AFIP Wednesday Slide Conference - No. 30

28 May 1997
Conference Moderator: Dr. Thomas P. Lipscomb
Diplomate, ACVP
Department of Veterinary Pathology
Armed Forces Institute of Pathology
Washington, D.C. 20306-6000
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Case I - 388 (AFIP 2578783)

Signalment: 5-year-old, castrated male, lop-eared rabbit.
History: In early January, this rabbit developed ocular discharge and was treated for Pasteurella infection. Soon after, the owner noticed a lump below the philtrum which was biopsied in mid-January and diagnosed as ameloblastoma. The ocular discharge never resolved, and the mass began growing back by late January and gradually deformed the right side of the face. Sneezing worsened and by
mid-February, the rabbit began having breathing difficulty and was euthanized.
Gross Pathology: A 1x1x2 cm exophytic mass is present within the oral cavity just below the nasal philtrum. The right nasal bones are markedly convex from the nasal planum to a point just rostral to the eye. The convex region has marked crepitus on palpation, and measures 2x2x3 cm with the skin removed. Longitudinal section of the skull reveals a mass associated with the oral mass. There is bone destruction of the maxilla, nasal bones, hard palate and turbinates. The mass is soft with numerous mineralized foci.
Laboratory Results: None.
Contributor's Diagnosis and Comments: Ameloblastoma - maxillary gingiva, nasal philtrum, maxilla and nasal cavity, extensive, asymmetric.
Ameloblastoma is a rare neoplasia of tooth root origin and has never been reported in the rabbit. The tumor is locally invasive and locally destructive to bone. Metastasis has not been reported. The histologic criteria to be alerted to are the irregular islands with peripheral palisading columnar cells with polarized nuclei away from the basement membrane, and the stellate reticulum within the central region.
AFIP Diagnosis: Nasal cavity: Ameloblastoma, with hard substance, lop-eared rabbit, lagomorph.
Conference Note: Odontogenic neoplasms are uncommon. Teeth develop from two embryonic tissues. The enamel cap is derived from the dental lamina, which is an invagination of squamous epithelium from the lining of the buccal cavity. All other parts of the tooth, including dentin, cementum, and pulp, arise from the embryonic mesenchyme. Classification of odontogenic neoplasms is based on the inductive concept of odontogenesis: ameloblastic epithelium induces differentiation of dental papilla mesenchyme into odontoblasts, which forms dentin. The dentin induces ameloblasts to form enamel.
During normal tooth development, an epithelial ridge (dental lamina) develops, grows, and extends into the underlying mesenchymal tissue. The invading epithelium continues to proliferate as a solidly cellular mass forming the cap stage. There is condensation of the mesenchymal component (dental papilla) at its base. Both the epithelium and dental papilla mesenchyme continue to grow convert the epithelium into a bell-like structure in the bell stage. The epithelium, now an enamel organ, is divisible into distinct regions. The inner enamel epithelium is composed of columnar ameloblasts. The center of the enamel organ is the stellate reticulum. The ameloblasts are separated from the dental papilla by a basement membrane. The region of contact between the stellate reticulum and ameloblasts is occupied by cuboidal cells (stratum intermedium). As the tooth develops, the stellate reticulum (enamel pulp) atrophies and the outer enamel epithelium collapses upon the inner enamel epithelium. The dental papilla is entrapped within the confines of the enamel organ. A thin layer of columnar cells (odontoblasts) differentiates from the mesenchyme along the inner surface of the basement membrane; the remaining papilla becomes the pulp. A condensed mass of connective tissue (dental sac) surrounds the enamel organ and dental papilla, giving rise to alveolar bone, the periosteum surrounding the root, cementoblasts, and the periodontal membrane. (Banks, 1993)
In animals, ameloblastomas are reported more commonly in dogs and cattle than in cats and horses and are most frequently located in the mandible. They tend to be slow growing and invasive, resulting in extensive bone destruction. They do not metastasize but tend to recur after incomplete excision. Histologically, ameloblastomas are composed of islands and anastomosing cords of epithelium with peripheral palisades of polarized, cuboidal to columnar cells that resemble the inner enamel epithelium and enclose stellate reticulum-like tissue. There may be occasional keratinization. There may be cysts originating from the degeneration of centers of epithelial islands or from stromal degeneration. In animals, the presence of dentin or osteodentin-like hard substance has been noted in ameloblastomas.
Contributor: University of California - Davis, Veterinary Medical Teaching Hospital, Davis, CA
1. Banks WJ (editor): Applied Veterinary Histology. Third edition, Mosby Year- book, pp. 331-336, 1993.
2. Dubielzig, RR, Thrall, DE: Ameloblastoma and keratinizing ameloblastoma in dogs. Vet Pathol 19:596-607, 1982.
3. Shafer, WG: A textbook of oral pathology, WB Saunders, pp 308-314, 1983.
4. Jubb KVF, Kennedy PC, Palmer N (eds): Pathology of Domestic Animals. Vol. 2, pp 21-26, 1993.
5. Moulton, JE (editor): Tumors in Domestic Animals. 3rd ed., Univ. of Calif. Press, Berkeley, pp. 364-370, 1990.
6. Gardner DG: Ameloblastomas in the horse: a critical review and report of an additional example. J Oral Pathol Med 23:41-4, 1994.
International Veterinary Pathology Slide Bank:
Laser disc frame #3336, 9349, 19928-9.

Case II - D95-203 (AFIP 2551585)

Signalment: 8-month-old, female, ferret (Mustela furo).
History: This ferret was obtained from a commercial vendor, where it had been maintained under artificial lighting conditions consisting of 16 hours of light and 8 hours of darkness. These lighting conditions were continued after the animal was received from the vendor. Weight loss occurred over the next 18 days, and the animal was submitted for a diagnostic necropsy. The animal had not been experimentally manipulated during this time.
Gross Pathology: The animal was moderately thin, with little body fat. The uterus was enlarged.
Laboratory Results: None.
Contributor's Diagnosis and Comments:
1. Uterus: Endometrial hypertrophy with symplasma formation (pseudopregnancy), Mustela furo.
2. Uterus: Endometritis, acute, multifocal, mild.
Pseudopregnancy in the ferret can develop following a sterile mating, or as result of hormonal imbalance caused by reduced light intensity one month before breeding. The history of this ferret prior to receipt from the vendor is unknown.
Histological changes in the endometrium are the same in the pregnant and pseudopregnant uterus. Features of the endometrium in the present case include dilated glands containing large amounts of secretory material, marked enlargement of luminal and glandular epithelial cells with extreme karyomegaly, symplasma formation, and sloughing of symplasmic masses into the uterine lumen. There are also small accumulations of neutrophils within some dilated glands. These features are similar to the appearance of the endometrium 20 to 25 days following breeding. Symplasma formation occurs as the most superficial hypertrophied epithelial cells lose their integrity and form masses of protoplasm containing whole or fragmented nuclei. The duration of pseudopregnancy is identical to pregnancy (40-42 days). The endometrium breaks down between day 35 and day 40, and resembles the anestrous state by day 45.
AFIP Diagnosis:
1. Uterus: Endometrial hypertrophy with symplasma formation, ferret (Mustela furo), mustelid.
2. Uterus: Endometritis, acute, multifocal, mild.
Conference Note: In ferret uteri, the pre-implantation period is characterized by general growth of the tissue and moderate secretory activity. At the time of implantation, the luminal epithelium undergoes hypertrophy and hyperplasia and shows much secretory activity. This area of altered activity sweeps progressively toward the gland fundi, and the epithelium behind it becomes progressively enlarged forming symplasmic masses. In the ferret, symplasma formation occurs in all regions of the uterus in both pregnant and pseudopregnant animals, in contrast to other carnivores that have been studied in which it develops only at implantation sites.
Contributor: The Procter & Gamble Company, Miami Valley Laboratories, P.O. Box 398707, Cincinnati, OH 45239-8707.
1. Buchanan GD: Reproduction in the ferret (Mustela furo). I. Uterine histology and histochemistry during pregnancy and pseudopregnancy. Am J Anat 118(1): 195- 216, 1966.
2. Fox JF: Biology and Diseases of the Ferret. Lea & Febiger, Philadelphia, 1988.
International Veterinary Pathology Slide Bank: None.

Case III - 1000194 (AFIP 2550496)

Signalment: Hare (Lepus europaeus), male, adult
History: The animal was shot in January 1994 together with six other hares from the same area in order to find out possible causes of the progressive diminishing of the hare population in Germany. The epidemiological study included parasitological, serological, toxicological and histopathological investigation on 88 hares from 4 adjacent areas altogether. Tissues from lungs, heart, pancreas, spleen, kidneys, adrenals, thyroid gland, brain and testes were submitted for histopathological examination.
Gross Pathology: Macroscopic changes in this animal were restricted to the liver which exhibited multiple firm yellowish grey patches.
Laboratory Results: Serologically, antibodies to Brucella spp., Leptospira spp. and Pasteurella tularensis were not detected. The Coxiella burnetii titer was suspicious (1:10). A hemagglutination inhibition test for rabbit hemorrhagic disease virus antibodies showed a positive result (titer 1:80). The parasitological investigation revealed eggs of Capillaria hepatica in the liver, as well as low contents of Trichostrongylus retortaeformisand Trichuris leporis in the intestine.
Contributor's Diagnosis and Comments: Liver: hepatitis, granulomatous, multifocal, chronic, severe, with eggs of Capillaria hepatica and caseous necrosis within granulomas.
Sections of the liver contain multiple coalescing granulomas characterized by central partially calcified caseous necrosis, cellular debris and granulocytes, epithelioid macrophages and giant cells. Lesions are surrounded by a zone of fibroblast proliferation and encapsulated by fibrous connective tissue. In adjacent areas, bile duct proliferation can be observed. In the centers of the granulomas, either multiple ovoid, intact parasite eggs with obvious polar caps or their disintegrated remnants are found in an intracellular or extracellular localization.
Additionally, two other hares from the same areas also showed a Capillaria hepatica infection. The remaining 85 animals examined within this study over a period of three years, were not affected. The reason for the local and temporary limitation of the infection remains unknown.
Rats and mice are the usual hosts of Capillaria hepatica. The parasite shows a direct life cycle with both female and male worms in the liver parenchyma. Eggs remain in the liver until the host is devoured or the liver undergoes postmortem decomposition. Embryonation occurs in the soil (CONLOGUE et al., 1979). Antemortem diagnosis is only possible by liver biopsy. The parasites are not highly pathogenic. Their importance is gathered by their ability to infect other mammals. Sporadically carnivores [dogs (see: AFIP 2415684), cats, coyotes), horses, hares, hedgehogs, and humans] may be affected (BRANDER et al., 1990;PANNENBECKER et al., 1990).
AFIP Diagnosis: Liver: Granulomas, eosinophilic, multiple, coalescing, with bioperculate barrel-shaped nematode eggs, hare (Lepus europaeus), lagomorph, etiology consistent with Capillaria hepatica.
Conference Note: Capillaria hepatica is apparently a widespread parasite of wild mice and rats; up to an 80% incidence has been reported in urban rats in some areas. Infection is usually inapparent in rodents, and is uncommon in laboratory-reared animals because of the unusual requirements of the life cycle. This parasite is occasionally seen in dogs and monkeys, has been described in several other wild animal species (beavers, muskrats, hares, and peccaries), and sometimes infects man. Capillaria spp. are aphasmids and are classified in the group Trichinellina, which includes both Capillariidae and Trichuridae; these aphasmids are unique among nematodes because they have stichosomes (a series of glands along their esophagus) and one or more bacillary or hypodermal bands (hypodermal gland cells that have pores through the cuticle) that give the cuticle a striated appearance, and distinguish it from the other trichurids. Their musculature is coelomyarian, polymyarian but may be inapparent. The intestine is composed of uninucleate cuboidal to columnar cells. Eggs are bioperculate, barrel- shaped, thick- shelled and the outer shell layer is striated.
Microscopically, both adult nematodes and masses of eggs can be seen. The adults cause some traumatic hepatitis and the eggs provoke the development of granulomas. The hepatitis may be severe enough in some animals to result in cirrhosis. In primates, the disease is severe and has been associated with some deaths.
C. hepatica is of public health significance where children play in rat-infested areas. Clinical manifestations in humans resemble visceral larva migrans. There is eosinophilia and hepatomegaly, and acute or subacute hepatitis.
Contributor: Institut für Veterinär-Pathologie, der Unversität Leipzig, Margarete- Blank-Str. 4, D-04103, Leipzig.
1. Brander P, Denzler T, Henzi M: Capillaria hepatica in a dog and hedgehog. Schw Arch Teirheilk 132:365-370, 1990.
2. Conlogue G, Foreyt W, Adess M, Levine H: Capillaria hepatica (Bancroft) in select rat populations of Hartford, Connecticut, with possible public health implications. J Parasitol 65:103-108, 1979.
3. Farhang-Azad A: Ecology of capillaria hepatic (Bancroft 1893) (Nemotoda). 1. Dynamics of infection among Norway rat populations of the Baltimore Zoo, Baltimore, MD J Parasitol 63:117-122, 1977.
4. Pannenbecker J, Miller TC, Müller J, Jeschke R: Severe Capillaria hepatica infestation in a young child. Monatsschr Kinderheilkd 138:767-771, 1990.
5. Chitwood, M, and Lichtenfels, JR: Identification of parasitic metazoa in tissue sections. Exp Parasitol 32: 407-519, 1972.
6. Jubb KVF, Kennedy PC, Palmer N (eds): Pathology of Domestic Animals, Fourth edition, Vol. 2, Academic Press, p. 376, 1993.
International Veterinary Pathology Slide Bank:
Laser disc frame #4131, 19337-40.

Case IV - 95P1056 (AFIP 2551662)

Signalment: 5-year-old, female, Holstein, bovine.
History: The herd has lost 18 cattle in the last 4 to 5 weeks. This cow calved 6 days ago and was down this morning. She died during calcium therapy.
Gross Pathology: There were multiple and numerous linear and punctate erosions and ulcers in the distal ½ of the esophagus. There were petechia in the abomasum. The ileum and colon were filled with serosanguineous fluid containing clots of blood and fibrin. The liver was pale and swollen. The uterine mucosa was diffusely gray, thickened, necrotic and foul smelling.
Laboratory Results: Florescent antibody test for bovine viral diarrhea (BVD) virus on esophagus and ileum was positive. Culture of Peyer's patches and colon yielded Salmonella serogroup E and liver yielded E. coli and Pasteurella hemolytica.
Contributor's Diagnosis and Comments:
1. Esophagitis, necrotizing, multifocal, acute, moderate.
2. Enteritis, necrohemorrhagic, diffuse, acute, severe with thrombosis and lymphoid (Peyer's patch) necrosis due to infection with BVD virus and Salmonella serogroup E.
The cow had classical mucosal disease and was also infected with Salmonellaserogroup E. Probably the cow was persistently infected with a non-cytopathic strain of bovine viral diarrhea virus and was recently exposed to a cytopathic BVD strain or a cytopathic mutant of the persisting strain. Two of the other affected herdmates were also positive for BVD virus and were infected with Salmonella serogroup E. By genomic typing, BVD isolates are divided in BVD VIRUS type 1 and type 2. Both cytopathic and non-cytopathic isolates are found among each subtype.
AFIP Diagnosis:
1. Small intestine: Enteritis, necrotizing, subacute, fibrinosuppurative and hemorrhagic, transmural, severe, with necrotizing vasculitis, thrombosis, lymphoid necrosis and depletion, bacilli and fungal hyphae, Holstein, bovine.
2. Esophagus: Esophagitis, necrotizing, subacute, multifocal, moderate, with intra- epithelial cleavage vesicles, Holstein, bovine.
Conference Note: The histopathologic findings are characteristic of mucosal disease. In addition to the evidence of viral and bacterial infection, a section stained by the GMS method demonstrated vaso-invasive fungal hyphae morphologically consistent with Aspergillus sp. The fungal hyphae are very difficult to discern in the HE stained sections. A Gram's stain demonstrated gram-negative bacilli wihin the inflamed intestinal wall. A variety of opportunistic infections have been reported in cases of mucosal disease.
Bovine viral diarrhea virus infection produces a wide spectrum of disease including subclinical infection (most common), bovine virus diarrhea, immunosuppression, infertility, abortion and mummification, congenital defects, immunotolerance and persistent infection, and acute and chronic mucosal disease.
The principle routes of infection are via inhalation or ingestion of infected saliva, oculonasal discharge, urine and feces. Transmission may also occur through infected semen, uterine secretions, amniotic fluid, placenta or via contaminated hypodermic needles. Blood-feeding flies can transmit the infection experimentally.
The virus can cross the bovine placenta and fetal blood-brain barrier and infect the fetus; a wide variety of developmental abnormalities and/or fetal death may result. Cows usually remain clinically normal; however, fertility is transiently reduced. Fetal damage is probably due to specific interference with tissue differentiation, maturation, and growth, since there are no placental lesions.
BVD virus is antigenically related to the Hog Cholera virus of pigs and the Border Disease virus (Hairy Shaker Disease) affecting sheep.

Contributor: Iowa State University, Department of Pathology, South 16th Street, Ames IA 50011.
1. Boling S. In Report of the committee on infectious diseases of cattle, bison and llama. Proc USAHA Ann mtg. Grand Rapids, MI, 1994, pg 266-268.
2. Baker JC. Bovine viral diarrhea virus: A review. JAVMA 190:1449-1458, 1987.
International Veterinary Pathology Slide Bank:
Laser disc frame #1302, 1328, 1561, 2030, 2031, 2668, 2847, 2848, 3511, 3512, 8868.
Lance Batey
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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