Primary hyperoxaluria (L-glyceric aciduria) in the cat: a newly recognised inherited disease

The clinical features of a newly recognised inherited disease, primary hyperoxaluria in the cat, are reported. Affected cats developed acute renal failure between five and nine months old owing to the deposition of oxalate crystals in the tubules of the kidney. In addition to the signs attributable to kidney failure the affected animals became profoundly weak; there was evidence of denervation atrophy in skeletal muscle, and accumulations of neurofilaments were found in the proximal axons of the ventral horn cells and dorsal root ganglion cells of the spinal cord. Examination of urine from affected cats revealed L-glyceric aciduria and intermittent hyperoxaluria suggesting that the disease is a feline analogue of the human disorder, primary hyperoxaluria type 2. This supposition was confirmed by liver enzyme studies.     

Acute pancreatitis: a newly recognised potential complication of canine babesiosis

This retrospective study describes 4 cases of canine babesiosis with histologically confirmed acute pancreatitis. In addition, 16 dogs with babesiosis are reported with serum amylase (>3500 U/l) and/or lipase (>650 U/l) activity elevations of a magnitude that would support a diagnosis of probable acute pancreatitis, although extra-pancreatic sources of the enzymes could not be excluded in these cases. Median time of pancreatitis diagnosis was 2.5 days post-admission, with primarily young (median age 3 years), sexually intact dogs affected. The development of pancreatitis was unrelated to the degree of anaemia at time of admission. In addition to pancreatitis, 80% of cases suffered from other babesial complications, namely icterus (13), acute respiratory distress syndrome (6), immune-mediated haemolytic anaemia (6), renal failure (3), haemoconcentration (2) and cerebral syndrome (2). Acute respiratory distress syndrome, renal failure and cerebral syndrome were associated with a poor prognosis, with 4 of the 5 dogs included in the overall 26% mortality rate having at least 1 of these complications. Haemolytic anaemia with ischaemia-reperfusion injury to the pancreas is proposed as a possible primary pathophysiological mechanism in babesial pancreatitis. Hypotensive shock, immune-mediated haemolytic anaemia, haemoconcentration and possibly altered lipid metabolism in babesiosis may also be involved. The previously postulated pro-inflammatory cytokine milieu of complicated babesiosis may underlie the progression, if not the primary initiation, of pancreatic pathology. Acute pancreatitis may represent the previously reported 'gut' form of babesiosis.     

Case-control study of canine infection by a newly recognised Babesia microti-like piroplasm

We did a case-control study to identify risk factors for prevalent infection of dogs by a newly recognised Babesia microti-like piroplasm. Clinical manifestations and haematology of infected dogs also were described. Forty-three laboratory-based cases and 86 individually matched controls were studied. Information on clinical signs and on risk factors was collected by a questionnaire and telephone interviews. Haematology was carried out for all the dogs. Variables were screened in a bivariable conditional logistic regression and checked for colinearity. The final multivariable model was selected by backward stepwise elimination. The odds of a case having ticks when examined at the clinic was 4 times that of a control and the odds of a case being a hunting or a house-guarding dog were, respectively, 24.2 and 2.7 times those of a control. The most consistently reported clinical signs were weakness (79%), tachycardia (43%) and haemoglobinuria (42%). Mean red-blood-cell count, haemoglobin concentration, platelet count, and mean platelet volume of infected dogs were lower than the reference values and those of non-infected dogs-but leukocyte count, mean corpuscular volume and red-blood-cell distribution width were higher.     

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.

     

Familial cutaneous vasculopathy and demodicosis in a German shepherd dog

A two-month-old female German shepherd dog was presented with a history of ulcerated central pads of all four feet. On physical examination, the footpads were swollen, soft and ulcerated. On the nasal planum there was a partially depigmented nodule. Multiple biopsies were taken from the cutaneous lesions and histological examination revealed focal collagen degeneration and vasculitis. A diagnosis of familial cutaneous vasculopathy was made. Seven months later the nasal nodule had disappeared and the footpads were still swollen but non-ulcerated. At this time, the dog manifested a generalised pustular demodicosis.     

Giant hypertrophic gastritis (Menetrier's-like disease) in an Old English sheepdog

An 11-year-old, male Old English sheepdog was admitted for weight loss and intermittent vomiting of 1 month's duration. A cranioventral abdominal mass, anemia, hypoproteinemia, and hypoalbuminemia were the prominent abnormal findings. Imaging studies identified a remarkably thickened gastric wall with multilobulated folds protruding into the gastric lumen. Gastrotomy revealed the presence of giant cerebriform rugal folds arising from the fundus and body of the stomach. Pronounced gastric glandular hyperplasia and lack of evidence of cellular atypia were suggestive of giant hypertrophic gastritis. The dog was treated with prednisolone, cimetidine, and hyoscine butylbromide, only to experience a short-term remission.     

Recurrent supraventricular arrhythmias in a dog with atrial myocarditis and gastritis

This report describes a dog with recurrent atrial fibrillation and atrial flutter associated with chronic gastritis. Although no underlying structural heart disease was apparent antemortem or on gross post-mortem examination, chronic atrial myocarditis was seen on histopathological examination. Atrial myocarditis is a recognised cause of atrial fibrillation in human beings with presumed lone fibrillation, and an association between supraventricular tachyarrhythmias and infectious agents has been made.     

Neuromuscular disease in a dog

Diffuse neuromuscular disease occurs sporadically in dogs. The most commonly reported diffuse neuromuscular diseases are polyradiculoneuritis (coonhound paralysis), tick paralysis, botulism, and myasthenia gravis (1,2,12). This clinical report describes an atypical presentation of a diffuse neuromuscular disease in a dog.