Scurvy, Past and Present

by Alfred F. Hess

Recently an intensive study of this subject has been made by Zilva and Wells, which is of special interest because it describes the first beginnings of these lesions, and particularly because we have no knowledge whatsoever of the dental changes which occur in human scurvy. These investigators found a fibroid degeneration of the pulp of the teeth, a pulpar fibrosis. “It is clear at once,” they write, “and it is an important fact that no trace of cellular organization, no trace of cell nuclei, no trace of interstitial cement substances can be found anywhere. Nerves, cells, blood-vessels, and odontoblasts have all shared the process of fibrication and are no longer recognizable.” These radical changes in the teeth, brought about by a deficiency of antiscorbutic vitamine, were demonstrated not only in guinea-pigs but also in monkeys. In some instances they were found where a histologic examination of the costochondral junctions showed nothing abnormal. “Profound changes were recorded where the scorbutic changes during life were so slight as to be almost unrecognizable,” and, they continue, “the mildest degree of scurvy which could just be discovered at the postmortem examination produced well-defined changes in the structure of the teeth.” If this work is confirmed, we must consider the teeth as one of the first tissues of the body to be affected by scurvy. The authors quite rightly raise the question whether the teeth of young children may not likewise be injured by a deficiency of antiscorbutic vitamine, whether this may not play a rôle in the dental caries so prevalent among civilized communities. It is evident, they state, that such transient conditions of infantile scurvy as have been described by Hess as “subacute” or “latent” scurvy, may occur more often than is usually suspected, and may reasonably be expected to influence dentition. It seems quite possible that the caries of the permanent teeth is due not only to infantile rickets but also to infantile scurvy.

Besides the typical histologic changes in the bones there are alterations in other organs which require mention. All investigators have found a degeneration of the muscles, showing a loss of their striations, swelling of the fibres, and the presence of irregularly-distributed vacuoles and granules. The interstitial tissue frequently is permeated with edema, as we should expect from gross appearances. Holst and Froelich have reported a fatty degeneration of the heart muscle, as well as of the epithelium of the mucous membrane of the glands of the stomach and of the intestine. Hart and Lessing, in their protocols of necropsies on monkeys, describe an interesting lesion associated with the degenerated muscle fibres—a collection of granules staining deep blue with hæmatoxylin and dissolving on the addition of acid. These granules, interpreted as being composed of calcium, were found in the muscles of the limbs, of the tongue, and in the heart. It is reasonable to attribute their formation to an absorption of bone throughout the body. Similar calcium deposits were seen frequently in the adrenal glands, in their cortex, or at the border of the cortex and medulla. This lesion gains special interest in view of the calcium deposits described so frequently in connection with mercurial poisoning, more particularly as the symptoms of scurvy and of this toxic condition have marked clinical resemblances.

There has been but little histologic investigation of the nerves in experimental scurvy. In fact, the only systematic study of the kind is that of Holst and Froelich, whose attention was drawn to this field in an attempt to solve the relationship between scurvy and ship beriberi. These writers found a true Wallerian polyneuritis in only two pigs, one of which had been fed on wheat bread made with yeast, and the other on decorticated barley. In many instances, however, there was extensive degeneration of the axis cylinders without degeneration of the sheaths. They do not, however, attribute great importance to these changes, as the same lesions were found in the nerves of animals fed on cabbage and fresh potatoes. In view of the confusing reports on the nerves of birds in experiments on polyneuritis, one cannot be too careful in drawing conclusions from histologic studies of this kind.

In the study by Jackson and Moore on experimental scurvy in guinea-pigs, the histology of the blood-vessels is carefully considered. “Marked thinning of the wall” was found and depicted; “the wall as a whole had partially melted away, leaving few traces.” These parts of the wall contained many small round bodies resembling cocci, which were stained a deep blue by the Wright and the Giemsa methods. These bodies were present also in the lumen of the vessel and in the inner layers of the more normal portions of the wall. In addition to such changes in the veins, “lesions having the shape, location, and characteristics of infarcts, were found in the ends of the diaphyses of the long bones.” As a result of this pathologic picture the authors are of the opinion that they may have been dealing with a mild infection. This is quite possible, as scurvy tends to render the tissues less resistant to the entrance of bacteria. We believe, however, that even if such were the case, the phenomenon must be regarded merely as secondary in its relation to the pathogenesis of scurvy.

Following the study on the pathology of experimental scurvy, Jackson and Moore undertook to determine primarily whether the small stained bodies seen in the sections of the scurvy lesions were bacteria. This investigation has been cited frequently as presenting cogent evidence in favor of the infectious nature of scurvy, so that it will be necessary to consider it fully; the general question of whether scurvy is a bacterial infection is discussed under the consideration of etiology.

As is well known, Morpurgo, a generation ago, claimed to have produced rhachitic lesions in young rats by means of artificial infection with a gram-positive diplococcus. Pappenheimer brought about similar lesions in rats by the injection of a suspension of bone marrow from a rhachitic animal. Koch injected a streptococcus longus intravenously into young dogs, occasioning gross bony changes of the epiphyses and costochondral junctions, and microscopic changes resembling scurvy—an irregular line of ossification and “a framework” marrow, which, however, showed regions of osteoid. Jackson and Moody were able to isolate from the crushed tissue of their guinea-pigs “a diplococcus of low virulence with a tendency to form chains and produce green (color) on blood agar.” Pure strains of these organisms inoculated into the circulation of guinea-pigs and rabbits, living under ordinary conditions (a mixed diet consisting of green vegetables, hay and oats), gave rise in most instances to hemorrhagic and other lesions in the bones, joints, muscles, lymph-glands or gums. Hemorrhages were found beneath the periosteum in the region of the lower incisor teeth and the acetabulum and ribs. These results are far from constituting evidence in favor of the microbic origin of scurvy. They show merely that the tissues of scorbutic animals frequently harbor bacteria, and that injections of these bacteria will bring about hemorrhages which may be subperiosteal in character. They are open to the specific criticism that scurvy was produced readily in the rabbit, an animal which otherwise does not develop scurvy, and, furthermore, they differ from feeding experiments in inciting scurvy notwithstanding the fact that the animals were receiving an antiscorbutic diet (green vegetables). Cultures of the hearts’ blood of the affected animals were sterile in every instance; a result obtained likewise by Holst and Froelich.

Further studies of this kind should be carried out and should include cultures of the blood and tissues of guinea-pigs in the various stages of scurvy, especially the early stage. In addition, a histologic study should be made of the bones of animals injected with bacteria (preferably streptococci), in order to ascertain whether notwithstanding an unrestricted diet, typical lesions can be produced by this means.

For further details of the pathology of scurvy, the reader is referred to the chapter on human pathology.

Symptoms.—Let us consider the symptomatology of guinea-pig scurvy. In the course of an observation of many hundreds of animals we have been struck by the striking uniformity of the signs and symptoms. The animals made use of were almost invariably of moderate size, weighing from 200 to 300 grams. Where heavier pigs were employed the disease progressed less rapidly, but the signs were the same; they were, however, more difficult to elicit, owing to the subcutaneous fat. Most of the animals were on a diet of hay, oats and water ad libitum, but there was no variation in symptoms where fat and fat-soluble vitamine were supplied by an addition of egg yolk or of cod liver oil, or where egg albumen was fed to render the protein adequate, or where the inorganic salts were supplemented by additions of sodium or calcium chloride.