126 Scurvy

Scurvy is a deficiency disease, arising from a lack of vitamin C (ascorbic acid) in the diet. It occurs most characteristically in the absence of fresh fruit and vegetables, but can still be avoided when these are not consumed if the diet is rich in uncooked meat as in the case of Eskimos (heat destroys the vitamin).

Etiology, Epidemiology, and Distribution

Human beings, like guinea pigs and monkeys but unlike many other animals, do not synthesize vita­min C. No doubt this reflects a period of evolution in a vitamin C-rich environment; and, with the expan­sion of the species to all parts of the Earth, less generous climates have inevitably taken a toll due to scurvy. The disease occurs where economic, social, or climatic factors prevent access to an appropriate diet, and frequently has appeared under circum­stances where diets are circumscribed, including long sea voyages, during military operations, in pris­ons, with the failure of crops, and during the Gold Rush. In the modem period, infantile scurvy has been a problem, for example, in Canada during the decades 1945-65, where it occurred mostly among the lower socioeconomic groups. As with other occur­rences of infantile scurvy, this period was associated with a trend away from breast feeding, combined with maternal ignorance about substitute foods. The same causes were at work in cases in Australia.

Scurvy occurs occasionally in slavish followers of fad diets, and more commonly in middle-aged men living on their own and neglecting their diets.

It can be said in general that scurvy is a disease of northern countries although, as observed, the tradi­tional diet of the Eskimo is sufficient to prevent it. Until recent times adult scurvy was endemic in Rus­sia. This was not the case with infantile scurvy, however, for properly suckled infants do better than adults when the general diet tends toward the scorbutic.

Clinical Manifestations

Various individuals in the modern period have sub­jected themselves experimentally to a diet free of vitamin C, and the characteristic features of the dis­ease have been carefully monitored. At about 12 weeks the first sign, a feeling of lethargy, appears. The first physical sign appears at 19 weeks, when the skin becomes dry and rough and the hair follicles form lumps. Small hemorrhages in the legs begin at about 23 weeks, and a bit later fresh wounds will no longer heal. One of the classical signs of scurvy, the swollen, purple, and soft gums, does not appear until about 30 weeks of a diet free of vitamin C. In a wartime study on a group of conscientious objectors, one of the volunteers developed a tubercular lesion at 26 weeks, and two more suffered what seems to have been cardiac hemorrhage, at 36 and 38 weeks. They were clearly close to that stage of the disease that had killed another self-experimenter in the eighteenth century, not to mention many thousands of sailors. At this point, the volunteers were given large doses of ascorbic acid, and all made complete recoveries.

In the young, scurvy produces reabsorption at the end of the long bones and a disappearance of carti­lage. Postmortem examination, particularly in ani­mals, reveals a characteristic subperiosteal hemor­rhage.

History

Outbreaks

Antiquity. No doubt scurvy appeared often in an­cient times - perhaps during sieges - and no doubt was treated by medical personnel. But we cannot claim that the disease was really known to the an­cients unless we can give evidence of some sort of consensus about it. To discuss an illness and write about it means, at least, that the disease has a name; but the ancients did not seem to have had a name for scurvy. In any event scurvy could not be found in the writings of Hippocrates or Galen by individuals of the late fifteenth and sixteenth century, to whom the disease was so obvious, and for whom medicine was founded on Hippocrates and Galen. As with the other apparently new disease of the Renaissance, syphilis, it was important for humanist physicians to believe that, notwithstanding a change of name, the old writers had known the disease. Only then could it be fitted into the newly classical body of theory and practice of medicine and an effective treatment sought. Attempts were made by scholars to show that Hippocrates was not ignorant of scurvy, but the disease was treated as new by practical per­sons like the ships’ surgeons who saw so much of it.

Renaissance Through the Eighteenth Century: Mari­time Scurvy. Of course, the circumstances sur­rounding scurvy’s appearance during the Renais­sance and Early Modern Europe were very different from those that Sturounded the diseases discussed by Galen and Hippocrates. The economic power of northern European countries was growing rapidly, and their desire to trade was matched by the techni­cal developments of shipbuilding and navigation. The Europeans’ theater of action was the Atlantic, not merely the enclosed Mediterranean, and all of these factors meant that the ships stayed at sea for periods long enough for scurvy to develop.

The earliest battles for trade routes were between Spain and Portugal, and Fernando Magellan, for example, saw much scurvy among his crew when at sea for 15 weeks in 1519. These two nations estab­lished control over the southern routes to the Far East, but were quickly followed by the French and English, who tried to find a northern route.

A French expedition of 1523 explored the east coast of North America, and a second expedition sent in 1534 that had to overwinter on the Saint Law­rence River suffered a great deal of scurvy.

The English, too, were interested in North Amer­ica since making an expedition to Newfoundland under the command of John Cabot in 1497. Francis Drake’s circumnavigation of 1577—80 indicates the extent of the technical developments in shipbuilding and navigation since the previous century, and the defeat of the Spanish Armada in 1588 was a stimu­lus to trading voyages. The next century saw the expeditions of the big trading companies like the East India Company, and the establishment of colo­nies by countries other than Spain and Portugal. It also, as a consequence, witnessed more and more sea voyages of long duration. The East India Company, for example, sent out an expedition to trade with Sumatra in 1601; it was 29 weeks at sea before reaching the Cape, and scurvy was widespread, al­most to the point of paralyzing the expedition. The only ship exempted from the disease was that of the expedition’s general, Sir James Lancaster, who had provided lemon juice for his sailors.

Observers of the early voyages noted the surpris­ingly rapid recovery of scorbutic sailors on reaching a port where fresh food was available. Empirical experience showed in particular the value of citrus fruits (the variant forms of “lime” and “lemon” in the different vernaculars are easily confused).

The answer lies partly in the logistical and techni­cal problems of provisioning the ever larger ships and squadrons: Citrus fruits are not native to the northern countries where big merchant fleets were based; these fruits did not keep well over long voy­ages; and attempts to concentrate or preserve the juice must have often reduced its effectiveness. The Dutch East India Company tried to ensure regular supplies by planting orchards at Mauritius and St. Helena, and even attempted laying out gardens on board ship. The Dutch Company’s statistics show that the mortality in its ships over a 5-year period during the last decade of the seventeenth century, from all causes, was a little more than 13 percent, although where distilled water was used, the rate dropped to 9.5 percent. It is not known what propor­tion of these deaths were due to scurvy, but it ap­pears that in regular trading voyages at least, with known landfalls and provisions for the crews includ­ing fruit juice, scurvy was not very deadly.

This was not the case, however, in the European navies, particularly during the following century. Their business was military, not commercial, and their operations were far from regular. In any mili­tary operation there is the expectation that the lives of men will have to be expended, and experience showed that disease would take many. Control of the seas rather than mere coastal defense was now the prize of naval warfare, and fully 855 men out of 1,000 succumbed, largely to scurvy, when Commo­dore George Anson fulfilled his commission of 1740 to capture the Spanish treasure-galleon.

Subsequent wars involved navies not only in long­distance operations but also in blockades of long duration. The supply of citrus fruits was simply not adequate for operations on this scale, when a comple­ment of 500 men for a single ship of the line was not unusual.

This was essentially a forced clinical experiment, a technique taken up (after correspondence with Ives) and used in a more elaborate way by the better known James Lind. Lind divided his scorbutic pa­tients into those taking fresh oranges and lemons, those taking cider, and those to whom he gave other current remedies. The first group improved rapidly, followed by those drinking cider; the remainder did not improve. Lind has been much celebrated for this early clinical trial, but doubt has recently been cast on his results on the grounds that modern research shows no vitamin C in cider. Yet modern cider is generally preserved in some way to give it a longer shelf life, whereas cider made in the eighteenth­century manner is high in vitamin C.

By 1753 Lind had incorporated his results into a large and very scholarly historical, bibliographical, and clinical work entitled A Treatise of the Scurvy. It was the most authoritative argument that had been made for the use of citrus fruits to prevent scurvy, but it was not until the end of the eighteenth cen­tury that, because of the work of an administrator, Sir Gilbert Blane, lime juice was issued to British sailors as a matter of course.

Nineteenth Century. The lessons learned at sea en­abled the occasional small-scale outbreak of scurvy in the prisons of the earlier nineteenth century to be handled adequately. But there was no remedy for the scurvy produced by the great failure of the potato crop in 1845-6. Potatoes are rich in vitamin C, and the population of Ireland, more than other European countries, depended upon them as food. Scotland also suffered. Scurvy later in the century appeared regularly where conditions prevented access to fresh fruit and vegetables. Examples are the California Gold Rush of 1848 and later, during which the long trek over mountains much resembled a long voyage at sea and the war in the Crimea (1854-6) and the siege of Sebastopol, when the French and British armies’ supply routes were interrupted. American experiences with scurvy also occurred during a cir­cumnavigation in 1838, during a blockade of the Mexican coast in 1846, and during the Civil War, particularly in prisoner-of-war camps, where the mortality rose to 9 percent per month.

The circumstances that made scurvy a disease of the northern countries made it a special danger in the Arctic regions. When there was regular commerce - for example, by the Hudson Bay Company - scurvy was only a minor threat, and, since its origin in the seventeenth century the Company had shipped out lime juice. Fresh meat killed locally was also recog­nized as valuable, a truth that had been learned the hard way in some early overwintering disasters. Government-backed explorations, however, gener­ally encountered scurvy, particularly when small par­ties left the iced-in ship for exploration on foot.

Perhaps the least expected occurrence of scurvy was that of the infantile variety from the 1870s to the First World War, in Europe and America. The odd feature was that infantile scurvy occurred in the higher social classes, where there was no economic reason for vitamin C deficiency. The reason was that mothers of the upper classes tended to avoid breast feeding their own children, and the various forms of preserved milk newly available did not contain vita­min C. Thus scurvy often occurred before the child began consuming adult food. In previous periods, upper-class mothers also avoided breast feeding, but then the infants would have been given to a wet nurse as a substitute mother.

Etiological Theories

Changing Concepts and Implications for Treatment. Theories on the causation of scurvy were, on the whole, more destructive than helpful to its success­ful treatment in the period before the discovery of vitamin C. By and large, government officials, offi­cers, and surgeons of big trading companies, and eventually naval and military administrators, were convinced of the empirical fact that certain fruits prevented and cured the disease. But when they took advice about scurvy from educated physicians, it was sometimes bad. Because medical theory had its impact upon practice, we must look briefly at theo­ries about scurvy.

There is one central feature of the story of scurvy theories which had an enormous effect. This was the rise of the germ theory of disease in the second half of the nineteenth century, which changed medicine more than anything else had done in the preceding 2,000 years. Disease was now seen to be caused by a living organism, in some cases visible under a micro­scope. The organism was s species of living thing, perceptible (perhaps) and classifiable. Here was the essence, the cause of the disease: Clinical symptoms were now viewed as secondary reactions, varying with the nature of the patient. And the new medi­cine, by the end of the century, proved spectacularly successful in combatting infectious diseases. The ef­fect was a whole new ontology of disease, centered on the infective organism; thus for scurvy, the effect of this revolution was to encourage a search for a causal organism, or at least a poison. In other words, the research ran counter to the previous consensus that incomplete diets could cause scurvy, and led to numerous disputes about the nature of the disease.

To understand why, we must look at the nature of medical theory in the earlier period. Up to and even including the eighteenth century in some places, the medical person had seen the human body as a micro­cosm located in a similar but larger macrocosm. Tra­ditional European medicine, based on Galen’s ratio­nalization of Hippocratic principles, recognized the body as consisting of seven “Naturals” - its humors, spirits, faculties, and parts. The “Non-Naturals” were the points at which the body intereacted with the macrocosm and the results of its activity - the regi­men of diet, exercise, sleep, and so on. “Contra­Naturals” were things that caused disturbance in the body. The microcosm corresponded to the macrocosm because they both consisted of the same principles, the four elements and four qualities, appearing in the body as the four humors. Food was elementary and qualitative and needed only refining to become the substance of the body. The effect of the environment - its airs, waters, and places - was similarly qualita­tive. The notion that scurvy was a disease that arose from an improper diet fitted naturally into this scheme. An impropriety of the diet was generally believed to affect bodily organs, and early writers such as Echthius in 1541 made scurvy a melancholic disease of the spleen.

He attributed it to the spleen because in discuss­ing splenetic diseases Hippocrates listed some symp­toms that look scorbutic; and Echthius^,s argument was the Hippocratic-Galenic one - that a disordered spleen could not fulfill its normal function of excret­ing black bile (melancholia, one of the four humors), and that the excess of black bile in the body in turn caused scurvy. Similar humoral theories of scurvy were widely held, and many writers attributed the presumed damage to the spleen to a dietary cause - the salt meat, stale water, and preserved food of long sea voyages.

The theory of the disease changed with the theory of medicine. In the later seventeenth century, when chemical notions of the body were proving attrac­tive, some writers distinguished an “acid” from an “alkaline” scurvy. When mechanism was employed in the medicine of the eighteenth century, doctors talked about sharp, corrosive particles in the blood. These were still humoral theories, and although the humors were no longer viewed as qualitative in ac­tion, their vice still derived from diet. Hermann Boerhaave, the most authoritative voice of the eigh­teenth century, blamed salt; dried and smoked meats, including fish and sea birds; ships’ biscuits (panis biscoctum); dried peas and beans; old, sharp, and salty cheese; and so on. Such a diet, he argued, led to the proximate cause of the disease: The blood became thin and sharp, whether acid or alkaline. From this all the symptoms could be deduced, and all treatment was to be directed to restoring the proper nature of the blood. Boerhaave had the whole armory of eighteenth-century medical techniques with which to attempt this, because some kind of disturbance of the blood was believed to be at the root of many diseases in the medical theory of the time.

Citrus fruits were mentioned by Boerhaave, but only in a long list of other remedies and without special attention, and without an explanation of how such remedies work. The use of citrus juice, after all, was a mere empirical discovery, which had little part in a medicine so rational as that of Boer- haave. Perhaps Boerhaave, like Beaudouin Ronsse (Ronsseus) more than a century before, was embar­rassed at something so empirical. His rationalist view attributed the cause of scurvy not to anything necessary lacking in the diet, but to the excess of things undesirable. His student Gerard L. B. van Swieten, however, took the more usual line that the cause of the disease was the lack of something. Scurvy, he argued, appeared more often in besieged cities than in the army besieging, which had access to fresh provisions.

The practice of treating scurvy was again affected by medical theory later in the eighteenth century. Contemporary interest in medical chemistry cen­tered on the nature of various “airs” (in our terms, “gases”) of which “fixed air” was sometimes held to prevent putrefaction. It was also commonly held that scurvy was a putrefactive disease, and attention natu­rally was given to the possibility that it could be treated with fixed air. There were attempts to use water impregnated with fixed air on board ship, and a wider movement to treat scurvy with malt. It was argued that just as malt digested in water became a wort that ferments into beer, giving off fixed air, so wort drunk by scorbutics would ferment in their bod­ies, correcting the tendency to putrefy.

Captain James Cook’s report to the Admiralty in 1776 spoke highly of malt, and also of sauerkraut, both of them in his view being preferable to the contemporary citrus fruit concentrate - “rob” - of oranges and lemons. The expense of the latter was clearly the reason for the search for substitutes. Cook’s apparently empirical observations agreed with theories of fermentation shared by his influen­tial colleagues in the Royal Society and elsewhere, and helped to lengthen the period of the use of malt­wort in the navy. In 1795, however, Gilbert Blane was appointed commissioner of the Board of Sick and Wounded Sailors, and, supported by some recent experiments with lemon juice, he persuaded the Lords of the Admiralty to authorize a daily dose of three quarters of an ounce of the juice to each sailor. Over the next 20 years, this amount totaled more than 1.5 million gallons; Admiral Horatio Nelson alone accounted for 50,000 gallons for the Mediterra­nean fleet.

Although, after this, scurvy virtually disappeared from the British fleet (but not from other fleets as, for example, the French, during the Napoleonic Wars), on land the theories of medical professionals continued to threaten practice. The Seige of Paris (1870-1) produced an outbreak of scurvy and once again focused attention on its cause at a time when ideas about contagion and germs were becoming more widespread. At a debate in the French Acad­emy of Medicine in 1874, the view was aired that scurvy was a contagious miasm, and was no more caused by a lack of fresh fruit than malaria was caused by a lack of the medicine quinine. The revolu­tion in medical thought about disease causation now made positive causes of scurvy (the presence of a noxious agent) more attractive than a negative (the absence of a factor).

A British expedition of 1894 spent three winters in Franz-Joseph Land, remaining healthy on a diet that included fresh meat but very little lime juice. The medical explanation for the absence of scurvy was that the disease was caused by chemical prod­ucts resulting from bacterial action in poorly kept meat, and it was realized that no one had studied scurvy in the light of Louis Pasteur’s germ theory. This new line of inquiry was made possible by a grant from the Royal Society, whose president was Lord Joseph Lister, the man who revolutionized sur­gery by killing Pasteurian germs with carbolic acid. It was Lister who presented the results of the in­quiry to the Royal Society, and those results were taken to support a germ theory of scurvy. So thor­oughly was germ theory implicated in the etiology of scurvy that one naval surgeon, at least, explained that the benefit obtained from lime juice was simply that it acted as an antibacterial mouthwash.

Evolution of the Deficiency Disease Concept. The final recognition of scurvy as a deficiency disease is a twentieth-century story. From the last years of the nineteenth century, there had been concern in Nor­way at the incidence of “ship beriberi.” It was stud­ied by Axel Holst, who had had experience at the Pasteur Institute and had also worked with Robert Koch. He knew of the experimental use of chickens in a study of beriberi in the Dutch East Indies, but chose guinea pigs as his experimental animals, feel­ing them to be more convenient and closer to hu­mans in physiology. Under a restricted diet, the ani­mals developed the symptoms of scurvy as it ap­peared in humans. Guinea pigs had also been used in Germany as models for “Barlow’s disease” (infan­tile scurvy, long thought a separate condition).

The work (up to 1913) of Holst and his collaborator Theodor Frolich (a specialist in infantile scurvy) was to show that scurvy was indeed a disease of a defi­cient diet. Meanwhile, in 1912, Casimir Funk, work­ing at the Lister Institute in London, proposed that scuιvy was one of a group of four diseases (the others were beriberi, rickets, and pellagra) that were caused by dietery deficiency. Each missing factor, he be­lieved, was a nitrogenous base, for which he coined the name “vitamine.” At the same time, in the United States E. V. McCollum and others showed that some fats contained a factor necessary for the growth of rats. The “deficiency” thesis met some oppo­sition from bacteriologists, and in 1916 and 1917 workers in the United States cultured bacteria from the tissues of scorbutic animals. Inoculated into healthy animals, this culture produced some signs of scurvy. Related to the bacterial theory was the “posi­tive” notion of McCollum that scurvy was due to poisons developing by bacterial action in the accumu­lating feces in the intestines of the experimental animals. (The animals were rats, which synthesize their own vitamin C.)

Despite all these opposing doctrines, however, the results obtained by Holst and Frolich prompted la­ter efforts to identify and isolate the active compo­nent. McCollum had already identified a fat-soluble factor - “A” — and a water-soluble factor - “B” - nec­essary for the growth of experimental rats, and it was natural for those who believed in the deficiency thesis to look for a “vitamine C.”

The presence of scurvy during the First World War and its aftermath in central Europe prompted sys­tematic assays on various antiscorbutics, particu­larly in guinea pigs at the Lister Institute. There too, from 1918, S. S. Zilva and others attempted to isolate the active component of vitamin C. This was achieved by the Hungarian Albert Szent-Gyorgyi, who was working in Hopkin’s laboratory in Cam­bridge on a different problem. He was interested in the powers of chemical reduction of organic sub­stances, including the sugars of lemon juice. Be­tween 1928 and 1932, Glen King at the University of Pittsburgh also had been trying to isolate vitamin C, and in the latter year published results that com­bined the findings of Szent-Gyorgyi with his own and with trials with guinea pigs. Vitamin C had been discovered, and scurvy was vanquished.

Roger K. French

Bibliography

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