No abstract

Corneal vascular neoplasms (hemangioma and hemangiosarcoma) are rare in all species. Reported cases are single case reports in a single species. Archived cases of corneal hemangioma and hemangiosarcoma from dogs, cats, and horses were obtained from the Comparative Ocular Pathology Lab of Wisconsin (COPLOW, Madison, WI), tabulated, and examined. This retrospective study describes the breeds, ages, tumor types, and characteristics of vascular neoplasms that appeared to be primarily corneal in location, in feline, canine, and equine patients, with gross and histologic images. There is a discussion of predisposing factors and speculated association with chronic ocular surface disease.

A 5-year-old male neutered Bernese Mountain Dog was presented for cutaneous plasmacytoma, which was treated by surgical excision. Four months later, the dog developed multiple skin masses, hyphema, pericardial and mild bicavitary effusions, myocardial masses, and marked plasmacytosis in the peripheral blood. Circulating plasma cells expressed CD34 and MHC class II by flow cytometry. Immunocytochemistry demonstrated that these cells were strongly positive for multiple myeloma oncogene 1/interferon regulatory factor 4 (MUM-1) and weakly to moderately positive for Pax5. The dog was hypoglobulinemic but had a monoclonal IgA gammopathy detected by serum immunofixation electrophoresis. The PCR analysis of antigen receptor gene rearrangements (PARR) by fragment analysis using GeneScan methodology revealed that plasmacytoid cells in the original cutaneous plasmacytoma and peripheral blood had an identical immunoglobulin heavy chain gene (IgH) rearrangement, indicating that both populations were derived from the same neoplastic clone. Canine cutaneous plasmacytoma rarely progresses to a malignant form and plasma cell leukemia is rarely diagnosed in the dog. This report describes a case of cutaneous plasmacytoma progressing to plasma cell leukemia with a rapid and aggressive clinical course. This report also highlights the utility of flow cytometry, immunocytochemistry, immunofixation electrophoresis, and PARR by fragment analysis using GeneScan methodology in the diagnosis of this hematopoietic neoplasm.

Due to the nonspecific nature of the ocular signs, a diagnosis of protothecosis generally is not made until enucleation and histopathologic examination of the globe(s). Retinal detachment and blindness were common. Cytologic sampling of retinal plaques and exudate may provide a rapid way to identify Prototheca.

Abstract. Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA), or Bland-White-Garland syndrome, is a rare congenital malformation described in children and adults. In this condition, the left coronary artery, which normally originates from the left coronary sinus in the aorta, instead originates from the pulmonary trunk, which results in retrograde flow of blood away from the myocardium into the lower-pressure pulmonary artery. Myocardial hypoxic-ischemic injury results in cardiac dysfunction, failure, and eventually in patient death if not surgically repaired. This report describes gross and microscopic findings in 4 beef calves with ALCAPA. All the calves had a history of being found dead with few or no premonitory signs, 2 shortly after sudden strenuous exercise. Gross necropsy lesions suggestive of heart failure included cardiomegaly with atrial and ventricular dilation and/or ventricular hypertrophy, and hepatomegaly. Dissection of each heart revealed the origin of the left coronary artery arising in the pulmonary trunk above the anterior cusp of the pulmonic valve. No other cardiac anomalies were identified. Histopathologic changes in the heart included cardiomyocyte degeneration; mineralization; and fiber loss, with replacement by fibrous connective tissue, predominantly in the left ventricular papillary muscle and the interventricular septum. Changes observed in the liver and lungs, including hepatomegaly, sinusoidal congestion, centrilobular fibrosis, and pulmonary congestion, edema, and intra-alveolar pigment-laden macrophages were consistent with heart failure.