While the acute stages of infantile scurvy are comparatively rare, incipient cases are more common, and not always easily recognised. Comby10 reports that 90 per cent of the 72 cases of this disease which he encountered had been wrongly diagnosed by the attending physician. Tobler11 states that in addition to the infants suffering from manifest scurvy there are a far larger number of latent cased with characteristic muddy complexion, lack of appetite, stationary weight, and fretful disposition. In a discussion of this disease Hess remarks:12

6 Abels, Wien. klin. Woch. 33, 899, 1920.

7 See Hess and Pish, Am. J. Dis. Child. 8, 386, 1914.

8 Hess, Am. J. Dis. Child. 12, 162, 1916.

9 Comby, J. MeU, Paris, 1920, 1, 673.

9a Seven children were cured of Barlow's disease by feeding them exclusively upon milk. In five of the cases the milk was heated for 10 to 35 minutes and in two cases the heating was prolonged to one hour. It is concluded that the vitamin is not as readily affected by heat as has been assumed. The concentration of the food, i. e., the water content, is important. Nobel (Z. Kinder-heilk. a8, 348, 1921).

Morikawa (Igakkwai 19, 9, 1920; Endocrinology 4, 615) concludes that the hypertrophy which is similar to that found in polyneuritis gallinarum indicates that the absence of a necessary vitamin is also an etiological factor in Barlow's disease.

10 Comby, Bull, 80c. Med. Hop. Par. 45, 288, 1921.

Infantile scurvy differs clinically from the other deficiency diseases mainly in the fact that it is characterised by the production of hemorrhage in various parts of the body, hemorrhage into the gums, into the skin, beneath the periosteum, into the kidneys, etc. A study of the pathogenesis of these hemorrhages has shown that they were not the result of alterations of the blood itself, a delayed coagulability, or a decrease of blood platelets, but that they were due to the alteration of the blood vessels which allow the blood to traverse its walls. This alteration probably should be regarded merely as a part of the general tissue changes which occur in this disorder.

Although hemorrhage is not encountered in beriberi, a careful consideration will show some clinical relationships between these two diseases. As is well known, signs of involvement of the nervous system are the characteristic manifestations in beriberi. A study of the cases which came under our view showed that infantile scurvy is not entirely free from nervous signs. The knee jerks are increased, there seem to be slight involvement of the optio disks in some cases and perhaps sensitiveness of the cutaneous nerves. Again, dilation of the right heart, a remarkable pathological condition which has been frequently described in beriberi and noted by Andrews in infants who had suffered from this disease, was found to occur likewise in infantile scurvy, as demonstrated in numerous Roentgen ray examinations. Oedema, which is such a common symptom in beriberi, is not frequently present in infantile scurvy. In fact, there is one form of this disorder, an exceptional type, where oedema is most marked.

In this connection it should be remembered that degeneration of the nerves has been found by Ingier in some animals suffering from scurvy, that Hoist and Frolich have noted that guinea pigs fed on decorticated or highly milled rice, developed scurvy and not beriberi, and that Darling has reported that in some African negroes a diet that caused scurvy in one set of men, caused neuritis in others. There is evidently, therefore, a definite interweaving in the symptomatology of these two deficiency diseases. As is well known, beriberi is produced by a diet of decorticated rice and may be cured by feeding the rice polishings. In this regard, there seems also to be some connection between the two diseases, for we found that the giving of wheat middlings, which may be regarded as the pericarp of the wheat, in some instances resulted in a prompt amelioration of the symptoms, although it was unable to bring about a complete cure of the disorder.

Certain of the lower animals, notably guinea pigs, are extremely susceptible to scurvy, while other species such as the rat and the prairie dog appear to be immune.18 Whether this immunity is real or only apparent is an interesting question, but one which is difficult to settle, since the only test known for the presence of the antiscorbutic factor in foods is the biological method and this may not be sufficiently delicate to detect small quantities present. A very interesting investigation has recently been made by Parsons 14 who has been able to show that the livers of rats fed on a typical antiscorbutic ration for from 213 to 247 days were high in antiscorbutic, as shown by the guinea pig test. Scarcely any difference in antiscorbutic content was demonstrable between the livers of these rats and those of control animals on a normal diet. This seems to show that the rat actually requires the factor for its metabolism, but whether it is synthesized in the body of the animals or received in small amounts in the food is at present unanswerable. Preliminary experiments are said to suggest the existence of the same phenomenon in newly hatched chickens. Plimmer 15 notes that pigs fed on cooked food, consisting of a mash composed of meals, sharps or middlings and turnips, developed scurvy.

The animals were cured by giving them the same food but in the raw condition and by increasing the quantity of turnips, which are rich in the antiscorbutic factor.

11 Tobler, Ztschr. f. Einderh. 18, 63, 1918.

12 Hess, Proc. 2nd Pan. Am. Sci. Cong. Sec. 8, Pt. 2, p. 49.

13 McCollum and Parsons, J. Biol. Ghem. 44, 603,1920; McClcndon, Cole, Engstrand, and Middlekanff, Ib.t 40, 367. 1019; Funk, Ib, 26, 409,1916; Harden and Zilva, J. Path. Baot. 1919; Hoist and Frolich, Zeitseh. f. Hyg. Infek. 72, 1,1912; J. Hyg. 7, 634, 1907; Dranmond, Bioeh. J. 13, 77, 1919.