Authors: Philip Ziegler
That the Black Death, in its original form, was bubonic plague has been commonly accepted for many years. Bubonic plague is endemic to certain remote areas of the world; those which have been identified with reasonable certainty are Uganda, Western Arabia, Kurdistan, Northern India and the Gobi Desert. From time to time it erupts there in the form of minor, localized
epidemics
. Far more rarely it breaks its bounds and surges forth as one of the great pandemics. Unlike influenza, bubonic plague in such a mood moves slowly, taking ten years or more to run its course across the world. When it comes, it comes to stay. The high mortality of its initial impact is followed by a long period in which it lies endemic, a period interspersed with occasional epidemics which gradually die away in frequency and violence. Finally, perhaps several hundred years after the original outbreak, the plague vanishes.
Three such pandemics have been recorded. The first,
beginning
in Arabia, reached Egypt in the year 542. It ravaged and perhaps even fatally weakened the Roman Empire of Justinian and moved on across Europe to England, where it was known as the Plague of Cadwalader’s Time, and Ireland, which it laid waste in 664. The second pandemic was that of the Black Death. One of its parting flourishes was the Great Plague of London in 1665; it seems to have died out in the seventeenth century. Finally came the pandemic which started in 1892 in Yunnan and reached Bombay in 1896. In India alone it is believed to have killed some
six million people. It made a brief and mercifully unsuccessful foray into Suffolk in 1910, finding only a handful of victims. Quite recently it has made itself felt in the Azores and parts of South America. In many parts of the world it has still to run its course.
Though on present evidence it is impossible to be categoric about the origins of the medieval pandemic, recent investigations by the Russian archaeologist Chwolson near Lake Issyk-Koul in the district of Semiriechinsk in Central Asia show that there was an abnormally high death rate in 1338 and 1339. Nestorian memorial stones attribute the deaths to plague.
34
Given the later course of the disease and the fact that this area is in the heart of one of the zones in which bubonic plague lies endemic, Dr
Pollitzer
, probably the leading authority on the subject, has
concluded
that this was almost certainly the cradle of the Black Death.
35
From thence it spread out, eastwards into China, south to India and west to reach the Crimea some eight years later.
In this remote fastness, since recorded history, the bacillus
Pasteurella
pestis
has lingered on, finding its home either in the bloodstream of an animal or the stomach of a flea. The flea
normally
favoured is
Xenopsylla
cheopsis
, familiarly X.
cheopsis
, an insect which, in its turn, chooses ideally to reside in the hair of some rodent. One can only guess which rodent was most readily to be found near Lake Issyk-Koul in 1338 but the experience of later epidemics points to the tarbagan or Manchurian marmot, a beguiling squirrel-like creature much hunted for its skin. The jerboa and the suslik probably also played their part and, of course, the rat too, though the latter’s main role was not to come till the disease was on the move.
To disturb the tranquil and largely harmless existence of
Pasteurella
pestis
something had to happen to make the rodents leave their homes. With them, inevitably, would travel their
attendant
fleas and, within the fleas, a cargo of deadly parasites. We are unlikely ever to know exactly what it was which caused this particular rodent migration. Such evidence as survives
suggests
that they were driven away by floods but, on other
occasions
, prolonged droughts have provided the necessary
incentive
or it could simply have been that an increase in the rodent population put too great a strain on the available supplies of
food. At all events a massive exodus took place and it was above all
Rattus
rattus
, the tough, nimble, by nature vagabond, black rat which made the move.
Without disputing the importance of the rat as a carrier of plague, Professor Jorge has suggested that its role, except in the earliest stages of an epidemic, is inessential, and that the lack of references to it in contemporary accounts of the Black Death indicates that the infection was mainly dependent on other means of transport.
36
He believed that
Pulex
irritans
, the flea which preys above all on human beings, was perfectly capable of carrying the plague direct from man to man without the
intervention
of an infected rat. Medically this is doubtful. There is no need to eliminate
Pulex
irritans
altogether as an extra factor but its capacity to drink in sufficient plague bacilli from one person so as to be able to implant a fatal dose in the next has been much questioned. Colonel MacArthur has recorded that, in blood cultures made from fatal cases of bubonic plague, he found ‘bacilli so sparse that theoretically one could have fed twenty thousand fleas on such a case and yet have infected none.’
37
There is certainly no doubt that the rapid spread of bubonic plague was greatly helped by the presence of infected rats. Nor was there any shortage of rats. By the middle of the fourteenth century they abounded in Europe, probably having been imported originally in the boats of the returning Crusaders. Their role was unobtrusive and, since there is no particular reason why
contemporaries
should have commented on their activities, their absence from the chronicle casts no doubt on their existence. Dead rats no doubt littered the streets and houses but this would hardly have seemed worthy of attention at a time when dead human beings were so much more conspicuous.
But though the rat helps greatly in the spread of bubonic plague, Professor Jorge is right in his contention that it is not essential. The Plague Research Commission of 1910 commented ‘… the transference of infected rats and fleas in merchandise, or in the case of fleas, on the body of a human being, must be
considered
.’
38
It has been, and Dr Hirst has shown that the adage ‘No ship rats, no plague’ is palpably untrue.
39
X.
cheopsis
, in ideal conditions, can live for a month away from its host.
Travelling with a cargo of grain or in a bale of cloth it could easily journey hundreds of miles without a rat. There is one
substantiated
case of a flea surviving unfed for six months in a rat
burrow
. The absence of rats, therefore, was far from a guarantee that bubonic plague could never strike.
The symptoms of bubonic plague as known today coincide
precisely
with those described by the medieval chroniclers. The ‘swollen and dropsical mass of inflamed lymphatic glands’ known as the bubo is the classic sign. Sometimes this is the size of an almond, sometimes of an orange; usually it is found in the groin but it may also grow in the armpit or, occasionally, on the neck. Equally familiar are the dusky stains or blotches caused by
subcutaneous
haemorrhages and the intoxication of the nervous system: ‘In Provence a man climbed on to the roof of his house and threw down the tiles into the street. Another executed a mad, grotesque dance on the roof …’
40
Modern medical
experience
suggests that, if the bubo breaks down and suppurates
within
a week, the victim will probably survive; few medieval doctors would have expected their patient to endure more than four or five days of the agonizing pain which accompanies the boil. But otherwise the cases observed by Boccaccio or Simon of Covino could be found in half a dozen plague centres today.
But though bubonic plague was the first and most conspicuous form taken by the Black Death, a variant known as primary pneumonic or pulmonary plague was more lethal. In the
epidemics
of the late nineteenth century, when methods of treatment were remarkably little more sophisticated than in the Middle Ages, between sixty and ninety per cent of those who caught bubonic plague could expect to die. In the case of pneumonic plague recovery was virtually unknown. Bubonic plague would generally take between four days and a week to kill; in the
Manchurian
epidemic of 1921 the expectation of life of the victims of pneumonic plague was a mere 1.8 days. Finally, bubonic plague is one of the less infectious epidemic diseases; the breath is not affected and the patient usually died or recovered before enough bacilli have accumulated in the blood to make it a source of
infective
material for the flea.
41
Pneumonic plague is perhaps the most infectious; it attacks the lungs so that there is coughing of
blood and the plague bacilli are sprayed out into the air every time that the patient exhales.
Hirst has remarked
42
that, if it were not known that they had a common origin and were linked by intermediate types, true pneumonic and uncomplicated bubonic plague would seem to be different diseases. The link between the two is to be found in an attack of bubonic plague during which the victim also develops pneumonia. This compound, though extremely dangerous to the victim, is not usually infectious. Yet, in certain cases, it may
become
so. The main outstanding problem of the Black Death, or indeed of the plague in any era, is what the factors are which make this happen, what it is which provokes an epidemic of the air-borne pneumonic variant of the disease.
‘Where the fourteenth-century plague is said to differ from later experience is that in its quite slow extension across Europe it seemed to change as the season of the year changed from
pneumonic
to bubonic, and then from bubonic to pneumonic without discontinuity’
43
The medieval doctor can hardly be blamed for finding the process incomprehensible. But if he had understood it he would even then not have mastered the full story. For there would still have remained unexplained those cases, already
mentioned
, in which a man would die within a few hours or go to bed in the best of health and never wake in the morning.
There seems no doubt that a third element in the Black Death, septicaemic plague, was here at work. This, like bubonic plague, is insect borne. The distinction is that the brunt of the infection falls on the bloodstream which, within an hour or two, is
swarming
with plague bacilli. The victim is dead long before buboes have had time to form. It is in this form of plague that
Pulex irritans
, the man-borne flea, has a chance to operate. So rich in bacilli is the blood of a sick man that the flea can easily infect itself and carry on the disease to a new prey without the need of a rat to provide fresh sources of infection. Septicaemic plague must have been the rarest of the three interwoven diseases which
composed
the Black Death but it was certainly as lethal as its
pneumonic
cousin and it introduced yet another means by which the plague could settle itself in a new area and spread hungrily among the inhabitants.
1
J. F. C. Hecker,
The
Epidemics
of
the
Middle
Ages,
(Trad. B. G. Babington) London, 1859, p.11. Cf. Abbé des Guignes,
Histoire
des
Huns,
Paris, 1757.
2
Voyages
de
Ibn-Batoutah, Société Asiatique, Paris, 1853.
3
De Smet, ‘Breve Chronicon clerici anonymi’,
Recueil
des
Chroniques
de
Flandres,
Vol. III, p.14.
4
Storie
Pistoresi,
Muratori 11, V. p.237.
5
Chronicon
Estense,
Muratori 15, III, p.160.
6
Hecker, op. cit., p.21.
7
Haeser,
Archiv
für
die
gesamte
Medizin,
Jena, Vol. II, p.29.
8
A. G. Tononi, ‘La Peste dell’ Anno 1348’,
Giornale
Ligustico,
Genoa, Vol X, 1883, p.139.
9
G. Vernadsky,
The
Mongols
and
Russia,
Yale, 1959.
10
Haeser, op. cit., Vol. II, pp.48–9.
11
C. S. Bartsocas, ‘Two 14th Century Greek Descriptions of the “Black Death”’,
Journ.
Hist
.
Med.,
Vol. XXI, No. 4, 1966, p.395.
12
Chronicon
Estense,
op. cit., p. 160.
13
De Smet, op. cit., Vol. III, pp. 14–15.
14
S. d’Irsay, ‘Notes to the Origin of the Expression: Atra Mors’,
Isis,
Vol. 8, 1926, p.328.
15
R. Kjennerud,
Journal
of
the
History
of
Medicine,
Vol. III, 1948, P.359.
16
Gasquet,
The
Black
Death,
London, 1908, p.8.
17
J. Michon,
Documents
inédits
sur
la
Grande
Peste
de
1348, Paris, 1860, p.11.
18
J. Nohl,
Der
Schwarze
Tod,
Potsdam, 1924, p.11.
19
Boccaccio,
Decameron,
Trans. J.M. Rigg, London, 1930, p.5.
20
e.g. Lechner,
Das
grosse
Sterben,
p.15; or plague tractates of Ibn Khātimah or Gentile da Foligno.
21
La
Grande
Chirurgie,
ed. E. Nicaise, Paris, 1890, p. 171.
22
Chronicon
Galfridi
le
Baker,
ed. E. Maunde Thompson, Oxford, 1889, p.99.
23
Simon of Covino,
Bibl.
de
l’École
des
Chartes,
1840–41 Ser. I, Vol. 2, p.241.
24
J. P. Papon,
De
la
Peste
ou
Époques
mémorables
de
ce
Fléau.
Vol. I, p.115.
25
Ibn Khātimah, Sudhoff,
Archiv
für
Geschichte
der
Medizin.
Vol XIX, 1927, p.30.
26
Ibn al Khatīb,
Sitzungsberichte
der
Königl:
bayer,
Munich, 1863, II, P.1.
27
Alfonso de Cordova, Sudhoff,
Archiv,
III, p.225.
28
‘Utrum mortalitas …’ Sudhoff,
Archiv,
XI, p.44. Cf. Konrade of Megenberg,
Buch
der
Natur
, ed. Pfeiffer, Berlin, 1870.
29
Hirst,
The
Conquest
of
Plague,
Oxford, 1953, p.28.
30
De Smet, op. cit.,
Breve
Chronicon,
Vol. III, p.15.
31
‘Tractatus de epidemia’, Michon,
Documents
inédits,
op. cit., p.46.
32
C. Creighton,
History
of
Epidemics
in
Britain,
Cambridge, 1891, p.175.
33
The most useful studies of bubonic plague which make special reference to the Black Death are Greenwood’s
Epidemics
and
Crowd
Diseases,
Pollitzer’s
Plague
and Hirst’s
The
Conquest
of
Plague,
34
J. Stewart,
The
Nestorian
Missionary
Enterprise,
Edinburgh, 1928, p.209.
35
R. Pollitzer,
Plague,
W.H.O. Publication, Geneva, 1954, p.13.
36
Jorge,
Bull.
Off.
Int.
Hyg.
Publ.
Vol. 25,1933, p.425.
37
MacArthur, ‘Old Time Plague in Britain’,
Trans.
Roy.
Soc.
Trop.
Med.
Hyg.,
Vol. XIX, p.355.
38
Reports
on
Plague
Investigations
in
India.
No. 39 of 1910.
39
Hirst, op. cit., p.324.
40
Nohl, op. cit., p.31.
41
Greenwood,
Epidemics
and
Crowd
Diseases,
London, 1935, p.308.
42
op. cit., p.28.
43
Greenwood, op. cit., p.291.