RELATION OF SCURVY TO OTHER DISEASES
In the foregoing there has been frequent reference to the close
relationship between scurvy and the incidence of the infectious
diseases--to the fact that a scorbutic condition increases the
susceptibility to infection. This is indeed one of the most
characteristic, as well as one of the most important phenomena
associated with scurvy and other disorders resulting from vitamine
deficiency. Mention has been made of the special susceptibility to the
diphtheria bacillus, and to the organisms leading to coryza and the
respiratory diseases, but no doubt this applies also to invasion by
other bacteria. We wish, however, to confine ourselves to the
nutritional disorders, first in their relationship one to the other, and
second, as a group of deficiency diseases, due to a lack of vitamines of
various kinds. As is well known, in addition to scurvy, this group
generally includes beriberi, a disease attributed to a lack of the
water-soluble vitamine, and xerophthalmia, an eye condition which
recently has been brought about in rats by placing them on a diet free
from fat-soluble vitamine. These, however, form only the nucleus of the
disorders which commonly are included in this category. Schaumann, the
first to formulate this classification, illustrated his conception of
the interrelationship by depicting the various members as spokes of a
wheel surrounding a central hub. He included scurvy, rickets,
osteomalacia, typical beriberi, ship-beriberi, pellagra and
mehlnaerschaden. Funk made a similar classification of disorders which
he termed the "avitaminosen." There is a tendency to enlarge rather than
to decrease the membership of this class, and recently war or hunger
edema, infantile atrophy and diarrhoea, sprue, coeliac disease,
leprosy and others have been proposed as suitable candidates. At the
present time it is impossible to determine which and how many of this
motley company should be associated with scurvy. Some, possibly, are the
result of a lack of vitamine, but for the present it will be well to
bear in mind that three vitamines only have stood the test of
experiment, and only these three therefore can be definitely connected
in a causal relationship with pathologic conditions. In addition to this
consideration of the interrelationship of the "deficiency diseases," the
kinship of allied disorders--more particularly of rickets--must be
discussed.
Although at first thought _beriberi_ and scurvy would seem far apart
from a clinical point of view, they have some important features in
common. In both there is a tendency to a rapidity of the heart's action
and a marked lability of the pulse, to an enlargement of the cardiac
ventricles, to an involvement of the vagus, and to an exaggeration of
the deep reflexes. It is unnecessary to describe these signs and
symptoms in detail, as they have been fully considered under
symptomatology. It has been recorded from time to time that under
certain circumstances scurvy has developed in man where one should have
expected beriberi, and _vice versa_. Darling, who has had a large
experience in this field, writes: "A deficient dietary in a tropical
African negro mine laborer causes severe scurvy, in a Cape Colony
African mine laborer, mild scurvy, and in some African negroes a diet
that causes scurvy in one set of men causes neuritis in others."
Possibly some minor differences in the dietary can explain this
difference in reaction--for we do not know all the sources of the
water-soluble vitamine, but such an experience deserves to be cited as
it is not an isolated instance. It is all the more worthy of attention
because it harmonizes to a certain extent with the everyday experience
of animal investigation. As has been stated elsewhere, a diet of
decorticated grain will lead to scurvy in the guinea-pig, to
polyneuritis in the pigeon, and to a combination of these diseases in
the hog! Results of this kind show that there must be a relationship
between the etiologic factors of scurvy and of beriberi. It is unwise at
present to attempt to define the relationship more precisely. The
remarkable observation, first made by Fuerst, and since confirmed by
numerous investigators, that seeds and legumes are devoid of
antiscorbutic potency but acquire this power on sprouting, constitutes
another link in the evidence of their kinship. Funk has suggested that
the antiscorbutic vitamine can be formed from the "antineuritic"
vitamine, a theory which is very attractive but needs confirmation and
experimental proof. It is quite evident that this change does not
usually occur in animals, in view of the specificity of the vitamines
for their respective diseases--of the antiscorbutic for scurvy and the
water-soluble for beriberi.
It will be noted that "_ship-beriberi_" is included in this group of
diseases. Very little is known about this condition, except what is
contained in the investigation of Nocht (1903) and that of Holst and
Froelich. It is a very rare condition but of interest because it is
characterized by spongy, hemorrhagic gums and other signs encountered in
scurvy. The feature which differentiates it sharply from scurvy,
however, is an anæsthesia of the extremities. Ship-beriberi is generally
regarded as a combination of beriberi and scurvy. Where these two
disorders occur concomitantly, the beriberi manifests itself some months
before the scurvy, as the latter takes much longer to develop.
In considering the vitamines in connection with diseases of the nervous
system, mention may be made of "central neuritis" and the "peripheral
neuritis" which has been reported from the West Indies. This bears only
a partial resemblance to beriberi, as there is no edema, nor dyspnoea,
and its course is more chronic. Judging from the report of Edwards from
Jamaica, the cases more closely resemble pellagra, terminating after
many years. A degeneration of the cells of the spinal cord was found and
"in some isolated patches of the cerebellum and in the roots of the
optic and auditory nerves." The disease occurs among the poor classes
whose diet is inadequate chiefly in nitrogen.
Eijkman was the first to draw an analogy between beriberi and
_pellagra_, and thus to suggest that the latter might be a disease due
to an unidentified factor; he compared the pernicious effect of a diet
of polished rice with that of decorticated corn. Of recent years,
largely as the result of the investigations of Goldberger and his
co-workers, pellagra has come to be regarded as a dietetic disorder
primarily due to a lack of adequate protein, rather than to a lack of a
specific vitamine. Its relationship to scurvy cannot, therefore, at the
present time, be discussed from an etiologic viewpoint. Apart, however,
from the question of etiology, the two diseases have certain clinical
symptoms in common. Weston states that "distinguished physicians, who
were really astute observers, have mistaken pellagra for scurvy, eczema,
various kinds of intestinal troubles, syphilis, and many other
diseases." In the chapter on symptomatology, attention has been directed
to the fact that an eczema which yields to antiscorbutic treatment may
occur in scurvy; at times it presents the symmetrical arrangement so
typical of pellagra. In other cases a fleeting erythema may be observed,
another sign noted frequently in pellagrins. In some instances
congestion of the gums has been recorded. In describing a little girl of
three who had pellagra, Weston writes: "The gums are also red and
swollen, suggesting scurvy." This child had eaten large amounts of
turnips, so that there could have been no question of complicating
scurvy. Lombroso and some of the earlier authors drew attention to the
fact that fragility of the bones, of the ribs and of the long bones, was
often associated with pellagra. These various clinical similarities
should not be construed as evidence in favor of the "avitamine" nature
of pellagra. They indicate, rather, that in nutritional disorders,
whatever may be their underlying cause, the vessels, the bones,
and other tissues may suffer and lead to similar--but not
identical--clinical pictures.[58]
[58] There is no adequate reason for placing in this group "coeliac
disease," a nutritional disorder of children recently described by
Still, and suggested by McCarrison as belonging to the category of the
vitamine deficiency diseases. A case of this kind has come to our
attention which resembled pellagra in many respects. It showed the
bright red, denuded tongue, the intestinal symptoms, the occasional
edema, marked loss in weight, and evanescent erythema--all symptoms of
markedly disturbed nutrition but not distinctive of a lack of vitamines.
The relation between scurvy and rickets is a subject which was discussed
by Glisson. With the renewed interest in infantile scurvy which followed
Barlow's work toward the end of the last century, children's specialists
ranged themselves into opposing camps on the question of the
interrelationship and interdependency of these two diseases. Some
accepted Barlow's dictum that infantile scurvy is an absolutely distinct
and separate entity; others, for example, Hirschsprung, declared that
the so-called scurvy was merely a form of rickets; whereas a third group
considered it a combination of rickets and scurvy. This last viewpoint
was actively maintained by Cheadle on the clinical side, and later by
Schoedel and Nauwerk on the pathologic side--the latter declaring that
rickets is "an inseparable component of infantile scurvy," and that the
entire disease should be regarded merely as "an episode in the course of
rickets." Even Barlow, in a paper published in 1894, wrote: "Rhachitic
changes already present may act as a physiological determinant of the
sites in which scurvy becomes manifest" and "rickets as a basis plus
inadequate food gives the simplest explanation of the typical case" (of
scurvy).
We had an exceptional opportunity to test this thesis in 1914, in an
institution where scurvy broke out among infants who were on a diet of
pasteurized milk. All these infants were receiving cod liver oil daily,
as prophylactic treatment against rickets. Many infants have been seen
since that time, who in spite of receiving cod liver oil developed
scurvy, and others in whom large doses of this oil failed to mitigate
the scurvy, although it prevented rickets. The same failure has been
encountered in the treatment of scurvy in guinea-pigs. This experience
has been without exception, both from a prophylactic and a curative
standpoint.
Confusion between the two diseases has resulted from the fact that the
majority of infants in the Temperate Zone have some degree of rickets.
Thus the two diseases have been found very frequently associated in
pathologic examination of the bones, leading some to infer that they are
in some way interdependent. They have been also confused clinically, as
mentioned in another connection, owing to the fact that beading of the
ribs--the rhachitic rosary--has been mistakenly regarded as a
pathognomonic sign of rickets, whereas it is also a sign common to
scurvy. It is important to bear in mind that from the pathologic
viewpoint scurvy and rickets present strikingly dissimilar pictures--the
former is characterized by an almost complete cessation of activity of
bone-forming elements, whereas the latter is distinguished by a
hyperplastic condition leading to a marked overgrowth of cartilage and
of abnormal bone. Viewed from the pathologic, etiologic and clinical
standpoint, we believe that there is no basis for assuming an
interrelationship between the two disorders, and that scurvy will
develop as readily and as rapidly where rickets is absent as where it is
present.[59]
[59] The only evidence in favor of a true interrelationship is furnished
by a necropsy report of Hart and Lessing on one of five monkeys fed on a
scorbutic diet. This animal died of disseminated tuberculosis, and the
bones showed "the classic picture of severe rickets." This occurrence
cannot be explained, although illness and lack of exercise no doubt
played a rôle. Until similar cases are reported, the incident must be
regarded merely as interesting and suggestive.
It is premature to discuss the relationship of these two disorders from
the vitamine standpoint. In 1910 Schaumann suggested that rickets was
due to a lack of a specific food factor, and somewhat later Funk
included it among the "avitaminosen." Recently Mellanby, as the result
of experiments on dogs, has affirmed that the fault lies in a lack of
the fat-soluble or a closely-related vitamine. Investigations of the
near future will probably decide the merits of this contention; our
experience is that rickets develops in infants even where the diet
contains adequate fat-soluble vitamine. If rickets is proved to be a
disorder depending on a vitamine, it belongs, naturally, in the same
group as scurvy. This would indicate relationship, but not
interrelationship. Just as the mere fact that a lack of vitamines leads
to scurvy and to beriberi does not signify, in theory or in practice,
the existence of pathogenetic interrelationship. However, as stated,
this is a subject which does not as yet rest on a secure foundation.
_Osteogenesis imperfecta and osteomalacia_ are disorders of dietetic or
metabolic origin characterized by fragility of the bones. The latter
has developed new significance and importance due to its increased
occurrence in almost epidemic form in the Central Empires at the close
of the World War. The etiology of both disorders is most obscure. In the
future in considering their pathogenesis it will be well to draw a sharp
distinction between them. Osteogenesis imperfecta is a disease in which
an injury occurs to the foetus without any manifest illness in the
mother, which seems to indicate a primary lesion of the foetus
(perhaps metabolic); osteomalacia, on the other hand, attacks the mother
who gives birth to an apparently healthy foetus. The latter gains
added interest because it is a disease of the bones which is attributed
to dysfunction of the endocrine glands, to a disturbance especially of
the parathyroid. If this observation is confirmed, it furnishes another
anatomical basis for associating the glands of internal secretion with
pathologic conditions of the bones.
One cannot survey the various diseases of the bones--scurvy, rickets,
osteoporosis, osteogenesis imperfecta, osteomalacia, etc.,--without
realizing that this group is at present in a state of great confusion
and will have to be rearranged and winnowed. The differentiation
between some of these diseases is not in every instance clear
morphologically--for instance, early cases of scurvy and
osteoporosis--so that it is difficult to consider them satisfactorily
from the standpoint of pathogenesis. Clinical differentiation is still
more difficult and uncertain. It seems probable that new entities will
be established, as has happened in the past. It is not so long since
rickets included almost all the bone diseases of infants. Gradually
congenital syphilis, scurvy, and achondroplasia were segregated as
distinct diseases. Probably a similar separation of other pathologic
conditions, now so entangled as to be indistinguishable, will be
evolved.
Among the diseases which have been attributed to a vitamine deficiency
are "war or hunger edema," sprue, the "mehlnaerschaden" of infants, and
the "exudative diathesis" described by Czerny and Keller. Future
investigation will disclose whether any of these disorders belong in the
group with scurvy. The _hunger edema_, noted in the late war and in
previous wars, seems to be a complex condition, quite dissociated from
scurvy, as many of the sufferers consumed comparatively large quantities
of potatoes or other vegetables. The "_mehlnaerschaden_" resembles
scurvy and the other vitamine disorders in its tendency to produce
hydremia and susceptibility to infection. It also develops in spite of a
liberal supply of antiscorbutic foodstuff in the dietary. As its name
implies, it comes about on a diet containing large quantities of
carbohydrate, of the cereal paps so commonly fed to infants. It is
conceivable that an unbalanced diet of this kind may not provide a
sufficiency of all the vitamines.
It does not seem probable that _exudative diathesis_, a term which
implies a predisposition to develop exudations or denudations of the
skin and mucous membranes, is the result of a lack of vitamine. This
condition does, however, predispose to scurvy. The association was very
evident in the group of cases reported by Hess and Fish in 1914. It is
not without significance that the blood-vessels in exudative diathesis
also show a decided weakness, an increased permeability, as judged by
the "capillary resistance test." In both scurvy and in exudative
diathesis eczema and petechial hemorrhages are encountered.
There may be _nutritional diseases due to an excess of food_ rather than
to a deficiency. A superfluity may be harmful by hindering the proper
utilization of the food, or may possibly lead to the formation of
deleterious products. Disturbances of this kind do occur. For example,
it is by no means uncommon for an infant which has been overfed with
milk to show the typical signs of rickets. Young guinea-pigs which are
fed liberal amounts of cow's milk develop a disease characterized by
fragility of the bones. The experience of Lubarsch, who produced
osteogenesis imperfecta in rabbits by means of a diet consisting mainly
of liver, or adrenal gland, is of interest, especially as this condition
did not come about when they were fed muscle tissue.
From what has been stated, it must be evident that this subject not only
is in a state of flux but that it is in a state of great confusion. This
applies not only to the relationship of vitamines to these disorders,
but to their identification and demarcation pathologically as well as
clinically. During the past few years we have begun to regard these
diseases from a new viewpoint, which no doubt will be helpful, but it is
probable that they will not be sharply defined and their relationships
determined until it is possible to bring about each disease definitely
and regularly in an experimental animal. Until this time we should
proceed slowly, and not bring about "confusion worse confounded" by
yielding to the vogue, and grouping together heterogeneous and
little-understood clinical conditions under the caption of deficiency
diseases. There is a growing danger of attributing every unexplained
nutritional disorder to the new, overworked, but ill-defined
vitamines--of their sharing with the secretions of the endocrine glands
the fate of becoming the dumping-ground for every unidentified disorder.
APPENDIX
Extract from "Treatise on Scurvy," by James Lind, London, 1772.
(a) _Recipe for preparing a stable orange or lemon juice._ Let the
squeezed juice of these fruits be well cleared from the pulp and
purified by standing for some time; then poured off from the gross
sediment; or, to have it still purer, it may be filtrated. Let it then
be put into any clean open vessel of china or stone-ware, which should
be wider at the top than bottom, so that there may be the largest
surface above to favor the evaporation. For this purpose a china basin
or punch-bowl is proper, and generally made in the form required; all
earthen glazed vessels are unfit, as their glazing will be dissolved by
the acid. Into this pour the purified juice, and put it into a pan of
water, upon a clear fire. Let the water come almost to a boil, and
continue nearly in that state (with the basin containing the juice in
the middle of it) until the juice is found to be of the consistence of a
thick syrup when cold. The slower the evaporation of the juice the
better; and it will require at least twelve or fourteen hours
continuance in the bath heat before it is reduced to a proper
consistence.
It is then, when cold, to be corked up in a bottle for use. Two dozen
good oranges, weighing five pounds four ounces, will yield one pound
nine ounces and a half of pure juice; and when evaporated, there will
remain about five ounces of rob, or extract; which in bulk will be equal
to less than three ounces of water. So that thus the acid, and the
virtues of twelve dozen lemons or oranges, may be put into a quart
bottle, and preserved for several years.
I have now some extract of lemons which was made four years ago.
Those who intend this extract for making punch may infuse some of the
fresh peel of the oranges or lemons into the spirit before it is used.
But for this purpose I find it is sufficient to add a very small
quantity of the outer peel to the extract a little before it is taken
off the fire, and there will be all that is requisite to make it
entirely equal to the freshest fruit.
(b) _How to preserve berries and other fruits for long periods._ And it
may be proper to acquaint them that most berries, and several fruits,
when gathered two-thirds ripe on a dry day, while the sun shines, if put
into earthen pots, or rather in dry bottles, well corked, and sealed up,
so that no air or moisture can enter, will keep a long time, and at the
end of a year, be as fresh as when new pulled.
(c) _Method of preparing an antiscorbutic decoction from fir-tops,
leaves, bark, etc._ When the Swedes carried on a war against the
Muscovites, almost all the soldiers of their army were destroyed by the
scurvy, having putrid gums, rigid tendons, etc. But a stop was put to
the progress of this disease by the advice of Erbenius, the King's
physician, with a simple decoction of fir-tops, by which the most
deplorable cases were perfectly recovered, and the rest of the soldiers
prevented from falling into it.
I am inclined to believe by the description given by Cartier of the
ameda tree, with a decoction of the bark and leaves of which his men
were so speedily recovered, that it was the large swampy American spruce
tree.
A simple decoction of the tops, cones, leaves or even green bark and
wood of these trees is an excellent antiscorbutic medicine; but it will,
I am apt to think, become much more so when fermented, as in making
spruce beer. By carrying a few bags of spruce or its extract to sea,
this wholesome drink may be prepared at any time. But where it cannot be
had the common fir-tops used for fuel in the ship should be first boiled
in water, and the decoction afterwards fermented with molasses in the
common method of making spruce beer; to which a small quantity of
wormwood and horse-radish root (which it is easy to preserve fresh at
sea) may be added. The juice of the cocoanut tree was experienced to be
of very great benefit to several persons afflicted with the scurvy.
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INDEX
A
Acid, effect on keeping qualities of antiscorbutics, 66, 161
Acidosis, 244 theory, 24
Adrenals, 102
in guinea-pig scurvy, 122
Adult, scurvy in, history of, 1
Age incidence, 51
Aging, effect on antiscorbutics of, 67
Agglutinins, effect of scurvy on, 68
Alimentary tract, gross pathology, 89
microscopic pathology, 100
Alkalization, effect on milk of, 50
on orange juice of, 66, 154
Amboceptor, effect of scurvy on, 68
Anasarca, 86, 196
Animals, scurvy in, 114
Anorexia, 206
Antiscorbutics, and antiscorbutic foods, 143, =149=, 157
history of use of, 9, 143
Antitoxin, effect of scurvy on, 68
Appendicitis, confused diagnosis, 183
Appetite, 206
Apple, antiscorbutic value of, 158
Armies, scurvy in, 3, 15
Army, use of canned tomatoes in ration of U. S., 231
B
Bacteria, fecal, in scurvy, 28
as etiological factor in scurvy, 134
in tissues, 133
Bacterial theory of scurvy, 30
Banana, antiscorbutic value of, 158
Beading of ribs, 197
in guinea-pig, 129, 137
pathology of, 94
Beans, germinated, 167, 231
Beef juice, 236
Beer, antiscorbutic value of, 20, =169=
Beriberi, differential diagnosis, 221
relation to scurvy, =249=
Berries, antiscorbutic value of, 156
Blindness, 182
Blood cells, changes in, 209-211
Blood cells, chemistry of, 244, 245
coagulability of, 211
Blood vessels, changes in, 68, =98=, 209
in guinea-pigs, 133
Blood, vitamine content of, 76
Bones, gross pathology, 93
microscopic pathology, 105
Brain, pathology, 93
Breast fed, scurvy in, 35
C
Cabbage, antiscorbutic value of, 159
dehydrated, 165
effect of heat on, 159
Calcium, deposits of, 98, 102, 103
metabolism, 241-247
"Capillary resistance test," =212=, 257
Carbohydrates, 34, 59
"Cardiorespiratory syndrome," 200
Cardiovascular system, 199
Carrots, antiscorbutic value of, 159, 160
Central nervous system, gross pathology, 93
microscopic pathology, =104=
Cereals, antiscorbutic value of, 170
germinated, 167
Cerebrospinal fluid, 203
Chlorides, 242-247
Citric acid theory, 23
Climate, 55
Complement, effect of scurvy on, 69
Complexion, characteristic change in, 176, 184
Complications of scurvy, 182, 202, 205, 217
Constipation, 27, =118-122=, 207
Cord, spinal, pathology, 93, 104
Creatinine, 244
Cure, 236
D
Death, causes of, 179, 227
Deficiency diseases, general discussion, 63, 248
Diagnosis, 176, 219
Diastase, blood content of, 244
Diet, general, 59
Digestive disturbances, 78
Diphtheria, antitoxin in blood, 68
as complication of scurvy, 217
Drying, effect on vitamines of, 66
Duodenum, pathology, 89
Dysentery, 59, 182
E
Economic status, 55
Eczema, 195
Edema, 178, 184, =196=
hunger, 256
war, 256
Eggs, antiscorbutic value of, 168
Endocrine organs, gross pathology, 92
microscopic pathology, 104
extracts of, as preventive, 172
theory of vitamine action, 72
Epidemics, 2, 217
Epiphyses, separation of, 96, 181, =198=
Etiology, =35=
exciting factors in, 60
Excretion of vitamine, 77
Expeditions, scurvy in Arctic, 10
Experimental scurvy, 111
pathogenesis, 116
pathology, 122
symptoms, 135
Exudative diathesis, 59, 256
Eyeball, proptosis, 193
F
Familial tendency, 58
Fats, in diet, effect on scurvy, 59
Fever, 181, =216=
Foetus, effect of scorbutic diet on, 125
Food, excess of, 257
Foods, antiscorbutic, 143, =149=
proprietary, 49
Fractures, 95
Frost-bite, 180
Fruit juices, 153
Fruits, fresh, 144
G
Generative organs, pathology, 104
Glands, endocrine, 72
changes in, 73, 92, 104
Glucose, blood content of, 244
Grapes, antiscorbutic value of, 158
Growth in scurvy, 213
Guinea-pig scurvy, 112, 114
Guinea-pig pathogenesis, 116
pathology, 122
relation to human, 115
symptoms, 135
Gums, 177, 181, 184
in infantile scurvy, =189=
pathology of, 89, 100
H
Hair, changes in, 194
Heart, =200=
gross pathology, 87
microscopic pathology, 99
Heat, effect on vitamine of, 65
Hemorrhages, 180, 189
as early symptoms, 178
distribution of, 84
gastric, 208
orbital, 193
subperiosteal, 95, =191=
urinary, 204
History of scurvy, 1
Hog, effect of scorbutic diet on, 115
Hypophysis, 104
I
Infantile scurvy, history, 10
in artificially fed, 40
in breast-fed, 35
increase during World War, 21-22
relation to epidemic scurvy of adults, 15, 37
relation to rickets, 11, =110=, =252=
symptomatology, =183=
Infection, as exciting factor, 60, 218
increased liability to, 68
effect on prognosis, 227
Intestines, gross pathology, 90
microscopic pathology, 100
Intravenous use of orange juice, 238
Irregularities in course of deficiency diseases, 78
J
Jaundice, 208
Joints, lesions of, 199
K
Kidneys, gross pathology, 91
microscopic pathology, 102
L
Latent scurvy, 179, 183, =187=
Laxatives, failure to cure with, 28, =207=
Lemon juice, antiscorbutic value of, 153, 234
dried, 155, 232
ration in British Navy, 9, 144
Lentils, value as antiscorbutic, 167, 231
Lice, theory of transmission of scurvy by, 30
Lime juice, antiscorbutic value of, 156
fallacy in regard to, 149
use in British Navy, 144
Liver, gross pathology, 91
microscopic pathology, 101
Lungs, gross pathology, 88
microscopic pathology, 99
Lymph-nodes, gross pathology, 92
microscopic pathology, 101
M
Malnutrition, general, 58
Malt soup, 50
Marrow, changes in, 107
Meat, fresh, 147, =168=
salt, 146
"Mehlnaerschaden" of Czerny, 256
Metabolism in scurvy, 241-247
Milk, alkalized, 50
amount necessary to prevent scurvy, 49, 117, =150=
boiled, 44, 65
condensed, 48
dried, 46, 66, =152=
effect of industrial methods on, 43
evaporated, 45
pasteurized, 40, 65
home vs. commercial, 42
sterilized, 44
breast, amount necessary to prevent scurvy, 36, 39, 153
as cause of beriberi, 39
cows, antiscorbutic value of, 40, 152
goats, antiscorbutic value of, 153
Mineral metabolism in scurvy, 241-247
Monkey, scurvy in, 114, =127=
pathology, 128
Muscles, pathology, 97
N
Nails, changes in, 194
Necropsy reports, 82
Nephritis, 205
Nerves, peripheral, in guinea-pig
scurvy, 132
pathology, 105
Nervous system, effect of scurvy on, 202
Nutrition, general, in scurvy, 58, 59, 213
Nyctalopia, 182
O
Orange juice, antiscorbutic value of, =153=, 234
"artificial," 33
dried, 155
effect of alkalization of, 154
intravenous use of, 238
subcutaneous use of, 155
peel, antiscorbutic value of, 234
Osteogenesis imperfecta, 255
Osteomalacia, differentiation of, from scurvy, 255
Osteomyelitis, differentiation of, from scurvy, 222
Osteoporosis, differentiation of, from scurvy, 255
Osteotabes infantum, 109
P
Pains, as early symptom, 176
Pancreas, gross pathology, 91
microscopic pathology, 104
Pasteurized milk, 40
Pathogenesis of scurvy, theories of, 23
Pathology of scurvy in guinea-pig, 122
in man, gross, 83
microscopic, 96
in monkey, 128
Peas, antiscorbutic value of, 167, 231
Pellagra, 251
Phenols, excretion of, 245
Phosphate metabolism, 241-247
Pigeon, effect of scorbutic diet on, 114
Pneumonia, 202
Posture, characteristic, in guinea-pig, 136
Posture, characteristic, infant, 183
Potassium deficiency theory, 23
metabolism, =241-247=
Potatoes, antiscorbutic value of, 6, 7, 146, =161=, 235
Prevention of scurvy, 230
Prognosis, 225
Protein in diet, effect on scurvy, 59
Psychic element in scurvy, 57
Pulse, 181, =201=
Pulses, germinated, 167, 231
Purpura, differential diagnosis, 221
Pyorrhoea, relation to lesion of gums, 181
R
Racial immunity, 56
Rats, effect of scorbutic diet on, 114, 115
Recurrent scurvy, 228
Respirations, 201
Retina, hemorrhages in, 105
Rheumatism, confusion with scurvy, 176, 220
Ribs, beading of, 197
pathology, 94
in guinea-pig, 129, 137
Rickets, relation of, to scurvy, =11=, =110=, =252=
Rosary, 94, 197
S
Sauerkraut, antiscorbutic value of, 145
Season, effect on incidence, 54
Sex, effect on incidence, 56
Shaking, effect on antiscorbutic factor, 68
Ship beriberi, 250
Skin, pathology, 96
Spleen, gross pathology, 91
microscopic pathology, 102
Sprue, 256
Starvation, pathology of, 125
Stomach, gross pathology, 89
microscopic pathology, 100
Storage of vitamine in body, 74
Streptococcus in blood in scurvy, 134
Subacute form of scurvy, 184
Subcutaneous use of antiscorbutics, 155
Swede, antiscorbutic value of, =162=, 235
Symptomatology, in adult, 176
in infant, 183
Syphilis, congenital, differential diagnosis, 222, 223
T
Teeth, in guinea-pig scurvy, 130, 137
in human scurvy, 177
Temperature, in guinea-pig scurvy, 141
in human scurvy, 181, =216=
Thymus, pathology of, 104
use of gland in treatment, 172
Thyroid, pathology of, 104
use of gland in treatment, 172
Tomatoes, canned, antiscorbutic value of, =166=, 231, 234
in U. S. Army ration, 231
Toxic theory of pathogenesis of scurvy, 25
Treatment of scurvy, 230
duration of, 237
non-dietetic, 239
U
Ultra-violet rays, effect on antiscorbutics, 67
Urea content of blood, 244
of tissues, 245
Urine in scurvy, =204-206=
V
Vegetable juices, keeping qualities of, 161
Vegetables, antiscorbutic value of 144, =158=
canned, 166
dehydrated, 163
effect of heat on, 159
fresh, 144, =158=
ripeness of, effect on antiscorbutic value, 160
Vitamine, antiscorbutic, general discussion of, 62
action of, 68, 69
as antitoxin, 69
as catalytic agent, 70
as nutriment, 69
blood content of, 76
effect of heat on, 65
of ultra-violet ray on, 67
excretion of, 77
Vitamine, experimental evidence for, 62
fate in body, 74, 77
relation to water-soluble factor, 65, 67
relation to antineuritic vitamine, 67
resistance to chemical and physical processes, 64
storage in body of, =74=
theory of scurvy, 32
W
Weight, loss of, 138, 213
"White line" of Fraenkel, =128=, =198=
World War, scurvy in, 15
X
X-ray in diagnosis of scurvy, 128, 192, 198
Y
Yeast, antiscorbutic value of, 171
End of Project Gutenberg's Scurvy Past and Present, by Alfred Fabian Hess