AFIP Wednesday Slide Conference - No. 24

16 April 1997
Conference Moderator: Dr. Anne L. Kincaid
Diplomate, ACVP
Antech Diagnostics
8831 Satyr Hill Road
Carney, MD 21234
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Case I - 96-599 (AFIP 2565887)

Signalment: Young adult female Hartley guinea pig.
History: This guinea pig was a control animal in a blast overpressure study. Approximately 39% of the guinea pigs in this study had similar hepatic lesions.
Gross Pathology: White streaks were present on the capsular surface of affected livers.
Laboratory Results: N/A
Contributor's Diagnosis and Comments: Liver: Hepatocytic mineralization, multifocal, random, moderate, with multifocal necrosis and hemorrhage.
Metastatic calcification has been reported in the guinea pig. Clinical signs may include unthriftiness and apparent muscle stiffness. Affected tissues have included lung, trachea, heart, aorta, liver, kidney, stomach, colon, uterus, sclera, and soft tissues around the elbows and ribs. The pathogenesis of the syndrome in guinea pigs is unclear, although dietary mineral imbalances have been implicated. Studies suggest that lowering the ratio of magnesium to calcium and phosphorus may be more critical than the level of any one mineral.
The cause of hemorrhage seen in these livers may be related to the more friable nature of the mineralized tissue.
AFIP Diagnosis:
1. Liver: Mineralization, midzonal and multifocal, moderate, with multifocal coagulative necrosis, Hartley guinea pig, rodent.
2. Liver, hepatocytes: Vacuolar change (lipid type), periportal to midzonal, diffuse, mild.
Conference Note: The conference participants agreed with the contributor's diagnosis and comments. Metastatic calcification occurs most often in guinea pigs over 1 year of age. Dietary factors such as low magnesium and high phosphorous and calcium intake have been implicated in this syndrome. High calcium or high phosphorous diets appear to interfere with magnesium absorption and metabolism. Therefore, this syndrome may not be the result of a deficiency of a single component but rather due to a dietary imbalance of magnesium, calcium, and phosphorous.
Contributor: Walter Reed Army Institute of Research, Washington, D.C. 20307- 5100.
1. Galloway JH, et al: Relationship of diet and age to metastatic calcification of guinea pigs. Lab An Care 14:6-12, 1964.
2. Maynard LA: Dietary mineral interrelations as a cause of soft tissue calcification in guinea pigs. J Nutr 64:85-97, 1958.
3. Morris ER and O'Dell BL: Relationship of excess calcium and phosphorus to magnesium requirement and toxicity in guinea pigs. J Nutr 81:175-727, 1963.
3. O'Dell BL, et al: Diet composition and mineral balance in guinea pigs. J Nutr 63:65-77.
4. Percy DH and Barthold SW: Pathology of Laboratory Rodents and Rabbits, p. 168, Iowa State University Press, 1993.
5. Sparschu GL and Christie RJ: Metastatic calcification in a guinea pig colony: A pathological survey. Lab An Care 18(5):520-526, 1968.
International Veterinary Pathology Slide Bank: None.

Case II - W501/96 (AFIP 2551735)

Signalment: 7-month-old Jack Russell, crossbreed, female dog.
History: Vomiting and depressed, with a normal appetite, for one week. Vomit comprises white froth which is sometimes bile stained. Two days ago developed tender soft tissue swellings in the region of the submandibular salivary glands.
Gross Pathology: Oedema of soft tissue overlying the salivary glands was noted at surgery; the salivary glands were firm with a "blotchy" grey-green discoloration.
Laboratory Results: None.
Contributor's Diagnosis and Comments: Acute to subacute idiopathic salivary gland necrosis.
Subtotal to total apparently ischemic necrosis of the mandibular salivary glands in the characteristic histologic finding in a sporadic disease of terrier-type dogs, notably of the Jack Russell breed. Originally described as salivary gland infarction, the term "necrotizing sialometaplasia" has been adopted from human medicine. However, unlike the situation in dogs, in people necrotizing sialometaplasia generally affects the intraoral minor salivary glands and also, in our experience, ductal metaplasia has not been a distinctive feature of the canine lesion.
In subtotally affected glands, the margin between affected and unaffected tissue is delineated by a band of fibro-vascular tissue accompanied by a mild infiltrate of inflammatory cells.
Although presumably vascular in origin, the precise etiology and pathogenesis of this condition are unknown.
AFIP Diagnosis: Salivary gland, mandibular: Necrosis, coagulative, diffuse, with multifocal neovascularization and rare multifocal squamous metaplasia of ductular epithelium, Jack Russell Terrier, canine.
Conference Note: Necrotizing sialometaplasia (NS) is a rare, distinctive disease of the salivary glands reported in humans and, more recently, dogs. Histologic findings in humans and dogs are somewhat similar but the distribution of affected glands and clinical course are very different. In humans, NS is a benign self-limiting ischemic disorder of the salivary glands which has histologic features that have caused confusion with neoplasia. The characteristic histologic findings are ischemic necrosis of salivary lobules and secondary squamous metaplasia of salivary ducts. The palatine glands are most commonly affected.
Salivary gland infarction / NS has been reported in at least six small breed dogs which included the Jack Russell Terrier, Wirehaired Fox Terrier, West Highland White Terrier, and Pomeranian. In contrast to the disease in humans, canine salivary gland infarction / NS affects the submandibular salivary gland and has much more severe clinical signs. Affected dogs appear to be in extreme pain and vomit frequently. Sialoadenectomy of affected glands results in little if any improvement, while sialoadenectomy followed by short-term administration of an anticonvulsant appears to be an effective treatment.
The Department of Otolaryngic Pathology reviewed this case. They do not consider the histologic findings consistent with necrotizing sialometaplasia because there is no true replacement of acinar tissue by well developed squamous metaplasia. They commented that this might represent an early stage of developing NS.
Given the clinical and pathologic differences between the human and canine diseases, it might be best to retain different names for the conditions: necrotizing sialometaplasia for the human disease and salivary gland infarction for the canine disease.
Contributor: The University of Melbourne, Veterinary Clinical Centre, Werribee, 3030 Australia.
1. Kelly DF, Lucke VM, Denny HR, Lane JF: Histology of salivary gland infarction in the dog. Vet Pathol 16:438-443, 1979.
2. Brooks DG, Hottinger HA, Dunstan RW (1995) Canine necrotizing sialometaplasia: a case report and review of the literature. JAAHA 31:21-25, 1995.
3. Wenig BM: Necrotizing sialometaplasia of the larynx. Am J Comp Pathol 103:609-613.
4. Spangler WL, Culbertson MR: Salivary gland disease in dogs and cats: 245 cases (1985-1988). JAVMA 198(3):465-469, 1991.
International Veterinary Pathology Slide Bank: None.

Case III - UFSM #2 (AFIP 2559048)

Signalment: 8-month-old, Charolais cross, male, bovine.
History: Rapidly growing mass noticed on the scapular region for the last 40 days. The steer showed marked weight loss. The mass was surgically removed but the animal was eventually euthanatized due to its poor body condition.
Gross Pathology: A 50 x 23 x 8 cm, firm, cream-white mass was submitted for histological evaluation. At the cut surface the mass had a fibrous firm aspect with whitish hard foci (foci of mineralization) scattered throughout.
Laboratory Results: Bacteriological examination of the mass yielded pure culture of Pasteurella granulomatis.
Contributor's Diagnosis and Comments: Subcutis, focal proliferative fibrogranulomatous panniculitis.
Etiology: Pasteurella granulomatis.
The slides show the typical histological features of bovine focal proliferative fibrogranulomatous panniculitis (Lechiguana). There is a mass of well-vascularized dense fibrous connective tissue with multifocal areas of calcification and with several scattered myofibers entrapped within the mass. Lymphatic are distended by eosinophils, and eosinophilic microabscesses are found scattered within the connective tissue. The microabscesses have rosette-like (Splendore Hoeppli phenomenon) structures in their centers and occasionally are surrounded by a small rim of epithelioid cells. Gram-negative coccobacilli are seen in the centers of the rosettes.

Bovine focal proliferative fibrogranulomatous panniculitis (Lechiguana) is a disease affecting cattle in southern Brazil and is characterized by rapidly growing, large solitary subcutaneous swellings occurring mostly over the scapula or adjacent areas. Both sexes and several breeds of cattle are affected. Ages of affected cattle vary from 1 to 10 years (average 4-5 years). The correlation between the distribution of lesions of Lechiguana and those caused by Dermatobia hominis suggests that this parasite may have a role in transmitting or initiating the disease. Histologically, the subcutaneous mass consists of well vascularized mature connective tissue, multifocally calcified and infiltrated by numerous eosinophils and lesser numbers of lymphocytes, plasma cells, and neutrophils. Numerous microabscesses composed mainly of eosinophils are found within the connective tissue. The mass extends into adjacent skeletal muscle destroying myofibers; scattered myofibers are found entrapped within the connective tissue mass. Lymphatics within the mass are dilated and filled with eosinophils. Bacteria can be seen in these lymphatics in sections stained by appropriate techniques (Geimsa and Steiner's). It appears that this eosinophilic lymphangitis evolves to micro- abscesses formed mainly by eosinophils in the centers of which there is formation of rosette-like structures with eosinophilic projections (clubs) at the periphery. In the centers of the rosettes, there are gram-negative bacilli or coccobacilli. Microabscesses are occasionally surrounded by a thin layer of epithelioid cells. Similar lesions are found in the regional lymph nodes.
AFIP Diagnosis: Subcutis and skeletal muscle: Panniculitis and myositis, fibrosing, chronic-active, diffuse, severe, with multifocal eosinophilic microabscesses, Splendore Hoeppli material, bacterial colonies and mineralization, Charolais cross, bovine.
Conference Note: The conference participants agreed with the contributor's diagnosis.
Contributor: Universidade Federal de Santa Maria, Departamento de Patologia, 97119-900, Santa Maria, RS, Brazil.
Riet-Correa F, Méndez MC, Schild AL, Ribeiro GA, Almeida SM: Bovine focal proliferative fibrogranulomatous panniculitis (Lechiguana) associated with Pasteurella granulomatis. Vet Pathol 29:93-103, 1992.
International Veterinary Pathology Slide Bank: None.

Case IV - 2274/96 (AFIP 2565964)

Signalment: Black crake (Limnocorax flavirostra), male, subadult.
History: A subadult, male black crake died unexpectedly at the Basle Zoo.
Gross Pathology: At necropsy, the crake was cachectic. Disseminated white, raised, firm, well circumscribed nodules, 1 to 3 mm in diameter, were noted throughout the lung parenchyma. No lesions were seen in other tissues.
Laboratory Results: Bacteriological investigation revealed a severe infection with Nocardia sp. in liver, spleen, kidney and lung. Parasitological investigation was negative.
Contributor's Diagnosis and Comments: Morphologic diagnosis: Pneumonia, granulomatous and necrotizing, severe with beaded, branching filamentous organisms.
Etiologic diagnosis: Nocardiosis.
Histologically, the lungs had multiple, often confluent, granulomas with moderate to severe central necrosis. The necrotic center was surrounded by a margin composed of heterophils, macrophages, lymphocytes, and some multinucleated giant cells. Various numbers of delicate, gram positive, 0.5 to 1.0 m wide, branching, occasionally beaded, filamentous organisms were visible in the necrotic centers. These organisms were acid-fast with the Fite-Faraco method, but not with the Ziehl-Neelsen acid-fast stain. No histologic lesions were recognized in other organs.
Natural nocardial infection has been reported in dogs, cats, cattle, goats, horses, pigs, rabbits, monkeys, dolphins, whales, fishes, birds and in man. Reports in birds are uncommon; whether nocardiosis is actually a very rare disease entity birds, or has just been poorly recognized, is not known. In the past, Nocardia has been often confused with Mycobacterium, Actinomyces and Streptomyces infections in both animal and man.
AFIP Diagnosis: Lung: Pneumonia, necrotizing, granulomatous, multifocal to coalescing, severe, with necrotizing vasculitis and filamentous bacilli, black crake (Limnocorax flavirostra), avian.
Conference: The conference participants agreed with the contributor's diagnosis and comments. Calcific bodies were also noted in many of the sections examined. Calcific bodies are often found within the caseated centers of granulomas, are readily stained with H&E and the PAS reaction and resemble yeast-like cells. When apposed, these bodies may look like budding yeast, and their laminated structure creates the illusion of a thick cell wall or capsule. Calcific bodies do not stain with GMS or Gridley's stains.
Nocardia sp. are gram-positive, non-motile, aerobic, filamentous rods that are partially acid-fast. The organism is a saprophyte and occurs commonly in soil and water. This bacterium is not well demonstrated by H&E stains; the organism stains well with Gram's stain, modified acid fast (Fite-Faraco or Cross-Coates modifications), and by the GMS method. Three species are associated with most animal disease: Nocardia asteroides (approximately 90% of cases); N. caviae; and N. brasiliensis.

Little information is available concerning the pathogenesis of nocardiosis. The organisms may gain entry by wound contamination, inhalation, or ingestion. Direct extension or hematogenous dissemination may then occur. Cell mediated immunity is apparently critical to control of infection. The glycolipid trehalose dimycolate (cord factor) present within nocardial cell walls has been proposed to play a major role in macrophage activation and release of tumor necrosis factor, which are important in host resistance to infection. In one study, injections of Nocardia rubra cell wall skeleton into enlarged subcutaneous lymph nodes of bovine leukemia virus positive cattle had an antitumor effect. N. asteroides has been reported to both inhibit phagosome-lysosome fusion and resist the microbicidal effects of neutrophils. Apparently, virulent strains of this species are resistant to hydrogen peroxide, myeloperoxidase, and halide through the production of superoxide dismutase and catalase.
Contributor: Institute of Animal Pathology, University of Berne, P.O. Box 2735, CH 3001 Bern, Switzerland.
1. Parnell MJ, Hubbard GB, Fletchter KC and Schmidt RE: Nocardia asteroidesInfection in a Purple-Throated Sunbird (Nectarinia sperapa). Vet Pathol 20, 497-500, 1983.
2. Long P, Choi G, Silberman M: Nocardiosis in two Pesquet's Parrots (Psittrichas fulgidus). Avian Dis 27(3):855-859, 1983.
3. Walton AM, Libke KG: Nocardiose bei Blauflügel-Königssittichen (Alisterus amboinensis hypophonius). Schweiz Arch Tierheilk 121:195-200, 1979.
4. Bergmann A, Schüppel KF, and Kronberger H: Nocardiose bei einem Türkisvogel (Cyanerpes cyaneus). Verh Ber Int Symp Erkrank Zootiere 15:293-296, 1977.
5. Timoney JF: Hagen and Brunner's Microbiology and Infectious Diseases of Domestic. Animals, Comstock Publishing, pp.267-269, 1988.
6. Gross TL; Ihrke PJ; Walder EJ: Veterinary Dermatopathology Mosby YearBook, Inc., pp. 163-166, 1992.
7. Onuma M; Yasutomi Y; Yamamoto M: Chemotherapy and Immunotherapy of bovine leukosis. Vet Immunol Immunopathol Oct;22(3):245-54, 1989.
8. Gyles CL and Thoen CO: Pathogenesis of Bacterial Infections in AnimalsIowa State University Press, pp. 124-126, 1993.
9. Jubb KVF, Kennedy PC, Palmer N (eds): Pathology of Domestic Animals Academic Press, Inc., pp. 466-467, pp 437-438, 1993.
10. Chandler FW, Watts JC: Pathologic Diagnosis of Fungal Infections. ASCP Press, Chicago, pg. 125 and 136.
International Veterinary Pathology Slide Bank: None.
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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