Causes of Medieval Leprosy.
What was there in the medieval manner of life to give rise to a certain number of cases of leprosy in all the countries of Europe? Granting that not all who were called leprosi and leprosae, were actually the subjects of lepra as correctly diagnosed, and that the misnomer was not unlikely to have been applied in the case of princes, nobles and great ecclesiastics, we have still to reckon with the apparition of leprosy among the people in medieval Europe and with its gradual extinction, an extinction that became absolute in most parts of Europe before the Modern period had begun.
Of the “importation” of leprosy into Britain from some source outside there can be no serious thought; the words are a meaningless phrase, which no one with a real knowledge of the conditions, nature and affinities of leprosy would care to resort to. The varying types of diseases, or their existence at one time and absence at another, are a reflex of the variations in the life of the people—in food and drink, wages, domestic comfort, town life or country life, and the like. No one doubts that the birth-rate and the death-rate have had great variations from time to time, depending on the greater or less abundance of the means of subsistence, on overcrowding, or other things; and the variation in the birth-rate and death-rate is only the most obvious and numerically precise of a whole series of variations in vital phenomena, of which the successions, alternations, and novelties in the types of disease are the least simple, and least within the reach of mere notional apprehension or mere statistical management. The apparition and vanishing of leprosy in medieval Europe was one of those vital phenomena. It may be more easily apprehended by placing beside it a simple example from our own times.
The pellagra of the North Italian peasantry (and of Roumania, Gascony and some other limited areas) is the nearest affinity to leprosy among the species of disease. Strip leprosy of all its superficial and sentimental characters, analyse its essential phenomena, reduce its pathology to the most correct outlines, and we shall find it a chronic constitutional malady not far removed in type from pellagra. In both diseases there are the early warnings in the excessive sensibility, excessive redness and changes of colour, at certain spots of skin on or about the face or on the hands and feet. In both diseases, permanent loss of sensibility follows the previous exaggeration, blanching of the skin will remain for good at the spots where redness and discoloration were apt to come and go, and these affections of the end-regions of nerves will settle, in less definite way, upon the nervous system at large,—the cerebro-spinal nervous system, or the organic nervous system, or both together. What makes leprosy seem a disease in a different class from that, is the formation of nodules, or lumps, in the regions of affected skin in a certain proportion of the cases. If leprosy were all anaesthetic leprosy, its affinities to pellagra would be more quickly perceived; it is because about one-half of it has more or less of the tuberculated character that a diversion is created towards another kind of pathology. But the fact that some cases of leprosy develop nodules along the disordered nerves does not remove the disease as a whole from the class to which pellagra belongs. In both diseases we are dealing essentially with a profound disorder of the nerves and nerve-centres, commencing in local skin-affections which come and go and at length settle, proceeding to implicate the nervous functions generally, impairing the efficiency of the individual, and bringing him to a miserable end. The two diseases diverge each along its own path, leprosy becoming more a hopeless disorder of the nerves of tissue-nutrition, and so taking on a structural character mainly but not exclusively, and pellagra becoming more a hopeless disorder of the organic nervous system (digestion, circulation, etc.) with implication of the higher nervous functions, such as the senses, the intellect, and the emotions, and so taking on a functional character mainly but not exclusively. The correlation of structure and function is one that goes all through pathology as well as biology; and here we find it giving character to each of two chronic disorders of the nervous system, according as the structural side or the functional side comes uppermost.
What, then, are the circumstances of pellagra, and do these throw light upon the medieval prevalence of leprosy? Pellagra has been proved with the highest attainable scientific certainty to be due to a staple diet of bread or porridge made from damaged or spoilt maize. It followed the introduction of maize into Lombardy at an interval of two or three generations, and its distribution corresponds closely to the poorer kinds of maize on colder soils, and to the class of the peasantry who get the worst kind of corn or meal for their food. The cases of the disease among the peasantry of Lombardy and some other maize-growing provinces of Northern Italy, were about one hundred thousand when last estimated; the endowed charitable houses and lunatic asylums are full of them. The connexion of the disease with its causes is perfectly well understood; but the economic questions of starvation wages, of truck, of large farms with bailiffs, and of agricultural usage, have proved too much for the chambers of commerce and the Government; so that there is as yet little or no sign of the decline of pellagra in the richest provinces of Italy. This disease is not mentioned in the Bible, therefore it has no traditional vogue; it is not well suited to knight-errantry, because it is a common evil of whole provinces; its causes are economic and social, therefore there is no ready favour to be earned by systematic attempts to deal with them; and there is absolutely no opening for heroism and self-sacrifice of the more ostentatious kind. These are among the reasons why this great object-lesson of a chronic disorder of nutrition, proceeding steadily before our eyes, has been so little perceived. It is in pellagra, however, that we find the key to the ancient problem of leprosy. The two diseases are closely allied in the insidious approach of their symptoms, in their implicating the tissue-nutrition through the nerves, or the nervous functions through the nutrition, in their cumulating and incurable character, and in their transmissibility by inheritance. Thus nosologically allied, they may be reasonably suspected of having analogous causes; and as we know the cause of modern pellagra to be something noxious in the habitual diet of the people, we may look for the cause of medieval leprosy in something of the same kind.
The dietetic cause is not far to seek, and it cannot be stated better than in the following well-known passage by the philosophical Gilbert White in his Natural History of Selborne[206]:—
“It must, therefore, in these days be, to a humane and thinking person, a matter of equal wonder and satisfaction, when he contemplates how nearly this pest is eradicated, and observes that a leper is now [1778] a rare sight. He will, moreover, when engaged in such a train of thought, naturally inquire for the reason. This happy change perhaps may have originated and been continued from the much smaller quantity of salted meat and fish now eaten in these kingdoms; from the use of linen next the skin; from the plenty of bread; and from the profusion of fruits, roots, legumes, and greens, so common in every family. Three or four centuries ago, before there were any enclosures, sown-grasses, field-turnips, or field-carrots, or hay, all the cattle which had grown fat in summer, and were not killed for winter use, were turned out soon after Michaelmas to shift as they could through the dead months; so that no fresh meat could be had in winter or spring. Hence the marvellous account of vast stores of salted flesh found in the larder of the eldest Spencer even so late in the spring as the 3rd of May (600 bacons, 80 carcases of beef, and 600 muttons)[207]. It was from magazines like these that the turbulent barons supported in idleness their riotous swarms of retainers, ready for any disorder or mischief. But agriculture is now arrived at such pitch of perfection, that our best and fattest meats are killed in the winter; and no man needs eat salted flesh, unless he prefers it, that has money to buy fresh.
“One cause of this distemper might be no doubt the quantity of wretched fresh and salt fish consumed by the commonalty at all seasons as well as in Lent, which our poor now would hardly be persuaded to touch.... The plenty of good wheaten bread that now is found among all ranks of people in the south, instead of that miserable sort which used, in old days, to be made of barley or beans, may contribute not a little to the sweetening their blood and correcting their juices.”
Let us add to this, that the meat diet of the poorer class, whether serfs or freemen, would be apt to consist of the more worthless portions, the semi-putrid pieces in the salted sides of bacon, mutton or beef, and that badly-cured pork was in many parts the usual kind of flesh-food; and we shall have no difficulty in finding the noxious element in the diet of the Middle Ages, which the dietetic hypothesis of leprosy requires. Some who have advocated that hypothesis for modern leprosy, have laid themselves open, notwithstanding the ability and industry of their research, to plausible objections which have no bearing if the hypothesis be sufficiently safe-guarded. Leprosy, like every other morbus miseriae, needs a number of things working together to produce it, its more or less uniform specific character or distinctive mark being determined by the presence of one factor in particular. The special factor should be generalised as much as possible, so as to cover the whole circumstances of leprosy: it is not only half-cured or semi-putrid fish[208], but half-cured or semi-putrid flesh of any kind. The most general expression for leprosy is a semi-putrid or toxic character of animal food, just as for the allied pellagra, it is a semi-putrid or toxic character of the bread or porridge. Moreover it is that noxious or unnatural thing in the food, not once and again, or as a bonne bouche, but somewhat steadily from day to day as a chief part of the sustenance, and from year to year. As the rain-drops wear the stones, so the poison in the daily diet tells upon the constitution. Once more, such special causes may be present in a country generally, among the poor of all the towns, villages and hamlets, and yet only one person here and there may show specific effects that are recognisable as a disease to which we give a name. Unless there be present the aiding and abetting things, the special factor will hardly make itself felt; and if there be not the special factor, there may be some other morbus miseriae but there will not be that one. These aiding things are for the most part the usual concomitants of poverty and hardships, wearing out the nerves far more than is commonly supposed and producing in ordinary an excessive amount of nervous affections among the poor. But among the poor themselves, as well as among the well-to-do, there are special susceptibilities in individuals and in families. One person may have the same unwholesome surroundings as another and the same poisonous element in his diet, but he may fall into no such train of symptoms as his leprous neighbour because he is not formed in quite the same way, because he has “no nerves,” or is of a hardier stock, or because his unwholesome manner of life comes out in some other form of disease (scrofula perhaps, less probably gout), or for some other reason deeply hidden in his ancestry and his personal peculiarities. The chances would be always largely against that particular combination of factors needed to make leprosy. It was a morbus miseriae of the Middle Ages, but on the whole not a very common one; and it was easily shaken off by the national life when the conditions changed ever so little. It was all the more easily shaken off by reason of the facilities for divorce, the prohibition of marriage, and the monastic discipline.
The staple diet as a cause of leprosy was suspected in the Middle Ages, and by writers as ancient as Galen. It is not without significance that the minute directions for the dieting of the lepers in the rich hospital of Sherburn, near Durham, urge special caution as to the freshness of the fish: when fresh fish was not to be had, red herrings might be substituted, but only if they were well cured, not putrid nor corrupt. Those directions were in accordance with the best medical teaching of the time on the dietetics of leprosy, or on how to prevent leprosy, as it is given with considerable minuteness in Gordonio and Gilbert[209].
On the other hand we find a singular ordinance of the Scots Parliament at Scone in 1386, or some forty years after the date of the Durham regulations: “Gif ony man brings to the market corrupt swine or salmond to be sauld, they sall be taken by the Bailie and incontinent without ony question sall be sent to the lepper-folke; and gif there be na lepper-folke, they sall be destroyed alluterlie[210].” Nothing could be more significant for the prevalence and persistence of leprosy in Scotland[211]. Putrid fish and pork did actually come to market; the dangers of them as regarded the production of leprosy were unsuspected; and the lepers (genuine or mistaken) were actually directed to be fed with them. Such food for “lepers” could only have fed the disease; and if it be the case that genuine leprosy was met with in Edinburgh and Glasgow more than two centuries after it ceased to be heard of in England, we need be at no loss to assign the reason why the disease was more inveterate in the one country than in the other.
CHAPTER III.
THE BLACK DEATH.
The most likely of the fourteenth-century English annalists to have given us a good account of the Black Death was the historian Ranulphus Higden, author of the Polychronicon, who became a monk of St Werburgh’s abbey at Chester about the beginning of the century, and lived to see the disastrous year of 1349[212]. That part of his history which relates to his own period he brings down year by year to 1348, with less fulness of detail in the later years, as if old age were making him brief. Under the year 1348 he begins the subject of the great mortality, speaks of the incessant rains of the second half of the year from Midsummer to Christmas, refers to the ravages of the plague at Avignon, the then ecclesiastical capital of Christendom, just mentions England and Ireland, and then lets the pen fall from his hand. Higden is believed to have resumed his annals after 1352; but he was then a very old man, and the last entries are unimportant. But the period from 1348 to 1352 is an absolute blank. He comes to the edge of the great subject of that time, as if he had intended to deal with it comprehensively, beginning with a notice of the previous weather, which is by no means irrelevant, and after two or three lines more he breaks off. Most of the monastic chronicles are interrupted at the same point; if there is an entry at all under the year 1349 it is for the most part merely the words magna mortalitas. The prevailing sense of desolation and despair comes out in the record made by a friar of Kilkenny, who kept a chronicle of passing events, and escaped the fate of his brethren in the convent only long enough to record a few particulars of the great mortality[213]:
“And I, friar John Clyn, of the Order of Friars Minor, and of the convent of Kilkenny, wrote in this book those notable things which happened in my time, which I saw with my eyes, or which I learned from persons worthy of credit. And lest things worthy of remembrance should perish with time, and fall away from the memory of those who are to come after us, I, seeing these many evils, and the whole world lying, as it were, in the wicked one, among the dead waiting for death till it come—as I have truly heard and examined, so have I reduced these things to writing; and lest the writing should perish with the writer, and the work fail together with the workman, I leave parchment for continuing the work, if haply any man survive, and any of the race of Adam escape this pestilence and continue the work which I have commenced.”
There is nothing in the English chronicles so directly personal as that, but there are some facts recorded of the mortality in four of them which have contemporary value, or almost contemporary. The best of these accounts, as a piece of history, is that of Henry Knighton, canon of Leicester[214], who acknowledges his indebtedness to Higden’s Polychronicon for the events down to 1326, but after that date either writes from his own observation or takes his facts from some unknown contemporary source. The next in importance is Geoffrey le Baker[215], a clerk of the abbey of Osney, near Oxford, whose account of the arrival of the Black Death in England has obtained wide currency as copied literally in the 1605 edition of Stow’s Annals. The third is Robert de Avesbury[216], whose History of Edward III. serves as a chronicle for the city of London more particularly. The fourth is the Malmesbury monk who wrote, about 1367, the chronicle known as the Eulogium[217].
From the systematic paragraphs of those writers, and from various other incidental notices, an outline of the progress of the pestilence in England, Scotland and Ireland, may be traced. It entered English soil at a port of Dorsetshire—said in the Eulogium to have been Melcombe (Weymouth)—in the beginning of August, 1348. It is said to have spread rapidly through Dorset, Devon and Somerset, almost stripping those counties of their inhabitants, and to have reached Bristol by the 15th of August. The people of Gloucester in vain tried to keep out the infection by cutting off all intercourse with Bristol; from Gloucester it came to Oxford, and from Oxford to London, reaching the capital at Michaelmas, according to one account, or at All Saints (1st November) according to another. Although the 15th of August is definitely given as the date of its arrival at Bristol from the Dorset coast, it must not be assumed that the infection covered the ground so quickly as that in the rest of its progresses. We have a measure of the rate of its advance south-westward through Devonshire to Cornwall, in a contemporary entry in the register of the Church of Friars Minor at Bodmin[218]: confirming the independent statements that the pestilence entered England at the beginning of August, the register goes on to record that it reached the town of Bodmin shortly before Christmas, and that there died in that town about fifteen hundred persons, as estimated.
The corporation records of Bridport, a town near to the place in Dorset where the infection landed, show that four bailiffs held office, instead of two, in the 23rd of Edward III., in tempore pestilentiae; the 23rd of Edward III. would begin 25 Jan. 1349, but the municipal year would probably have extended from September 1348, so that Bridport may have had the infection before the end of that year[219]. It seems probable that the smaller towns, and the villages, all over the South-west, had been infected in the end of 1348, but somewhat later than Bristol and Gloucester. The mandate of Ralph, bishop of Bath and Wells, “On confessions in the time of the pestilence,” is dated Wynchelcomb, 4. id. Jan. M.CCC.XLVIII. (10 January, 1349) and it speaks of the contagion spreading everywhere, and of many parish churches and other cures in his diocese being left without curate and priest to visit the sick and administer the sacraments[220].
The autumn of 1348 may be taken, then, as correct for the South-west; and there is no doubt that the infection had been severe enough in London before the end of that year to move the authorities to action.
“Owing to the increasing severity of the sudden plague day by day at Westminster and places adjoining,” Parliament was prorogued on the 1st of January, 1349[221]. There was a further prorogation on the 10th of March, for the reason given that “the pestilence was continuing at Westminster, in the city of London, and in other places, more severely than before” (gravius solito)[222]. This agrees with Avesbury’s statement that the epidemic in London reached a height (in tantum excrevit) after Candlemas, 1349, and that it was over about Pentecost. One of the best proofs of the season and duration of the Black Death in London is got from the number of wills enrolled in the Husting Court of the city in the successive months. Those who died of the plague leaving wills were, of course, but a small fraction of the whole mortality; but the wills during some eight months of 1349 are ten or fifteen times more numerous than in any other year before or after, excepting perhaps the year of the pestis secunda, 1361. Starting from 3 in November, 1348 (none in December), the probates rise to 18 in January, 1349, 42 in February, 41 in March, none in April (owing to paralysis of business, doubtless), but 121 in May, 31 in June, 51 in July, none in August and September, 18 in October, 27 in November, and then an ordinary average[223]. Thus it would have had a duration of some seven or eight months in the capital, with a curve of increase, maximum intensity, and decrease, just as the great London epidemics of the same disease in the 16th and 17th centuries are known from the weekly bills to have had.
It does not appear to have been felt at all in Norwich and other places in the Eastern Counties until the end of March, 1349, its enormous ravages in that part of England falling mostly in the summer. There is a definite statement that it began at York about the feast of the Ascension, by which time it had almost ceased in London, and that it lasted in the capital of the northern province until the end of July. The infection almost emptied the abbey of Meaux, in Holdernesse, of its monks, and the abbey lands of their tenants; and the date given in the abbey chronicle is the month of August, 1349. The spring and summer of that year appear to have been the seasons of the great mortality all over England, excepting perhaps in the southern counties where the outbreak began; even at Oxford, which is one of the towns mentioned as on the route of the pestilence from Dorsetshire to London, the mortality is entered under the year 1349, which was also the year of its enormous prevalence among the farmers and peasants on the manor of Winslow, in the county of Bucks.
Its invasion of the mountainous country of Wales (by no means exempt from plague in the 17th century) may have been a season later—anno sequenti, says Le Baker, which may mean either 1349 or 1350. In the Irish annals, the first mention of the pestilence is under the year 1348; but it was probably only the rumour of the mortality at Avignon and elsewhere abroad that caused the alarm in Ireland among ecclesiastics and in gatherings of the people. It was first seen on the shores of Dublin Bay, at Howth and Dalkey, and a little farther north on the coast at Drogheda; it raged in Dublin “from the beginning of August until the Nativity[224],” which may mean the year 1348, although the year 1349 is the date given for the great mortality in Ireland in later chronicles.
The experience of Scotland illustrates still farther the slow progression of the plague, and its dependence to some extent upon the season of the year. Two English chroniclers (Le Baker and Knighton) mention that it got among the Scots assembled in the forest of Selkirk for an invasion at the time when the mortality was greatest in the northern counties, the autumn of 1349. But the winter cold must have held it in check as regards the rest of Scotland; for it is clear from Fordoun that its great season in that country generally was the year 1350. Thus the Black Death may be said to have extended over three seasons in the British Islands—a partial season in the south of England in 1348, a great season all over England, in Ireland and in the south of Scotland in 1349, and a late extension to Scotland generally in 1350. The experience of all Europe was similar, the Mediterranean provinces receiving the infection as early as 1347, and the northern countries, on the Baltic and North Seas, as late as 1350.