Lanny W. Pace

Retrospective Study of 338 Canine Oral Melanomas with Clinical, Histologic, and Immunohistochemical Review of 129 Cases

Diagnostic records from 338 canine oral melanomas in 338 dogs received at the Veterinary Medical Diagnostic Laboratory (1992-1999) were reviewed. Of these tumors, 122 plus an additional 7 metastatic melanomas of unknown origin were selected for clinical follow-up, histologic review, and immunohistochemistry. Chow Chow, Golden Retriever, and Pekingese/Poodle mix breeds were overrepresented, whereas Boxer and German Shepherd breeds were underrepresented. There was no gender predisposition and the average age at presentation was 11.4 years. Forty-nine dogs were euthanized due to recurrence or metastasis. The average postsurgical survival time was 173 days. The gingiva and the labial mucosa were the most common sites. Most tumors were composed of either polygonal cells (27 cases, 20.9%), spindle cells (44 cases, 34.1%), or a mixture of the two (polygonal and spindle) (54 cases, 41.9%). Clear cell (3 cases, 2.3%) and adenoid/papillary (1 case, 0.8%) patterns were uncommon. The metastases of 6/6 oral melanomas had morphologic and immunohistochemical features similar to those of the primary tumors. Immunohistochemically, Melan A was detected in 113/122 oral (92.6%) and 5/7 (71.9%) metastatic melanomas. Only 4/163 nonmelanocytic tumors were focally and weakly positive for Melan A. Antibodies against vimentin, S100 protein, and neuron-specific enolase stained 129 (100%), 98 (76%), and 115 (89.1%) of 129 melanomas, respectively. Antibodies against other melanocyticassociated antigens (tyrosinase, glycoprotein 100) did not yield adequate staining. We conclude that Melan A is a specific and sensitive marker for canine melanomas.

Cutaneous Neoplasia in 340 Cats

A total of 340 cases of cutaneous neoplasia were diagnosed in 340 of 3,564 cats that were examined by biopsy or necropsy during a 41-month period from January 1, 1986 through May 31, 1989. Eighteen types of tumor occurred, but four types comprised 77% of the cases. These were basal cell tumor, 89 cases (26%, mean age 10.3); mast cell tumor, 72 cases (21%, mean age 8.6); squamous cell carcinoma, 52 cases (15%, mean age 11.6); and fibrosarcoma, 50 cases (15%, mean age 10.2). For each of these four types of tumors, peak number of cases occurred in cats older than 10 years. Mast cell tumor was the only tumor diagnosed in cats younger than 1 year. The head was the most common site for basal cell tumors, mast cell tumors, and squamous cell carcinomas. The legs were the most common location of fibrosarcomas. Siamese cats had approximately three times as many mast cell tumors as statistically expected, but only one-fourth as many squamous cell carcinomas. Breed predilection for other skin tumors was not apparent. Sex predilection was not detected for any skin tumor.

Uterine neoplasia in 13 cats.

Thirteen uterine tumors were diagnosed in 13 cats and accounted for 0.29% of all feline neoplasms received during a 9.6-year period. Age at diagnosis ranged from 3 to 16 years; median 9 years. Six were Domestic Shorthair cats, and 7 were purebred cats of 5 different breeds. Eight adenocarcinomas and 1 mixed Müllerian tumor (adenosarcoma) comprised the endometrial tumors. Myometrial tumors included 3 leiomyomas and 1 leiomyosarcoma. One of the adenocarcinomas developed in the uterine stump of an ovario-hysterectomized cat; the other cats were sexually intact. Concurrent mammary adenocarcinoma was diagnosed in 1 cat with uterine adenocarcinoma and in another with uterine leiomyoma. Tumors were discovered during elective ovariohysterectomy in 2 cats, but at least 3 others had experienced reproductive problems (infertility or pyometra). Five cats presented for abdominal or pelvic masses. Endometrial adenocarcinomas were positive immunohistochemically for cytokeratins and negative for smooth muscle actin (SMA); 1 of 6 cats was positive for vimentin and 4 of 8 were positive for estrogen receptor—α (ERα). Adenosarcoma stromal cells were positive for vimentin and ERα but negative for cytokeratins and SMA. Smooth muscle tumors were positive for vimentin and SMA and negative for cytokeratins. Leiomyomas, but not the leiomyosarcomas, were positive for ERα. Adenocarcinomas in 4 cats had metastasized by the time of ovariohysterectomy. Two other cats were euthanized 5 months after ovariohysterectomy; at least one of these cats had developed an abdominal mass that was not examined histologically. Only 2 cats with endometrial adenocarcinoma had disease-free intervals longer than 5 months after surgery. Metastasis was not detected in any mesenchymal tumor; however, these cats were either euthanized on discovery of the tumor or the tumor was first detected at necropsy.

Gastrointestinal pythiosis in Missouri dogs: eleven cases.

Pythium insidiosum is the cause of gastrointestinal and muscularis of the stomach, pylorus, and small intestine, with subcutaneous pythiosis of dogs. Pythium spp. are aquatrare involvement of the mesentery, mesenteric lymph nodes, ic oomycetes of the kingdom Protoctista found in tropical and pancreas. The pyogranulomas typically consisted of neand subtropical climates where high temperatures favor their crotic foci infiltrated and surrounded by neutrophils, eosingrowth. Canine gastrointestinal pythiosis, formerly included ophils, epithelioid macrophages, plasma cells, and multiamong the gastrointestinal phycomycoses, is characterized nucleated giant cells (Fig. 1). Etiologic agents were not apparent by severe granulomatous inflammation of the alimentary tract in HE-stained sections, although Splendore Hoeppli reacand associated tissues. Prevalence is highest among young tions surrounded clear spaces within the granulomas. Exmale dogs of large breeds, with case reports from the United amination of Grocott’s methenamine silver-stained sections States limited to states bordering the Gulf of Mexico. In revealed branching, rarely septate hyphae, 5-8 μm in dithis report, we describe 11 cases of gastrointestinal pythiosis, ameter with nearly parallel walls within the granulomas (Fig. confirmed by immunohistochemical techniques, in dogs from 2). A presumptive diagnosis of gastrointestinal pythiosis was the midwestem state of Missouri. based on histologic findings. Formalin-fixed tissue samples from 11 dogs with gastrointestinal pythiosis were received by the University of Missouri Veterinary Medical Diagnostic Laboratory from November 1987 through January 1991. Information regarding these dogs is contained in Table 1. The average age of the dogs was 2.5 years, 8 of 11 were female, and several large and small breeds were represented. Clinical histories were typified by chronic anorexia, weight loss, vomiting, and diarrhea. The tissue samples were collected during exploratory celiotomy or necropsy and were identified by the submittors as masses or neoplasms of the gastrointestinal tract or associated tissues. The diagnosis was confirmed by an indirect immunoperoxidase technique specific for Pythium as previously described. Rabbit serum containing primary antibody specific to Pythium antigen was applied to formalin-fixed tissue sections, which were subsequently stained using an avidin-biotin immunoperoxidase technique and examined microscopically. Negative controls with no primary antibody were run with all samples.

Immunohistochemical Detection of Thyroid Transcription Factor-1, Thyroglobulin, and Calcitonin in Canine Normal, Hyperplastic, and Neoplastic Thyroid Gland

Immunohistochemistry for thyroid transcription factor-1 (TTF-1), thyroglobulin, and calcitonin was done in normal, hyperplastic, and neoplastic canine thyroid glands that had been fixed in formalin and embedded in paraffin. Prolonged fixation did not significantly alter the immunostaining for TTF-1. Staining for TTF-1 was always nuclear and usually strong. One of two C-cell adenomas, five of five follicular cell adenomas, 5 of 11 C-cell carcinomas, 38 of 42 follicular cell carcinomas, two of five cases of C-cell hyperplasia, two of two cases of follicular epithelial hyperplasia, one of two metastatic C-cell carcinomas, and three of four metastatic follicular carcinomas were positive for TTF-1. One follicular carcinoma that was positive for TTF-1 was negative for thyroglobulin. Thirty-nine of 42 follicular cell carcinomas were positive for thyroglobulin, including two cases that were negative for TTF-1. All C-cell lesions were positive for calcitonin. Of a variety of normal canine tissues and 278 nonthyroid tumors, only normal lung (airway and alveolar epithelial cells) and four of five pulmonary carcinomas were positive for TTF-1. TTF-1 is a good marker of thyroid differentiation and can be used in conjunction with thyroglobulin and calcitonin to increase the detection and differentiation of thyroid tumors and their metastases.

Endocarditis and Pulmonary Aspergillosis in a Horse

Brown CM, Kaneene JB, Taylor RF: 1988, Sudden and unexpected death in horses and ponies: an analysis of 200 cases. Equine Vet J 20:99-103. Bush LP, Crowe MW: 1989, Nicotiana alkaloids. In: Toxicants of plant origin, ed. Cheeke PR, 1st ed., vol. 1, pp. 87-107. CRC Press, Boca Raton, FL. Crowe MW, Swerczek TW: 1974, Congenital arthrogryposis in offspring of sows fed tobacco (Nicotiana tobacum). Am J Vet Res 35:1071-1073. Keeler RF, Balls LD: 1981, Teratogenic effects of Nicotiana glauca and concentrations of anabasine, the suspect teratogen in plant parts. Cornell Vet 71:47-53. Marsh CD, Clawson AB, Roe GC: 1927, Wild tobaccos (Nicotiana trigonophylla Dunal and Nicotiana attenuata Torrey) as stock poisoning plants. USDA Tech Bull 22:25-30. Plumlee KH, Holstege DM, Blanchard PC, et al.: 1993, Nicotiana glauca toxicosis of cattle. J Vet Diagn Invest 5:498-499. Taylor P: 1985, Ganglionic stimulating and blocking agents. In: Goodman and Gilman’s the pharmacological basis of therapeutics, ed. Gilman AG, Goodman LS, Rall TW, Murad F, 7th ed., pp. 215-221. Macmillan, New York, NY.

Immunoreactivity of A103, an antibody to Melan A, in canine steroid-producing tissues and their tumors

The monoclonal antibody A103 to the melanocytic differentiation antigen Melan A stains human steroid-producing cells and their tumors. A total of 200 formalin-fixed, paraffin-embedded canine normal tissues and hyperplastic and neoplastic lesions of the adrenal gland, testis, and ovary were immunohistochemically tested for Melan A with antibody A103. Leydig cell tumors (23/23, 100%), Sertoli cell tumors (14/15, 93%), and adrenocortical adenomas (12/13, 92%) were consistently positive. Adrenocortical carcinomas (23/35, 65%) and granulosa cell tumors (10/17, 59%) were less frequently positive. All pheochromocytomas, seminomas, and dysgerminomas were negative. The pattern of staining was cytoplasmic, but nuclear staining was also frequently seen in normal Leydig cells and their tumors. As in human tumors, immunohistochemistry for Melan A stains many canine steroid-producing tumors and can be used to distinguish these tumors from those of nonstereidogenic cells.

Acute Arsenic Toxicosis in Five Horses

Five adult horses presented with acute clinical signs of watery diarrhea, excessive salivation, muscle tremors, ataxia, and depression. Four died within 24 hours and the fifth was euthanatized approximately 48 hours after onset of clinical signs. Necropsy findings in two of the horses included hyperemia of gastric mucosa, intestines filled with green to black watery fluid, and multifocal to coalescing, hemorrhagic 1.0-2.0-cm-diameter ulcers of the mucosa of the cecum and large colon. Histopathologic changes in the cecum and large colon consisted of mucosal necrosis and ulceration, vascular thrombosis, necrosis of submucosal blood vessels, and infiltration by mixed mononuclear inflammatory cells and neutrophils. Arsenic toxicosis was suspected. The owner had not been feeding the horses any grain; however, a mixture of grain and pink powder was found in the pasture. Liver arsenic concentrations in the two horses were 14.0 and 11.0 ppm, a sample of renal cortex contained 108 ppm arsenic, and the grain/powder mixture found in the pasture was positive for arsenic at <3,000 ppm. Kidney lead concentrations were 6.5 and 4.2 ppm. Results were consistent with lead arsenate or lead arsenite poisoning.

Botryoid Rhabdomyosarcoma of the Urinary Bladder in a Filly

complex. Proc Annu MeetUS Anim Health Assoc 66:498-501.3. Jensen R, Lauerman LH, Braddy PM, et al.: 1980, Laryngealcontact ulcers in feedlot cattle. Vet Pathol 17:667-671.4. Jensen R, Lauerman LH, England JJ, et al.:1981, Laryngealdiphtheria and papillomatosis in feedlot cattle. Vet Pathol 18:143-150.5. Kersting K, Thompson J: 1989, Tracheal collapse and stenosisof calves. Proc Am Assoc Bovine Pract 22: 18.6. Minnigerode B, Richter HG: 1987, Pathophysiology of subtra-cheal stenosis in childhood. Prog Pediatr Surg 21:1-7.7. Panciera RJ, Williams DE: 1981, Tracheal edema (honker)syndrome of feeder cattle. In: Current veterinary therapy-foodanimal practice, ed. Howard JL, p. 800. WB Saunders Co.,Philadelphia, PA.8. Pearson BW: 1976, Trachea: tracheal stenosis. In: Scientificfoundations of otolaryngology, ed. Hinchcliffe R, Harrison D,pp. 919-933. Year Book Medical Publishers, Chicago, IL.9. Sasaki CT, Horiuchi M, Koss N: 1979, Tracheostomy-relatedsubglottic stenosis: bacteriologic pathogenesis. Laryngoscope 89:857-865.10. Shaw RR, Paulson DL, Kee JL: 1961, Traumatic tracheal rup-ture. J Thorac Cardiovasc Surg 42:281.11. Squire R, Brodsky L, Rossman J: 1990, The role of infectionin the pathogenesis of acquired tracheal stenosis. Laryngoscope100:765-770.12. Vestweber JB, Leipold HW: 1984, Tracheal collapse in threecalves. J Am Vet Med Assoc 184:735-736.J Vet Diagn Invest 5:451453 (1993)

Serum levels of tumor necrosis factor-α in calves experimentally infected with Pasteurella haemolytica Al

The purpose of this study was to document the levels of tumor necrosis factor-alpha (TNF) in serum of calves experimentally infected intratracheally with Pasteurella haemolytica A1 and to determine if elevated TNF levels correlate with development of pneumonic pasteurellosis in the bovine. Serum samples were collected at sequential time periods from 0 h to 72 h post inoculation with P. haemolytica. TNF levels in those sera were measured by a cytotoxicity assay utilizing the TNF-sensitive WEHI 164 mouse fibrosarcoma cell line. Serum TNF levels in infected cattle began to rise at 2 h post inoculation, peaked at approximately 8 h, and decreased to near control levels by 72 h. There was extreme variability in serum TNF among the inoculated animals with levels varying from 120 pg ml-1 to 5000 pg ml-1 at 8 h post inoculation. These levels did not correspond with the degree of lung involvement. All inoculated calves developed lesions of pneumonic pasteurellosis characterized by fibrinous pleuritis with necrotizing, hemorrhagic pneumonia. These results suggest that TNF is probably a significant inflammatory mediator involved in the pathogenesis of bovine pneumonic pasteurellosis.