THORACIC METASTASES OF CANINE MAMMARY GLAND TUMORS

The absence or presence of metastases on thoracic radiographs in 55 female dogs with mammary gland tumors was assessed by comparing the results of a single radiographic examination, using dorsoventral and left lateral views, with clinical and histologic follow-up data. Radiographic abnormalities found in dogs with thoracic metastases were classified as well-defined pulmonary nodules, ill-defined pulmonary nodules, and involvement of pleural effusion. No obvious difference in the effect on the right or left lung lobes was found. The sensitivity, specificity and accuracy for the detection of thoracic metastases were 65%, 97%, and 87%, respectively.     

0–7–21 Radiation Therapy for the Treatment of Canine Oral Melanoma

Eighteen dogs with malignant melanoma of the oral cavity were treated with high-dose per fraction (0–7–21) radiation therapy. Eight hundred cGy was administered on days 0, 7, and 21 for a total dose of 2,400 cGy in 3 weeks. Of 17 dogs evaluated, 9 (53%) had a complete remission and 5 (30%) achieved a partial remission with an overall response rate of 83%. Local failure occurred in 2 of the 9 dogs where a complete response was initially observed. One dog died of intercurrent disease, and one died of metastatic disease without evidence of local recurrence. Five dogs are alive and free of disease 9 to nineteen months from the initiation of therapy. The 0–7–21 protocol was well-tolerated, and acute radiation reactions were low-grade and limited to the skin. The results of this study demonstrate that oral melanomas in dogs are responsive to radiation. 0–7–21 radiation therapy offers a viable alternative to radical excision, especially when tumor volume or location would require cosmetically or functionally debilitating surgery.     

Use of 64Copper Measurements to Diagnose Canine Copper Toxicosis

Inherited canine copper toxicosis is a serious problem in Bedlington terriers and West Highland White terriers, and may also be a problem in other less-studied breeds. Affected dogs become ill at midlife with progressive and ultimately fatal liver disease. Treatments for removal of copper and prevention of copper accumulation are available, but are most effective if begun before the dog becomes ill. Until recently diagnosis has not been available until the dog is 1 year of age, and then only by an invasive liver biopsy with determination of liver copper concentration. The authors studied the use of 64copper for early diagnosis of canine copper toxicosis. Two procedures were evaluated. The first involved measuring the concentration of 64copper in blood 24 hours after oral administration of the radioisotope. At this time, 64copper was associated primarily with ceruloplasmin secreted into the blood by the liver. This procedure is useful in the diagnosis of the human counterpart, Wilson's disease. However, the authors found it to be nondiscriminatory between affected and unaffected dogs. In contrast, the second procedure, which involved measuring 64copper excreted in stool during 48 hours after an intravenous dose of radioisotope, yielded results that differentiated most affected and unaffected dogs.     

Plasma Cell Myeloma in the Horse

Plasma cell myelomas in horses have been reported infrequently. Data from 10 cases, 9 from the literature and 1 new case, are used to characterize the disease in the horse. Hot-blooded horses (7/10), specifically Quarter Horses (4/10), were most often affected. Median age at diagnosis was 11 years (range, 3 mo-22 yr) and both male (5) and female horses (5) were represented equally. Clinical findings included weight loss (6/8), anorexia (4/8), fever (4/8), limb edema (4/8), pneumonia (3/8), rear leg paresis/ataxia (3/8), epistaxis (3/8), palpable lymphadenopathy (2/8), and bone pain (2/8). Anemia (8/8) was present routinely, and in three horses, RBCs were macrocytic. Leukopenia (2/8), thrombocy-topenia (2/8), and circulating plasma cells (3/8) were variable findings. Except for abnormal protein concentrations and hyponatremia (3), abnormal results from serum biochemical analysis including hypo-cholesterolemia (1), hypercalcemia (1), and azotemia (1) were reported infrequently. Hyperproteinemia (8/9), hypoalbuminemia (7/9), and hyperglobulinemia (8/9) were characteristic but not invariable findings. Monoclonal proteins (7/7) were detected in the α₂, β, or γ region by serum electrophoresis. The paraprotein's heavy chain, determined in four horses, was a subclass of IgG. Three horses had decreased concentrations of normal immunoglobulins. Variable proteinuria (trace to 4+) was detected by routine urinalysis in four of six horses. Bence Jones proteinuria was detected in one of five horses (heat precipitation) and monoclonal proteins were detected in two of three electrophoresed urine samples. Three of the horses had lytic bone lesions detected radiographically. Bone marrow aspirates were diagnostic in two of five horses. Atypical plasma cells or increased numbers of plasma cells or both were present in histologic sections of bone marrow in six of eight horses. Common extraosseous sites of plasma cell infiltration included lymph nodes (8/8), kidney (5/8), spleen (5/8), liver (3/8), lung (3/8), brain (2/8), and orbit (2/8). Two horses had intracellular and extracellular crystalline deposits.     

Application of Airway Pressure Therapy in Veterinary Critical Care: Part II: Airway Pressure Therapy

As the specialties of emergency medicine and critical care have grown and evolved in both human and veterinary medicine, so has the need for more advanced care of patients with primary lung disease. Treatment of acute respiratory failure has been the focus of several articles in the human medical literature of the past few years.^1,8 This paper deals with airway pressure therapy and its application in cases of acute respiratory failure in veterinary medicine. The reader is referred to part I of this paper for a reveiw of respiratory mechanics and hypoxemia as they apply to respiratory therapy.     

Pasteurella haemolytica A1 and Bovine Respiratory Disease: Pathogenesis

The severe fibrinonecrotic pneumonia associated with pneumonic pasteurellosis usually results from colonization of the lower respiratory tract by Pasteurella haemolytica biotype A, serotype 1(A1). Despite recent research efforts, the authors lack a detailed understanding of the interactions and host response to P. haemolytica in the respiratory tract. The authors hypothesize that management and environmental stress factors or viral infection alters the upper respiratory tract (URT) epithelium allowing P. haemolytica to colonize the epithelium. Once the URT is colonized, large numbers of organisms enter the lung where they interact with alveolar macrophages. Endotoxin, released from the bacteria, crosses the alveolar wall where it activates pulmonary intravascular macrophages, endothelium, neutrophils, lymphocytes, platelets, complement, and Hageman factor leading to complex interactions of cells and mediators. It is the progression of this inflammatory response with neutrophil influx that is ultimately responsible for the pulmonary injury. Leukotoxin is a major virulence factor of P. haemolytica that allows it to survive by destroying phagocytic cells. At subcytolytic concentrations it may also enhance the inflammatory response by activating cells to produce mediators and release reactive oxygen metabolites and proteases.