Borodino numbered 120,000 men, but 10,000 of these were
raw, hastily trained militia. Opposing them were 130,000 seasoned
French troops with 600 guns. The Russian artillery was slightly superior
in number and weight. Kutusov entrenched his infantry on a slope above
the Moscow River, centring them on the village of Borodino, and
prepared redoubts for his cannon. There, for two days, the Russian army
awaited battle.
The engagement which followed bore some resemblance to
Waterloo, probably for similar reasons. Napoleon was a sick man at
Waterloo, unable to give undivided attention to the battle. The same is
true of Borodino. He was in great pain from an acute attack of cystitis,

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inflammation of the bladder. He also suffered from a heavy feverish
cold. The two days’ delay in attacking may have resulted from his
indisposition but the question also arises of how far was Napoleon in
charge of the actual battle and to what extent, if any, did his illness affect
the issue. He disregarded Davout’s advice to attempt an encircling
movement by turning the Russian left wing, which seems a sensible
method of destroying an entrenched army. The excuse has been made
that Napoleon had already experienced the Russians’ agility in
disengaging when threatened on the flank. Whatever the reason, the
French mounted massive cavalry attacks upon the well-defended Russian
centre, the same disastrous tactics which Marshal Ney employed against
the unbroken British line at Waterloo.
Battle was joined at dawn on 7 September. The French cavalry
charged repeatedly but the Russians succeeded in reforming the line and
were not driven from their entrenched position until the evening. At the
height of the engagement, when it seemed a spectacular Russian defeat
was in reach, Davout urged Napoleon to throw in his most trusted
Imperial Guard. Napoleon refused: ‘If I throw in the Guard, with what
shall I fight tomorrow?’ he asked. Whether by foresight or by chance, the
decision to withhold his best troops prevented absolute disaster two
months later.
Both sides suffered heavy casualties, the Russians losing about
fifty thousand men and the French just over half that number. Obviously
the French loss was the more serious, since they were operating in
hostile country with little opportunity for reinforcement. But at least it
was victory of a kind, though meaningless in the long term. The Russians
retired, retaining freedom to manoeuvre and with the certainty of
receiving ample supplies and fresh troops. Kutusov plainly appreciated
the situation. He had fought this token battle for Moscow and withdrawn
in good order. Now disease, the winter cold and hunger would
effectively do his work for him. On 13 September he held a council of

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war and said to his officers: ‘The salvation of Russia is in her army. Is it
better to risk the loss of the army and of Moscow by accepting battle, or
to give up Moscow without a battle?’ His reasoning was accepted and
the army retreated through Moscow in a south-easterly direction towards
the town of Ryazan.
So the French marched unopposed into Moscow on 14 September
and typhus marched with them. They had already lost ten thousand men
from sickness in the past week. Of over 300,000 who had formed and
reinforced Napoleon’s task force, only 90,000 reached Moscow. Seven
out of ten had fallen on the way. But the tattered remnant at last saw the
gilded and multicoloured domes shining before them. All the church
bells were ringing. Napoleon expected to be met by a humble deputation
of leading citizens offering him the keys of the city, but the gates
remained shut. That primitive but effective weapon, the battering-ram
which had been dragged across the length of Poland, was brought
forward. The gates were battered down and the army entered to find
empty streets and silent houses. Within a few hours fires broke out in
several districts.
The true story of these fires will probably never be known. The
population of early nineteenth-century Moscow numbered about
300,000. For some days the governor, Count Rostopchin, had been
organizing the evacuation of the city and only about 50,000 people
remained at the time of Napoleon’s entry. Immense quantities of stores
and valuables had also been removed. In the last phase of the evacuation,
Rostopchin released prisoners from the city gaols. Legend has it that he
released them on the condition that they remained in the city to harass
the French by pillaging and arson. Rostopchin’s action in sending all the
fire engines out of the city suggests that the fires were deliberate rather
than that they were caused by drunken French soldiers.
Napoleon, overjoyed that Moscow had been won, clung to his
opinion that Alexander must now sue for peace. His judgement here was

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at fault. Alexander could not submit. He had been warned by his sister
that the capture of Moscow would stiffen national feeling against the
French to such an extent that peace negotiations might endanger his life.
Alexander well knew, with the example of the assassination of his father
Tsar Paul in mind, that he was not safe from even his intimate advisers.
The late French ambassador to Russia, de Caulaincourt, tried to convince
Napoleon that Alexander neither would nor could accept defeat and
refused to act as an intermediary. On 4 October Napoleon sent General
Lauriston on a peace mission to St Petersburg.
Kutusov learned of Lauriston’s mission and ordered his Cossack
patrols to fraternize with the French outposts, thereby lulling Napoleon
into a false sense of security and providing a rational basis for his peace
fantasy. Kutusov was again playing for time. He knew that nearly three-
quarters of Moscow had been destroyed by fire. He was also aware of the
sickness that increasingly reduced his enemy. Typhus spread unchecked
among the French, the sick finding such shelter as they could in the
burnt-out ruins or in improvised hutments. Army morale fell to a low ebb
as the idle soldiers, disappointed of the ample supplies they had been
promised, spent their time in plundering and drinking such stocks of
alcohol as they could find in the city cellars.
The hot dry summer had passed into an unusually warm autumn.
De Caulaincourt, the one man in Napoleon’s entourage who had
experience of a Russian winter, warned him that the wasted, ruined city
would be untenable when the cold weather set in. Napoleon, misled by
the mild season, replied that de Caulaincourt was exaggerating and must
know that a Russian winter could be little worse than a winter at
Fontainebleau. Thus his futile peace parleys combined with a mild
October to lead Napoleon into the final mistake of this disastrous
campaign. The remnant of his army could only be saved by adopting one
of two courses: either to return immediately to Smolensk or march north,

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join with his Prussian allies, and invest St Petersburg. A bold, successful
attempt on the capital might possibly have brought Russia to her knees.
Squadrons of moving cavalry ringed Moscow with the result that
the French had lost touch with the main body of the Russian forces. They
had retreated to the east, then rapidly marched in a half-circle south and
west to cut Napoleon off from the chief centres of supply and arms
manufacture at Kaluga and Tula. Murat’s army was stationed at Tarutino,
south of Moscow. Here, on 18 October, Kutusov launched a surprise
attack, inflicting six thousand casualties and forcing Murat to withdraw.
This comparatively small engagement warned Napoleon that the
Russians had taken the offensive, that his peace bid had failed, and that
he was now in danger of encirclement. On 19 October his army at last
began the retreat from Moscow.
Fifteen thousand reinforcements had joined the French army
during their month’s stay in the city, but nearly ten thousand soldiers
succumbed to disease and wounds. The army which left Moscow on 19
October amounted to just over ninety-five thousand dirty, half-starved,
unhealthy men. They were encumbered with their sick and wounded, six
hundred cannon and insufficient horses to draw them, an immense mass
of loot including the enormous and quite useless gilded copper cross
from the cupola of the Kremlin tower called Ivan Veliki. Napoleon
turned south to avoid the already devastated direct route to Smolensk. On
24 October the Russians met him at Malojaroslavetz. A heavy day’s
fighting ended indecisively. Napoleon, having suffered too many
casualties, declined to press the attack next day and Kutusov also lost the
opportunity of victory.
The southern route being effectually barred, Napoleon had no
option but to turn north, rejoining the Smolensk road at Borodino. The
cold had now become intense and snow started to fall heavily on 5
November. Fast-riding bands of Cossacks, aided by guerrillas, rendered
foraging almost impossible. No preparations had been made for a winter

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campaign. De Caulaincourt managed to obtain ice-shoes for the horses of
Napoleon’s suite, but not a single cavalry or artillery horse was properly
shod. This and not the cold is the reason for Napoleon’s dispatch of 7
November: ‘the cavalry is on foot’.
The army pressed on to the promised food and shelter of Smolensk.
Napoleon arrived with the vanguard on 8 November, to find his reserve,
under Claude Victor, wasted by typhus fever and the hospitals already
crowded with their sick. Discipline had deteriorated to such an extent
that rations could no longer be fairly distributed. The greatest blow of all
was the lack of food, for the reserves and communication troops had
consumed most of the supplies stored against the army’s return. Finding
no succour in Smolensk, Napoleon evacuated the town on 13 November,
leaving over twenty thousand sick in the makeshift hospitals and ruined
houses. Next day he found Kutusov barring the road leading west.
The Russians, now entrenched at Krasnoi, expected that the
depleted French army would try to avoid battle but the men had straggled
to such an extent that Napoleon decided his only hope was to give them
time to concentrate. He therefore ordered the Imperial Guard to attack.
These valiant troops, preserved so carefully at Borodino, now prevented
complete and humiliating defeat. Kutusov, hurled back by their fury,
could not reform to attack. Leaving Ney to fight a magnificent rearguard
action, Napoleon pushed on to his next supply base at Minsk. On 22
November he received the appalling news that Minsk had already fallen
to the enemy.
Two days later he learned that the Russians had destroyed his
bridgehead over the River Beresina. The pontoon bridges had already
been abandoned for lack of transport. The position now seemed hopeless,
for Napoleon’s flanking armies, also in retreat, had been heavily defeated
by Prince Wittgenstein in the north and by Admiral Tchitchagov in the
south. The Russian pincers were closing in from either side and
Kutusov’s army blocked the way to the west. The French were saved by

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their brilliant engineer General Jean Baptiste Eblé. While a small force
made a feigned crossing of the river to the south of Studianka,
misleading Tchitchagov into believing that the whole army intended to
make the attempt, Eblé improvised two bridges on the north side of the
town. But, despite the heroism of the rearguard, only fifty thousand men
succeeded in continuing the retreat.
The army now began to degenerate into an undisciplined rabble.
On 29 November Napoleon wrote: ‘Food, food, food – without it there
are no horrors that this undisciplined mass will not commit at Vilna.
Perhaps the army will not rally before the Niemen. There must be no
foreign agents in Vilna. The army is not a good sight today.’ Fifteen
thousand men died on the road between the Beresina and Vilna. But
there was worse in store.
The starving vanguard reached Vilna on 8 December, having
marched through thickly falling snow driven by a bitter north-east wind.
Only twenty thousand sick and disheartened men comprised the effective
force. The rest were stragglers, stumbling along as best they could,
starving and frozen, harried by Cossack patrols. Just twenty men
remained of Ney’s Third Corps, who had fought so valiantly in the
rearguard. The town of Vilna offered no relief. Already starving, it was
crowded with sick, and typhus fever had spread throughout the
surrounding countryside. Men suffering from typhus, dysentery and
pneumonia lay on rotten straw soaked with their own excrement, without
medical attention or means of warmth, so hungry that they gnawed
leather and even human flesh. By the end of December over twenty-five
thousand sick and frost-bitten men had struggled into the town. Fewer
than three thousand of these were alive in June 1813.
On 5 December Napoleon had received news from Paris of his
rumoured death and of a conspiracy led by General François de Malet.
Next day, at Smorgoni to the west of Vilna, he decided on a hasty return
to France before the full extent of the disaster could be understood. He

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drafted a bulletin for dispatch in the usual manner, giving a frank account
of the horrors experienced during the retreat but not mentioning the
breakdown of supply arrangements and laying blame entirely on the
atrocious weather. Napoleon then set out, first by chaise, later on
horseback. After a furious ride across the whole of Germany and eastern
France, he arrived at the Tuileries in Paris on the night of 18 December,
anticipating his catastrophic bulletin by two days. He handled a
dangerous, indeed a desperate, situation with supreme skill, from the
understatement of his report to the Senate on 20 December – ‘My army
has had some losses, but this was due to the premature rigour of the
season’ – to his successful mobilization of 470,000 fresh troops by the
autumn of 1813. This, perhaps the most remarkable episode of
Napoleon’s astonishing career, bears witness to his tenacity and speed of
action when faced with a threat to his power.
He could save himself but he could not save his army. Murat, left
in command, proved a broken reed. He refused to make a stand at Vilna
and on 10 December abandoned the last guns, the remaining baggage
and the army’s treasury to the Russians. On 12 December Berthier sent a
private report ahead to Napoleon that the army no longer existed, and
that even the Imperial Guard, now reduced to five hundred men, had lost
all semblance of a military formation. Ney, still stubbornly fighting a
rearguard action, crossed the Niemen on 14 December. When the last
stragglers had shuffled over to the German bank, there remained fewer
than forty thousand of the brilliant Grand Army which Napoleon had
reviewed on 24 June. It is said that only a thousand of those who
returned were ever again fit for duty. So ended Napoleon’s dream
fantasy, the conquest of Russia and of India. There were, of course, other
causes of defeat besides typhus fever. Cold, hunger, the Russians, all
helped to destroy the army – and so did Napoleon Bonaparte himself.

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 Napoleon was born by a precipitate labour on 15 August 1769. At
the age of twenty-six in 1795 he was only five feet six inches tall, with a
square face, a strangely sallow complexion, a well-formed nose, grey
eyes and dark brown hair. His most striking physical characteristic at this
time was excessive thinness. Although well muscled and fairly powerful,
he looked a runt of a man. He had a lively, rather impressive expression
provided his interest had been aroused, but at other times often looked so
miserable that people thought he must be in actual pain. He took little
care of his person in early life. His long ill-powdered hair hung over his
collar, his clothes and boots were shabby and his hands dirty. Napoleon
had been a bookish youth, intelligent, eager to learn, a brilliant
mathematician. He had shown little interest in sex during adolescence.
Napoleon’s swift and dazzling rise to supreme power depended
on a combination of controlled imagination, unusual intelligence
tempered by downright common sense, and an acute perception of the
correct moment for any course of action. His magnificent brain seemed
as if divided into separate compartments which he could open and close
at will. Thus, he dictated orders and plans to a number of secretaries,
turning from one subject to another as he walked between their desks.
His notorious anger was a weapon calculated to inspire fear and was
entirely under his control. He lived for power and knew that power
largely comes from the master’s ability to instil fear: ‘Abroad and at
home I reign only through the fear I inspire.’ Later in his career, he was
to imagine himself as his own ideal of a gloomy, cold-blooded,
inaccessible tyrant, but he never achieved that character for, although
formidable, he remained fascinating. Talkative, gregarious, possessed of
great charm which, like his anger, could be switched on and off at a
moment’s notice, he aroused a genuine love and devotion among those
who came in contact with him. Even his enemies were impressed. The
ship’s company of HMS Bellerophon which took him to St Helena
agreed that ‘if the people of England knew him as well as we do, they

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would not hurt a hair of his head’. His veterans worshipped him, for his
fantastic memory enabled him to call any one of them by name – and it
was the duty of his aide-de-camp to prompt that memory should it fail.
Napoleon also achieved his success by a phenomenal capacity for
hard work. Pressure of work caused him to neglect his natural body
requirements. He slept for only three hours each night and developed the
ability, not uncommon among hard-pressed administrators, of falling
deeply asleep for short periods at intervals during the day. Anthelme
Brillat-Savarin dismissed Napoleon as ‘an undiscerning eater’. He bolted
his food, often taking only twelve minutes over dinner, and ate when
business permitted rather than at set hours. Despite this unhealthy
regimen, Napoleon seems to have kept remarkably fit during his earlier
years in power.
He had certain disabilities which became more troublesome as he
aged. The story of infertility, half believed by himself, came to a happy
end with the birth of his bastard sons. The rumour of epilepsy possibly
has a firmer foundation. As a lad at Brienne he fell unconscious to the
ground, but this was probably nothing more than a faint. During the near-
disaster of Brumaire in November 1799, when he was physically
menaced by members of the Five Hundred, friends dragged him to safety
in an almost unconscious state. This, although it has been cited as
evidence, was probably reaction to a totally unexpected crisis. But three
attacks bearing some resemblance to epileptic fits are recorded between
January 1803 and September 1805.
The suggestion has also been made that Napoleon suffered from
syphilis. This story is based on some urinary trouble during the
Consulate of 1802–4. Napoleon himself wrote that the opinion of his
doctor, Alexis Boyer, caused him to ‘conceive strange suspicions of
Josephine, for I was quite sure of myself’. But his urinary symptoms
(which we have already noticed at the battle of Borodino) are more

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suggestive of small stones, ‘gravel’, in the bladder. There is nothing here
to support a diagnosis of syphilis.
The most serious of Napoleon’s illnesses to be diagnosable with
any certainty is migraine, the distressingly painful ‘sick headache’ which
is only too common among highly strung people who work under great
pressure. The first report of migraine comes towards the end of the
Italian campaign in 1796 and he suffered from similar attacks at times of
stress throughout his life. Another symptom of Napoleon’s highly strung
temperament is his itching skin. This must have been a dermatitis of
nervous origin but may well have been induced by the true ‘itch’ or
scabies which he contracted at Toulon in December 1793.
Two other disabilities, neither serious in itself, profoundly
affected Napoleon’s later career. Napoleon was certainly a man of
‘irregular habits’, which resulted in constipation, and the straining at
stool, a natural sequel of constipation, rendered him liable to prolapsed
haemorrhoids, generally known as piles. The first mention of this very
common and very painful ailment is in 1797, when he was twenty-eight
years old. Five years later, in 1802, irregular eating habits produced
another painful condition, equally common among those who live at high
pressure and without due care. Fauvelet de Bourrienne, Napoleon’s chief
secretary, recorded that his master began to suffer from abdominal pain
early in 1802. He would quite often lean against the right arm of his
chair, unbutton his waistcoat and exclaim ‘Oh what a pain I feel!’ This is
possibly gall-stone colic or simple indigestion but the later history
suggests that bane of the harassed financier, a peptic ulcer.
In 1805 Napoleon, crowned Emperor on 2 December 1804, was
thirty-six years of age. From now on he started to deteriorate, both
physically and mentally. This fairly rapid change was noticed by all
those in close contact with him. He began to fill out, developing a
paunch. His thin face became rounded and his neck thickened. The long
straggling hair receded from his forehead, grew sparser and finer in

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texture. His skin was softer and his hands, once long and ‘beautiful’
(although dirty), were covered with fatty tissue and so gave the
appearance of being small and pudgy. The lean, haggard Corsican Ogre
of the James Gillray caricatures changed into the better-known stocky
little Napoleon of school history-book pictures.
This physical deterioration was accompanied by a marked
alteration in temperament and mentality. Basically, he lost self-
discipline. From 1806 onward his rule became more absolute and his
ministers little better than yes-men. Denis Decrès, Minister of Marine,
declared: ‘The Emperor is mad and will destroy us all.’ In 1807 Prince
Metternich observed that ‘there has recently been a total change in the
methods of Napoleon. He seems to think that he has reached a point
where moderation is a useless obstacle.’ His temper was not under the
same control as before. His rages were less frequent but he could no
longer switch them on and off at will. He lost the common sense which
had nearly always guided his actions and now allowed his fantasies to
take charge of his plans. Hand-in-hand with lust for power and dream-
fantasies there went an unwonted impatience. But the body refused to
obey the dictates of the mind. His magnificent vitality slackened and he
lost the old capacity for prolonged constructive work. By the age of forty
Napoleon had changed into a lethargic and hesitant but irritable man.
What was the cause of this dramatic change? Many reasons have
been suggested but not one wholly explains the facts. His obesity and
lethargy suggest a physical rather than a mental cause. Thyroid
deficiency, myxoedema, might produce changes of this kind, but
portraits of Napoleon’s features do not favour the diagnosis. Fröhlich’s
Syndrome, deficient secretion of the pituitary gland at the base of the
brain, has been suggested, but it is unlikely that a person suffering from
this disorder would be capable of siring children. Neither of these
theories takes into account the three ‘fits’ or epileptiform convulsions
reported in 1803–5. These are unlikely to have been true epilepsy but

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may be associated with his known migraine. Ordinary migraine can
occasionally develop into the syndrome now called ‘complicated
migraine’ in which fits or paralyses or disturbances of speech may occur.
These severe symptoms result from spasm of the cerebral arteries which,
though transient, can lead to brain damage. If this is the case, Napoleon’s
lethargy resulted from minor brain damage and his obesity was
consequent on the lethargy. The damage must have been only minor, for
it is evident that Napoleon could react violently and swiftly when faced
with a direct challenge to his power, nor is there evidence that he showed
any of the grosser signs of severe brain damage.
Whatever the cause may have been, and it is certainly unwise to
be dogmatic on this point, the new Napoleon lacked the quickness and
decision of the old. Nevertheless he successfully recruited a new army of
470,000 between December 1812 and July 1813. His army was superior
in numbers to that of the Allies, but was poorer in quality since it mainly
comprised raw recruits, the type always more susceptible to campaign
diseases than seasoned veterans. On the way back from Moscow the
retreating French and pursuing Russians had infected Germany with
typhus fever. All central and eastern Europe suffered an epidemic in the
autumn and winter of 1813–14. Thousands of Napoleon’s new army
succumbed until, by the late autumn of 1813, fewer than half remained
fit for service.
Towards the end of August 1813 the French had seemed on the point of
inflicting decisive defeat upon the Allies at Dresden. After two days of
bitter fighting, during which Napoleon directed the battle in person, the
Allied armies were forced to retreat, leaving the French poised for an
annihilating stroke on the next day. But now one of Napoleon’s
comparatively minor disabilities attacked him and helped to change the
course of history. On the evening of the second day, he was exhausted,
soaked to the skin and famished with hunger. He ate hurriedly and
ravenously. During the night of 27/28 August abdominal pain and

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vomiting became so severe that he was forced to return to the rear,
leaving Marshal Mortier, Marshal Laurent de St Cyr and General
Dominique Vandamme to resume battle next day. The defeat of
Vandamme prevented a rout of the Allies.
Two months later, on 17 October, a similar attack of abdominal
pain and vomiting prostrated Napoleon during the decisive battle of
Leipzig, but in this case probably did not affect the issue. By November
the French had been driven back across the Rhine. Prussians under
Prince Blücher, Austrians under Prince Schwarzenberg and Russians
under Tsar Alexander gave chase and poured along the roads to Paris.
Wellington was fighting his way up from the Pyrenees. The days of the
Napoleonic Empire were numbered. At this critical, hopeless time
something of Napoleon’s old magic returned. Wellington said of the
campaign of 1813–14: ‘the study of it has given me a greater idea of his
genius than any other … but he wanted patience’. On 6 April 1814 the
Marshals insisted on unconditional abdication and on 11 April Napoleon
made a declaration renouncing the thrones of France and Italy.
There followed an attempt at suicide, probably by means of
strychnine, on the night of 12 April. Then came the terrible journey
through southern France, when the fallen Emperor narrowly escaped
lynching at Avignon and saw himself hanged in effigy at Orgon, and his
departure into exile as monarch of Elba. Here he seems to have been
reasonably happy, administering his tiny kingdom, exercising his toy
army, no doubt supported by his dreams and his plans. Then came the
dramatic, almost insanely adventurous return to France. On 1 March
1815 Napoleon landed at Antibes and started on his triumphant progress
through Mouans-Sartoux, Grasse, Digne, Grenoble and Lyons back to
Paris.
The ill-health which had now dogged him for ten years almost
brought the adventure to an end before it had really started. The
returning hero rode triumphantly on horseback at the head of an

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impressive cavalcade from Antibes to Grasse. Here the haemorrhoids,
which had troubled him on and off since 1797, became excruciatingly
painful. Even to walk was agonizing, to ride unthinkable. Napoleon
commanded a carriage to be brought forward and for a time found some
comfort, but the rough road and the jolting wheels made relief only
temporary. A sick and deposed monarch lolling on cushions is very
different from a returning conqueror prancing on his warhorse. But the
attack passed fairly quickly and Napoleon found himself able to continue
the march after two days. Had the bout been more prolonged, his
triumphant progress might well have ended at Grasse.
These same troublesome piles, together with Napoleon’s somnolence and
lethargy, largely account for what the French still call the enigma of
Waterloo. Of all the armies which Napoleon recruited, that which fought
at Waterloo was the one most needing inspiring and coherent command.
They were a ‘scratch lot’, unaccustomed to their leaders, hastily enrolled
during the Hundred Days. But these troops cannot be blamed for the
disaster of Waterloo. Napoleon lost the battle of 18 June by losing his
opportunity on the previous day. On the evening of the 16th the strategic
position looked most favourable for the French army. Considering the
poor quality of his troops, this fact itself testifies to Napoleon’s skill as a
military leader.
Napoleon, commanding about 124,000 men, faced a Prussian
army of 120,000 under Prince Blücher and a mixed British-Dutch-
German-Belgian force of 100,000 under the Duke of Wellington.
Napoleon’s admirable plan was to operate with two wings and a large
reserve. Headquarters having been established at Charleroi, he ordered
one wing under Marshal Ney to hold Wellington on the Brussels road
while the other, under General Grouchy, engaged the Prussians. These
were still about ten miles to the east of the nearest point where they
could make contact with their British allies and so face Napoleon with
numerical superiority. On 16 June Ney duly attacked Wellington at

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Quatre Bras, while Grouchy and Napoleon defeated and partially routed
the Prussians at Ligny. Neither battle was decisive, but the opportunities
for the following day were immense. Napoleon with his reserve could
either complete the rout of the Prussians on his right flank or take an
easy swing to the left and smash Wellington. But, as the military
historian Becke has written: ‘it was in these twelve hours from 9 p.m. on
the 16th to 9 a.m. on the 17th that the campaign was lost.’
Napoleon had been in the saddle for the whole day of 16 June.
This obese, prematurely aged man of forty-six was completely worn out.
Worse still, his piles had once more become agonizingly painful. He
remained sleepless, in pain, throughout the night of 16/17 June. Whether
Larrey did or did not administer opium will probably never be known for
sure, but Napoleon stayed in his bed until eight in the morning. He did
not resume active command until eleven, when he ordered Grouchy to
pursue the Prussians. By this time contact had been lost and Napoleon
made the mistake of ordering pursuit to the east, whereas Blücher had
retired to the north. At the same time Napoleon ordered the Guard to
support Ney at Quatre Bras. Wellington, having learned of Blücher’s
retreat to the north, moved his army back up the Brussels road to parallel
the Prussians and to establish a defensive position on the high ground
before the village of Waterloo. For some time the British were entangled
in the narrow village street and single bridge of Genappe, an easy target
for Ney. Meanwhile Grouchy, feeling his way east and south, was every
moment increasing his distance from the coming battle.
On 17 June the sun rises at about 3.45 GMT. Over four hours of
daylight were wasted before Napoleon awoke from his uneasy sleep,
over seven hours before he was able to assume control of strategy. It is
certain that he had the opportunity of inflicting decisive defeat and it is
certain that he lost the chance. The young Napoleon would never have
missed the opportunity offered but would have risen triumphantly to the
occasion, exhaustion or no exhaustion, pain or no pain. The lethargic,

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impatient, pain-ridden Napoleon of June 1815 was no longer capable of
the effort required. To the medical historian Saturday 17 June is the fatal
day and the Sunday of Waterloo itself comes as something of an
anticlimax. Napoleon was still in no fit state to exercise control of the
battle, yet despite his ill-health and the mistakes made by Ney he very
nearly defeated Wellington at Waterloo. If we accept the victor’s own
opinion – ‘It was the most desperate business I ever was in. I never took
so much trouble about any battle and never was so near being beat’ –
then Napoleon’s ill-health may well have provided the necessary weight
to tip the balance.
Six years later, on 5 May 1821, the deposed Emperor died on the
island of St Helena. The second period of exile had been a time of
hopeless frustration, of petty quarrelling, of sulky seclusion.
Undoubtedly the Governor, Sir Hudson Lowe, lacked the tact and
intelligence to handle so difficult a prisoner as Napoleon, but the legend
of the ‘Martyrdom of St Helena’ has no basis of fact. Political necessity
prompted the British to present the island as something in the nature of a
health resort. Conversely, similar considerations encouraged Napoleon’s
sympathizers to depict it as more akin to Devil’s Island. Even Pope Pius
VII, whom Napoleon had arrested and exiled, made a plea for his release
on the ground ‘that the craggy island of St Helena is mortally injurious to
health and the poor exile is dying by inches’.
A form of liver disease, an acute infective hepatitis, was endemic
on St Helena. Napoleon may have fallen sick of it but, if so, he quickly
recovered. His terminal illness lasted six months. Much has been written
about it and many theories have been advanced. In fact the history is
quite clear. During his last days he suffered from ‘tarry stools’ and
‘coffee-grounds vomit’, both of which are caused by digested or semi-
digested blood. The treatment given to him does not seem very sensible.
One of the last drugs administered was a large dose of calomel, which
can have done not the slightest good and may have actually hastened

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death. The post-mortem reports vary as to the condition of Napoleon’s
liver, but all mention a large ‘scirrhous growth’ of the stomach. This,
taken together with the tarry stools, coffee-grounds vomit and the
obstinate hiccups described by General Bertrand, make the cause of
death certain. Napoleon died of a cancer which had invaded the stomach
wall, piercing an aperture of sufficient size to admit a finger. The cancer
had eroded a blood vessel and the immediate cause of death was
exhaustion from haemorrhage and peritonitis, both secondary to
perforation of the stomach wall by the malignant growth.
Although the cause of death is plain, a number of allegations
were made. Among these is poisoning, a very common allegation when
the deaths of prominent persons are under consideration. Napoleon
ordered in his Will that his head be shaved and locks of hair distributed
to various friends and followers. Some excitement was caused in 1960
by the report that traces of arsenic had been found in samples of his hair.
Poisoning by arsenic cannot have been the immediate cause of death.
Arsenic is, however, a known carcinogen and, if taken inadvertently or
purposely administered for any length of time, might have been the
causative agent. It is conceivable but unlikely.
Napoleon died nearly six years after Waterloo and lost Waterloo
three years after the Moscow campaign. His disastrous fall began and
became inevitable when his own health and judgement began to fail. His
Grand Army was destroyed by his own impatience and by the ill-luck of
encountering typhus fever. His empire never recovered from the
destruction of that army. On 29 November 1812, during the crossing of
the River Beresina, Marshal Ney wrote to his wife: ‘General Famine and
General Winter, rather than the Russian bullets, have conquered the
Grand Army.’ This is the accepted opinion but, to tell the whole truth, we
must add the names of General Typhus and General Napoleon.

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 C S
CHOLERA AND SANITARY REFORM

There is an important group of diseases, known as enteric fevers, which

are caused by human excrement contaminating food or drinking water
with the relevant bacteria. These include typhoid, paratyphoid and
dysentery. To them must be added cholera, often known as Asiatic
cholera to differentiate it from infantile cholera, better called infantile
diarrhoea. Until recently these afflictions, together with typhus fever,
were often classed as campaign diseases, that is illnesses which were
particularly prevalent in the special conditions of warfare.
Before the Battle of Crecy in 1346 the French rudely spoke of the
English invading force as the breechless or bare-bottomed army because
they so often squatted to defaecate. It would be impossible now to decide
which disorder had attacked them but typhoid or dysentery seem the
most likely. Until the twentieth century endemic enteric diseases of this
group, together with typhus fever and eventually the exotic Asiatic
cholera, killed many more soldiers than any weapon. In the grossly
mismanaged Crimean War of 1854–6 (‘the army was destroyed by its
military leaders and saved by a civilian woman’) out of 97,000 British
troops dispatched to the theatre of war, 2,700 were killed in action, 1,800
died of wounds, and 17,600 died of disease. Cholera was rampant in the
British forces and, during the winter months, scurvy (Vitamin
deficiency) also caused a number of deaths. In the American Civil War
of 1861–5 the Northern Armies lost 93,443 men killed on the battlefield
or later dying from their wounds. The toll from disease amounted to
almost exactly double at 186,216, the deaths of 81,360 being ascribed to
typhoid and dysentery. Again, cholera was partially responsible for the

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high mortality. Accurate figures are not available for the Confederates
but it is believed that typhoid caused even more deaths than in the North.
The Boer War of 1899–1901 is also of considerable medical
interest. British military commanders have been less noted for
intelligence than for their refusal to accept civilian advice, but the Boer
War generals must surely have been unusually wooden-headed. The
organisms causing typhoid and bacillary dysentery had already been
discovered and measures for prevention, including anti-typhoid
inoculation, were available. Long before 1899 typhoid had been
recognized as primarily a water-borne disease and it was well-known
that contaminated water could be rendered harmless by boiling or
filtration. About 400,000 troops in all were engaged in South Africa, the
field army numbering 200,000 at any one time. From February 1900
until the end of 1901, 6,425 British soldiers died in battle or from
wounds. The Boers used the high-velocity Mauser rifle which either
killed outright or inflicted a clean and fast-healing wound. The terrain
was largely uncultivated, not highly populated, and so relatively free
from the organisms which cause human disease such as wound sepsis.
Despite this comparative freedom from pathogenic organisms, 42,741
men fell sick of typhoid fever alone and the total who died from all
forms of disease amounted to 11,237, nearly double the deaths from
enemy action. There is no doubt whatsoever that the armed forces
themselves introduced infection and that the incidence of typhoid and the
number of deaths from enteric disease could have been greatly reduced
had proper water discipline and sanitary measures been ordered by the
high command.
This may appear a severe and unfair judgement, so let us see
what happened only four years later in the Russo-Japanese War of 1904–
5. The Russians did not issue exact figures but claimed that of 709,587
men engaged, less than one in a hundred suffered from illness. The
report may be an underestimate but observers remarked that the health of

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the troops remained excellent throughout the Russian débâcle. The
Japanese lost 58,357 men from enemy action and 21,802 from disease,
thus reversing the previously recorded battle casualty/sickness ratio. Of
the Japanese who died from sickness, 5,877 died from typhoid fever and
dysentery. These water-borne diseases were as prevalent, if not more
prevalent, in Manchuria as in South Africa. The enormous improvement
in the sick rate largely depended on forbidding troops to drink unboiled
water, providing constant supplies of hot water for making tea, provision
of latrine areas, and, so far as possible, never billeting men in villages.
We can understand that the common soldiers on active service
suffered badly from these infections but it is more surprising to find that
even royal commanders were affected. Of English monarchs who led
their armies in person, William the Conqueror died in 1087 from a
ruptured ulcer in the bowel, a late result of typhoid fever. Edward I died
of dysentery in 1307 as did the hero of Agincourt. Henry V, in 1422.
Edward the Black Prince, heir to Edward III, died of the same disease,
and may thereby have changed the course of English history, for his
weak young son came to the throne during the land and labour crisis
following the Black Death, one of the more difficult periods in social
development. King John’s romantic death in 1216 from ‘a surfeit of
peaches and new cider’ is likely to have been the plebeian effect of
resultant diarrhoea violent enough to rupture a bowel already weakened
by typhoid fever. The demise in 1135 of the second royal glutton, Henry
I, was undoubtedly from another of the enteric group, food poisoning:
‘He ate voraciously of a lamprey, which he was accustomed to delight in
more than anything else, and paid no attention to his physicians when
they forbade it him.’ It is said that a man who helped embalm the body
fell ill and died in great pain a few days later.
In rather more recent times, the death in 1861 of Albert the
Prince Consort, husband of Queen Victoria, was most probably due to
typhoid (although some commentators now prioritize intestinal

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inflammation). His son, Edward VII, very nearly lost his life from the
same disease ten years later, and Edward’s nephew, Tsar Nicholas II, fell
seriously ill of typhoid fever in 1900. His mother, Maria Feodorovna,
complimented him on his strength of mind when the physician reported
to her that Nicholas had refused to eat a mutton cutlet until it had been
minced, a precaution commonly adopted in the recovery stage of typhoid
fever.
The early story of this group of diseases is impossible to
disentangle because they were commonly lumped together under the
term ‘continuing fevers’. Many physicians suspected that the group
contained more than one disease but many more thought the appreciable
differences to be variations in behaviour of the same type of illness. In
the late summer and autumn of 1839 William Budd, a doctor in North
Tawton, Devon, had under his care the inhabitants of several cottages
notorious for the number of ‘fever cases’ they produced. Budd studied
the problem and concluded that he was dealing not with one but with two
types of disease. He found that, although both were characterized by
fever and a blotchy pink rash, one tended to be acute, killing within days,
and the other chronic, sometimes causing months of sickness. It is not
clear whether Budd himself named the two infections, because he did not
publish his findings until 1873, by which time credit for the
differentiation had already been attached to Sir William Jenner in Britain
(1849) and to William Wood Gerhard of Philadelphia (1837). The acute
disease was named ‘typhus fever’ and the more chronic one was called
‘typhoid’ because it resembled typhus in some respects without being
identical.
Continuing his observations, Budd found that the majority of his
typhoid patients came from a single group of cottages which all drew
their water from the same shallow well. In view of the unmistakable
bowel symptoms, he concluded that the excreta of the sick individuals
must be leaking from the earth privy which served the cottages into the

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well from which the cottagers drew their water. After one or two
inconclusive experiments, he treated the privy with massive doses of
chloride of lime. The number of typhoid cases gradually dwindled and
finally reached a low which might be expected in any village community
of the time. Local historians who search old parish registers often find a
pattern of deaths obviously from small localized epidemics affecting all
age groups and occurring at any time of the year. Sometimes it is
possible to trace the names of the dead to a group of families living in
close proximity and even to identify the disused well from which they
drew the water.
The village system of drawing water from a surface supply,
streams or shallow wells, and disposing of human excreta by spreading
over the fields had worked quite satisfactorily for centuries without
producing unbearable living conditions and persisted in the remoter
country districts almost down to the present day, until the thatched hovel
with its unreliable well and earth privy became the desirable residence
ripe for conversion. But during the eighteenth century living conditions
of the labouring class started to be changed by the industrialization
which first developed in the relatively small country of Britain. Here the
population of England and Wales rose from 8.9 to 17.9 millions between
1801 and 1851. The problem caused was greater than even this increase
suggests. As the Industrial Revolution quickened, there developed a
swiftly accelerating movement from country to town. It is for this reason
that our primary consideration will be the problems and the solution of
the problems as they affected Britain.
As in all European countries, the life and economy of Britain had
been sustained by agriculture for centuries. Now the villages and small
market cities of a farming community burst their bounds and sprawled
over the countryside until, in many districts, the intervening fields
disappeared and individual hamlets lost identity to become parish names
in one coalescent mass. Unfortunately for the health of the public,

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landlords, speculative builders and the inhabitants themselves regarded
these new towns simply as enlarged villages, which they were not. As
the towns expanded and spread over the fields, so the difficulty of waste
disposal intensified. The temptation to pour excremental waste into the
river could not be resisted. This river also supplied much of the drinking
water. A swiftly flowing stream carried most of the waste away from the
town and its water supply. A tidal river, such as the Thames in London or
the Avon in Bristol, returned a large part of the noxious material on the
incoming flow and so increased the risk of pollution. Use of steam power
diminished an already inadequate water supply and mills used the river
as a convenient waste pipe for their effluent. By 1830 no large
manufacturing town in England possessed water entirely safe to drink
and rivers in these areas had become so polluted that fish could no longer
survive.
More and more houses had to be built as the country people
continued to pour into the town. The new houses must be close to the
mill, for neither master nor worker desired that time be wasted on
travelling. Contractors used any available land to the best advantage,
cramming a maximum number of dwellings into a minimum of space.
Speed was essential since the mill could not start work until the
operatives were housed, so builders did not waste time on digging out
foundations, building weight-supporting walls and erecting tower blocks.
They built skimpily of readily available material, back to back in rows or
narrow courts. These new houses were serviced on the same principle as
the village dwelling, one house or part house to a family, with a shared
water supply and outside privy, often no more than a single earth closet
for each court or row of houses.
As time went on and the number of factories increased, building
could no longer keep pace with the influx into manufacturing towns nor
was there any more available land close to the existing mills. Taking in
lodgers and sub-letting became the rule. Few families occupied more

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than a single room and a two-roomed cottage might contain as many as
twenty people. Cleanliness, privacy, decency, proper sanitation and clean
water supply were all impossible in conditions such as this. The
uncleaned privies, in daily use by dozens of people, overflowed and
filled the courts with a morass of excrement which permeated the soil to
contaminate the shallow wells from which the inhabitants drew a scanty
supply of water.
We should rid our minds of the common fallacy that all this
sordidness was entirely new. All the major evils of the industrial town
already existed in the rural village. Underfed families lived in
overcrowded hovels, women and young children worked in the fields,
labourers toiled from dawn to dusk for a starvation wage. A child of
seven scaring crows on a bleak hillside in midwinter does not command
the same sympathy as a child of that age labouring in a mill. We
remember the overseer’s strap but forget the farmer’s whip. We are not
so horrified by the picture of a pregnant woman engaged in the back-
breaking task of hand weeding a cornfield as we are by that of her sister
harnessed to a coal-truck underground. The modern city-dweller’s
Cloud-cuckoo-land of a rural Arcady, a Merrie England that never
existed, has blinded us to the fact that every evil of the industrial town
originated in the agricultural village and resulted from the transfer not of
people only but of their manner of living. This way of life did not
become intolerably dangerous in the countryside because communities
were small, cottages widely separated, and work performed in the open
air. The disaster of epidemic illness became inevitable when the
community was cramped for space, houses lay cheek by jowl and factory
hands worked close together for long hours in an enclosed atmosphere.
The cholera which was to cause huge mortalities in communities
such as this and to become a world-wide pestilence during the early
nineteenth century had never before been endemic in Europe. Even in
India, where cholera probably formed part of the ancient disease pool, it

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seems to have been confined to a quite small area for centuries. It is, like
typhoid, one of the water-borne infections and there is reason to believe
that the Hindu ritual of river bathing, while probably encouraging
human-to-human spread, also limited the range of distribution because
the illness is typically a short one, often not more than a few hours. Older
reports of cholera by Europeans in India cannot be regarded as
trustworthy because of its similarity to the much more widely prevalent
bacterial dysentery, but the true disease was certainly existent in Madras
during the years 1770–90. In June 1814 it appeared among native troops
on a march of many hundred miles from Trichinopoly, a district of
Madras, to Jaunpur or Jawalpur, both towns in the United Provinces, the
latter standing on the River Ganges. In 1817 cholera broke out with great
violence over the whole Ganges delta, which became notorious as a
focus. Medical men in the area stated that it had not been seen in the
delta before 1817 and considered it a new disease. Their opinion is now
regarded with some doubt. A possible explanation is that cholera was
endemic in Central India, then largely unexplored by Europeans, and
made its way down river to the coast, carried by troop movements and
river shipping.
Cholera was on the move at the beginning of the nineteenth
century. In 1817–18 came the first known export from India, eastward to
China and the Philippines, south to Mauritius and Reunion, north-west to
Persia and Turkey. By 1823 a pandemic covered the whole of China,
Japan and Asiatic Russia. Then, for some unknown reason, the advance
halted for three years, only to recommence in 1826. This may or may not
have been a new export from India which followed the same route to
Persia and the Caspian Sea area, from where it travelled to Europe. The
first English cases appeared at Sunderland in October 1831. The whole
of the British Isles had been invaded by the winter of 1832/3 and most of
Europe by the end of 1833, Italy remaining free until 1835. Quebec and
New York received cholera by ship in 1832 and the disease spread

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slowly south through North America to Mexico and beyond. This slow
advance is typical and we cannot improve upon John Snow’s account of
a later pandemic in 1849:

There are certain circumstances connected with the progress of

cholera which may be stated in a general way. It travels along the great
tracks of human intercourse, never going faster than people travel, and
generally much more slowly. In extending to a fresh island or continent,
it always appears first at a seaport. It never attacks the crews of ships
going from a country free from cholera to one where the disease is
prevailing, till they have entered a port, or had intercourse with the
shore. Its exact progress from town to town cannot always be traced,
but it has never appeared except where there has been ample
opportunity for it to be conveyed by human intercourse.

This slow, relentless progress, which of course also characterized

the first waves of 1817–32, aroused a peculiar horror fed by rumour and
superstition. There was a widespread return to the medieval idea of
Divine Punishment. Cholera is an agonizingly painful illness, producing
intolerable vomiting and diarrhoea until the gut is entirely emptied and
the whole body dehydrated. Dehydration brings on terrible cramps of the
limbs and often of the abdominal muscles, while attempts to empty the
already empty stomach cause continual retching and hiccupping. A
cholera patient is a pitiful sight, whether he or she lives or dies, but the
most terrifying aspect of the illness is its sudden onset and the speed of
development. Heinrich Heine wrote a letter on 9 April 1832 describing a
scene in Paris of which this is a much edited version. On 29 March a
masked ball had been in progress, the ‘chahut’ in full swing. Suddenly
the merriest of the harlequins collapsed, cold in his limbs and,
underneath his mask, violet-blue in the face. Laughter died out, dancing
ceased, and in a short while carriage-loads of people were hurried from
the dance hall to the Hôtel Dieu (the oldest of the Paris hospitals) to die.

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To prevent a panic among the patients already there, the dead were
hastily thrust into rude containers still wearing their dominoes. Soon the
public halls were filled with dead bodies sewed in sacks for want of
shrouds or coffins. Long lines of hearses stood in queues outside the
cemetery of Père Lachaise. The rich gathered up their belongings and
fled the city. Among the poor, the suspicion of secret poisoning caused
the cry of ‘à la lanterne’ to be raised again. Six persons were murdered
and their naked bodies dragged through the streets in the belief that they
were culprits.
The horror of this disease and the rumours which preceded its
appearance demanded that action be taken by those in authority and the
slow progress gave time to prepare. Britain, closely followed by some of
the German states, was the first country to attempt centralized control of
‘public health’ and enforcement of health regulations upon the whole
civilian population. For example, a Board of Health had already been
instituted for this object in 1804 when a sea-borne epidemic of yellow
fever threatened. However, this was dissolved two years later once the
immediate danger had receded and no rules had been implemented. In
practice the government could only exert influence through such local
authorities as existed. The only ones available were composed of parish
officers and justices of the peace, whose primary duty was to implement
the Poor Law under the titular control of the Privy Council. The system
dated from the reign of Elizabeth I and in the course of time had become
so decentralized that every parish was virtually a self-governing unit.
Towards the end of 1830, when it appeared likely that Britain
would soon be endangered by cholera, there were some people
determined to make good use of the little time that might be left. In
January 1831 Charles Greville, Clerk of the Privy Council, asked Dr
Walker of St Petersburg for a description of the epidemic already
affecting northern Russia. Walker seems to have left the city, for he did
not reply until March and then with a second-hand account. Cholera

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reached the west Baltic coast in early summer and on 17 June Greville
sent Dr William Russell and Dr David Barry to investigate and report.
Four days later, on 21 June, government established a Central Board of
Health under the aegis of the Privy Council.
However, the authorities made a serious mistake by appointing
leading members of the medical profession and high officials instead of
waiting for the return of Barry and Russell or employing doctors from
the East India Company who had first-hand experience of cholera. The
Board met almost daily from 21 June until 11 November 1831, preparing
‘such Rules and Regulations as they may deem most effectual for the
adoption of the most approved method of guarding against the cholera’.
The Privy Council received its first recommendations on 29 June. This
historic document is the first attempt to influence public health through a
centrally directed coordination of local government but was of little
value at the time as no member of the Board had yet seen a case of
cholera.
The Board advised the establishment of local Boards of Health,
consisting of members of the medical profession, clergymen and leading
citizens, which would maintain contact with the General Board in
London. They provided a few obvious but not inspired directions for
dealing with patients and their belongings and promised more detailed
instructions and a description of the disease in due course. On 3
September The Lancet carried an announcement of the scheme, which
was violently attacked by the editor Thomas Wakley.
On 12 October danger became acute with the appearance of
cholera in Hamburg, a port of regular communication with the British
Isles. The Rules and Regulations, with an additional statement on the
nature and treatment of cholera, were published on 20 October. A week
later, on 27 October, an army surgeon named James Kell reported the
first British death from cholera at Sunderland. Four more deaths were
reported before 1 November. The Home Secretary now issued

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instructions that the regulations published on 20 October must be
enforced. The Privy Council decided that a Central Board of Health
composed of members who knew something about cholera might be
useful, and dismissed the physicians on the pretext that they were too
busy to attend the almost perpetual sessions required. The new Board
consisted of Dr Russell and Dr Barry, a customs official named Edward
Stewart and Sir William Pym of the quarantine service. The Board was
full-time and did not confine its meetings to London. Barry left
immediately for Sunderland and other members travelled the country
encouraging formation of Local Boards, instituting isolation hospitals,
and advising on segregation and treatment. By February 1832 the Central
Board of Health employed four deputy inspectors-general of hospitals,
twenty-one medical officers and seventeen surgeons. At the end of the
epidemic these officers were advising 1,200 local Boards of Health in
England and Wales and about 400 in Scotland. Cholera caused some
twenty-two thousand deaths before the end of May 1832, then started to
decline rather rapidly until the epidemic had virtually ceased in
December and the Central Board of Health was dissolved. In February
Parliament had authorized a Cholera Prevention Act permitting local
authorities to provide nurses and medicines, cleanse infected houses,
destroy bedding, clothing and other articles, cover drains and cesspools
and abate nuisances in general, the cost to be chargeable to the poor-rate.
There had been some rioting in the worst slum areas of industrial
towns leading to apprehension that the close-packed, insanitary streets
might prove breeding grounds not of disease only but of social unrest.
Fear was intensified by the riots preceding the 1832 Reform Act. The
government set up a Royal Commission to enquire into the working of
the Poor Law, and to make recommendations for ameliorating the lot of
the working class. The Commission invited the help of Edwin Chadwick,
a lawyer-journalist who had been secretary to Jeremy Bentham, the
social reformer and co-founder of the University of London. Chadwick

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later became secretary and the most active member of the Poor Law
Commission.
He is chiefly remembered by the British public as the originator
of the hated Union, the central workhouse in which men, women and
children, paupers, the sick and the disabled, were herded in prison-like
conditions, including segregation of the sexes. The memory is unjust
because Chadwick had recommended hospitals for the sick, orphanages
for the fatherless, homes for the aged and workhouses for the healthy
unemployed, but a parsimonious government bungled the whole scheme
and it was further mismanaged by incompetent local authorities
interested only in lowering the Poor Rate paid by householders.
In 1836, when the first Registration of Deaths Bill came before
Parliament, Chadwick secured addition of a clause requiring registrars to
insert the cause of death. He persuaded the first Registrar-General to
appoint a statistician named William Farr. In 1838, the first full year of
registration, there occurred a major epidemic of typhus fever. About
fourteen thousand people fell sick in London, of whom 1,281 died. Many
of the manufacturing towns reported similar figures. Some of the better
local authorities noticed a relation between the number of typhus deaths
and the level of the poor rate. A few took advantage of the Cholera
Prevention Act to indict landlords who refused to abate nuisances. The
cost of prosecution was charged to the poor rate but auditors refused to
allow this as a reasonable expense on the ground that the Act only
covered prevention of cholera. The dispute was taken to Chadwick as
secretary of the Poor Law Commission. He saw the chance for an
investigation with the possible outcome of introducing some of the
reforms omitted from his Union scheme.
Chadwick enlisted the help of three doctors. They examined
conditions in the worst fever districts and concluded that the high
incidence was largely caused by dirty habits and drunkenness but that the
poor could do nothing to better themselves while living conditions

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remained filthy. In August 1839 the House of Lords pressed for an
extended enquiry largely undertaken by Chadwick himself with the help
of his three medical assistants. They published their findings on 9 July
1842 under the title Report of an Inquiry into the Sanitary Conditions of
the Labouring Population of Great Britain.
It is virtually impossible to overestimate the importance of this
document. On a relatively minor plane it was Chadwick’s Report that
first roused Florence Nightingale’s interest in social science and
particularly in hospitals, ultimately making her the leading authority on
the subject. Chadwick is one of those prophets of whom it can be said
that he was honoured save in his own country – though he did receive a
belated knighthood. His fame now is world-wide. His report directly
stimulated action on public health in the United States. The brilliant
American medical historian Fielding Garrison wrote: Through Lemuel
Shattuck, Chadwick may be said to have started public health activities
in the USA and latterly influenced even Billings.’ There had been no
advance in public hygiene until Shattuck instigated a sanitary survey of
Massachusetts in 1849. The survey report stressed the enormous amount
of ill-health in American cities consequent upon insanitary conditions
and the need for investigation and control. State Boards of Health were
instituted which did excellent work but there was no national
organization until John Shaw Billings urged the United States Public
Health Service in 1889. Chadwick also influenced Max von Pettenkoffer
who designed a sewerage system for Munich, did much work on cholera,
and was appointed their first Professor of Hygiene in 1859.
Chadwick covered an enormous field. Having examined returns
from 533 districts, he produced ‘sanitary maps’ clearly showing the
relationship between infectious disease and overcrowding. He pointed
out that disease was propagated by atmospheric pollution resulting from
filth, overcrowding, lack of drainage and defective water supply. He
proved his point by taking the ages of death from eight districts and

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showing that average expectation of life was related to class: forty-three
years for gentry, thirty for tradesmen and only twenty-two for labourers.
The last low figure entailed a very large number of widows and orphans,
all of whom must be supported by parish relief. Early loss of the
breadwinner, overcrowding and neglect forced children on to the streets
to beg, thieve and sell themselves as prostitutes. Disease thinned the
ranks of higher age groups leaving a ‘young, passionate and dangerous
population, easily deceived by anarchist fallacies’. Chadwick’s
biographer R.A. Lewis wrote that he ‘drew his respectable hearers to the
edge of the pit and bade them observe the monsters they were breeding
beneath their feet’.
The Chadwick report shook government and bourgeoisie out of
their complacency. Implementation of the necessary legislation would
require heavy expenditure. The government referred the problem to a
committee, usually known as the Health of Towns Commission, and a
number of semiofficial associations recommended action in the larger
towns. Liverpool was one of the first to obtain a Sanitary Act in 1846,
empowering appointment of a Borough Engineer, an Inspector of
Nuisances and a Medical Officer of Health. On 1 January 1847
Liverpool appointed Dr William Henry Duncan to be the first MOH in
Britain.
Meanwhile Chadwick turned from broad policy to detail. He had
no knowledge of sanitary engineering but set himself to learn and
enlisted the help of two efficient advisers. Piped water was coming
increasingly into use but the supplying companies were obsessed by the
ancient type of main, a bored elm trunk which split under the pressure
required. They therefore supplied water under very low pressure by
ground-level standpipes usually only for an hour or two on stated days.
Thomas Hawksley, one of Chadwick’s advisers, proved that flow and
pressure could be maintained at no extra cost by using metal piping.

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The problem of sewage disposal was solved by Chadwick’s second
adviser, John Roe. A few sewers already existed to take storm water off
the streets but they were simply brick channels with flagstone covers
which could be lifted to remove mud and rubbish by hand. Roe
demonstrated that it would be economical to replace these ‘sewers of
deposit’ by narrow-bore self-cleaning drains. This type of sewer, circular
or oval in section and running in smooth curves, required a constant flow
of water for efficient cleansing. If to be used for disposal of human
excrement, a sewer of this kind demanded the installation of flushing
water closets in place of the dry earth privy.
Self-cleansing sewers carrying noxious waste posed a major
difficulty. The ultimate outfall of the sewer could only be into a river,
almost certainly the river from which the town drew its drinking water.
Chadwick tackled the problem himself and devised the ‘arterio-venous
system’, exchanging rural water for town sewage. Land drainage was
coming increasingly into use as more acreage was needed for the
growing population and this substandard ground required heavy
manuring, much of which had been provided by ‘night-soil’, the term
used for the contents of privies. Chadwick proposed to pump water from
the land drains into the town and pump liquid town sewage through
return pipes on to the land. The term ‘sewage farm’ still commemorates
Chadwick’s scheme. This simple exchange of sewage for water proved
uneconomic in Britain although it was adopted in a number of other
countries.
Now came two disasters. Chadwick was a rather unpleasant,
dictatorial man who eventually quarrelled with the Poor Law
Commissioners and was dismissed from the secretaryship on 8 July
1847. The threat of another cholera epidemic had been growing since
1845, so the Prime Minister immediately put Chadwick in charge of an
enquiry into the sanitary defects of London, thought to be at special risk.
He produced a startlingly adverse report which, together with the

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imminent threat of cholera, terrorized even the British Parliament into
embarking on panic legislation. The Public Health Act (‘Chadwick Act’)
was rejected in March 1847 but became law on 31 August 1848.
The Act resurrected the General Board of Health for a term of
five years and gave local authorities power to form their own Boards of
Health. The General Board would no longer be under the control of the
Privy Council; it was responsible to no ministry and had no spokesman
in any department. In fact it had no definite duties, and could count on no
support except by engendering good will. The Board consisted of two
peers and Edwin Chadwick, later joined by a medical adviser, Dr T.
Southwood Smith. They held their first full meeting on 21 November
1848.
By this time cholera had appeared in Edinburgh. It reached
London in December and infected the whole country by June 1849. The
epidemic was much more serious than that of 1831. The ten-year-old
Registration of Deaths apparatus collapsed under the strain and the
figures are approximate rather than exact. At least fifty thousand and
probably more nearly seventy thousand died in England and Wales.
London suffered about fourteen thousand deaths out of at least thirty
thousand cases of cholera. The mortality gave the General Board of
Health the power denied to them by Parliament. Within three days of
their first meeting, sixty-two towns asked for application of the Public
Health Act. Local authorities demanded advice on how to implement the
vague powers accorded them. The Board secured passage of a Nuisances
Removal and Diseases Prevention Bill, which gave power of compulsion
but only in times of emergency. Now the General Board could order
abatement of nuisances, cleansing of streets, disinfection of houses and
provision of isolation hospitals. Chadwick used these powers to recruit a
corps of health inspectors, increase the number of Poor Law surgeons
and press local authorities to appoint Medical Officers of Health.

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 The General Board of Health undoubtedly worked hard and did
well but it became increasingly unpopular. Chadwick antagonized both
medical profession and local authorities by his dictatorial attitude. The
medical profession, local authority and public did not understand the
reason for insisting on clean water, disposal of sewage and abatement of
nuisances in time of epidemic illness. For this the prevalent ideas on the
cause of infection were to blame. Microbes, germs or micro-organisms
still lay in the future. The majority firmly believed in the theory of
miasma – impurity of the air – as the cause of disease. They believed that
the impurity arose from cesspits and dungheaps, was carried by
movement of the air from person to person to produce the illness which
was then carried on the air from the sick to the healthy individual.
The Board’s term of office ended in 1853 but the government
extended it for another year because of the continuing threat of cholera.
On 31 July 1854 a motion to extend the Board’s life for another term of
five years was defeated by 74 votes to 65. The debate took the form of a
venomous attack on Chadwick in which MPs made intemperate and
quite unjustified accusations: ‘England wanted to be clean but not to be
cleaned by Mr Chadwick’. He had been removed from the Poor Law
Board ‘for his rules of atrocious stringency’ (an allusion to the now
universally hated Unions). One member announced himself to be ‘quite
at a loss to know what services this man has rendered to the community’.
Next day a leader in The Times approved Chadwick’s dismissal with the
words ‘we prefer to take our chance with cholera and the rest than to be
bullied into health’.
So Chadwick went. The curious point is that his ideas on clean
water and sewage disposal had been completely vindicated by a
pamphlet published five years before, in 1849, although the author knew
nothing of microbes. John Snow, a London physician better remembered
as the first specialist anaesthetist, became interested in cholera in 1832
when he was nineteen years old and working as a surgeon’s apprentice in

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Newcastle-on-Tyne. He concluded that infection was transmitted not by
bad air (miasma) but by shared food and unwashed hands. Snow, now in
London, followed up his idea during the 1849 epidemic and decided that
the hands of a person attending the sick would inevitably become soiled
with the cholera evacuations and that, if this person prepared food, there
would be great risk to any uninfected person who ate it. Such might
account for the massive spread of cholera among the crowded poor, but
how did infection reach the houses of the wealthy? Snow thought a likely
explanation to be that cholera evacuations somehow got mixed ‘with the
water used for drinking or culinary purposes either by permeating the
ground and getting into wells or by running along channels and sewers
into the river from which entire towns are sometimes supplied with
water’. Then came the dramatic incident of the Broad Street pump, the
only item in Snow’s research to have entered folk memory. In 1849 the
majority of houses in the Golden Square area of London were not served
by piped water but depended on ‘pump wells’ of which that in Broad
Street yielded one of the best supplies. At the end of August cholera
caused over six hundred deaths in the district. The outbreak took an
explosive form in the Broad Street area, 344 deaths occurring in four
days. Snow investigated eighty-nine deaths in Broad Street itself and
found that all except ten of the dead lived close to the pump and drew
their water from the well. Of the remaining ten, five would have been
expected to draw water from another well but preferred the Broad Street
supply. Three more were children living in other districts who attended a
school served by the pump. Such is the genesis of the story that when the
local Vestry asked Snow’s advice on the prevention of further outbreaks,
he replied: ‘Take the handle off the Broad Street pump.’ The site of the
pump is now covered by a public house named in his honour The John
Snow, despite his having been a strict teetotaller.
Snow now traced the pipelines of various water companies and
showed convincingly that cholera abounded in districts served by one

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company but was almost absent in those served by another. He found
streets in which the pipes ran side by side, each company supplying
different houses in the same street. Cholera was rife in those served by
Company A and infrequent in those served by Company B.
John Snow had proved that cholera is a water-borne disease in
1849. He confirmed his findings in the epidemic of 1853–4 when he
compared two of the largest water suppliers in London. The water
supplied by one company produced a death rate of 315 persons per
10,000 houses, the other a rate of 57 per 10,000. He tentatively advanced
the theory that the materies morbi of cholera is a living organism. Dr
William Budd of North Tawton, mentioned earlier in connection with
typhoid fever, had moved to Bristol where he studied the 1849 cholera
epidemic and formed the opinion that the causative agent was capable of
multiplying in the human intestine and was disseminated by
contaminated drinking water. John Snow and William Budd not only
proved Chadwick’s contention that pure water and efficient disposal of
sewage are essential to the health of town dwellers, but came close to
anticipating Pasteur’s germ theory. From the latter there followed the
identification by Robert Koch of the causative organism Vibrio cholerae
in 1883, although Felix Pouchet had seen and described the vibrio in
1849 when examining the stools of a cholera victim under the
microscope – without realizing that he was looking at the cause of the
disease.
After the dismissal of Chadwick and his fellow members, the
General Board of Health was reconstituted on a year-to-year basis with
an Advisory Medical Council containing among others William Farr the
statistician and John Simon the Medical Officer of Health for London.
Farr and Simon determined to prove whether Chadwick’s views on water
and sewage were or were not correct. They examined the records of
London water companies, comparing the death rates in the areas served,
just as Snow had done on a small scale. The results were startling,

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ranging from a high of 130 to a low of 37 per 10,000. The company with
the best record used the method of sand filtration, introduced over twenty
years previously by James Simpson.
John Simon presented these results to the Board in May 1856.
Parliament again made public health the responsibility of the Privy
Council and empowered it to appoint a Medical Officer with the duty of
investigating health problems and preparing reports preliminary to
legislation. The Privy Council appointed John Simon to this office where
he remained until 1876, five years after public health passed into the
hands of the Local Government Board.
The two decades of Simon’s work as Medical Officer are
undoubtedly the most fruitful period in the world history of public health
but he and workers in many other countries covered so huge a field that
it cannot be dealt with adequately here. Simon possessed in a marked
degree the ability to choose men and lead them as a team. He had no
permanent assistant staff but was allowed to appoint paid inspectors for
specific tasks. The majority of the sixteen doctors specially associated
with Simon were young and at first inexperienced. Almost without
exception they rose to high rank in their profession. No fewer than eight
became Fellows of the Royal Society. Only three failed to attain
distinction and two of those were sick men.
They were not office workers. Simon and his team did not
depend on reports but visited in person. In times of epidemic illness they
tried to visit every town, every street, every infected house. They
gathered a mass of information about cholera, smallpox, diphtheria and
typhus fever. Infant mortality (death in the first year) then stood at an
average of 150 per 1.000 live births and was much higher in the working
class and especially high when mothers were in employment. An
inspector discovered the frightful truth that excessive mortality was
largely caused by drugging the babies with opium. Another inspector,
working on deaths from lung disease, produced evidence that many

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trades put the worker at risk. Others proved that the majority of manual
workers suffered from malnutrition, partly because they worked long
hours without adequate food, partly because of their wives’ lack of
domestic education. But polluted water, inefficient sanitation and
overcrowding were the major evils. One inspector discovered a mining
community where over three hundred families living in single rooms
took in lodgers.
By 1866 Simon had gathered an immense body of evidence and
the time had come for legislation. He showed himself a skilled diplomat,
lobbying Members of Parliament, feeding his own ideas into their minds,
flattering them into the self-delusion that they had themselves conceived
his plans. In 1871 Parliament established a new department, the Local
Government Board, to which the Medical Department of the Privy
Council was transferred. Simon the inspired leader became Simon the
desk official. He shared the work of drafting ‘The Great Public Health
Act’ of 1875, a remarkable piece of legislation embodying almost all the
recommendations made by his team and so wide in its scope that it
permitted implementation of most sanitary improvements in Britain
during the next sixty years. But the Medical Branch lost ground,
becoming increasingly subservient to lay officials. In 1876 Simon found
his power so eroded that his usefulness had almost gone. After a last
fierce battle with the Treasury he resigned ‘with extreme pain’ and
retired into private life, received a knighthood and died aged eighty-eight
in 1904.
Chadwick, Simon, Shattuck, Koch and many others in many
lands conditioned the public mind to the need for sanitary reform,
showed the way, and made the crowded cities cleaner and more
comfortable to live in. But it was the terror-striking cholera which
provided the initial and greatest impetus. Unfortunately this disease does
not have a history that can be neatly completed by the total eradication
described in the case of smallpox. Further visitations of cholera came in

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1863 and 1881, the first lasting for eleven and the second for fifteen
years. The 1881 pandemic is notable for providing the final proof that
cholera is water-borne by a terrible outbreak at Hamburg in Germany.
Hamburg was a self-governing city which drew its water supply directly
from the River Elbe. Adjoining it lay the town of Altona, part of the
Prussian State, where the government had installed a water-filtration
plant. Cholera caused a great mortality on the Hamburg side of the street
dividing the two cities but spared the Altona side completely. What may
be termed the final episode in the emigration of cholera from India in
1817 broke out in 1899 and lasted until 1923 but did not seriously affect
Western Europe and the Americas.
Another and unrelated pandemic started in the early 1960s with a
new strain of vibrio, given the name of El Tor. First identified in
Indonesia, it spread to Asia, Africa and South America. Another variant
was detected in India and Bangladesh early in the 1990s. Cholera
currently affects some 4 million people worldwide, predominantly in
developing countries, and causes at least 100,000 deaths per annum. So
this disease is still very much with us and there is yet a great deal to be
done. Even today we live our own comfortable lives in a world where
millions have to fight for survival under conditions of filth and
deprivation as bad as any that the Victorian sanitary reformers strove to
ameliorate. Indeed, to poverty and pollution we have added other
contributing factors. One of these – to which we return in our Epilogue’s
discussion of Covid-19 – is an unprecedented level of global movement
which serves only to increase our problems in seeking to control cholera
and other diseases with pandemic potential.

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 C S
GIN, FLU AND TUBERCULOSIS

Cholera and other water-borne diseases were not the only ills to affect
the industrial population. At the time of the Boer War (1899–1901)
medical examination of British recruits for South Africa revealed a
deplorably low standard of physical fitness. Young men, especially from
industrial areas, were found to be undersized, of poor physique, and
suffering from a range of deformities and chronic illnesses, many of
them preventable. The revelation came as a jolting blow to the pride of a
nation which then believed itself divinely created to rule the earth.
National arrogance found it impossible to accept that a large proportion
of the British people had been turned into chronic invalids by the very
processes which made Great Britain the most wealthy and highly
civilized nation in the world.
Three of the major evils attending the Industrial Revolution were
syphilis, alcohol and respiratory infections, of which last tuberculosis
was the greatest scourge. All three of these existed in the agricultural
village but each was also exacerbated by the conditions which developed
in the industrial town. A close-packed community will obviously
encourage promiscuity, entailing risk of transmitting venereal infection,
which is much increased by the loss of control engendered by alcohol.
Alcoholic drink is a means of escape from reality, harmless and even
beneficial in moderation, but one which, like all escapes, tends to be
addictive and is harmful in excess. It is easy to become dependent and, in
this respect, alcohol resembles any other means of escape, whether
smoking tobacco, taking various drugs by mouth and by injection, or
deliberately losing oneself in fantasies. Dependence upon any escape,

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not the means of escape itself, is the cause of disaster. This simple fact is
not well understood even today and was certainly not appreciated in the
nineteenth century.
Alcohol cannot have been a major social problem while beer
remained the staple drink of all classes. The thick, muddy liquid
contained much free yeast and had a variable but generally low alcoholic
content. It was food rather than drink, adding some desirable vitamins to
the diet of the predominantly meat-eating baron as well as to that of the
peasant living almost exclusively upon bread.
Alchemists succeeded in distilling the essence or spirit of wine
and chemists started to elaborate the method of fractional distillation in
the sixteenth century. The small quantities of spirit they produced were
medicines rather than drinks. The names eau-de-vie and usquebaugh,
both meaning water of life, remind us that brandy and whisky originated
as cordials, preparations alleged to stimulate the heart’s action. In
London the Company of Distillers received its charter in 1638 but the
drinking of distilled spirit did not become popular until after the Battle of
Ramillies in 1706. British troops developed a taste for Hollands, a Dutch
spirit flavoured with juniper berries. Brandy and whisky were expensive,
one being distilled from wine made of grapes and the other from grain or
malt. Gin could be spirit of any kind flavoured with juniper (in French
genièvre which gave gin its name) or even with turpentine. Distillers
soon found that any fermentable material yielded a spirit that could be
sold to merchants who diluted (‘broke’) it with water and added
flavouring. It was much cheaper to ferment waste grain, vegetables of all
kinds, rotten fruit or sawdust and distil the result than to brew good ale.
The distillate contained a higher percentage of alcohol than wine or beer
and, particularly if sawdust or wood shavings entered the mixture, it was
more or less poisonous.
Over five million gallons of unbroken spirit, which had paid duty
of 2d a gallon, were sold yearly in England during the 1730s. No one can

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possibly estimate the amount of illicit spirit consumed, for the crude
distillation of fermented liquid required only primitive apparatus and
little knowledge or skill. In 1736 the Government tried to check gin
drinking by imposing higher taxation, but the move caused rioting rather
than decreased consumption. One of the more tragic and less obvious
effects of heavy drinking is the noticeably increased number of deaths of
infants suffering from measles in the mid-eighteenth century. Measles
itself rarely caused death; rather death resulted from complications such
as pneumonia or ear infections, generally avoidable by good nursing. It
is a sad fact that drunken mothers do not make good nurses.
The problem had become so serious by the middle of the century
that action was essential. In 1751 the government again raised the tax
and prohibited retail sale of less than two gallons by distillers and
shopkeepers. This did reduce drinking in the street and the home quite
considerably but introduced the notorious ‘gin-palace’, owned by the
distiller or brewer and managed by the publican who retailed the drink.
Gin-palaces acquired a thoroughly bad reputation but, arguably, it may
not have been altogether deserved. They did not sell the more poisonous
concoctions but gin which had been distilled from a grain liquor. It is for
this reason that the series of bad harvests in the years following 1780 did
more to check gin-drinking than any legislation. The worst was over by
1790 but heavy drinking persisted among all classes until almost the end
of the next century.
No stigma attached to drunkenness. The tough hunting man, the
squire and the parson all regarded the dark evenings as a time for
enjoying the bottle. There was not much else to do. Music, dancing,
reading and writing all require light which was an expensive item only to
be provided on special occasions. Talking does not need light and a
single candle will reveal cloudiness in the wine. The king and his court,
the manor house, the rectory provided no example for the working man
to follow. The gin-palace remained the only place of relaxation and

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good-fellowship open to the illiterate and poverty-stricken mechanic and
his family, living among a crowd of similar workers. The failure to
provide any alternative to cheap alcohol and to the gin-palace as a place
of escape from crowded, comfortless living quarters is the primary
reason for heavy drinking in slum areas and industrial towns during the
eighteenth and nineteenth centuries.
In 1852 a Swede named Magnus Huss coined the term
‘Alcoholism’ which he defined as a chronic disease resulting from
dependence upon alcohol. Thus he almost instantly turned the problem
of drunkenness into a scientific craze throughout much of Europe.
Discussion of the virtues and evils of alcohol in the press (then as now!)
aroused public interest and in many countries associations were formed
to fight ‘the demon drink’. For instance in England the Church of
England Temperance Society, the Blue Ribbon Army and the Rechabites,
among others, preached the virtue of sobriety, induced drunkards ‘to sign
the pledge’ and demanded repressive legislation. Such legislation
implied a threat to the liberty of the subject as Dr Magee, Bishop of
Peterborough, made plain to the House of Lords in 1872: ‘If I must take
my choice whether England should be free or sober, I declare, strange as
such a declaration may sound coming from one of my profession, that I
should say it would be better that England should be free than that
England should be compulsorily sober.’
In view of opposition such as this, it is not surprising that the first
Licensing Act did not reach the Statute Book until 1904. Alcoholic
intake was reduced by social opinion rather than by legislation. Overt
drunkenness became unacceptable. As usually occurs, whether it be a
fashion in curtain material or in manners, moderation in drinking
gradually filtered down from the upper to the lower strata, immensely
helped in Britain by muscular Christianity as preached and practised in
public schools. By 1895 heavy drinking had quite gone out of fashion at
the Universities, to be replaced by chain-smoking of cigarettes, for which

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we must blame introduction of the White Burley tobacco cultivar by
George Webb in 1864, which made the straight-cut, flue-cured Virginian
cigarette popular. At first limited by price to the university undergraduate
and gilded youth of cities, the firm of W.D. and H.O. Wills brought
cigarettes within the workers’ budget, so much so that the years 1914–18
may justly be called the Age of the Woodbine. One of the perils of
civilization is that most members of the human race will periodically
demand escape from reality and as soon as one means of escape goes out
of favour, it will be replaced by another, no less addictive or dangerous.
The public attitude towards drinking took a different turn in the
United States. The American temperance movement was largely
political. Drinking saloons played a major part in corrupt politics and
many people thought it would be impossible to clean up local
government until the saloon had been abolished. The first State to
become ‘dry’ was Maine in 1851. Others followed and a growing
temperance lobby, rather than an abnormally high incidence of
alcoholism, prompted the Volstead Act, the eighteenth amendment to the
Constitution, which banned all intoxicating liquor throughout the United
States from 16 January 1920.
The battle against the evil drinking saloon had produced the
innocent drug-store, a curious mixture of pharmacy and refreshment
room, where respectable citizens, with their wives and children, could
enjoy cooling drinks such as ice-cream sodas. The opposite counter sold
a variety of patent medicines with names such as Mrs Pinkham’s
Vegetable Compound, Colonel Hostetter’s Stomach Bitters and Peruna.
These famous remedies contained about 20 per cent of absolute alcohol,
some herbal flavouring and little else. Sales of ‘whisky tonics’, always
high in the ‘dry’ states, rose to astronomical figures throughout the
country after January 1920. A Supplemental Act of 23 November 1921
imposed drastic regulations on physicians’ prescriptions and practically

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banned the whisky tonics by limiting alcohol content to half of 1 per
cent.
There had been little serious opposition during 1920–1 but now
the rum barons moved in. America was flooded with the kind of spirit
that had almost ruined England in the eighteenth century. The saloon
became the speakeasy. The majority of citizens carried a hip flask and
dealt with their bootlegger every week just as they dealt with the grocer.
Cocaine and heroin, more easily concealed than alcohol, became a
national vice. One in every four hundred Americans was a drug addict in
the early 1920s. During the late 1920s and early 1930s the United States
was synonymous with lawlessness. After thirteen years of gang-fighting
and murder, almost amounting to civil war, the prohibition lobby at last
gave in and the laws were repealed by the twenty-first amendment to the
Constitution on 5 December 1933. The American experiment clearly
showed the danger of the single factor or ‘pet abomination’. Until a safe,
universally acceptable and non-addictive means of escape can be found,
it is both hopeless and dangerous to attempt to cure the ‘Disease of
Addiction’ by prohibition of a single agent.

Respiratory diseases, or more correctly diseases that are

transmitted by close contact and especially by the breath, will obviously
be more prevalent in a close-packed community. It is not so much
density of population as occupancy of room space which will determine
incidence. When a single individual occupies one room, the infection
will be passed only by casual contact with outsiders, but the risk will
increase proportionately with the number of persons who occupy and
sleep in that room because individuals are continually brought into close
contact with one another. Thus the family of eight or more adults and
children housed in a single room may increase the risk of infection by as
much as eight times and if the family takes in lodgers, as was often the
case, then the risk will be still greater.

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 The common cold must have infected such a family whenever
one member introduced it and probably none would have escaped. As the
breadwinner worked in an almost equally crowded mill, the chance of
introduction from a sufferer outside the family circle was high.
Epidemics rapidly developed and the infection could be more serious
than the comparatively harmless cold. Some forms of influenza would
have swept through factory and home with the speed and intensity of a
prairie fire, causing numbers of deaths among the aged and the very
young from resultant pneumonia.
Influenza is a mysterious disease, not yet fully understood and
with a controversial history. It is really not a single entity but a collection
of diseases, caused by a mixture of quickly mutating viruses or even by
crossbreeding between an existing human form of the influenza virus
with some related virus of an avian or other animal origin. This
instability has so far defeated efforts to produce a truly comprehensive
vaccine and, as we re-emphasize in Chapter Eleven and in our Epilogue,
this is the reason why new types of the disease still remain a global
danger. Most known types are characterized by a very short incubation
period, a short but acute illness, and an almost complete lack of
increased resistance or conferred immunity to a future attack. Three
strains of virus, labelled A, B and C, are recognized and a bacillus,
named after the German discoverer R.F.J. Pfeiffer, was once believed to
be one of the causative organisms. It has been said of this bacillus that ‘it
inveigled many scientists into wasting a lot of time discovering its
insignificance’. Certainly when Alexander Fleming first prepared crude
penicillin in 1928, he used it as a ‘laboratory antiseptic’ to obtain
uncontaminated cultures of Pfeiffer’s bacillus, then often named Bacillus
influenzae, and for over ten years totally neglected the potential of
penicillin as an antibiotic for human medication.
Influenza may or may not be a comparatively modern infection.
The name is Italian, dating from the eighteenth century or earlier, and

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implies that it was caused by the influence of heavenly bodies. One of
the peculiarities of this common infection is that it disappears for quite
long periods and then reappears as wide-spread epidemics of varying
severity. Typically, though not invariably, an illness of the winter
months, it may take the form of ‘two-day flu’, little more than a raised
temperature, sore throat and headache, in one epidemic, to reappear a
year later as a much more lethal sickness, carrying risk of pneumonia,
and leaving the patient suffering from severe depression for many weeks.
So variable is influenza in its behaviour that no certain diagnosis can be
made on the evidence of ancient records. In fact it is doubtful whether
the disease existed as an infection of the human before the fifteenth
century. A much disputed theory identifies influenza with the first
appearance of the sweating sickness or ‘English sweat’ in the year 1485
when Henry Tudor defeated King Richard III at the battle of Bosworth
Field on 22 August. It is said that a hitherto unknown illness struck the
victorious army and that they carried the infection to London. Henry was
proclaimed king on the battlefield and it was very necessary that he
should establish his Divine Right by being crowned as soon as possible.
The illness carried by his troops caused so many deaths and such
disorganization that the ceremony had to be postponed until 30 October.
This is the first recorded appearance of the Sudor Anglicus. An attack
was of short duration, the victim either dying in a matter of hours or
remaining severely ill for several days before recovery. Symptoms were
high fever, burning thirst, headache and painful joints, sometimes
abdominal pain and vomiting, and always the profuse, stinking sweat
which gave the infection its name. In those unwashed times any profuse
sweat would probably have smelt badly, but the fact that sweating is
described as the most noticeable symptom indicates that the disease
caused a high temperature. Accounts suggest that the wealthier class
suffered heavily and that many deaths occurred among young adults.

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This first epidemic seems to have lasted only a few weeks and then to
have disappeared as mysteriously as it came.
Epidemics of a similar kind recurred for a century. Four have
been identified, in 1507, 1528, 1551 and 1578. That of 1528 also spread
to Germany where the infection was named ‘the English Pestilence’.
Meanwhile another form had appeared in Europe, bearing more
resemblance to the modern ‘ordinary flu’. That of 1516 which affected
all Europe is often regarded as the first definite appearance of influenza.
There were further European pandemics in 1557 and 1580. Then, for just
over a century, there seem to have been small regional epidemics but
nothing in the nature of a European pandemic until 1729. Major
outbreaks followed in 1732, 1781 and 1788. That of 1781–2 not only
became widespread but was very infectious. About three-quarters of the
British population are said to have fallen ill and it reached as far as the
Americas. The disease again receded, no epidemic being recorded until
1830. This was followed by a second in 1833 and a third in 1847. Then
influenza seems to have disappeared almost entirely until 1889.
The pandemic of 1889–92 was much more serious than most of
the previous outbreaks and is better documented. It is also the first type
of influenza to be named after its supposed place of origin. ‘Russian flu’
appeared in the St Petersburg district during December 1889, and by
March 1890 had spread over most of the world. This is also the first
certainly known epidemic of influenza to occur in ‘waves’ of varying
severity, acute in the winter of 1889, still worse in spring 1891, mild in
autumn and winter 1891–2. It killed at least 250,000 Europeans and the
total global death toll may have been as high as a million or more. This
‘Russian flu’ seems to have persisted for a number of years, gradually
becoming less prevalent and less severe.
In 1918 the world had been ripened for a pestilence. Four years
of trench warfare, fought under conditions of privation previously
unknown to those engaged, had produced a breeding ground for

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infection. Starvation or near-starvation affected most of the peoples of
Europe as well as the less privileged countries of the world. One would
have expected a disease far worse than ‘mere flu’ to have ravaged
Europe and been carried by the swiftly moving steamship to all other
parts of the globe. In fact when the pandemic arrived, it took the form of
an exceptionally virulent strain of influenza (now labelled as H1N1).
One of the peculiarities of flu is that it seems to attack a number
of widely scattered areas at the same time. For this reason it is difficult,
if not impossible, to decide where the 1918 pandemic originated. The
contemporaneous name ‘Spanish flu’ is certainly misleading and for an
interesting reason. Belligerent governments, fearful that reported loss of
manpower would encourage the enemy, imposed censorship upon reports
of serious epidemic illness. Spain, not being a belligerent, permitted
publication of the fact that the country was suffering from an unusually
severe type of influenza.
The first wave occurred in the early summer of 1918, starting
either in the USA or in American army camps in France, and attracted
little attention because it was a mild illness. The second wave was quite
different and appeared in several localities during August. Freetown, the
capital of Sierra Leone, Brest, the French port of disembarkation for
American troops, and Boston, Massachusetts, appear to have been all
infected at the same date. The illness was not only unusually infectious
but also exceptionally lethal. The symptoms were those of a typical
severe influenza – high temperature, sore throat, headache, generalized
pains in the limbs and prostration – but abdominal pain was frequent and
pneumonia much more prevalent. Although the elderly and the very
young suffered badly, there was an unusually high proportion of deaths
from pneumonia in the 20–30 age group. At a military camp in
Massachusetts the first case of influenza was diagnosed on 12
September. Less than a fortnight later 12,604 soldiers had been taken ill.
Boston itself was severely affected, about 10 per cent of the total

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population suffering, of whom nearly two-thirds died. The San Francisco
Hospital admitted 3,509 patients suffering from pneumonia, of whom a
quarter perished. It is reckoned that 20 per cent of the United States
Army fell ill between August and October. In all, about 24,000 American
service personnel died from influenza and resultant pneumonia,
compared with a total of 34.000 battle casualties.
These figures indicate the kind of morbidity and mortality experienced in
the second wave. The third came in the spring of 1919 and was almost as
severe but less wide-spread. During the whole pandemic only St Helena,
New Guinea and a few Pacific islands are certainly known to have
escaped infection, although there must have been unknown areas in
Central Africa, Asia and South America which were not attacked. The
death toll was appalling – over 150,000 in Britain alone – while between
twenty-one and twenty-five million of the world population died. (Even
that huge number may be an underestimate. A more modern accounting
doubles the world-wide toll and adds 50,000 to the British figure.) The
pandemic of 1918–19 undoubtedly produced the largest loss of lives by a
single invasion of disease since the Black Death, though on a percentage
of the population basis, the mortality rate was probably much smaller
than in 1347–50.
Hunger, bad living conditions, stress and war-weariness lowered
resistance on a massive scale and contributed to the incidence and death-
toll. Travel was perhaps quicker than in 1889 and the war entailed large
troop movements between nations. But, even making allowance for these
abnormal factors, the pandemic of 1918–19 remains unique. The great
killer was not influenza itself but the superimposed viral pneumonia.
Never before, nor since (while we are as yet only in the opening phase of
the Covid-19 pandemic discussed in the Epilogue to this book), has
a respiratory infection produced such a concentrated death-toll
as this. At the time, and at intervals in the following years, blame was
laid upon an animal infection, perhaps the organism of swine-fever,

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which transferred to the human. Pigs have been farmed as human food
for centuries with the result that pig and human have lived in close
contact. If pigs suffer from epidemics of a fever, then the infection could
have been transferred to the pig-keeper without interposition of any
vector such as a louse or flea.
For this reason and because of the similarity between the
symptoms, there are those who believe that the pandemic of 1918 was a
recurrence of the ‘English Sweat’. But such a belief does not imply that
the 1918 visitation was not influenza. Rather it suggests that the Sweat
may have been the first recorded influenza epidemic, originating in and
at first confined to England. The theory that it was a disease of pigs,
poultry, or any other domestic animal, that transferred to the human
might also account for the comparatively late appearance of influenza in
the European disease pool. If this is correct, then influenza is one of the
less acceptable gifts that Britain has made to the world.

It was said above that never before nor since has a respiratory
infection imposed so great a mortality as that in 1918–19. But the
statement has to be qualified if we think in terms of a prolonged time-
scale and include the insidious effect of pulmonary tuberculosis upon the
world. Here we have a disease that is more ancient than Man, caused by
an organism possibly descended from the oldest living thing on earth.
Many scientists believe that the tubercle bacillus derives from a
saprophyte, feeding on dead tissue, which transferred to living cold-
blooded creatures, then to warm-blooded animals and so to the human.
Part of this theory is borne out by the great prevalence of tuberculosis in
the animal kingdom and the number of recognizably different strains of
the causative bacillus.
We are concerned here with only two, the bovine and human
strains, both of which can cause the disease in humans and cattle. The
bovine type, usually acquired by drinking milk from tuberculous cows,

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tended to be a disease of childhood. The human type, usually acquired by
direct spread from one person to another, tended until quite recently to be
a disease of the young adult. Tuberculosis can affect every body
structure, forming ‘tubercles’, from which the name derives, which are
tiny nodes of inflamed tissue. These are formed by reaction to the bacilli
which they contain and are sometimes microscopic, sometimes just
visible to the naked eye. The bovine type more commonly affected
glands or lymph nodes, which hardened in texture and became enlarged,
or joints which developed the classical ‘white swelling’. For a similar
reason bones softened and lost their shape. This kind of lesion was
known as scrofula or the King’s Evil. The human type more often
attacked the lungs, being known as phthisis or consumption. The
invading organism caused increasing destruction of lung tissue, starting
as ‘the patch’, typically in the apex of the lung, and extending throughout
the whole organ, often causing collapse of the tissues and a massive
exudate, heavily tinged with blood, purulent or serous. Symptoms were a
cough, a high temperature with night sweats, rapid wasting and
expectoration of blood.
One attack of the bovine type protects the patient against
infection by the human type. Being almost confined to children, the
bovine infection was an actual safeguard against a more lethal illness in
later life. Although bovine infection could result in death or crippling
deformity, many children suffered nothing more than an enlarged gland
or a slight and temporary rise in temperature. They had been infected by
the bovine bacillus but their natural resistance had been sufficient to
overcome the small invasion. This ‘attack’ was sufficient to protect
against further infection by the bovine type and also to protect against
the human type. The importance of this fact must be emphasized. In
closely packed communities, such as the industrial town, human invasion
was likely to be far more massive and more difficult to resist, so that the
immunity conferred by the bovine type was positively advantageous. In

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the years of high incidence many doctors, especially in industrialized
Britain, believed treatment of milk to render it free of tubercle bacilli
carried a danger because, although such treatment might save some
children from death or deformity, it would place many more at risk
through later and almost inevitable contact with a human source.
Evidence of tuberculous infection has been found in Eurasian and
African remains at least from the Neolithic period onward and in
Amerindian skeletons from about 800 BC. One of the more interesting
medical-archaeological discoveries is the mummified body of an
Ammonite priest named Nesperehan who died about 1,000 BC. He
shows not only the typical hunchback (kyphosis) of advanced spinal
tuberculosis but also a cavity formed in the lower part of the abdomen
above the hip-joint which would now be known as a psoas abscess.
Hippocratic texts record recognizable symptoms and appearances.
Aretaeus of Alexandria, writing in the second century AD, described the
habitus phthisicus, accepted by nineteenth-century physicians as ‘the
tubercular diathesis’, the appearance of a person in positive danger of
pulmonary tuberculosis: ‘the slender, with prominent throats, whose
shoulder blades protrude like wings, who are pale and have narrow
chests’. All civilizations and all nations have been subject to
tuberculosis. Physicians have attempted cures in all ages. The Hindus
advised out-door living, exercises and sleeping in goat-stables. Galen
taught that the disease is contagious and warned against contact with
infected persons. He sent his patients to Stabia, a resort on the coast of
Italy opposite the Isle of Capri, just as an early twentieth-century
physician might have advised his wealthy ‘lungers’ to live on the French
Riviera. Rhazes and Avicenna of the medieval Arabian school
recommended draughts of asses’ milk and powdered crab shells. The
latter, a long-lasting popular remedy, provided additional calcium, a
treatment revived in the late nineteenth century.

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 Magic or miraculous cure played its part and took a strange form.
The King’s Evil or scrofula, commonly affecting the glands of the neck,
was supposed to respond to the royal touch. Touching is an ancient
custom, which may have been introduced by Clovis the Frank about AD
496 and is said to have been first used in England by Edward the
Confessor, although there is no certain record until the twelfth century.
Charles II of England touched in exile and dealt with 6,275 sufferers in
1660, the year of his restoration. By the time of his death in 1683 he had
touched no fewer than 92,107 people. History does not relate how many
he cured, but the figure suggests a high incidence of glandular
tuberculosis in the seventeenth century. William III continued the
ceremony but had little faith in its value for he accompanied each
touching with the words ‘God grant you better health and more sense.’
Queen Anne touched no less a person than the two-year-old Samuel
Johnson in 1711/12. Johnson must have been among the last English
subjects of this curious rite, for George I abolished it when he came to
the throne in 1714. French kings regularly touched until 1775 and the
custom was briefly resurrected by Charles X, an ardent believer in the
Divine Right, when he ascended the throne in 1824. The last recorded
ceremony took place in 1825.
The early history of the pulmonary form of tuberculosis is not
altogether clear, partly because of confusing nomenclature. In England
the word ‘tissic’ may have been attached to the disease. If so, the Tudor
dynasty of kings suffered badly for both Henry VII and his elder son
Arthur died of this mysterious ailment. So did the Duke of Richmond,
illegitimate son of Henry VIII, and it has already been mentioned that
Henry’s only legitimate son, Edward VI, appears to have died of a
combination of syphilis and tuberculosis which was a quite common end
for town children in the nineteenth century. Some historians maintain
that consumption was a disease of the well-nourished upper class rather
than of the underprivileged until the eighteenth century. Deaths of

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notabilities attract attention, whereas deaths of lesser persons do not, so
it is equally logical to infer from the large number of known royal and
upper-class victims that pulmonary tuberculosis was wide-spread,
attacking all classes including the highly privileged.
From the second half of the eighteenth century until the Second
World War, roughly two hundred years, pulmonary tuberculosis was far
more common among the under-privileged than among the privileged,
though the latter suffered badly by modern standards. Tuberculosis
became equated with poverty. The term ‘consumption’ was taboo among
the more wealthy class who preferred to be afflicted with a ‘decline’. The
present view is that, while poverty was a major factor, poor living and
working conditions combined with an inadequate and unhealthy diet do
not wholly account for the very high incidence among the labouring
population. The rise in the incidence of tuberculosis during all major
wars may be mainly due to these causes but suggests that physical and
psychological strain also play a part. This concept of ‘strain’ or ‘stress’ is
supported by a markedly increased prevalence among pregnant women
who are employed in industry. The industrial town was not solely to
blame although it lacked those amenities supposed to lessen risk of
infection: fresh air, sunlight, adequate leisure and proper facilities for
personal hygiene. The sum of these inadequacies cannot wholly account
for the high urban incidence in the nineteenth century, because all had
existed in earlier if smaller towns. The new factors were exacerbation of
previous evils, gross overcrowding in home and factory, acute strain
consequent on overwork and stress caused by the nagging fear of losing
the means of livelihood. The last is a particular phenomenon of
tuberculosis because the illness is prolonged and the sufferer too weak to
carry out heavy work.
The scientist Thomas Young stated in 1815 that phthisis caused
the ‘premature death’ of one person in every four. At about the same
time in Paris, autopsy showed that 40 per cent of all deaths were due to

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consumption. John Brownlee, a statistician and co-founder of the science
of epidemiology, believed that the highest mortality in London occurred
about 1800 and that provincial industrial towns reached their zenith a
few years later. From 1838 to 1843 the pulmonary form, consumption,
caused an average of over sixty thousand deaths a year in Britain. The
death rate then started to fall, although pathologists stated that autopsy
revealed that almost all individuals examined had suffered from some
form of tuberculosis during their lifetime. The Registrar-General’s
figures show that in the decade 1881–90, 664,963 persons died from all
forms of tuberculosis (that is about sixty-six thousand a year as
compared with sixty thousand from consumption alone in 1838–43). In
the following decade, 1901–10, deaths from all forms amounted to
566,162, an average improvement of ten thousand a year.
There is no simple explanation for this decline in mortality. The
legislation briefly described in the last chapter was beginning to take
effect at the end of the nineteenth century with the result described by
William D. Johnston: ‘The early stages of an industrial economy are
generally those in which crowded and impoverished living conditions
prevail for numerous people and lead to increased tuberculous mortality.
Eventually, however, industrialization’s material benefits improve
housing and nutrition, and reduce risks for infection and reinfection,
thereby lowering both morbidity and mortality rates.’ This combination
of social legislation, improved amenities and increased personal
prosperity in the end made the industrial town more healthy than the
agricultural countryside. But, as regards the single problem of
tuberculosis, the continuing reductions in mortality are not attributable to
any specific treatment until the 1940s.
The belief that tuberculosis is contagious dates from very early
times but was not proven until 1865 when Jean Antoine Villemin, a
young surgeon in the French army, showed that the infection could be
transmitted to animals by inoculation. Even then, the cause of

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tuberculosis remained unknown until Robert Koch of Wollstein in
Germany isolated the causative bacillus, now known as Mycobacterium
tuberculosis, in 1882. Despite Koch’s discovery, almost the most
important in the whole history of medicine and certainly in the history of
bacteriology, no direct attack upon the bacillus could yet be made.
Attempts to destroy the organism by inhalations of ‘antiseptics’ such as
carbolic acid ended in disaster. Until the Second World War treatment of
tuberculosis depended on good food, sunlight, fresh air and rest. In the
early years fresh air encountered much opposition because so many
doctors believed ‘miasma’ carried by the air to be the cause of disease. A
Birmingham doctor, George Boddington, appears to have been the first
to establish a fresh-air sanatorium for consumptives at Sutton Coldfield
in 1843, but he was forced to abandon his project. Hermann Brehmer
opened a sanatorium at Göbersdorf, Silesia, in 1859 and one of his
patients, Peter Dettweiller, built a similar institution at Falkenstein in
1876. By now the germ theory was replacing the theory of miasma,
which accounts for the success of Edward Livingstone Trudeau at
Saranac Lake in the healthy Adirondack Mountains of America.
Trudeau, himself a sufferer, planned a number of small separate cottages
surrounding a central laboratory in 1884. His sanatorium formed the
prototype of many others in many countries. Thomas Mann’s famous
novel of 1924, based on his own experience of Davos, relentlessly details
the therapy available to those dwelling on the slopes of ‘The Magic
Mountain’.
The concept of pulmonary tuberculosis as a familial disaster
rather than an illness of the individual was first understood by Thomas
Beddoes who founded his Preventive Medical Institution at Little Tower
Court, a Bristol slum area, in 1803. He purposed to examine not only the
sick patient but the seemingly healthy members of the family with the
object of detecting disease at the earliest possible moment. In 1799
Beddoes had noted that brassworkers and stonecutters were unusually

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prone to consumption and so confirmed the finding by Paracelsus in
1567 that there is a relation between pulmonary disease and mining.
Gradually it became recognized that dusty trades, particularly when the
dust is from silica, placed workers at special risk and legislation was
introduced to protect them. One of the more beneficial advances in this
field accidentally occurred during an attempt to make synthetic
diamonds, resulting in the discovery of the harmless and efficient
abrasive, carborundum, by Edward G. Acheson of Pennsylvania in 1891.
Beddoes’s ‘social approach’ was not pursued until 1887 when
Robert Philip, an Edinburgh physician, founded the Victoria Dispensary
for Consumption. Philip taught the need to consider the whole family as
the unit for investigation. Thus he started the tracing of tuberculous
contacts. He also campaigned for notification, isolation, sanitorium care
and formation of colonies to provide light work. Two years later three
physicians, H.M. Biggs, T.M. Prudden and H.P. Loomis, developed a
similar dispensary and investigation system in New York.
Attempts to prevent or to cure by vaccines prepared from tubercle
bacilli failed. Tuberculin or ‘Koch’s fluid’, an extract of killed bacilli,
proved not only useless but actively dangerous as a treatment. Through
the work of an Austrian, Clemens von Pirquet, and a Frenchman, Charles
Mantoux, a much purified Koch’s fluid has, however, proved invaluable
as a skin test to indicate whether a person has suffered infection or not.
The search for a safe and efficient vaccine continued, resulting in some
strange but ultimately valueless treatments. In 1902 Emil von Behring of
Marburg prepared an attenuated strain of human bacilli with which he
hoped to stamp out tuberculosis in cattle. In 1906 Albert Calmette of the
Pasteur Institute in Paris and his colleague Camille Guérin started work
on von Behring’s idea of using an alien bacillus, seeking a cure for
human tuberculosis by using a bovine strain. Calmette worked for over
thirteen years before satisfying himself that he had an attenuated and
stable vaccine. He had moved to Lille just before the First World War.

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The Germans occupied the town from 1914 to 1918 and requisitioned all
cattle so Calmette transferred his experiments to an avian strain of
tubercle bacillus, using pigeons as his subjects. The number of pigeons
aroused German suspicion and Calmette narrowly escaped being shot as
a spy.
Bacille-Calmette-Guérin, the famous BCG, was first used for
protection of very young children and calves in 1921. Calmette
distributed a free supply for human use throughout France in 1924,
warning that it must be given only to infants. By the end of 1925 1,317
babies had been treated, of whom 586 were known to have been in
contact with a tuberculous relation. Six children died from tuberculosis
within six months of inoculation, which aroused mistrust of the method.
Then, in 1930, there occurred a frightful disaster at Lübeck in Germany
which has never been satisfactorily explained. A total of 230 infants
were inoculated from a single batch of BCG, of whom 173 developed
pulmonary tuberculosis and 68 died, all within a few months. As a result
BCG did not come into use again until after the Second World War when
better laboratory control and standardization made such accidents
virtually impossible. By 1963 a hundred and fifty million BCG
vaccinations had been performed with only four known deaths.
Meanwhile Wilhelm Konrad Röntgen of Würzburg in Germany
had discovered X-rays in 1895 and so revolutionized diagnosis,
permitting foreign bodies to be located and broken bones examined
much more exactly. The first satisfactory X-ray photographs of lungs in
1922 were greatly improved by introduction of a radio-opaque contrast
fluid, lipiodol, in 1924. As methods improved and experience grew,
tuberculous lesions could be detected at an earlier and earlier stage and,
eventually, before any symptoms or clinical signs of disease appeared.
Simplification made possible the use of mobile units for mass
radiography which revealed an unexpectedly large number of sufferers
not detected clinically. In the late 1940s screening revealed that the

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global incidence of tuberculosis had hitherto been underestimated by at
least one-third.
There had been much controversy about the bovine type of
tuberculosis. Was it or was it not a safety factor? Theodore Smith of
Harvard University isolated the responsible bacillus in 1898 and showed
that it would cause tuberculosis in the human as well as in cattle. In 1907
a British Royal Commission on tuberculosis reported that milk from
infected cows is a potent cause and stressed the urgent need to prevent
sale of infected milk. Louis Pasteur had already proved that heated milk
will not sour if sealed from the air. In 1880 the German firm of Ashborn
made the first commercial apparatus for ‘pasteurization’ of milk, the
purpose being simply to delay souring. In 1907 Dr Charles North of New
York introduced a pasteurizing plant that not only killed all disease-
producing organisms but also delayed souring and was therefore
commercially desirable. Meanwhile Smith’s work had suggested an
attempt to eliminate tuberculosis from dairy herds. This is comparatively
easy, for cows can be tuberculin tested as can humans. But it is also
expensive because the only practicable solution is to kill the infected
cow. In 1917 about 16 per cent of dairy cattle in USA and 25 per cent in
Britain were tuberculous. A programme of eradication started that year
in the United States which reduced the incidence of tuberculosis among
American children to about half that obtaining in Britain at the
equivalent date. Britain did not take strenuous action until 1922. From
then onwards, the incidence of the bovine type affecting glands, bones
and joints was very greatly reduced.
Direct attack upon the tubercle bacillus did not become possible
until after the Second World War. Penicillin proved to be useless for the
purpose. In 1944 Selman Waksman of New Jersey, USA, investigated a
mould found growing in the throats of chickens reared in a heavily
manured field. The mould proved to be one of a group, the Actinomyces,
from which he prepared an antibiotic, actinomycin, lethal to a range of

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bacteria but too toxic for human medication. This led him to the
discovery of a related mould to which the name Streptomyces griseus
was given and from which he isolated the antibiotic streptomycin. In
1948 Professor W.H. Feldman of the Mayo Clinic tried it on a large scale
for the treatment of tuberculosis. Unfortunately, streptomycin was too
often followed by emergence of resistant strains of the tubercle bacillus.
The potential was so good, however, that Professor Feldman determined
to find some means of preventing bacillary resistance. After much
experimental work, he found that a course of streptomycin combined
with two drugs, para-aminosalicylic acid and isonicotinic acid hydrazide
(PAS and isoniazid), could be used with excellent effect and with less
danger of producing resistant strains.
A modernized tuberculin test, mass radiography, BCG vaccine
prepared under strict control, and chemotherapy based on streptomycin
have all contributed to producing a situation in which the estimated
numbers of those currently affected by this disease are now relatively
stable. Even so, the latest available figures suggest that in 2018 no fewer
than 10 million people were suffering from tuberculosis (with highest
incidence among young adults), and that 95 per cent of the 1.5 million
TB-related deaths for the same year had occurred in low- and middle-
income countries. Thus in the less privileged parts of the world this
condition still persists as a health problem despite all attempts at mass
prevention. The reasons are largely overcrowding of the home and
malnutrition. Until those social ills are rectified, and solutions are
devised for meeting the increasing challenge of drug resistance to
effective treatment (considered further in the Conclusion as being an
overarching issue of current concern), tuberculosis will remain a major
scourge.

Even the partial defeat of an illness such as this must have

affected world history. Though a cynic would probably remark that

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tuberculosis has killed as many budding Hitlers as potential Elizabeth
Frys, the premature deaths of so many young people must have robbed
us of potentially brilliant scientists, artists, and similar creative workers.
Let us take as a single example one young Englishman whose story not
only stresses the characteristically familial nature of the infection but is
all the more apposite precisely because it encouraged the nineteenth-
century habit of dignifying ‘the decline’ as essentially a romantic
affliction. If ever there was a ‘fashion’ in disease, we have ample
evidence of it here (though it seems often to have been confused with the
less fatal but equally romantic ‘vogue’ malady known as chlorosis,
where a similarly wan appearance resulted from iron-deficiency
anaemia). In the novel and in the opera, in painting and in poetry, we
repeatedly encounter pallid heroes and still paler heroines, all of whom
project an increasingly ethereal radiance. However, such ivory beauty
serves to reveal their consumption not only by the fires of love but also
by the relentless advance of a paradoxically purifying corporeal decay. If
such romanticism inspires us to shed a tear over the fictional fate of
Verdi’s Violetta or Puccini’s Mimi, then we should be all the more
affected by the reality of the final illness suffered by John Keats.
Born in London, John was the eldest child of Thomas Keats,
manager of a livery stable owned by his father-in-law, Mr Jennings, on
29 October 1795. John was the eldest of four children; he had two
brothers, George and Tom, and a sister named Fanny. They were well
off, a happy and united family. The boys were sent for their education to
a good school in Enfield under the headmastership of the Revd John
Clarke. John Keats developed as a typical schoolboy, good at athletics,
not so good at lessons, and in his early years rather too pugnacious for
the comfort of others.
Then came tragedy. His father was killed after falling from his
horse on 16 April 1804, a few months before John’s ninth birthday. The
widow married again within two months but the couple soon separated

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and she went to live with her mother at Edmonton which became the
family home for the next five years. Edmonton being not far from
Enfield, the boys stayed at school. When in his fourteenth year and
entering puberty, John changed in character, becoming less pugnacious
and more sensitive, a kindly and popular boy who spent less time on
games and read widely in addition to his ordinary schoolwork.
At this point his mother fell ill of consumption. John, passionately fond
of her, helped to nurse the patient devotedly but she died in February
1810. Not only was her death a terrible loss, but it left him the eldest of
four orphans with little money. Their grandmother Jennings entrusted
them to two guardians, one of whom, Richard Abbey, removed John
Keats from school at the end of 1810 and apprenticed him to an
Edmonton surgeon named Thomas Hammond. John had become a close
friend of his late headmaster’s son, Cowden Clarke, and often walked
over from Edmonton to the school at Enfield. On one of these visits the
master lent John a copy of Edmund Spenser’s great verse-epic The
Faerie Queene. This is the work that inspired Keats to write his poetry.
He had been apprenticed to Hammond for a term of five years,
which meant that he could set up for himself as a surgeon at the end of
1815 when twenty years old. But something happened in the autumn of
1814. It is commonly said that he quarrelled with Hammond but the
more likely explanation is that Hammond was an unqualified surgeon
and Keats cherished the ambition to become fully qualified. The
Apothecaries’ Act, which empowered the Society of Apothecaries to
regulate medical practice, was then under discussion and would become
law in 1815. In October 1814 Keats moved to London to register for
classes and walk the wards of one of the largest teaching hospitals, the
United Hospital of St Thomas’s and Guy’s, then in the Borough on the
south side of London Bridge. At first he lodged with some fellow-
students in St Thomas’s Street, but when his two brothers came to
London to work in Abbey’s office they lived together in Cheapside.

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Keats studied hard and seems to have shown himself to be a promising
student although one of his contemporaries, Henry Stephens, recorded
his surprise when Keats passed the examination for the Licence of the
Society of Apothecaries at his first attempt on 25 July 1816. His
certificate is numbered 189 and he was elected to the coveted post of
surgeon’s dresser (now known as house surgeon) at Guy’s Hospital. But
his experiences in the wards and particularly in the theatre, where he
himself operated, sickened him. We must remember that operations were
performed without anaesthesia in those days and surgeons were
becoming more ambitious, so that, despite the patient’s agony, their
procedures took longer than the one-minute lithotomy or the two-minute
amputation. In the winter of 1816/17, Keats decided that he could not
face a medical career.
Earlier in 1816 his old headmaster John Clarke had introduced
Keats to James Leigh Hunt, the critic, poet and editor. Keats now became
member of a circle of artists and writers, most of them of the second
class but including Shelley and also an elderly merchant named Charles
Brown who enjoyed helping young people of this kind. After spending
some months on the Isle of Wight and the Kent coast, John joined with
his younger brother Tom to share a house in Hampstead with Charles
Brown. By now he had firmly decided to make his living by writing
poetry.
Leigh Hunt had already published some of Keats’s poems in his
newspaper The Examiner. The circle of friends, Shelley in particular,
urged publication of a book of verse which came out in March 1817, but
it was not well received. Keats now started on the very long poem
Endymion which he published in May 1818. In the summer of 1818 he
went on a walking tour in the Lake District and Scotland with Charles
Brown. The occasion was not a happy one, for his brother Tom was
showing signs of consumption and had been sent to Teignmouth in
Devon, while the other brother George had married and part of John’s

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reason for going north was to see the couple off at Liverpool on the start
of their voyage to a new life in America. John returned to Hampstead in
September to find Tom very much worse. As he had done for his mother,
he helped to nurse his brother devotedly but Tom died in the first week
of December 1818.
In the autumn of 1818 John Keats met Fanny Brawne, the
daughter of a man who had rented Charles Brown’s house while they
were in the north and had now become a neighbour. The two fell
passionately in love and were engaged at Christmas. But now Keats
himself began to show the first signs of the disease that had killed his
mother and his younger brother. In April 1819 he met Samuel Taylor
Coleridge who recorded his premonition of Keats’s approaching death.
This is of pathetic interest because Coleridge had been one of the circle
surrounding Thomas Beddoes and his assistant, the young Humphry
Davy, at Bristol where they experimented with inhalation of various
gases in attempts to cure or relieve consumption.
There followed eighteen months of feverish composition in
which Keats produced a new poem nearly every day. Almost the last of
his poems, La Belle Dame sans Merci, contains a verse which in effect
describes his own appearance in the terminal phase of consumption:

I see a lily on thy brow

With anguish moist and fever dew,
And on thy cheeks a fading rose
Fast withereth too.

It was during this period that he wrote the odes, To a Nightingale,

On a Grecian Urn and To Autumn, among others, which many critics not
only regard as his best work but declare to be some of the finest English
poetry ever written.
Keats had been staying alone in London when, on a night in early
January 1820, he turned up at the Hampstead house in a state resembling

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advanced intoxication. Charles Brown realized that the trouble was not
drink but illness. Keats explained that he had come on an outside seat of
the coach and, it being a bitter night, had caught a chill, adding ‘I do not
feel it now, but I am a little feverish.’ Brown hastened to put him to bed
and, as he climbed in, Keats gave a cough, put a handkerchief to his
mouth and brought it away stained with bright blood. ‘Bring me a
candle. I must see that blood.’ He looked steadily into his friend’s face
and calmly said ‘I know that colour – it is arterial blood. I must die.’
He was better in the spring and experienced the spes phthisica,
the false hope and sensation of well-being that is a quite common
symptom of advanced pulmonary tuberculosis. He wrote hardly at all
now and had spent his share of the small capital which came to him after
his mother’s death. Brown lent him sufficient for his needs and Fanny
Brawne looked after him. His doctor ordered him to winter in a warmer
climate and he received an invitation to join Shelley in Pisa, but Keats
had never liked Shelley. The young artist Joseph Severn had won a
Royal Academy scholarship to study in Rome for three years. He offered
to take Keats with him and place him under medical care when they
arrived. Keats accepted the offer and they sailed on 18 September.
Owing to stormy weather in the Channel, the ship put in at Lulworth
where Keats landed and wrote the last of his poems Bright star! Would I
were faithful as thou art. When they arrived at Naples, Severn took him
to Rome and put him under the care of Dr Clark, later Sir James Clark,
the trusted physician and adviser of Queen Victoria.
Clark and Severn looked after their patient well and he seemed to
improve but had a severe haemorrhage on 10 December from which he
never really recovered. During the final month of his life he woke every
morning disappointed that he had not died during the night. On the last
morning he whispered to Severn that he wanted to be lifted up: ‘I shall
die easy – don’t be frightened – be firm, and thank God that it has come.’

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John Keats died from consumption on that day, 23 February 1821, aged
twenty-five.
Here, then, is one telling example of the loss that tuberculosis has
inflicted on the world.

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 C E
MOSQUITOES, FLIES, TRAVEL AND
EXPLORATION

Men and women have encountered and overcome terrible dangers as

they have forced their way into every corner of the earth. A long sea
voyage in tiny ships led the Spanish Conquistadores to a hostile terrain in
Central and South America. The vast featureless plains and high
mountain ranges of North America, inhabited by hostile indigenous
tribes, failed to deter the pioneers in their covered wagons as they
journeyed from the Atlantic to the Pacific. Geographical barriers can be
overcome and even the fiercest of human opponents or the most
aggressive of predatory creatures were powerless before a well-aimed
musket.
It was not the larger animals that presented the greatest danger
for, until almost the end of the nineteenth century, minute forms of life
were the unbeatable enemy – the mosquitoes breeding in steamy
swamps, the tsetse flies of the African savannahs and forests. While
these were not dangerous in themselves, the saliva of their bites carried
even smaller organisms: the tiny parasites that cause malaria, the virus of
yellow fever, the trypanosomes that produce sleeping sickness. Tropical
heat, damp and dirt also provide ideal conditions for the bacteria of
disease.
We briefly noted in the first chapter that malaria contributed to
the end of the Roman Empire. Greece had contact with Egypt, while
Rome conquered and settled the Mediterranean coast of Africa, and it is
probably by this means that malaria reached Europe, for there is little

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doubt that it is of African origin. Malaria is in fact the most dangerous
and widespread of the African diseases. It is caused by a minute
protozoon, known as a plasmodium, of which there are several strains.
Plasmodium malariae or P. vivax is more common in Europe and
America while P. falciparum is the prevalent African parasite. A
European who has developed a resistance to the type of malaria caused
by P. vivax will still be susceptible to the type caused by P. falciparum.
The parasites have a complicated life history, multiplying
asexually in the human bloodstream and completing their sexual life-
cycle in the body of the mosquito. To put it very briefly, the parasites are
injected into the human by the bite of a female Anopheles mosquito, go
through various phases, take up their lodging in the red blood cells, feed
on the haemoglobin and burst the cell envelope, so releasing toxic
products formed by the digestion of haemoglobin.
These toxins cause the typical malarial attack: a cold stage, a hot
stage and a stage of sweating. The first signs of malaria appear about a
fortnight after being bitten by a mosquito, the onset varying slightly
according to the number of parasites injected by the bite. This
‘incubation period’ is the time taken for the rapidly dividing parasites to
form a sufficient number – several hundred in every cubic millimetre of
blood – to affect the victim’s health. It takes between forty-eight and
seventy-two hours to invade a red blood cell, grow to fill it, divide into
six or twelve new individuals and burst the cell wall to release the toxins.
As all the parasites injected by one mosquito bite are in the same
stage of development and as they keep to a fairly rigid developmental
timetable, attacks of malaria occur at regular intervals. For this reason
one kind of malaria was given the name ‘tertian ague’, describing an
attack occurring every forty-eight hours, that is on the first, third, fifth
day and so on. ‘Quartan ague’, with an attack every seventy-two hours
(first, fourth, seventh day), is caused by a different but similar
plasmodium which has a longer developmental cycle. The predominant

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African type, caused by P. falciparum. known as ‘sub-tertian’ or
‘quotidian (daily)’ malaria in which attacks are almost continuous, is a
far more dangerous disease. It often causes quick death but, if death does
not occur in the first attack and the subject is regularly reinfected by the
parasite, the resultant attacks may be little more than chills and slight
fever.
Untreated tertian or quartan malaria rarely kills of itself but is a
chronic illness, which progressively weakens those who suffer from it,
rendering them less resistant to other diseases. The chief reason for
chronic ill-health is anaemia resulting from the parasites’ destruction of
the haemoglobin in the red blood cells, the iron-containing pigment
essential for carrying oxygen to all parts of the body. Therefore if
malaria attacks a community on a large scale, the vigour of the people
will decline. This is why nineteenth-century travellers to malaria-infested
regions such as the Pontine Marshes remarked on the feebleness of the
population and their squalid life.
Malaria seems to have attained its widest distribution in Europe
during the seventeenth century when very few countries, if any at all,
escaped infection. Oliver Cromwell, born in the English Fenland,
suffered from malaria all his life and died on 3 September 1658 ‘of a
tertian ague’. A post-mortem examination revealed his spleen to be ‘a
mass of disease and filled with matter like the lees of oil’. This is a fairly
common termination of malaria. The spleen is enlarged and may either
be ruptured by a quite minor accident or suffer a spontaneous
haemorrhage into its substance. The blood clot then becomes infected
and forms an abscess which will cause death from toxaemia. Malaria was
relatively common in England until 1840, after which incidence rapidly
declined until by 1860 it had become a rarity except in the Isle of
Sheppey off the Kentish coast. One of the present writers, while going
through old case-notes in his hospital, found details of a patient who had
never travelled abroad yet acquired malaria in 1874. He lived on the

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Plumstead Marshes, a waterlogged area bordering the River Thames and
only separated from the London Docks by the river. This should remind
us that the Anopheles mosquito is still found in malaria-free countries
and people can be infected by a casually introduced malarial parasite.
Until the seventeenth century doctors treated malaria in the same
manner as any other fever. Many physicians recognized only two kinds
of fever, ‘intermittent’ and ‘continuous’, a classification which
sometimes led to disaster. Purging, starvation diet and bleeding were the
accepted remedies and must have hastened the end of many unfortunates
who suffered from the anaemia of malaria. In 1632 the Spaniards sent
from Peru a bark which was found to be an effective medicine. ‘The
Bark’ as it was generally called has a curious story.
For many years it was taught that the bark known as cinchona
took its name from the Countess of Chinchon, wife of the Governor of
Peru, who had been cured of an obstinate fever by taking an infusion of
this native remedy. As a thank-offering she distributed free supplies to
the citizens of Lima and it was she who brought the original import on
her return to Spain. The true story is less romantic. The Peruvian Indians
applied the name quina-quina, meaning bark of bark, to a tree,
myroxylon, which yielded a gum known as Balsam of Peru. This became
such a popular remedy in Europe that apothecaries could not meet the
demand and adulterated the extract with gums from other barks including
that of the cinchona tree. The latter mixture proved particularly effective
and so was the one most often prescribed. Physicians gradually realized
that it was not the much-vaunted Balsam of Peru but the adulterating
cinchona which helped to cure fevers. In 1820 two French chemists,
Pierre Pelletier and Joseph Caventou, extracted the active alkaloid from
cinchona bark but mistakenly gave it the name Quinine from the
Amerindian quina-quina, the bark which produced Balsam of Peru.
Quinine is lethal to the malarial parasite and so can be used in the
cure of the active disease. Quinine is also fairly effective in preventing

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malaria if taken regularly so as to maintain the blood-level necessary to
kill the parasite. The drug is perhaps the classical example of effective
empirical treatment. No one knew the cause of the illness or why the
cure worked, but it did work. Quinine is not a pleasant medicine for, if
taken in sufficiently large doses to kill the parasite, it has side-effects
such as vomiting, headache, rashes, disturbance of vision and hearing.
Many regular takers of quinine suffered from such severe tinnitus or
‘singing in the ears’ that they were almost stone-deaf. Later a synthetic
analogue medicine called chloroquine proved to be a better agent of
treatment. Shortly before the Second World War an entirely new drug,
mepacrine hydrochloride or atebrin, was found to be effective as a
prophylactic and a suppressant (that is, it did not cure the developed
disease but suppressed the worst symptoms). Mepacrine proved very
successful during the campaigns in Burma and New Guinea and
practically stamped out the most lethal form of malaria known as
blackwater fever. This drug, too, had unpleasant side-effects. Not only
did it stain the whole skin yellow but it caused vomiting and, sometimes,
cerebral excitement. More recently two drugs, pyrimethamine and
sulphormetoxine, used in single doses, have protected against the
parasite. After the war in Vietnam a number of cases of malaria occurred
in the United States and these were traced to returning soldiers who
neglected prophylactic treatment. Sporadic cases still occur in
plasmodium-free countries because travellers to malarial areas have
thought it unnecessary to take precautions when going for a stay of only
a few days. Even more generally, as we note in the Conclusion, the
campaign against malaria has become hindered in recent times by factors
such as increasing resistance to the drugs available to combat it.

Malaria, especially the malignant African type, was for many

years confused with Yellow Fever, often known as Yellow Jack because
it was a common cause for the quarantining of ships, which would then

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have to fly a yellow flag. Yellow fever is caused by a virus harboured by
another type of mosquito, Stegomyia or Aëdes, injected into the human
when the insect sucks blood. The distressing and dangerous symptoms
include high fever, jaundice, vomiting, intractable diarrhoea, suppression
of urine and profound exhaustion. One attack protects the patient for life.
Thus, in areas where the disease is endemic, a considerable mass
immunity develops and, as in measles, some maternal resistance is
conferred upon uninfected children. Yellow fever is therefore at its most
dangerous when introduced to communities which have never
experienced it. Yellow Jack became particularly feared by seamen who
plied between Africa and America in the eighteenth and nineteenth
centuries. A single case occurring on board a ship that had never been
infected could wipe out the whole crew.
The original habitat of yellow fever is not certain. There is a
legend, which may well be true, that the Aëdes mosquito had a
preference for breeding in ships’ water butts. This would certainly
account for the wide distribution and the mosquito may well have been
carried by ship from Africa to the West Indies. Some epidemiologists
believe the reverse: that the disease originated in the West Indies and was
transported to the West Coast of Africa. They base their theory on the
fact that the first well-documented epidemic occurred in Barbados,
Guadeloupe and Yucatan in 1647. For a long time it was believed that the
first known African outbreak was that described by J.P. Schotte at St
Louis de Senegal in 1778. More recently it has been found that John
Williams, a surgeon of Kingston, Jamaica, described a West Indian
epidemic and continued: ‘I do not apprehend this fever is what we call a
local disorder, for I have seen it on the coast of Africa and am well
informed that in the River Benin they have a bilious or yellow fever
acuter than what is here, at the time of the expedition to Carthagena. The
person seized with this fever dying there in less than twenty-four hours.’
John Williams had been surgeon on a Guineaman, a slaving ship plying

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between Guinea and the West Indies. The date of his own African
experience is not clear but the Carthagena expedition took place in
1740–1, nearly forty years earlier than the supposed first African
epidemic.
Williams tried to differentiate between yellow fever and malaria.
He was probably the first practitioner to understand the difference and
the reason must be his experience in both Africa and the West Indies.
The very prevalent and severe type of malaria endemic in West Africa,
often associated with the lethal blackwater fever, may have obscured the
presence of true yellow fever on the African coast. Williams’s theory
aroused much opposition in Jamaica. So angry were the arguments that
his chief critic, Dr Parker Bennet, challenged Williams to a duel in which
both men were killed.
Whether yellow fever originated in Africa or America, it became
a common disease in many parts of the world during the seventeenth,
eighteenth and nineteenth centuries. Particularly severe epidemics
developed on the eastern seaboard of America, extending as far north as
Halifax, Nova Scotia, which experienced a severe outbreak in 1861. New
York suffered at the end of the seventeenth century and a hundred years
later in 1793 Philadelphia was ravaged by an epidemic that must have
equalled in its horrors a visitation by the Black Death. At least one-tenth
of the population died between April and September. Morale fell to a low
level. In his Devils, Drugs and Doctors Howard W. Haggard quotes the
following comment from a witness of the epidemic:

While affairs were in this deplorable stage and the people at the
lowest ebb of despair, we cannot be astonished at the frightful scenes
that were enacted, which seemed to indicate a total dissolution of the
bonds of society in the nearest and dearest connections. Who, without
horror, can reflect on a husband deserting his wife, united to him
perhaps for twenty years, in the last agony, a wife unfeelingly

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abandoning her husband on his deathbed, parents forsaking their only
child without remorse, children ungratefully flying from the parents
and resigning them to chance without an enquiry after their health or
safety?

A shining light in this dark tale is provided by the behaviour of

Philip Syng Physick, sometimes called the Father of American Surgery.
Physick left America for London to study under the great John Hunter
who pressed him to remain as his assistant but he preferred to return.
Only twenty-five years old, he had just settled in practice in Philadelphia
when the epidemic started. Physick attended his patients devotedly until
he was himself attacked. He recovered but never regained his previous
strength. Later he was appointed surgeon to the Pennsylvania Hospital
and Professor at the University.

The battle against malaria and yellow fever is of great importance

in the history of travel, as are any of the attempts to combat major
transmissible diseases, so the story will be very briefly told here. In 1857
Louis Pasteur, Professor of Chemistry in the University of Lille, studied
the problem of fermentation and concluded that the cause was not
miasma, or bad air, as previously thought, but microscopical particles
carried in the air. He thought that these particles were endowed with life
and could multiply, as did other living creatures. He gave the particles
their name on 7 April 1864 when telling his audience at the Sorbonne of
a flask of milk which he had sterilized and kept airtight for some months:

And I wait, I watch, I question it, begging it to recommence for

me the beautiful spectacle of the first creation. But it is dumb, dumb
since these experiments were begun several years ago. It is dumb
because I have kept from it the only thing Man cannot produce, from
the germs which float in the air. from Life, for Life is a Germ and a
Germ is Life.

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 So was born the germ theory, not yet applied to the cause of
infection and wrongly applied to the genesis of life. Joseph Lister, taught
the use of the microscope by his father, a wine merchant, could
appreciate the existence of micro-organisms as the agents of
fermentation. He applied Pasteur’s theory to the prevention of surgical
sepsis by trying crude carbolic acid, then used to deodorize sewage, as a
wound dressing for the first time on 12 August 1865. There were many
who believed that germs were not the cause but the product of disease.
The large bacillus causing anthrax had been seen under the microscope
by Franz Pollender as early as 1849 but Pollender did not understand
what he had discovered. In 1876 Robert Koch succeeded in isolating the
bacillus and growing it in a culture medium.
Louis Pasteur, unaware of Koch’s work, started to investigate
anthrax, then a plague among French cattle, early in 1877. He found by
experiment that the bacilli would multiply rapidly in urine. He took one
drop of blood from an infected animal and added it to 50 cubic
centimetres of sterilized urine in a flask. He allowed the culture to grow,
then seeded a second 50 cc of sterilized urine with one drop of the first.
Proceeding in the same manner, he produced a dilution of the original
drop approximating to 1 in 1,000 million. The blood was now
imperceptible but the urine teemed with anthrax bacilli. Pasteur found
that one drop of his end product when injected into a warm-blooded
animal caused death from anthrax just as certainly as did one drop of
blood from an anthrax-infected animal.
Robert Koch widened the scope of his own investigations. In
1878 he identified six different types of bacteria which caused surgical
infections and proved that each of the six bred true through several
generations. His preparations had been more or less contaminated by
alien micro-organisms but in 1881 he succeeded in producing pure
cultures by transplanting selected colonies from generations grown on
glass plates covered with a medium of gelatine and meat extract,

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protected from the air. In 1882 he made perhaps his most important
discovery, the bacillus which causes tuberculosis, and in the same paper
laid down the rules governing the relationship between bacteria and
disease:

• The organism must be found constantly in every case of the

disease.
• It must be possible to cultivate the organism outside the body of the
host in pure cultures for several generations.
• The organism, isolated and cultured through several generations,
must be capable of reproducing the original disease in susceptible
animals.

These are known as Koch’s Postulates and, when they are

applicable, prove conclusively that a specific disease is caused by a
specific organism.
The work of Pasteur, Koch and others made it possible to
uncover the microscopical cause of infections but the method of
transmission had yet to be demonstrated. In 1877 (Sir) Patrick Manson,
then of Hong Kong, showed that embryos of a minute worm called
Filaria, one of the causes of elephantiasis, were ingested at night from
human blood by the Culex mosquito, that they developed in the insect’s
body, and were transmitted when the mosquito bit another individual.
Manson’s theory was not believed but in 1881 Carlos Finlay of Cuba
made a similar suggestion that yellow fever was spread by mosquito
bites, although he could produce no evidence in support. Meanwhile in
1880 a French army surgeon stationed in Algeria, Alphonse Laveran, had
observed malarial parasites in the red blood corpuscles of infected
patients when examined under a microscope. The parasites were also
observed by an Italian, Camillo Golgi, who noted a difference between
the parasites of tertian and quartan malaria.

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 In 1894 Manson, now working in London, met Ronald Ross, a
young surgeon on leave from the Indian Army, and showed him
Laveran’s parasites in a blood film. Manson told Ross that he believed
the parasites developed in ‘some suctorial insect’, just as the eggs of
Filaria were incubated in the body of the Culex mosquito. Back in India
Ross undertook a long investigation and eventually, on 20 August 1897
(a date which he thereafter always called ‘Mosquito Day’), discovered
malarial parasites in the stomach of the Anopheles mosquito. His finding
was confirmed in the following year by Giovanni Grassi of Rome, who
also showed that the female Anopheles is the only type of mosquito
capable of transmitting malaria. The parasite’s life cycle was gradually
worked out. In 1900 infected mosquitoes, sent from Italy to London,
were allowed to bite Ross’s son who developed malaria. A control
experiment was equally successful when three of Ross’s assistants lived
for some months in specially mosquito-proofed huts in the heavily
infested Roman Campagna and failed to develop malaria.
These findings renewed interest in Carlos Finlay’s unproven
theory that yellow fever is spread by mosquito bites. Walter Reed was an
army surgeon who had studied under the eminent pathologist William
Welch of Baltimore. In 1900 Reed joined Carlos Finlay in Havana with
two assistants from Baltimore, James Carroll and Jesse Lazear, to form a
Yellow Fever Commission. Lazear and Carroll allowed themselves to be
bitten by the Stegomyia mosquito. Both developed yellow fever. Lazear
died within a few days but Carroll recovered after a severe illness. Walter
Reed carried on with the work and, having proved the association
between mosquitoes and yellow fever, suggested methods of control
which virtually freed Havana from infection within three months,
although the causative virus was not isolated until 1928. Reed died in
1902 and was succeeded at Havana by William Crawford Gorgas who
had himself suffered from yellow fever earlier in his career as an army
surgeon in Texas. Colonel Gorgas took command of the dramatic

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campaign which now opened against malaria and yellow fever during the
construction of the Panama Canal.
If ever disease has hindered the travels of Man and the defeat of
disease has demonstrably removed the hindrance, it is in the first failure
and later success of driving the Canal through an infected terrain. The
Pacific Ocean could only be reached from Europe by the long and
notoriously dangerous voyage round Cape Horn at the extreme tip of
South America. In 1879 Ferdinand de Lesseps, engineer of the Suez
Canal, started to investigate the possibility of digging a canal across the
narrow Isthmus of Panama, following the line of a railway which had
already been constructed. It is said that a labourer died for every sleeper
laid upon that railway track. De Lesseps estimated that completion of the
canal would take about eight years. He encountered immense problems,
and some financial difficulties, but the terrible sickness rate among his
workmen was the primary cause of failure. Mosquitoes abounded in the
undrained lakes and swamps through which the canal must pass. The
death rate from all causes among the workers amounted to 176 per 1,000.
Lesseps abandoned his project in May 1889. No more work was
attempted for eighteen years and at one time the idea of the Panama
route was entirely given up and a much longer canal through Nicaragua
proposed.
In 1904 the United States became actively interested in reopening
the Panama route and put William Gorgas in charge of health. One of the
preventive measures introduced by Walter Reed in Havana had been
isolation of all yellow fever patients in mosquito-proof rooms. This,
combined with an active campaign against mosquitoes, had been the
reason for success. Gorgas now proposed a similar campaign but
encountered stubborn opposition from the authorities who failed to
appreciate that mosquitoes and not dirt caused malaria and yellow fever.
After a hard battle, lasting nearly a year, he at last persuaded the
American Government-run Canal Commission to take action on the

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Havana lines. He organized sanitary brigades on a large scale and
conducted intensive warfare against the mosquito. Special buildings
were prepared for workers and officials, all of them protected by fine
copper-gauze netting. Stagnant pools were drained and filled in wherever
possible. Very good results followed spraying of choked drainage
channels with weedkiller, which not only allowed a freer flow but
destroyed the resting places of adult mosquitoes. When drainage proved
impossible, water surfaces were regularly sprayed with kerosene to
destroy the larvae. The work of digging started again in 1907 and by then
yellow fever had been beaten, the last case occurring in 1906, and the
incidence of malaria had fallen very considerably. On 17 November
1913 the first ship passed through the Panama Canal which opened fully
for traffic in August 1914. The ‘official’ opening arranged for 1 January
1915 had to be delayed because of an earth-slide in the previous October
and, owing to the First World War, did not take place until 1920. By
1913 mortality from all causes among workers on the project had fallen
to only six per thousand. This compared with an overall death rate of
fourteen per thousand throughout the United States and fifteen per
thousand in London. Colonel Gorgas, whose efforts had achieved this
magnificent triumph, organized the medical services of the United States
Army in the First World War.

Exploration of Africa was delayed by fly-borne, mosquito-borne

and water-borne diseases which so weakened expeditions that the
interior long remained impenetrable. The white man clung precariously
to the coastal areas. James Lind, a naval surgeon well remembered for
his introduction of lemon juice to prevent scurvy aboard ship, believed
that the upland interior must provide better living conditions for the
European. The practical difficulties of reaching the central plateau were
unknown and unsuspected. The rivers teemed with mosquitoes;
dysentery and other enteric fevers waited all along the route; wounds

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caused by thorns or other means festered and refused to heal. The terrible
trypanosomiasis affected humans in the form of sleeping sickness and
horses with the fatal infection called nagana. Borne by the tsetse fly, this
last was perhaps the decisive factor. Because of it the horse – which in
the different circumstances of Central America had flourished even in
the same tropical latitudes – could not be used for transport in equatorial
Africa. There all cross-country journeys had to be made on foot, goods
being carried on the heads of natives.
Hardy men attempted the hopeless journey for four hundred
years. In 1569 a party of Portugese settlers started from the coastal plain
on horseback, explored part of the lower and middle Zambezi River, then
struck inland searching for gold. Much later news came back that all the
horses had died and the men had succumbed to disease and attack by
hostile tribes. In the late 1770s a Scottish surgeon named Mungo Park
endeavoured to find the source of the Niger River. Having failed once he
tried again, setting out on 28 April 1805 with a party of forty-four
Europeans, including scientists, soldiers, four carpenters and two
seamen. He reached the Niger on 19 August after travelling over five
hundred miles through disease-infested country. By now all the party
were suffering from dysentery and fevers and by 11 October all except
four were dead. Park, probably with the only remaining white man
Lieutenant Martin, contrived a canoe with which they tried to reach
safety by river. He appears to have been drowned or killed by hostile
natives while negotiating rapids with the remnant of his party. One native
servant escaped to recount this tale about five years later. A few
belongings were recovered but Mungo Park’s journal has never been
found.
In 1816 Captain James Tuckey RN tried to explore up the River
Congo. He took his ship as far as the rapids where he landed with a shore
party containing one or two scientific assistants. They found the climate
‘pleasant, the thermometer seldom exceeding 76°F or being lower than

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60°F, with scarcely any rain and the atmosphere dry’. Despite these
favourable conditions the whole expedition was attacked by an intense
‘remittent fever’ with black vomit, almost certainly the African type of
malignant malaria. Fourteen men died on land and four more after
boarding the ship. The total European mortality can be expressed as 37
per cent. The dead included Captain Tuckey and the scientists.
In 1832 Major M’Gregor Laird headed an expedition carried by two
ships, Quorra and Albrukah, intending to explore the Niger delta and
push on up the river. They entered a tributary, the Benue, on 18 October.
By 12 November nearly all the crew were sick with fever and two days
later only one European was fit for duty. The Quorra reached the sea in
August 1833, only five of the Europeans having survived. Albrukah
returned in November having lost fifteen out of nineteen Europeans.
Travel by steamship proved no more successful. A much larger
expedition led by Captain H.D. Trotter in 1841 consisted of 145 white
Europeans, 25 non-Europeans recruited in Britain and 133 Africans
recruited in Sierra Leone travelling in three iron-built steamboats, Albert,
Wilberforce and London. The steamers reached a point on the Niger
about a hundred miles from the sea on 26 August. Fever broke out at the
beginning of September and ‘paralysed the whole expedition’. They
pushed further on but sickness became so prevalent that Wilberforce and
London were sent back to the coast on 19 September laden with their
own sick and those from Albert. Albert steamed on further but was
forced to return on 4 October, reaching the coast ten days later, having
been on the river for nine weeks. Of the 145 Europeans, 130 fell sick of
fever and 50 died. Eleven of the non-Europeans from Britain fell ill but
all recovered. None of the 133 Africans recruited in Sierra Leone
developed fever. The fate of these expeditions – and there were many
more, equally disastrous – clearly shows why the interior of Africa
remained unknown territory for so long a time.

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 We now know that many Africans in malarial areas suffer from a
genetic disorder known as sickle-cell anaemia. The malarial parasite
cannot develop in the thin crescent shaped red blood corpuscles and so
the subject is immune, although anaemic. The susceptibility of
Europeans to ‘fever’ compared to the exemption of Africans puzzled
medical men who put forward many theories to account for the immunity
of the natives. Perhaps God had purposely arranged matters thus so that
the Africans might live in peace. Or perhaps they did not develop fevers
because they had not experienced the European’s more luxurious style of
life. A favourite theory maintained that Africans had a greater capacity
for perspiration and so were better able to throw off the ‘foul and nasty
vapours’ which poisoned the European body in hot climates.
Most medical authorities held that Africans must be differently
constituted. They invented a pseudo-scientific or at least a pseudo-
medical basis for racism. The African could perform manual labour in a
tropical climate without falling sick while the white man inevitably
succumbed. Therefore the function of the latter was to direct and govern
leaving the native population to carry out the heavy work. These
vacillating and erroneous ideas resulted in gross injustice and the
abandonment of hopeful policies. They also explain why, in its early
stages, so much of tropical medicine had to be concentrated on avoiding
‘white men’s graves’ rather than on the afflictions of the natives
themselves.
For four centuries the European exploited the tropical coast of
Africa. Unable to penetrate further inland, he made treaties with native
chiefs and Arab traders who searched out unknown inland communities,
overwhelmed them, and herded the survivors to the coast. The white man
eagerly bought their captives for a handful of shoddy goods, packed
them head to foot in his insanitary sailing ship and sold those who
survived the sea passage to Bristol or across the Atlantic for a hundred
times the price he had paid in Africa. Some of these slaves, particularly

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boys in the eighteenth century, were bought as servants for fashionable
houses and probably enjoyed a much better life than in their native land.
Many more laboured in the sugar plantations of the West Indies and in
the cotton fields of the Southern States of North America under masters
of varying degrees of kindness and brutality who paid them with scanty
food and primitive lodging. Often regarded and treated as animals, the
bitter resentment of these slaves outlasted manumission and even today
helps to shape the folk-memory of their descendants.
Experience of the African terrain, greater knowledge of disease
and massive dosage with quinine enabled white explorers to penetrate
more deeply in the second half of the nineteenth century. There remained
the deadly infection known as sleeping sickness which attacked native
Africans and, to a lesser degree, immigrant Europeans too. Sleeping
sickness is caused by a minute parasite belonging to the genus
Trypanosoma carried by the tsetse fly, a species of Glossina, a genus of
which many varieties infest different areas in Africa. There is also a form
of trypanosomiasis called Chagas Disease, carried by a louse, which is
found only in Latin America.
African trypanosomiasis occurs widely in the area lying roughly
between the Gambia River on the north-west coast and the Limpopo
River on the south-east, thus embracing the whole of the Great Central
Plateau and all equatorial Africa. Two types of sleeping sickness affect
the human: the gambiense, distributed in west and central Africa, and the
rhodesiense occurring in east and central areas. The two types are carried
by different varieties of tsetse which also differ in habitat. Those which
carry gambiense thrive in shade and high humidity, while the vectors of
rhodesiense live in open, scrub-covered country. This differing habitat
implies that few parts of central Africa are free from one or other form of
the disease, the first belonging to the humid forest regions, the second to
the dry savannahs.

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 The bite of the tsetse is described as like a red-hot needle,
commonly in the soft skin behind the ear or on the neck. The spot bitten
swells up and then subsides, much like the bite of a common horse-fly. If
the tsetse is infected, the bitten place again becomes swollen and painful
about ten days later. This swelling is sometimes called the chancre, on
the analogy of the chancre produced by syphilis. The trypanosomes
invade the subject’s bloodstream within two or three weeks and the
generalized disease process then begins. The clinical picture varies with
the type.
Gambiense is the more chronic, and by far the more frequently
encountered. There are irregular bouts of mild fever and the glands,
particularly at the back of the neck, become enlarged with a distinctive
rubbery feeling when palpated. The bouts of fever now last longer, often
for as much as a week. The liver and spleen enlarge. After some months
the central nervous system is affected. Those afflicted complain of severe
headache and their behaviour is not entirely rational, unusual lethargy
alternating with outbursts of senseless anger accompanied by physical
violence. Typically, there is reversal of the normal sleep rhythm,
insomnia at night and somnolence by day. They develop tremors and
paralyses of the limbs, lose their appetite, and start to waste away until
reduced to little more than skin-covered skeletons. Gradually the sufferer
sinks into coma which deepens until death.
Rhodesiense is a much more acute illness. Fever is higher and
constant rather than intermittent, the patient is seriously ill within only a
few weeks of being bitten and death often occurs quickly from the direct
effect of high fever on the heart. If this does not happen, the final stages
will resemble gambiense, with tremors of the limbs, increasing
drowsiness and coma.
Sleeping sickness is undoubtedly of ancient African origin but
the first and classic description comes from Cuba. In 1803 Doctor T.M.
Winterbottom, an Englishman working in the West Indies, observed this

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strange illness in slaves imported from the west coast of Africa, who
must have shown the first symptoms on the long Atlantic crossing. He is
still remembered by ‘Winterbottom’s sign’ – the prolonged swelling and
peculiar rubbery texture of glands at the back of the neck. David
Livingstone, the great missionary-explorer, described the tsetse fly in
1857 and stated that horses and cattle died from its bite. Livingstone
treated horses suffering from ‘nagana’ or stallion sickness with arsenic.
His treatment must have been empirical because the cause was not yet
known, but arsenical preparations were the first hopeful medicines even
after the trypanosome had been identified.
Tsetse flies tend to colonize belts of countryside rather than
spreading haphazardly. This fact was recognized by the African native
but not by the European. Epidemics of sleeping sickness among the
indigenous populations became more frequent in the last years of the
nineteenth century because white men opened new trade routes and there
was increased movement and ecological disruption in the hitherto almost
static equatorial area. At the same time there was a corresponding
increase in the nagana of horses and cattle. Prevalence of nagana limited
mobility. In 1894 (Sir) David Bruce, an army medical officer, arrived in
Natal to investigate the problem, accompanied by his wife who actively
assisted him in the work. They examined the blood of all infected horses
and cattle brought to them and discovered the parasite which became
known as Trypanosoma brucei. Bruce showed that the parasite was
conveyed to animals by the bite of tsetse flies, thus confirming and
expanding Livingstone’s observation of 1857.
In 1901 Joseph Everitt Dutton, a doctor working in Gambia,
found trypanosomes in the blood of human patients suffering from
sleeping sickness, hence the name T. gambiense. Dutton’s investigation
ended prematurely in the following year when he died while researching
another insect-borne disease, relapsing fever, on the Congo River. In
1903 a large epidemic of sleeping sickness caused many deaths in

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Uganda. David Bruce and his wife went to investigate with a team
including the famous Italian expert on tropical diseases, Aldo Castellani.
Castellani was particularly interested in the nervous symptoms, the
tremors and paralyses, the alternating violence and drowsiness. He
examined the cerebro-spinal fluid, which is contained between the two
membranes enclosing the brain and spinal cord, and found a minute
parasite. Bruce, informed of this finding, turned his attention to the blood
of patients suffering from sleeping sickness and discovered similar
parasites, identical to the trypanosomes he had discovered in the blood of
cattle suffering from nagana. All the pieces of the puzzle fell into place.
Bruce showed beyond question that both nagana of animals and sleeping
sickness of humans are due to a trypanosome carried by tsetse flies. He
advocated control of spread by restricting movement of infected humans
and cattle, and by destruction of the flies.
Unfortunately it was not so easy as that. Control of the gambiense
type is comparatively simple, for the vector fly is not common and will
only thrive in humid shade. Stripping the hot, damp river banks of their
vegetation destroyed the breeding grounds and soon diminished the fly
population. But rhodesiense is carried by the fly of the arid scrubland
savannahs. The parasite infests domestic cattle causing a high mortality
which limits production of meat and milk. This is the chief reason for
prevalence of the disease known by the Ghanaian name Kwashiorkor
which affects fast-growing children and is due to a deficiency of high-
grade protein foods. Control of the fly depends on clearing wide areas of
scrub and restricting movement of cattle. The latter derives from the
ancient observation of African herdsmen, for the fly is only active by day
and the herdsmen found that they could safely drive cattle from one
grazing ground across scrub country (the fly belt) to another ground at
night. Farming of herded wild game in large reserves has been suggested
as an alternative means of providing protein. Wild animals have
developed sufficient resistance not to be affected but they may act as a

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reservoir of parasites and so spread the disease to domestic animals and
humans unless kept under conditions of strict control.
Treatment of both types of sleeping sickness was practically
useless until the early 1920s. A drug, atoxyl, and very large doses of
tartar emetic, given intravenously, were often prescribed. European
travellers to fly-infested districts were advised to wear gauze veils over
the face and neck, gloves, and long trousers tucked into boots, an
uncomfortable kind of attire in a hot and humid climate, but the reason
why the European was much less commonly infected than the naked or
semi-naked African. In 1922 the German firm Bayer introduced a useful
drug, the arsenical compound tryparsamide, and this has been followed
by increasingly effective compounds both in treatment of the developed
disease and as prophylactics. Combined with intensive warfare against
tsetse flies, using persistent insecticides, these measures brought sleeping
sickness and nagana under some measure of control by the 1960s.
However, since then political instability in many areas has resulted in
displacement of populations with consequent disruption of public health
services on a scale that has brought these diseases again into prominence.
For example, over the last decade or so 70 per cent of the reported cases
have come from the Democratic Republic of Congo where inter-tribal
civil war has itself become endemic.
The long battle of almost four centuries against the African pool
of disease has presented the native peoples with an extraordinary
problem. The northern areas – Morocco, Algeria, Tunisia and Libya –
have evolved more or less in parallel with their European neighbours.
The ancient civilization of Egypt succumbed to barbarian attack but has
also developed on lines similar to Europe. The pleasant climate and rich
farmland of South Africa, curiously neglected by the early Portuguese
settlers, has attracted first Dutch and then British emigrants since the
early seventeenth century. With the discovery of diamonds and gold in
the 1870s and 1880s a migratory flood from all parts of the world

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brought both the benefits and the ills of the European type of civilization
into South Africa.
None of this penetrated to the African interior. When the
conscience of the white man awoke to the fact that traffic in humans is
offensive and the slave trade ended in the 1830s, communication
between the coast and the Central Plateau practically ceased. Then
interest in the mysterious interior was aroused. Missionaries and doctors,
battling against immense difficulties, forced their way inland. As
knowledge of disease increased and as quinine became more readily
available, they met with greater success. Most notable of these devoted
men is David Livingstone who, from 1841 until his death on 1 May
1873, founded mission stations, preached to the natives, treated their
illnesses and explored large areas of equatorial Africa. His exploratory
work was continued by another remarkable man, the Welsh orphan John
Rowland, who ran away from the workhouse at the age of fifteen and
sailed to America as a cabin boy, to be adopted by a New Orleans
merchant, Henry Morton Stanley, whose name he assumed. Dispatched
by the New York Herald to search for Livingstone after his reported
death in 1869, Stanley found him alive but reduced almost to a skeleton
on 28 October 1871. Disease had most certainly not yet been conquered.
Both Stanley and Livingstone almost succumbed to attacks of malaria
and dysentery on many occasions, and not one of the mission stations
founded by Livingstone survived for more than a few months.
The true importance of Livingstone and Stanley lies not in what
they directly accomplished but in the enthusiasm which their example
inspired. They were the first in a long line of later nineteenth-century
pioneers who stimulated international interest in the potential
opportunities of unexplored Africa. They found communities, often
uncivilized by European standards, sometimes entirely unclothed, living
the kind of existence described in the introduction to this book. Their
reports suggested that here were whole nations, not only to be saved by

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Christianity and educated to be citizens of the modern world, but also to
be commercially exploited.
Until 1877, in which year Stanley completed his journey down
the Congo River, the only foreign powers established in Africa were
Great Britain, Portugal and France. The Portuguese claimed sovereignty
over 700,000 square miles but effectively controlled less than 40,000.
The French, almost confined to the Mediterranean sea-board, held
170,000 square miles, and the British with the Dutch Boers held
250,000, largely in the south. The total area ‘ruled’ by the European
amounted to 1,271,000 square miles, about one-tenth of the continent.
Apart from the large deserts of Sahara and Libya, roughly half the total
area of Africa was wholly inhabited and ruled by native tribes. Much the
larger part lay in the unexplored tropical zone.
The Franco-Prussian War of 1870–1 greatly affected the future.
Victorious and united, Germany became eager for overseas dominions.
Defeated France saw her own hope of renaissance in an enlarged colonial
empire. The struggle for African colonies was intensified by an initiative
from King Leopold II of Belgium. In September 1876 he summoned
representatives of all the powers to a conference in Brussels, the object
being to suppress the slave trade and discuss the future exploration and
civilization of Central Africa. Delegates to this conference did not
represent their governments, who gave no official support. The
conference agreed to set up an International African Association with its
headquarters in Brussels. As the result of international jealousy and lack
of cooperation, the Association failed and the venture became purely
Belgian. The Congo Free State came under the personal sovereignty,
rapidly approaching the personal ownership, of Leopold II.
Leopold’s rule very soon aroused hostility and other countries
were not slow to see the material advantages that they themselves might
gain by opposing his unenlightened and brutal management. The Congo
River, which Stanley had shown to be a navigable waterway from its

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deep estuary on the coast for nearly a thousand miles inland, was an
attractive feature. In January 1879 Stanley received an appointment as an
accredited agent of Leopold II in the Congo Free State. He established
trading stations and entered into treaties with native chiefs along the
south bank of the Congo. Portugal made renewed claims, traditional
rather than justified. The French became suspicious of Belgian
penetration. In 1880 Savorgnan de Brazza, acting for France, made
treaties and founded stations along the north bank of the Congo, in an
endeavour to link the coast with Timbuktu, the theoretical southern
extremity of the French colonial empire. In 1884 Germany announced
the annexation of a long stretch of the west coast together with the
hinterlands of Togo and Cameroon. The British, who had lagged behind
except in South Africa, now formally declared their sovereignty over the
Niger Delta, Lagos and Sierra Leone.
The great land-grabbing operation had clearly got out of hand and
would inevitably lead to large-scale warfare unless the countries could
reach some kind of agreement. The Berlin conference of powers, opened
on 15 November 1884, decided that possession by a European country of
any part of Africa must be actual and effective to be valid and that all
signatory powers must be notified of intention to annex any part of the
continent. The ominous phrase ‘spheres of influence’ appeared for the
first time in this treaty. The ‘scramble for Africa’ occupied slightly less
than a quarter of a century. By 1914 nearly eleven million square miles
had passed into European possession, leaving only 613,000 independent.
The consolidation of effective control over the partitioned regions owed
as much to quinine as it did to the rifle.
Only three independent states remained at the beginning of the
Second World War in 1939. the Union of South Africa, Egypt and the
Republic of Liberia which had originally been founded by American
abolitionists as a home for freed slaves. Just over twenty years later, in
1962. twenty-eight independent African states had become voting

215
members of United Nations. Within twenty-three years the whole
population of Central Africa acquired the rights of self-government and
self-determination. There is no doubt that the change had been too rapid.
In 1962 there were many equatorial Africans who had hurtled from a
Stone Age civilization into the Atomic Age within their own lifetimes.
We can gain some idea of the headlong speed of this change by
estimating the length of railroad in the Africa of 1934, at a time when
steam transport was giving way to the internal combustion engine in
Europe and America. In the whole of equatorial Africa there existed only
318 miles of track and the total mileage for the huge continent, including
that of ‘white’ South Africa, was 42,750, just double that of the
relatively tiny Britain at the same date. The equivalent figure for Europe
and Russia is 235,719. Africa, hardly touched by the horse or steam
power, passed directly from pedestrian transport to the internal
combustion engine.
The continent of Africa is in fact the seat of a vast technological
and social experiment. By the early twenty-first century this process was
by no means complete, for poverty, famine, sickness, primitive housing,
tribal hostility and race-hatred still remained. No one can usefully
prophesy what the future holds or what the result of the experiment will
be. The difficulties are derived not least from the sheer speed of change.
This is the sense in which the danger of African diseases still existing in
the last quarter of the nineteenth century, and the rapid but incomplete
social and medical advances directed against them since that era, may
well have posed one of the greatest world problems of the future.

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 C N
QUEEN VICTORIA AND THE FALL OF
THE RUSSIAN MONARCHY

At first thought, Queen Victoria would be a most unlikely candidate for

the dubious honour of bringing Lenin and his Bolsheviks to power. But
strange things happen in history and, in fact, the ‘Great Queen’ was one
of the primary causes of the troubles which overwhelmed tsardom during
its last years, even if her contribution was made only indirectly and
unwittingly. The royal families of Europe may have begun to doubt that
they ruled by Divine Right but still clung to the absurd principle that
only they were fit to wear a crown. No commoner might be allowed to
debase the royal blood. Marriage was limited to the royal circle and,
since that circle was a comparatively small one, a wife would often be
quite closely related to her husband.
Until the late nineteenth century no one seems to have fully
understood just how dangerous intermarriage of closely related spouses
can be. The Christian Church forbade union between the closest degrees
of affinity but even first cousins, that is the children of brothers or
sisters, were permitted to intermarry. It could be, and was, argued that if
two brothers showed exceptional intelligence then the grandchildren,
issue of a son and daughter of the brothers, would be likely to possess an
even higher degree of intelligence. There was a tendency to forget that
intelligence is not the only attribute which may be transmitted by both
mother and father.
To understand Victoria’s role in the collapse of tsardom, we need
to turn back to the middle of the nineteenth century when a quite

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unknown Roman Catholic monk named Gregor Mendel became
interested in the growth of peas. He worked in the garden of his abbey at
Brunn in Austria and was puzzled by the fact that if he sowed seed from
tall peas the plants produced were not always tall. He tried crossing a
short breed of pea with a tall breed, sowed the seed, and to his surprise
found that the plants produced were nearly all tall, not half tall and half
short or all medium as he had expected. He worked on until he had one
strain that produced all tall peas and another that produced all short.
Then he crossed a tall with a short and sowed the seed. Three quarters of
the resultant plants were tall and only a quarter short.
Mendel decided that there must be a ‘hereditary factor’ that
determined tallness and shortness but that the factor must be double, as it
appeared that the factor for tallness would override the factor for
shortness. If the factor was double and a true tall pea (T) was crossed
with a true short pea (t) then the two factors could form four possible
combinations: TT, Tt, tT and tt. But what really interested Mendel was
that tallness must be dominant because three-quarters of the progeny
proved to be tall (TT, Tt, tT) and only the remaining quarter were short
(tt). But of the tall peas only one-third (TT) would breed true when
crossed with another TT to produce uniformly tall progeny and two-
thirds (Tt and tT) contained a factor for shortness and even if crossed
with a TT would produce a proportion of short plants.
After over ten years of research Mendel described his theory of
‘hereditary factors’ in 1866. Unfortunately he buried his findings in the
pages of an obscure journal and they attracted no attention at the time.
The history of Europe might conceivably have been a little different had
their implications been understood more swiftly. In fact thirty-five years
elapsed before three botanists in three different countries had the same
idea. During the course of their researches they came across Mendel’s
paper and. having proved his theory correct, assured him posthumous
fame. In 1905 William Bateson, working on the hybridization of sweet

218
peas at Cambridge, gave to Mendel’s hereditary factors or elements the
name ‘genes’.
These genes, derived from each parent, decide the physical
appearance of the child and the basic manner in which he or she will
react to environmental influences. The human is derived from a single
female cell, the ovum, and a single male cell, the sperm. Both cells
contain a nucleus and each nucleus contains a material called chromatin,
visible under the microscope as fine tangled threads, largely composed
of nucleic acid – the very important constituent now usually termed
DNA. When the ovum is fertilized by the sperm, the two nuclei fuse and
form a single cell. The billions of cells that compose the adult body are
all ultimately derived from this single cell. When the single cell first
divides into two, the new cells contain equal male and female elements
and this process continues throughout growth of the embryo and of the
developing body. Before the fertilized cell first divides, the tangled
threads of chromatin coalesce to form a number of roughly X-shaped
bodies called chromosomes. It is these chromosomes that carry the genes
of inheritance.
Mendel’s original theory was based on naked-eye observation.
He could not see what was happening when he crossed his peas. Modern
microscopical studies have confirmed his postulate that his hereditary
factor or element (TT or Tt for instance) is always doubled in the
individual and that only half of this element is transmitted by each parent
to the offspring. In the human, the female ovum and the male sperm cells
each contain twenty-three chromosomes so the fertilized cell will contain
forty-six, although very occasionally an extra chromosome is transmitted
with unfortunate results. The number of chromosomes remains constant
with each cell division in all members of the human race, but the size
and shape of the chromosomes differ, and this difference affects the
nature of inheritance.

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 As chromosomes bear differing genes and as only half the
maternal and paternal chromosomes are transmitted to the offspring, it is
extremely unlikely that a child, deriving twenty-three gene-bearing
chromosomes from one parent and twenty-three from the other, will
exactly resemble either of the parents. It is also extremely unlikely that
there will be no resemblance. It is also unlikely that one child in a family
will exactly resemble any other, except in the case of identical twins who
are formed from the splitting of a single fertilized cell and are therefore
genetically the same.
Quite often a familial resemblance can be traced back for
centuries by examining portraits, such as those of the Habsburgs with
their drooping lips and narrow chins. However, if we could find a full-
length picture of a Habsburg who existed as far back as one million years
BC, we should not expect any resemblance to the descendant who ruled
Austria at the beginning of the twentieth century. The differences would
be even greater than any that could be explained by the constant infusion
of fresh genes by marriage. Face and body would in fact bear little
resemblance to any human who lives today.
This is because the genes themselves change and it is the
mutation of genes which has, in the course of many centuries, produced
the human from his more ape-like ancestor and, going back to an
unknown period in time, from creatures that preceded the hominids.
Such genetic changes are essential to the orderly process of evolution
because they enable a creature to adapt itself to a gradually changing
environment and to a more complex life. In our present state of scientific
knowledge and technical ability there is a temptation to encourage the
mutation artificially. One of the chief reasons why we must recognize
that ‘genetic engineering’ is risky derives from our knowledge of the
accidents which have already occurred during the natural process.
For things sometimes do go wrong. The mutant gene produces an
undesirable trait which was not present in the genetic pattern before. The

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change may take the form of a disease. True genetic disease is by no
means common because, if the disease limits viability of the individual,
the family is likely to die out completely within only a few generations.
An exception, and one of the first genetic disorders to be recognized, is
Huntington’s Chorea which causes progressive mental deterioration
accompanied by continuous involuntary twitching movements. It was
first fully described in 1872 by an American physician George
Huntington, who attended several patients in Long Island suffering from
these symptoms. Some of the patients belonged to families treated by
Huntington’s father and grandfather, who had started practising there in
1797. The Huntington grandson was thus able to trace the families back.
He showed that the disease – that is the mutant gene – existed in a family
from Bures, a small village in Suffolk, who landed at Boston in 1630.
The violent twitching and mental symptoms aroused suspicion and
caused some of those affected to be accused in the notorious Salem witch
trials of 1692. Huntington’s Chorea is a rare example of persistent
genetic disorder because, although incurable, it most commonly appears
in middle age. Thus there is time for children to be born before onset and
about half of these will be affected. In one case, the unbroken line could
be traced back through an immigrant for twelve generations.
Among other genetic diseases, porphyria is of particular interest
because it stimulated a famous (though still controversial) piece of
medical detective work, and may also have had some effect on the
course of history. The name ‘porphyria’ means ‘purple urine’ and refers
to the most common sign, occasional passing of urine which turns a
purplish-brown colour on standing. The disorder usually becomes
apparent in the second or third decade of life, taking the form of a
sudden attack associated with abdominal pain and constipation, local
nervous symptoms such as a hypersensitive skin, rheumatic pains and
mental disturbance. In the 1960s the investigations of Ida Macalpine and
Richard Hunter led them to conclude that King George III of Great

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Britain and Hanover was a victim of this ailment. Cruelly treated in his
lifetime as ‘mad’ or, in modern terminology, as beset by a manic-
depressive psychosis, George is now considered by many physicians to
have been afflicted by porphyria. Macalpine and Hunter traced the
disease back through six generations to Mary Queen of Scots. Among
those in whom they found evidence of the disease were Queen Anne,
Mary’s great-granddaughter, and King Frederick I of Prussia. Four of the
sons of George III showed symptoms as did two tactfully unnamed royal
personages still living in the 1960s, one descended from Frederick I and
the other from a sister of George III.
King George III, born in 1738 and dying in 1820, had eight
attacks of illness, all of a similar character, between 1762 when he was
twenty-four years old and 1804. In October 1810 he again fell ill and,
after two years of exacerbations and remissions, lapsed into hopeless
insanity. He died, mad, blind and stone deaf at the age of eighty-one. His
final illness, which started when he was seventy-two, was probably not
related to porphyria, bearing more resemblance to advancing senility of
the Alzheimer type.
Many attempts have been made to link his ‘madness’ with the
most notable event of his reign, the loss of Britain’s colonies in America
and the birth of the independent United States. Undoubtedly George was
a stubborn, not very intelligent, unimaginative man and he backed his
Prime Minister, Lord North, in the foolish provocation that precipitated
the War of Independence in 1775. But he showed no sign of mental
aberration between attacks. He was garrulous, prone to ask strange
questions such as ‘How does the apple get into the dumpling?’, often
seemed more interested in turnips than statecraft, but he ruled adequately
and with some firmness. He had no attack between 1762 and January
1766, when he suffered a mild one lasting for a month. He was then free
of symptoms until July 1788. Since there is no evidence of ‘madness’
between 1766 and 1788, we can hardly blame porphyria for the loss of

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the American colonies in the war of 1775–81. The king’s bad judgement
may have helped to precipitate the crisis and his obstinacy may have
prevented an amicable settlement, but his faults were shared by his
ministers, the majority of the House of Commons and a large proportion
of the British public.
It was on Irish rather than American issues that George’s malady
had the greater impact. During the eighteenth century Protestant settler
and Catholic native lived fairly amicably together in Ireland, although
Catholics were not allowed to sit in the Dublin Parliament. In the last
years of the century Republican France offered to liberate Ireland from
the yoke of England, an offer which provoked the rebellion of 1798
when Catholics attempted to set up a Celtic Republic dominated by
priests. After the revolt had been cruelly suppressed by a combination of
English troops and Irish Protestants, the Prime Minister, William Pitt,
decided that union of the two islands in one Parliament at Westminster
offered the best hope of restoring order and justice. He induced the Irish
Parliament to abolish itself and to declare for union with Britain in 1800,
on the understanding that Catholics would be eligible to sit in the new
United Parliament. In other words Pitt committed himself to Catholic
emancipation.
But Pitt omitted to inform King George III of his intention.
George regarded himself as the Defender of the true Protestant Faith.
When the Lord Chancellor drew the king’s attention to Pitt’s proposal, he
at once objected and Pitt resigned. Ten days later, in February 1801,
George suffered another attack of porphyria with severe mental
derangement. He recovered in March and Pitt made the solemn promise
that he would never again mention Catholic emancipation in the king’s
lifetime. ‘Now my mind will be at ease,’ George answered. So, to set the
royal mind at rest, the subject of Catholic emancipation was shelved for
twenty-eight years. Lacking this essential ingredient, Pitt’s scheme for
the pacification of Ireland was doomed to failure. Union with Britain

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denoted to the Irish Catholic nothing more than domination by the alien
and oppressive Protestant. Perhaps porphyria is partly to blame for the
Irish troubles of the nineteenth and twentieth centuries.

Queen Victoria’s most fateful role in history was to transmit the

rare genetic disorder known as Haemophilia A to a number of her
descendants. An almost invariable characteristic of this condition is that,
while females are the means of passing on the disease, it is their male
progeny who suffer the ill-effects. Even an afflicted father cannot
transmit haemophilia directly to his sons, as distinct from siring
daughters who may act as carriers to their own male offspring. A female
can suffer from haemophilia only if the mother is a carrier and the father
is a haemophiliac. The disease itself involves the failure of blood to clot
within the normal time. This abnormality has been noticed for centuries,
particularly among people, such as the Jews, who practise circumcision.
The first clear description was given by a physician, John C. Otto of
Philadelphia, in 1803: ‘an haemorrhagic disposition existing in certain
families. It is a surprising circumstance that the males only are subject to
this strange affection. Although the females are exempt, they are still
capable of transmitting it to their male children.’ The defect is lack of a
protein in the serum, the liquid part of the blood, which is essential for
clotting. Whereas normal blood takes from five to fifteen minutes to clot,
the haemophiliac’s blood will take at least half an hour and generally
several hours or even days. Thus the haemophiliac lives in extreme
danger. A small wound, trivial in the normal individual, will place him at
risk. A bruise, caused by a subcutaneous wound to a blood vessel, will be
exceptionally painful as the extravasated blood forces its way into the
tissues. Such internal bleeding is particularly dangerous because the
surgeon can deal with it only by making an open wound.
The defect or mutant gene seems to have originated with Queen
Victoria or perhaps her mother the Duchess of Kent. Victoria was an

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only child, so there can be no certainty. There is no known history of
haemophilia in either the British royal family or that of Saxe-Coburg-
Saalfeld, the mother’s family. One of Victoria’s four sons, Prince
Leopold, died from haemophilia. Of her five daughters, two transmitted
haemophilia to their sons or grandsons. The worst history is that of the
youngest, Princess Beatrice, who married Prince Henry of Battenberg.
Two sons of the marriage died of the defect. A daughter, Ena, married
King Alfonso XIII of Spain. Two haemophiliac sons of this marriage
died aged twenty and thirty-one. This is a family history typical of the
disorder and, since no sufferers can be traced on either the maternal or
the paternal side of Victoria’s acknowledged ancestry, questions have
inevitably been raised about illegitimacy. Was she really the Duke of
Kent’s daughter, or rather the child of some man unknown? Despite her
facial resemblance to the Duke and to his father George III, and the
possibility that a genetic mutation might have spontaneously occurred
for the first time (as happens in about a quarter of recorded cases of
haemophilia) in Victoria or in either of her ducal parents, a trace of doubt
about her paternity remains.
Victoria’s third child and second daughter, Alice, was born in
1843 and married Louis IV, Grand Duke of Hesse-Darmstadt. There
were two sons of the marriage, of whom one died of haemophilia aged
three. Of their five daughters, the youngest survivor, always known as
Alix, married Nicholas II, Autocrat, Tsar and Emperor of All the
Russias, thus bringing Queen Victoria’s haemophiliac gene into the
Romanov family.
Alix or, to give her full name, Alice Victoria Helena Louise
Beatrice, Princess of Hesse-Darmstadt, was born at Darmstadt on 6 June
1872. At the age of six she lost her mother and her younger sister during
an epidemic of diphtheria. The family had regularly visited ‘Granny
Victoria’ once a year. After her daughter’s death, the Queen tended to

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regard the widower as her own son and the visits to the British court
became more frequent.
Alix grew up to be beautiful, a tall slender woman with red-gold hair,
blue eyes, a pink and white complexion, her classical features marred
only by a withdrawn, cold expression. If not outstandingly clever as an
adolescent, she was by no means unintelligent for she was well grounded
in history, geography, literature and music by the age of fifteen. She also
developed an interest in medicine. The great ideals of the Victorian Age,
hard work, discipline and service, remained with her throughout her life.
She became a prude, the typical Victorian ‘lady’ who was secretly
obsessed by sex but regarded any overt discussion of the subject as
disgusting. Pathologically shy, she lacked charm, that essential quality of
royalty. Not many people knew her well but. to those who did, she was
‘Sunny’, a name given as tribute to her bright hair and sparkling eyes.
In 1884 this quite unimportant twelve-year-old princess of a
minor royal family travelled for the first time to the court of the
mightiest land empire in Europe, the occasion being the marriage of her
elder sister to Grand Duke Serge, brother of Tsar Alexander III. Here she
met Alexander’s sixteen-year-old son, the Tsarevitch Nicholas, born on
18 May 1868. It was a case of love at first sight.
If Alix had genetic problems, so did Nicholas. The root of his
trouble lay in the first ‘hereditary factor’ observed by Mendel, the
vagaries of tallness. Alexander III was gigantic, six foot six inches in
height, and broad in proportion. He could bend a silver coin in his
fingers and once held up the roof of a wrecked railway carriage on his
shoulders while his family escaped. When the Austrian ambassador
tactlessly remarked at the dinner table that it might be necessary to
mobilize an army division or two on the frontier. Alexander picked up a
heavy silver fork, casually tied it in a knot, and threw it at him with the
words ‘That is what I will do with your divisions.’ This great strong bull
of a man, practically solid wood from the neck up but downright in word

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and action, married a tiny woman of more complex character. Nicholas
inherited much more from his mother. Maria Dagmar, than he did from
his awe-inspiring father. Charming, brave, athletic, shy and hesitant,
intelligent but fatally at the mercy of stronger personalities. Nicholas
grew into a small, slight man, only just over five feet six inches in
height, surrounded by a mob of gigantic Romanov relations.
Queen Victoria warmly supported the couple, because their
marriage seemed a brilliant opportunity for one of her favourite
granddaughters. But a shadow overlaid it from the start. Neither
Alexander nor his wife approved, for both of them disliked Germans.
Also, the future Tsaritsa of Russia must be a member of the Orthodox
Church and Alix was a fervent Lutheran. The dutiful son Nicholas told
his diary: Tor a long time I resisted my feeling, trying to deceive myself
by the impossibility that my dearest dream will come true.’ His dream
did come true two years after he wrote those words. In April 1894 the
Tsar fell seriously ill with a kidney disease and his son’s marriage quite
suddenly became a matter of state importance. Nicholas would hear of
no one else but Alix, and there was nothing his parents could do but give
in.
Alexander went downhill rapidly. In October he was obviously
close to death. Alix, hastily summoned, reached Livadia in the Crimea
on 23 October and the formal ceremony of betrothal took place in the
Tsar’s bedroom. Typically the dying man insisted on dressing in full
uniform for the occasion. On 28 October Alix wrote in Nicholas’s diary
an inter-polation prophetic of the future: ‘Sweet child, your Sunny is
praying for you and the beloved patient. Be firm and make the doctors
come alone to you every day – so that you are first always to know –
don’t let others be put first and you left out – show your own mind and
don’t let others forget who you are.’ On 1 November 1894 the mighty
Alexander died aged forty-nine and at the age of twenty-six Nicholas II
assumed the title of Autocrat, Tsar and Emperor of All the Russias.

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 Alix’s reception into the Orthodox Church under the name of
Alexandra Feodorovna and the marriage, on 26 November, took place in
an atmosphere of deep mourning. Nicholas, flung into the business of
state, could afford no time for a honeymoon. But the prime purpose of a
royal marriage, whether a love match or one of policy, had to be fulfilled
and Alexandra did not show herself laggard in her duty. The first child
was born in October 1895 and three more followed in the next six years.
Each birth proved an increasing disappointment, for all four of these
children were girls. At last, on 12 August 1904, in the middle of the
disastrous Russo-Japanese War, the cannon of St Petersburg thundered
news of the event which, more than any other, was to change the course
of Russian history. That day was born the unfortunate boy Alexis, the
longed-for son to whom Alexandra transmitted Victoria’s mutant gene
for haemophilia.
The first sign showed itself by bleeding from the umbilicus when
Alexis was six weeks old. Very soon the appearance of bruises, resulting
from quite minor knocks while crawling or toddling, confirmed the
diagnosis beyond doubt. Alexandra, a devotedly possessive mother to all
her children, was forced to recognize that she had transmitted the terrible
disease to her innocent son. The revelation came as a shock from which
she never recovered. No one who has not experienced the bearing of a
haemophiliac boy can fully enter into the mother’s agony. She enters a
dark, sunless world of loneliness. If the boy is heir to a throne, the
distress must be all the greater, for no one can be told and life becomes a
lie.
Such is the reason for the withdrawal of Nicholas and Alexandra
into seclusion at Tsarskoie Selo, for their bourgeois family life amid a
dull and restricted court circle. In many ways Alexandra resembled her
grandmother Victoria. She hid her despair at Tsarskoie just as did
Victoria in the suburban castle of Windsor when robbed of her beloved
Albert. They were both dominant personalities, but both demanded to be

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dominated and both chose their masters from the lower ranks of society.
Victoria had her John Brown and her Munshi, Alexandra had her
drunken peasant. Existence such as this inevitably bred rumour. At one
time popular gossip told that the hidden Victoria had followed her
grandfather into insanity. Petersburg society whispered that the
Tsarevitch could not be allowed in public because he suffered from
epilepsy or congenital idiocy. And, as the haemophiliac boy was the only
direct heir to the throne of Russia, the truth could not be told.
Nicholas could do nothing, nor could the doctors or courtiers.
The prayers of royal chaplains were equally unavailing and supplications
to orthodox saints went unanswered. But God could not entirely desert
one who, like Alexandra, believed in His goodness so fervently, who
worshipped Him so wholeheartedly. Somewhere there must exist a
human of sufficient spiritual purity and strength to wring from God the
miraculous intervention which alone could save the child Alexis.
Because such a being was so ardently desired, his appearance was
inevitable. It just happened that he took the form of Rasputin, a staretz or
wandering holy-man.
In July 1907 Alexis lay for three days at the point of death.
Rasputin was summoned to Tsarskoie Selo by the Empress, on the advice
of either a grand duchess or her dowdy but intimate friend Anna
Vyroubova. The holy man sat quietly beside the boy’s bed, held his hand,
and whispered to him fairy stories and Siberian folk tales. Next day
Alexis was free of pain and able to sit up. A temporary ‘cure’ by this
kind of treatment is quite possible, for keeping the patient quietly at rest
is half the battle.
The next incident falls into a quite different category. In
September 1912, when Alexis was eight years old, the imperial family
paid a visit to Bialowieza in East Poland. The boy fell when jumping out
of a boat and sustained a large bruise on the upper part of his left thigh.
He complained of severe pain so the family physician, Dr Eugene

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Botkin, confined him to bed for a few days. Two weeks later, when he
seemed to have recovered, the family moved to Spala, a cramped and
dark hunting box in dense forest. Alexis made no progress in these
gloomy surroundings, seemed in discomfort, pale and unhappy.
Alexandra decided that a long drive in an open carriage would do him
good, but the roads were uneven and the carriage jolted unmercifully.
After a few miles, Alexis began to suffer agonizing pain in his upper
thigh and lower abdomen. His terrified mother ordered an immediate
return. The homeward journey became a nightmare. It was obvious that
Alexis must be put to bed under medical care as soon as possible, but
any attempt to speed the horses resulted in increased jolting which
caused the boy to scream in pain. By the time they reached Spala he was
only semi-conscious.
When jumping out of the boat two weeks earlier, Alexis had
fallen heavily on the butt end of an oar. The superficial bruising misled
the doctors. He had ruptured a small blood vessel, deeply situated in
either the upper part of the thigh or the internal abdominal wall. The
bleeding was minimal so long as he remained quiet. The jolting of the
carriage not only caused fresh bleeding but probably widened the wound
in the small blood vessel which had already been injured.
Nothing would stop the haemorrhage. For eleven days Alexis
hovered between life and death, exsanguinated, with a high temperature,
tortured by pain. For eleven days Alexandra sat beside his bed, hardly
sleeping, snatching brief moments of rest on a sofa in his room. At last
the surgeon Feodorov warned the Tsar that his people must be prepared
for the heir’s death. National prayers were ordered, bulletins issued, but
the nature of the illness was not mentioned. On 10 October priests
administered the Last Sacrament and that day the bulletin was worded in
such a manner that the next could announce the death of the Tsarevitch.
That night Alexandra decided to call in Rasputin. He had gone
home to Siberia and could only be reached by telegraph. He did not

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immediately board a train and rush to Spala. Instead he telegraphed back:
‘God has seen your tears and heard your prayers. Do not grieve. The
Little One will not die. Do not permit the doctors to bother him too
much.’
Twenty-four hours later the bleeding stopped.
There is no doubt that this story is substantially true. Unless the
doctors were parties to some mysterious plot, it is also inexplicable. But
that does not affect the outcome. Can we wonder that Rasputin now
became essential to the mother of Alexis? Is it probable that any report
of bad behaviour would turn her against him? Here is the one man for
whom she had been praying, a man who possessed the miraculous power
to intercede directly and successfully with God. Since God listened to
him. Rasputin must be a good man. Since he was a good man, anyone
who opposed his will or spoke evil of him must be bad. It was as simple
as that.
Many books and learned articles have been written about the man
Grigori Efimovich, known as Rasputin, but he remains a mystery. Here
we are concerned only with his strange relationship with the Tsaritsa and
her son, and the effect his domination of her exerted upon the future of
Russia. Rasputin, born in the Siberian village of Pokrovskoie about 1860
or 1865, first appeared on the St Petersburg scene in 1903. On 1
November 1905 the Tsar entered in his diary: ‘We have today met a man
of God, Gregory, from the province of Tobolsk.’ ‘Holy fools’,
soothsayers and monstrosities had always formed part of the Russian
court retinue. Rasputin was not the first wonderworker to gain access to
the closed circle of the imperial family. Alexandra, desperate for a male
child, had at one time been so influenced by a charlatan named Philippe
Nizier-Vachot that she had developed a pseudocyesis or false pregnancy.
Rasputin rarely visited the royal family, probably not more than half a
dozen times in any one year, but his association with Tsarskoie Selo, his
intimacy with some of the grand duchesses, wealthy industrialists and

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wives of the nobility, his public drunkenness and open lechery, were
reported in the press (uncensored after 1905) and alarmed many
responsible Russian leaders.
As one of the few outsiders to gain admission to the closed circle
of Tsarskoie Selo, Rasputin was obviously of use to anyone who desired
to influence governmental policy. He could hardly be expected to choose
his clientele wisely, and this is the worst, most disastrous aspect of his
hold on the imperial family. But, even in the days when he was
unknowingly destroying all confidence in the regime, Rasputin’s advice
was by no means always bad. He possessed plenty of common sense and
he knew his fellow peasants. During the 1914 war he continually urged
more equitable division of food supplies and he prophesied serious
trouble unless something was done to speed up distribution and so
prevent long queues waiting for hours in the bitter cold. His prophecy
proved correct, for the revolution of March 1917 would start in the food
queues of Petrograd. Had the Empress been less dependent on him, his
presence at court could have been a stabilizing influence, for the majority
of peasants were less impressed by stories of his orgies than by the fact
that one of their own number had broken through the barrier of the
nobles to reach their Little Father the Tsar.
And what of his ability to arrest the internal bleeding which
caused Alexis agonizing pain and jeopardized his life? Was he in league
with the royal physicians who told him the exact moment at which to
exercise his alleged power? Did he have access to ‘mysterious Tibetan
remedies’ supplied by the quack doctor Peter Badmaiev? Was it done by
hypnosis? Had he stumbled on the possibility that all disease, even
uncontrollable haemorrhage, may be psychosomatic and that cure can be
aided by psychiatric treatment? Or was it just luck? We shall never know
the answer to these questions, but the essential fact is that Alexandra
firmly believed in Rasputin’s power.

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 There is evidence that the Tsar did not altogether share his wife’s
obsession. Nowhere in his diary nor in his letters to his mother and to
Alexandra, does he so much as mention the miraculous power of
Rasputin. He attributed the recovery at Spala to administration of the
Last Sacrament. Nicholas regarded Rasputin as an ordinary Russian
peasant: ‘He is just a good, religious, simple-minded Russian,’ he wrote.
‘When in trouble or assailed by doubts, I like to have a talk with him,
and invariably feel at peace afterwards.’ The Tsar, who received the
police reports, must have known much better than Alexandra of
Rasputin’s scandalous life, and he was no doubt at times disturbed by her
dependence upon one who, however good and simple, behaved in so
dissolute a fashion. There is a story that one of his favourite courtiers,
Admiral Nilov, dared to ask the Tsar why he continued to put up with
Rasputin’s insolent behaviour. ‘Better Rasputin than hysterics,’ answered
Nicholas shortly.
In July 1914, when war with Germany became imminent,
Rasputin was at home in Siberia, convalescing from a stab wound. On
hearing of the order for mobilization, he telegraphed to Tsarskoie Selo:
‘Let Papa not plan war for with war will come the end of Russia and
yourselves and you will lose to the last man.’ The Tsar angrily tore the
telegram to pieces. He wished to take immediate command of his
beloved army and was only with great difficulty persuaded to appoint as
commander-in-chief Grand Duke Nicholas Nicholaievitch, the most
experienced soldier in the imperial family. The war went badly for
unprepared Russia. The Battle of Tannenberg on 26–30 August saved
France by diverting German troops from the western front but almost
destroyed the regular army. Lack of munitions continually hampered
recovery. Although Russia achieved some startling successes against
Austria, she could make no headway against Germany. By August 1915
most of Russian Poland had been lost, and nearly four million men
killed, wounded or captured. The Tsar now decided to take supreme

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command. He did so against the advice of all his ministers, but with the
enthusiastic support of Alexandra.
Her eagerness for this absurd if understandable move on the
Tsar’s part was dictated by her determination that her husband must
never be second to anyone in the empire. The royal couple usually
corresponded with each other in English whether by letter or telegraph.
On 24 June 1915 Alexandra had written to Nicholas, then touring the
front line, ‘Sweetheart needs pushing always and to be reminded that he
is the Emperor and can do whatsoever pleases him – you never profit of
this – you must show you have a way and will of yr. own, and are not led
by N [Grand Duke Nicholas] and his staff, who direct yr. movements and
whose permission you have to ask before going anywhere. No, go alone,
without N by yr. very own self, bring the blessing of yr. presence to
them.’
From 5 September 1915, when Nicholas left Tsarskoie Selo to
take over command of his armies, until 20 March 1917, the day before
his arrest at Moghilev, we can follow the tragic and almost incredible
events of these last months of tsardom through the letters which passed
between Nicholas and his wife. This series of letters forms one of the
most astonishing and important of historical archives. But we cannot
possibly understand them unless we recognize and sympathize with the
terrible dependence of these unfortunate parents upon the only person
who could restore their beloved son to health.
On 4 September 1915 Alexandra wrote her husband a letter to
await his arrival at headquarters: ‘Do not fear for what remains behind
… Lovy, I am here, don’t laugh at silly old wifey, but she has trousers on
unseen.’ Nicholas was overjoyed: ‘Think, my wifey, will you not come
to the assistance of your hubby now that he is absent? What a pity that
you have not been fulfilling this duty for a long time or at least during
the war!’ On 10 September Alexandra accepted her commission: ‘Oh
Sweetheart I am so touched you want my help, I am always ready to do

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anything for you, only never liked mixing up without being asked.’ So,
by these few absurdly childish words, was the supreme government of
Russia handed over to the Empress. Loving power, she gladly accepted.
But she still demanded to be dominated. There was only one man upon
whom she could lean and that man was Rasputin.
The scandal of Rasputin did not become an urgent problem until
the Empress Alexandra began tampering with governmental affairs at the
end of 1915. The Tsar started his reign determined to uphold the
principle of autocracy but, in the near revolution of 1905, he accepted a
compromise, a form of parliamentary government known as the Imperial
Duma. Alexandra detested the Duma for two reasons. First, this body
instigated a public enquiry into the scandalous behaviour of Rasputin in
1911. Secondly, the very existence of an elected Duma implied a check
on the absolute authority of her husband and, worse still, upon the future
autocracy of her son. Her sick fear for the child’s life was translated into
a determination that he must reign as the all-powerful monarch. To this
end, Nicholas must himself be Ivan the Terrible, Peter the Great, a harsh
tyrant who could transmit unchallenged power to his son. She returns to
the theme again and again: ‘For Baby’s sake we must be firm as
otherwise his inheritance will be awful, as with his character he won’t
bow down to others but be his own master.’ ‘We must give a strong
country to Baby, and dare not be weak – for his sake, else he will have a
yet harder reign, setting our faults to right and drawing the reins in
tightly which you have let loose.’ ‘He has a strong will and mind of his
own, don’t let things slip through your fingers and make him have to
build up all again.’ Such was the driving force which steered Nicholas
into the fatal and avoidable errors of his last eighteen months in power.
At the outbreak of war the Premier had been a wily old
bureaucrat named Goremykin, who held that ministers were no better
than butlers to the Tsar. Even he protested against the Tsar’s decision to
take command and was unexpectedly dismissed on 2 February 1916, to

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be replaced by B.V. Stürmer, a Master of Ceremonies at the Palace.
There is little doubt that Alexandra had suggested his name. At first he
showed himself a firm friend of Rasputin and received Alexandra’s
support, being granted the additional and key appointment of Minister of
the Interior. He knew nothing of his duties and made less attempt to carry
them out. Even had he been capable. Stürmer’s Teutonic name would
have rendered him suspect. As it was, many influential people, among
them the allied ambassadors, thought he would urge the Tsar to conclude
a separate peace with Germany. The Duma launched an angry attack on
him at the beginning of November. Having already described him as
‘such a devoted, honest, sure man’, on 7 November 1916 Alexandra
wrote to Nicholas: ‘for the quiet of the Duma, Stürmer ought to say he is
ill and go and rest for three weeks – being the red flag for that madhouse,
it’s better he should disappear for a bit and then in December when they
will have cleared out – return again.’
Nicholas agreed with his wife’s description: ‘He, as you say
rightly, acts as a red flag not only to the Duma, but to the whole country,
alas! I hear this from all sides, nobody believes in him. Alas! I am afraid
he will have to go altogether.’ On 22 November he dismissed Stürmer
from both offices and appointed the senior member of the Cabinet, the
Minister of Transport A.F. Trepov, to be temporary Premier. Alexandra
was not in the least pleased: ‘Trepov, I personally do not like and can
never have the same feeling for him as to old Goremykin and Stürmer …
if he does not trust me or our Friend, things will be difficult. I told
Stürmer to tell him how to behave about Gregory and to safeguard him
always.’
Trepov lasted until January 1917, to be replaced by the final
Tsarist prime minister, Prince Nicholas Golytzin, whom Bernard Pares
described as ‘an honest old gentleman in weak health, who was known to
the empress as her deputy-chairman of a charitable committee’.
Golytzin, horror-struck at the proposal, pleaded his infirmities and

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inexperience but could not disobey the direct imperial command. He
certainly need not have worried for neither he nor Trepov counted for
anything in these last days of tsardom. The Empress and Rasputin had
found the ideal partner to complete a triumvirate in the person of A.D.
Protopopov, first an acting minister, then the last tsarist Minister of the
Interior.
At first sight Protopopov seems a very sensible choice, for he was
a Vice-President of the Duma. In fact he was hopelessly unsuited even
for his first post, to which he was appointed on 23 September 1916, after
repeated appeals from Alexandra to the Tsar. Some years before, he had
suffered from syphilis and been treated with ‘mysterious Tibetan
remedies’ by the charlatan Badmaiev, who was a possible source of
Rasputin’s success with the Tsarevitch and one of the more unsavoury
members of ‘the Rasputin gang’. There is little doubt that Protopopov
now suffered from the cerebral form of late syphilis known as GPI.
Many Russians who had contact with him as minister regarded him as
insane. He knew nothing of his work and spent most of his time when
Minister of the Interior in drawing up fantastic plans, illustrated by
complicated graphs and charts, for sweeping reforms of the army, the
government and the whole empire. He rarely troubled to attend meetings
of the Cabinet and wisely kept away from the Duma.
Nicholas doubted the wisdom of retaining a lunatic as minister in
charge of internal affairs. On 10 November 1916 he wrote to his wife: ‘I
am sorry for Prot – he is a good, honest man, but he jumps from one idea
to another and cannot make up his mind on anything. I noticed that from
the beginning. They say that a few years ago he was not quite normal
after a certain illness (when he sought the advice of Badmaiev). It is
risky to leave the Ministry of Internal Affairs in the hands of such a man
in these times. … Only, I beg of you, do not drag our Friend into this.
The responsibility is with me, and therefore I wish to be free in my
choice.’ But the Tsar was not ‘free in his choice’, for ‘our Friend’

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Rasputin had decided that Protopopov must remain. Alexandra delivered
one of her heaviest broadsides on her husband: ‘I entreat you don’t go
and change Protopopov now – he is honestly for us. Oh Lovy, you can
trust me. I may not be clever enough – but I have a strong feeling and
that helps more than the brain often. Don’t change anybody until we
meet, I entreat you, let’s talk it over quietly together. Protopopov
venerates our Friend and will be blessed. He is not mad, the wife sees
Badmaiev for her nerves only. Quieten me, promise, forgive, but it’s for
you and Baby that I fight.’
Alexandra had already arranged a visit to her husband at
Moghilev. On 12 November, two days after writing this letter, she set out
for headquarters and stayed for three weeks. It was not an easy visit, for
Nicholas proved uncharacteristically obdurate. He argued that there was
antipathy to Protopopov on every side. She pleaded with him to be
‘firm’, to be ‘sharp and bitter’, to show that he was the master who took
no account of popular clamour. Above all, he must trust in Rasputin. A
little while before the present crisis she had written: ‘Ah, Lovy, I pray so
hard to God to make you feel and realize that He is our caring, were He
not here I don’t know what might have happened. He saves us by His
prayers and wise counsels and is our rock of faith and help.’ It should be
noticed that Rasputin is now not only ‘our Friend’ but merits the divine
capital when referred to by a pronoun. On 4 December, the day that
Alexandra left him, Nicholas wrote apologizing for having been so
‘moody and unrestrained’ during her visit. But she had got her way.
Protopopov was confirmed in his office.
The Tsar, his wife and Rasputin were now, in the autumn of 1916,
intensely unpopular among all classes in Russia. This hatred had
developed in little less than eighteen months. Many well-meaning
attempts were made to open the Tsar’s eyes to the true position. His
mother, several Grand Dukes, the British and French ambassadors, the
President of the Duma, besought him to get rid of Rasputin and ‘throw in

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his lot with the people’. Grand Duke Paul, Alexandra’s favourite uncle
by marriage, and her own elder sister Grand Duchess Elizabeth, pleaded
with her to rid herself of Rasputin’s evil influence. They tried to make
her understand that his interference in military matters gave the
impression that she was treacherously helping the German High
Command. They all failed, for she would hear nothing against Rasputin.
As a result, certain members of the imperial family decided upon direct
action.
Unfortunately they could not agree on the best way to set about
it. Most were of the opinion that Alexandra could now be considered
insane, but they saw no method of removing her unless the Tsar
abdicated. This extreme course was considered but rejected as too
dangerous. At last they decided on the murder of Rasputin, arguing that
his loss would force Alexandra into a state requiring asylum treatment
and the pliable Tsar could then be persuaded to stop acting the
commander-in-chief and rule in cooperation with the Duma. The murder
was planned by Prince Felix Yusupov, nephew of the Tsar by marriage.
He was assisted by Grand Duke Dmitri who was the Tsar’s favourite
cousin and son of Grand Duke Paul, and by V.M. Purishkevitch, an
ardent monarchist and extreme right-wing member of the Duma.
The story of the sordid and ill-planned killing of Rasputin, on 30
December 1916, has been recounted so many times and with so many
variations that it need not be discussed in detail here. There must be
considerable doubt about the quantity of cyanide (if any at all) in the
wine that he drank and the cakes that he ate, but he was certainly shot
once with a revolver at point-blank range and a second time from a little
further off. He was then thrust under the ice covering the River Neva,
and subsequently found to have died only after inhaling water. All of this
suggests that, if the other Romanovs were so inefficient as murderers,
they would not have made better Tsars than Nicholas. The effect of
Rasputin’s death on Alexandra seems to have been the reverse of that

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expected. So far from relapsing into hopeless mania, she quickly
recovered after the initial shock. One of the most remarkable chapters in
the whole story is the amazing fortitude of this sick woman who
supported the family throughout the miseries and indignities of the next
eighteen months.
The Tsar was the one who collapsed. On his wife’s urgent
demand, he hurried back from headquarters to Tsarskoie Selo where he
stayed for just over two months. All who met him during this time were
startled by his changed appearance and manner. The old charm had gone,
his face became lined and apathetic, the whites of his eyes yellowed and
the pupils lacked lustre. He was moody, hesitant, sometimes seeming not
to know the day of the week nor to be aware of his surroundings. Some
thought that he drank heavily or took drugs (‘supplied by Badmaiev’).
There is no evidence in support of either allegation but we can postulate
both a psychological and a physical reason for his collapse. During the
past eighteen months the Tsar had not only lived under intense strain but
had become almost completely isolated, for all his advisers and his old
devoted friends had either resigned or been removed by order of
Alexandra. He must have known that his isolation resulted from loyalty
to his wife and her concept of Rasputin. The latter had become essential
to her and therefore must be retained at all costs. Now Rasputin had gone
and Alexandra seemed virtually unmoved. All these sacrifices and errors
had been unnecessary.
The physical reason is to be found in two of the Tsar’s letters.
Back in June 1915 he had replied to Alexandra’s enquiry: ‘Yes, my
darling, I am beginning to feel my old heart. The first time it was in
August of last year, after the Samsonov catastrophe, and again now – it
feels so heavy in the left side when I breathe.’ On 11 March 1917, when
he had returned to headquarters, there is a much more ominous
paragraph: ‘This morning during the service, I felt an excruciating pain
in the chest, which lasted for a quarter of an hour. I could hardly stand

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the service out, and my forehead was covered with drops of perspiration.
I cannot understand what it could have been, because I had no palpitation
of the heart, but later it disappeared, vanishing suddenly when I knelt
before the image of the Holy Virgin. If this occurs again I shall tell
Feodorov.’ The Tsar appears to have suffered a small coronary infarct or
perhaps an attack of angina.
Three days earlier Nicholas had left Tsarskoie Selo for
headquarters, having been urgently summoned by General Alexeiv,
probably because the discipline of some units gave cause for alarm. On
the same day disorders broke out in Petrograd. The weather had been
unusually severe, even for a Russian winter. The railways were brought
almost to a standstill by the number of engines with boilers cracked by
frost, and little coal or food could reach the city. There is said to have
been plenty of flour but too little fuel to bake bread. The Duma furiously
attacked the government’s food policy, while large crowds wandered
aimlessly about the streets demanding bread, but doing little damage and
quietly dispersing when ordered by the police. Next day the crowds
increased and some food shops were looted. Cossacks helped the police
to restore order, but neither demonstrators nor law enforcers seemed
willing to attack one another.
Not until Saturday 10 March did any political flavour appear in
the demonstrations. A few of the crowd carried red flags and there were
some shouts of ‘Down with the German woman.’ In other respects the
disorders were little more than a rather widespread food-riot. On Sunday
the mood became more ugly and the police summoned troops who fired
on the crowd. The Pavlovsky Regiment mutinied and refused to fire but
were disarmed by the famous Preobrazhensky Guards. Order had been
restored by nightfall but during the day the Volynsky Regiment had
proved unreliable and returned to barracks. That night they mutinied and
killed at least one officer. On Monday morning, 12 March, they joined

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the crowd on the streets. This was the action which changed an aimless
bread-riot into a revolution.
In fact Russia had had no effective government since the
preceding Friday. That day Alexis and his sister Olga went down with
measles, to be followed shortly by the three other girls and Anna
Vyroubova. Alexandra nursed them all devotedly and had no time left to
spend on business. Protopopov ruled almost alone with such help as he
could receive from the shade of Rasputin conjured up in a series of
spiritualistic seances.
Later on Monday 12 March Alexander Kerensky, a left-wing
Duma deputy, advised the Volynsky to go to the Tauride Palace where
the Duma met. The Volynsky sent deputations to all regiments in the
garrison inviting them to leave their barracks and join them ‘in defence
of the Duma’. By evening the whole of the Petrograd garrison had
mutinied except for three companies of the Ismailovsky Guards and three
companies of Chasseurs. Urgent messages were sent from the Duma to
the Tsar at headquarters.
The Duma had now become the centre of a kind of mob rule,
feebly trying to restore order with the alternate help and opposition of the
Council (Soviet) of Workers and Soldiers, hastily elected by show of
hands on the basis of one representative per thousand. During the night
of 14/15 March, after much angry discussion, Duma and Soviet agreed
that Nicholas must abdicate but the Tsardom should continue with Alexis
as constitutional monarch under the regency of his uncle Grand Duke
Michael. Nicholas had attempted to reach Tsarskoie Selo but had been
turned back and was now at Pskov in contact with Army command. Two
members of the Duma, Alexander Guchkov and Basil Shulgin, drew up a
deed of abdication and left for Pskov at dawn on 15 March.
Meanwhile the generals had been conferring and had also
decided that Nicholas must abdicate. He consented after some hesitation
and in the afternoon of 15 March composed his own deed, naming

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Alexis as his successor and his brother Michael as regent. Then he
consulted the surgeon Feodorov and changed his mind. When Guchkov
and Shulgin arrived at ten o’clock that night he told them he could not be
parted from his haemophiliac son. He would abdicate, but only in favour
of Grand Duke Michael.
The Duma representatives, both monarchists, were horrified, for
Nicholas had wrecked the whole plan. A boy of twelve under the
tutelage of the Duma might have been acceptable. Michael would be just
another Romanov autocrat. And so it turned out, for when the deputies
proclaimed Tsar Michael at the Petrograd station, they were howled
down by the crowd and had difficulty in escaping from an angry mob.
Twenty-four hours later Michael, too, abdicated the crown of Russia.
Haemophilia had destroyed the last chance of saving the Romanov
dynasty.
There followed a summer of anarchy, disillusion and defeat under
the ineffectual rule of a Provisional Government awaiting confirmation
by a Constituent Assembly to be elected in December. But the only call
which would rally the despairing people of Russia in the autumn of 1917
was that of bread and land and peace. These the minority Bolshevik
party promised them and so came to power. In the civil war which
followed, the imperial family were taken to the Bolshevik-held mining
town of Ekaterinberg on the eastern side of the Ural Mountains. There,
on the night of 16 July 1918, they were all shot by order of the
Ekaterinberg Soviet. They died as they had always lived, a united family.
Eighty years later, to the very day, the remains of most of the Romanov
victims killed in Ekaterinberg were given a ceremonial reburial in the
former capital of the tsarist empire. By 1998, after the ending of Soviet
rule some seven years earlier, their bones were returned to a city no
longer called Leningrad, but to one with the restored name of St
Petersburg. There the coffins containing the remains of Nicholas and
Alexandra, with those of their daughters Olga, Tatiana and Anastasia,

243
and of four faithful servants, were entombed together in a chapel of the
Romanov mausoleum within the fortress cathedral of St Peter and St
Paul. Two further charred and partial skeletons were found near
Ekaterinberg in 2007. After DNA testing the Russian authorities declared
one to be that of the third-born daughter Marie. The other was identified
as the remains of the boy who is surely the most tragic single figure in
the tale which links Queen Victoria to the fate of the Russian imperial
house – the haemophiliac Tsarevich Alexis himself.
One notable feature of the 1998 ceremonies in St Petersburg was
the attendance of about fifty Romanov relations of varying degrees of
kinship to Nicholas II. Some of these visitors took the opportunity of
inspecting, at her moorings on the River Neva, the cruiser Aurora of the
former Imperial Navy, the guns of which had threatened the ministers of
the Provisional Government in the Winter Palace at the start of the
Bolshevik coup and thus inaugurated the seven decades of communist
dictatorship. No doubt these members of the imperial family derived
some satisfaction from the recent collapse of the Soviets, but they were
clearly less pleased to discover that the funeral service of the last of the
Romanov rulers had been denied the personal presence and spiritual
approval of the Patriarch of St Petersburg. He had dismissed the
obsequies as meaningless, giving as the reason his dogmatic belief that
forensic DNA-testing was utterly incapable of authenticating the
imperial remains. Sadly, such conduct merely served to demonstrate -
nearly fifty years after Watson and Crick established the structure of the
DNA molecule and no less than a century after the rediscovery of
Mendel’s hereditary elements – that no understanding of genetics had yet
penetrated the minds of those who simply found it convenient to ignore
or deride much of modern science and of biology in particular. As the
twentieth century drew to a close. Russians were experiencing grave
difficulty in elaborating stable governmental and economic structures for
their post-Soviet era of development. It was therefore all the more

244
regrettable that, in July 1998, at the solemn moment of political
reconciliation symbolized by the reburial of the Tsar, they should find
ecclesiastical obscurantism, one of the major defects of the tsarist
regime, again added to the many problems facing Russia. Recalling the
agonies of the Revolution and civil war, followed by the terrors of
Stalin’s Gulag system, one is moved to wonder whether the change from
an inefficient tsarist dictatorship to an even more oppressive communist
regime had been of any benefit to the world in general and to the Russian
people in particular. A great opportunity wasted may have been the true
legacy of Victoria’s haemophiliac gene.

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 C T
MOB HYSTERIA AND MASS SUGGESTION

Broadly speaking there are two main types of disease, somatic and
psychiatric. Somatic, sometimes called organic disease, is demonstrable
by lesions which doctors can identify by the patient’s description of the
symptoms and the physical signs which they can elucidate, using the
ancient methods of palpation and auscultation or more modern aids such
as X-rays and blood tests. In psychiatric or emotional disease there is no
demonstrable physical lesion but the patient suffers from very real
symptoms. Cancer is a somatic disease recognizable by definite signs
and symptoms. Cancerophobia is a fairly common psychiatric disorder in
which the patient may be able to present symptoms suggestive of cancer
but no signs demonstrable on physical examination. The above is an
oversimplification because disease is seldom purely somatic or purely
psychiatric. The very fact that the patient is ill may give rise to
symptoms which cannot be related to a physical cause. Troubles such as
financial difficulties, frustration, sleeplessness and loss of appetite may
result in psychiatric symptoms that are not part of the somatic disease
from which the patient is suffering. Conversely, a psychiatric illness will
often produce physical signs such as tics, paralyses or disorders of
appetite which are not symptoms of the disease itself.
For these reasons it is arguable that all disease is to a greater or
lesser degree psychosomatic. Consider two examples, discussed in
previous chapters. Henry VIII almost certainly suffered from the somatic
infection syphilis. If so, the effects were exaggerated by his powerful
position, by his arrogance and intolerance. The two latter are psychiatric

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defects. His main trouble was undoubtedly a somatic disease (or
diseases, if preferred) and the psychiatric element was secondary.
Napoleon, in contrast, suffered from a number of minor somatic ills
throughout his life but his real illness was psychiatric. He conceived
himself to be master of the world and thus a greater man than he really
was.
We find an instructive example of this psychosomatic
combination in the puzzling case of Joan of Arc. Born of a prosperous
peasant family at Domremy in Lorraine, Joan began to hear mysterious
voices at the age of thirteen, about the year 1425. She later claimed that
her voices came from St Michael, St Margaret and St Catherine. The
voices told her that she had been chosen by God to deliver France from
the English invader. They commanded her to go to the Dauphin and
persuade him to be crowned king. His mission must be to drive the
English and Burgundians from France and to dedicate his cleansed
kingdom to the service of God. In this, Joan was undoubtedly abnormal,
for normal people do not hear supernatural voices nor do they see visions
of saints. But Joan was certainly not insane, any more than Florence
Nightingale can be regarded as insane because she heard God speaking
to her in her seventeenth year. Joan showed herself to be thoroughly
practical, as did Miss Nightingale, and elaborated a policy which was
ultimately successful. It is therefore unwise to dismiss her voices and her
visions as the hallucinations of a diseased mind. While admitting that she
was a ‘strange girl’, that is she did not behave as would an ordinary girl,
we ought to look for a somatic cause of these aberrations of sight and
hearing.
The only real evidence is to be found in the statements which she
made at her trial before the Bishop of Beauvais in February-March 1431.
At first Joan showed great unwillingness to speak of her heavenly
visitors. Her judges were anxious to show that the Black Arts had
inspired her and, at one point, suggested drug addiction. They asked

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what she had done with her mandragora. Joan replied: ‘I have no
mandragora and never had any. I have heard it said that near to my town
there is one. I have heard it said that it is a thing evil and dangerous. I
know not what use it is.’
She defended herself bravely and firmly throughout the trial.
Asked about the voices, she told the Court that she first heard them at
age thirteen and that they frightened her. She could not understand what
they tried to tell her until the third time they spoke to her. They spoke
again and again but she could never understand their meaning unless her
surroundings were perfectly quiet. The figures of the saints, who seemed
to be speaking, did not appear until later. She refused to give any details
of their physical appearance but said she embraced them and they had a
pleasant odour. On further questioning, she twice declared that the
apparitions frightened her so much that she fell on her knees. Then
comes, from a medical point of view, her most significant statement: ‘I
heard the voice on the right hand side … and rarely do I hear it without a
brightness. The brightness comes from the same side as the voice is
heard. It is usually a great light.’ On one occasion she was asleep and the
Voice woke her, not by touch but by sound alone. The Voice did not
seem to be in the cell where Joan slept but she was sure it was
somewhere in the castle building. She thanked the Voice by getting up,
sitting down on the bed and clasping her hands.
A little more evidence is to be found in the Trial of Rehabilitation
held in 1456, twenty-five years after Joan died at the stake. Two priests
testified that they visited her in her cell on the morning of her burning.
She told them that her saints, or spirits, appeared to her in the form of
minute specks, in great numbers and of the smallest size. The only other
suggestive evidence is the rather mysterious illness which attacked her
during her trial, causing it to be adjourned for three days. Her gaolers
attributed this to eating shad, a great Loire delicacy, while Joan herself
blamed a carp sent to her by the Bishop of Beauvais. John Tiphaine, the

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surgeon who attended her, made enquiry and found that she had been
unwell, with vomiting, on several occasions and that the present attack
only differed from the others in being rather more prolonged.
There is not enough here to attempt a definite and exact diagnosis
but sufficient to hazard a guess. Joan’s disability started at the age of
puberty. She suffered from intermittent attacks of tinnitus, the singing or
ringing in the ears, which some people translate into speech. (A patient
of one of the present writers complained of the hymn Onward Christian
Soldiers repeated over and over again in her ears). Joan’s tinnitus was
unilateral, on the right side only, again a quite common manifestation.
She also suffered from visual disturbance which took the form of bright
or flashing light mingled with dancing black specks. The specks are a
common symptom of nausea, in Joan’s case sometimes so severe that she
actually vomited. At the same time she experienced giddiness, which
forced her to sit down or fall on her knees. Joan probably suffered from
the syndrome first described by Prosper Menière as aural vertigo in
1861, now usually known as Menière’s Disease.
But Joan’s somatic disorder, whatever it may have been, is
obviously only of secondary importance in the story. She had convinced
herself that her Voices required her to liberate France. So convinced was
she of her mission that she convinced many others and thus sparked off a
great mass movement. France was in a dreadful state, her people
hopeless after seventy years of unsuccessful warfare and foreign
occupation. Joan infused her countrymen with a new hope by her own
example. In her case we can identify with certainty the one person who
triggered off a great mass-change in behaviour. There are many examples
in history of these mass changes. Sometimes we can select the individual
or the incident which has started a chain reaction but in other cases we
can detect no individual stimulus, for there seems to have been a general
perception that something which has been accepted without question is
no longer desirable. A simple example is the attitude of the British to the

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hunting of foxes and deer. At the beginning of the twentieth century
hunting was generally regarded as a desirable and colourful ‘sport’, the
meet being an occasion when all classes mingled together and those who
could not afford horses followed on foot. Less than a hundred years later
the ‘sport’ had aroused massive opposition as being cruel to animals and
there was wide demand for its abolition. In this case no one could
possibly identify an individual who started a considerable mass
movement, a change in the way of thinking and pattern of behaviour.
Foxes have been hunted as vermin and deer as human food for
many centuries and it is only in very recent years that the feelings of the
animal have aroused concern. Consideration for the animal may be
regarded as an advance in human civilization, the imposition of another
in a series of covering skins. Underneath the skins there still lie hidden
the primitive instincts of animal Man. Fear, hate, anger, greed, self-
preservation and preservation of the human race are ever-present. There
comes a time in the life of any individual when the skins break and a
primitive instinct emerges. Then the control imposed by civilization is
lost and we may rightly speak of the individual’s bestial rage or animal
fear.
But Man is a gregarious animal and such creatures do not like to
be different from their fellows, for fear that they may be cast out of the
pack. This is why we tend to copy one another and, given the right
conditions, why unreasoning and causeless fear or anger can pass from
the individual into a crowd. Men and women who are apparently sensible
in their face-to-face dealings with each other as individuals may, as part
of the mass, suffer a persistent delusion that whole categories of their
fellow-beings are inimical. There are all too many instances in world
history when one crowd has regarded another, very similar crowd, as
monstrous, as tools of the devil, as non-men, as instruments of
destruction. This is one of the phenomena to which the name mob
hysteria has often been attached.

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 Mob hysteria in its simplest form can be exemplified by the not
infrequent occurrence of mass fainting. One worker faints on the factory
floor, another follows, and a dozen are ‘Out’ within a few minutes.
Sometimes an organic cause – perhaps an overheated workshop or
noxious fumes – is apparent. Quite often there is no obvious cause. In
fact the first girl fainted because she was suffering excessive blood-loss
from her period, or the man had come to work without breakfast. The
remainder were cases of ‘sympathetic fainting’. The fainting is hysterical
or emotional in that it has no physical cause.
Fear can also be contagious and hysterical, sometimes with tragic
results. A well-known example occurred on 30 May 1883, soon after the
new Brooklyn to Manhattan bridge was first opened. Somehow an
unreasoning fear that the structure was on the point of collapse swept
through the crowd. In the rush to get off the bridge, which was perfectly
safe, twelve people were trampled to death and twenty-six injured. The
precipitating cause of panic has never been identified. A similar baseless
panic fear caused many deaths on the stairway leading to a deep air-raid
shelter during a flying-bomb attack on London in 1944.
Sympathetic fainting and panic fear depend upon mass
suggestion, the fainting or panic of one individual suggesting to others
that they should do the same. This is how the crowd can be manipulated.
A good example is the hysteria which followed the tragic death of
Princess Diana on 31 August 1997. Death of a passenger, sometimes
attractive or well-known, when the car driver is under the influence of
alcohol, is unfortunately too common an event to arouse much public
attention. The princess was certainly attractive, her marital difficulties
aroused sympathy, and a relatively small circle of people knew of and
admired her love of children and her humane efforts to outlaw land-
mines. Had an enquirer gone from house to house anywhere in Britain a
few days before the accident and asked the simple question ‘What do
you know of Princess Diana?’, many of the answers would have run

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along the lines of ‘Not very much at all.’ Yet, less than a week later,
thousands of these people, united by a mass process of imitative
behaviour, would be depositing bunches of flowers at the Kensington
Palace gates as though mourning a close relation or an intimate friend.
Such is the power of the media today and such has been the
power of demagogues in the past, whether ranting from their cathedral
pulpits or on a street corner soapbox. The wise ruler knows only too well
that the crowd which cheered him vociferously last week may be crying
for his blood tomorrow. Patriotic loyalty to the crown can be aroused by
appeal to the mob, but so too can the more primitive urges of fear, hate
and anger. These suggest to the individual that he or she should take
immediate and preferably violent action, but there may be nothing to hit
or the object of our protest may be too strong for us. When this demand
for immediate action transfers itself from the individual to the crowd a
mass movement will result. This may take a bizarre form because the
participants cannot translate their protest effectively.
The dancing mania of medieval Germany is an example of the
latter. We can probably uncover an initiating cause, ergot of rye. Rye, a
common bread-corn in northern Europe, sometimes becomes infected
with Claviceps fungus in wet seasons. The resultant product, ergot, is
chemically complex. One of the compounds present is D-lysergic acid
diethylamide, commonly known as LSD, the initials of its Swiss name.
This was one of the drugs which used to be taken at pop-music sessions
in the 1960s because it increases the response to rhythm. Other effects
include hallucinations, agitation and intensely coloured vision.
Small outbreaks of dancing mania occurred in Germany from
early in the Middle Ages until late in the sixteenth century. The
phenomenon was not confined to Germany but has been reported from
many countries. The last known ‘dancing epidemic’ affecting a number
of people was observed in 1911 close to the Mediterranean outlet of the
Dardanelles. The most serious incident started at Aix-la-Chapelle in July

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1374. Sufferers danced uncontrollably in the streets, screaming and
foaming at the mouth. Many suffered hallucinations, some declaring they
were immersed in a sea of blood, others claiming to have seen the
heavens open to reveal Christ enthroned with the Virgin Mary.
At first these dancers had no definite aim but they rapidly gained
adherents who imitated their unrestrained movements. Thousands
became affected and, as the craze grew, it crystallized into anti-clerical
protest largely directed against the hated Prince-Bishops. Streams of
dancers invaded the Low Countries and moved along the Rhine,
gathering new adherents throughout Germany. Mobs stormed monastic
houses, chased out abbots and priors, shouted filthy abuse at priests. It is
interesting that no ruling Prince-Bishop was killed or even dislodged. In
the later stages, the dancers often appeared insensitive to quite severe
pain or other external stimuli, a symptom of hysteria rather than LSD
intoxication. The mania bears a marked resemblance to the flagellant
movement which we noticed in Chapter Two. It will be remembered that
this started as an intercession against plague and developed into a protest
against riches, the Church and established government.
Both flagellant movement and dancing mania produced increased
sexual activity. Violent action and violent emotion both stimulate the
most primitive instinct, the sexual urge or instinct of race preservation.
This is why the dance is part of the ritual of witchcraft. The witch craze
is mysterious in more than one respect. It has been convincingly argued
that it is essentially a devil doctrine purposively established by the
Church during the early Middle Ages, which might account for the
marked similarity in witch practices in widely separated countries. There
is little evidence that apostles of the diabolical religion travelled
extensively in search of converts, but there is much to suggest a wide
distribution of knowledge through the written denunciations made by
churchmen.

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 The mob hysteria of the cult and the hysteria of those who would
suppress the cult are of equal interest. We cannot divorce the craft from
the hunt. If witch-hunting took the form of a mass movement at times,
then so did witchcraft itself. The cult became widespread at the same
periods as did suppression. Thus, when we speak of the witch craze, we
should apply the term both to the witch and to the hunter. The three main
periods of witch hysteria roughly coincide with the Renaissance, the
Protestant Reformation and the Catholic Counter-Reformation. Within
each of these we observe a loosening of the hold of conformity which in
turn stimulated aberrations and repression. Witchcraft was only one of
these aberrations and witch-hunting was only part of a general repression
of non-conformity, practised by Catholic and Protestant alike.
The practice of witchcraft bears the stigmata of hysteria. The
myth of the witch flying long distances on her broomstick to the sabbat
is levitation, the sensation of being airborne, a symptom of hysteria. The
sabbat itself with its wild exhausting dance, weird music and sexual orgy
is mass hysteria. The feast of nauseous delicacies lacks any taste, the kiss
or copulation with a diabolical leader holds no warmth. The witch often
complains of formication, the sensation of ants crawling over her skin.
The witch-finder searched with his bodkin for areas of anaesthesia on the
suspect’s body. All these are well-known symptoms of hysteria.
A witch, endowed with supposed diabolical power to bring
disease and ill-fortune, must be an object of terror to the uninitiated. But
we may be able to uncover an even more primitive urge for the witch-
hunt. The witch is commonly, although by no means invariably, a woman
who possesses the supernatural power. She is the embodiment of
feminine evil. To the celibate priest, to the grim Protestant who believed
in the subjection of women, she was a special object of hatred and fear.
Such men saw in witchcraft not only an obscene parody of religion but a
threat to male supremacy. The witch became a symbol of the primitive

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love-hate relationship, the age-old struggle for domination between the
sexes.
The real increase in witch practices that occurred in times of
unbridled repression bred panic exaggeration. Fear bred fear, hatred bred
hatred, witches were seen everywhere. The gentle, scholarly Nicolas
Remy of Lorraine sent between two thousand and three thousand victims
to the stake in the years 1595 to 1616. The pious Archbishop of Trier
burned 368 witches from twenty-two villages between 1587 and 1593,
leaving only one woman alive in each of two villages in 1595. From
1623 until 1631 the Prince-Bishop of Würzburg burned over nine
hundred people for witchcraft, including his own nephew, a number of
children and nineteen priests. France, Germany, Switzerland, Spain,
Sweden and Scotland all joined in this form of mass murder. Germany
was the country worst affected, a fact that will have some significance
later in the story. At the height of the terror, belief in witchcraft became
an article of faith and to deny the existence of witches could lead to
condemnation.
The worst excesses in England and the American colonies were
associated with extreme puritanism. Though repression never equalled
that on the European continent, two outbreaks are notorious. The first
affected the eastern counties of England in 1644–7 when the puritanical
parliamentary army was in the ascendant. The hysterical denunciations
and accusations were instigated by Matthew Hopkins who, in 1645,
procured a commission as Witch-finder General. An Ipswich lawyer, he
journeyed about the countryside in search of witches, supported by a
barrister named John Godbolt who had been appointed a judge for this
special purpose by vote of parliament. Within just over a year the two
villains hanged over sixty women in Essex alone, besides many others in
Norfolk and Huntingdonshire. Hopkins published a treatise, The
Discovery of Witches, in 1647, and in the same year was denounced as an
imposter. He failed to pass the trial of swimming; that is, he floated when

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thrown into water with his hands and feet tied. He was condemned to be
hanged as a sorcerer.
The American episode occurred at Salem, then a village about
fifteen miles north-east of Boston, Massachusetts. The witch-craze began
in 1692 with an accusation made by ten young girls that they had been
bewitched by two old women and a West Indian slave named Tituba,
property of the Revd Samuel Parris. The latter seems to have been
largely responsible for fanning the hysteria which spread rapidly. Within
four months hundreds of women had been arrested and tried. The judges
condemned nineteen women to be hanged, one to be pressed to death for
refusing to plead, and many to imprisonment. The hysteria passed almost
as quickly as it had arisen and a swift reaction against the witch-hunters
followed. In May 1693 Governor Phelps ordered the release of all
prisoners held on a charge of witchcraft.
Cotton Mather, the Boston Congregational minister who was to
become a Fellow of the Royal Society in 1713, played a curious part in
this episode. He is sometimes named as the instigator of the hunt and
there is no doubt that he firmly believed in witchcraft and wrote several
papers on the subject before 1700. On the other hand he warned the
judges of their unfair methods and that they had unjustly sentenced some
of their victims. Whatever the truth may be, it is certainly of interest that
a serious scientist, as was Mather, could have believed in the existence of
witches.

Over two hundred years later the rise of Adolf Hitler and the Nazi
party was to show what terrors can be inflicted when a diseased
individual, a capacity for mass suggestion, a persecutory craze and a
state of mob hysteria are brought together to infect a whole nation. Hitler
himself unwittingly exemplifies how history may be affected not only by
disease itself, but by the individual’s ideas about disease. His concept of
a diseased nation was based upon two assumptions. The first was that

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society is not merely comparable to a biological organism but that
actually and for all purposes it is such an organism. Society is often
compared to an organism in phrases such as ‘the body politic’. But
Hitler, like many before him, mistook the metaphor for reality. In Mein
Kampf he declared: ‘As Aryans, we can consider the state only as the
living organism of a people.’ His second assumption followed from the
first and is the linchpin of his racist ideology: since human society is a
biological organism, it can become diseased or degenerate in much the
same way as the individual. Further, just as the union of two individuals
may produce a physically or mentally inferior second generation, so the
union of two societies or ‘races’ can result in the degeneration of the
product.
In order to justify this hypothesis, Hitler had to postulate the
existence of a ‘pure stock’. So he intensified and developed the ‘Aryan
myth’: the fallacy that Nordic Teutons are pure Aryans. Since he thought
that the most immediate threat to Aryan rule and culture came from the
supposed ‘Jewish race’, the Jew was represented as the leading
degenerate element. Hitler’s theory of heredity was based on the ancient
idea of the literal blending of blood. Thus he was able to use such
meaningless expressions as ‘poisonous contamination of the race’ and
‘the pestilential adulteration of the blood’. Logic suggested a further
extension of the disease metaphor. Since he regarded the ‘Jewish race’ as
the major contaminant, he depicted the Jew as a bacillus or parasite
sapping the vitality of the society in which he lived: ‘On putting the
probing knife carefully to that kind of abscess, one immediately
discovered, like a maggot in a putrescent body, a little Jew who was
often blinded by the sudden light.’ This concept of disease lies at the
heart of Hitler’s vision of the universe and thus contributed to the most
horrifying events in all recorded history. Yet, in one curious sense, Hitler
was right. From 1918 until 1945 he did live in a diseased community.
The disease was not physical but of the mind.

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 In the First World War Germany made greater sacrifices than any
other belligerent. Victory seemed at last to be in sight in the spring of
1918. Russia had signed a humiliating peace treaty at Brest-Litovsk,
Romania had surrendered, the German armies had broken the stalemate
of trench warfare and were hurling the Allies back to Paris and the
Channel ports. All this was announced to the German people in exultant
communiques. But when the advance faltered, halted, turned to retreat,
no inkling of the truth appeared in the press. Knowledge that the position
was rapidly becoming hopeless remained almost confined to the High
Command. The announcement at the beginning of October that the
government was seeking peace terms stunned and bewildered the
German nation. Up to that moment the home front stood unbroken and
the news came as a shattering blow which produced near-panic. It is
often forgotten that even on 11 November, when the world learnt of the
Armistice, the German armies still held their lines on foreign soil and not
a single Allied soldier had penetrated German territory.
The economic situation in Germany now moved from bad to
worse. During the next months a demobilized army flung on to a labour
market already staggering under a burden of unemployment, added to the
general discontent. Demand for reparation payments caused a fall in the
mark, from 4 to the dollar in mid-1914 to 75 in July 1921 and to more
than 17,000 in January 1923. In that month French troops occupied the
industrial district of the Ruhr, cutting off 80 per cent of Germany’s coal
and steel production. By August 1923 the mark had fallen to four million
to the dollar and to an unbelievable 4,200,000 million by 15 November.
Total collapse of the currency resulted in loss of all savings, bankrupt
businesses, mass unemployment and renewed food shortages. The
foundations of German society were far more shaken by the collapse of
the mark than by the war, the revolution of 1918 and the Treaty of
Versailles combined.

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 Slowly Germany began to recover, only to be faced with the
world depression which began in the USA in 1929 and intensified during
the years 1930–1. German industry could not cope. In 1929
unemployment rose towards two million and by 1932 the figure was
growing well beyond five millions. Germany was now a sick nation in
that so many of her individual members were half-starved and idle,
defeated and disillusioned, translating their sufferings into a fantasy of
persecution.
This was the only Germany known to Hitler. He had no personal
experience of the efficient, prosperous Germany of pre-1914, for he was
not a German national. The son of a minor official in the Habsburg
customs service, he was born on 20 April 1889 at Braunau on the border
between Austria and Bavaria. His father Alois was an illegitimate child
of Maria Anna Schicklgruber, the father not being certainly known but
presumed to be Johann Georg Hiedler. Alois legally adopted the name
‘Hitler’ thirteen years before Adolf’s birth. There is no evidence that J.G.
Hiedler was a Jew, but Adolf may have believed this disputed
grandfather to be partly Jewish. Here is one possible basis for Adolf
Hitler’s virulent anti-semitism, for there would have been no stigma of
illegitimacy in the family tree had his grandmother not been seduced by
a Jew. At the very least this seems a more likely explanation than the
theory propounded by more than one writer that his obsession derived
from some sexual experience with a Jewish prostitute.
Adolf Hitler spent his boyhood in a small village outside Linz in
Upper Austria, where his father died in 1903, a few months before his
son’s fourteenth birthday. He made little progress in the local school
except in such subjects as he himself desired to learn. Aged sixteen in
1905 he left school without acquiring the customary Leaving Certificate.
He continued to live with his widowed mother whom he loved in his
own strange way though he did nothing to support her financially. He
became fired with the ambition to be a brilliant architect but made no

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attempt to undergo any regular training, preferring to fill notebooks with
drawings and elaborate plans for rebuilding Linz. In 1907 he decided on
an artist’s career and applied to join the Academy of Fine Arts at Vienna.
He failed the entrance examination and, when he applied again a year
later, was not even permitted to retake it. His mother had died at the end
of 1907. Early in 1908 Adolf, friendless, incompetent and work-shy,
disappeared for five years into the Viennese world of cheap boarding-
houses and odd jobs, shifting to Munich in 1913.
But Hitler was something more complex than a mere work-shy
dropout. It is now known that he invented some of the more squalid parts
of his autobiographical account. In doing so, he was excusing himself,
for Hitler is a good example of that most pathetic of beings, the would-be
creative artist without talent or acquired ability. Of such are the dreamers
who make dreams their master, in whose fantasies the great book is
written, the picture painted, the symphony composed without any
intermediate step from inception to completion. Their dreams never
produce anything second-rate, for the figment of their minds is always a
masterpiece. It naturally follows that they are themselves great and find
themselves surrounded by a crowd of petty beings, who will not
acknowledge their pre-eminence or allow them their dominating place,
through jealousy, misunderstanding and ignorance. Thus the persistent
illusion of grandeur is accompanied by hatred and contempt for their
worthless fellows.
Adolf Hitler’s early history clearly shows that he suffered from
this type of paranoia, behaviour dependent on a fixed belief totally
divorced from reality. He was of the schizophrenic type which believes
itself to be the subject of persecution and whose actions are dictated by a
revulsion against the supposed persecutors. Paranoia caused his
indolence, his sudden bursts of feverish work when work was
inescapable, his maniacal rages when affairs would not arrange
themselves exactly as he wished, his alternating moods of sullen despair

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and irrational hope. But how on earth did such a man ever achieve
supreme power?
He would never have done so had it not been for his service in
the First World War. He was twenty-five years old in 1914 and war
conditions gave him exactly what he urgently needed: inescapable
reality, an outlet for violence, membership of a gang, the security of
strict discipline. Hitler had managed to evade compulsory military duty
before the war, but the moment it broke out he enlisted voluntarily. He
did not join his own national Austrian army, but asked to be recruited
into a Bavarian regiment forming part of the German forces. Hitler made
a good soldier because he had voluntarily offered his services to a
country which he admired and because he found in its army the
stabilizing conformity he could no longer avoid. For this reason he ended
the war more competent and more stable than he had been in 1914. But
he had not been cured. He still suffered from paranoia, was still obsessed
by the delusion that he towered far above his fellow-men.
Hitler seems to have always been mildly interested in politics, the
type of political thought found in the beer-cellar and at the street corner.
He is said to have expressed extreme opinions with intemperate violence,
showing no control in face of reasoned opposition or restrained debate.
Such a man, whether of the political right or left, has no use for the
forms of democratic government. The Aryans must be the Master Race
solely because he, as a Teuton, was a member of that elite. Therefore it
was their mission, but only under his leadership, to restore broken
Germany to her former greatness. This Hitler could do only by winning
absolute power.
Hitler’s following or gang was the party of discontent, of envy, of
resentment. The ex-officers like Hermann Goering, disappointed
intellectuals such as Alfred Rosenberg and Joseph Goebbels, out of work
labourers, small shopkeepers ruined by inflation, all these found a place
in it. Hitler refused to permit a class or age identification. He wrote of his

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mass following: ‘These fine chaps, what sacrifices they were willing to
make, all day at their jobs, and all night off on a mission for the Party. I
specially looked for people of dishevelled appearance. A bourgeois in a
stiff collar would have bitched up everything.’ The Austrian bourgeoisie
had failed to support the great Hitler, had forced him to scratch a living
in the gutters of Vienna. As it turned out, he had to have middle-class
support, for unlike Lenin he could not ride to power on the shoulders of
the workers alone. Yet he often felt nothing but contempt for his white-
collar supporters.
During the thirteen years of Hitler’s struggle towards absolute
power, his organization reached its tentacles into the heart of German
youth, creating new and aggressive gangs. Hitler Youth, that frightful
parody of scouting, was founded about 1926 and grew quickly in
numbers until in 1931 over a hundred thousand members paraded before
their leader in the torch-lit stadium at Potsdam. The Students’ League
and the Nazi Schoolchildren’s League were other ways of indoctrinating
youth. The active spearhead of Nazism, the SA, rose rapidly in numbers
from 27,000 in 1925 to 178,000 in 1929. But Nazism itself, the party of
militant discontent, could make little headway while Germany was
struggling back to prosperity in the years 1923–9. The turning point
came with the global economic depression. In 1928 the Nazi Party polled
810,000 votes in the Reichstag elections. In the first year of depression,
1930, they polled 6,409,600, nearly a fifth of the total cast, and in July
1932 they gained no fewer than 13,745,000. Hitler had now become a
major political figure. More ominous was his turbulent SA which he
himself found difficulty in controlling. A paramilitary force, largely
drawn from the unemployed, they now numbered over four hundred
thousand – four times the size of the regular army permitted to Germany
by the Treaty of Versailles.
Adolf Hitler came to power as Chancellor on 30 January 1933.
Having dropped two million votes in yet another Reichstag election as

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late as November 1932, he commanded only 33 per cent of the national
vote, and he achieved his ambition, not by a great upsurge of patriotic
heroism (as the carefully fostered legend declared) but by a shoddy deal
with the parties of the Right, the ‘Old Guard’ whom he and his followers
had been attacking for years past. The Right aimed to regain its old
function as the ruling class, to destroy the Republic and restore the
Hohenzollern monarchy, to repress the workers and their trades unions,
to reverse the Treaty of Versailles and rebuild the military power of
Germany. Led by the octogenarian Hindenburg, now in his dotage, and
the aristocratic Franz von Papen, they made the fatal mistake of
believing that in Adolf Hitler they had found the man who would help
them attain those ends. So they did not doubt their own ability to control
Hitler and trusted the promises that he made. They were not alone.
Neville Chamberlain, Edouard Daladier and Joseph Stalin among others
fell into a similar error with disastrous results. Psychiatry is not a
compulsory subject in the training of politicians, so we cannot altogether
blame them if they failed to understand that no one should rely upon the
behaviour or promises of a paranoiac.
So Germany passed into the rule of the gang. The gang demanded
conformity with its laws and usages. Any person who did not conform
was an outcast, a non-man. Hitler and his associates, the narcissist
Goering, the malignant Goebbels, the sadistic Himmler, preached the
virtues of Nazism to the mass which responded with mobs shrieking
hysterical admiration, just as mobs of mindless teenagers screamed
hysterical worship of their adored pop stars forty years later. But the
teenager, though silly, was harmless. The German mob was not. They
attacked their supposed enemies, destroyed their property, condoned
their murder.
Within months of taking over the chancellorship, the Führer had
ensured that his was the only political party officially remaining in
Germany. There followed a modern version of the witch-hunt, aimed at

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the extermination of every person who would not conform to the pattern
of the gang. Since Hitler had labelled the Jews as the diabolical agents or
instruments of organic decay, it logically followed that the ‘Jewish race’
suffered the greatest hardship. They were persecuted, just as witches had
been persecuted in sixteenth- and seventeenth-century
Germany, but to a greater extent and with all the refinements
made possible by technological advance. Some five million Jews died in
German-controlled concentration and extermination camps during the
Third Reich. In places such as those, the rhetoric of bacillus and parasite
was converted into a hideously literal reality. To the earnest Nazi, the
Jew was not human. Those who shared Hitler’s world-view had reverted
to the thinking of their remote ancestors who described their tribe as ‘the
men’, thus implying that other tribes, groups or villages had no part in
human virtues or even in human nature.
The Nazis aimed to preserve their supposed race uncontaminated,
fearing and hating anything that menaced their self-preservation. Thus
the primitive instincts of fear and hate, self-preservation and race-
preservation broke through the skins of civilization and came to the
surface. The despairing Germans of the 1920s and 1930s sloughed off
those thin skins or veneers under which Primitive Man still lies hidden.
They found their immediate satisfaction in violence and in conformity
with the Gang. The whole Hitler episode, with its hysterical Nuremburg
rallies, indoctrinated youth, witch-hunts and insane racial theories, was
in part spurred by the distinctive anxieties of the inter-war years. Yet it
also embodied a return to the hates and lusts and fears of a primitive era.
It is a terrible example of the dangers and delusions consequent upon
mass suggestion and mob hysteria.

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 CHAPTER ELEVEN
CURRENT PROBLEMS OF SURVIVAL

Earlier parts of this book have already made clear many of the
remarkable achievements registered by the ‘scientific’ medicine of the
West, particularly over the last century or so. Even allowing for the
various insights afforded by different versions of ‘traditional’ medical
practice rooted in other regions of the world, there is no alternative
approach to the treatment and cure of major diseases which has proved
more generally effective, nor any rival system which has attained
comparable influence on a global scale. In this sense it is understandable
that historians of modern Western medicine should have had such
frequent resort to the rhetoric of ‘progress’. Yet the present volume has
also suggested that instances of complete conquest over particular
diseases have remained rare, and that in many other respects as well the
overall story is far too complex to be properly presented as a simple
chronicle of unbroken advance.
We need to note, for example, that the development of scientific
medicine has brought with it a formidable set of social, economic, and
ethical dilemmas. The earlier achievement of figures such as Chadwick
and Simon in promoting the notion of health care as an ongoing
responsibility to be discharged by society as a whole was one of the
foundations for the twentieth-century experience of an ever-closer
linkage between, on one hand, the growing authority of medicine and, on
the other, the enlargement of state power within liberal as well as more
autocratic regimes. Almost regardless of their particular ideological
stance, governments became leading agents of collective mobilization
for the preventative and therapeutic battles against disease. This process

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was assisted by the tendency of doctors (who themselves were now
increasingly likely to be public employees) to urge the greater
medicalization of an expanding range of policy issues, such as those
dealing with the quality of the environment, or of diet, or of housing and
working conditions, or of other components of a ‘welfare’ society.
These developments meant that, by the early twenty-first century,
medicine within the advanced economies was also big business. Here,
whatever the particular balance between public and private outlay in
each instance, the expenditure on health care within the most prosperous
societies of the West had risen generally to around 10 per cent of Gross
National Product. In the trend-setting case of the USA, however, the
figure had already spiralled higher – to one of 18 per cent by 2011,
which reflected more than a doubling since the early 1970s. Such
statistics indicate that the processes by which these societies were now
seeking to combat disease and produce a healthier and longer lifespan
had turned medicine into a major service industry. Its operation required
huge investment in various forms of professional education, as well as in
the construction and servicing of the complex hospital systems which
now served as the principal sites of ‘high-tech’ innovation. It was also an
enterprise offering the prospect of huge commercial gain to companies
active in fields such as health insurance or the production of
pharmaceuticals. All too often patients were becoming mere units of
accountancy, especially when viewed from the perspective either of
those intent on maximizing private profit or of those seeking to limit
public expenditure.
Nothing about the health economics of the late twentieth century
had been more striking than the inclination of Western societies to
generate an almost infinite demand for improved medical care. Recent
scientific and technical advances had fuelled far more hopes than
available resources could readily meet, under circumstances where rising
expectations constantly clashed with rising costs. As the new millennium

266
dawned those who lived in the West were generally healthier than any
preceding generation. But, at the same time, they seemed ever more
anxiously obsessed about their health. Among the more justifiable of
their concerns was a fear that the ‘rationing’ of medical services, which
had already become prominent as a topic for public debate, would prove
to be an increasingly pressing problem as a longer-living, and thus
longer-ageing, population made ever greater demands upon resource.
However, when contrasted with the fate of those living on poorer
continents, these anxieties appeared simply as side-effects stemming
from the fact that the relative prosperity of the West had generated an
enlarged range of difficult choices. As the twenty-first century began
there remained extensive regions of Africa, Asia and Latin America
where chronic political instability and unsolved poverty precluded all
such choice and imposed far more radical limitations on the diffusion of
scientific medicine as a potentially vital means of combating disease. In
Ralf Dahrendorf’s words, ‘the globalized world has an underside of
destitution and death’.
Some of the prevailing dilemmas and anxieties were linked to an
understandable ambivalence about much of the impact of science. In the
domain of medicine this was particularly clear from the attention devoted
to ‘iatrogenic’ conditions – illnesses or disabilities attributable to the
intervention of physicians themselves. Such problems demonstrated the
complexity of modern treatment. A drug might be invaluable in the cure
of a certain disease, yet have distinct and sometimes dangerous
disadvantages too. Perhaps the most notorious example from the modern
epoch was thalidomide, first introduced during the 1950s in West
Germany and soon widely available without formal prescription. As a
means of inducing sleep, it seemed safer than any of the barbiturates,
being non-addictive and having a margin of safety wide enough to make
lethal overdose virtually impossible. Around 1960, however, German
paediatricians found themselves dealing with an unprecedentedly large

267
number of babies suffering from phocomelia, or ‘seal extremities’, a
hitherto rare congenital deficiency of the long bones which produces
normal or rudimentary hands and feet springing directly from the trunk.
These children also presented deformities of the eyes, ears, and heart, as
well as of the alimentary and urinary tracts. It soon became evident that
there was a connection between these defects and a drug retailing as
Contergan, which had been taken by the babies’ mothers during early
pregnancy (the second month being the crucial phase). Other
thalidomide-based agents, such as that being sold as Distaval in Britain
and that being trialled as Kevadon in the USA, were soon similarly
implicated. It is reckoned that about 20 per cent of the women who had
taken the drug at the relevant stage of their pregnancies produced
deformed offspring. In West Germany the Ministry of Health estimated
that about 10,000 abnormal babies had resulted, of whom only half
survived. Britain experienced 500 cases, with much the same rate of
mortality. The USA escaped the worst of the disaster only because there
the pharmacologist and drug regulator Frances Kelsey had remained so
sceptical about the safety of the product, and had been so successful in
resisting strong commercial pressures to license its general marketing.
Thalidomide was an outstanding example of something which
appeared to meet a public need, to add an amenity to life, to replace a
more perilous agent, yet which carried an unsuspected and even graver
danger. In other instances doubts about the side-effects of drug usage,
especially over the longer term, have been frequently but less
conclusively expressed. Such unresolved worries have shadowed the
history of ‘the pill’, as a means of female chemical contraception that
proved so convenient as to have played a major role in the rapid increase
of sexual ‘permissiveness’ during the later twentieth century. Some
similar anxieties surrounded Viagra, a ‘cure’ for male impotence which
was launched with huge publicity in 1998 and which seemed destined

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quickly to become an object more of recreational than of strictly medical
usage.
Even more generally, there were serious dangers stemming from
drug resistance. This is the process whereby chance genetic mutations
among bacteria, viruses, fungi, and parasites confer upon such harmful
microorganisms a relative immunity from the effects of medications
previously used to tackle them. Strains that do not display this ability to
resist treatment are selectively wiped out so that ‘superbugs’ become
dominant. We observe this development, for example, in the cases of
some severe hospital-acquired infections caused by bacteria such as
methicillin-resistant Staphylococcus aureus (MRSA). The situation has
been worsened by the often complacent over-prescription of antibiotics,
where the perils are partly attributable to the fact that it has often been
the patients themselves who were pressing most eagerly for this kind of
chemical ‘fix’. It is now increasingly clear, however, that the genetic
mutations producing resistant strains of microorganism are
fundamentally natural phenomena which have to be countered not
ignored if medicine is to avoid retreat into the conditions of the pre-
antibiotic era.

That particular issue also illustrates the point that, by the turn of
the millennium, the areas of interaction between physicians and
geneticists were precisely those where prospects for further scientific
breakthroughs looked not only brightest but, in other ways, also most
threatening. Fifty years or so after Crick and Watson’s decoding of DNA,
the principal focus of fundamental science in relation to the battle against
disease was increasingly directed towards molecules rather than cells.
This emphasis was reflected in the Human Genome Project, launched as
a scheme of international collaboration in the 1980s and completed by
2003. Here scientists had succeeded in mapping the position of every
gene on every chromosome, and in plotting the sequence of three billion

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molecular ‘base pairs’ running through the double helix of DNA. Having
established such a matrix, investigators hoped to be able to identify the
precise genetical origin of any disease or other defect attributable to
inheritance. Thereafter the most pressing challenge would almost
inevitably become that of manipulating the hereditary material so as to
eliminate the disorders at issue. By the year 2000 genetic screening was
already being increasingly applied during pregnancy to check the unborn
for their vulnerability to such inherited disorders as cystic fibrosis or
haemophilia, and techniques of adult testing were also being refined in
ways that might permit predictions concerning the susceptibility of
particular individuals to the eventual onset of afflictions like
Huntington’s Chorea or Alzheimer’s disease. However, it was also
within this same broad context that the ethical dilemmas associated with
the potentialities of modern science seemed constantly to deepen,
especially where questions arose about the nature and limits of justifiable
alterations to genetical processes. Under what circumstances did
beneficial ‘improvement’ become potentially perilous ‘tampering’? After
cloned sheep, for example, the chilling prospect of a Huxleyesque ‘brave
new world’ where human babies might be ‘bio-engineered’ into
supposed physical perfection moved significantly closer. Similarly, with
respect to patterns of nutrition, there were growing fears that rapid
advances in the genetic modification of food-crops were being most
strongly driven by considerations of imminent commercial profit, and in
a manner that paid inadequate heed to the dangers of triggering
unanticipated, and even uncontrollable, risks to health over the longer
term.

Towards the end of the 1970s, those inclined to interpret the

modern history of mankind’s battle against disease in broadly
triumphalist terms seemed to have something very substantial to
encourage them. Most specifically, as we saw in Chapter Four, this was

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the epoch that witnessed the final stage in the global eradication of the
scourge of smallpox. On the basis of such an undoubted achievement, it
was tempting to argue that scientific medicine would now swiftly
continue to register major advances against epidemic infections in
general. Yet one can see with hindsight that, in strictly relative terms,
smallpox had actually been one of the easier targets. As Geoff Watts has
noted: ‘It had no animal reservoir; it was easily recognized and
diagnosed; there was a very effective vaccine against it; and it was
widely feared.’ These considerations had far less bearing on a number of
other familiar major diseases. Still more crucially, however, none of
these factors (not even, at the very outset, that of fear as distinct from
sheer ignorance) proved immediately applicable to the particular form of
epidemic illness which began to be identified as a new and dramatic
threat to global health very shortly after the campaign against smallpox
had been won.
This was the infection soon labelled as AIDS (Acquired Immune
Deficiency Syndrome). Allan M. Brandt has commented on the historical
significance of the timing of its eruption as follows: ‘The epidemic
began at a moment of relative complacency, especially in the developed
world, concerning epidemic infectious disease. Not since the influenza of
1918-20 had an epidemic with such devastating potential struck. The
Western, developed world had experienced a health transition from the
predominance of infectious to chronic disease and had come to focus its
resources and attention on systemic non-infectious diseases. AIDS thus
appeared at a historical moment in which there was little social or
political experience in confronting a public-health crisis of this
dimension.’ Neither the nature nor the potential scale of the problem was
fully appreciated during the initial phase of investigation, commencing in
1980. Although there had almost certainly been a few earlier but as yet
undiagnosed cases, this was the point at which some puzzling
immunological deficiencies started to be observed among a small

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number of male homosexuals resident in Los Angeles, and then among
similar communities in San Francisco and New York. Before long the
same problem began to appear in major European cities too. At this early
stage the names given to the illness included ‘gay plague’ and ‘GRID’
(gay-related immune deficiency). The sufferers showed severely
weakened resistance to infection, especially in the forms of pneumonia
and tuberculosis. By 1983 the causative agent had been recognized as an
RNA retrovirus, subsequently called HIV (Human Immunodeficiency
Virus), and the means of infection had been identified as the transmission
of blood and other body fluids. It had also become worryingly plain that
someone could carry the virus for a number of years before any signs of
the infection (and thus of a previous capacity to pass it on unknowingly)
became apparent, and that once the symptoms did reveal themselves then
an AIDS-related death was eventually inevitable.
The disease appeared to be unprecedented, at least in the sense
that it had not been previously the object of specific identification nor
had it ever taken epidemic form. Yet virologists soon strongly suspected
that HIV itself had been around for quite a long time. In 1985 the
discovery within West Central Africa of a second strain (designated as
HIV-2) suggested that these kinds of virus might well have been present
for many years among isolated communities living in that region. By the
late 1990s the work of an international team coordinated from the
University of Alabama would indeed be demonstrating that the human
infection almost certainly originated as a result of the ‘bushmeat trade’
common in countries such as Gabon and Cameroon. It is now known that
chimpanzees, of the sub-species Pan troglodytes troglodytes, with a very
high degree (98 per cent) of genetic similarity to Homo sapiens, have
long been carriers of a virus almost identical to HIV. Though seemingly
harmless to the apes themselves, this was capable of bringing disease to
humans once the species barrier had been crossed through the blood
contamination that must have stemmed from the slaughtering and eating

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of these animals. Thus AIDS – even if undiagnosed as such while it
remained masked by the many other infections ravaging West Central
Africa – appears to have become endemic in a number of self-contained
localities before breaking out of the region as an epidemic illness.
The nature and speed of this eventual eruption testify to an
increased human mobility, as well as to other behavioural changes
(including a more ‘permissive’ climate of sexuality) which help to
characterize the life of our globalized epoch. As William H. McNeill
observed, ‘The exact path whereby the HIV virus escaped the older
limits on its habitat before being propagated along truck routes in Africa
and then around the world by aeroplane is not known, but its global
propagation in less than two decades is not in doubt.’ Nor could there be
any reason for doubting that other previously unrecorded viral diseases
might also have the potential to reach epidemic level – a consideration
sharpened by the discovery of the dangerous Marburg, Lassa, Rift Valley
and Ebola fevers (the last of which was beginning to spread
uncontrollably during 2014 in parts of Guinea, Liberia and Sierra
Leone). With regard to HIV-AIDS, the fact that in the West this was first
transmitted largely by sexual activity between men provoked a great deal
of scapegoating (reminiscent, for example, of responses to leprosy in
past ages) and of facile moralizing in a homophobic mode. Just as
harmfully, it also lured many into supposing that there was nothing more
to this affliction than the ‘gay plague’ of their initial imaginings.
However, by the time that the WHO established its global AIDS
programme in 1986, there was urgent need to raise public consciousness
about a far wider range of risk. It was now becoming more evident that
modes of infection included heterosexual contact (markedly so in the
case of HIV2), perinatal transmission between mothers and infants,
blood transfusions, and shared use of needles on the part of those
engaged in the intravenous consumption of illegal drugs. There was also
increasing evidence that the viruses causing AIDS were capable of even

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more rapid mutation than those causing influenza, where transformation
into new strains had already frustrated any comprehensive control.
By the 1990s epidemiologists were tracing the pattern of HIV
distribution in terms of three broad areas. The first of these covered
North America, Western Europe, Australasia and urban parts of Latin
America. There most of the impetus for diffusion had come from
homosexual activity, even though there was also a rise in the rate of
heterosexual transmission as a result of intravenous drug use and thus in
the number of paediatric cases generated by perinatal infection too. A
second pattern of spread, apparent in sub-Saharan African and in much
of rural Latin America was far more heavily dependent on heterosexual
infection and took as much toll upon women as upon men. The third
region embraced North Africa, the Middle East, Eastern Europe, Asia
and the Pacific, where HIV seems not to have been present at all until the
mid-1980s and where the illness then developed principally through
contacts with those already infected in the other two areas mentioned. By
2019 the WHO was reporting that the tally of global mortality since the
start of the epidemic had risen to around 33 million; and that best
estimates of those currently living with HIV amounted to around 38
million, with nearly 70 per cent of their cases being located in sub-
Saharan Africa. Despite the importance of California and New York as
primary foci for the epidemic diffusion of AIDS during the 1980s, it
must be stressed that by the opening decades of the twenty-first century
the disease had become predominantly yet another affliction of the
developing world. Most tragically, it had now ‘returned’ to Africa in an
unprecedentedly virulent way. There its continuing advance served only
to enlarge the potential for further social and political destabilization
across a particularly troubled continent.
The international mobilization not simply of governments but
also of medical science against this pandemic threat was in many
respects impressive. As Mirko Grmek commented, ‘The grandeur of

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modern medicine – its highs – may be displayed in the rapidity with
which some complex problems of AIDS are resolved: its semiotics and
pathology, the nature of the causal agent, its routes of infection and
epidemiologic surveillance.’ However, as he went on to concede, the
progress ‘from understanding to action, from knowledge to power’ has
been far from straightforward. The vital role that had been increasingly
played by immunology in modern battles against disease was never more
clearly evident than at the juncture when scientists were suddenly
outflanked by an infection which radically subverted the workings of the
immune system itself. Even with the impressive developments that have
occurred in molecular medicine over the last two decades or so, no cure
for this particular disease has yet been devised. Nonetheless the more
encouraging news concerns the increasing (though very far from
universal) availability of treatments for HIV infection that use a
combination of anti-retroviral drugs which possess the capability to
delay the onset of full-blown AIDS, often to the extent of restoring near-
normal life expectancy. But even these therapies carried the danger of
prompting reduced concern for the stricter precautions about sexual
activity which, after massive publicly funded campaigns of health
education, had served to slow the advance of the affliction in North
America and Western Europe. As for the regions of the world that were
now in the direst need of rescue from HIV-AIDS, poverty continued to
limit their access to any prophylactic more sophisticated than condoms
or to any significant pharmaceutical palliative. Here millions have
entered the new millennium under the shadow of a ‘plague’ as dark as
any in recorded history.
That same epoch had barely begun when, in 2003, the sudden
eruption of yet another unfamiliar disease, generated by a so-called
coronavirus, produced something close to global panic. This was a lethal
kind of pneumonia, soon labelled ‘SARS’ (Severe Acute Respiratory
Syndrome). It originated in China, where the notoriously secretive

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authorities of the People’s Republic were initially reluctant about alerting
the WHO to the nature and scale of the emerging problem. By the time
that the alarm was properly raised, intercontinental air-travel had already
complicated the situation. In the absence of a vaccine, the first line of
defence was the protective surgical mask, which soon transformed the
street-scene in parts of Beijing and Toronto alike. International financial
markets were badly jolted, and significant damage was done to the global
transportation and tourist industries as well. On this occasion, the WHO
still had just enough time to coordinate an effort capable of averting the
worst of the destructive potential carried by the virus. Even so, the rapid
death-toll of around 800 extended across no fewer than twenty-seven
countries. Scientists swiftly concluded that, as with HIV-AIDS, the
human form of the disease had been unleashed after some kind of cross-
species transmission – with the civet cat, a Chinese gastronomic
delicacy, then becoming the main animal suspect.
Although the international response to SARS in 2003 had proved
impressive, the return of yet another type of coronaviral pneumonia
remained a very real threat – as eventually demonstrated by the Covid-19
pandemic, which erupted in 2020 and which is further discussed in the
Epilogue to this book. Similarly worrying were other viral diseases such
as influenza, whether in forms that were radically unfamiliar or were
significant mutations from earlier appearances. The 2009-10 eruption of
‘swine flu’, for example, proved to be a variant of the H1N1 strain that
had been so deadly in 1918-19. ‘Bird flu’, caused by a virus of the H5N1
subtype, is another peril in waiting. Where people have fallen victim to it
their illness has usually been triggered by contact with infected poultry,
dead or alive. Since a major Asian outbreak in 2003-4 this avian virus
has spread to Europe and Africa, becoming entrenched in many poultry
populations and retaining the potential to mutate into versions highly
transmissible among humans who as yet possess very limited immunity.
Even more generally, early in a millennium that more or less opened

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with the horrors of the falling towers of Manhattan on 11 September
2001, the kind of dangers just mentioned are accentuated by the
possibility of political terrorists being increasingly tempted to exploit
various modes of biological warfare as weapons of mass destruction.

Many of the broader expectations aroused by the specific

achievement of eradicating smallpox have been disappointed not only
because of the AIDS epidemic but also due to the intractability of other
major diseases of a more familiar kind. One of these was cancer. In the
West ‘the Big C’ was the affliction that aroused the most generalized
anxieties during the second half of the twentieth century, at least until the
threat from HIV produced a surge of rival fears. In contrast to AIDS,
here was a chronic degenerative illness of a non-infective kind which
took its principal toll upon those who had reached middle or old age.
Though known since ancient times, cancer was something which most of
those living in previous eras had simply not survived long enough to
face. Thus this disease could be viewed, paradoxically, as witness to the
generally improved longevity registered within Western societies. No
less important, however, is the fact that by the early twenty-first century
more than half of all new cases were occurring in developing countries.
The affliction is, strictly, not a single disease at all. Rather, the
term ‘cancer’ has come to cover a cluster of disorders, numbering more
than a hundred according to the tally kept by the WHO. The overall
linking feature is a change in the nature of cells, so that they escape from
the processes which normally control their division. The consequent
unchecked multiplication of cells leads most typically to the formation of
tumours. Sometimes, through the process known as metastasis, such
‘malignant’ cells spread elsewhere in the body and set up secondary
lesions as well. Areas most vulnerable to attack include the stomach,
lungs, breast, cervix, colon, rectum, prostate, and liver.

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 Despite long years of major investment in research, no unifying
explanation of the causes behind these cancerous processes – let alone
any comprehensive approach to cure – has yet been achieved. Even so, it
is now generally recognized that genetic predisposition or mutation plays
an important part in shaping the incidence of at least some cancers, while
other forms have dietary, environmental or other exogenous factors as
their more likely triggers. As early as 1755, the London surgeon
Percivall Pott had already described a cancer of the male genitals which
seemed to be confined to chimney sweeps and other workers whose
clothing was persistently contaminated with sooty tars. Since then the list
of chemicals known to be carcinogenic has vastly grown. During the
1920s questions began to be raised in Germany about possible linkage
between smoking and cancer of the lung in particular. By the early 1960s
both the Royal College of Surgeons in London and the Advisory
Committee of the US Surgeon-General were expressing their
unequivocal confirmation of such a connection. Thereafter the medical
profession found itself engaged in a long (and still unfinished) struggle
against a rich and powerful lobby of tobacco industrialists prone to self-
delusive denial of increasingly damning evidence, as well as against the
reluctance of governments to forgo the immense tax revenues generated
by addictive smoking. As for nuclear technology, its development over
the last fifty years or so has also prompted growing and justifiable fears
about the carcinogenic effects of atomic radiation. Similar concerns have
surrounded other environmental issues, such as the connection between a
rising incidence of skin cancer and changes in the intensity of solar
ultraviolet light.
Towards the end of the 1990s it was already being estimated that
some kind of cancerous invasion would affect at least one-third of those
then living within the advanced economies. More recently the WHO’s
World Cancer Report for 2018 has suggested that, on the broader global
scale, some 18 million people a year were now being newly diagnosed

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with the disease. Such statistics appear all the more alarming in so far as
the most commonly available surgical, chemotherapeutic, and
radiotherapeutic responses to at least some of the major cancers (for
example, those attacking the lungs and the pancreas) have not yet
produced any really radical transformation in survival rates. However,
more encouragingly, at the end of 2013 the prestigious journal Science
had recorded as ‘breakthrough of the year’ a new potentiality for
deploying immunotherapy as the basis for more effective treatment of a
considerable range of cancers. Here, it argued, was a ‘paradigm shift’
stemming from research done principally in the USA which – over the
longer term at any rate – might offer some reliable prospect of
mobilizing even against tumour cells those same defence systems that
generally serve to protect us from viral and microbial invasion.
It may well be correct to claim that in the course of the twentieth
century cancer replaced consumption as what David Cantor has called
‘the dominant disease metaphor’ of the age. However, as we observed
towards the end of’ Chapter Seven, even tuberculosis itself has proved
much more difficult to eradicate than medical scientists anticipated a
couple of generations ago. It remains a far from defeated force,
stubbornly persisting as a widespread problem that affects especially but
not exclusively the populations of the developing world where it takes a
particularly high toll among young adults. Further examples of the
continuing intractability of certain major diseases are the cholera whose
latest manifestations we noted in Chapter Six, and also the malaria
whose role in the nineteenth-century exploration of Africa we surveyed
in Chapter Eight. By the 1950s and 1960s, the latter affliction had
become the object of an international eradication programme,
comparable in aim to that which eventually conquered smallpox. Sadly
the campaign against malaria met with only limited success. Although it
has been largely eliminated from North America, Europe and most of the
former USSR, there remains a large band of tropical and subtropical

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areas in Africa, Asia and Latin America where this illness persists as a
major hazard. The increasing resistance shown by mosquitoes against
insecticides has been matched by that of the malarial parasites
themselves when exposed to drugs like chloroquine, and meanwhile the
expansion of international air-travel has also threatened to facilitate
distribution of the infected insects. Though the eradication effort has
certainly reduced mortality in recent years, the WHO’s estimates for
2018 suggested that there was still an annual death-toll of some 400,000,
that there existed over 200 million cases of the disease, and that nearly
half of the global population stood at some degree of potential risk.
Malaria also suggests a linkage between disease and the
unprecedentedly rapid changes which have recently been affecting the
world’s ecosystem. The most disturbing of these is man-made global
warming. Despite some obdurate campaigns of denial from certain
quarters, this is now endorsed as a perilous reality by an overwhelming
majority of scientific experts. As with the tsetse fly in relation to
sleeping sickness, it would take only a couple of degrees of further rise
in average temperatures to produce a very dramatic enlargement of the
areas which the anopheline mosquito might succeed in colonizing or
recolonizing. Diseases such as dengue fever and various diarrhoeal
infections are similarly sensitive to current climatic shifts, while enlarged
patterns of drought and malnutrition are also readily predictable.
Prominent among other environmental concerns has been the fouling of
air, soil, and water, particularly by industrial chemicals. Widespread
emissions of the CFC refrigerant have certainly contributed to that
depletion of the ozone layer in the upper atmosphere which has led to
less effective filtering of ultraviolet radiation and thus to greater risk of
skin cancers. Perhaps most dramatic of all have been the disasters
affecting nuclear reactors: the explosion that wrecked the Ukrainian
plant at Chernobyl in 1986, and the destruction of the cooling systems at
Fukushima when the Japanese coast was swamped by a tsunami in 2011.

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Nor has the international community yet managed to resolve a related
issue with even longer-term implications – that of how and where to
store radioactive waste so as to keep it safe for the necessary thousands
of years ahead. Such considerations serve to underline the globalized
perils to health which have become inseparable from mankind’s
harnessing of atomic power, even in avowedly peaceful forms.
Current debates on the poisoning of our planet, and thus of
ourselves, cannot be detached from the extra strain imposed upon the
global environment by the forces of population growth. Here the very
success of modern medicine – for example, in deploying antibiotic and
immunological techniques against the scourge of infant and child
mortality – eventually proved to be a source of problems as well.
Between 1750 and 1900 the global population grew, roughly, from 1
billion to 1.6 billion. By 1950 the figure had climbed to 2.6 billion, and
thereafter the numbers rose at a pace unparalleled in any previous era.
The United Nations Organization records that the 6-billion mark was
passed during 1999; and its best recent estimate indicates 7.8 billion for
2020, with a projection of 9.7 billion for 2050. Thus the history of the
last hundred years or so suggests that humanity is already in the midst of
a process of quantitative transformation huge enough to carry vast
qualitative implications as well. These are perhaps most evident from the
prediction that at least 90 per cent of the continuing demographic
increase will be concentrated in the poorer regions of the globe. But what
might prove to be the significance of the fact that many of these areas are
also the ones where, in the early twenty-first century, HIV and other
major diseases held strongest sway? Even now, the work of Malthus and
Darwin still serves to remind us of the possibility that massive mortality
– whether produced by AIDS, or indeed by some other epidemic force
similarly arising unforeseen amid the environmental and social
upheavals of the contemporary world – might slow the demographic
surge altogether sooner than present projections suggest.

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 As a result of its continuing battle against disease, modern
medicine – social, therapeutic, and preventative – has offered much of
the human race a prospect of longer and healthier life. Yet, in promoting
the expansion of global population, it has generated difficulties which
may be insoluble. Similarly the advance of technology, while spreading
to many societies the kind of comforts and amenities that were virtually
unimaginable even as little as a century ago, has also brought some
problems which may defy solution. With respect to material things, the
combination of these two processes has caused mankind to run ahead of
its own state of civilization. The primitive is not buried deeply enough
for safety. This may be why humans continue to breed unchecked, to foul
their surroundings, to exhaust their resources, and to take inadequate
thought for their future. Governments tell us that ‘we must come to terms
with our environment’, but this is begging the question. Rather, mankind
must first come to terms with itself. If we do not learn self-discipline and
if we fail to tackle the difficulties which we ourselves have largely
created, then our problems seem destined to be resolved, at least
temporarily, in an altogether harsher way. The solution will then surely
lie in the hands of one or all of humanity’s age-old enemies, Famine,
Pestilence, and War – those Horsemen of the Apocalypse who also bring
with them Death upon his Pale Steed.

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 EPILOGUE
THE COVID-19 PANDEMIC

The previous chapter surveyed some of the major dangers that disease
was still presenting to humanity in the opening decades of the twenty-
first century. Early in 2020 one of the potential perils, that of a hitherto
unknown infection, was identified as developing very abruptly into a
widespread mortal threat. On 30 January the World Health Organization
(WHO) announced a public health emergency of international concern,
and five weeks later declared the disease to have reached pandemic
scope. Designated as Covid-19, it was beginning to emerge as the most
rapidly spreading outbreak of severe illness since the ‘Spanish flu’ of
1918-19. By early November official figures for its accelerating advance
suggested that it was now present in nearly all the countries of the world;
that more than 50 million cases had been globally recorded; and that the
death-toll had risen to 1.25 million. Epidemiologists were also united in
predicting that, unless and until a worldwide programme of effective
vaccination might be developed, a severe worsening of the pandemic
was almost inevitable.
The WHO attributed Covid-19 to a hitherto unknown strain of the
same family of coronaviruses that had been responsible in recent years
for two other forms of previously unrecorded disease. All three varieties
were distinct from influenza, though they did resemble it especially
through a shared tendency to culminate in pneumonia. The first of the
new infections, mentioned in the preceding chapter, was the Severe
Acute Respiratory Syndrome (SARS) that emerged from China in 2003.
The second was Middle East Respiratory Syndrome (MERS), which
originated from Saudi Arabia in 2012 and produced a second cluster of

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cases in South Korea from 2015 onward. Like SARS, this seemed to be
the product of animal-to-human transfer and, though popularly
associated with camels, its more probable source was bats. Both these
respiratory disorders were highly lethal to the victims who did contract
them. However, the speed and scale of spread was limited by the fact that
transmission from person to person required particularly close contact.
Thus, even in the absence of any specific counter-vaccine, it became
possible to bring SARS and MERS under a good measure of control
while fatalities from each of them could still be counted in hundreds
rather than many thousands. This was, in itself, good news: but such an
outcome certainly nurtured some complacency about the scale of risk
still presented by viruses of this kind.
Covid-19 presented an altogether more formidable challenge. This
disease stemmed from a coronavirus that was soon formally labelled as
SARS-CoV-2. The epicentre of origin was Wuhan, a densely populated
city of some 11 million people in the Hubei province of central-southern
China where it served as a major hub for domestic and international
travel. Here the live-animal and seafood marketing that featured as a
major everyday business appeared to be the most likely source for the
initial cross-species transfer. It soon became clear that signs of the
disease had first emerged early in December 2019, and that the
government of the People’s Republic had been somewhat slow (though
perhaps not as badly so as in its 2003 response to SARS) about
publicizing this as an issue of public health. It was only on 31 December
that a state website first drew attention to ‘pneumonia of unknown
cause’. On 1 January 2020 a Wuhan ophthalmologist, Li Wenliang, was
officially reprimanded for having reported to students his own viral
analysis that appeared to indicate a return of SARS. Ten days later other
Chinese scientists confirmed that a coronavirus was indeed the causative
agent, albeit in a previously unknown form – one from which Li himself
would soon die, and so become widely recognized as a martyr not simply

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to the infection but also to an excessively secretive state bureaucracy.
During the fourth week of January the Chinese government at last
imposed full-scale ‘lockdown’ on Wuhan and its wider region. However,
by then the virus had escaped, with new cases arising not only in Beijing
and Shanghai but also abroad in the USA, Japan, and South Korea. At
the end of the month came similar confirmation of the disease’s first
appearance in parts of western Europe, including Spain, Italy, France,
and the UK.
As the year went on some of the main features of Covid-19
emerged more clearly. Whatever its animal source, the new CoV-2
coronavirus was found to be passing between humans much more easily
than the types involved in the earlier SARS and MERS outbreaks. The
principal mode of transmission appeared to be exhaled droplets, which
entered through the mucous membranes of eyes, nose, and mouth either
directly or after lingering on exposed surfaces. Inhalation of suspended
aerosol particles of the virus was also likely to play a role, especially in
confined spaces. Unlike the earlier SARS and MERS, Covid-19 often
produced only mild to moderate symptoms. However, some studies
suggested that an even larger number of potential carriers were
remaining altogether asymptomatic – a feature that plainly promoted
‘silent transmission’ and complicated the tracing and isolation of
contacts. The most common symptoms were a dry painful cough and a
high fever, with loss of taste or smell being also sometimes indicative.
Where infection did become severe the sufferers encountered breathing
difficulties and then pneumonia plus kidney or more general organ
failure. Initial evidence from patients who had managed to survive a bout
of the virus suggested that many of them would then go on to suffer from
‘long Covid’ – not only persistent lung damage but also continuing
severe fatigue as well as chronic coronary, neurological, and other major
weaknesses. Six months or so into the pandemic, some cases of

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reinfection (albeit relatively small in number as yet, but very relevant to
debates on limits of immunity) also began to be recorded.
The pattern of incidence showed men proving to be rather more
vulnerable than women. Equally clear was a strong correlation between
serious attacks and advancing age, with the over-70s generally at greatest
risk. While children under 10 or so seemed to have the best resistance,
Covid-19 certainly presented a higher threat to all other age-groups and
especially to people falling into further specific categories: for example,
those who had received certain kinds of transplant or were undergoing
some forms of cancer treatment, those who were obese, and those who
were already suffering badly from a severe respiratory condition or
receiving significant doses of immuno-suppressant medication. More
speculative discussions focused on the extent to which ethnicity might be
disentangled from socio-economic circumstances as a potentially
independent contributory factor towards explaining varying degrees of
susceptibility. For example, in Britain there was a disproportionate
impact on black, Asian, and other ethnic minorities, as was also the case
with African Americans and Latinos in the USA.
Following the eventual declaration of pandemic in early March,
the disease-tracking centre at Johns Hopkins University in Baltimore
provided the most helpful daily bulletins on the overall global advance of
Covid-19. However, the reliability of the ‘official’ and other publicly
available statistics being processed there differed greatly from country to
country. The most consistent feature was substantial underestimation
both of cases and of deaths – due partly to the intrinsic difficulties that
all governments (especially those in developing countries) faced when
calculating accurate running tallies but also, in some instances, to active
concealment of the scale of mismanaged response to the disease. In
general, the published figures were better at indicating relevant mortality
within hospitals than they were in adding deaths that had been directly or
indirectly caused by coronavirus in other settings. Similarly, the statistics

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on the overall extent of infection across communities usually reflected
only those cases that officials were prepared to designate as formally
confirmed. Here calculation was further complicated by differential
scales of testing: best estimates available in September suggested that
high-income countries were generally processing tests at a rate per
million of population that was at least twenty times greater than that
operative among lowest-income states.
Initially it was China that headed the tally of caseload, but from
April onwards the figure officially announced by Beijing remained
frozen at around 85,000 (with 4,634 deaths), even though there was
evidence of further but unquantified outbreaks. By mid-March the WHO
had already identified the major epicentres of a broader international
diffusion as being parts of Western Europe and the USA. In both of these
contexts the sudden impact proved all the more startling precisely
because here were regions that had become accustomed to relative
insulation from the worst of the killer diseases still prevalent across
much of the wider world. Within Europe the largest mortality was borne
early on by Italy (especially its northern provinces), Spain, and France;
but from early May onwards it became the UK that was recording an
even greater cumulative death-toll. As for the USA, its losses were
already far higher than for any of these European countries. In mid-May
the WHO then deemed the Americas to be the new epicentre of major
spread, as the incidence of cases also began to rise rapidly across central
and southern parts of the continent, most notably in Brazil, Mexico,
Peru, Colombia, Argentina, and Chile. Nine months or so after the
WHO’s original declaration of global emergency other major countries
where Covid-19 had greatly advanced included Russia and Turkey; Iraq,
Iran and Saudi Arabia; and – now continuing with particular rapidity –
India and Indonesia as well.
By then South Africa too was in a crisis of over-strained
response, at one end of a continent that seemed unlikely to escape the

287
full force of the virus for much longer. The full roster of global statistics
was certainly showing that the disease had established some presence in
all the world’s poorest countries where, as earlier parts of this book have
shown, endemic disease was already a longstanding problem. Thus a
surge in Covid-19 cases from Africa and Asia, as well as South America,
was now to be expected. Across those regions the new disease, whose
first tide of infection had threatened to overwhelm more advanced
systems of public health protection, posed an even graver threat – one
that also had implications for the extent of any resurgences occurring
within those richer countries which had borne the initial brunt of the
pandemic.
While the worldwide scale of mortality linked to the 2020
outbreak remained as yet dwarfed by the figures for the ‘Spanish flu’ or
indeed for HIV-AIDS, massive multiplication of the toll from Covid-19
still loomed as an imminent threat. The Table as presented below, based
on the Johns Hopkins figures current in early November, indicates the
reported scale of global incidence and mortality at that stage as well as
statistics for the twenty countries then recording the largest cumulative
number of infections. For reasons previously mentioned the data tend
towards significant underestimation and they are at best suggestive rather
than definitive. Particularly striking are the differing proportions
reported as between the quantities of cases and of deaths (Columns 1 and
3), as well as the range of highly variable figures covering mortality in
proportion to overall population (Column 4). Further contrasts, relating
to growth rates in caseload during the previous 25 days, are similarly
evident (Column 2); and here the increases also reflect in varying
degrees some enlargement of these states’ infection-testing activity.
The significance of any such statistical snapshot is clearly limited
by a realization that various countries were at different stages of their
trajectory through the crisis, under circumstances where it was often
difficult to differentiate between the prolongation of a first wave of

288
Covid-19 and the onset of a second. Moreover, with the pandemic still in
progress and with a typical time-lapse of two to three weeks between
infection and death, the highly variable ratios between quantities of cases
and of mortality could not be easily explained by any one factor in
isolation. However, there were grounds for believing that during the first
three or four months of the pandemic the relatively limited proportion of
deaths evident in Germany and South Korea, for example, had been
linked to previously well-prepared schemes of diagnostic and
immunological testing together with prompt contact tracing.
Among the less impressive examples of governmental responses
were those made by the UK and the USA. Despite Britain recording its
first coronavirus death on 5 March, Boris Johnson’s administration had
begun by avoiding the stricter border controls and other major limitations
on movement that were already being imposed in much of Europe, and
most swiftly in Italy and Spain. Although it was wise for the UK
government to prescribe rigorous handwashing as an essential first line
of defence, it was foolish not to have resorted speedily to even tougher
protective measures. In the early stages the official approach taken
ostensibly with some expert backing was that, while the most vulnerable
must isolate themselves at home, a majority of the population should be
exposed to what was expected to be a predominantly modest infection –
the aim being to achieve a protective level of ‘herd immunity’. However,
on 23 March (especially after a dramatic acceleration of Covid-19 across
much of northern Italy) the UK government was persuaded into a sudden
and radical change of course by a new projection from a research group
at Imperial College, London. Their modelling indicated that, without the
more extensive policy of enforced isolation and physical distancing that
was already having some success in other countries, the death rate in
Britain would be on a trajectory heading towards catastrophe. Even after
the resulting changes of policy the outcome (which included a period of
intensive care for Johnson himself) was still bad enough to leave the UK

289
in a particularly parlous position. The slowness of initial response –
combined with confused public messaging, inadequate testing and
tracing arrangements, shortages of protective and other equipment, and a
policy of reducing pressure on hospitals by discharging many of their
untested patients into other parts of the care system – meant that the UK
would soon be suffering the highest mortality toll in Europe. Moreover,
by early November, its total fatalities remained the fifth highest in the
world.

290
 COVID-19: TABLE OF CASES AND DEATHS
Cumulative Figures at 9 November 2020
Col.1 Total number of Recorded Cases
Col.2 Percentage Increase in Recorded Cases over the previous 25 days
Col.3 Total number of Recorded Deaths
Col.4 Recorded Deaths per Million of Population
Column 1 Column 2

WORLD 50,523,502 32%

USA 10,066,916 27%

India 8,507,754 18%
Brazil 5,664,115 11%
Russia 1,796,132 34%
France 1,787,324 136%
Spain 1,328,832 48%
Argentina 1,242,169 35%
UK 1,192,013 88%
Colombia 1,143,887 24%
Mexico 967,825 17%
Italy 935,104 156%
Peru 922,333 8%
South 737,278 6%
Africa
Iran 692,949 36%
Germany 672,507 101%
Poland 568,138 303%
Chile 521,558 8%
Iraq 498,549 22%
Belgium 494,168 199%
Ukraine 469,018 17%

[Based on Johns Hopkins University Tracking Data]

291
 In Washington the handling of the crisis was similarly dismal.
There medical experts had to confront in Donald Trump a leader who
showed stubborn resistance to proper recognition of the dire realities.
Back in 2018 the President had closed down the White House pandemic
response team that his predecessor had maintained. In mid-February
2020 Trump then repeatedly misled his nation with unfounded assertions
about the efficacy of untested therapies and with promises that, come the
warmer spring weather, the threat would ‘miraculously go away’ almost
as a form of seasonal flu. Even when events soon disproved such
nonsense there was continuing presidential bluster about early and
widespread restoration of ‘business as usual’. All this was accompanied
by attacks on the WHO’s allegedly over-friendly treatment of China.
These culminated in Trump’s disgraceful withdrawal of US membership
at a juncture when that organization, for all its faults, had never been
more needed as an agent of international cooperation. There was also
bitter wrangling over policy and authority as between the White House
and many of the Governors bent upon promoting wiser responses to
Covid-19 within various states of the Federal Union. By late April the
US death-toll already exceeded that suffered in the Vietnam War. During
the early months of the pandemic the heaviest price for Trump’s over-
optimistic misjudgments had fallen on New York State. But the main
areas of accelerating infection had then shifted to a swathe of southern
states running from the Atlantic coast across to the Pacific one, and then
increasingly to the Midwest as well. Early in October, at the final stage
of his eventually unsuccessful campaign for presidential re-election,
Trump himself (having been recklessly casual over matters of face-
covering and ‘social distancing’, not least amongst his own White House
staff) needed a short spell of hospital treatment after testing positive for
the virus. Before that, one of his most fervent admirers, President Jair
Bolsonaro of Brazil, had also been infected. Even so, the latter had
remained similarly cavalier in his refusal fully to confront the general

292
danger, to the point where his own country’s death-toll was exceeded
only by that of the USA itself.
As the pandemic progressed, governments were endeavouring
rapidly to enlarge the capacity of their hospital systems; to increase
supplies of oxygen, ventilators, and other respiratory equipment; and to
provide adequate protective clothing for doctors, nurses, and others in
the front line of care. Of all the challenges the most fundamental was
identification – and then mass production, global distribution, and
extensive take-up – of a safe and effective vaccine to counter the disease.
Prompt sequencing of Covid-19’s genetic code by Chinese scientists had
certainly helped to launch a huge international effort towards this
preventive goal. The venture was partly co-operative, but also showed
many signs of a competitive race marked by divisive geopolitical,
nationalistic, and capitalistic rivalries. These raised the possibility of an
inadequately tested and eventually ineffective or damaging product
getting prematurely into mass circulation, thus harming the credibility of
any later and better-developed versions. By mid-2020 the WHO was
tracking the accelerated development of over 300 candidate vaccines.
They reflected a range of methods: for example, using existing viruses to
introduce a harmless section of coronavirus that might stimulate an
immune response, or employing messenger RNA to trigger the
production of antibodies. It remained uncertain as to how many, if any,
of these candidate schemes would prove viable and according to what
timescale. Nor was there yet an adequate picture of the depth and
duration of any immunity that might be generated either by preventive
vaccination or by post-infection survival.
Meanwhile there had been some progress in assessing the
contribution that existing drugs might make towards mitigating the
impact of the disease upon those who had become infected. Most notable
here was the realization that dexamethasone – an immuno-suppressant
steroid very widely and cheaply available – could improve the survival

293
rates of those already undergoing the most intensive care. Effective
response to Covid-19 also involved much wider testing, to detect not
only the direct presence of the virus but also the development of
antibodies within those who had recovered from infection. Here other
relevant measures included contact tracing and the imposition of ‘social
distancing’, even to the point of full isolation in many instances.
Within a few weeks of Covid-19’s eruption an extensive social
transformation was already afoot – progressing thereafter with a speed
and geographical scope hitherto unparalleled even in wartime. The
distinguished Canadian historian Margaret MacMillan was soon arguing
that the year 2020 should be seen as constituting, like the great
landmarks of 1789 and 1917, a juncture ‘when the river of history
changes direction’. Now the disease was plunging country after country
into a revolution in patterns of everyday living and even of political
control. Governments attempted to break the chain of transmission by
imposing some mix of quarantine, curfews or other bans on movement,
together with varying degrees of tighter official surveillance and police
enforcement. Among the most dramatic features of the cultural upheaval
associated with lockdown were the almost total cancellation of
international passenger travel by air as well as restrictions on much other
public transport, the closure of schools and churches, the banning of
mass gatherings for sport or other entertainment, the shutting of
‘hospitality’ enterprises and non-essential retail outlets, the shift of much
office work into more dispersed home-based settings, the surge in
‘Zooming’ and similar electro-visual means of distanced social and
business interaction, and the increasing usage of face-coverings. Only
time could tell whether, from state to state, adequate levels of public
compliance would be maintained either by protective self-discipline or
more crudely by force; and whether such counter-measures might
eventually take an even greater toll on health than the coronavirus itself

294
(for example, by escalating mental illness or causing postponement of
many regular medical procedures).
The controls were such that governments soon came under
pressure to heed the growing ‘response fatigue’ of their citizens and to
publicize phased ‘exit strategies’ from these new constraints. Here the
needs of public health had to be weighed particularly against those of
economic wellbeing. For example, in April 2020 the World Trade
Organization’s broad projections for shrinkage of commerce through the
rest of the year had ranged from 13 to 32 per cent: threatening to exceed
at the first of these levels the impact of the 2008-9 banking crisis, and to
match at the second the kind of falls experienced in the Great Depression
of 1929-32. In this domain of economic vulnerability as well as in that of
strained medical resources it would be those countries already at the
weaker end of the global scale that now had most to fear. Even within
more prosperous societies the harshest consequences, especially relating
to huge rises in unemployment, were similarly bound to fall upon those
citizens who were already most disadvantaged. Wherever possible the
amount of governmental spending and borrowing was significantly
enlarged, not simply to meet the extra healthcare costs but also to fund
policies aimed at mitigating the extent of job losses and the huge strain
placed by the pandemic upon many other aspects of socio-economic
welfare.
Across the middle months of 2020 it became clear at the complex
interface between physical and economic health that managing any
sustained release from lockdown was, if anything, even more difficult
than imposing it, and that any expectations of full return to social
‘normality’ were unsustainable. For instance, those countries of Western
Europe that had suffered worst in the opening months of the pandemic
but had now passed a first major peak of infection were also among the
earliest to experience ‘spikes’ of viral resurgence. By autumn these were
especially sharp in France, Spain, and the UK, where nothing less than a

295
second wave appeared to be developing. The response across much of
Europe was to re-impose various forms of lockdown or other restriction
on a regional or even national basis, as well as to re-tighten the border
controls and the quarantine requirements that would affect many
international travellers. Moreover, as the whole northern hemisphere
entered its regular flu season there remained the possibility of needing to
enforce even tougher social controls aimed at avoiding a dual pneumonic
catastrophe over the coming winter.
During the course of 2020 the pandemic had already served to
underline many of the issues discussed in the previous chapter with
regard to ongoing problems of human survival in the face of major
disease. On one side stand the many modern advances of medical science
and of international co-operation in matters of health monitoring. On the
other, we face the more negative aspects of the globalization that has
been so rapidly accelerating in recent decades. Bearing such threatening
features in mind, many historians were becoming increasingly attracted
to the argument that they should be chronicling a radically new epoch of
global development, deserving to be known as the Anthropocene. Here
was a label designed to express the unprecedented extent to which
human behaviour had now become the most powerful source of
potentially irreversible damage to the environmental and ecological
systems essential to the survival of our own species.
Although the coronavirus driving Covid-19 was not in itself man-
made, the conditions that facilitated its transmission from animal sources
and then speeded its infectious diffusion from person to person were
largely human creations. So, even if the current pandemic were
eventually to develop into something just as deadly as the global
influenza of 1918-19, the outbreak that began in 2020 would be unlikely
to constitute the last such crisis, whether this might be triggered by a
coronavirus different from that producing Covid-19 or by some other
agent. As we have seen elsewhere in this book, such threats from disease

296
have been a constant, and sometimes decisive, influence on the course of
human history. However, our potential exposure to them can only deepen
while we maintain a form of over-populated civilization where global
warming remains inadequately constrained; where pressures on food
production and increasingly disruptive penetration into wild habitats
render animal-to-human transmissions of infection more frequent; where
people crowd ever more densely into mega-cities; and where modern
international travel (in the form prevailing under more ‘normal’
circumstances) allows fewer and fewer communities to enjoy the
protection of relative isolation. At the beginning of the third decade of
the twenty-first century, and amidst the wider challenges of the
Anthropocene epoch, the spread of the Covid-19 pandemic had already
served to demonstrate that the four Horsemen of the Apocalypse who
haunt our histories were continuing to circle us, but now on swifter
steeds.

297
298
 FURTHER READING

GENERAL

Ackernecht, E.H., A Short History of Medicine (Baltimore, MD: Johns

Hopkins University Press, 1968)
– – –, History and Geography of the Most Important Diseases (New
York, NY: Hafner, 1965)
Bett, W.R. (ed.), The History and Conquest of Common Diseases
(Norman, OK: University of Oklahoma Press, 1954)
Burnham, J.C., What is Medical History? (Cambridge: Polity, 2004)
Bynum, W.F. & Porter, R. (eds), Companion Encyclopedia of the History
of Medicine (2 vols, London: Routledge, 1993)
Bynum, W., The History of Medicine: A Very Short Introduction
(Oxford: Oxford University Press, 2008)
Cartwright, F.F., A Social History of Medicine (London: Longman, 1977)
Crawford, D.H., Deadly Companions: How Microbes Shaped our
History (Oxford: Oxford University Press, 2007)
Duffin, G. (ed.), Clio in the Clinic: History in Medical Practice
(Toronto: University of Toronto Press, 2005)
Friedman, M. & G.W., Medicine’s 10 Greatest Discoveries (New Haven,
CT: Yale University Press, 1998)
Gale, A.H., Epidemic Diseases (Harmondsworth: Penguin, 1959)
Grob, G.N., The Deadly Truth: A History of Disease in America
(Cambridge, MA: Harvard University Press, 2002)
Harrison, M., Disease and the Modern World: 1500 to the Present Day
(Cambridge: Polity, 2004)

299
Hays, J.N., The Burdens of Disease: Epidemics and Human Response in
Western History (New Brunswick, NJ: Rutgers University Press, 1998)
Henschen, F., The History of Diseases (London: Longman, 1966)
Hudson, R.P., Disease and Its Control: The Shaping of Modern Thought
(Westport, CT: Greenwood, 1983)
Huisman, F. & Warner, J.H. (eds), Locating Medical History: The Stories
and Their Meanings (Baltimore, MD: Johns Hopkins University Press,
2004)
Jackson, M. (ed.), The Oxford Handbook of the History of Medicine
(Oxford: Oxford University Press, 2011)
Jackson, M., The History of Medicine: A Beginner’s Guide (Oxford:
Oxford University Press, 2014)
Kiple, K.F. (ed.), The Cambridge World History of Human Diseases
(Cambridge: Cambridge University Press, 1993)
– – –, The Cambridge Historical Dictionary of Disease (Cambridge:
Cambridge University Press, 2003)
Lindemann, M., Medicine and Society in Early Modern Europe
(Cambridge: Cambridge University Press, 2010)
McGrew, R.E., Encyclopedia of Medical History (New York, NY:
McGraw-Hill, 1985)
McNeill, W.H., Plagues and Peoples (Harmondsworth: Penguin, 1979)
Morton, L.T., A Medical Bibliography (Garrison and Morton): An
Annotated Checklist of Texts Illustrating the History of Medicine (4th
edn, Aldershot: Gower, 1983)
Porter, R., The Greatest Benefit to Mankind: A Medical History of
Humanity from Antiquity to the Present (London: Harper Collins, 1997)
– – – (ed.), The Cambridge Illustrated History of Medicine (Cambridge:
Cambridge University Press, 1996)
– – –, Blood and Guts: A Short History of Medicine (London: Penguin,
2003)

300
Ranger, T. & Slack P. (eds), Epidemics and Ideas: Essays on the
Historical Perception of Pestilence (Cambridge: Cambridge University
Press, 1992)
Rotberg, R.I. (ed.), Health and Disease in Human History (Cambridge,
MA: MIT Press, 2000)
Scott Stevenson, R., Famous Illnesses in History (London: Eyre &
Spottiswoode, 1962)
Shrewsbury, J.E.D., The Plague of the Philistines and other Medical-
Historical Essays (London: Gollancz, 1964)
Sigerist, H.E., Civilization and Disease (Ithaca, NY: Cornell University
Press, 1943)
Singer, C. & Underwood E.A., A Short History of Medicine (2nd edn,
Oxford: Oxford University Press, 1962)
Snowden, F.M., Epidemics and Society: From th Black Death to the
Present (New Haven, CT: Yale University Press, 2019)
Sournia, J-C., The Illustrated History of Medicine (London: Starke,
1992)
Waddington, K., An Introduction to the Social History of Medicine:
Europe since 1500 (Basingstoke: Macmillan, 2011)
Walton, J., Barondess, J.A., & Lock, S. (eds), The Oxford Medical
Companion (Oxford: Oxford University Press, 1994)

DISEASE IN THE ANCIENT WORLD

Chadwick, H., The Early Church (Harmondsworth: Penguin 1967)

Grmek, M.D., Diseases in the Ancient Greek World (Baltimore, MD:
Johns Hopkins University Press, 1989)
Harper, K., The Fate of Rome: Climate, Disease, and the End of an
Empire (Princeton, NJ: Princeton University Press, 2017)
Hornblower, S. & Spawforth, A. (eds), The Oxford Classical Dictionary
(3rd edn, Oxford: Oxford University Press, 1996)

301
Jackson, J., Doctors and Diseases in the Roman Empire (London: British
Museum, 1988)
Jones, A.H.M., The Later Roman Empire (3 vols, Oxford: Clarendon
Press, 1964)
Little, L.K. (ed.), Plague and the End of Antiquity: The Pandemic of
541-750 (Cambridge: Cambridge University Press, 2008)
Lloyd, G.E.R. (ed.), Hippocratic Writings (Harmondsworth: Penguin,
1978)
Nutton, V. (ed.), Galen: Problems and Prospects (London: Wellcome
Institute, 1981)
Phillips, E.D., Greek Medicine (London: Thames & Hudson, 1973)
Procopius, The Persian War (Loeb Classical Library, London:
Heinemann, 1914)
Scarborough, J., Roman Medicine (Ithaca, NY: Cornell University Press,
1969)
Schouten, J., The Rod and Serpent of Asklepios (Amsterdam: Elsevier,
1967)
Sherwin-White, S., Ancient Cos (Göttingen: Vandenhoeck & Ruprecht,
1978)
Smith, W.D., The Hippocratic Tradition (Ithaca, NY: Cornell University
Press, 1979)
Stathakopoulos, D.C., Famine and Pestilence in the Late Roman and
Early Byzantine Empire (Aldershot: Ashgate, 2004)
Temkin, O., Hippocrates in a World of Pagans and Christians
(Baltimore, MD: Johns Hopkins University Press, 1991)
Thucydides, History of the Peloponnesian War: Book Two
(Harmondsworth: Penguin, 1954)

THE BLACK DEATH

Aberth, J., The Black Death: The Great Mortality, 1348-1350 (London:
Palgrave Macmillan, 2005)

302
Bell, W.G., The Great Plague in London in 1665 (London: John Lane,
1924)
Cohn, N., The Pursuit of the Millennium (London: Seeker & Warburg,
1957)
Creighton, C., A History of Epidemics in Britain (2 vols, Cambridge:
Cambridge University Press, 1891)
Dols, M.W., The Black Death in the Middle East (Princeton, NJ:
Princeton University Press, 1977)
Gottfried, R.S., The Black Death: Natural and Human Disaster in
Medieval Europe (New York, NY: Free Press, 1983)
Hatcher, J., Plague, Population and the English Economy, 1348-1530
(London: Macmillan, 1977)
Hirst, L.P., The Conquest of Plague (Oxford: Clarendon Press, 1953)
Langland, W., Piers the Ploughman (Harmondsworth: Penguin, 1959)
Nutton, V. (ed.), Pestilential Complexities: Understanding Medieval
Plague (London: Wellcome Trust Centre, 2008)
Ormrod, W.M. & Lindley, P. (eds), The Black Death in England
(Stamford: Watkins, 1996)
Poliakov, L., The History of Anti-Semitism (Vol. 1, London: Elek, 1966)
Slack, P., The Impact of Plague in Tudor and Stuart England (London:
Longman, 1988)
– – –, Plague: A Very Short Introduction (Oxford: Oxford University
Press, 2012)
Southern, R.W., The Medieval Church (Harmondsworth: Penguin, 1970)
Ziegler, P., The Black Death (Harmondsworth: Penguin, 1970)

THE MYSTERY OF SYPHILIS

Chapman, H.W., The Last Tudor King (London: Cape, 1958)

303
Crosby, A.W., The Columbian Exchange: Biological and Cultural
Consequences of 1492 (Westport, CT: Greenwood, 1972)
Elton, G.R., England under the Tudors (3rd edn, London: Routledge,
1991)
Goodman, H., Contributors to the Knowledge of Syphilis (New York,
NY: Froben, 1944)
Guy, J., Tudor England (Oxford: Oxford University Press, 1988)
Holcombe, R.C., Who Gave the World Syphilis? (New York, NY: Froben,
1937)
Hudson, E.H., Non-Venereal Syphilis (Edinburgh: Livingstone, 1958)
Maclaurin, C., Post Mortem (London: Cape, 1923)
Macnalty, Sir A., Henry VIII: A Difficult Patient (London: C. Johnson,
1952)
Pavlov, A. & Perrie, M., Ivan the Terrible (London: Pearson Longman,
2003)
Quétel, C., History of Syphilis (Oxford: Polity, 1990)
Scarisbrick, J.J., Henry VIII (Harmondsworth: Penguin, 1971)
Uden, G., They Looked Like This (Oxford: Blackwell, 1965)
Yanov, A., The Origins of Autocracy: Ivan the Terrible in Russian
History (Berkeley, CA: University of California Press, 1981)

SMALLPOX, OR THE CONQUEROR CONQUERED

Elliott, J.H., The Old World and the New, 1492-1650 (Cambridge:
Cambridge University Press, 1970)
Fisher, R.B., Edward Jenner, 1749-1823 (London: Deutsch, 1991)
Gruzinski, S., The Conquest of Mexico (Cambridge: Polity, 1993)
Hassig, R., Mexico and the Spanish Conquest (London: Longman, 1994)
Hemming, J., The Conquest of the Incas (London: Macmillan, 1970)
Hopkins, D.R., The Greatest Killer: Smallpox in HIstory (Chicago, IL:
University of Chicago Press, 2002)
Parry, J.H., The Spanish Seaborne Empire (London: Hutchinson, 1970)

304
Prescott, W.H. (intro. by Fernández-Armesto, F.), History of the
Conquest of Mexico (London: Folio Society, 1994)
Rolleston, J.D., The History of the Acute Exanthemata (London:
Heinemann, 1937)
Williams, G., The Angel of Death: The Story of Smallpox (Basingstoke:
Palgrave Macmillan, 2010)
World Health Organization, The Global Eradication of Smallpox
(Geneva: WHO, 1980)

GENERAL NAPOLEON AND GENERAL TYPHUS

Cooter, R., Harrison, M., & Sturdy, S. (eds), Medicine and Modern
Warfare (Amsterdam: Rodopi, 1999)
Ellis, G.J., The Napoleonic Empire (London: Macmillan, 1991)
Emsley, C., The Longman Companion to Napoleonic Europe (London:
Longman, 1993)
Esdaile, C., The Wars of Napoleon (London: Longman, 1995)
Gates, D., The Napoleonic Wars, 1803-1815 (London: Arnold, 1997)
Herold, J.C., The Age of Napoleon (Harmondsworth: Penguin, 1969)
Kemble, J., Napoleon Immortal (London: Murray, 1959)
Markham, F., Napoleon (London: Mentor, 1966)
Prinzig, F., Epidemics Resulting from Wars (Oxford: Clarendon Press,
1916)
Zinsser, H., Rats, Lice, and History (4th edn, London: Routledge, 1942)

CHOLERA AND SANITARY REFORM

Brockington, C.F., A Short History of Public Health (2nd edn, London:

Churchill, 1966)
Durey, M., The Return of the Plague: British Society and the Cholera,
1831-2 (Dublin: Gill & Macmillan, 1979)
Evans, R.J., Death in Hamburg: Society and Politics in the Cholera
Years, 1830- 1910 (Oxford: Oxford University Press, 1987)

305
Finer, S.E., The Life and Times of Sir Edwin Chadwick (London:
Methuen, 1952)
Halliday, S., The Great Stink of London: Sir Joseph Bazalgette and the
Cleansing of the Victorian Metropolis (Stroud: Sutton, 1999)
Hamlin, C., Public Health and Social Justice in the Age of Chadwick
(Cambridge: Cambridge University Press, 1997)
– – –, Cholera: The Biography (Oxford: Oxford University Press, 2009)
Lambert, R., Sir John Simon 1816–1904 and English Social
Administration (London: MacGibbon & Kee, 1963)
Morris, R.J., Cholera, 1832: The Social Response to an Epidemic
(London: Croom Helm, 1976)
Pelling, M., Cholera, Fever and English Medicine, 1825-1865 (Oxford:
Oxford University Press, 1978)
Porter, D. (ed.), The History of Health and the Modern State
(Amsterdam: Rodopi, 1994)
Snow, J., On Cholera (reprint, New York, NY: Hafner, 1965)

GIN, FLU AND TUBERCULOSIS

Bloch, M., The Royal Touch: Sacred Monarchy and Scrofula in England
and France (London: Routledge, 1973)
Breitnauer, J., The Spanish Flu Epidemic and its Influence on History
(Barnsley: Pen and Sword, 2018)
Brown, J., Influenza: The Hundred Year Hunt to Cure the Deadliest
Disease in History (Atria: New York, 2018)
Bryder, L., Below the Magic Mountain: A Social History of Tuberculosis
in Twentieth-Century Britain (Oxford: Clarendon Press, 1988)
Bynum, H., Spitting Blood: The History of Tuberculosis (Oxford: Oxford
University Press, 2012)
Crosby, A.W., Epidemic and Peace 1918 (London: Greenwood, 1976)
Daniel, T.M., Pioneers in Medicine and their Impact on Tuberculosis
(Rochester, NY: Rochester University Press, 2000)

306
Dormandy, T., The White Death: A History of Tuberculosis (London:
Hambledon, 1999)
Dubos, R. & J., The White Plague: Tuberculosis, Man, and Society
(Boston, MA: Little Brown, 1952)
Holt, M.P. (ed.), Alcohol: A Social and Cultural History (Oxford: Berg,
2006)
Mann, T., The Magic Mountain (Penguin: Harmondsworth, 1960)
Philips, H. & Killingray, D. (eds), The Spanish Influenza Pandemic of
1918-19 (London: Routledge, 2003)
Rosenkrantz, B.G. (ed.), From Consumption to Tuberculosis: A
Documentary History (New York, NY: Garland, 1994)
Smith, F.B., The Retreat of Tuberculosis, 1850-1950 (London: Croom
Helm, 1988)
Sournia, J-C., A History of Alcoholism (Oxford: Blackwell, 1990)
Spinney, L., Pale Rider: The Spanish Flu of 1918 and How it Changed
the World (London: Cape, 2018)

MOSQUITOES, FLIES, TRAVEL, AND EXPLORATION

Brock, T.D., Robert Koch: A Life in Medicine and Bacteriology

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QUEEN VICTORIA AND THE FALL OF THE RUSSIAN

MONARCHY

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MOB HYSTERIA AND MASS SUGGESTION

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Índice
PREFACE 4
INTRODUCTION 6
CHAPTER ONE 9
Chapter Two 31
Chapter Three 56
Chapter Four 84
Chapter Five 109
Chapter Six 141
Chapter Seven 164
Chapter Eight 192
Chapter Nine 217
Chapter Ten 246
CHAPTER ELEVEN 265
EPILOGUE 283

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