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Five 3-month-old foals presenting with fever and respiratory disease were found to have pulmonary abscesses with patchy to diffuse alveolar and interstitial pneumonia on post-mortem examination. All affected foals had evidence of Rhodococcus equi infection and had few to abundant Pneumocystis carinii cysts in the sections of affected lung. Of the 5 foals examined radiographically, 3 had a distinct reticulonodular (miliary) pattern which may aid in the ante-mortem diagnosis of P. carinii pneumonia (PCP). Leukocyte counts of foals with PCP were significantly greater than in the control group of foals with uncomplicated bacterial pneumonia. Foals with PCP tended to be more tachypnoeic than the control foals and 4 of the 5 PCP+ foals appeared dyspnoeic before death. The ante-mortem recognition of PCP may be expedited by bronchoalveolar lavage and successful treatment of foals with PCP may require the administration of adequate levels of potentiated sulphonamides.

The most characteristic morphologic features of the pancreatic islets of human non-insulin-de- pendent diabetes mellitus (NIDDM, or type 2 diabetes mellitus) and of similar forms of diabetes in cats and macaques are the deposition of amyloid (islet amyloid) and the loss of beta cells. Islet amyloid is derived from islet amyloid polypeptide (IAPP), which is a normal secretory product of the beta cells. Therefore, knowledge of the IAPP gene is of potential importance in defining the pathogenesis of NIDDM. To identify the feline chromosome(s) on which the IAPP gene is located, we screened genomic DNA obtained from 38 feline-rodent hybrid cell lines that have a known feline chromosome content. Feline IAPP DNA was amplified and detected using the polymerase chain reaction technique. Discordancy analysis for each feline chromosome showed that chromosome B4 had the lowest discordancy (P syntenic relationship with human chromosome 12, on which the human IAPP gene is located. This study therefore extends and confirms the homology between human chromosome 12 and feline chromosome B4 and provides an additional genetic marker for feline chromosome B4.

Papillomaviruses (PVs) are highly species- and site-specific pathogens of stratified squamous epithelium. Although PV infections in the various Felidae are rarely reported, we identified productive infections in six cat species. PV-induced proliferative skin or mucous membrane lesions were confirmed by immunohistochemical screening for papillomavirus-specific capsid antigens. Seven monoclonal antibodies, each of which reacts with an immunodominant antigenic determinant of the bovine papillomavirus L1 gene product, revealed that feline PV capsid epitopes were conserved to various degrees. This battery of monoclonal antibodies established differential expression patterns among cutaneous and oral PVs of snow leopards and domestic cats, suggesting that they represent distinct viruses. Clinically, the lesions in all species and anatomic sites were locally extensive and frequently multiple. Histologically, the areas of epidermal hyperplasia were flat with a similarity to benign tumors induced by cutaneotropic, carcinogenic PVs in immunosuppressed human patients. Limited restriction endonuclease analyses of viral genomic DNA confirmed the variability among three viral genomes recovered from available frozen tissue. Because most previous PV isolates have been species specific, these studies suggest that at least eight different cat papillomaviruses infect the oral cavity (tentative designations: Asian lion, Panthera leo, P1PV; snow leopard, Panthera uncia, PuPV-1; bobcat, Felis rufus, FrPV; Florida panther, Felis concolor, FcPV; clouded leopard, Neofelis nebulosa, NnPV; and domestic cat, Felis domesticus, FdPV-2) or skin (domestic cat, F. domesticus, FdPV-1; and snow leopard, P. uncia, PuPV-2).

Acute fulminant hepatic necrosis was associated with repeated oral administration of diazepam (1.25 to 2 mg, PO, q 24 or 12 h), prescribed for behavioral modification or to facilitate urination. Five of 11 cats became lethargic, atactic, and anorectic within 96 hours of initial treatment. All cats became jaundiced during the first 11 days of illness. Serum biochemical analysis revealed profoundly high alanine transaminase and aspartate transaminase activities. Results of coagulation tests in 3 cats revealed marked abnormalities. Ten cats died or were euthanatized within 15 days of initial drug administration, and only 1 cat survived. Histologic evaluation of hepatic tissue specimens from each cat revealed florid centrilobular hepatic necrosis, profound biliary ductule proliferation and hyperplasia, and suppurative intraductal inflammation. Idiosyncratic hepatotoxicosis was suspected because of the rarity of this condition. Prior sensitization to diazepam was possible in only 1 cat, and consistent risk factors that could explain susceptibility to drug toxicosis were not identified. On the basis of the presumption that diazepam was hepatotoxic in these cats, an increase in serum transaminase activity within 5 days of treatment initiation indicates a need to suspend drug administration and to provide supportive care.

Granular cell tumor (GCT) is a morphologic designation for tumors of varied histogenesis. Most GCTs in human beings are derived from Schwann cells, and rat meningeal GCTs are believed to originate in the neural crest. Three equine pulmonary GCTs from aged horses were studied immunohistochemically with primary antibodies directed against vimentin, cytokeratins (AE1/AE3), S-100, Leu 7, desmin, and neuron-specific enolase (NSE) using a steptavidin–biotin procedure. All three tumors stained similarly with strong and diffuse staining of neoplastic cells for vimentin and S-100 and negative staining with all other antibodies. On the basis of the immunohistochemical results and the previously described histologic and ultrastructural characteristics, equine pulmonary GCT is designated as neural crest and possibly Schwann cell derived, similar to GCT in rats and human beings.

Assays were validated for the measurement of urinary concentrations of cortisol and creatinine in domestic ferrets (Mustela putorius furo). Urinary concentrations of cortisol and creatinine and the calculated urinary cortisol:creatinine ratio (UCCR) values were determined for 29 clinically normal female ferrets, 22 clinically normal male ferrets, and 12 ferrets with adrenal gland tumors. The UCCR values for the 51 clinically normal ferrets ranged from 0.04 x 10(-6) to 1.66 x 10(-6), with a median value of 0.22 x 10(-6). The UCCR values were significantly (Por = 0.01) higher in the 12 ferrets with adrenal tumors, with a range of 0.5 x 10(-6) to 60.13 x 10(-6) and a median of 5.98 x 10(-6). We concluded that determination of UCCR values was useful in the diagnosis of hyperadrenocorticism associated with adrenal neoplasia in domestic ferrets.

Adrenocortical tumors were diagnosed in 5 adult spayed ferrets. Four ferrets had bilaterally symmetrical alopecia of the caudal femoral region, abdomen, and tail, and 1 had alopecia of the distal limbs and feet. All 5 ferrets had vulvar swelling. During abdominal ultrasonography, irregular masses, believed to involve the adrenal glands, were seen in all 5 ferrets. Unilateral adrenalectomy was performed successfully in each ferret by use of ventral midline celiotomy. On histologic examination of biopsy samples, 4 ferrets were found to have adrenocortical adenomas, and 1 ferret was found to have an adrenocortical adenocarcinoma. All clinical signs resolved after adrenalectomy, suggesting that the adrenocortical tumors had been secreting adrenocortical hormones.

A 9-year-old Quarter Horse mare was examined because of progressive weight loss, weakness, muscle atrophy and tremors, and behavioral change. Selenium and glutathione peroxidase assays, blood lead analysis, erythrocyte transketolase analysis, pseudorabies and Borrelia burgdorferi serology, electromyography, and CSF analysis were performed. Motor neuron degeneration was diagnosed by microscopic examination of neural tissues. The cause of the disease was not substantiated, but several possibilities were excluded via diagnostic testing. Diagnosis of motor neuron degeneration in horses may be made from an accurate history, thorough neurologic examination, and ancillary testing. In particular, antemortem diagnosis may be based on finding scattered angular atrophy of predominantly type-1 or of type-1 and -2 skeletal muscle fibers in frozen sections of muscle biopsy specimens.

Administration of trimethoprim-sulfadiazine in a dog was associated with vomiting, inappetence, and icterus, and high values of alanine transaminase, aspartate transaminase, alkaline phosphatase, gamma-glutamyltransferase, and total bilirubin concentration. The clinical signs and biochemical abnormalities resolved after discontinuation of the treatment. Histologic examination of sections from a liver biopsy specimen revealed moderate, predominantly portal hepatitis with cholestasis.

Morphological information is presented for syntype material of the etiologic agent of equine protozoal myeloencephalitis, Sarcocystis neurona. A clinical description of the horse from which the organism was isolated and the methodology used to immunosuppress the horse in an attempt to increase parasite numbers are also given. The description includes microscopic details observed both with light and transmission electron microscopy. Mainly stages from tissue are illustrated, but information is also presented on the development of the organism after inoculation onto monolayers of bovine monocytes. It is believed that the large numbers of organisms observed in this horse were due to its having not received prior treatment with trimethoprimsulphonamide and the large amounts of corticosteroids that were administered in order to facilitate isolation of the pathogen.

Cutaneous plasmacytomas associated with local deposition of amyloid were diagnosed by light microscopy in a series of six older dogs (mean age 10.7 years) consisting of two Cocker Spaniels, a Poodle, a Weimeraner, and two mixed-breed dogs. The neoplasms occurred on the digits (2 dogs), forelimb (2 dogs), lip (1 dog), and ear (1 dog). In most cases, groups of neoplastic plasma cells were widely separated by large homogeneous islands of amyloid. The neoplastic cells had characteristic plasmacytoid features, but the degree of pleomorphism varied greatly between different neoplasms. In four of the six tumors, the diagnosis of plasmacytoma was confirmed by the demonstration of a monoclonal plasma cell population using immunofluorescent staining for anti-canine immunoglobulins. In these tumors, the neoplastic cells reacted with only one class of immunoglobulins (IgG). The amyloid did not react with any of the reagents used. The suspicion that the amyloid was of immunoglobulin origin (primary amyloid) was supported by its retention of birefringence under polarized light after treatment with potassium permanganate and staining with Congo red.

A 12-year-old Morgan gelding was examined for colic of 3 days duration. Signs of depression, colic, diarrhea, and endotoxemia persisted despite aggressive medical therapy and surgical exploration. Culture results from gastric fluid and feces yielded many colonies of Clostridium perfringens. This organism also was recovered from peritoneal fluid 10 days after admission; consequently, the horse was euthanized. At necropsy, a localized gas-filled, necrotic stomach wall was found; many mucosal and submucosal gas blebs were visible. Culture of this tissue yielded Clostridium perfringens. Emphysematous gastritis is a fulminant infection of the stomach wall caused by gas-forming organisms that gain access to the submucosa via mucosal defects such as ulcers. This condition has been reported infrequently in people, and the case reported herein represents the first instance of emphysematous gastritis in the horse.