Klippel-Trenaunay syndrome in a Border collie

A Border collie was presented at the age of 9 weeks with several lesions of the right forelimb, including a reddish-blue haemangiomatous macula in the medio-dorsal part of the elbow, multiple, scattered small cavernous haemangioma-like lesions at the plantar part of the foot and a general hypertrophy of the limb. X-rays of the limb showed osteolysis. On skin biopsy, telangiectatic veins were observed. The rest of the body did not show any skin lesions or hypertrophy. The dog was otherwise healthy. Due to the extension of the lesions and worsening of the limb swelling, it was decided to amputate the affected limb. The dog remained healthy for 2 weeks, but then passed through episodes of anaemia, and finally died suddenly with signs of shock. Dissection of the limb after amputation revealed hypoplasia and aplasia of the deep venous system in the lower part of the leg. No arterio-venous shunts were noticed. ln man, this syndrome, characterised by an insufficiently developed deep venous system associated with local overgrowth of the limb and cutaneous telangiectasia, is known as Klippel-Trenaunay syndrome.     

Lipoid pneumonia in a rough collie dog

The incidence of lipoid pneumonia in dogs is not known and confirmed cases do not appear to have been reported. Three forms of lipoid pneumonia are recognised in mammalian species; exogenous lipoid pneumonia (ELP), endogenous lipoid pneumonia (EnLP), and post-obstructive endogenous lipoid pneumonia (PEnLP). All forms share similar microscopic characteristics of fat accumulation in the cytoplasm of alveolar macrophages and are otherwise clinically indistinct from other forms of pneumonia. A case of lipoid pneumonia in a seven-year-old rough collie dog which was presented with recurrent bronchopneumonia over several months is reported here. Diagnosis was made from biopsy of resected lung tissue and from detection of fat-containing vacuoles in macrophages obtained by bronchoalveolar lavage. ELP could not be differentiated from PEnLP in this dog, but a complete recovery followed removal of the affected right accessory and caudal lung lobes.     

Infective endocarditis of the aortic valve in a Border collie dog with patent ductus arteriosus

Infective endocarditis (IE) in dogs with cardiac shunts has not been reported previously. However, we encountered a dog with concurrent patent ductus arteriosus (PDA) and IE. The dog was a 1-year-old, 13.9-kg female Border collie and presented with anorexia, weight loss, pyrexia (40.4°C) and lameness. A continuous murmur with maximal intensity over the left heart base (Levine 5/6) was detected on auscultation. Echocardiography revealed a PDA and severe aortic stenosis (AS) caused by aortic-valve vegetative lesions. Corynebacterium spp. and Bacillus subtilis were isolated from blood cultures. The dog responded to aggressive antibiotic therapy, and the PDA was subsequently surgically corrected. After a series of treatments, the dog showed long-term improvement in clinical status.     

Sensory neuropathy in two Border collie puppies

A peripheral sensory neuropathy was diagnosed in two Border collie puppies. Neurological, electrophysiological and histopathological examinations suggested a purely sensory neuropathy with mainly distal involvement. Urinary incontinence was observed in one of the puppies and histological examination of the vagus nerve revealed degenerative changes. An inherited disorder was suspected.     

Hyperammonaemic encephalopathy secondary to selective cobalamin deficiency in a juvenile Border collie

An eight-month-old Border collie was presented with anorexia, cachexia, failure to thrive and stupor. Laboratory tests demonstrated a mild anaemia, neutropenia, proteinuria and hyperammonaemia. Serum bile acid concentrations were normal, but an ammonia tolerance test (ATT) was abnormal. The dog responded to symptomatic therapy for hepatoencephalopathy. When a low serum cobalamin (vitamin B12) concentration and methylmalonic aciduria were noted, the dog was given a supplement of parenteral cobalamin. Two weeks later, a repeat ATT was normal. Cobalamin supplementation was continued every two weeks, and all clinical signs, except for proteinuria, resolved despite withdrawing all therapy for hepatoencephalopathy. A presumptive diagnosis of hereditary selective cobalamin malabsorption was made, based on the young age, Border collie breed, low serum cobalamin concentration and methylmalonic aciduria. Although hereditary selective cobalamin malabsorption in Border collies, giant schnauzers, Australian shepherd dogs and beagles has previously been reported in North America, to the authors' knowledge this is the first report of the condition in the UK and the first to document an abnormal ATT in a cobalamin-deficient dog.     

An unusual myopathy in a dog

A nine-month-old Cavalier King Charles Spaniel was examined because it could not withdraw its tongue into its mouth and had difficulty eating and drinking. These clinical signs were first observed when the dog was two months of age. On percussion of the tongue a dimple could be produced and there was electromyographic evidence of myotonia. Histological examination showed replacement of muscle fibres by adipose tissue, focal areas of myonecrosis, neutrophil infiltration and proliferation of sub-sarcolemmal nuclei. These changes were considered to be consistent with a primary myopathy similar to paramyotonia in man. No related dogs were found to be affected.     

Acute necrotizing myopathy in a dog

A 9 yr old spayed female cocker spaniel presented for an acute onset of weakness. Rhabdomyolysis and myoglobinuria were found 36 hr after presentation. The dog was managed for several electrolyte and mineral abnormalities and rhabdomyolysis-induced acute renal failure. The diagnosis of idiopathic necrotizing myopathy was determined by histopathology and by the exclusion of underlying infectious agents and metabolic defects. The dog recovered completely from the acute crisis and acute renal failure.     

An unusual myopathy in a dog

A nine-month-old Cavalier King Charles Spaniel was examined because it could not withdraw its tongue into its mouth and had difficulty eating and drinking. These clinical signs were first observed when the dog was two months of age. On percussion of the tongue a dimple could be produced and there was electromyographic evidence of myotonia. Histological examination showed replacement of muscle fibres by adipose tissue, focal areas of myonecrosis, neutrophil infiltration and proliferation of sub-sarcolemmal nuclei. These changes were considered to be consistent with a primary myopathy similar to paramyotonia in man. No related dogs were found to be affected.     

Glomerular polycystic kidney disease in a dog (blue merle collie)

Glomerular polycystic kidney disease was diagnosed in an 11 month old, female, Blue Merle Collie. Clinical signs (polyuria, polydipsia, vomiting, diarrhea, partial anorexia) and laboratory work (blood urea nitrogen, creatinine, serum phosphorus, specific gravity, proteinuria, nonregenerative anemia) indicated chronic renal failure.

However, after the study of a biopsy specimen, a definitive diagnosis was reached and the prognosis was determined. Necropsy findings and histopathological studies revealed: presence of glomerular cysts, atrophy of glomerular tufts and sclerosis of the interstitial tissue.

     

Mitochondrial myopathy in a german shepherd dog

A 9-month-old male German Shepherd dog was referred for evaluation of progressive exercise intolerance. Clinical examination revealed a stiff, stilted gait and marked atrophy and hypotonia of skeletal muscle. The dog had raised creatine kinase (181 U/liter), lactate dehydrogenase (510 U/liter), and aspartate aminotransferase (123.6 U/liter) levels, suggesting a muscle disease. Histochemical evaluation of muscle biopsies revealed the presence of subsarcolemmal oxidative activity, reduced nicotinamide adenine dinucleotide, and succinate dehydrogenase, and the absence of cytochrome oxidase activity. Ragged red fibers were demonstrated with Gomori trichrome stain. Ultrastructural examination of the muscle confirmed the presence of subsarcolemmal accumulations of mitochondria and morphologically atypical mitochondria.     

Fibrotic myopathy of the iliopsoas muscle in a dog

Fibrotic myopathy of the iliopsoas muscle developed in a dog, following extensive migration of a grass awn within the muscle and adjacent subcutaneous tissue. The dog was initially presented for evaluation of a fluctuant swelling over the right flank region. The clinical and imaging findings were suggestive of iliopsoas fibrotic myopathy and the diagnosis was confirmed by histopathology. This is the third report of iliopsoas fibrotic myopathy in a dog, the first report to describe the postmortem pathologic changes and the first report of iliopsoas fibrotic myopathy subsequent to foreign body migration.     

Teres minor myopathy as a cause of lameness in a dog

A case of a teres minor myopathy causing chronic lameness in a flve-yearold working iabrador retriever Is described. Uitrasonography was used to assist in detection of the condition and a definitive diagnosis was made by histological examination after muscle excision. Medical treatment was ineffective, but excision of the affected muscle resulted in complete resolution of the lameness with no apparent adverse affects on joint function. The aetiology of this condition Is unknown.     

Extrahepatic biliary atresia in a border collie

Progressive lameness and leg pain were the predominant clinical signs in a 17-week-old male border collie presented for examination. On clinical investigation, extrahepatic cholestasis in association with rickets due to inadequate vitamin D resorption was diagnosed. The dog was treated parenterally with vitamin D and a cholecystoduodenostomy was performed. At 25 days postsurgery the lameness had resolved and bone structure was radiographically normal. However, at six weeks postsurgery, the dog's condition deteriorated rapidly and euthanasia was finally performed at eight weeks postsurgery. At postmortem examination, Toxocara canis nematodes were found to have invaded the biliary system via the anastomosis between the gallbladder and duodenum, causing biliary and hepatic toxocariasis. The cause of the primary extrahepatic cholestasis was atresia of the common bile duct at the hepatic end. The liver tissue showed microscopic lesions of chronic extrahepatic cholestasis as well as acute inflammation associated with the nematode invasion. There was no postmortem evidence of bone lesions. Extrahepatic biliary atresia is extremely rare in animals and has not been described before in dogs. In contrast, it represents the most common cause of congenital cholestasis in children, occurring in approximately one per 10,000 to 15,000 live births.