AFIP Wednesday Slide Conference - No. 16
January 13, 1999

Conference Moderators:
Dr. Richard J. Montali and Dr. James T. Raymond
Department of Pathology
National Zoological Park Washington, D.C. 20008
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Case I - 98-317-7 (AFIP 2652613)
Signalment: A 23-year-old, female, Matschie's tree kangaroo (Dendrolagus matschiei).
History: This animal originated from a breeding colony of tree kangaroos held at the National Zoological Park Conservation & Research Center in Front Royal, Virginia. The animal had a chronic history of coughing and had been treated for mycobacteriosis for the past four years. In September of 1998, she was moved to a new area at the research center. Her eating habits became erratic, and she developed gastric bloating and died after a surgical procedure to relieve the gas accumulation.
Gross Pathology: At necropsy, the animal presented in good nutritional condition with adequate subcutaneous and cavitary fat. Externally, a small amount of a cloudy, serous fluid was dripping from the left naris, and a circumscribed, firm mass measuring 1.0 x 0.75 centimeters was found at the base of the left teat; it contained a firm, gritty, yellow material. Internally, there was petechiation of the serosa and intestines, and the spleen was diffusely dark black. The pleurae were diffusely opaque, moderately thickened, and there were multiple, stringy, fibrous attachments between the parietal and visceral pleura. The upper left lung lobe was severely consolidated, mottled pink, red, and yellow, and contained multiple, white, nodules measuring up to 7 millimeters in diameter which were filled with a creamy discharge when cut. The remaining lung lobes were mottled dark red and pink. The bronchial lumens occasionally contained casts of green, pasty material that extended to the level of the bronchioles.
Laboratory Results: Mycobacterium avium was cultured from the lungs.
Contributor's Diagnosis and Comments: Lung, pneumonia, caseonecrotic, cavitating.

Etiology: Mycobacterium avium.

The National Zoological Park has maintained a breeding colony of Matschie's tree kangaroos (Dendrolagus matschiei) since 1975 with a documented history and continued prevalence of Mycobacterium avium complex (MAC) infections. No evidence of immunosuppressive retrovirus infections or loss of heterozygosity that may have led to an immune dysfunction in these animals was found. Isolates of MAC organisms from affected tree kangaroos and from their environment had no common restriction fragment DNA types. Cellular immune reactivity in apparently healthy tree kangaroos was three to six-fold lower than in humans and other marsupial and eutherian mammals, as determined by lymphocyte proliferative assays. Thus, while MAC infections are typically opportunistic in humans and other mammals, tree kangaroos commonly develop primary progressive disease with MAC from random sources. Comparative information derived from this study should benefit both the endangered tree kangaroo and humans with immunosuppressive disorders that lead to mycobacterial infections.
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Case 16-1. Lung. Central area of cavitary necrosis is surrounded by congested, consolidated lung parenchyma.
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Case 16-1. Lung. Numerous acid fast bacilli are scattered throughout caseous necrotic debris.
AFIP Diagnosis: Lung: Pneumonia, granulomatous and necrotizing, diffuse, severe, with cavitation and mineralization, Matschie's tree kangaroo (Dendrolagus matschiei), marsupial.
Conference Note: Marsupials are more susceptible to infection with mycobacteria than true placental mammals, and the earliest report of a tuberculous disease in a captive tree kangaroo was described in the middle of the 19th century. More recently, a number of Mycobacterium avium complex (MAC) infections have been documented in several managed colonies of tree kangaroos in North America. The prevalence of MAC infections of marsupials in the wild is currently unknown.
Disease due to MAC in captive Matschie's tree kangaroos begins insidiously and progresses over a period of two to three years. The disease predominantly affects males that are between the ages of 5 and 16 years, with a reported male to female ratio of 3:2. Clinical signs vary from none to lethargy, anorexia, and weight loss; coughing is occasionally reported, but is not a prominent sign in most animals. Radiographic evidence of pneumonia is present in advanced cases, and cytological evaluation of tracheobronchial lavage samples sometimes reveals the presence of inflammatory cells admixed with filamentous acid-fast bacilli.
In the group of diseased tree kangaroos studied by the contributor, gross and microscopic lesions due to MAC infection have been observed in several organ systems. However, the most extensive lesions have occurred in the lungs and bones, and were histologically characterized by necrotizing pyogranulomatous pneumonia and osteomyelitis with numerous acid-fast bacilli. The Ziehl-Neelsen and Fite's staining methods performed at the AFIP demonstrated acid-fast bacilli in a section of lung from this tree kangaroo.
The recent study cited by the contributor indicates that tree kangaroos in captivity are very sensitive to MAC infections. Infected animals often develop progressive pulmonary mycobacteriosis that may disseminate and become fatal. The in vitro studies examining lymphocyte responses in healthy tree kangaroos seem to indicate that cellular immune reactivity is lower in this species compared to other marsupials and eutherian mammals resistant to MAC infections. This lowered cell-mediated immune response may significantly contribute to the susceptibility to opportunistic MAC infections in tree kangaroos. However, tree kangaroos do not appear to be predisposed to other opportunistic infections, and there may be additional factors which contribute to increased susceptibility to MAC, including genetic influences, stress, and environmental exposure. Additionally, the respiratory tracts of many tree kangaroos have been found to be colonized with mycobacteria, but some animals remain asymptomatic for more than three years; this is another unusual feature of MAC disease in Matschie's tree kangaroos.
Contributor: National Zoological Park, Department of Pathology, 3001 Connecticut Ave. NW, Washington D.C. 20008.
1. Montali RJ, Bush M, Cromie R, et al.: Primary Mycobacterium avium complex infections correlate with lowered cellular immune reactivity in Matschie's tree kangaroo (Dendrolagus matschiei). J Infect Dis 178(6), 1998 (in press).
Case II - UCD 1 (AFIP 2648197)
Signalment: Five-month-old, female, black-tailed deer (Odocoileus hemionus columbianus).
History: This fawn was experimentally infected with deer adenovirus isolated from a naturally infected fawn in Yuba County, California that died during the 1993 epizootic of adenovirus hemorrhagic disease. The adenovirus was isolated in black-tailed deer pulmonary artery endothelial cells, purified on a CsC1 gradient, and dialyzed in PBS. This female fawn was inoculated by intravenous injection and died five days post-inoculation.
Gross Pathology: Necropsy findings included blood-stained perineum, hemorrhage throughout the lumen of the small and large intestines, and pulmonary edema. Color photo transparencies of the lungs and intestinal tract are included.
Case 16-2. Lung. Interlobular septa are markedly expanded by edema fluid.
Case 16-2. Spiral colon and jejunum. Colon & small intestine is segmentally filled with dark red hemorrhage-stained ingesta. The mesentar appears diffusely edematous.
Laboratory Results: Fluorescent antibody test using fluorescence-labeled bovine antiserum to bovine adenovirus type 5 (BAV-5) and immunohistochemistry using BAV-5 antiserum stained endothelial cell nuclei in the lungs, alimentary tract, lymph nodes, and other organs.
Contributor's Diagnoses and Comments:
1. Pulmonary vasculitis with endothelial hypertrophy, necrosis, and intranuclear inclusion bodies.
2. Interstitial pneumonia, moderate, acute, lymphocytic, neutrophilic, with pulmonary edema.

Etiology: Adenovirus.
Ten fawns were inoculated with adenovirus, half of which were inoculated through the mucous membranes and the other half intravenously. Eight fawns developed clinical disease with either systemic or the localized form of the disease. Lesions reproduced were similar to those described in black-tailed deer that died during the natural epizootic that occurred in California in 1993. The epizootic started in July of 1993 and continued into the spring of 1994. Thousands of deer were believed to have died during this outbreak. Other than two outbreaks in rehabilitation centers, no other cases were reported in California until July of 1998. Adenovirus has thus far been confirmed in deer from three counties in California associated with high mortality in free ranging deer herds. In addition, adenovirus has been confirmed associated with increased mortality in farmed white-tailed deer in Iowa.
In the tissue section of this experimentally infected animal, the pulmonary parenchyma is multifocally atelectatic, and the interlobular septa and subpleural spaces are moderately to severely expanded by edema and very mild inflammation (lymphocytes, plasma cells, and neutrophils). Small to medium-sized arterioles throughout the tissue are lined by endothelium in which the nuclei are prominent and rounded, are darkly basophilic, bulge into the vascular lumina, and contain darkly amphophilic viral inclusion bodies. Many of these arterioles contain sloughed luminal endothelial cells admixed with moderate numbers of mononuclear and polymorphonuclear cells, and in some of the arterioles, inflammation extends into the vessel wall where it is admixed with rare, brightly eosinophilic hyalinized material (fibrinoid necrosis). Throughout the remaining parenchyma there is multifocal atelectasis, alveolar capillaries are expanded by neutrophils, and there is expansion of alveolar septa by moderate numbers of neutrophils and lymphocytes. Transmission electron microscopy demonstrated endothelial cell necrosis in the lungs and alimentary tract and adenovirus particles in the nuclei with protein crystalline arrays.
Differential diagnosis should include the orbiviruses, bluetongue virus and epizootic hemorrhagic disease virus. Definitive diagnosis depends on the presence of endothelial intranuclear inclusions in the lungs with the systemic adenoviral infection. Transmission electron microscopy or immunohistochemistry demonstrates adenovirus in endothelial cells in the lungs, alimentary tract, and other organs. Animals with the localized form of the disease may die of starvation or bacterial sepsis with chronic lesions in the upper alimentary tract. Finding inclusions or virus by transmission electron microscopy or immunohistochemistry in chronic lesions is more difficult.
Case 16-2. Transmission Electron Micrograph. The cytosol is expanded by electron dense hexagonal particles (virions) layered between multiple needle-like crystal lattices of moderately electron dense granular material.
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Case 16-2. Lung. The pulmonary arteriole (20x view) is expanded by lymphocytes and plasma cells. The endothelium (both views) is lined by piled up, hypertrophic, endothelial cells which rarely bear smudgy amphophilic intranuclear inclusions (arrow head).
AFIP Diagnosis: Lung: Endothelial degeneration and hypertrophy, diffuse, with multifocal vasculitis, interstitial pneumonia, diffuse edema, and endothelial intranuclear inclusion bodies, black-tailed deer (Odocoileus hemionus columbianus), cervid.

Note: A fat embolus was observed in some sections.
Conference Note: A novel adenovirus closely related to bovine adenovirus-5 was identified as the cause of the 1993 epizootic of hemorrhagic disease of mule deer (Odocoileus hemionus) in California. The gross and histologic lesions of systemic adenovirus in mule deer are remarkably similar to the those found in the hemorrhagic disease of white-tailed deer (Odocoileus virginianus) caused by orbiviruses (bluetongue virus and epizootic hemorrhagic disease virus). Outbreaks of hemorrhagic disease in mule deer in California previous to 1993 were attributed to bluetongue but may have been caused by deer adenovirus. As noted by the contributor, the presence of endothelial intranuclear inclusions distinguishes adenovirus from orbivirus infection in deer presenting with signs of hemorrhagic disease. Additionally, hemorrhage in deer caused by orbivirus appears to be more widespread, while hemorrhage and edema seem to be confined to the lung and intestinal tract in adenoviral infections.
The most significant gross pathologic findings in deer with natural and experimental systemic adenovirus infections are pulmonary edema and hemorrhagic enteropathy. The virus consistently infects the endothelial cells of the lungs and intestines, causing endothelial necrosis associated with intranuclear inclusions. Disruption of the endothelium leads to hemorrhage and edema. Endothelial necrosis exposes the subjacent basement membrane, triggering platelet adhesion and agglutination that may culminate in disseminated intravascular coagulation. The endotheliotropic character of this strain of adenovirus resembles that of bovine adenovirus-10, infectious canine hepatitis virus, and porcine adenovirus. Localized vasculitis with necrotizing stomatitis, pharyngitis, glossitis, and/or osteomyelitis of the jaw were other lesions frequently found in mule deer that died during the 1993 California epizootic.
Diseases caused by adenoviruses in other species are most often observed in neonatal or juvenile animals, or in immunocompromised individuals. Mule deer with clinical disease caused by adenovirus in the 1993 California epizootic were predominantly fawns, though a few juveniles and adults were also affected. Adenovirus or adenovirus-like infection has been reported in a red deer from New Zealand and a fallow deer in Hungary, but the viruses in these cases primarily targeted the bronchiolar epithelium and are likely a different strain of adenovirus from the one associated with hemorrhagic disease of deer in California.
Contributor: California Veterinary Diagnostic Laboratory Services, School of Veterinary Medicine, University of California, PO Box 1770, Davis, CA 95617.
1. Woods LW, et al.: Systemic adenovirus infection associated with high mortality in mule deer (Odocoileus hemionus) in California. Vet Pathol 33:125-132, 1996.
2. Woods LW, et al.: Experimental adenovirus hemorrhagic disease in yearling black-tailed deer. J Wildl Dis 33:801-811, 1997.
3. Woods LW, et al.: Lesions and the transmission of experimental adenovirus hemorrhage disease in black-tailed deer fawns (in press), 1998.
Case III - 537-98 (AFIP 2656747)
Signalment: Seven-week-old broiler breeder pullets (chicken).
History: There was increased mortality of 3-4 days duration. Affected birds were lethargic, inappetent, and had ruffled feathers and mild to moderate loss of pectoral muscle mass. A few birds had red-brown feces.
Gross Pathology: Moderate to marked loss of pectoral muscle mass was present. Gross lesions varied with chronicity, ranging from marked hyperemia and mild ulceration of the cecal mucosa to extensive ulceration of the cecal mucosa with large fibrinonecrotic casts within the lumens. In virtually all birds, there was moderate to marked thickening of the cecal walls. The livers of several birds contained variably-sized, often coalescing, foci of necrosis. In a few of the birds, there was rupture of the cecum with extensive fibrinous peritonitis and airsacculitis. Small numbers of cecal worms (Heterakis gallinarum) were variably present in the cecal lumen.
Laboratory Results: Clinical pathology was not performed. Liver cultures revealed a mixed aerobic growth including moderate numbers of Escherichia coli and a variety of other bacteria. Salmonella sp. were not isolated.
Contributor's Diagnoses and Comments:
1. Cecum: Ulcerative, lymphocytic, histiocytic typhlitis, multifocal to coalescing, subacute, severe with intralesional protozoa and intraluminal nematodes.
2. Liver: Necrotizing, lymphocytic, histiocytic hepatitis, multifocal to coalescing, acute to subacute, severe, with intralesional protozoa.

Etiology: Histomonas meleagridis and Heterakis gallinarum.
While typically associated with morbidity and mortality in turkey flocks, infections with Histomonas meleagridis have caused significant morbidity and mortality in young broiler breeder flocks (pullets and cockerels) in recent months. The exact cause of this recent re-emergence is not clear, however. Factors including changes in anticoccidial programs and availability of antiprotozoal drugs may have contributed to these outbreaks.
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Case 16-3. Liver. Liver parenchyma is multifocally necrotic and partially replaced by myriad Histomonas trophozoites, 10-20u in diameter, which are fragmented, pale, amphophilic, and surrounded by narrow rims of clear space.
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Case 16-3. Colon. The lamina propria is diffusely expanded by macrophages, lymphocytes, heterophils, and fragmented, pale, granular Histomonas amoeba. At points of mucosal erosion, these inflammatory cells stream into the gut lumen.
AFIP Diagnoses:
1. Liver: Hepatitis, granulomatous, necrotizing, multifocal to coalescing, moderate, with numerous protozoa, chicken, avian.
2. Cecum: Typhlitis, lymphoplasmacytic, histiocytic, and heterophilic, diffuse, moderate, with protozoa and cecal core.
Some microslides contain cross-sections of intraluminal cecal nematodes.
Conference Note: Histomoniasis, caused by the protozoan Histomonas meleagridis, is a disease of several gallinaceous birds including turkeys, chickens, peafowl, grouse, quail, and other species. Major lesions in infected and clinically diseased birds are necrotizing hepatitis and typhlitis. The disease has been referred to as infectious enterohepatitis and "blackhead" in turkeys. Bacteria, such as Clostridium perfringens, seem to play a pivotal role in the pathogenesis of the disease, and experimentally, in the absence of bacteria, the histomonad does not appear to be pathogenic.
Histomoniasis is a ubiquitous disease. Infected chickens often have only mild illness. Chickens serve as the principal reservoir of infection for turkeys, which are extremely susceptible and often succumb to the disease. Turkey poults between 3 and 12 weeks of age and chickens between 4 and 6-weeks-old are the most susceptible to infection. The chukar partridge and ruffed grouse are also severely affected. Milder forms of disease occur in peafowl, guinea fowl, bobwhite quail, and pheasants. While development of safe antihistomonal drugs has significantly limited disease in domestic poultry, histomoniasis remains an important cause of death among many other galliformes.
Transmission of H. meleagridis to susceptible birds may occur by one of three mechanisms. First, birds may ingest fresh feces containing histomonads; this route is probably unimportant with the exception of spread among closely confined animals within a flock. Second, birds may ingest embryonated eggs of the ascarid cecal nematode Heterakis gallinarum which contain the histomonads. The protozoa are liberated from the nematode eggs when the larvae break out, and the histomonads subsequently invade the cecal wall. Protozoa are then carried to the liver via the hepatic portal system. Finally, birds may become infected through ingestion of earthworms containing histomonad-bearing cecal worm larvae in their tissues. Interestingly, histomoniasis occurs infrequently in areas lacking earthworms or other mechanical vectors, or in areas with sandy, dry soil. Historically, infection in turkeys occurred when the animals were reared together with chickens, or when raised on ground previously inhabited by chickens. Histomonads may survive several years within cecal worm eggs.
The classical macroscopic lesions of histomoniasis include bilaterally enlarged, hemorrhagic ceca that have a thickened mucosa and are filled by caseo-necrotic, yellow-green, laminated material (cecal cores). The cecal mucosa may also be necrotic and ulcerated. In the liver, there are multifocal to coalescing, circular, depressed, greenish-yellow areas of necrosis that are circumscribed by a thin raised ring of parenchyma. The hepatic lesions have been described as target-like. Microscopically, the histomonads can be identified within areas of inflammation in the cecae and within necrotic areas of the liver on routine hematoxylin and eosin stained sections. Visualization of the protozoal trophozoites may be enhanced by the periodic acid-Schiff reaction, especially in chronic lesions that contain few organisms.
Contributor: Laboratories of Veterinary Diagnostic Medicine, University of Illinois, 2001 South Lincoln Ave., Urbana, IL 61801.
1. American Association of Avian Pathologists Committee on Disease Reporting: 1986 summary of commercial poultry disease reports and 1986 pet, zoo, and wild bird disease report. Avian Dis 31:926-987, 1987.
2. McDougald LR: Other protozoan diseases of the intestinal tract. In: Diseases of Poultry, Calnek BW, ed.,10th ed., pp. 890-899, Iowa State University Press, Ames, Iowa, 1997.
3. Kemp RL, Reid WM: Staining techniques for differential diagnosis of histomoniasis and mycosis in domestic poultry. Avian Dis 10:357-363, 1966.
4. Lee DL: The structure and development of Histomonas meleagridis (Masticamoebidae: protozoa) in the female reproductive tract of its host, Heterakis gallinae (nematoda). Parasitol 59:877-884, 1969.
5. Charlton BR, et al.: Histomoniasis. In: Avian Disease Manual, 4th ed., pp. 178-180, American Association of Avian Pathologists, University of Pennsylvania New Bolton Center, PA, 1996.
Case IV - V98-7693 (AFIP 2643018)
Signalment: Five-year-old, male, hedgehog.
History: Lethargy, weak hind limbs, and a fifty gram weight loss were noted over one year. Physical examination revealed a caudal abdominal mass, which on exploratory laparotomy, was not associated with the gastrointestinal tract, liver, kidneys, or bladder. Multiple small omental masses were noted.
Gross Pathology: The caudal abdominal mass measured 1 x 2.7 x 3 centimeters and was firm and irregular. The omental masses were 1-3 millimeters in diameter and were disseminated throughout the omentum.
Laboratory Results: None.
Contributor's Diagnoses and Comments:
1. Testicle: Interstitial cell tumor, with multifocal infarction.
2. Testicle: Moderate to severe diffuse atrophy of seminiferous tubular epithelium, multifocal mineralized intratubular debris and occasional spermatozoa.
3. Omentum: Metastatic interstitial cell tumor.
Interstitial cell tumors (ICT) are derived from Leydig cells and rarely metastasize. A continuum was noted from a less well differentiated cell type which had a hyperchromatic central round nucleus and a modest amount of a lightly basophilic cytoplasm, to larger round polyhedral cells with abundant lightly eosinophilic to vacuolated cytoplasm in the more well differentiated cells. There was mild cytomorphologic atypia and a slightly higher mitotic rate (2-4/hpf) in well differentiated areas of the tumor. The sharply demarcated focus of tumor necrosis is suggestive of vascular compromise due to possible tumor emboli. Numerous tumor metastases were noted in the omentum. The mineralized debris in the seminiferous tubules appeared to obstruct flow, trapping the few spermatozoa present in the nearby tubules resulting in mild distention.
Hedgehogs are popular exotic pets in which neoplasia is quite common. However, reference material is rather scarce. There are a few isolated case reports in the literature1, 2 and one review of hedgehog necropsy lesions from the Baltimore Zoo from 1984-1991.3 Thirty-two percent of 74 hedgehogs necropsied at the Baltimore Zoo from 1984-1991 had neoplasms. Neoplasia was common in the integumentary, respiratory, reproductive, hematopoietic, and endocrine systems.3 Multiple skeletal sarcomas have been associated ultrastructurally with probable type C retrovirus in two African hedgehogs.
Interstitial cell tumors are common in older animals and in cryptorchid testicles. Hedgehog testicles are often located intra-abdominally. Interstitial cell tumors are classified as solid diffuse, cystic vascular, and pseudoadenomatous. This interstitial cell tumor (ICT) is an intermediate type between the solid diffuse and cystic vascular types. The atrophic seminiferous tubules may have been a result of mechanical obstruction, an aging change, seasonal variation, or less likely, humoral inhibition.
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Case 16-4. Testis, Epididymis. Replacing seminiferous tubules and extending around adjacent epididymal tubules, there is an expansile, infiltrative mass consisting of sheets of polygonal cells bearing pale granular, often vacuolated cells with oval to round nuclei with granular basophilic chromatin.
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Case 16-4. Testis. Seminiferous tubules are atrophic, lack mature spermatozoa, and contain reduced numbers of spermatids. Tubules are separated by clear space (edema) and free RBCs (hemorrhage).
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Case 16-4. Mesentary. Multifocally expanding mesothelium lined adipose tissue, there are numerous irregularly sized nodules of pleomorphic polygonal cells like those described above (metastatic foci).
AFIP Diagnoses:
1. Testis: Interstitial cell tumor, malignant, hedgehog, insectivore.
2. Adipose tissue (omentum per contributor): Interstitial cell tumor, malignant, metastatic.
Conference Note: A densely cellular neoplasm has effaced the testis and infiltrated the epididymis. It is composed of polygonal cells arranged in broad cords, nests, packets and solidly cellular areas, supported by a fine fibrovascular stroma. In some areas, neoplastic cells palisade along the vascular stroma. Neoplastic cells have indistinct cell borders, moderate amounts of eosinophilic cytoplasm, and oval to elongate nuclei. Some polygonal cells contain very distinct, clear, cytoplasmic vacuoles. The mitotic rate is high, and some mitotic figures are bizarre. Similar neoplastic cells are found within the submitted sections of mesentery. Based on histomorphology, conference participants agreed with the contributor's diagnosis. The differential diagnosis that was considered included seminoma, Sertoli cell tumor, lymphoma, mast cell tumor, and mesothelioma.
Among domestic species, testicular tumors occur most commonly in geriatric dogs, are found less frequently in aged bulls and stallions, and are unusual or rare in other animals such as cats, sheep, and swine. The three most common testicular tumors are seminoma, interstitial cell tumor and Sertoli cell tumor, and they arise, respectively, from germ cells, interstitial (Leydig) cells, and Sertoli (sustentacular) cells. In the dog, cryptorchidism is an important predisposing factor for development of seminomas and Sertoli cell tumors. Cryptorchidism is not a recognized predisposing condition for development of interstitial cell tumors, except in the horse and possibly the cat. Interestingly, most interstitial cell tumors in the horse occur in cryptorchid testes.
Leydig cells normally produce androgens, and interstitial cell tumors in humans may elaborate excess androgens and/or estrogens, and occasionally corticosteroids. Most canine interstitial cell tumors do not produce excess hormones. Hormonally active canine interstitial cell tumors are associated with perianal gland hyperplasia, prostatic enlargement, and tail-gland hyperplasia, suggesting androgen excess. Less frequently, signs of hyperestrogenism may occur including alopecia and attraction of other male dogs.
Contributor: Marshfield Laboratories, 1000 North Oak Avenue, Marshfield, WI 54449.
1. Raymond JT, et al: Malignant mast cell tumor in an African hedgehog. J Wildl Dis 33:140-142, 1997.
2. Rivera RY, et al: Oronasal squamous cell carcinoma in an African hedgehog. J Wildl Dis 28:148-150, 1992.
3. Done LB, et al: Necropsy lesions by body systems in African hedgehogs. In: Proceedings of the Annual Meeting of American Association of Zoo Veterinarians, pp. 113-115, Oakland, CA, 1992.
4. Peauroi JR, et al: Multicentric skeletal sarcomas associated with probable retroviral particles in two African hedgehogs. Vet Pathol 31:481-484, 1994.
5. Ladds PW: The male genital system. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th ed., volume 3, pp. 504-511, Academic Press, San Diego, CA, 1993.
6. Kennedy PC, et al.: Histological classification of tumors of the genital system of domestic animals. In: World Health Organization International Histological Classification of Tumors of Domestic Animals, Schulman FY, ed., Second series, volume 6, pp. 15-19, Armed Forces Institute of Pathology and American Registry of Pathology, Washington DC, 1998.
Conference Coordinator:
Ed Stevens, DVM
Captain, United States Army
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
* The American Veterinary Medical Association and the American College of Veterinary Pathologists are co-sponsors of the Registry of Veterinary Pathology. The C.L. Davis Foundation also provides substantial support for the Registry.
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