|
|
CASE I – 00Z 1743 (AFIP 2739529)
Signalment: 2-year-old, female red-tail boa snake (Boa constrictor constrictor).
History: This snake had a history of “not doing well” for several weeks. The snake was lethargic, refused food, and had lost weight. The snake died during initial examination by the referring veterinarian.
Gross Pathology: A necropsy was performed by the submitting veterinarian. Formalin-fixed tissues and a fresh sample of coelomic fluid were sent to the diagnostic laboratory. The described gross findings included dehydration with significant loss of adipose stores and muscle mass. The coelomic cavity contained a considerable amount of pale yellow, slightly cloudy, watery fluid. The spleen was enlarged, multifocally friable, and mottled red/tan on section. The liver was similarly enlarged and contained disseminated pinpoint to 2 mm white/tan nodules on surface and section. There were multifocal petechial hemorrhages, small yellow/tan nodules, and firmer white/tan nodules scattered throughout the omentum, lung, and kidneys. The brain and spinal cord were not examined or submitted.
Laboratory Results: Bacterial culture of the coelomic fluid yielded heavy growth of Citrobacter freundii.
Contributor’s Diagnoses and Comment: 1. Liver, spleen, kidney, lung, heart, gastrointestinal tract, pancreas, and adipose tissue: Lymphoma, intermediate to large cell, diffuse.
2. Liver, kidney, pancreas, and gastrointestinal tract: Epithelial and lymphocytic eosinophilic intracytoplasmic inclusion bodies (boid inclusion body disease).
3. Liver, spleen, kidney, lung, gastrointestinal tract, and adipose tissue: Granulomas, disseminated, with intralesional bacteria.
Throughout all parenchymal organs, in all levels of the gastrointestinal tract, and infiltrating the coelomic adipose tissue there are multifocal to coalescing sheets of medium-sized to large lymphocytes with scant, eosinophilic to pale basophilic cytoplasm and large, predominantly round, nuclei with coarsely clumped chromatin and inconspicuous nucleoli. Mitotic activity varies between sections, but is generally high (5-20/10 hpf). The lymphocytes efface normal architecture in most organs, most obviously in the spleen and kidney. In many tissues, multifocal small blood vessels contain similar neoplastic lymphocytes, and a diagnosis of lymphoid leukemia was considered. Leukemia could not be confirmed because a hematology profile was not available and no blood smears were made antemortem, but the infiltrative pattern in the liver submitted (portal tracts and sinusoids) certainly suggests leukemia. Both lymphoma and lymphoid leukemia have been reported in snakes of several species, including boa constrictors.
The eosinophilic, intracytoplasmic inclusion bodies in epithelial cells of most tissues, and occasionally observed in lymphocytes, are consistent with a diagnosis of boid inclusion body disease (IBD). This is a chronic, progressive disease affecting snakes in the family Boidae, including boas (subfamily Boinae) and pythons (subfamily Pythoninae).
The etiology of IBD is thought to be a retrovirus based upon ultrastructural observations of type-C retrovirus-like particles associated with the inclusions, demonstration of reverse transcriptase activity in the plasma of affected snakes and in the supernatant of kidney cell cultures from affected snakes, and recent isolation of a retrovirus (yet uncharacterized) from several snakes with IBD. Routes of transmission for IBD are unknown, but the snake mite, Ophionyssus natricis, has been suggested as a potential vector.
Clinical signs differ slightly between affected boas and pythons; in boas, intermittent and recurrent regurgitation of food is often the first sign observed, while pythons generally do not regurgitate. Snakes of both subfamilies become lethargic and anorexic, lose weight, and may develop secondary bacterial, fungal, or other infections (especially stomatitis and/or pneumonia). Neurologic signs may begin early and progress, but are consistently observed terminally and include: disorientation, incoordination, inability of animals to right themselves, head tremors, opisthotonos, loss of motor function, paresis, flaccid paralysis, and occasionally behavioral changes, including aggression. Neurologic disorders are generally more pronounced in pythons than in boas.
Gross lesions observed at necropsy are variable and occasionally lacking, but sometimes include splenic atrophy, pancreatic atrophy with fibrosis, evidence of secondary bacterial or fungal infections (granulomas in tissues), and hepatomegaly with pallor. Ascites or effusions, as observed with the snake in this report, have been described in other cases occasionally.
Characteristic histological lesions include variably sized, 1-8 um, eosinophilic, intracytoplasmic inclusions in epithelial cells of most tissues and also in lymphocytes, ependymal cells, and neurons in the CNS. Inclusions are more common in the CNS of boas, while inflammation (nonsuppurative meningoencephalitis with neuronal degeneration and necrosis, demyelination, and gliosis) is typically more severe in pythons. Other lesions reported include pancreatic acinar vacuolar degeneration, pancreatic atrophy, pancreatic necrosis, hepatocellular vacuolar degeneration, and thymic and splenic atrophy (lymphoid and reticuloendothelial depletion). Evidence of localized or systemic bacterial, fungal, or other infections is often found in tissues of affected snakes (granulomas with intralesional organisms), as in the case presented here.
There are several reports of type-C retrovirus particles associated with neoplasms in snakes. The association between lymphoma/lymphoid leukemia and IBD (presumptively caused by a retrovirus) in this snake may be coincidence, but this coincidence should raise concerns about the potential for the development of neoplasia in putative IBD virus-infected snakes.
AFIP Diagnoses: 1. Liver; spleen: Malignant lymphoma, red-tail boa (Boa constrictor constrictor), reptile.
2. Liver, hepatocytes and bile duct epithelium: Inclusion bodies, eosinophilic and intracytoplasmic, many, consistent with boid inclusion body disease.
3. Liver; spleen: Granulomas, with bacterial colonies.
4. Liver: Hepatitis, necrotizing, random, acute, multifocal, mild, with sinusoidal fibrin thrombi.
Conference Comment: The controversial association of a type C retrovirus and boid inclusion body disease (IBD) was discussed during conference. Because of the inability to fulfill Koch’s postulates, a causal relationship between a retrovirus and IBD has not been established. The intracytoplasmic inclusions reported in a California king snake (Lampropeltis getulus californiae), in the provided reference, were visible only by transmission electron microscopy, and were not attributed to IBD. However, a disease resembling IBD of boids, with similar intracytoplasmic inclusion bodies when viewed by light and electron microscopy, was recently reported in captive palm vipers (Bothriechis marchi).
Bacterial infections of reptiles are most often caused by gram-negative organisms. Citrobacter rodentium (formerly C. freundii) is commonly found in moist reptilian environments and was likely an opportunistic pathogen in this debilitated snake.
Contributor: Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, 1174 Snowy Range Road, Laramie, Wyoming 82070
References: 1. Carlisle-Nowak MS, Sullivan N, Carrigan M, Knight C, Ryan C, Jacobson ER: Inclusion body disease in two captive Australian pythons (Morelia spilota variegata and Morelia spilota spilota). Australian Vet J 76:98-100, 1998
2. Frye FL, Carney JD: Acute lymphatic leukemia in a boa constrictor. Vet Med Small Anim Clin 68:653-654, 1973
3. Jacobson ER, Seely JC, Novilla MN: Lymphosarcoma associated with virus-like intranuclear inclusions in a California king snake (Colubridae: Lampropeltis). J Natl Cancer Inst 65:577-579, 1980
4. Jacobson ER, Calderwood MB, French TW, Iverson W, Page D, Raphael B: Lymphosarcoma in an eastern king snake and a rhinoceros viper. J Am Vet Med Assoc 179:1231-1235, 1981
5. Oros J, Tucker S, Jacobson ER: Inclusion body disease in two captive boas in the Canary Islands. Vet Rec 143:283-285, 1998
6. Raymond JT, Garner MM, Nordhausen RW, Jacobson ER: A disease resembling inclusion body disease of boid snakes in captive palm vipers (Bothriechis marchi). J Vet Diagn Invest 13(1):82-86, 2001
7. Schumacher J, Jacobson ER, Homer BL, Gaskin JM: Inclusion body disease in boid snakes. J Zoo Wildl Med 25:511-524, 1994
CASE II – 2000-193-6 (AFIP 2744082)
Signalment: 2-year-old, male redhead duck, Aythya americana
History: This duck was seen alive in the morning but was found floating dead in the pond at noon.
Gross Pathology: The carcass was in poor nutritional condition with no subcutaneous or cavitary fat. Approximately 150 ml of cloudy yellow fluid was in the coelomic cavity. Numerous tan-yellow caseous masses, measuring 0.5–3.0 cm in diameter, were scattered throughout the hepatic parenchyma. Similar, but smaller, nodules were present in the small and large intestine serosae, mesentery, and spleen.
Laboratory Results: Mycobacterium avium complex was cultured from the liver lesions.
Contributor’s Diagnoses and Comment: 1. Liver, amyloidosis, diffuse, severe.
2. Liver, hepatitis, granulomatous and heterophilic, multifocal, moderate.
Etiologic Diagnosis: 1. Hepatic amyloidosis; 2. Mycobacterial hepatitis
Etiology: 1. Amyloid-associated (AA) protein deposition; 2. Mycobacterium avium
Amyloidosis is the pathological deposition of hyaline-like proteinaceous material in various organs. Although this condition may be classified into several categories in humans, only reactive amyloidosis, which occurs secondary to chronic inflammatory processes, has been recognized in birds. Activated macrophages produce IL-1 and IL-6 that induce hepatocytes to synthesize serum amyloid-associated (SAA) protein, an acute phase reactant. SAA is normally completely degraded, but in reactive amyloidosis there is incomplete breakdown of SAA resulting in deposition of insoluble amyloid-associated (AA) protein.
In birds, amyloidosis commonly occurs in association with chronic infectious diseases such as tuberculosis, aspergillosis, and bumblefoot. Amyloid deposits are most frequently seen in the liver and spleen, and occasionally kidneys; other organs are rarely affected in most species. Waterfowl appear to be especially prone to develop amyloidosis.
In this case, amyloidosis developed secondary to avian tuberculosis. Granulomas containing myriad acid-fast bacilli were located throughout the intestinal tract, mesentery, and spleen. Granulomas were also located in the liver; however, many of the hepatic lesions consisted primarily of necrosis and heterophilic inflammation. The degree of hepatocyte loss due to necrosis and pressure atrophy from the amyloid deposits was severe enough to have caused liver failure. Amyloid was also present in the spleen.
AFIP Diagnoses: 1. Liver: Amyloidosis, diffuse, severe, with hepatic cord atrophy, redhead duck (Aythya americana), avian.
2. Liver: Hepatitis, necrotizing, granulomatous and heterophilic, multifocal, moderate.
Conference Comment: Secondary amyloidosis is a common disease of waterfowl that is characterized by the deposition of extracellular amyloid A (AA) protein fibrils within the space of Disse, resulting in compression atrophy and necrosis of surrounding hepatic cords.
Although secondary amyloidosis is most often attributed to chronic stimulation of the immune system, diet, stress, and genetics also may play a role.
Contributor: Smithsonian National Zoological Park, 3001 Connecticut Avenue, NW
Washington, DC 20008
References: 1. Cotran RS, Kumar V, Robbins SL: Diseases of Immunity. In: Robbins Pathologic Basis of Disease, 5th ed., pp. 231-238. WB Saunders Co, Philadelphia, PA, 1994
2. Guo J-T, Aldrich CE, Mason WS, Pugh JC: Characterization of serum amyloid A protein mRNA expression and secondary amyloidosis in the domestic duck. Proc Natl Acad Sci USA 93(25):14548-14553, 1996
3. Montali RJ, Bush M, Thoen CO, Smith E: Tuberculosis in captive exotic birds. J Am Vet Med Assoc, 169(9):920-927, 1976
4. Nakamura K, Tanaka H, Kodama Y, Kubo M, Shibahara T: Systemic amyloidosis in laying Japanese quail. Avian Dis 42:209-214, 1998
5. Pepercamp NHMT, Landman WJM, Tooten PCJ, Ultee A, Voorhout WF, Gruys E: Light microscopic, immunohistochemical, and electron microscopic features of amyloid arthropathy in chickens. Vet Pathol 34:271-278, 1997
6. Sanford SE, Rehmtulla AJ, Josephson GKA: Tuberculosis in farmed rheas (Rhea americana). Avian Dis 38:193-196,1994
CASE III – R95-1228 (AFIP 2739042)
Signalment: This tissue specimen is from a 1.24 meter long, male green iguana (Iguana iguana).
History: This male green iguana was kept in a local zoo. He was listless, anorexic, and had mucoid diarrhea. He died due to cachexia.
Gross Pathology: The lesions were confined at the lower intestine and liver. The lower intestinal lumen was enlarged and was filled with a large amount of dark colored, viscid necrotic substance. The intestinal mucosa had multiple to coalescing ulcerations and was covered by a thick layer of yellowish pseudomembrane. There were multifocal pinpoint white spots over the hepatic surface.
Laboratory Results: Fecal examination revealed developmental stages of a protozoan parasite. Escherichia coli was isolated from the intestine. Histochemistry revealed many PAS positive trophozoites scattered throughout the necrotic foci of intestine, primarily along the margins of the necrotic lesion.
Contributor’s Diagnosis and Comment: Intestine: Enteritis, necrotizing and ulcerative, diffuse, subacute, severe, with intralesional amoeba spp., green iguana (Iguana iguana), reptile.
Microscopic features confirmed the gross observation of necrotizing enteritis in cecum-colon sections. Heavy cellular debris was present in or along the edge of the necrosis. Inflammatory reaction was minimal. Other findings were edema, hemorrhage, vascular thrombosis, bacterial colonies, and hyperemia, as well as pericolonic peritonitis. The amoebic trophozoites that were recognized in tissue sections were irregularly spherical in shape, ranging from 10 to 30 um in diameter. They had a variably distinct nucleus, with abundant vacuolated cytoplasm.
The most commonly reported amoebic pathogen in primates is Entamoeba histolytica, in amphibians is Entamoeba ranarum, and in reptiles is Entamoeba invadens. These organisms usually inhabit the intestinal tract and cause amoebic dysentery in man, nonhuman primates, and less frequently, other animals including dogs, cats, rats, and pigs. Amoebic lesions are typically confined to the colon and cecum and produce characteristic flask-shaped ulcers in affected animals. Extra-intestinal dissemination of amoebae in advanced cases, with abscessation in other organs, especially liver, lung, and brain, is a relatively common complication in humans and nonhuman primates.
Transmission occurs through ingestion of mature quadrinucleate cysts most commonly in fecal-contaminated water, hands, and food. Cockroaches, house flies, and other arthropods may mechanically transfer infected feces on their legs or mouthparts to food. In an experimental study of germ-free and conventional guinea pigs infected with amoebae, results showed that intestinal bacteria such as Aerobacter aerogens and Escherichia coli probably play an important role in the pathogenesis of amoebiasis.
Although the precise host and parasite factors promoting invasion and necrosis are not known, the killing reaction is initiated by the binding of the amoeba to the target cell. This binding is mediated by an amoebic galactose-specific adhesion on the amoebae surface. Once the cell to cell contact is established, massive surface blebbing of the target cell occurs, suggesting that amoebae secrete factors that alter membrane permeability. Amebapore, a pore-forming peptide, and granule vesicles, that resemble the cytotoxic granules of lymphocytes, mediate the subsequent cytotoxic activity. In addition to the killing effect, amoebae release other virulence factors that inhibit macrophage motility, degrade type I collagen, and destroy extracellular matrix to aggravate lesions.
Treatment of the surviving green iguana in the affected diorama with metronidazole, at the dose rate of 250 mg/kg, proved rapidly effective. This is the first report of reptilian amoebiasis in a green iguana in Taiwanese zoos.
AFIP Diagnosis: Cecum: Typhlitis, necrotizing, transmural, acute, diffuse, severe, with edema and amoebic trophozoites, etiology consistent with Entamoeba invadens, green iguana (Iguana iguana), reptile.
Conference Comment: Chelonians and crocodilians are considered more resistant to infection by Entamoeba invadens, and may serve as a reservoir for infection of snakes and lizards in captivity. The mixing of chelonians and crocodilians with snakes and lizards in the same exhibit, or the recirculation of water through separate exhibits can result in high morbidity and mortality of susceptible reptiles in an outbreak of amoebiasis.
In histologic sections, amoebae are scarce and are usually found in small clusters within the colonic mucus. They may exhibit erythrophagocytosis. Iron hematoxylin and trichrome stains can aid in identifying the pathogenic amoebic trophozoites in tissue sections and in distinguishing them from macrophages among the necrotic debris. The characteristic flask-shaped submucosal ulcer seen in histologic section is due to the difficulty of trophozoite invasion and penetration of the intestinal muscular tunics, resulting in expansion laterally within the submucosa. Invasion of blood and lymphatic vessels can result in Gram negative sepsis, and allow dissemination of trophozoites to other organs, such as the liver.
Contributor: Pig Research Institute Taiwan, Department of Pathobiology, P.O. Box 23, Chunan, Miaoli, Taiwan 350
References: 1. Donaldson M, Heyneman D, Dempster R, Garcia L: Epizootic of fatal amebiasis among exhibited snakes: epidemiologic, pathologic, and chemotherapeutic considerations. Am J Vet Res 36:807-817, 1975
2. Jakob W, Wesemeier H-H: Intestinal inflammation associated with flagellates in snakes. J Comp Path 112:417-421, 1995
3. Fowler ME: Zoo and Wild Animal Medicine, 2nd ed., pp. 162-164. WB Saunders Co., Philadelphia, PA, 1986
CASE IV – 99-96-2 (AFIP 2740760)
Signalment: Adult, female ball python (Python regius).
History: Respiratory distress with audible open mouth breathing.
Gross Pathology: The cranial half of the trachea contained 10-15 masses that were adhered to the inner surface of the trachea. Several masses occluded about 75-85% of the lumen.
Laboratory Results: None.
Contributor’s Diagnosis and Comment: Trachea: Chondromas, multiple intraluminal.
Microscopically, the lesions were all similar and composed of well-demarcated, expansile masses of disorganized chondrocytes separated by variable amounts of chondroid matrix. Serial sections revealed that the masses were continuous with the mineralized tracheal cartilage ring. In some sections, the tracheal epithelium-lined surface was cuboidal, flattened, and/or focally eroded. Some sections in which there was loss of the surface epithelium also exhibited focal degeneration of the subjacent chondroid tissue.
Primary tracheal neoplasms are uncommon in all species and those originating from tracheal cartilage are rare. The most common benign tumors of tracheal origin are papillomas and fibromas. Squamous cell carcinoma is the most common malignant tumor of the trachea. Ball pythons are apparently predisposed to the development of tracheal chondromas.
AFIP Diagnosis: Trachea: Chondroma, ball python (Python regius), reptile.
Conference Comment: By definition, this lesion represents a chondroma: a benign proliferation of chondrocytes, composed of hyaline or myxohyaline cartilage, and usually arising from cartilaginous tissues. Conference discussion raised the question as to whether this lesion represented a true neoplasm, or some other benign proliferation of cartilage cells, possibly as an idiosyncratic response of ball pythons to some sort of trauma or inflammatory insult. Reported cases show no apparent sex predilection, age association, distribution or location within the trachea, or association related to inbreeding.
In humans, most pulmonary chondromas occur in the setting of Carney’s triad, which consists of pulmonary chondromas, epithelioid smooth muscle tumors of the stomach, and extra-adrenal paragangliomas. Certainly, more detailed reports and studies of ophidian chondromas are needed.
Contributor: The Procter & Gamble Company, 8700 Mason-Montgomery Road, Mason, OH 45040-9462
References: 1. Diethelm G, Stauber E, Tillson M, Ridgley S: Tracheal resection and anastomosis for an intratracheal chondroma in a ball python. J Am Vet Med Assoc 209(4):786-788, 1996
2. Drew ML, Phalen DN, Berridge BR, Johnson TL, Bouley D, Weeks
BR, Miller HA, Walker MA: Partial tracheal obstruction due to
chondromas in ball pythons (Python regius). J Zoo Wildl
Med 30(1):151-157, 1999
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
 |
