B-cell lymphoma invading and compressing the heart base and pericardium in a cat.

A 3-year-old, 3.5-kg, neutered male, domestic shorthair cat presented with progressive lethargy, anorexia, coughing, and acute respiratory distress of two-week duration. Auscultation detected diffuse pulmonary crackles. Lung sounds were absent over the left cranial thorax. Sinus tachycardia was recorded. Thoracic radiographs revealed cardiac silhouette enlargement, dorsal displacement of the carina, and uniform, soft tissue opacity in the left cranial hemithorax. Transthoracic two-dimensional echocardiography revealed a large mass within and external to the pericardial space, effacing the pericardium, and compressing basal cardiac structures. The point-of-care feline immunodeficiency virus and feline leukemia virus test was negative. Euthanasia was elected, and permission for necropsy granted. Gross postmortem evaluation revealed a prominent mediastinal mass that effaced the left cranial lung lobe and invaded the heart base and pericardium. The mass was confirmed as B-cell lymphoma by histopathology and immunohistochemistry.

Sudden death in a dog with aortic coarctation.

A previously healthy, one-year-old, intact female Vizsla dog collapsed and experienced cardiopulmonary arrest after a stressful event. Postmortem examination identified juxtaductal aortic coarctation (AoCo) with complex morphology. Located in the isthmus aorta adjacent to the ligamentum arteriosum, the AoCo comprised a shelf-like structure caused by invagination of the aortic wall into the lumen. Just distally, a second region of aortic occlusion resulted from an obstructing aortic membrane that restricted blood flow into the descending aorta through a small, eccentric ostium. Plausibly, the AoCo contributed to high afterload which led to reduction of coronary blood flow, myocardial hypoxia, and sudden death during physical stress. Although AoCo is a well-recognized congenital defect in humans, it has been reported only rarely in animals. The present case details the gross and histologic features of a complex, juxtaductal AoCo in a dog who died suddenly after stress. These morphologic findings may be informative when contemplating diagnosis of this anomaly.

Giant pericardial-occupying compressive primary cardiac hemangiosarcoma in a cat.

Hemangioarcoma in the cat is an infrequently diagnosed tumor, and cardiac involvement is rare. We report a previously healthy, 8-year-old, domestic shorthair cat with acute collapse associated with pericardial effusion and cardiac tamponade. Following pericardiocentesis and removal of 15 mL of fluid, the cat improved rapidly. A massive, space-occupying, intrapericardial tumor adhered to and compressing the right atrium and ventricle was detected by echocardiography. Approximately 5 weeks following initial presentation, bicavitary effusion and tachypnea developed, and the cat was euthanized. Necropsy revealed a giant intrapericardial mass adhered to and impinging upon the right heart. Histologic and immunohistochemical examination confirmed hemangiosarcoma with no gross or histologic evidence of metastasis. To the authors' knowledge, this is the first account of a pericardial-occupying, primary feline cardiac hemangiosarcoma resulting in compression of the right heart and cardiac tamponade, Further, this report describes novel clinicopathological relationships between radiographic and echocardiographic findings and gross and microscopic pathology.

Bartonella spp. as a Possible Cause or Cofactor of Feline Endomyocarditis-Left Ventricular Endocardial Fibrosis Complex.

Endomyocarditis is a commonly detected post-mortem finding in domestic cats presenting for sudden onset cardiovascular death, yet the aetiology remains unresolved. Cats are documented reservoir hosts for Bartonella henselae, the infectious cause of cat scratch disease in man. Various Bartonella spp. have been associated with culture-negative endocarditis, myocarditis and sudden death in man and animals. We hypothesized that Bartonella spp. DNA could be amplified more often from the hearts of cats with feline endomyocarditis-left ventricular endocardial fibrosis (FEMC-LVEF) complex compared with cats with hypertrophic cardiomyopathy (HCM) or cats with grossly and microscopically unremarkable hearts (designated non-cardiac disease controls). Formalin-fixed and paraffin wax-embedded, cardiac tissues from 60 domestic and purebred cats aged 3 months to 18 years were examined, and histological features were recorded. Cardiac tissue sections were tested for Bartonella DNA using multiple 16-23S intergenic transcribed spacer region polymerase chain reaction (PCR) primer sets, including two Bartonella genera, a Bartonella koehlerae species-specific and a Bartonella vinsonii subsp. berkhoffii-specific assay, followed by DNA sequence confirmation of the species or genotype. Special precautions were taken to avoid DNA cross-contamination between tissues. Bartonella spp. DNA was amplified by PCR and sequenced from 18 of 36 cats (50%) with FEMC-LVEF and 1/12 (8.3%) cats with HCM. Bartonella spp. DNA was not amplified from any non-cardiac disease control hearts. Based on PCR/DNA sequencing, one Bartonella spp. was amplified from 10 cats, while the remaining eight were coinfected with more than one Bartonella spp. To our knowledge, this study represents the first documentation of B. vinsonii subsp. berkhoffii genotype I infection in cats (n = 11). Fluorescence in-situ hybridization testing facilitated visualization of Bartonella bacteria within the myocardium of four of seven PCR-positive FEMC-LVEF hearts. Collectively, these findings support the hypothesis that Bartonella spp. may play a primary role or act as a cofactor in the pathogenesis of FEMC-LVEF. Studies involving cats from other geographical regions and definitive demonstration of Bartonella spp. within regions of inflammation are needed to confirm an association between Bartonella spp. and FEMC-LVEF induced morbidity and mortality in cats.

Assessment of the efficacy and potential complications of transjugular liver biopsy in canine cadavers.

BACKGROUND: Transjugular liver biopsy (TJLB) is used in humans at risk of bleeding. There are no reports of its use in veterinary medicine. OBJECTIVE: To assess the efficacy and potential complications of TJLB in canine cadavers, and compare with samples obtained via needle liver biopsy (NLB) and surgical liver biopsy (SLB). ANIMALS: Twenty-five medium and large breed canine cadavers. METHODS: Prospective study. TJLBs were procured through the right jugular vein. After biopsy, intravenous contrast and gross inspection were used to assess the biopsy site. Minor and major complications were recorded. NLBs and SLBs were then obtained. Histopathology was performed, and TJLB and NLB were compared for number of complete portal tracts (CPTs), length, and fragmentation. Pathologic process and autolysis were assessed in all samples. RESULTS: All TJLBs yielded liver tissue. The proportion of minor complications was 12/25 (48%), and major complications 16/25 (64%); 13/16 (81%) of the major complications were liver capsule perforation. In 21/25 (84%), the histopathology in the SLB was reflected in the TJLBs. For cases with minimal autolysis, median number of CPTs in TJLBs was 7.5, compared with 4 in NLBs (P = .018). Median length of TJLB specimen was 28 mm compared to 22 mm in NLBs (P = .007). Fragmentation rate was median of 1.25 for TJLB compared to 1.50 in NLBs (P = .11). CONCLUSIONS AND CLINICAL IMPORTANCE: TJLB is technically feasible and achieves comparable results to NLB and SLB. The number of complications, in particular liver capsule perforation, was greater than expected. Further studies are indicated before clinical use is recommended.

Malignant peripheral nerve sheath tumour of the urinary bladder in a cat.

A 14-year-old domestic shorthair cat presented with a 5-month history of urinary incontinence and inappro-priate elimination. Ultrasonography revealed a well-marginated, vascular mass of mixed echogenicity ex-tending from the dorsal wall of the urinary bladder into the lumen. Partial cystectomy was performed for re-moval of the urinary bladder mass; histopathological evaluation revealed a spindle cell neoplasm with a prominent palisading pattern. Histomorphologic features and immunohistochemical demonstration of vimentin, glial fibrillary acidic protein and S-100 protein, combined with negativity for smooth muscle actin and desmin were consistent with malignant peripheral nerve sheath tumour. This case report describes a novel location of malignant peripheral nerve sheath tumour; to the authors' knowledge, the bladder has not been described as a site of origin in the cat or any other domestic species.

Meningoencephalitis in a polar bear caused by equine herpesvirus 9 (EHV-9).

A 12-year-old female polar bear (Ursus maritimus) developed a sudden onset of muscle tremors, erratic circling, increased blinking, head shaking, and ptyalism, which progressed to partial and generalized seizures. Ancillary diagnostic tests were inconclusive, and the only significant laboratory finding was nonsuppurative pleocytosis of cerebrospinal fluid. Euthanasia was elected. Microscopic evaluation demonstrated multifocal, random nonsuppurative meningoencephalitis involving most prominently the rostral cerebral cortex, as well as the thalamus, midbrain, and rostral medulla. Lesions consisted of inflammation, neuronal necrosis, gliosis, and both neuronal and glial basophilic intranuclear inclusion bodies. Immunohistochemistry with a polyclonal antibody reactive to several equine herpesviruses was positive within affected areas of the brain, and polymerase chain reaction conclusively demonstrated the presence of only equine herpesvirus 9. The clinical and morphologic features of this case resemble other fatal herpesvirus encephalitides derived from interspecies transmission and underscore the need for extreme caution when managing wild or captive equids.

The preparation of deglycosylated ricin by recombination of glycosidase-treated A- and B-chains: effects of deglycosylation on toxicity and in vivo distribution.

Deglycosylation of ricin may be necessary to prevent the entrapment of antibody-ricin conjugates in vivo by cells of the reticuloendothelial system which have receptors that recognise the oligosaccharide side chains on the A- and B-chains of the toxin. Carbohydrate-deficient ricin was therefore prepared by recombining the A-chain, which had been treated with alpha-mannosidase, with the B-chain, which had been treated with endoglycosidase H or alpha-mannosidase or both. By recombining treated and untreated chains, a series of ricin preparations was made having different carbohydrate moieties. The removal of carbohydrate from the B-chain did not affect the ability of the toxin to agglutinate erythrocytes, and alpha-mannosidase treatment of the A-chain did not affect its ability to inactivate ribosomes. The toxicity of ricin to cells in culture was only reduced in those preparations containing B-chain that had been treated with alpha-mannosidase, when a 75% decrease in toxicity was observed. The toxicity of the combined ricin preparation to mice varied from double to half that of native ricin, depending on the chain(s) treated and the enzymes used. Removal of carbohydrate greatly reduced the hepatic clearance of the toxin and the levels of toxin in the blood were correspondingly higher. These results suggest that antibody-ricin conjugates prepared from deglycosylated ricin would be cleared more slowly by the liver, inflict less liver damage, and have greater opportunity to reach their target.

The removal of carbohydrates from ricin with endoglycosidases H, F and D and alpha-mannosidase.

Recently, several investigators have explored the possibility of targeting ricin to designated cell types in animals by its linkage to specific antibodies. There is evidence, however, that the mannose-containing oligosaccharide chains on ricin are recognised by reticuloendothelial cells in the liver and spleen and so cause the immunotoxins to be removed rapidly from the blood stream. In the present study we analysed the carbohydrate composition of ricin and examined enzymic methods for removing the carbohydrate. The carbohydrate analysis ricin A-chain revealed the presence of one residue of xylose and one of fucose in addition to mannose and N-acetylglucosamine which had been detected previously. The B-chain contained only mannose and N-acetylglycosamine. Ricin A-chain is heterogeneous containing two components of molecular weight 30 000 and 32 000. Strong evidence was found that the heavier form of the A-chain contains an extra carbohydrate unit which is heterogeneous with respect to concanavalin A binding and sensitivity to endoglycosidase H. The lower molecular weight form of A-chain did not bind concanavalin A and was insusceptible to endoglycosidases. Only one of the two high mannose oligosaccharide units on the isolated B-chain could be removed by endoglycosidases H or F, whereas both were removable after denaturation of the polypeptide by SDS. Both the isolated A- and B-chains were sensitive to alpha-mannosidase. Intact ricin was resistant to endoglycosidase treatment and was only slightly sensitive to alpha-mannosidase. The addition of SDS allowed endoglycosidase H to remove both of the B-chain oligosaccharides from intact ricin and increased the toxin's sensitivity to alpha-mannosidase. In conclusion, extensive enzymic deglycosylation of ricin may only be possible if the A- and B-chains are first separated, treated with enzymes and then recombined to form the toxin.

The use of anti-ricin antibodies to protect mice intoxicated with ricin.

Antibodies raised in rabbits to ricin or its constituent polypeptide chains are effective at rescuing mice from ricin intoxication if given soon enough after administration of the toxin. The maximum safe period for intravenous injection of 100 micrograms antibody is 40 min after intravenous injection of 1 microgram ricin, increasing to 640 min in the case of subcutaneously injected ricin. The antibodies raised against the isolated A and B chains are as effective as those against whole ricin. The antibody is as effective when administered intracerebrally as by the intravenous route; this result, combined with the very high toxicity for ricin administered intracerebrally suggests a neurotoxic role for the lectin.