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sixth years covered by the statistics, 30,714 cases of scurvy were reported; and 383 deaths were attributed directly to that disease."

Munson writes: "It prevailed among our troops during the Civil War and its recognition was a surprise and shock to professional ideas preconceived from practice in civil life."

As is well known, the besieged in Paris during the Franco-Prussian War in the winter of 1870-71 suffered severely from scurvy. The accounts of their pitiable condition have been portrayed for us by numerous French writers . The people lived mainly on rice and bread, with an occasional addition of potatoes or horse meat. The winter was exceptionally severe, which was supposed to have intensified the scorbutic condition. Not only were the inmates of the prisons on the Seine attacked, numbering about one thousand, but even the patients in the military hospitals developed the disease. It is of interest to remember that the siege lasted but little over four months, from September 17th to January 27th, the date of the armistice.

In the Russo-Japanese War, after the siege of Port Arthur, it was found that one-half of the garrison of 17,000 men had scurvy.

Although there are certain parts of the world where scurvy is of frequent occurrence, no country has been entirely free from it. As might be expected, it has been particularly prevalent in the North, where vegetation is scanty--in Greenland, Alaska, Russia and the Baltic States. It has likewise prevailed in the tropics when the crops have failed. India has been conspicuous for its large number of epidemics; some years ago scurvy occurred in Arabia among the English troops stationed at Aden, both among the British and the native troops. A recent communication from Aruba, a small island of Dutch Guiana, lying north of Venezuela, illustrates how devastating scurvy still is in some parts of the world. This account tells of 3000 cases of this disease which occurred in 1915 among a population of less than 10,000, owing to the fact that the crops had failed almost entirely during the years 1912, 1913 and 1914.

It is important for us to realize that we are still dependent on the annual crops for our protection from scurvy; in other words, the world is leading a hand-to-mouth existence in regard to its quota of antiscorbutic food. The truth of this condition has been realized for Ireland, sadly illustrated by numerous epidemics, notably the great epidemic of 1847 reported by Curran. It was demonstrated by the outbreaks of scurvy in Norway in 1904 and 1912, and was brought to the attention of many in the United States in the spring of 1916. In this year our potato crop fell far below the normal, with the result that scurvy appeared in various parts of the United States, especially in institutions .

The fact that scurvy may occur in any land and climate, even in the garden spots of the world, is strikingly shown by the epidemics reported from Algiers, and the ravages of this disease among the gold seekers in California in 1849. Nothing could be more incongruous than the occurrence of a deficiency disease in this land of plenty.

The fact that crews of vessels which set sail in winter were more subject to scurvy than those which set out in the summer must be attributed to the existence of latent scurvy among the sailors at the time of sailing, rather than to the season of the year.

The earliest account of the outbreak of scurvy at sea is that of Vasco de Gama, who in 1497 discovered a passage to the East Indies by way of the Cape of Good Hope. The narratives of subsequent explorers, especially those of Cartier and of Drake, are replete with descriptions of the ravages of scurvy. The expedition of Lord Anson in 1740 is always cited as a memorable example of an undertaking which foundered as the result of scurvy. After a cruise of four years, this expedition had lost from this disease more than four out of five of the original number of its crews. In striking contrast to this picture, and to that furnished by the voyages of earlier navigators, is that of Captain Cook, who in 1772 undertook a voyage lasting over three years, sailing from 52? north to 71? south, with a loss of but one of his crew from disease, and that not from scurvy. This remarkable feat, more than any other, centered attention on the feasibility of preventing scurvy, and resulted in measures tending to eradicate it from the navy. Captain Cook attributed the absence of scurvy among his crew to "sweetwort," an infusion of barley, which he prepared fresh and served liberally. He also prized the antiscorbutic value of sauerkraut.

We find accordingly in 1795, at the instance of Sir Gilbert Blaine, that improvements were introduced in the victualling of the fleet. As the result of a regular ration of lemon juice, the incidence of scurvy fell precipitously. It is due largely to this provision that between the years 1779 and 1813, according to the statistics of Sir Jay Barrow, the morbidity and the mortality in the British Navy was decreased by 75 per cent.

It has been shown that it took a generation after the efficacy of antiscorbutics had been demonstrated in various expeditions, for an antiscorbutic to be included in the ration of the navy. The merchant marine of England was far more conservative, and for many years after scurvy had been eradicated from the navy we still read of its occurrence on the vessels making voyages to India, China and Ceylon. Gradually, however, its incidence became less and less. Its toll of death, before preventive measures were employed, may be appreciated from the fact that it has been estimated that scurvy destroyed more sailors than all other causes incidental to sea life, including the great slaughter of naval warfare. Sir R. Hawkins stated in the latter part of the sixteenth century that he could give an account of 10,000 mariners who had been destroyed by scurvy during the twenty years that he had been at sea.

As is well known, scurvy has played an important r?le in Arctic and Antarctic explorations, and has been the cause of the failure of many of these expeditions. It is now realized that the development of scurvy is quite preventable, that if a sufficient quantity of meat is consumed, explorers can be entirely independent of a supply of fresh vegetables. This fact was brought out by the Arctic Survey Committee , who "were appointed to enquire into the causes of the outbreak of scurvy in the recent Arctic expedition" , and who reported that it may result from an absence of fresh meat. That this conclusion was sound has been proved by the experiences of Nansen and of Johansen, who wintered safely in Franz-Josefsland on a diet of meat and bacon. More recently Stef?nsson has carried out successful Arctic explorations, depending entirely on fresh meat as antiscorbutic foodstuff and making no provision whatsoever for vegetable food.

"The scurvy is sometimes conjoyned with the affect. It is either hereditary, or perhaps in so tender a constitution contracted by infection, or lastly, it is produced from the indiscreet and erroneous Regiment of the infant, and chiefly from the inclemency of the air and climate where the child is educated."

"The scurvy complicated with this affect hath these signs: 1. They that labor under this affect do impatiently indure purgations; but they who are only affected with the Rachites do easily tolerate the same. 2. They are much offended with violent exercises, neither can they at all endure them. But although in this affect alone, there be a kind of slothfulness and aversation from exercise, yet exercise doth not so manifestly, at least not altogether so manifestly hurt them, as when the scurvy is conjoyned with the Rachites. 3. Upon any concitated and vehement motion they draw not breath without much difficulty, they are vexed with diverse pains running through their joynts, and these they give warning of by theyr crying, the motion of the Pulse is frequent and unequal, and somethimes they are troubled with a Palpitation of the Heart, or threatened with a Lypothymie, which Affects are for the most part soon mitigated, or altogether appeased by laying them down to rest. 4. Tumours do very commonly appear in the Gums. 5. The urin upon the absence of the accustomed feavers is much more intense and increased."

Glisson's description of scurvy was entirely lost sight of, overshadowed by his description of rickets, so that for over two hundred years no word of infantile scurvy is to be found either in the English or other literature. There is no doubt that from time to time cases must have occurred, but they were looked upon probably as rickets or as a manifestation of one of the hemorrhagic diseases.

In 1859 Moeller described some cases which evidently were scurvy, but which he termed "acute rickets." He realized that they presented a novel clinical picture but failed to recognize that they represented a disorder quite distinct from rickets. This article was followed within the next few years by reports of other German writers who, accepting Moeller's point of view, considered these cases merely as an acute form of rickets. They were led to this erroneous conclusion chiefly on account of the lack of marked involvement of the gums, which they considered an essential sign, influenced by their conception of adult scurvy. This viewpoint has pervaded the German literature even to the present day, when it is still considered necessary to bring further evidence that infantile scurvy in its pathogenesis and pathology is identical with adult scurvy.

Infantile scurvy is frequently termed "Die Moellersche Krankheit." There seems to be no occasion for giving Moeller credit for discovering this disease, as he believed that he was dealing with rickets merely in an acute form. He recognized the clinical similarity to scurvy, but in one of his cases sharply differentiates it from adult scurvy by the fact that "lemon juice and fresh vegetables" were of no avail in the treatment.

In 1871 Ingerslev, an assistant of Hirschsprung in Copenhagen, wrote a paper on "A Case of Scurvy in a Child," which is quite convincing. Two years later Jalland, an English physician, reported a similar case of "Scurvy in a Ten-Months-Old Infant." In 1878 Cheadle reported three cases of infantile scurvy with typical tumefaction of the gums, and obscure tenderness of the legs, and followed this paper by two others, which appeared in 1879 and 1882. Cheadle clearly recognized the disease as scurvy. However, as the title of his first paper--"Three Cases of Scurvy Supervening on Rickets in Young Children"--indicates, he considered it a condition engrafted upon rickets. About this time Gee presented a brief but accurate account of five cases of scurvy which he termed "osteal or periosteal cachexia."

In 1883, Barlow published his classical paper on this subject, the first to furnish anatomical proof that this disorder of infants presented the pathological changes characteristic of adult scurvy. Previous to this publication there had been but one autopsy report, that by Moeller, which had been incorrectly interpreted. The work of Barlow was accepted remarkably quickly in England and in America, but less promptly on the Continent. This was probably due to the fact that infantile scurvy was occurring far more frequently in these two countries, and that the subject was open therefore to more prompt investigation. This increased prevalence of infantile scurvy in the two great English-speaking nations has continued to the present time, and no doubt is due to the extensive employment of artificial feeding and of proprietary foods. In 1894 not less than 106 cases were reported to the Academy of Medicine of New York City by various physicians, and in 1898 the comprehensive investigation of the American Pediatric Society appeared, which was based on 379 cases.

It was soon evident that infantile scurvy occurred to a greater or less degree throughout the civilized world. In France, Monfalcon had reported a case in 1820 which is sometimes referred to as the earliest case of infantile scurvy mentioned in the literature. It relates, however, to an older child and was published as a case of scorbutic rickets. Netter was one of the first in France to recognize the true nature of the disorder, and published several papers in 1898 describing typical cases. Infantile scurvy was, however, almost unknown in that country until what is termed "lait maternis?" and "lait fix?" came into vogue. This is apparent from a table prepared by Lecornu, which gives a list of all cases in the French literature between 1894 and 1904, and of the diets on which they came about. The former of these milk preparations is subjected to various manipulations and then heated to a temperature above the boiling point; the latter is shaken violently in a machine to render the fat globules smaller, and is then sterilized by one of the usual methods.

Switzerland has undergone an experience similar to that of France. Previous to 1903 only five cases of infantile scurvy had been published from that country. In this year Stoos published an additional five. In 1907 Bernheim-Karrer reported nine cases, all of which had developed on homogenized milk, a process very similar to that employed by the French to break up the fat globules. The increase of infantile scurvy in Switzerland may be judged by the fact that a commission was formed in the following year to investigate its occurrence.

In Germany there was for many years continued discussion as to the true nature of scurvy. Some believed it to be a form of rickets, others a form of scurvy; still others a combination of scurvy and rickets. Some thought it merely hereditary syphilis, and not many years ago Naegeli looked upon it as an entity distinct from scurvy on rickets. The subject attained additional importance through an epidemic of infantile scurvy, which broke out in Berlin in 1898, among infants who received milk from one of the largest dairies. The episode led to prolonged discussion in the Berlin Medical Society, and to several excellent papers, among which that by Neumann deserves particular mention.

The disorder has been reported in Holland by DeBruin, who recorded numerous cases; in Denmark, by Hirschsprung, who refused to recognize its scorbutic nature; in Italy, by Concetti, and by others. It was not long before there were reports of cases from almost every part of the world, including Australia and East India .

In view of the fact that scurvy is endemic among adults in Russia, we should also expect to find infantile scurvy widespread in that country. In point of fact, quite the contrary seems to be the case. In connection with the great scurvy epidemic in Russia , Tschudakoff personally examined over 10,000 persons and found 11.11 per cent. of the people sick with this disease. He states that in the course of this large experience he did not meet with a single case under the age of five years. Fuerst writes that Filatow, the great Russian children's specialist, declared that he knew of no case of Barlow's disease described in the Russian literature. This is not literally correct, as Doepp described an epidemic of scurvy in the St. Petersburg Foundling Asylum occurring in 1831. It serves to emphasize, however, the paucity of cases among infants in this great land of endemic adult scurvy. Lyabmow, in referring to the scurvy in Kazan, tells us that among 28,000 cases only a few infants were affected, and Rauchfuss made the statement at the International Congress at Copenhagen, in 1884, that although he had seen a great many cases of scurvy, he had never seen it in children one to two years of age. We shall not, in this place, comment on this interesting and apparently paradoxical situation, but shall have occasion to refer to it in considering the pathogenesis. It may be added that in Norway and Sweden, where scurvy is to some extent also endemic among the adult population, there is a similar lack of scurvy among infants.

Scurvy occurred next in frequency among the nations neighboring Russia. Speyer tells us that a German sanitary commission was sent to Bulgaria largely with the object of investigating scurvy in that country. The excellent monograph on the pathology of scurvy just written by Aschoff and Koch was founded on an experience in Roumania among Turkish, German and Austrian soldiers. Added to its other woes the Servian army was visited by scurvy. Wiltshire gives us a description of this disease based on an observation of 3000 cases in the first half of the year 1917. In regard to scurvy in this part of the world, Morawitz writes that when he reached Roumania he was surprised to find scurvy the most prevalent disease in the army, and that since the spring of 1917 it was widely disseminated among the German troops. Lobmeyer writes of scurvy among the Turkish troops, and Disqu? reports 500 cases among prisoners captured in Turkestan.

Along the Western front very few cases are described. There is an account by Korbsch of 51 cases in this area in 1915. Schreiber describes 30 cases among the German prisoners of war captured in the beginning of 1917, which were diagnosed as purpuric rheumatism. Arneth recounts that sporadic cases of scurvy occurred among the German troops, especially among the older soldiers, and that in many cases this was combined with the hunger edema. He attributes the scurvy to a dependence on dehydrated vegetables in the ration.

From all these accounts it is evident that scurvy played an important r?le in the general nutrition of the troops on the Eastern front. Probably it was of the latent variety, which is exceedingly difficult to diagnose, but which increases the susceptibility to infection, and intensifies the severity of all medical or surgical diseases. Von Niedner takes this point of view, stating that although scurvy had been largely prevented in this war, the obscure rudimentary type had not been eradicated. He remarks upon a fact, noted in our Civil War and other wars, that under these conditions eruptions assume a hemorrhagic character in typhoid fever, cerebrospinal fever, rheumatism and other infections. Pick made a similar observation at a medical meeting in Vienna in reference to scurvy in the Austrian army, drawing attention to the hemorrhagic diathesis existing among the troops and expressing the opinion that scurvy was occurring in this war as in previous wars.

Very little scurvy seems to have broken out among the British troops in Europe. Thirty-two cases were reported as occurring in the middle of 1915 at a divisional rest station in France. It made marked inroads, however, on the health of the Colonial troops in Mesopotamia. In the report of the Mesopotamia Commission we read that 7500 men were lost to the force in 19 weeks as a result of scurvy, and that this happened in the summer of 1916 although additions had been made to the ration in the previous spring. A conception of the extent of the scurvy may be formed from the accompanying table, published by Willcox:

Scurvy Beriberi

It will be noted that thousands of cases occurred among the Indian troops. This was due to the fact that the British ate more potatoes and fresh meat. In his official report of the outbreak of scurvy among Indian troops, Colonel Hehir writes: "The only vegetable now allowed is 2 ounces of potatoes and the only fresh meat 28 ounces a week. It is very doubtful whether this authorized ration, if not supplemented by other vegetables and more meat, is sufficient to prevent scurvy." In the account which this officer gives of the medical conditions during the siege of Kut-el-Amara, it is stated that there were 1050 admissions for scurvy, fully developed, incipient and latent. It is remarked that those Indians who ate horseflesh were decidedly less affected. From the fact that special hospitals for scurvy were established in June, 1916, at Bagdad, Amora and Basrah, it is evident that a large number of cases must have been encountered. Most significant in this connection, however, are the preventive measures which were instituted by the British government. A body of 256 men, designated as the Madras Gardener's Corps, were dispatched to Mesopotamia to plant gardens all over the country and to supply packets of seeds to various units. At Bagdad alone their output of vegetables was over 400,000 pounds. This certainly constitutes a remarkable innovation in the hygiene of armies.

The French army was not entirely spared from scurvy. In 1917 Harvier, an army surgeon, was surprised to discover that 95 per cent. of the 800 troops of which he had charge suffered from scurvy; he tells us that other epidemic centres were recognized later outside this sector. Elsewhere we read of the occurrence of scurvy in France, involving 40 per cent. of the 1700 men of the South African Labor Corps, and that this disorder was still more serious in another company owing to the fact that it was not recognized . Benoit reported 63 cases which he discovered in 1917 among 300 laborers. According to his account, all these laborers received the same food, and those with scurvy recovered quite independently of any change in the dietary.

The writer adds that he believes that the health of the natives at home is protected by Kaffir beer, which they consume even to the amount of 3 gallons a day, and which is made from germinated Kaffir corn. This cereal is germinated by steeping it in water for forty-eight hours and is then dried in the sun. Only enough is prepared for one brew. The French prepared a similar fermented beverage for these South African laborers; the sole difference in its mode of preparation was that the corn had not been germinated.

There are many accounts of scurvy among the Italian troops. Vannutelli gives a description of an epidemic of some 200 cases of infectious purpura with manifestations of hemorrhagic scurvy. Another writer informs us that in June, 1916, scurvy broke out among some Italian troops stationed at an altitude of 1500 to 2000 metres . Vallardi gives an account of 180 cases among Italian troops in Macedonia, accompanied by slight jaundice and enlargement of the glands.

The American soldiers seem to have been practically spared from scurvy. This was due probably to their ample ration and to the fact that they were in the field for a comparatively short period. The Surgeon-General's report to date, which has been kindly furnished me, showed but 5 cases in 1917 occurring in Europe and the United States, and but 15 cases reported during the year 1918.

That scurvy must have occurred extensively among the infants in Vienna may be gathered from the report of Erdheim, who records 31 autopsies on infants under the interesting title of the "Barlow Heart." In Berlin scurvy occurred also in the foundling asylums, as reported by Eric Mueller and by Brandt. This was caused by a diet of pasteurized milk and dehydrated vegetables. In an article bearing the suggestive title of "On a Marked Increase in Barlow's Disease in the Years of the War 1917-1918," Epstein states that in Prague there had been an endemic increase of infantile scurvy since August, 1917. The only information regarding scurvy among the adult civilian population of Germany is that furnished by Morawitz, who states that this disorder occurred sporadically. Here again it is probable that there were many latent or rudimentary cases which were not recognized.

In Great Britain there are reports which show that scurvy manifested itself in institutions caring for the poor. In Glasgow we learn of 50 cases developing in the Poor Law Hospital in the course of fifteen months, and in Newcastle of 16 cases appearing in the Poor Law Infirmary in the course of three months.

It is probable that when more detailed reports are available, it will be found that there was far more scurvy than was appreciated during the course of the war. It will be impossible, however, to gain even an approximate knowledge of the extent to which this disorder prevailed, as in many instances it was inextricably interwoven with other nutritional diseases. The situation which Enright describes in Cairo among the Turkish prisoners suffering from war edema, where there was "evidently a scorbutic factor involved," probably held true for many other parts of the world. War and scurvy must still be regarded as associated evils, for war is closely linked with famine and food deprivation--the dominant factor in the production of scurvy.

PATHOGENESIS AND ETIOLOGY

At the outset it may be stated that there is no longer any reason to doubt that adult scurvy and infantile scurvy are one and the same disease, having an identical pathogenesis. For many years, far longer than the facts warranted, there was discussion whether Barlow's disease was true scurvy or merely a form or a complication of rickets, or perhaps a distinct hemorrhagic disease. This question may be relegated to the past, so that we may proceed to consider the pathogenesis of scurvy in the infant and in the adult under a common heading.

The cases on which Wright based his theory were soldiers who developed scurvy during the siege of Ladysmith. It is probable that the men were suffering from starvation, purpura and dysentery. That they did not have scurvy is proved by the fact that they were cured by giving lactate and bicarbonate of soda.

A consideration of the clinical course of scurvy sheds but little light on this aspect, and can be interpreted as well for as against the action of a toxin. The nervous system, which is well known to be particularly vulnerable to toxins, is but slightly affected--the cardiorespiratory phenomena , the occasional changes in the optic disks, and the abnormality of the tendon reflexes constitute the aggregate. In a general way it may be stated that the symptoms resemble those brought about by poisons of various kinds--the cottonseed poisoning in swine, the toxic products of the wheat embryo, or even mercurial poisoning in man. The nervous symptoms, especially the irritability of the heart, remind one of the enterogenous intoxication or enterotoxic polyneuritis described by Von Noorden. Such analogies are interesting and suggestive, but can be accorded little weight in deciding the question at issue.

In chronic mercurial poisoning the following suggestive symptoms occur: anemia, bleeding and spongy gums, loosening of the teeth, a quickened pulse, ulcers of the extremities. At times mercury attacks the nervous system, producing palsy. The resemblance is heightened by the fact that calcium metastases have been found in the muscle in experimental scurvy comparable to those characteristic of mercurial poisoning.

If a toxin is to be regarded as the proximate cause of infantile scurvy, the question naturally arises as to the nature of the toxin. Is it exogenous or endogenous? There is sound basis for believing that the hypothetical poison is not introduced preformed in the food. In the first place, infantile scurvy frequently develops in babies who receive milk of the very best grade indeed, in contradistinction to rickets, this is not pre?minently a disease of the poor. Furthermore, there is no relation between the concentration of the food mixture and its liability to induce scurvy. For example, if among a large number of infants receiving pasteurized milk from a common source, some are given the milk diluted by one-half, others given it diluted by one-third, and still others whole milk, the last group will show the least tendency to scurvy, which we should not expect were the poison contained in the food. Nor is it at all uncommon to encounter scurvy in an infant which has been fed with a very dilute milk mixture. Another side of this question should, however, be mentioned--stale pasteurized milk is more apt to produce scurvy than the freshly pasteurized, but here again the injury is in inverse ratio rather than in direct ratio to the amount consumed. There are reports of adult scurvy having been occasioned by decomposed food, such as Torup's investigation of Nansen's polar expedition, but the diet had not been faultless in other respects. The experiments of Jackson and Harley, who produced scurvy in monkeys by feeding tainted tinned meat, cannot be unreservedly accepted, as they are substantiated by no pathological examination of the bones, and the diarrhoea and the blood and mucus in the stools do not suggest simple scurvy.

Of those who held to the toxic origin of scurvy the majority had in mind an endogenous toxin, although the conception of the nature of this poison varied greatly. The minority report of the American Pediatric Society states that "scurvy appears to be a chronic ptomaine poisoning due to the absorption of toxins." Neumann considered scurvy a chronic poisoning, formed probably from the albumin of the milk, and considered the fact that the infant refused to take the harmful food as weighty evidence of its toxic nature. Kohlbrugge included scurvy in his group of "fermentive diseases," due to the overgrowth of harmful bacteria in the intestine, which are normally restrained by the acid reaction of the chyme. McCollum and Pitz, on the basis of a study of experimental scurvy, suggested that as the result of a break in the metabolism it might be due to the retention of faeces and consequent absorption of toxins. Still more recently Gerstenberger suggested that as the result of the break in the metabolism of carbohydrates, a defunctioning substance, possibly oxalic acid, is produced, which has a strong affinity for calcium.

There can be no question whether retention of faeces of itself can bring about scurvy; this is excluded by the marked instances of constipation frequently encountered among thriving babies. The majority of bottle-fed babies and a large number of the breast-fed suffer from a greater or less degree of constipation. On looking over our records of infantile scurvy from this point of view, and comparing them with non-scorbutic infants, we have not been able to note a characteristic distinction. Some of the infants had normal stools, others suffered from constipation, while the records of a great number showed occasional loose stools. Furthermore, in cases of latent or subacute infantile scurvy, it was of no moment whether a laxative was given or whether constipation was induced by means of opium. The report of the American Pediatric Society shows that the majority have had a similar experience; the bowels were regular in seventy-four instances, irregular in fifteen, constipated in one hundred and twenty-six, and diarrhoeal in seventy-seven. In this connection, it may be pointed out that the preparation termed "malt soup," the diet which in our experience has been most frequently associated with scurvy, is essentially laxative, and, on the other hand, that one of the most potent antiscorbutics is potato, which has no definite laxative property. It may be added, as noted elsewhere, that scurvy developed in infants in spite of their receiving cod liver oil or olive oil for long periods. It is evident, therefore, that the retention of faeces is not the essential factor in the etiology of scurvy. Its secondary r?le, especially after scurvy has developed, will be considered later in this chapter.

In order to elucidate this question Torrey and Hess made a study of the relation of the intestinal flora to the scurvy of guinea-pigs and of infants. In guinea-pigs they found in the intestinal tract merely such bacteria as are encountered on the oats and hay fed these animals. The bacteria were few in number and hardly any were actively proteolytic. Furthermore, there was no change in the flora on adding antiscorbutic food, although the scorbutic symptoms disappeared. Recently Givens and Hoffman, as the result of a similar study, have come to the same conclusion. The investigation of infants led to similar results, and is illustrated in Table 1. It will be seen that the infants were all on a high carbohydrate diet, and that in two instances the flora was compared, not only during the active scorbutic process, but after orange juice had been given for a week or more. The bacteria were such as one should expect on a diet rich in carbohydrates; putrefactive organisms were present only in small numbers; and in the case in which they were most numerous , they had disappeared upon the subsequent examination, although the scurvy had become more marked. It is evident, therefore, that in the scurvy of infants as well as of guinea-pigs there is no overgrowth of putrefactive bacteria in the intestinal tract, and therefore no basis for the hypothesis of ptomaine or similar intoxication. Other poisons may, however, be absorbed from the intestine as the result of a prolonged deprivation of an essential vitamine.

Almost all of these cases were receiving liberal daily amounts of cod liver oil, which should exclude the possibility of complicating rickets.

It is evident from the limited data concerning the blood chemistry of scurvy that it is a field which has been inadequately explored and will repay more intensive study. Investigations of this kind have recently been made possible by the introduction of accurate methods requiring only small quantities of blood.

Studies of the metabolism of animals suffering from scurvy are almost as few as those on man. The work of Morgan and Beger, which is frequently quoted in this connection, is not applicable, as it concerns rabbits, which do not develop scurvy. They found that rabbits fed solely on oats and water suffered in their nutrition , and could be cured by the addition of sodium bicarbonate to the dietary. In 1916 Lewis and Karr published a paper on the constituents of the blood and the tissues of guinea-pigs fed on an exclusive oat diet. They found the urea content several times greater than normal, but that it fell to normal once more if cabbage or orange juice was given. From the standpoint of scurvy, this investigation is open to the criticism that the diet was too incomplete, and also, as the authors suggest, that the animals suffered from partial starvation and a lack of water.

In the following year Karr and Lewis published a paper on a different phase of this subject, and came to the following conclusions: "No changes in urinary elimination of phenols, nor in the degree of conjugation of the phenols, were observed, provided the factor of partial starvation was ruled out. This is believed to indicate that no increased bacterial action occurs in the intestine of scorbutic guinea-pigs despite the difficulty of evacuation of the faeces." These results are in harmony with the bacteriological study of Torrey and Hess, who found that there was no increase in the proteolytic flora of the intestine in infants or in guinea-pigs suffering from scurvy.

In 1917 Baumann and Howard published the only metabolism study which has been carried out on guinea-pigs suffering from scurvy, and they are of the opinion that this disorder has a profound effect on the mineral metabolism of this animal. The calcium was excreted in notably large amount; potassium was also lost, and to a greater extent than sodium; the only element which was consistently retained during the active stage as well as during the period of recovery, was magnesium. This study was followed shortly by one from the same laboratory, by Howard and Ingvaldsen, carried out on a monkey suffering from scurvy. It was inconclusive, not conforming to the experiments on the guinea-pigs; the authors state that the "changes in the mineral excretion of the monkey during the scorbutic period were not sufficiently significant to admit of easy interpretation." "The marked loss of the various mineral substances encountered in experiments with man and guinea-pig was not observed in the present series." It should be remembered, however, that the diets of the guinea-pigs and the monkeys were quite different, the former consisting mainly of oats, and the latter of condensed milk. It is quite possible that the basic diet may play a r?le in the metabolism of this disease, although, as stated elsewhere, its effect cannot be noted clinically. Special attention should be paid to this factor in metabolic studies, in view of the widely-held opinion that the carbohydrates exert a potent influence in the development of beriberi.

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