Part 34

Gouty arthritis has been recorded but three times, although on several occasions small uratic deposits in tendon sheaths have been observed in birds; gout has not been seen in mammals. An illustrative case in a Boat-billed Heron (_Cancroma cochlearia_) will be given in the section on gout.

Arthritis as an acute infectious disease such as rheumatism of the human being, has not been observed, but copious examples of acute, subacute or chronic monoarticular inflammation are recorded. Nearly all of these have a definite explanation—traumatism or acute general disease, and there are a few cases of polyarthritis with chronic disease. Notable among the last are two instances of chronic dry ossifying arthritis and synovitis, one with tuberculosis, the other with actinomycosis, both occurring in ungulates. A third case similar in character deserves special mention. The Indian elephant “Bolivar” (_Elephas indicus_) died from pulmonary tuberculosis, myocarditis, nephritis and hepatic cirrhosis. The joints of all extremities showed atrophic arthritis with fluid, the synovial membranes being ulcerated or retracted and fibrotic. The articulating surfaces where not roughened by erosion, were flattened. It is perhaps worthy of mention that this old and familiar animal was the occupant of the same enclosure, floored with cement, for over thirty years, conditions which might be partly instrumental in the arthritic changes as well as in the flattening of articular surfaces.

The Ungulata frequently suffer with wounds, ulcers and abscesses about the lips, nose, and soft tissues of the jaws which may at times be confusingly like actinomycosis. This disease we have seen in gazelles and tapirs but have had to exclude it in several other members of this order. A number have come to autopsy with osteitis of the lower mandible, some evidently traumatic in origin, others probably due to infection _via_ the teeth. Figure 44 represents the jaw bone of an Isabelline gazelle (_Gazella isabella_) suffering with a rarefying osteitis from a root abscess, and illustrates well the possibility of focal infection from this source.

DEGENERATIVE SKELETAL DISEASES.

While the foregoing instances of disease in the osseous system are interesting examples of individual pathological lesions, they are insignificant in comparison with the forms of bony change known under the names of rickets, osteomalacia, osteogenesis imperfecta and the like—systemic conditions which are chiefly degenerative but have certain evidences of inflammation in addition. The modern knowledge of the first two named is so far from complete that it cannot be said that there is any certainty of their identity. Indeed there seem to be some reasons to think that there is more than one variety of rickets, that all cases are not dependent upon the same cause, and that in essence it is the same process as osteomalacia, the latter, however, occurring at a later age. We shall show that in the same order, Primates, both diseases may occur in animals fed upon the same diet, and that one family tends to have one disease, another family the other.

RICKETS.

Since the two conditions are diagnosed separately in veterinary practice and each seems to have a distinct place in medical ideas, it may be well to outline upon what criteria the two diagnoses have been made in this Garden. Rickets is essentially a disease of early life. The animal is noted as having a large head, squatty station, heavy extremities and a prominent belly. Death occurs as the result of enteritis or pneumonia. Occasionally such a young specimen seems to recover from the disease but retains the distortion of his skeleton; this is important, for we believe that osteomalacia, except the variety confined to periods of pregnancy, rarely ends in recovery when once thoroughly established. At autopsy the cranial bones are the seat of osteotabes, the face is broad, the epiphyseal junctions are swollen by irregular osteogenesis and granulation tissue, the periosteum shows an irregular fibrous tissue overgrowth—the last two processes producing bones of irregular contour and thickness. Section through the osteogenetic ends of the long bones shows actively congested marrow up to the articular cartilages with very tortuous strands of spongy bone or cartilage, and when considered transversely, there is a bone-forming layer of many times the normal thickness but bloody red instead of pink.

OSTEOMALACIA.

Osteomalacia appears in mature animals or at least those well able to care for their own nourishment. The earliest observations are not referable to the skeleton but to the change in the activity of the beast. He will be noted as less active in running, jumping or searching for his food. The customary position is a sitting or lying one. No change is noted in the head or face. As the disease progresses, the animal becomes quite inactive, seeks solitude but will eat well if the food be conveniently available and he does not have to fight for it. The movements are stiff and seem painful. About this time definite alteration in the shape of the chest is perceptible, and in some cases there is anterior curvature of the legs. Movement becomes so difficult, probably from weakness and pain, that it seems as if paraplegia actually existed. The inability of affected monkeys to climb has given rise to the term “cage paralysis,” but this term should not be restricted to weakness, the result of osteomalacia since it is used by dealers and keepers to imply the cramped station and gait of an animal long housed in quarters too small for it, an appropriate application because it suggests cause and effect. However, the appellation is widely and loosely used insuring its employment in diagnosis for entirely different conditions such as degenerative bone disease and hind-quarter laming from enteric intoxications; for these affections one might use the term in an adjectival or descriptive sense.

Our Primate collection has suffered considerably with osteomalacia, and we have devoted much time to the study of its cause and treatment. However, the Garden is not alone in this experience, for wherever certain species are kept the disease appears. The description of cases in the New York Garden by Blair and Brooks[46] is excellent, and with the exception of data concerning the nervous system, almost exactly parallels our own observations. They lay much stress upon the changes in the brain, cord and ganglia as constant in well developed cases but as probably secondary to the osseous, hemic and metabolic disturbances. We have been unable to find any pathological lesions in four thoroughly studied brains and cords from well developed cases. As will appear later, our most satisfactory findings were in the dietary and metabolic chemistry and in the osseous pathology. The cases recorded by Campbell and Cleland[47] would seem to be undoubted instances of myelitis, but the osseous changes are not sufficiently discussed. In many cases it would seem, therefore, that there is some change in the nervous system, but there may be some examples without this and with predominant osseous lesions. We are inclined to think that these two groups differ qualitatively, and we look upon the confusion as demanding for its ultimate solution the use of exact nomenclature, especially the exclusion of “cage paralysis” as a diagnostic term. The only division we can understand at the present time depends upon the gross changes in the bones, those with and those without definite irregularities in contour due to periosteal overgrowth. Certain of the former may show no unevennesses at all, the deformity being due to softness of the skeleton. The other group has shafts of irregular thickness, swellings around the joints and much beading of the middle of the ribs.

Whether or not there be true paralysis is difficult to settle, but in our cases we have decided always in the negative because of the ability of the monkeys to grasp firmly with the hind digits. The animals tend to lie in one position, determined probably by comfort, the result being that they develop sores at the points of contact with their cage floor, and deformities of the skeleton (see Fig. 45). These deformities are especially well exhibited by the chest, the vertebræ and the pelvis and are referable to the almost constant squatting of the animal; the long bones may be bowed but not as much as in rickets, nor is the epiphyseal junction so knobby as in that disease.

The foregoing description is based chiefly upon observations on monkeys but may be closely paralleled in carnivores and rodents. These latter, however, lie rather than sit during the development of the disease, so that thoracic and pelvic deformity is relatively less than in monkeys. Death is due to enteritis, anemia, shock from fractures and respiratory inflammation.

In so far as the deformities of the skeleton may serve to distinguish between rickets and osteomalacia, I can only point to the preponderance of changes in the skull and extremities in the former and of the trunk bones in the latter. Deformity of the chest, barrel-shape shortening and pigeon breast, is due more to posture than to the essentially osseous changes. “Rachitic rosary” may occur in both, but it is always better exhibited in rickets; in this disease the swellings occur at the costochondral junction, while in osteomalacia rosary-like nodules may develop anywhere along the ribs.

Examination of the anatomical lesions is, however, somewhat more helpful, and the following description for osteomalacia may be contrasted with that already given for rickets. The peculiar change is a thinning of the shaft of long bones and reduction of the subperiosteal plates of flat bones.

In mammals the long bones are more affected than in birds whose sternum, ribs and beak show the severest changes. The skull is frequently not affected to a serious degree, but may, however, show advanced lesions, the cranial plates being thinned in places so that they may be bent in, or occasionally a periosteal thickening may be found; the head as a whole is not misshapen. The ribs are softened and may be of paper thickness although there may be found a periosteal overgrowth, perhaps a kind of splinting, which makes the diameter variable. At costochondral junctions, beading may be found, but without the active congestion seen in rickets. Similar alterations may be found in the long bones, here in characteristic degree in that the shaft walls are thin, by removal of the endosteal and periosteal layers sometimes with definite retraction of the marrow. Occasionally subperiosteal thickenings, made of osteofibrous tissue are encountered. At the epiphyses there are strands of gelatinous tissue, fibrous and cartilaginous, separating pink or blood-red areas of marrow. These strands may contain calcareous matter and are probably the remains of the cancellated tissue. Despite all this activity at the ends of the long bones there is not the extreme prominence of articulations so characteristic of rickets. Gelatinous or cartilaginous islands may be seen in the deep red shaft marrow.

Fractures may be found and around them may form a blood clot or loose fibrous tissue entirely devoid of bone salts. If a break has existed for some time a very pronounced fibrous overgrowth from the periosteum is apt to occur, indeed an excessive fibrosis may exist, but this is ineffective for healing of the fracture or splinting of the shaft. Certain cases, notably in Carnivora, seem to have especial activity in and around joints so that when the member is dissected one gets the impression of osteoarthritis. In such cases the synovia may be fibrotic and the articular surfaces dry. The pelvic deformities are similar to those in the human being—lateral contraction with bending in of the superior rami of the pubis with the production of a beak, to which the name “duckbill” has been given. The anterior curvature of the lumbar spine makes an acute angle at the upper end of the sacrum.

Histological examination of a number of our cases of osteomalacia and rickets have failed to show any lesion different from those known for the human being and for domesticated animals. It is noteworthy that not all bones of a given case will show the changes to the same degree even though grossly they may seem comparably affected. So too there is no certain relation between the degree of deformity as shown by the body as a whole and the advancement of osteoporosis as seen under the microscope. These observations are in accord with those of Brooks and Blair. Just why this is cannot be stated, but as the cause of these two bone diseases may not always be the same, variations in gross and minute anatomy are not remarkable.

Analysis of the bones shows a loss of calcium and an excess of sulphur and magnesium. The loss of the first is chiefly _via_ the intestinal discharges but also _via_ the urine. The metabolism of one monkey showed a high calcium and phosphorus loss with moderate retention of sulphur and magnesium.

Because of the importance of osteomalacia and rickets in cebus monkeys and certain other animals, Dr. E. P. Corson-White has been investigating its etiology. I shall refer briefly to her results as they affect our present subject but shall leave for discussion in the chapter on diet, which she has written, the broader question of food and systemic disease.

It must be understood that the instances included in this general discussion of degenerative osseous disease are cases of definite character and development. There may have been, in addition to the numbers cited in the list on page 357, many more animals at autopsy with early or unrecognized constructive or destructive abnormalities, and we are thoroughly familiar with the imperfect skeletal development of specimens, inbred or reared in captivity or even those adult when caught yet under Park conditions for many years. In these latter groups the changes vary from incomplete construction (an example of atrophy was quoted on page 24) to actual degeneration as in osteomalacia. Inbreeding seems to be a potent factor in many cases, a well known fact in human and veterinary medicine. The importance of inactivity in the causation of degenerative bone disease, the unused muscles giving the bones nothing to do, is certainly admitted but it is immeasurable. It is probably not great in a cage of mixed varieties of monkeys. The effect of the absence of sunlight in osseous degeneration is no factor in our material. The exhibition house is well lighted and many animals are out of doors all year around.

The ductless glands have repeatedly been accused of responsibility for these disorders. In our seventy-nine cases of osteomalacia and thirty- four of rickets, no abnormality has been observed in ovary, testes or adrenals except for moderate congestions. Two cases were associated with pancreatic disease, once acute, once chronic. The thyroid body has been found to have been definitely abnormal only once—secondary hyperplasia with colloid in a carnivore. In the Primates this body was frequently congested and has shown small colloid cysts but was not uniformly enlarged or atrophic. As a therapeutic measure I have administered adrenalin to two monkeys, one for a few weeks, one for nearly six months; this treatment was without any perceptible effect upon the process.

Dr. Corson-White has, by the study of some cases during the life of the monkey, confirmed the decreased alkalinity of the blood in connection with the increased output of calcium in the feces and urine.

Since the explanation of the disease by blaming the ductless glands has failed, Dr. Corson-White has undertaken a study of the diet given our monkeys to see if any fault in it were a part of the etiology. Analysis of this diet (see list page 426) computed from Atwater’s table, and by actual analysis of the amounts of food consumed by the animal in four four-day periods, gave:

1. Protein—low in quantity and poor in quality; especially low in phosphorus content.

2. Fat—very low.

3. Carbohydrate—very high, almost eleven times the value of all other ingredients.

4. Ash—decidedly low and predominatingly acid. Further analysis of this ash showed a trace only of calcium and phosphorus and iron and only a small amount of sodium; potassium, sulphur and magnesium were slightly higher.

5. Vitamines A, B, C, were present in extremely small amounts—A was exceptionally deficient, and in the rations of some days was entirely lacking.

There are in this monkey diet several factors of importance. 1. Low vitamine contents—especially Vitamine A—factors which are essential for life and growth. 2. A high carbohydrate diet—which in oxidation yields an acid ash and which favors the growth of intestinal bacteria producing acid and gas. The acid from these two sources must be neutralized either by the alkali derived from food, or from the body storage. This diet, however, is abnormally low in ash and especially in the alkaline salts of the ash, therefore making it an ideal diet for the production of osteomalacia.

The following table shows the additions necessary for corrections of the separate ingredients of the diet:

Monkey diet Corrected by Rice Casein, Salt mixture, Carrots, or Lettuce. Bread Casein, Butter fat, Salt mixture, especially Phosphorus. Potato Salt mixture, especially NaCl and CaCO_{3}. Raw peanuts Salt mixture. Bananas Casein, Yeast, or Carrots. Corn Casein, Tryptophan, Lacto-albumin. Apple Casein, Gelatin, Butter fat. Onion Casein, Gelatin, Butter fat.

The complete diet may therefore be rendered adequate by the addition of fresh, whole milk and leafy vegetables, or by butter fat, salt mixtures and leafy vegetables.

It would seem from these data that in this inefficient diet we have, if not the cause of osteomalacia, at least a very potent factor in its production. The disturbance of the calcium and phosphorus metabolism may be due primarily to the deprivation of the alkaline salts from the diet (famine osteomalacia) or to a drain from the alkaline storage of the body, associated with a deficient diet (as in the cases of osteomalacia of pregnancy and lactation) or in the combined action of a diet faulty in more than its salt content, which by the production of acid in its oxidation and by favoring the development of acid-forming bacteria, causes the drain of the body alkali for the neutralization of this acid, or it is due to the combination of all these factors acting through their influence on the ductless glands.

It is important also that while this disease is very common among the Cebidæ it has never been found among the macaques. This may be due to the fact that, owing to the storage sacs in the mouth of the macaques, more food proportional to body weight is consumed, or there may be an essential difference in the basal metabolism of the families and individuals. All the factors enumerated do tax the metabolic resources of the body and depress the functions of the endocrine glands. Only detailed and accurate quantitative studies of normal metabolism and the effect of alterations of it on the ductless glands will give a more definite answer to the problem.

This work indicates clearly the alterations to be made in the diets to meet the requirements of the Cebidæ and is to be followed by investigations along similar lines for other families.

TABLE 17. _A List of the Orders Exhibiting Definite Lesions of Osteomalacia and Rachitis._ ═══════════════════════╤═══════════════════════╤═══════════════════════ │ Osteomalacia │ Rachitis ───────────────────────┼───────────────────────┼─────────────────────── Primates │ 29 │ 10 Lemures │ 4 │ 2 Carnivora │ 3 │ 8 Hyracoidea │ 2 │ 1 Rodentia │ 5 │ 3 Marsupialia │ 1 │ 10 │ 44 │ 34 Passeres │ 3 │ Psittaci │ 9 │ Accipitres │ 2 │ Columbæ │ 12 │ Galli │ 9 │ │ 35 │ ───────────────────────┼───────────────────────┼─────────────────────── │ 79 │ 34 = 113 ───────────────────────┴───────────────────────┴───────────────────────

Having discussed the nature of these diseases and some of the factors in their causation, analysis of their distribution may be appropriately added. The accompanying list (Table 17) illustrates the orders in which the two diseases have been found. Veterinarians are familiar with systemic osseous diseases in all the domesticated herbivores, but Hutyra and Marek note them as uncommon in dogs and birds. Among the Primates, osteomalacia occurs almost exclusively in New World monkeys, Cebidæ and Hapalidæ, whereas rickets is much more common among macaques (Cercopithecidæ). Eight of the ten cases of rickets in monkeys seem to have arrived at the Garden with evidences of this disease. Half of the cases were arrested, or at least not florid, when the beast came to autopsy. All of the osteomalacic lemurs belonged to the ring tailed species, born in the Garden and dying at ages from three to seven years. The cases of rickets among the Carnivora were four Felidæ, three Canidæ and one Procyonidæ while all the osteomalacia cases were in the last family. Six of the eight cases among the rodents affected squirrels. The large number of cases of rickets among the marsupials is due to a litter of small opossums thrown by an apparently healthy mother and dying in from six weeks to three months.

The avian varieties which show the most definite osteomalacic changes are the pigeons and pheasants, with the parrakeets presenting nearly as characteristic lesions. Birds when affected with this disease, may come to autopsy in fairly good plumage and without any very marked emaciation. This is remarkable, for when the _cresta sterni_ is palpated this ridge may sometimes be bent enough laterally to touch the _alæ sterni_. How the bird can sit upon a perch when it is possible to bend the femora almost double, is difficult to understand. Deformity is by no means so frank as in mammals although periosteal overgrowth may be quite marked at times. Anemia is undoubted in nearly every instance, the pallor of the muscles seeming to be as great as if the specimen were intentionally bled to death.

OSTEITIS DEFORMANS.

Dr. Corson-White was fortunate enough, during the course of her work upon osteomalacia of monkeys, to detect a specimen which did not show the usual excessive excretion of calcium but on the other hand retained this element and evinced alkali hunger. The general appearance of the specimen was similar to that of monkeys having osteomalacia but at autopsy a definite picture of Paget’s disease or osteitis deformans was discovered. This led to a search for cases in the literature and to the following study, which I paraphrase and condense from Doctor Corson- White’s notes.