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CASE I – 95-106660 (AFIP 2513017)
Signalment: 6-month-old, intact female, Dutch rabbit
History: Relatively sudden onset of a skin mass (2 cm in diameter) arising from the medial digit, left rear foot. Digital amputation was performed.
Gross Pathology: 2 cm ulcerated skin mass, digit.
Laboratory Results: Not applicable
Contributor’s Diagnosis and Comment: Dermal and subcutaneous mass, medial digit of right rear foot (Shope fibroma)
Etiology: Poxvirus
Shope fibroma is a relatively common diagnosis for skin nodules from rabbits received as biopsy specimens during late summer and early fall. The etiology of these tumors is a poxvirus related antigenically to myxomatosis virus and to the hare and squirrel fibroma viruses. In this case, intracytoplasmic eosinophilic inclusions typical of poxvirus infection could be found in some dermal spindle cells as well as some cells within the epidermis. Many cases spontaneously regress.
AFIP Diagnosis: Haired skin: Atypical mesenchymal cell proliferation, focally extensive, with eosinophilic intracytoplasmic inclusion bodies, heterophilic inflammation and ulceration, consistent with Shope fibroma, Dutch rabbit, Oryctolagus cuniculus, lagomorph.
Conference Comment: Shope fibroma virus is a Leporipoxvirus of the family Poxviridae. In natural infections, it causes proliferative, dermal fibromas to form in immunocompetent wild cottontail rabbits (Sylvilagus spp.) and domestic rabbits (Oryctolagus spp.). Clinical signs, other than tumors, do not occur in infected adult rabbits. The disease is rare in hares (Lepus spp.), which are naturally resistant to the virus.
Mechanical transmission by biting arthropods appears to be the primary means of spread. Tumors may persist for several months, and in some cases for nearly a year. Cell-mediated immunity is important in spontaneous tumor regression. Many tumor cells have large, eosinophilic intracytoplasmic inclusion bodies characteristic of poxvirus infections. Because the disease is endemic and of little significance in cottontail rabbits, no control measures have been developed.
Contributor: Tufts School of Veterinary Medicine, Veterinary Diagnostic Laboratory, 200 Westboro Road, North Grafton, MA 01536
References: Percy DH, Barthold SW: In: Pathology of Laboratory Rodents and Rabbits, pp. 182-183. Iowa State University Press, 1993
CASE II – 472/2000 (AFIP 2741839)
Signalment: 5-week-old castrated male, large white crossbred pig
History: Two litters of pigs had yellow diarrhea and some had respiratory distress. The owner dosed them with lincospectin and ampicillin by injection without any veterinary consultation (farmers can get ready access to antibiotics in this area). When no response was shown in several days, the litters were culled.
Gross Pathology: The carcass was in poor body condition and appeared dehydrated. Subcutaneous tissues and muscle appeared pale. Visceral surfaces in the abdomen and the lung and pleural surfaces appeared dull and rough with a yellowish fibrous appearance. The joint fluid was slightly turbid and synovial linings were dull and discolored. There were fibrous adhesions between intestines, liver, spleen and stomach and between pericardial sac, heart and lungs. Small intestine had yellowish pasty contents and large intestinal contents were quite fluid and had no formed feces.
Laboratory Results: Moderate growth of b -hemolytic E. coli (O149, nK91 and K88a,c positive) was recovered from liver, lymph nodes and intestines.
Haemophilus parasuis was isolated from lung tissue.
Tracheal swabs and lung tissue were negative for hemagglutinating viruses by chick embryo allantoic cavity and MDCK cell culture inoculation.
Homogenized, pooled lymph nodes and tonsil were negative for classical swine fever virus by antigen capture ELISA and PCR tests and by PK15 cell culture inoculation. No inclusion bodies suggestive of porcine circovirus were detected in PK15 cell cultures.
Rotavirus latex agglutination test on small intestinal content was negative.
Contributor’s Diagnoses and Comment: 1. Lung, fibrinopurulent pleurisy, subacute, diffuse, severe.
2. Lung, suppurative bronchopneumonia, acute, lobular, moderate severity.
3. Heart, fibrinopurulent pericarditis, subacute, diffuse, severe.
Other histopathological changes present for the case included polyserositis in all abdominal organs examined and a mild subacute meningoencephalomyelitis. The serositis and meningoencephalomyelitis appeared to be subacute based on the increased presence of plasma cells within the inflammatory cells. The isolation of Haemophilus parasuis from lung tissue, together with presence of fibrinopurulent polyserositis, polyarthritis and meningoencephalitis are consistent with a diagnosis of Glasser’s disease. Other possible causes of polyserositis and polyarthritis syndrome in pigs of this age would be Mycoplasma hyorhinis and Streptococcus suis type II infections. In M. hyorhinis infection, a predominantly lymphocytic infiltration would be expected and with S. suis infection a more purulent response would be likely.
AFIP Diagnoses: 1. Heart: Epicarditis and subepicardial myocarditis, fibrinous and necrotizing, subacute, diffuse, moderate, crossbred pig, porcine.
2. Lung: Pleuritis, fibrinous and necrotizing, subacute, diffuse, moderate, with bronchopneumonia.
Conference Comment: The etiologic agent of porcine polyserositis and arthritis (Glässer’s disease) is Haemophilus parasuis. It is a small, gram-negative rod whose growth is supported only on media containing nicotinamide-adenine dinucleotide (NAD) or on blood agar in the vicinity of a streak of a staphylococcus strain (satellitism). It is typically seen in young pigs after weaning, but can be found in pigs of all ages, particularly after periods of stress.
Haemophilus parasuis is commonly found in the upper respiratory tract of swine and is considered an opportunistic secondary invader causing pulmonary infection. Collapse of peripheral circulation can produce cyanosis of the skin and diseased animals often have swollen, painful joints. In many cases, pigs have signs of meningoencephalitis with muscular tremors and incoordination. The histopathologic features are those of a fibrinopurulent inflammation with infiltration of many neutrophils and some mononuclear cells.
Isolation of the organism, particularly from joints or visceral pleura, is required to differentiate Glässer’s disease from other septicemic bacterial infections. Streptococcus suis or Mycoplasma hyorhinis can cause similar pulmonary or arthritic lesions; however, mycoplasmosis is generally a milder, more chronic infection and is rarely accompanied by meningitis. Nervous symptoms may be observed with Escherichia coli enterotoxemia and viral infections such as pseudorabies (porcine herpesvirus). Erysipelothrix rhusiopathiae can cause arthritis and cutaneous lesions.
Contributor: Castle Peak Veterinary Laboratory, Agriculture, Fisheries and Conservation Department, San Fuk Road, Tuen Mun, New Territories, Hong Kong, SAR
References: 1. Buddle JR: Bacterial and Fungal Diseases of Pigs: Glasser’s disease. In: Animal Health in Australia, vol. 6, pp. 88-91. Australian Government Publishing Service, Canberra, Australia, 1985
2. Nicolet J: Haemophilus parasuis. In: Diseases of Swine, ed. Leman AD, Straw BE, Mengeling WL, D’Allaire S, Taylor D, 7th ed., pp. 526-528. Iowa State University Press, Ames, Iowa, 1992
3. Palmer N: Glasser’s disease of swine. In: Pathology of Domestic Animals, ed. Jubb KVF, Kennedy PC, Palmer N, 4th ed., vol. 1, pp. 169-170. Academic Press, San Diego, CA, 1992
CASE III – 00-246 (AFIP 2741244)
Signalment: 9.5-year-old, female spayed, Dalmatian (Canis familiaris), canine
History: Progressive inability to rise for one week. Physical examination revealed cold cyanotic hindlimbs with no palpable pulses.
Gross Pathology: Both kidneys were normal in shape and size and had slightly mottled tan and white cortices and pale yellow-pink medullas. They were slightly firmer than normal on sectioning, and treatment of sections with iodine, followed by sulfuric acid, stained the glomeruli and the medullary interstitium black.
In the abdominal aorta at the bifurcation, there was a pale brown, granular thrombus attached to the vessel wall. It extended proximally for 3 cm, and 5 cm and 6 cm distally down the left and right eternal iliac arteries, respectively. No other thrombi were found in any other sites.
Laboratory Results: Urinalysis: SG= 1.032; 4+ protein
Protein:Creatinine Ratio = 32.4 (normal = < 0.5)
Coagulation screen (PT and PTT): within normal limits
Serum albumin = 1.8 g/dL (normal = 2.3 – 3.9 g/dL)
Globulin = 3.3 g/dL; A/G ratio = 0.5
Cholesterol = 345 mg/dL (normal = 126–359 mg/dL)
BUN = 18 mg/dL (normal = 5–30 mg/dL)
Creatinine = 1.4mg/dL (normal = 0.5–1.0 mg/dL)
Contributor’s Diagnoses and Comment: 1. Kidney: severe generalized glomerular and moderate multifocal medullary amyloidosis; moderate segmental subacute tubular necrosis with regeneration; mild multifocal chronic lymphoplasmacytic interstitial nephritis; mild multifocal tubular and interstitial mineralization
2. Abdominal aorta: acute thrombus; focal intimal fibrosis; mild focal acute arteritis
Microscopic examination of the kidneys revealed extensive, pale eosinophilic, amorphous hyaline material effacing the normal architecture of most of the glomeruli. Further deposits of the same material were seen in the interstitium, most notably within the medulla. This material stained positively with Congo red and exhibited typical apple-green birefringence when viewed under polarized light, confirming it to be amyloid. The congophilia was lost following pretreatment of the section with acidified potassium permanganate solution, suggesting that the amyloid is of the AA rather than AL type.
The tubular necrosis was considered to be due to localized ischemia caused by compression of the vasculature by the extensive amyloid deposits, possibly exacerbated by the altered blood flow resulting from the aortic thrombus.
Examination of the aorta and thrombus revealed intimal fibrosis at the site of attachment and a mild infiltrate of neutrophils within the vessel wall, also at this site.
Amyloidosis in dogs is usually idiopathic, and can involve many organs such as the liver or spleen, but the kidney is most commonly affected, with deposits most often found in the glomeruli. This type of amyloid is usually of the AA rather than the AL type, and leads to progressive renal disease with proteinuria.
According to Virchow, one or more of the following three factors can lead to thrombosis: endothelial damage; alterations in blood flow, and changes in blood coagulability (either hypercoagulable or hypofibrinolytic states). In animals, a number of conditions have been associated with a predisposition to thrombosis including hyperadrenocorticism, immune-mediated hemolytic anemia, neoplasia, sepsis, disseminated intravascular coagulation, acute pancreatic necrosis, heart disease, dirofilariasis, and renal disease.
Renal diseases that have been associated with thromboembolism include glomerular amyloidosis, glomerulonephritis, chronic interstitial nephritis, and acute tubular necrosis. Of these, chronic glomerular diseases leading to a protein-losing nephropathy are the most usual cause.
Typically, affected animals develop signs of the nephrotic syndrome characterized by proteinuria, hypoalbuminemia, ascites and hypercholesterolemia. Three of these four findings were present in this dog, the exception being the lack of ascites. In this case there was a severe proteinuria, with a urine protein: creatinine ratio of 32.4. A value of less than 0.5 is considered normal, greater than 1.0 is positive, while a ratio of greater than 3.0 suggests that it is of glomerular origin. Furthermore, the highest ratios are seen with amyloidosis.
The pathogenesis of the ensuing thromboembolic disease is believed to stem from the loss of anticoagulant and pro-fibrinolytic factors from the serum through the leaky glomeruli into the urine. Among these, the most important is the loss of antithrombin III, which is one of the major components accounting for anticoagulant activity in the blood.
In dogs with renal amyloidosis, thromboembolic disease has been reported in a number of sites, the lungs being the most common, with other sites including the heart, kidneys, intestine, aorta, iliac arteries and other tissues. It is interesting to speculate whether the localized intimal fibrosis in the caudal abdominal aorta in this case predisposed it to thrombosis at this site through either endothelial damage or alterations in local blood flow leading to increased turbulence. Certainly this is not an uncommon lesion that is generally regarded as “benign”.
Cats with aortic thromboembolism usually present with peracute to acute signs of hindlimb lameness, pain and lack of palpable femoral pulses. This contrasts to some extent with affected dogs in which signs may be present and slowly progress over a matter of days to weeks. The prognosis for dogs is, also, less guarded.
AFIP Diagnoses: 1. Kidney: Amyloidosis, generalized glomerular and multifocal medullary, moderate, Dalmatian, canine.
2. Kidney: Nephritis, interstitial, lymphoplasmacytic, multifocal, moderate, with mild tubular mineralization.
3. Large elastic artery: Thrombus.
4. Large elastic artery: Fibrosis, intimal.
Conference Comment: The pathogenesis of thromboembolism in dogs with renal amyloidosis is likely multifactorial. The contributor provided an excellent discussion of many factors which may be involved. Canine aortic/iliac thrombosis is an uncommon condition, which usually occurs secondarily to underlying disease processes that interfere with blood flow, disrupt vascular integrity, or cause hypercoagulable or hypofibrinolytic states. When found, efforts should be made to search for an underlying cause.
Contributor: University of Pennsylvania, School of Veterinary Medicine, Laboratory of Pathology & Toxicology, 3800 Spruce Street, Philadelphia, PA 19104-6008
References: 1. Boswood A, Lamb CR, White RN: Aortic and iliac thrombosis in six dogs. J Sm Anim Prac 41:109-114, 2000
2. DiBartola SP, Meuten DJ: Renal amyloidosis in two dogs presented for thromboembolic phenomena. J Amer Anim Hosp Assoc 16:129-135, 1980
3. Slauson DO, Gribble DH: Thrombosis complicating renal amyloidosis in dogs. Vet Pathol 8:352-363, 1971
4. Van Winkle TJ, Hackner SG, Liu SM: Clinical and pathological features of aortic thromboembolism in 36 dogs. J Vet Emerg Crit Care 3(1):13-20, 1993
CASE IV – 10893 (AFIP 2741042)
Signalment: 5-year-old, female, Japanese domestic cat
History: This cat was administrated anti-estrual drug for several years at an animal hospital and had a vaginal discharge for the last 2 years. She was presented to another animal hospital where the veterinarian palpated an enlarged hard uterus and performed an ovariohysterectomy.
Gross Pathology: At biopsy, uterine horn was greatly enlarged and many whitish nodules of up to 1 mm diameter were disseminated in the surface. Whitish nodules were also formed on the surface of the bladder. The uterine wall was thickened by white to yellow tissue and the uterine lumen was filled with hemorrhagic pus.
Laboratory Results: None
Contributor’s Diagnosis and Comment: Adenocarcinoma, uterus.
Although the uterine tumor is one of the rare tumors in animals, there are comparatively many reports in the cat. The gross and microscopic images of the previously reported cases of uterine adenocarcinoma were similar to this case, and many had similar suppurative inflammation. The biological behavior of feline uterine cancer seems to be also highly malignant, because there is metastasis and implantation in most reported cases. Our case also had implantation of neoplastic tissue in the urinary bladder mucosa.
Among Felidae, uterine adenocarcinoma in a tiger has been reported, and it was considered that the administration of long-term implants of progesterone and progestin to suppress estrus was a cause of the carcinogenesis. A long-term estrus suppressant was also administered in this case and the possibility of carcinogenesis by a similar mechanism was considered.
AFIP Diagnosis: 1. Uterus: Adenocarcinoma of endometrium, Japanese cat, feline.
2. Uterus: Endometritis, suppurative, multifocal, severe.
Conference Comment: Uterine adenocarcinoma, comparatively rare in the cat, usually arises from endometrial glands and often invades the myometrium. Squamous metaplasia and stromal fibrosis are seen. Reported metastatic sites include lung, brain, ovary, liver, kidney, lymph nodes and eye.
Of the domestic animals, carcinoma of the endometrium is reported more frequently in cattle. The tumors may be single or multiple, nodular masses in the uterine wall. The serosal surface is often umbilicated. Metastasis occurs to regional lymph nodes and the lungs. Uterine adenocarcinoma is the most commonly encountered spontaneous neoplasm in rabbits. Metastasis and tumor implantation within the liver and lung are similar to the primary neoplasm, often with a prominent stromal component.
Conference participants cited tissue identification as the most challenging aspect of this case. Urinary bladder and prostate were considered by many. When given the animal’s gender, conference participants had little trouble with the diagnosis. By immunohistochemistry, small clusters of cytokeratin-positive neoplastic cells were demonstrated within the uterine stroma; vascular invasion was not evident.
Contributor: Setsunan University, Research Institute of Drug Safety, Faculty of Pharmaceutical Sciences, 45-1 Nagaotouge-cho, Hirakata, Osaka 573-0101, Japan
References: 1. Moulton JE: Tumors in Domestic Animals, 3rd ed., pp. 509-510. University of California Press, Berkley and Los Angeles, CA, 1990
2. Buergelt CD: Color Atlas of Reproductive Pathology of Domestic Animals, pp. 122-125. Mosby Year Book, St. Louis, MO, 1997
3. McEntee K: Reproductive Pathology of Domestic Animals, pp. 182-183. Academic Press, San Diego, CA, 1990
*Sponsored by the American Veterinary Medical Association, the American College of Veterinary Pathologists and the C. L. Davis Foundation.
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