Disease in captive wild mammals and birds

Part 26

Chapter 263,582 wordsPublic domain

The most decided example of the lobulated kidney is to be found in the class Aves, wherein the organ consists of two or three large lobes lying in concavities of the sacrum, each lobe being made up of tiny lobules. The latter appear to the unaided eye as fairly distinct divisions whether viewed on the exterior or by cross section. There is a cortex and a medulla to each, the separation being clear in a large specimen, vague in a small one. These lobulations are quite well observed when the kidney is full of urates, a common finding in birds. Magnification of the avian kidney reveals an apparently simpler tubular arrangement than is found for mammals[33][34], yet the relation of vascular plexuses and secreting tubules remains similar.

From the standpoint of comparative pathology attention can be drawn to the glomerulus, to the interstitial tissue, and to the character of the epithelium. The tuft of intricately wound capillaries called the glomerulus has always been viewed as the part of the secretory unit chiefly concerned in urine production whether one accept the older idea that it excretes only fluid or the modern belief of many observers that all parts of the urine go out through it. In the mammal the tuft is closely wound, is surrounded by a distinct space and a limiting membrane of appreciable width called Bowman’s capsule; all this so-called Malpighian body has a breadth varying from 120 to 300 micra. There is however great variation in the size of this body when seen in the peripheral and deeper zones of the same organ, amounting at times to seventy per cent. of the diameter. The capillary congeries forming the avian tuft is by no means so delicate and one can see individual capillaries with more ease. It may be impossible to discover a space between the tuft and its exceedingly delicate capsule, the latter being usually applied closely to the vascular corpuscle. The whole breadth varies from 70 to 140 micra with an average of 110. There is more uniformity in size than in the mammalian organ.

Supporting tissues between the tubules seem less definitely nuclear in the bird than in the mammal, at least in so far as connective tissue is concerned, there being in the former only a few groups of mononuclears to be seen in the cortex. Perivascular tissues are reasonably rich. The epithelium of proximal and distal tubules is not easily fixed by our customary laboratory techniques, the best results being obtained by Zenker’s fluid. As seen in a routine specimen of a normal organ it is vacuolated or very palely stained. The individual cells stand out clearly and many present a pointed end to the tubular lumen.

KIDNEY WEIGHTS.

According to the work of Mangan[35] and of Alezais[36], the bird has an average kidney-to-body weight of 6.9 grams per kilo while man has a ratio of 4.3 grams, dog 5.9 grams and guinea-pig 8.5 grams. The first author would show that the fish-eating birds have the heaviest and vegetarian birds the lightest organ. Our own figures are limited to the weights of apparently normal organs in thirty-one mammals and five birds; they are as follows:

│per kilo of body weight Primates (5)│ 7.7 grams│ Carnivora (6)│ 7.6 grams│ Rodentia (2)│ 15. grams│ Hyracoidea (1)│ 7.5 grams│ Ungulata (9)│ 3.5 grams│ Edentata (1)│ 5.6 grams│ Marsupialia (7)│ 7.6 grams│ Monotremata (1)│ 11.2 grams│ │ │Average 7. Steganopodes (1)│ 9.1 grams│ Anseres (1)│ 3.9 grams│ Struthiones (3)│ 7. grams│ │ │Average 6.7 ────────────────┴───────────┴───────────

This to be sure is not a very exhaustive list but is the result of our routine observations and subject to all limitations of such work. Grossly diseased organs are naturally excluded. More avian weights are not available because of the difficulty of removing the organ from its bed, in a manner assuring us of completeness. I am inclined to view our mammalian records as fairly representative. Figures to be found in text- books of human and veterinary anatomy correspond to those given by the authors just quoted and in our own list. The values for rodents, hyraces, edentates and monotremes may be modified by more figures.

There is however one point which does not appear in the list. Small animals have relatively larger kidneys than large animals. This is perhaps most strikingly illustrated among the ungulates which have the lowest value quoted. A small deer had a kidney-to-body index of 5.9 grams per kilo while a camel had only 2.8. Judging by the work of Magnan the avian kidney should be larger than the mammalian, a conclusion with which I am inclined to coincide, even though the weights cited do not bear this out.

In so far as the function and chemistry of the kidney and its excretion are concerned this study can supply little. The general metabolism is known for most animals, it being dependent upon diet and gastrointestinal discharge of excrement. What lessons can be learned will be discussed by Dr. Corson-White in the section on diet. Our observations upon the ability of the kidney to excrete normal urine are limited to the examination of vesical contents at death or of the occasional specimen obtained in cages in the quarantine room. Renal disease was formerly considered of little or no importance in veterinary medicine or at least was studied only as a specific separate and occasional occurrence. Kitt[37] systematized the knowledge of the subject at the time he wrote but it remained for Hutyra and Marek in their text-book to emphasize its general importance and to clarify diagnostic measures. Breindl[38] pointed out that nephritis occurs more often in acute general diseases, notably the specific infections, than was customarily thought, thus placing the subject for the lower animal where it is in human medicine.

Renal disease is quite common among wild animals albeit there are certain orders in which the lesions are less conspicuous. Clinical diagnoses of nephritis, and this is the only diagnosis attempted, have been made on monkeys by examination of urine which shows the same characters as in the human disease. In ungulates more attention is to be placed upon the cellular contents of the urine since renal epithelium is apparently shed more readily and casts less often formed. Signs and symptoms of renal disease are limited to edema and uremia; cases of the latter are rare enough to discuss separately at the proper place.

ABSENCE OF ABNORMALITIES.

Abnormalities of size, shape and position of the kidney are frequently reported in literature of veterinary medicine and aplasia has been described. Our material has failed to present cases of horse-shoe kidney well known to occur in horses, cows, sheep and dogs. Wandering kidneys are also known but have not been seen in our wild animals. Shall these abnormalities be considered as due to degenerative changes in cross bred animals or as the result of the strain of domestication? To such a speculative question our material affords no answer.

HYPERTROPHY.

That the kidney has the power of hypertrophy in a compensatory manner is illustrated by two cases. A Japanese Macaque (_Macacus fuscatus_) ♂ apparently had suffered with a unilateral nephritis which had gone into a contracted stage. At all events much functionating tissue was gone, the organ irregular and small, being half or less of the size of the other organ which was larger than is considered normal for the species. Histologically the large organ was practically normal. A common opossum (_Didelphys virginiana_) suffered with a complete suppurative nephritis of the right side which completely destroyed the organ; the origin of this is not clear as no ascending disease could be determined and no certain acute infection had existed; decomposition precluded satisfactory bacteriology. The left kidney was nearly twice its normal size and involved in an early diffuse nephritis, with miliary abscesses, in which the glomeruli did not participate. There were in these sections evidences of regeneration, swollen reduplicated epithelial coverings presenting a picture similar to those seen in so-called chronic nephritis secondary to interstitial change.

INFILTRATIONS.

Pathological infiltrations of the renal structures are exceedingly uncommon. Early in our experience we were often perplexed at the appearance of certain organs, notably in carnivores and marsupials to which we were inclined to apply the term fat infiltration. However the absence of reasons for considering this picture pathological seemed sufficient cause to ignore the finding, and later Pfeiffer[39] called attention to the apparent inability of these kidneys to emulsify fat or at least to combine it in an invisible form, an ability possessed by the herbivorous organ. A monkey and a passerine bird only showed sufficient fat visible in the renal epithelium to warrant a denomination of fatty infiltration; these were both obese specimens. Amyloid infiltration occurred in four mammals and six birds, being a sequel of its usual causes, tuberculosis, chronic suppuration and osseous system disease. It is perhaps well to emphasize the fact that every organ the seat of amyloid deposit need not be enlarged. This teaching is common but I have seen human cases without enlargement and only two of the ten cases in these animals are noted as bulkier than normal.

DEGENERATIONS.

Degenerations represent the reaction of the kidney to toxic or infectious agents and might be considered as indicating the vulnerability of the organ. Their incidence does not coincide with that of nephritis as we shall see later. Any discussion of degenerative phenomena, and especially in the kidney, should be limited by a definition of what they are believed to be and their separation from inflammations. Degenerations are swellings, granularities, vacuolizations or infiltrations of tubular epithelium, changes which destroy the outline and internal structure, perhaps including the nucleus. No changes of the glomerular tuft or interstitial tissue are necessary for this conception since when these occur the picture becomes that of nephritis. In border-line cases it is safer to include the case under the latter heading since then the physiology is apt to be disturbed, albumen and casts appearing in the urine. Degenerations appear in various pathological states—toxemia, infection, prolonged congestion and others. The first named cause seems to be the most important in our records and the seat of the toxine production seems to be the intestine. Enteritis stands very high in the list of accompanying factors, especially in Carnivora, Primates and in Aves. Perhaps the most instructive cases are to be found in the Ungulata with toxic duodenitis. The kidney in these animals is deep red or purple, with a spanned capsule. The section surface bulges slightly, is of an opaque, dull purple color and shows a congested zone between cortex and medulla. Tubular epithelium may be found, under the microscope, sufficiently swollen to fill the lumina, in places being like ground glass, in others distinctly vacuolated. It cannot be stated absolutely which part of the tubule is usually affected; it seems more often the distal convoluted portions than other subdivisions. Glomeruli may be full of blood but there is no increase in cells nor any material in the capsular space. The urine is dark and may or may not show albumen. The kidney of kangaroos with streptothricosis is similar to the picture just given.

Mammals have shown a percentage incidence of renal degenerations of 4.8 per cent. while Aves show only 3. per cent. In order of incidence the carnivores head the list followed by Lemures, Accipitres, Rodentia, Primates and Marsupialia; the remaining groups show but a few cases. A form of degeneration is sometimes seen in the avian kidney the seat of excess urate collections, especially when these are arranged as so- called uratic infarcts. This last term has been applied to the streaking and mottling of human kidneys by the accumulations of these salts in a manner believed by some to be related to the formation of uratic calculi. The epithelium of such a kidney may show granularity and collections of acids and salts have been found in the lumina. In the bird on the other hand one frequently sees masses of urates in one lobule, or a part thereof, arranged to simulate closely the common infarct shape. Secretory cells in the affected area are hydropic, with absent or dislocated nucleus, or again they present a densely basic staining protoplasm. This form of kidney is well seen in what has been called here an uratic serositis, a coating of all somatic free membranes with a thin, white, granular film. We have tried with many techniques to preserve one of these cases but the deposit either dissolves or the whole specimen becomes opaque. Although the term infarct is applied to these lesions, they are of course not infarcts in the customary use of the term. True infarcts are exceedingly uncommon and, with the exception of one case which became infected and suppurated, have been negligible in our material.

HEMORRHAGES.

Hemorrhages into the kidney are found in acute infections and certain diseases like leucemia; they are of little moment. Perirenal hemorrhage is a somewhat striking and unusual affair. Recently I saw at a human autopsy of a young subject a subcapsular hemorrhage from the renal substance probably due to vascular rupture in an acute nephritis; there was no history of injury. There have been three cases of subcapsular hemorrhage in our records and as two of them represented the immediate cause of death, are interesting enough to record. An armadillo suffered an acute diffuse nephritis with much congestion but not enough to call it hemorrhagic. There was a large hemorrhage around the left organ, probably from a vessel near the hilum, sufficient to compress the kidney and cause it to atrophy. A lion presented an acute vegetative endocarditis with all its usual complications. The right renal capsule was distended with recent clot to a size which reached to the pelvic brim. Presumably an embolism caused thrombosis, ulceration and rupture of some middle size vessel. A dormouse suffering with an acute general infection probably emanating from the intestine, had several small recent clots separating the kidney from its capsule.

NEPHRITIS.

Nephritis, whether one begin its conception with the clinicopathological picture originally given by Bright, with the purely pathological classification of Weigert and Virchow or the modern tendency to subordinate all physical changes to clinical phenomena, is nevertheless a process of degeneration and inflammation affecting the secreting and supporting structures of the kidney and leading to some degree of impaired function. The disease is bilateral in so nearly every case that for practical purposes unilateral cases may be ignored. This implies that for some reason the renal tissues are generally susceptible to etiological agents so that when one side is affected its fellow seems always to participate or to follow. It seems desirable in studying nephritis to evaluate fully the mutual relations of functionating and supporting tissues and of the various sections of the first named. It is taught in many places that inflammations of one or another of these parts may occur independently, as for example a tubular nephritis, a glomerulonephritis and an interstitial nephritis. If however one reflect upon the dependence of the tubular function upon the glomerulus and _vice versa_ or upon the effect of inflammatory exudates in the supporting tissues upon the blood supply of the tubule, it becomes evident that only the most trivial or evanescent pathological changes in one can be without effect upon the others. It is difficult to see how, for examples, a glomerulus could remain normal if its associated tubule were destroyed or how if round cell infiltration or pus surround a capsule for any length of time, this structure could fail to be doomed. All this is by way of directing attention to the progress of physical damage in a kidney which has received injury sufficient to cause nephritis, but of course it does not explain the cause.

In classification of nephritis different commentators have employed different standards according as they viewed the acuteness or chronicity of the process, or as the principal functionating structures, glomerulus, tubular epithelium, blood vessels, or supporting connective tissues, presented the most conspicuous changes. To these, clinicians have added phenomena of constitutional complication or of direct renal insufficiency. These latter being unavailable for us, we must fall back upon a classification based upon physical changes and to this end we have always used a slight modification of the Weigert method. This classification offers little in the direction of etiology except that toxins are believed to cause tubular changes, bacteria to produce glomerular lesions and vascular deficiencies to lie at the root of chronic interstitial nephritis.

The origin of acute nephritis of chiefly degenerative character seems best explained by reference to some form of toxemia, whereas exudative processes, be they in glomerulus or supporting structures, seem to depend upon the direct action of bacteria. The origin of a chronic nephritis cannot be explained quite so readily. No one has answered with complete satisfaction whether a chronic process always begins with and proceeds from a single attack of acute disease, whether many acute attacks succeed upon one another or whether many small crops of agents successively attack the organ over a long time. Nor has an adequate explanation of the rôle of damaged blood vessels been given. It is reasonably easy in man to discover the existence of nephritis and of a possible cause; this is only true of acute cases in wild animals. Focal infections, those which might be the point of mobilization for bacteria sent to the kidneys, are frequently found in man but with exception of an occasional carious tooth, or a chronic osteitis are to be localized with difficulty in lower animals. In so far as the rôle of a single acute attack in the causation of chronic disease is concerned our material offers nothing, but some collateral or presumptive evidence may be mustered in regard to multiple infections.

Wild animals do not give evidence of repeated attacks of acute disease and indeed it would seem that they more often die of an acute infection than live to have it repeated. Evidences of chronic infection, not focal, are reasonably definite in forty-eight per cent. of the cases of chronic nephritis encountered here. This suggests strongly that in this material protracted infectious states offer opportunities for renal damage of progressive character. Vascular disease has been found twenty- eight times (see also section on arteries), in twenty-six of which the nephritis seemed due to or advanced by the damage to the vessels. This means further that only 14.3 per cent. of the chronic forms and 4 per cent. of the total seem closely related to disease of blood vessels.

Nephritis has been found in 12.2 per cent. of our total autopsies. Mammals show an incidence of 20.6 per cent., birds 7.7 per cent. Only the orders upon which more than one hundred autopsies have been held are subjected to separate analysis. Some of the remaining orders give very high figures which may indicate great renal vulnerability but it is deemed unfair to make statements upon them. Carnivorous mammals and birds lead their respective classes, the succeeding order of renal vulnerability being marsupials, ungulates, rodents, Primates, Galli, Striges, anserine birds, parrots, and doves. The leaders of this list, Carnivora and Accipitres, occupy a definite position in the analysis of acute and chronic lesions. Their kidneys show the smallest percentages of acute lesions and the highest percentages of chronic lesions. This would seem to indicate a resistance to acute injuries but susceptibility to prolongated or repeated infections or intoxications. The relation of chronic infection of some sort to chronic renal disease is not as clear as the influence of acute infection to acute nephritis. Taking Carnivora for example with 34.2 per cent. of chronic nephritis we find 22.4 per cent. with evident chronic inflammation while in the 55 per cent. of acute forms 40 per cent. are of acute infectious origin—the relation is as 64 is to 74.

While the relation of infection to nephritis is a consistent and perfectly acceptable one, the frequency of this disease in the carnivorous orders obliges one to think of high protein diet as a favoring factor. Renal disease is common enough in other orders, some strictly herbivorous, and it is fair only to emphasize which are the leaders in incidence. In so far as anatomy or habits are concerned no generalizations seem permissible. There is no relation of nephritis to the size of the kidney as given on a previous page, to the length of the alimentary tract, or to the expected longevity.

Toxic nephritis is a term applied when the kidney is the seat of epithelial degeneration, much congestion, perhaps leading to tiny hemorrhages, and definite swelling of the tuft without exudation into the capsular space. It is a severe grade of the degenerations already mentioned and is exemplified by the organ in cases of acute duodenitis of ungulates and in some monkeys dying after tuberculin injection. It seems especially to follow gastrointestinal diseases believed to be due to food intoxications. It seems important in monkeys and wild rodents. No adequate explanation is at hand for the latter.

As has already been stated vascular disease was present in twenty-six cases in a manner suggesting some relation to the cardiorenal complex but the only organ to which the term renal sclerosis of arteriosclerotic origin could be applied is that of an eagle; the autopsy is cited.