AFIP Wednesday Slide Conference - No. 30
May 12, 1999

Conference Moderator: LTC Thomas P. Lipscomb
Division of Veterinary Pathology
Armed Forces Institute of Pathology
Washington DC 20306-6000
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Case I - E98-127 (AFIP 2638228)

Signalment: Adult Holstein cow.
History: The lungs were harvested from an adult Holstein cow at a slaughter house.
Gross Pathology: Close examination of the lungs revealed small grey spots in many of the lobules. Several pulmonary arteries contained variably-sized, non-adherent, soft, white-grey material.
Laboratory Results: None.
Contributor's Diagnoses and Comments:
1. Bronchiolitis, severe, multifocal, chronic, nonsuppurative with bronchiolar smooth muscle hyperplasia (Bovine Farmer's Lung; extrinsic allergic alveolitis).
2. Pulmonary embolization of brain tissue.
Bovine farmer's lung (extrinsic allergic alveolitis) is a disease primarily of adult cattle in areas with wet summers and severe winters leading to a combination of moldy hay and housing of cattle in winter. Baling or stacking high moisture hay (>30%) results in overheating and proliferation of thermophilic molds such as Micropolyspora faeni and Thermoactinomyces vulgaris. Billions of spores and the metabolic products of these molds are released when the hay is distributed during feeding. Inhalation of spores by previously exposed animals results in activation of both humoral and cellular immune effector functions resulting in allergic reactions. The hypersensitivity response leads to widespread infiltration of interalveolar septa by lymphocytes and plasma cells. Extensive peribronchial accumulations of lymphocytes, plasma cells, histiocytes, and smaller numbers of eosinophils are accompanied by bronchiolar smooth muscle hypertrophy. Interstitial epithelioid granulomas, an important diagnostic feature, may be absent unless there has been recent antigenic exposure. These lungs were harvested in late spring, presumably after the cows had been turned out from the barn, which likely accounts for the lack of granulomas.
Humane euthanasia in slaughter plants involves various methods of stunning to render an animal insensible followed by exsanguination.2 A pneumatic-actuated penetrating captive bolt gun was used to stun this animal. While the bolt is in the cranial cavity, injected air disrupts the brain structure. Momentary severe increases in intracranial pressure and simultaneous rupture of dural venous sinuses or the development of a large cerebral venous defect likely allows lacerated brain tissue to enter the venous system. Brain emboli can lodge in various organs such as in pulmonary arteries in the lung, as in this case, or in the liver, presumably due to retrograde travel through the posterior vena cava.
AFIP Diagnoses:
1. Lung: Bronchitis and bronchiolitis, chronic and active, lymphoplasmacytic and eosinophilic, multifocal, moderate, with peribronchial and peribronchiolar lymphoid follicles, chronic interstitial pneumonia, peribronchiolar and interstitial fibrosis, and bronchiolitis obliterans, Holstein, bovine.
2. Lung, pulmonary artery: Brain embolus.

Note: Not all sections contain embolized brain in the pulmonary artery.
Conference Note: Inflammatory cells expand peribronchial and peribronchiolar interstitium, multifocally compress bronchiolar lumens and extend into adjacent alveolar septa. Inflammatory cells include lymphocytes, plasma cells, macrophages, and eosinophils. The walls of several bronchioles are expanded by eosinophilic fibrillar material, which occasionally extends into airway lumens. Participants interpreted this material as fibrous connective tissue; a Masson's trichrome stained the material blue confirming this interpretation. The lumens of some bronchioles contain mucin, eosinophils, neutrophils and macrophages. In some sections, globule leukocytes and eosinophils are present within the epithelium of larger bronchioles and bronchi.
This case was reviewed by the Department of Pulmonary and Mediastinal Pathology. They interpreted the lesion as primarily chronic interstitial pneumonia with a prominent bronchiolocentric distribution, and noted that extrinsic allergic alveolitis (or "farmer's lung") in humans is classically characterized by a histologic triad of bronchiolocentric chronic inflammation, poorly-formed non-necrotizing granulomas, and areas of organizing pneumonia. They did not identify the latter two histologic features in this case, but commented that the bronchiolocentric inflammation is consistent with hypersensitivity pneumonitis given the correct clinical setting. In humans, the differential diagnosis for this lesion would also include infection, collagen vascular disease and drug reaction.
While the clinical history is not available in this case, the histologic lesions and signalment are compatible with extrinsic allergic alveolitis as described in cattle. Many participants considered mycoplasmal bronchitis and bronchiolitis of calves in the differential diagnosis; however, histologic lesions of that condition are characterized by suppurative bronchitis and bronchiolitis with peribronchiolar lymphoid hyperplasia and atelectasis. The paucity of neutrophils, the presence of globule leukocytes and eosinophils, and the fibrosis are more consistent with hypersensitivity pneumonitis.
In humans, hypersensitivity pneumonitis includes a variety of immune-mediated, predominately interstitial lung diseases caused by intense, prolonged exposure to inhaled organic dusts and related occupational antigens. Affected individuals have heightened immune response or abnormal sensitivity to the antigen, and lesions primarily involve alveoli with progression to chronic fibrotic lung disease. Sources of antigens vary, and may include thermophilic bacteria, fungi, animal proteins, and several others. Experimental and human studies support type III immune complex reaction for the early lesions, followed by type IV delayed hypersensitivity reaction for the granulomatous component.
Contributor: Department of Pathology, Cornell University, Ithaca, New York 14853-6401.
1. Breeze R: Hypersensitivity pneumonitis. Vet Clin N Am Food Anim Pract 1:324-330, 1985.
2. Grandin T: Euthanasia and slaughter of livestock. J Amer Vet Med Assoc 204:1354-1360, 1994.
3. Kobzik L: The lung. In: Robbins Pathologic Basis of Disease, Cotran RS, Kumar V, Collins T, eds., 6th ed., pp. 737-738 and 356, WB Saunders, Philadelphia, PA, 1999.
4. Jones TC, Hunt RD, King NW: The respiratory system. In: Veterinary Pathology, Jones TC, Hunt RD, King NW, eds., 6th ed., pp. 694-695, Williams & Wilkins, Baltimore, MD, 1997.
5. Dungworth DL: The respiratory system. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th ed., vol. 2, pp., 575-576, 658-659, 676-677, Academic Press, San Diego, CA, 1993.
6. Van Metre DC: Allergic respiratory disease. Vet Clin N Amer Food Anim Pract 13:495-512, 1997.

Case II - CP94-150 (AFIP 2459067)

Signalment: 15-year-old, male, mixed breed, canine.
History: The owner observed pigmented nodules in the left flank region.
Gross Pathology: The skin specimen consisted of a dark, pigmented, raised nodule measuring 1.8 x 1.5 cm.

Laboratory Results: None.
Contributor's Diagnosis and Comments: Nodular cutaneous amyloidosis.

Etiology: May be directly related to the plasma cell infiltrate.
Multiple amyloid deposits are scattered throughout the dermis. Some deposits are associated with plasma cells, and other deposits are associated with giant cells. The eosinophilic deposits stained positive with Congo red and were birefringent (green) when polarized.
AFIP Diagnosis: Haired skin: Atypical plasma cell infiltrate, favor plasmacytoma, with amyloid and granulomatous inflammation, mixed breed, canine.
Conference Note: Most participants agreed with the contributor and diagnosed cutaneous amyloidosis associated with plasmacytic and granulomatous inflammation. However, the moderator and a few participants noted that, aside from the macrophages and multinucleate giant cells (that appeared to represent a foreign body reaction to the amyloid), the cellular infiltrate is composed of almost exclusively plasma cells. Additionally, although most of the plasma cells are well differentiated, scattered cells are up to five times the size of normal plasma cells, some plasmacytoid cells have atypical nuclear features such as nucleoli, and rarely, plasmacytoid cells contain mitotic figures. These features support a neoplastic proliferation. Unfortunately, immunohistochemical stains for light chains did not work properly, and insufficient material was available for further testing to determine whether or not the plasma cells are monoclonal. Canine cutaneous plasmacytomas range from very well differentiated to very poorly differentiated.
A recent study of canine extramedullary plasmacytomas confirmed the previously reported, predominantly benign biological behavior of these tumors, but noted rare instances of local recurrence and metastasis by the most pleomorphic subtype. Aside from this observation, histopathologic grading of plasmacytomas was not found to be useful.
Contributor: St. Jude Children's Research Hospital, Comparative Medicine/ARC, 332 North Lauderdale, Memphis, TN 38105.
1. Gross TL, Ihrke PJ, Walder EJ: Dysplastic and depositional diseases of the dermal connective tissue. In: Veterinary Dermatopathology, Reinhardt RW, ed., pp. 229-232, Mosby-Yearbook Inc., St. Louis, MO, 1992.
2. Jones TC, Hunt RD, King NW: Intracellular and extracellular depositions; degenerations. In: Veterinary Pathology, Jones TC, Hunt RD, King NW, eds., 6th ed., pp. 50-54, Williams & Wilkins, Baltimore, MD, 1997.
3. Rowland RH, et al.: Cutaneous plasmacytomas with amyloid in six dogs. Vet Pathol 28:125-130, 1991.
4. Cotran RS, Kumar V, Collins T: Diseases of immunity. In: Robbins Pathologic Basis of Disease, Cotran RS, Kumar V, Collins T, eds., 6th ed., pp. 251-257 and 356, W.B. Saunders, Philadelphia, PA, 1999.
5. Jager JA, Scott DW, Wilcock BP: The skin and appendages. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th ed., vol. 1, pp. 628, Academic Press, San Diego, CA, 1993.
6. Platz SJ, Breuer W, Pfleghaar S, Minkus G, Hermanns W: Prognostic value of histopathologic grading in canine extramedullary plasmacytomas. Vet Pathol 36:23-27, 1999.

Case III - 60929-C (AFIP 2460487)

one 2x2 histology color photo transparency
Signalment: 4½-year-old, male, German Shepherd dog.
History: The dog came from Fort Walton Beach, Florida. He had exophthalmia and prolapse of the third eyelid for approximately 1½ months. The referring veterinarian examined the dog five weeks previously and had treated the dog with KeflexÔ (500mg, TID) and prednisone (20mg, BID) for seven days. The exophthalmia improved slightly. The referring veterinarian then treated the dog with a tapering dose of dexamethasone over the next 25 days. At the time the dog was examined at Auburn University, no medications had been administered for one week. According to the owners, the exophthalmia was less prominent than originally noted.
At Auburn, the dog was depressed, lethargic, and had dark-coated, soft stool. He had lost 1½ lbs. in the last week. The temperature was 103.3°F; pulse was 80 beats/minute; and the respiratory rate was 40 breaths/minute. On physical examination, the dog had a nasal discharge and appeared to have a nasal mass. A mass near the left eye was identified in skull radiographs; however, no tumor was identified by CT. In the process of performing a rhinoscopic examination and obtaining a nasal biopsy, the dog went into cardiac and respiratory arrest. Resuscitation was progressing poorly using external cardiac compression. Upon opening the thoracic wall to facilitate cardiac massage, 500-800 ml of gray, flocculent fluid spilled out.
Gross Pathology: Necropsy was not allowed, but observations were made during resuscitation attempts. Pericardial fluid was present, but was not as flocculent as that found in the thoracic cavity. The pericardium was thickened. There were numerous pleural adhesions, and several intra-thoracic lymph nodes were enlarged. Cytologic preparations were made from aspirates of the nasal mass and the thoracic effusion. Sections for histopathologic examination were obtained from lung, bronchial lymph nodes, pericardium, and the nasal mass.
Laboratory Results
Cytologic findings: Nasal and thoracic effusions are similar. Neutrophils are numerous and often surround or appear attached to the surface of hyphal elements that are irregularly branching, variably septate or twisted/compressed, and have thick nonparallel walls often with bulbous ends or sections. There is abundant gray-blue, amorphous proteinaceous material in the background.

Cytologic opinion: Purulent inflammation with numerous mycotic organisms; evidence of necrosis.

Mycotic culture performed at Auburn University resulted in growth of Conidiobolus sp. (probably not C. coronatus). Mycotic culture performed at the Fungus Testing Laboratory in San Antonio, Texas resulted in the growth of Conidiobolus (not consistent with C. coronatus).
Contributor's Diagnosis and Comments: Lymph node: Pyogranulomatous, necrotizing, mycotic lymphadenitis.

Etiologic agent: Conidiobolus sp.
The architecture of this bronchial lymph node is effaced focally to locally extensively. Multifocal areas have increased numbers of large epithelioid macrophages, often in sheets. Other areas have necrotic centers with neutrophils, cellular debris, and scattered negative reliefs of oval to irregular structures that are sometimes surrounded by intensely acidophilic amorphous material. Macrophages, fewer neutrophils, and scattered multinucleated giant cells are adjacent to the necrotic centers. Plasma cells are increased in lymphoid follicular structures nearest the granulomas and necrotic areas. The submitted photomicrograph of a Grocott's methenamine silver (GMS) stained section demonstrates many thin-walled, irregularly shaped, broad hyphae within and adjacent to areas of necrosis.
In other tissues (not submitted), the left nasal cavity has abundant purulonecrotic material on the surfaces with numerous fungal hyphae. The pericardium has mild, diffuse infiltration of neutrophils and several wide, septate hyphae on the surface. The lung tissue has thickened pleura and an infiltration of macrophages and fewer neutrophils. Wide, septate hyphae are on the surface.
Conidiobolus sp. are classified as follows (according to Goodman and Rinaldi):
Superkingdom: Eukaryotae
Kingdom: Fungi
Division: Zygomycotina
Class: Zygomycetes
Order: Entomophthorales
Family: Ancylistaceae
Genus: Conidiobolus
Subgenus: Conidiobolus
Pathogenic species:
1. Conidiobolus coronatus
2. Conidiobolus incongruus
Conidiobolus coronatus infections are typically limited to the nasal cavity with occasional extension into the cerebrum (rhinocerebral infections) and have been diagnosed most often in horses from tropical and semitropical areas (Chandler, Bridges) and in one llama (French). Conidiobolus incongruus infections have been reported in sheep in Australia (Ketterer, Carrigan) and have had nasal, pulmonary, and thoracic cavity involvement. A case of disseminated Conidiobolus infection (species not compatible with any known variant) has been reported in a man who was a crack cocaine addict (Jaffey). This dog was suspected to be immunosuppressed owing to the prolonged administration of corticosteroids.
AFIP Diagnosis: Lymph node and perinodal adipose tissue: Lymphadenitis, granulomatous and eosinophilic, necrotizing, multifocal and coalescing, moderate, with perinodal steatitis, lymphangitis and fungal hyphae surrounded by radiating eosinophilic hyaline material (Splendore-Hoeppli material), German Shepherd Dog, canine.
Conference Note: In some sections, sinus histiocytosis, hemosiderosis, and erythrophagocytosis are present. Participants noted a paucity of lymphoid follicles, but the presence of many plasma cells. Significant numbers of eosinophils are associated with fungal hyphae. Several participants observed anisotropic crystals within macrophages (silicosis), suggesting that the lymph node drained the respiratory tract.
Zygomycosis is a disease of humans and animals caused by fungi belonging to the class Zygomycetes. The pathogenic Zygomycetes include members of two orders that are histomorphologically similar but cause differing types of disease: Mucorales and Entomophthorales. The Mucorales cause mucormycosis and include the genera Rhizopus, Mucor, Rhizomucor, Mortierella, Absidia, and others. The Entomophthorales include Basidiobolus and Conidiobolus sp., and disease induced by these fungi is termed entomophthoromycosis.
Generally, the Mucorales cause invasive, disseminated disease in humans and animals. Mucormycosis commonly occurs in debilitated hosts, and systemic zygomycosis is usually caused by the Mucorales. Rhinocerebral zygomycosis is a fulminating, often fatal disease in humans which most commonly occurs in individuals suffering from acute diabetes mellitus or other immunosuppressive conditions.
The Entomophthorales tend to cause localized subcutaneous and nasal granulomas in humans and animals. In humans, for example, infections with Conidiobolus coronatus are limited to the nasal mucosa and sinuses, and the subcutaneous tissue of the nose and face. With few exceptions, zygomycosis caused by Basidiobolus and Conidiobolus occurs in healthy individuals and does not disseminate. Exceptions to these generalities include rhinocerebral and disseminated infections of sheep in Australia caused by Conidiobolus incongruus, and a few reports of invasive and disseminated infections in humans caused by C. incongruus and other Conidiobolus sp.
In addition to variation in clinicopathologic presentation between infection with the Mucorales and Entomophthorales, differences in histologic lesions have also been observed. The presence of Splendore-Hoeppli material and eosinophilic inflammation is more consistent with infection by the Entomophthorales. The Mucorales tend to invade vessels, causing necrotizing vasculitis, thrombosis, and infarction while the Entomophthorales do not typically cause vascular lesions.
Differential diagnosis for zygomycosis includes Pythium insidiosum and Aspergillus sp. The fungal hyphae of the Zygomycetes are broad (3-25 mm, avg. 12), thin-walled, infrequently septate, have nonparallel sides, and measure up to 200 mm in length. They are characterized by nondichotomous, irregular branching that sometimes occurs at right angles. Frequently, the hyphae of Mucorales are easily observed in standard hematoxylin and eosin stained sections. The hyphae of Entomophthorales are often surrounded by Splendore-Hoeppli material. The hyphae of the protist Pythium of the phylum Oomycetes, are narrower (2 to 6 mm), have thicker walls, and are found most often at the periphery of necrotic areas. In general, the hyphae of Aspergillus are 3 to 6 mm, have dichotomous branching, parallel walls, numerous septa, and may be difficult to observe in standard H & E stained tissue sections. Special stains, such as the periodic acid-Schiff reaction and the Gomori's methenamine silver method, frequently stain the hyphae of Aspergillus more intensely than the Zygomycetes.
Contributor: Auburn University, Department of Pathobiology, College of Veterinary Medicine, Auburn University, AL 36849-5519.
1. Goodman NL, Rinaldi MG: Agents of zygomycosis. In: Manual of Clinical Microbiology, Balows A, et al., eds., 5th edition, pp. 674-690, American Society for Microbiology, Washington, 1991.
2. Bridges CH, Romane WM, Emmons CW: Phycomycosis of horses caused by Entomophthora coronatus. J Amer Vet Med Assoc 140:673-677, 1962.
3. Chandler FW, Kaplan W, Ajello L: In: Color Atlas and Text of the Histopathology of Mycotic Diseases, Chandler FW, Kaplan W, Ajello L, eds., pp. 122-127, Year Book Medical Publishers, Chicago, 1980.
4. Carrigan MJ, Small AC, Perry GH: Ovine nasal zygomycosis caused by Conidiobolus incongruus. Aust Vet J 69:237-240, 1992.
5. French RA, Ashworth CD: Zygomycosis caused by Conidiobolus coronatus in a llama (Llama glama). Vet Pathol 31:120-122, 1994.
6. Jaffey PB, Haque AK, El-Zaatari M, Pasarell L, McGinnis MR: Disseminated Conidiobolus infection with endocarditis in a cocaine abuser. Arch Pathol Lab Med 114:1276-1278, 1990.
7. Ketterer PJ, et al.: Rhinocerebral and nasal zygomycosis in sheep caused by Conidiobolus incongruus. Aust Vet J 69:85-87, 1992.
8. Jager JA, Scott DW, Wilcock BP: The skin and appendages. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N, eds., 4th ed., vol. 1, pp. 670-672, Academic Press, San Diego, CA, 1993.
9. Jones TC, Hunt RD, King NW: Diseases caused by fungi. In: Veterinary Pathology, Jones TC, Hunt RD, King NW, eds., 6th ed., pp. 523-525, Williams & Wilkins, Baltimore, MD, 1997.
10. Foil CS: Miscellaneous fungal diseases. In: Infectious Diseases of the Dog and Cat, Greene CE, ed., 2nd ed., pp. 423-425, W.B. Saunders, Philadelphia, PA, 1998.

Case IV - A41168 (AFIP 2638283)

Signalment: Five-year-old, male, Belgian Malinois, dog.
History: The dog had a history of seizures and had been treated with barbiturates for more than a year. Recently, the dog also had a history of anorexia, vomiting, and weight loss. The dog developed ulcerative hyperkeratotic lesions on all four feet.
Gross Pathology: There was bilateral ulceration on the skin of the elbows. All four feet had ulcerative skin of dorsal terminal digits and hyperkeratosis on the paws. The liver was nodular, smaller than normal in size, and had a thick, opaque, fibrotic capsule.
Laboratory Results:
Blood chemistry tests revealed alkaline phosphatase was increased (1823 IU/L); SGPT (ALT) was increased (101); CPK was increased (656 IU/L); BUN was decreased (6 mg/L); and total bilirubin was increased (0.5 mg/L).
Urinalysis results were bilirubin 3+; blood 3+; protein 3+.
Contributor's Diagnosis and Comments: Superficial necrolytic dermatitis (hepatocutaneous syndrome).
Morphologically, the skin had marked parakeratosis and necrosis in the stratum corneum, vacuolization of the epithelium in the stratum spinosum, epidermal necrosis with occasional presence of bacterial colonies, and infiltration of neutrophils. These lesions are typical of superficial necrolytic dermatitis (hepatocutaneous syndrome). The dog also had severe hepatic cirrhosis. The lesions are similar to those in the pig or dog with zinc deficiency.
AFIP Diagnosis: Footpad and adjacent haired skin: Parakeratosis, diffuse, severe, with moderate epidermal hyperplasia, multifocal superficial epidermal pallor, mild lymphoplasmacytic and histiocytic superficial dermatitis, dermal edema, and intracorneal colonies of cocci, Belgian Malinois, canine.
Note: Some sections contain folliculitis, furunculosis, and intracorneal and subcorneal pustules.
Conference Note: Superficial necrolytic dermatitis (SND) is an uncommon skin disease of dogs with similarities to necrolytic migratory erythema (NME) in humans. The human disease is primarily a paraneoplastic syndrome associated with pancreatic endocrine tumors that secrete glucagon (glucagonoma) resulting in high blood levels of glucagon. Although a minority of canine cases have been associated with glucagon producing pancreatic endocrine tumors, the condition most often has been associated with chronic hepatic disease and diabetes mellitus, thus the term hepatocutaneous syndrome. The disease in the dog is primarily a manifestation of internal metabolic derangement rather than a manifestation of a specific diagnostic entity as in humans. The disease is primarily seen in older dogs, and seems to occur more frequently in females.

Gross lesions are usually bilateral, and the affected skin is erythematous, eroded, ulcerated, and crusted. Lesions occur on the footpads, mucocutaneous junctions, edges of the pinnae, pressure points on the distal extremities, ventral thorax, and scrotum. Microscopically, diagnostic features include the presence of pale staining keratinocytes in the superficial half of an acanthotic stratum spinosum (white), located between the parakeratotic, crusted stratum corneum (red) and the hyperplastic basal cell layer and deeper stratum spinosum (blue). Pallor of the upper stratum spinosum may not be present in all sections. Clefts and vesicles may form in the outer stratum spinosum as cells degenerate, and subcorneal pustules may be present. Secondary bacterial and fungal infections may occur.
The pathogenesis of SND in dogs and NME in humans is not completely understood, but hypoaminoacidemia caused by metabolic disease or hormonal abnormalities may be the common underlying etiology in both conditions. High glucagon levels in functional glucagonomas in humans are known to induce hypoaminoacidemia through prolonged gluconeogenesis, depleting the serum and skin of essential amino acids and leading to degeneration and necrosis of keratinocytes. In dogs, chronic hepatic and metabolic diseases may have a similar result. Indeed, dermatoses associated with poor quality diets (generic dog food dermatosis) and zinc-responsive dermatoses have similar histologic features and probably have a similar pathogenesis.
In addition to zinc deficiency and generic dog food dermatosis, other parakeratotic hyperplastic dermatitides which might be considered in the differential diagnosis include lethal acrodermatitis of Bull terriers and thallium toxicosis. The clinical differential diagnosis might also include erythema multiforme, toxic epidermal necrolysis, systemic lupus erythematosus, and pemphigus foliaceus.
Contributor: Department of Pathology, The Animal Medical Center, 510 East 62nd Street, New York, NY 10021.
1. Miller WH, et al.: Necrolytic migratory erythema in dogs: A hepatocutaneous syndrome. J Amer Anim Hosp Assoc 26:573-581, 1990.
2. Kasper CS, McMurry K: Necrolytic migratory erythema without glucagonoma versus canine superficial necrolytic dermatitis: Is hepatic impairment a clue to pathogenesis? J Amer Acad Dermatol 25:534-541, 1991.
3. Kernkamp HCH, Ferrin EF: Parakeratosis in swine. J Amer Vet Med Assoc 123:217-220, 1953.
4. Robertson BT, Burns MJ: Zinc metabolism in zinc-deficiency syndrome in the dog. Amer J Vet Res 24:997-1002, 1963.
5. Gross TL, Ihrke PJ, Walder EJ: Diseases of the epidermis In: Veterinary Dermatopathology, Reinhardt RW, ed., pp. 46-48, 102-105, Mosby-Yearbook Inc., St. Louis, MO, 1992.
6. Gross TL, Song MD, Havel PJ, Irhke PJ: Superficial necrolytic dermatitis (necrolytic migratory erythema) in dogs. Vet Pathol 30:75-81, 1993.
7. Munson L, Koehler JW, Wilkinson JE, Miller RE: Vesicular and ulcerative dermatopathy resembling superficial necrolytic dermatitis in captive black rhinoceroses (Diceros bicornis). Vet Pathol 35:31-42, 1998.
8. Lewis DT: Life-threatening dermatoses. Comp Contin Med Ed Small Anim Pract 20:271-282, 1998.
Wednesday Slide 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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