A six‐year‐old male castrated domestic shorthair cat was evaluated for a six‐month history of haematochezia, mucoid diarrhoea, tenesmus and rectal prolapse. Colonic histopathology revealed multifocal mucosal ulceration and lamina propria infiltration with large numbers of periodic acid‐Schiff‐positive macrophages. Large clusters of intracellular Escherichia coli were confirmed with fluorescence in situ hybridization testing, similar to that seen in dogs with granulomatous colitis. An eight‐week course of marbofloxacin resulted in resolution of clinical signs; however, recurrence occurred four weeks later. A 12‐week course of marbofloxacin resulted in disease remission for which the cat still remains free of clinical signs (15 months). Escherichia coli‐associated granulomatous colitis, although reported with rarity in this species, is an important infectious cause of chronic large intestinal disease in the cat.
Background Ureteral atresia is the congenital absence of a ureteral opening, resulting in a blind-ended ureter that fails to terminate at the urinary bladder. Consequently, severe hydroureter and hydronephrosis occur ipsilateral to the atresic ureter. However, hydronephrosis contralateral to severe hydroureter, although reported in humans, is not documented in the dog. Additionally, ureteral atresia has not been reported as a cause for lower urinary tract signs directly related to extramural urinary bladder compression. This report aims to describe these unique manifestations of this congenital urinary tract disease, as well as follow-up findings after successful treatment. Case presentation A 4-month-old male Husky puppy was evaluated for pollakiuria, stranguria, and urine dribbling of 1-month duration. During the physical examination, a mass was palpated in the mid-abdomen. Diagnostic imaging and cystoscopy findings were diagnostic for right-sided ureteral atresia with secondary hydroureter and hydronephrosis. The severe right hydroureter caused lower urinary tract signs and contralateral hydronephrosis secondary to regional compression of the left distal ureter and urinary bladder. A right-sided ureteronephrectomy was performed, resolving the stranguria and pollakiuria. Significant reduction in the contralateral (left) hydronephrosis also occurred. Clinical Relevance Ureteral atresia should be considered as a differential diagnosis for lower urinary tract signs and/or bilateral hydronephrosis in a young dog. Reporting this case expands our knowledge of congenital lower urinary tract disease and the etiology of their manifestations in dogs. Surgical resolution of the congenital ureteral abnormality can result in preservation of renal function in the contralaterally obstructed kidney.
Background The pathogenesis of gallbladder (GB) mucoceles in dogs is unknown. It has been proposed that hyperlipidemia could impair GB motility and contribute to GB mucocele formation. Hypothesis/Objectives The objective of this study was to compare GB motility in dogs with hyperlipidemia to control dogs using ultrasonography. We hypothesized that hyperlipidemic dogs will have decreased GB motility compared with controls. Animals Twenty‐six hyperlipidemic and 28 healthy, age‐matched control dogs were prospectively enrolled. Methods Cholesterol and triglyceride concentrations were measured in all dogs. Hyperlipidemia was defined as hypercholesterolemia (>332 mg/dL) and/or hypertriglyceridemia (>143 mg/dL) using a biochemical analyzer. Ultrasound was performed before feeding, and 60 and 120 minutes after ingestion of a high fat diet. Gallbladder volumes (GBV) and ejection fractions (EF) were calculated. Results Hyperlipidemic dogs had significantly larger GBVs (ml/kg) before feeding and 60 minutes after feeding of 1.2 (0.4‐7.5; P = .008) and 0.6 (0.1‐7.2; P = .04) compared with controls 0.6 (0.2‐2.6) and 0.4 (0.1‐1.9), respectively. Severely hyperlipidemic dogs had significantly larger GBV at baseline, 60 minutes, and 120 minutes of 1.7 (0.6‐7.5; P = .03), 1.3 (0.4‐7.2; P = .02), and 1.3 (0.2‐8.2; P = .04), respectively compared with mildly hyperlipidemic dogs. EFs at 60 and 120 minutes between controls, hyperlipidemic, and severely hyperlipidemic were all 0.3 at 60 minutes and 0.5, 0.3, and 0.3 at 120 minutes, respectively which were not statistically different. Conclusions and Clinical Importance Hyperlipidemia leads to GB distention in dogs which could lead to retention of bile and gallbladder disease.
A 7 yr old male beagle was examined because of lethargy, anorexia, and cranial abdominal discomfort. Significant clinicopathologic abnormalities included severe liver enzyme elevations and hypercholesterolemia. Abdominal imaging identified vascular compromise of the left lateral liver lobe and a gallbladder mucocele. Following liver lobectomy and cholecystectomy, the dog’s clinical signs resolved, and liver enzymes substantially improved. Diffuse hepatocellular infarction and necrosis secondary to multifocal atherosclerosis was present on histopathology of the liver. Hypothyroidism was subsequently diagnosed. Restoration of euthyroidism with oral levothyroxine therapy resolved the remaining liver enzyme elevations and hypercholesterolemia. To the author’s knowledge, this is the first case report of hypothyroidism resulting in a clinically apparent and resolvable acute hepatopathy due to atherosclerosis. Clinicians should include atherosclerosis as a differential diagnosis for dogs with an acute hepatopathy and investigate dogs for hypothyroidism if atherosclerosis is diagnosed on liver biopsy.
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