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.
There is no need of studying all the theories which have been advanced to account for scurvy. They have been manifold and most of them have died a natural death. For many years thepotassium deficiency theory, suggested by Garrod, gained wide acceptance. That scurvy should be attributed to a lack of this salt is readily comprehensible in view of the abundance of potassium in the antiscorbutic foodstuffs, the fruits and the vegetables. It was not long before it was evident that this was not the correct solution, as the salts of potassium served neither to prevent nor to cure scurvy. This theory was accordingly modified to include only organic potassium. Experiment, however, failed to support the validity of this hypothesis, and it was gradually abandoned.
Another theory which had a short but popular career was thecitric acid theory, which was maintained vigorously by Netter. This explanation seemed logical in view of the marked potency of the citrous fruits, and particularlywhen it was shown that human milk contains a greater percentage of the salts of citric acid than cow’s milk, and that some of these salts are lost in the course of heating. This hypothesis withstood neither the practical test nor chemical investigation. It was found that the various salts of citric acid, either singly or in combination, are unable to cure scurvy. This treatment has been employed repeatedly on man and on animals with little or no success; we also have resorted to it in vain. It was shown, furthermore, that it rested on an insecure chemical basis, as boiled milk contains but 0.1 g. per litre less citric acid than raw milk—an amount which is negligible from a therapeutic point of view.
Before considering what may be termed the prevailing theories, a few lines must be devoted to theacidosis theorychampioned by Sir Almroth Wright. According to this writer scurvy is due primarily to an excess of acid compared with alkaline food.5A theory of this nature was open to verification, and soon collapsed when put to the test. It was found, in the first place, that an addition of alkali was unable to cure experimental scurvy. It may be added that we have found it of no value in infantile scurvy. Holst and Froelich pointed out that potatoes and peas, two excellent antiscorbutic vegetables, have an alkaline and not an acid ash; that adding hydrochloric acid to dandelion juice improves rather than diminishes its potency; that 1 g. of cabbage, which suffices to protect a guinea-pig from scurvy, does not contain sufficient alkali to neutralize an acid state; and, finally, that scurvyis not encountered in the well-established acidosis of diabetes.
Let us turn to some of the current theories of the etiology of scurvy. For years many have held to thetoxic theory, believing that poisons either were consumed in the food or formed in the intestine by means of bacterial action. At present this view is held by the minority. The situation in this respect may be compared to that of beriberi, about which there is also no consensus of opinion, a minority attributing it to the action of an unknown toxin.
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 (indicating an involvement of the pneumogastric nerves), 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.6The 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.
If a toxin is to be regarded as the proximate cause ofinfantile 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 preëminently 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 diarrhœa 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 theconception 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 fæces 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.
It is of no avail to discuss these various hypotheses—the formation of intestinal toxins—except where they are based on observations which can be tested and controlled. This is true solely ofthe relation of constipation to scurvy, and we shall confine ourselves therefore to a consideration of this aspect of the question.
There can be no question whether retention of fæces 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 notbeen 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 diarrhœal 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 fæces is not the essential factor in the etiology of scurvy. Its secondary rôle, especially after scurvy has developed, will be considered later in this chapter.
TABLE 1
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 sameconclusion. 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 (S), 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.
There are those who believe that scurvy is ofbacterial origin, some going so far as to regard it as a communicable disease. This viewpoint was maintained by the famous Boerhaave and supported with all the weight of his authority by Villemin in the seventeenth century. It is a view held by many, if not by the majority, of physicians in Russia to-day, and recently has been advanced by European army surgeons. This question illustrates in an interesting manner how the trend of the day influences medical thought—it has been suggested lately by Much and Baumbach that the scurvy microörganism may be carried by means of lice. But clinical experience points absolutely against the infectious nature of scurvy. Indeed, the only episode which lends any support to this opinion is its widespread and seemingly epidemic character;the fallacy of such deductions has been well illustrated in regard to beriberi, which for many years was regarded as an infectious and communicable disease. The fact that whenever scurvy occurs among a body of troops the officers are spared, constitutes convincing evidence against its communicability. This peculiarity of incidence was noted by Hoerschelman and others in the recent World War, and is referred to in the Report of the War of the Rebellion. Many of the earlier writers, in discussing the occurrence of ship scurvy, drew attention to the paucity of cases among the officers.
When we turn to bacteriological studies we find that some years ago Ausset claimed to have isolated “a pasteurella type of organism” from a case of infantile scurvy, and suggested it as the causative agent of this disorder. On the other hand, Hart, Rehn, Hirschsprung, von Starck, Schmorl, and recently Boerich, have failed to find bacteria in the blood, although the total number of cultures must be admitted to have been small. Czerny and Keller report negative bacterial growth from fluid aspirated from affected joints.
The only articles considering this important question from the experimental side are those of Jackson and Moody, and of Moore, who conclude tentatively that scurvy may be a bacterial infection. Jackson and Moody cultivated a diplococcus from the tissues of scorbutic animals after death, reproduced hemorrhages by inoculating cultures of these microörganisms into the circulation, and recovered the bacteria from the tissues some weeks later. Their results are open to the criticism that bacteria were found only after death, and that all blood cultures during life proved negative. An article by Moore, however, which has just appeared from this samelaboratory, states that “an organism of the streptococcus viridans type was isolated from the blood” in a case of adult scurvy. In one instance we recovered an organism of this type from the blood of an infant suffering from scurvy. It is highly important that more blood cultures should be carried out in the course of human or animal scurvy, and that particular note should be made of the stage of the disorder when they are taken.
There is no doubt that invasion of the blood-stream does occur readily in the course of scurvy, but this takes place generally after the disease has developed and must be regarded as a secondary phenomenon and therefore unessential from an etiologic standpoint. Indeed one of the striking and important symptoms of scurvy is the marked susceptibility to infection (furunculosis, nasal diphtheria, “grippe,” etc.), which comes about as the result of the nutritional disturbance. An excellent example of this interrelationship is the “epidemic” of hemorrhagic scurvy described in the chapter on symptomatology. Hemorrhages coming about in this way should be regarded as focal complications rather than as truly scorbutic. It should be realized that, at the present time, it is not possible to distinguish between local symptoms which are truly nutritional or scorbutic in nature, and those which are bacterial and of secondary origin.
The newest theory, and the one at present most widely accepted, is thevitamine(accessory factor)theory. It was evident to Lind in the seventeenth century that scurvy could be prevented and cured by means of fruits or vegetables, a fact which became increasingly clear to succeeding generations. Until the latter part of the nineteenth century, however, this miraculous virtue of plants stimulated little inquiry and no research. As far back as 1841 Buddrealized that “the explanation depended on the study of organic chemistry, and the experiments of physiologists,” but until recently it was not perceived that the solution of the problem involved the introduction of a new chemical factor. This view suddenly took shape after Eijkman in 1897 showed the nature of polyneuritis in fowl, and Hopkins in 1906, going a step farther, demonstrated the necessity of one or more unidentified food factors for the normal nutrition of the rat. The work which established this novel theory on a scientific basis in relation to scurvy was the classic investigation of Holst and Froelich, referred to so frequently in connection with experimental scurvy. These investigators showed that the mere drying of vegetables was sufficient to deprive them of their antiscorbutic power, although from a chemical standpoint they seemed unaltered; that high degrees of heat had generally the same effect; that under certain conditions these foods withstood prolonged heating, demonstrating that the antiscorbutic factor was not a ferment; that acids and alkalies played no essential rôle in the etiology; that fats, proteins and carbohydrates were not significant factors; that as little as 1.0 g. of cabbage suffices to afford protection to a guinea-pig. In other words, by a process of exclusion they showed that it is a disorder due to the lack of an unidentified food factor.
Subsequent studies, carried out within the past few years, have served only to strengthen this viewpoint. For example, an “artificial orange juice” composed of the various salts, citric acid, and sucrose in the proportions in which they are found in the natural juice, failed, in the experience of Hess and Unger, to protect or to cure guinea-pigs—demonstrating that this preparation did not contain the essential factor. In the same way, Harden andZilva were able to protect animals from scurvy with a preparation of lemon juice which had been almost entirely deprived of its salts. It is needless to multiply these examples. It is sufficient to state that there has been no investigation during the last years of intensive study of scurvy, which has tended to weaken the vitamine hypothesis. It may be stated, therefore, that experiments have demonstrated that scurvy is due essentially to the lack of a specific vitamine. It is unwise to proceed farther and place it in the group of so-called “deficiency diseases,” including beriberi, pellagra, etc., unless the reservation is made that these several diseases may present marked differences. It is quite possible that one may be what might be termed a simple deficiency disease, whereas another may have important additional etiologic factors. At any rate, unless it is realized that there has been no proof that all are due to similar deficiencies, we may, by stamping them all alike and by grouping them together, be misled into taking their close relationship for granted. In regard to scurvy, there may well be other etiologic factors, but they are of a secondary character. Bacterial invasion has been referred to in this connection, and it is possible that toxins are absorbed from the intestine after nutrition has been disturbed. Diarrhœa and digestive disturbances may play a rôle. Whether the total intake of food or the correlation of its constituents—protein, carbohydrate, fat and salts—affects the action of the vitamine, is one which has not been well studied clinically or experimentally. In regard to beriberi, it is claimed that there is a direct ratio between the quantity of carbohydrate ingested and the amount of vitamine required. No such interrelationship exists in regard to scurvy. This was evident a few years ago (1917) whensome infants receiving pasteurized milk, prepared with the addition of 3 per cent. flour, did not tend to develop scurvy more readily than others receiving simple pasteurized milk. A consideration of the antiscorbutic vitamine will be postponed for a subsequent chapter.
Etiology.—In considering infantile scurvy we are concerned almost entirely with the artificially-fed baby. It is true that in the literature we meet with scattered reports ofscurvy in breast-fed babiesand that these cases seem to constitute a noteworthy group; in point of fact, they are comparatively few. The collective investigation of the American Pediatric Society includes ten infants who had been given breast milk exclusively, and Concetti adds another ten in his compilation of 682 cases.7In spite of their paucity these cases require separate consideration because they represent an important aspect from an etiologic standpoint. How are we to explain the fact that human milk may lead to rather than protect against this disorder? On investigating more closely it is found that these cases differ in several important respects from the group which has been artificially fed. They are of a different age; instead of being in the second half year of life they are generally but a few months old. Furthermore, the signs are not the same. The hemorrhages involve the upper extremities fully as frequently as the lower extremities, and often appear at unusual sites—for example, on the scalp or as large subcutaneous effusions at various parts of the body. In many instances it has been noted that the nursing mothers were suffering from some debilitating disease such astuberculosis or syphilis, or had an insufficient supply of milk, or that there had been some other unusual factor, as Freund has shown in an article devoted to this particular aspect. It is not necessary, however, to fall back on these attendant circumstances to exclude from consideration many of the cases. For example, Crandall’s case of “scurvy in an infant of six weeks” should be invalidated, not because, as Freund suggests, the mother had rheumatism and insufficient milk, but because of the age of the infant, and the course of the disease; first one arm was involved, then the other, then hemorrhages appeared on the skin, and finally it was cured by giving a teaspoonful of fresh cream before each nursing. Had the baby really suffered from scurvy it could not have been cured by this means. Southgate’s case must also be rejected, not because the mother was tuberculous but in view of the symptoms—the arms and legs were pseudoparetic, “the legs, feet and hands were double their normal size,” and moderately large hemorrhages were present on the back and chest. It seems hardly necessary to discuss in detail the score of cases which comprise this group, as, in general, the same criticism applies to all. Some evidently were congenital syphilis, still more must be regarded as sepsis, and others as unknown toxic conditions. Apart from these cases the question must be considered whether scurvy can occur in a breast-fed infant. Personally, we have never met with a case of this kind, and, as Finkelstein aptly remarks, there has been “no necropsy of a breast-fed case or conclusive X-ray picture.” It seems possible only if an infant, for a period of months, has obtained a scanty supply of milk, or when the milk has been exceedingly deficient in the antiscorbutic vitamine.Even under such conditions it does not seem possible for scurvy to become manifest in six weeks (Crandall’s case), or in four weeks, as in a case reported by the American Pediatric Society, unless we believe that the infant suffered also from a certain degree of intrapartum or congenital scurvy. In view of the fact that an infant requires about one pint of milk to furnish it with an adequate daily quota of the antiscorbutic factor, it is theoretically possible, under extreme conditions, for it to become scorbutic, in spite of being nursed at the breast. Such an occurrence must be regarded as exceedingly rare, far more so than the current statistics illustrate, for considerably less than a pint of milk a day will prevent the appearance of manifest scurvy for a period of several months. Some of the reported cases may have been latent scurvy, rendered acute by a complicating bacterial infection.
It might be expected that by ascertainingthe occurrence of infantile scurvy in countries where it is endemic, we could learn under what conditions and how frequently breast-fed babies develop this disorder. Approaching the question from this angle, it is found that the available data is meagre and not entirely convincing. Peculiarly enough infantile scurvy has rarely been reported from Russia, where scurvy is, in many sections, endemic. For example, although Tschudakoff, who personally examined over 10,000 persons, in connection with the great scurvy epidemic in Russia (1898–99) found 11.11 per cent. of the people suffering from this disease, he did not meet with a single case under the age of five years. Fuerst writes that Filatow, the celebrated Russian children’s specialist, declared that he knew of no instance of Barlow’s diseasedescribed in the Russian literature.8Shortly after the recent war scurvy broke out among the wet-nurses in an infant asylum in Vienna. A very few of the infants nursed by these women developed the disorder, far fewer than might have been expected (personal communication). Hopkins recently wrote a communication to the effect that in the island of Aruba, in the Dutch West Indies, they had been unable to grow any crops in 1912, 1913, 1914, that 3000 cases of scurvy had developed there during the year 1915, and that in 1917 it was again being noted. In answer to a personal inquiry regarding the occurrence of scurvy among the infants of Aruba, he wrote that “infantile scurvy is very rare,” although “most all of the babies are breast-fed for about a year.”9
On the other hand, descriptions of the coincidence of scurvy in mother and nursling are even more fragmentary; in fact, we have been able to find but two reports of this kind. The one most frequently cited is that of Cheadle, which consists merely of the following bald statement: “With the exception of one or two doubtful cases, of which the details of breast-feeding and diet are imperfectly given, the only instances of scurvy arising in sucklings are those when the nursing mother has been suffering from scurvy at the time.” The other report has been gleaned from a recent editorial in theBritish Medical Journal, which refers to the above mentioned outbreak of scurvy in Vienna, affecting in some cases both mothers and breast-fed infants.
It is difficult to pass judgment on this question in viewof the paucity of data. In the near future, probably, when we learn in detail about the epidemics of scurvy which occurred during and immediately following the war, we shall be in a better position to weigh its pros and cons. In view of the above data it does not seem that nursing infants readily develop scurvy, even though their mothers do not obtain a full quota of antiscorbutic vitamine in their food. This appears to be the clinical result, whatever its interpretation may be. It cannot be explained on the assumption that human milk contains a particularly large quota of this factor. In a test carried out to elucidate this question it was found that eight ounces a day of breast milk was insufficient to alleviate the symptoms in a case of scurvy, and that twelve ounces barely sufficed. This milk was from a woman who was on a liberal diet containing an adequate supply of vegetables. It had been previously demonstrated that sixteen ounces of cow’s milk is sufficient to cure infantile scurvy, so that it is evident that human and cow’s milk do not differ essentially in this respect. There are, however, other factors to be considered—for example, the incomparable freshness of the milk suckled from the breast, which may endow it with additional potency, or the possibility that the lack of vitamine may be compensated for by the large quantity of milk consumed. It also may not be entirely immaterial whether the vitamine is supplied in one dose, as, for example a daily feeding of orange or tomato juice, or whether this factor is furnished to the infant in frequent small quantities in the mother’s milk throughout the day. In this connection we cannot help contrasting the relation of beriberi to breast feeding. As is well known, infants which develop beriberi are almost always nursed and not bottle-fed, and show signs of this disorder, although themothers are in apparent health, and give no clinical evidence of disease.
Turning to a consideration ofthe artificially-fed infant, there exists a somewhat similar situation in regard to the occurrence of scurvy on a diet of raw cow’s milk. In almost all reports of this kind the quantitative viewpoint is entirely disregarded, and little or nothing is stated to indicate how much milk the infant consumed. And yet this factor is of essential importance in interpreting the cause of the nutritional failure. It is clear, for example, that if a baby receives but eight ounces daily of raw milk—one-half the requisite amount—it may well develop scurvy, notwithstanding the fact that the milk has not been heated. In addition to the quantity, there are other factors which play a greater or less rôle in the relation of raw milk to the etiology of scurvy. It is no doubt of consequence whether the fodder of the cows was rich or very poor in the antiscorbutic factor, and, accordingly, whether the baby received what may be termed an “antiscorbutic-rich” or an “antiscorbutic-poor” milk. Furthermore, the age of the milk must be borne in mind, for we have found that even raw milk loses some of its potency on becoming stale.10
One of the mooted questions relative to the etiology of scurvy is the rôle of heated milk, and more particularly ofpasteurized milk. In view of the vogue which pasteurization has acquired in the large municipalities, especially in the United States, this aspect has assumed increasing importance, and deserves detailed investigation. Pasteurization has achieved so much in limiting theinfectious diseases, especially the diarrhœal disorders of infancy, that it has come to be looked upon as heresy to deprecate its virtues in any regard.
It has become increasingly evident that in the course of pasteurization milk loses an important measure of antiscorbutic vitamine. The term pasteurization, when employed in this connection, is not meant to be synonymous merely with the heating of milk to 140° to 165° F., but embraces the entire commercial process—the heating, handling, subsequent cooling, aging and all other factors involved. There can be no doubt that milk which has undergone this elaborate treatment has suffered in its antiscorbutic property. In 1914 Hess and Fish reported mild cases of scurvy occurring among infants who had received milk heated to a temperature of 165° F. for thirty minutes. This degree of heat is claimed by many physicians and hygienists, including the National Commission on Milk Standards, not to destroy its chemical constituents. Nevertheless typical cases of scurvy supervened after this diet had been followed for a period of six to nine months. Subsequent experience, published by Hess in 1917, with milk heated to only 145° F., served to confirm the previous observations. That these cases were true scurvy was proved by the fact that a cure resulted when raw milk was substituted. A similar experience in Berlin reported by Neumann and others was convincing, but was not heeded in this country. In 1901 one of the largest dairies in that city established a pasteurizing plant where all milk was raised to a temperature of about 60° C. After an interval of some months infantile scurvy began to be reported from various sources throughout the city. Neumann depicts the situation as follows: “Whereas, Heubner, Cassel and myself had seen only thirty-two cases ofscurvy from 1896 to 1900, the number of cases suddenly rose from the year 1901, so that the same observers—not to mention a great many others—treated eighty-three cases in 1901 and 1902.” At a spirited meeting held by the Berlin Medical Society in 1903 to discuss this subject, Heubner was able to report 65 cases. An investigation was made, and the pasteurization discontinued. The result was almost immediate, the cases decreasing just as suddenly as they had increased. These reports and others demonstrate that unless additional antiscorbutic food is given, a diet of pasteurized milk will lead to the development of scurvy. As the antiscorbutic vitamine is not entirely destroyed by pasteurization, the severity of the disorder will be in inverse ratio to the amount of milk which is consumed.
It has been our experience that milk pasteurized in the home or institution did not lead to scurvy to the same extent as that which was commercially pasteurized. Babies fed on home-pasteurized milk did not develop manifest scurvy. The difference in the two processes consists mainly in the amount of handling during the process of heating and the subsequent aging which the milk undergoes. An interval of forty-eight hours usually elapses between commercial pasteurization and the delivery of the milk to the consumer. In New York city most of the better-grade milk is pasteurized at the farm, so that it is subjected to a longer period of aging than the poorer grade, which is not pasteurized until it reaches the city. Although our results indicated the effect of freshness or staleness on milk which had been heated, they showed also that other factors must be involved, for home-pasteurized milk which is forty-eight hours old is superior to the commercial product of the same age. This differencewe believe is due to the handling which the milk undergoes, to the mechanical processes involved in commercial pasteurization.
In considering this aspect of the development of infantile scurvy on a diet of heated milk, it is of interest to refer to the experience of Switzerland and of France. In 1907 Bernheim-Karrer reported nine cases of scurvy which occurred on “homogenized” milk. This milk is forced between rapidly-rotating surfaces at a temperature of 55° to 65° C. at a pressure of 150 atmospheres. This process had been introduced the year previous by a large dairy which was well known for its excellent grade of milk. Before this innovation, milk usually had been boiled for a long while before being fed to infants. In France a similar epidemic of scurvy followed the introduction of the use of homogenized milk (lait fixé). Lecornu gives an interesting account of this episode, remarking on the large number of cases of scurvy occurring on this milk compared with sterilized milk, which was employed so much more extensively. These experiences furnish excellent examples ofthe harmful effect of industrial methods on milk, especially on its antiscorbutic vitamine. Lecornu also emphasized the scorbutic influence of “lait maternisé,” which is similar to the German Gaertner milk, and is subjected to dilution, centrifugation, and sterilization.11He states that before this preparation was introduced scurvy was practically unknown in France. Lecornu attributes the deleterious effect of the “lait maternisé” and the “lait fixé” to bacterial contamination, as does Bernheim-Karrer.We believe, rather, that its loss of potency is due to the mechanical processes to which it has been subjected.
Boiled and, more particularly, sterilized milk, is regarded as a common cause of infantile scurvy and figures prominently among the foods held accountable for this disorder. It has been pointed out, however, that thousands of infants, especially in Europe, receive milk of this kind, and do not develop scurvy. Statistics such as those of Variot, who has distributed in his out-patient department, during a period of twelve years, 400,000 quarts of sterilized milk (heated in half-litre bottles and hermetically sealed at the farm) without observing a case of scurvy, must be accorded weight in this connection.12Escherich, some years previously, stated that he did not meet with scurvy in Graz, although he was accustomed to feed babies on sterilized milk. Budin, the celebrated French children’s specialist, writes: “As for the so-called infantile scurvy which is alleged to follow the use of sterilized milk, I have heard a very great deal about it during the last few years, but I am still looking for my first case.” Evidence from such sources cannot be summarily cast aside, but must be given due consideration. It is evident that the mere heating or sterilization of milk, although it reduces the antiscorbutic vitamine, does not do so to a degree sufficient to lead to the production of clinical scurvy. Our experience accords with that of the above observers. Some years ago we fed infants with milk which had been boiled for five minutes, and, at another time, made use ofhome-made evaporated milk which had been heated for a period of seventeen hours, until it had been reduced to one-eighth its volume. This evaporated milk was well borne for months, although slightly caramelized in the course of heating, and did not lead to any signs of scurvy. Clearly there are other factors involved in this question besides the mere subjection to heat. We believe that every step in the process is important—the freshness of the milk, whether or not it is agitated and exposed to the air, whether it is sealed carefully and used soon after sterilization,13and, finally, whether the baby receives a sufficient quantity. If this milk, which has certainly lost some of its vitamine content, is given in small amount, it will not supply an adequate amount of the antiscorbutic factor.
Neumann, Czerny, and others state that they have even cured infantile scurvy by giving boiled milk obtained from a different source. In the Berlin epidemic, Neumann laid particular emphasis on the fact that the milk which induced scurvy had been doubly heated, having been pasteurized commercially and later boiled in the home before it was fed to the baby. Plantenga has also laid stress on the influence oftwo-fold heating, citing an interesting experience with scurvy in his clinic. When the milk was pasteurized one day and boiled for five minutes on the subsequent morning, 23 cases of infantile scurvy developed among the 200 infants attending his dispensary. The following year when the procedure was altered so that the milk was merely pasteurized, no case of this disorder developed. There can be no doubt that milk whichhas been heated twice must have lost more of its antiscorbutic properties than milk which has been heated but once, and that aging also must contribute to this loss. Whether there is what may be termed a peculiar sensitization of milk following pasteurization, has not been definitely shown.
Up to the present timedried milkhas played an insignificant rôle in the etiology of infantile scurvy. One of the factors which has hindered the general acceptance of dried milk by physicians and laymen has been the fear that its use might lead to the development of Barlow’s disease. It is therefore important to consider this aspect of the subject, especially as dried milk seems destined to be used to an increasing extent. A recent report to the Local Government Board by Coutts states that “Millard and Naisch in England confirmed the testimony of Miele in Belgium, and Gautier and Genevoix in France, that scurvy is not to be feared” from this foodstuff. This coincides with our experience, namely, thatdried milk not only does not lead to scurvy, but may contain sufficient antiscorbutic vitamine to cure this disorder. Recently a scorbutic baby was fed with milk which had been dried by the so-called Just-Hatmaker process—whereby it is subjected on a drum for a few seconds to about 230° F.—with the result that the hemorrhages of the gums began to be absorbed in about three days, and all symptoms to disappear shortly thereafter. This infant received dried milk to the equivalent of 24 ounces of fresh milk, and this preparation had been dried and canned somewhat over three months before it was used. Recently two infants, suffering from marked scurvy, were treated with milk which had been dried six months previously. The one received only sixteen ounces a day and the other aquart; both recovered within a few days after this food had been substituted for malt soup. Not long ago, as reported elsewhere in a paper by Unger and myself, after curing a baby of scurvy by means of this milk, it was maintained in health for a subsequent period of three months on a diet which contained no additional source of antiscorbutic vitamine. These results are emphasized as illustrating the peculiar relationship of drying and of the application of heat to the antiscorbutic vitamine, and because recently several reports have appeared, for example, that of Barnes and Hume in England, and of Hart, Steenbock and Smith in this country, to the effect that dried milk is devoid of antiscorbutic value. The difference of opinion is due to the assumption that dried milk is a uniform product and has identical antiscorbutic properties. For milk to retain its antiscorbutic value, notwithstanding drying, it must have been rich in vitamine before desiccation, it must have been dried quickly, and packed within the shortest possible interval in air-tight, preferably hermetically sealed, containers. As in relation to the heating of milk, so in regard to its drying, it is not the degree of heat to which it is subjected which is all important, but rather the associated conditions. The merits of each process will have to be tested individually and perhaps even each particular brand of milk.14
In the foregoing, the dictum has been accepted without comment that fresh milk may be either rich or poor in antiscorbutic vitamine. This point of view has recentlygained general acceptance, on the assumption that the milk of the stall-fed cow is markedly deficient in this factor. Recent work by Hart, Steenbock and Ellis gives evidence that “summer pasture milk is much richer in this nutritive factor than dry feed milk or winter produced milk, involving the use in the ration of corn silage or sugar mangels.” In some experiments (unpublished) we have found that dried milk shows similar variations, being a much more potent antiscorbutic when obtained from cows fed on fresh fodder than a similar milk from the same cows on fodder containing a minimum amount of antiscorbutic vitamine. The supposition of a direct quantitative ratio between the antiscorbutic intake in the food and output in the milk needs confirmation, especially as it does not quite coincide with the experience among human beings in countries where adult scurvy is endemic. In such countries—for example, Russia—nursing infants do not develop scurvy to the extent that would be expected, and it is possible that this exemption is due in part to a selective secretion of antiscorbutic vitamine into the milk.
As is well known, a diet ofcondensed milkleads to scurvy. This is not surprising, considering the prolonged heating to which this milk has been subjected. It is probable that many cases of mild scurvy developing on this food and characterized by beading of the ribs (rosary) and other indefinite manifestations, have been erroneously diagnosed as rickets.
It is hardly necessary to discuss separately the various kinds of milk which have led to scurvy in the course of infant feeding.15The principles laid down in the precedingdiscussion hold good for milk of all kinds. Heat will destroy a certain amount of vitamine, and, if the heating is followed by aging, still more will be lost. If an interval elapses and a second heating ensues, there will be further loss of vitamine. It should never be forgotten in considering foods in their relation to the causation of scurvy, thatthe amount of foodgiven must not be overlooked. For example, a pint of ordinary pasteurized milk will lead to scurvy, whereas a quart in most cases will be sufficient to tide the baby over until the period of mixed feeding. No general rule can be laid down, however, as may be judged from the fact that dried milk which has been subjected to almost all the influences which are deleterious to the antiscorbutic vitamine—heating, drying, aging, all carried out in a neutral medium—nevertheless retains its specific potency.
Infantile scurvy has always been far more prevalent in England and in America than in Europe, notwithstanding the fact that on the continent practically all milk for babies is boiled or sterilized. This has been ascribed, and probably rightly so, to the widespread usage ofproprietary foodsin the English-speaking countries. Among the cases reported by the American Pediatric Society about 60 per cent. had been given foods of this description. How is this relationship to be explained? These preparations in general may be stated to consist of cereals, sugar, with occasionally a small amount of dried milk; they are mixed with varying proportions of water and milk and then cooked. It is evident that two important causative factors of scurvy are thus furnished, namely, a small and inadequate quota of milk and the application of heat. In most instances not more than sixteen to twenty ounces of milk are used to make up the day’s feeding, and frequentlythis has been previously pasteurized. But there is an additional factor which comes into play in this connection, one to which we have recently drawn attention in treating of “The Deleterious Effect of the Alkalization of Infants’ Food.” It has been shown that the antiscorbutic vitamine is peculiarly sensitive to the faintest alkaline reaction, in which medium it rapidly undergoes deterioration, and even total destruction if heat is applied. Proprietary foods, with but few exceptions, are alkaline, having been rendered so by the addition of potassium carbonate or bicarbonate, in order to prevent acid fermentation of the fat and to counterbalance the relative poverty of potassium in cow’s milk. Little or no regard has been paid to this reaction; the textbooks on children’s diseases give this point no consideration whatsoever, expressing the salt content merely in terms of total ash. By this means ideal conditions are furnished for the destruction of a large part of the vitamine, and if this factor is not present in excess, scurvy will readily develop. It is to these various circumstances—the deficiency of milk, the alkalinity and the heating—that the scorbutic quality of proprietary foods is to be ascribed.
The most flagrant example of an infant’s food leading to scurvy is “malt soup”—an alkaline preparation of malt, which is prepared with flour and a small amount of milk.16This food brings about scurvy almost invariably unless an antiscorbutic is added to the dietary. That this effect is due to the alkaline potassium carbonate was shown by a recent test which is illustrated in chart. (Fig. 2). Here we see that in a case of scurvy, when thefood was altered and prepared with the same amount of milk and alkali, the disorder did not abate (although the carbohydrate had been discontinued), but when the potassium carbonate was omitted a gain in weight ensued, and, we may add, the symptoms disappeared.