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CASE I – 95-1 (AFIP 2503050)
Signalment: Tissue from a healthy pigtailed macaque, Macaca nemestrina.
History: A 10 cm diameter uterine mass was discovered during routine uterine ultrasonography. The mass was removed and submitted for examination.
Gross Pathology: None given.
Laboratory Results: None given.
Contributor’s Diagnosis and Comment: Uterus: Leiomyosarcoma.
An unencapsulated, well-demarcated cellular mass infiltrates uterine smooth muscle and submucosa. The mass is composed of round eosinophilic cells arranged in cords and sheets that are supported by a fine fibrovascular tissue. In several foci, the cells appear to be in packets or bundles. The cells have moderate amounts of fibrillar cytoplasm and distinct margins. Their nuclei are round to indented and markedly anisokaryotic. The nuclei contain vesiculate to marginated clumped chromatin and one to two small nucleoli. Mitotic figures are rare. Rare binucleate cells are scattered through the mass. Infiltrating neoplastic cells entrap large vessels and islands of smooth muscle. These foci contain hemosiderin-laden macrophages and hemorrhage. Entrapped smooth muscle cells are often heavily vacuolated and hyaline (degeneration and necrosis). In some sections, a cluster of neoplastic cells is present within a large blood vessel in the muscularis. A mild, multifocal lymphohistiocytic infiltrate is present in the perivascular tissue of the adjacent muscularis.
The cellular origin of this undifferentiated round cell tumor was not clear from microscopic examination alone. Immunocytochemical analysis demonstrated that the neoplastic cells stained positively for desmin, muscle actin, and smooth muscle alpha-actin but did not stain for cytokeratins. In addition, the cells were outlined or encapsulated by material that stained positive for collagen type IV, indicative of basement membrane material. This staining pattern was consistent with that expected with smooth muscle cells and indicated a diagnosis of leiomyosarcoma in this case. Proliferative and neoplastic lesions of the uterus are relatively common in nonhuman primates, and uterine neoplasms are cited as the third most common neoplasm in nonhuman primates. Uterine leiomyoma and endometriosis appear to be the most frequently described lesions. To our knowledge, uterine leiomyosarcoma has not been described in Macaca nemestrina.
2X2 Photomicrograph: The photomicrograph contains the mass and adjacent uterus. It demonstrates the presence of smooth muscle alpha-actin within the cytoplasm of the neoplastic cells.
AFIP Diagnosis: Leiomyosarcoma, epithelioid, pigtailed macaque, Macaca nemestrina, nonhuman primate.
Conference Comment: As the contributor states, the origin of this neoplasm is not clear based on histomorphology alone. The nests and packets of neoplastic round to polygonal cells that infiltrate the myometrium led conference participants to consider neuroendocrine carcinoma, endometrial carcinoma and poorly differentiated carcinoma in their differential diagnosis, as well as the more common uterine neoplasms of leiomyosarcoma and leiomyoma.
Leiomyosarcomas may have cellular morphology ranging from strap-like muscle fibers to rounded anaplastic cells that may not suggest a particular cell lineage. In this case, the presence of binucleate cells, nuclear folding and occasional vacuolation of cells provided hints of a smooth muscle origin. Immunohistochemical staining was helpful in determining the cell of origin and making the diagnosis.
Contributor: University of Washington, Department of Comparative Medicine, Box 357190, Seattle, WA 98195-7190
References: 1. Birkebak TA, Wang NP, Weyhrich J: Uterine epithelioid leiomyosarcoma in a pig-tailed macaque. J Med Primatol 25:367-369, 1996.
2. Brunnert SR, Herron AJ, Altman NH: Subcutaneous leiomyosarcoma in a Peruvian squirrel monkey. Vet Pathol 27:126-128, 1990
3. Lowenstine LJ: Neoplasms and proliferative disorders in nonhuman primates.
In: Primates: The road to self-sustaining populations, ed. Beinirschke K, pp. 781-814. Springer-Verlag, New York, NY, 1986
4. Seibold HR, Wolf RH: Neoplasms and proliferative lesions in 1065 nonhuman primate necropsies. Lab Anim Sci 23(4):533-539, 1973
CASE II – 95:962M (AFIP 2514767)
Signalment: 4-month-old, castrated male, Yorkshire crossbred pig.
History: A group of 100 pigs was moved into the region. The pigs were 3 months of age, and approximately 4 pigs died after this move but were not necropsied. Four weeks later, the pigs were moved to a new facility within the region and within one week six animals were dead or dying. Dyspnea, weight loss, difficulty walking and pyrexia were reported. The ear pinnae of affected pigs became markedly cyanotic.
Gross Pathology: The specimen was submitted live and was moderately emaciated upon presentation. The animal was euthanized by an overdose of barbiturate administered by intracardiac injection. There were multiple, irregular, coalescent and locally extensive regions of red-purple discoloration to the skin of the ears.
The trachea contained a small amount of white froth. The ventral one-half of the right apical, cardiac and diaphragmatic lung lobes were very firm, non-pliable, sunken, consolidated and brown and were sharply demarcated from the dorsal aspects of the right lung lobes, which were firm, pink and pliable. On cut section, these non-pliable, sunken and consolidated regions yielded yellow mucoid fluid from small caliber bronchi. There were multiple, sunken, brown, sharply demarcated foci scattered throughout the left lung lobes.
The liver was firm, smooth and brown, and the gall bladder contained thick green bile. The kidneys were smooth, firm and tan, and there were numerous petechiae disseminated throughout the cortices and medulla of the left and right kidneys. The urinary bladder contained approximately 20 ml of straw-colored urine, and there were few and scattered petechiae along the mucosal surface. The spleen was markedly enlarged and very firm with adhesions of mesentery distributed over its capsular surface. There were multifocal, irregular and coalescent, firm, pale white and dark red regions distributed randomly throughout the spleen on both the capsular and cut surfaces. The adrenal glands were firm and smooth, and the adrenal cortices were diffusely red-brown. The stomach contained mucous and refluxed bile, and there was a focus of petechiation of the gastric mucosa. The small intestine contained yellow fluid, and scattered petechiae were present in the mucosa. The cecum and colon contained thick, green feces, and the colonic mucosa was segmentally hyperemic with petechiations. The submandibular, tracheobronchial, gastrohepatic, mesenteric and sublumbar lymph nodes were enlarged, hemorrhagic and edematous. There were petechiae disseminated throughout the mesentery. No lesions were noted in the brain prior to fixation.
Laboratory Results: Bacterial cultures of spleen, kidney, liver, lung, mesenteric and tracheobronchial lymph nodes and bile yielded pure culture of Salmonella cholerae-suis. Direct fluorescent antibody stains against classical swine fever and African swine fever virus performed at the Plum Island Foreign Animal Disease Diagnostic Laboratory on fresh frozen tissue sections of tonsil were negative. Animal inoculation tests performed at Plum Island using tissue extracts from kidney, spleen, lymph node and blood were negative. An agar gel immunodiffusion test for pseudorabies was negative.
Contributor’s Diagnosis and Comment: Spleen, infarction, severe, locally extensive, with fibrinoid necrosis and thrombosis of intralesional blood vessels and with intralesional bacteria, porcine, cross-bred.
Etiologic diagnosis: Septicemic salmonellosis.
A triangular section of spleen is examined. A locally extensive zone of coagulation necrosis of red and white pulp is present with thrombosis of numerous intralesional blood vessels. There is fibrinoid necrosis of mural elements of thrombosed blood vessels with infiltration of adventitial and medial zones by neutrophils, macrophages and perivascular accumulations of small numbers of necrotic neutrophils and macrophages around scattered arterioles. Clusters of slender, lightly basophilic, rod-shaped bacteria are dispersed within fields of necrosis. The zone of coagulation necrosis is bordered by a thin layer of neutrophils and macrophages which, in turn, is surrounded by a wider layer of fibroblasts, macrophages and fibrous connective tissue. Small clusters of histiocytes accompanied by low numbers of neutrophils are present in the remaining red pulp, and there is proliferation of small blood vessels with local accumulations of low numbers of lymphocytes and histiocytes along segments of the capsule.
AFIP Diagnosis: Spleen: Necrosis, focally extensive (infarct), with intralesional bacilli and adjacent necrotizing vasculitis, Yorkshire crossbred pig, porcine.
Conference Comment: Salmonella choleraesuis typically infects feeder pigs at 2-4 months of age and is often associated with the containment of many young animals in limited areas. The pathogenesis of salmonellosis, following ingestion, involves colonization and invasion of the intestinal mucosa through ileal M cells using fimbriae or pilar adhesins, and subsequent plasmid-mediated survival within macrophages. The lipid A portion of lipopolysaccharide within gram-negative cell walls is responsible for the endotoxin-mediated effects seen in the systemic form of the disease. Acute enterocolitis with ulcerative colonic lesions (button ulcers) is common. Stressed young animals often have compromised cell-mediated immunity that can lead to dissemination of organisms with rapidly fatal consequences. Interstitial pneumonia and multifocal hepatic necrosis or microgranulomas (“paratyphoid nodules”) are the most consistent systemic lesions. Peripheral cyanosis of the tail, snout and ears, dyspnea and terminal convulsions can be seen clinically with septicemia. Splenomegaly with infarction and petechial hemorrhages in many organs are associated with endothelial damage due to endotoxin.
The differential diagnosis in this case could include other bacterial septicemias (e.g., Erysipelas rhusiopathiae, Haemophilus, Streptococcus), African swine fever virus (Asfarviridae; asfarvirus) and classical swine fever virus (Flaviviridae; porcine pestivirus). The presence or absence of splenic infarcts cannot be used to distinguish between salmonellosis and classical swine fever, as shown in this case.
A Brown and Hopps Gram’s stain demonstrated that the bacilli within the infarct are gram-negative.
Contributor: University of Connecticut, Department of Pathobiology, 61 North Eagleville Road, U-89, Storrs, CT 06269-3089
References: 1. Barker IK, Van Dreumel AA: The alimentary system. In: Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 2, pp. 213-217. Academic Press, New York, NY, 1993
2. Jones TC, Hunt RD: Diseases due to simple bacteria. In: Veterinary Pathology. 5th ed., pp 622-625. Lea & Febiger, Philadelphia, PA, 1983
3. Van Kruiningen HJ: The gastrointestinal system. In: Special Veterinary Pathology. ed. Thompson R, Decker BC, p. 211. Toronto, Canada, 1988
CASE III – 1906709 (AFIP 2642675)
Signalment: 4-month-old, castrated male, mixed breed, feline
History: This kitten developed coughing and progressed to severe dyspnea.
Gross Pathology: There was a serosanguinous nasal discharge. The right lung was darkened, edematous and firm in texture and sank in formalin. The left lung was mottled. There were no other significant gross lesions.
Laboratory Results: Fluorescent antibody examination for feline viral rhinotracheitis was positive on the trachea and lung, as was virus isolation. Mycoplasma felis was isolated from the lung at >1,000 cfu.
Contributor’s Diagnosis and Comment: Severe, acute, necrotizing and suppurative bronchointerstitial pneumonia with peribronchial and perivascular lymphoid cuffing and intranuclear inclusion bodies; consistent with feline herpesvirus-1 (feline viral rhinotracheitis, FVR) and respiratory mycoplasmosis.
The most significant changes were in the lung that had a severe necrotizing process that targeted airways and the interstitium. Airway epithelium was obliterated leaving only necrotic exudate that extended into the underlying submucosal glands and also affected alveolar walls in the adjacent parenchyma. Intranuclear inclusion bodies were present in sloughed cells of the airways, and within the submucosal glands and occasionally in alveolar walls. Alveolar lumens contained sloughed necrotic cells, fibrinous exudate, erythrocytes and neutrophils, with hyaline membranes in some regions. There was a concomitant “cuffing” pneumonia with lymphoid infiltrates of a variable degree surrounding airways and in perivascular regions. The histologic findings correlate well with the identification of the FVR virus via FA and VI, and the isolation of Mycoplasma felis. Necrosis of airway epithelium with interstitial extension is commonly seen with herpesviruses due to their cytopathic nature, but is apparently uncommon in cats. Complication of FVR with Mycoplasma felis and other bacteria has been described. In man, herpes simplex may cause similar lesions with targeting of the airways and the interstitium, inducing diffuse alveolar damage (DAD). Cytomegaloviruses, measles virus, and adenovirus may induce similar lesions. “Cuffing” pneumonias are characteristic of mycoplasmosis in numerous species. The pathogenesis of mycoplasma pneumonias is in part related to ciliary stasis. In this case, it was difficult to determine which etiology was primary and which was secondary.
AFIP Diagnoses: 1. Lung: Pneumonia, bronchointerstitial, necrotizing and fibrinous, acute, diffuse, severe, with eosinophilic intranuclear inclusion bodies and rare syncytia, cat, breed not specified, feline.
2. Lung: Pneumonia, perivascular, lymphocytic, multifocal, mild.
Conference Comment: Feline herpesvirus-1 (FHV-1) and feline calicivirus are major components of the feline respiratory disease complex. Feline reovirus and a feline-adapted strain of Chlamydia psittaci are considered minor components with Mycoplasma felis and secondary bacterial invaders such as Streptococcus felis, Bordetella bronchiseptica, and Pasteurella multocida often present as opportunistic infections. FHV-1, like most alphaherpesviruses, is primarily cytolytic in its pathogenesis and causes a necrotizing pneumonia, bronchitis and bronchiolitis with prominent eosinophilic intranuclear inclusion bodies within infected respiratory epithelial cells. Intranuclear inclusion bodies are difficult to find after the first week of infection and most cats recover in 1-2 weeks. More than 80% of recovered cats remain carriers with latent infection of the trigeminal ganglia, optic nerves, olfactory bulbs, and corneas. Intermittent viral shedding may occur during periods of stress or immunosuppression. Alphaherpesviruses that cause upper respiratory disease in other species include infectious bovine rhinotracheitis (bovine herpesvirus-1), equine rhinopneumonitis (equine herpesvirus-4) and infectious laryngotracheitis of chickens (gallid herpesvirus-1).
Contributor: Animal Health Diagnostic Lab, PO Box 30076, Lansing, MI 48909-7576
References: 1. Dungworth DL: The respiratory system. In: Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., pp. 558-559. Academic Press, Inc., New York, NY, 1993
2. Gaskell R, Dawson S: Feline respiratory disease. In: Infectious Disease of the Dog and Cat, ed Greene CE, 2nd ed, pp. 97-106, WB Saunders, Philadelphia, PA, 1998
3. Sykes JE, Anderson, GA, Studdert VP, Browning GF: Prevalence of feline Chlamydia psittici and feline herpesvirus 1 in cats with upper respiratory disease. J Vet Intern Med 13:153-162, 1999
CASE IV – 95:973P (AFIP 2514858)
Signalment: A young adult (1 to 2-years-old), female, red fox (Vulpes vulpes).
History: This fox was observed to be limping and emaciated in a residential neighborhood. The fox was trapped by animal control officers and was transported to a wildlife rehabilitation center. It was lame on the left front limb on presentation. It died after 3 days of treatment. A partial necropsy was performed by the attending veterinarian.
Gross Pathology: The specimen was in fair condition. The thorax and abdomen had been entered, and the heart had been removed. The left and right ventricular free walls had been incised. The specimen was emaciated, and there were multiple extensive, irregular and coalescent regions of skin that were alopecic and greasy with excessive scaling. These regions covered the head, dorsum, inguinal region and lateral aspects of the limbs.
The lungs were firm, pliable and mottled red and tan. Within the primary and secondary bronchi, there were numerous 0.5 cm to 1 cm long slender worms. There were few and scattered, minute (2-3 mm), oval, tan, smooth foci within the endocardium of the left and right ventricles.
The liver and kidneys were firm, smooth and brown. There were numerous tan striations throughout the renal cortices along the corticomedullary junction, and there were tan striations within the papillae. The stomach contained several soft, pliable, red-brown trichobezoars, the smallest was 0.5 cm in length, the largest was 2.0 cm in length. The small intestine contained watery yellow fluid, and there were scattered loci in the jejunum that contained small numbers of small, 1 cm, slender worms. The enteric mucosa was tan and smooth. Soft green feces were present in the colon.
Laboratory Results: Direct fluorescent antibody tests performed on impression smears of the brainstem, cerebellum and hippocampus are negative for rabies.
Contributor’s Diagnosis and Comment: Skin, dermatitis, suppurative, diffuse, mild to moderate, with parakeratotic hyperkeratosis, intralesional acarids, bacteria and yeast, red fox.
A rectangular section of haired skin is examined. There is diffuse, mild to moderate, parakeratotic hyperkeratosis with numerous adult acarids present within pockets scattered throughout the stratum corneum. Small foci of necrosis with accumulations of low to moderate numbers of neutrophils are dispersed throughout the stratum corneum. Clusters of coccoid bacteria, along with aggregates of ovoid yeasts are scattered among the shards of keratin present along the epidermal surface. Within the dermis there is a mild, diffuse accumulation of histiocytes and lymphocytes along the interface with the epidermis; occasional perivascular lymphohistiocytic aggregates are present. The acarids are limited to pockets in the stratum corneum, and they possess a chitinized cuticle and jointed appendages when distinguishable. The body cavities of the mites are dorsoventrally compressed and the somatic musculature is striated. Salivary glands, nervous tissue and excretory tubules are identified in various sections. The chitinous exoskeletons of numerous mites possess dorsal spines characteristic of Sarcoptes sp.
AFIP Diagnosis: Haired skin: Dermatitis, proliferative and hyperkeratotic, superficial, mastocytic, eosinophilic and neutrophilic, diffuse, moderate, with numerous intracorneal acarids, cocci and yeasts, red fox (Vulpes vulpes), canine, etiology consistent with Sarcoptes sp.
Conference Comment: Sarcoptes scabiei var. canis is the most debilitating skin disease diagnosed in wild red foxes. The parasite spends its entire 17-21 day life cycle on the host causing a diffuse crusting dermatitis and pruritus. It is not possible to differentiate the varieties of Sarcoptes scabiei using morphologic characteristics, but the different varieties are thought to be members of the same species, each having become adapted to a specific mammalian host. Cross-infections between host species are often transient and self-limiting. Red foxes appear to be highly susceptible to developing sarcoptic mange and, in the absence of treatment, become extremely debilitated and die within 2 to 3 months. Unlike other species, red foxes do not develop cell-mediated immunity in response to infection. Foxes that are treated with ivermectin develop similarly severe lesions upon subsequent infection.
Infected foxes develop strong, IgE-mediated, type 1 hypersensitivity reactions that can persist as long as 4 months after treatment and complete resolution of clinical signs. Dermal mast cell hyperplasia and increased eosinophils, indicative of immediate hypersensitivity reactions, predominate throughout infection. IL-4 stimulates production of T helper 2 cells and binds B cells to trigger the isotype switch to IgE. IgE binding on mast cells, basophils, eosinophils and dendritic cells causes increased production of IL-4, stimulating more T helper 2 cells in a perpetuating “allergy loop.” IgE binding to mast cells also causes activation and degranulation, with release of vasoactive amines, and activation of the arachidonic acid and complement cascades, leading to production of the C3a and C5a anaphylatoxins. T helper 2 cells and mast cells also produce IL-5, which triggers eosinophil release from bone marrow. Mast cell granule contents (including histamine, platelet activating factor, and eosinophil chemotactic factor) as well as C5a and leukotriene B are chemotactic for eosinophils. Most S. scabiei-related lesions are the result of self-trauma induced by severe pruritus. “Norwegian scabies” is a chronic form of scabies seen in animals with a weak hypersensitivity reaction or immunosuppression. These animals exhibit a severe crusting dermatitis with extremely large numbers of mites.
Diagnosis of the typical allergic form of the disease may be difficult in domestic animals since the mites are characteristically difficult to demonstrate even with multiple skin scrapings or in microscopic section. The most useful diagnostic procedure is often response to therapy.
Contributor: University of Connecticut, Department of Pathobiology, 61 North Eagleville Road, U-89, Storrs, CT 06269-3089
References: 1. Gardiner CH, Poynton SL: An Atlas of Metazoan Parasites in Animal Tissues, pp. 56-58. Armed Forces Institute of Pathology, Washington, DC, 1999
2. Little SE, Davidson WR, Rakich PM, Nixon TL, Bounous DI, Nettles VF: Responses of red foxes to first and second infection with Sarcoptes Scabiei. J Wild Dis 34(3):600-610, 1998
3. Tizard IR: Veterinary Immunology An Introduction, pp. 307-321. WB Saunders, Philadelphia, PA, 2000
4. Yager JA, Scott DW: The skin and appendages. In:
Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer
N, 4th ed., vol. 1, pp. 681-683. Academic Press, New York, NY,
1993
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
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