John H. Keating

Chronic Hepatitis in Labrador Retrievers: Clinical Presentation and Prognostic Factors

BACKGROUND An increased incidence of chronic hepatitis has been reported in Labrador Retrievers. HYPOTHESIS A breed associated hepatopathy occurs in Labrador Retrievers. ANIMALS Twenty-four client-owned Labrador Retrievers. METHODS Medical records of dogs with histopathologic confirmation of chronic hepatitis were retrospectively reviewed. A clinical score based on clinical signs and the results of biochemical tests was generated for each dog. Hepatic biopsy specimens were scored for disease activity, fibrosis, and copper accumulation. RESULTS The median age was 9.3 years (range, 3.9-14.0 years). Clinical signs included inappetence, vomiting, lethargy, and weight loss. All dogs had increases in serum activity of one or more hepatobiliary enzyme. Hyperbilirubinemia and hypoalbuminemia were present in 45% and 21% of dogs, respectively. The median clinical score was 2.9, with a range of 0-8. The median histopathology activity and the fibrosis scores were 3.5 (range, 1-6) and 3.0 (range, 0-4), respectively. Rhodanine-positive copper staining was present in 15 of 17 biopsy specimens, with a median score of 2.0 (range, 0-3). Median survival was 374 days (range, 1-2645 days). A prolonged prothrombin time (P = .013) and thrombocytopenia (P = .041) were associated with survival < 2 months. The presence of anorexia (P = .049), hypoglobulinemia (P = .045), or prolonged partial thromboplastin time (P = .033) were associated with shorter overall survival times. The clinical score correlated with survival time (P = .030) and histopathologic staging (P = .049). CONCLUSIONS AND CLINICAL IMPORTANCE A progressive hepatopathy in Labrador Retrievers in this study was marked by chronic inflammation, fibrosis, and copper accumulation. A clinical scoring system that correlates with survival time may be useful as a noninvasive method to predict prognosis.

Clinical Characterization of a Familial Degenerative Myelopathy in Pembroke Welsh Corgi Dogs

BACKGROUND Adult dogs with degenerative myelopathy (DM) have progressive ataxia and paresis of the pelvic limbs, leading to paraplegia and euthanasia. Although most commonly reported in German Shepherd dogs, high disease prevalence exists in other breeds. OBJECTIVE Our aim was the clinical and histopathologic characterization of familial degenerative myelopathy (FDM) in Pembroke Welsh Corgi (PWC) dogs. ANIMALS Twenty-one PWCs were prospectively studied from initial diagnosis until euthanasia. METHODS Neurologic examination, blood tests, cerebrospinal fluid (CSF) analysis, electrodiagnostic testing, and spinal imaging were performed. Concentrations of 8-iso-prostaglandin F2alpha (8-isoprostane) were measured in CSF. Routine histochemistry was used for neuropathology. Deoxyribonucleic acid and pedigrees were collected from 110 dogs. RESULTS Median duration of clinical signs before euthanasia was 19 months. Median age at euthanasia was 13 years. All dogs were nonambulatory paraparetic or paraplegic, and 15 dogs had thoracic limb weakness at euthanasia. Electrodiagnostic testing and spinal imaging were consistent with noncompressive myelopathy. No significant difference was detected in 8-isoprostane concentrations between normal and FDM-affected dogs. Axonal and myelin degeneration of the spinal cord was most severe in the dorsal portion of the lateral funiculus. Pedigree analysis suggested a familial disease. CONCLUSIONS AND CLINICAL IMPORTANCE Clinical progression of FDM in PWC dogs was similar to that observed in other breeds but characterized by a longer duration. Spinal cord pathology predominates as noninflammatory axonal degeneration. Oxidative stress injury associated with 8-isoprostane production is not involved in the pathogenesis of FDM-affected PWC dogs. A familial disease is suspected.

Degenerative Myelopathy in 18 Pembroke Welsh Corgi Dogs

Postmortem examination was performed on 18 Pembroke Welsh Corgi dogs (mean age 12.7 years) with clinical signs and antemortem diagnostic tests compatible with a diagnosis of degenerative myelopathy. Tissue sections from specific spinal cord and brain regions were systematically evaluated in all dogs. Axonal degeneration and loss were graded according to severity and subsequently compared across different spinal cord segments and funiculi. White matter lesions were identified in defined regions of the dorsal, lateral, and ventral funiculi. The dorsolateral portion of the lateral funiculus was the most severely affected region in all cord segments. Spinal cord segment T12 exhibited the most severe axonal loss. Spinal nerve roots, peripheral nerves, and brain sections were within normal limits, with the exception of areas of mild astrogliosis in gray matter of the caudal medulla. Dogs with more severe lesions showed significant progression of axonal degeneration and loss at T12 and at cord segments cranial and caudal to T12. Severity of axonal loss in individual dogs positively correlated with the duration of clinical signs. The distribution of axonal degeneration resembled that reported in German Shepherd Dog degenerative myelopathy but differed with respect to the transverse and longitudinal extent of the lesions within more clearly defined funicular areas. Although these lesion differences might reflect disease longevity, they could also indicate a form of degenerative myelopathy unique to the Pembroke Welsh Corgi dog.

Portal Vein Thrombosis in Cats: 6 Cases (2001–2006)

BACKGROUND Portal vein thrombosis (PVT) in cats is sparsely reported. PURPOSE OF STUDY To evaluate the clinical signs and diseases associated with PVT in cats. ANIMALS 6 client-owned cats. METHODS Medical records for cats with a portal vein thrombus diagnosed on abdominal ultrasound or at necropsy were reviewed. Signalment, historical data, underlying disorders, clinical findings, clinicopathologic and histopathologic data, diagnostic imaging findings, treatment, and outcome were recorded. RESULTS All 6 cats identified with PVT also had hepatic disease. Evidence of a congenital portosystemic shunt was present in 3/6 cats. Two cats had primary or metastatic hepatic neoplasia. One cat had acute cholangitis, acute pancreatitis, and locally extensive acute centrilobular hepatic necrosis. Two cats were suspected to have acute thrombi and 4 cats had chronic thrombi. CONCLUSION AND CLINICAL SIGNIFICANCE PVT might be an important concurrent finding in cats with hepatic disease.

Safety and correlation of test results of combined ultrasound-guided fine-needle aspiration and needle core biopsy of the canine spleen.

The safety and diagnostic value of combined splenic fine-needle aspiration (FNA) and needle core biopsy (NCB) is unknown. Forty-one dogs with splenic lesions were studied prospectively. Safety was assessed in 38 dogs and no complications were encountered. Initially, clinical and anatomic pathologists reviewed each FNA and NCB sample, respectively, without knowledge of the others results. Diagnoses were categorized as neoplastic, benign, inflammatory, normal, or nondiagnostic. The level of agreement between sampling methods was categorized as complete, partial, disagreement, or not available. Test correlation was performed in 40 dogs. Nondiagnostic results occurred in 5/40 NCB (12.5%) and no FNA samples. Neoplasia was diagnosed in 17/40 dogs (42.5%), benign changes in 20/40 dogs (50%), inflammatory disorders in 0/40 dogs, and normal 2/40 dogs (5%). One of the 40 dogs (2.5%) had a diagnosis that was equivocal for neoplasia on both tests and therefore was not categorized. Of the 35 dogs that had diagnostic samples, cytopathologic and histopathologic diagnoses agreed completely in 18/35 dogs (51.4%), partially in 3/35 dogs (8.6%), and were in disagreement in 14/35 dogs (40.0%). Pathologists collaboratively reviewed diagnoses that were in disagreement or partial agreement and altered their individual diagnoses in 6/17 dogs (35.3%) to be within partial or complete agreement, respectively. Percutaneous FNA and NCB can be performed safely in dogs with sonographic splenic changes. Results suggest that adding NCB to FNA provides complementary information in dogs with suspected splenic neoplasia. This combined protocol may improve detection of splenic neoplasia and provide neoplastic subclassification.

Disseminated candidiasis secondary to fungal and bacterial peritonitis in a young dog.

OBJECTIVE To describe a severe case of bacterial sepsis and disseminated candidiasis in a previously healthy dog. CASE SUMMARY Fungal sepsis was identified in a 2-year-old dog following intestinal dehiscence 4 days after abdominal surgery. Septic peritonitis was identified at admission and evidence of dehiscence at the previous enterotomy site was found during an exploratory laparotomy. Both gram-positive cocci and Candida albicans were cultured from the abdominal cavity. Candida sp. was also subsequently cultured from a central venous catheter. Euthanasia was performed due to failure to respond to therapy. Fungal organisms, morphologically consistent with Candida spp., were found in the lungs and kidney on postmortem histopathologic examination indicating disseminated candidiasis. NEW OR UNIQUE INFORMATION PROVIDED Candida peritonitis is a well-recognized entity in humans and contributes to morbidity and mortality in critically ill patients. Abdominal surgery, intestinal perforation, presence of central venous catheters, and administration of broad-spectrum antibiotics are all considered to be suspected risk factors. This report describes the first known case of systemic candidiasis occurring secondary to Candida peritonitis and bacterial sepsis in a critically ill dog.

Multiple meningiomas in three dogs.

Three dogs with seizures were diagnosed with multiple intracranial meningiomas. Two of the three dogs were golden retrievers, and ages ranged from 9 to 11 years. Treatment consisted of surgery and radiation (n=2) or chemotherapy (n=1). In all three cases, the masses were two distinct tumors as determined by imaging, surgery, or necropsy. In two dogs, the meningiomas had the same histological pattern, while in one dog the histological subtypes were different.

Clinicopathological and ultrasonographic features of cats with eosinophilic enteritis

Eosinophilic enteritis (EE) in cats is poorly characterized. The aim of the current study was to retrospectively evaluate the clinical and ultrasonographic findings in cats with histologic evidence of eosinophilic inflammation on gastrointestinal biopsy. Twenty-five cats with tissue eosinophilia on surgical (10) or endoscopic (15) biopsy of the gastrointestinal tract, having an abdominal ultrasound performed within 48 h of biopsy acquisition, were enrolled. History, clinical presentation, clinical pathology and abdominal ultrasound findings were reviewed. Intestinal biopsies were evaluated by a single pathologist and separated into two groups based on the degree of eosinophilic infiltrate: mild (<10 eosinophils/high-power field [HPF], 11/25 cats), or moderate/marked (>10 eosinophils/HPF, 14/25 cats). The former were considered primary lymphoplasmacytic or lymphocytic inflammatory bowel disease (LPE) with subtle eosinophilic infiltrates, and the latter to have EE. Signalment, history and clinical signs were similar in all cats. Only cats with EE (6/14) had palpably thickened intestines. The only distinguishing clinicopathological feature of cats with EE was the presence of peripheral eosinophilia (6/14). On ultrasound, when compared with cats with LPE, cats with EE had a greater mean jejunal wall thickness (3.34 mm ± 0.72 mm vs 4.07 mm ± 0.58 mm, respectively) and an increased incidence of thickening of the muscularis layer (1/11 and 11/14, respectively). In conclusion, ultrasonographic evidence of a prominent intestinal muscularis layer, palpably thickened intestines and peripheral eosinophilia can serve as biomarkers for the presence of EE in cats with chronic intestinal signs.

Ultrasonographic and clinicopathological features of feline gastrointestinal eosinophilic sclerosing fibroplasia in four cats.

Four cats with feline gastrointestinal eosinophilic sclerosing fibroplasia (FGESF) are described. Clinical signs included decreased appetite, weight loss, vomiting and diarrhea. Bloodwork abnormalities included mild neutrophilia (n = 2) and hyperglobulinemia with concurrent hyperproteinemia (n = 2). Ultrasonographically, a total of five solitary masses with mural thickening and loss of layering were identified in the stomach, duodenum, jejunum and colon. In one cat a second, separate lesion was diagnosed 3 weeks following surgical resection of one mass. Histopathologically, lesions were characterized by collagen trabeculae and mixed inflammatory cell infiltrates, predominantly eosinophils. Multiple areas of necrosis were also noted, which contained bacteria in 2/4 cats. In two cats, changes consistent with FGESF were also noted in the liver. All cats had surgical resection of their lesions. Two cats are still living at time of publication (43 and 24 months post-surgery). FGESF should be considered as a differential for intestinal masses in cats.

Dermatitis in a Siberian hamster (Phodopus sungorus). Bacterial pseudomycetoma.

circumferentially subcutaneously in the distal right forelimb. We collected a 2.0-mm punch biopsy sample from an active skin lesion. The biopsy site was closed using sterile surgical tissue glue. The biopsy sample was fixed in 10% neutralbuffered formalin. We gave the hamster fluids (lactated Ringers solution, 100 ml per kg body weight administered subcutaneously) and meloxicam (0.2 mg per kg body weight administered subcutaneously) for post-operative analgesia. The hamster recovered uneventfully from the procedure. Pending biopsy results, treatment with enrofloxacin (Baytril, 10 mg per kg body weight administered orally every 12 h) was initiated. What are your differential diagnoses? Is the condition metabolic, infectious or neoplastic?