Disease in captive wild mammals and birds (part 3 of 4)

Disease in captive wild mammals and birds (part 3 of 4)

The development of the genital tract seems to be essentially the same through all orders in that the genital ridge forms the ovary and its attachments while the Mullerian ducts supply the tubes, uterus and vagina. Early in fetal life these two longitudinal ducts begin to approach one another, and by the end of the third month should be in the position which they are to retain for the full development of their end result. In the human being this position is complete union and fusion, with the production of a single tube from the uterine fundus to the exterior, while in the lowest mammals, edentates and marsupials, the two Mullerian ducts retain their lateral position, and upon completion of embryonal life a double tube from the ovaries to the exterior is found. If the normal fusion of the ducts does not take place, and if for any reason their proper relation is not reached, an abnormality will result varying according to the stage of development that has been reached. Thus in man instead of a single uterus of triangular shape and a single cervix, a double set of tubes may be found. It can be shown that the abnormalities of the human uterus are of definite and fixed types corresponding to an arrest of fusion or completion of the developmental cycle as given for the Mullerian ducts and further that these very deformities are comparable to normal organs of lower orders. In other words abnormalities in arrest of development in the human uterus represent normal types of lower uteri at various evolutionary stages. In monotremes there are two ovaries, tubes, uteri, cervices, a urogenital passage and a clitoris. This corresponds with Uterus didelphys with a single vagina. This abnormality while occurring in the lowest mammal, does not represent the most marked deformity known for the human being— that in which the double tube remains to the vaginal outlet, a condition found in the marsupials. In this order the uteri are entirely separate, and each is fitted with its own vagina. The next higher order, Edentata, seems somewhat out of place if it be judged by its female genitalia since it is possessed of a triangular uterus and single vagina but without distinct cervical segment; the tract is very similar to that of the Primates.

Rodents, in the various families, present no uniform uterine construction, there being four kinds corresponding to as many degrees of Mullerian duct fusion and differentiation. The lowest forms simulate the marsupials, another group is like the monotremes, a third shows a complete fusion with a single cordiform uterine body, while the last resembles somewhat the first, but the uterine divisions are bound together and the vagina is divided only half way down. The Insectivora occupy a transitional position resembling higher and lower groups in having a long uterovaginal canal, without distinct cervix, extending upward into long curved cornua. Cetacea (whales) have a highly rugous single vagina, a distinct, short uterine segment divided into two separate horns. The genitalia of Sirenia resemble those of the last group, but the cervix is better developed. In the last three orders the clitoris begins to be well developed and to present externally. Proboscidea have a single vagina separated from the short uterine body by three transverse folds corresponding to the cervix; the two cornua are long and wide.

“The foregoing orders present in their uteri all the essential characteristics of uterus bicornis unicollis with single vagina and are therefore the homologues of this anomaly in man.”

In the Perissodactyla, the bicornate uterus has a body of a little less than half the whole length; there is a sphincter at the lower end of the body but no projecting cervix. The cornua are longer still in the Artiodactyla and are coiled in a manner suggesting spiral sheep’s horns; there is a differentiated projecting cervix. In cats the length of the uterine body and of the cornua are almost equal and both are flat tubes; the cervix is prominent and the vagina long and rather smooth. The dog’s uterus is similar but the two cornua are bound together or fused before the point at which their termini enter that of the uterine body; the cervix is not very prominent, but well formed and the vagina is rugous. These types correspond to the uterus cordiformis. Lemurs have a common uterovaginal cavity like the Edentata. The lower monkeys possess a long slender uterus with definite superior lateral angles, the last vestiges of the cornua, a prominent cervix and a short rugous vagina. The higher apes have a uterine construction almost identical with that of man at the stage of infantile development.

“From the foregoing study it is clearly shown that every anomaly of the female genitalia in Man is in reality the result of atavism and hence, a degenerative change, and inasmuch as every special form of anomaly finds its counterpart in the normal anatomical arrangement of the analogous structures in one or another of the great mammalian groups, one additional item of proof is offered in support of that greatest of biological doctrines, the descent of Man from the lower forms of life.”

ANATOMY OF LABOR.

In a second article Schumann reviews the comparative anatomy of labor, demonstrating that the basic principles are essentially the same, alterations only being in the direction of accommodation to the pelvic construction. In order to make the analysis comparable with human conditions the pelvis is studied as if the animal were standing erect upon the hind limbs.

The salient points of difference between the quadruped pelvis and the biped, human type may be epitomized as follows: (a) The entire pelvis lies (with the animal in its normal station) in a generally horizontal position with a slight slope downward anteriorly. (b) The false pelvis is almost entirely wanting, there being practically no bony structures above the brim with the exception of the small upper portions of the ilia. (c) The pelvis in quadrupeds is never basin-shaped, the lateral walls from the iliac crests to the tuberosities of the ischia lying roughly parallel to each other and enclosing a pelvic cavity rectangular in outline. Only in the highest apes does the basin-shaped pelvis appear. (d) The angle of the axis from the promontory of the sacrum to the symphysis is always greater in the quadrupeds than in man, averaging in the former from 70 to 80 degrees, in the latter about 55 degrees, (e) The symphysis pubis is an extremely long joint, being frequently greater than half the length of the entire pelvis, (f) The sacroiliac joint is more or less movable in all quadrupeds, especially in young animals. The rotation of the sacrum on the ilia increases the anteroposterior (dorsoventral) diameter of the outlet and at the same time wedges apart the ilia, thus increasing the lateral diameter.

In regard to the forces of labor it is to be pointed out that in the lower mammals the pregnant uterus hangs below the pubic arch so that the fetus must rise at an angle of about 45 degrees to pass over the pelvic brim. In so doing it meets the narrowest part of the triangular bony pelvic inlet, the anterior pubic angle. Since the sacrum is above and out of the way, the lateral diameter is the one which must be suitable to the passage of the presenting part. This is the head in homo, the largest part of the fetus, but in lower animals either head or breech often accompanied by one or more extremities, may present; the head is not the largest part in lower mammalian fetuses. The uterine contraction proceeds as in man, the fundus and cornua acting alone until the cervix contains the fetus, at which time all parts contract. In the bicornate organ both sides must contract or the fetus might be forced from the gravid to the empty side. In multiparous animals with both uterine horns occupied, the fetuses lie head to head, breech to breech and are expelled alternately from each side.

In uniparous animals rotation is in the nature of an accommodation of the greatest diameter of the fetal body in cross section to greater axis of the mother—the dorsoventral. Uterine contractions cause the fetus to unfold from its elliptical form and to assume an extended position, permitting head or breech to enter the lower pelvis. The pubic angle having been passed and the extension of the presenting part being successfully accomplished, there is no striking difference in the manner of external expulsion of the fetus.

DYSTOCIA.

Dystocia in domesticated animals is a well studied subject, and its general clinical phases are fairly well known. Several cases have been observed, details of which are worthy of note since some of them are entirely complete.

Inertia uteri as a single non-obstructive condition seems not to have been observed here, although well enough known to veterinarians. Nor has a case of dystocia been seen as the result of excessive expulsive force. Obstruction to natural passage by bony deformities or malformations is a common occurrence in man but not so in lower animals. There may also be dystocia by reason of a normally formed but too small pelvis when the female has been impregnated by a much larger male, or if the female conceived before the pelvis has achieved its full growth.

Deformities may be due to irregularities of bony development, exostoses, fracture or diseases of the osseous system. A most interesting case of this type occurred in a Barbary ape (Macacus innuus) which had been in the collection for two years and was apparently in good health when discovered in labor.

No progress being made and the animal becoming shocked, an ineffectual attempt was made to deliver by version, the monkey dying during the operation. Upon autopsy the uterus contained a fetus apparently at term. The head was extended so that the face presented, but the head was not engaged. The cervix was fully dilated but the uterine muscle was relaxed and flaccid. The fetus was dead when the animal was first examined. The uterus contained two placentæ as is normal for these apes, the left placenta being the place of attachment of the fetus while the right one was somewhat smaller and presented no umbilical cord. The fetus was normal in size and form, the face was extended and its lower portion far advanced in a caput succedaneum. The measurements of the fetal were as follows: bitemporal 5.5 cm., biparietal 6 cm., occipitomental 8.5 cm., occipitofrontal 7.5 cm. The pelvis (dried specimen) presents a most interesting condition. The sacrum is bent sharply forward, carrying with it the border of the ilia, which are bent upon themselves forward and downward. The lateral walls of the pelvis are greatly narrowed, the ischia drawn inward. The pubes and the symphysis are fairly normal. The pelvic measurements are: diagonal conjugate 6 cm., true conjugate 4 cm., greatest transverse 4 cm.

It is apparent at a glance that here was an impossible labor, since the head of the fetus could not possibly enter the pelvis, the size of which, intra vitam, must have been less than the above measurements by reason of the soft parts. “This is in the experience of the writer a unique case of a complete obstetric history, plus the specimens, of labor with an osteomalacic pelvis in a wild animal.”

Another case may be added to those already reported by Dr. Schumann, as follows:

Hairy rumped Agouti (Dasyprocta prymnolopha). Dystocia. An apparently normal fetus occupies the left uterine horn. The nose was engaged in the pelvis and has been moulded in a curve pointing to the right. The fetus measures—bitemporal 30 mm., cervical-coronal 31 mm., length of fetus 17 cm. Pelvic inlet in the fresh state measures 18 mm. transversely and about 17 mm. anteroposteriorly. The umbilical cord is 10 cm. long and appears normal as do the membranes. Placenta presents as a spherical mass of hard dense consistency, 35 mm. in diameter and with apparently normal placental tissue occupying the lower border of this spherical mass. On section the mass shows areas of alternating soft red tissue separated by communicating trabeculæ of dense white fibroid tissue. This mass is distinctly encapsulated, but the nature of the enclosing membrane is indeterminate. The pelvis in dry state shows evidences of malformation due to trauma. The right ileum is pushed forward and inward carrying the acetabulum a short distance inward and backward. There is a marked thickening about the right acetabulum. At the upper portion of the symphysis there is marked bending backward toward the sacrum with thickening of the bone. The last sacral vertebra is sharply bent and anchylosed, forming an angle of sixty degrees. The pelvic measurements in the dry state—at superior strait-transverse 24 mm., right oblique 23 mm., left oblique 26 mm., true conjugate 22 mm., outlet 17 mm., between the ischiatic spines.

This is obviously a traumatic malformation and forms a relatively contracted pelvis. The delivery of an adult fetus is impossible.

Cape Hyrax (Hyrax capensis). Impossible labor due to malformation of the pelvis. This animal died as the result of shock and exhaustion of labor. She was pregnant of two fetuses, one of which was extracted manually by the keeper but was dead at birth. Twenty-four hours later the animal was found dead. On autopsy there was present a fully developed fetus in the right cornu, the head just above the pelvic inlet. The left cornu was large and boggy. The myometrium of the right side was so thin as to be almost transparent. On examining the bony pelvis the reason for the dystocia is at once apparent. The sacrum is tilted to the right, and the body of the left ileum is bent sharply to the right, the pelvic inlet being obliquely contracted, the right oblique diameter being 16 mm. while the left is 23 mm.

The pelvic obliquity made the birth of a full sized fetus impossible, the one delivered being under developed. The myometrium was evidently stretched almost to the point of rupture when death occurred.

Obstruction to the birth canal by abnormalities in the soft parts, such as muscular rigidity, edema, or inflammation, tumors, atresia or developmental defects are occasionally seen by veterinarians but have not been encountered here.

Dystocia from uterine displacements are uncommon except such as may depend upon the failure of support by the abdominal wall, since this is the principal support of the organ especially when gravid. Hernia or hysterocele is known and anteflexion has been seen. Torsion, a rare human condition, is not uncommon in lower animals probably due to the loose dependent position of the pregnant cornua, attached only to the pelvic walls by slender inactive suspensory ligaments. A case may be reported, not originally described.

Canada Porcupine (Erethizon dorsatus dorsatus). Obstructed labor. This animal died from exhaustion due to an impossible labor. On autopsy the abdomen contained a moderate amount of clear serous fluid with one small blood clot. The right uterine cornu was distended with a fetus to about the same diameter as the uterine body. This cornu was congested and edematous and its walls very thin. The cornu was twisted one-half full turn from right to left, so that the pregnant portion overlaid the uterine body anteriorly. The torsion produced a compression of the vessels on the right side to the point of violent congestion of the cornu. There was no apparent rupture of the uterine walls, death having occurred from exhaustion. The fetus and its membranes were normal.

Many forms of abnormalities in position are recognized for domesticated animals, but since we know so little of the early stage in the wild specimens no data can be given.

Complicated labor in lower varieties of animals will follow lines similar to those for man and domesticated animals. Hemorrhage from trauma is not common at term, but several cases of abortion following injury have been seen. Postpartum hemorrhage might be expected in the higher apes which have a large discoid placenta similar to the human form, but when the placenta is more loosely attached and is subdivided as in lower forms, such bleeding is of no danger; when a cotyledon is torn from the ungulate uterine wall, a free hemorrhage sometimes occurs.

Geoffroy’s Marmoset (Leontocebus geoffroyi). Puerperal relaxation of the uterus with fatal hemorrhage. The uterus is 4 cm. long, 15 mm. wide at intertubal line. Uterine wall averages 2 mm. in thickness. Peritoneal surface is smooth, glistening and intact. Uterine musculature is soft and relaxed. Entire organ is intensely congested and on section uterine cavity contains a large firm blood clot completely filling it. Mucosa is of deep purple color, shows many fragments of decidua and is the seat of profuse hemorrhage.

Placenta previa is very rare. A row of cotyledons may form near the internal os, therefore like a placenta previa, but it appears to be of no consequence. Premature separation of the placenta is known to veterinarians, and is exemplified by the following case in our records:

Black Lemur (Lemur macaco) was found dead in its cage. Upon autopsy the uterus contained a small fetus with one leg and the tail protruding from the vulva. The fetus was normal in size. There was a large amount of free blood in the uterine cavity and extensive extravasation into the myometrium. The placenta was completely detached.

Rupture of the uterus and cervix have not been seen, but a traumatism of the vagina gave occasion for the following death:

Bactrian Camel (Camelus bactrianus) died of shock in labor. Upon autopsy the animal was found to have hydatid disease of the liver, lungs, and spleen, cirrhosis of the liver, and nephrolithiasis. Protruding from the vulva was a portion of the fetal membranes, the whole vaginal wall and several coils of intestine which had escaped through a large rent in the posterior vaginal wall. The anterior wall was swollen and edematous, the whole region surrounded by clotted blood. The cervix was obliterated, the membranes unruptured, the fetus in the normal extended head presentation. The veil-like placenta was somewhat injected but otherwise normal. There was some hemorrhage about the rectum but none in the free peritoneum.

This animal had broken her hind leg just above the fetlock three weeks before falling into labor, and was unable to stand. It is evident that the difficulty of delivery associated with an unnatural and forced posture due to the fractured leg was sufficient cause for the rupture of the vagina where the tissues were degenerated as a result of the coincident general disease.

Inversion of the uterus is one of the common accidents of labor among all animals, most frequently seen in ruminants. It is a condition more to be expected in lower animals than in man because of the long slender relaxed suspensory ligaments, the length of the uterus and the rigor of the contractions. The immediate causes are those operative for human beings. Three cases are recorded—one in an axis deer, one in an opossum, one in a mouse, the last being detailed in the following notes:

A Japanese Waltzing Mouse (Mus wagnerii rotans) died a few hours after an uneventful labor. On autopsy the entire uterus was found inverted and prolapsed, the organ the seat of a violent congestion, the animal having died of shock.

THE PELVIS.

A study of the dynamics of the female pelvis from an evolutionary standpoint may explain some of the difficulties attending parturition. Starting from the biological law that morphology follows function and that the anatomy of a part alters to suit a changed physiology with such modifications as are necessary to fit each part properly to interact with other structures comprising the entire animal, it is evident that two great changes have occurred in the evolution of homo—the assumption of the upright posture and an increase of intellectual power necessitating a larger cranium of modified form. To this end also the pelvis would have to change both for support and to allow the passage of the enlarged head. The functions of the pelvis are (1) to attach the legs or hinder limbs to the trunk; (2) to furnish points of attachment and fulcra for the great muscles which move the limbs, and in the case of man, hold the trunk erect; (3) to provide egress and support for the terminal canals of the intestinal and urinary systems; (4) to provide for a birth passage; (5) to act as a shelf and support for the abdominal viscera. In quadrupeds the first four functions being perfectly served, there are fewer abnormalities of reproduction (and in the positions of viscera as well—ED.). In man natural selection weeded out narrow pelves, but the present product is as yet an imperfect structure for one of its main uses, parturition. It should be a funnel-shaped basin of the shape of the fetal head and of the same height at all points—that is not oblique, there should be no promontory, the pelvic symphysis should be short and the sacrum of the same height. This would obviate internal rotation now necessitated by the oblique pelvis; this does not occur in quadrupeds.

Tracing the evolution of the pelvis, it is to be found first in fishes where it is a loose disjointed, variable structure not attached to the spine; in some it consists merely of ischia. In reptiles the box assumes a form suggesting higher types. Passing from the toads to turtles and to the crocodiles, the elements which go to make up the pelvis assume a more and more osseous character and become more and more definitely articulated with the spine or with the differentiated sacrum. Its purpose in these low forms is mostly as a support for the muscles of the legs and back. Birds present an advance in pelvic construction but with a great preponderance of the vertebral column since thirteen to seventeen bones may fuse to form a sacral “roof.” The ilia, ischia and pubis are firmly combined. The box is long and narrow with a heavy part for the acetabulum and broad surfaces for muscular insertions. The pelvis of birds differs from that of cold-blooded vertebrates in the greater number of vertebral segments entering into its composition, and in their bony confluence. It differs from that of mammals by being unclosed by an anterior symphysis and by a widely perforate acetabulum. The ossification of the pelvic bones is to afford a support for the legs, and the open pelvis allows passage of the large brittle egg. The shape of the pelvis is of little importance in parturition in the foregoing animals, except for birds which bear large eggs when the pubis anteriorly is open for that purpose.

In monotremes one finds the reptilian type of pelvis with the three divisions of the innominate bone remaining separate. The pelvis is short, heavy and flat and is fitted with marsupial bones. The marsupial pelvis, possessing parallel walls made by the ilia and ischia and a long symphysis, resembles roughly a triangular prism. The sacrum is wedge- shaped, without a promontory and has a considerable movability. The marsupial bones are quite long. The triangular outlet is many times the size necessary for the passage of the fetus.

The rodent pelvis is difficult to summarize morphologically by reason of the great diversity of form occurring in the many genera of the order, but it may be said that here the pelvis is usually of a type rather higher in the scale than the other structural characteristics of the order would indicate. The outlet is more commonly ovate than rectangular, the ischia and ilia lie at a more marked angle to each other, and the true conjugate forms a lesser angle than is common in quadrupeds. The sacroiliac joint is, in general, freely movable.

The female insectivorous pelvis is relatively large, the sacroiliac junction usually being long and well knit while the pubes are slender, wide of angle as to their descending rami and there may be no symphysis, as in bats. Edentates have distinct bony unions of the elements of the innominate bone and of this to the sacrum which increases in width downward permitting a long synostosis with ischia and pubes; these joints are not movable. The pubes are slender and the symphysis short. The sacrosymphyseal angle is 80 degrees in the armadillo. The inlet is roughly triangular to almost round. Cetacea have no clearly developed pelvis, its place being represented by two long bones, larger in males, which seem to be the insertion of the genital erector muscles. There is no junction to form a pelvis nor is there an acetabulum. A pelvic box is absent in the Sirenia, but lateral processes from the lumbar vertebræ form a sort of ileum between which an ischium is located.

Proboscidea have a massive pelvis lying vertical to the spine. The iliac alæ are wide and deeply concave; the ischia are short, heavy and parallel to the ilia; the pubes are short and combined in a heavy symphysis; the sacroiliac joint is short, heavy and slightly movable; the outlet is ovate. In one specimen examined the length was 4 feet, symphysis 18 inches, true conjugate 19 inches, transverse diameter 17.5 inches; crests of iliac were 28 inches long.

Perissodactylic animals throughout this suborder have similar pelves except in so far as the obliquity is concerned. In the rhinoceros it is 90° with the spinal column, in the horse 135°; the angle of the true conjugate is 10° in the former, 50° in the latter. The lateral halves of the box are heavy and parallel; the symphysis is short in the rhinoceros, large in the horse; the outlet is ovoid. Artiodactyla, including pachyderms and ruminants, show a variety of shapes and constructions. Hippopotami have a short massive box tilted at about 150° from the spine, with widely flaring ilia and ischia; the pubes are slender but not combined in a strong symphysis. In ruminants the sacrum consists of four fused units; the sacroiliac joint is fairly movable; the obliquity is about 145°; ilia are long and slender and flaring; the ischia are broad and parallel with the ilia; pubes are slender but form a symphysis about two-fifths the total pelvic length; the infrapelvic angle is wide; the outlet of the pelvis is almost rectangular.

The general characteristics of the carnivorous pelvis may be summarized as consisting of a long strong symphysis, parallel lateral pelvic walls, a great sacrosymphyseal angle, and a marked separation of the bodies of the ischia. The sacroiliac joint is in general moderately movable.

The pelvis of lemurs is narrow, attached lightly to the slender sacrum, tilted at an angle of 140° and is possessed of a short weak symphysis; it resembles the structure in bats. In macaques the box is long, the sacrum wide, with a short iliac synostosis, the ilia long, narrow and curved out sharply, the ischia are continuous with the ilia and widely separated; the symphysis is short, about one-sixth the pelvic length; the angle of the superior strait is about 60°; the outlet is oval, the transverse diameter being short. The chimpanzee pelvis is made up of a wedge-shaped sacrum composed of three vertebræ, wide, flaring, concave ilia, stout well separated ischia with flattened tuberosities and a short symphysis parallel to the sacrum; the outlet is ovoid; true conjugate angle is 65°; the sacroiliac junction has little motility. In the gorillas the following points differ from the last described structure. Five vertebræ comprise the sacrum and the anterior surface is distinctly concave; the pelvic contour while still ovoid, has the two diameters more nearly equal; the pelvic angle is obtuse; the true conjugate is at an angle of 70°.

In man the salient features of the pelvis are—a broad, wedge-shaped sacrum, concave anteriorly, with wide articular surfaces and a limited motility; widely flaring ilia including the concave curvature of the body of the bone whereby the lateral diameter of the pelvic inlet becomes wider than in lower orders; short stout pubes with a narrowed angle beneath them; heavy blunt ischia with large tuberosities; true conjugate is at an angle of 55°. The human fetal pelvis resembles that of quadrupeds.

Study of these data indicates that the quadruped pelvis retains many things in common through all the orders especially in being a roughly rectangular structure lying chiefly horizontally, with a poorly developed false pelvis, straight ischia and a long symphysis pubis; the angle of the true conjugate is greater than in man and may be up to 80°. The long pubic synostosis changes the relation of the true and diagonal conjugate, but the former is no indicator of pelvic capacity, since in lower mammals the promontory of the sacrum lies anterior to the symphysis; the vertical diameter is a better measure of pelvic size and form. Sacral movement seems greater in lower animals especially in youth. The shape of the pelvic inlet is triangular in the lowest forms, the posterior base of this becoming wide as one ascends in a zoological line; the concavity of the ilia also increases so that the higher the animal the more curved are the lateral borders. In quadrupeds the anteroposterior diameter is greater than the lateral; the reverse is true in man. The long straight-sided quadruped pelvis is retained because of the direction of the forces from the legs, which is as much or more upon the anterior or pubic arch as upon the sacroiliac junction. In the semiupright position of the monkey the force is directed backward and downward upon the sacrum, this aiming to widen the pelvis by forcing the ilia apart. The effect of the upward force from the femora is to throw the pelvis upward and anteriorly by directing the line of action through the acetabula more toward the ventral surface. The sacroiliac ligaments hold the ilia firmly, their alæ being spread outward by the force from above. Elevation of the pubes shortens their symphysis and the true conjugate. By these changes the birth canal is shorter, entirely bony, with the upper inlet on the same plane, and promontory and symphysis are near enough the same level to be met at the same time by the engaging head. In these pelves the anteroposterior diameter is still long and superior rotation is not necessary.

In Man the force exerted on the pelvis from above is greatest among all animals and is greater when he is in active motion. The force is directed from above to the sacroiliac joint, the iliac bodies and the acetabular region while from below the pressure is directly exerted upon the last named. The force from above rotates the sacrum downward at its upper end, the attached sacroiliac ligaments at the same time pulling the alæ inward and throwing outward the lower end, the acetabular part. This tends to widen the pelvic box and to reduce its anteroposterior diameter. But the force acting from the legs and the adductors of the thigh push the lower parts of the ilia and the ischia and pubes apart, thus counterbalancing the effort of the force from above. The combined forces tend to bend the iliac bodies, thereby producing the curved lateral margins of the superior strait and making the lateral axis long. As between these two forces that from above is certainly the greater.

The effect of these forces can be followed by comparing a quadruped pelvis, a human fetal pelvis and an adult human one. The first two are similar chiefly in the shape of the inlet and the flat character of the ilia. This is strongly corroborative of the evolutionary development of the pelvis to meet the demand of the upright position. The effects of this evolution are as follows: First, to develop a forward inclination of the sacrum and a concavity in its surface anteriorly, second to increase greatly the iliopubic and ilioischiatic angles, third to cause the acetabula to move forward of the lumbosacral axis, fourth to shorten the bodies of the ilia and to develop in them a regularly curved surface, the concavity of which faces forward and inward, fifth to decrease the interpubic angle and accordingly to remove the triangular quality of the pelvic contour, sixth to increase the transverse diameter at the expense of the anteroposterior, and seventh to decrease greatly the sacrosymphyseal angle with the result that the entire pelvic cavity lies in one plane.

The effect of forces in alterations of the pelvic architecture may be seen in their several stages by the observation of the mammalian pelvis in the course of its evolution and development. The transitions in form are very gradual, but their gradations are well shown in the characteristic forms which have been described; the quadruped, monkey, anthropoid ape, human fetal and adult human type.

By an examination of the adult pelvis and fetal skulls it will be seen that the shape of the quadruped birth canal accommodates the fetal head nicely when in extension since there is no large posterior cranial development, the head and neck being of nearly the same thickness. In the monkey, where the facial angle increases, the head does not advance as a pointed presentation but as an irregular surface—the chin, forehead or occiput. It is only when the head has assumed a high facial angle and a well developed occipital lobe and the pelvic inlet has become transversely wide, that internal rotation is necessary.

Resuming a discussion of our records I shall at this place introduce additional cases of pathology in the parturient genital organ and then discuss the general system. Beside the cases of dystocia discussed in preceding pages there occurred in a deer a complete eversion of the uterus, which was incompletely involuted, accompanying prolapse of the rectum and bladder due to straining after severe injuries, probably inflicted by a male. The animal lived long enough to develop a purulent cystitis which spread to the vagina, uterus and pelvic soft parts. The left uterine cornu of an American bison was found to contain a decomposing fetus at about half term; general sepsis had supervened which led to the animal’s death in about a week, according to the keeper’s observations. The history of a monkey, followed through two pregnancies and finally dying of tuberculosis and sepsis is interesting.

Pigtailed Macaque (Macacus nemestrinus). Received March 5, 1903, died October 29, 1904. This animal gave birth on December 28, 1903 to a young one which appeared feet first; the arms appeared to have penetrated the septum between the vagina and rectum and protruded through the anus. Had to be cut off before delivery. She had a second young one October 21, 1904, which was properly delivered but was weak and lived two days, having received little attention from the mother. The mother since has been weak in the hind legs, eaten almost nothing and several times has passed a little blood in the stool. Lungs are partially collapsed; contain scattered small pinhead tubercles; right lower lobe contains a caseous nodule about the size of a cherry. Both pleuræ contain clear fluid. Abdomen contains a half pint of cloudy fluid. Omentum adherent along lower border and region of spleen and contains pinhead tubercles. Surface of the liver is studded with numerous pinpoint, pinhead and (old) pea sized tubercles. Some places in the liver seem to be the result of two invasions. Spleen presents small cherry sized tubercles thickly grouped together leaving small amount of splenic tissue to be seen. Kidneys contain pinhead to barley grain tubercles. Uterus is somewhat enlarged. External surface smooth. Section shows wall to be about one-quarter inch thick. Uterine cavity enlarged. Considerable bloody pus in uterine cavity. No communication can be found between the bladder and the vaginal wall or between the vaginal wall and the rectum. The intestines are negative. Mesenteric glands enlarged and caseous.

Abortion and miscarriage are occasionally seen in the monkeys, rodents and ungulates. The underlying reason for this can seldom be determined. A few cases seem to depend upon annoyance or abuse by cage-mates, a few to immaturity of the mother and some others seem the result of bone diseases such as osteomalacia. It does not occur regularly in any group or enclosure and appears to have no comparative pathological value.

Injuries of the external genitalia of the nature of lacerated wounds are occasionally seen in ungulates and carnivores, but never in monkeys. Acute vaginitis, sometimes localized into an abscess of the wall has been known to follow these traumata. Chronic changes have been met but once, which example will be detailed under another heading.

INFLAMMATIONS.

Endometritis has been observed sixteen times, as follows: Carnivora 10, Rodentia 3, Ungulata 2, Edentata 1. In searching for causes it was found that the association with a recent delivery of young, an abortion or the retention of a fetus, was responsible five times. Association with tumors of the uterus was noted four times. Injury preceded the condition on two occasions, while one instance seemed to be hematogenic, being secondary to a septic pneumonia. On four occasions the actual cause could not be established with satisfaction. Pathologically the traumatic and parturient cases were purulent while tumors seemed to produce a more exfoliative or hypertrophic inflammation.

Inflammation of the Fallopian tube has been observed but five times, and only in one of these did the uterine wall fail to participate in the disease. The animals affected were three carnivores, one rodent and one marsupial.

No particularly important association of this salpingitis and other pathology was noted, and indeed the only noteworthy lesion of the organ under discussion is now to be cited.

Nylghaie (Boselaphus tragocamelus). Chronic vaginitis, fibroma uteri, chronic tuberculous salpingitis. The vulva and lower half of the vagina are covered by a thin coating of yellowish mucus. Mucosa is mottled purple, irregular, in some places smooth and flat, and in others showing clear cysts with yellowish fluid contents. The upper part of the vagina shows a pedunculated fibroid extending from the cervix. This tumor measures 32 × 20 mm., and is attached to the posterior cervical wall by a broad pedicle and is of smooth surface. The right uterine wall shows a large fibroid which twists the uterine lumen to the left. The tumor in the right uterine cornu is nodular, measures 11 × 9 × 7 cm., shows many dilated veins coursing over the surface and one section shows a soft central necrotic area. The left uterine cornu shows a small fibroid at the lower end. There is a chronic endometritis present. The outer half of the right tube is the seat of firm nodular swellings, one of which proves to be a purulent salpingitis (tuberculous), the others calcareocaseous salpingitis. Both ovaries are fibroid and cystic. Microscopic section shows some exfoliation of the epithelium of the vagina. The uterine cornu is thickened and the fibrous tissue is greatly increased. The tube is the seat of a purulent salpingitis with an occasional broken down tubercle present. The ovaries show a mild degree of oöphoritis (Fig. 23).

OBSTRUCTIONS TO CONTINUITY OF BIRTH CANAL.

Obstruction to the lumen of the genital canal was observed in three mammals.

An American Bison (Bison bison), five years old and known to have been in captivity three years died of a chronic gastroenteritis and pulmonary parasites after many weeks of failing health. At autopsy a double hydrosalpinx, and probably unilateral hydrometra, with low grade cystic oöphoritis were found. A picture is reproduced. The notes are not perfectly clear as to the anatomy but from the gross specimen in preservative it would seem that the left uterine cornu was involved in the dilatation (Fig. 24).

Lion cub (Felis leo) had congenital cystic uterus. The only abnormality found is in connection with the internal genitalia. The vagina is 50 mm. long, uterus 23 mm. long, horns of uterus each 90 mm. long. The diameter of the uterus measures 10 mm. in both body and cornua, the latter being distended by clear watery fluid. They are symmetrically curved downward. They show no adhesions or obliteration of the os uteri to account for fluid retention. The probe is readily passed from the vagina to the end of the uterine horns. Vagina is patulous through its whole course. Ovary and tube normal.

An Axis Deer (Cervus axis) showed congenital hydrometra. This specimen is from a day old animal, consists of the genitalia in which the entire body of the uterus and both uterine cornua have been transformed into a thin-walled translucent cystic cavity containing clear fluid. The body of the uterus measures 15 mm. diameter, each cornu reaching the diameter of 5 mm. The cornua are curled not unlike ram’s horns, and are united by a line of adhesions above the body in the midline. From the ends of the convoluted and cystic uterus and cornua spring the normal tubes each with its ovary.

CYSTS.

Cysts have not been noticed in the lower genital canal, but it is true that this region is not exhaustively studied in routine autopsies; however, no large cysts have occurred there. Cysts of the ovary have been limited to the so-called cystic disease of this organ; one parovarian cyst has been found. These animals, two ungulates, two carnivores and a rodent, are noted as being young adults, only one of which was known to have borne young. In only one, the rodent, was there evidence of chronic peritoneal disease. The notes of the parovarian cyst case are as follows:

An Aoudad (Ovis tragelaphus) showed a ruptured parovarian cyst with normal right side pregnancy. The fetus, its placenta and membranes show no change. The right broad ligament and ovary are negative, the latter containing a red and gray corpus luteum. The left ovary is fibrotic and the left ligament is the seat of a large hematoma, which on section is found to contain thin sheets of gray translucent membrane, like walls of a cyst. The vessels are all distended. Arteries have stiff walls and are empty. Veins have well formed clot. The whole uterus and adnexa were slightly turned to the right, but the twist does not seem to have been sufficient to cause rupture of a broad ligament vessel. Microscopic section of the broad ligament shows a parovarian cyst into which there has been hemorrhage. The cyst is separated from the ovary proper by a short band of tissue which apparently consists of thinnedout ovarian cortex.

TUMORS.

Tumors of this tract in the mammals have been confined to the uterus proper, none having been found in the vagina, tubes or ovaries; in birds one oviductal growth and two ovarian tumors are recorded. These tumors are reported briefly according to their histological structures, a brief summary being added at the end.

A Black Lemur (Lemur macaco) showed a local leiomyofibromatous nodule on the lateral aspect of the uterine body near the cornu.

A nine banded Armadillo (Tatu novemcinctus) gave an interesting specimen which can be described as follows: The uterus is enlarged so that it measures 90 mm. from external os to fundus. Tubes and ovaries apparently normal. There is considerable grumous blood in the vagina and cervix; the former is normal. The cervix is pale and opaque in its lower half; upper half is slightly congested and mucosa decidedly rugous. The uterus itself shows an attenuated muscular wall with a thickened irregular mucosa which is the seat of pseudomembranous tabs of a dull red color, while the mucous membrane itself is irregularly red and yellow; also some grumous blood in the cavity. The size of the uterus is due to a large fibroma attached to the left lateral wall near the cornu. The mucous membrane of this is irregularly disturbed in some places, the tumor being partly bare. Here and there the mucous membrane shows the same degenerating hypertrophic character as seen on uterine wall. The tumor is attached to the wall by a narrow peduncle (Fig. 25).

A nylghaie with multiple fibromata has already been described.

A Jaguar (Felis onca) presented in the middle of the right uterine cornu a cystic resilient tumor 3 × 4 cm., which proved to be a fibroadenoma.

A lioness (Felis leo) presented a penetrating malignant adenoma of the uterine cervix upon which an active endometritis was implanted. The tumor penetrated the uterine wall, which gave way, an acute fatal peritonitis resulting. Metastases had occurred to the lung.

A Wild Boar (Sus scrofa) had a generalized ulcerating carcinoma of the uterine body.

An instance of chorionepithelioma in a Canada porcupine is worthy of separate description.

Canada Porcupine (Erethizon dorsatus dorsatus). Acute suppurative catarrhal endometritis, hemorrhage in myometrium, chorionepithelioma. In anterior abdominal wall a short quill was found imbedded. A very small quill was imbedded in the retrocervical muscles. A quill about 2 cm. long lies free in the peritoneal cavity attached by recent plastic adhesions to peritoneum over left pubic ramus. A fourth quill was adherent by recent fibrous lesions to anterior wall of cecum. Peritoneum contains a moderate excess of thin watery fluid. Liver and spleen are negative. Kidney is large, greenish yellow, firm, smooth and glistening. The right uterine cornu is subinvoluted (the animal was delivered of a fetus before arrival at the Garden, which was sixteen days before death). Its walls are thick and distinctly congested, the congestion being of inflammatory type. Microscopic section of uterus shows a regular, not ulcerated serosa. Subjacent fibrous tissue is loose and contains a granular precipitate together with a few red blood cells. Muscular bundles under this are widely separated evidently partly by trauma, but certainly also by edematous interstitial tissue in which fibrillæ are widely separated and between which free red blood cells and plasma cells are seen. Capillaries ramifying through muscular bundles are greatly distended and congested. Numerous large arteries are present in addition. Some of these contain pink granular material within their walls together with diffuse collection of red blood cells. Fibroblasts extend into this necrotic mass from other sections of the walls. Lumen of such arteries is diminished and in places quite obliterated by recent organization tissue. At many places in muscularis are large cells of irregular rounded form and some cytoplasms incline toward the basic tint with one or several large hyperchromatic nuclei. They are especially likely to occur close to a capillary. There is an especially large accumulation of these cells at that point of section farthest from fundus. Here these cells occur in chord-like masses which infiltrate the muscularis both internally and externally. This particular mass lies in the muscularis internal to great arteries and well removed from mucosa. In this mass are giant cells with multiple nuclei scattered through the whole cytoplasm together with smaller cells with exceptionally large hyperchromatic nuclei. Subepithelial tissue is especially congested and contains numerous fibroblasts together with a few well formed glandular acini. Lining epithelium is discontinuous, of simple tall columnar type, in places becoming flattened or even lost. Lumen of organ is practically completely occupied by pus.

The Indian Elephant “Empress” (Elephas indicus) showed calcified fibroids of the fimbriæ; gross and microscopic notes and a photograph are given. The uterus is bicornate in type. In its body there are numerous fibrous nodules 1 to 4 cm. diameter. They can be traced from the cervix to the ends of both horns and tubes. At the end of each tube there is a great mass of calcified partly conglomerate tumors some of which are partly, others quite, pedunculated. One specimen measuring 2 × 1 × 1½ cm. has a peduncle 15 cm. long. The mass on the right side weighs 3,926 grams, that on the left side about the same. Section of tumor from uterine cornu shows the classical appearance of a leiomyoma with usual whorling and interlacing bundles of involuntary muscle fibres. Degenerative and vascular changes not seen nor is there any notable addition of fibrous tissue. This latter tissue is shown only in small amounts at one end of section.

The preceding data record the discovery of three fibromata of the uterus and one of the fimbriæ; one fibroadenomata of the cystic type, one malignant adenoma, one adenocarcinoma, and one chorionepithelioma. They were found in Lemures 1, Carnivora 2, Ungulata 2, Proboscidea 1, Rodentia 1, and Edentata 1. Metastases occurred but once, to the lung. No secondary tumors were found in the uterus.

While upon the subject of neoplasms of the female genitalia, it may be well to describe the three instances found in the avian organs. A very definite case of adenocarcinoma occurred in the oviduct of an Undulated Grass Parrakeet (Melopsittacus undulatus), a variety of bird very susceptible to neoplasms. The notes in an abbreviated form are given:

Immediately under the ovary is an irregular mass measuring 2 cm. long, 1 cm. wide, 1 cm. deep. The lower part of the tumor thus comes to press against the cloaca. It is adherent anteriorly to the peritoneum. It apparently consists of two parts, an upper rounded larger, and a lower spherical smaller. Both parts are well encapsulated and separated from each other by a well defined constriction. The upper part has a pale opalescent appearance. It cut easily with moderate resistance. The lower portion externally has an egg-yellow color streaked with red. Upon section it has the same general appearance but contains in addition numerous small, irregular, yellow areas which mask the general opalescent appearance. The centre of this node contains an empty space (cyst) 1 × 2 mm. Microscopic section consists of an oval or elliptical mass showing over one convexity a depression simulating a constriction. A thin fibrous capsule extends over most of the section which is extra thick at the point of constriction. Constriction roughly divides the section into two. The upper portion consists of one or two coarse septa of fibrous tissue. From these central areas a delicate connective tissue framework extends peripherally. In this framework are great numbers of irregular gland spaces. These gland spaces are so closely placed in most cases that room is afforded for but one nucleus of the bundle. The gland spaces vary in size, some large, some small, and show grotesque shapes. The larger gland spaces here contain granular debris and pyknotic nuclei. Compound granule cells suggesting colostrum corpuscles may be seen in this debris. The epithelium of the gland spaces consists of a single layer of columnar epithelium of low cuboidal type. In places it is heaped up so as to present several layers. In places too it is not applied in a regular manner to the basement membrane but breaks through and then the cells extend in most disorderly fashion into the lymphatics of the stroma. At these points the nuclei are hyperchromatic. The lower portion follows closely the description given above save that the glandular spaces are much larger. They contain pink glandular material with admixture of compound granule cells. At the convexity of the tumor the acini are especially large. Here they contain a pink granular material which stains more intensely than the other granular contents and, too, inside of this intense pink material are sharply circumscribed areas of yet more intensely pink staining material. This latter substance has a streaming appearance under the high power. This streaming appearance is due to elongated areas of less dense material which are placed with their long axes parallel. This lower portion shows, furthermore, even with the naked eye, two large cysts which are lined by epithelium and contain a very small number of compound granule cells. The capsule at the lower pole is worthy of note from the extreme dilatation of its capillaries.

A papillary adenoma was found in a wild turkey (Fig. 26) and a mixed cell sarcoma in a King parrakeet (Apromictus cyanopygius). None of these tumors sent out metastases.

Interest in the avian reproductive tract from a pathological standpoint centres around the tumors as already given, and abnormalities in egg- bearing. Among our specimens there have been many cases of soft shelled eggs apparently blocked in the oviduct, of “egg-binding” and of the inspissated-egg-remains in the abdominal cavity. These conditions are well known to veterinarians and are explained on the basis of improper food, immaturity of the bearing fowl, injury and inflammations of the cloaca and oviduct. I made an attempt to associate these conditions with infectious disease incidence and with the normal egg size. The results are not harmonious. No relation existed between general or local infection and any of these conditions. Gallinaceous birds with their large eggs show the highest percentage (2.3 per cent.), but Anseres with a somewhat larger relative egg size show 1.6 per cent. Passeres, with eggs of very variable size but relatively large pelves, have an incidence of .6 per cent. Struthiones’ eggs are relatively small; their incidence is 1.5 per cent.

Salpingitis occurred in seven cases, but there have been no evidences of an acute infectious disease such as is responsible for gleet.

THE MAMMARY GLAND.

This structure has been the seat of three inflammatory conditions and four tumors. The former occurred twice in nursing animals, one of which seemed to be suffering with distemper, another from puerperal sepsis, while the third case was probably traumatic. The animals were in order, a raccoon, a coati and a skunk. Four cancers of the breast have been observed, all richly cellular or glandular in type; none of the scirrhous variety has been encountered. Two of them were ulcerating and one was about to become so. One gave extension to the axilla and lung, one had penetrated the abdominal wall and grown around the kidney; the remainder had not yet extended. The animals were Black Bear (Ursus americanus) (thoracic mamma with extension), Common Opossum (Didelphys virginiana) (two sections of breast in pouch), two White footed Mice (Peromyscus leucopus) (posterior abdominal right gland and whole side). These animals were all adult but not old.

SECTION X THE MALE GENITALIA

Affections of the penis are limited to phimosis and occasional inflammations on a traumatic basis. The latter is best seen in carnivorous animals like raccoons and coatis, but has little pathological interest. Two cases of phimosis have been seen at the autopsy table and one in an animal (hyena) still living. The last was operated upon some years ago and has given no trouble since. The prepuce of this beast is seldom retracted, but no swelling or retention of urine has occurred. A Red River Hog (Potamochœrus porous) dying of a variety of lesions, was found to have contracted preputial opening, the edges of which were tight and adherent to the glans penis at various spots. The prepuce had been dilated with urine to a large size from which collection the fluid could be pressed dropwise only by considerable pressure. Opening the sac revealed forty to fifty gray white sand granules about the size of millet seeds. A gray fox (Canis cinereo argenteus) had a mild grade of phimosis; in this case probably traumatism had some etiological relation, for it is the one referred to before in which a terminal urethral stricture was followed by rupture of the bladder.

The testes have been peculiarly free of disease, only a small number of lesions having been found. A raccoon had an acute inflammation, traumatic in origin, and a few passerine birds were noted as showing involvement of this organ in the presence of some general infectious diseases. Two tumors were found in birds, none in mammals. The avian cases both occurred in Red shouldered Parrakeets (Palæornis eupatrius) and were round cell sarcomata, without metastases.

Acute inflammations of the prostate and Cowper’s glands occurred only once as secondary to pelvic infection. Chronic change was observed in these bodies on two occasions, and prostatic hyperplasia, commonly called hypertrophy, was seen thrice. The mammalian prostatic area is known to become overfilled with secretion and to be affected by inflammation when it is not discharged. This occurred in a wood rat (Neotoma pennsylvanica) and a wild boar (Sus scrofa), the former having the condition so marked that prostate and seminal vesicles were swollen backward into the pelvis like a tumor. Histologically one finds in these conditions an engorgement of the glandular and ductal spaces with a mucoid substance and a mild round and plasma cell infiltrate in the connective tissue; there are no marked evidences of active inflammation. The testes were not abnormal in these cases.

The three cases of “hypertrophy” of the prostate are worthy of separate record.

Indian Paradoxure (Paradoxurus niger) the prostate is greatly enlarged, of pale orange color, soft and does not exude pus on section or pressure.

Common Opossum (Didelphys virginiana) The prostate is enlarged, soft, gray-yellow. Urethra contains a little gray mucus but seems patulous. Seminal vesicles negative.

Rhesus Macaque (Macacus rhesus). Glandular hyperplasia of prostate. The bladder is collapsed. The opening of the urethra is occupied by a firm, friable yellow-white cast of matter apparently inspissated semen. Urethral mucous membrane normal. Prostate is 7 × 4.5 × 3 cm. firm, resilient, dull purple-gray, capsule negative. Section shows normal lobulations containing apparently normal secretion. Vasa negative. Testes negative. Microscopic section of prostate shows acini of various sizes lined by a single layer of tall vacuolated cells with nucleus at the bottom. Cells probably nowhere reduplicated. Acini nowhere grossly atypical but everywhere hyperplastic and dilated irregularly. Mass is adenomatous in general increase but no part is truly neoplastic. Interstitial tissue rather less than normal proportionately. No “amyloid” bodies.

Still another case of accessory sex gland enlargement was found in a Ring tailed Lemur (Lemur catta), this time, however, with more suggestion of a neoplastic change. The prostate of the lemur is normally large, pale gray-pink and rather firm. Histologically it is about equally glandular and fibrous. In this case the cellular activity is undoubted, and one must consider it adenomatous. The cause of death was enteritis, being perhaps more serious in the presence of the urethral obstruction.

The seminal vesicles are distended to 7 × 2 cm. with a thick boiled- starch-like material. Wall and mucosa are negative. Prostate large, tense and injected. Its cut surface is pale purple, homogeneous; character of fluid is normal although excessive. Urethra is occupied by a cast of rather tenacious starch-like matter which begins at neck of bladder and runs almost to meatus. Openings of excretory ducts are prominent. Mucosa and submucosa of urethra are deep purple and the former seems to be slightly opaque as if covered with desquamated epithelium. Testes and epididymes seem normal. Vasa deferentia are slightly distended with excess of normally turbid fluid. Microscopical section shows hyperplastic epithelial condition with accumulation of droplets of hyaline matter but there is no amyloid deposit. In places it is possible to see a hyperplastic and loosened epithelium with nuclei becoming vacuolated, and the whole being cast off. Less granular free globules suggest that this is the method of origin of the hyaline globules free in the acini. The picture is one of papillary adenoma. In some places there is surely reduplication of the lining cells. Connective tissue is deeply staining, compact and with adult nuclei. Growth is not very vascular. There are no corpora amylacea.

A case of tuberculous prostatitis and seminal vesiculitis was seen in a Japanese Macaque (Macacus fuscatus). Judging by the advanced stage of these lesions and their more recent character in other viscera, the disease was suspected as pelvic in origin, possibly due to infection by a thermometer. Whether or not such be the case cannot be established, but at all events, separate thermometers kept in carbolated vaseline were employed after this death. The females caged with this animal did not develop tuberculosis of the pelvic organs.

SECTION XI THE DUCTLESS GLANDS

THE THYROID BODIES.

The ductless glands occupying the anterior cervical regions, known as the thyroids and parathyroids are structures to be found in some form in all vertebrates, but increase in distinctness of outline and construction upward in the zoological scale. In the bird they present themselves as discrete rounded bodies lying well to the side of the midline resting usually upon the carotid artery or jugular vein or both. As one removes the skin reddish brown globular masses will be exposed to view, sometimes showing an irregular lobular outline, a variation due to separate but attached masses of parathyroid glandules; the latter may be yellowish or even white. For the most part, however, distinct thyroid and parathyroid bodies are separated with difficulty, and one must discover the latter by microscopical section. In the mammal these organs are by no means so readily found when removing the cervical integument, for they are usually buried beside the trachea and covered by sternohyoid and sternothyroid muscles. Their position, relative to the larynx and upper end of the sternum, varies considerably but this seems to have little importance in the enlargements to which the gland is liable. It is, however, lower, that is more posterior, than in the human being, rarely rising as high as the lateral thyroid cartilages. The principal lobes are elliptical or roughly triangular masses with their long axis corresponding to that of the animal’s body and apposed mesially to the trachea. When enlargement occurs it develops in the anterior or ventral direction, pushing through the cleft between the muscles and the trachea to present under the cervical skin. In quadrupeds it may become dependent and the swelling is nearer the sternum than is the case in man. The isthmus is a very variable structure, and its presence or absence cannot be said to be a constant character in any order, or indeed in any family. I have seen in old animals a fibrous band extending over the face of the trachea connecting the capsule of the lateral lobes, which might have been an isthmus at one time. From these few observations the idea of atrophic fibrosis occurred to me. Such may be the reason for the absence of this transverse link in some adult specimens.

The amount of thyroid tissue possessed by an animal might be judged by measurement or weight. The former is misleading since the density might vary, as it certainly does in the two classes and between certain orders in mammals. Actual weights would afford little comparison, whereas the weight in terms of total body weight may supply a guide to the amount of gland normal to an animal. There are given in Table 15 the grams-per- kilogram-body-weights of the thyroid bodies (thyroid and parathyroids both sides combined) of twenty animals whose gland seemed entirely normal at autopsy. They are all adult specimens, free of cretinoid characters and of bone or heart diseases, conditions which might reflect abnormalities to these glands. The list is too small to warrant any conclusions, but in one respect confirms Murray’s[41] observation and certain experimental work, notably of Vincent and Jolly[42] and Carlson, Rooks and McKie[43]. The carnivores have more thyroid than ungulates (averages .55 gm. vs. .18 gm.), but the marsupials on our list have nearly as high an average as the former, namely .44 gm. To these figures might be added others which I have worked out from the list given by Murray; it is only possible to compute the gram-perkilogram value for a few of his examples since the body weights are not given in all. Using 2.2 pounds as equal to one kilogram, the seal of 432 kilos had .03 gm. of thyroid, lion had .18 gm., leopard had .46 gm., a serval .36 gm., a skunk 2.35 gm., (was this normal?) while a single herbivore with the weight given was a porcupine having .25 gm. per kilo. The average of Murray’s carnivores is therefore .67 gm. per kilo of body weight, whereas our figure is .55 gm. That the incidence of thyroid abnormalities stands in direct relation to carnivorous character has been recognized before, and is abundantly borne out by our statistics, as will appear at a later place.

TABLE 15 _Showing Weights of Animals, of Their Thyroid Bodies and the Relation of These Weights Per Kilogram._ ═════════════════════════════╤═════════════╤═════════════╤═════════════ │Grams of Body│ Grams of │ Grams of │ │ Thyroid │ Thyroid per │ │ │Kilo of Body ─────────────────────────────┼─────────────┼─────────────┼───────────── Primates: │ │ │ Woolly Monkey │ 2,370│ 2.│ .84 Lagothrix lagotricha │ │ │ Carnivora: │ │ │ Wild Cat │ 8,180│ 2.│ .24 Felis ruffus │ │ │ Silver Fox │ 3,325│ 4.│ 1.2 Canis chama │ │ │ Kamchatkan Bear │ 31,800│ 22.│ .63 Ursus beringiana │ │ │ Lynx │ 9,500│ 1.│ .1 Felis canadensis │ │ │ Jaguar │ 29,500│ 16.│ .54 Felis onca │ │ │ Rodentia: │ │ │ Ground Squirrel │ 550│ 2.│ 3.6 Xerus capensis │ │ │ Ungulata: │ │ │ Zebra │ 340,000│ 64.│ .19 Equus burchelli │ │ │ Giraffe │ 384,000│ 45.│ .12 Giraffa camelopardalis │ │ │ Barasingha Deer │ 56,800│ 8.│ .14 Cervus duvanceli │ │ │ Kashmir Deer │ 56,800│ 20.│ .35 Cervus cashmirianus │ │ │ Urial │ 22,700│ 2.5│ .11 Ovis vignei │ │ │ Marsupialia: │ │ │ Kangaroo │ 18,000│ 10.│ .55 Macropus robustus (?) │ │ │ Tasmanian Devil │ 3,120│ 4.│ .13 Sarcophilus ursinus │ │ │ Wombat │ 26,000│ 7.│ .27 Phascolomys mitchelli │ │ │ Wallaby │ 3,360│ 3.│ .9 Genus and species (?) │ │ │ Edentata: │ │ │ Anteater │ 3,300│ 2.│ .6 Myrmecophaga tetradactyla│ │ │ Accipitres: │ │ │ Wedgetailed Eagle │ 2,300│ 1.│ .43 Aquila audax │ │ │ Struthiones: │ │ │ Rhea │ 18,000│ 5.│ .27 Rhea americana │ │ │ Emu │ 36,300│ 23.│ .63 Dromæus novæ-hollandiæ │ │ │ ─────────────────────────────┴─────────────┴─────────────┴─────────────

ANATOMY.

The minute anatomy of the normal thyroid is fully given in text-books, and is doubtless pictured in the minds of all but students of the subject as a fixed and definite affair. Such is not the case. There is certainly a variation in gross size under conditions of seasonal and sexual activity, and it would seem acceptably demonstrated that changes in diet, especially where meat is concerned, are associated with swellings or shrinkage of the glands. These gross changes must be due to alterations in histology. In youth also the bulk is larger, a condition due to cellular activity, while as middle age advances the thyroid becomes smaller and more balanced in its colloid and cellular proportions. I need not detail the ultimate constituents of the gland, but it is well to emphasize a few points which must be taken into consideration in microscopical diagnosis. In the first place, the lobules or acini are not all of the same size in normal organs. This is especially true in the normal adult gland but may be so in youth. The cells which form the inner lining of the acinus are low cuboidal in shape but the elements which lie under them are oval and do not change with hyperplasia of the former. The colloid which fills the glandular spaces is very susceptible to mechanical and chemical agencies. In material preserved in alcohol it may be shrunken away from the cells or heavily vacuolated, while in tissue preserved a long while in any liquid it may be found contracted or broken. Large vacuolated or vesicular cells are characteristic of the human parathyroid; this type is by no means so prominent in the lower animals, and in the few examples studied closely the arrangement is less definitely glandular than in man.

The avian thyroid is distinct from the mammalian in the delicacy of its fibrous framework and the flatter character of its epithelia. Acini are usually of more uniform size. Capsular vessels are prominent but internal vascularity is less in birds than in mammals and their goitres are not solid.

PHYSIOLOGY.

The physiological value of the thyroid-parathyroid complex has been the subject of extensive study and voluminous literature without exhaustion of the possibilities, but with the result that we are possessed of knowledge explaining certain phases of abnormality, even if the normal functions be not unexceptionally demonstrated. The accepted alterations of functions are hypothyroidism—inadequate physiology, and hyperthyroidism—excessive activity. Absence or atrophy of the thyroid bodies is usual in hypothyroidism, while enlargements, collectively called goitre, commonly accompany excessive function. Exemplifying the former, cretinism is the result of failure of normal function and development during fetal life while myxedema is the expression of the disappearance of thyroid secretion after it has once been operative; the latter may occur in infancy after nursing has ceased, or at any time that the thyroid may atrophy, during some of the forms of goitre for example. Hyperthyroidism may express itself, with or without visible enlargement of the thyroid body, in nervousness, gastrointestinal disturbances, tachycardia, loss of weight and exophthalmos. The first group, which might be called athyroidism, is often associated with alterations in the bony skeleton in the form of chondrodystrophy or of rickets, while some degree of osseous change is observed with myxedema. Goitre, be it simple or exophthalmic, may be followed by cardiac enlargement or by myocarditis.

The character of the thyroid secretion is not known except that it is influenced by the availability of iodine in the diet, but there are some other as yet unexplained features. The normal thyroid fed to cretins or persons suffering with myxedema, has the power to improve the condition apparently by supplying iodine and the other essential elements. Iodine is an important constituent of the gland, being present in combination with protein. Its quality varies indirectly with the amount of colloid and of hyperplasia (Marine). The administration of this element is beneficial in colloid goitre but is harmful in the toxic variety. Even though the administration of thyroid extract may relieve athyroidism, this procedure in normal animals fails to produce typical pictures of hyperthyroidism. Carnivora fed thyroid gland do not show toxic symptoms until excessive amounts are given, whereas herbivorous varieties are much more sensitive to this feeding.[44] Tachycardia, nervousness and exophthalmos are not produced by these experiments, an interesting observation since these signs are not recorded in wild animals, and only vaguely reported by veterinarians. Man is apparently very sensitive to thyroid dysfunction.

On the other hand, meat-eating animals are more sensitive to excision of the thyroid body than are grain eaters.[45] Chemical studies have shown that the thyroid is concerned in basal metabolism since this is increased in hyperthyroidism and decreased in myxedema; nitrogen output is much elevated.

Thyroid physiology stands probably in some relation to the cardiac mechanism since in simple colloid or simple hyperplastic goitre if of long duration, cardiac enlargement and disease may be greater than the excess work occasioned by the mere physical bulk of the enlarged gland in the neck would seem to warrant. A detoxicating function has been ascribed to the gland, but Murray discredits this on the ground that congestion occurs in infectious disease of warm blooded animals but not in snakes. He thinks the gland more likely stands in some connection with the thermoregulatory mechanism.

It is evident from the foregoing that the thyroid is closely related to protein metabolism, and that this is in some way connected with the ability the body possesses to use iodine in the food if it can get it. Feeding of meat to fish was found by Marine to increase the size of the thyroid. With all this in mind it is not astonishing that two-thirds of our cases of thyroid abnormalities were found in the order Carnivora.

The anatomical changes of the human thyroid that precede or accompany the various clinical pictures cannot be said to be uniform to a degree that one can even approximately predict in every case what will be found at operation, at autopsy or by the microscope. Furthermore, much discussion has existed upon the importance of the several changes, the association with clinical phenomena and the nomenclature. I shall not enter the academic discussion with our material because so much has depended, in human medicine, upon symptoms, signs and chemistry—data that we cannot adduce. Upon many occasions I have seen animals with very evident goitres, but have not been able to detect bulging of the eyes or especial nervousness. One striped hyena carried his mass for several years. It swelled up occasionally and seemed to cause dyspnœa. At one examination of the beast, to see if anything could be done for him, a large cyst broke under the examining hand, whereupon a deep inspiration was heard and relief was apparent. This handling was repeated twice, these times with the purpose of breaking cysts and when this was successful disappearance of the dyspnœa was observed. However, a similar attempt upon another hyena and a wolf failed possibly because no large thin-walled cyst was present. These and the case of the lion cub (page 170) are the only instances in which the enlarged thyroid seemed to have given serious difficulty, and the symptoms were probably due to pressure. Many, indeed most, enlarged thyroids have been found at autopsy, when the Garden personnel was unaware of their existence. Interesting notes of familial cretinism will be found under the appropriate heading.

PATHOLOGICAL ANATOMY. CLASSIFICATION.

And now to return to the question of morbid anatomy of the thyroid gland, I shall begin by outlining briefly the classification to be used in analyzing our cases, a system which combines those of many pathologists, yet which I believe contains the essentials of all. The changes in the gland being hyperplastic and recessive, at times to a stage of atrophy, no clear cut definite line of demarcation separates all these pictures; instead they must be thought of as merging into one another. When the thyroid enlarges more or less continuously with a maintenance of considerable colloid, the picture is that of COLLOID GOITRE. The gland is pale, gelatinous, tense but resilient and may show large cystic areas with fluid contents. Microscopically studied the acini are overfilled with colloid yet the lining cells are retained but flattened. The cysts may show the ruptured septa of the original acini. Enlarged soft reddish glands are found at times to contain much colloid, nearly every acinus being distended with it, but in such organs the epithelia are high or even reduplicated; the amount of contents is the striking feature. These are termed HYPERPLASIA WITH COLLOID. Hyperplasia may go on with the absorption of colloid, HYPERPLASIA WITHOUT COLLOID. The gland is then a darker body of more solid character, red, dull purple or uniformly pale pink, somewhat dependent upon the blood content. By magnification one sees smaller acini with prominent high cuboidal or cylindrical epithelia and little or no colloid. The increase of cells seems to be due both to an increase in their size and number. As the proliferation increases the lining layer must be accommodated so that it bulges out into the lumen as a bud or papilla which, if it be extensive or universal in the thyroid, gives rise to the ADENOMATOID GOITRE OF PAPILLOMATOUS type. This growth is accompanied by much congestion and small or large hemorrhages may occur, forming cysts containing a blood stained fluid. Grossly such a gland has solid and cystic areas, is mottled red and gray or brown from old pigmentation and is usually of very irregular shape. These forms are more or less uniform and general, but in certain instances the hyperplasia tends to remain in isolated areas or nodules, and in these develop solid masses of thyroid epithelium, sometimes with a small lumen usually devoid of colloid, and a rather rich but loose fibrous supporting tissue, the whole picture resembling the microanatomy of the fetal gland; to these the name fetal adenoma has been given, but since they are not fetal in origin and do not behave like tumors I have called them NODULAR ADENOMATOID HYPERPLASIAS. The next step in hyperplasia would remove it from benign to malignant in pathological character, and the term NEOPLASTIC HYPERPLASIA is used; this must of course be limited to the epithelial growths, since sarcomata, while they occur in the gland, come from other cells.

The changes in atrophy consist in irregular distortion of the gland by fibrous tissue to which may be added large colloid or fluid cysts. There is no uniform finding in the thyroid for the diseases believed to be due to its atrophy, functionally at least, namely cretinism and myxedema. In the former there may be no thyroid, or it may rather closely resemble the normal organ while in the latter definite scarring and distortion is the rule. The gland acini are compressed, the cells vacuolated or crushed out of existence or there may be colloid cysts.

Inflammations occur as swellings of the interstitial tissues and of the acinus cells during many acute infections. Repetitions of this may leave a definite increase of connective tissue with large cells in the acini, a lesion which many observers have looked upon as underlying certain goitres and myxedema.

HYPERPLASIAS.

The cause of progressive hyperplasias has been ascribed to infection, to chemical substances in water and food, endogenous toxins, heredity and many other factors. While we can add nothing definite in this matter it is worthy of notice that all our animals are exposed to the same general climatic conditions, receive the same water, are fed from the same stocks and many varieties may be in charge of the same keeper. The influence of preëxisting infections cannot of course be measured. Inbreeding or captive breeding seems to have a very definite effect upon thyroid insufficiency as is well known and so sharply emphasized by McCarrison in his reference to intermarriage among certain Moslems; I shall cite the history of a wolf bitch which gave birth to three cretin litters while apparently well but mated to a goitrous male. These facts concerning the etiology are given merely to emphasize the high degree of probability that the distribution of the lesions of the thyroid gland among our specimens indicates the susceptibility of the various orders. This perhaps needs no emphasis for the carnivores, but it does for the marsupials. The literature contains many references to goitre in domesticated ungulates; this would give the impression that they are common among them, and so they may be, but this is not the case for wild ungulates. There being no doubt that the Carnivora have the highest incidence of thyroid enlargement, man being especially prone to it, and since goitre may be induced in fish by feeding meat, the inference is direct that high protein diet stands in some relation to this condition. Thirty-nine of our sixty thyroid lesions occurred in the order Carnivora; all the families of land varieties are represented; 8.1 per cent. of the specimens coming to autopsy showed definite thyroid alterations. However, marsupials have also a decided thyroid vulnerability as indicated by 4 per cent. of the specimens presenting abnormalities at death. Four of the seven cases were among the carnivorous opossums and “devils,” the remaining three being in herbivorous kangaroos. The influence of high protein diet is not evident in birds.

A discussion of the essential pathology can be based upon the accompanying table. In making a diagnosis care was used to exclude mild swelling of the gland seen in acute infectious disease and under conditions of sexual activity. The gross diagnosis was checked by microscopical section, and all but a very few have been reëxamined for the purpose of making the table.

TABLE 16. Showing Distribution of Lesions in the Thyroid Body by Giving the Number of Cases Met in the Autopsies upon the Various Orders, According to the Classification Given in the Text.

═══════════╤═══════╤═══════╤═══════════╤═══════════╤═══════════ Order │ Cases │Colloid│Hyperplasia│Hyperplasia│ Papillary │ of │Goitre │ with │ without │Adenomatoid │Thyroid│ │ Colloid │ Colloid │Hyperplasia │Disease│ │ │ │ ───────────┼───────┼───────┼───────────┼───────────┼─────────── Carnivora │ 39│ 7│ 6│ 5│ 4 Rodentia │ 1│ │ │ │ Ungulata │ 2│ 1│ │ │ Marsupialia│ 7│ 1│ 1│ 1│ 1 Passeres │ 2│ 2│ │ │ Psittaci │ 2│ │ │ │ 1 Accipitres │ 1│ │ 1│ │ Galli │ 2│ 1│ │ 1│ Alectorides│ 1│ │ 1│ │ Anseres │ 3│ │ 2│ │ ───────────┼───────┼───────┼───────────┼───────────┼─────────── Total │ 60│ 12│ 11│ 7│ 6 ───────────┴───────┴───────┴───────────┴───────────┴───────────

═══════════╤═══════════╤═══════════╤══════╤═══════╤═══════ Order │ Nodular │ Malignant │Mixed │Sarcoma│Atrophy │Adenomatoid│Hyperplasia│Tumors│ │ │Hyperplasia│ │ │ │ │ │ │ │ │ ───────────┼───────────┼───────────┼──────┼───────┼─────── Carnivora │ 9│ 1│ 1│ 1│ 7 Rodentia │ │ │ │ 1│ Ungulata │ │ │ │ │ 1 Marsupialia│ 3│ │ │ │ Passeres │ │ │ │ │ Psittaci │ │ 1│ │ │ Accipitres │ │ │ │ │ Galli │ │ │ │ │ Alectorides│ │ │ │ │ Anseres │ │ │ │ │ ───────────┼───────────┼───────────┼──────┼───────┼─────── Total │ 12│ 2│ 1│ 2│ 8 ───────────┴───────────┴───────────┴──────┴───────┴───────

This rather diversified group of pathological lesions would warrant one to expect a notable number of instances of disease observed during life, suggesting that the thyroid was at fault; such, however, is not the case. In the first place, no case of exophthalmic goitre, as the symptom complex is known in man, has been observed, yet the anatomical alterations, hyperplasia without colloid, and with papillary or solid adenomatoid character, are abundantly represented. For the pathologist to accept a case as toxic goitre I would ask evidence of enlargement of the heart and perhaps in addition degeneration of the myocardium. The animal showing the closest resemblance to the disease in man was a Raccoon-like Dog (Canis procyonoides) whose history and notes are given in brief.

Raccoon-like dog (Canis procyonoides) ♀ . Acute hemorrhagic splenitis. Acute fermentative gastritis. Subacute catarrhal enteritis. Acute general infection. Hypertrophic cirrhosis of liver. Chronic interstitial nephritis. Hypertrophy of heart with acute myocarditis- infiltrative and parenchymatous. Chronic lymphadenitis with acute exacerbation. Epigastritic and gastric venous stasis. Nodular adenomatous goitre. The right thyroid is lower, both measure 4 × 3 × 2 cm., are soft, resilient with dense gray capsule. Section shows cysts filled with blood separated by pale septa of soft tissue of varying thickness. One similar mass under angle of jaw seemed like a lymph node but on section is like thyroid. Parathyroids not found. Pleuræ negative. Lungs are gray, collapsed except lower half of lower lobes which are slightly emphysematous and edematous. No consolidations. Pericardium contains about 3 cc. clear, colorless fluid. Epicardium is glistening, transparent and pale. Heart muscle is soft flaccid, pale mottled gray-brown. All chambers are distended with mixed clot. The coronary muscles and columnæ are mottled brown and gray. The tips at insertion of chordæ are pale. Streaks of gray run through muscles. One area 1 × 2 cm. of softening found in middle of left auricular muscle. Aorta negative. The liver is enlarged, surface rough and irregular, edges rounded and uneven, consistency firm and tough, color mottled deep red-brown. Section surface glistening, moist, granular, opaque. Lobular markings not lost but obscured. Connective tissue lines not clear but surely diffuse in lobules. Scars on surface leading to definite connective tissue strands about vessels and irregularly placed. Gall-duct patulous with limpid bile. Spleen is well forward in front and below stomach. It is much enlarged, soft, tough, has a smooth, tense capsule. Section surface shows homogeneous purple pulp with faint, narrow but tough trabeculæ. Follicles distinctly outlined, slightly large but merely of a slightly paler purple than pulp. On surface are many round 2–5 mm. sharply outlined gray thickenings of the capsule and immediately subjacent pulp. The right kidney’s lower half has been replaced by a thin-walled clear cyst 3 × 2.5 × 2 cm. The left kidney is small, capsule strips with difficulty tearing surface slightly. Surface and section are mottled pink and gray, glistening and opaque. It is firm, dense and tough, cortex narrow, medulla wide. Cortex has obscure, irregular markings with few small cysts, striæ and glomeruli, faintly visible, margin between layers irregular. Veins are distended over surfaces of stomach, under surface of diaphragm, in peritoneum over liver but not in abdominal wall. Stomach contains sour gas and water. Mucosa especially near cardia is deep purple. Rugæ are large and permanent but mucosa and submucosa are soft and on section congestion does not extend deep. The tips of the rugæ near pylorus are infiltrated and the infiltration is surrounded by a zone of congestion. Mucosa seems about to slough but has not separated. At pylorus mucosa becomes deep brown-red, dense, swollen, opaque and covered with a slimy, soft brown mucus. Folds are prominent but temporary. In jejunum and ileum mucosa is still swollen and opaque and rugæ are still larger than normal and temporary with a dense sensation on compressing them. The color is not brown but deep pink and yellow with areas of submucous injection. Follicles not visible. Colon is negative except for slight thickening of mucosa unaccompanied by congestion or opacity. Lymph glands of small omentum are small, firm, yellow, homogeneous; those of the mesentery are large, edematous, yellow brown and tense with lymph which escapes on section. Lymph channels up to mesenteric stalk can be traced.

HISTOLOGICAL NOTES.—Liver architecture much altered by passively dilated hepatic capillaries chiefly toward the centre of the distorted lobules. This distortion is in the form of irregular liver columns separated by irregular vessels and interlobular connective tissue. This latter is increased everywhere but is abnormal in distribution within the lobules. The connective tissue at the portal spaces is not so much increased but it shows most around arteries. Bile ducts seem not increased in numbers. Much bile pigment in large, coarse, dark brown masses chiefly settled within portal spaces. The cells show slight fatty infiltration. No multinucleation. Organ is not seriously robbed of functionating tissue. Alterations are not equally distributed over section. Spleen shows enormous congestion with edema of the few chords and perifollicular tissue left unengorged with blood. Follicles are negative. No connective tissue increase. Blood destruction not now active but there are many hemosiderotic masses irregularly scattered. The subcapsular areas are loose edematous follicles. Heart muscle fibres have lost all transverse striations, some are hyaline while others are fibrillar. The nuclei are decreased in number but there is no increase of connective tissue nuclei. No pigmentation. There are several areas of round and polynuclear cell infiltration and one distinct abscess in section. The perivascular tissues are edematous. Muscle fibres are large and wide. Thyroid made up largely of slightly enlarged acini in most of which a slightly eosin-stained hyaline collection is found. There are a few cysts containing a thrombus and hemorrhage. There are no typical colloid cysts. Some scars from old hemorrhages may be seen. There is much free blood in and between acini. Blood pigment free and in granule cells is abundant. Some acinus cells show fat droplets. Lung shows old interstitial tissue increase especially about vessels and a few scars, some of which are forming cartilage. These are deeply encapsulated. Mesenteric lymph nodes show trabecular thickening with active connective tissue formation which is also present about follicles and along edges of chords. Follicles lack germ centres, solidly lymphatic. About them and in and along chords are many tissue cells some of Maximov type and a few eosinophiles. Many of these and endothelial cells are phagocytic of red blood cells. (Fig. 32.)

Just at the time of completing this book another case strongly resembling exophthalmic goitre in man was encountered in a Gray wolf (Canis lupus). This animal had a history of enlarged neck and enlarging abdomen for about six months. His appetite and discharges remained about normal but weight was lost and activity reduced to a minimum. Attempts at removing the fluid believed to be in the peritoneum, by the use of diuretics, failing and the beast being in such poor shape, he was killed. An enormous adenomatoid goitre, concentric hypertrophy of the heart, passive dilatation of all cervical and thoracic veins, passive congestion of the liver and congestion of the portal area were autopsy diagnoses. It will be noted that no exophthalmos and nervousness were observed during life.

Bone disease and atheroma are at times associated with thyroid insufficiency in man. The former, aside from osteogenesis imperfecta of cretinism, occurred only once in a carnivore and once in a marsupial. There is but one case of atheroma among the sixty cases of thyroid disease.

The reaction of the avian thyroid in its hyperplasias is somewhat different from that of the mammalian. The delicacy of the septa and the relative paucity of vessels is perhaps the reason that the gross and microscopic pictures differ from those found in mammals. It should be emphasized, however, that while one can perceive a hyperplasia of the gland of both classes when the testes or ovaries are active, there appears less participation of the thyroid in birds in infectious diseases than is the case for mammals. In simple functional hyperplasia the capsular vessels are prominent, but the cross section need show no change. In the continued hyperplasias the organ remains more solid, being less apt to develop cysts; large cysts are occasionally seen, however, and in one case the entire gland was composed of them. Microscopically the differences are largely of degree in that the process is less frank in development, but the essential changes of swollen epithelia and condensed colloid remain the same.

ATROPHIES.

The thyroid gland in its functional capacity, may be considered to undergo hyperplasia and then atrophy of the parenchyma cells. Normally this would leave the colloid, the epithelia and the supporting tissue in proper balance, but in the presence of low grade inflammation or where an abnormally hyperplastic process retrogresses, the connective tissues may exceed their norm, the epithelia may be shed or remain high and the colloid be irregular in distribution. Such a state of atrophy may exist in fetal life, arise from unknown cause during a course of toxic goitre, or perhaps insidiously in chronic toxic conditions. When this occurs in fetal life cretinism or myxedema arises, when in later life, only the latter appears. Judged entirely by microscopic findings, eight instances of atrophic changes in the thyroid have been found. Three of these were in Carnivora and were secondary to definite goitres, but were not followed by myxedema; one of these three was a cretin. A brother of this cretin but not himself a cretin, died at the age of five months from acute dilatation of the heart, and with a decidedly atrophic thyroid gland. A lion showed a distorted gland, the result of chronic inflammation, a condition also present in a leopard, in the latter possibly in association with a general infection of the heart, vessels and kidneys of long standing. A case in a bear can only be explained on the basis of chronic intestinal toxemia. A camel is the only other variety of animal to show this regressive change. The beast suffered with a marked anemia with marrow atrophy and hydatid disease; calcification was found in the thyroid.

As has been repeatedly stated, myxedema has not been seen, but hypothyroidism has expressed itself in these animals as cretinism. The most interesting pathological fact concerning the relation of the thyroid to this maldevelopment is that there is absolutely no uniform gross or microscopical change constantly present in the typical cases. This will become more evident as the following records of our cases are perused. In 1914 an apparently normal Gray Wolf bitch threw two normal young ones which died of lack of maternal care; they were not posted. The father of this litter died shortly and was found to have a sarcomatous hyperplasia of the thyroid. A year after the first lot a second litter was born of an apparently perfect father which still lives. This animal was purchased in the same lot with the mother, and the two could be related. The first father was not related to the female. This litter consisted of seven, two dying almost at once and burned, the other five not being especially good specimens. They died at ages ranging from two to five months and were all cretins or cretinoid. Two showed hemorrhagic pachymeningitis, one external, one internal, and the usual bulky skeleton of cretinism (Fig. 34). The bones were constructed in a rather orderly and somewhat graceful manner, the uncalcified epiphyses being only occasionally distorted. The same two animals, mated again in 1916, had as offspring seven pups. One evident cretin was killed while another runt was sacrificed and found to have fractures of both femora around which no trace of callus was discoverable (Fig. 35). Two other cubs were apparently normal, while the remaining three did not develop and soon showed the cretin characters. When this group was about three months old they were fed chopped horse thyroid; one improved decidedly, one slightly, the third not at all, but it might have been too weak to get its share. These animals lived from eight months to three years; the two good ones remain alive. In 1919 the mother was killed by her cubs, probably because she was weakened by long sickness. A papillary adenomatoid goitre, endocarditis, nephritis and chronic enteritis were found. The pathological changes in the thyroids of the cretins were as follows: In the second litter two cubs had hyperplasia with colloid, one had nodular adenomatoid change and the fourth showed distinct atrophy secondary to colloid increase. In the third group two had distinct colloid changes, once pure and once as a secondary process with some evidence of atrophy to alter the fibrous tissue and shape of the acini. The remaining four seem to be all colloid in character, but I am not satisfied with the description or sections so that I shall not offer an unqualified diagnosis. The adrenals of these animals all showed some medullary congestion but no change in the chromaffin or lipoidal content.

The deformative lesions of bones are frequently associated with lesions in the pituitary body. Several of our thyroid cases have been studied for such changes without their discovery. Indeed no gross alterations have been noted among many hundreds of hypophyses seen in removing the brain nor in a small number studied histologically. Those examined under the microscope have seemed to correspond to the descriptions given by Stendell in Oppel’s Handbook of Comparative Microscopic Anatomy.

TUMORS.

True malignant hyperplasias of the thyroid epithelium in man are being more thoroughly studied in recent times so that similar lesions in the lower animals gain interest. The notes given below are of value as individual observations only, but since three were in carnivores, another indication is at hand of the vulnerability of this order. One of the cases is admitted upon diagnosis alone, the slides and records having been lost, but since the determination was made by Dr. C. Y. White, I am satisfied to accept it. The four of which notes are at hand are as follows:

Raccoon-like Dog (Canis procyonoides) ♂ . Adenocarcinoma sarcomatodes. Metastases to liver and lungs. Fatty degeneration of liver and kidney. Acute diffuse splenitis. Submucous hemorrhages in stomach. At level of thyroid cartilage on each side and removed 1 cm. from same is a rounded encapsulated nodule measuring 2.5 × 2 × 1 cm. Portions are hard, others fluctuate suggesting cystic degeneration. Below these nodules are two bodies also bilateral, evidently lobes of thyroid, each measuring 5 × 2.5 × 2.5 cm. They are firm with some foci of cystic softening. From a ruptured cyst of the right lobe grumous, red, malodorous material exudes. Peripheries of such cyst show greenish discoloration. Bodies as a whole are greenish black in color. They are well encapsulated, do not meet in midline but are joined at lower pole by firm, apparently colloid, material. All through lung especially under pleura there are dark red, rounded, firm, well circumscribed foci measuring 2–8 mm. diameter. They project markedly on pleural surface. No capsule can be made out. Upon incising they have lighter red centres and deeper peripheries. They cut with resistance and have no inclination toward a wedge shape. Surface is for most part smooth except where tumors are present. Organ is soft and distinctly yellow. All portions of liver contain rounded and irregular nodules, some deep, others superficial. They vary in size from 2 mm. to 3.5 cm. diameter. No capsule can be made out, yet they are circumscribed. The central portions of larger nodules are dirty gray and friable. Peripheral parts dark red. Smaller lesions are solid red and of fleshy consistency. Spleen is deep dark red, homogeneous. Histological section of thyroid shows firm, old, dense capsule very irregular in thickness seemingly on account of the penetration of the enclosed tumor cells. Such infiltration gives the inner outline of capsule a very irregular, bizarre appearance, and at times thins the capsule until it is reduced to nil. In one place the tumor elements appear outside the capsule at a point where a large vessel is apposed to outside capsule. The appearances within this capsule vary; in places the picture is that of a carcinoma. Small, round, interspersed with larger irregularly shaped acini are seen lined by a single layer of low cuboidal epithelium. Very frequently indeed the lining cells contain fine granules of golden brown pigment even where their lumina contain no blood. Some of the larger acini contain altered blood cells and a smooth, pink material, knife streaked and vacuolated peripherally. In some parts of section these acini are regular and well formed, in others they are very irregular and appear to be eroding the capsule. A second appearance concerns the connective tissue. Appearing in almost any part of the section and bearing no regular relation to the epithelial elements or the section in general are areas of closely packed large spindle cells with hyperchromatic nuclei. In another place such spindle cells are arranged purposefully to form irregular capillaries containing blood. A third appearance results from a combination of the first two. Here there are acini, between which run blood capillaries with remarkably rich and numerous embryonic lining cells. A section stained by Van Gieson stain proves that part of the pink intra-alveolar material is colloid. Every gradation can be made out in tint of this material from pink to salmon to orange. It is often very difficult or impossible to state whether a given blood-filled space is a blood vessel or an acinus with hemorrhage. In both structures the lining consists of flattened cells. In one there is the possibility of colloid, in the other of hematogeneous hyaline, both with peripheral vacuolization. Lung shows walls of alveoli thickened by young type of cells. Nuclei of cells lining bronchi are prominent, in good condition. Much coal pigment through whole section. Air sacs empty. There are several rounded nodes through section consisting of closely packed spindle and round cells. Blood is abundant in such nodules both in small lined spaces like capillaries and in larger necrotic foci where there is abundant blood pigment. In one place an irregular, large acinus is seen containing a smooth pink material. A large part of the interstitial tissue is diffusely infiltrated by the large, round cells with hyperchromatic nuclei (Figs. 36 and 37).

Prairie Wolf (Canis latrans) ♂ . Mixed tumor of thyroid. Metastases to lungs. The neck of the animal is enormously enlarged, the diameter exceeding that of the body. Thyroid is enormously enlarged to about the size of a child’s head, rather firm before incision. When incised about 300 cc. blood stained fluid drained. It is rather soft and quite friable looking as if made up of fatty and hemorrhagic matter. The lung is of mottled deep red color with here and there on surface small hemispherical areas about the color of the surrounding tissue but of slightly increased resistance. They are raised above the surface and measure 2–7 mm. in diameter. Histological section of thyroid shows a mixed tumor. It is not possible to say that it is a pure thyroid gland tumor. It is largely sarcomatous, the round cell alveolar arrangement dominant at one place, at another the short spindle cell but not typical, so-called spindle celled type. There are many areas of small and a few of large hemorrhage. Cartilaginous deposit is occurring at some places in the field showing the latter type of sarcoma. Section of lung contains a large sarcoma nodule. The cells consist of round cells without the large cartilage-like cells found in the original tumor mass.

Coypu (Myocastor coypus) ♂ . Sarcoma of right thyroid. The thyroids occupy a position deep in the neck upon the anterior vertebral muscles, the left higher than right, being up to level of top of thyroid cartilage. Only a half-inch of lower pole of right remains and it is like the left which is soft, deep brown-red, delicately lobulated, closely bound to trachea but movable in fascia. It is 30 × 10 × 3 mm. The upper part of the right organ is occupied by, or at least within the same capsule as a 25 × 15 × 10 mm. encapsulated, pink mass with many small vessels on its exterior. It is soft and on section the surface is mushy, of gray-pink-yellow, and seems to have an exceedingly delicate trabecular network. Posterior and superior to this, lying near the salivary glands but back of them is a similar mass 15 × 12 × 5 mm. Still another lies anterior to what remains of the right thyroid and is about 8 × 5 × 4 mm. The adrenals are 30 × 13 × 8 mm. slightly hard and not unlike a long kidney in arrangement. The cortex is wide, regular, brown or tawny, the medulla rich in vessels and deep brown. Histological section of thyroid is an almost completely cellular mass with here and there delicate and incomplete trabeculations. Small blood vessels are numerous and consist of a delicate line with a cell nucleus here and there, that is no true wall. It seems as if the blood channels were simply regular spaces through the cell mass. The cell type is mononuclear with definitely acidophilic “granuloid” somewhat vacuolated protoplasm. The nucleus is almost without exception eccentric, rather poor in chromatin but in places diffusely staining. Mostly, however, the nuclear skein is in spots or threads and fairly dense around margins, therefore not unlike a thyroid cell and a plasma cell. Here and there one finds compressed remains of thyroid acini. There is decided irregularity of size and shape in these cells. Its origin is not clear but this seems like a sarcoma of the thyroid.

Undulated Grass Parrakeet (Melopsittacus undulatus) ♂ . Medullary carcinoma of thyroid. On opening the body a mass 10 × 6 × 4 mm. is found in the upper thoracic region on the right side. A similar mass measuring 5 × 3 × 2 mm. lies in similar position on the left side. They are identified as thyroid glands only from their position and from the numerous large vessels which radiate from them. An especially large vessel leads directly to the heart. Long axes extend anteroposteriorly. The masses are of a firm gelatinous consistency, the color of carpenters glue in lower portions, shading off to a dirty canary yellow above. They have a translucent appearance in lower portions. The surface is fairly smooth, adherent latterly and posteriorly. They are well circumscribed. At one end of the histological section thyroid tissue is easily identified. It varies from normal in that its spaces are often very large, contain villus projections or may be completely filled by large compound granule cells with no colloid. Other acini are atypical and contain typical colloid. Continuous to such thyroid tissue is a very large, rounded tumor. It consists of round cells with round nuclei in which many mitotic figures may be seen. An arrangement into acini cannot be made out nor is colloid material abundant. In one or two places an irregular collection of such material may be seen with peripheral vacuolization but its confines are always indefinite. As far as section goes the mass is well encapsulated but the lymphatics are infiltrated by the tumor cells. The tumor, too, is sharply separated from the relatively normal thyroid. Irregularly scattered through section are remarkable cells with nuclei three or four times the size of other nuclei. They may be hyperchromatic or normally staining. (Figs. 38 and 39.)

The THYMUS BODY is a structure encountered in our specimens with greater regularity than is the case in human autopsy experience. However, no great size of the gland is observed, and there is no record or recollection of anything which could resemble an enlargement suggesting status thymicolymphaticus nor has a tumor with this organ as its origin been observed. In one case only did the thymus present what was believed to be an unusual size. An adult Gray Lagothrix (Lagothrix lagotricha) died with an acute intestinal infection. Its thymus was a large, soft, deep pink body lying in the anterior mediastinum, running up to the clavicular joints and down along the sternum. The death had ample explanation without any state of this organ. The thymus body has not been found enlarged in association with thyroid disease.

The SUPRARENAL or ADRENAL BODY is an organ of essentially the same general construction in the two classes here studied except that in birds the cortical portion may be imperfectly developed and in some of the lower groups is decidedly narrow. This outer zone may indeed be entirely missing since tissue comparable to it is distributed elsewhere in the body, notably with ganglia along the vertebral column. The organ is infrequently the seat of alterations, detectable either grossly or microscopically. Congestion and small hemorrhages are rather common in acute infectious disease especially when the respiratory system is involved, but these rarely destroy tissue or materially reduce the chromophilic cells. These circulatory disturbances have, however, been predominatingly among the mammals although birds have suffered with infections to a high percentage. The medulla is much more often the seat of congestion while, when hemorrhage has occurred, the cortex is apparently always involved. Lipoidal reduction has been seen in a few mammals, Primates and Carnivora, once to a state of complete exhaustion. More serious lesions have occurred eleven times, and since the cause and meaning of disease in this body are so vague it seems well to recite briefly each one.

A Weeper Cebus (Cebus capucinus) suffered for several months with constantly but slowly increasing skeletal deformity of the osteomalacic variety. He died after moving him to a new cage, his end being hurried by a scalp wound. At autopsy the skeletal condition was determined to be of the above named kind. The organs were in good condition. The adrenals were decidedly enlarged for a monkey of this size, measuring 1.8 cm. in length. The medulla was a solid, brownish, homogeneous portion covered with a very narrow, barely discernible cortical zone. This was apparently due to a uniform hypertrophy of the cells of the medulla. The testes were slightly atrophied and fibrotic. A Black Spider Monkey (Ateles ater) had a history of stiffness of legs for six months. This was probably a sign of osteomalacia since at autopsy this condition was found together with a secondary anemia, chronic gastritis, acute enteritis and brown atrophy of heart. The adrenal was knob-shaped, the cortex was wide, brown, regular, the medulla small gray-purple. “Histologically the capsule of the adrenal is thicker than is commonly seen in Primates and connective tissue bands between the units of the zona glomerulosa are somewhat stouter than common. The cells of this layer take the stain a little more deeply than usual, but are otherwise negative. The layer separating cortex and medulla is occupied by a band of well formed connective tissue which is not proceeding inward but outward and so encroaching upon the zona reticularis as to remove it completely in places, in others to make isolated islands of its cell groups. Fine lines of connective tissue are penetrating from this into the middle layer but not disturbing it as yet. The connective tissue septa penetrating the medulla are somewhat wider than one would expect but show no activity in their growth. The medulla is somewhat broken up, vacuolated and the chromophilic cells are not especially prominent, indeed some of them seeming to have undergone necrosis.” A puma (Felis concolor) died after a sickness of two weeks from acute gastroenteritis with its usual visceral associations, including acute nephritis, and with calcifications in the adrenals. These structures were quite firm and nodular, on section tough and resilient. “The cortex is irregular, brown, with paler brown medulla. Areas of calcifications appear as small dots, as linear formations and in some places seemingly around blood vessels. Histological section shows marked vacuolization of cells, particularly of cortex. There is a diffuse overgrowth of connective tissue which has become hyaline. Here and there small calcareous deposits may be seen but no massive areas as mentioned above.”

A Himalayan Thar (Hemitragus jemlaicus) came to his end, after a history of convulsions, from nephritis, which had resulted in general edema including the serous sacs, and an associated cardiac dilatation. His adrenal was egg-shape, of normal size, with a wide, irregular dull brown cortex and a homogeneous opaque, darker brown medulla. “Histologically the cellular structure of the cortex is partly destroyed, partly dropped out and partly disturbed by overgrowth of connective tissue. This connective tissue is quite prominent in the medulla where it is surely increased although it is made more prominent by absence of cells, some of which have been degenerated and some dislodged.” A Japanese Macaque (Macacus fuscatus) after drooping three weeks presented at autopsy the following numerous lesions: anemia, chronic atrophic gastritis, atrophy of heart muscle with regeneration, hemosiderin pigmentation of liver, perilobular fibrosis of liver, chronic diffuse nephritis (subcapsular type), congestion of spleen, fibrillar fibrosis of spleen, hemosiderin pigmentation of spleen, local amyloid infiltration of spleen, calcareous infiltration in medulla of adrenal. Grossly the adrenal showed a thick, orange yellow cortex and small solid, brown medulla. “Histologically the organ appears normal in all respects save for the presence of a few small irregular areas of calcification in the medulla. These occur apart from any recognizable necrotic or fibrous areas. In one place one appears to lie within the lumen of a blood vessel. No fibroses or special congestions found anywhere in the organ and cells show normal details and normal numbers of vacuoles.”

A California hair seal (Zalophus californianus) which had been refusing food and having loose stools for about ten days presented after death the following diagnosis: Hypernephroma of adrenal, chronic hypertrophic enteritis with acute exacerbation, hemorrhagic splenitis, passive congestion of liver, congestion and edema of lungs with catarrhal pneumonia, acute fibrinous pericarditis, chronic lymphadenitis, chronic interstitial nephritis. His right adrenal seemed about normal, being 5 × 2 × 1 cm. with a narrow, dull yellow cortex and a large mottled gray-brown medulla. The left one was 5 × 3 × 1 cm. The upper pole is swollen and contains in its centre a spherical tumefaction which is red, mottled, sharply outlined, with a suggestion of a capsule and slightly firmer than surrounding organ. “Histological section shows a capsule of very noticeable thickness but possibly not much in excess of normal. The cortex particularly in its deeper layers is much injected and in some places there has been hemorrhagic diffusion. In many places in the zona fasciculata, more especially near the periphery, there is breaking up of the cell tubes with an infiltration of large round cells and some chromatophilic cells. In other places this seems to have gone on to fibrous tissue increase and necrosis of the cortical fibrous cell types. The connective tissue layer below the cortex is wide and the spaces filled with blood. This connective tissue also surrounds islets of medullary cells which are not specially chromatophilic. The mass in the medulla is made up of varying sized alveoli surrounded by rather rare, highly vascularized connective tissue and enclosing islets of medullary cells. These alveoli may be subdivided by septa. Hemorrhage has occurred into many of them. The individual cell masses are made up of groups of rather large cells with illy defined margin, a granular, opaque but not vacuolated protoplasm. They have a bladder-like nucleus in which the centrosome is large and prominent. Definite mitotic figures could not be found, but mitosis is probably present. A few cells with double nuclei were seen and one with four. In many of these large islands the centre has gone to pieces from hemorrhage or necrosis. Some of the vessels are thrombotic and one shows a very pronounced periarteritis.” A brown cebus (Cebus fatuellus) was killed because of a poor tuberculin test chart. His organs were negative except the right adrenal body which was 3 × 1.5 cm., or four times the size of its fellow. It was a tense body with a smooth, mottled, deep yellow surface. On section there were deep yellow islands separated by pale brownish septa; the structure did not resemble adrenal. Histological section showed a hypernephroma of vacuolated cell type, roughly alveolar. Two other cases, which because of their microanatomy are to be called hypernephroma can be added to those just cited. One occurred in an undulated grass parrakeet (Melopsittacus undulatus), the other in a black duck (Anas obscura). As illustrative of this tumor the former will be cited in brief. “Hypernephroma of adrenal with hemorrhage into body cavity. A tumor approximating in size the head of the host extends from the region of the internal genitalia and adrenals lying more on the right than on the left side extending fully to cloaca and shoving all abdominal viscera forward. It has a pedicle springing from between the two upper lobes of the kidney where adrenals and internal genitalia are not distinguishable. Tumor is coarsely lobulated, well encapsulated, nowhere adherent. It has a pale, dirty yellow color, richly marked by red lines of congested vessels. It is fairly soft, i.e., about consistency of normal liver. Upon incising, the cut surface bulges markedly, is a dirty gray-yellow, blotched with darker gray areas, shows no internal hemorrhages or markings of special import. No metastases noted to any other organ. Microscopic section shows a light capsule surrounding the tissue of the tumor. The latter has a very scanty fibrous reticular framework showing no orderly or purposeful arrangement. Upon and between the reticulum, irregular and for the most part elongated collections of cells are placed. At times these present an elongated fascicular form, but this is not by any means a prominent feature. The cells themselves are large, rounded or polygonal, have coarsely granular cytoplasm which only in rare cases contains vacuoles. Nuclei of these cells stain very poorly, but it can be made out that they are of large epithelial type and of vacuolar appearance.”

A somewhat unusual tumor was encountered in a Polar bear (Ursus maritimus), an adenocarcinoma of the adrenal, when judged purely by its histology but a secondary tumor in the lung displayed the more familiar picture of large vacuolated cells as seen in hypernephroma. The diagnosis follows: “Scirrhous adenocarcinoma of adrenals, secondary carcinoma of lymph glands, secondary hypernephroma of lung, secondary carcinoma of diaphragm, acute mucopurulent bronchitis, acute catarrhal enteritis, chronic diffuse fibrous cholecystitis, cholelithiasis, slight acute interstitial pancreatitis, follicular hyperplasia of spleen with fibrosis, hydrothorax, hydropericardium, chronic hypertrophic osteoperiostitis, encysted trichina in diaphragm, fatty infiltration of diaphragm, chronic diffuse nephritis, chronic productive lymphadenitis, pigmentation of lymph gland. Both adrenals are smaller than normal, of woodeny consistency, the pale cortex and medulla are poorly separated from each other. The cut surface shows gray white and tawny mottling and occasional calcareous points. Histological section shows an extra capsule of fibrous tissue containing highly distended veins; the lining contains masses of tumor cells, many of which are necrotic. It is distinctly denser in type than normal and more abundant in places showing a proceeding fibrosis. Parenchyma shows but few irregular islands containing non-neoplastic cells, some of which are highly vacuolated, others are not. Interstitial tissues in peripheral parts are often grown together with the deeper portion where are intermixed tumor areas. The latter consist of small round acini of variable size lined by cells of active type. Nuclei are large and hyperchromatic, cytoplasm broad and disintegrating. Parts show necrosis and hemorrhage. Upon search transitionals from non-neoplastic to neoplastic cells can be discovered in same fasciculus.”

SECTION XII THE SKELETON AND ITS JOINTS

The bones with their articulations have been the subject of extensive study and research by zoologists in the direction of classification and evolution. Adaptation of the osseous construction to the needs of the animal is well appreciated biological knowledge. For example, the keel of the sternum in birds affords broad origins for the flying muscles, the pectorals, which also insert on the alæ of this bone and on the clavicle, and in addition use these latter formations as fulcra. So too the extremities of quadrupeds are angular in their upper two segments for the purpose of supplying a direct action of the flexors employed in running and leaping. The thick masseter muscle of carnivores is accommodated in the deep zygomatic fossa. Many other examples might be cited, but these serve to direct attention to the adaptation of function and construction. Pathological changes in our materials are however too few to permit conclusions as to possible relation of zoological position and development except such as may refer to deformity incident to the degenerative processes—rickets, osteomalacia and osteogenesis imperfecta, and in these conditions the alterations are merely passive accommodations to weakened support in order to obtain comfort. To put the matter in other words, it would seem that, aside from the diseases just named, there is no outstanding change in the skeletal tissues peculiar to zoological orders that might indicate vulnerability of the system or the methods of response to injury or disease.

EFFECTS OF TRAUMA.

There must be considerable reserve or reconstructive power in the bones of animals since it is a common thing at autopsy to see unmistakable evidences of repair of fractures, dislocations and inflammations. Some illustrations are introduced to exemplify this healing ability, one of which was found in an animal shot by a hunter, the other an incidental autopsy discovery. Even though there be no definite relationship between the zoological order and osseous disease, it is interesting to record a very simple observation. Animals with long extremities, especially when the bones are quite near the skin, have a rather high incidence of fractures and inflammations. Thus the ungulates have of all orders the highest percentage of these traumatic and infective lesions; herons and gallinaceous birds follow the ungulates. Marsupials, primates and carnivores, in this order, are susceptible to inflammations but not to fractures. Bones are often broken, among the Cervidæ, Bovidæ and Camelidæ, when as they are chased by mates, they fall upon the slippery floor of the cages; or again the mounting of a small animal by a large buck may crush the former to the earth. Two cases of fractured pelvis have been seen in antelopes from a fall with extended hind legs.

It would seem that repair is usually satisfactory if the animal has a quiet retreat where callus may form and union occur. A heron is known to have broken both bones of the leg; at autopsy a very insignificant circumferential callus remained, the member being as straight and strong as normal. Figure 40 shows the femur of a deer shot by a hunter; the shortening was considerable, but function was doubtless good because the hunter could perceive no limping as the animal ran. The most interesting fracture among our records was an intracapsular fracture of the hip in a Huanaco (Lama huanacos) shown in Figure 41. This animal slipped on the ice in December and was thought to have broken something near the hip, but it limped around without any great show of pain until the following May, when it died of meningitis secondary to an otitis media et interna. At autopsy an unhealed, complete fracture of the neck of the right femur was found, apparently separating the head from the neck, the former being dislocated to the upper angle of the obturator foramen. Everywhere about the joint callus had been thrown out, but not in a manner to effect a junction of the broken ends nor to seal the edge of the acetabulum to the femoral neck. This was probably due in part to the irregularity of the line of fracture and to the interposition of the upper part of the dislocated head between the lower rim of the acetabulum and the surgical neck of the bone. When the specimen was fresh traces of capsule were found over the upper half of the acetabulum. While it is usually difficult to decide the manner in which these injuries effect their damage and deformity, it might be ventured to explain this case as due to extreme posterolateral extension of the leg driving the head of the femur downward and inward, rupturing the capsule and the ligament bridging the acetabular notch, to rest on the pubis at the upper edge of the obturator foramen where it could find a sort of joint cavity made by the pubic and ischial segments of the old acetabulum, but about an inch and a half below its normal location.

Another injury to the hip joint was noted in a Livingstone’s eland (Taurotragus oryx livingstonii). This beast was not positively known to have fallen, although it was suspected that such an accident had occurred by reason of sudden inability to rise. At autopsy, death having succeeded on signs of shock, a complete upward and backward dislocation of the right femoral head was found; there was also an intracapsular rupture of the left round ligament, but on this side the femoral head had not left the acetabular cavity.

Many other fractures have been observed but generally without interesting features. The conclusions which may be drawn from our experience are that animals with long bones, and liable to chase have the greatest liability to fractures, and that the healthy beast, given seclusion and quietude, possesses great ability to heal its broken bones. Pathological fractures are occasionally seen. (Consult notes on cretin wolves.)

Before entering upon a discussion of the most important of osseous lesions, rickets and osteomalacia, certain inflammatory states may be appropriately described.

INFLAMMATIONS.

Hypertrophic osteoperiosteitis: A male lion (Felis leo) at the Garden three years died, after being out of condition for a long time, from chronic ulcerative pulmonary tuberculosis with terminal pneumonia, nephritis and enteritis. Both hind feet had been observed as enlarged and apparently painful for some weeks before death. Upon dissection the bones of both hind feet are the seat of extensive hypertrophy, and the periosseous fibrous tissues are thickened. A large mass about the size of a small orange lies attached to the outer side of each ankle. The hypertrophic periosteitis extends up the tibia a distance of about three inches and the fibula for about the same distance. These two bones are adherent to each other for about 1½ inches. The joint between them and the tarsal bones is apparently perfectly free. The calcaneum is the bone most severely involved; on this is a large rounded mass which extends on the bone for a distance of about 2½ inches. The small bones of the foot are more or less severely involved but are not bound together, the joints being practically free. The terminal and next phalanges are entirely free from disease while the metatarsals are severely involved and grown together into one large mass. On section this appears as a mass of spongy bone lying on top of the cortex. In the dried specimen this looks very like old pumice stone. Histological section shows the periosteum raised from the bone by mononuclear infiltration. The bone marrow spaces are filled by a very delicate gelatinous material. The lamellæ are thickened. A photograph of the foot with a normal example is given. (Fig. 42.) (See also Tuberculosis section—Carnivora.)

A cockatoo died from acute miliary tuberculosis; the upper thoracic and lower cervical vertebræ are involved in an S-shaped scoliosis which reduces the height of the thorax by perhaps a centimetre. Thorough dissection was not made, the trunk being kept as a museum specimen and for study in event another avian scoliosis occurred; but from palpation, separation of the muscles and stretching of the spinal column it does not appear that a tuberculous osteitis of the vertebra existed. It seems that this may be due to congenital deformity or old injury.

A white-nosed coati (Nasua narica) suffered with generalized tuberculosis which also affected the wrist joint with a caseous and ulcerative arthritis.

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.

Osteitis deformans is a chronic constitutional affection characterized by the absorption of compact bone, chiefly in the cranium and long bones, and the laying down of fibro-osteoid tissue in such an excess as to enlarge the affected bones. This material, which is soft and cuts with reasonable ease, has calcareous matter in it as shown by Röntgen- ray examination. Paget described it in a classical article in 1876[48] since which time the reported cases have mounted to three hundred and fifty. Because it has only been recognized in its best developed stages, it may be that early mild or arrested cases have been overlooked. Judging by the instances claimed to have been found in museum collections of bones, it is probably an affection dating to antiquity. So far these remarks apply only to man but in lower animals the reports are very few and those are not available in the original. The abstracts and references show considerable confusion. The names osteitis deformans, osteoporosis, osteitis fibrocystica, osteodystrophia deformans and osteosarcoma, leontiasis ossei, etc., are used almost interchangeably. In 1901 Barthelemy[49] described a condition (Maladie du Son) in horses in which there was a marked enlargement of the head and of the epiphyses of the long bones. His cases were more allied to osteitis fibrosa cystica. Paget’s disease always attacks the diaphyses of the bones and not the epiphyses. Goldman[50] described typical examples of this condition in fowls. Jöst[51], in one communication, described a case in a horse which he says was identical with that condition described by Paget as osteitis deformans and by Virchow as leontiasis ossei; he also refers to similar cases in goats and monkeys. Rossweg[52] found it in goats. In wild animals the only suggestive article found was by Jöst but the description was probably of an osteoporosis and a craniosclerosis which occurred in a young lion and a monkey. All the communications deal with either domesticated animals or those in captivity.

The etiology of this condition is as obscure to-day as it was at the time of Paget’s first description. Prince thought it might be due to a defect in some peripheral nerve or nerve centre or to a tract degeneration. Cases have been reported in conjunction with a myelitis. There has been however little on which to base these suppositions. Paget felt that the process was at least upon an inflammatory basis and deduced this from the enlargement and the excessive production of an imperfectly developed structure with increased blood supply. Many felt that rickets, osteomalacia and osteitis deformans were all manifestations of the same disease. A bacterial cause was proposed by Arcangelli who claimed the discovery of diplococci and improvement from a vaccine. Lancereaux[53] and Richards felt that focal infection played a profound rôle in the etiology. However all other observers fail to isolate an organism from the bones or to get improvement from removal of infectious foci. Heredity has been held responsible in seven per cent. of the cases in human beings.

That some inflammatory factor is partly responsible seems plausible when one considers the active growth of fibrocellular tissue in the endo- and periosteum. The more interesting theories go back to perversions of internal secretions, pituitary, parathyroid etc., (Macallum & Vogtlein). Higbee and Ellis[54] say in relation to the neurotrophic theory that if the neurotrophic mechanism governs metabolism and is influenced by the activity of the ductless glands, there is considerable likelihood that its disturbance may possibly be found to be the cause.

Da Costa[55] believed the disease to be a disorder of bone metabolism probably dependent on the absence or perversion of some internal secretion. There is much evidence on hand to indicate that disorders of the ductless glands do influence bone metabolism, and changes in these glands have been reported in cases of Paget’s disease, although the findings and lesions have been far from uniform or distinctive or even confined to one gland. Eight cases were reported as possibly due to a hypothyroid condition; pituitary changes were found in three; adrenal changes in one; parathyroid reported missing in two; three had sclerotic thyroids. Many case reports make no mention whatever of the glands of internal secretion.

Da Costa interprets the retention of calcium, phosphorus and magnesium, with the sulphur loss found in these cases, as indicating a stimulated osseous or osseoid formation accompanying the resorption of a highly sulphurized organic matrix. In the course of this calcification procedure we suppose a certain quota of the sulphur of the matrix is replaced by other elements, a process which must entail retention of calcium, phosphorus and magnesium and increased elimination of sulphur. He shows the close parallelism between the mineral metabolism of a growing boy, a case after parathyroidectomy and a case of osteitis deformans, and suggests that this depends in some way either on the absence or perversion of some internal secretion, possibly of the parathyroids, which controls calcium exchange in the body. Substances from some cause arise which have the power to abstract calcium from the body tissues, the abstraction of these salts being the first step in the production of the disease.

The example which is reported in full was the first to be encountered in our 5,365 autopsies but shortly after this series was concluded two more came to autopsy and Dr. Corson-White’s studies were made to embrace these.

A reddish woolly monkey (Lagothrix infumatus) received November 25, 1919, was a particularly active specimen and as far as we could determine a perfectly healthy adult animal. He passed the tuberculin test and was placed on exhibition. In April, 1920, he was first reported as crippled and was removed to the laboratory in June, 1920. At that time the long bones of the legs and arms were bowed anteriorly and laterally, the degree of curvature making the hands and feet seem disconnected. The monkey could stand but made no voluntary effort to do so. There was evidently some pain although it could not have been at all severe. He resented handling, especially of his arms and legs. The head was rounded, resembling that of a baby, and the eyes were protuberant suggesting an exophthalmos. The maxillary bones were so excessively thick that the mouth could not close and the monkey drooled saliva. His blood on admission to the infirmary in May was—Hg eighty-nine per cent., R. B. C. 4,370,000, W. B. C. 5,800; one week before death it was Hg fifty-four per cent., R. B. C. 2,860,000, W. B. C. 6,000. Routine urine examination showed a constant trace of albumin, hyaline and granular casts. There was at no time a Bence-Jones protein reaction, excess of indican, indol, or diacetic acid. He had a constant slight diarrhœa with some flatulence, the semifluid, constantly acid feces presenting a preponderance of Gram-positive coccoid organisms. His appetite was fair and he showed marked craving for lime, eating plaster from the walls when he could get it. Because of this desire for lime he was given a salt mixture to see if it would have any effect on the bone condition. The mixture used was the following:

NaCl 0.874 grams KCl 0.548 grams CaH(PO) H_{2}O 3.608 grams Ca lactate 0.386 grams Mg citrate 0.848 grams K citrate 1.953 grams

This mixture the animal ate with avidity and seemed more comfortable; other than that no change was noted.

An inorganic metabolism examination was attempted on the ordinary diet and the diet plus the salt mixture. Under the circumstances at our disposal this was not entirely accurate but showed such marked variation from the control animals examined—normal and osteomalacic—and such marked correspondence on the four separate four-day periods of each intake that it seemed acceptable. The result of this investigation on the first series of four four-day periods was:

═══════════╤═════════╤═══════════════════╤═════════════════════════════ │ Intake │ Output │ Total ───────────┼─────────┼─────────┬─────────┼───────────────────────────── „ │ „ │ Feces │ Urine │ „ ───────────┼─────────┼─────────┼─────────┼───────────────────────────── Calcium │0.0280 │0.014 │0.0022 │0.0162 = 0.0118 retention Magnesium │0.0640 │0.034 │0.0123 │0.0463 = 0.0177 retention Phosphorus │0.1540 │0.027 │0.0430 │0.07 = 0.084 retention Sulphur │0.1440 │0.002 │0.1680 │0.17 = 0.026 loss ───────────┴─────────┴─────────┴─────────┴─────────────────────────────

The result on the higher salt content was practically the same, the retention being in proportion slightly less. The diet for these small monkeys is two apples, two bananas, six small sweet potatoes, with a lump of boiled rice about the size of an egg. The content of this diet has been found very low in calcium, phosphorus, sodium, chlorine and iron, while potassium, magnesium and sulphur were high. To this diet lime water was added to increase its inorganic content.

This Reddish Woolly Monkey died August 20, 1920, and was immediately posted. There was marked thickening of the frontal, occipital and parietal bones, upper and lower jaws. The increase in the size of the alveolar margins prevented the closing of the mouth; only the last four teeth could be brought into apposition. The enlargement of the mandibles reduced the capacity of the mouth cavity. The skull while decidedly thickened did not enlarge at the expense of the cranial cavity. There was a cervical and dorsal kyphosis. The chest was increased anteroposteriorly and contracted laterally. The long bones were thick, bulky and deformed. (Fig. 46.)

A Black Spider Monkey (Ateles ater) showed a general hyperplasia of the whole shaft of the long bones. She was much deformed by curvatures and swellings of the skeleton—head enlarged, face deformed by the swelling of the upper and lower alveolar processes, jaws do not close and the palatal bones were flattened, skull irregularly thickened, elastic but not soft, slight subperiosteal growth. Thickening of the long bones was largely due to subperiosteal growth; section of the ulna showed a subperiosteal osseoid layer surrounding the old shaft. This tissue seemed to be very poor in lime salts, cutting without any grit. Marrow cavity was filled with a fairly firm, deep red marrow which did not bleed on section. The third monkey, a Brown cebus (Cebus fatuellus) showed exactly the same general picture but was less severely affected than the other two.

“The more minute study of the bones of these monkeys shows a variety of pictures while preserving one general form. The skull was smooth, mottled by irregularly placed areas of congestion; it was asymmetrically thickened; differentiation between cortex and diploe, internal and external tables was lost; calcareous matter was absorbed and the resultant bone was soft, elastic and porous; lacunæ enlarged and lined with bone corpuscles and giant cells. Other areas show more dense bone, the reparative processes being more active in that the lamellæ are wide and the vascular spaces narrower. As a rule the compact bone is absorbed, the Haversian canals are more or less confluent and there is generally a marked increase of newly formed osseoid tissue. The ossifying periosteitis obliterates the depressions for the cranial arteries and the sutures. The skull cap becomes finely porous, cancellous and even cavernous. The spaces are filled with a soft, red marrow-like material. The bones at the base of the skull are much less involved; the pericranium, dura and brain are normal.

“The long bones show interlacing narrow strands which are in some regions wide, in others narrow or thin as in spongy bone. Large irregular cavities are present and there is a disappearance of the compact bone and an encroachment on the medullary canal of a relatively dense new bone with small irregular trabeculæ surrounded by osteoblasts and a fibrous connective tissue which fills the outer trabecular spaces. The new bone is often both subperiosteal and subendosteal, the latter often gaining on the former. It is always soft and irregularly calcified. The general arrangement of the strands in the deep layers is longitudinal but in the subperiosteal bone they are very irregular and almost at right angles with the central strands. In this new osseoid tissue cysts are frequent, varying in size from very small to rather large cavities filled with a cloudy gelatinous material. The picture here is very like osteitis fibrosa cystica. Endosteal cells proliferate and may fill up the marrow spaces so that solid masses of fibrous tissue result. Frequently the osteoid material shows fibrillæ. The compact bone may be irregular with well marked Haversian systems. Toward the periosteum the cells may become scanty, the bone dense in structure while toward the interior the cells are more numerous and in the more cancellous portions, the trabeculæ become slender and far apart; here they may be covered by a single row of osteoblastic cells. The intertrabecular spaces are large, irregular and filled with a delicate alveolar tissue containing only a minimal number of normal bone marrow cells, large capillaries and no giant cells. Periosteum may be of usual thickness; the bone immediately beneath is spongy. The sclerosis of the bone in its densest areas is entirely due to the ossification of spindle cells which have remained in the place of the original marrow of the bone. As a whole the bone is nowhere normal in amount or proportion but the small Haversian systems are properly made, the abnormality being chiefly due to cellular and fibrous growth around the large lamellæ which at times is normal in amount but usually much in excess. In places this consists wholly of fibroblasts, at others of giant and round cells very suggestive of sarcoma. All histologists apparently agree that Paget’s disease starts as a resorption of already calcified bone.”

These data seem to supply ample evidence that the autopsy diagnosis of Paget’s osteitis deformans was correct. While the anatomy and course and chemical changes presented by these monkeys do not settle the causation of the disease, they offer very definite suggestions which Dr. Corson- White summarizes in the following cautious conclusions.

“Many of the cases of Paget’s disease first came under the observation for fractures, accidents common in osteomalacia but very rare in developed cases of osteitis deformans. Early cases all presented diarrhœa, which was present in all the early human cases seen, and in all the cases reported in monkeys. This symptom was mentioned in fourteen of the cases from the literature. It was also a constant symptom in primate osteomalacia. The diet of these monkeys was exceedingly low in those substances essential to bone development, and Sherman has shown that the calcium balance is regulated to a certain extent by the calcium ingested, and that when the diet was poor in this element, the output materially exceeds the intake, a fact which is immediately changed where the animal is put on a diet high in calcium. So far as we could find there are no studies on the mineral metabolism of beginning cases of Paget’s disease. It seems possible from the osteomalacic animals previously studied, that the low mineral and otherwise faulty content of the diet might so disturb the chemical equilibrium directly, through the neurotrophic mechanism or through the perversion of the ductless glands, that the mere addition of lime water might entirely change the pathological picture. This is in accord with the histology. The initial histological picture is always resorption of bone, a general decalcification which later presents an irregular proliferation. The disease then progresses along different lines ending as osteitis fibrosa cystica, Paget’s or Von Recklinghausen’s diseases, etc., dependent upon the strength of the reparative stimulus and the organism upon which it acts.

“These cases are of interest (1) because they are typical examples of Paget’s disease as it has been described in man both clinically and pathologically, (2) because the disease shows the same general type of inorganic metabolism that was exhibited in man, (3) because of the alkali hunger shown by one monkey, and by two human cases, a hunger which was severe, which preceded the deformity and disappeared after the deformity was established, (4) because the disease developed in animals fed on a diet insufficient in its inorganic and vitamine content to which an excess of calcium was added.

“From this study it seems possible that Paget’s disease may be just one stage in a deficiency disease, a reparative response through a neurotrophic mechanism or through the perversion of the glands governing calcium metabolism which has been perverted by an improperly balanced diet.”

TUMORS.

Neoplastic diseases of the bones have yet to be classified to everyone’s satisfaction. All gradations of hyperplasia of osteogenetic cells and fibres and of the marrow elements, from simple inflammation to true sarcoma, are recognized. As one reviews a large series of lesions, clearly defined types may be found, but there are transition stages to which an exact name is difficult or impossible to apply. Nor does the pathological diagnosis always fit with the clinical course. Thus, for example, the giant cell tumor of bones looks malignant, and is not, and its structure may be simulated in such diseases as fibrous osteitis and Paget’s disease. As we have seen in the discussion of the latter of these two, abnormalities of fibre and cell growth simulate neoplasms very closely. In addition it might be mentioned here that actinomycosis may produce bony growths resembling sarcoma. When osteitis deformans affects the facial bones especially, it has been called leontiasis ossium, and it is then a more nodular, tumor-forming process, the enlargement consisting of fleshy masses occupying the whole bone, but especially the marrow cavity. Histologically the lesion is fibrocellular, frequently with numerous giant cells; accumulations of small sarcoma-like alveoli may be found. We have encountered four cases among common opossums (Didelphys virginiana) and one in an Isabelline Gazelle (Gazella isabella) and, because of the localization and fleshy consistency of the tumor, we have called them osteosarcomata for descriptive purpose, but not for classification among neoplasms (where they will not be found). Two of the opossums had osteoporosis and gelatinous marrow in the ribs. All these animals had been in the exhibition under a year, and as far as known are not related. Figure 47 shows the gross character, while the following is the description from one protocol.

Common Opossum (Didelphys virginiana) ♀ . Osteosarcoma of alveolus, rarefying osteitis deformans of skull, hypertrophy of thyroid, acute catarrhal enteritis, acute hyperplasia of spleen. About the middle of both lower rami and involving the posterior half of each upper maxilla is a uniform elliptical growth apparently emanating from alveolus. Teeth not loose, but can be moved in tumor to be described. On section a white glistening homogeneous growth is seen apparently originating in the body of the alveolus and around the teeth. The shaft of bone is soft and easily broken. What remains of marrow is irregularly injected. In upper jaw there is a distinct porosis of facial bones; they and the enclosed sinuses are deeply injected. Lower four ribs on both sides show distinct nodulations of pale color along a bluish bone. All ribs are very soft and section shows osteoporosis of shaft with injected marrow and distinct cartilaginous periosteal bone formation. The skull is everywhere soft and the bone is apparently increased in thickness, rich in blood, but porotic. Rest of skeleton seems well calcified. Microscopic section of tumor shows practically the same picture. Bone is nowhere normal in amount and proportion but the Haversian systems seem properly made, the abnormality consisting chiefly of cellular and fibrous growth around larger lamellæ, which at times is normal in amount but usually much in excess. In places this consists wholly of fibroblasts, at others of giant and round cells very suggestive of sarcoma; indeed all areas must be called giant cell sarcoma. There is an attempt to lay down osteoid tissue at places particularly beneath periosteum. The giant cells are in great numbers and some seem osteoclastic. As the lamellæ disappear young connective tissue seems to take their place but giant cells do not remain numerous at such places. Despite its atypical nature it must probably be looked upon as an osteosarcoma. The tooth socket is not much involved save for hyalinization of root matrix immediately about dentinal zone.

In another Isabelline Gazelle (Gazella isabella) there was a fibro- osteoma localized to one side of the superior maxilla (Fig. 48); this has been included among the tumors, while the above mentioned cases have not been so grouped.

True osteosarcoma seems not to have occurred. One tumor was seen upon the wing of a Cuvier’s Toucan (Rhamphastos cuvieri) which was formerly diagnosed as sarcoma, but later examination reveals some giant cells in arrangement suggestive of tuberculous osteitis; since this is the only case and not unequivocally a tumor its record is hardly warranted. Osteomata of the hard variety have been seen on the ribs of a pigeon and a pheasant as small rounded compact well outlined tumors. It is thought that they represent products of healing after osteomalacia or rickets. An osteochondroma growing from the nasal cartilage was found in a caracal (Felis caracal), a fibro-osteoma was found on the vertebra and clavicle of a Beechy’s spermophile (Citellus grammurus beecheyi) and a fibroma occurred on the clavicle of a lesser snow goose (Chen hyperboreus hyperboreus). The only other tumor from a bone was an endothelioma from the periosteum of the clavicle in a moorhen (Gallinula chloropus). It corresponds to the usual idea of this tumor. It probably caused death by cachexia, and by its size, interference with respiration. The only secondary tumor was a metastasis in the tibia from a spindle cell sarcoma of the kidney in a scaly ground dove (Scardapella squamosa).

THE MUSCLES.

The skeletal muscles of the wild animals of our collection have been quite free of pathological lesions such as atrophies and dystrophies and indeed seem relatively seldom affected by disease. Occasionally hyalinization will accompany infectious disease or local suppurations will spread into the muscles. Much more often filaria, sarcocystis, flukes and larval insects will be found resident within or between muscle bundles; this will be discussed at a later time. Six tumors have been found, three of which certainly developed in a muscle, while for a fourth case no primary growth was discovered. This last one, to dispose of it at once because of its peculiarity, was an adenocarcinoma found as a firm, conglomerate, encapsulated mass in the sheath of the gluteal muscles of a waltzing mouse (Mus wagneri rotans). No other growth was discovered although it must be admitted the body was not exhaustively searched for some tiny nodule to which primary focus this muscle mass could have been secondary. That metastases may be larger than original growths is well known. The gross diagnosis was sarcoma. If this be an original tumor it might be explained as arising from ectopic mammary tissue.

The five other tumors were sarcomata, one of large cells almost syncytial in size, shape and number of nuclei, two definite spindle cell growths and two of fibrosarcoma type. The first occurred in an all green parrakeet (Brotogerys tirica), the second in an undulated grass parrakeet (Melopsittacus undulatus), the third in a larger Egyptian gerbille (Gerbillus pyramidum), the fourth in a white-footed mouse (Peromyscus leucopus), and the last in a bean goose (Anser fabalis).

SECTION XIII THE CENTRAL NERVOUS SYSTEM AND THE SPECIAL SENSES

Diseases of this system and its specialized end organs of sense in the eye, ear and nose are recognized by veterinarians as occurring among domesticated animals, in which however they are by no means so common as in human beings. Because of the natural reserve of wild beasts and because their habits and manners are not so familiar to the observer, it would seem that clinical evidences of disease of the nervous system are rarest among them. The brain, cord and nerves of our specimens have not been studied with the minuteness accorded to the examination of other viscera since we have not had the personnel to devote the time to this really colossal undertaking, our work with these tissues being directed toward the accumulation and preservation of apparently normal brains from every species; there are now some nine hundred brains on the shelves. However, whenever the history of the animal before death has suggested that disturbance in the nerve organs might exist, they have been dissected grossly and examined microscopically. Had we subjected all our material to microscopic study it is quite possible that we might have discovered more lesions. This is still possible by reason of our gross material and autopsy protocols.

We have been fortunate in having Dr. W. B. Cadwalader, Secretary of the Society, and Dr. J. H. W. Rhein with their broad experience in neurology, take interest in this phase of the subject and study our material. The number of cases in which definite lesions have been found is surprisingly small, so that no generalizations can be attempted except perhaps in a negative sense. After the study of thirty-nine brains and cords from animals in whose history some suggestion of nervous system disease existed, Doctor Cadwalader could find abnormalities in only twenty-two cases, mostly however of a very indefinite character. This observer further points out that in his experience with our material, his observations of our animals and a review of the literature, he is unable to find satisfactory instances of the so-called system or tract diseases such as tabes and lateral sclerosis. This he suggests is due to the absence of arterial sclerosis in the lower types of brain, intimating further that perhaps the relation of syphilis to human arteriosclerosis and degenerative nervous system disease is thereby strengthened. These facts being true it is not astonishing that massive cerebral apoplexy and cerebral softening do not occur[56]. The lesions that have been found were either definitely infectious, as encephalitis or acute septicemia, tuberculosis, poliomyelitis, meningitis, or the minute hemorrhages and vague granularities or vacuolizations of nerve cells in toxemic conditions. The material being limited and broad statements being impossible, the important cases will be cited individually or in small groups.

CONVULSIONS.

Before entering upon the special subjects, a word might be added concerning the clinical evidences of neurologic conditions as seen in the Garden. Perhaps the most common and certainly the most definite clinical sign of nervous disturbance is the convulsion. General spasms or fits are fairly common among the carnivores and monkeys, in the former most often associated with intestinal parasitism, in the latter with no especial relationship unless it be renal disease. The convulsions have been general, with and without the preservation of consciousness. No cases of focal or Jacksonian spasms are recorded although we shall cite two instances of tuberculoma reasonably near the motor area in the cerebrum. The exact cause of many cases cannot be set down since intracranial disease does not often exist.

Intoxication from chemical products of disturbed digestion or from worms themselves is the usual explanation of spasms associated with intestinal parasitism; if this be true, intoxication in the absence of demonstrable parasites may also be the cause in certain cases of enteritis. However we have seen fits when enteritis, parasites and renal disease were not found. If these were true epilepsy, they are instances of perhaps the rarest disease of animals, which I do not presume to diagnose.

Convulsive seizures in herbivorous animals are exceedingly rare although I have seen clonic movements of a spasmodic character in antelopes and deer shortly before death from gastroenteritis. Ataxia and incoördination are much more common. Birds, notably parrots and soft- billed insectivorous varieties, are not uncommonly afflicted with fits but as they are rarely observed except by the keeper the exact nature is difficult to describe. Those seen by the writer have been of two kinds.

The first and more common consists of falling from the perch in a dazed and stiff condition, with dilated fixed eyes, stiffened and spread-out legs and wings. Recovery follows shortly and the bird resumes its perch either in excitement, or slowly and uncertainly, perhaps to have another attack in a few minutes. These cases, in the few instances in which they could be followed, were due to faulty feeding and enteritis and showed either nothing or a mild congestion of the brain. The other variety of fit is epileptiform, a rapidly developing clonic spasm of all parts of the body with a tendency to opisthotonos. In one case of this character, a parrot, no lesions were found in the brain, an enteritis existing however. Another case concerned a pet Indian Shama I had at my home. He had been doing well and singing loudly, until one evening he was allowed to remain in a tobacco-smoke-filled room whereupon next morning he stopped eating and singing. Later that day the clonic form of convulsions appeared, growing worse for thirty-six hours or until death. At autopsy no food was found in the alimentary tract. The brain and cord were congested grossly, while minutely, perivascular hemorrhages and marked vacuolization and diffuseness of staining were found in ganglion cells of the bulb, pons, anterior spinal horns and in the pyramidal cells of the cerebellum. Happening so promptly after exposure to tobacco smoke, when the bird was doing well, I venture to associate the two.

ATAXIA.

Incoördination and ataxia are so often observed and under so many conditions that it is well nigh impossible in any individual case to give an adequate explanation before death. They are in all probability the expression of sickness and nothing more in the vast majority of instances. When they are observed in such cases as the tyromata of the cerebrum or in certain of the ungulates, they may mean something definite. In this latter order and to a less extent in carnivores, one frequently sees weakness and uncertainty of gait in the hind quarters, the legs being usually coördinate but tending to give way under the weight of the body.

From a study of veterinary literature and our own material it would seem that this may have many explanations. In the first place, it may simply indicate weakness expressing itself in the heaviest part of the body, the animal inclining its femora forward to assist in supporting the heavy abdomen. It may be an expression of abdominal pain, the recti becoming rigid and the quadriceps of the thigh participating in the protection of the belly. Almost any of the intra-abdominal conditions, gastroenteritis, mesenteric thrombosis, peritonitis, or diseases of the psoas muscle and lumbar vertebra, might occasion this attempt at support. Disease of gluteal muscles, as hemoglobinuric fever, may produce a palsy of the whole pelvic girdle with weakness of the hind legs. There may be associated with the weakness of the hind legs a humped-up condition of the lumbar spine and retraction of the abdomen, sometimes called “tucked in;” in two definite cases of this last sort we have found renal pelvic stones and once intestinal sand. Some instances are undoubtedly due to meningomyelitis or to poliomyelitis and at the place for this subject a few cases will be discussed. Meningitis has not been found in the ungulates showing this weakness. There have been however cases of ataxia in the hind legs of deer and antelopes, which did not have a ready explanation fitting in with the foregoing. Two of these we thought might be due to certain grasses in the enclosures and have changed the exhibition spaces. No conclusion can be drawn from this as yet. No enterocolic disease could be found nor any lesion of the sciatic nerve and lumbar enlargement of the cord. We have however discovered sciatic neuritis in a case like hemoglobinuric fever in a Burchell’s zebra. The history of the animal is similar to that of this disease in domestic animals in so far as symptomatology is concerned; in so far as confinement in a stall is concerned no data is at hand but death occurred on December 26th in the zebra house whereas he had been accustomed to go out into the yard all summer and autumn.

MENINGITIS.

The coverings of the brain and cord have not been the seat of the well known acute inflammations seen in domestic horses and cattle. Eleven instances of disease in the meninges are recorded but, with very few exceptions, have been accompanied by other lesions offering a ready etiological explanation. These cases are however not very instructive except perhaps three in monkeys where the meningitis seemed to be secondary to gastroenterocolitis. In one case a colon bacillus was apparently responsible, in a second no bacteriology was undertaken and a third was too rotten for the results to be dependable. A focus of infection aside from the intestinal area could not be found. The only noteworthy finding was the scantiness of the cerebrospinal fluid and the almost exclusive subpial exudate; these facts would seem to strengthen the thought that the virus came through the blood stream. Another case was due to extension, through the temporal bone to the lateral sinus, of a necrotizing process beginning in the buccal muscles or parotid gland; the necrosis bacillus and a host of Gram-positive cocci were found. A Canadian porcupine suffered with a mucopurulent nasopharyngitis which involved the deep sinuses, the middle ear and the temporal bone; smears from the pus over the corresponding cerebral hemisphere and from the nasal pus showed pneumococcus forms; the lungs were not affected. The llama which showed the intracapsular fracture of the femur (page 344) had also hemorrhage into a fibrinous exudate in the mastoid cells with deep opaque congestion and edema of the pia above the petrous portion of the temporal bone. Decomposition precluded satisfactory bacteriology but it is suggested that probably injury in falling started a hemorrhage in the ear upon which a secondary infection was implanted. What seems a true meningitis secondary to otitis media and mastoid suppuration was seen in a marmoset.

A case of the well known but obscure condition known as chronic productive pachymeningitis was observed in a badger. Although it cannot be explained it is cited as a matter of record and interest.

American Badger (Taxidea taxus). Pachymeningitis externa. The dura is fast to the skull and cannot be removed. Scattered irregularly over the entire inner surface of the skull are pale pinhead sized hard nodules. It is impossible to tell if they are in the dura or the bone. The brain shows engorged vessels but is otherwise negative.

Two instances of hemorrhagic pachymeningitis associated with cretinism were seen in wolf cubs. The following notes illustrate both cases.

American Gray Wolf (Canis mexicanus). Cretinism. Hemorrhagic external pachymeningitis with craniotabes. Upon removing the calvarium a marked craniotabes of the under surface is found and with it a deep red and purple staining of outside of dura and inner table of skull. These changes are most marked along the longitudinal sinus at internal occipital protuberance and along left parietal region. Dura on left side is distinctly congested. This is also true of pia. The brain and its base seem normal.

Cyst of the brain. A sooty mangabey (Cercocebus fuliginosus) had been in the Garden for about four months and was apparently an adult normal animal. It died rather suddenly after a distinct convulsion with semiconsciousness. At autopsy in addition to a nephritis, a large cyst was found to occupy the posterior third of the left hemisphere. Its walls were composed of a thin (one-sixteenth inch) rim of cerebral substance and the meninges; its contents were clear. The notes do not record any examination for parasites. This monkey showed no localizing signs.

TUBERCULOSIS.

Gross tuberculous lesions have been found in the brain in several specimens with generalized disease but only two cases are of special interest. A Rhesus macaque (Macacus rhesus) suffering with generalized but chiefly lymphatic tuberculosis, showed a large plaque on the external surface of the dura over the vertex where it was adherent to a yellow, fairly firm nodule about ten mm. across. This nodule was deeply imbedded in the brain substance, barely projecting above the surface, generally spherical and not encapsulated. There was no peripheral reactive zone. The meninges were not altered anywhere except as above. The blood vessels were not especially congested. The pia arachnoid contained no excess of fluid but the summits of the convolutions were flattened. The mass was located in the posterior frontal convolution, near the longitudinal fissure, occupying nearly its whole breadth and penetrating about one centimetre. It did not enter the fornicate gyrus. There was a completely degenerated core about two mm. across. The adjacent bone was beginning to erode. No localizing signs were reported.

The other case, that of a young Drill baboon (Papio leucophæus), was studied with Dr. J. H. W. Rhein and can be reported in the following condensed notes.

The baboon appeared to be perfectly well until October 18, 1906, when some lameness in the anterior and posterior extremities on the right side was observed. This gradually increased, and was associated with general convulsions. On November 30th, I made an examination and found the following condition: The right upper and lower extremities were weaker than on the left side. On the left side the power seemed to be fair. He was able to hold on to an iron bar with the fingers of the upper and lower extremities on the right side but in withdrawing the bar it was not difficult to overcome his grasp and the power on this side was distinctly less than on the left. The movements of the right arm were somewhat ataxic, as observed when he made efforts to grasp the bar. The knee jerks were increased on both sides and appeared to be equally so. There was no evidence of facial palsy. He moved both sides of the face equally well at times when he expressed anger or fear in the facial expression. The tongue seemed to be retracted equally well on both sides. Tests for hemianopsia were, of course, unsatisfactory, but he seemed to recognize readily the approach of the iron bar from both sides. There was no disturbance of the rectal or bladder functions, although at autopsy the bladder was full. Death occurred on December 2, 1906. At the autopsy the brain and spinal cord, with the other organs were examined. The dura was adherent to the left side of the brain, in the prefrontal region, in the upper third and when the brain was removed it was observed that an area of softening lay beneath this point. A small caseous mass was also observed at the base of the right lung, and beneath the diaphragm on the right side was a large abscess, partly involving the liver. The tubercle bacillus was found in the pus removed from the area of softening beneath the left cortex. A study of the brain revealed the presence of three foci of softening. The largest one was situated in the left hemisphere in the prefrontal region, and extended from just beneath the cortex in the upper third of the region, downward almost to the base of the brain. This area was cylindrical in shape and measured 2.5 cm. in its greatest diameter. The area of softening consisted of caseated material and pus, in which the tubercle bacillus was found present. The second area of softening was found on the right side of the brain, much smaller in extent and measuring 1.5 cm. diameter. There was no pus present in this area, but it consisted of a circumscribed mass of caseous material. The apex of this area of softening was just beneath the cortex in the prefrontal region on the right side, and in the removal of the brain the cortex was torn just above this area of caseation. This point was .5 cm. in front of the central fissure and about 1 cm. below the superior surface of the brain. A third area of softening was observed posteriorly, in the white substance, in the parieto-occipital region, and measured about 6 mm. in diameter. A study of the sections of the brain shows beautifully the extent of the destruction of the brain tissue. The optic thalamus and the lenticular nucleus, and the posterior limb of the internal capsule, on the left side, are destroyed in part. The anterior limb of the internal capsule in one section, is preserved, notwithstanding the fact that the optic thalamus on the same side has been in large part destroyed. In spite of the fact that the posterior limb of the internal capsule has been destroyed at some levels, it is interesting to note that the degeneration of the pyramidal tracts of the pons and medulla on the opposite side and the lateral columns of the spinal cord are not intensely—although distinctly—degenerated. It is very interesting to note that in view of the severe damage to the posterior limb of the internal capsule on the left side, there was not more paralysis, for it will be remembered that there was considerable power of prehension in the right upper and lower extremities.

ENCEPHALOMYELITIS, POLIOMYELITIS.

While, as has been stated, no well defined cases of the recognized meningocephalic infectious diseases have been observed in the Garden, there have been several animals in whose cord and brain changes were found comparable to the infections disease known in man as poliomyelitis. On several occasions since this disease was recognized as occurring in epidemic form it has been observed that domestic mammals and fowls suffered from a similar condition. The general vicinity of Philadelphia had a low grade epidemic among children during the years from 1907 to 1912 and it is during this time that most of the cases of a comparable character were observed among our animals. It is to be emphasized that attacks were entirely sporadic and the cases did not appear to bear a relation to one another. This character is quite in accord with certain of the outbreaks in man. However we cannot state that the disease is exactly the same as seen in the human being for, as will be noted in the cited examples, all the pathological features were not fulfilled.

It is not always possible to differentiate between myelitic disease and polyneuritis of man or animals. Studied symptomatically the cases in our records which proved to have degenerative and infiltrative lesions comparable to poliomyelitis showed gradual but progressive paralysis expressed by inability to move rather than disinclination—in other words loss of power rather than restriction because of pain. None of the animals in which poliomyelitis was demonstrated have exhibited the ataxia of the hind legs discussed on a previous page nor have we found myelitic lesions in the few cords from animals suffering with this weakness. The nearest approach to a cerebrospinal explanation for weakness and palsy was in a zebra which died with constipation, acute nephritis, and hepatic perilobular fibrosis. In this animal a pronounced subpial mononuclear infiltrate was observed, in places involving the superficial parts of the cerebral gray matter, especially about the congested vessels of this area. This condition was present to a slight degree in the cord. There was then a low grade meningoencephalitis but no nerve cell changes. So far as is known to me no animal showing a definite local paresis or paraplegia recovered from the attack; had this occurred we might have observed residual palsies.

In so far as lesions are concerned they are perhaps best illustrated by the appended cases, but since even in them there is a lack of uniformity, it may be well to discuss the basic changes of all. The outstanding abnormality in the microscopic anatomy is the richness of small mononuclear cells beneath the pia, both spinal and cerebral, around the smaller blood vessels and to a lesser extent around the multipolar cells of the gray matter. These do not present the dense colonization often seen in the acute cases of infantile paralysis in man but are prominent in comparison to normal nervous tissue. Hemorrhages or at least small groups of erythrocytes outside of blood vessels are seen here and there. Vacuolization of ganglion cells is variable, being prominent in some, trifling or absent in others. Glial proliferation is often quite marked, and in one case to be cited seems the prominent lesion.

The animals in which meningopoliomyelitis has been found were three monkeys, two Canadian lynx, a bear and a raccoon; about a score of cords from other animals with some kind of palsy have been studied microscopically without discovering it. The following cases illustrate our material. The only instance of two cases in close relation concerns the lynx (Felis canadensis). They occupied the same cage and died twelve days apart. No symptoms were recorded until a few days before death when a general paralysis appeared, deepening to completeness on the day of death. No case occurred in neighboring cages. Doctor Rhein studied all these cases, and his notes are used for these records. Portions of the lumbar and cervical enlargements and of the thoracic regions of the cord were stained with hemalum and acid fuchsin and with thionin. The pia was slightly infiltrated. There was some cellular infiltration of the anterior septum, and the vessels here showed an increase in the nuclei of the walls and a slight perivascular infiltration. The pial infiltration seemed to be equally distributed in the entire circumference of the cord, although perhaps a little more marked over the anterior and posterior septa. The vessels of the gray matter were congested and the walls of the vessels in most part showed a proliferation of the nuclei. There were a few small hemorrhages into the gray matter, probably agonal. As compared with the human cord and the cords of monkeys, antelopes and dogs, there was an unusually large number of glia nuclei, which, if found in the human cord, would be looked upon as a proliferation process. In some cases these nuclei were heaped together in masses, and were evidently pathological. There was also, about the ganglion cells, some pericellular round cell infiltration, and this was more marked around a few cells which were almost entirely destroyed. The ganglion cells themselves were swollen. Some showed eccentric nuclei, and many of them stained poorly, while one or two showed distinct vacuolization. In one field a ganglion cell was partly destroyed by a recent hemorrhage. There were, however, a number of cells which appeared normal. This process seemed to be fairly distinct in the lumbar and cervical enlargements, but was not clearly demonstrated in the sections from the dorsal region. The cellular infiltration of the horns was evidently not leucocytic, but presented the appearance of a connective tissue proliferation. Although these are not the exact lesions found in poliomyelitis in the human animal, they are at least suggestive of the same process since the infiltrating cells are of the lymphatic or connective tissue types. There is no acute inflammatory leucocytic infiltrate.

A weeper cebus (Cebus capucinus) ever since he was received acted in such a peculiar manner, seeming to have only partial control of his movements, that he was known as the “Crazy Monkey.” There was no history of illness before death. Pathological diagnosis: Chronic enterocolitis, chronic adhesive pericarditis, early interstitial change in kidney, edema of lungs, meningitis and poliomyelitis. The pia of the paracentral cortex was thickened and was the seat of a round cell infiltration of moderate degree, the cells being of the mononuclear type. The blood vessels of the cortex were congested and the nuclei of the walls were increased. The round cell infiltration of the pia had in some places extended into the cortical layers. The pia surrounding the medulla oblongata was also the seat of a slight round cell infiltration. The pia of the spinal cord, however, did not show any cellular infiltration. The cells of the anterior horns of the spinal gray matter were extensively diseased, being swollen in places, some surrounded by a glia proliferation and many with marked vacuolization.

A common raccoon (Procyon lotor) was observed in the laboratory to have complete paralysis of the anterior and partial paralysis of the posterior extremities. This latter was almost complete in muscles controlling the feet, while the thigh and hip muscles showed some irregular incoördinate movements. Respiration shallow but regular. History shows that the power of the extremities began to fail about a month before death and was absolutely lost in the fore extremities three days before the animal was killed. Diagnosis: Poliomyelitis. Examination of the central nervous system showed the presence of marked round cell infiltration of pia of cortex and of spinal cord, more particularly in the lower thoracic and lumbar regions. Ganglion cells in the lumbar region were markedly diseased. There were numerous old and fresh hemorrhages and a moderate degree of round cell infiltration in the anterior horns. Two young of this animal, born three months before its death, showed weakness and gradual increasing paralysis of their extremities beginning when three months old (that is at the time of the death of their mother), and lasting until their death, one in the seventh and one in the eighth month of life. These were found not to have changes in the central nervous system, but there was sufficient rachitis to account for this paralysis.

The only tumor of the central nervous system found among these animals occurred in an Undulated Grass Parrakeet (Melopsittacus undulatus). The gross notes are very vague but the microscopy is suggestive of a glioma. The growth in the brain consists of large irregular masses of large cells with vesicular nuclei and pale homogeneous protoplasm. “Scattered between these accumulations are irregular strands of spindle cells, with spindle-shaped nuclei, taking the hematoxylin very deeply. The supporting tissue is almost without cells, taking the eosin faintly, and is quite loosely arranged. No fibrils are seen among the cells. The blood vessels are congested, and at one place there is a small hemorrhage. The vessel walls are the same as the rest of the connective tissue. There is a slightly atypical metastasis in the liver.”

A case, the identity of which is still undecided, was observed in a Green Monkey (Cercopithecus callitrichus); it may belong among the gliomata or glioses. There was in the middle of this monkey’s cerebrum a gray area about 3 × 2 × 1 cm. with a softened centre, the more solid parts being found under the microscope to consist of glia tissue, blood vessels and degenerated cells. No true gliomatous formations could be discovered. Because of the indefiniteness of the lesion, it is not included in the tumors or inflammations. Clinically the effect of the change was to cause blindness and ataxia but motor power was not greatly impaired.

A very small number of tumors of the brain in wild animals is on record in the English and German literature, perhaps the most interesting being what resembles in description a subdural neurocytoma reported by Wilson in the Proceedings of the London Zoological Society, 1908. The mass was separate from the cerebellum, but had hollowed out a place for itself in this part of the hind-brain.

BRAIN WEIGHTS.

The policy of preserving the brain of all species enables us to record in the accompanying list the weights of a large number of specimens. In order that the figures may have a representative and comparative value only those are given where the total body weight of the animal is also known. The specimens were removed by the laboratory staff, most of them by one person, and by the same technique. All brains were weighed immediately upon removal from the body, no preservative being near the organ. The brains were themselves externally normal. Our technician is skillful in removing the organ, practically always getting the pituitary body, and cutting off the brain stem at the foramen magnum, the pia remaining but the dura removed. Because the specimens were taken, in practically all cases, from animals that died in the Park, and because of the shortness of the list (196), it seems wise not to attempt conclusions referable to comparative weights of the different orders and families. However, the data seem worthy of record because it is doubtful if anywhere one can find so many weights taken under comparable conditions by the same personnel. One can find a considerable list of brain weights and values in many publications throughout the literature, notably in an article by Ziehen in Bardeleben’s Handbuch der Anatomie (Vol. IV, Abt. III 363), but from no single source are there so many varieties or so long a list. Ziehen’s tables are compiled from the literature and therefore represent data collected under different conditions, many of which were probably pathological. The appended figures are to be considered as raw material collected under uniform conditions.

Examination of the figures bears out in a measure some of the remarks made by Ziehen, notably those which indicate that between large and small varieties of the same general group, the smaller has the greater brain weight value and that the youthful animal has more brain than the adult.

The brains at the museum are fixed in saline-formaldehyde—sufficient strength of the former to suspend the organ in the container and four percentage of the latter. When fixation is complete, as indicated by density, preservation is done in one per cent. formaldehyde, the organ, usually bound in gauze, being laid in cotton. A list of important references is added to the weight tables—some antedating Ziehen’s articles, but principally those that have appeared since the publication of his monograph.

PRINCIPAL REFERENCES TO THE RELATIVE WEIGHT OF THE BRAIN

ZIEHEN: In Bardeleben’s Handbuch der Anatomie des Menschen, Vol. 4, pt. 3. ZIEHEN: Handbuch der Anatomie des Nervensystems, Jena, 1903. GIRARD: Bulletin de l’Institut Gen. Psychologie, Vol. 7, p. 53. VON BUSCHAU: Real Encyclopedie der Gesamten Heilkunde 3. Aufl. VON BUSCHAU: Neurologisches Zentralbl., 1897, March. BRANDT: Bull. de la Soc. Imperial des Naturalistes de Moscow, 1867, 40, pt. 2, 525. MIES: Verhandl. der Gesellsch. deutscher Naturforsch und Arzte, 1898, 353. DHERE ET LAPICQUE: Archives de la Physiologie, October, 1898. LAPICQUE ET GIRARD: C. R. des Sceances de l’Academie de Science, Paris, 1905, 140, 1057. LAPICQUE: Bulletin de Museum d’Histoire Naturelle, 1909, No. 7, 408. LAPICQUE: Revue du Mois, Paris, April, 1908, 445. LAPICQUE: Bulletin et Memoires de la Société d’Anthropologie de Paris, 1907, 5, Vol. 8, No. 3, 261. LAPICQUE: Biologica, Vol. 2, 1912, p. 257. FUNK: Inaug. Dissert. Wurzburg, 1911. POYNTER: Cerebral Anthropology, Lincoln, 1913. MOLLISON: Arch. für Anthropologie, 1914, XIII, 388. HULTGREN: Das Hirngewicht des Menschen, Upsala, 1912. WEBER: Festschrift für Karl Gegenbauer, 1898. DUBOIS: Bulletin de la Soc. Anthropologie, Paris, 1897, 337. DUBOIS: Archiv. für Anthropologie, Vol. 25, 1898. DUBOIS: Proc. Sci. K. Acad. Wet., Amsterdam, 1914, 16, 647. DUBOIS: Zeitschrift für Morph. und Anthropologie, 1914, Vol. 18, 323. MARCHAND: Hirngewicht des Menschen, Leipsig, 1902. RUDOLPH: Beiträge zur Path. Anatomie, Jena, 58, 1914, 48. KRAEMER: Mitt. der Deutsch. Landwehrgesell, 29, 1914, 55.

TABLE 18.—Giving the Actual Weight of the Brain and the Relation of this to that of the Body in 196 Animals. ════════════════════╤═══╤══════╤═══════════╤══════╤═════════╤════════╤══════╤══════ Order Family │Sex│Known │Development│ Time │Condition│ Body │Brain │Grams │ │Age at│ │ in │ │ Weight │Weight│Brain │ │Death │ │Garden│ │in Grams│ in │ Per │ │ │ │ │ │ │Grams │ Kilo │ │ │ │ │ │ │ │ of │ │ │ │ │ │ │ │ Body │ │ │ │ │ │ │ │Weight Genus Species │ „ │ „ │ „ │ „ │ „ │ „ │ „ │ „ Common Name │ „ │ „ │ „ │ „ │ „ │ „ │ „ │ „ ────────────────────┼───┼──────┼───────────┼──────┼─────────┼────────┼──────┼────── PRIMATESA: │ │ │ │ │ │ │ │ SIMIADÆ: │ │ │ │ │ │ │ │ Simia satyrus, │ │ │ │ │ │ │ │ Orang utan │ ♂ │ │Immature │4 yrs.│Good │ 15,500.│ 405.│ 26.1 │ │ │ │6 mo. │ │ │ │ Orang utan │ ♀ │ │Immature │4 yrs.│Thin │ 22,178.│ 300.│ 13.4 │ │ │ │2 mo. │ │ │ │ Hylobates │ │ │ │ │ │ │ │ hainanus, │ │ │ │ │ │ │ │ Hainan Gibbon │ ♂ │ │Mature │4 yrs.│Good │ 5,900.│ 115.│ 19.4 │ │ │ │3 mo. │ │ │ │ Hylobates │ │ │ │ │ │ │ │ leuciscus, │ │ │ │ │ │ │ │ Silver Gibbon │ ♀ │ │Mature │14 │Very thin│ 3,030.│ 75.│ 24.7 │ │ │ │days │ │ │ │ │ │ │ │ │ │ │ │ CERCOPITHECIDÆ: │ │ │ │ │ │ │ │ Presbytis │ │ │ │ │ │ │ │ cephalopterus, │ │ │ │ │ │ │ │ Ceylon Entellus │ ♂ │ │Mature │1 mo. │Good │ 4,080.│ 58.│ 14.2 Cercopithecus │ │ │ │ │ │ │ │ sabæus, │ │ │ │ │ │ │ │ Grivet Monkey │ ♀ │ │Mature │14 │Good │ 3,530.│ 65.│ 18.4 │ │ │ │yrs. │ │ │ │ Cercopithecus │ │ │ │ │ │ │ │ patas, │ │ │ │ │ │ │ │ Red Monkey │ ♂ │ │Mature │2 yrs.│Good │ 5,060.│ 105.│ 20.7 │ │ │ │9 mo. │ │ │ │ Cercocebus │ │ │ │ │ │ │ │ fuliginosus, │ │ │ │ │ │ │ │ Sooty Mangabey │ ♀ │ │ │3 mo. │Good │ 3,342.│ 105.│ 31.4 Macacus arctoides,│ │ │ │ │ │ │ │ Brown Macaque │ ♂ │ │ │3 yrs.│Good │ 3,161.│ 100.│ 31.7 │ │ │ │6 mo. │ │ │ │ Macacus │ │ │ │ │ │ │ │ nemestrinus, │ │ │ │ │ │ │ │ Pigtailed │ ♀ │ │ │4 yrs │Very Thin│ 4,560.│ 100.│ 21.9 Macaque │ │ │ │3 mo. │ │ │ │ Pigtailed │ ♀ │10 mo.│Baby │10 mo.│Good │ 1,390.│ 67.│ 48.2 Macaque │ │ │ │ │ │ │ │ Macacus rhesus, │ │ │ │ │ │ │ │ Rhesus Macaque │ ♂ │6 mo. │Baby │6 mo. │Good │ 462.│ 67.│ 145. Papio porcarius, │ │ │ │ │ │ │ │ Chacma Baboon │ ♂ │ │Mature │1 wk. │Thin │ 12,300.│ 180.│ 14.6 Papio │ │ │ │ │ │ │ │ cynocephalus, │ │ │ │ │ │ │ │ Yellow Baboon │ ♂ │ │Mature │4 yrs.│ │ 8,942.│ 140.│ 15.6 │ │ │ │6 mo. │ │ │ │ │ │ │ │ │ │ │ │ CEBIDÆ: │ │ │ │ │ │ │ │ Ateles ater, │ │ │ │ │ │ │ │ Black Spider │ ♀ │ │ │1 mo. │Good │ 1,790.│ 125.│ 70. Monkey │ │ │ │ │ │ │ │ Black Spider │ ♀ │ │ │2 mo. │Good │ 2,475.│ 105.│ 42.5 Monkey │ │ │ │ │ │ │ │ Black Spider │ ♂ │ │ │2 mo. │Good │ 3,630.│ 125.│ 34.4 Monkey │ │ │ │ │ │ │ │ Lagothrix │ │ │ │ │ │ │ │ lagotricha, │ │ │ │ │ │ │ │ Woolly Monkey │ ♀ │ │ │9 mo. │Thin │ 1,634.│ 82.│ 50.3 Cebus fatuellus, │ │ │ │ │ │ │ │ Brown Cebus │ ♀ │ │ │2 yrs.│Thin │ 1,500.│ 60.│ 40. Cebus albifrons, │ │ │ │ │ │ │ │ White fronted │ ♂ │ │ │ │ │ 1,750.│ 61.│ 34.8 Cebus │ │ │ │ │ │ │ │ Aotes vociferans, │ │ │ │ │ │ │ │ Noisy │ ♂ │ │ │2 wks.│Good │ 480.│ 20.│ 41.7 Douroucouli │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ CALLITRICHIDÆ: │ │ │ │ │ │ │ │ Callithrix │ │ │ │ │ │ │ │ pencillata, │ │ │ │ │ │ │ │ Black eared │ ♂ │ │ │1 yr. │Good │ 135.│ 10.│ 73. Marmoset │ │ │ │ │ │ │ │ Black eared │ ♂ │ │ │6 mo. │Good │ 250.│ 15.│ 60. Marmoset │ │ │ │ │ │ │ │ Leontocebus │ │ │ │ │ │ │ │ œdipus, │ │ │ │ │ │ │ │ Pinche Marmoset │ ♂ │ │ │1 wk. │Good │ 167.│ 14.│ 84. │ │ │ │ │ │ │ │ LEMURES: │ │ │ │ │ │ │ │ LEMURIDÆ: │ │ │ │ │ │ │ │ Lemur catta, │ │ │ │ │ │ │ │ Ring tailed │ ♀ │Mature│ │7 yrs.│Good │ 1,470.│ 30.│ 20.4 Lemur │ │ │ │ │ │ │ │ Ring tailed │ ♀ │ │ │1 yr. │Good │ 1,240.│ 20.│ 16. Lemur │ │ │ │3 mo. │ │ │ │ Lemur mongoz, │ │ │ │ │ │ │ │ Mongoose Lemur │ ♀ │ │ │2 yrs.│Good │ 1,457.│ 20.│ 13.8 Galago maholi, │ │ │ │ │ │ │ │ Maholi Galago │ ♂ │5 yrs.│Mature │5 yrs.│Good │ 100.│ 4.│ 40. │ │3 mo. │ │3 mo. │ │ │ │ │ │ │ │ │ │ │ │ CARNIVORA: │ │ │ │ │ │ │ │ FELIDÆ: │ │ │ │ │ │ │ │ Felis viverrina, │ │ │ │ │ │ │ │ Fishing Cat │ ♂ │ │ │10 mo.│Good │ 7,000.│ 60.│ 8.5 Felis chaus, │ │ │ │ │ │ │ │ Jungle Cat │ ♀ │ │Mature │5 yrs.│Good │ 3,640.│ 45.│ 12.2 │ │ │ │3 mo. │ │ │ │ Felis ruffus, │ │ │ │ │ │ │ │ American Wild │ ♀ │ │ │4 yrs.│Thin │ 4,402.│ 50.│ 11.1 Cat │ │ │ │ │ │ │ │ Felis onca, │ │ │ │ │ │ │ │ Jaguar │ ♀ │20 │Mature │15 │Very thin│ 29,500.│ 170.│ 5.7 │ │yrs. │ │yrs. │ │ │ │ Felis eyra, │ │ │ │ │ │ │ │ Eyra │ ♂ │ │ │3 mo. │Good │ 5,000.│ 44.│ 8.8 Felis canadensis, │ │ │ │ │ │ │ │ Canada Lynx │ ♀ │ │Mature │4 yrs.│Very thin│ 7,270.│ 80.│ 11. │ │ │ │6 mo. │ │ │ │ Felis │ │ │ │ │ │ │ │ chibigonazon, │ │ │ │ │ │ │ │ Brazilian Ocelot│ ♀ │ │Young │1 mo. │Thin │ 1,350.│ 35.│ 26. Felis pardalis, │ │ │ │ │ │ │ │ Common Ocelot │ ♀ │ │ │10 mo.│Good │ 5,800.│ 50.│ 8.6 Common Ocelot │ ♂ │ │Young │2 mo. │Thin │ 2,700.│ 45.│ 16.6 Felis concolor, │ │ │ │ │ │ │ │ Puma │ ♂ │ │ │ │Good │ 52,700.│ 150.│ 2.8 Puma │ ♀ │ │Mature │8 yrs.│Very thin│ 29,500.│ 50.│ 1.69 │ │ │ │6 mo. │ │ │ │ Puma │ ♂ │ │Baby │ │Good │ 1,067.│ 55.│ 51.5 Puma │ ♀ │ │Baby │ │Good │ 998.│ 55.│ 55. Felis tigris, │ │ │ │ │ │ │ │ Bengal Tiger │ ♀ │ │Mature │12 │Fair │ 66,000.│ 250.│ 3.8 │ │ │ │yrs. │ │ │ │ Bengal Tiger │ ♂ │ │Mature │12 │Very thin│ 91,000.│ 240.│ 2.6 │ │ │ │yrs. │ │ │ │ Felis uncia, │ │ │ │ │ │ │ │ Snow Leopard │ ♀ │ │Mature │8 yrs.│Good │ 22,700.│ 120.│ 5.3 │ │ │ │ │ │ │ │ HYÆNIDÆ: │ │ │ │ │ │ │ │ Hyæna hyæna, │ │ │ │ │ │ │ │ Striped Hyæna │ ♂ │ │Mature │4 yrs.│Poor │ 27,200.│ 92.│ 3.3 │ │ │ │ 3 mo.│ │ │ │ Striped Hyæna │ ♂ │ │Mature │8 yrs.│Good │ 36,300.│ 90.│ 2.4 │ │ │ │10 mo.│ │ │ │ │ │ │ │ │ │ │ │ CANIDÆ: │ │ │ │ │ │ │ │ Canis │ │ │ │ │ │ │ │ procyonoides, │ │ │ │ │ │ │ │ Raccoon-like Dog│ ♀ │ │Mature │3 yrs.│Good │ 4,770.│ 25.│ 5.2 Raccoon-like Dog│ ♀ │ │ │ │Good │ 4,900.│ 35.│ 7.1 Canis familiaris, │ │ │ │ │ │ │ │ Eskimo Dog │ ♂ │ │Mature │ │Very thin│ 36,300.│ 100.│ 2.7 Canis cinereo │ │ │ │ │ │ │ │ argenteus, │ │ │ │ │ │ │ │ Gray Fox │ ♀ │ │Mature │3 yrs.│Good │ 2,652.│ 40.│ 15. Canis cinereus │ │ │ │ │ │ │ │ argenteus scotti, │ │ │ │ │ │ │ │ Scott’s Gray Fox│ ♀ │ │Mature │2 yrs.│Good │ 2,200.│ 53.│ 25. │ │ │ │6 mo. │ │ │ │ Canis chama, │ │ │ │ │ │ │ │ Silver Fox │ ♂ │ │ │7 mo. │Good │ 3,325.│ 40.│ 12. Canis mesomelas, │ │ │ │ │ │ │ │ Blackbacked │ ♂ │ │ │2 yrs.│Good │ 6,000.│ 60.│ 10. Jackal. │ │ │ │6 mo. │ │ │ │ Blackbacked │ ♀ │ │ │ │ │ 3,500.│ 70.│ 20. Jackal │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ MUSTELIDÆ: │ │ │ │ │ │ │ │ Mustela foina, │ │ │ │ │ │ │ │ Beech Marten │ ♀ │ │Mature │3 yrs.│Good │ 810.│ 15.│ 18.3 Mustela americana,│ │ │ │ │ │ │ │ Pine Marten │ ♂ │ │Mature │4 yrs.│Good │ 680.│ 13.│ 19. Gulo gulo, │ │ │ │ │ │ │ │ Wolverine │ ♀ │ │ │3 yrs.│Good │ 5,700.│ 75.│ 13.1 │ │ │ │3 mo. │ │ │ │ Galictis barbara, │ │ │ │ │ │ │ │ Tayra. │ ♂ │ │ │7 mo. │Good │ 1,480.│ 55.│ 37. Mephitis │ │ │ │ │ │ │ │ mephitica, │ │ │ │ │ │ │ │ Common Skunk │ ♀ │ │ │6 mo. │Good │ 1,755.│ 6.│ 3.4 Common Skunk │ ♀ │ │ │2 wks.│Good │ 1,700.│ 7.│ 4.1 Meles meles, │ │ │ │ │ │ │ │ European Badger │ ♂ │ │ │3 yrs.│Good │ 7,473.│ 46.│ 6. │ │ │ │ │ │ │ │ PROCYONIDÆ: │ │ │ │ │ │ │ │ Procyon lotor, │ │ │ │ │ │ │ │ Common Raccoon │ ♂ │ │Mature │7 yrs.│Good │ 9,000.│ 42.│ 4.6 │ │ │ │3 mo. │ │ │ │ Common Raccoon │ ♀ │ │Mature │9 yrs.│Good │ 5,450.│ 37.│ 6.9 │ │ │ │2 mo. │ │ │ │ Procyon lotor │ │ │ │ │ │ │ │ hernandezi, │ │ │ │ │ │ │ │ Mexican Raccoon │ ♀ │ │ │2 yrs.│Good │ 6,130.│ 40.│ 6.5 Nasua nasua, │ │ │ │ │ │ │ │ Ring tailed │ ♂ │ │ │1 yr. │Good │ 1,600.│ 40.│ 25. Coati │ │ │ │4 mo. │ │ │ │ Ring tailed │ ♂ │ │ │10 mo.│Good │ 1,600.│ 35.│ 24.3 Coati │ │ │ │ │ │ │ │ Nasua narica, │ │ │ │ │ │ │ │ White nosed │ ♂ │Mature│ │8 yrs.│Very thin│ 5,000.│ 44.│ 8.8 Coati │ │ │ │ │ │ │ │ Potos │ │ │ │ │ │ │ │ caudivolvulus, │ │ │ │ │ │ │ │ Kinkajou │ │Mature│ │3 yrs.│Good │ 1,440.│ 35.│ 24.2 │ │ │ │2 mo. │ │ │ │ │ │ │ │ │ │ │ │ URSIDÆ: │ │ │ │ │ │ │ │ Ursus malayanus, │ │ │ │ │ │ │ │ Sun Bear │ │ │ │1 yr. │Good │ 41,000.│ 125.│ 3.5 │ │ │ │9 mo. │ │ │ │ Ursus beringiana, │ │ │ │ │ │ │ │ Kamchatkan Bear │ ♀ │ │ │ │Very thin│ 31,800.│ 315.│ 9.9 │ │ │ │ │ │ │ │ PINNIPEDIA: │ │ │ │ │ │ │ │ OTARIIDÆ: │ │ │ │ │ │ │ │ Eumetopias │ │ │ │ │ │ │ │ stelleri, │ │ │ │ │ │ │ │ Steller’s Sea │ ♂ │ │ │4 yrs.│Very thin│120,400.│ 515.│ 4.27 Lion │ │ │ │ │ │ │ │ Zalophus │ │ │ │ │ │ │ │ californianus, │ │ │ │ │ │ │ │ California Hair │ ♂ │ │Mature │6 yrs.│Very good│ 94,000.│ 420.│ 4.46 Seal │ │ │ │9 mo. │ │ │ │ │ │ │ │ │ │ │ │ RODENTIA: │ │ │ │ │ │ │ │ MURIDÆ: │ │ │ │ │ │ │ │ Peromyscus │ │ │ │ │ │ │ │ leucopus, │ │ │ │ │ │ │ │ White footed Mouse│ ♀ │5 yrs.│Mature │5 yrs.│Good │ 39.│ 1.│ 25.6 │ │ │ │ │ │ │ │ CASTORIDÆ: │ │ │ │ │ │ │ │ Castor canadensis,│ │ │ │ │ │ │ │ American Beaver │ ♀ │ │ │8 yrs.│Good │ 10,000.│ 40.│ 4. │ │ │ │2 mo. │ │ │ │ │ │ │ │ │ │ │ │ OCTODONTIDÆ: │ │ │ │ │ │ │ │ Myocastor coypus, │ │ │ │ │ │ │ │ Coypu │ ♀ │ │ │ │Good │ 2,000.│ 20.│ 10. │ │ │ │ │ │ │ │ HYSTRICIDÆ: │ │ │ │ │ │ │ │ Hystrix │ │ │ │ │ │ │ │ longicauda, │ │ │ │ │ │ │ │ Malaccan │ ♀ │ │Mature │18 │Thin │ 6,000.│ 26.│ 4.3 Porcupine │ │ │ │yrs. │ │ │ │ Erethizon dorsatus│ │ │ │ │ │ │ │ dorsatus, │ │ │ │ │ │ │ │ Canada Porcupine│ ♀ │ │ │2 mo. │Good │ 4,065.│ 20.│ 4.9 Coendon │ │ │ │ │ │ │ │ prehensilis, │ │ │ │ │ │ │ │ Brazilian Tree │ ♀ │ │ │1 wk. │Good │ 480.│ 14.│ 29.1 Porcupine │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ CAVIIDÆ: │ │ │ │ │ │ │ │ Cavia porcella, │ │ │ │ │ │ │ │ Wild Guinea-Pig │ ♂ │ │Mature │6 yrs.│Good │ 320.│ 4.│ 12.5 │ │ │ │2 mo. │ │ │ │ Hydrochœrus │ │ │ │ │ │ │ │ hydrochœrus, │ │ │ │ │ │ │ │ Capybara │ ♂ │ │ │1 mo. │Good │ 19,000.│ 50.│ 2.63 │ │ │ │ │ │ │ │ PROBOSCIDEA: │ │ │ │ │ │ │ │ Elephas maximus, │ │ │ │ │ │ │ │ Asiatic Elephant│ ♂ │3 yrs.│Young │1 mo. │Good │241,000.│3,432.│ 14.1 │ │ │ │ │ │ │ │ HYRACOIDEA: │ │ │ │ │ │ │ │ HYRACIDÆ: │ │ │ │ │ │ │ │ Procaria capensis,│ │ │ │ │ │ │ │ Cape Hyrax │ ♂ │ │ │8 mo. │Good │ 1,800.│ 15.│ 8.3 Cape Hyrax │ ♀ │ │ │1 yr. │Good │ 2,170.│ 20.│ 9.2 │ │ │ │9 mo. │ │ │ │ │ │ │ │ │ │ │ │ UNGULATA: │ │ │ │ │ │ │ │ TAPIRIDÆ: │ │ │ │ │ │ │ │ Tapirus indicus, │ │ │ │ │ │ │ │ Malayan Tapir │ ♀ │ │Mature │7 yrs.│Thin │250,000.│ 300.│ 1.2 │ │ │ │4 mo. │ │ │ │ Malayan Tapir │ ♂ │ │Young │3 mo. │Good │ 80,000.│ 225.│ 2.8 │ │ │ │ │ │ │ │ EQUIDÆ: │ │ │ │ │ │ │ │ Equus prjivalskii,│ │ │ │ │ │ │ │ Wild Horse │ ♀ │1 wk. │Baby │1 wk. │Good │ 22,700.│ 330.│ 14. Equus burchelli, │ │ │ │ │ │ │ │ Burchell’s Zebra│ ♂ │ │Mature │6 yrs.│Good │341,000.│ 645.│ 1.9 │ │ │ │ │ │ │ │ BOVIDÆ: │ │ │ │ │ │ │ │ Strepsiceros │ │ │ │ │ │ │ │ capensis, │ │ │ │ │ │ │ │ Greater Kudu │ ♂ │ │ │4 mo. │Thin │285,000.│ 290.│ 2.2 Cobus leche, │ │ │ │ │ │ │ │ Leche Antelope │ ♀ │ │Mature │10 │Good │ 52,700.│ 200.│ 3.8 │ │ │ │yrs. 6│ │ │ │ │ │ │ │mo. │ │ │ │ Damaliscus │ │ │ │ │ │ │ │ albifrons, │ │ │ │ │ │ │ │ Blessbok │ ♂ │ │Mature │11 │Good │ 58,100.│ 245.│ 4.2 │ │ │ │yrs. │ │ │ │ Boselaphus │ │ │ │ │ │ │ │ tragocamelus, │ │ │ │ │ │ │ │ Nylghaie │ ♀ │ │ │2 yrs.│Good │136,300.│ 310.│ 2.3 │ │ │ │2 mo. │ │ │ │ Poephagus │ │ │ │ │ │ │ │ grunniens, │ │ │ │ │ │ │ │ Yak │ ♂ │3 yrs.│Young runt │3 yrs.│Runt │114,000.│ 290.│ 2.5 │ │6 mo. │ │6 mo. │ │ │ │ Yak │ ♀ │ │Mature │5 yrs.│Thin │177,000.│ 385.│ 2.2 Taurotragus oryx │ │ │ │ │ │ │ │ livingstonii, │ │ │ │ │ │ │ │ Livingstone’s │ ♀ │ │Old │13 │Good │327,000.│ 415.│ 1.3 Eland │ │ │ │yrs. │ │ │ │ Hemitragus │ │ │ │ │ │ │ │ jemlaicus, │ │ │ │ │ │ │ │ Himalayan Thar │ ♂ │ │ │2 yrs.│Good │ 31,800.│ 165.│ 5.2 │ │ │ │2 mo. │ │ │ │ Himalayan Thar │ ♂ │9 mo. │Young │9 mo. │Good │ 9,100.│ 130.│ 16. Ovis tragelaphus, │ │ │ │ │ │ │ │ Aoudad │ ♂ │ │ │3 yrs.│Good │ 77,200.│ 233.│ 3. │ │ │ │2 mo. │ │ │ │ Aoudad │ ♀ │ │Old │3 yrs.│Good │ 41,000.│ 195.│ 4.8 │ │ │ │6 mo. │ │ │ │ │ │ │ │ │ │ │ │ GIRAFFIDÆ: │ │ │ │ │ │ │ │ Giraffa │ │ │ │ │ │ │ │ camelopardalis, │ │ │ │ │ │ │ │ Giraffe │ ♀ │ │ │5 yrs.│Good │500,000.│ 630.│ 1.2 │ │ │ │8 mo. │ │ │ │ Giraffa capensis, │ │ │ │ │ │ │ │ Giraffe │ ♂ │ │Old │7 mo. │ │383,000.│ 670.│ 1.7 (Southern) │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ CERVIDÆ: │ │ │ │ │ │ │ │ Cervus duvanceli, │ │ │ │ │ │ │ │ Barasingha Deer │ ♀ │1 mo. │Baby │1 mo. │Good │ 9,500.│ 121.│ 13. Cervus eldi, │ │ │ │ │ │ │ │ Eld’s Deer │ ♂ │ │ │ │Good │ 59,000.│ 225.│ 3.8 Cervus elaphus, │ │ │ │ │ │ │ │ Red Deer │ ♀ │ │ │ │Good │ 72,700.│ 310.│ 4.4 Cervus porcinus, │ │ │ │ │ │ │ │ Hog Deer │ ♂ │11 mo.│Young │11 mo.│Good │ 25,000.│ 130.│ 5.2 Hog Deer │ ♂ │ │ │3 yrs.│Good │ 41,000.│ 125.│ 3. │ │ │ │4 mo. │ │ │ │ Cervus sika │ │ │ │ │ │ │ │ manchuricus, │ │ │ │ │ │ │ │ Manchurian Sika │ ♂ │ │Mature │6 yrs.│Good │ 56,800.│ 265.│ 4.6 Deer │ │ │ │3 mo. │ │ │ │ Cervus │ │ │ │ │ │ │ │ cashmirianus, │ │ │ │ │ │ │ │ Kashmir Deer │ ♂ │ │ │3 yrs.│Fair │ 56,800.│ 275.│ 4.6 │ │ │ │4 mo. │ │ │ │ │ │ │ │ │ │ │ │ CAMELIDÆ: │ │ │ │ │ │ │ │ Camelus │ │ │ │ │ │ │ │ bactrianus, │ │ │ │ │ │ │ │ Bactrian Camel │ ♂ │ │Mature │11 │Fair │430,000.│ 610.│ 1.4 │ │ │ │yrs. │ │ │ │ Camelus │ │ │ │ │ │ │ │ dromidarius, │ │ │ │ │ │ │ │ Common Camel │ ♀ │ │Mature │5 yrs.│Fair │472,700.│ 465.│ .98 │ │ │ │ │ │ │ │ HIPPOPOTAMIDÆ: │ │ │ │ │ │ │ │ Hippopotamus │ │ │ │ │ │ │ │ amphibius, │ │ │ │ │ │ │ │ Hippopotamus │ ♂ │1 mo. │Baby │1 mo. │Good │ 40,000.│ 195.│ 4.87 │ │ │ │ │ │ │ │ SUIDÆ: │ │ │ │ │ │ │ │ Macrocephalus │ │ │ │ │ │ │ │ africanus, │ │ │ │ │ │ │ │ Wart Hog │ ♀ │ │Mature │7 yrs.│Good │ 59,000.│ 151.│ 2.5 │ │ │ │9 mo. │ │ │ │ Wart Hog │ ♂ │ │ │2 yrs.│Good │ 82,700.│ 150.│ 1.8 │ │ │ │9 mo. │ │ │ │ Wart Hog. │ ♂ │ │ │ │Good │ 90,000.│ 158.│ 1.7 │ │ │ │ │ │ │ │ TAYASSUIDÆ: │ │ │ │ │ │ │ │ Tayassu tajacu, │ │ │ │ │ │ │ │ Peccary │ ♀ │ │Mature │6 yrs.│Good │ 19,650.│ 95.│ 4.8 │ │ │ │6 mo. │ │ │ │ Peccary │ ♂ │ │ │3 yrs.│Good │ 22,700.│ 75.│ 3.3 │ │ │ │6 mo. │ │ │ │ │ │ │ │ │ │ │ │ ENDENTATA: │ │ │ │ │ │ │ │ DASYPODIDÆ: │ │ │ │ │ │ │ │ Tatu novemcinctus,│ │ │ │ │ │ │ │ Nine banded │ ♀ │ │ │2 yrs.│Good │ 1,840.│ 10.│ 5.4 Armadillo │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ MYRMECOPHAGIDÆ: │ │ │ │ │ │ │ │ Myrmecophaga │ │ │ │ │ │ │ │ tetradactyla, │ │ │ │ │ │ │ │ Tamandua Anteater │ ♀ │ │ │1 wk. │Good │ 3,300.│ 24.│ 7.3 │ │ │ │ │ │ │ │ MARSUPIALIA: │ │ │ │ │ │ │ │ DIDELPHYIDÆ: │ │ │ │ │ │ │ │ Didelphys │ │ │ │ │ │ │ │ virginiana, │ │ │ │ │ │ │ │ Common Opossum │ ♂ │ │ │2 wks.│Good │ 2,500.│ 6.5│ 2.6 Common Opossum │ │ │Young │3 mo. │Good │ 351.│ 6.│ 17. │ │ │ │ │ │ │ │ DASYURIDÆ: │ │ │ │ │ │ │ │ Sarcophilus │ │ │ │ │ │ │ │ ursinus, │ │ │ │ │ │ │ │ Tasmanian Devil │ ♂ │ │Mature │4 yrs.│Thin │ 2,950.│ 8.│ 2.7 │ │ │ │6 mo. │ │ │ │ Dasyurus │ │ │ │ │ │ │ │ viverrinus, │ │ │ │ │ │ │ │ Common Dasyure │ ♀ │ │ │2 yrs.│Good │ 680.│ 4.5│ 6.6 │ │ │ │2 mo. │ │ │ │ Common Dasyure │ ♂ │ │ │8 mo. │Good │ 1,130.│ 5.5│ 4.8 Common Dasyure │ ♂ │ │ │1 yr. │Good │ 1,430.│ 7.│ 4.9 │ │ │ │6 mo. │ │ │ │ │ │ │ │ │ │ │ │ PHASCOLOMYIDÆ: │ │ │ │ │ │ │ │ Phascolomys │ │ │ │ │ │ │ │ mitchelli, │ │ │ │ │ │ │ │ Wombat. │ ♂ │ │Mature │9 yrs.│Excellent│ 25,900.│ 70.│ 2.7 │ │ │ │6 mo. │ │ │ │ │ │ │ │ │ │ │ │ MACROPODIDÆ: │ │ │ │ │ │ │ │ Macropus │ │ │ │ │ │ │ │ giganteus, │ │ │ │ │ │ │ │ Great Gray │ ♂ │ │Mature │3 yrs.│Good │ 34,000.│ 65.│ 1.9 Kangaroo │ │ │ │2 mo. │ │ │ │ Macropus rufus, │ │ │ │ │ │ │ │ Red Kangaroo │ ♂ │ │Mature │5 yrs.│Good │ 63,600.│ 70.│ 1.1 │ │ │ │8 mo. │ │ │ │ Macropus unguifer,│ │ │ │ │ │ │ │ Nailtailed │ ♂ │ │ │2 wks.│Good │ 4,600.│ 12.│ 2.6 Wallaby │ │ │ │ │ │ │ │ Macropus thetidis,│ │ │ │ │ │ │ │ Thigh striped │ ♂ │ │ │2 wks.│Good │ 5,150.│ 25.│ 4.8 Wallaby │ │ │ │ │ │ │ │ Macropus │ │ │ │ │ │ │ │ ualabatus, │ │ │ │ │ │ │ │ Black Wallaby │ ♀ │ │ │1 yr. │Good │ 8,170.│ 35.│ 4.2 │ │ │ │6 mo. │ │ │ │ Aepyprymnus │ │ │ │ │ │ │ │ rufescens, │ │ │ │ │ │ │ │ Rufous Rat │ ♀ │3 yrs.│Mature │3 yrs.│Good │ 1,130.│ 15.│ 13.3 Kangaroo │ │1 mo. │ │ │ │ │ │ Rufous Rat │ ♀ │6 yrs.│Mature │6 yrs.│Good │ 1,485.│ 15.│ 10.+ Kangaroo │ │9 mo. │ │9 mo. │ │ │ │ │ │ │ │ │ │ │ │ PASSERES: │ │ │ │ │ │ │ │ ICTERIDÆ: │ │ │ │ │ │ │ │ Quisculus │ │ │ │ │ │ │ │ quiscula, │ │ │ │ │ │ │ │ Purple Grackle │ ♂ │ │ │2 yrs.│Good │ 115.│ 2.7│ 23.4 │ │ │ │7 mo. │ │ │ │ Icterus icterus, │ │ │ │ │ │ │ │ Common Troupial │ ♂ │ │ │2 yrs.│Good │ 53.│ 2.│ 27.7 │ │ │ │7 mo. │ │ │ │ Common Troupial │ ♂ │ │ │4 yrs.│Thin │ 68.│ 2.│ 29.4 │ │ │ │7 mo. │ │ │ │ │ │ │ │ │ │ │ │ PLOCEIDÆ: │ │ │ │ │ │ │ │ Amadina │ │ │ │ │ │ │ │ erythrocephala, │ │ │ │ │ │ │ │ Red headed Finch│ ♀ │ │ │4 yrs.│Good │ 25.│ 1.2│ 48. Munia malacca, │ │ │ │ │ │ │ │ Black headed │ ♂ │ │ │3 yrs.│Good │ 13.│ .7│ 52.6 Finch │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ TANAGRIDÆ: │ │ │ │ │ │ │ │ Euphonia violacea,│ │ │ │ │ │ │ │ Violet Tanager │ ♀ │ │ │2 days│Good │ 15.│ 1.│ 66.6 Violet Tanager │ ♂ │ │ │2 days│Good │ 16.│ 1.│ 62.5 Tanagra cana, │ │ │ │ │ │ │ │ Silver blue │ ♂ │ │ │6 mo. │Good │ 29.│ 1.│ 34.5 Tanager │ │ │ │ │ │ │ │ Silver blue │ ♀ │ │ │1 yr. │Good │ 30.│ 1.│ 33.3 Tanager │ │ │ │2 mo. │ │ │ │ │ │ │ │ │ │ │ │ FRINGILLIDÆ: │ │ │ │ │ │ │ │ Zonotrichia │ │ │ │ │ │ │ │ albicollis, │ │ │ │ │ │ │ │ White throated │ ♂ │ │ │1 yr. │Good │ 35.│ 1.5│ 42.8 Sparrow │ │ │ │6 mo. │ │ │ │ White throated │ ♂ │ │ │6 mo. │Good │ 32.│ 1.5│ 46.9 Sparrow │ │ │ │ │ │ │ │ White throated │ ♂ │ │ │1 yr. │Good │ 23.│ 1.3│ 56.5 Sparrow │ │ │ │8 mo. │ │ │ │ Eophona melanura, │ │ │ │ │ │ │ │ Black tailed │ ♂ │ │ │2 mo. │Good │ 31.│ 2.│ 64.5 Hawfinch │ │ │ │ │ │ │ │ Black tailed │ ♂ │ │ │1 mo. │Good │ 30.│ 1.7│ 56.6 Hawfinch │ │ │ │ │ │ │ │ Java Sparrow │ ♂ │ │ │ │Good │ 28.│ 1.2│ 42.8 Passerina ciris, │ │ │ │ │ │ │ │ Nonpareil │ ♂ │ │ │9 mo. │Good │ 15.│ .5│ 33.3 Bunting │ │ │ │ │ │ │ │ Pipilo │ │ │ │ │ │ │ │ erythropthalmus, │ │ │ │ │ │ │ │ Towhee │ ♀ │ │ │1 yr. │Good │ 16.│ 1.2│ 75. │ │ │ │2 mo. │ │ │ │ │ │ │ │ │ │ │ │ TURDIDÆ: │ │ │ │ │ │ │ │ Turdus iliacus, │ │ │ │ │ │ │ │ Red winged │ ♀ │ │ │5 yrs.│Good │ 55.│ 1.5│ 27.2 Thrush │ │ │ │6 mo. │ │ │ │ │ │ │ │ │ │ │ │ PITTIDÆ: │ │ │ │ │ │ │ │ Pitta strepitans, │ │ │ │ │ │ │ │ Noisy Pitta. │ │ │ │1 yr. │Good │ 92.│ 2.5│ 27. │ │ │ │8 mo. │ │ │ │ │ │ │ │ │ │ │ │ CRATEROPODIDÆ: │ │ │ │ │ │ │ │ Garrulax │ │ │ │ │ │ │ │ leucolophus, │ │ │ │ │ │ │ │ White crested │ ♀ │ │ │2 yrs.│Good │ 105.│ 2.7│ 25.7 Jay Thrush │ │ │ │6 mo. │ │ │ │ │ │ │ │ │ │ │ │ PICARIÆ: │ │ │ │ │ │ │ │ RHAMPHASTIDÆ: │ │ │ │ │ │ │ │ Rhamphastos │ │ │ │ │ │ │ │ cuvieri, │ │ │ │ │ │ │ │ Cuvier’s Toucan │ ♀ │ │ │11 │Thin │ 356.│ 8.│ 22.4 │ │ │ │yrs. 9│ │ │ │ │ │ │ │mo. │ │ │ │ │ │ │ │ │ │ │ │ BUCEROTIDÆ: │ │ │ │ │ │ │ │ Lephoceros │ │ │ │ │ │ │ │ flavirostris, │ │ │ │ │ │ │ │ Yellow billed │ ♀ │ │ │1 yr. │Good │ 177.│ 6.│ 33.8 Hornbill │ │ │ │9 mo. │ │ │ │ │ │ │ │ │ │ │ │ STRIGES: │ │ │ │ │ │ │ │ ALUCONIDÆ: │ │ │ │ │ │ │ │ Aluco pratincola, │ │ │ │ │ │ │ │ Am. Barn Owl │ ♂ │ │ │1 mo. │Good │ 470.│ 11.│ 23.4 │ │ │ │ │ │ │ │ BUBONIDÆ: │ │ │ │ │ │ │ │ Bubo virginianus, │ │ │ │ │ │ │ │ Great Horned Owl│ ♀ │ │ │1 yr. │Good │ 1,415.│ 12.│ 8.4 Otus asio asio, │ │ │ │ │ │ │ │ Screech Owl │ ♂ │ │ │1 day │Good │ 122.│ 6.│ 49. Strix varia varia,│ │ │ │ │ │ │ │ Barred Owl │ ♀ │ │ │11 │Good │ 1,022.│ 12.│ 11.6 │ │ │ │yrs. │ │ │ │ │ │ │ │ │ │ │ │ PSITTACI: │ │ │ │ │ │ │ │ PSITTACIDÆ: │ │ │ │ │ │ │ │ Conurus cactorum, │ │ │ │ │ │ │ │ Cactus conure │ ♀ │ │ │1 yr. │Good │ 64.│ 4.│ 62.5 │ │ │ │6 mo. │ │ │ │ Chrysotis │ │ │ │ │ │ │ │ leucocephala, │ │ │ │ │ │ │ │ White fronted │ │ │ │1 yr. │Good │ 251.│ 8.5│ 33.8 Amazon │ │ │ │ │ │ │ │ Chrysotis │ │ │ │ │ │ │ │ levaillanti, │ │ │ │ │ │ │ │ Levaillant’s │ │ │ │1 yr. │Good │ 300.│ 12.│ 40. Amazon │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ ACCIPITRES: │ │ │ │ │ │ │ │ SERPENTARIIDÆ: │ │ │ │ │ │ │ │ Serpentarius │ │ │ │ │ │ │ │ serpentarius, │ │ │ │ │ │ │ │ Secretary │ ♂ │ │ │2 wks.│Good │ 3,768.│ 15.│ 4. Vulture │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ FALCONIDÆ: │ │ │ │ │ │ │ │ Haliæetus │ │ │ │ │ │ │ │ leucocephalus, │ │ │ │ │ │ │ │ Bald Eagle │ ♀ │ │ │1 yr. │Good │ 2,860.│ 15.│ 5.2 │ │ │ │3 mo. │ │ │ │ │ │ │ │ │ │ │ │ COLUMBÆ: │ │ │ │ │ │ │ │ COLUMBIDÆ: │ │ │ │ │ │ │ │ Ocyphaps lophotes,│ │ │ │ │ │ │ │ Crested Pigeon │ │ │ │3 mo. │Thin │ 142.│ 2.│ 14. Lophophaps │ │ │ │ │ │ │ │ leucogaster, │ │ │ │ │ │ │ │ Plumed Pigeon │ ♂ │ │ │ │Good │ 52.│ 1.2│ 23. Phaps chalcoptera,│ │ │ │ │ │ │ │ Bronze winged │ ♀ │ │ │4 yrs.│Good │ 219.│ 1.5│ 6.8 Pigeon │ │ │ │2 mo. │ │ │ │ Columba phæonata, │ │ │ │ │ │ │ │ Dark backed │ ♂ │ │ │2 yrs.│Good │ 360.│ 2.│ 5.05 Pigeon │ │ │ │9 mo. │ │ │ │ Scardapella │ │ │ │ │ │ │ │ squamosa, │ │ │ │ │ │ │ │ Ground Dove │ ♀ │ │ │2 yrs.│Good │ 23.│ 1.7│ 64. │ │ │ │9 mo. │ │ │ │ Zenaidura macroura│ │ │ │ │ │ │ │ carolinensis, │ │ │ │ │ │ │ │ Carolina Dove │ ♂ │ │ │2 yrs.│Thin │ 92.│ 1.│ 10.8 │ │ │ │9 mo. │ │ │ │ │ │ │ │ │ │ │ │ GALLI: │ │ │ │ │ │ │ │ PHASIANIDÆ: │ │ │ │ │ │ │ │ Coturnix │ │ │ │ │ │ │ │ pectoralis, │ │ │ │ │ │ │ │ Stubble Quail │ ♀ │ │ │2 yrs.│Good │ 70.│ .7│ 10. Lophortyx │ │ │ │ │ │ │ │ californica │ │ │ │ │ │ │ │ californica, │ │ │ │ │ │ │ │ California Quail│ ♀ │ │ │1 yr. │Good │ 180.│ 1.5│ 8.33 │ │ │ │4 mo. │ │ │ │ Arboricola │ │ │ │ │ │ │ │ atrogularis, │ │ │ │ │ │ │ │ Black throated │ ♀ │ │ │1 yr. │Good │ 151.│ 2.5│ 16. Hill Partridge │ │ │ │2 mo. │ │ │ │ Meleagris │ │ │ │ │ │ │ │ gallopavo │ │ │ │ │ │ │ │ silvestris, │ │ │ │ │ │ │ │ Eastern Wild │ ♂ │ │ │ │Good │ 6,340.│ 12.│ 1.9 Turkey │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ CRACIDÆ: │ │ │ │ │ │ │ │ Ortalis vetula, │ │ │ │ │ │ │ │ Mexican Guan │ ♀ │ │ │2 yrs.│Thin │ 442.│ 5.│ 11.3 │ │ │ │2 mo. │ │ │ │ │ │ │ │ │ │ │ │ MEGAPODIDÆ: │ │ │ │ │ │ │ │ Catheturus │ │ │ │ │ │ │ │ lathami, │ │ │ │ │ │ │ │ Brush Turkey │ ♂ │ │ │3 mo. │Good │ 1,487.│ 5.│ 3.37 │ │ │ │ │ │ │ │ ALECTORIDES: │ │ │ │ │ │ │ │ GRUIDÆ: │ │ │ │ │ │ │ │ Grus lilfordi, │ │ │ │ │ │ │ │ Lilford’s Crane │ ♂ │ │ │1 yr. │Good │ 3,790.│ 18.│ 4.7 │ │ │ │4 mo. │ │ │ │ Tetrapteryx │ │ │ │ │ │ │ │ paradisea, │ │ │ │ │ │ │ │ Stanley Crane │ ♂ │ │ │3 yrs.│Good │ 4,450.│ 13.│ 2.9 │ │ │ │3 mo. │ │ │ │ │ │ │ │ │ │ │ │ STEGANOPODES: │ │ │ │ │ │ │ │ ANHINGIDÆ: │ │ │ │ │ │ │ │ Anhinga anhinga, │ │ │ │ │ │ │ │ Darter │ ♂ │ │ │3 yrs.│Good │ 251.│ 8.5│ 33.8 Darter │ ♀ │ │ │7 yrs.│Good │ 998.│ 6.│ 6. │ │ │ │6 mo. │ │ │ │ │ │ │ │ │ │ │ │ HERODIONES: │ │ │ │ │ │ │ │ ARDEIDÆ: │ │ │ │ │ │ │ │ Nycticorax │ │ │ │ │ │ │ │ nyctanassa, │ │ │ │ │ │ │ │ Yellow crowned │ ♂ │ │ │1 yr. │Good │ 620.│ 7.│ 11.3 Night Heron │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ CICONIIDÆ: │ │ │ │ │ │ │ │ Leptoptilus │ │ │ │ │ │ │ │ dubius, │ │ │ │ │ │ │ │ Adjutant Stork │ │ │ │ │ │ 7,873.│ 36.│ 4.5 Leptoptilus │ │ │ │ │ │ │ │ crumeniferus, │ │ │ │ │ │ │ │ Marabou Stork │ │ │ │ │ │ 4,580.│ 24.│ 5.2 │ │ │ │ │ │ │ │ PLATALEIDÆ: │ │ │ │ │ │ │ │ Carphibis │ │ │ │ │ │ │ │ spinicollis, │ │ │ │ │ │ │ │ Straw necked │ │ │ │ │ │ 1,665.│ 89.│ 4.8 Ibis │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ PALAMEDES: │ │ │ │ │ │ │ │ Palmadea derbiana,│ │ │ │ │ │ │ │ Derbian Screamer│ ♂ │ │ │3 yrs.│Good │ 2,730.│ 10.│ 3.6 Derbian Screamer│ ♂ │ │ │1 wk. │Thin │ 1,700.│ 8.│ 4.7 │ │ │ │ │ │ │ │ ANSERES: │ │ │ │ │ │ │ │ ANATIDÆ: │ │ │ │ │ │ │ │ Cygnopsis │ │ │ │ │ │ │ │ cygnoides, │ │ │ │ │ │ │ │ Chinese Goose. │ ♂ │ │ │2 yrs.│Good │ 2,740.│ 15.│ 5.5 │ │ │ │6 mo. │ │ │ │ Plectropterus │ │ │ │ │ │ │ │ niger, │ │ │ │ │ │ │ │ Black Spurwinged│ ♂ │ │ │9 yrs.│Good │ 2,735.│ 13.│ 4.7 Goose │ │ │ │ │ │ │ │ Cereopsis novæ- │ │ │ │ │ │ │ │ hollandiæ, │ │ │ │ │ │ │ │ Cereopsis Goose │ ♀ │ │ │2 yrs.│Good │ 2,370.│ 9.│ 3.6 │ │ │ │3 mo. │ │ │ │ Cereopsis Goose │ ♂ │ │ │1 yr. │Good │ 2,748.│ 11.│ 4. Anser domesticus, │ │ │ │ │ │ │ │ Sebastopol Goose│ ♂ │ │ │3 yrs.│Good │ 3,106.│ 19.│ 6.1 │ │ │ │2 mo. │ │ │ │ Anser fabalis, │ │ │ │ │ │ │ │ Bean Goose │ ♂ │ │ │12 │Good │ 2,640.│ 13.│ 4.9 │ │ │ │yrs. 6│ │ │ │ │ │ │ │mo. │ │ │ │ Chloephaga │ │ │ │ │ │ │ │ magellanica, │ │ │ │ │ │ │ │ Upland Goose │ ♂ │ │ │2 wks.│Thin │ 1,822.│ 8.│ 4.4 Coscoroba │ │ │ │ │ │ │ │ coscoroba, │ │ │ │ │ │ │ │ Coscoroba Swan │ ♂ │ │ │1 mo. │Good │ 1,915.│ 9.│ 4.7 Anas │ │ │ │ │ │ │ │ platyrhynchos, │ │ │ │ │ │ │ │ Mallard Duck │ ♀ │ │ │3 yrs.│Good │ 1,471.│ 8.│ 5.4 Mallard Duck. │ ♀ │ │ │3 yrs.│Good │ 525.│ 6.│ 11.4 Dafila acuta, │ │ │ │ │ │ │ │ Pintailed Duck. │ │ │ │3 yrs.│Good │ 489.│ 6.│ 12.2 Fuligula ferina, │ │ │ │ │ │ │ │ Pochard │ ♂ │ │ │4 yrs.│Good │ 600.│ 6.│ 10. │ │ │ │6 mo. │ │ │ │ │ │ │ │ │ │ │ │ STRUTHIONES: │ │ │ │ │ │ │ │ STRUTHIONIDÆ: │ │ │ │ │ │ │ │ Struthio │ │ │ │ │ │ │ │ molybdophanes, │ │ │ │ │ │ │ │ Samoli Ostrich │ ♀ │ │ │9 yrs.│Thin │ 60,000.│ 37.│ .65 │ │ │ │3 mo. │ │ │ │ │ │ │ │ │ │ │ │ CASUARIIDÆ: │ │ │ │ │ │ │ │ Casuarius │ │ │ │ │ │ │ │ papuanus, │ │ │ │ │ │ │ │ Papuan Cassowary│ ♂ │ │ │8 yrs.│Good │ 24,000.│ 30.│ 1.3 ────────────────────┴───┴──────┴───────────┴──────┴─────────┴────────┴──────┴──────

SECTION XIII-PART II THE EYE

INFLAMMATIONS.

Conjunctivitis is rather rare but does occur in all varieties of animals, seldom however, to the extent that the specimen has to be sacrificed. So far as the daily reports can be relied upon we have had no epidemic inflammations of the eye. The parrots and monkeys are the only animals that can be handled enough for treatment, and in them the applications have not seemed very efficacious. Two cases of conjunctivitis and iritis have had a tuberculous basis and two other specimens have had tuberculosis in the eye. Two parrots had, in association with generalized tuberculosis, semisolid masses in the orbit which dislocated the bulb, thickened the lids and presented as yellowish granulating tumors under the conjunctiva; a Swainson’s long-tailed jay (Calocitta formosa) had this lesion on both sides. The only case in a mammal concerned an Anubis baboon (Papio anubis) in which one eye had been enucleated, two weeks before death, for purulent ophthalmitis. The other eye became affected shortly after the extraction and the animal was killed; it was found to have caseous pneumonia. The tuberculous process had probably begun in the region of the optic nerve and involved the whole bulb. Secondary infection with pyogenic cocci had been superimposed upon the original process. Keratomalacia, encountered on a few occasions, will be discussed by Doctor White.

Iridocyclitis was found in a white browed guan (Penelope superciliaris) the notes of which are condensed as follows:

The internal organs show nothing of value pathologically. The right eye shows moderate conjunctivitis and a marked thickening of the cornea with complete opacity. The lens is destroyed and the retina infiltrated by gelatinous material. Humors are watery, non- suppurative, but the fundal portion of the retina shows several poorly circumscribed, yellowish white, gelatinous collections. Microscopical section of cornea shows replacement of normal bundles by wavy ones intermixed with small numbers of nuclei. These are never of inflammatory type, but always of connective tissue type. Conjunctival mucosa defective in centre, puckered but shows no subjacent inflammatory features. Ciliary body richly infiltrated by lymphocytes and vessels distinctly congested. This condition extends over whole anterior surface of iris and for a short distance over posterior. Sclera shows much bone formation. Chronic interstitial keratitis, subacute interstitial iritis and cyclitis.

CATARACT.

Opacities of the cornea are quite common among our specimens, most often due we believe, to local trauma; ungulates exhibit them more than other varieties. Cataractous opacities of the lens are frequently observed in senile animals but, while I have no figures for the statement, I believe they are not as common among our specimens as can be observed in domestic horses and dogs. No record has been made of streaky clouds or spots in the lens but only of complete opacities. There are three only, an aoudad (Ovis tragelaphus) a macaw (Ara macao) and a summer duck (Aix sponsa) the last of which alone is interesting. This bird, a fully developed adult female, was killed because of total blindness and found to have a low grade chronic pancreatitis and a bilateral Morgagnian cataract, the lens capsule containing a thin cloudy fluid with the nucleus quite freely movable in it.

AMBLYOPIA.

A very interesting case of amblyopia in a young monkey was studied and reported by Dr. H. M. Langdon and Doctor Cadwalader in the Journal of Comparative Pathology and Therapeutics, Vol. XXVIII, Part 4. Because of its unusual character and careful investigation, the report is reproduced here:

Pigtailed macaque (Macacus nemestrinus) was born June 9, 1913, in the monkey house, a well developed baby. He thrived and was as good as any for his age. He was never known to have anything wrong with him until on the morning of June 3, 1914, when he was found on the bottom of the cage in the monkey house. He had clenched hands and feet, jaws tightly closed, lips drawn back, eyes staring and glassy, with convulsive shaking of the extremities. At intervals he would become limp, with fists still clenched, and with only occasional jerks in the extremities. This would last about a minute, and then convulsive movements would be resumed. The entire “fit” lasted about ten minutes. He was immediately removed from the large cage in the monkey house to a small one in the back room of the laboratory. When put in the small cage he staggered as if dazed, and groped about apparently blind. He never recovered his sight entirely, but at times seemed to see better than at others. He was not seen in a “fit” in the laboratory. On June 24th, a small piece of banana was offered by a person who stood directly in the sunlight. The monkey came to the front of the cage, reached out and grasped very firmly the thumb of the hand holding the banana but did not take the banana although he very plainly wanted it. The banana was thrown into the cage, hitting the monkey on the back. He turned very quickly, then smelled over the floor of the cage until he found the banana. On June 30th, he was examined by Doctor Langdon and the following condition was noted:

“Pupils react to the light of the ophthalmoscope. Optic discs are normal. Arteries possibly a little small. No other fundus changes.” On July 1, a cloudy day, he was laid facing a window. A coat sleeve was laid over his eyes for a minute and then quickly removed. His pupils were seen to react slowly but distinctly to the light. His gaze would not follow a finger moved in front of his eyes. When put back in the cage he climbed up on the wire at the back and then tried to climb the plain sheet-iron side. He groped and felt for a support and then fell. This he did several times. About August 1, when the eyes were examined, there seemed to be more visual perception and very distinctly prompter pupillary reflex, which condition remained about the same when examined October 1. He died October 10, 1914, of a compound fracture of the right femur inflicted by a monkey in the adjoining cage.

At autopsy the viscera appeared normal throughout. The animal was fairly well nourished. There was about 5 cc. clear, pale yellow fluid under the dura. It escaped upon removal of the brain. There were adhesions of the dura over the temporal lobe (inferior surface), posterior and external to the optic tract, so firm as to remove some periosteum and superficial bone. Rest of dura seemed normal.

Examination of the brain. Sections were made from different parts of the cerebral cortex, all of which were more or less alike. There was swelling of the endothelium of the pial lymph spaces, with some separation of the fibres of the pia itself which extended into the sulci. The perivascular lymph spaces of the larger arteries of the cortex were dilated, and the adjacent cerebral tissue was edematous. A well marked endothelial swelling and hyperplasia affected a number of the arteries and capillaries producing marked general or nodular thickening in some places. Accompanying these hyperplastic changes there was a marked calcification of some of the arteries. This was not confined to one tunic, but in some instances it extended almost completely through the vessel wall, and here and there the lumen of a vessel was nearly obliterated. The main features were endothelial hyperplasia, edema of the pia and of the subpial cortex with some calcification of the vessels. It was perhaps less well marked in the occipital lobes than in other parts. The optic nerve and other portions of the brain appeared to be normal.

MOON BLINDNESS.

It seems also profitable to repeat here a report Dr. H. M. Langdon and I made in 1911 upon a horse with periodic ophthalmia or “moon blindness,” a widespread condition and one upon which there is even to-day little known and much contradictory theorizing. It is worthy of record that Dr. J. H. W. Eyre of Guy’s Hospital, had a case to study at the same time as ours. He did not find the protozoön-like body discussed below, but laid weight upon the isolation of St. aureus, an organism often mentioned in the literature about this disease. I cite the whole report since our publication in the 1911 Report of this Garden seems not to have been quoted in any of the reference articles on “Moon blindness.” Those who are interested in the clinical and pathological sides of the question will find a good summary in Veröff. aus der-Jahres. Vet. Berichten der beamt. Tierärzte Preussens, 1908, and the bacteriology of the equine eye by Karsten, Inaug. Disser. Giessen, 1909.

“During the latter part of 1909 and first part of 1910 we had a horse referred to us suffering with recurrent ophthalmia or moon blindness. This affection, suggested by its name, is supposed to have some relation to the lunar periods. Some points in our work showed that such may be the case. Attacks appear not infrequently at the time of the full moon, and in our only experimental infection twenty-eight days elapsed between inoculation and a general ocular inflammation.

“This affection manifests itself as a conjunctivitis early in the attack, but rapidly progresses to an iridocyclitis and lastly to a panophthalmitis. After each attack the ball is smaller until it is so shrunken as to be sightless from chronic thickening and opacities. The causation is not known. The disease behaves not unlike an infectious one, remaining in a stud for years at a time. Not every horse may be affected. It has been connected with dampness, bad fodder, overwork and the like. Again others have connected it with malaria or rheumatism. Potapenke, Vigezzi, Koch and others have found various microörganisms, no two of which seem to be the same. Even an animal organism like malaria has been described. (Whether or not malaria has anything to do with the disease, it must be said that our horse was favorably affected in regard to temperature as well as to the eye condition by repeated subcutaneous injections of Quinine Bisulphate, Grain xx daily.) The attacks last five to nine days. One or both eyes may be attacked and not uncommonly do they alternate. One eye may cease to have attacks while the other continues. The experiments here recorded were made with the idea of transmitting the disease to other horses. They were only partially successful. During eight months the affected animal referred to us had six attacks of ophthalmia. The attack was observed for study on the first occasion, but during the second his anterior chamber was entered by a needle attached to a syringe, the exudate aspirated and injected into the eye of a horse with apparently healthy eyes. The history of this second horse will be given later. The attacks of the first horse ranged from six to twelve days. Five of the six affected the left eye and one the right. In January, 1910, the left eye was used for further inoculation, and following this traumatism complete recovery never took place. The corneal scar left by the needle tract almost disappeared, but an inferior anterior synechia formed and was followed by a spreading opacity of the cornea, much wrinkling of the iris and opacity of the depths. After the fourth attack in this eye it was completely blind. Material was obtained from this eye during its last attack, but it was merely serous fluid containing a few blood cells and epithelium, but no bacteria.

“In transferring the affection from this animal, the conjunctival sac was washed with 1–5000 bichloride of mercury solution and well rinsed with salt solution. The anterior chamber was then entered with an aspirating needle and the exudate removed. This consisted of 0.4 cc. slightly turbid straw colored fluid containing a few shreds of lymph. Bacteriological cultures, moist and dry preparations were made from a part of this, while the remainder was introduced into the anterior chamber of the second horse. This animal’s eye showed the effects of the traumatism for eight days, and then was normal save for a small opaque spot in the cornea left from needle puncture. After twenty-three days a small patch of lymph collected in the pupil. This increased slowly accompanied by lacrymation until the twenty-seventh day, when a sudden and violent conjunctivitis arose. The lymph in the anterior chamber likewise suddenly increased and rapidly became pus, forming a hypopyon. The conjunctivitis became purulent. The violent stage lasted five days and slowly subsided, leaving an ectropion with a densely injected bulbar conjunctiva, almost complete corneal opacity and an irregular contraction of iris, apparently due to several small synechiæ. The depths could not be seen because of the corneal condition. This stage of affairs remained during the rest of the animal’s life, two months. He was permitted to live to see if an exacerbation of this chronic process or involvement of the other eye would appear. Such not occurring in two months, he was killed and the eyes removed. Fluid removed from the left eye of the first horse when killed during the last attack was injected into the anterior chamber of a third horse. This animal’s eye received the operation well and the trauma had entirely disappeared when the animal died on the eighth day.

“LABORATORY EXAMINATIONS.—From fluid removed from horse eye (No. 1) anaerobic cultures made on milk and blood serum, blood agar, glycerine agar; cultures were made directly from the fluid, while the coagula were dried upon slides and stained as follows: Loeffler’s, Gram’s, Giemsa. In all there are very few recognizable bodies. They are red blood cells, polynuclears and a very few small mononuclear cells. In regard to microörganisms three structures present themselves. A well staining Gram-positive, rounded end rod of fairly uniform size but tending to grow in pairs and stain rather irregularly with Loeffler and Giemsa. These forms are sometimes called ‘dumbbell’ in that they are bipolar, or even seem to have a constriction in their centre. Another form is peculiar and cannot be said to be recognized as a bacterium. It is circular, of fairly regular size and contour and in many places looks like a very large coccus. In Loeffler’s stain it is colored deeply in the centre with a paler marginal zone and an unstained halo about it, which, however, is not like a capsule. In the Gram and Giemsa method it is deeply blue or purple with a retractile centre and very sharply outlined contour. These forms varied from 3 to 5 microns. The third form is a wavy delicate short mycelium-like thread. Smears from the cultures as made above showed chiefly a Gram-positive, rounded end rod but which did not grow on planting out. It grew on aerobic media, but was not found on anaerobic. The Gram-positive organism would not grow beyond the fourth generation. It was not identified with any known species by the characters manifested during the short time we were able to keep it alive but could be placed in the Hog Cholera group. The mycelium was found to be an aspergillus. In regard to the large coccus-like body, little can be added to the above description. Further examination did not reveal characters permitting us to place it among the protozoa. No evidences of division were seen. The body is quite uniform in appearance, varying only in size. Whatever this is it seems to be an organized body.”

“Cultures from pus in the anterior chamber of the second horse showed the palely staining rod, an aspergillus and Micrococcus aquatilis. The first was planted on horse serum bouillon, but did not grow after the first generation. These cultures were made after death, but the cultures made during the acute attack direct from conjunctival sac contained such a host of organisms that no judgment could be formed of their relative importance. The polar staining rod was found in smears. No large coccus- like bodies were observed in the second horse. Fluid taken from the first horse’s eye at death was sterile.”

“These observations are at variance with those of others but such results are not unique in this respect. It seems as if the polar staining rod deserves some consideration, and we expect to devote some attention to it if another horse suffering from recurrent ophthalmia come to our notice. The large coccus-like bodies are very interesting and may be protozoa. The finding of the amœba in the cases of Potapenke, increases their importance. Before, during and after the fourth attack of the first horse twenty grains of quinine bisulphate were given hypodermically daily for twenty days. The attack was very mild. Before the drug was given his temperature had ranged from 99° to 101° F. Immediately after the first dose the temperature fell to below 99° F., and remained at a very regular level during the entire twenty days. No malarial organisms were found in the blood.”

The ear is without special interest except as a place of localization of sarcoptes, demodex and fly larvæ. A few cases of acute catarrhal otitis media have been found in association with nasopharyngitis both of the nonspecific variety and that which resembles distemper. One case which led to meningitis has been mentioned.

SECTION XIV CONSTITUTIONAL DISEASES

There is a long list of diseases including among others such conditions as hyperthyroidism, osteodystrophies, diabetes and gout which are spoken of as constitutional but which in reality are usually dependent upon some lesion peculiar to a definite organ. Several have been discussed under systemic diseases so that there remain for consideration in this section only two, gout and diabetes.

Constitutional diseases are recognized in wild animals either not at all or by some happy chance which permits of examination direct enough to elicit diagnostic criteria. Gout has been discovered for example in some parrots and herons because of their swollen feet and their movements. In veterinary practice fairly accurate diagnoses are possible but in wild collections they are nearly always hit or miss. Therapeutics naturally follow this rule.

GOUT.

Gout in mammals has been observed in the London Zoological Garden but has not been encountered here or we have overlooked it. Avian gout on the other hand in one of its forms comes to our attention not infrequently. It occurs most often in parrots, gallinaceous and anserine birds and herons; occasionally accipitrine birds will suffer with it, an observation more often recorded in European collections than with us. The figures show no predominance of percentage for any order but the records indicate that the most beautiful examples of internal uratic deposits occur in the anserine birds and parrots, while the best specimen of general gout, including the joints, was found in a boat- billed heron (Cancroma cochlearia) quoted below.

In so far as etiology of this disease is concerned in domestic stock, too rich food, especially in protein, and restriction of activity seem to be credited with the greatest influence. These factors, while doubtless of importance for birds as they are believed to be for man, do not seem to fill all the requirements since all our specimens are confined and, because of their lack of exercise, possibly receive too much food. Judging by our observations and by publications from other gardens, carnivorous birds are not conspicuous for the incidence of gout whereas grain- seed- and fish-eaters suffer more often. This suggests that these varieties cannot dispose of dietary protein which might be excessive for their metabolism while in captivity, whereas carnivorous species have a digestive and chemical reserve to take care of excess protein. Some such accommodative power must exist in human beings since not every large meat-eater develops gout. Heredity, often blamed for the human disease cannot help us with these birds. Examination of the diet list at the Garden does not reveal a great percentage of concentrated protein in the feed of the grain- and seed-eaters. The disease occurs too seldom to disturb the accepted dietary for its possible elimination. Studies now going on may indicate appropriate changes in the dietaries that might be responsible.

Arthritic gout appears usually in the pedal joints but may be found in the wings. Irregular, sometimes very deforming swellings appear which must be tender judging by the quietness of the bird and by its behavior if the joints be touched. Most often the swelling seems greater upon the flexor (palmar) surfaces of the toes or in the end of the tarsal articulation. Aside from these few observations there is nothing peculiar about the attack or the specimen during its sickness. Chronicity seems to be the rule and little emaciation may be found. Appetite is normal or excessive, provided the food can be reached.

Internal or serous membrane gout cannot be recognized during life so far as I know. The bird may seem in its usual condition of feather, activity, appetite and elimination, when suddenly it will fade in a day or so and die. At autopsy the serous surfaces of the heart and peritoneum will be white with uric acid crystals and the kidneys a pale yellow brown with markings indicating that the pelves and tubules are choked with urates.

The boat-billed heron (Cancroma cochlearia) had had bad feet for three months. The general condition is poor as to plumage and flesh. The tarsal and metatarsal joint areas of both legs are surrounded by firm tough swellings involving skin and periarticular tissue. That on left foot has ulcerated and bled. On section the swelling is found to consist of reddened fibrous tissue around tendons, the latter apparently running through smooth sheaths. At both ankles are urate deposits clearly seen in this inflammatory tissue but at the lower end of the tarsus there are no distinct deposits. The joint surfaces do not seem to be involved. Knee, hip, and wing joints seem uninvolved. Internally all surfaces are opaque by sprinkling of whitish or yellowish dots like urates; this is especially marked over heart. Pleuræ aside from urates are negative. Lungs very slightly uniformly congested throughout. Aorta and branches are stiff, intima smooth. The liver is soft, deep brown color, architecture seems normal. The kidney has a smooth capsule and a smooth pale yellow surface. Organ is firm. Section surface is glistening and opaque, every lobule clear, pelves filled with pale yellow material, cortical areas irregular. Alimentary tract negative. Microscopical section of kidney shows general topography retained, vessels very much injected, some showing thrombosis. Cortex slightly irregular probably by swelling of medulla. Tubular epithelium swollen and granular or desquamating and degenerating. Glomeruli vary in size and shape, mostly fill out the capsule. Capillary cells show some vacuoles. Some urate collections in tubules; practically all pelvic tubules have some urates. Interstitial tissue not increased. Blood vessel walls somewhat loose. Endothelium prominent. No areas of degeneration seen.

DIABETES.

Diabetes is an infrequent but well recognized disease among domestic animals. Its detection depends on a rather vague chain of symptoms confirmed by the discovery of sugar in the urine. For the suspicion that a wild animal was suffering with diabetes one would have to rely upon great thirst, loss of flesh, depression, excessive urination and possibly cataractous opacity of the eye. Such a chain of symptoms has not been detected. At every occasion at postmortem that the bladder is full of urine, a routine examination is made. In this way we detected one case which seems to have been diabetes, the diagnosis being based upon the glucosuria and the lipemia. For some unknown reason a section of the pancreas was not made, a regrettable matter since a definite purulent gingivitis existed and may have lain at the basis of an infective pancreatitis, well known to be the cause of certain cases of diabetes. The case is recorded in full since it is unique, no other case in a wild animal being fully reported.

The arctic fox (Canis lagopus) ate and appeared well the day before it was found dead. Diagnosis—Diabetes mellitus. The animal was in good condition. The left conjunctiva was reddened, congested, edematous, with slight mucopurulent discharge in canthus. Muscles have a cloudy appearance. Fat lacks rich yellow color. The general impression of anemia is present. Lungs and pleura are normal throughout. Heart muscle is pale, firm and tough. The tricuspid shows thickening of the edge of posterior leaflet, the mitral shows slight sclerosis of edge of mesial leaflet. The auricles are distended with clot. Left ventricular wall is greatly thickened. Upon incising the heart the surface of blood shows fine fat globules. Peritoneum is normal. Liver is slightly increased, surface smooth, edges rounded, consistency soft, color brownish red with yellow mottlings which are without definite boundaries; the section surface is moist, granular and opaque. The bile is fluid, green-yellow and the duct is patulous. The spleen is slightly enlarged and soft. The kidney is slightly enlarged, capsule strips easily leaving a smooth, purplish red surface; section surface is glistening, moist and exudes blood; consistency is slightly softened; cortical striæ very distinct. The bulging cut surface and poor demarkation of cortex and medulla characteristic of acute nephritis are present. The organ shows fat globules in the expressed blood. The adrenals are very small, firm, brown, bean-shaped bodies with a brownish medulla. The bladder is slightly distended with turbid urine. Urine shows dark granular casts, compound granule cells, spermatozoa and a positive Fehling’s test. Prostate is large and firm and a turbid material exudes from external meatus. The mouth shows several decayed teeth. In the neighborhood of last molars on left side of upper jaw a bead of pus exudes; further pressure results in no greater flow. The stomach is distended with a great quantity of undigested food and gas; no worms. Serosa and wall normal but anemic. Duodenum normal. Jejunum contains numerous worms about 1 to 1.5 cm. long; it is distended with gas. The pancreas is large, soft, like fat, white; it extends between the layers of mesentery along the course of the duodenum; at first the pancreas was mistaken for fat.

HISTOLOGICAL NOTES.—Spleen shows a distinct overgrowth of trabeculæ. Beyond this there is nothing pathological. Liver shows distended portal venules in which there are chains of bacilli. There is no especial fibrous overgrowth of capsule of Glisson; capillaries are choked with shadow corpuscles and here too, long chains of bacilli may be seen; parenchyma cells show postmortem change. Adrenal is the seat of postmortem degeneration, not congested, nor is there any evidence of bacterial invasion. The kidney shows no interstitial changes, in fact the section seems to be entirely normal save for moderate congestion. Vessels show no bacteria.

SECTION XV THE RELATION OF DIET TO DISEASE

BY

DR. E. P. CORSON-WHITE

Food in the widest acceptation of the term, means every thing ingested that goes, directly or indirectly, to growth, repair of the body, or production of energy, all of which phenomena must continue when food is withheld or supplied in insufficient quantities. Under the latter condition the processes go on at the expense of the body tissues as these are protected only when the diet is adequate in every way. A proper diet, therefore, must be one on which an animal will attain maximum development, maintain a normal weight curve, show a minimum susceptibility to disease, live out a full term of life, breed normally, and rear healthy offspring, capable of normal independent life after they are weaned. It must fulfill the caloric needs of the body, and in young animals it must also supply the growth impulse. In its physical properties it must fit the morphological demands of each type of gastrointestinal tract. In its chemical content it must supply all the elements found in the body in usable form, and in amounts sufficient to cover the needs of the body for growth, repair and waste. To evaluate fully the influence of food on the individual animal it is necessary to study its relation: (1) to the type of alimentary tract, (2) to the type of bacterial flora and their metabolic processes, (3) to the chemical needs of the body, (4) to the changes arising in the catabolism and anabolism of all types of food, (5) to exercise or its lack, keeping in mind always the constant interdependence of all factors. Our knowledge of nutrition has to a very large extent paralleled the advances in chemistry, especially the researches into the structural makeup of living cells, the intermediate stages in their upbuilding and degradation and the products resulting from their physiological activities.

Incorrect feeding both qualitative and quantitative undoubtedly plays an important rôle in producing disease. In the early works on nutrition, the proportion of fats, carbohydrates and proteins was regarded as the essential point of a normal diet. The researches on the composition of foods marked the first real epoch in this history and Fischer’s[57] studies on the variation in the composition of proteins from different sources first introduced the idea of quality. Later Mendel and Osborne investigated the biological values of purified proteins, while at the same time McCollum and others were studying the value of the groups of proteins occurring in a single natural food stuff, were calling attention to the so-called vitamines, and were emphasizing the need of balanced inorganic materials. These studies have practically revolutionized our knowledge, particularly of the effects of badly balanced foods. They have clearly demonstrated that dietary values can, in all probability, be discovered only by careful biological study of feeding experiments together with the finer analysis of the components of the diet, especially of the protein and fat radicles. At the same time a definite appreciation of the rôle of each element in metabolism must be kept in mind.

These varied studies on nutrition have shown that the chemical requirements of a diet are in their ultimate analysis essentially the same for all species of the higher animals—that is all require approximately the same amount of protein, fat, carbohydrate, etc., per kilo of body weight, while the morphology of the tract decides the physical properties of the diet.

RELATION OF FOOD TO ALIMENTARY TRACT.

Food derived from animal sources is high in protein, readily digested, and highly putrefactive. This type of diet is suited to an alimentary tract which permits rapid passage through its length, and is fitted with sturdy walls. The gastric section is simple, the intestine short and narrow with ill-defined separation of its parts into small gut, cecum and colon. This type is found in all land Carnivora. The fish-eating carnivores have a strong tubular stomach and an enormous length of intestine, but no cecum. The omnivores occupy a middle place. In them the alimentary tract consists of a simple stomach, a short wide intestinal tube, and a more complex, although still comparatively simple, cecum which is generally longer than that found in the carnivores. This tract is too small to manipulate the bulky vegetable masses necessary to provide their minimum protein requirement, and too long and complicated to dispose quickly of the putrefactive animal tissue. Among these animals colitis is common, due to the fact that the shape and position of this part of the tract favors stasis, or at least a sluggish movement of its contents at a point in the digestive scheme where the food residue is rich in protein by-products, ready for bacterial growth.

The herbivores with food derived from plants which requires a long period of time for its digestion, have, on the other hand, voluminous stomachs, or large ceca or both; and very long small intestine. In this tract the concentrated food of the carnivores would provide an enormously excessive protein intake or if only the protein requirement is supplied would leave the tract so empty that it would be unable to functionate.

All studies in comparative anatomy demonstrate the fact that while neither a complex stomach nor a large cecum is essential to the digestion of vegetable food, a capacious and complex alimentary canal, as a whole, bears a relation to vegetable diet, particularly in the mammals. Either a highly developed concentrated glandular apparatus is added to the stomach, as in the wombats, beavers and dormice, or the stomach is subdivided, sacculated, or otherwise amplified as in the ruminants and herbivorous marsupials. Sometimes both complexities are combined as in the case of the sloths. If the simple stomach is retained, it is supplemented by a large sacculated colon or cecum, as in the horse. In birds, the proventricle is larger in meat- and fish- eaters, while the gizzard is more muscular in grain- and insect-feeders, and the intestines are longer in those devouring coarse green grass and leaves. The length of the ceca is related entirely to the diet, the long ones corresponding to the diet which needs protracted periods of time to exhaust its nutriment.

THE BACTERIAL FLORA.

The bacterial flora harbored in the intestinal tract is closely related to the type of food and to the character of the alimentary tract. Levin[58] found sterile intestinal tracts in white bears, seals, reindeer, eider ducks and penguins when in the Arctic regions; but these same animals when they are brought to a temperate climate rapidly acquire intestinal bacteria. The function of the normal inhabitants of the tract is, probably, to protect the body against invasions of obnoxious species. Herter found in man that a few species adapt themselves to the digestive tract and control the growth of newcomers capable of doing injury. These common varieties become a source of danger only when present in large numbers.

Bacteria which produce decomposition of food in the digestive tract are of three types: (1) Pure putrefactive anaerobes, (2) organisms both fermentative and putrefactive, but tending generally to antagonize the putrefactive anaerobes, and (3) fermentative organisms. In the stomach, fermentation of carbohydrates with the production of organic acids is a frequent occurrence. Putrefactive types are very rare except with pyloric stenosis, a condition which favors excessive fermentation by diminishing the tone and motility of the stomach and the amount of hydrochloric acid. This condition is further increased by excessive carbohydrate food. In general the products of fermentation tend to restrict putrefaction, yet both may be operative. In the small intestines, bacteria are always present because of the protein richness of secretions, the rapid digestion of food and the slight or ineffectual antiseptic properties of intestinal juice, bile and pancreatic secretions. The putrefactive bacteria rapidly increase and decompose any protein that is unabsorbed—a process most marked in the colon because its shape and position favor stasis or slow movement of its contents. In general the greater the amount of unabsorbed and digestible protein and the longer the material stays in the intestinal tract, the greater the putrefaction. The meat-eating animals develop Gram-negative bacilli, while the carbohydrate-eaters show a predominance of Gram-positive types.

Ingested food never contains the enormous amount of bacteria found in the feces. The alimentary tract with its contents forms a most efficiently combined incubator and culture medium, in which bacterial growth exceeds that of any known location both in intensity and complexity. The range of reaction and composition of nutritive substances at different levels of the intestinal tract is such that a great variety of bacteria capable of growth at body temperature develop. The prominent types that appear in the flora of each order of mammals are fairly constant in their occurrence. They depend primarily on food ingested, and show well marked seasonal variations, dependent again on changes in food. Faulty feeding may itself give rise to a toxic condition of the gastrointestinal tube, and thus often prepares this soil for the development of organisms.

The intestinal flora also changes along rather definite lines as the diet of the host changes from the monotony of the infant to the variety of the adult. At birth the tract is sterile, but bacteria soon make their entry through the mouth in food and water. The majority of these organisms pass to the stomach where many are destroyed, but a number travel to the intestines where they may gain a foothold. There is always a mechanical transportation of intestinal bacteria from higher to lower levels. A continued preponderance of protein in the diet of all animals leads to a partial or complete suppression of the Gram-positive acid- forming groups and an increase of the proteolytic Gram-negative types; while on the other hand an excess of carbohydrate leads to diminution or suppression of proteolytic activity and an increase in the fermentative organisms. Therefore the most important normal factor in determining the intestinal flora in health is the chemical composition of the ingested foods.

The nature of the dominant organisms which develop in diets rich in carbohydrates varies with the carbohydrate itself. In all ordinary diets there are (1) starches—forms not readily fermentable, and (2) sugars— which are largely absorbed from the higher levels of the small intestine, leaving residual starches and proteins in relatively great concentration in the lower levels. Therefore the obligate fermentative organisms are prominent only in the higher levels, the facultative appear in the intermediate places, and the obligate proteolytic organisms in the lower intestines. This accounts in a measure for the great increase of lower intestinal disturbances in omnivores. Complete proteins resist putrefaction, but the products of protein digestion and of the intestinal secretions constitute the main substrata for putrefactive bacteria. Animal protein develops more active proteolytic bacteria than vegetable protein, which accounts for the greater predominance of putrefactive infections in carnivores than in omnivores.

There are two important factors to consider in discussing the influence of diet on intestinal bacteria: (1) The substitution of types, which frequently follows a monotonous diet, and (2) the change in metabolism of existing types of bacteria when dietary conditions are such that the intestinal medium at one or another level fluctuates in its content of usable carbohydrate and other nutrient. The nature and extent of these modifications and their effects upon the host vary greatly, not only qualitatively but quantitatively. An invasion of the tract by exogenous bacteria, as the dysentery bacillus, cholera, typhoid, etc., in food or water may lead to a more or less pronounced replacement of some of the normal intestinal types by these alien organisms, and to the production of disease.

The importance of all the foregoing facts concerning the changes in the food, in the intestinal cultural substrata and in the advent of new kinds of organisms was emphatically demonstrated in the marked fall in gastrointestinal diseases in carnivores after proper screening of meats. The simple protection of the food given to these animals eliminated the air bacteria which, entering from dust and flies, alter the chemistry of the meat before consumption or change the flora of the intestine after consumption. Normal organisms, or types indistinguishable from them, may multiply, through unusual conditions, extend their normal habitat, and eventually lead to abnormal reactions detrimental to the host. These facts throw considerable light on the site and character of gastrointestinal lesions found in various orders, a subject to be discussed more fully later.

There are many intestinal disturbances of unknown causation, in some of which bacteria presumably play a secondary part. The primary disturbance is due to the products resulting from the action of bacteria upon food. Many toxic bodies are produced either before or after ingestion by the bacterial decomposition of carbohydrate, fat or protein, independent of any actual infection. The symptoms arising from bacterial decomposition of foods depend largely on the organism concerned and vary from a mild intoxication to a severe toxemia.

RELATION OF DIETARY GROUPS TO AUTOPSY DIAGNOSES.

Analysis of the autopsies on file from sole point of view of dietary habits of the animals gives rather interesting groupings of disease states, which apparently and, in some cases definitely, emphasize the relationship between food, metabolism and disease. (Table 19.)

From this table a few facts stand out prominently. It is definitely shown that both birds and mammals on a diet of mixed animal and plant tissue show a low percentage of disease in the gastrointestinal tube, liver, pancreas and kidney. The mammals on this diet give the highest figures for anemias and degenerative osseous conditions. Birds on this diet show very little osteomalacia, but a fair amount of anemia. Possibly this may be accounted for by the fact that all of them pick gravel and may be able from this to supply some of the inorganic deficiency. Carnivorous birds and mammals, on the other hand, show an exceedingly large assortment of gastrointestinal disorders, diseases of the accessory glands of digestion, and of the kidneys. Disorders of the thyroid gland are almost entirely confined to carnivorous mammals—7.5 per cent., compared to 0.25 per cent. in all other orders. Gout, while common among birds, was not present in any mammalian autopsy, while arthritis in mammals reached its highest record among grass- and grain- eating herbivora. The percentage of rickets was highest in the young carnivores (2.6 carnivores as against .4 per cent. in all other mammals), and was very rare among all birds.

The succulent vegetable diet was lowest in its relation to degenerative visceral disorders and highest in acute gastritis; the latter fact was probably due to the fermentation of soft moist food that requires rather a long time for its primary digestion. This type of food has also a high and easily available sugar content which makes it a very favorable medium for many of the fermentative types of bacteria. Most of the lesions in this group were around the pylorus and upper duodenum.

TABLE 19. An Analysis of the Pathological Findings Described in the 5,365 Autopsies from the Point of View only of the Dietary Habits of the Animals. The Percentage Results Represent the Proportionate Number of Cases of Each Pathological Lesion Found in the Entire Group of Animals on Each Special Diet without Reference to Zoological Orders. ═════════════════╤═══════════════════════════════╤═══════════════════════════════ Disease states │ Mammalia 1860 │ Aves 3505 ─────────────────┼──────┬───────┬────────────────┼──────┬───────┬──────────────── „ │Omniv-│Carniv-│ Herbivora │Omniv-│Carniv-│ Herbivora │ ora │ ora │ │ ora │ ora │ ─────────────────┼──────┼───────┼──────────┬─────┼──────┼───────┼─────┬────────── „ │ „ │ „ │Succulent │Grain│ „ │ „ │Seeds│Succulent │ │ │Vegetables│ │ │ │ │Vegetables ─────────────────┼──────┼───────┼──────────┼─────┼──────┼───────┼─────┼────────── Malnutrition │ .1│ 1.6│ .6│ 2.2│ .05│ .4│ .1│ Food Poisoning │ .3│ │ │ 2.5│ .05│ .2│ .08│ Acute Gastritis │ 3.2│ 6.3│ 9.3│ 3.1│ .9│ 2.│ 1.3│ 13.5 Acute Duodenitis │ .5│ .3│ │ .5│ .1│ 1.4│ 1.2│ 5.4 Acute Enteritis │ 2.5│ 3.4│ 3.│ 3.1│ 7.│ 1.│ 8.│ 5.4 Acute │ 26.3│ 53.2│ 19.9│ 29.2│ 25.3│ 38.6│ 35.6│ 64.8 Gastroenteritis│ │ │ │ │ │ │ │ Chronic Gastritis│ 1.1│ 6.│ 2.│ .8│ .2│ 1.4│ .3│ 5.4 Chronic Enteritis│ 2.│ 5.6│ 3.│ 2.2│ 1.1│ 3.3│ 1.3│ 13.5 Colitis │ 1.9│ │ │ │ │ │ │ Acute │ .1│ 2.2│ 1.│ 3.1│ .4│ .6│ .08│ Pancreatitis │ │ │ │ │ │ │ │ Chronic │ .5│ 1.7│ │ │ .2│ 1.2│ .5│ Pancreatitis │ │ │ │ │ │ │ │ Acute Liver │ .8│ 1.3│ .3│ 1.4│ 4.2│ 2.8│ 2.5│ 2.7 Disease │ │ │ │ │ │ │ │ Chronic Liver │ 3.│ 6.3│ 3.3│ 6.│ 1.1│ 2.5│ 1.6│ 13.5 Disease │ │ │ │ │ │ │ │ Acute Nephritis │ 9.1│ 12.2│ 12.7│ 12.4│ 5.1│ 6.7│ 4.1│ 8.1 Chronic Nephritis│ 4.5│ 11.6│ 6.7│ 7.8│ 2.9│ 6.7│ 2.1│ 13.5 Myocardial │ .1│ .34│ │ 1.1│ .3│ 2.│ .4│ 8.1 Degeneration │ │ │ │ │ │ │ │ Arterial Disease │ .1│ 3.1│ .3│ 2.2│ .3│ 3.1│ .66│ 1.8 Anemia pernicious│ .3│ .32│ │ │ │ │ │ Anemia secondary │ 4.2│ .32│ 1.2│ 1.5│ 1.1│ 2.5│ 1.5│ Thyroid Disease │ │ 7.5│ .3│ .7│ .3│ .2│ .3│ Adrenal Disease │ 1.6│ 1.3│ .3│ 1.5│ │ │ .08│ Diabetes │ │ .2│ │ │ │ │ │ Osteomalacia │ 5.2│ .4│ 2.3│ .2│ .1│ .6│ 2.8│ Osteitis │ .6│ │ │ │ │ │ │ deformans │ │ │ │ │ │ │ │ Arthritis │ │ .3│ .3│ 2.2│ │ .2│ .08│ Rickets │ .1│ 2.6│ .6│ .7│ │ │ .08│ Gout │ │ │ │ │ │ .4│ .08│ Sore Eyes │ │ .3│ │ .2│ .1│ │ .3│ Malignancy │ .05│ .9│ .6│ │ .05│ │ .6│ Tuberculosis │ 32.6│ 3.5│ 4.5│ 9.6│ 12.│ 1.7│ 17.2│ 5.7 ─────────────────┴──────┴───────┴──────────┴─────┴──────┴───────┴─────┴──────────

Overeating is a factor that must be borne in mind when considering the hay- and grass-eating herbivora. Packing of the rumen is a not infrequent discovery. This condition is also found in certain seed- eating birds. As a supply of food is constantly at the disposal of these animals and exercise is prevented by captivity, continuous eating becomes their principal diversion. In this group also food poisoning was highest, a condition which may be due to (1) spoiled food, (2) poisonous substances in the foods, (3) fermentation of grass foods (spoiled hay or musty fodder). Malnutrition also, is higher than with any other diet, due probably to the somewhat meagre nutritious value of the food. This group also shows a high percentage of acute pancreatitis, degeneration of the liver, myocardium and arteries. Arthritis was present in this group 2.2 per cent., against 0.2 per cent. in all other groups.

A study of Table 19 demands a constant recollection of the morphology of the tract involved and its main points of vulnerability, the bacteria capable of living on the particular type of food or its constituents and the by-products produced during the digestion and absorption of these foods. Not one of these factors can be ignored in evaluating the influence of diet, which to be correct must supply elements in proportions that are chemically available for body needs (for instance, Von Wendt[59] found that more iron was required if the diet was deficient in calcium). These proportions must be worked out by carefully combined chemical and biological experiments.

MALNUTRITION.

There was one omnivorous beast, a Hamadryas Baboon, which represented the only true case of starvation, probably induced by nostalgia, as it never ate after coming into the Garden. Thirty cases of partial starvation or malnutrition are listed in our records, the majority among the rarer specimens, ten carnivorous, seven herbivorous and one omnivorous mammals, ten carnivorous and two seed-eating birds, due possibly to inappropriate diet or to some unknown factor that rendered the diet inadequate. At the autopsy nothing was found to account for death except the draining of all storage supplies.

STARVATION.

The reports of studies conducted during long laboratory fasts have been among the most valuable records for the understanding of the chemical requirements of diet and of the close chemical interrelationship existing between the different food factors. In absolute starvation life is very short, primarily because water is necessary for respiration, for dissolving products of metabolism and for preventing changes in digestive intestinal secretions. The amount of water needed varies with different species of animals. If the water is supplied, the organism is enabled to maintain its energy for continued existence from the destruction of its own tissues. The length of life depends upon the amount of protein ingested before the fast commenced, and the amount of stored fat and glycogen, especially that stored in the liver. The mechanism of the results is similar. The animal body uses first its available glucose, and when this is partially exhausted burns its stored fat and protein. The fat combustion is usually defective, ketone bodies appearing in the urine in large quantities. The change from fat to protein metabolism accounts for the premortal rise in metabolism which occurs usually a few days before death. The chemical composition and corpuscular richness of the blood is tenaciously preserved; glucose and protein concentration are practically normal up to the day of death. There is at times a slight increase in globulins and always an increase in fat due to its transportation from storage depots. The cause of death is primarily due to loss of substance in organs necessary to life and to an acid intoxication.

Wasting occurs first in stored substances, fat, glycogen, etc., then in the least used organs. The bones usually show some rarefication. The animal, as a rule, dies from acid intoxication before atrophy of the organs is marked.

In the wild, when animals are forced to seek their food with the expenditure of much energy and where feasts are often followed by fasts, this using up of storage supplies cannot help being a factor in preserving the integrity of the storage and eliminative organs. In captivity this cannot occur. Food is supplied regularly, exercise is lacking, consequently overloading and disease of storage and eliminative organs is more or less constant—a situation very marked in the Carnivora.

TABLE 20. _Detailed Analysis of the Various Diets Used at the Philadelphia Garden on Basis of 100 Grams of Mixed Food._ ═════════════╤══════════════╤═════════════╤══════════════╤═════════════ │ Omnivora │ Carnivora │ Herbivora │ Herbivora │ │ │ Succulent │ Coarse Food │ │ │ Vegetables │ ─────────────┼───────┬──────┼──────┬──────┼───────┬──────┼──────┬────── „ │Mammals│Birds │ Meat │ Fish │Mammals│Birds │ Hay │ Seed │ │ │ │ │ │ │ Food │ Food ─────────────┼───────┼──────┼──────┼──────┼───────┼──────┼──────┼────── Protein │ 14.3│ 11.5│ 15.6│ 17.2│ 6.1│ 3.2│ 6.4│ 7.1 Fat │ 9.5│ 7.2│ 18.8│ .3│ 2.6│ .5│ 2.2│ 1.3 Carbohydrate │ 26.7│ 41.2│ │ │ 18.5│ 25.7│ 35.9│ 51.2 Calcium │ .034│ .068│ .058│ .109│ .067│ .025│ .071│ .044 Magnesium │ .058│ .093│ .118│ .133│ .164│ .119│ .289│ .16 Potassium │ .497│ .713│ 1.694│ 1.671│ .538│ .242│ .644│ .324 Sodium │ .103│ .284│ .421│ .373│ .08│ .291│ .089│ .261 Phosphorus │ .263│ .484│ 1.078│ 1.148│ .556│ .342│ .692│ .458 Chlorine │ .117│ .377│ .378│ .528│ .038│ .044│ .073│ .063 Sulphur │ .338│ .486│ 1.146│ 1.119│ .134│ .125│ .217│ .163 Iron │ .0032│ .0063│ .015│ .0055│ .0018│ .0012│ .0022│ .0012 ─────────────┴───────┴──────┴──────┴──────┴───────┴──────┴──────┴──────

A further study of Table 19 in the light of the finer analysis of the ingredients of the diets, shown in Table 20, explains, at least in part, the high percentage of certain types of disease in relation to particular diets.

In the food of the first group, the omnivorous mammals, there is a moderately increased carbohydrate content and an unevenly balanced inorganic content, the last being the factor most at fault. The calcium and phosphorus are both so low that at the best the animal could only be in equilibrium, while any drain of the fixed bases would sooner or later have to be replenished from the calcium and phosphorus storage depots, the bones. Osteomalacia is most marked in the Cebidæ, monkeys whose diet is even lower in these same elements: calcium .025, phosphorus .116, and iron .0008 per 100 grams of food. The inorganic composition of all animals is grossly similar; the typical digestion developed from the habitual diet of the animal explains the more apparent changes and variations in their reactions to certain deprivations.

IRREGULARITIES OF INORGANIC METABOLISM.

Twelve essential elements are present in the body, namely: carbon, nitrogen, hydrogen, oxygen, phosphorus, calcium, sulphur, sodium, chlorine, potassium, iron, magnesium. Of these, five are furnished by the protein molecule and three of the five are duplicated in the fats and carbohydrates; the remaining seven must be present in the mineral ash. These elements functionate in three ways, (1) as constituents of bone, (2) as essential elements of organic compounds, (3) as soluble salts in body fluids. Chlorine, sodium, sulphur are supplied in sufficient quantity with most diets. In the case of chlorine, marked differences exist between the herbivores and carnivores. The meat-eating mammals easily acquire sufficient sodium chloride from the flesh and blood of their victims, while the herbivores on the other hand, find in their vegetable food large amounts of potassium and very little sodium or chlorine which must therefore be acquired separately. Both omnivores and herbivores crave salt, probably because this large potassium content of vegetable food tends to increase the sodium elimination. A deprivation of salt always leads to a distaste for foods rich in potassium. So far as is known excessive sodium stimulates protein catabolism, and through the overstimulation of the digestive tract, may interfere with the absorption of food.

Sulphur is largely taken into the body in organic combination with the protein, (a very little inorganic sulphur appears in the drinking water) therefore if the protein requirements are adequate the sulphur will usually be adequate.

Magnesium is abundant in meat and most plant tissues; so that except in diets of highly refined foods, it is more often excessive than deficient.

The other elements, calcium, phosphorus and iron are frequently insufficient, especially for animals on omnivorous diet (cf. Table 20). Phosphorus enters into every living cell, and in cases of starvation is excreted up to the last. It is involved in practically all the cell functions. In the body it is present (1) as an inorganic compound in the bone tissues and blood where it helps to maintain neutrality, (2) as phosphorus-containing protein, phosphatids and phosphoric esters of a carbohydrate, all closely associated with the cell and its nucleus. In foods, phosphorus occurs in the same positions, that is, inorganically or combined with protein, fat or carbohydrate. It is not entirely proved but is very probable that the phosphorus in organic combination has the greater metabolic value, inasmuch as there is greater storage of nitrogen and stimulation of tissue growth on foods containing phosphorized proteins, fats, etc. It has been shown, however, that the animal body can satisfactorily supply its phosphorus requirements by inorganic phosphates. The omnivorous diet, even the widely varied diet of man, is very often deficient in phosphorus, a fact which becomes very important when we consider that the omnivorous diet produces many acid residues which must be neutralized, and that phosphorus is largely responsible for the maintenance of tissue neutrality. Voit showed that the phosphates excreted during starvation were withdrawn from the bones; and there is much proof that during the daily metabolism a certain slight movement of phosphorus takes place. The metabolized phosphorus is excreted by carnivores practically from the kidney alone; by herbivores almost entirely through the intestinal wall, while in the omnivores it is excreted by kidney and intestinal tract. Whether these facts have any real influence on the phosphorus need of different types is not altogether determined.

Calcium also enters into many of the essential functions of life, coagulation of the blood, contractility of the heart, etc. Omnivorous diet is usually deficient in this element, which is very irregularly distributed both in animal bodies and plants. Insufficient amounts lead to deprivation of body tissues and to the production of osteomalacia- like conditions. Voit produced marked thinning of the skull bones and sternum by a diet poor in calcium. Steenbok and his associates had the same results in cattle by feeding “shorts” a diet rich in magnesium. Etienne[60] showed that an excess of magnesium in an otherwise well balanced food caused a continual loss of calcium. Adults stand a deprivation of calcium much better than children or young animals. They often show no symptoms and retain a normal blood content as the losses from the blood and soft tissues are promptly replaced from the bones. Sooner or later all these animals show weakness and flexibility of the bones. Osteomalacia occurred in 5.2 per cent. of the animals on an omnivorous diet, that is this number showed gross evidence of absorption of bone salts. This condition occurring in man and the lower animals is a generalized softening of adult bones that were at one time normally calcified. Three clinical varieties are recognized in man: a mild form seen in pregnant, puerperal and lactating women, a senile form in which the lesions are usually limited to the pelvis, and a severe progressive form encountered in both sexes and at any age. This last form ends in marasmus. Its chemical characteristic is a loss of calcium and phosphorus with retention of sulphur and magnesium.

The progressive type has occurred very frequently among the Cebidæ whose diet on careful examination, showed a protein content low in quantity, poor in quality, and especially deficient in the phosphorus-containing proteins and total fat. The carbohydrate was high. The ash was small in amount and predominatingly acid. The daily ration often showed only an unweighable trace of calcium, phosphorus or iron. Sodium, potassium, sulphur and magnesium, on the contrary, were present in amounts sufficient for equilibrium or in excess. The Vitamines A.B.C. were present but were not always correctly proportioned. The fat soluble A was low and in some daily rations was entirely lacking.

Diet has at various times been proposed as at least one factor in the production of this condition, a premise that has gained considerable weight through the increase in the number of cases, both in man and in the domesticated animals, reported from the war-famine district of Central Europe where the dietary was restricted and unbalanced. It has been shown that when calcium is low in the diet, the amount excreted materially exceeds the intake. Benedict[61] has further shown that even during absolute fasts calcium is excreted. The requirements of this element for man have been fairly well worked out, but for animals we have no standards. Still it seems certain from the foregoing observations that storage supplies are called upon very early in cases of deprivation, while in pregnancy and lactation when the calcium requirements are greatly increased, a reason is found for a higher incidence of osteomalacia, Steenbok and Hart[62] have shown that the skeletons of cows and goats gave evidence of a drain of inorganic salts during the production of milk unless the calcium and phosphorus of the diet were liberally supplied. In osteomalacia it would seem that inefficient diet, if not the cause, was at least a very potent factor in pathogenesis. The disturbance of the calcium-phosphorus-metabolism may be due to the deprivation of the alkaline salts as in the famine osteomalacia, to a drain from the alkaline storage of the body associated with an inefficient diet as in the osteomalacia of pregnancy and lactation or to 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 a drain of the body alkali for neutralization of the acid; or it may possibly be due to a combination of all these factors acting through their influence on the ductless glands.

Paget’s disease or Osteitis Deformans is a chronic constitutional process which usually involves all the bones of the adult skeleton. DaCosta[63] believed it to be a disorder of bone metabolism probably dependent upon absence or perversion of some internal secretion. We have had the unique opportunity of observing three cases of this disease in Cebidæ, the family of monkeys which has presented the highest incidence of osteomalacia. The experience is all the more interesting because of the typical picture presented by the specimens, and of the absence of references in the literature on the subject, to the occurrence of the malady in wild animals. The interesting point about these cases lies in the fact that the disease appeared in all three only after lime water was added to the diet to supply the deficiency of calcium.

Search for literary record of the disease brought to light a case in a horse that Barthelemy[64] described, but this involved the epiphyses of the bone while osteitis deformans is confined as a rule to the diaphyses. This case was probably more closely allied to osteitis fibrosa cystica. Goldman[65] described examples in fowls and Rossweg[66] refers to specimens in domestic goats and monkeys. Many of these cases first come under observation through fractures, an accident common to osteomalacia, but very rare in well developed osteitis deformans. The diet of our monkeys was exceeding low in those substances essential to bone development. Sherman[67] has shown that the calcium balance is regulated to a certain extent by the calcium ingested, and that when the diet is poor in this element, the output materially exceeds the intake, a condition which is definitely changed when the animal is put on a diet high in calcium.

So far as we could find there are no recorded studies of the mineral metabolism of beginning cases of Paget’s disease. It seems possible from the study of osteomalacia that the low mineral and otherwise faulty diet, added to the symptoms produced by that diet might so disturb the chemical equilibrium, directly through the neurotrophic mechanism or through the perversion of the ductless glands, that the mere addition of the lime water might entirely change the pathological picture. This is in accord with the histology where the initial lesion is resorption of bone followed by irregular proliferation. It is also in accord with the probable chemistry of calcification. These animals all showed a lowered carbon-dioxide-carrying-power of the blood, and therefore lowered ability to carry calcium in solution. It is possible that Paget’s disease is but a stage in a deficiency disease, a faulty reparative response through a disordered neurotrophic mechanism, or through a perversion of the glands governing calcium metabolism. Such perversion could be caused by an improperly balanced diet, or by the addition of an excess of calcium to the diet of an animal whose body fluids were unable by reason of previous faulty diet or other disorder, to hold it in solution. In young animals the calcium demands are much higher than in adults, a need met in the high calcium content of breast milk, a content in excess of almost every other food, but apparently just sufficient to maintain calcium equilibrium. After it is weaned the young animal frequently shows disorders of its inorganic metabolism. Herter estimated that a child should store at least 0.1 gram of calcium daily and he described many cases of arrested bone development occurring during infancy and early childhood, because of an inefficient assimilation of calcium. One case, probably of this character, was found in a Hamadryas Baboon (Papio hamadryas) a typical example of infantilism. The animal was an adult male about half the size of an adult female. His skin was fine and more delicate than normal, the bones were small and slender, contour of body was that of a young animal, genitalia were imperfectly developed, thyroid gland apparently normal, gastrointestinal tract atrophic, associated was a slight arthritis, portal cirrhosis of liver and diffuse nephritis.

First among the results of inorganic insufficiency in youth stands Rickets. This disease occurs in children starting usually at about the sixth month and continuing with irregular remissions for several years. The bone changes, which are the most prominent, are always associated with more or less severe anemia, a general lowered resistance and flabby musculature. The excretion of calcium is very high in the feces and low in the urine. There is a frequent negative calcium balance dependent upon the great loss in the feces. Healing is preceded by a hyperretention of calcium and a relative increase in the urinary calcium. The excessive loss of calcium in the feces is not brought about through the agency of fats because fat could only remove calcium as insoluble soaps and these are not at all increased. This fact contradicts the idea of fat starvation as a cause of rickets. Howland and Kramer found that the blood in active rickets had a normal or slightly lowered calcium content, but a regularly reduced phosphorus content. The latter deficiency was extreme at times. They ascribe to this deficiency the failure of the bones to calcify. It can be readily understood that a decrease of phosphorus in the blood would render difficult the precipitation of calcium phosphate.

Recently two series of studies, the first by Pappenheimer, Zucher and McCann and the second by Shipley, McCollum, Park and Simonds have shown that rats fed on a diet low in calcium but with a sufficient amount of fat soluble vitamine and phosphorus develop a bone condition with many fundamental resemblances to rickets. They were also able to produce the condition with an excess of calcium and deficiency of phosphorus. On the first diet, the condition differs from rickets in that the arrangement of the proliferating zone of cartilage cells is maintained and the evidence of bone resorption in the diaphyses is excessive. A diet deficient in both calcium and phosphorus leads to an atypical rickets.

In the animals autopsied at this Garden rickets occurred very much more frequently in the flesh-eaters than in any of the other dietary groups. On closer analysis it was found that rickets in almost every case appeared in the carnivores which did not receive bones as a part of the food. Rickets occurred frequently in the omnivorous macaques which however did not show osteomalacia, although they belong to the same dietary group as the Cebidæ. The reason they did not suffer the latter disease while adult but had rachitic young is probably due to the fact that this monkey group, which breeds best in our Garden, receives in addition to the diet given to Cebidæ one raw egg. This increased the calcium content of their food more nearly to the requirements of these mammals. These monkeys also have mouth sacs, which enable them to acquire more food per kilo of body weight than the smaller Cebidæ which are not so advantageously equipped. The food even in the amounts consumed by the macaques is low in calcium, phosphorus and iron. It is very possible that there are enough of these ingredients present as a rule, to maintain the animal in organic equilibrium, during normal life, and possibly even enough to supply the needs of the embryo but not sufficient to maintain the young during the period of lactation. A few macaques dying during the delivery of young showed slight osteomalacic changes in the pelvis. This was notably present in one described in detail by E. A. Schumann.

The calcium requirements of the female are always much increased during pregnancy and lactation due to the withdrawal from the mother to meet the needs of the embryo and nursling. Forbes and Beegle[68] found that lactating animals made heavy drains on their storage calcium even when the diet was liberal and the animal was storing nitrogen.

Iron is the essential element of hemoglobin and chromatin—the body constituent most directly concerned with the process of oxidation, secretion, reproduction and development. The iron of the food is absorbed from the small intestines, enters the circulation through the lymphatics, is deposited in the liver, spleen, and bone marrow and eliminated through the intestinal walls. There is very little iron reserve in the adult body; and as a result any failure of the intake to equal the output causes an immediate reduction of the hemoglobin. Voit found that the iron eliminated in the feces of starving dogs, or dogs on a diet low in iron comes from the body through the intestinal walls. Medicinal iron stimulates the production of hemoglobin and red blood cells but whether it is directly employed in the production of hemoglobins has not been proved. Undoubtedly most of the extra iron given with the food passes through the alimentary tract without being absorbed or metabolized. The greater the amount of iron in the food, the greater the influence of the inorganic iron. Anemia occurred in all the animals we examined at least four times as frequently in omnivorous as in all the other dietary groups, a fact probably explained by the low content of iron and calcium in this diet. Both Von Wendt[69] and Sherman[70] demonstrated that larger amounts of iron were required to maintain the iron equilibrium when the amount of calcium was low.

Herter has shown that many anemias are associated with intestinal putrefaction. The carnivores, however, on a diet that putrefies very easily and on one in which the iron content is apparently of distinctly lower nutritive value than that of the iron found in milk, eggs and vegetables, presented an anemic incidence of only 0.32 per cent. This is probably due to the excellent hygienic care of the meat foods and to the morphology of the carnivorous intestinal tract, which is short, straight and fashioned for quick elimination. The cases of anemia steadily increase among the animals as the conformation of the tract approaches the omnivorous type with the longer and wider hind-gut.

Herbivora, obtaining their iron from vegetable sources, are much less liable to blood disorders. The iron needs of the female are greater than those of the male because of the drains of pregnancy and lactation. Young animals demand more iron than adults. All exclusively breast- feeding animals have a considerable storage of iron in the body at birth, while those that eat food immediately have no such supply. Bunge’s[71] experiments showed that breast-fed animals contained about six times as much iron as the milk that nourished them. The iron content of all these animals is highest at birth, remains constant during the suckling period and then rapidly decreases to the adult standard. After this level is reached the iron metabolized must be supplied from the food if the hemoglobin is to be spared.

The functions of all these inorganic substances are intimately interrelated and in places interchangeable. Calcium is capable of correcting disturbances of inorganic equilibrium in the animal body whatever the direction of the deviation from the normal may be. These interrelationships are most involved in the maintenance of body neutrality. The normal processes of metabolism involve a continual production of carbonic, phosphoric and sulphuric acid which must be immediately disposed of if the neutrality of the body is to be permanent.

The factors involved in this are carbonates, phosphates, ammonia and proteins. Carbon dioxide is the chief excretory product but is at the same time a normal constituent of the blood and as such, is an important factor in this physicochemical regulation. There is a tendency for the respiratory mechanism to hold its carbon dioxide tension nearly constant. Late investigations have shown that lowering of this tension is an early sign of beginning acidosis. When food such as protein, is taken in excess the strongly acid residues are neutralized by the sodium and potassium carbonates which are eliminated with a corresponding loss of sodium and potassium. The carbon dioxide tension diminishes, 37.2 per cent. on a high protein as against 43.3 per cent. on a vegetable diet. If this excess is long continued, the result may be, and often is, an increased elimination of the base-forming elements which if not made good tends to diminish the body’s reserve alkalinity. A diet with a preponderance of basic elements leads to an alkaline urine with an increased uric acid solvency and an increased carbon dioxide tension and reserve alkalinity. A diet with a preponderance in the acid-forming elements, on the contrary, leads to an increased urinary acidity and urinary ammonia, decreased ability to dissolve uric acid and lowered carbon dioxide tension and alkaline reserve.

DEFICIENCIES OF VITAMINES.

Recent investigations have shown that diets furnishing sufficient amounts of protein, fat, carbohydrate and inorganic salts may yet prove inadequate for growth or even for maintenance. Hopkins,[72] feeding rats on purified food mixture was unable to obtain any growth until he added small quantities of milk or of the ether-soluble portion of milk but with this addition growth progressed in the normal manner, but it was out of all proportion to the energy or protein value of the addition. Five substances of this character, called by Funk[73] Vitamines, have been described, two of which have definitely established a place as essential food factors. According to him, pellagra, rickets, scurvy and beriberi are the result of a lack of these unidentified but specific and indispensable food complexes.

The first vitamine isolated was the fat soluble A, an adequate supply of which is necessary, not only because of its stimulating growth properties, but because its absence produces a serious condition of the eyes and, at times, marasmus leading to death. Xerophthalmia is a common condition in animals on experimental diets. The eyes are swollen, the cornea inflamed and often opaque while blindness and death invariably occur unless the dietary error is corrected. McCollum[74] rescued animals almost at the point of death by butter or other fat rich in this vitamine. Opacities of the cornea are often seen in the animals in this and other gardens among ungulates—hay-eating mammals; four advanced cases were found, three in seed-eating birds and one in a fox on a diet made up solely of horse muscle. The quantity of vitamine A present in muscle, hay and seeds is very small. It is supplied in largest amounts in milk, eggs, glandular organs and leaves, substances which were very low or absent in the diet of all the affected animals. This xerophthalmia has been reported in man on several occasions, especially by Hrdlicka[75] in American Indians, by Mori[76] in 1400 Japanese during a period of food shortage (this epidemic was cured by the addition of chicken livers to the diet), by Bloch[77] in forty-seven children of Copenhagen fed on a fat free milk who were cured by the administration of cod liver oil. The disease is not however a fat starvation, as it is entirely uninfluenced by vegetable fats which do not contain this vitamine.

Beriberi is an established deficiency disease, frequently seen among the poorer classes of the Orient whose diet is limited to polished rice and fish. It has appeared in Labrador coincident with the excessive use of bolted flour. A similar condition has been induced in pigs and cattle by a diet made up of an excess of cotton seed meal and tankage. Two forms of the disease are described: (1) acute or wet, characterized by marked edema, ascites, hydropericardium, hydrothorax, edema of the lungs, and a congestion of the spleen, liver, kidney, and heart muscle, (2) chronic or dry, characterized by polyneuritis. The disease was first produced experimentally in pigeons by Eijkman[78] in 1897 by means of a diet of polished rice. The paralysis appeared in 2–3 weeks after the diet was initiated. Fraser and Stanton[79] in 1907, found that it could be cured by an alcoholic extract of rice polishings. Funk[80] later determined the vitamine character of this extract. In pigeons and fowls experimental feeding usually results in the chronic or polyneuritic form, expressed by a typical degenerative inflammatory condition of the peripheral nerves. In pigs, on the contrary, Rommel and Vedder[81] produced both types, though the acute or wet beriberi appeared more frequently. In rats the same deficiency causes multiple hemorrhages in the cerebellum and midbrain followed by a degeneration of the associated nervous structures. It is possible that the pathology following a lack of the vitamine B or in fact any of the vitamines will vary with the different species or with varying demands of different individuals. This antineuritic vitamine affects more than the nervous system, and it is possible that all vitamines may have wider effects than are at present described.

Scurvy was the first condition to call attention to diet as a cause of disease. It occurs in man when deprived of fresh vegetables. That faulty diet was in some way the cause of scurvy has been known for many years, but only since 1905 has there been any systematic attempt to determine the peculiar value of the curative foods. At this time Theobald Smith[82] called attention to a disease suggestive of scurvy which developed in guinea-pigs fed on a diet of oatmeal. This observation was confirmed by Holst and Frölich[83] who stated that the disease could be prevented by the addition of fresh milk or cabbage, because in these foods there was present an antiscorbutic or C vitamine. This unidentified substance was easily destroyed or diminished by heat or an alkaline medium. It was found in rather large amounts in succulent vegetables and fruits. McCollum[84] and his coworkers showed that the oat kernel was low in inorganic salts and vitamine A and poor in the quality of its protein; but with these faults corrected it proved to be a complete food for rats. McCollum also found that scurvy developed more readily in animals if the physical properties of the diet favored constipation. He was able to delay the onset of the disease in guinea- pigs for a considerable period by the addition of mineral oil which has no food value, or phenolphthalein, a cathartic. At the same time, Jackson and Moore,[85] found the cecum of all guinea-pigs dying of scurvy, packed with putrefying feces. They were able to produce a mild type of the disease by the injection of the diplococci isolated from the swollen joints.

From these observations it seems safe to conclude that scurvy may not be purely a deficiency disease, or even a simple dietary one, although the presence of a vitamine influence is not excluded; but it is probably the result of a bacterial invasion of tissues debilitated by a faulty diet and by the toxins produced by the putrefactive bacteria developing in a diet unsuited to the anatomical demands of the alimentary tract. This theory receives support from the fact that pasteurization destroys all aciduric bacteria, allowing only the spore-forming putrefactors to develop; and from the fact that scurvy develops more frequently in children on stale pasteurized than on stale raw or boiled milk. In this Garden no suggestion of scurvy has been noted.

Pellagra is very definitely a disease of poverty endemic for years among the poor, especially in the mountains of Northern Italy. It has been under observation in the United States since 1907. So far as is known no cases have been observed among animals. Opinions differ as to the rôle of diet in the etiology but the results of recent studies seem to show that uncomplicated cases of average severity clear up entirely on a diet rich in animal protein. No vitamine deficiency has so far been determined. Wilson’s careful studies of the diets known to have produced the condition show that the etiological factor lies in a deficiency of the protein molecule. The results of Goldberger[86] corroborate this fact, and he concludes from his latest studies that “the dominating rôle of diet in the prevention and causation of pellagra is referable primarily to the character of the protein supply or to the specific quality of the aminoacid makeup of the protein supply.” Just what aminoacid or combination of aminoacids it is, has not been determined, nor has the possibility of a vitamine alone or in combination with the aminoacid factor been absolutely excluded.

The principal influence of the omnivorous diet is toward those degenerations arising primarily from imbalances in the inorganic makeup, or to insufficiencies of certain necessary factors. The vitamine deficiencies are markedly less prevalent in animals than in man whose food is less often consumed in its natural state. It is now known that much of the injury and loss of nutritive value in foods is produced by the processes involved in preparation, preservation, refinement and storage. Whenever the choice of food is not restricted, vitamine deficiencies do not occur. The vitamine requirements probably differ in different species and in individuals from the same species according to their environmental and individual variations. It is very possible that if the diet is low in vitamine content there may arise conditions of relative deficiencies; and McCarrison has shown that a vitamine deficiency associated with a high fat or carbohydrate content may disturb the balance of the endocrine glands. It is however to the inorganic content of the omnivorous food that most of the disturbances peculiar to this diet are to be assigned.

With the flesh eating animals and birds the records present a very different picture. Disorders of the digestive tube, of the storage organs, of the organs of elimination and of the endocrine glands predominate. Their diet is low in carbohydrates and, at times, in fats and very high in protein. Bone supplies the inorganic salts, which in this Garden is fed only to the larger mammals. The carnivorous birds get their inorganic supply from mice which are eaten entire. The carnivores are as a rule large and are given to active fighting or to long flights. In the wild, very probably there are long periods between feasts, while in captivity the food is always plentiful and regularly supplied. This regularity added to the lack of exercise, particularly among the larger animals, must lead to excessive demands upon the storage and eliminating organs. Storage is always promoted by rest and liberal diet, and cleared away by exercise and starvation. The life of these birds and mammals, moreover favors inactivity of the bowels, which, together with the highly putrefactive diet adds another serious factor to a problem which in gardens is almost insurmountable.

IRREGULARITIES OF CARBOHYDRATE METABOLISM.

The carbohydrates are derived from the glucose and glycogen of the meat and from the protein molecule. They are absolutely less than in the diet of herbivores but become a factor in the disorders of this group because of the lack of exercise and the regularity of feeding. In digestion the carbohydrate becomes available for absorption and bacterial growth in the upper small intestine and appears on the other side of the intestinal wall as blood glucose in which form it is burned for energy or stored as glycogen for the future maintenance of the blood glucose.

The blood of different animals has a glucose concentration between 0.05–0.1 which for each species is quite constant, as it is regulated by the coadaptation of four factors: combustion, fermentation of glycogen, formation of fat, and elimination from the kidney. In excessive feeding the amount needed for energy is burned, the remainder is stored in the liver up to its capacity, then in the muscles and other cells, after which fat is formed and all further excess is eliminated by the kidney. Overfeeding causes an immediate overloading of the oxidative mechanism with symptoms of gastric disorder, achylia, and at times acid fermentation with irritation of the stomach walls and the development of bacteria in the organ. This is frequently followed by glycosuria, several types of which are described: (1) associated with an increased concentration of glucose following excessive ingestion exceeding the normal glycogenic function of the liver, a form common among the Herbivora, (2) that due to a reduction of the glycogenic function of the liver, (3) that associated with disease of the ductless glands in which the resulting glycosuria probably depends upon the influence of these glands upon the pancreas, (4) that dependent upon the defect of glycolysis or to an overstocked liver seen in gout, obesity or hypertrophic cirrhosis, and (5) renal glycosuria due to a lowering of the renal threshold and usually associated with gout, arteriosclerosis or chronic nephritis; this last is best explained on the ground of increased renal permeability. Normally when the blood sugar concentration rises above a certain level the elimination via the kidney begins and continues until the blood has again reached its normal concentration. The relation of the kidney to glucose concentration is not constant and variation is always toward the side of lesser elimination while the kidneys become accustomed to the higher level.

Diabetes, a disease of the islands of Langerhans in the pancreas, is essentially a disturbance of sugar metabolism always associated with an exaggerated and defective fat and protein combustion. It is not only that the diabetic has lost the faculty of combustion but these abnormalities all establish states of intoxication to which the diabetic must sooner or later succumb. Among lower animals the disease is rare. Dogs are most frequently affected (about 1 in 12,000 deaths). It has also been described in horses, cattle and monkeys. In our records there was one case an Arctic fox (Canis lagopus) presenting a typical picture. Degeneration of the islands of Langerhans was seen in three other animals, but there was no other evidence of diabetes. This disease is not due to diet but to the absence of a normal ferment (pancreaticozymo-excitor) for one particular type of food.

IRREGULARITIES OF FAT METABOLISM.

Disorders of fat metabolism are very rare among lower animals notwithstanding the fact that fat even in the carnivorous diet, represents about 13 per cent. of the whole intake. It plays two important rôles in the body, storage for energy reserve, and as a most essential structure in cellular protoplasm, in which position it joins with protein in complex combinations of still unknown composition which present to a striking degree the phenomenon of absorption. Very marked biological differences exist in the value of fats from different sources, due to the presence or absence of vitamines. The body fat is derived from the fat of the diet or is synthesized from glucose. The former is specific to the fat consumed while the latter is specific to the animal. In omnivores the type depends upon the varying extent to which animal fats enter the diet, in carnivores it depends almost entirely on the fat intake, while in the herbivores practically all the fat is synthesized from the carbohydrate. On digestion, fat splits, yielding a glycerol and fatty acid which are collected in the lymph spaces of the intestinal mucosa, there changing to some complex combination which is not only soluble but diffusible.

Fatty infiltration and fatty degeneration are conditions of much pathological interest and of great frequency in captive animals. The researches of Mansfield[87] have thrown considerable light upon these conditions. He found that the total fat content in cases of most marked degeneration was normal or reduced. The proportion of fat free from protein was increased and the firmly bound fat decreased. This increase is due to neutral fat brought from without the organ by the blood when for any cause the oxidative powers are decreased, and setting free of the previously invisible intercellular fat and lipoids, which are normally present in the cells, by autolytic or physicochemical changes. This condition is pretty evenly distributed among the dietary groups, the liver being most commonly involved. The hepatic cells are easily degenerated by the toxins or other harmful substances passing through the organ and become passive and unable to throw off or to utilize the deposited fat. In all probability the same general situation occurs in the atheromatous changes in arteriosclerosis which on this diet shows a high incidence. The causative agent is probably some poisonous substance, possibly a protein degradation product, indol, pressor substance, acting on the intima over long periods, or at irregular but often repeated periods causing first destruction then fat accumulation. It is also possible that it may be caused by repeated absorption of some sensitizing protein. Arteriosclerosis in these animals is often closely associated with nephritis.

Obesity may result from excessive ingestion of food in individuals whose habits are sedentary and whose digestions are active or it may come from an inherent abnormality of metabolism dependent upon ductless gland disease. It is very common in castrated animals. The obesity of overeating is always of milder type than that associated with endocrine disturbance.

So far as is known there are two main disorders of fat metabolism—the failure of the diabetic to form fat from glucose, and acidosis, the inability of the organism to burn fat beyond betaoxybutyric acid, acetoacetic acid, or acetone. The symptoms are unsteadiness of gait, stupor, coma, air hunger, in all of which the essential features are due to the impoverishment of the body in available bases. In infants this frequently follows an excessive fat diet. It is also common in starvation due to the deprivation of sugar. It is associated with phosphorus poisoning, narcosis, carcinoma, liver disease, inanition, etc. It has been produced experimentally by the administration of acids or by foods deprived of their bases. The excess of acid in the body whether produced in the body or introduced from without must be neutralized in part by the ammonia manufactured in the ultimate metabolic transformation of the protein and by the alkaline salts of the blood and tissues. When alkali is reduced the carbon dioxide accumulates in the tissues, blocking oxidation. The urine immediately shows an increase of ammonium salts, a decrease of the urea and an increase in the output of sodium, potassium, calcium and magnesium, which last two are drawn from the bones.

Symptoms do not arise until the fixed alkalies are exhausted; and they are immediately relieved by the administration of alkalies, except in those cases of starvation where the administration of sugar and the subsequent sparing of the fats relieves the situation. In herbivores, acidosis does not follow starvation, but, on the other hand, it is markedly easier to excite it in herbivores than in carnivores whose heavy protein diet produces more ammonia, which better enables the animals to protect their fixed alkalies. The acid intoxication of infections arises from different causes and is dependent on the intensity of the type of infection; but ultimately it also depends upon the depletion of the fixed alkalies.

IRREGULARITIES OF PROTEIN METABOLISM.

Fat and carbohydrate disturbances are not infrequent in carnivores, but it is with the protein fraction of the diet that most of the trouble is connected. Natural foods contain several proteins or groups of proteins, whose biological adequacy depends upon their yield of aminoacid. Experiment has shown that many proteins are entirely lacking in one or more of these essential radicles; and no food can be adequate unless it contains at least all the aminoacids that the individual animal is unable to manufacture for itself. So far as is known, no animal can produce in itself either lysin or tryptophane. Gliadin, the principal protein of wheat and lacking in lysin, is unable to support growth even when given in amounts sufficient to insure the storage of nitrogen, and is associated with a diet adequate in all other factors. Absence of tryptophane prevents not only growth but maintenance. Any of the aminoacids, whose radicles are contained in tissue proteins, may contribute to the maintenance of adult equilibrium; but no growth occurs unless all the necessary groups are present. Except in laboratories, diets are never made up of isolated proteins, but they are often composed of proteins derived from one plant and are often deficient. McCollum and his associates in their studies showed that while there were pronounced differences in the composition of many foods used by men and animals not only in their protein content but in water, fats, carbohydrates, etc., yet in the combinations found even in rather restricted diets, the errors, as a rule, corrected each other.

During digestion the protein molecule is broken down into the component aminoacids which are absorbed and synthesized in the intestinal walls, and appear on the other side as the specific blood protein, which serves as the substrate for the anabolism of all the special tissue proteins. Excessive protein is stored to a slight extent as aminoacid for the future maintenance of the blood protein, the integrity of which is tenaciously protected during hibernations, sexual migrations, and even during starvation. The animal body tends to adjust its nitrogen metabolism to its nitrogen supply; the adjustment requires an appreciable amount of time. A diet changed to a lower nitrogen level results in a continued loss of nitrogen, increased combustion of fats and carbohydrates. The animal makes no apparent effort to reëstablish equilibrium, and sooner or later digestive disturbances and loss of strength occur.

If, on the contrary, the protein is steadily increased after an animal has established equilibrium, the nitrogen metabolism increases and the level of nitrogen equilibrium rises to higher and higher levels. There is, at the same time, a lowering of the fat combustion, an increase in the respiratory quotient and in the heat production. The excess protein must be split, deaminated, burned and eliminated. Fifty-five per cent. of the intake is converted into glucose which is burned and the excess stored as glycogen. The sulphuric acid formed during the protein cleavage is neutralized by the body alkalies. In these cases the liver is often congested and enlarged. The urine shows excess of urea and ammonia. At times the excess, being so great that it cannot be absorbed, undergoes chemical and bacterial decomposition which causes digestive disturbances, torpor and constipation.

The organisms associated with protein food are usually the putrefactive types which break the protein molecule into the aromatic bodies, phenols, indolacetic acid, indolpropionic acid, skatol, etc. These bodies on absorption are believed to give rise to hypertrophy of the adrenal, interstitial changes in the kidney, and arteriosclerosis. Another group of substances, pressor bases and amines, are manufactured by certain anaerobes acting on proteins. These, when fed by mouth, are detoxicated by the liver cells, but when formed below the portal circulation, give rise to anaphylactic phenomena—urticaria, etc. Certain other organisms give rise to soluble toxins as in botulism and thyrotoxicon poisoning. All these types of toxins will destroy if they act acutely in sufficient concentration; or as is more common, if they act persistently over long periods, or at oft recurring intervals they will cause serious injury to the tissues coming in contact with them, and have a part in the production of cirrhosis of the liver, chronic nephritis, myocarditis, arteriosclerosis, etc.

All foods have a limit beyond which they are excreted untouched or imperfectly oxidized. Many of these partial oxidation products of protein are in themselves toxic and may also be a source of these degenerative organ conditions. The pathological material studied by us showed a marked decrease in gastrointestinal diseases in close association with the more hygienic care of the meat foods.

Always associated with the protein foods are the nucleoprotein complexes, which are split by both bacteria and digestive juices into globulins and nucleic acid, and then through the agency of a special enzyme, into purin bases and uric acid, in which forms they are excreted in the urine and feces. The oxidation of purins is never complete.

Gout, representing the pathology of purin metabolism, is a paroxysmal inflammatory disturbance, due to the deposition of sodium urates in the joints or in the internal organs, usually accompanied by a fibrosis especially in the liver, kidney, arteries, etc. The disease occurs almost exclusively in birds. Isolated cases have been described in dogs, horses and hogs, but among lower animals it is undoubtedly very rare. In birds it is most frequent in the carnivores—4 per cent., as against 0.02 per cent. in all other groups. It is higher in fish-eating birds than among the flesh-eaters. The avian gout is usually of the visceral type and was most marked in its distribution over the organs in the Anseres and Psittaci, birds whose diet apparently is not unduly heavy in nucleoproteins, but whose tract approaches the carnivorous type. The only arthritic cases occurred in Boat-billed herons (Cancroma cochlearia), fish-eaters. Our records show examples in Accipitres, Galli and Columbæ, although the number of cases in the last order were few and slight in extent. This disease stands in close relation to diet, as it develops on generous protein food, high in nucleoprotein or hypoxanthin, especially if this be associated with restricted activity.

The carnivorous mammals lead in the disease of the thyroid glands. Thyroid disease occurs among the birds, but is equally distributed among the dietary groups. Thyroid activity has a marked influence on metabolism probably through the influence of the iodine-containing protein of its secretion. There are some experimental evidences in favor of a detoxicating function of the thyroid, of which the following are quoted: (1) The effects of thyroidectomy are most marked in the carnivores; Herbivora are often capable of several years of life without thyroid tissue; (2) administration of meat to thyroidectomized omnivores or herbivores caused a marked increase in all symptoms. The importance of the relation of the meat diet, detoxication and thyroid disease receives considerable confirmation from the fact that among the 1,860 mammalian postmortems thyroid disease occurred in 2.6 per cent. of all mammals, 94.9 per cent. of which were found in flesh eating varieties. Wells[88] suggested that possibly this could be interpreted as an indication that toxic materials found in the meat in the intestinal tract were, under normal conditions, detoxicated by the thyroid. Against a local neutralization, however, is the improvement following the administration of dried thyroid substance. The function is either neutralization of toxic substances or the stimulating action on intracellular metabolism, both of which might be called into play by an excessive protein diet.

THE CARNIVOROUS DIET.

The pathology of the more prominent diseases developed in carnivores points at least to diet as a predisposing or determining factor. This diet is very high in a distinctly putrefactive protein and yields products, chemical and bacterial, which are toxic and which give rise to acute or more often chronic diseases of the alimentary tract and its adnexa. By reason of the amount ingested, excessive because of lack of exercise, there is a severe tax on the storage organs and on the detoxicating glands, as the liver and thyroid. The constant absorption of these toxic substances gives rise to chronic degenerative or fibrotic changes in the organs through which they pass: liver, kidneys, arteries, heart. In birds the degenerative diseases are even more marked than in mammals on the same diet. The ultimate fault of this diet, especially for mammals and birds with restricted activity, lies in the production of toxic bodies, produced either in the incomplete degradation or oxidation of the protein molecule or as the result of bacterial action on the protein molecule, a poisonous quality which is probably enhanced by the chemical changes occurring while the digested protein is passing through the intestinal mucosa. Garden conditions are such that these factors are almost unsurmountable unless the substitution of vegetable protein could be accomplished. Failure is often caused by limited feeding to carnivores of muscle and bones, whereas they should be supplied with glandular organs and blood.

THE HERBIVOROUS DIET.

Herbivorous diet must be divided into two groups, (1) that composed of succulent vegetables, and (2) of grasses, grains and seeds. In the first group there is an apparent variation in the results found in mammals and birds. In both there is a marked decrease in the chronic degenerative pathology. In both, acute gastritis is more prominent, far outstripping the incidence of this condition in other classes.

This diet yields a large and quickly available amount of carbohydrate which in conjunction with the moisture, heat and bacteria which are unavoidably associated with raw vegetables, makes an ideal situation for infection. These foods carry many saprophytic bacteria, moulds, etc. In birds the conditions are aggravated by the injuries that may occur from the sharp objects picked up with the gravel. The incidence of acute infection is higher among birds than among mammals of this group, and often there is involvement of the whole tract. The explanation of the other pathological findings occurring among birds must be found in the frequently repeated low grade infections which result finally in the production of chronic lesions in the digestive tract, liver, pancreas and kidney. Toxins as an etiological factor cannot be altogether excluded, but as a rule they are not important because the by-products of vegetables are distinctly less toxic than those derived from animal sources. Arteriosclerosis is much less frequent and less intensive in herbivorous birds than among the carnivorous, probably because of differences in the concentration and character of toxins in the two groups.

SOFT HERBIVOROUS DIET.

The diet of succulent vegetables is composed of tubers, edible roots and leaves. The tubers and edible roots are high in water and carbohydrate and poor in the amount and quality of the protein, most of which is not even a true protein but a mixture of aminoacids. The leaves, on the contrary, are rich in organic ash, especially calcium, sodium, chlorine, and fat soluble A vitamine, and as a rule contain a good quality of protein. They often, however, contain injurious substances. This diet, while measurably less nutritious than that of the carnivores, can satisfactorily nourish many animals with an extensive intestinal tract during growth and even throughout their entire life, but proves entirely inadequate when fed to an omnivorous tract.

SEED DIET.

Closely allied in general character to the diet of succulent vegetables are the seed diets, eaten only by birds and having no parallel among mammalian foods. All seeds, in contradistinction to tubers, contain true proteins which, however, are of poor quality because of the deficiencies in the aminoacid content. They are as a rule low in the fat vitamines and in the amount of calcium, sodium and chlorine carried. In three pathological conditions only do these birds show any oversusceptibility: (1) Sore eyes, (2) acute enteritis, (3) osteomalacia. Sore eyes were frequently noted in this group. The lesions were very like those described in animals deprived of the fat vitamine, which was present in this food in very small amounts or entirely absent, thus giving a very plausible explanation of this condition, especially as in some of the cases no other cause could be found. Gastric disease of any type is rare in this group because the food at the gastric stage is highly resistant to bacterial action. In the duodenum, however, the conditions are early changed because the bacteria carried with the food through the stomach become active in the presence of available carbohydrate and protein decomposition products.

Osteomalacia is confined almost as exclusively to the seed-eating birds as it was to the omnivorous mammals, and it is also associated with the same deficiencies, calcium and phosphorus (cf. Tables 19 and 20). It is also interesting to note that these two diets, the omnivorous and seeds, yield the greatest number of cases of tuberculosis. Mammals showed 32.6 per cent., as against 5.8 per cent. in all the other dietary groups, an observation which becomes more striking when man is added to the omnivorous group. Seed-eating birds showed 17.2 per cent., as against 6.4 per cent. in other groups. In both diets the fat, fat vitamine and inorganic salts, especially the calcium, are deficient in amount. In the wild, birds vary their diet of seeds with insects, worms, soft fruits and the tender shoots of plants, and at the same time they increase their inorganic intake by the minerals picked up with the gravel and from the water which has penetrated the soil.

GRAIN AND GRASS DIET.

The hay-eating animals constitute a large and well studied group— including practically all the domestic varieties. Table 19 shows that these animals yield the greatest number of cases of malnutrition, food poisoning, acute pancreatitis, acute degenerative conditions of liver and myocardium.

Recent literature describes many cases of osteomalacia, especially among horses and cows, in the famine districts of Europe. In our collection of 1,860 postmortems only one case was found, that of an Isabelline gazelle (Gazella isabella), a hay-eating animal, and in this case it was secondary to infection.

Arthritis, occurring in 3.4 per cent. of all the autopsies, was almost entirely confined to the hay-eating animals. The literature describes many cases of arthritis almost entirely confined to ungulates, of which many were associated with calving and subsequent infection. Bacteriological researches have found it most often associated with streptococci, staphylococci, or Bact. perfringens, organisms that require a certain amount of carbohydrate for their proper development. The relation of diet to this condition probably lies only in the fact that it provides an excessive carbohydrate substrate suitable for the optimum development of these organisms. Folin and Bergland, noting glycoresis in Herbivora, thought that it represented the absorption and excretion of unusable carbohydrate, present in grains, vegetables, fruits, etc., and that it was sharply separated from the main carbohydrate metabolism. These products were absorbed from the blood exactly as they were ingested like lactose, dextrose, etc., are absorbed, but do not enter into the economy although they might cause disorders, especially forms of arthritis.

The grain foods are composed largely of carbohydrates (principally in the form of cellulose and starch) small amounts of protein and little or no fat. They have a very low nutritive index so that large amounts must be consumed to supply adequate calories. This food is constantly present, and during the enforced idleness of captivity is almost continuously eaten. Despite these facts, however, malnutrition is present in 2.2 per cent. of the animals on this food. Associated with the plentiful food and lack of exercise are overeating and pica. Overfilled stomachs occurred thirty-four times. They were limited to these mammals and to the seed-eating birds whose environmental conditions are practically the same. Pica or excessive appetite for abnormal food, is also more frequent in these groups, but is usually associated with badly balanced diets, and thus represents an effort on the part of the animal to supply its own deficiency. It is present in osteomalacic monkeys and has been reported in cattle from regions where osteomalacia is common and following crop failures where the rations are restricted. In cattle it very often accompanies food poisoning, especially that produced by ingestion of peat hay.

Disturbance of the alimentary tract and its adnexa occurs in two forms: (1) Infection which is quite common and involves the duodenum, pancreas and liver, and (2) toxic. Compared with other diets alimentary disorders are not frequent among grain feeders, despite the ease with which grass foods ferment and the great variety of organisms found in them such as moulds (aspergillus), Bact. coli, paratyphosus, enteritidis, suipestifer, oidium lactis, etc. Few bacteria can attack whole protein, cellulose or starch, and the decomposition products, peptone, glucose, etc., are not available in any quantity until the lower stomach and duodenum are reached. The inflammation of the alimentary tracts of these animals is confined to the fourth stomach and duodenum, with, in many cases, extension to liver and pancreas.

Acute and chronic degenerative changes occur very frequently, and as a rule are the result primarily of absorbed toxins. After ingestion of new hay this often appears. The toxic substance probably is a terpinol ester, cumarin, which is produced by an enzyme in the cut grass.

The result is a gastroenteritis with jaundice, thirst and marked flatulence. It is very probable that many of the gastrointestinal and degenerative lesions are the result of the combined action of toxin and bacteria.

FOOD POISONING.

Food poisoning occurs in all diets, but especially among the grass- eating mammals. To-day under the general heading of food poisoning are included those cases due to (1) some injurious substance inherent in the food itself, true food poisoning, (2) those due to toxic substances liberated or produced in food contaminated by parasites or bacteria, (3) those due to bacteria that are carried by food and develop into true infection after ingestion. Most of the cases of meat poisoning described in literature undoubtedly belong to this third class, i.e., flesh is infected during the life of the animal or during its preparation for food and the virus develops in the host after ingestion. A fourth and more rare class of food poisoning is due to the condition of the individual consuming the food-protein sensitization.

Injurious constituents of normal flesh foods are very uncommon. There are a few poisonous fish, notably the balloon, puffer, and Fuga fish of Japan, which when eaten give rise to cholera-like conditions ending in convulsions and paralysis. A marked intoxication has been described in dogs which have fed upon the Greenland shark. Some fish are poisonous at certain periods as spawning season, the poison then being confined to the roe. Still others are harmless unless rendered toxic by some injurious food. This poisoning of muscle meats is seen in quail and partridges fed on mountain laurel, in some fish after consuming certain marine plants, and in cattle poisoned by amanita.

The most common sources of poisoning are spoiled meat and flesh of diseased animals, both of which are serious factors in the production of the gastrointestinal disorders of omnivores and carnivores. Practically all the reports of meat poisoning from the literature have been traced to the use of raw or insufficiently cooked flesh, and have yielded on bacteriologic examination Bact. paratyphosus, Bact. enteritidis, Bact. suipestifer, Bact. coli, or Bact. proteus.

The bacteria may produce toxin in the food previous to ingestion causing in the host only a severe intoxication. This is the situation developed after eating sturgeon infected with Bact. piscidus agilis, an organism which manufactures a highly poisonous alkaloid. A similar intoxication follows the ingestion of potatoes infected with Bact. proteus or containing the poisonous alkaloid, solanin, which is produced in diseased and sprouting potatoes. Other examples of this are (1) ergotism—due to an infection of rye and wild grasses with Claviceps purpurea which produces three poisonous bodies, ergotinic acid, which is not poisonous when taken into the stomach, sphacetinic acid and cornutin which act on the nervous system, brain, cord, vagus and vasomotor centre giving rise to toxic polyneuritis, and (2) favus, an acute febrile anemia with jaundice and hemoglobinuria probably due to a bacterial infection or fungus growth of the bean. Infected food may also produce soluble heatresisting toxins that produce immediate symptoms and increase the animal’s susceptibility to infection. This is the more common finding in cases of poisoning with milk and milk products. Non- pathogenic saprophytes carried in milk produce (1) a poison closely allied to tyrotoxicon, (2) a toxalbumin which in itself causes serious disturbances. Botulism, also probably of this group, is a disease initiated by a toxin elaborated by Bact. botulinus acting on a protein. There is, however, some evidence that Bact. botulinus can also establish a real infection.

The toxemias from food infected with bacteria may not occur until the food is ingested or the bacteria implanted. This result occurs in infections with Bact. bovis morbificans, Gärtner’s bacillus, etc., or after the feeding of meat from animals infected with Bact. paratyphosus and enteritidis.

The plant poisons are more frequently due to inherent injurious substances, although even among them, bacterial and fungus diseases play an important rôle. Among the 16,673 plants indigenous to North America, almost 500 are more or less poisonous and about 30 are of great economic importance. The toxic factor may be confined to the leaf, seed or root, but more often it is associated with all parts of the plant. Through the efforts of the Department of Agriculture a more or less complete list of the plants implicated in the poisoning of stock has been compiled. This list includes the following: Amanita muscaria; A. phalloides; Veratrum viride; Phytolacca decandra; Agrostemma githago; Delphinium, 25 varieties; Astragalus mollissimus; Aragallus lambertii; Crotalaria sagittalis; Euphorbia lathyris; E. marginata; Rhus radicans; R. diversiloba; R. vernix; Aesculus pavia; A. hippocastanum; A. glabra; A. Californica; Cicuta maculata; C. vagans; Conium maculatum; Kalmia latifolia; K. augustifolia; Leucothöe catesbaei; Rhododendron maximum; Pieris mariana; Datura stramonium; Solanum nigrum; S. dulcamara; Helenium autumnale; Asclepias pumila; A. verticullata; A. galoides; A. mexicana; A. eriocarpa; A. speciosa; A. fremonti; Eupatorium agertoides; E. urticarfolium; Isocoma wrightii; Daubentonia longifolia; Senecio jacobia burchelli latifolius.[89] Some of these as the Amanita are only occasional sources of disaster, but as they frequently involve man they are important. The Amanita muscaria symptoms appear very soon after eating the fungus and consist of a deepening stupor. A. phalloides, on the contrary, starts with severe abdominal pain, cramps, discharges of blood and mucus and later convulsions. The meat of animals dying from fungus poisoning is distinctly poisonous. This transfer of poison to the muscles of the animal partaking of these plants occurs also in poisoning with Kalmia.

The other plants of this list are closely associated with the grass foods and are consumed usually when the food on a range is scarce. Some groups as the Asclepias contain a distinct neurotoxin and give rise to a condition known as trembles or staggers. It affects mostly cows and sheep, causing staggering, trembling gait, bloating and salivation and death with convulsions. There is marked congestion of alimentary tract, liver and kidney. In the cerebrospinal axis there are marked changes in the nerve cells of the medulla and spinal cord. The Purkinje cells show the effect of extreme fatigue. Other plants causing stiffness or weakness of the extremities, show on microscopic examination no definite lesions in the cerebrospinal axis. Loco weed—Astragalus mollissimus and Aragallus lambertii—causes maniacal disturbances but no gross lesions. This weed in Colorado costs the state enormous amounts of money yearly.

Helenium poisons domestic animals by means of a toxic glucoside, dugaldin, which produces stiffness, salivation and nausea with mild depression (“spewing sickness”). The alimentary tract shows severe inflammation of the rumen and reticulum which may at times be hemorrhagic. The liver usually presents an interstitial hepatitis. This toxin is decidedly hemolytic. The effects of this plant are always permanent, total recovery being very rare.

The larkspur (25 different varieties), on the contrary, shows prompt recovery after treatment, but no establishment of toleration. These plants give rise to nausea, vomiting and great agitation and destroy many animals yearly. The poisons are included in four alkaloids, all spinal cord depressants resembling aconite in general character.

These poisonous plants all produce more or less gastrointestinal inflammation and practically all are destructive in their action on the liver, pancreas and kidney. It is impossible to form even approximate estimates of the damage done by them because of the general ignorance of the subject. The Division of Botany has been collecting for the past few years specific information concerning these plants, but the individual plants are not equally poisonous, and all animals do not show the same susceptibility to the poison. Veratrum viride, for instance, is eaten with relish by sheep and elk and is decidedly toxic for the horse. In many the toxic factor has not been isolated. Some, as Euphorbia, are poisonous only when fed in honey derived from its flowers.

The influence of diet on the general health of animals is very far reaching and very inclusive. Metabolic disturbances are undoubtedly at times the result of unbalance—deficiencies on the one side, excesses on the other, at times are probably much more the results of bacterial invasions aided and abetted by the food administered, at still other times are poisonous either in their own content or from the degradation products resulting from digestion or bacterial decomposition.

SECTION XVI NEOPLASMS

The occurrence of true neoplasms in domesticated animals has always been well known and thoroughly studied while for beasts in the wild the data has been fragmentary. That tumors exist in natural environment has been accepted upon the testimony of hunters but there is an impression, and nothing more, of their extreme scarcity probably because only younger vigorous animals come to the attention of the sportsman or collector. This matter will of course not be settled until some natural historian with a knowledge of pathology, makes a survey of a large number of specimens taken during a collecting expedition. Observations in menageries are valuable to the extent that they show what tumors may occur, the orders most commonly affected and the incidence under captive conditions. It is unfortunate that too seldom do we know the history of our specimens in regard to the age, manner of capture or breeding, data which if at our disposal would permit of a very fair idea of the probable incidence in the wild and of the effect of captivity. Some observations in this direction are however possible by using the figures of known captivity and breeding.

The facts gleaned from a study of neoplasms under captive conditions may be of interest to the experimental pathologist, especially when considering the relation of the origin from the embryological layers. I have tabulated this with great care, using Jordan’s[90] table for the source of the various tissues, and further have studied the destination of metastatic emboli in terms of the blastoderm.

The following observations are based entirely upon our own data for while it might be valuable to include the cases in the literature their descriptions are often so meagre that they would not combine readily with our records. Plimmer, Seligmann, and Murray have published in the Proceedings of the London Zoological Society since 1903, their annual report of the pathological service in which they have recorded very many interesting tumors. So too from time to time Harlow Brooks and W. R. Blair in the Annual Report of the New York Zoological Park, have presented cases occurring in their service. Joest [91] discusses tumors in the lower animals in a broad way and analyzes their incidence and characters. C. Y. White and I [92] have already published articles on this subject. Numerous single references may be found in the Jahresber. der Veterinär-Medicin.

In so far as the incidence of tumors in wild animals is concerned this literature can scarcely give an adequate measurement but it would seem that they are less than in domestic varieties. Exact figures for the occurrence of tumors in the latter seem not available in the literature, but one can find that in the Prussian army horses about one hundred are observed each year. In our 5,365 specimens collected during nineteen years, 94 tumors in 92 animals have been found, 1.7 per cent. or about one in every sixty specimens, not at all a low figure. If one were to include all fibromata of the feet and the blood collections to which the name angioma might be applied, this incidence would be greater; they are excluded because few in number and vague in history; only one true angioma was seen.

The gross and microscopical appearances of tumors in the lower animals are essentially the same as one encounters in human beings or at least it is possible to apply the pathological nomenclature used in human medicine to all the neoplasms we have discovered. There is appended a list of all the animals and their tumors, a table of zoological orders, tumors and organs (Table 21) and an analytical table of the histological data. (Table 22)

TABLE 21. Table of Orders and Families Showing Type of Tumor and Principal Organ of Origin.

═══════════════════╤═══════╤═══════╤═════════╤══════╤══════════╤══════ Order Family │Fibroma│Osteoma│Chondroma│Lipoma│Myoma and │Glioma │ │ │ │ │Fibromyoma│ │ │ │ │ │ │ ───────────────────┼───────┼───────┼─────────┼──────┼──────────┼────── „ „ │ „ │ „ │ „ │ „ │ „ │ „ │ │ │ │ │ │ ───────────────────┼───────┼───────┼─────────┼──────┼──────────┼────── Primates, │ │ │ │ │ │ Cercopithecidæ │ │ │ │ │ │ Cebidæ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Lemures, Lemuridæ │ │ │ │ │ │ │ │ │ │ │ │ Carnivora, Felidæ │ │ │ 1│ │ │ │ │ │ │ │ │ Viverridæ │ │ │ │ │ │ Canidæ │ │ │ │ │ │ Procyonidæ │ │ │ │ │ │ Ursidæ │ │ │ │ │ │ │ │ │ │ │ │ Phocidæ │ │ │ │ │ │ │ │ │ │ │ │ Rodentia, Sciuridæ │ │ 1│ │ │ │ Muridæ │ │ │ │ │ │ Heteromyidæ │ │ │ │ │ │ │ │ │ │ │ │ Octodontidæ │ │ │ │ │ │ Hystricidæ │ │ │ │ │ │ Dasyproctidæ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Proboscidea │ │ │ │ │ 1│ Ungulata, Equidæ │ 1│ │ │ │ │ Bovidæ │ │ │ │ │ 1│ Cervidæ │ │ │ │ │ │ Camelidæ │ │ │ │ │ │ Suidæ │ │ │ │ │ │ Edentata, │ │ │ │ │ 1│ Dasypodidæ │ │ │ │ │ │ Marsupialia, │ │ │ │ │ │ Didelphyidæ │ │ │ │ │ │ Dasyuridæ │ │ │ │ │ │ Peramelidæ │ │ │ │ │ │ Macropodidæ │ │ │ │ │ │ Passeres, Turdidæ │ │ │ │ │ │ Crateropodidæ│ │ │ │ │ │ Tanagridæ │ │ │ │ 1│ │ Fringillidæ │ │ │ │ 1│ │ Icteridæ │ │ │ │ │ │ Striges, Bubonidæ │ │ │ │ │ │ Psittaci, Loridæ │ │ │ │ │ │ Cacatuidæ │ │ │ │ 2│ │ Psittacidæ │ │ │ │ 3│ │ 1 │ │ │ │ │ │ Accipitres, │ │ │ │ 1│ │ Falconidæ │ │ │ │ │ │ Columbæ, Columbidæ │ │ │ │ │ │ Galli, Phasianidæ │ │ │ │ │ │ Fulicariæ, Rallidæ │ │ │ │ │ │ Anseres, Anatidæ │ 1│ │ │ │ │ Struthiones, Rheidæ│ │ │ │ │ │ ───────────────────┼───────┼───────┼─────────┼──────┼──────────┼────── Total │ 2│ 1│ 1│ 8│ 3│ 1 ───────────────────┴───────┴───────┴─────────┴──────┴──────────┴──────

═══════════════════╤═══════╤════════════╤═══════╤═════════╤═══════════ Order Family │Angioma│Endothelioma│Sarcoma│Papilloma│Epithelioma │ │ │ │ │ │ │ │ │ │ ───────────────────┼───────┼────────────┼───────┼─────────┼─────────── „ „ │ „ │ „ │ „ │ „ │ „ │ │ │ │ │ ───────────────────┼───────┼────────────┼───────┼─────────┼─────────── Primates, │ │ │ │ │ Cercopithecidæ │ │ │ │ │ Cebidæ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Lemures, Lemuridæ │ │ │ │ │ │ │ │ │ │ Carnivora, Felidæ │ 1│ 1│ │ │ │ │ │ │ │ Viverridæ │ │ │ │ │ Canidæ │ │ │ 1│ │ Procyonidæ │ │ │ │ │ Ursidæ │ │ │ │ │ 1 │ │ │ │ │ Phocidæ │ │ │ │ │ │ │ │ │ │ Rodentia, Sciuridæ │ │ │ │ │ Muridæ │ │ │ 2│ │ Heteromyidæ │ │ │ 1│ │ │ │ │ │ │ Octodontidæ │ │ │ 1│ │ Hystricidæ │ │ │ │ │ Dasyproctidæ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Proboscidea │ │ │ │ │ Ungulata, Equidæ │ │ │ │ │ Bovidæ │ │ │ 1│ │ Cervidæ │ │ │ │ │ Camelidæ │ │ │ │ │ Suidæ │ │ │ │ │ Edentata, │ │ │ │ │ Dasypodidæ │ │ │ │ │ Marsupialia, │ │ │ │ │ Didelphyidæ │ │ │ │ │ Dasyuridæ │ │ │ │ │ 1 Peramelidæ │ │ │ │ │ Macropodidæ │ │ │ │ │ Passeres, Turdidæ │ │ │ │ │ Crateropodidæ│ │ │ │ │ Tanagridæ │ │ │ │ │ Fringillidæ │ │ │ │ │ Icteridæ │ │ │ │ │ Striges, Bubonidæ │ │ │ │ 1│ Psittaci, Loridæ │ │ │ │ │ Cacatuidæ │ │ │ │ │ Psittacidæ │ │ │ 7│ │ 1 │ │ │ │ │ Accipitres, │ │ │ 1│ │ Falconidæ │ │ │ │ │ Columbæ, Columbidæ │ │ │ 1│ │ Galli, Phasianidæ │ │ │ │ │ Fulicariæ, Rallidæ │ │ 1│ │ │ Anseres, Anatidæ │ │ │ 1│ │ Struthiones, Rheidæ│ │ │ │ │ ───────────────────┼───────┼────────────┼───────┼─────────┼─────────── Total │ 1│ 2│ 16│ 1│ 3 ───────────────────┴───────┴────────────┴───────┴─────────┴───────────

═══════════════════╤═══════╤═════════╤═══════════╤═════════════╤══════ Order Family │Adenoma│Carcinoma│ Chorion- │Hypernephroma│Mixed │ │ │epithelioma│ │Tumors │ │ │ │ │ ───────────────────┼───────┼─────────┼───────────┼─────────────┼────── „ „ │ „ │ „ │ „ │ „ │ „ │ │ │ │ │ ───────────────────┼───────┼─────────┼───────────┼─────────────┼────── Primates, │ 1│ │ │ │ Cercopithecidæ │ │ │ │ │ Cebidæ │ │ │ │ 1│ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Lemures, Lemuridæ │ 1│ │ │ │ │ │ │ │ │ Carnivora, Felidæ │ 2│ 1│ │ │ │ │ │ │ │ Viverridæ │ │ 2│ │ │ Canidæ │ 3│ 1│ │ │ 1 Procyonidæ │ 1│ │ │ │ Ursidæ │ │ 2│ │ │ │ │ │ │ │ Phocidæ │ │ │ │ 1│ │ │ │ │ │ Rodentia, Sciuridæ │ 1│ │ │ 1│ Muridæ │ │ 3│ │ │ Heteromyidæ │ │ │ │ │ │ │ │ │ │ Octodontidæ │ │ │ │ │ Hystricidæ │ │ │ 1│ │ Dasyproctidæ │ │ 1│ │ │ │ │ │ │ │ │ │ │ │ │ Proboscidea │ │ │ │ │ Ungulata, Equidæ │ │ │ │ │ Bovidæ │ │ │ │ │ Cervidæ │ 1│ │ │ │ Camelidæ │ │ 1│ │ │ Suidæ │ │ 1│ │ │ Edentata, │ │ │ │ │ Dasypodidæ │ │ │ │ │ Marsupialia, │ 1│ 1│ │ │ Didelphyidæ │ │ │ │ │ Dasyuridæ │ │ 1│ │ │ Peramelidæ │ │ 1│ │ │ Macropodidæ │ │ 2│ │ │ Passeres, Turdidæ │ │ │ │ 1│ Crateropodidæ│ 1│ │ │ │ Tanagridæ │ │ │ │ │ Fringillidæ │ │ 2│ │ │ Icteridæ │ │ │ │ 1│ Striges, Bubonidæ │ │ │ │ │ Psittaci, Loridæ │ │ 1│ │ │ Cacatuidæ │ │ │ │ │ Psittacidæ │ 5│ 4│ │ 1│ 1 │ │ │ │ │ Accipitres, │ │ │ │ │ Falconidæ │ │ │ │ │ Columbæ, Columbidæ │ │ │ │ │ Galli, Phasianidæ │ │ 1│ │ │ Fulicariæ, Rallidæ │ │ │ │ │ Anseres, Anatidæ │ 1│ │ │ 1│ Struthiones, Rheidæ│ 1│ │ │ │ ───────────────────┼───────┼─────────┼───────────┼─────────────┼────── Total │ 19│ 25│ 1│ 7│ 2 ───────────────────┴───────┴─────────┴───────────┴─────────────┴──────

═══════════════════╤═══════════════════════════════════════════ Order Family │ Organic Source of Tumor │ │ ───────────────────┼────┬──────┬───────┬──────┬──────┬───────── „ „ │Lung│Muscle│Thyroid│Uterus│Kidney│Bone and │ │ │ │ │ │Cartilage ───────────────────┼────┼──────┼───────┼──────┼──────┼───────── Primates, │ │ │ │ │ │ Cercopithecidæ │ │ │ │ │ │ Cebidæ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Lemures, Lemuridæ │ │ │ │ │ │ │ │ │ │ │ │ Carnivora, Felidæ │ │ │ │ 2│ │ 1 │ │ │ │ │ │ Viverridæ │ 1│ │ │ │ │ Canidæ │ │ │ 3│ │ │ Procyonidæ │ │ │ │ │ │ Ursidæ │ │ │ │ │ │ │ │ │ │ │ │ Phocidæ │ │ │ │ │ │ │ │ │ │ │ │ Rodentia, Sciuridæ │ │ │ │ │ 1│ 1 Muridæ │ │ 3│ │ │ │ Heteromyidæ │ │ │ │ │ │ │ │ │ │ │ │ Octodontidæ │ │ │ 1│ │ │ Hystricidæ │ │ │ │ 1│ │ Dasyproctidæ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Proboscidea │ │ │ │ 1│ │ Ungulata, Equidæ │ │ │ │ │ │ Bovidæ │ │ │ │ 1│ │ 1 Cervidæ │ │ │ │ │ │ Camelidæ │ │ │ │ │ │ Suidæ │ │ │ │ 1│ │ Edentata, │ │ │ │ 1│ │ Dasypodidæ │ │ │ │ │ │ Marsupialia, │ │ │ │ │ 1│ Didelphyidæ │ │ │ │ │ │ Dasyuridæ │ │ │ │ │ │ Peramelidæ │ 1│ │ │ │ │ Macropodidæ │ 1│ │ │ │ │ Passeres, Turdidæ │ │ │ │ │ 1│ Crateropodidæ│ │ │ │ │ 1│ Tanagridæ │ │ │ │ │ │ Fringillidæ │ │ │ │ │ 2│ Icteridæ │ │ │ │ │ 1│ Striges, Bubonidæ │ │ │ │ │ │ Psittaci, Loridæ │ 1│ │ │ │ │ Cacatuidæ │ │ │ │ │ │ Psittacidæ │ │ 2│ 1│ 1│ 5│ │ │ │ │ │ │ Accipitres, │ │ │ │ │ │ Falconidæ │ │ │ │ │ │ Columbæ, Columbidæ │ │ │ │ │ 1│ Galli, Phasianidæ │ │ │ │ │ │ Fulicariæ, Rallidæ │ │ │ │ │ │ 1 Anseres, Anatidæ │ │ 1│ │ │ 1│ 1 Struthiones, Rheidæ│ │ │ │ │ │ ───────────────────┼────┼──────┼───────┼──────┼──────┼───────── Total │ 4│ 6│ 5│ 8│ 14│ 5 ───────────────────┴────┴──────┴───────┴──────┴──────┴─────────

═══════════════════╤═══════════════════════════════════════════════ Order Family │ Organic Source of Tumor │ │ ───────────────────┼────────────────┬──────┬──────────┬──────┬───── „ „ │Gastrointestinal│Liver,│Peritoneum│Lymph │Mamma │ Tract │ &c. │ │Tissue│ ───────────────────┼────────────────┼──────┼──────────┼──────┼───── Primates, │ 1│ │ │ │ Cercopithecidæ │ │ │ │ │ Cebidæ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Lemures, Lemuridæ │ │ │ │ │ │ │ │ │ │ Carnivora, Felidæ │ │ 1│ │ 1│ │ │ │ │ │ Viverridæ │ 1│ │ │ │ Canidæ │ │ 2│ │ │ Procyonidæ │ │ │ │ │ Ursidæ │ │ │ │ │ 1 │ │ │ │ │ Phocidæ │ │ │ │ │ │ │ │ │ │ Rodentia, Sciuridæ │ │ 1│ │ │ Muridæ │ │ │ │ │ 2 Heteromyidæ │ │ │ │ │ │ │ │ │ │ Octodontidæ │ │ │ │ │ Hystricidæ │ │ │ │ │ Dasyproctidæ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Proboscidea │ │ │ │ │ Ungulata, Equidæ │ │ │ 1│ │ Bovidæ │ │ │ │ 1│ Cervidæ │ │ 1│ │ │ Camelidæ │ │ 1│ │ │ Suidæ │ │ │ │ │ Edentata, │ │ │ │ │ Dasypodidæ │ │ │ │ │ Marsupialia, │ │ │ │ │ 1 Didelphyidæ │ │ │ │ │ Dasyuridæ │ 1│ │ │ │ Peramelidæ │ │ │ │ │ Macropodidæ │ 1│ │ │ │ Passeres, Turdidæ │ │ │ │ │ Crateropodidæ│ │ │ │ │ Tanagridæ │ │ │ │ │ Fringillidæ │ │ │ │ │ Icteridæ │ │ │ │ │ Striges, Bubonidæ │ 1│ │ │ │ Psittaci, Loridæ │ │ │ │ │ Cacatuidæ │ │ │ │ │ Psittacidæ │ 1│ 3│ │ │ │ │ │ │ │ Accipitres, │ │ │ 1│ │ Falconidæ │ │ │ │ │ Columbæ, Columbidæ │ │ │ │ │ Galli, Phasianidæ │ │ │ │ │ Fulicariæ, Rallidæ │ │ │ │ │ Anseres, Anatidæ │ │ │ │ │ Struthiones, Rheidæ│ 1│ │ │ │ ───────────────────┼────────────────┼──────┼──────────┼──────┼───── Total │ 6│ 9│ 2│ 2│ 4 ───────────────────┴────────────────┴──────┴──────────┴──────┴─────

═══════════════════╤══════════════════════════════════════════╤════════════ Order Family │ │Notes Extra │ │ cases not │ │ tabulated. ───────────────────┼─────┬────────┬────┬──────┬───────┬───────┼──────────── „ „ │Ovary│Pancreas│Skin│Testes│Adrenal│Unknown│ „ │ │ │ │ │ │ │ ───────────────────┼─────┼────────┼────┼──────┼───────┼───────┼──────────── Primates, │ │ │ │ │ │ │ Cercopithecidæ │ │ │ │ │ │ │ Cebidæ │ │ │ │ │ 1│ │Adenoma of │ │ │ │ │ │ │ prostrate │ │ │ │ │ │ │suggesting │ │ │ │ │ │ │ cancer in │ │ │ │ │ │ │ places. Lemures, Lemuridæ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Carnivora, Felidæ │ │ │ │ │ │ │Endothelioma │ │ │ │ │ │ │ of pleura. Viverridæ │ │ 1│ │ │ │ │ Canidæ │ │ 1│ │ │ │ │ Procyonidæ │ │ 1│ │ │ │ │ Ursidæ │ │ │ │ │ 1│ │Epithelioma │ │ │ │ │ │ │ of tongue. Phocidæ │ │ │ │ │ 1│ │ │ │ │ │ │ │ │ Rodentia, Sciuridæ │ │ │ │ │ │ │ Muridæ │ │ │ │ │ │ │ Heteromyidæ │ │ │ │ │ │ │Sarcoma of │ │ │ │ │ │ │ bladder. Octodontidæ │ │ │ │ │ │ │ Hystricidæ │ │ │ │ │ │ │ Dasyproctidæ │ │ │ │ │ │ │Squamous │ │ │ │ │ │ │ carcinoma │ │ │ │ │ │ │ of larynx. Proboscidea │ │ │ │ │ │ │ Ungulata, Equidæ │ │ │ │ │ │ │ Bovidæ │ │ │ │ │ │ │ Cervidæ │ │ │ │ │ │ │ Camelidæ │ │ │ │ │ │ │ Suidæ │ │ │ │ │ │ │ Edentata, │ │ │ │ │ │ │ Dasypodidæ │ │ │ │ │ │ │ Marsupialia, │ │ │ │ │ │ │ Didelphyidæ │ │ │ │ │ │ │ Dasyuridæ │ │ │ 1│ │ │ │ Peramelidæ │ │ │ │ │ │ │ Macropodidæ │ │ │ │ │ │ │ Passeres, Turdidæ │ │ │ │ │ │ │ Crateropodidæ│ │ │ │ │ │ │ Tanagridæ │ │ │ │ │ │ 1│ Fringillidæ │ │ │ │ │ │ 1│ Icteridæ │ │ │ │ │ │ │ Striges, Bubonidæ │ │ │ │ │ │ │ Psittaci, Loridæ │ │ │ │ │ │ │ Cacatuidæ │ │ │ │ │ │ 2│ Psittacidæ │ 1│ │ │ 2│ 1│ 5│Glioma of │ │ │ │ │ │ │ brain. Accipitres, │ │ │ │ │ │ 1│ Falconidæ │ │ │ │ │ │ │ Columbæ, Columbidæ │ │ │ │ │ │ │ Galli, Phasianidæ │ 1│ │ │ │ │ │ Fulicariæ, Rallidæ │ │ │ │ │ │ │ Anseres, Anatidæ │ │ │ │ │ 1│ │ Struthiones, Rheidæ│ │ │ │ │ │ │ ───────────────────┼─────┼────────┼────┼──────┼───────┼───────┼──────────── Total │ 2│ 3│ 1│ 2│ 5│ 10│ ───────────────────┴─────┴────────┴────┴──────┴───────┴───────┴────────────

TABLE 22. _Analytical Table Showing Data of Incidence, Sex, Breeding, Duration of Captivity, Metastases and Embryological Origins and Distributions According to Order._

════════════╤═══════╤═════╤════════╤═══════════════╤══════════╤═══════ Order │ Total │ Per │ Sex │ Breeding │ Range │Average │animals│cent.│ │ │ known │ for │ │ per │ │ │captivity │ tumor │ │order│ │ │ │animals ────────────┼───────┼─────┼──┬──┬──┼────┬───────┬──┼──────────┼─────── „ │ „ │ „ │♂ │♀ │? │Wild│Captive│? │ „ │ „ ────────────┼───────┼─────┼──┼──┼──┼────┼───────┼──┼──────────┼─────── Primates │ 2│ .4│ 2│ │ │ 2│ │ │3–4 yrs. │3½ yrs. Lemures │ 1│ 1.1│ 1│ │ │ 1│ │ │4 yrs. │ Carnivora │ 17│ 3.5│ 8│ 9│ │ 14│ 3│ │1–18 yrs. │9 yrs. Rodentia │ 12│ 6.│ 7│ 4│ 1│ 8│ 2│ 2│1 mo.–7 │2 yrs. │ │ │ │ │ │ │ │ │yrs. │8 mo. Insectivora │ 0│ │ │ │ │ │ │ │ │ Chiroptera │ 0│ │ │ │ │ │ │ │ │ Proboscidea │ 1│33.│ │ 1│ │ 1│ │ │38 yrs. │ Hyracoidea │ 0│ │ │ │ │ │ │ │ │ Ungulata │ 7│ 1.9│ 2│ 5│ │ 5│ 1│ 1│2–16 yrs. │9 yrs. Edentata │ 1│6.2│ │ 1│ │ 1│ │ │10 yrs. │ Marsupialia │ 7│ 4.│ 6│ 1│ │ 6│ 1│ │1 wk.–12 │5 yrs. │ │ │ │ │ │ │ │ │yrs. │6 mo. Monotremata │ 0│ │ │ │ │ │ │ │ │ ────────────┼───────┼─────┼──┼──┼──┼────┼───────┼──┼──────────┼─────── Totals │ 48│ 2.58│26│21│ 1│ 38│ 7│ 3│ │ │ │ │ │ │ │ │ │ │ │ Passeres │ 7│ .51│ 4│ 2│ 1│ 6│ │ 1│1–14 yrs. │6 yrs. Picariæ │ 0│ │ │ │ │ │ │ │ │ Striges │ 1│ .75│ │ 1│ │ 1│ │ │7 yrs. │ Psittaci │ 26│ 3.7│ 9│ 8│ 9│ 8?│ 16?│2?│5 mo.–9 │3 yrs. │ │ │ │ │ │ │ │ │yrs. │ Accipitres │ 2│ 1.│ 2│ │ │ 2│ │ │(1)[93]–4 │ │ │ │ │ │ │ │ │ │yrs. │ Columbæ │ 1│ .63│ │ 1│ │ 1│ │ │4 yrs. │ Galli │ 1│ .33│ │ 1│ │ 1│ │ │? │ Hemipodii │ 0│ │ │ │ │ │ │ │ │ Fulicariæ │ 1│2.8│ 1│ │ │ 1│ │ │6 yrs. │ Alectorides │ 0│ │ │ │ │ │ │ │ │ Limicolæ │ 0│ │ │ │ │ │ │ │ │ Gaviæ │ 0│ │ │ │ │ │ │ │ │ Impennes │ 0│ │ │ │ │ │ │ │ │ Steganopodes│ 0│ │ │ │ │ │ │ │ │ Herodiones │ 0│ │ │ │ │ │ │ │ │ Odontoglossæ│ 0│ │ │ │ │ │ │ │ │ Palamedes │ 0│ │ │ │ │ │ │ │ │ Anseres │ 4│ 1.2│ │ 3│ 1│ 3?│ 1│ │(1)[93]-10│ │ │ │ │ │ │ │ │ │yrs. │ │ │ │ │ │ │ │ │ │(1)[93]-4 │ │ │ │ │ │ │ │ │ │yrs. │ Struthiones │ 1│3.1│ 1│ │ │ 1│ │ │(1)[93]-5 │ │ │ │ │ │ │ │ │ │yrs. │ Crypturi │ 0│ │ │ │ │ │ │ │ │ ────────────┼───────┼─────┼──┼──┼──┼────┼───────┼──┼──────────┼─────── Totals │ 44│ 1.23│17│16│11│ 24│ 17│ 3│ │ ────────────┼───────┼─────┼──┼──┼──┼────┼───────┼──┼──────────┼─────── Grand Totals│ 92│ 1.7│43│37│12│ 62│ 24│ 6│ │ ────────────┴───────┴─────┴──┴──┴──┴────┴───────┴──┴──────────┴───────

════════════╤══════════════╤════════════════════════════════════ Order │Embryological │ Metastases │ layer │ │ │ │ │ ────────────┼────┬────┬────┼────┬─────┬──────┬───────────┬────── „ │Ecto│Meso│Ento│Lung│Liver│Kidney│Lymphocytes│Spleen ────────────┼────┼────┼────┼────┼─────┼──────┼───────────┼────── Primates │ │ 1│ 1│ │ │ │ │ Lemures │ │ │ 1│ │ │ │ │ Carnivora │ 2│ 8│ 7│ 5│ 1│ │ 1│ Rodentia │ 2│ 7│ 3│ │ │ │ │ │ │ │ │ │ │ │ │ Insectivora │ │ │ │ │ │ │ │ Chiroptera │ │ │ │ │ │ │ │ Proboscidea │ │ 1│ │ │ │ │ │ Hyracoidea │ │ │ │ │ │ │ │ Ungulata │ │ 5│ 2│ │ 1│ 1│ 1│ Edentata │ │ 1│ │ │ │ │ │ Marsupialia │ 2│ 2│ 3│ 1│ 2│ 1│ 1│ 2 │ │ │ │ │ │ │ │ Monotremata │ │ │ │ │ │ │ │ ────────────┼────┼────┼────┼────┼─────┼──────┼───────────┼────── Totals │ 6│ 25│ 17│ 6│ 4│ 2│ 3│ 2 │ │ │ │ │ │ │ │ Passeres │ │ 7│ │ 1│ 1│ │ │ Picariæ │ │ │ │ │ │ │ │ Striges │ │ │ 1│ │ │ │ │ Psittaci │ 1│ 17│ 8│ │ 2│ │ │ 1 │ │ │ │ │ │ │ │ Accipitres │ │ 2│ │ │ │ │ │ │ │ │ │ │ │ │ │ Columbæ │ │ 1│ │ │ │ │ │ Galli │ │ 1│ │ │ │ │ │ Hemipodii │ │ │ │ │ │ │ │ Fulicariæ │ │ 1│ │ │ │ │ │ Alectorides │ │ │ │ │ │ │ │ Limicolæ │ │ │ │ │ │ │ │ Gaviæ │ │ │ │ │ │ │ │ Impennes │ │ │ │ │ │ │ │ Steganopodes│ │ │ │ │ │ │ │ Herodiones │ │ │ │ │ │ │ │ Odontoglossæ│ │ │ │ │ │ │ │ Palamedes │ │ │ │ │ │ │ │ Anseres │ │ 4│ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Struthiones │ │ │ 1│ │ │ │ │ │ │ │ │ │ │ │ │ Crypturi │ │ │ │ │ │ │ │ ────────────┼────┼────┼────┼────┼─────┼──────┼───────────┼────── Totals │ 1│ 33│ 10│ 1│ 3│ │ │ 1 ────────────┼────┼────┼────┼────┼─────┼──────┼───────────┼────── Grand Totals│ 7│ 58│ 27│ 7│ 7│ 2│ 3│ 3 ────────────┴────┴────┴────┴────┴─────┴──────┴───────────┴──────

════════════╤═════════════════════╤══════════════ Order │ Metastases │Embryological │ │ layer of │ │ metastases │ │ ────────────┼─────────┬────┬──────┼────┬────┬──── „ │Intestine│Bone│Muscle│Ecto│Meso│Ento ────────────┼─────────┼────┼──────┼────┼────┼──── Primates │ │ │ │ │ │ Lemures │ │ │ │ │ │ Carnivora │ │ │ 1│ │ 5│ 5 Rodentia │ │ │ │ │ │ │ │ │ │ │ │ Insectivora │ │ │ │ │ │ Chiroptera │ │ │ │ │ │ Proboscidea │ │ │ │ │ │ Hyracoidea │ │ │ │ │ │ Ungulata │ │ │ │ │ 1│ 1 Edentata │ │ │ │ │ │ Marsupialia │ │ 1│ │ │ 2│ 3 │ │ │ │ │ │ Monotremata │ │ │ │ │ │ ────────────┼─────────┼────┼──────┼────┼────┼──── Totals │ │ 1│ 1│ │ 8│ 9 │ │ │ │ │ │ Passeres │ 1│ │ │ │ 1│ 2 Picariæ │ │ │ │ │ │ Striges │ │ │ │ │ │ Psittaci │ 1│ │ │ │ 1│ 3 │ │ │ │ │ │ Accipitres │ │ │ │ │ │ │ │ │ │ │ │ Columbæ │ │ 1│ │ │ 1│ Galli │ │ │ │ │ │ Hemipodii │ │ │ │ │ │ Fulicariæ │ │ │ │ │ │ Alectorides │ │ │ │ │ │ Limicolæ │ │ │ │ │ │ Gaviæ │ │ │ │ │ │ Impennes │ │ │ │ │ │ Steganopodes│ │ │ │ │ │ Herodiones │ │ │ │ │ │ Odontoglossæ│ │ │ │ │ │ Palamedes │ │ │ │ │ │ Anseres │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ Struthiones │ │ │ │ │ │ │ │ │ │ │ │ Crypturi │ │ │ │ │ │ ────────────┼─────────┼────┼──────┼────┼────┼──── Totals │ 2│ 1│ │ │ 3│ 5 ────────────┼─────────┼────┼──────┼────┼────┼──── Grand Totals│ 2│ 2│ 1│ │ 11│ 14 ────────────┴─────────┴────┴──────┴────┴────┴──── For meaning of italics see foot note Table 1.

INCIDENCE OF TUMORS.

Examination of the table, (21) from the standpoint of differential percentage reveals that mammals have 48 tumors giving an incidence of 2.58 per cent. whereas birds have 44 new growths equivalent to 1.23 per cent. Were it not for the high figures for one single variety of bird (Undulated Grass Parrakeet) this value for Aves would be still lower. At all events our figures would indicate that the mammal is at least twice as productive of neoplasms as is the bird. In our material the latter class has had a better chance than Mammalia to show its susceptibility since there have been nearly twice as many autopsies.

Within the classes the comparative figures have less value because of the smaller and varying numbers. Such high percentages as are shown by the elephants and armadillos cannot be taken as indicators for their orders since too few specimens were examined. Judging by orders with more than one hundred autopsies the rodents stand at the head of the list followed by the marsupials and carnivores. It is interesting that the animal nearest to man, the monkey, and with greatest number of autopsies in its zoological class, has the lowest tumor incidence. Psittaci lead the avian orders, followed by the Fulicariæ, but as there are but thirty-five autopsies upon these, the second place rightly belongs to the Anseres. All the principal orders are represented but the only one of importance is the leader. The Psittaci are very prone to have tumors in the renal area, sometimes of the kidney, at others of the adrenal and occasionally of the sex glands. Some remarks have already been given to this matter in the sections devoted to the kidney and genitalia but it will be discussed again under tumor morphology.

Among these ninety-two animals, one bore multiple tumors, a Jaguar (Felis onca) with adenomata of the liver and uterus and angiomata of the mesentery. Careful study failed to reveal any parasitism as the cause of the growths and since the first two were of slightly varying structure it is not believed that one is a metastasis from the other.

The sex incidence stands in direct relation to the proportion of total males and females posted or in other words it is the same for the two. The figures might be somewhat affected were the gender of all the parrakeets available but the tumors growing in the upper renal area frequently destroy the sex gland.

Definite statements concerning the importance of breeding in the causation of neoplasms cannot be made since we cannot quote figures for the percentages of wild- and captive-born of our entire autopsy list. The data are confused by scanty information concerning the twenty-six parrots, the history of which is vague and I am perhaps too severe in accrediting the birth of sixteen of them to captivity. This was done because of a lack of exact information concerning these specimens and, because their variety is known to breed when captive by the residents of their habitat[94], the distribution into wild- and captive-born is based upon what information we have. If the order Psittaci be subtracted entirely, it leaves a total of 62 tumor-bearing animals of known breeding, 49 of which were born in the wild, thirteen in captivity, a fact which strengthens the thought that unnatural breeding increases the chance of neoplasms.

The known length of captivity has also a direct bearing on this point. The figures given in the columns “known captivity” and “average for tumor bearers” were compared with figures obtained by averaging the lives of fifty others (when possible) of the same order or of at least three times as many as bore tumors. Animals dying from injury were excluded. With one exception the average for “tumor bearers” exceeded that for “non-tumor bearers”; the exception, the Ungulata, had the same average for both groups. It seems then that tumors occur in animals in captivity longer than the average for their order, or in specimens that have the power to live under confined conditions until neoplasms develop. In this respect I recall the statements made by Harlow Brooks[95] that tumors will probably be found more commonly in animals when they live in a manner comparable to that of urban man and that racial degeneracy will favor their development. There is adduced here perhaps the first definite evidence that long captivity allows tumor tendency to express itself but it does not prove that confinement increases tumors. Nor does the expectation of life, average or potential, stand in any direct and definite relationship to the frequency of neoplasms. The only clear case of long life and high tumor incidence is to be found in Parrots; we feel however that some unknown factor increases tumors of the renal-adrenal region in these birds and that unqualified statements about age and tumor growth are not permissible. Since tumors grow in many wild-born specimens, a high percentage of which become known in the first few years of captivity, is it not highly probable that tumors are reasonably common in the wild and that we do not observe enough purely natural specimens to assume an immunity on the part of free living beasts.

One of the undesirable features of captive breeding is consanguinity of parents and there is good reason to believe that tumor susceptibility can be bred into or out of a line of animals by mating tumor bearers and non-tumor bearers, the tendency following the rules of Mendelian inheritance (Slye). Is there any proof that inbreeding does not occur in the wild and if it do, it is perfectly possible that tumor tendency may be transmitted as a dominant character; the effect of artificial or intentional inbreeding in captivity would only offer an opportunity for a summation of these influences.

If injury and animal parasitism have any importance in neoplasmata then this opportunity certainly occurs under natural conditions. Fibiger observed gastric tumors in rats arising under the influence of nematodes while Slye and Wells report facial neoplasms in mice apparently arising at points of old injuries. It seems to me that we have no right to assume an immunity of wild animals, in their native environment, to tumors; the incidence is another matter but it may be considerable.

It was thought possible that there might be some light shed upon the matter by an analysis of our sarcomatous and epitheliomatous tumors in wild- and captive-born animals. In our second paper[96] upon this subject I ventured the statement that sarcomatous growths occurred more frequently in captive-born, epitheliomatous in wild-born specimens. Greater data have not borne out this conclusion and information was sought as to the embryonal derivation of tumor-bearing tissue. Analyzing the cases in which all the factors could be obtained, it seems that among seven tumors of captive-bred animals, five came from the entoderm, two from the mesoderm, whereas in wild-bred animals, of the fifty-seven tumors, five came from the ectoderm, thirty-two from the mesoderm and fourteen from the entoderm. These figures do not include the parrots. The sex values have no significance.

It is interesting and noteworthy, that, as in the human being, the majority of the tumors came from tissues arising in the mesoderm and that the entodermic derivatives received the largest number of metastases; no ectodermic tissues were sites of secondary tumors. The visceral seats of metastases are probably of little value for comparison in so small a number; the lung and liver however occupy the prominent places.

Interesting as the foregoing facts may be, they do not shed light upon the question of breeding and degeneracy in the causation of neoplasms. Attention is arrested however by the paucity of tumors in derivatives of the ectoderm since in man new growths are common in the breast, at the rectal and labial mucocutaneous junctions and on the skin. The immunity of the ectodermic tissues to secondary growths is very distinct; this holds true in man.

SPECIAL TUMORS.

The diagnosis of fibroma offers the same difficulty in the zoological material as it does in man and even more care must be exercised for solid tumors in certain localities. The bird often presents hard nodular masses on the palmar and lateral aspects of the feet, sometimes surmounted by callosities, to which the term fibroma or fibromatous corns might be applied. Section of some of these will reveal areas of granulation tissue about points of inflammation so that we have considered them as infectious or the result of incorrect perches and excluded them from the tumors. True fibromata have been encountered thrice but in combination with muscle tissue as a fibromyoma thrice in addition. The “fibroids” seen in the elephants and armadillo have already been described.

The nodular growth sometimes accompanying degenerative disease of the osseous system followed by attempts at repair as discussed under osteitis deformans, leontiasis ossium and actinomycosis, are often productive of masses to which it is easy to apply the term osteoma. If one demand that an osteoma shall be a distinct neoplastic, localized bony growth of unnatural or greatly exaggerated structure, then the tumor is quite rare. We have seen one growing from the vertebræ and clavicle of a gerbille and a fibro-osteoma on one jaw of an Isabelline gazelle. The chondromata have been limited to one case, a unilateral mass growing from the nasal cartilage of a caracal.

Lipomata are localized collections of fat consisting of cells with greater fat capacity than normally, sometimes surrounded by an indefinite capsule. Judging by the observations of Joest and Johne they are reasonably common in horses and cows. We have not seen a single case in mammals but eight cases appeared in the birds. These were with one exception disposed under the skin mostly over the abdomen and chest and once under the scalp. In a hawk the tumor grew as a pelvic mass surrounding the cloaca and apparently caused decided obstruction to the lumen. The lipomata of the Psittaci usually grow as pendulous masses on the abdominal wall covered by thin, featherless, delicate skin, often showing dilated veins. Upon section they are rather rich in blood supply, “angiolipoma,” but fail to show any angiomatous or solid cellular areas under the microscope. The frequency of the growths in one variety (Roseate cockatoo—Cacatua roseicapilla) led to an attempt to transplant the tumor. The plant seemed to thrive in the recipient for a while but soon disappeared. Breeding experiments on the tumor bearers are now under way.

Angiomata of lymph channels were observed in the omentum and mesentery of a jaguar (Felis onca); this is the animal with three apparently separate and distinct tumors. “The omentum is normally fatty and slightly congested. In its meshes are myriads of tiny cysts containing gray fluid. The main peritoneal area is negative but in the pelvic region on anterior rectal wall, in the superior edge of the broad ligament and in Douglas’ pouch, are cysts from a few millimetres to several centimetres, with clear contents. The microscopic section of omentum shows the multiple cysts as cavities of varying size, from that of an arteriole to the diameter of a two-third lens field. They are lined with flat, closely placed pavement cells with well stained but vesicular nucleus. The septa are adult connective tissue. No contents or granular eosin-staining material. No swollen cells like in adenomata. No parasites seen.”

Two endotheliomata have been found, one of the flat variety with warty excrescences common on serous surfaces, located in the pleura of a leopard (Felis nebulosa), and one of the nodular variety, growing from the clavicle of a Moorhen (Gallinula chloropus).

The sarcomata present their usual morphology grossly and minutely and with the exception of the cases arising from the pectoral muscle and from the genital area offer little of interest. Two instances in the former location, observed in parrakeets, presented several puzzling features. The component cells were spindle in shape, similar to a muscle cell but were fitted with the round or elliptical nuclei of embryonal cells. In a few places they were exceedingly large and had shadowy outlines like a syncytium or they would be so arranged as to suggest a glandular structure. The dominant type of cell was, however, everywhere the spindle as it is seen in sarcoma. The sarcomata when they occur in the genital area usually assume the alveolar arrangement and are of the round or mixed cell variety. Only three of the sixteen sarcomata gave metastases.

Papillomata of minor character appear occasionally on the skin of animals as warts, but only one instance of any greater importance has been found. The duodenal mucosa of an owl (Bubo virginianus) presented a soft growth which partly obstructed the intestinal lumen. Papillary adenomata, on the other hand, have been observed several times, but since they have more importance as irregular hyperplasias of glandular origin have been included in the next group. An interesting case was seen in a baboon (Papio hamadryas) in which a large part of the gastric wall was the seat of adenomata, presenting in addition several distinct papillary outgrowths. A similar picture was found in the duodenum of the rhea (Rhea americana).

The greatest interest in the adenomata centres around these growths in the renal area in parrakeets, and as they have much in common with all the glandular tumors of this region, a general discussion of this subject may be introduced here. We have observed seven tumors constructed on a glandular basis of renal or adrenal character. Grossly these tumors develop as irregular masses usually of distinct brown color, constructed on a lobular plan, delicate barely visible septa dividing the growth. They seem devoid of large vessels, a gross observation confirmed microscopically. There is no criterion to the naked eye, which will distinguish the variety of epithelial hyperplasia or permit separation of these neoplasms from some sarcomata; the latter are usually gray but need not be so. Minutely studied, three of these tumors proved to be adenomata, all papillary, one cystic as well. Three had to be denominated carcinoma because of their distinct separate crowded nests and incomplete acini. The cells comprising these growths are comparable to the lining elements of the collecting tubules of the renal lobule in that they have relatively large nuclei and a tendency to basic staining protoplasm. The adenomatous picture is, however, more comparable to the cortex than to the medulla. The remaining tumor was a hypernephroma of the usual large cell, acinus-forming type and seemed to originate in the adrenal. None of these tumors in the parrakeets sent out metastases. Other hypernephromata have been diagnosed, to the number of six. Upon review of their descriptions and sections, the determinations are to be confirmed. However, it must be recorded here that none of the three in mammals gave metastases, while two of the three in birds did so. They are all of the usual type with large vacuolated cells in glandular groups or strands.

Three rather interesting examples of epithelioma have been observed. The first and most important was a basocellular growth of the tongue in a black bear (Ursus americanus). The local damage—ulceration and infiltration—and swelling sufficient to interfere with deglutition, were quite considerable. The basal cell nests had penetrated deeply into the muscle, but extension had taken place only to a single submaxillary gland. A squamous epithelioma was found on the skin of the thigh of a Tasmanian devil (Sarcophilus ursinus). The construction was somewhat unusual in that it was cystic but lined with squamous and keratinized plates. It could not be decided that it originated from glands like a trichoepithelioma; it was not like a basal cell cancer. No metastases had occurred. The third case was that of a tumor within the abdomen of an Amazon (Chrysotis leucocephala). It consisted of an illy defined basement membrane upon which were irregular stratified squamous epithelial cells. Upon the surface were wavy bands of horny material, very much like dried and cast-off epithelial scales, except more compact and extensive. These latter seemed to form the bulk of the mass. Beneath the membrane a few irregular accumulations of cells bearing a similarity to those on the surface could be found, but they were probably large plasma cells. The epithelial layer dipped down like in epithelioma. No pearls or separate nests were found. While this mass was not localized, it was doubtless an epithelioma, and should be included in this series. Its possible origin in the small intestine has been considered.

The question of the occurrence of tumors in wild animals seems fairly well settled when twenty-five examples of malignant epithelial neoplasms can be discovered in fifty-three hundred autopsies. It is interesting to note the incidence of these tumors in wild- and park-bred animals. Exclusive of the parrakeets there are twenty-one cancers, seventeen in known wild-bred, two in known park-bred specimens, and two with breeding uncertain. The average known duration of captivity of the wild-bred animals is about four years, while the two park-bred animals lived eight and eighteen years. Thirteen of the twenty-one cases were males, eight females. Adenocarcinoma was discovered twelve times, simplex nine times, medullary and squamous each twice. Three tumors of the pancreas and mammary gland were seen in which fibrotic or scirrhus areas were found, but in no case was there detected that hard cicatrizing cancer so commonly found in the human breast. All the interesting cases of carcinoma have been recorded in the discussion of organs from which they took origin. The only case of chorionepithelioma has been reported in detail on page 308. The two cases of mixed tumors are as follows: Mixed tumor of the thyroid and adenocarcinoma sarcomatodes in the liver; they have been discussed in detail on pages 334 and 242 respectively.

Analysis of the incidence of tumors according to organs is disturbed by the large number of cases in Psittaci. Including this order the first place is taken by the kidney, followed by the liver, uterus, muscle, gastrointestinal tract, bone and cartilage, thyroid, adrenal and lung in this order. Curiously enough, if these birds be subtracted the degree of organ susceptibility to new growths is not greatly altered. The lead is still held by the kidney, the uterus occupying the second place and then in sequence the liver, gastrointestinal tract, muscle, thyroid and adrenal. Examination of the figures for mammals shows the uterus to lead in numbers, followed by the liver, thyroid, and mammary gland. For the birds the kidney takes the undisputed head of the column with a total of twelve tumors (27 per cent. of all avian tumors); the next figures are shown by the liver, gastrointestinal tract and muscle.

ZOOLOGICAL AND PATHOLOGICAL LIST OF TUMORS

MAMMALIA PRIMATES (2) Cercopithecidæ—Hamadryas Baboon (Papio hamadryas) Papillary adenoma of gastric mucosa Cebidæ—Brown Cebus (Cebus fatuellus) Hypernephroma of right adrenal

LEMURES (1) Lemuridæ—Ring tailed Lemur (Lemur catta) Papillary adenoma of prostate

CARNIVORA (17) Felidæ—Clouded Leopard (Felis nebulosa) Endothelioma of pleura Caracal (Felis caracal) Osteochondroma of nose Lion (Felis leo) Malignant adenoma of cervix uteri Metastases to lung Jaguar (Felis onca) Fibroadenoma of uterus Fibroadenoma of bile ducts Lymphangioma of mesentery Viverridæ—Indian Paradoxure (Paradoxurus niger) Adenocarcinoma of pancreas Malayan Civet (Viverra tangalunga) Carcinoma of lung Canidæ—Corsac Fox (Canis corsac) Adenoma of pancreatic ducts Red Fox (Canis vulpes pennsylvanicus) Cystic adenoma of bile ducts Raccoon-like Dog (Canis procyonoides) Adenocarcinoma sarcomatodes of thyroid Gray Fox (Canis cinereo argenteus) Papillary cyst adenoma of bile ducts Prairie Wolf (Canis latrans) Sarcoma of thyroid region Metastases to lungs Prairie Wolf (Canis latrans) Sarcoma of thyroid region Procyonidæ—Common Raccoon (Procyon lotor) Adenoma of pancreas Ursidæ—Polar Bear (Ursus maritimus) Adenocarcinoma of adrenals Metastases to lungs, lymph nodes, diaphragm Black Bear (Ursus americanus) Medullary carcinoma of breast Metastases to lungs Black Bear (Ursus americanus) Epithelioma of tongue Phocidæ—California Hair Seal (Zalophus californianus) Hypernephroma of adrenal

RODENTIA (12) Sciuridæ—Beechy’s Spermophile (Citellus grammurus beecheyi) Osteoma of sternum Gray Squirrel (Sciurus carolinensis pennsylvanicus) Hypernephroma of kidney Woodchuck (Arctomys monax) Adenoma simplex of liver Muridæ—Waltzing Mouse (Mus wagneri rotans) Adenocarcinoma of thigh muscles White footed Mouse (Peromyscus leucopus) Carcinoma simplex of mammary gland White footed Mouse (Peromyscus leucopus) Spindle celled sarcoma of leg White footed Mouse (Peromyscus leucopus) Carcinoma of mammary gland Larger Egyptian Gerbille (Gerbillus pyramidum) Fibrosarcoma of shoulder region Heteromyidæ—Kangaroo Rat (Perodipus richardsoni) Sarcoma of urinary bladder Octodontidæ—Coypu Rat (Myocastor coypus) Sarcoma of thyroid Hystricidæ—Canada Porcupine (Erethizon dorsatus) Chorionepithelioma uteri Dasyproctidæ—Azara’s Agouti (Dasyprocta azara) Squamous carcinoma of larynx

PROBOSCIDEA (1) Indian Elephant (Elephas indicus) Leiomyoma, uterine cornua and fimbria

UNGULATA (7) Equidæ—Chapman’s Zebra (Equus burchelli chapmani) Fibroma peritonei with sarcomatous and osseous change and metastases to lung Bovidæ—Isabelline Gazelle (Gazella isabella) Osteofibroma of jaw with mucoid degeneration Nylghaie (Boselaphus tragocamelus) Fibroma uteri Dorcas Goat (Capra hircus) Lymphosarcoma of mediastinum with metastases to liver, kidney and lymph nodes Cervidæ—Common Deer (Mazama virginiana) Fibroadenoma of bile ducts Camelidæ—Alpaca (Lama pacos) Carcinoma of liver or bile ducts with extension to intestine Suidæ—Wild Boar (Sus scrofa) Carcinoma uteri

EDENTATA (1) Dasypodidæ—Nine banded Armadillo (Tatu novemcinctus) Fibroma uteri

MARSUPIALIA (7) Didelphyidæ—Common Opossum (Didelphys virginiana) Adenoma of kidney Common Opossum (Didelphys virginiana) Adenocarcinoma of mammary gland Dasyuridæ—Spotted tailed Dasyure (Dasyurus maculatus) Adenocarcinoma of intestines with metastases to lymphatics, liver, spleen, lungs Tasmanian Devil (Sarcophilus ursinus) Cystic epithelioma of skin of thigh Peramelidæ—Rabbit eared Bandicoot (Thylacomys lagotis) Carcinoma of lung Macropodidæ—Red Kangaroo (Macropus rufus) Malignant papilloma of stomach Metastases to liver, spleen, kidney Red Kangaroo (Macropus rufus) Carcinoma of lung Metastases to spleen and gastric wall

AVES

PASSERES (7) Turdidæ—American Robin (Planesticus migratorius) Hypernephroma of kidney, metastases to intestine Crateropodidæ—Jungle Babbler (Crateropus canorus) Adenoma of kidney Tanagridæ—Palm Tanager (Tanagra palmarum) Lipoma of abdominal wall Fringillidæ—Saffron Finch (Sycalis flaveola) Adenocarcinoma of kidney Chestnut-eared Finch (Amadina castanotis) Adenocarcinoma of kidney with metastases to lung Chestnut headed Bunting (Emberiza luteola) Lipoma of scalp Icteridæ—European Blackbird (Merula merula) Hypernephroma of kidney region with metastases to liver

STRIGES (1) Bubonidæ—Great Horned Owl (Bubo virginianus) Papilloma of duodenum

PSITTACI (26) Loriidæ—Musky Lorrikeet (Glossopsittacus concinnus) Carcinoma of lung

Cacatuidæ—Roseate Cockatoo (Cacatua roseicapilla) Lipoma of abdominal wall Roseate Cockatoo (Cacatus roseicapilla) Multiple lipomata of abdominal wall Psittacidæ—Undulated Grass Parrakeet (Melopsittacus undulatus) Glioma of brain with metastases to liver Undulated Grass Parrakeet (Melopsittacus undulatus) Hypernephroma of adrenal Undulated Grass Parrakeet (Melopsittacus undulatus) Papillary adenoma of kidney Undulated Grass Parrakeet (Melopsittacus undulatus) Cystic papillary adenocarcinoma of kidney Undulated Grass Parrakeet (Melopsittacus undulatus) Adenocarcinoma sarcomatodes of liver Undulated Grass Parrakeet (Melopsittacus undulatus) Papillary cyst adenoma of kidney Undulated Grass Parrakeet (Melopsittacus undulatus) Adenoma of kidney Undulated Grass Parrakeet (Melopsittacus undulatus) Adenoma of kidney Undulated Grass Parrakeet (Melopsittacus undulatus) Adenocarcinoma of oviduct Undulated Grass Parrakeet (Melopsittacus undulatus) Carcinoma simplex of liver with metastases to liver, spleen Undulated Grass Parrakeet (Melopsittacus undulatus) Carcinoma simplex of liver Undulated Grass Parrakeet (Melopsittacus undulatus) Multiple lipomata Undulated Grass Parrakeet (Melopsittacus undulatus) Multiple lipomata Undulated Grass Parrakeet (Melopsittacus undulatus) Sarcoma of pectoral muscle with metastases to liver Undulated Grass Parrakeet (Melopsittacus undulatus) Round cell sarcoma in region of liver, spleen, kidney Undulated Grass Parrakeet (Melopsittacus undulatus) Carcinoma simplex of thyroid Blue fronted Amazon (Chrysotis æstiva) Adenocarcinoma (?) of proventricle White fronted Amazon (Chrysotis leucocephala) Epithelioma in peritoneum (?) All Green Parrakeet (Brotogerys tirica) Sarcoma of pectoral muscle Red shouldered Parrakeet (Palæornis eupatrius) Sarcoma of testes Red shouldered Parrakeet (Palæornis eupatrius) Sarcoma of testes

King Parrakeet (Apromictus cyanopygius) Sarcoma of ovary Crested Ground Parrakeet (Calopsitta novæ-hollandiæ) Lipoma of muscle of abdomen and chest walls

ACCIPITRES (2) Falconidæ—Red shouldered Buzzard (Buteo lineatus) Retroperitoneal sarcoma Sparrow Hawk (Sparverius sparverius) Lipoma around cloaca

COLUMBÆ (1) Columbidæ—Scaly Ground Dove (Scardapella squamosa) Sarcoma (spindle) of kidney with metastases to tibia

GALLI (1) Phasianidæ—Wild Turkey (Meleagris gallopavo) Papillary adenocarcinoma of ovary

FULICARIÆ (1) Rallidæ—Moorhen (Gallinula chloropus) Endothelioma of clavicle

ANSERES (4) Anatidæ—Red headed Duck (Fuligula ferina americana) Papillary adenoma of kidney Black Duck (Anas obscura) Hypernephroma of adrenal Lesser Snow Goose (Chen h. hyperboreus) Fibroma on clavicle Bean Goose (Anser fabalis) Myxosarcoma of pectoral muscle

STRUTHIONES (1) Rheidæ—Common Rhea (Rhea americana) Cystic papillary adenoma of duodenum

SECTION XVII THE COMMUNICABLE DISEASES—PART I

TUBERCULOSIS.

Nearly all infectious diseases have either a limited natural zoological distribution or are encountered chiefly in one order or division. Thus typhoid fever is peculiar to man, hog cholera to swine, foot-and-mouth disease to cows. A second group, including for example anthrax, variola, hemorrhagic septicemia and malignant edema, is somewhat less specific, and may occur in several varieties. There is no more widespread, important infection, zoologically, economically and hygienically, than tuberculosis, and it would seem that all kinds of vertebrates are subject to it. Its manifestations too, are sufficiently similar to support the idea that there must have been originally a common ancestor of the viruses which we now designate separately by a term to indicate their immediate source (human, avian, etc.), and moreover it has been shown that any of the artificially separated varieties or subspecies may under certain circumstances infect all zoological families.

There is, however, a varying resistance to the tubercle bacillus, certain zoological groups standing out preëminently as more or less susceptible to it. There is also a tendency for each animal group to present features more or less peculiar to itself, but nevertheless the characteristics, both gross and minute, of the disease caused by the Bacillus tuberculosis are sufficiently similar to permit close analogy and to establish a diagnosis when the bacteria are found.

The data collected at this Garden are well suited to elucidate the susceptibility of wild animals under captive conditions and to illustrate the nature of lesions in them. Perhaps they do not offer a perfect cross section of zoological distribution of tuberculosis because of the predominance in the display of birds, of monkeys and of ungulates, but the figures will be found significant in certain respects. Such records cannot be compared with those obtained for domesticated animals in farms or breeding places, nor can our material be used to show the incidence for individual species, such as cows, dogs and the like, in a manner commonly used in veterinary literature. Those who are interested in this phase of the problem can find in Lubarsch- Ostertag’s Ergebnisse, 1917–18, No. 2, a summary by Eber of all recent literature, covering nearly 1,700 references, which really amounts to a review of all modern knowledge of tuberculosis in the lower animals. The article does not, however, attempt to compare or contrast the incidence per order or family in wild varieties since little information is available on these points. There are no reliable data concerning the existence of tuberculosis in the wild. It is noted in the report of the British Tuberculosis Commission that monkeys were received with this disease; Eber mentions that wild swine from a private preserve presented undoubted evidence of tuberculosis and another similar experience with pheasants, but these and other citations can give no proper estimate of exact conditions nor allow a decision that the infection exists at all under natural environment for in all cases the association with human beings or domesticated animals cannot be excluded. Tuberculosis is usually described as a disease of civilization and its incidence surely varies directly with crowding.

THE TABLE.

Description of Table 23. The study of our autopsy records was begun by the preparation of the accompanying table, which is based first upon the zoological classification per order with subdivisions for families where there are sufficient examples within important orders, and second, upon percentage of total cases. For the analysis of the pathological types, headings of probable origin, gross anatomical lesions and visceral distribution were then made. The first vertical column shows the total autopsies per order, and where families are given, for each of them. In three instances Primates, Ungulata and Galli, not all families are represented, so that the total for the order is greater than that for the subdivisions quoted. It is noteworthy that we have had no tuberculosis among nine families of ungulates; this will be discussed later. The second column gives the total cases of tuberculosis for the order and family, respectively, followed by a third line of percentages. For the analysis of the pathology in these animals all the protocols were reviewed. Forty-eight of them being found unsuitable, deductions were made according to the natural group, thereby leaving the number shown in the fifth column for separation according to origin and type. Analyses in the succeeding columns are made upon number of cases and not upon percentages, because of the confusion arising from small decimals. The actual relationships will be pointed out in the notes. Percentage is not so necessary because comparisons and contrasts are usually made with classes or orders where the figures are comparable.

TABLE 23. _Analytical Table Showing Incidence of Tuberculosis per Order and for Some of the Principal Families, to Which are Added Columns Showing Probable Origin of Infection, Pathological Type of the Disease and the Visceral Distribution of the Morbid Process._

════════════════════╤═════════╤════════════╤══════════╤════════════ Order Family │ No. of │ Cases of │Percentage│ Cases not │autopsies│Tuberculosis│ │sufficiently │for order│ │ │ described │or family│ │ │for analysis ────────────────────┼─────────┼────────────┼──────────┼──────────── „ „ │ „ │ „ │ „ │ „ │ │ │ │ │ │ │ │ │ │ │ │ ────────────────────┼─────────┼────────────┼──────────┼──────────── Primates │ 498│ 192│ 38.5│ 8 Simiadæ │ 7│ 3│ 43.│ 0 Cercopithecidæ│ 353│ 171│ 48.4│ 8 Cebidæ │ 106│ 18│ 16.9│ 0 Lemures, Lemuridæ │ 86│ 23│ 26.7│ 3 Carnivora │ 481│ 17│ 3.5│ 4 Rodentia │ 199│ 5│ 2.5│ 0 Ungulata │ 365│ 35│ 9.6│ 2 Equidæ │ 11│ 1│ 9.│ 0 Bovidæ │ 123│ 12│ 9.7│ 1 Cervidæ │ 171│ 19│ 11.1│ 1 Camelidæ │ 25│ 3│ 12.│ 0 Proboscidea │ 3│ 2│ 66.│ 0 ────────────────────┼─────────┼────────────┼──────────┼──────────── Totals for Mammalia │ [97]1860│ [97]274│ [97]14.7│ 17 Passeres │ 1355│ 18│ 1.3│ 6 Picariæ │ 87│ 11│ 13.│ 0 Psittaci │ 698│ 38│ 5.4│ 3 Loriidæ │ 24│ 3│ 12.5│ 0 Cacatuidæ │ 80│ 7│ 8.7│ 1 Psittacidæ │ 585│ 28│ 4.8│ 2 Striges │ 133│ 6│ 4.5│ 3 Accipitres │ 196│ 11│ 5.6│ 1 Columbæ, Columbidæ │ 157│ 50│ 32.│ 5 Galli │ 299│ 42│ 14.│ 5 Phasianidæ │ 252│ 22│ 8.3│ 3 Cracidæ │ 38│ 17│ 44.│ 1 Megapodidæ │ 5│ 3│ 60.│ 1 Fulicariæ │ 35│ 9│ 27.│ 0 Hemipodii │ 2│ 1│ 50.│ 0 Alectorides │ 37│ 10│ 27.│ 2 Odontoglossæ │ 6│ 2│ 33.│ 1 Anseres │ 317│ 16│ 5.│ 5 Struthiones │ 32│ 3│ 9.4│ 0 Crypturi │ 5│ 2│ 40.│ 0 ────────────────────┼─────────┼────────────┼──────────┼──────────── Totals for Aves │ [97]3505│ [97]219│ [97]6.2│ 31 ────────────────────┼─────────┼────────────┼──────────┼──────────── Grand Totals │ [98]5365│ [98]493│ [98]9.1│ 48 ────────────────────┴─────────┴────────────┴──────────┴────────────

════════════════════╤════════╤══════════════════════╤═══════════════ Order Family │Net no. │ Probable origin │Pathological Type │of cases│ │ │ in │ │ │analysis│ │ ────────────────────┼────────┼──────────┬───────────┼───────┬─────── „ „ │ „ │Pulmonary-│Intestinal-│ Acute │Massive │ │aerogenic │ lymphatic │Miliary│caseous │ │ │ │ │ │ │ │ │ │ ────────────────────┼────────┼──────────┼───────────┼───────┼─────── Primates │ 184│ 86│ 98│ 3│ 52 Simiadæ │ 3│ 3│ │ │ 2 Cercopithecidæ│ 163│ 76│ 87│ 2│ 46 Cebidæ │ 18│ 7│ 11│ 1│ 3 Lemures, Lemuridæ │ 20│ 6│ 14│ │ 5 Carnivora │ 13│ 6│ 7│ │ 1 Rodentia │ 5│ 3│ 2│ │ 3 Ungulata │ 33│ 27│ 6│ │ 6 Equidæ │ 1│ │ 1│ │ 1 Bovidæ │ 11│ 10│ 1│ │ 1 Cervidæ │ 18│ 14│ 4│ │ 4 Camelidæ │ 3│ 3│ │ │ Proboscidea │ 2│ 2│ │ │ ────────────────────┼────────┼──────────┼───────────┼───────┼─────── Totals for Mammalia │ 257│ 130│ 127│ 3│ 67 Passeres │ 12│ 9│ 3│ │ 5 Picariæ │ 11│ 1│ 10│ │ 2 Psittaci │ 35│ 13│ 22│ 1│ 9 Loriidæ │ 3│ 1│ 2│ │ 1 Cacatuidæ │ 6│ 4│ 2│ │ 1 Psittacidæ │ 26│ 8│ 18│ 1│ 7 Striges │ 3│ 3│ │ │ 1 Accipitres │ 10│ 5│ 5│ │ 2 Columbæ, Columbidæ │ 45│ 10│ 35│ │ 12 Galli │ 37│ 10│ 27│ │ 12 Phasianidæ │ 19│ 2│ 17│ │ 4 Cracidæ │ 16│ 7│ 9│ │ 7 Megapodidæ │ 2│ 1│ 1│ │ 1 Fulicariæ │ 9│ 1│ 8│ │ 1 Hemipodii │ 1│ 1│ │ │ 1 Alectorides │ 8│ │ 8│ │ 2 Odontoglossæ │ 1│ │ 1│ │ Anseres │ 11│ 2│ 9│ │ 4 Struthiones │ 3│ 3│ │ │ Crypturi │ 2│ │ 2│ │ ────────────────────┼────────┼──────────┼───────────┼───────┼─────── Totals for Aves │ [99]188│ 58│ 130│ 1│ 51 ────────────────────┼────────┼──────────┼───────────┼───────┼─────── Grand Totals │ [99]445│ 188│ 257│ 4│ 118 ────────────────────┴────────┴──────────┴───────────┴───────┴───────

════════════════════╤════════════════════════╤════════════════════════ Order Family │ Pathological Type │ Visceral Distribution │ │ │ │ │ │ ────────────────────┼───────┬──────────┬─────┼─────┬─────┬──────┬───── „ „ │Nodular│ Chronic │Pearl│Lungs│Liver│Spleen│Lymph │caseous│ fibrous │type │ │ │ │nodes │ │ and │ │ │ │ │ │ │ulcerative│ │ │ │ │ ────────────────────┼───────┼──────────┼─────┼─────┼─────┼──────┼───── Primates │ 108│ 16│ 5│ 173│ 122│ 149│ 145 Simiadæ │ │ │ │ 3│ 2│ 3│ 3 Cercopithecidæ│ 96│ 16│ 3│ 156│ 111│ 136│ 128 Cebidæ │ 12│ │ 2│ 14│ 9│ 10│ 14 Lemures, Lemuridæ │ 15│ │ │ 17│ 14│ 17│ 12 Carnivora │ 8│ 4│ │ 11│ 4│ 2│ 6 Rodentia │ 2│ │ │ 4│ 2│ 2│ 4 Ungulata │ 1│ 24│ 2│ 28│ 7│ 3│ 25 Equidæ │ │ │ │ │ │ │ 1 Bovidæ │ 1│ 9│ │ 9│ 4│ 2│ 7 Cervidæ │ │ 13│ 1│ 17│ 2│ │ 14 Camelidæ │ │ 2│ 1│ 2│ 1│ 1│ 3 Proboscidea │ │ 2│ │ 2│ │ │ ────────────────────┼───────┼──────────┼─────┼─────┼─────┼──────┼───── Totals for Mammalia │ 134│ 46│ 7│ 235│ 149│ 173│ 192 Passeres │ 7│ │ │ 9│ 5│ 5│ Picariæ │ 8│ │ 1│ 2│ 9│ 6│ 1 Psittaci │ 25│ │ │ 18│ 24│ 14│ 2 Loriidæ │ 2│ │ │ 3│ 3│ 1│ Cacatuidæ │ 5│ │ │ 5│ 5│ 2│ Psittacidæ │ 18│ │ │ 10│ 16│ 11│ 2 Striges │ 2│ │ │ 3│ 3│ 2│ Accipitres │ 7│ 1│ │ 8│ 6│ 8│ 1 Columbæ, Columbidæ │ 33│ │ │ 24│ 40│ 34│ 1 Galli │ 24│ 1│ │ 20│ 34│ 29│ 2 Phasianidæ │ 15│ │ │ 7│ 18│ 15│ 1 Cracidæ │ 8│ 1│ │ 12│ 15│ 13│ Megapodidæ │ 1│ │ │ 1│ 1│ 1│ 1 Fulicariæ │ 8│ │ │ 4│ 8│ 8│ 1 Hemipodii │ │ │ │ 1│ 1│ 1│ Alectorides │ 6│ │ │ 4│ 8│ 7│ 2 Odontoglossæ │ 1│ │ │ │ 1│ 1│ Anseres │ 5│ 2│ │ 4│ 7│ 8│ 1 Struthiones │ │ 3│ │ 3│ 2│ 3│ 2 Crypturi │ 2│ │ │ 1│ 2│ 2│ ────────────────────┼───────┼──────────┼─────┼─────┼─────┼──────┼───── Totals for Aves │ 128│ 7│ 1│ 101│ 151│ 128│ 13 ────────────────────┼───────┼──────────┼─────┼─────┼─────┼──────┼───── Grand Totals │ 262│ 53│ 8│ 336│ 300│ 301│ 205 ────────────────────┴───────┴──────────┴─────┴─────┴─────┴──────┴─────

════════════════════╤══════════════════════════════════════════════════════ Order Family │ Visceral Distribution │ │ │ ────────────────────┼─────────┬──────┬─────────┬──────┬─────┬─────┬──────── „ „ │Intestine│Kidney│ Serous │Bones │Brain│Heart│Pancreas │ │ │membranes│ and │ │ │ │ │ │ │joints│ │ │ │ │ │ │ │ │ │ ────────────────────┼─────────┼──────┼─────────┼──────┼─────┼─────┼──────── Primates │ 30│ 84│ 70│ 2│ 2│ 7│ 3 Simiadæ │ 2│ 1│ 1│ │ │ │ Cercopithecidæ│ 24│ 76│ 63│ 2│ 2│ 7│ 2 Cebidæ │ 4│ 7│ 6│ │ │ │ 1 Lemures, Lemuridæ │ 2│ 7│ 1│ │ │ │ 1 Carnivora │ 1│ 4│ 3│ 1│ │ │ Rodentia │ 1│ 2│ 2│ 1│ │ │ Ungulata │ 1│ 2│ 7│ │ │ │ Equidæ │ │ │ │ │ │ │ Bovidæ │ 1│ 1│ 1│ │ │ │ Cervidæ │ │ │ 5│ │ │ │ Camelidæ │ │ 1│ 1│ │ │ │ Proboscidea │ │ │ │ │ │ │ ────────────────────┼─────────┼──────┼─────────┼──────┼─────┼─────┼──────── Totals for Mammalia │ 35│ 99│ 83│ 4│ 2│ 7│ 4 Passeres │ 4│ │ 4│ │ │ │ Picariæ │ 4│ 1│ 3│ 1│ │ │ Psittaci │ 12│ 6│ 6│ │ │ 1│ Loriidæ │ 1│ 1│ 1│ │ │ │ Cacatuidæ │ │ 1│ 1│ │ │ 1│ Psittacidæ │ 11│ 4│ 4│ │ │ │ Striges │ │ │ 3│ │ │ │ Accipitres │ 4│ 3│ 6│ │ │ 2│ Columbæ, Columbidæ │ 16│ 13│ 20│ │ │ 1│ Galli │ 20│ 7│ 15│ │ │ │ 1 Phasianidæ │ 10│ 2│ 6│ │ │ │ 1 Cracidæ │ 10│ 5│ 7│ │ │ │ Megapodidæ │ │ │ 2│ │ │ │ Fulicariæ │ 3│ 3│ 4│ │ │ │ Hemipodii │ 1│ 1│ 1│ │ │ │ Alectorides │ 3│ 3│ 7│ │ │ │ Odontoglossæ │ 1│ │ │ │ │ │ Anseres │ 3│ 4│ 4│ │ │ │ Struthiones │ │ 1│ 1│ │ │ │ Crypturi │ 2│ 1│ │ │ │ │ ────────────────────┼─────────┼──────┼─────────┼──────┼─────┼─────┼──────── Totals for Aves │ 73│ 43│ 74│ 1│ 0│ 4│ 1 ────────────────────┼─────────┼──────┼─────────┼──────┼─────┼─────┼──────── Grand Totals │ 108│ 142│ 157│ 5│ 2│ 11│ 4 ────────────────────┴─────────┴──────┴─────────┴──────┴─────┴─────┴──────── See page 484, for description of tabulation. For meaning of italics see foot note Table 1. These and figures set opposite them are cases not percentages.

It is generally conceded that the principal and only significant routes of origin for tuberculosis are via the respiratory and alimentary tracts. The criteria upon which to decide the route that has been followed are by no means definite and may not be for any given case unexceptionable. In birds the alimentary tract is conceded to be the important one, while in mammals an aerogenic route is believed to be the rule. However, since feeding experiments have shown that tubercle bacilli can gain the lungs by passing through the intestinal wall and abdominal lymphatics without leaving gross traces, the decision that one or the other route has been taken may be erroneous, and statistics therefore can often be fallacious. It is usually the rule to assume that the oldest or best developed lesions occur where the originally settled organisms exerted their maximum effect. The questions of infection-path and of original lesion not having been settled it is obvious that decision as to the route must be in the nature of an estimate. With these limitations in mind I have divided the cases into probable respiratory and alimentary origins according to the following criteria. Where the lesions were wholly respiratory or within the lymph glands of the trachea and bronchi the decision was not so difficult. Predominance of the pulmonary disease with recent lesions in other organs was taken to indicate an aerogenic origin. The chronic ulcerative or fibrous pulmonary lesions were also ascribed to those beginning in the lungs. The alimentary tract was considered for this purpose as beginning in the tonsillar area and ending at the anus. This is as I understand the customary teaching. When the lymph nodes of the alimentary area were advanced in the process, the intestinal method was held responsible. It is of course not to be forgotten that organisms coughed up from the lungs and swallowed may be responsible for lesions within the alimentary system. However, a predominance of intestinal, splenic, hepatic and lymphatic lesions caused me to place the case with those originating from the alimentary tract. Granting the limitations of our knowledge, of the criteria and of my own judgment, it is noteworthy that the results of this division of the table are not contradictory to the usual teaching, the most conspicuous being the predominance of the alimentary infection of Aves and in the order Primates, whereas the pulmonary route has the highest figures for the Ungulata.

The next subdivision of the table concerns the gross pathological type. Beginning with the most acute form, the acute miliary, progression is made in terms of chronicity—then following in order the massive caseous form including caseous pneumonia, the caseous miliary or nodular form so well represented by the monkey, then the fibroulcerative type such as one encounters in human consumption, including also forms in which fibrosis predominates, and lastly the rather uncommon pearl disease. This classification has been relatively easy to follow and can be readily imagined by the reader. There are of course intermediate cases or transition forms and there have been instances partaking of more than one character. The groupings present only gross appearances and, with few exceptions, are not to be taken as direct indications of type incidence in special groups.

Visceral distribution is shown in the last gross section of the table; single cases or unusual locations are not tabulated but will be separately discussed. The visceral distribution is made upon evident gross lesions or their discovery in organs whose condition suggested the need of microscopic study for confirmation. The figures in the table will be reviewed first upon the incidence as a whole and then between classes and orders. This will be succeeded by an analysis of the particulars for each order and then for each of the pathological headings.

TOTAL AND CLASS INCIDENCE.

The autopsies upon 5,365 animals have revealed the existence of tuberculosis in 492, a percentage of 9.1. This means that lesions due to the Bacillus tuberculosis were present, but they were not always the cause of death, since many specimens have been executed and others have had sufficient pathology to kill, aside from the tuberculous changes. Deaths due to the disease alone are difficult to estimate, but seem to be about 325 or 6 per cent. These figures, while they represent the total incidence, lose considerably in significance when the factors are analyzed. Mammalian incidence is 14.7 per cent., Avian 6.2 per cent., but the former is based upon figures obtained from six of twelve orders numbering 1,860 animals, whereas the latter represent the cases in fourteen of twenty orders numbering 3,505 birds. The percentages are considerably increased by high figures for a few orders, Primates, Lemures, Columbæ for examples. There are missing from the list very few orders of which we have any notable number of autopsies, Marsupialia and Herodiones being the only important ones; it would seem that these orders have a high resistance to the disease.

Investigation into the origin of the disease in mammals and birds shows with definiteness the preponderance of the alimentary route influence in the latter, but for the former the figures cannot be said to be conclusive. The bird excretes large numbers of bacilli with the feces thereby soiling the feed and the ground. This is due to the frequency of intestinal open lesions and to the really enormous numbers of bacilli which are in the morbid tissue. I think it can be said with safety that, other things being equal, the bird excretes bacilli constantly and in greater numbers than does the mammal, and that in physically comparable lesions there are more bacilli in the avian than in the mammalian.

The inconclusive figures for the origin of the disease in the mammal can be clarified very little by the subtraction from the tables of the figures for the very susceptible Primates. By doing this it would seem that the respiratory route dominates as 43 to 29, whereas if the reasonably susceptible Lemures be also deducted the ratio becomes as 38 to 15. It would seem that the evidence favors the aerogenic route in the mammal.

PATHOLOGICAL TYPES.

An inquiry into the gross pathological types reveals at once the frequency with which the nodular and massive caseous forms appear. If the number of cases be reduced to percentage it will be found that 59 per cent. of all specimens presented the nodular variety and 26.6 per cent. the massive caseous form. These large figures (equaling when combined 85 per cent.) coupled with the fact that only 12 per cent. of the total were fibroulcerative and 1.8 per cent. of the pearl type, would seem to indicate that the nodular and massive caseous processes are the lesions to be expected in wild animals. Furthermore, if these nodular and caseous forms speak for recent infection or acuteness of the morbid process, it would seem that wild animals have a low tissue resistance to tuberculosis. It is a widespread belief, in some degree well supported, that a disease new to an animal species is highly fatal and that the survival of the race depends upon an active self- immunization or the survival of the pathologically least susceptible. If tuberculosis be a disease of civilization, these figures would suggest that it is absent in nature. As a further support of this idea it can be said that with the exception of two cases in ungulates, no fibroid tuberculosis, approaching the quiescent type as seen in man and rarely in domestic animals, was encountered. Very rarely calcareous deposits will be found in both simian and ungulate lesions but these need not indicate a tendency to general healing although at that place the process may be inactive. The bird uses considerable fibrous tissue in the construction of its tuberculous mass but fibrosis never masters the situation with the formation of scar tissue sufficient to wall off the process. Pearl disease, a fibrocaseous condition, is not a healing fibroid procedure and is, in our material, of no numerical significance.

VISCERAL DISTRIBUTION.

The distribution of the morbid lesions in the viscera presents some interesting features. In the first place the data leave no doubt that the most susceptible tissue in the wild animal body is, as in the case of human and domestic animals, the lung. The susceptibility of this organ in the two classes is however a different matter since in the mammal 91.4 per cent. show pulmonary lesions while only 53.7 per cent. of birds are so affected. Part of the reason for this appears in the figures for the principal abdominal organs, of which the liver and spleen occupy the prominent places. The mammalian livers show 58.2 per cent., the avian 80.3 per cent.; 67.5 per cent. of mammalian spleens, 68.0 per cent. of avian spleens have tuberculous lesions. The figure for the mammalian spleen is distorted because of the peculiar susceptibility of this organ in the monkey, it being conspicuously free of lesions in most mammalian orders. The intestines presented discernible lesions in practically 40 per cent. of birds but only in 13.5 per cent. of mammals. Renal involvement was found in 38.4 per cent. of mammals and 22.9 per cent. of birds.

A study of the changes in the serous surfaces is complicated by the difference of anatomy in the two classes. The mammal has separate closed serous sacs well guarded against invasion from mucous surfaces whereas in the bird the air sacs and serous cavities are closely related, the latter being loosely applied to viscera they are intended to cover. Moreover in Aves direct infection of the air sacs seems a definite possibility. Notwithstanding the fact that the bird’s sacs and serous surfaces appear so open to infection there is no great preponderance of lesions within them—Aves 39.3 per cent. Mammalia 32 per cent. The lymph nodes were tabulated as a tissue rather than according to location, the latter method being found profitable for discussion in a few orders only. As might be expected the abundant lymph nodes of the mammal were affected out of all proportion to those in the bird. These matters will be discussed later. The remaining figures on the table have no comparative value.

ORDINATE CHARACTERISTICS.

The Primates as an order have shown low resistance to tuberculosis, a fact well known to general observation. How much this is due to the unsanitary surroundings to which these naturally free active beasts are subjected, in catching, transporting and storing for sale, must at present remain conjectural, but they are probably infected with ease as our experience in this laboratory suggests. Desiring a tuberculous monkey for certain tuberculin tests, I injected one hundredth of a milligram of a human culture, known to produce definite lesions in rabbits; the animal died in three months with advanced general tuberculosis. The unexpected and interesting feature of our figures is the susceptibility of different families within the order. The Old World monkeys, Simiadæ and Cercopithecidæ have a combined incidence two and one-half times as great as the New World Cebidæ, and the marmosets had no tuberculosis at all in the thirty-two specimens. Possibly this is a matter of transportation and handling, which reduces the resistance and offers chance to infect apes and baboons. The New World capucin monkeys have their exposure too since many of them are household pets before the Garden receives them. Their usual life in captivity is however shorter than that of Old World varieties, they therefore being exposed to infection for a shorter time. It would seem however that American Primates are more resistant to the disease than African and Australasian.

The form of tuberculosis to which this order is liable is well described in text-books, it being so characteristic that the term “monkey tuberculosis” is used to distinguish it. The purpose of the term is to compare the lesions with certain cases of generalized tuberculosis in children. It is characterized by a nodular involvement of the liver and of the spleen particularly, sometimes also of the lungs but in fatal cases the last organ is commonly the seat of massive caseation or caseous pneumonia. The prominence of the pulmonary lesions often makes a decision of origin difficult since important changes may be found in the liver and abdominal nodes. Blair at New York, and Rabinowitsch at Berlin are of the impression that many cases of monkey tuberculosis start by pharyngeal and tonsillar infection because they found cervical adenitis so commonly. Our records and specimens would support this idea in only fourteen instances and I am of the impression that the lower intestinal route is more often responsible, even to a higher figure than is recorded in the table. This view is based upon the frequent occurrence of enlarged glands in the mesentery, retroperitoneum and posterior mediastinum, in the latter location being quite as prominent if not more so than in the bronchial and tracheal area. Occasionally deposits of calcareous matter will be found in old caseous glands but in such animals there has always been some other spot of activity of tuberculosis. The frequency with which the liver and spleen are affected gives opportunity for hematogenic spread, a method of no small importance in the opinion of Eber. The chronic ulcerative form is quite well displayed in monkeys, interestingly enough to cite an illustrative case at the end of this division of the discussion. Five cases of distinct chronic cavitation were encountered; several small recent cavities were found in the massive caseous pneumonic cases. The two acute miliary cases and one of the pearl type will be discussed briefly on a later page.

Despite the prominence of the liver, spleen and lymph nodes, the lungs stand ahead of all others by a safe margin of visceral incidence. The spleen stands in the third place in this order and in the next, Lemures, but in no other mammalian group does this organ occupy so prominent a position. The susceptibility of lymphatic tissue in the monkey is further illustrated by the large number of cases showing lesions in lymph nodes. It is rather striking however that our material showed very few active ulcerations in the lymphoid plaques of the intestinal wall nor indeed do the intestines present a large numerical involvement. Serous membrane tuberculosis is chiefly that of the pleura, upon which early precaseous tubercles are frequently found, usually in conjunction with pulmonary disease. Tuberculous peritonitis of the plastic and nodular variety occurred only six times, though light adhesions to nodules in the liver and spleen were quite common. Pericarditis was found five times, in three of which there was myocardial disease; which of the two was primary was not indicated in the notes but from present reading it would seem that the heart muscle was involved first.

The next order, Lemures, has a susceptibility of about half that of the monkeys judging by the percentage incidence. Analytically the members of this group react quite like the preceding order in having the same types of origin, pathology and organic distribution. Since they are so close zoologically, present similar lesions and are tested in the same manner as the monkeys, we group them together and shall proceed to discuss special cases of interest in both orders.

Special Cases in Primates and Lemures. Acute general miliary tuberculosis occurred thrice in Old World and once in New World monkeys. The first case took its origin in a caseous gland in the bronchotracheal area, the lung showing a minor degree of involvement with milia but no older process. The second took its origin in the mesenteric area and the organs of this section of the body were most affected. The only case in the Cebidæ seemed to be of intestinal origin since an acute plastic peritonitis with fluid exudate accompanied the generally miliary disease.

Pearl disease of the bovine type has been encountered on four occasions but it cannot be said to have developed to the state of perfection seen in the cow. There is lacking the masses of nodules growing together in a fungoid character usually seen on the pleura and peritoneum. The monkey form is in isolated nodules of gray-yellow color which may show caseous centres. The visceral lesions are in firm separate areas not tending to soften or coalesce. Two of these monkeys died from recent pulmonary exacerbations. From one of the cases a bovine bacillus, judging from culture and rabbit virulence, was isolated.

As a good example of monkey tuberculosis, illustrating at the same time a chronic ulcerative pneumonitis with cavitation, the following case is cited:

Green Monkey (Cercopithecus callitrichus) ♀ . Was coughing and drooping for two days before death. Chronic ulcerative tuberculosis of lungs with cavity formation; early conglomerate tuberculosis of liver; conglomerate caseous tuberculosis of spleen; early conglomerate tuberculosis of ileum (Peyer’s patches); acute catarrhal enteritis; miliary tuberculosis of right kidney. The animal is well preserved, sleek, with a moderate amount of fat. The left pleura is largely obliterated by adhesions in the lower portion. As lung is freed it is torn, showing a cavity measuring 3 × 3 × 4 cm., which is filled with a curdy gray material. Cavity has well defined walls. Rest of lower lobe in which this cavity lies is solidified, red and edematous and contains numerous conglomerate tubercles. Upper lobe practically free of tubercles; shows compensatory emphysema. The right lung closely resembles the left but lacks the cavity. The liver is enlarged, soft and friable, of red color, spotted yellow. Serous and section surfaces show closely packed early conglomerate tubercles. The spleen is of normal size, soft, has red pulp with large conglomerate tubercles which project slightly on the capsule. The kidneys are apparently normal except for the presence of two or three subcapsular large, solitary tubercles in the right organ. The duodenum has thickened walls, mucosa bright, brilliant scarlet hue. In the ileum the walls are thickened, mucosa bright red, agminated follicles hyperplastic elevated and display several (4–12) miliary tubercles. These may be seen shining through on the serous surface but there is no peritoneal tuberculosis. No ulceration of Peyer’s patches. Contents of large intestine is rather dry and here the mucosa shows exaggerated rugæ which cannot be smoothed out. Walls are thickened, and ulceration, while suggested, cannot surely be determined.

An interesting case of primary tuberculosis in the larynx detected at postmortem after a tuberculin injection is as follows:

Black and White Lemur (Lemur varius) ♂ . Miliary tuberculosis of larynx; perilaryngitis and retropharyngeal lymphadenitis. Killed because of unsatisfactory chart after injection of tuberculin. The only tuberculous lesion to be found in the body, which is in excellent shape, is in and about the larynx. The lesions within are on the epiglottis, false and true vocal cords and the main ventricle. On either side of the root of the epiglottis, there are a few recent tubercles. The lesion in the retropharyngeal lymphatics is recent and diffuse. This is probably primary as it is not known that the retropharyngeal glands drain to or from the larynx. About the lesions on the laryngeal mucosa there is an area of congestion probably due to the tuberculin injection.

Local lymphatic tuberculosis of comparative interest was encountered a few times. Three cases of cervical adenitis, large enough to be visible, were seen, of which one broke down about two weeks before death, and discharged. The others did not ulcerate through the skin but, contrary to the usual rule for the human being, remained as isolated glands only lightly adherent to one another where they lay adjacent. There was also seen an ulcerating tuberculous lymph node in the groin of one monkey, the animal having rather pronounced abdominal and pelvic tuberculosis. Two instances of tonsillar tuberculosis are recorded, in both of which the lesion was of some duration and associated with caseation in the lymph node lying immediately behind and below it. A Guinea Baboon (Papio sphinx) had as an unusual part of his general tuberculosis, an active caseopurulent collection in the antrum of Highmore, which attacked the upper maxilla and immediately adjacent muscle; tubercle bacilli could be demonstrated.

One of the cases of nodular or massive peritoneal tuberculosis is quite like the tumor-forming variety of human adolescents; it is as follows:

Reddish Macaque (Macacus rufescens). Caseous tuberculosis of mesentery and spleen; miliary tuberculosis of lungs, pleura and liver; chronic myocarditis. The lymphatic glands of the posterior and superior mediastinum and bronchi are slightly enlarged, soft and anthracotic but do not show any tuberculous change. Both lungs are riddled with small, firm, gray miliary tubercles, some surrounded by a clear mantle of connective tissue. The intervening lung is practically normal. Pleura over base of right lung on both surfaces shows small, pale miliary tubercles. The liver contains various sized miliary tubercles. There is a large caseous mass in posterior end of spleen with adhesions to kidney, stomach and colon. Retroperitoneal glands are much enlarged, firm, homogeneous—probably tuberculosis of a different type. Lesser omentum contains one caseous gland. Few caseous glands in great omentum. In the right iliac region there is a large mass involving many coils of intestine. It is found to arise probably from the ileocecal glands and can be traced along the mesentery to the central lymphatic stalk. The mass involved the tissues of the mesentery and surrounds many coils of intestine. Cecum and first part of colon can be traced over its right side. Rectum is free except on right side where it is lightly attached to the mass. Epicardium is gray and irregularly thickened and the muscle just beneath serous membrane is pale and streaked with red lines.

There have been three cases of tuberculosis of the internal male genital area, one of which was suspected of having been the primary seat of the disease; it was described on page 315. The other two could have been secondary since other points of morbid change were as old or older. One of these cases formed a tumor as large as a goose egg at the vesical neck, obstructing the flow of urine and blocking up the seminal vesical, in consequence of which paralytic distention occurred in the bladder while the vesicles were tightly filled with inspissated semen. A case of Fallopian salpingitis has also been cited. Two instances of cerebral tuberculomata have already been described.

Carnivora. This order has the reputation of being quite resistant to the tubercle bacillus, based upon the relative infrequency among cats and dogs in contrast to cows and swine. Some veterinary statistics cite the incidence up to 5 per cent., and occasional references may be found to tuberculosis in circus lions and tigers. Our records would suggest that in gardens the wild varieties of this order have about as much of the infection as the domestic carnivores, 3.5 per cent. The group is made of six Felidæ, one Viverridæ, three Canidæ, six Procyonidæ, and one Ursidæ. The first family includes a lion, tiger, a jaguar and three smaller cats. The Canidæ are all small foxes. The Procyonidæ are all coatis. The features of this order are the occurrence of the fibroulcerative variety with cavitation in the Felidæ and the caseous nodular abdominal and glandular disease in the coatis. All these animals, even those of the last named variety and pathological type, tend to show some tissue resistance to the tuberculous disease. Connective tissue activity is characteristic of the process, considerable distortion being produced by the fibrosis. This feature is borne out where the tissues are studied microscopically. Definite milia are sometimes found, but they consist of epithelioid and round cells with imperfect caseation, giant cells being often missing. About the miliary tubercles a diffuse and not essentially specific tuberculous granulation tissue is found, mixed with which is much connective tissue growth. The fibrotic adhesion-forming serous membrane tuberculosis of carnivores seems worthy of emphasis by the citing of a case in point. White nosed coati (Nasua narica), was received in poor condition and died in a few days. Upon dissection a slightly turbid yellowish fluid was found to occupy what remained of the peritoneal cavity which was reduced in size by dense adhesions of the intestines into an inflammatory mass. The omentum was a diffuse thickened apron, also beset with fine tubercles, lying over the mass. Fine young tubercles could also be found upon the intestines and liver while the mesenteric lymph nodes were early in caseation; thoracic organs not infected.

One of the most interesting cases concerned hypertrophic osteitis in a chronically tuberculous lion; the feet are discussed on page 346. This process was described by Marie for human beings many years ago, and was reported in dogs by Cadiot[100] in 1912. This beast was one of five large cats which have died from tuberculosis in its chronic ulcerative form. Three of the cats, one fox and the bear showed definite cavitations of a ragged loculated form. The cavities were usually of the multiple variety and were found in the posterior, that is lower lobe.

Rodentia. The paucity of cases in this order permits little information to be drawn from the form of tuberculosis. The total seems to have been swollen by a group of three beavers, all of which came in one shipment. The remainder were a Capybara and an Agouti. The general type is that of much caseation with little or no surrounding fibrosis. One illustrative case is cited:

American Beaver (Castor canadensis). General tuberculosis. The animal presents generalized tuberculosis. The regional lymph nodes show caseous nodules. The right hip joint shows caseous material about the acetabulum with necrosis and pathological fractures in the os innominatum immediately above the acetabulum and including its cavity. Lungs show almost no normal respiratory tissue, the process being a diffuse precaseous, partly gelatinous pneumonic phthisis. The superior and posterior mediastina show caseous glands. There is miliary tuberculosis of the liver. Nodular caseous tuberculosis of the spleen with small tubercles and some cirrhosis of the intervening tissue. There are caseous nodules in all perirenal glands and in the kidney cortices. The psoas muscle glands are densely caseous. The pelvic organs except about the right acetabulum escape involvement. Adrenals not opened but probably not involved.

Ungulata. This order shows the most definite figures among those for the order of mammals. Nearly one-tenth of the whole number of specimens have had some form of tuberculosis and of a very definite character. It is well at first to mention, however, that only four of thirteen families are represented, from which four came 328 of the total 365 autopsies. The remaining thirty-seven were such animals as tapirs, giraffes, swine, and peccaries, in all of which tuberculosis has been reported from elsewhere.

Pulmonary disease with less prominent lesions in other organs, especially the intestines and their related glands, speaks in favor of the aerogenic route being the common one. This of course has been a bone of contention among veterinarians, and I do not presume to settle the matter with these figures.

This order resists tuberculosis to a certain degree as attested by the fibroulcerative character of the majority of the cases. Two instances, one in a buffalo and one in a deer, showed very highly fibrotic pulmonary lesions with a partial attempt to surround and wall off numerous areas of caseation. So too in this order there is a greater tendency to calcification, both in the intra- and extrapulmonary nodes. It is to be emphasized that in our material the thoracic lymph nodes are affected more than the abdominal and regional as 3 to 1. The apparent immunity of the spleen of this order is well illustrated.

The paucity of serous surface involvements in the wild Bovidæ and their prominence in the Cervidæ cannot be ignored in the figures, but it seems misleading since pleural growths and adhesions are quite common in the domestic Bovidæ. The case in the Equidæ was that of a Zebra with a large tuberculous abscess in the retroperitoneal glands forming a tumor in the left renal region. It was quite well surrounded by fibrosis, and the infection had not extended; it seemed quite recent. Analysis of the figures for the remaining three families of ungulates offers little for contrast and much for comparison; it is the usual picture as seen in the domestic cow. Some special cases are worthy of review.

An interesting specimen of softened glands chiefly on one side of the neck was found in a Fallow deer (Cervus dama). It resembled the juvenile human cases that require surgical attention. Although palpable lymph nodes can be found in practically all cases of generalized tuberculosis in the Ungulata, this is the only case in our records in which they have presented a large tumefaction and broken down. Pulmonary cavitation is recorded but thrice, one for each of the last three families. Fibrocaseous tuberculosis of the testes was discovered in a Nylghaie (Boselaphus tragocamelus), but there is no knowledge of mating or offspring. An ischiorectal abscess was found in an American Bison (Bison bison) showing nodular precaseous tubercles of the lung. The former was the cause of death. No tubercle bacilli could be found in the abscess contents, so that the tuberculous basis is inferred, not proven. Tuberculous salpingitis in a Nylghaie was discussed on page 306.

Proboscidea. Eber mentions in the article already referred to that there are three reports in the literature of tuberculosis in elephants. When looking for an explanation of tuberculosis in this animal it must be remembered that it is one of the most attractive objects in a zoological garden and receives perhaps more attention, including feeding, from visitors than any other specimen. The beast while possessing some tissue resistance to tuberculosis, is by no means immune thereto, as has been thought by some persons on account of its reputed longevity, and therefore he is to be protected from infection just as much as other animals. It would appear that he may present caseous pneumonia or nodular caseous disseminated lesions. Our two cases, in animals at the Garden twenty and thirty-eight years respectively, were both of the fibrocaseous variety; the lesion was confined to the lungs. A brief description of their lesions is as follows:

Indian Elephant (Elephas indicus) ♂ . Chronic polyarthritis. Chronic myocarditis. Chronic hepatitis (cirrhosis). Parenchymatous nephritis. Chronic tuberculosis of the lungs, partly encapsulated. Pigmentation of the spleen. The pleuræ are very fat but the surfaces are smooth and devoid of adhesions. The lymph nodes of the mediastinum are about 10 × 20 cm. for the largest while the smaller ones vary around 2 × 4 cm. They are firm, deep red-brown without clear divisions into medulla and follicular cortex. There are several large, firm, pale rather cheesy follicles in all the large ones and a few of the small. These do not appear like tuberculosis. The lungs are flaccid and soft; gray and red mottled. The bronchi are firm and stand open. Around one in the upper lobe of the right lung, there is a large area of cheesy degeneration around which a zone of connective tissue has formed. This extends about the bronchus about halfway in a sheath-like manner. There is also a separate nodule the size of a cherry with a cheesy centre. The trachea appears normal. Tubercle bacilli could be demonstrated in the cheesy material. Microscopic section of lung around the cheesy area shows a low grade chronic granulation tissue in some places enclosing cheesy masses with giant cells on the margin. The neighboring septa are slightly thickened and in some places broken, forming emphysematous cavities. Some of these cavities are edematous.

Indian Elephant (Elephas indicus) ♀ . Miliary and conglomerate caseous tuberculosis of lung. Edema of lungs. Endarteritis deformans of lung. Cloudy swelling of liver. Chronic passive congestion of liver. Hemosiderin pigmentation of liver. Acute parenchymatous nephritis. Chronic passive congestion of spleen. Chronic hyaline perisplenitis. Multiple calcified fibroid tumors of uterus. Leiomyoma of uterine cornu. Senile atrophy of ovaries. Acute catarrhal enteritis. There are some adhesions of the upper lobes of the lung to the ribs. The lungs are large, increased in weight, color pink and mottled red, air content diminished. There are several masses of tubercles, each as large as a cocoanut, in both lobes. In one such the tubercles are yellow and caseous; some are fibroid but none are liquefied or calcified. The fibrous tissue of the lung parenchyma here is much overgrown. In one instance the terminus of a bronchus is solidly plugged by caseous material. Mucosa of bronchi is reddened, markedly ulcerated, ulcers overlaid by mucopus.

INDIVIDUAL FEATURES OF AVIAN TUBERCULOSIS.

The avian form of tuberculosis is somewhat peculiar in its physical appearance as well as in its distribution. The isolated nodular type is far and away more common by more than 100 per cent. than all the other types combined. These nodules are usually well circumscribed, and to the naked eye suggest that they have a restraining fibroid wall. This is, however, not the case, the impression being due to the dense but actively growing fibrocellular cortical zone of the tubercle. The centre of the nodule, instead of having the soft character like Camembert cheese, resembles the firm but brittle American dairy cheese. Upon opening such an area the central necrotic mass may split away from its cortex and even shell out, leaving a cavity lined by a gray-yellow membrane. These characters are best displayed in nodules of moderate size, the small ones being like the yellow mammalian analogue, the large being like indefinite cheesy masses. In the surrounding tissue evidences of inflammatory processes seem decidedly greater in our material than I am accustomed to see in human and veterinary pathology. This, it seems, should be emphasized since secondary infection with pus cocci and other pathogenic germs appears less often in birds than in mammals.

The difference speaks, therefore for a difference either in the tubercle bacillus of birds or the avian physiology. Judging by the limited morbid processes produced by injecting avian bacilli into rabbits and guinea- pigs the reaction of the bird itself would not seem wholly responsible for the difference. The local tissue reaction in all avian lesions is mononuclear and fibrous, softening and pus being rare. It would seem from this and similar operations that the bird expresses its resistance to the bacteria by a fibrocellular reaction which goes on to fibrosis without softening; perhaps this means also that their polynuclears are not sufficiently active, but the pathogenic power of the bacillus itself doubtless is individualistic.

The character of the cheesy degeneration is likewise different from the mammalian. It seems like an abrupt hyaline necrosis of a large central mass and not the slower cell death seen in the other types of tubercle. At times the degenerated area, instead of having the yellowish color of caseation, will present what we have designated “gelatinous tuberculosis,” the whole infiltrated area resembling boiled sago or tapioca. This seems to be a complete homogeneous coagulation or hyaline necrosis of the whole mass out to the delicate fibrous mantle supplied by the tissue in which the tubercle lies.

The organic distribution of tuberculous lesions has already received some attention and is to be discussed with the orders. There are, however, some localities affected conspicuously in the bird. The skin lesions often attract attention during life. They occur around the eye, at wing joints, on the cresta sterni and on the legs. Parrots and jays have shown nodular or diffuse growths around the eye, originating both in the lids and orbit, which on section have proved to be tuberculous. These seldom ulcerate, but those upon the skin of the breast and wings tend to have superficial erosions or deep ulcers. The latter lesions are more common upon pigeons but have been seen in Psittaci and Galli. Toucans and pigeons when pinioned, have on three occasions shown a tuberculous mass on the stump.

Two parrots with hyperkeratosis of the beak and of the skin of the feet, have also had tuberculosis. These have been mentioned in literature as of tuberculous origin. One case well studied failed to show tubercle bacilli in the corns. In the absence of tubercle bacilli, one is inclined to think that this might be explained on the basis of a circulating toxin such as is assumed to be responsible for hypertrophic periosteitis. This latter condition has not been seen in birds.

Still another type of occasional occurrence deserves mention. While most of the lesions in birds correspond to the description given in the preceding pages, some lesions fail to degenerate in the centre, retaining instead a solid homogeneous fleshy character of dull gray- yellow color. Upon section these have been found wholly cellular in construction. To distinguish them from the ordinary nodules they have been designated tuberculomata. Lesions of this kind may occur along the lymphatic paths, indeed seem more common in the lateral cervical and thoracic chain, and upon bones and nerves. When they are numerous the nodular caseous type is inconspicuous. They suggest the bovine infection (Pearl disease), but one attempt to prove this failed. We are of the opinion that this is the avian lymphatic form, as our examples correspond to the literary descriptions of cervical tuberculous lymphatics in birds. No especial variety of bird is more often affected by this process.

Intestinal tuberculosis among the Aves may be said to assume three forms. The best known, indeed the form usually spoken of as representing the common picture, is that which produces varying sized nodules upon the serosa, sometimes associated with adhesions to neighboring intestines. Just how this type develops is not known. In some quarters it is believed to originate by the penetration of the tuberculous granulation tissue from the mucosa through the intestinal wall by following lymphatic channels and that irregular contractions of the musculature squeeze the exudate outward under the serosa. Other observers think that the bacilli are carried via the lymphatics to the superitoneal tissue, there starting the tubercle. The truth of the matter will probably be that both methods are operative although we have seen more cases suggestive of the second than of the first explanation. When these peritoneal nodules are numerous and prominent, mucosal ulcers are uncommon and vice versa.

The second form is the ulcerative, flat ragged or crateriform defect situated in a diffusely thickened wall. This was well illustrated in cases of pulmonary infection in doves and guans, suggesting reinfection of the gut tract from swallowed tubercle bacilli or a backward development of the disease after the lungs were nearly solid.

The third form of tuberculous enteritis is quite interesting and striking. It is best seen in the duodenal loop but may occur anywhere. Diffuse thickening of the enteric wall is noted, and when palpation is practiced a resilient but leathery sensation is obtained. Careful inspection reveals the mucous surface to be velvety, a condition due to a swelling, that is widening, of the villi which retain their erect position and, when washed in flowing water, will be seen to move like a field of grain in a breeze. The serosa may be, usually is, negative. Studied microscopically the peculiarity of this form is in the development of tubercles and diffuse cellular exudation in the villus stalk, sometimes extending into the submucosa also. Round cell masses like lymph follicles are sometimes prominent. This form is not associated with any peculiar organic distribution so far as my studies go.

Passeres. The peculiarity of this order seems to be in the predominance of the pulmonary route as origin of tuberculosis. Perhaps in no other order has there been such extensive and advanced lesions as in these little birds. Sometimes one whole lung will be solid while its fellow will be half occupied by caseous material. The doves alone seem to approximate the Passeres in ability to live with so much tuberculous exudate.

Picariæ. Specimens from this order illustrate well the intestinal origin and distribution of tuberculosis. There was, among these birds, one case showing tuberculomata which was, because of its gross anatomy, listed as the pearl type. Its description is as follows:

Lesson’s Motmot (Momotus lessoni). The region above and behind the right clavicle in front of the brachial plexus on the internal surface of the thorax, exterior to the first and second ribs, and on the internal surface of the ribs at the junctions of ribs with the alæ of the sternum, there are many small, irregular, smooth, firm, yellowish white nodules varying in shape from spherical to sweet potato and in size from 3 × 3 mm. to 3 × 7 mm. These are found quite homogeneous on cross section. They do not resemble tubercle or mould infection but make one think of neuromata. There are also a few present in the left lateral air sacs, close to but not joining the intestine. The lungs are apparently normal. Histological section of the masses described as distributed along the nerves consist of sharply outlined but not well encapsulated masses made up of irregularly disposed bunches of large cells with vesicular nuclei in a stroma of loose connective tissue very inconspicuous in amount. There is also quite a number of small round cells and a few leucocytes. The large cells first described have the nucleus eccentric for the most part. Many of them have two nuclei and a few three and occasionally a giant cell is observed. Blood vessels have a very delicate wall and are frequently encountered in the centre of these masses. Atypical mitoses can be found. Here and there a seal ring placement of the nucleus can be found. A few eosinophiles are present not definitely placed. Necroses, with large quantities of nuclear fragments, are scattered irregularly through the mass. The diagnosis rests between an infectious granuloma, false neuroma and sarcoma. Tubercle bacilli were found by stain in great numbers both within and without the cells.

Psittaci. Tuberculosis occurs in this order somewhat more frequently in the varieties whose habitat is the Eastern world, although South American birds also suffer from it in the characteristic manner. There seems to be no difference in the pathology of these two groups. Parrots present very beautifully the separate solid or semisolid nodules of avian tuberculosis, whether they be in the lungs, liver, or spleen. When the lung becomes riddled with masses, coalescence occurs and the whole mass turns into a cast of the hemithorax. Lesions in the liver are mostly isolated, but the spleen often appears like one large pink tuberculous nodule. The liver occupies as usual the first place in organic incidence.

Striges. Owls (and Struthiones—see below) present the interesting exception to the rule of intestinal origin of tuberculosis in birds. Perhaps the platting is incorrect but the birds in the order under discussion had older and much more advanced lesions in the lungs and thoracic serosa than they did in the abdominal organs. That this was true in all three examples is in itself noteworthy. Perhaps they possess less pulmonary and more intestinal resistance. One of these birds showed a small recent cavitation in the posteroinferior angle of one lung.

Accipitres. With one exception the cases of this order occurred among the Falconidæ, that is in hawks, buzzards, and eagles. Their lesions are usually generalized as indicated by the figures for visceral distribution, but that half the number should have the oldest, most prominent lesions in the lungs is curious. Their intestinal tuberculosis seems mostly of the diffuse infiltrative type.

Columbæ. These birds are obviously the most susceptible of all the varieties of which there are sufficient autopsies to make a comparison. Generalized nodular lesions emanating from the intestinal tract comprise their usual form, while most of the hepatic lesions are small miliary and nodular; occasionally one sees caseous masses destroying large sections of the organ. Their intestinal lesions may assume any of the three forms described.

Galli. This is an order of something over the average percentage incidence for the birds but containing families that seem very susceptible to tuberculosis. The small number of Brush Turkeys (Catheturus lathami) had 60 per cent. of the disease, while South American Cracidæ had 44 per cent. These two groups raise the incidence for the order. Galli as a group have generalized nodular tuberculosis originating by the intestinal route. This is especially seen in the Phasianidæ, while the very susceptible Cracidæ have much more prominent lesions in the lungs, often of a massive caseous type. It is really astonishing at times how much of the pulmonary tissue is occupied by infiltrate before death has supervened.

Fulicariæ are represented by a special contingent of rails and gallinules. Avian characters are well illustrated in the order. So too the succeeding order, Alectorides, another variety of shore birds, run true to the avian form. It is interesting to note that in the two cases from each of these orders tuberculosis and aspergillosis have been combined. The former has assumed the firm nodular type, while the mycosis has been of the air sac variety. The following case is worth citing as possibly illustrating infection per cloacam. There is, however, no trace of this bird having been with a male with the disease.

Demoiselle Crane (Anthropoides virgo) ♀ . General tuberculosis including the oviduct. All organs are thickly beset by caseous tuberculous nodules except the lungs which have only a few scattered ones. The oviduct is, for its lower two-thirds, much enlarged, firm, tough, pale yellow, thickly beset with caseous nodules; upper parts uninvolved. The kidneys are definitely enlarged, irregular, almost mulberry-like, brownish yellow, firm and tough. On section the lobules are irregular, connective tissue increased, urates in pelves. Tubercles in intestines seem to be wholly peritoneal. This seems like a tuberculosis of genital origin judging from condensation of tubercles in the lower abdomen (mass around cloaca). The ovaries are not involved. Lungs and thoracic air sacs relatively free. The pericardium shows a whitish thickening of both layers due to the presence of whitish granules like urates. Histological section of kidney shows the capsule not greatly altered. Glomeruli largely negative but a few show hyaline capsular thickening of vacuoles in tufts or fibrosis in tufts or obliteration of whole structure. Tubules largely degenerated, distended or distorted. Interstitial tissue between the tubules definitely but irregularly increased. No real attempt at regeneration. Few vessels show perivascular fibrous change. One tubercle seen.

Anseres. These birds present no especial features so far as percentage or organic incidence are concerned. The individuals are mostly geese and swans, ducks being somewhat more often affected by mycosis than by tuberculosis. However, both these diseases tend to assume the nodular type in Anseres so that the diagnosis should be supported by bacteriological discovery of the respective organisms.

Struthiones. The marked feature of this order is the prominence of the isolated and confluent nodules in the lungs, of apparently greater age, certainly of great size, than similar lesions in the abdominal viscera. Caseation of the avian variety is well illustrated in these birds. The thyroid body was involved in two of the three cases, the ovary in one. The representatives of the Crypturi, two tinamous, came at the same time and lived only a few months. Miliary tuberculosis of the small precaseous variety was the form exhibited by both specimens.

HISTOLOGY OF THE TUBERCULOUS LESIONS.

The initial and characteristic unit of tuberculosis, the miliary tubercle, seems to be constructed upon the same general principles in all cases of the disease and in all members of the zoological groups in our study and in a manner entirely comparable to that well known for man and for the domestic animals. There are, however, certain minute differences which are interesting and may at some time become important. It is customary to speak of the bovine tubercle and of the human variety, but there are also slight variations of the microanatomy of each of these, while one may find on occasion a tubercle of the human type in a cow and vice versa. Not all the domestic animals show the bovine form, although in sheep and swine it is approximated very closely. In the horse there is much greater tendency to a central softening and fibrosis is not so common as in the bovine tubercle. I have attempted to study the histological anatomy of each of the zoological orders, but it has not resulted in any profitable discovery. It is, however, possible to contrast the type commonly found in monkeys with that characteristic for man and the ungulates and also to emphasize the construction of the avian tubercle that it may be distinguished from mammalian tuberculosis and from avian mycosis.

The tubercle of the Primates is a loosely constructed affair lacking the fibrous mixture of the bovine and the close cellular packing of the human form. Studied from the periphery to the centre, there will be found very little fibrocellular reaction in the immediately surrounding organ, while the mantle of round cells, rather prominent in the human tubercle, is often quite inconspicuous. The principal cellular component of the miliary granuloma is the large pale endo- or epithelioid cell, which is abundant, loosely arranged and without apparent purpose. In the centre is an irregular necrosis usually retaining some chromatic matter, probably the remains of recently destroyed nuclei, but this caseous midpoint does not assume the dense acid staining common for many milia. Giant cells of the Langhan’s or foreign body type are often entirely missing, and when present are scanty. There may be large cells, resembling the aforementioned epithelioid cells, with two or even three large palely staining nuclei, but these latter are arranged irregularly and not like the spokes of a wheel near the cell wall.

This picture suggests a rapidly growing inflammatory mass and indeed this is the type that tuberculosis follows in monkeys. In a few cases gross evidence of fibrosis in the serous surfaces and in the lungs has been observed, but they are too rare to permit one to think that connective tissue activity is an important part of the reaction of this beast to the disease.

The avian tubercle as it rests in the tissue seems like a sharply outlined almost encapsulated body. This is in part due to the homogeneity of its structure and in part to the fibrocellular condensation around the caseous part of the growths. Examined from without inward, there is a round cell mantle, between the elements of which course fine but easily perceptible fibrils; elastic tissue has been seen among them. The small cells continue more deeply than the fibres, to be succeeded in prominence by epithelioid cells of rather dense character, the nuclei especially seeming quite rich in chromatin and round. The rotundity of the nuclei remains not only in the single separate cells forming the middle zone of the cellular cortex, but can be found in the nuclei of the compound or giant cells which comprise the internal layer lying upon the necrotic centre. These giant cells are characteristic for the avian tubercle in assuming a form like syncytia with nuclei arranged in irregular radiating columns. This internal large cell area may completely surround the central necrosis or it may be interrupted by the large single cells. Tubercle bacilli are more common in and between single cells than multinuclear ones. Within the cellular zone lies the necrotic centre, often, indeed usually, full of chromatic debris. This centre is commonly quite amorphous but occasionally one will see what is probably the remains of a coarse coagulum. Between the necrosis and the cells one usually finds a split, a sort of separation of the gangrenous from the living part. Old tubercles with denser fibrous capsule retain this microanatomy in part, but the cellular zone gradually becomes thinner and thinner until all that remains is a narrow cortex of round cells and imperfectly retained multinuclear cells.

Tuberculous granulation tissue without definite milia consists entirely of the round cells with small vacuoles and a fine but definite fibrosis. Tuberculomata consist of cells of varying sizes with small round nuclei. Interstitial fibrosis is delicate and barely visible unless especially sought. Giant cells may be encountered but are not so large as in milia. Necrosis occurs but not in an orderly manner in relation to cells as in an isolated tubercle. Tubercle bacilli are very numerous.

TYPES OF BACILLARY INFECTION.

According to experimental and statistical research, all the tubercle bacilli of the higher vertebrate classes can be infective for any member of these classes. Thus, for example, human bacilli have been found in many orders of mammalia and in birds. The bovine form has been found in swine. The lesson from this is that while the special predilection of a variety of the tubercle bacillus may be for one kind of animal, it is potentially a virus for other kinds. Hygienic principles have therefore been laid down at the Garden which aim at the protection of all specimens from every variety of tubercle bacillus. For this reason and because the laboratory has not attempted extensive research on bacteriology, few type determinations have been made and those at hand offer nothing new or unusual; they are noted here as a matter of record. Bovine bacilli have been judged by their slow growth and infectivity for rabbits, human bacilli by the reverse of these characters. Avian tubercle bacilli can be cultivated with reasonable ease directly from lesions not bearing a mixed bacterial flora, and grow in a yellow, moist, even, spreading colonization. In our two attempts at infection of guinea-pigs, no success was had, although Rabinowitsch and others had no difficulty in so doing; this strain may vary in virulence as do other tubercle bacilli. No avian culture was obtained from a mammal, but a bovine was found in a parrot and a human in a duck. Bovine bacilli were isolated once from a monkey (see page 496) and in another case of lymphatic type, bacilli of the short heavy blunt shape, supposed to be characteristic of this variety of the germ, could be stained. Monkey tuberculosis in our experience is usually due to the human tubercle bacillus, judging by the staining characters and two successful cultures.

DISCOVERY OF TUBERCULOSIS DURING LIFE.

Fully developed chronic tuberculosis may be recognized with reasonable ease in the human being and some domestic animals. The diagnosis rests largely upon the history and symptoms and partly upon the appearance of the individual and upon signs elicited by physical examination. There is good reason to believe that these latter methods are entirely applicable to certain wild animals, notably those that can be caught and held quiet, but because of their naturally great reserve many specimens offer little reason for suspicion as to their tuberculous condition until near death. Certain ungulates with chronic pulmonary disease get thin and weak but remain on their feet with good appetite and satisfactory discharges for many months. Primates, Carnivora, Rodentia and Aves not uncommonly come to autopsy with very good coats and without great emaciation and yet are heavily infected. It can be stated with fair positiveness that no chain of historical data or gross observations are certainly known to us as indicative of tuberculosis in the wild beast. Coughing is not necessarily characteristic of chronic pulmonary infection, although when continuous it rouses considerable suspicion, especially in the Ungulata. It is to be interpreted with care in all animals that have loose bedding as bits of straw or seeds get into the throat causing irritation; the dust of hay may cause coughing in horses.

However much chronic or fatal tuberculosis may be interesting from the standpoint of pathology or of zoological or visceral incidence, the most important factors in our knowledge of the disease are its early recognition and treatment, either for curative or hygienic purposes. Since we have learned that advanced lesions may exist in an animal without materially affecting its external appearance and behavior, it naturally follows that early cases, possibly of an “open” or infectious character are still less likely to give evidence of their existence. This is well recognized by veterinarians as being true of cattle, but is perhaps less well known, or possibly admitted, by those who handle the very susceptible monkey.

Upon a visit to a foreign garden I was told that experience alone is sufficient to enable an observer to detect tuberculosis, and that the disturbance entailed in physical examination and tuberculin tests is prejudicial to the well-being of all varieties, but especially the delicate ones. I learned later that they had the disease in their exhibition cages all the time but decided to put their method to the test. Shortly after my return from abroad a splendid specimen of Grivet Monkey (Cercopithecus sabæus) was condemned by the tuberculin test. He was well studied by the superintendent and two very experienced keepers, all of whom pronounced him one of the finest specimens they had ever seen, and stated that he was behaving quite normally. Despite their protests he was sacrificed, tuberculosis with early cavitation being found in the upper lobe of the left lung. Incidentally vague physical signs were found by auscultation, but as the monkey was unruly and had long pectoral hairs little weight was placed on the observation. However, it is frequently possible to make very thorough physical examination of the lungs of the more tractable specimens, diagnoses of pneumonia and bronchitis being frequently made in this and other parks, so that treatment may be instituted.

IMPORTANCE OF TRANSMISSION AND KNOWN SUSCEPTIBILITY.

Some light upon possible reasons for the poor condition of an individual animal is of course shed by a knowledge of the disease to which that particular variety is most susceptible, to which may be added the data obtained from previous deaths in the same group or enclosure. Thus, for example, a sickly monkey would be suspected of having tuberculosis or early osteomalacia, whereas no suspicion of these diseases would fall upon the marsupials. The same position would be assumed if a dove and a heron were out of condition.

In so far as enclosures are concerned, the matter is somewhat different. Whenever a case of tuberculosis occurs in a cage, the remaining specimens if any are removed and the place cleaned by soap and water and disinfectant and paint. The naked flame from a blast lamp is used when possible. Out-of-doors enclosures are vacated, spread with lime and allowed to lie fallow for as long a time as practicable. These methods have been in the main successful in clearing a cage of the disease, and all our experience demonstrates the effect of cage hygiene and the selection of non-infective replacements. A few places such as those occupied by doves and guans have not been freed of infection, if one judge by its appearance when new specimens are placed in them, but they may of course be due to the infection from elsewhere. The history of seven years in the new bird house where the hygienic conditions are excellent, seems to indicate that a cage thoroughly cleaned is no longer a source of danger, and that a repetition of tuberculosis in such an enclosure is due to its importation with new exhibits.

The spread of the disease to nearby cages seems to depend upon two factors. If the number of cases has been large and the infection virulent, immediately adjoining cages are involved, but the tendency to spread is directly proportional to the proximity of orders or families that have a high susceptibility for tuberculosis. This second factor seems to be the more important and is illustrated by our experience in one corner of the new bird house. In this area are exhibited certain doves and pheasants, among which are many cases, while the passerine varieties nearby are little affected. So too in the flying cage the disease has occurred in varieties with high general susceptibility. There are at the present writing ten orders on exhibition in this large enclosure and there have been more. An occasional case of the disease occurs, but only in the orders which show it elsewhere. The Herodiones, of which we have had nearly one hundred autopsies and many now are on exhibition, are always well represented in this cage and yet show no tuberculosis. In the ten orders mentioned above three show no cases of the disease.

These observations illustrate the spread of tuberculosis, especially to the most susceptible varieties, and how non-susceptibles under good hygienic conditions fail to become infected even when infected animals are near them. The freedom of activity in the large enclosure is doubtless an important factor.

The history of the past three years with regard to the control of tuberculosis in the small cages shows that twenty-nine were infected, but by the measures employed nineteen have remained free of the disease for one year; three of the remaining ten are known to have received newly arrived and possibly infected specimens.

The accredited method of transmission in birds, the swallowing of material soiled with the feces richly laden with germs, is the principal reason why infected enclosures and their immediate environment are the principal breeding places for tuberculosis. To be sure air currents may blow the virus around, allowing it to light upon food in other cages but this cannot be a great menace if for no other reason than that we have had no epizoötic outbreak of the disease, when there were groups of deaths in doves and guans.

Evidences with which to trace transmissions are much clearer in the birds than in the mammals with the exception of monkeys and some ungulates. Of course cases are perhaps too few in the carnivores and rodents to permit correct deductions but it is very rare that more than one case occurs in the same enclosure containing groups of these varieties. Nor do animals in adjoining cages seem to “catch” the infection. This observation does not suggest that any relaxation of hygiene need be allowed but probably it implies that not many bacilli are excreted by these animals; they cough very rarely. Groups of ungulates (bison and deer) are often known to be infected but just how it has arisen is seldom clear. Transmission from monkey to monkey has been observed so frequently that it cannot be doubted, nor will anyone wonder at it if reflection is given to the close personal contact of these animals during their natural behavior. They huddle, pluck lice from one another, take food from the mouth of another, bite and perform many other actions greatly facilitating the transfer of any virus. Bacilli may also be disseminated by coughing, drooling and with the fecal discharges, for which latter there seems ample opportunity since a notable percentage of cases have intestinal lesions. Monkeys do not seem to raise sputum and expectorate it but they do eject saliva from their lips.

Contraction of the disease from infected cages is believed to have occurred at least once in our experience but the lesson of complete sanitary cleaning of the enclosure learned from that happening, seems to have enabled us to forestall its repetition.

THE TUBERCULIN TEST.

Tuberculosis presents the greatest single problem among the specific infectious diseases which the director of a menagerie must attempt to solve. Even though one may possess a knowledge of its zoological distribution, clinical characters and pathological effects, these are insufficient criteria for its detection at a stage when the animal might be saved by treatment or, what is most important, removed from its companions that they might be protected. To this end there remains but a single procedure for the discovery of the existence of tuberculosis—the use of tuberculin in one of its forms by one of its methods of application. The use of this test in veterinary medicine needs no commentary, having made its place in clinical and hygienic practice for a quarter century or more. Armed with the knowledge of the satisfactory use of the toxins of tubercle bacillus in cows, Dr. Penrose, Dr. C. Y. White, Dr. A. E. Brown and Dr. Leonard Pearson began in 1901 a series of experiments with old tuberculin of Koch which have led to the development of a technique for its use in the detection of infected monkeys. These interesting and instructive animals, being known as highly susceptible since most of the collection died of the disease in those days, and being handled with reasonable ease by experienced men, were investigated as the most important specimens upon which to perfect the method. Other varieties have been studied since and I shall refer to them individually. The greatest amount of work and the most conspicuous success attended the observations upon monkeys and the results of this study are now in daily use in this Garden.

The work, conclusions and results, originated by Doctor Penrose, Doctor White, and Doctor Brown can be described as one of the most completely satisfactory series of observations in scientific medicine. Applying the principle that a tuberculous animal reacts to the injection of tuberculin by a temperature rise, the normal temperature curve of the monkey was studied, that of the tuberculous monkey determined by killing many specimens. This enabled them to state which animal was infected, which was not and to place on exhibition only healthy specimens. Added to this, strict hygienic principles in the housing and handling of the animals have resulted in the elimination of the disease from our exhibition house. Occasionally a case may develop, perhaps from feeding by visitors, but the matter is no longer a problem. I know of no more complete and satisfactory experiment and its practical application than this work, which is condensed in the succeeding paragraphs.[101]

THE TEMPERATURE OF MONKEYS.

The success of the tuberculin test in the lower animals as in man depends chiefly upon the alterations in temperature following the injection of the toxin. It is generally admitted to-day that a healthy animal’s temperature will not be affected by the introduction of this material. There are in addition changes in the pulse and respiration rate and in the physical signs but these are detected with difficulty and are much less definite than thermometric records. The first essential was therefore a thorough familiarity with the normal temperature of the monkey, a requirement which met with considerable difficulty from the beginning since the earliest observations revealed puzzling irregularities. This necessitated the establishment of certain regulations of technique which, after the preliminary tests, have been found satisfactory enough to continue until the present day. All monkeys are received in the quarantine rooms of the laboratory where they are observed by the officials of the Garden and of the laboratory and there they remain in separate cages until passed, as free from tuberculosis, to the exhibition house.

The handling of monkeys for the purpose of taking temperatures is a matter of no small importance since excitement will quite definitely increase the registration. We have been fortunate enough to have in charge of this work since its inception the same man, Keeper McCrosson, who is thoroughly experienced in the care of these beasts and who can catch and hold them with a minimum of disturbance. To him and to the interested laboratory helpers much credit is due. Small specimens like capucins and spider monkeys are caught with the gloved hand or with the protection of a piece of heavy cloth. Larger specimens may be caught in a net while strong monkeys are fitted with a collar and chain by which they are pulled into the corner of the cage and held, while the door is opened to permit a helper to catch the feet and arms. Two experienced men can take the temperature of any monkey that can be handled at all safely. The knowledge of how to do such work reduces the excitement of the animal and renders more accurate the observation of its temperature. During the period of temperature-taking food is given in small quantities and only after the record is made.

Temperatures are taken in all animals by rectum,[102] the thermometer, a separate instrument but always the same for each animal, well greased with plain vaseline, being passed along the anterior rectal wall and allowed to register for twice its indicated speed. During the preliminary work, special instruments of officially standardized accuracy were obtained by Doctor Brown but once the normals were obtained, ordinary good thermometers registering from 94°F. to 108°F. have been employed. If the record vary very much from the expected, such as the figures obtained at the same time on the preceding day, or if the rectum be crowded with feces, the instrument is shaken down and reintroduced. In order to facilitate timing of exposures we use sand glasses of three minute run.

After some experimentation by taking records at various times of day it was found that monkeys as a group do not have a uniform temperature during twenty-four hours but register a higher figure during daylight than during darkness. This is probably due, as I shall discuss, to the period of activity, not to the time of day. Figures obtained at various hours indicated that the highest and lowest temperature would be obtained if records were made at four-hour intervals at three, seven and eleven o’clock AM. and PM. To give the normal temperature of a monkey, the kind and the time of day are necessary adjuncts. Reference to forty- eight hour charts which are used for the illustration of normal records, and for contrast with tuberculin reactions later, will convey to the reader a better idea of the normal daily rhythm of the simian heat regulating system than would verbal description.

NOTE.—In the temperature charts degrees indicated by circles and connected by dashes are from records made after diagnostic tests by injecting tuberculin.

The anthropoid apes (Curves A and B) have on the whole a mean temperature nearer the human being than do the lower monkeys, but they too present daily variables far greater than man. The high point of their curve, at three PM., is in the neighborhood of 100°F. the lower point around 97.5°F. From these charts and other records it can be said that while the higher apes have a daily temperature curve with its high point at three PM. and its low point at three AM., there is in them not by any means the regularity of curve to be found in Cercopithecidæ and Cebidæ. Our records of temperatures in the Hylobates (Gibbons) are not extensive enough to quote but what we have approach those of the lower monkeys.

Graphic curves of the normal temperatures of the various genera of Cercopithecidæ and Cebidæ present striking similarities in the regularity with which the daily rhythm is performed. In the seven genera of which we have accurate records the normal high points fall between 102°–103°F. and the low points between 99°–100°F. while the curve of the four-hourly steps is closely comparable. The curves D to J are composites from charts of animals that have been tested with tuberculin, which thereafter died or were killed and found free from tuberculosis. Not every individual chart that may come to hand necessarily follows the exact course detailed in these illustrative curves but these latter offer a guide as to what is to be expected of the different varieties. They show unequivocally the V-shaped curve of the temperature of the monkey during twenty-four hours.

The Callitrichidæ or Hapalidæ have failed to show tuberculosis in our Garden and little has been done upon them. As a matter of record there is reproduced the only satisfactory chart at hand (K) taken very early in the researches. It shows a similarity to those of the higher monkeys; because of its very high afternoon record the animal was killed; no tuberculosis was found.

The Lemures, being close to the Primates zoologically and presenting a high incidence of tuberculosis, were included in this study. Observations upon their normal temperature were hampered more than upon that of monkeys and even to-day we cannot feel the same confidence in the records. Irregularity is most marked and they seem easily disturbed by handling. Chart C shows a composite temperature for forty-eight hours of twenty-two proven non-tuberculous Lemures. The tendency for the “night drop” is certainly existent but with much less definiteness than in the Primates.

CONDITIONS WHICH MODIFY THE TEMPERATURE.

Observations by A. E. Brown[103] and by Simpson and Galbraith[104] would seem to indicate that the diurnal variation in monkeys is due to periodicity of activity. Doctor Brown found that the temperature of a night monkey is reversed, that it is higher during the dark than the daylight hours. See chart of Potto (Perodictus potto) chart L. The Scotch observers report that if the activity of day monkeys were reversed, daytime being made artificially dark and activity forced during the night, the temperature curves were likewise reversed.

Perhaps the most important discoveries of these investigators concerned the influence of excitement upon the temperature records. These observers indicate definitely that the greater the physical activity and nervous excitement the higher the thermometric record. We have noted that the substitution of a strange keeper who may not be gentle and tactful with the monkeys can serve to raise the temperature above the records obtained by an experienced man with whose methods the animals are familiar.

A knowledge of these facts dictates at least two important precautions on our part—our specimens must be kept under identic conditions peculiar to their kind, and surroundings must be established offering comfort with a minimum of annoyance in transfer and handling. To this end all specimens upon receipt are put into separate cages suitable to their size and allowed to become accustomed to their surroundings for several days before attempt at temperature-taking is made. Mention has already been made of the experience and interest of the principal keeper; the regularity of records is an attest to his work. Daily three o’clock afternoon temperatures are taken first to accustom the animal to the matter, before test records or tuberculin injections are made.

The existence of pathological states undoubtedly affects normal temperature curves and tuberculin reactions. Gastroenteritis has the effect of increasing the whole level and of making irregular the midday and afternoon records. Respiratory tract disease cannot be said to have a very definite effect; its most frequent influence seems to be to drive the night records lower so that there is a long fall between seven and eleven PM. and a long rise between seven and eleven AM.

THE TEST.

The preliminary rest of the new arrivals having passed daily three o’clock afternoon temperatures are taken until an even level is obtained; this requires usually four days but in very nervous specimens it may be much longer. The afternoon temperature course provides not only a means of teaching the monkey what is coming but supplies us with a high point record for comparison. When a new variety is received, a full normal twenty-four hour record is usually made. This preparatory routine being fulfilled, the animal is injected under the skin of the thigh or flank with freshly diluted mixed bovine and human tuberculin.

THE DOSAGE.

Early trials with this substance revealed the fact that a dosage based upon the weight in comparison to man failed to elicit a definite response whereas if based upon relative weight of cow was too large. The finally determined quantity was arrived at, as was the case in early human and bovine work, by experiment and trial and was as follows: A monkey of five to ten pounds (2.3 to 4.5 kilos) received an initial dose of 1. milligram and for each additional five pounds (2.3 kilos) 0.5 mg.; this is 0.2 to 0.4 mg. per kilo. The amount given to man varies from 2. to 5. mg.; if the body weigh 60 kilos this is 0.03 to 0.08 mg. per kilo. Cows are given usually in this country 400 mg. or, for a cow of 250 kilos, 1.6 mg. per kilo. In the early work, doses comparable to the figure for man failed, whereas at least two animals died very quickly after 1.+ mg. per kilo; 5. mg. was the original high dose. While the death of a monkey after a large dose was of no moment and was perhaps desirable, it would only be the heavily diseased specimens and this would give no criterion upon which to judge the appropriate dose for all. Experience seems to warrant us in continuing with our present figures since all tuberculous monkeys have reacted to it. Subsequent cases for retest are increased from 50 to 100 per cent. depending upon the size of the monkey, the very robust and vigorous ones receiving an increase represented by the higher figure. One monkey injected eight times has risen from 1. to 24. mg. with constantly a negative response over a period of nine years.

Doses for Lemures are relatively higher, averaging 1.5 mg. or about 0.5 mg. per kilo; they are increased in the same manner as above.

THE TEMPERATURE TAKING.

Injections are usually made in the late forenoon, temperature records being started at the usual three PM. hour and continued at four-hour intervals for forty-eight hours, giving thirteen records over two days, a time period presenting two complete cycles of diurnal variation. This was found necessary because certain cases do not react during the first day. Explanation of this was sought in the nature of the lesion but could not be found further than that mild early lesions may give it but it cannot be read as indicative of low activity since one case of laryngeal tuberculosis had this “delayed reaction.” At times it has seemed to occur when the injection fluid formed a blister under the skin, a pocket in the areolar subcutaneous tissue, whence absorption would be slow. Whatever the correct explanation, experience has justified the recording of temperatures for full forty-eight hours.

THE REACTION.

The experience gained with these monkeys supported definitely the general opinion that tuberculin injected into healthy animals will not disturb the temperature but will produce decided changes in that of tuberculous animals. The reaction in the tuberculous animals may assume several characters, of which usually two are combined in a chart. The commonest and most convincing is a definite rise in the first twelve hours, amounting to one degree or more; rarely it may be three degrees (W). This is followed either by a maintenance of a high level or an attempt to perform the night drop. It may be said that in general there is an abortive attempt in nearly all tuberculin reactions to simulate the V of the normal cycle; this can be seen in charts M, N, O and P. Another rise may be attempted during a similar period of the second twenty-four hours or the whole course may at that time approximate the normal. A modification of this type of reaction is the performance of the whole daily rhythm on a high level, set, as it were, by the initial three PM. record. This form is confusing at times and has been responsible for at least one of our mistakes. Combined with this high level of curve is a tendency for the second twenty-four hours to be higher than the first day (See Variegated Cebus Q and Sooty Mangabey R and Chacma Baboon W). The second type of reaction, illustrated by chart S, fails to resemble the normal daily cycle of the monkey temperature but has sudden rises and falls as its characteristic feature. We have learned to look with suspicion on all charts with sudden marked changes of record even if they follow in the main a rhythmic course. The sudden fall exhibited by a very sick monkey illustrated by Grivet Monkey (T) and Campbell’s Monkey (U) is a bad sign. It has been met more often in advanced caseous pulmonary tuberculosis than in any other tuberculous lesion. On two occasions it has been seen in the absence of tuberculosis so that retest is indicated if the specimen be valuable; such animals however rarely survive the disturbance incident to the test as they are usually suffering with some serious disease. Illustrative charts of several positive reactions serve to elucidate their character better than description. If comparison and contrast of the normal and post- injectional temperature be made, the conclusions are definite.

It cannot be said that any type of reaction indicates a particular form of disease although the last type, the falling of the temperature beyond the thermometric registration point, usually means advanced lesions especially of the caseous pneumonic form. A very small lesion may give a definite reaction as in Cebus (V).

The examples given are those of a definite character but there are many charts that vary from the normal upon which a decision is extremely difficult to make. Such animals are held in quarantine to be retested after the lapse of three months. Early in the work a suspected specimen was reinjected after two weeks, failed to give a reaction but died in about two months of tuberculosis. The nullification of the test by previous injections of tuberculin is well known. Three months’ interval permits a disappearance of the non-sensitivity and allows any latent tuberculosis, possibly stimulated by the toxin, to develop. Repetition upon the same monkey has occurred as high as ten times without apparent harm.

There are sometimes in human beings local reactions at the point of injections. These have been entirely lacking from our monkey specimens. Nor have we ever seen secondary tuberculous lesions appear at the point of the needle-stick. Aseptic syringes and generally cleanly technique have also protected against local abscesses. When an animal is injected he may scratch or pick at the spot for a minute or two but thereafter seems to ignore it entirely.

RESULTS.

The value of the test can best be estimated by a recital of the mortality of monkeys, from tuberculosis, since its inception. Before the test was started practically every monkey in the collection for sufficient length of time to be exposed died from the disease. The average duration of exhibition life of all specimens up to 1903 did not exceed eleven months. The time has risen almost uninterruptedly until now it is thirty-five months. There are, at time of writing, sixty-eight specimens in the cages which have been on view from one to one hundred and eighty-five months with an average of fifty-four months. These figures speak for themselves as evidence of the reduction of infection. The average mortality from enteritis and degenerative bone disease has remained about the same through all these years. Percentage figures such as are recorded in our yearly report are misleading because all monkeys written into the property record of the Garden are listed and since some of these specimens remain in quarantine, they do not properly belong to the exhibition collection. Up to 1906 when the test technique was perfected nearly all deaths were due to tuberculosis, the figure for 1906 (including experimental animals) being 78 per cent. However from February 1906 to October 1907 and from then until May 1910 no case of tuberculosis occurred in the exhibition cages and both deaths at these given times seem like infection from visitors. During the next three years thirteen monkeys died of the disease in the exhibition and many more in quarantine. By 1913 the outbreak was stamped out. Its explanation is not so very far to seek. In the fall of 1910 we obtained some suspected monkeys which were kept in one of the quarantine rooms. After repeated testing two were passed. From them five cases are known to have originated and it was not until in 1912 when the whole exhibition house was cleaned of specimens, thoroughly disinfected and fumigated and until every specimen was retested, that the infection passed. In 1914 no cases occurred, while in 1915 a case either slipped through undetected or was a visitor infection; 1916 two cases, 1917 one case, 1918 one case (see orangutan charts), 1919 and 1920 none and 1921 one case, 1922 no cases. Since 1912 the whole monkey collection has been tested every two years, a method which enabled us to catch a small group in 1916 and has protected the collection since then. Three of the six monkeys specified above were never placed free in the general cages of the exhibition house, they being segregated in smaller cages. One, the orang, was with its mate in an isolated cage. The other two were in larger cages and their history suggests visitor infections.

We have never underestimated the possibility that an occasional very early case might evade detection by this test but we believe the history just outlined warrants us in depending upon it for the protection of the exhibition. By the tuberculin test we have detected the existence of the disease in twenty-three per cent. of specimens. Every condemned specimen, forty-one, showing tuberculosis, gave a positive test. Fifteen monkeys condemned on their temperature charts failed to show the disease. Eight per cent. of the tests resulted in suspicious charts, and the animals finally died of the disease in quarantine. Fifty-six tuberculous monkeys died on exhibition, of which thirty-one were original there and twenty-five their contacts. Twelve of the thirty-one were in the early stages of the work, thirteen due to our misadventure of 1910 and the remainder, six, scattered over nine years.

Another interesting experience concerns the exhibition of a group of Rhesus Macaques in an open “band stand” cage. The idea arose in an attempt to find a separate exhibition space for some good specimens that gave unsatisfactory charts, with the purpose of applying at the same time the “open air” treatment if tuberculosis existed. The experiment has been entirely successful since in the eleven years during which this enclosure has been used there has been but a single case of tuberculosis among twenty-six monkeys. Curiously enough this exception gave a good chart and we suspect it was a visitor infection; no secondary case arose from it. The animals housed in this cage keep in excellent condition, their coats responding to our severe winter by increasing in thickness and glossiness. Frozen toes, fingers and tails are sometimes seen but these monkeys seem just as happy as the others. Breeding is active and the young are lusty and husky. Practically the only deaths are due to accident, or to abuse of old and less vigorous members of the colony. We are unable to give comparative exhibition periods and death rates for monkeys in the large house and this open cage because some specimens have been changed from one to the other but it is certain that the appearance of the “band stand” monkeys is better than those in the house and there are four of eleven animals in the former which have been there eleven years and only four among the seventy in the exhibition house for that length of time.

The results of the foregoing work seem to demonstrate that the tuberculin test permits the separation of tuberculous and non- tuberculous monkeys and that its employment serves the purpose of maintaining a healthy exhibition by excluding infected specimens. These experiences form further corroboration of the facts that tuberculosis begets tuberculosis, that a healthy individual is not a source of infection. It follows that an obviously tuberculous animal should not, need not, be a source of danger; the hidden or unrecognized case is the menace. There is little or no problem when an unequivocally good or bad temperature record is obtained; it is when there are slight variations from the standard for the group that decision as to the disposition of the specimen must be made. Nearly always such specimens are retested until the records are definite. If they be constantly irregular the animal is either sacrificed or exhibited in a separate cage far from other monkeys. It is by the sacrificing of infected specimens or the segregation of suspected ones that our collection is kept clear of disease.

Hygiene of a general character must be maintained also. Our quarantine rooms are disinfected by formaldehyde and mechanical cleansing after every case detected as tuberculosis, and painted every two years. Monkeys associated with infected ones, are retested and then given a bath of carbolized water before being put on exhibition. The exhibition house is mechanically and chemically disinfected at the injection time each two years. All keepers are examined for tuberculosis upon beginning their employment and those handling monkeys, periodically thereafter. When a case of tuberculosis dies, all animals in the same and adjoining cages are removed for retest and the enclosure scrubbed and disinfected.

There is a source of tuberculosis upon the importance of which we can only speculate—the visitor. There were two isolated cases in animals which had passed the test with unexceptionable charts, three and four months on exhibition; curiously enough no other cases occurred in their cages. These we have laid to visitor infection since no previous exposure can be traced for the specimens and no secondary cases occurred.

I can conclude this discussion of the tuberculin test and of the control of tuberculosis by its use, by mentioning the possibilities for the solution of the problem in man. While the eradication of the disease cannot be accomplished as easily as if a potential source could be eliminated by sacrifice, it will come in direct relation to the earliness of detection of infection and isolation of the sources of danger. Not so much the cough-racked consumptive but the unrecognized early lesion whose bearer hawks and spits in public places or at home, unaware of his malign power!

THE SKIN AND EYE TESTS WITH TUBERCULIN.

The first of these can be dismissed briefly, for in a few cases it was absolutely of no value. A known tuberculous monkey was injected into the skin of the chest with 0.5 mg. of old tuberculin. The small bleb disappeared in a few hours and was followed by no reaction whatsoever. Other attempts likewise failed, some of them I believe due to the technical difficulty of injecting into the skin. This tissue is very thin, delicate and loose at the less hairy places where a reaction might be read—arm, chest, abdomen. The hairless parts of the rump might be used, but are so often scratched and soiled with dirt that readings might be misleading. The Von Pirquet test was done on the first mentioned specimen and was likewise negative. His tuberculin test was afterward positive.

The ophthalmic reaction is highly spoken of in the New York Zoological Park and has been used elsewhere. It was tried by me at the time Doctor Blair first discussed it, but with variable results. One set of two monkeys was treated with Calmette’s purified tuberculin into the conjunctival sac and given a subcutaneous dose of old tuberculin. Another set received 1 per cent. old tuberculin into the conjunctivæ and the usual subcutaneous dose. Although all these monkeys gave a temperature reaction only one gave a conjunctival reaction. Fearing that the two tests simultaneously might be an unfair trial, another poor specimen was given an eye test which resulted negatively; a later subcutaneous test and autopsy revealed the disease. Because of these experiences and the fear that any reacting conjunctivæ might become secondarily infected from the uncertain personal hygiene of the beast, we decided to omit this method and rely upon the temperature test.

PATHOLOGICAL EFFECTS OF THE INJECTION OF TUBERCULIN.

It is generally believed that tuberculin injected into tuberculous animals, in doses large enough to produce a marked reaction at the site of disease, may stimulate the process to growth and spread and that certain parenchymatous organs in such bodies undergo degenerative changes. We can give little information concerning the first point because known infected animals have not been sacrificed during the test and we are not informed of the degree of morbid lesion in those dying, since we had no previous knowledge of its existence.

An interesting and practically useful observation has, however, been made upon the kidneys of several monkeys dying shortly after tuberculin injection. It consists in a marked cloudy swelling of the renal epithelium and a congestion or even thrombosis of the glomerular capillaries, accompanied sometimes by increase of nuclei in the tuft and by amorphous material in the space of Bowman. Grossly such kidneys are but little changed, albeit the cortical zone may be dull and opaque and swell out slightly on section; very occasionally bloody streaks may separate the cortical and medullary striæ. In a few kidneys there have been suggestions of preëxisting nephritis but usually the findings are confined to those given above. At all events true glomerulonephritis is not often found. Monkeys which have this condition may or may not exhibit a behavior suggesting its existence. Sometimes it will be noted that the animal is dull and eats little, at other times the keeper will report that the cage is seldom wetted and we know of cases in which only an ounce or two of urine has been passed in a day. Two monkeys were distinctly ataxic and incoördinate and one of these had a convulsion. From one a specimen of urine showed albumen but no casts.

These signs of renal affection are not always alone nor are the kidneys necessarily the only part diseased since postmortem records show a variety of accompanying lesions, bronchitis and enteritis, for example. There are, however, several cases dying in a few days after tuberculin injection, both with and without tuberculosis, in which the renal changes were quite prominent; two examples, without tuberculosis, exhibited the damage to the kidneys very well and with no other evident visceral pathology. The relation of cause and effect may not be unequivocal, but these findings suggest that the condition of the kidneys deserves attention when tuberculin is to be injected. My associate, Dr. Corson-White, is firmly convinced that the substance whips up a preëxistent parenchymatous disease and wants to see a urinalysis from every monkey that is in any way abnormal.

THE TUBERCULIN TEST IN OTHER ANIMALS.

Two cases of tuberculosis occurred in White nosed Coatis (Nasua narica) so that it was decided to test their neighbors in the next cage. There is reproduced a composite (Y) of the temperature record of three of these animals after receiving 2 mg. of tuberculin under the skin. No tuberculosis was found in them at death, all dying within two years. The similarity to the primate type of temperature curve is striking.

Chart Z shows the course of temperature before and after tuberculin injection in a Bactrian Camel (Camelus bactrianus) ♀ which lived for some months and showed no infection at autopsy.

Charts AA and BB show the temperature ranges of respectively a healthy and a tuberculous Bison (Bison bison.)

Chart CC is that of a Malayan Sambur Deer (Cervus equinus) which died a week after injection, showing fibrocaseous tuberculosis. The failure to make an initial rise is noteworthy, but the fall in temperature may be explained by the severity of the lesions and the approaching death.

Chart DD represents daily and post-injection records of a Virginia Deer (Cervus virginianus) which at death was found free of the disease. Chart EE is that of a healthy American Elk (Cervus canadensis).

SECTION XVII—PART 2 MYCOSIS

This is a general term applied to the infections with Hyphomycetes, but in the zoological material discussed here it refers chiefly to the growth of aspergillus in the air sacs and viscera of birds. A few cases of cutaneous mould growth have been seen in mammals but are of trifling importance; brief mention will be made of them on a later page.

Under the names of Aspergillosis and brooder pneumonia, the infection with Aspergillus fumigatus, A. glaucus and others is well known to breeders of chickens, ducks and ostriches. Literary references to its occurrence in zoological collections are numerous, but there seems to be no record indicative of its frequency in the various orders nor discussion of the pathological types best exhibited by different birds. There has indeed been some discussion of the actual entity, mould disease, the picture found at autopsy being referred to secondary contamination with fungi in the presence of bacterial infection. Experiments by DeLong and others have been indifferently successful in the production of the disease by inhalation of mould spores. The appearance of groups of cases in breeding places, apparently all exhibiting the same organism, in the absence of other varieties of avian epizoötics seems to warrant the conclusion that the hyphomycetes can at least be associated with a fatal morbid lesion of quite uniform character whether or not they be the original invaders.

Judging by our experience it would seem probable that the aspergillus can, under conditions not fully explained, cause inflammation of the avian air sac and tubercles in viscera, in the absence of other evident causes of illness and death. Over three-fourths of our cases have no other diagnosis than “mould disease”; this may be in part due to overlooking other things, but to a much greater extent to the very extensive mould growth which obscures all other changes. That unexplained preparatory conditions may exist is indicated by general observation and some experimental work. Whereas in breeding establishments this disease occurs in epizoötics, or in groups of cases, with us it is enzoötic, constantly present, never, however, bursting forth in virulent form with high mortality. Nor is the condition highly contagious.

In an attempt to explain its source I examined over forty varieties of feed and found therein several strains of aspergillus and of mucor; the latter occurs occasionally in the avian air sac. The infective material is therefore constantly present, and it would seem that if it were capable of initiating a fatal disease many more cases should come to our attention. Perhaps these moulds do gain access to the avian air sac and are killed off, or only assume a pathogenic rôle when they are in large numbers or a preëxisting disease assists them. Since our records do not support the idea that a preceding condition must exist for a growth of mould to be successful, and yet pathological and experimental observations suggest that something helps its colonization in the air sac, what are such conditions? Moulds grow on feed and litter in which birds pick; from this it is quite possible for a piece of grain or even inorganic matter laden with spores to be inhaled and lodged in a secondary alveolus near the air sac whence extension into the air spaces could occur. In addition I think it quite conceivable that a whole colony of mould might be inspired with the same result, the mechanical obstruction being sufficient physical damage to incite inflammation. The continuous moist surfaces of the bronchial passages and air sacs afford conditions favorable to the growth of mould and as inflammation is not vigorous, little resistance is presented to its spread.

The mode of operation of these hyphomycetes has usually been assumed to be a mechanical one, local colonization replacing healthy tissue or spreading along surfaces so that function is physically impossible. A support of this idea is to be found in the fact that inflammation, as produced by schizomyces, is trifling or absent; the necrosis that occurs is due to choking off of tissue by the intricately tangled masses of mycelia and blocking off of air or blood supply. The existence of an infiltrating and necrotizing form in some parrots and gallinaceous birds, suggested to me that a toxin might be responsible for some part of mould action. Proof for this speculation was sought by injecting into the pectoral muscles of pigeons an emulsion of a dead mould and a filtered broth culture. Necroses occurred but only to an extent which I interpreted as due to the physical destruction of muscle by the injected material; they were larger with the dead mould than with broth filtrate. I concluded therefore that aspergillus perhaps has no toxin as usually described for bacteria.

TYPES OF MYCOSIS.

Avian mycosis occurs in three different forms, two of which are probably of similar nature and two are frequently combined. The first variety, most often seen in gallinaceous and anserine birds, consists of thickening and opacity of the air sac walls, upon the surface of which either a curd-like pseudocoagulum or a velvety or fluffy mould growth appears. This variety usually begins about the anteroinferior pulmonary stoma on the right side extending thence to the related sac, upward toward the wing and downward to the abdominal spaces. Occasionally the middle thoracocervical space is involved, probably via the opening in the syrinx. Extension takes place by the way of normal passages, but when the growth is dense it also seems to occur by continuity through tissue. This variety may or may not be associated with the second, an infiltrative type of lesion best seen in the lung. Under what seems to be a true picture of mycotic pneumonia, dirty gray consolidated areas will be found around the bronchial space, infiltrating in all directions and without definite boundaries. A similar lesion has been seen also in the liver on rare occasions, but the lung is its usual seat. Judging from microscopic appearances this is a process complicated by the addition of bacteria.

The third variety is nodular or tubercular mycosis, a process of probably more chronic nature since around the isolated lesions connective tissue is perceptible, it being absent or inconspicuous in the other types. The formation of gray or yellow-white nodules from a few millimetres to a centimetre in cross section, is the characteristic production in this variety. Lungs, liver, spleen, intestines and air sacs are involved in about this order. Attempts at explanation of this peculiarity of growth were made in the direction of identification of the species of mould, kind of bird and probably degree of resistance. No conclusions could be drawn since the same variety of mould was found in this as in other types; no bird showed a special susceptibility or resistance to it. It is quite difficult to obtain a culture from nodular mycosis, it being necessary to crush or grind the solid masses before making cultural implants. This variety should always be differentiated from tuberculosis by staining for the organisms.

Histologically studied these three types are not as easily separated as the gross appearances would warrant one to expect. The original mould nodule begins in essentially the same manner in all, a small colonization of mycelia and spores which grow centrifugally, but ever becoming more intricately wound in their first location. As the tissue is invaded, total necrosis takes place, no recognizable cellular architecture being left. When fully formed the mycotic tubercle consists from the centre outward of a necrotic mass, in which spores and mycelia stain indifferently well, surrounded by a dense zone of fully formed mould beyond which mononuclear cells and a few loose fibrils may be found. The circumferential tissue of the viscus supplies a mild congestion and perhaps a moderate connective tissue capsule. Giant cells, as known for tuberculosis, do not appear.

Where the process involves loose tissue like the lung, especially when growing rapidly, the sporulating heads of the mycelia stretch out in advance of the main mass and resemble rays. So too in a rapidly growing nodule radiating mycelia are sometimes seen but never with the regularity of arrangement typical for actinomycosis. Diffuse and irregular mycelial spread is characteristic of the second or infiltrative type of lesion and between the mould stalks one may discover well preserved tissue cells and at times bacterial forms like cocci or bacilli. This picture, suggesting as it does bacterial admixture and more active inflammation, leads one to the conclusion that the morbid process in which it is found does not represent mould disease per se, but a mixed infection. Whether or not the bacterial disease exists first and paves the way for the mould I am unprepared to say; I am inclined to the view that mycosis can start by itself.

INCIDENCE IN AVIAN ORDERS.

Mycosis may be said to occur in all birds although the appended list fails to show cases in a few of the orders included in this study; the sum total of autopsies from missing orders is only 45, so that they may be ignored.

═══════════╤═══════════ │ per cent. Passeres │ 3.7 Picariæ │ 1.2 Psittaci │ 3.9 Striges │ 6.7 Accipitres │ 5.1 Columbæ │ .6 Galli │ 2.7 Fulicariæ │ 8.6 Alectorides│ 2.7 Gaviæ │ 10. Impennes │ 40. Herodiones │ 2. Anseres │ 6. Struthiones│ 9.4 ───────────┴─────────── For meaning of italics see foot note Table 1.

These figures hardly permit conclusions as to relative vulnerability unless the large percentage of cases for the small number of Impennes, Gaviæ and Struthiones be permitted to stand. Judging from orders upon which there are at least one hundred autopsies, owls, ducks and eagles are most likely to suffer with mycosis. The percentages are, however, not very convincing, and it would seem better with these data to conclude for the present that any variety of bird is susceptible to mould. Ostriches have long had the reputation of succumbing to this affection, so that their outstanding position in the list is more easily credited.

It was to be hoped that the various susceptibilities would assist in an explanation of the genesis of mould disease, but the result of the analysis is suggestive only in one direction which can be stated quite briefly. Ostriches, owls, shore and swimming birds have large stomata between the lungs and the lateral air sacs and show a high mould disease incidence. The natural thought is that access of mycelia and spores to the air sacs is facilitated. More comparative data is being assembled upon this point. Water birds are more susceptible to mould than land birds; the percentages based upon cases and totals for orders is 5.4 to 3.7.

The hygiene of mycosis is that of scrupulous cleanliness. Being hampered by incomplete knowledge as to its genesis one can only apply common sense measures. The germs having been found upon all the vegetable feeds, it naturally follows that they cannot be eradicated, but their colonization in large numbers can be prevented by repeated cleansing or sterilization of bins and pans so that no mouldy or musty material is given to the animals. At times of serious outbreaks sterilization by burning all old feed, starting fresh with good material in bins painted or saturated with disinfectant and then deodorized, is the only salvation. Where the blast lamp can be applied, it is the safest procedure. Autoclave sterilization should be thorough if practiced. By constant vigilance we believe that our large exhibition house is protected, but the sanitation of the pond, where many ducks have the disease, can never be so satisfactory.

Mycosis among mammals as an organic pathological entity is certainly a rare condition, indeed almost always to be considered an accidental or secondary one. In so far as human pulmonary disease is concerned it is among the pathological curiosities deserving of individual report. Moulds of several varieties have been found in intestinal ulcers, in cranial sinuses and in the ear, while generalized mycosis from thrush and favus are reported (cases of thrush in kites with fatal outcome has been described on page 168). Cutaneous infestation with mould is quite another matter for ring worms and similar conditions are now believed to be due solely to the penetration by spores and mycelia into the superficial dermis and into hair follicles. Numerous small lesions have been detected on dogs and cats that correspond to the ring worms described for them; to these we have devoted little study, because when discovered the animal is removed, treated or killed to protect others. Doctor Weidman has discovered several varieties of hyphomycetes which he will report upon at a later time. No case of generalized mould disease has been found in mammals, but Doctor Weidman has discovered a hitherto undescribed mould in ulcers and cutaneous abscesses of seals; no extension beyond subcutaneous areolar tissue occurred in these cases.

Botryomycosis, while not strictly belonging to the foregoing group, may be mentioned here because of its nodular tumor-forming superficial growths. The case to be cited certainly belongs to this illy defined group of diseases even if the organism was not isolated. It cannot be accepted as wholly demonstrated that the disease described under this name is always the same or that it has a single cause.

California Hair Seal (Zalophus californianus) ♀ . Had sore spots on side for several months. Ate well up to three days before death but ate something to time of death.

DIAGNOSIS.—Chronic enteritis with acute hemorrhagic exacerbation. Low grade chronic diffuse nephritis. Botryomycosis. General condition poor, subcutaneous fat practically absent. On the left side of the thorax there is a warty and nodular thickening of the skin overlying diffuse and flat thickening of subcutaneous tissues. There are warty, pustular, fistulous communications in four places between surface and deep mass. They are covered over with light crust. On dissection mass is found to be in subcutaneous tissue well outlined and encapsulated and consisting on section of dense, white, firm trabeculæ forming a mesh around yellow, soft areas which can be squeezed out. An adjoining lymph node is much enlarged, dense, tough, resilient, on section showing great connective tissue increase and solid brown medulla. The thyroids are solid, brown, 3. x 2. x .6 cm. and 3.7 × 1.8 x .6 cm. Trachea and bronchi contain pink froth but mucosa is negative. Anterior edges of lungs are distinctly emphysematous. Remainder of lung is uniformly congested and lobules are quite prominent. No consolidations. Bronchial lymph nodes are slightly large, anthracotic and wet. The heart is dilated, filled with mixed clot, muscle firm and deep brown color. The liver surface is smooth, edges sharp, size normal, color dull brown with greenish cast, consistency firm and tough. Section surface is glistening, smooth, moist, lobules indistinct but probably normal. The gall-bladder is full of fluid yellow bile. The common duct is patulous. The spleen is of normal size and shape, capsule opaque gray. The trabeculæ are prominent, the pulp stippled rusty brown. The kidney is of normal size, capsule is smooth, strips easily leaving a smooth purple surface. The organ is firm. The lobules and lobular markings are distinct. The adrenal has a narrow regular brown cortex and gray homogeneous medulla. The stomach contains whole fish. The mucosa shows digestion, congestion and mucus formation. Beginning at the pylorus and extending to the colon the mucosa is swollen and edematous, yellow brown. In the lower part it is quite firm and opaque. In the upper part it is more translucent except where there are diffuse hemorrhagic mottlings of the submucosa. Here and there are shallow erosions but no ulcers. The lymphatics of the mesentery are definitely enlarged, white, pale and very firm. Smear from the surface of the growth in side fails to show any definite yeasts or moulds by Loeffler’s or Gram’s stains. It is largely made up of polynuclear cells with many large mononuclears, many of which are phagocyting polynuclears and nondescript bodies. Cultures failed to grow. Microscopic section of liver shows marked congestion with slight hydropic degeneration of the epithelium. The kidney capsule is not thickened. Interstitial tissue not grossly exaggerated but connective tissue nuclei fairly numerous. Some tufts have decidedly more elongated nuclei than others and connective tissue around the stalk vessels seems hyaline. Capsule for most part not thickened but space contains cells and detritus in many instances. Epithelium of the tubules for the most part swollen, loosened and without nuclei. Some imperfectly formed casts. The intestine shows distinct congestion of the whole mucosa with here and there definite small hemorrhages well out in the villi. Slight round cell increase but no definite fibrosis. In submucosa around vessels connective tissue is hyaline in many places. The tumor on side consists of dense strands of connective tissue forming alveoli of varying size containing an exudate of fibrin and cells, about three-fourths of the latter being mononuclears. Neither connective tissue nor cells are arranged in a characteristic or peculiar manner so the observer is forced to conclude that this is one of the conditions of the group called Botryomycosis.

SECTION XVII—PART 3 THE STREPTOTHRICOSES

The organisms belonging to the genera Streptothrix, Actinomyces, Discomyces and Nocardia as named by various authors have in common the power to produce local chronic inflammation of gradually spreading character and chronic course. Their most conspicuous representative, the ray fungus, is best known as the producer of lumpy jaw in cattle and as an occasional pathogen in man. Other members of the group cause certain lymph-channel disease in domestic animals and pulmonary disease in man. Pathogenic power, it is believed, lies in the ability of these organisms to colonize and irritate, thus producing continuously enlarging tumefactions, no evidence being at hand that any of them produce a toxin either in their surroundings or within their own bodies. Because of their constant irritation, bacterial mixed infection often ensues so that purulent degeneration may occur at the original site of disease and thence may spread via the blood vessels, or by continuity of tissues or, if the mucous membrane of the pharynx be diseased, by the air passages.

The study of the genesis of actinomycosis is by no means a closed one. While it is believed that pastures and fodder carry the organism and that it gains access to the tissues by passing into small wounds that are made by sharp sticks or grain beards, the exact origin of the disease is not understood. The original lesion is certainly trifling and the fully developed one may not be discoverable until it is well under way and causes external deformity. Even when sloughing has occurred, the disease is not very communicable. The method of contraction of lymphatic streptothricosis in cattle is believed to be from other cases via skin wounds or if abrasions be soiled by infective dirt. Just how human beings contract these infections, in the absence of infected cattle is unknown, but for the pulmonary form the route usually followed in tuberculosis is probably taken.

The material of our zoological collection permits few observations of value upon “lumpy jaw” but we have encountered a streptothricosis of kangaroos which may throw some light upon the whole subject and to these cases I shall devote considerable space since no description of it occurs in the literature.

ACTINOMYCOSIS.

This disease has been diagnosed with certainty in two American Tapirs and with reasonable satisfaction in three deer. Two Malayan Tapirs have also had lumpy jaw clinically but the organisms were not found. It is interesting and noteworthy that other zoological collections have observed the disease in this same animal, a fact which suggests the high susceptibility of the tapir to actinomycosis. There are recorded in the protocols a few times sluggish ulcers on the tongue in other ungulates but I am not prepared to label them as actinomycotic since on one occasion smears and sections were studied with great care and nothing found to justify such a diagnosis; nor were there maxillary or pulmonary lesions. Before passing to a discussion of the diagnosis and morbid characters it seems worthy of emphasis that our cases of this disease should appear in one family of Perissodactyla and in one family of Artiodactyla, in the latter not affecting Bovidæ, the family to which domestic cattle belong.

The diagnosis of lumpy jaw depends upon the growth of tumors in the neck and maxillary regions which tend to break down and discharge a thick pus containing “sulphur granules,” little masses of necrotic matter surrounding colonies of the ray fungus. When these conditions are fulfilled, the matter is easily enough settled. This was possible with the tapirs but in the deer the conclusion was not so easily reached and the diagnosis had to be made partly by exclusion. Anatomically the gross and microscopic appearances of lumpy jaw in the tapirs follows the text- book descriptions but our cases in the deer deserve separate comment. Whether or not these differences mean a peculiarity of resistance on the part of the animal or a new variety of streptothrix only further study can settle.

The beginning of the lesion in the deer was in the jaw bone as circumscribed or fusiform swellings appearing on the under surface. Growth usually progressed into the pharyngeal cavity and backward under the ear, but a large tumor stretching down the neck was only observed once. Suppuration and ulceration occurred twice but only once were bacteriological observations possible before death, and then they were negative. The fatal outcome seemed to be due to inanition, possibly because the animal could not eat, for respiratory tract involvement was only present once and then to a trifling degree. At autopsy, actinomyces in ray form were found in one animal only, the diagnosis resting upon histology in the other two. Nor did the degenerated centre of the swelling contain the sulphur granules in any case.

The microscopic characters of the tumors resembled those of giant cell sarcoma and chronic rarefying osteoperiosteitis with areas of round cell infiltration but no granulomata as are occasionally seen in lumpy jaw. I have always felt that a “giant cell sarcoma” with inflammation when seated in the jaw of a lower animal should be looked upon with grave suspicion and be searched diligently for fungi. The organisms could not be found in sections of any of these cases, although present in the pus from a pocket in one. Reference has been made in discussing tumors of the bones in gazelles and opossums to their resemblances to osteofibroma and actinomycosis. The diagnoses were made after long study of the notes and sections. Actinomycosis is usually unilateral while leontiasis ossium is commonly bilateral; the tumors have not broken down nor spread into the neck. In one macerated jaw bone the osteoporosis and hypertrophic periosteitis were comparable to those of the bovine form but the masses were not so extensive as is common for domestic cattle.

Treatment of this disease was attempted in the tapirs but not in the deer; the latter are too nervous to be handled repeatedly with safety to themselves. Following the usual method, potassium iodide was administered in saturated solution on bread, beginning at twenty grains thrice daily and rising in two cases to sixty grains thrice daily. It cannot be stated that any material improvement followed this heavy dosage although in one case the disease was very protracted—some six months, so that it may have modified the progress of the lesion. However, other things were done for the beast so that the effect of any one kind of treatment is difficult to evaluate. It was noted that iodide served to keep the stools quite loose and that its withdrawal was followed by constipation; upon resumption of the drug normal bowel movements appeared. Every soft spot was opened surgically to allow the pus to drain away. A vaccine of Act. bovis was prepared and injected under the hide beginning at 0.5 mg. and rising to 2.5 mg. in five doses after which the animal became so unruly that the injections had to be discontinued. On the whole we are not impressed with the probability of success in the treatment of actinomycosis in tapirs. In the future we propose to try operation and the use of Dakins solution or Dichloramin T.

STREPTOTHRICOSIS OR NOCARDIOSIS OF KANGAROOS.

A fatal disease of Australian marsupials characterized by swellings and ulcerations about the lips, teeth, tongue and cervical tissues is known apparently all over the world by observers of these animals in collections. From commercial shippers of animals, from zoologists and naturalists we have reports that wherever kangaroos and wallabies are exhibited this disease makes its appearance and carries off a considerable percentage of the collection. A fully developed case bears a noteworthy resemblance to lumpy jaw, being called “jaw disease” by non-medical observers. However, it is highly probable that, while the most conspicuous morbid changes occur around the jaw, the agent provocative of the disease is capable of causing different pathological effects and that certain cases of septicemia and gastroenteritis are due to it; Doctor Blair of New York concurs in this opinion. Our study of the problem would inculpate a variety of Nocardia, possibly assisted by certain schizomyces. I have seen in the literature, but unfortunately cannot locate, a reference to an article by a Russian who observed the disease and was convinced that its cause is to be found in a streptothrix[105] obtainable from the necroses in the soft tissues of the jaw, a view entirely in accord with our findings.

The disease is not very communicable because its appearance in a pen need not be followed by secondaries in the mates of the sick beast. It appears chiefly in newly acquired specimens but may develop sporadically in those exhibited a long time and apparently not associated with recent acquisitions. This suggests two or three possibilities. It may be imported by new arrivals, or newcomers may meet a germ to which they are unaccustomed and therefore less resistant, the strange surroundings reducing their opposition to it. Old specimens may have enough resistance to withstand infection entirely or only succumb to large doses. Lastly one comes to the explanation commonly employed for actinomycosis, the presence of the organisms in fodder or pasture, perhaps all the time, but gaining entrance to the animal’s body via wounds made by sharp sticks or the beards of grain.

While circumstantial evidence offers some support to this general idea, it cannot be accepted as proven. I have not made studies of the feed for the purpose of isolation of the streptothrix but cultures from the lips and gingival margin of healthy and infected animals were made for its cultivation. These attempts were fruitless, and without wonder since the germ when isolated from a fully developed case is quite finical in its manner of growth; there are so many kinds of bacterial life that they may easily overgrow the one in quest. So, too, cultures made directly from subcutaneous necrotic areas may not always give a positive growth although smears from the same material may reveal numerous threads under the microscope.

The idea that sharp grasses are responsible for the origin of Kangaroo disease finds a protagonist in Dr. A. S. LeSouef, Director of the Zoological Garden at Sidney, Australia, a gentleman whose judgment carries weight. He writes: “We have found that it is entirely due to getting spear or barley grass in their food; owing to the formation of the mouth, this grass gets wedged in between the teeth and the cheeks, penetrates the flesh and allows the bacteria to get a footing, this in time heaps up on the inside and forms an abscess that bursts exteriorly. Formerly all the Australian Zoos lost animals through this cause, but now, through being very careful not to give any rough spined grasses, we never have the trouble.” Since receiving this letter we have removed straw bedding, and feed only soft alfalfa which is carefully inspected for foreign substances. During this time we have had two cases but the period of observation is too short for final judgment as to the value of feeding grasses without sharp beards and spines. The appearances of cases sporadically without reference to the arrival of new specimens, the low communicability of the disease, its beginning in the jaw in most cases and the prominence of pulmonary and gastric lesions, all seem to support the thought that the virus is received with the fodder or drink. The anatomy of the kangaroo’s buccal cavity favors the collection of material between the gums and cheeks and between the root of the tongue and the molars, while the “hare lip” also affords a crevice in which food particles or foreign bodies may accumulate. These three places seem to be the starting points of most of the cases.

THE COURSE OF THE ATTACK.

Despite careful watching of the exhibition specimens it is often difficult to detect the beginning stages of the disease. Since our last outbreak it has been the practice to examine all kangaroos thrice yearly by catching them, inspecting the buccal membranes, teeth, tongue and nose and by palpating the jugular and sublingual regions. This procedure succeeded in catching one very early case from which the original changes can be described.

The animal appeared in generally good condition but close inspection revealed a “running nose,” a purplish mottling along the gingival margin of one lower jaw below which was a doughy swelling; no internal ulceration had appeared nor was there a visible change in the external contour of the jaw. Within a few days a small fusiform lump appeared along the body of the lower maxilla which spread gradually backward, the nearby soft parts becoming involved very shortly. This particular animal died without ulceration but with evidences of septicemia. Usually at the time that the lump is noticeable the animal loses appetite, becomes inactive and seems depressed; no especial change in the coat need be perceptible although it may be lusterless or at times ruffled. In the cases with great involvement of the cervical tissues, dyspnœa is an early sign but I lay this more to pulmonary disease than to mechanical obstruction of the upper air passages. The loss of appetite is in large part due no doubt to the discomfort of chewing and swallowing in the presence of an inflammatory mass in the neck. The eyes usually remain normal until quite late. No change in the character of the droppings is recorded.

A slightly different course is followed by the cases that have the primary lesion in the “hare lip” and nose; from these the masses along the jaw may be entirely missing. After an initial stage of “running nose” with or without swelling of the upper lips and alæ of the nose, the animal rapidly goes down hill, with dyspnœa, loss of flesh, perhaps loose stools, lusterless eyes and a “dead” coat, a series of signs indicative of a septicemic state not pronounced in the first variety; any form of this infection may however present course and pathology of a septicemic character. If the beast live long enough ulceration may appear on the upper lips or a large area of necrosis between them may be discovered.

There have been in our series two cases, believed to be due to the same virus, which gave a picture of septicemia with pulmonary localization; they will be discussed in detail later but are of interest here because they were not known to be sick until the day before their death. A similar failure to evince signs of sickness is found in the gastrointestinal cases, those with ulcerations in the stomach and perhaps an accompanying catarrhal intestinal inflammation. At most the report will be that the specimen was “off its feed.”

The signs of Kangaroo disease with exception of those applying directly to the nose and jaw are therefore very vague and one is limited to observation of the contour of the head and of the discharge from the nostrils. Because of the indefinite nature of the earliest changes, the duration of the disease cannot be stated with accuracy but from the time that the swellings are perceptible it is not very protracted if no treatment be given. Some cases die in four or five days while others may last up to three weeks and we believe that two of our cases may have been existent longer than that. It is impossible to estimate the duration of the septicemic and gastric forms although the latter, judging by the appearance of the ulcers, are believed to be chronic. We believe that frequent inspection and the precautions as to the character of fodder are the only special hygienic measures indicated.

THE INCIDENCE OF THE DISEASE.

Not the least puzzling character of the disease is the variability of its appearance. There have been groups of cases in our records; for example the following periods showed several while the intervening years lacked them entirely—1905, 1907–8, 1911–2, and 1920–1. The second and fourth outbreaks were definitely related to a new arrival but the records do not show that such was the case for the other two. Mr. Joseph who supplied us with many specimens, tells us that he has had an experience of fifty-four cases in 200 kangaroos and then failed to encounter the disease for years. Perhaps this irregularity of appearance has something to do with the character of food supplied to the animals.

Among seventy deaths of Macropodidæ we have had thirty-three cases of the varieties which I have included in this infection, made up of the following forms: cases limited to the jaws, pharynx and neck, six; cases of this sort with extension to lungs and stomach, ten; cases of this sort with general spread suggesting septicemia, five; gastrointestinal and hepatic, eight; nasal and sinus infection without necrosis in the jaw and with general spread including the lungs, four. The total incidence in Kangaroos is therefore 47 per cent., the necrotizing forms being 30 per cent., the gastrointestinal 11.4 per cent.

THE PATHOLOGY.

The essential features of the necrotizing variety of this disease are similar to those of actinomycosis—an inflammation giving rise to much fibrous tissue overgrowth enclosing pockets of softening, the whole process causing a deforming tumefaction. While primarily developing in the soft parts, this streptothricosis behaves like the ray fungus in that it spreads not only along clefts of tissue but directly through muscles and organs and even bones. Rarefying osteitis with irregular attempt at repair in the form of productive periostitis may be found in both infections. There is however a greater tendency to ulceration and general disease in the marsupial form, variations which seem referable to secondary invaders. When however the massive tumorous, necrotic and ulcerative characters of this streptothrix disease are insignificant or absent, the pathology is modified to the extent of obvious bacterial mixed infection, there then being catarrhal and fibrinous inflammations with degenerations of the viscera.

BACTERIOLOGY.

Since the pathology varies with the bacteriology as seen at this laboratory, it is well to pause at this time in a discussion of the former subject to introduce a brief statement of our findings in the latter, leaving however a full description thereof for later paragraphs. It is relatively easy to find in smears from necrotic masses threads of streptothrix, straight or curved with heavy blunt, but not bulbous, ends and never branched. Similar forms may be found in the necrotic tissue, both free in the softened area and near the margin of the healthy tissue, as irregular colonies growing in a tangled mass from the edge of which radiating threads may be seen. It has not been possible to find a “ray” growth with anything like the regularity so characteristic of the actinomyces nor do the ends present the bulb distinctive of that organism. Branching has been found once only, it being very uncommon in tissues although beautifully developed in cultures. While not especially sought, cocci and bacilli have not been seen, by Gram stains, within or immediately around the streptothrix colonies. Surrounding the mycelial groups is a necrotic zone about which is a loose connective tissue full of mononuclears and a few polynuclears. The centre of the colony is made up of tangled mycelial threads and necrotic debris. From uncontaminated necrotizing masses we have obtained cultures three times out of very many attempts.

When ulceration or suppurative softening has taken place mixed infection with lower bacterial forms naturally occurs and the whole picture changes. Pulmonary complications, with or without evident ulceration in the pharynx, also admit other bacteria. Streptothrical forms are often easy to detect in stained smears and in cultures but the very extensive bacterial flora soon overgrows them and attempts at isolation are fruitless. Under the best of conditions their colonial development is slow and tiny until they are well accustomed to saprophytic life. The complicating bacteria that have been identified are Streptococcus pyogenes, pneumococcus, pyocyaneus and colon bacilli to which may be added moulds of the Aspergillus group but these all have been variable in numbers and appearance; the most frequent and therefore probably most important secondary invader is an organism we have not been able to identify.

This germ, a tiny, Gram-negative, non-motile rod with a tendency to bipolar staining, will appear in smears from an ulcerated necrotic mass, from the nasopharyngeal exudate and from pulmonary lesions and may develop upon agar or blood media for the first generation but refuses to grow after that despite our best efforts. At present we hope to have it by growing material a long time in blood broth. Microscopical examination has not revealed it in the tumor-forming variety but on one occasion it was found in the lung; its Gram-negative characters make its detection in tissue very difficult. For obvious reasons the importance of this germ cannot be estimated but it seems from the frequency with which it is encountered that in some manner the streptothrix may be aided by this unidentified bacillus especially in the ulcerative and septicemic varieties of Kangaroo disease.

In so far as the diagnosis of this infection in the uncomplicated form, like lumpy jaw, is concerned the finding of streptothrix by stain seems adequate and its presence in the gastric ulcers and hepatic necroses identifies this variety. The most difficult question to decide is the identity of the cases without one or the other of these distinctive features but with mucocatarrhal or purulent nasosinusitis followed by pneumonia or septicemia, and of cases of primary pulmonary involvement. These instances have been diagnosed as belonging to the same category because of the presence of streptothrix in the exudate at the site of the important lesions and because the type of lesion is similar to that which complicates accepted characteristic cases. Inability to reproduce experimentally any of these infections limits our criteria for judgment in the matter. I am inclined to view these septicemic cases therefore as initiated by the streptothrix, growing in the nose and sinuses or inhaled into the lungs, aided by lower bacteria, an unidentified Gram- negative bacillus being the most important.

Having reviewed briefly the bacteriology of Kangaroo disease, its strict pathology may be discussed more definitely in terms of the type of infection. Reference has already been made to the method of pathogenesis employed by the streptothrix and its congeners. Whether or not a toxin is elaborated by these organisms is an unsettled question, especially for the marsupial variety because as yet it cannot be made to produce lesions in other animals. It is highly probable that all these organisms find colonization easy in the animal’s body once they get well settled, and that they act mechanically, producing necroses by their growth and by attracting leucocytes in such large numbers that digestion of devitalized tissue occurs, to an extent that resembles pus. The inflammatory tissue is not distinctive, except in so far that fibrosis enclosing pus pockets is peculiar to it. In softer tissue, like the liver, fibrosis is not so prominent, whereas diffuse and irregular spread is more pronounced. At the margin with the healthy tissue, reactive, that is resistant, inflammation is no more in evidence than within the tumor growth itself and as a matter of fact the tissues do not seem to put up a good fight against the spread of the inflammation.

Histologically, aside from the finding of the streptothrix colonies, there is nothing distinctive, the peculiar expressions of the disease being most manifest in their gross characters. For the purpose of describing the pathological features, the cases have been divided into the necrotizing form around the jaw, a similar process in the stomach and liver, necrotic cervical cases followed by lung involvement, the nasal variety upon which pneumonia succeeds and a septicemic form arising from any locality. Illustrative cases will be cited for each of these forms, a method of presenting the pathology thought to be superior to a general discussion.

The first illustrative case is one localized in the tongue and pharyngeal wall; it is quoted because of its strict localization.

Great Gray Kangaroo (Macropus giganteus). Sick four days, tongue swollen so he could not eat.

DIAGNOSIS.—Necrotizing process of floor of mouth and pharyngeal wall, dilatation of heart, passive congestion of liver, acute diffuse nephritis, inflammatory edema of lungs. General condition good. Jaws and teeth negative. Floor of mouth firm in places, boggy in others, but generally infiltrated. Anterior two-thirds of tongue purple and green as if gangrenous. Root of tongue and adjacent floor of mouth yellowish, wet as if from recent coagulation necrosis. In the muscle of the tongue a line of demarkation is shown at end of hemorrhagic zone behind which muscle is fairly good. Sides of pharynx, palate, tonsillar region show superficial pseudomembranous inflammation and yellowish gray, wet infiltration of muscles. Epiglottis purple and swollen to twice normal size. Laryngeal mucosa deeply injected, swollen and covered with tenacious gray mucus. Trachea and bronchi deeply injected and slimy. The lungs are uniformly deeply injected and along course of bronchi in lower lobe, lung tissue is distinctly more boggy than elsewhere. On section this area is slightly paler and more granular than the rest of the lung. Lung is everywhere slightly edematous. The bronchial lymphatics are swollen, pale pink and edematous. The heart is dilated acutely judging from the left ventricle wall which is nowhere over 1 cm. The liver is slightly enlarged, surface smooth, edges sharp, color deep purple, section surface very bloody. The spleen is soft, capsule smooth, pulp homogeneous purple, follicles not visible, trabeculæ normal. The kidney is slightly large, capsule smooth, strips easily leaving purple surface. The cut surface swells out, has irregular striæ, congested lines between, glomeruli visible and large. Smear from centre of tongue muscle shows staphylococci in some places in colonies, and long, slender rods.

The following case is one of gastric, intestinal and hepatic involvement, apparently primary, the last possibly arising by a hematogenic or lymphogenic route. Judging by the slides of the gastric wall the process started deeply and broke through the mucosa. This cannot be asserted definitely since kangaroos are susceptible to gastritis so that the streptothrix may have been implanted upon a preëxisting inflammation.

Black Wallaby (Macropus ualabatus). Congestion and edema of lungs, abscess of stomach and liver (streptothrix), ulcerative enteritis, necroses of spleen and lymph nodes, congestion of kidney. The animal is thin, hair loose. The mouth and nose seem to be absolutely healthy. The weight of the lungs is increased by congestion, they are solid, homogeneously red, with no air in any lobe except at edges. A piece cut from centre of lung sinks quickly in water. The trachea contains frothy blood. The heart muscle is soft, flabby and lustreless, chambers dilated, valves normal. The liver is of normal size, firm, smooth surface, sharp edges, red-brown color. The small sublobe of the liver which lies between the gall-bladder and the pyloric end of the stomach shows a large abscess 4 × 3 cm., apparently starting in the substance of the liver via the bile ducts. This is certainly not extension from the stomach abscess as the liver lying against the stomach is nearly normal. The abscess is sharply circumscribed with a zone of congestion about it. Aside from congestion the rest of the liver is normal. The common bile duct is large and freely patulous. The capsule of the spleen is thick, consistency firm, pulp deep red, irregularly mottled by pale areas of necrosis. The kidney capsule is smooth, strips easily leaving a smooth, brown surface. The organ is firm. The section surface is glistening, the cortex wide and congested, the medulla normal. The adrenal medulla is deep purple with congested line between it and the pale cortex. Most of the gastric mucosa seems good. At about the middle of the lesser curvature is an ulcer about 4 cm. across. The shelving edges are covered with apparently normal mucosa. The centre contains bloody pus and nodular masses of the submucosa extending in finger-like projections through the pus. At one point on the greater curvature there is a small pocket of pus on the serous side which has not ulcerated through to the mucosa nor broken into the peritoneum. The large intestine is deep red and the follicles appear from the serosa as darker areas. On the mucus side the follicles have ulcerated, having a necrotic centre and shelving edges. The rest of the mucosa in the neighborhood is swollen and deep red. The colon mucosa is dry and the contents are hard, dry “baked” feces. The main pancreatic duct and the common bile duct form a thick, firm, cord-like mass running through the pancreas and enlarging the papilla of Vater into the duodenum. All abdominal lymph nodes are large, firm and on section mottled with red areas. Culture from the liver abscess failed to grow. Histological section of lung shows moderate congestion, collapse of alveoli or their filling by edema, epithelial and small round cells. There seems to be no fibrin. This could be an early stage of pneumonia. Bronchi are for the most part negative, little peribronchial round cell infiltration. No streptothrix in two areas of round cell infiltration or in bronchi. Liver section shows a part of the liver destroyed by hemorrhage, degeneration and necrosis. The abscess consists of necrotic matter surrounded by a zone of about equal numbers of mono- and polynuclears and around this a loose fibrocellular zone. Streptothrix abundant in the abscess. Lymph nodes show chronic inflammation and coagulation necrosis without abscess formation. No streptothrix in areas of necrosis. Kidney is very much congested with little or no damage to secreting parts. Spleen shows enormous congestion, moderate amount of pigmentation, connective tissue both trabeculæ and through pulp increased, no areas of necrosis. In the stomach the mucous membrane shows slight cellular activity and some degeneration—this amounts to a true catarrhal gastritis especially in view of the submucous cellular infiltration and the granulation tissue which has separated the muscularis and involved most of the connective tissue. The edge of the necrotic part begins abruptly, the mass of necrosis lying on an active fibrocellular submucous and muscular layer. Streptothrix can be seen at edge and in necrosis.

Pneumonia originating either by inhalation or via the blood stream, is illustrated in two stages by the succeeding cases. The first history illustrates the pulmonary involvement as secondary to necrotic streptothricosis around the jaw and tongue while the second animal’s disease began in the nose and related sinuses. These two protocols provide material for a discussion of two phases of the subject.

The character of the early bronchopneumonia in the first is peribronchial, and there is distinct indication of a generalized process suggesting a hematogenic origin, whereas there is but one area of bronchopneumonia in the second—a necrotizing lesion beginning in the bronchus. Streptothrices are rare in the first case but reasonably easy to find in the second. This latter is one of the cases which seem to support the idea that nasosinusitis may have a streptothrix as its basis in the absence of the usual picture of necrotizing “lumpy jaw.” These cases also indicate that pneumonia may originate either by inhalation or by the blood stream, and that perhaps the hepatic lesion may have the latter origin. There have been two instances of necrotizing periarthritis, in one of which the threads could be found. This also suggests that spread through the blood stream can occur, possibly in this respect to places where previous injury prepares for the reception of the organisms.

Thigh striped Wallaby (Macropus thetidis). Streptothricosis of soft tissues of jaw. Early bronchopneumonia. Acute fermentative gastritis. Acute general infiltrative enteritis. Cloudy swelling of myocardium. The general condition of coat and of nutrition is good. The jaws are wide and the maxillocervical region full, both due to an indurative inflammation of the gums, tongue, floor of mouth and upper cervical tissues. At either side of the tongue and running around body of maxilla both sides, the inflammatory tissue becomes softer and there is an area about one inch long where it is soft, gray and contains yellow gray bodies in a grumous matrix. The teeth seem sound as do the external buccal tissues. The nasopharynx is free from induration. The bone on the left side shows a periosteitis with involvement of the superficial layers of bone, while on the right side the periosteum is swollen and opaque but the bone is free. The thyroid is imbedded in the edematous infiltration of the lower cervical tissues. The pleuræ are free of fluid and adhesions. Lungs are collapsed, uniformly pink somewhat emphysematous at places but give the impression of being lumpy. On palpation numerous nodular areas are detected. These prove to be peribronchial areas of gray-red solidity which swell out on section. The bronchus contains a gray and bloody thick mucoid matter. There is distention of the mesenteric vessels especially near the enteric insertion. The liver surface is smooth, edges very sharp, consistency firm, tough, resilient, color deep red, the section surface is glistening, moist, opaque, architecture probably normal. The gall-bladder is distended with viscid green bile; the common duct is patulous. The spleen has a rough, thin capsule, consistency tough and resilient, the section surface is mottled red with purple points; on section two small, pale objects seem to be squeezed out. The kidney capsule is smooth, strips easily leaving a smooth, deep red surface, the consistency is soft, the cortex is deep red, then a purple line between it and the red medulla, striæ invisible. The stomach contains frothy grayish mush. The mucosa is finely mammillated, deep pink until the last third when it becomes deep red, deeply injected and somewhat thickened. The pylorus is closed. Externally the gut is congested, in places translucent but for most part seems thickened by reddish swelling of both external layers and mucosa. The mucosa is granular or pebbly with here and there a small bloody suffusion. The histological section of lung shows alveoli open, septa relatively thin but somewhat congested, bronchi mostly open and connective tissue not increased. Some few bronchi, especially the larger, show a slight catarrhal bronchitis but mostly an infiltrative peribronchitis. The nearby veins and arteries show the most striking change, there being in nearly all of them a distinct thrombosis without circumferential pneumonia. In one place a distinct peribronchial pneumonitis was found. The kidney shows very marked congestion of all parts, causing compression, cloudiness and granularity of the epithelium. Glomeruli and connective tissue about normal. The intestinal serosa is negative save for congestion. Submucosa is densely infiltrated with mononuclears, some in definite groups. Section does not show areas mentioned in notes but these could be accumulations of cells with congestion. No streptothrix forms. Section from the infectious focus of face consists of active granulation tissue, densely injected and filled with mononuclears of two types, one the lymphoid cell, the other of the young connective tissue type. Areas of grouping like abscesses are seen and some necroses. Streptothrix in small numbers in the cellular collections.

Nail tailed Wallaby (Macropus unguifer). Kangaroo disease of nasal region. Necrotizing bronchopneumonia (Aspergillus fumigatus and Micrococcus albus). Acute diffuse splenitis. Congestion of liver and kidney. The general condition of coat and nutrition is good. The face is wide just below the eyes. About the “hare lip” and the nose the soft tissues are soft, gray, necrotic. All the internal nasal tissues seem swollen, gray-red. There is subcutaneous edema, bloody in places, around the right face, eye and jugular angle. Tissues of nasopharynx swollen, deeply injected and covered by a thick mucus. Pharyngeal and buccal cavities negative. Tonsillar areas pink and flat. Larynx and trachea slightly swollen but pale on mucosa. Salivary glands and cervical glands normal in size and pale pink. Pleuræ pale and empty. Lungs swollen out uniformly, quite cottony except at lower right base where there is a nodule about 3 × 5 cm. firm and doughy. On section it is found to be a peribronchial consolidation of pale reddish gray color and indefinite outline. The bronchus itself is deeply congested and contains a grumous mass. The peribronchial lymph nodes are small, soft, pink, homogeneous. The heart is negative. The liver is large, surface smooth, edges sharp, color deep purple, consistency soft. Section surface is glistening, smooth, moist, very dark purple with obscure markings. The gall-bladder contains fluid brown bile; common duct is patulous. The spleen is soft, tough, capsule pebbly, section surface is mottled, light and deep pink, follicles and trabeculæ not distinguished. The kidney capsule is smooth, strips easily leaving a smooth purple surface, section surface is glistening, deeply congested, striæ obscure but seem normal, glomeruli not visible, organ is soft. The gums and teeth are not involved in the mycosis. The stomach contains mushy digesting food. The mucosa is mottled pink, soft, digesting, at lower half submucosa is deep pink, a few small ecchymoses. From pylorus to ileum, serosa is deeply injected, edematous, mucosa swollen and edematous, deep pink, loosened in places, but translucent. Below this the mucous membrane becomes smooth, flat, pink-yellow. Lower ileum and colon contain rather firm fecal balls. Follicles nowhere prominent. The pancreas is small, soft, yellow pink. The follicles of the mesentery are small, pink gray and homogeneous. Smears from the bronchopneumonia show a threadlike Gram- positive form and a few Gram-negative rods. Cultures from lung show Aspergillus fumigatus and Micrococcus albus. Nose too foul for culture. Histological section of lung shows the alveoli mostly open but the septa widened by congestion. Blood vessels are open and contain recent clots; one vessel near lesion below is thrombotic. The two large bronchi in section show catarrhal bronchitis and infiltrative peribronchitis of which the latter is more severe and advanced. Beside the larger is a necrotizing pneumonitis from which nearly all the architecture has disappeared. The exudate is chiefly mononuclear around the edges; centre no cellular identity. Another mononuclear process not connected with bronchus in section is found with an early necrosis. Streptothrix strands may be found in the bronchial exudate and near the margin of the necrotic patch. They do not grow in colonies however. The spleen shows general congestion without pigmentation. Follicles large, solidly lymphoid. Connective tissue about normal. The kidneys show marked congestion everywhere. Capsule and intrarenal fibrous tissues about normal. Very severe congestion which seems to have caused compression and granularity of the epithelium.

The last case, judging by stained smears, is one of pure nasosinusitis from streptococci and streptothrices. Cultures were not tried because of the enormous bacterial flora.

Robust Kangaroo (Macropus robustus). Acute purulent ethmoiditis. General acute purulent anterior cranial sinusitis. Acute necrotizing glossitis and pharyngitis. Cloudy swelling of kidney. The face seems a little full and the subcutaneous tissues slightly edematous. The nasopharynx contains a thick tenacious mucopus. Ethmoid and frontal sinuses and turbinate spaces contain a thick purulent matter, the mucosa being densely injected, swollen and velvety. Pharyngeal wall and right half of posterior half of tongue are involved in a dull brown and necrotizing process, quite sharply outlined by zone of congestion. This process is comparable to the necrotizing gingivitis seen in front of jaw in kangaroos. Larynx, trachea and lungs seem uninvolved save for slight generalized congestion. Cervical lymph nodes especially those about the larynx are definitely enlarged, soft, moist and brown. Mediastinal nodes slightly enlarged, soft and pink. The heart is negative. Liver normal. Spleen is soft, homogeneous dull red. The capsule of the kidney is smooth, strips easily leaving a purple surface. The glistening section surface swells slightly, vasa recta are congested, striæ wide and pale, glomeruli not visible; consistency is resilient. The mouth and teeth are not involved in the process mentioned above. There is a small quantity of properly digesting food in the stomach. Stomach and intestines negative. Brain not involved. No extension from anterior cranial sinusitis. Smears from the mucopus confirm the gross appearance and contain short chains of streptococci and large diplococci. Smear from cut surface of tongue shows innumerable small bacilli and diplococci but especially mycelia with rather heavy clubbed ends but without true branching. One group was found arranged like ray fungus. It is noteworthy that there is no aspiration pneumonia and very slight evidences of septicemia.

BIOLOGY OF N. MACROPODIDARUM.

The original discovery of the streptothrical forms was made in stained smears from necrotizing lesions. They were considered as secondary invaders until repeated observations of a similar character aroused the suspicion that they stood in some important relationship to the lesion. Early attempts at their cultivation were made under anaerobic precautions, a method now known to be almost certainly doomed to failure because a strain long under cultivation requires two to three weeks to make an appreciable growth in the absence of air. Finally in 1911 a successful cultivation occurred by searing the surface of an unopened mass in a freshly dead animal and planting bits of the interior upon aerobic blood serum plates. Colonies grew after three or four days and from them the first strain was started. It grew for several generations, long enough for the preparation of a vaccine, which will be described later, when by mischance it was lost. In 1920 another successful cultivation occurred, this time by incising a mass in the soft sublingual tissue and plating in the same manner; upon this culture the biology is described. Smear preparations offer no more than has already been mentioned.

Colonies develop upon blood serum plates as opaque, pale yellow, circular, discrete masses with a slightly depressed uneven centre, but without umbilication. They remain smooth and slightly glistening for several days, then become slightly wrinkled and twisted with a more definitely raised edge and a tendency to an uneven sinking in of the centre. Transfers to agar slants show wrinkled continuous opaque, dull yellow, sharply outlined growths which soon wrinkle, fold, and twist like certain tubercle bacillus cultures. Spreading occurs, but is slow after forty-eight hours. As medium becomes drier it is possible to see a thin, colorless, wrinkled film stretching out from the main growth. If the medium be dry or old or if only a small portion of seed material be used and this scattered over the surface of the slant, discrete colonies arise. These are circular, seldom exceeding 3 mm., dirty yellow-white, distinctly umbilicated and without clear film of spreading around them.

In nearly all quite old cultures, a white chalky efflorescence appears over the surface.

The morphology of the young agar culture is chiefly mycelial or filamentous, whereas from a culture on dried media and those showing efflorescence, the organisms are short, heavy, deeply granular and of the mycobacterial type.

Glycerine agar.—Corresponds to agar.

Blood agar.—Similar to agar but much less luxuriant.

Blood serum.—Limited dirty yellow, raised, dull, wrinkled and granular, tightly adherent to the medium.

Potato.—Spreading, dirty yellow, much wrinkled, friable, tightly adherent.

Gelatine.—Limited growth as a wrinkled, tough scum only on surface.

Litmus milk.—No change for six days, then beginning slight alkalinity which increases very little, shows digestion of the caseinogen, slight, thin filmy growth on surface.

On media such as litmus lactose agar and old Endo it grows slowly on surface and assumes the color of the medium.

Broth.—Only surface growth appearing during early generations, after 3–6 days as a wrinkled, pale yellow scum very much like the tubercle bacillus growth; later generations grow perceptibly in one to three days. Medium perfectly clear. If a large mass be seeded into neutral broth there is a perceptible increase in the growth after ten days. The medium thereafter tends to a faint turbidity. Titration of broth growth after twelve days shows alkalinity requiring 0.3 cc. decinormal acid, while the control tube incubated same length of time showed an acidity requiring 0.57 cc. of decinormal NaOH.

On the following sugars there is a slight surface growth without change in the color, Andrade indicator—dextrose, lactose, saccharose, maltose, mannite, dextrin, galactose, salicin.

Cultures observed on two per cent. neutral agar.

A.—Stained by Loeffler’s stain.

Twenty-four hours.—Shows threads growing out from a central amorphous mass, but the whole does not retain the regularity or parallelism of actinomyces. Threads are poorly stained and rather disconnected but not jointed. Small number of metachromatic bodies apparently in older individuals, certainly in the better formed ones. No intercalary spores, unless the metachromatic bodies be so considered. Individual threads measure from one-third to one micron in width. Metachromatic bodies measure on the average one micron.

The threads in the forty-eight hour preparation seem distinctly wider, up to one micron and possibly become heavier toward the end, but do not have a distinct bulbous extremity.

In three days the threads are much longer, show distinct branching and a tendency to transverse segmentation. More than one metachromatic body may be present in one segment.

Four days.—Still coarser, short segments have appeared separately. Metachromatic body is coarser and blacker; some of the masses have gone to pieces and show only a diffusely staining smudge of metachromatic bodies. The short segments show a tendency to grow out into threads.

Fifth day.—Condition is much the same plus many young, delicate, poorly staining threads.

Sixth day.—The same but all seem to be somewhat wider and diffusely staining.

Seventh day.—More diffuse staining and decidedly fewer metachromatic bodies.

A.—Stained by Gram’s stain.

Twenty-four hours.—All forms are light purplish. The threads stain much more clearly than by Loeffler’s and show distinct transverse segmentation of rather uniformly long bacilliform shape. Metachromatic bodies not so distinct but seem larger where found. Coarser threads have swellings in some of the areas which are not segmented and this type seems to have more branching and metachromatic bodies; in other words it would seem that this is a form that reproduces by budding or intercalary spore formation.

Forty-eight hours.—Much the same, more long threads with transverse division, somewhat more delicate, generally fewer coarse threads with swellings and spores. Still pale purple and not distinctly Gram- positive.

Three days.—Condition much the same.

Four days.—Two forms present—definitely Gram-negative delicate slender threads, nearly Gram-positive, and heavier, curved and twisted long bacillary forms, some streptococcoid threads and a few bulbous short threads. Very few metachromatic bodies.

Five days.—Condition much the same except that the delicate threads are inconspicuous and the darker purple bacilli have increased. Metachromatic bodies increased as have swellings in coarser threads.

Six days.—Much the same but for the appearance of young, delicate definitely Gram-negative threads. There are fewer metachromatic bodies and internal spores.

Seven days.—The same.

B.—Grown on Loeffler’s blood serum.—Loeffler’s stain.

Twenty-four hours.—Delicate, poorly stained short threads, few tiny metachromatic bodies.

Two days.—Not well stained, relatively short threads show numerous metachromatic bodies varying from exceedingly tiny dots to coarse granules wider than the thread. These may be numerous in the same segment and form a row from six to ten. Many short bacillary forms.

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