AFIP Wednesday Slide Conference - No. 18

26 February 1997
Conference Moderator: COL William Inskeep II
Diplomate, ACVP
Chairman, Department of Veterinary Pathology
Armed Forces Institute of Pathology
Washington, DC 20306-6000

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Case I - A96-64 (AFIP 2549328)

Signalment: Adult (aged), spayed-female, domestic long-haired, grey feline.
History: This cat was adopted from an animal shelter three years ago with a history of chronic renal disease. Later, hyperthyroidism was diagnosed which was partially controlled by Tapazole therapy. A few days before presentation, the cat became anorexic with progressive weight loss and eventual lethargy. Palpation revealed a large mass in the abdominal cavity and the cat was euthanatized at owners request.
Gross Pathology: The cat was emaciated with no subcutaneous or intra- abdominal fat. The left thyroid gland was markedly enlarged (3 cm by 1 cm by 1.2 cm) and the right was markedly atrophied. A multi-lobulated, smooth, soft tissue mass was present in the mesentery, 4.5 cm by 4 cm by 3 cm, with firm attachments to the ileocecal junction and the pancreas. On cut surface, the mass consisted of homogeneous, grey- white tissue that bulged slightly from the cut surface. Some areas had small, dark, red to black foci. The liver had numerous discrete round to oval masses scattered throughout the parenchyma which often bulged from the capsular surface. Most consist of soft, grey-white tissue similar to the mesenteric mass but a few were cavitated and filled with clotted blood or serosanguinous fluid.
Two similar mass 4 mm and 1 cm diameter were present in the spleen. Two small (<2mm diameter), round, soft tissue masses were also present in the lungs. The kidneys were bilaterally shrunken and had diffusely rough, pitted to granular cortical surfaces.
Laboratory Results: Immunohistochemistry: Sections of the mass in the mesentery and liver were positive for antibodies directed against vimentin, factor VIII (von Willebrand's factor) and MIB-1 (proliferating cells marker) and negative for cytokeratin, synaptophysin, S-100 protein, BCL-2 (associated with inhibition of apoptosis), and desmin.
Contributor's Diagnosis and Comments: Hemangiosarcoma, mesentery, feline.
Hemangiosarcoma, metastatic, liver.

Additional diagnoses (tissues not provided): Hemangiosarcoma, metastatic, lung, spleen.
Adenomatous hyperplasia, thyroid gland, unilateral.
Nephritis, chronic, interstitial, diffuse, bilateral, idiopathic.
Hemangiosarcomas are more common in dogs than cats but several feline cases have been reported (1,2). Several cases of primary hemangiosarcoma have been reported in the root of the mesentery and/or mesenteric lymph nodes(1,2). Intra- abdominal hemangiosarcomas also tend to metastasize more frequently than those in the skin. In this case, the largest mass was found within the mesentery and histologic sections contained clusters of lymphocytes suggesting it may have arisen from with a mesenteric lymph node.
Although a few blood-filled spaces lined by plump endothelial cells projecting into the lumens were observed in some areas of the tumors, the solid and anaplastic appearance displayed in the majority of the masses prompted immunohistochemical analysis to determine the cell of origin. Neoplastic cells were positive for vimentin and factor VIII confirming a mesenchymal and vascular endothelial cell origin, respectively. Although lymphangiosarcoma cannot be ruled out with certainty, the presence of red blood cells and fibrin in some of the vascular clefts and spaces is more consistent with a hemangiosarcoma.
AFIP Diagnosis: Liver; mesentery: Sarcoma, poorly differentiated, Domestic Longhair, feline.
Conference Note: Although careful consideration was given to the contributor's diagnosis of hemangiosarcoma, the conference participants favored the less specific diagnosis of poorly differentiated sarcoma. In immunohistochemical stains performed at the AFIP, neoplastic cells did not stain positively for factor VIII-related antigen. Neoplastic cells were also negative for lysozyme, glial fibrillary acidic protein, smooth muscle actin, S-100 protein, desmin, and cytokeratin. Although the origin of this neoplasm could not be determined, the differential diagnosis includes malignant peripheral nerve sheath tumor, malignant fibrous histiocytoma, rhabdomyosarcoma, and leiomyosarcoma. The Department of Soft Tissue Pathology considered this an "unclassified malignancy" and favored a sarcoma.
Contributor: New England Regional Primate Research Center, Harvard Medical School, P.O. Box 9102, One Pine Hill Drive, Southborough, MA 01772.
1. Carpenter JL, Andrews LK, Holzworth J: Tumors and tumor-like lesions. In : Holzworth J, ed. Diseases of the cat, Philadelphia: Saunders WB Co., pp. 406-583, 1987.
2. Scavelli TD, Patniak AK, Mehlhaff CJ, Hayes AA: Hemangiosarcoma in the cat: Retrospective evaluation of 31 surgical cases. J Amer Vet Med Assoc 187:817- 819, 1985.

Case II - S-900-96 (AFIP 2549333)

Signalment: Canine, mixed breed, spayed female, 6-years-old.
History: The dog was presented with a vague history of previous anterior uveitis in both eyes. At presentation, the right eye had buphthalmia and moderate corneal edema was present. There was iris hypopigmentation, retinal vessel attenuation, and atrophy and cupping of the optic nerve. Both direct and consensual pupillary light reflexes (PLR) were absent in the right eye. Aqueous flare, slight iris hyperpigmentation, multifocal pigment deposits on anterior lens capsule, and a normal retina were present in the left eye. Direct PLR was normal and consensual PLR was partial in the left eye. The intraocular pressures (IOP) were recorded as 19 mm Hg and 7 mm Hg for the right and left eyes, respectively. The diagnosis of anterior uveitis was made for the left eye and glaucoma, likely secondary to previous uveitis, was made for the right eye. The animal was treated conservatively with medical therapy for a period of approximately three months. The IOP of the right eye had risen to 33 mm Hg (9mm Hg, left eye) and the owners elected enucleation of the eye.
Gross Pathology:.The eye was generally enlarged and the sclera was thin. Diffuse cloudy yellow staining, as a result of Bouin's solution fixation, prevented more detailed gross evaluation.
Laboratory Results: None.
Contributor's Diagnosis and Comments: Retinal, scleral, corneal, and iridial atrophy, severe, optic nerve herniation (consistent with chronic glaucoma).
Preiridial and postiridial fibrovascular membrane formation, moderate to marked, with entropion uveae and focal iridociliary synechiae.
The glaucoma in this case was considered to be secondary to filtration angle obstruction by the relatively thin, but extensive, preiridial fibrovascular membrane. The fibrovascular membrane in this case extends posteriorly over the inverted and adherent iridial free margin and across the posterior face of the iris where focal synechia have formed between the iris, fibrovascular membrane, and ciliary processes. Although there was virtually no uveal inflammatory cell infiltration, it is likely that the preiridial fibrovascular membrane in this case developed as a consequence of previous anterior uveitis. Preiridial fibrovascular membranes have been identified in dogs, cats, horses, and cattle and occur most often in globes with retinal detachment, ciliary body adenomas, chronic glaucoma, and anterior uveal melanomas. Preiridial fibrovascular membranes in human beings, known as rubeosis iridis, occur commonly and are most often present in patients with diabetic retinopathy, central retinal vein occlusion, or primary intraocular neoplasia. Occurrence secondary to chronic uveitis is also likely. Glaucoma resulting from fibrovascular membrane formation in human beings is known as neovascular glaucoma.
AFIP Diagnosis:
1. Eye, iris, ciliary body, and filtration angle: Fibrovascular membrane, pre-iridal and post-iridal, with entropion uveae and anterior peripheral synechiae, mixed breed, canine.
2. Eye, retina, sclera, cornea, and iris: Atrophy, diffuse, moderate.
3. Eye, lens: Cataractous change, subcapsular.
Conference Note: The conference participants agreed with the contributor's diagnosis and comments. A diagnosis of optic nerve herniation was not included above because in the sections reviewed during the conference, this structure was absent.
Iridal fibrovascular membrane formation is probably more common than the literature suggests. In a study by Peiffer, et al., membrane formation was commonly found in association with retinal detachment, chronic endophthalmitis, chronic glaucoma, ocular melanoma, and ciliary epithelial tumors. The membranes are often composed of a mixture of plump spindle-shaped cells, capillaries, and collagen fibers cover that cover the surface of the iris, or less commonly, the pectinate ligaments and ciliary body. Lesions attributed to the presence of iridal fibrovascular membranes can include, hyphema, eversion or inversion of the pupillary margin, and occlusion of the pupil or filtration angle. The pathogenesis of iridal fibrovascular membrane may be related to production of angiogenic factors by ischemic retina, by neoplasms, or by leukocytes involved in ocular inflammation.

Contributor: The Animal Medical Center, 510 East 62nd Street, New York, NY, 10021.
1. Peiffer RL, Wilcock BP, Yin H: The pathogenesis and significance of pre-iridal fibrovascular membrane in domestic animals. Vet Pathol 27:41-45, 1990.
2. Spencer WH: Glaucoma. In: Ophthalmic Pathology, An Atlas and Textbook. ed. Spencer WH, 3rd ed., Vol. 1, pp. 480-547, W.B. Saunders Company, 1985.
3. Jubb KVF, Kennedy PC, Palmer N (eds): Pathology of Domestic Animals, 4th ed., Vol. 1, pp. 441-521, Academic Press, 1992.
International Veterinary Pathology Slide Bank:
Laser disc frame #10204, 11999, 12000, 12007, 12010, 12011, 12019, 12044, 12046, 16818.

Case III - 1453-96 (AFIP 2549334)

Signalment: 6-year-old spayed Domestic Shorthair cat.
History: This cat presented recently with persistent cough and weight loss. Radiographs and ultrasound showed a large (20 cm), cystic, complex anterior mediastinal mass and pleural effusion.
Gross Pathology: 11 x 7 x 2 cm multi-cystic grayish mass.
Laboratory Results: The hematologic and biochemical findings were within normal limits.
Contributor's Diagnosis and Comments: Cystic thymoma containing both epithelial and lymphocytic components with diffuse cystic degeneration.
Post surgically the cat is doing well.
AFIP Diagnosis: Thymus: Thymoma, cystic, with marked mastocytosis, Domestic Shorthair, feline.
Conference Note: The conference participants agreed with the contributor's diagnosis.
Thymoma is an uncommon tumor in humans and animals. These neoplasms have been associated with myasthenia gravis, polymyositis, myocarditis, and dermatitis. Thymomas are rarely reported in cats. Several of the reported cases contained cysts lined by thymic epithelial cells, most often of the fusiform type, that were separated by prominent fibrous bands . Mast cells, which are preseent in small numbers in the normal feline thymic medulla, can be numerous in feline thymomas.

Thymic epithelial cells are derived from endoderm of the third and fourth pharyngeal pouches and are the neoplastic cells in thymoma. These cells may have round, oval, or fusiform nuclei, and may be arranged in solid, trabecular, cribriform, whorled, cystic, or rosette patterns. Thymomas often contain numerous non-neoplastic lymphocytes which may obscure the true nature of the neoplasm. In this case, thymic lymphoma must be ruled out.
Normal thymic epithelial cells produce several small polypeptide hormones including thymosin, thymopoietins, thymic humoral factor, thymulin, and the thymostimulins. Thymulin is interesting, since it is a zinc-containing peptide that can partially restore T cell function in thymectomized animals. Thymic epithelial cells also secrete IL-1.
Contributor: The Animal Medical Center, 510 East 62nd Street, New York, NY 10021.
1. Suster S and Rosai J: Cystic thymomas: A clinicopathologic study of ten cases. Cancer 69:92-97. 1992.
2. Carpenter JL, Holzworth J: Thymoma in 11 cats. JAVMA 181(3):248-251, 1982.
3. Tizard IR (ed): Veterinary Immunology. 5th ed., W.B. Saunders, pp. 78-80, 1996.
4. Moulton JE (ed): Tumors in Domestic Animals, 3rd ed., University of California Press, pp. 267-268, 1990.
5. Holzworth J (ed): Diseases of the Cat: Medicine and Surgery, Vol. 1, W.B. Saunders, pp. 439-441, 1987.

International Veterinary Pathology Slide Bank:
Laser disc frame #1134, 1135, 5967, 5968, 7911, 21559.

Case IV - 96:1186 (AFIP 2558107)

Signalment 26-week-old White Leghorn Dekalb XL layer chicken.

History: During June, July and August, a chronic mortality rate of 5-10% was identified in a 600-bird flock of layers. The birds were lethargic and weak and had droopy combs. A mild to moderate drop in production was noted. The mortality peaked in August. The birds were 25 weeks of age and had been raised from Day 1 on the farm. The layers were maintained on litter flooring and were fed 16% layer feed. Marek's disease was diagnosed in this flock earlier, and coccidiostats were withdrawn at 18 weeks.
Gross Pathology: Multiple laying chickens were examined. The small intestines were markedly dilated and contained bloody fluid with flecks of tissue and blood clots. The serosa of the middle one-third of the small intestine was red-grey with prominent blood vessels. Numerous, minute, 1-2 mm, smooth foci were disseminated across the serosa of the middle one-third of the small intestine, and petechiae were dispersed along the associated mucosa. The wall of the middle one-third of the small intestine was markedly thickened. The layers were in production, and one bird had symmetrically enlarged liver, spleen, and kidney with numerous, slightly raised, white, parenchymal foci ranging from 1-8 mm in diameter.
Laboratory Results: Serologic tests for antibodies to Mycoplasma gallisepticum, Mycoplasma synoviae, avian influenza, and Newcastle disease virus were negative. Bacterial cultures of liver and small intestine yielded no significant growth.
Contributor's Diagnosis and Comments: Morphologic diagnosis: Small intestine. Marked, segmental, subacute, lymphohistiocytic enteritis with intralesional protozoal schizonts and hemorrhage.
Etiology: Eimeria necatrix.
The sections are of the middle one-third of the small intestine. Dispersed throughout the lamina propria are numerous aggregates of closely-packed coccidian schizonts. The schizonts contain large numbers of densely-packed, comma-shaped merozoites that are limited by a thin membrane. In some foci, aggregates of schizonts are surrounded by mantles of foamy macrophages and occasional multinucleate giant cells. In other foci, mononuclear infiltrates of large numbers of lymphocytes and macrophages with occasional plasma cells and few eosinophils are present in the lamina propria surrounding schizonts. Spotty proprial hemorrhage is present. Along the mucosal surface, there is a layer of hemorrhage, fibrin, and proteinaceous fluid within which are scattered rafts of displaced, necrotic epithelial cells and aggregates of very large numbers of closely-packed, comma shaped, uninucleate merozoites. There is mild to moderate reduction and fusion of villi.
Eimeria necatrix is a severe pathogen and can cause high mortality in chicken flocks. Outbreaks of coccidiosis usually occur when environmental parameters favor sporulation of oocysts; for example, warm temperatures, wet litter, and the presence of old carrier birds. Probably because of its comparatively low reproductive capability, E. necatrix is not able to compete well with other coccidia and is diagnosed mostly in older birds such as brooder pullets or layer pullets (9 - 14 weeks or older). Gross lesions of E. necatrix are characterized by ballooning of the middle one-third of the small intestine with petechiae and disseminated white foci (i.e. schizonts). The intestinal contents are mucoid and bloody. Microscopically, large diameter second-generation schizonts (up to 66 µm) containing hundreds of merozoites penetrate the deep mucosa and can penetrate the submucosa and muscularis externa. Only large diameter schizonts and merozoites are identified in the small intestine; sexual stages and oocysts develop in small numbers in the cecal mucosa only and cause little pathogenic effect.
Immunosuppressive disease may act in concert with coccidiosis to produce more severe disease. Marek's disease may interfere with the development of immunity to coccidiosis.
The tissue damage resulting from proprial infiltration by second-generation schizonts of E. necatrix may allow for subsequent infection by Salmonella sp or Clostridium perfringens, the latter leading to necrotic enteritis.
AFIP Diagnosis: Small intestine: Enteritis, proliferative, subacute, diffuse, moderate, with villar atrophy, necrosis, hemorrhage, and coccidial schizonts, White Leghorn Dekalb XL chicken, avian.
Conference Note: The conference participants agreed with the contributor's diagnosis. The term "proliferative" was added to the diagnosis because of the prominent mucosal hyperplasia.
Eimeria necatrix has a typical eimerian life cycle. After ingestion of an oocyst, it is crushed in the gizzard and sporozoites are released. Sporozoites enter cells in the mucosa of the intestine and begin the cell cycle leading to reproduction. At least two generations of asexual reproduction, called schizogony or merogony, lead to a sexual phase, where small, motile microgametes seek out and unite with macrogametes. The resulting zygotes matures into oocysts, which are released from the intestinal mucosa and shed in the feces. This entire process takes from 4 to 6 days depending on species. In some species such as E. necatrix and E. tenella, maximum tissue damage occurs when second-generation schizonts rupture to release merozoites. Characteristics useful in identification of species of Eimeria in chickens are: 1) location of the lesion in the small intestine; 2) gross appearance of the lesion; 3) oocyst size; 4) size of schizonts and merozoites; and 5) location of parasites (epithelial versus subepithelial) in intestinal tissue sections.
Contributor: Department of Pathology, University of Connecticut, 61 North Eagleville Road, U-89, Storrs, CT 06269-3089
1. Biggs PM, Long Pl, Kenzy SG, and Roots DG: Investigation into the association between Marek's disease and coccidiosis. Acta Vet 38:65-75, 1969.
2. Helmbolt CF, and Bryant ES: The pathology of necrotic enteritis in domestic fowl. Avian Dis 15:775-780, 1971.
3. McDougald LR, Reid WM: Coccidiosis, In: Diseases of Poultry, 9th ed., Calrek BW, Barnes HJ, Beard CW, Reid WM and Yoder HW Jr.(eds), Iowa State University Press, Ames, Iowa. pp. 780-797, 1991.
4. Riddell, C: Alimentary System. In: Avian Histopathology, 1st ed. The American Association of Avian Pathologists, University of Pennsylvania, New Bolton Center, Kennett Square, Pennsylvania. pp. 47-56, 1987.
5. Whiteman CE and Bickford AA: Coccidiosis. In: Avian Disease Manual. 2nd American Association of Avian Pathologists, University of Pennsylvania, New Bolton Center, Kennett Square, Pennsylvania, 1983.
International Veterinary Pathology Slide Bank:
Laser disc frame #19550.
Lance Batey, DVM
Captain, VC, USA
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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