# 1911 Encyclopædia Britannica/Plague

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​PLAGUE (in Gr.) λοιμός, in Lat. pestis, pestilentia), in medicine, a term given to any epidemic disease causing a great mortality, and used in this sense by Galen and the ancient medical writers, but now confined to a special disease, otherwise called Griental, Levantine, or Bubonic Plague, which may be shortly defined as a specific infectious fever, one variety being characterized by buboes (glandular swellings) and carbuncles. This definition excludes many of the celebrated pestilences recorded in history-such as the plague of Athens, described by Thucydides; that not less celebrated one which occurred in the reign of Marcus Aurelius and spread over nearly the whole of the Roman world (A.D. 164–180), which is referred to, though not fully described, by the contemporary pen of Galen; and that of the 3rd century (about 253), the symptoms of which are known from the allusions of St Cyprian (Sermo de mortalztate). There is a certain resemblance between all these, but they were very different from Oriental plague. " Plague " was formerly divided into two chief varieties: (1) mild plague, pestis minor, larval plague (Radcliffe), paste fruste, in which the special symptoms are accompanied by little fever or general disturbance; and (2) ordinary epidemic or severe plague, pestis major, in which the general disturbance is very severe. Cases which are rapidly fatal from the general disturbance without marked local symptoms have been distinguished as fulminant plague (pestis siderans, paste foudroyarzte).
History up to 1880.—The first historical notice of the plague is contained in a fragment of the physician Rufus of Ephesus, who lived in the time of Trajan, preserved in the Collections of Orzbasius. Rufus speaks of the buboes called pestilential as being specially fatal, and as being found chiefly in Libya, Egypt and Syria. He refers to the testimony of a physician Dionysius, who lived probably in the 3rd century B.C. or earlier; and to Dioscorides and Posidonius, who fully described these buboes in a work on the plague which prevailed in Libya in their time. Whatever the precise date of these physicians may have been, this passage shows the antiquity of the plague in northern Africa, which for centuries was considered as its home. The great plague referred to by Livy (lx. Epitome) and more fully by Orosius (Histor. iv. 11) was probably the same, though the symptoms are not recorded. It is reported to have destroyed a million of persons in Africa, but is not stated to have passed into Europe.
It is not till the 6th century of our era, in the reign of Justinian, that we find bubonic plague in Europe, as a part of the great cycle of pestilence, accompanied by extraordinary natural phenomena, which lasted fifty years, and is described with a singular misunderstanding of medical terms by Gibbon in his forty-third chapter. The descriptions of the contemporary writers Procopius, Evagrius and Gregory of Tours are quite unmistakable. The plague of Justinian began at Pelusium in Egypt in A.D. 542; it spread over Egypt, and in the same or the next year passed to Constantinople, where it carried off 10,000 persons in one day, with all the symptoms of bubonic plague. It appeared in Gaul in 546, where it is described by Gregory of Tours with the same symptoms as lues inguinaria (from the frequent seat of buboes in the groin). In Italy there was a great mortality in 543, but the most notable epidemic was in 565, which so depopulated the country as to leave it an easy prey to the Lombards. In 571 it is again recorded in Liguria, ​ and in 590 a great epidemic at Rome is connected with the pontificate of Gregory the Great. But it spread in fact over the whole Roman world, beginning in maritime towns and radiating inland. In another direction it extended from Egypt along the north coast of Africa. Whether the numerous pestilences recorded in the 7th century were the plague cannot now be said; but it is possible the pestilences in England chronicled by Bede in the years 664, 672, 679 and 683 may have been of this disease, especially as in 690 pestis inguinaria is again recorded in Rome. For the epidemics of the succeeding centuries we must refer to more detailed works.
It is impossible, however, to pass over the great cycle of epidemics in the 14th century known as the Black Death. Whether in all the pestilences known by this name the disease was really the same may admit of doubt, but it is clear that in some at least it was the bubonicThe Black Death. plague. Contemporary observers agree that the disease was introduced from the East; and one eyewitness, Gabriel de Mussis, an Italian lawyer, traced, or indeed accompanied, the march of the plague from the Crimea (whither it was said to have been introduced from Tartary) to Genoa, where with a handful of survivors of a Genoese expedition he landed probably at the end of the year 1347. He narrates how the few that had themselves escaped the pest transmitted the contagion to all they met. Other accounts, especially old Russian chronicles, place the origin of the disease still farther east, in Cathay (or China), where, as is confirmed to some extent by Chinese records, pestilence and destructive inundations are said to have destroyed the enormous number of thirteen millions. It appears to have passed by way of Armenia into Asia Minor and thence to Egypt and northern Africa. Nearly the whole of Europe was gradually overrun by the pestilence. It reached Sicily in 1346, Constantinople, Greece and parts of Italy early in 1347, and towards the end of that year Marseilles. In 1348 it attacked Spain, northern Italy and Rome, eastern Germany, many parts of France including Paris, and England; from England it is said to have been conveyed to the Scandinavian countries. In England the western counties were first invaded early in the year, and London in November. In 1349 we hear of it in the midlands; and in subsequent years, at least till 1357, it prevailed in parts of the country, or generally, especially in the towns. In 1352 Oxford lost two-thirds of her academical population. The outbreaks of 136: and 1368, known as the second and third plagues of the reign of Edward III., were doubtless of the same disease, though by some historians not called the black death. Scotland and Ireland, though later affected, did not escape.
The nature of this pestilence has been a matter of much controversy, and some have doubted its being truly the plague. But when the symptoms are fully described they seem to justify this conclusion, one character only being thought to make a distinction between this and Oriental plague, viz. the special implication of the lungs as shown by spitting of blood and other symptoms. Guy de Chauliac notes this feature in the earlier epidemic at Avignon, not in the later. Moreover, as this complication was a marked feature in certain epidemics of plague in India, the hypothesis has been framed by Hirsch that a. special variety of plague, pestis indica, still found in India, is that which overran the world in the 14th century. But the same symptoms (haemoptysis) have been seen, though less notably, in many plague epidemics, even in the latest, that in Russia in 1878–1879, and, moreover, according to the latest accounts, are not a special feature of Indian plague. According to a Surgeon-General Francis (Trans. Epidern. Soc. v. 398) “hemorrhage is not an ordinary accompaniment” of Indian plague, though when seen it is in the form of haemoptysis. It seems, therefore, impossible to make a special variety of Indian plague, or to refer the black death to any such special form. Gabriel de Mussis describes it even in the East, before its arrival in Europe, as a bubonic disease.
The mortality of the black death was, as is well known, enormous. It is estimated in various parts of Europe at two thirds or three-fourths of the population in the first pestilence, in England even higher; but some countries were much less severely affected. Hecker calculates that one-fourth of the population of Europe, or 25 millions of persons, died in the whole of the epidemics.
In the 15th century the plague recurred frequently in nearly all parts of Europe. In the first quarter it was very destructive in Italy, in Spain (especially Barcelona and Seville), in Germany and in England, where London was severely visited in 1400 and 1406, and again in 1428. In 1427, 80,000 persons died in Dantzic and the neighbourhood. In 1438–1339 the plague was in Germany, and its occurrence at Basel was described by Aeneas Sylvius, afterwards Pope Pius II. In 1448–1450 Italy (Kircher), Germany (Lersch, from old chronicles), France and Spain, were ravaged by a plague supposed to have arisen in Asia, scarcely less destructive than the black death. England was probably seldom quite free from plague, but the next great outbreak is recorded in 1472 and following years. In 1466, 40,000 persons died of plague in Paris; in 1477–1485 the cities of northern Italy were devastated, and in 1485 Brussels. In the fifteenth car of Henry VII. (1499–1500) a severe plague in London caused the king to retire to Calais.
The 16th century was not more free from plague than the 15th. Simultaneously with a terrible pestilence which is reported to have nearly depopulated China, plague prevailed over Germany Holland, Italy and Spain, in the first decade of the century, and revived at various times in the first half. In 1529 there was plague in Edinburgh; in London in 1537–1539, and again 1547–1548; and also in the north of England, though probably not absent before. Some of the epidemics of this period in Italy and Germany are known by the accounts of eminent physicians, as Vochs, Fracastor, Mercuria is, Borgarucci, Ingrassia, Massaria, Amici, &c., whose writings are important because the question of contagion first began to be raised, and also plague had to be distinguished from typhus fever, which began in this century to appear in Europe. The epidemic of 1563–1564 in London and England was very severe, a thousand dying weekly in London. In Paris about this time plague was an everyday occurrence, of' which some were less afraid than of a headache (Borgarucci). In 1570, 200,000 persons died in Moscow and the neighbourhood, in 1572, 50,000 at Lyons; in 1568 and 1574 plague was at Edinburgh, and in 1570 at Newcastle. When, however, in 1575 a new wave of plague passed over Europe, its origin was referred to Constantinople, whence it was said to have spread by sea to Malta, Sicily and Italy, and by land through the Austrian territories to Germany. Others contended that the disease originated locally; and, indeed, considering previous history, no importation of plague would seem necessary to explain its presence in Europe. Italy suffered severely (Venice, in 1576, lost 70,000); North Europe not less, though later; London in 1580–1582. In 1585 Breslau witnessed the most destructive plague known in its history. The great plague of 1592 in London seems to have been a part of the same epidemic, which was hardly extinguished by the end of the century, and is noted in London again in 399. On the whole, this century shows a decrease of plague Europe.
In the first half of the 17th century plague was still prevalent in Europe, though considerably less so than in the middle ages. In the second half a still greater decline is observable, and by the third quarter the disease had disappeared or was disappearing from a great part of western Europe. The epidemics in England will be most conveniently considered in one series. From this time ​ onwards we have the guidance of the “Bills of Mortality” issued in London, which, though drawn up on the evidence of ignorant persons, are doubtless roughly true. The accession of James I. in 1603 was marked by a very destructive plague which killed 38,000 in London. In this and subsequent years the disease was widely diffused in England-for instance, Oxford, Derbyshire, Newcastle. It prevailed at the same time in Holland, and ad done so some years previously in northern Germany. In the same year (1603) one million persons are said to have died of plague in Egypt. This plague is said to have lasted eight years in London. At all events in 1609 we have the second great plague year, with a mortality of 11,785. After this there is a remission till about 1620, when plague again began to spread in northern Europe, especially Germany and Holland, which was at that time ravaged by war. In 1625 (the year of the siege of Breda in Holland) is the third great London plague with 35,417 deaths—though the year 1624 was remarkably exempt, and 1626 nearly so. In 1630 was the great plague of Milan, described by Ripamonti. In 1632 a severe epidemic, apparently plague, was in Derbyshire. 1636 IS the fourth great plague year in London with a mortality of 10,400, and even in the next year 3082 persons died of the same disease. The same year 7000 out of 20,000 inhabitants of Newcastle died of plague; in 1635 it was at Hull About the same time, 1635–1637, plague was prevalent in Holland, and the epidemic of Nijmwegen is celebrated as having been described by Diemerbroeck, whose work (Tractatus de peste, 4to, 1641–1665) is one of the most important on the subject. The English epidemic was widely spread and lasted till 1647, in which year, the mortality amounting to 3597, we have the fifth epidemic in London. The army diseases of the Civil Wars were chiefly typhus and malarial fevers, but plague was not unknown among them, as at Wallingford Castle (Willis, "Of Feavers, " Works, ed. 1681, p. 131) and Dunstar Castle. From this time till 1664 little was heard of plague in England, though it did not cease on the Continent. In Ireland it is said to have been seen for the last time in 1650.
In 1656 one of the most destructive of all recorded epidemics in Europe raged in Naples; it is said to have carried off 300,000 persons in the space of five months. It passed to Rome, but there was much less fatal, making 14,000 victims only-a result attributed by some to the precautions and sanitary measures introduced by Cardinal Gastaldi, whose work, a splendid folio, written on this occasion (Tractatus de avertenda et profliganda peste politicolegalis, Bologna, 1684) is historically one of the most important on the subject of quarantine, &c. Genoa lost 60,000 inhabitants from the same disease, but Tuscany remained untouched. The comparatix ely limited spread of this frightful epidemic in Italy at this time is a most noteworthy fact. Minorca is said to have been depopulated. Nevertheless the epidemic spread in the next few years over Spain and Germany, and a little later to Holland, where Amsterdam in 1663–1664 was again ravaged with a mortality given as 50,000, also Rotterdam and Haarlem. Hamburg suffered in 1664.
The Great Plague of London.—The preceding enumeration will have prepared the reader to view the great plague of 1664–1665 in its true relation to others, and not as an isolated phenomenon. The preceding years had been unusually free from plague, and it was not mentioned inGreat Plague of London. the bills of mortality till in the autumn of 1664 (Nov. 2) a few isolated cases were observed in the parishes of St Giles and St Martin's, Westminster, and a few occurred in the following winter, which was very severe. About May 1665 the disease again became noticeable, and spread, but somewhat slowly. Boghurst, a contemporary doctor, notices that it crept down Holborn and took six months to travel from the western suburbs (St Giles) to the eastern (Stepney) through the city. The mortality rapidly rose from 43 in May to 590 in June, 6137 in July, 17,036 in August, 31,159 in September, after which it began to decline. The total number of deaths from plague in that year, according to the bills of mortality, was 68, 596, in a population estimated at 460,000, out of whom two-thirds are supposed to have fled to escape the contagion. This number is likely to be rather too low than too high, since of the 6432 deaths from spotted fever many were probably really from plague, though not declared so to avoid painful restrictions In December there was a sudden fall in the mortality which continued through the winter, but in 1666 nearly 2000 deaths from plague are recorded.
According to some authorities, especially Hodges, the plague was imported into London by bales of merchandise from Holland, which came originally from the Levant, according to others it was introduced by Dutch prisoners of war; but Boghurst regarded it as of local origin. It is in favour of the theory that it spread by some means from Holland that plague had been all but extinct in London for some seventeen years, and prevailed in Holland in 1663–1664. But from its past history and local conditions, London might well be deemed capable of producing such an epidemic. In the bills of mortality since 1603 there are only three years when no deaths from plague are recorded. The uncleanliness of the city was comparable to that of oriental cities at the present day, and, according to contemporary testimony (Garenciéres, Angliae flagellum, London, 1647, p. 85), little improved since Erasmus wrote his well-known description. The spread of the disease only partially supported the doctrine of contagion, as Boghurst says: “ The disease spread not altogether by contagion at first, nor began only at one place and spread further and further as an eating sore doth all over the body, but fell upon several places of city and suburbs like rain.” In fact dissemination seems to have taken place, as usual, by the conversion of one house after another into a focus of disease, a process favoured by the fatal custom of shutting up infected houses with all their inmates, which was not only almost- equivalent to a sentence of death on all therein, but caused a dangerous concentration of the poison. The well known custom of marking such houses with a red cross and the legend “God have mercy upon us!” was no new thing: it is found in a proclamation in the possession of the present writer dated 1641; and it was probably older still. Hodges testifies to the futility and injurious effects of these regulations. The lord mayor and magistrates not only carried out the appointed administrative measures, but looked to the cleanliness of the city and the relief of the poor, so that there was little or no actual want; and the burial arrangements appear to have been well attended to. The college of physicians, by royal command, put forth such advice and prescriptions as were thought best for the emergency. But it is clear that neither these measures nor medical treatment had any effect in checking the disease. Early in November with colder weather it began to decline; and in December there was so little fear of contagion that those who had left the city “crowded back as thick as they fled.” As has often been observed in other plague epidemics, sound people could enter infected houses and even sleep in the beds of those who had died of the plague “before they were even cold or cleansed from the stench of the diseased” (Hodges). The symptoms of the disease being such as have been generally observed need not be here considered. The disease was, as always, most destructive in squalid, dirty neighbourhoods and among the poor, so as to be called the “poor’s plague.” Those who lived in the town in barges or ships did not take the disease; and the houses on London Bridge were but little affected. Of those doctors who remained in the city some eight or nine died, not a large proportion. Some had the rare courage to investigate the mysterious disease by dissecting the bodies of the dead. Hodges implies that he did so, though he left no full account of his observations. Dr George Thomson, a chemist and a disciple of Van Helmont, followed the example, and nearly lost his life by an attack which immediately followed.
The plague of 1665 was widely spread over England, and was ​ generally regarded as having been transmitted from London, as it appeared mostly later than in the metropolis, and in many cases the importation by a particular person could be traced. Places near London were earliest aflected, as Brentford, Greenwich, Deptford; but in July or August 1665 it was already in Southampton, Sunderland, Newcastle, &c. A wider distribution occurred in the next year. Oxford entirely escaped, though the residence of the court and in constant communication with London. The exemption was attributed to cleanliness and good drainage.
After 1666 there was no epidemic of plague in London or any part of England, though sporadic cases appear in bills of mortality up to 1679; and a column filled up with “0” was left till 1703, when it finally disappeared. The disappearance of plague in London was attribute; to the Great Fire, but no such cause existed in other cities. It has also been ascribed to quarantine, but no effective quarantine was established till 1720, so that the cessation of plague in England must be regarded as spontaneous.
But this was no isolated fact. A similar cessation of plague was noted soon after in the greater part of western Europe. In 1666 a severe plague raged in Cologne and on the Rhine, which was prolonged till 1670 in the district. In the Netherlands there was plague in 1667–1663, but there are no definite notices of it after 1672. France saw the last plague epidemic in 1668, till it reappeared in 1720. In the years 1675–1684 a new plague epidemic appeared in North Africa, Turkey, Poland, Hungary, Austria and Germany, progressing generally northward. Malta lost 11,000 persons in 1675. The plague of Vienna in 1679 was very severe, causing 76,000 or probably more deaths. Prague in 1681 lost 83,000 by plague Dresden was affected in 1680, Magdeburg and Halle in 1682*lIl the latter town with a mortality of 4397 out of a population of about 10,000. Many North German cities suffered about the same time; but in 1683 the plague disappeared from Germany till the epidemic of 1707. In S ain it ceased about 1681; in Italy certain cities were attacked till the end of the century, but not later (Hirsch).
Plague in the 18th Century.—At the beginning of this period plague was very prevalent in Constantinople and along the Danube. n 1703 it caused great destruction in the Ukraine. In 1704 it began to spread through Poland, and later to Silesia, Lithuania, Prussia and a great part of Germany and Scandinavia. In Prussia and Lithuania 283,000 persons perished; Dantzig, Hamburg and other northern cities suffered severely. Copenhagen was attacked in 1710. In Stockholm there was a mortality of 40,000. Certain places near Brunswick (10° E.) marked the western limit of the epidemic; and cholera was arrested at the same spot in later years (Haser).
At the same time the plague soread westward from the Danube to Transylvania and Styria, and (1713) appeared in Austria and Bohemia, causing great mortality in Vienna. Thence it passed to Prague and Ratisbon-to the former, possibly to the latter, almost certainly conveyed by human intercourse. This city (12° E.) was the western limit reached in this year. Haser states that the plague disappeared everywhere in Europe after the great hurricane of the 27th of February 1714.
In 1717 plague raged severely in Constantinople; and in 1719 it made a fresh progress westward into Transylvania, Hungary, Galicia and Poland, but not farther (about 20° E.). It thus appears that each successive invasion had a more easterly western limit, and that the gradual narrowing of the range of plague, which began in the 17th century, was still going on.
This process suffered a temporary interruption by the outbreak of plague of southern France in 1720–1722. In 1720 Marseilles became ailected with an epidemic plague, the origin of which was attributed by some to contagion through the slnp of a Captain Chataud which arrived on the 20th of May 1720, from Syria, where plague at that time prevailed, though not epidemically when e sailed. Six of the crew had died on the voya e to Leghorn, but the disease was declared not to be plague. Cases of plague occurred, however, on the ship, and on the 22nd of June among porters unloading the cargo. Hence, according to believers in contagion, the disease passed to families in the “old town,” the poorest and unhealthiest quarter. In the meantime other ships ad arrived from Syria, which were ut in quarantine. According to others the plague arose in Marseilles from local causes; and recently discovered data show that suspicious cases of contagious disease occurred in the town before the arrival of Chataud’s ship Opinions were divided, and the evidence appears even now nearly balanced, though the believers in contagion and importation gained the victory in public opinion. The pestilence was fearfully severe. Thousands of unburied corpses filled the streets, and in all 40,000 to 60,000 persons were carried off. In December 1721 the plague passed away, though isolated cases occurred in 1722 It passed to, or at least broke out in, Arles and Aix in 1720, causing great mortality, but in Toulon not till 1721, when it destroyed two-thirds of the population. The epidemic spread generally over Provence, but not to other parts of France, notwithstanding that, as confessed by D’Antrechaus, consul of Toulon, a believer in the exclusive power of contagion, there were abundant opportunities. The disease was in fact, as in other cases, self-limited. In all 87,659 persons are said to have died out of a population of nearly 250,000.
This great epidemic caused a panic in England which led to the introduction (under Mead’s advice) of quarantine regulations, never previously enforced, and also led to the publication of many pamphlets, &c., beside Mead’s well-known Discourse on Pestilential Contagion (London, 1720).
Plague in Sicily in 1743.—An outbreak of plague at Messina in 1743 is important, not only for its fatality, but as one of the strongest cases in favour of the theory of imported contagion. Messina had been free from plague since 1624, and the Sicilians prided themselves on the rigour of the quarantine laws which were thought to have preserved them. In May 1743 a vessel arrived from Corfu, on board of which had occurred some suspicious deaths. The ship and cargo were burnt, but soon after cases of a suspicious form of disease were observed in the hospital and in the poorest parts of the town; and in the summer a fearful epidemic of plague developed itself which destroyed 40,000 or 50,000 persons, and then became extinct without spreading to other parts of Sicily.
Spread of Plague from the East.—Independent of the episodes of Marseilles and Messina, the spread of plague from the East continued to exhibit the above-mentioned law of limitation. In 1738–1744 the disease was in the Ukraine, Hungary, the borders of Carniola, Moravia and Austria, extending along the Carpathians as far as Poland (20° E.), and also in Bukowina (25° E.). It lasted till 1745, and then disappeared from those parts for fifteen years. In 1755–1757 plague prevailed in parts of European Turkey, whence it on one occasion extended into Transylvania, in the neighbourhood of Cronstadt, where it was checked (25.5° E.).
In 1770 a destructive plague arose in Moldavia during the Russo-Turkish War, and shortly afterwards in Wallachia, apparently endemic in the former country at least. It affected also Transylvania and part of Hungary, and still more severely Poland, but was confined to Podolia, Volhynia, the Ukraine and east Galicia (5° E.), not even penetrating as far as Warsaw. After destroying, it is said, 300,000 persons, and without being checked by any quarantine regulations, the plague died out finally in March 1771, being remarkable for its short duration and spontaneous limitation (Haser).
In another direction the plague spread over Little Russia in 1770, and desolated Kieff, while in the next year it broke out in Moscow and produced one of the most destructive epidemics of modern times. More than 50,000 persons, nearly one-fourth of the population, were carried off.
The remaining European plague-epidemics of the 18th century were inconsiderable, but on that very account noteworthy. Transylvania was again affected in 1785, Slavonia and Livonia (a district of eastern Galicia) in 1795–1796 (25° E.), Volhynia in 1798. The disease, while reappearing in the seats of the terrible earlier epidemics, was more limited in its range and of shorter duration. An epidemic in Dalmatia in 1783–1784 is noteworthy in connexion with later outbreaks in the same region. In the last years of the century (1799–1800) there was a new epidemic in Syria and Egypt, where it affected the French and afterwards the English army.
Plague in the 19th Century.—Plague appeared at Constantinople in 1802–1803, about the same time in Armenia (Kars), and in 1801 in Bagdad. It had prevailed since 1798 in Georgia and the Caucasus, and in 1803–1806 began to spread from the north of the Caucasus into Russia, till in 1806 it was established at or near Astrakhan, and in 1807 reached Zareff, 200 m. higher up the Volga. These localities are interesting as being near those Where plague appeared in 1877–1878. It is also said to have entered the government of Saratov, but probably no great distanced. The plague remained in the Caucasus and Georgia till 1819 at least. In 1828–1831 it was in Armenia, and again in 1840–1843, since which time it has not been heard of in that country.
​ In 1808 plague was at Constantinople, in 1809 at Smyrna. In 1812 was a more general epidemic affecting these places and also Egypt. An outbreak at Odessa is supposed to have been brought from Constantinople, and thence to have passed to Transylvania. In 1813 a severe plague at Bucharest is supposed to havc been brought from Constantinople. About the same time plague prevailed in Bosnia, and is supposed to have passed thence to Dalmatia in 1815. In 1814–1815 it again appeared in Egypt, and once more invaded the continent of Europe in Albania and Bosnia. Two insular outbreaks, Malta in 1813 and Corfu in 1815, attracted much attention as being both thought to be cases of importation by sea-traffic and there seems good reason for this opinion.
A panic spread through Europe in 1815 in consequence of an outbreak in Noja on the eastern coast of Italy. According to one view it was imported from the opposite coast of Dalmatia, though no definite history of contagion was established; according to others, it originated endemically in that place. It remained, however, strictly confined to a small district, perhaps in consequence of the extraordinarily rigorous measures of isolation adopted by the Italian government. In 1828 an isolated epidemic appeared in Greece in the Morea, supposed to have been brought by troops from Egypt. In 1824–1825 an outbreak took place at Tutchkoff in Bessarabia, the town was strictly isolated by a military cordon and the disease did not spread. Croustadt in Transylvania was the scene of a small outbreak in 1828, which was said to be isolated by similar measures (Lorinser). A far more serious epidemic was connected viith the campaign of the Russian army against Turkey in 1828–1829 Moldavia, Wallachia and Bessarabia were widely affected, the disease broke out also in Odessa and the Crimea, and isolated cases occurred in Transylvania. The most northerly points reached by the plague were near Czernowitz on the frontier of Bessarabia and Bukowina, and its limitation vias as before attributed to the Russian and Austrian military cordons.
In 1831 another epidemic occurred in Constantinople and Roumelia, in 1837 again in Roumelia and in Odessa-its last appearance in these regions, and the last on the European continent except an isolated outbreak in Dalmatia in 1840, and one in Constantinople in 1841.
The plague-epidemics in Egypt between 1833 and 1845 are very important in the history of plague, since the disease was almost for the first time scientifically studied in its home by skilled European physicians, chiefly French. The disease was found to be less contagious than reported to be by popular tradition, and most of the French school went so far as to deny the contagiousness of the disease altogether. The epidemic of 1834–1835 was not less destructive than many of those notorious in history; but in 1844–1845 the disease disappeared.
In 1853 plague appeared in a district of western Arabia, the Asir country in North Yemen, and it is known to have occurred in the same district in 1815, as it did afterwards in 1874 and 1879 In 1874 the disease extended within iour days' march of Mecca From the scantiness of population the mortality was not great, but it became clear that this is one of the endemic seats of plague.
In June 1858 intelligence was received in Constantinople of an outbreak of disease at the small town Benghazi, in the district of Barca, province of Tripoli, North Africa, which though at first misunderstood was clearly bubonic plague. From later researches there is reason to believe that it began in 1856 or in 1855. The disease did not spread, and ceased in the autumn, to return with less violence in 1859, when it died out. In the autumn of 1873 it returned, but came again to a spontaneous termination.
After the epidemic of Benghazi in 1856–1859, plague was next heard of in the district of Maku, in the extreme north-west of Persia in November 1863. It occurred in a scattered population, and the mortality was not absolutely large.
In 1867 an outbreak of plague was reported in Mesopotamia (Irak), among the marshes of Hindieh bordering on the lower Euphrates The epidemic began in December 1866 (or probably earlier) and ceased in June 1867. But numerous cases of nonfatal mild bubonic disease (mild plague or pestis minor) occurred both before and after the epidemic, and according to Tholozan similar cases had been observed nearly every year from 1856 to 1865.
The next severe epidemic of plague in Irak began in December 1873. But facts collected by Tholozan show that pestis 1/nnor, or sporadic cases of true plague, had appeared in 1868 and subsequent years. The outbreak of 1873–1874 began about 60 m. from the origin of that of 1867. It caused a much greater mortality and extended over a much wider area than that of 1867, including the towns of Kerbela and Hilleh. After a short interval it reappeared at Divanieh in December 1874, and spread over a much wider area than in the previous epidemics. This epidemic was carefully studied by Surgeon-Major Colvill. He estimated the mortality at 4000. The epidemic ceased in July, but broke out again early in 1876, and in this year extended northwards to Bagdad and beyond. The whole area now affected extended 250 m. from north-west to south-east, and the total number of deaths was believed to be 20, oo0. In 1877 plague also occurred at Shuster in south-west Persia, probably conveyed by pilgrims returning from Irak, and caused great mortality.
After its customary cessation in the autumn the epidemic began again in October 1876, though sporadic cases occurred all the summer. The disease appeared in 1877 in other parts of Mesopotamia also with less severity than in 1876, but over a wider area, being now announced at Samara, a town 70 m. above Bagdad on the Tigris. The existence of plague in Bagdad or Mesopotamia was not again announced till the year 1884, when accounts again appeared in the newspapers, and in that July the usual official statement was made that the plague had been stamped out.
In 1870–1871 it appeared in a district of Mukri in Persian Kurdistan to the south of Lake Urumiah (far removed from the outbreak of 1863). The epidemic appears, however, to have died out in 1871, and no further accounts of plague there were received. The district had suffered in the great epidemic of plague in Persia in 1829–1835. In the winter 1876–1877 a disease which appears to have been plague appeared in two villages in the extreme north of the province of Khorasan, about 25 leagues from the south-east angle of the Caspian Sea. In March 1877 plague broke out in Resht, a town of 20,000 inhabitants, in the province of Ghilan, near the Caspian Sea at its south-west angle, from which there is a certain amount of trade with Astrakhan. In 1832 a very destructive plague had carried off half the inhabitants. In 1877 the plague was very fatal. From March to September 4000 persons were calculated to have died. The disease continued till the spring of 1878. In 1877 there was a doubtful report of the same disease at Astrabad, and also in some parts near the Perso-Afghan frontier. In 1878 plague again occurred in Kurdistan in the district of So-uj-Bulak, said by Dr Tholozan to be the same as in the district of Mukri where it occurred in 1870–1871. These scattered outbreaks of plague in Persian territory are the more remarkable because that country ​ had been generally noted for its freedom from plague (as compared With Asiatic Turkey and the Levant).
A few cases of plague occurred in January 1877 at Baku on the west shore of the Caspian, in Russian territory.
An outbreak of plague on European soil in 1878–1879 on the banks of the Volga caused a panic throughout Europe. In the summer of 1877 a disease prevailed in several villages in the neighbourhood of Astrakhan and in the city itself, which was clearly a mild form of plague (pestis minor). It caused no deaths (or only one due to a complication) and died out apparently spontaneously. An official physician, Dr Kastorsky, who investigated the matter for the government, declared the disease to be identical with that prevailing in the same year at Resht in Persia; another physician, Dr Janizky, even gave it the name of pestis nostras. In October 1878 some cases appeared in the stanitza or Cossack military settlement of Vetlanka, 130 m. from Astrakhan on the right bank of the Volga, which seem to have puzzled the physicians who first observed them, but on the 30th of November were recognized as being but the same mild plague as had been observed the year before near Astrakhan by Dr Doppner, chief medical officer of the Cossacks of Astrakhan. His report on the epidemic is the only original one we have. At the end of November the disease became suddenly more severe, and most of those attacked died; and from the 21st of December it became still more malignant, death occurring in some cases in a few hours, and without any buboes being formed. No case of recovery was known in this period. At the end of the year it rapidly declined, and in the first weeks of January still more so. The last death was on the 24th of January. In the second half of December, when the disease had already lasted two months, cases of plague occurred in several neighbouring villages, all of an extremely malignant type, so that in some places all who were attacked died. In most of these cases the disease began with persons who had been at Vetlanka, though this was not universally established. The inhabitants of these villages, terrified at the accounts from Vetlanka, strictly isolated the sick, and thus probably checked the spread of the disease. But it evidently suffered a spontaneous decline. By the end of January there were no cases left in the district except at one village (Selitrennoye), where the last occurred on the 9th of February. The total number of cases in Vetlanka, out of a population of about 1700, was 417, of whom 362 died. In the other villages there were about 62 deaths from plague, and not more than two or three cases of recovery. In consequence of the alarm excited by this appearance of plague upon European soil, most European governments sent special commissions to the spot. The British commissioners were Surgeon-Major Colvill and Dr J. F. Payne, who, like all the foreign commissioners, reached the spot when the epidemic was over. With respect to the origin of this epidemic, the possibility of its having originated on the spot, as in Resht and on the Euphrates in very similar situations, is not to be denied. An attempt was made to show that the contagion was brought home by Cossacks returning from the Turkish War, but on absolutely no evidence. In the opinion of Dr Payne the real beginning of the disease was in the year 1877, in the vicinity of Astrakhan, and the sudden development of the malignant out of a mild form of the disease was no more than had been observed in other places. The Astrakhan disease may have been imported from Resht or Baku, or may have been caused concurrently with the epidemics of these places by some cause affecting the basin of the Caspian generally. Plague in I ndia.-It used to be held as a maxim that plague never appeared east of the Indus; nevertheless it was observed during the 19th century in more than one distinct centre in India.. So long ago as 1815 the disease appeared in Guzerat, Kattywar and Cutch, “after three years of severe famine.” It reappeared early next year, in the same locality, when it extended to Sind as far as Hyderabad, and in another direction south-east as far as Ahmedabad and Dhollerah. But it disappeared from these parts in 1820 or early in 1821, and was not heard of again till July 1836, when a disease broke out into violence at the town of Pali in Marwar in Rajputana. It spread from Pali to the province of Meywar, but died out spontaneously in the hot season of 1837. The origin of these two epidemics was obscure. No importation from other countries could be traced.
In 1823 (though not officially known till later) an epidemic broke out at Kedarnath in Gurwhal, a sub-district of Kumaon on the south-west of the Himalayas, on a high situation. In 1834 and 1836 other epidemics occurred, which at last attracted the attention of government. In 1849–1850, and again in 1852, the disease raged very severely and spread southward. In 1853 Dr Francis and Dr Pearson were appointed a commission to inquire into the malady. In 1876–1877 another outbreak occurred. The symptoms of this disease, called maha murree or mahamari by the natives, were precisely those of oriental plague. The feature of blood-spitting, to which much importance had been attached, appeared to be not a common one. A very remarkable circumstance was the death of animals (rats, and more rarely snakes) at the outbreak of an epidemic. The rats brought up blood, and the body of one examined after death by Dr Francis showed an affection of the lungs.
Oriental plague was observed in the Chinese province of Yunnan from 1871, and also at Pakhoi, a port in the Tongking Gulf, in 1882—being said to have prevailed there at least fifteen years. In both places the symptoms were the same, of undoubted bubonic plague. At Pakhoi it recurs nearly every year.
In 1880 therefore plague existed or had existed within ten years, in the following parts of the world: (1) Benghazi, Africa; (2) Persian Kurdistan; (3) Irak, on the Tigris and Euphrates; (4) the Asir country, western Arabia; (5) on the lower Volga, Russia; (6) northern Persia and the shores of the Caspian; (7) Kumaon and Gurhwal, India; (8) Yunnan and Pakhoi, China.
Literature.—See the following works, besides those already quoted. Kamintus, Regimen contra epidimiam sive pestem, 4to, c. 1494 (many editions); Jacobus Soldus, Opus insigne de peste, 4to (Bologna, 1478), Alex. Benedictus, De observatione in pestilentia, 4to (Venice, 1493), Nicolaus Massa, De febre pestilentia, 4to (Venice, 1556, &c.); Fioravanti, Regimento della peste, 8vo, Venice, 1556; John Woodall, The Surgeon’s Mate, folio (London, 1639); an Helmont, Tumulus pestis, 8vo (Cologne, 1644, &c.); Muratori, Trattato del governo della peste, Modena, 1714; John Howard, An Account of Lazarettoes in Europe, &c., 4to London, 1789); Patrick Russel, A Treatise of the Plague, 4to London, 1791); Thomas Hancock, Researches into the Laws of Pestilence, 8vo (London, 1821); Foderé, Leçons sur les épidémies, &c., 4 vols. 8vo (Paris, 1822–1824); Ségur Dupeyron, Recherches historiques, &c., sur la peste (1837); Bulard, La Peste orientale, 8vo (Paris, 1839); Griesinger, Die Infectionskrankheiten (2nd ed., 8vo, Erlangen, 1864). (J. F. P.)
History since 1880.—The most striking feature of the early history of plague summarized above is the gradual retrocession of plague from the west, after a series of exceedingly destructive outbreaks extending over several centuries, and its eventual disappearance from Europe. It appears to have come to a sudden end in one country after another, and to have been seen there no more. Those lying most to the west were the first ​ to be freed from its presence, namely, England, Portugal and Spain. From all these it finally disappeared about 1680, at the close of a period of pandemic prevalence. Northern and central Europe became free about 1714, and the south of France in 1722. The last outbreak in northern Russia occurred in 1770. After this plague only appeared in the south-east of Europe, where in turn it gradually died away during the first half of the 19th century. In 1841 its long reign on this continent came to an end with an isolated outbreak in Turkey. From that time until quite recently it remained extinct, except in the East. The province of Astrakhan, where a very small and limited outbreak occurred in 1878, is politically in Europe, but geographically It belongs rather to Asia. And even in the East plague was confined to more or less clearly localized epidemics; it showed no power of pandemic diffusion. In short, if we regard the history of this disease as a whole, it appears to have lost such power from the time of the Great Plague of London in 1665, which was part of a pandemic wave, until the present day. There was not merely a gradual withdrawal eastwards lasting nearly two hundred years, but the outbreaks which occurred during that period, violent as some of them were, showed a constantly diminishing power of diffusion and an increasing tendency to localization. The sudden reversal of that long process is therefore a very remarkable occurrence. Emerging from the remote endemic centres to which it had retreated, plague has once more taken its place among the zymotic diseases with which Western communities have to reckon, and that which has for more than a century been little more than a name and a tradition has become the familiar object of investigation, carried on with all the ardour and all the resources of modern science. In what follows an attempt will be made to summarize the facts and indicate the conclusions to be drawn from recent experience.
Diffusion.—At the outset it is characteristic of this subtle disorder that the present pandemic diffusion cannot be traced with certainty to a definite time or place of origin. Herein it differs notably from other exotic diseases liable to similar diffusion. For instance, the last visitation of cholera could be traced clearly and definitely to a point of origin in northern India in the spring of 1892, and could be followed thence step by step in its march westward (see Cholera). Similarly, though not with equal precision, the last wave of influenza was shown to have started from central Asia in the spring of 1889, to have travelled through Europe from east to west, to have been carried thence across the sea to America and the Antipodes, until it eventually invaded every inhabited part of the globe (see Influenza). In both cases no doubt remains that the all-important means of dissemination is human intercourse The movements of plague cannot be followed»in the same way. With regard to origin, several endemic centres are now recognized in Asia and Africa, namely, (1) the district of Assyr in Arabia, on the eastern shore of the Red Sea; (2) parts of Mesopotamia and Persia; (3) the district of Garwhal and Kumaon in the North-West Provinces of India; (4) Yunnan in China; (5) East and Central Africa. The last was recently discovered by Dr Koch. It includes the district of Kisiba in German East Africa, and extends into Uganda. In applying the term “endemic centres” to these localities, no very precise meaning can be attached to the word. They are for the most part so remote, and the information about them so scanty, that our knowledge is largely guesswork. What we mean is that there is evidence to show that under various names a disease identical with plague has been more or less continuously prevalent for a number of years, but how long and how continuously is not known Whether any of them are permanent homes of plague the evidence does not enable us to say. They seem, at any rate, to have harboured it since its disappearance from Europe, and probably further investigation would disclose a still wider prevalence. For instance, there are good reasons for believing that the island of Réunion has been subject, since 1840 or thereabouts, to outbreaks under the name of “ lymphangite infectieuse, ” an elegant euphemism characteristically French. In all the countries named plague appears to behave very much as it used to do in Europe from the time of the Black Death onwards. That is to say, there are periods of quiescence, with epidemic outbreaks which attract notice at irregular intervals.
Taking up the story at the point where the earlier historical summary leaves off, we get the following list of countries in which plague is known to have been present in each year (see Local Government Board's Reports): 1880, Mesopotamia; 1881, Mesopotamia, Persia and China; 1882, Persia and China.; 1883, China; 1884, China and India (as mahamari); 1885, Persia; 1886, 1887, 1888, India (as mahamari); 1889, Arabia, Persia and China; 1890, Arabia, Persia and China; 1891, Arabia, China and India (as mahamari); 1892, Mesopotamia, Persia, China, Russia (in central Asia); 1893, Arabia, China, Russia and India (as mahamari); 1894, Arabia, China and India (as mahamari); 1895, Arabia and China; 1896, Arabia, Asia Minor, China, Japan, Russia and India (Bombay), 1897, Arabia, China, Japan, India, Russia and East Africa; 1898, Arabia, Persia, China, Japan, Russia, East Africa, Madagascar and Vienna; 1899, Arabia, Persia, China, Japan, Mesopotamia, East Africa, West Africa, Philippine Islands, Straits Settlements, Madagascar, Mauritius, Réunion, Egypt, European Russia, Portugal, Sandwich Islands, New Caledonia, Paraguay, Argentine, Brazil: 1900, to the foregoing should be added Turkey, Australia, California, Mexico and Glasgow; in 1901, South Africa and in 1902 Russia chiefly at Odessa.
This list is probably by no means exhaustive, but it sufficiently indicates in a summary fashion the extent of that wave of diffusion which set in during the closing years of the 19th century. It did not fully gather way till 1896, when plague appeared in Bombay, but our modern knowledge of the disease dates from 1894, when it attacked Hong Kong and first presented itself to accurate observation. From this point a more detailed account may be given. Plague was recognized at Hong Kong in May 1894, and there can be little doubt that it was imported from Canton, where a violent outbreak-said to have caused 100,000 deaths-was in progress a few months earlier, being part of an extensive wave of infection which is believed to have come originally out of the province of Yunnan, one of the recognized endemic centres, and to have invaded a large number of places in that part of China, including Pakhoi and other seaports. Hong Kong was severely affected, and has never since been entirely free from plague. In two intermediate years—1895 and 1897—very few cases were recorded, but more recently the epidemic has gathered force again. The following table gives the cases and deaths in each of the six years 1894–1899:—
The excessively high rate of mortality is probably due in part to under-statement of the number of cases. Concealment is practised by the Chinese, who are chiefly attacked, and it is easier to conceal sickness than death. Plague appears to have been equally persistent and destructive on the mainland in southern China during the period indicated, but no accurate details are available. In 1897 the Portuguese settlements of Lappa and Macao were invaded. In addition to the provinces of Yunnan, Kwang-si and Kwang-tung in southern China, plague is reported to have been present for several years in a district in Mongolia to the north of Peking, and distant about “twelve days' ride.” More recently several localities in Mongolia and Manchuria have been affected. Formosa was attacked in 1896, and suffered considerably in subsequent years; in 1899 the Japanese government officially reported 2633 cases, with ​ 1974 deaths. Japan itself has had a certain amount of imported plague, but not on a large scale. Speaking generally, the disease has persisted and spread in the Far East since 1894, but Precise information is lacking, except with regard to Hong Kong. W. J. Simpson in his Report on the Causes of the Plague in Hong Kong (1903) reports the endemicity of the plague in that colony to be maintained by (a) infection among rats often connected with infectious material in rat runs or in houses, the virus of which has not been destroyed, (b) retention of infection in houses which are rat-ridden, and (c) infected clothing of people who have been ill or died of plague. He considers the outbreaks are favoured by the seasonal heat and moisture of the spring and early summer, and the movement from place to place of infected rats or persons. He also believes that human beings may infect rats. In 310 cases of plague examined by Simpson 56% were bubonic, 40% septic and 4% pneumonia.
In 1896 plague appeared in the city of Bombay. It was certainly present in August, but was not recognized until the 23rd of September, and the diagnosis was not bacteriologically confirmed until the 13th of October. This fact should be remembered when failure to recognize the disease on its first appearance occurs elsewhere. The origin of the Bombay invasion is shrouded in obscurity. It is not even known when or in what part of the city it began (Condon, The Bombay Plague). Several theories have been put forward, and importation by sea from China is the theory which has met with most acceptance. The native form of plague, known as mahamari, is confined to the southern slopes of the Himalaya. It is described above, but that account may be supplemented by some earlier references unearthed by the Bombay Gazetteer (vol. iv.). Ibn Batesta notices two destructive pestilences in the 14th century, and Ferishta one in 1443, which he calls ta’un, and describes as very unusual in India. At the end of the 16th century there was a pestilence following a prolonged famine, and in the 17th century two violent epidemics are recorded under the names ta’un and waba. In the second of these, which occurred in the Ahmedabad district of the Bombay Presidency in 1683–89, buboes are distinctly described. In the 18th century several pestilences are recorded without description. It is at least probable from these notes that even before the undoubted outbreak, which began in Cutch in 1812, India was no stranger to epidemic plague. To return to Bombay and 1896: the infection spread gradually and slowly at first, but during the first three months of 1897 not only was the town of Bombay severely affected, but district after district in the presidency was attacked, notably Poona, Karachi, Cutch Mandvi, Bhiwandi and Daman. The number of cases and deaths reported in the presidency, exclusive of the city, in each year down to the end of 1899, was as follows:—
The corresponding figures for Bombay city are:—
The total for the presidency, including the city, in four years was 325,632 cases with 252,549 deaths in a. population of 26,960,421 (census of 1891). The population of the city is 821,764, but during the earlier plague period large numbers fled, so that the foregoing figures do not give the true plague incidence according to population. Moreover, concealment was extensively practised. The most striking fact brought out by the tables just given is the large and steady increase year by year in the presidency, in spite of all efforts to arrest the spread of infection. It has gone on since 1899, and it has not been confined to Bombay, but has extended over the whole of India. In 1897 it had already penetrated to Rajputana, the Punjab, the North West Provinces and the Central Provinces. In the following year Bengal, Madras, Haidarabad and Mysore were invaded. Not all these provinces suffered alike, but on the whole plague steadily strengthened its hold on India generally, and hardly relaxed it in any part. The most noteworthy details available are as follows, taken from the plague mortality returns published June 1908. In the Punjab from 179 deaths in 1897 the mortality reached a maximum of 334,897 in 1905, in Agra and Oudh they rose from 72 in 1897 to 383,802 in 1905, and in Madras Presidency from 1658 in 1899 to 20,125 in 1904.
The most striking figures, however, are those for Bombay and Bengal which are given below as well as the total mortality in India.
Outside China and India plague has caused no great mortality in any of the countries in which it has appeared, with the exception perhaps of Arabia, about which very little is known. But some of the outbreaks are interesting for other reasons, and require notice. The first case is the singular occurrence of three deaths at Vienna in October 1898. The earliest victim was an attendant named Barisch, employed in the pathological laboratory of the Vienna General Hospital, and told off to look after the animals and bacteriological apparatus devoted to the investigation of plague, cultures of which had been brought from India. by the medical commissioners sent by the Royal Academy of Science in 1897. Barisch was drunk and out all night on the 8th of October, on the 14th of October he fell ill. Plague was suspected, but Dr Müller, who attended the man and had studied the disease in India, would not admit the diagnosis on clinical grounds, nor was it bacteriologically established until the 19th of October. Barisch died on the 18th of October. On the 20th one of the nurses, and on the 21st Dr Müller, fell ill. Both died of pneumonia plague, from which also Barisch had undoubtedly suffered. A second nurse and a sister of mercy had feverish attacks, but no further case occurred. Barisch was shown to have been careless in the performance of his duties, and to have disregarded instructions; and the inference is that he conveyed the infection to his mouth, and so to the lungs, from the bacteriological specimens or inoculated animals. The melancholy incident illustrates several points of interest: (1) the correctness of the bacterial theory of causation, and the identity of the bacillus pestis as the cause; (2) the infectious character of the pneumonia type of disease; (3) its high fatality; (4) the difficulty of diagnosis.
The next occurrence of special interest is the appearance of plague in Portugal in 1899, after an absence of more than 200 years. Its origin is shrouded in obscurity. Oporto, the seat of the outbreak, had no connexion by sea with any place known to be infected, and all attempts to trace introduction ended in speculation or assumption. The most probable theory was that soldiers returning home from infected Portuguese possessions in the East brought it with them, but this does not explain the selection of Oporto and the escape of other places. The earliest ​ cases, according to retrospective inquiry, occurred in June 1899; suspicions were aroused in July, but the diagnosis was not established until August. The conclusion reached, after careful investigation by Dr Jorge, the medical officer of health, that the commencement really dated from June, is confirmed by the fact that about that time the riverside labourers, who were first affected, began to notice an illness among themselves sufficiently novel to attract their attention and that of an English shipowner, who from their description suspected plague. Through him the suspicion was conveyed to the Medical Times and Gazelle, in which the suggestion of plague at Oporto was made before any public mention of it in the town itself. The outbreak never assumed large proportions. It gained ground by degrees until October, after which it declined, and eventually ceased in February 1900. No recrudescence has been officially announced. The number of cases recorded in a population of 150,000 was 310, with 114 deaths, representing a case mortality of 36·7%. They were widely scattered about the town and outlying suburbs, but no further extension occurred, except some isolated cases at Braga, a town 35 m. distant, and one at Lisbon, in the person of the distinguished bacteriologist, Professor Camara Pestana, who contracted the disease in making a post-mortem at Oporto, and died in Lisbon.
The only other appearance of plague in Europe in 1899 was on the Volga Three places were affected, namely, Kolobovka, and Krasnoyarsk, in the province of Astrakhan, and Samara, higher up the river. All three outbreaks were small and limited, and no further extension took place. A commission appointed by the Russian government pronounced the disease to be undoubtedly plague, and it appears to have been very fatal. The origin was not ascertained.
The most interesting extensions of plague in 1900 were those in Australia and Glasgow. The following towns were affected in Australia: Sydney, in New South Wales; Adelaide, in South Australia, Melbourne, in Victoria; Brisbane, Rockhampton, Townsville, Cairns and Ipswich, in Queensland; Freemantle, Perth and Coolgardie, in West Australia. In none of these, with the exception of Sydney, did plague obtain a serious hold. The total number of cases reported in Queensland was only 123, with 53 deaths. In Sydney there was 303 cases, with 103 deaths, a case mortality of 34%. The infection is supposed to have been brought from Noumea, in New Caledonia, where it was present at the end of 1899, and the medical authorities believe that the first case, which occurred on the 19th of January, was recognized The outbreak, which hardly reached epidemic proportions, lasted about six months. That in Glasgow was on a still smaller scale It began, so far as could be ascertained, in August 1900, and during the two months it lasted there were 34 cases and 1 5 deaths. Once more the disease was not at first recognized, and its origin could not be traced. In 1901 plague invaded South Africa, and obtained a distinct footing both at Cape Town and Port Elizabeth. The total number of cases down to July was 760, with 362 deaths; the number of Europeans attacked was 196, with 68 deaths, the rest being natives, Malays, Indians, Chinese and negroes. With regard to Great Britain, a few ship-borne cases have been dealt with at different ports from time to time since 1896, but except at Glasgow the disease has nowhere obtained a footing on land.
Causation.—Plague is a specific infectious fever, caused by the bacillus pestis, which was identified in 1894 by Kitasato, and subsequently, but independently, by Yersin (see Parasitic Diseases). It is found in the buboes in ordinary cases, in the blood in the so-called “septicaemic” cases, and in the sputum of pneumonia cases. It may also be present in the urine. Post mortem it is found in great abundance in the spleen and liver. Nothing is known of its natural history outside the body, but on cultivation it is apt to undergo numerous involution forms Its presence in a patient is regarded as positive diagnostic proof of plague, but failure to find or to identify it does not possess an equal negative value, and should not be too readily accepted, for many instances are recorded in which expert observers have only succeeded in demonstrating its presence after repeated attempts. It is clear, from the extreme variations in the severity of the illness, that the resisting power of individuals varies greatly. According to the Plague Research Committee of Bombay, the predisposing causes are “those leading to a lower state of vitality,” of which insufficient food is probably the most important. There is no evidence that age, sex or race exercises a distinct predisposing influence. The largest incidence in Bombay was on young adults, but then they are more numerous and more exposed to infection, because they go about more than the younger and the older. Similarly, the comparative immunity of Europeans in the East may be explained by their different conditions of life. It is doubtful whether the distinction drawn between peslis minor and peslis major has a real etiological basis. Very mild cases occurring in the course of an outbreak of typical plague may be explained by greater power of resistance in individuals, but the epidemic prevalence of a mild illness preceding the appearance of undoubted plague suggests some difference or modification of the exciting cause. “It is impossible,” writes Sir Richard Thorne (Local Government Board Report, 1898–1899), “ to read the medical history of this disease in almost every part of the world without being impressed with the frequency with which recognized plague has been pre- ceded by ailments of such slight severity, involving some bubonic enlargement of glands and some rise in body-temperature, as to mask the real nature of the malady.” Considering the great importance of arresting the spread of infection at the outset, and the implicit reliance placed upon bacteriological criteria, the aetiology of such antecedent ailments deserves more attention than has hitherto been paid to it Of course plague does not stand alone in this respect. Epidemic outbreaks of other diseases—for instance, cholera, diphtheria and typhoid fever are often preceded and followed by the prevalence of mild illness of an allied type; and the true significance of this fact is one of the most important problems in epidemiology. In plague, however, it is of special importance, on account of the peculiarly insidious manner in which this disease fastens itself upon a locality.
The path by which the bacillus enters the body varies. In pneumonia cases it is presumed to enter by the air-passages, and in bubonic cases by the skin. The Bombay Plague Research Committee, whose experience is unequalled, say: “ In a number of instances points of inoculation were found on the extremities of patients, from which plague cultures were obtained, and in these cases buboes were found above the point of inoculation. In the majority of instances, however, no local indication could be found marking the point at which the microbe was implanted” From the fact that bacilli are hardly ever found in the blood of bubonic cases it may be inferred that they are arrested by the lymphatic glands next above the seat of inoculation, and that the fight-which is the illness-takes place largely in the bubo; in non-bubonic cases they are not so arrested, and the fight takes place in the general circulatory system, or in the lungs. As might be expected from these considerations, the bubonic type is very little infectious, while pneumonia cases are highly so, the patients no doubt charging the surrounding atmosphere by coughing. Whether infection can be introduced through the digestive tract by infected food is doubtful. The bacillus is non-resistant and easily killed by heat and germicide substances, particularly acids. Little is known of its toxic action; only a weak toxin has been obtained from cultures. Of the lower animals, mice, rats, guinea-pigs, rabbits, squirrels and monkeys are susceptible to the bacillus; horses, cattle, sheep, goats, pigs, dogs and cats are more or less resistant, but cats and dogs have been known to die of plague (Oporto, Daman, Cutch and Poona). In the Great Plague of London they were believed to carry the infection, and were killed in vast numbers The bacillus has been demonstrated in the bodies of fieas, flies, bugs and ants.
Clinical Characters.—One of the results of recent observation is the classification of plague cases under three heads, which have already been mentioned several times: (1) bubonic, (2) pneumonia, (3) septicaemic. (The word “pesti-caemic” is ​ also used instead of “septi-caemic,” and though etymologically objectionable, it is otherwise better, as “septicaemic” already has a specific and quite different meaning.) It should be understood that this classification is a clinical one, and that the second and third varieties are just as much plague as the first. It is necessary to say this, because a misleading use of the word “bubonic” has given rise to the erroneous idea that true plague is necessarily bubonic, and that non-bubonic types are a different disease altogether. The word “plague”—or “pest,” which is the name used in other languages—had originally a general meaning, and may have required qualifications when applied to this particular fever; but it has now become a specific label, and the prefix “bubonic” should be dropped.
The illness varies within the widest limits, and exhibits all gradations of severity, from a mere indisposition, which may pass almost unnoticed, to an extreme violence, only equalled by the most violent forms of cholera. The mild cases are always bubonic; the other varieties are invariably severe, and almost always fatal. Incubation is generally from four to six days, but it has been observed as short as thirty-six hours and as long as ten days (Bombay Research Committee). Incubation, however, is so difficult a thing to determine that it is unwise to lay down any positive limit. As a rule the onset is sudden and well marked. The symptoms may be described under the headings given above. (1) Bubonic cases usually constitute three-fourths of the whole, and the symptoms may therefore be called typical. In a well-marked case there is usually an initial rigor—in children convulsions—followed by a rise of temperature, with vomiting, headache, giddiness, intolerance to light; pain in epigastrium, back and limbs; sleeplessness, apathy or delirium. The headache is described as splitting; delirium is of the busy type, like delirium tremens. The temperature varies greatly; it is not usually high on the first day—from 101° to 103°—and may even be normal, but sometimes it rises rapidly to 104° or 105° or even 107° F.; a fall of two or three degrees on the second or third day has frequently been observed. The eyes are red and injected, the tongue is somewhat swollen, and at first covered with a thin white fur, except at the tip and edges, but later it is dry, and the fur yellow or brownish. Prostration is marked. Constipation is the rule at first, but diarrhoea may be present, and is a bad sign. A characteristic symptom in severe cases is that the patient appears dazed and stupid, is thick in speech, and staggers. The condition has often been mistaken for intoxication. There is nothing, however, in all these symptoms positively distinctive of plague, unless it is already prevalent. The really pathognomonic sign is the appearance of buboes or inflamed glands, which happens early in the illness, usually on the second day; sometimes they are present from the outset, sometimes they cannot be detected before the third day, or even later. The commonest seat is the groin, and next to that the axilla; the cervical, submaxillary and femoral glands are less frequently affected. Sometimes the buboes are multiple and on both sides, but more commonly they are unilateral. The pain is described as lancinating. If left, they usually suppurate and open outwards by sloughing of the skin, but they may subside spontaneously, or remain hard and indurated. Petechiae occur over buboes or on the abdomen, but they are not very common, except in fatal cases, when they appear shortly before death. Boils and carbuncles are rare. (2) Pneumonic plague was observed and described in many of the old epidemics, and particularly by two medical men, Dr Gilder and Dr Whyte, in the outbreak in Kathiawar in r8r6; but its precise significance was first recognized by Childe in Bombay. He demonstrated the presence of the bacilli in the sputa, and showed that the inflammation in the lungs was set up by primary plague infection. The pneumonia is usually lobular, the onset marked by rigors, with difficult and hurried breathing, cough and expectoration. The prostration is great and the course of the illness rapid The breathing becomes very hurried—forty to sixty respirations in the minute—and the face dusky. The expectoration soon becomes watery and profuse, with little whitish specks, which contain great quantities of bacilli. The temperature is high and irregular. The physical signs are those of broncho-pneumonia; oedema of the lungs soon supervenes, and death occurs in three or four days. (3) In septicaemic cases the symptoms are those of the bubonic type, but more severe and without buboes. Prostration and cerebral symptoms are particularly marked; the temperature rises rapidly and very high. The patient may die comatose within twenty-four hours, but more commonly death occurs on the second or third day. Recovery is very rare.
There is no reason for doubting that the disease described above is identical with the European plagues of the 14th and subsequent centuries. It does not differ from them in its clinical features more than epidemics of other diseases are apt to vary at different times, or more than can be accounted for by difference of handling. The swellings and discolorations of the skin which play so large a part in old descriptions would probably be equally striking now but for the surgical treatment of buboes. Similarly, the comparatively small destructiveness of modern plague, even in India, may be explained by the improved sanitary conditions and energetic measures dictated by modern knowledge. The case mortality still remains exceedingly high. The lowest recorded is 34% in Sydney, and the highest 95% at Hong Kong in 1899. During the first few weeks in Bombay it was calculated by Dr Viegas to be as high as 99%. It is very much higher among Orientals than among Europeans. In the Bombay hospitals it was about 70% among the former, and between 30 and 40% among the latter, which was much the same as in Oporto, Sydney and Cape Town. It appears, therefore, that plague is less fatal to Europeans than cholera. The average duration of fatal cases is five or six days, in the House of Correction at Byculla, where the exact period could be well observed, it was five and a half days. Patients who survive the tenth or twelfth day have a good chance of recovery. Convalescence is usually prolonged. Second attacks are rare, but have been known to occur.
Diagnosis.—When plague is prevalent in a locality, the diagnosis is easy in fairly well-marked cases of the bubonic type, but less so in the other varieties. When it is not prevalent the diagnosis is never easy, and in pneumonia and septicaemic cases it is impossible without bacteriological assistance. The earliest cases have hardly ever been even suspected at the time in any outbreak in a fresh locality. It may be taken at first for almost any fever, particularly typhoid, or for venereal disease or lymphangitis. In plague countries the diseases with which it is most liable to be confounded are malaria, relapsing fever and typhus, or broncho-pneumonia in pneumonia cases.
Treatment.—The treatment of plague is still symptomatic. The points requiring most attention are the cerebral symptoms—headache, sleeplessness, delirium, &c.—and the state of the heart. Alcohol and cardiac stimulants may be required to prevent heart failure. Speaking generally, it is important to preserve strength and guard against collapse. Extracts of supra-renal gland have been found useful. Buboes should be treated on ordinary surgical principles. An antitoxic serum has been prepared from horses by the Institut Pasteur in France, but has not met with success. The results in India obtained by British and various foreign observers were uniformly unfavourable, and the verdict of the Research Committee (1900) was that the serum had “failed to influence favourably the mortality among those attacked.” Success was somewhat noisily claimed for an improved method tried in Oporto, but the evidence is of little or no value. Of 142 cases treated, 21 died; while of 72 cases not treated, 46 died; but the former were all hospital patients, and included several convalescents and many cases of extreme mildness, whereas the non-serum cases were treated at home or not at all, some being only discovered when death had made further concealment impossible. Later observations have, however, established that the Yersin-Roux serum is of undoubted benefit when used early in the case, in fact during the first twenty-four hours. Very large doses, so much as 150 cc. may be injected subcutaneously or preferably intravenously, and it is stated to modify the whole course of ​ the disease. Another serum has been prepared by Lustig and Galeotti.
Morbid Anatomy:—(1) Bubonic cases. A bubo is found to consist of a chain of enlarged glands, surrounded by a mass of engorged connective tissue, coagulated blood and serum. Nearly all the lymphatic glands in the body are a little swollen, but the lymphatic vessels show little or no change. The spleen and liver are always enlarged, the former to sometimes twice or thrice its natural size. The lungs are engorged and oedematous, and often show haemorrhages. The kidneys are enlarged and congested. The serous membranes show petechiae and haemorrhages. The right side of the heart is frequently dilated, with clots in the cavities. The heart muscle is normal, or soft and friable. The substance of the brain, spinal cord and nerve-trunks is normal, but the membranes are engorged. (2) Pneumonic cases. The lymphatic glands are hardly affected. There is general engorgement and oedema of the lungs, with pneumonia patches varying in size and irregularly distributed. (3) Septicaemic cases. Nearly all the lymphatic glands in the body are involved, and have a characteristic appearance. They are enlarged to the size of an almond, rounded, firm and pink; there is some engorgement and oedema on section; the substance is rather soft, and can be scraped off with a knife. The surrounding tissue is not engorged or oedematous. The description of the other organs given under (1) applies also to (2) and (3).
Dissemination.—Given the bacillus, the questions arise, How is it disseminated? and What are the conditions that favour its propagation? That it is conveyed from person to person is an undoubted fact, proved by innumerable cases, and tacitly implied by the word “infectious,” which is universally allowed. The sick are a source of danger and one means of dissemination, and, since the illness may be so slight as to pass unrecognized, an obviously insidious one. The ambulatory plague patient goes far to explain the spread of the disease without leaving any track. But there is evidence that persons may carry the infection and give it to others without being ill at all themselves. One such case occurred at Glasgow, and another at Oporto. In the Glasgow case the wife of a laundryman employed in handling plague linen contracted the disease. She was brought into connexion with it in no other way, and there can be no doubt that she took it from her husband, though he was not ill at all himself. The Oporto instance is still more conclusive. Two little girls had plague at Argoncilhe, a suburb some miles from Oporto, and were the only cases which occurred in that place. Their father was a riverside labourer, who lodged during the week in Oporto, but went home for Sunday. He was not ill, but several cases of plague occurred in the house in which he lodged. How the poison passes from one person to another is less clear. In pneumonia cases patients no doubt spread it around them by coughing, and others may take it up through the air-passages or the skin; but even then the range of infection is small, and such cases are comparatively rare. In the vast majority of cases the bacilli are in the lymphatic or the circulatory system, and aerial convection, even for a short distance, seems highly improbable. This view is borne out by the experience in hospitals and with “contacts,” which goes to show that with reasonable care and under fair conditions the risk of infection from ordinary plague patients is very small. When persons live crowded together in closing contact, and when they are careless with regard to discharges of all kinds from patients, the risk is obviously much increased. Discharges-vomited matters, sputa, urine and faeces-are possible media by which plague is spread from person to person. They also contaminate clothing, which thus becomes another means of dissemination capable of acting at a distance. This is the most probable explanation of the two cases of indirect infection related above. Failure to catch or induce plague from clothing that has been worn by plague patients proves nothing Such cloth.ng is not necessarily infectious; indeed, the probability is that it is not, unless contaminated by discharges. There is no evidence that merchandise and foodstuffs are means of dissemination, but a great deal of evidence against such a theory. Then we come to the lower animals. Attention has been concentrated on rats, and some observers seem disposed to lay upon them the whole blame for the propagation and spread of plague, which is held to be essentially a rat-borne disease. The susceptibility of rats has been noted from remote times and in many countries, particularly in China, but it has never attracted so much attention as during the recent prevalence of plague. From one place after another a great mortality among rats was reported, and the broad fact that they do die of plague IS incontestable. It is therefore easily intelligible that they may play an important part in multiplying and fixing the poison on a locality. As to how they convey it from man to man the greatest probability is in favour of the fiea as an intermediary. Mortality among rats is said to precede the appearance of human plague, but the evidence of this is always retrospective and of a very loose character. At Sydney a careful investigation was made; and the conclusion reached by Dr Tidswell was that “there was no ground for even a suspicion that our epidemic was being maintained by any process of direct contagion between man and man,” but that rats were the carriers. In Glasgow the experience was just the contrary. Personal connexion was traced in every case, and rats excluded; there was no mortality among them, and of 300 caught and examined none had plague (Chalmers). Similarly, at Oporto, personal connexion was traced in all the earlier cases; there was no mortality among rats, and no evidence to connect them with the outbreak (Jorge). Again, a comparison between rat infested and rat-free districts in Bombay showed a much higher incidence of plague in the latter. A campaign against rats in Bombay, by which 50,000 or 60,000 were killed in a short time, had no effect in checking the disease. Plague-rats have rarely been found in ships sailing from infected ports; and though millions of these animals must have been carried backwards and forwards from quay to quay between Hong-Kong, Bombay and the great European ports, they have not brought the disease ashore.
By far the most important communication on the role of rats in the spread of plague is formed by the “Report on the Plague Investigations in India” (Journal of Hygiene, vol. vi. No. 4; vol. vii. No. 3, 1907). The chief conclusions arrived at in the report as the result of experiments are the following:—
1. Healthy rats contracted plague from infected rats when the only apparent means of communication between the two was the rat flea (pulex cheopis).
2. In 21 experiments out of 38, 55% of healthy rats living in flea-proof cages have contracted plague after receiving fleas collected from rats either dead or dying of septicaemic plague; consequently it is proved the rat flea can transmit plague from rat to rat.
3. Close and continuous contact of plague-infected animals with health ones does not infect the latter if fleas are excluded.
4. Should fleas be present an epizootic at once starts and spreads in proportion to the number of fleas present.
5. Guinea-pigs set free in plague-infected houses become infected with the rat flea and develop plague in a certain percentage.
6. Fleas caught on plague-infected rats are able to infect rats placed in flea-proof cages.
7. Guinea-pigs placed in plague-infected houses do not contract plague if they are protected from fleas; those placed in cages protected by a border of sticky paper at least six inches in radius, which the fleas cannot jump over, do not contract plague; the Others not similarly protected, do.
8. Chronic plague may prevail in rats.
On this report it may, therefore, be taken that aerial infection, except, perhaps, in pneumonic cases, may be excluded, and that the chief source of infection is the flea. It was also shown that animals may become infected through the faeces of a Bea which has been fed on plague-infected rats. This may serve to explain the manner in which plague-infected linen and clothing may convey the disease. The report also considers it proved that the bacillus pestis multiplies in the stomach of a flea and may remain a considerable time within its host.
Browning Smith says the following facts are admitted as known. (1) Plague can be carried by fleas rom an unhealthy rat. (2) A flea can retain the plague bacilli alive for seven or eight days. (3) Man is, in the majority of cases, infected through the skin, though the puncture may not be seen. (4) The rat flea, when finding no rats, will attack man and it will also attack other animals.
​ Very little light has been thrown on the conditions which favour the prevalence of plague. We do not know why it has developed a diffusive activity of late years, nor why it has attacked some places and consistently passed by others, such as Singapore. The words “dirt” and “insanitary conditions” are much used, but such general terms explain nothing. Singapore, where plague has several times been introduced, but never taken hold, is probably quite as dirty and insanitary as Hong-Kong, and it is pertinently remarked by the Bombay Research Committee that filth per se has but little influence, inasmuch as “there occurred in the House of Correction at Byculla, where cleanliness is brought as near to perfection as is attainable, an outbreak which exceeded in severity that in any of the filthy chawls and tenements around.” Again, in Oporto there is an area which combines every possible sanitary defect—dense overcrowding, great poverty, no light, no air, no drainage, no scavenging, water brought in buckets. Plague got into this quarter, but did not spread there; on the other hand, it appeared in other and vastly superior parts of the town Yet in at least one case neither the patient nor the “contacts” were removed, but were all shut up in one room with a sentry at the door and another in the street. The seasonal variations have been well marked and extremely regular in Bombay. The disease begins to be active in late autumn or the beginning of winter, and reaches its height in February or March, dying down in the summer. Baldwin Latham made an elaborate examination of the meteorological conditions, and more particularly of the vapour tension, from which he draws the conclusion that the seasonal variations are due to exhalation from the ground. His observations are original and worth attention A simpler explanation is that the people live more indoors, and are so more exposed to infection during the plague season. The curve shows two rises, one at the beginning of winter, and the other at the commencement of the monsoon, and at both these times the people are driven indoors. A broad survey of the epidemiological facts suggests some general conclusions. The outbreaks fall into two well-defined groups. (1) those in which the disease is destructive and persistent, (2) those in which its effects are slight and transient. In the former the poison clearly fastens on the locality, and gradually increases its hold. The place is infected, not merely the people in it; for if they evacuate it, the disease soon ceases among them, and if they return in a short time, they are again attacked. Now the poison is contained, as we have already seen, in the discharges from patients, and in such infected localities the standing conditions and the habits of the people combine to retain the discharges on the premises. The floors, mostly of mud covered with dung, are fouled with spittle, vomit, and urine, and, being seldom or never cleaned out, foster a gradual accumulation of poison, to which infected rats and the concealment of illness contribute. These are just the conditions which prevailed in Europe in the old plague days. They do not prevail now in those “white countries” which have been invaded but have repelled the attack with comparative ease and little loss. It may be concluded, with some confidence, from experience and theory alike, that localities where they do not prevail may fail to keep plague out, but have very little to fear from it, except the disturbance of trade caused by the traditional terrors that still cling to the name.
Prevention.—The principles are the same as those which govern the prevention of other infectious diseases. “Sanitary cordons” and the like are obsolete. International procedure is supposed to be regulated by the Venice convention of 1897 (see Quarantine), but that instrument contains an optional clause, which allows countries to do as they please with their own frontiers Except Great Britain and Germany, they all retain quarantine in a more or less stringent form at seaports. It is generally used as a system of local extortion imposed upon travellers and shipping According to the Venice convention, ships are divided into (1) healthy, (2) suspected, (3) infected. (1) Healthy are those free from plague throughout the voyage; (2) suspected, those in which plague has occurred, but no fresh case within twelve days; (3) infected, those in which plague has occurred within twelve days. Great Britain relies on medical inspection, removal of sick or suspected cases, and supervision of the healthy arriving on an infected ship, infected clothing is burnt and infected ships are disinfected. The procedure is the same as for cholera, but it has been equally successful. Ships passing through the Suez Canal are subject to similar inspection, sick persons are landed at Moses Wells, and suspected ones detained. The risk of importing plague from India has been materially lessened by medical inspection of outward-bound ships at the principal ports. This has been very thoroughly carried out at Bombay with good results. In 1897 pilgrimages from India to the Hedjaz were prohibited. By the Venice convention a number of articles of merchandise are classed as susceptible and liable to be refused admission, but the only ones which there is any reason to consider dangerous are used clothing and rags. A watch should be kept on rats at ports of arrival and on board ships from infected countries.
When plague is present in a place, the measures to be taken are the usual ones for dealing with infectious disease, with some additions. The sick and suspected should be removed in special ambulances to an isolation hospital, their soiled linen, &c., should be burnt, and the premises disinfected. Corrosive sublimate in an acid solution is the best disinfectant, but sulphuric acid, 1 in 250, is efficient and cheaper. Suspected cases should be bestowed in a special isolated building until the diagnosis is fully determined. “Contacts” should be kept under observation. Rats should be exterminated as far as possible, especially by means of the Danysz virus, which spreads a disease amongst rats which cannot be communicated to man. The greatest care should be taken in dealing with the hospital linen and discharges from patients. Hospital staffs should be kept apart. Inoculation with Haffkine’s prophylactic fluid should be offered to all persons willing to avail themselves of it. It is especially desirable for hospital and ambulance staffs to be inoculated with a vaccine prepared from sterilized cultures of plague bacillus. Inoculation is harmless, and the results obtained in India justify a favourable opinion of its protective efficacy. At Hubli, where nearly the whole population was inoculated between the 11th of May and the 27th of September ​1898, the mean mortality among the inoculated was 1·3%; among the uninoculated 13·2%. At Daman the mortality was—inoculated 1·6%, uninoculated 24·6%; at Dharwar, inoculated 1·2%, uninoculated 5·2%. In all these cases the numbers dealt with were large and the test fair.
Simpson, in The Practitioner (Dec. 1906), gives an analysis of the results of Haffkine’s serum inoculations as follows:—
In Poona, out of 5595 uninoculated cases the incidence was 6·8%, while in 1500 inoculated cases it was only 0·33%. Klein also prepares a new prophylactic from the dried organs of a guinea-pig, and one of the most interesting experiments is that of Strong (Archiv für Schiffs- und tropische Hygiene, April, 1906), who uses for producing immunity in man a living virulent culture of the bacillus pestis. He immunized 40 persons without mishap and with no more unpleasant results than those occurring after vaccination. Inoculation protects against attack, and greatly modifies the illness when it fails to protect. How long the protection lasts has not been determined, but it appears to be several months at least.
The main authorities for the researches into plague are in the official reports of recent years from India and elsewhere. See generally W. J. Simpson, A Treatise on Plague (1905).  (A. Sl.; H. L. H.)
* ↑ Amm. Marcell. xxiii. 7; see Hecker, De peste Antoniana (Berlin, 1835).
* ↑ Lib. xliv. cap. 17—Œuvres de Oribase, ed. Bussemaker and Daremberg (Paris, 1851), iii 607.
* ↑ Evagrius, Hist. eccles. iv. 29; Procopius, De bello persico, ii. 22, 23.
* ↑ See Noah Webster’s History of Epidemic Diseases, 8vo (2 vols., London, 1800) (a work which makes no pretension to medical learning, but exhibits the history of epidemics in connexion with physical disasters—as earthquakes, famines, &c.); Lersch, Kleine Pest-Chronik (8vo, 1880) (a convenient short compendium, but not always accurate); “Athanasii Kircheri Chronologia Pestium ” (to A.D. 1656), in Scrutinium pestis (Rome, 1658; Leipzig, 1671, 4to); Bascome, History of Epidemic Pestilences (London, 1851, 8vo). The most complete medical history of epidemics is Haser’s Geschichte der epidemischen Krankheiten (3rd ed., Jena, 1882), forming the third volume of his History of Medicine.
* ↑ See the original account reprinted with other documents in Haser, op. cit.; also Hecker, Epidemics of the Middle Ages, trans. by Babington, Sydenham Soc. (London, 18); Volkskrankheiten des Mittelalters, ed. Hirsch (Berlin, 1865); R. Hoeniger, Der schwarze Tod in Deutschland (Berlin, 1882).
* ↑ Vochs, Opusculum de pestilentia (1537); Fracastorius, “De Contagione, &c..” Opera (Venice, 1555); Hieron. Mercurialis, De peste, praesertim de Veneta et Patavina (Basel, 1577); Prosper Borgarutius, De peste (Venice, 1565), 8vo; Filippo Ingrassia, Informatione del pestifero morbo . . . Palermo e . . . regno di Sicilia (1575–1576, 4to, Palermo, 1576–1577); A. Massaria, De peste (Venice, 1597651 Diomedes Amicus, Tres tractatus (Venice, 1599), 4to; Victor de Bonagentibus, Decem problemata de peste (Venice, a 556), 8vo; Georgius Agricola, De peste libri tres (Basel, 1554) 8vo. he works of English physicians of this period are of little medical value; but Lodge s Treatise of the Plague (London, 1603) deserves mention.
* ↑ Josephus Ripamontius, De peste anni 1630 (Milan, 1641), 4to.
* ↑ For this period see Index to Remembrancia in Archives of City of London 1579–1664 (London, 1878); Richardson, Plague and Pestilence in North of England (Newcastle, 1852).
* ↑ Graunt, Observations on the Bills of Mortality (3rd ed., London, 1665).
* ↑ On the plague of 1665 see Nath. Hodges, Loimologia sive pestis nuperae apud populum londinensem narratio (London, 1672) 8vo—in English by Quincy (London, 1720), (the chief authority); Λοιμογραφία. or an Experimental Relation of the last Plague in the City of London, by William Boghurst, apothecary in St Giles’s-in-the-Fields (London, 1666),—a MS in British Museum (Sloane 349), containing important details; George Thomson, ΛΟΙΜΟΤΟΜΙΑ, or the Pest Anatomized, 8vo (London, 1666); Sydenham, “Febris pestilentialis et pestis annorum 1665–1666,” Opera, ed. Greenhill, p. 96 (London, 1844); Collection of Scarce Pieces on the Plague in 1665 (London, 1721), 8vo; Defoe’s fascinating Journal of a Citizen, which should be read and admired as a fiction, but accepted with caution as history; T. Vincent (minister of the gospel), God’s Terrible Voice in the City, 8vo (London, 1667); Calendar of State Papers (1665–1666; “Domestic” series), by M. E. Green.
* ↑ Relation historique de la pests de Marseille (Cologne, 1721, Paris, 1722, &c); Chicoyneau, Verny, &c., Observations et reflexions . . de la peste (Marseilles, 1721); Chicoyneau, Traité de la peste, Paris, 1744); Littré, article “Peste,” in Dictionnaire de médicine, xxiv. (Paris, 1841).
* ↑ D’Antrechaus, Relation de la peste de Toulon en 1721 (Paris, 1756); G. Lambert, Histoire de la peste de Toulon en 1721 (Toulon, 1861), quoted by Haser, Gesch. der epidem. Krankh.
* ↑ Adam Chenot, Abhandlung von der Pest (Dresden, 1776); De Peste (Vienna, 1766).
* ↑ Samoilowitz, Mémoire sur la peste en Russie, 1771 (Paris, 1783); Mertens, De la peste en 1771 (Paris, 1784)
* ↑ Lorinser, Pest des orients (Berlin, 1837) p. 103; Schraud, Pest in Syrmien, 1795 (2 vols, Pest, 1801).
* ↑ From the annals of the Moravian community of Sarepta on the Volga, Geschuhte der Bruder-Gememde Sarepta, by A. Glitsch (Sarepta and Berlin, 1865); also Tholozan, Epidémies de peste du Caucase (Paris, 1879).
* ↑ On the Plague in Malta (London, 1820), 8vo; J. D. Tully, History of the Plague in Malta, Gozo, Corfu and Cephalonia (London, 1821), 8vo; White, Treatise on the Plague (at Corfu) (London 1847); Calvert, " On the Plague in Malta, 1813," Med.-Chi. Transactions, vi. 1.
* ↑ A. Gosse, Relation de la peste en Grece, 1827–1828 (Paris, 1838).
* ↑ Lorinser, Pest des orients, p. 319.
* ↑ For the authorities, see Haser, Op. cit.
* ↑ Report of Local Government Board 1879–1880, suppl., p. 42.
* ↑ Tholozan, La Peste en Turquie dans les temps modernes (Paris, 1880).
* ↑ J. Netten Radcliffe, Report of the Medical Officer of the Privy Council, &c. (1875); also in Papers on Levantine Plague, presented to parliament (1879), p. 7.
* ↑ Tholozan, La Peste en Turquie, p. 86.
* ↑ See his report cited by Radcliffe, Papers on Levantine Plague (1879).
* ↑ J. Netten Radcliffe, Reports; Tholozan, Histoire de la peste bubonique en Perse (Paris, 1874).
* ↑ See Radcliffe, Reports (1879–1880); Hirsch and Sommerbrodt, Pest-Epidemie 1878–1879 in Astrachan (Berlin, 1880); Zuber, La Peste d’Astrakhan en 1878–1879 (Paris, 1880); Colvill and Payne, Report to the Lord President of the Council (1879).
* ↑ The dates are all reduced to new style.
* ↑ On Indian plague, see Francis, Trans. Epidem. Soc. Lond. iv. 407–408; John Murray, ibid., vol. iv. part 2; J. N. Radcliffe, Reports of Local Government Board (1875, 1876, 1877 and for 1879–1880); Parliamentary Papers (1879); Frederick Forbes, On Plague in North-West Provinces of India (Edinburgh, 1840) (Dissertation); Hirsch, Handbuch der historischen-geogr. Pathologie, i. 209 (1860), (Eng. trans. by Creighton, London, 1883); Hecker’s Volkskrankheiten des Mittelalters (Berlin, 1865), p. 101; Webb, Pathologia indica (2nd ed., Calcutta, 1848).
* ↑ See J. N. Radcliffe’s Report for 1879–1880, p. 45; Manson in Reports of Imperial Chinese Customs, special series No. 2, for half-year ended the 31st of March 1878, 15th issue (Shanghai); Lowry, “Notes on Epidemic Disease at Pakhoi” (1882), ibid., 24th issue, p. 31.
* ↑ The system of inoculation against plague with a fluid prepared from sterilized virus of the disease was introduced in India by Professor Haffkine earl in 1897. The composition of this fluid was subjected to a searching inquiry by the Indian Plague Commission, who pronounced its employment to be free from danger, and it was used on a large scale in various parts of India without producing injurious effects. In September 1902 the standard method of manufacturing this fluid was changed) b the director of the Plague Institute on his own authority, with the object of expediting the process, and thus meeting the heavy demand then being made by the Punjab government in connexion with a large scheme of inoculation. The change involved the omission of a small proportion of carbolic acid which had up till then been added to the original fluid as a further precaution against contamination. The new fluid, or water agar process, contained no carbolic acid, other methods being relied upon to ensure its purity. On the 6th of November 1902, nineteen persons who had been inoculated on the 30th of October in the villa e of Malkowal from a single bottle (labelled 53-n) of the new fluid were found to be suffering from tetanus, and all of them subsequently died. A commission, consisting of Sir Lawrence Tenkins, Lieut.-Colonel Bomford, M.D., principal of the Medical College, Calcutta, and Major Semple, R.A.M.C., director of the Pasteur Institute, Kasauli, was appointed by the government of India to inquire into the disaster. They found that the germ of tetanus had been introduced into the fluid before the bottle was opened at Malkowal, and they thought it probable that this might have occurred owing either to insufficient sterilization or to the process of filling the bottle from a larger flask having been performed with defective precautions. They also expressed the opinion that carbolic acid was a valuable agent in restraining tetanus growth when added to plague prophylactic, and they, therefore, thought that its omission was a grave mistake. Experiments undertaken in India by two independent inquiries appeared to confirm the view, and their conclusions, together with the data on which they were based, were submitted with the report of the commission for examination and further experiment to the Lister Institute in London. With reference to the findings of the Malkowal commission the Institute were asked to report: (1) On the comparative efficacy of the standard and new fluids as a protection against plague; (2) on the comparative liability of each fluid to contamination, and (3) on the probable origin of tetanus virus in the Malkowal cases. Their report on these points (Dec. 1904) contained the following conclusions: (1) “The Institute sees no reason to differ from the conclusions of the commission that the new prophylactic is not less efficacious than the old. (2) The Institute is of opinion that in the hands of more or less unskilled workers it is easier to ensure freedom from contamination by Haffkine’s ‘standard method’ of manufacturing plague vaccine than with the ‘water agar process’ as employed by him. (3) The Institute is in entire agreement with the commission as to the value of 5% carbolic acid in restraining tetanus growth when added to plague prophylactic, and its experiments emphasize still further the importance of this addition in preventing growth and toxin formation in a vaccine which might be liable to the possibility of contamination with spores of tetanus. (4) The conclusions of the Institute coincide with those of the commission that in all probability tetanus was at the time of inoculation in the fluid contained in the bottle, but that it is impossible to determine at what stage in its history or in what way the bottle (53-n) became contaminated.”  The government decided, on the advice of the director, that only the standard fluid should be manufactured at the lague institute. This fluid was sterilized by methods approved by tile Indian Plague Commission and contained the requisite proportion of carbonic acid It was bottled by a new method patented by Dr E. Maynard.  The result of the inquiries by the commission and the Lister Institute led to a protracted controversy with regard to the responsibility of Mr Haffkine’s laboratory, and to his subsequent treatment by the government of India; and the leading bacteriologists in England warmly took up his cause. A parliamentary “Return of Papers” was issued in June 1907, and in The Times of the 29th of July there appeared a letter signed by the distinguished pathologists, Ronald Ross, R. T. Hewlett, A. S. Grunbaum, W. J. Simpson, R. F. C. Leith, W. R. Smith, G. Sims Woodhead, E Klein, S. Flexner and C. Hunter Stewart, pointing out that the evidence, so far from showing that Mr Haffkine’s laboratory was to blame, made it clear to those acquainted with bacteriological work that It could have had nothing to do with the occurrence They agreed that there was strong evidence to show that “the contamination took place when the bottle was opened at Malkowal, owing to the abolition by the plague authorities of the technique prescribed by the Bombay laboratory, and to the consequent failure to sterilize the forceps which were used in opening the bottle, and which during the process were dropped on the ground”; and they complained of the inadequacy of the inquiries made by the Indian government, and called for Mr Haffkine’s exoneration The evidence showed that It had been much too readily believed that the tetanus germs llad entered the fluid before the bottle was opened, and that a grave injustice had been done to Mr Haffkine. Acting on this view, in November 1907, the Indian government invited Mr Haffkine again to take up work in India.