Results
AFIP Wednesday Slide Conference - No. 26
30 April 1997
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- Conference Moderator: Dr. Charles G. McLeod,
Jr.
Diplomate, ACVP
Antech Diagnostics
8831 Satyr Hill Road
Carney, MD 21234
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Case I - 95E 9853-3 (AFIP 2550323)
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- Signalment: 18-year-old, thoroughbred gelding, horse.
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- History: This horse suffered recurrent, prolonged,
severe episodes of dyspnea that were unresponsive to medical
treatment. Euthanasia was performed during a dyspneic episode.
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- Gross Pathology: The lungs were pink, spongy, and
normally collapsed, with the exception of mild firmness and darkening
of a cranial portion of the left lung. The diaphragm was diffusely
thickened (hypertrophy). The carcass was in good flesh.
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- Laboratory Results: None.
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- Contributor's Diagnoses and Comments: 1. Bronchiolitis
and bronchitis, diffuse, chronic, moderate, nonsuppurative, with
mild goblet cell metaplasia (all slides).
2. Bronchiolitis and bronchitis, diffuse, chronic, moderate,
nonsuppurative, with moderate goblet cell metaplasia and mucopurulent
exudate (95E9853-3).
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- Etiology: Presumptive respiratory hypersensitivity
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- The clinical signs and histological lesions in this horse
are indicative of the syndrome know variably as heaves, chronic
obstructive pulmonary disease, broken wind, chronic bronchiolitis-emphysema
complex, and chronic bronchitis/bronchiolitis. Heaves occurs
more commonly in stabled horses as compared to pastured horses.
Moving acutely affected horses from stables to pasture is often
an effective treatment. The condition is believed to be caused
by hypersensitivity to inhaled allergens; molds and hay dust
have both been implicated.
- Emphysema is often not observed in "heavy" horses.
Horses with severe, prolonged clinical signs may develop an easily
observed "heave line" which represents the thickened
edge of hypertrophic external abdominal oblique muscles, caused
by forced expiratory efforts. The horse in this case had severe,
recurrent clinical signs, but little evidence of gross lesions,
other than apparent hypertrophy of the diaphragmatic muscle.
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- AFIP Diagnosis: Lung: Bronchiolitis and bronchitis,
lymphoplasmacytic, diffuse, moderate, with airway epithelial
hyperplasia, diffuse congestion, and multifocal alveolar edema,
thoroughbred, horse, equine.
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- Conference Note: Conference participants agreed with
the contributor's diagnoses. The most consistent finding in horses
with clinical signs of chronic obstructive pulmonary disease
is a generalized chronic bronchiolitis. Emphysema is less common.
Constant features of the chronic bronchiolitis are epithelial
hyperplasia, goblet cell metaplasia, peribronchiolar fibrosis,
and infiltration by lymphocytes and plasma cells. Lumina of bronchioles
are narrowed by accumulation of exudate and peribronchiolar fibrosis.
Mucus is usually a major component of the exudate. The presence
of eosinophils is quite variable ranging from very few to numerous.
There are usually increased numbers of mast cells around bronchioles.
Neutrophils are less common than eosinophils but sometimes the
lesion has the appearance of a mucopurulent bronchiolitis.
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- Contributor: Wyoming State Veterinary Laboratory,
1174 Snowy Range Rd., Laramie, WY 82070.
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- References:
1. Jubb KVF, Kennedy PC, Palmer N: Pathology of Domestic Animals,
4th ed., vol 2, pp. 582-583, Academic Press, 1993.
- 2. Rooney JR, Robertson JL (eds): Equine Pathology. Iowa
State University Press, pp. 46-50, 1996.
- 3. Smith BP (editor): Large Animal Internal Medicine. Mosby,
St. Louis, pp. 533-536, 1990.
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- International Veterinary Pathology Slide Bank:
Laser disc frame #2628, 9575, 15543, 15580-3.
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Case II - HB1787 (AFIP 2554540), 1 photo
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- Signalment: Japanese Cat, female, adult.
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- History: The tumorous mass had been recognized in
the perianal area and gradually increased in size with ulceration
of the surface. The mass was initially excised in December 1994,
and thereafter recurrence of the tumor has taken place two times.
The cat harboring the tumor is still alive.
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- Gross Pathology: The primary tumor measured 5 x 5
x 6 cm and had an irregular ulcerated surface. Cut surface of
the tumorous mass was grayish-white and revealed fibrous septa
which divided the tumor into lobules.
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- Laboratory Results: None.
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- Contributor's Diagnosis and Comments: Carcinoma of
the anal sac- associated sebaceous gland.
- The tumorous mass was composed of lobules of basaloid and
sebaceous cells separated by fibrovascular septa. The neoplastic
cells were polyhedral or angular with vesiculate nuclei and brightly
eosinophilic granular cytoplasm. Occasionally, the tumor cells
showed definite cytoplasmic vacuoles. Frequently, there was squamous
differentiation towards the center of the neoplastic lobules.
In some lobules, there was intermingling of basaloid cells with
the sebaceous cells. The morphology of the present tumor is likened
to that of canine hepatoid tumor. It is worth mentioning that
cats have no perianal (hepatoid) gland which is a peculiar anatomical
structure of dog. Accordingly, based upon the morphologic features,
we suppose that the origin of the present tumor is the anal sac-associated
sebaceous gland. The contribution of the sweat gland, the other
glandular structure associated with the anal sac, was eliminated
as the histologic criteria of the present tumor are different
from that of apocrine carcinoma. There is no previous report
of a similar case of perianal tumor in cat. Yager and Wilcock
(1994) mentioned that they have seen only one case of feline
perianal carcinoma which they reclassified as a perianal adenoma.
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- AFIP Diagnosis: Haired skin, perianal area: Carcinoma,
sebaceous, Japanese cat, feline.
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- Conference Note: The conference participants agreed
that the histologic findings are diagnostic of sebaceous carcinoma.
The exact origin is not evident in the sections examined.
- Sebaceous carcinomas are infrequent in dogs and rare in cats.
These lesions are locally infiltrative, solitary, poorly circumscribed
tumors made up of pleomorphic cells, a proportion of which have
evidence of sebaceous differentiation. Lobule formation is often
present but is not a prominent feature. Neoplastic cells are
often pleomorphic with marked anisocytosis and anisokaryosis;
mitoses can be numerous. All neoplastic cells seem to make an
attempt at forming a sebaceous cell. In contrast, basal cell
tumors with sebaceous differentiation (also known as sebaceous
epitheliomas) have a preponderance of basal cells with variable
amounts of orderly and often complete sebaceous differentiation.
The sebaceous carcinoma lacks these two distinct and mature cell
populations.
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- Contributor: Laboratory of Comparative Pathology,
Department of Veterinary Clinical Sciences, Graduate School of
Veterinary Medicine, Hokkaido University, Sapporo 060, Japan.
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- References:
1. Dellman HD: Textbook of Veterinary Histology. Lea and
Febiger, Philadelphia, pp. 825-313, 1993.
- 2. Goldschmidt MH, Shofer FS: Skin Tumors of the Dog and
Cat. Pergamon Press, pp 66-75, 1992..
- 3. Greer MB, Calhound ML: Anal sac of the cat (Felis domesticus).
Am J Vet Res 27:773-781, 1996.
- 4. Gross TL, Ihrke PJ, Walder EJ: Veterinary Dermatopathology.
A macroscopic and microscopic evaluation of canine and feline
skin disease. Mosby-Year Book, pp. 381-384, 1992.
- 5. Pully, TL, Stannard AA: Tumors of the skin and soft tissues.
In: Tumors of the Domestic Animals, Moulton, JE (ed), Univ. of
California Press, pp 23-87, 1990.
- 6. Scott DH, Miller WH, Griffin CE: Small Animal Dermatology.
Saunders WB Company, pp. 956-989, 1995.
- 7. Yager JA, Wilcock BP: Surgical Pathology of the Dog and
Cat. Mosby-Year Book pp. 257-270, 1994.
- International Veterinary Pathology Slide Bank: None.
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Case III - 96-7927-5 (AFIP 2551386)
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- Signalment: 10.5-year-old, female, spayed, Domestic
Shorthair cat.
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- History: Diagnosed with diabetes one year ago. Controlled
with insulin. Six weeks ago became anorectic. Inflammatory bowel
disease was diagnosed. A gastric tube was placed for feeding.
- The cat had a distended abdomen when presented to the referring
veterinarian several weeks later. 60ml of fluid was removed from
the abdomen. Feline infectious peritonitis was diagnosed. After
presentation to the teaching hospital, ultrasound showed an enlarged
liver. 75ml of fluid was removed from the abdomen on the day
prior to death; 120 ml was removed on the day of death. Respiratory
difficulties and an absence of gastric emptying were noted.
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- Gross Pathology:
- Multiple neoplastic masses in liver.
Sessile mass on colonic wall constricting lumen.
Multiple mesenteric implants of neoplastic tissue.
Ascites.
- Laboratory Results: None.
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- Contributor's Diagnosis and Comments: Liver, cholangiocellular
carcinoma with biliary hyperplasia, rupture and inspissation
with transcoelomic metastasis.
- All sections of liver have multiple areas of poorly demarcated
glandular proliferations. Many of these have areas of necrosis
centrally. The cells in these areas replace hepatic parenchyma
and consist of a tall cuboidal epithelium forming glands and
tubules. Bile ducts are prominent in all sections and have multiple
extensions (biliary proliferation) of short tubules into the
adjacent hepatic parenchyma. There are many larger bile ducts
with an eosinophilic inspissated material in their lumina. Some
of these secretions are partially covered by a biliary epithelium.
In some areas, the bile ducts are ruptured and biliary epithelium
extends into the adjacent hepatic parenchyma. Occasional glands
and cysts contain eosinophilic material with variable numbers
of neutrophils. Adjacent remaining hepatocytes have marked centrilobular
vacuolization and atrophy with dilated sinusoidal spaces filled
with erythrocytes. There is mild fibrosis of the centrilobular
vein. There is also hemosiderin laden macrophages scattered throughout
the interlobular zone.
- Cholangiocellular carcinoma can spread by transcoelomic metastasis
as noted in this case. The ascites noted in this case would be
consistent with the widespread liver involvement. Metastatic
sites included colonic wall, mesentery, omentum, diaphragm, and
abdominal body wall. There was no evidence of lung involvement.
The metastatic sites had a marked desmoplastic response which
was contributory to the constriction of the colon associated
with the mass on the colonic wall.
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- AFIP Diagnosis: Liver: Adenocarcinoma, Domestic Shorthair,
feline.
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- Conference Note: Although the histopathologic findings
are compatible with cholangiocellular carcinoma, there are no
pathognomonic features of this neoplasm. Thus, metastatic adenocarcinoma
from such sites as pancreas, gastrointestinal tract, lung, extrahepatic
bile duct and gallbladder must be reliably excluded to reach
a conclusive diagnosis of cholangiocellular carcinoma.
- Cholangiocellular carcinomas are unusual in that they are
very frequently multiple or diffuse, suggesting that the cause
acts at multiple sites or that there is extensive intrahepatic
spread. Metastasis to the regional lymph nodes is common. In
the cat, there is a tendency of this neoplasm to invade Glisson's
capsule and implant on the peritoneum. In humans and some carnivores,
chronic infection with opisthorchid liver flukes (Opisthorchis
viverrini and Clonorchis sinensis) has been associated with bile
duct carcinomas.
- Grossly, cholangiocellular tumors can usually be distinguished
from hepatocellular tumors by their multiplicity, firmness, whitish
color and the typical umbilication of those that involve the
capsule.
- Microscopically, cholangiocellular carcinomas produce ductules
and acini, and sometimes papillary formations. The cells are
cuboidal or columnar, with a moderate amount of clear or slightly
granular cytoplasm. The tubules do not contain bile, but in well-differentiated
specimens may contain mucin. A desmoplastic reaction and vascular
invasion are common. Vascular invasion was particularly prominent
in the present case.
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- Contributor: University of Illinois, Department of
Pathobiology, College of Veterinary Medicine, Urbana, Illinois
61801.
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- References:
1. Feldman BF, Strafuss AC, Gabbert N: Bile duct carcinoma
in the cat: Three case reports. Feline Pract Jan:33-39, 1976.
- 2. Lawrence HJ, Erb HN, Harvey HJ: Nonlymphomatous hepatobiliary
masses in cats: 41 cases (1972 to 1991). Vet Surg 23:365-368,
1994.
- 3. Moore FM: Tumors of the liver and biliary system. In:
Diseases of the Cats (J Holtzworth, ed). Saunders, 1987. Pg 500-504.
- 4. Patnaik AK: A morphologic and immunocytochemical study
of hepatic neoplasms in cats. Vet Pathol 29:405-415, 1992.
- 5. Postorino NC: Hepatic tumors. In: Clinical Veterinary
Oncology (SJ Winthrow & E.G. MacEwen, eds), Lippincott, pp.
196-200, 1989.
- 6. Jubb KVF, Kennedy PC, Palmer N (eds): Pathology of Domestic
Animals, 4th ed., vol 2, Academic Press, pp. 405-406, 1993.
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- International Veterinary Pathology Slide Bank:
Laser disc frame #692, 693, 694, 1054, 6457, 6458, 12789,
12790, 12791.
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Case IV - A96121098 (AFIP 2550447)
Signalment: An adult female black buck antelope (Antelope cervicapra).
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- History: Pregnant female discovered near death, died
during C-section.
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- Gross Pathology: The liver is swollen with rounded
margins and diffusely dark red. There are fibrous adhesions between
the liver and diaphragm.
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- Laboratory Results: No significant bacterial pathogens
cultured. Fecal floatation revealed strongylid eggs.
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- Contributor's Diagnosis and Comments: Deposition,
amyloid, hepatic sinusoids, rumen submucosa, and spleen.
- Amyloid deposits were also detected in the renal medullary
interstitium. Oxidation with potassium permanganate abolished
the congophilia and green birefringence indicating the deposits
were of AA-type. Systemic reactive amyloidosis is observed in
a variety of domestic and exotic animals. Amyloid-A (AA) is derived
from an acute phase reactant protein designated serum amyloid
A produced mainly by the liver. Serum amyloid A is elevated in
inflammatory conditions and may have an antiinflammatory function.
Systemic reactive amyloidosis is often associated with chronic
inflammatory disease. In this case, except for the fibrous adhesions
between liver and diaphragm, lesions suggesting chronic inflammatory
disease were lacking. Deposition of amyloid is a multistep process
requiring elevated levels of serum amyloid A, generation of a
tissue factor termed amyloid enhancing factor that may serve
as a focal point for fibrillization and lastly, heparan sulphate
proteoglycan may be involved in the resistance of amyloid to
proteolysis.
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- AFIP Diagnosis: 1. Liver: Amyloidosis, diffuse, severe,
with hepatocellular atrophy and loss, blackbuck antelope (Antelope
cervicapra), bovid.
2. Liver: Hepatitis, portal, lymphoplasmacytic, diffuse, mild.
3. Spleen, red pulp: Amyloidosis, diffuse, severe.
4. Spleen: Hemosiderosis, diffuse, moderate.
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- Conference Note: Amyloid is a pathologic extracellular
proteinaceous substance deposited between cells in multiple tissues
and organs in various clinical and subclinical diseases. The
term amyloidosis encompasses a group of diseases sharing in common
the deposition of similar appearing extracellular proteins. Amyloid
proteins are predominantly AL (amyloid light chains) associated
with plasma cell dyscrasias or AA (amyloid-associated protein)
deposited secondary to chronic inflammation. The characteristic
appearance and staining reaction of amyloid are due to the conformation
of the constituent polypeptides into cross- -pleated sheets (
-fibrilloses) on x-ray crystallographic analysis.
- The clinicopathologic classification of amyloidosis is determined
by tissue distribution of the deposits and the presence or absence
of predisposing disease.
Systemic or generalized amyloidosis is subdivided into primary
(in association immunocyte abnormalities) and secondary (when
associated with chronic inflammation). In localized amyloidosis,
deposits are restricted to a single organ or tissue in the body
and are usually associated with aggregates of lymphocytes and
plasma cells.
Amyloidosis consists of about 90% fibril proteins and 10% glycoprotein
(P component). AL (amyloid light chain) is derived from plasma
cells, contains immunoglobulin light chains and is the predominant
deposit in primary amyloidosis. It is associated with multiple
myeloma and is composed of homogeneous light chains of the (
-VI type) and type or their N-terminal fragments ( -Bence Jones
protein, amyloid fibril protein in multiple myeloma), or both.
AA (amyloid-associated) proteins are derived from large protein
precursors in the serum (SAA-serum amyloid associated) that are
produced in the liver in response to interleukin-1, and perhaps
other cytokines, and are associated with the HDL3 subclass of
lipoproteins. SAA is an acute-phase protein associated with inflammatory
reactions. AA proteins have been isolated in vitro from the digestion
of delipidated SAA by monocytic serine proteases (u-PA, urokinase-type
plasminogen activator-macrophages and granulocytes). This is
the predominant deposit in secondary amyloidosis.
- Recent studies have revealed several other proteins in amyloid
deposits:
1. Transthyretin: A serum protein that binds and transports thyroxine
and retinol. A mutant form of transthyretin and its fragment
are isolated in familial amyloid polyneuropathies (Familial Mediterranean
fever) and amyloidosis associated with aging (Alzheimer's disease)
in humans.
2. 2 Microglobulin: component of the MHC class 1 molecule has
recently been isolated in amyloidosis that complicates long term
hemodialysis.
3. 2 Amyloid protein (A 4 protein) constitutes the core of cerebral
amyloid plaques as well as the deposits found in the walls of
cerebral vessels in Alzheimer's disease.
4. IAAP (islet amyloid polypeptide): major component of human
and feline pancreatic islet amyloid and of amyloid in human pancreatic
endocrine tumors, occurs in normal pancreatic cells of numerous
species, is located in the outer lucent zone and dense core of
the cell secretory vesicle in the cat and man, respectively,
and is probably co-secreted with insulin. It inhibits basal and
insulin-stimulated glycogen synthesis in skeletal muscle and
is believed to play a role in the insulin resistance seen in
type 2 diabetes mellitus in man.
5. AEF (Amyloid-enhancing factor): a glycoprotein that appears
to alter the metabolism of SAA and may be essential for the deposition
of AA amyloid in experimental models. Note that additional elements
must be required for the deposition of amyloid in tissue since
SAA when reacted to IL-1 in the presence of AEF does not give
rise to amyloid.
6. GAG's (sulfated glycosaminoglycans) have been reported in
several forms of amyloid deposits.
7. In addition to those proteins already described, amyloid deposits
derived from hormone precursors (pro-calcitonin, proinsulin,
medullary carcinoma of the thyroid) and keratin have been reported.
8. P Component (AP), also synthesized in the liver, is structurally
similar to C-reactive protein and is associated with all forms
of amyloidosis.
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- The pathogenesis of amyloidosis is unknown. Current evidence
suggests that amyloid proteins are derived by partial degradation
(monocyte-associated serine esterases, u-PA) of parent proteins.
On the other hand, in some cases, there is an increase in the
level of serum precursors (i.e. Ig light chains, SAA, 2-microglobulin)
that appear to be structurally normal. In others (transthyretin),
a genetic abnormality results in the production of a chemically
abnormal precursor protein. Additionally, the conversion of these
soluble precursors to their insoluble form (amyloid) involves
the action of proteolytic enzymes or some other form of processing.
In absence of conclusive evidence, both quantitative and qualitative
changes in the precursor proteins, coupled with defective proteolysis,
are implicated by recent research findings. Progressive accumulation
of these proteins between cells produces pressure atrophy, degeneration,
necrosis and loss of adjacent cells.
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- Contributor: Texas Veterinary Medical Diagnostic Laboratory,
P. O. Box 3200, Amarillo, TX 79116-3200.
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- References:
1. Husby G: Classification of amyloidosis, Bailliers Clin
Rheumatol 8(3):503-511, 1994.
- 2. Kisilivesky R, et al: A critical analysis of postulated
pathogenic mechanisms in amyloidogenesis. Crit Rev Clin Lab Sci
29(1):59-82, 1992.
- 3. Linke RP, et al: Immunohistochemical identification of
generalized AA- amyloidosis in a mountain gazelle (Gazella gazella).
Vet Pathol 23:63-67, 1986.
- 4. Rideout BA, et al: Renal medullary amyloidosis in Dorcas
gazelles. Vet Pathol 26:129-135, 1989.
- 5. Yakar S, et al: The molecular basis of reactive amyloidosis.
Sem Arthritis Rheumatism 24(4):255-261, 1995.
- 6. Inoue S, et al: Effect of polyvinylsulphonate on murine
AA amyloid: A high resolution ultrastructural study. Lab Invest
74(6):1081-1090, 1996.
- 7. Cheville, Norman, F. Cell Pathology, Iowa State University
Press, 2nd edition, pp. 173-79, 1983.
- 8. Maxie MG: The urinary system. In: Pathology of Domestic
Animals, eds. Jubb KVF, Kennedy PC, Palmer N, Academic Press
Inc., 4th edition Vol 2, pp 484-486, 1993.
- 9. Obrien, T.D. et al Islet Amyloid polypeptide and Calcitonin
Gene-related Peptide Immunoreactivity in Amyloid and Tumor Cells
of Canine Pancreatic Endocrine Tumors. Vet. Path. 27:194-198,1990.
- 10. Robbins SL, Cotran RS, Kumar V (eds): Pathologic Basis
of DiseasePhiladelphia, Pa.. W.B. Saunders Company, 2nd edition,
pp. 210-220; 1989.
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- International Veterinary Pathology Slide Bank:
Laser disc frame #4725, 5400, 9218, 9253.
- Lance Batey
Captain, VC, USA
Registry of Veterinary Pathology*
Department of Veterinary Pathology
Armed Forces Institute of Pathology
(202)782-2615; DSN: 662-2615
Internet: Batey@email.afip.osd.mil
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- * 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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