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 of the 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 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 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.
| Infant. | Diet. | Date. | Scorbutic condition. | Source of material. | Types of bacteria. | Remarks. |
|---|---|---|---|---|---|---|
| M. | Malt soup and cereal | Dec. 1 | Subacute | Rectum | B. acidoph. B. bifidus M. ovalis B. coli | {Normal infant’s flora. {Gram + bac. predominant. {No spore-bearing or putrefactive types. {B. acidoph. about 40% viable bact. |
| Do. | Dec. 4 | Do. | Do. | Do. | Do. | |
| Same, also 20 c.c. liquid petrolatum, one week | Dec. 11 | Subperiosteal hemorrhage | Do. | Do. | {Relatively more B. coli. {Many B. bifidus {No putrefactive bact. | |
| Same diet, oil stopped, orange juice 10 days | Dec. 21 | Markedly improved | Do. | Do. | Normal infants’ flora. Bacteria as above. | |
| K. | Malt soup and cereal | Dec. 11 | Subperiosteal hemorrhage | Rectum | Streptococci B. coli M. ovalis | {Gram - bacteria predominant. {B. coli gram + diploc. numerous. {B. acidoph. few. |
| Do. + orange juice (60 c.c.), 8 days | Dec. 21 | Markedly improved | Do. | B. bifidus B. coli Streptococci | {Gram + bac. predominant. {Many B. bifidus {Streptoc. unchanged. | |
| S. | Formula: Cream, water, flour, sugar, also cereal | Dec. 21 | Mild scurvy | Rectum | B. lact. aerog. B. coli M. ovalis B. bifidus B. welchii | {Gram + and - bact. about equal. {Many lact. aerog. {Putrefactive bact. in minority. |
| Malt soup and cereal | Feb. 11 | More marked | Do. | B. lact. aerog. M. ovalis B. bifidus Dipheroids | {Gram + bact. in great majority (B. bifidus). {Spore bearers very few. {Flora not at all putrefactive. |
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 (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 of bacterial 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 same laboratory, 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.