Taurine deficiency syndrome in cats

Taurine deficiency occurs in a large number of cats fed unfortified commercial diets. Deficiency arises because cats are unable to absorb all the taurine in processed diets and/or are unable to synthesize the deficit between absorption and requirement, which makes taurine an essential amino acid for cats. Taurine-depleted cats develop retinal degeneration, cardiomyopathy, altered white-cell function, and abnormal growth and development. Taurine deficiency is best estimated from the plasma-taurine concentration, with values less than 30 mumol/l considered deficient.     

Hypertensive retinopathy in a cat

A 12-year-old cat presented for sudden blindness was diagnosed with hypertensive retinopathy on the basis of ophthalmologic and ultrasonic examination. Renal failure due to a large intranephric cyst obstructing the right ureter and renal artery was the suggested cause of the systemic hypertension. The cat died 8 hours after unilateral nephrectomy.     

Hypertensive retinopathy and choroidopathy in a cat

Bilateral hypertensive retinopathy and choroidopathy with bullous retinal detachment was diagnosed in a 17-year-old, female spayed Domestic Short-haired cat. The underlying cause of the systemic hypertension could not be determined. The blood pressure was lowered successfully with the oral application of the L-type calcium channel blocker amlodipine besylate. The cat subsequently regained vision. The improvement in retinal function was documented using electroretinography.     

Diabetic retinopathy in a cat with megestrol acetate-induced diabetes

A case of diabetes mellitus in a cat is described, associated with prolonged administration of megestrol acetate for miliary dermatitis. The cat was presented with blindness due to diabetic retinopathy. Following the diagnosis, megestrol acetate was withdrawn. The diabetes proved to be transient and resolved after insulin therapy; however, severe visual impairment remained. The mechanism by which megestrol acetate induces diabetes is discussed.     

Taurine deficiency in Newfoundlands fed commercially available complete and balanced diets

OBJECTIVE: To determine taurine status in a large group of Newfoundlands related by environment, diet, or breeding to a dog with dilated cardiomyopathy and taurine deficiency. DESIGN: Prospective study. ANIMALS: 19 privately owned Newfoundlands between 5 months and 11.5 years old that had been fed commercial dry diets meeting established nutrient recommendations. PROCEDURE: Diet histories were obtained, and blood, plasma, and urine taurine concentrations and plasma methionine and cysteine concentrations were measured. In 8 dogs, taurine concentrations were measured before and after supplementation with methionine for 30 days. Ophthalmic examinations were performed in 16 dogs; echocardiography was performed in 6 dogs that were taurine deficient. RESULTS: Plasma taurine concentrations ranged from 3 to 228 nmol/mL. Twelve dogs had concentrations < 40 nmol/mL and were considered taurine deficient. For dogs with plasma concentrations < 40 nmol/mL, there was a significant linear correlation between plasma and blood taurine concentrations. For dogs with plasma concentrations > 40 nmol/mL, blood taurine concentrations did not vary substantially. Taurine-deficient dogs had been fed lamb meal and rice diets. Retinal degeneration, dilated cardiomyopathy, and cystinuria were not found in any dog examined for these conditions. The taurine deficiency was reversed by a change in diet or methionine supplementation. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate a high prevalence of taurine deficiency among an environmentally and genetically related cohort of Newfoundlands fed apparently complete and balanced diets. Blood taurine concentrations indicative of taurine deficiency in Newfoundlands may be substantially less than concentrations indicative of a deficiency in cats.     

Haemophilia A (Factor VIII deficiency) in the cat

A case of haemophilia A (classical haemophilia, factor VIII deficiency) in a cat is described. The cat presented with persistent bleeding from an oral wound, and protracted haemorrhage after castration. The diagnosis and management of this case is described. Subsequent investigation of the dam and a recent litter identified a further affected male kitten.     

Partial deficiency of antidiuretic hormone in a cat

Marked polydipsia and polyuria developed subsequent to trauma in a 1 1/2-year-old male Abyssinian cat. Diabetes insipidus was suspected, inasmuch as intramuscualr vasopressin administration resulted in amelioration of polydipsia and polyuria. However, hypertonic (3%) saline solution given intravneously resulted in anuria, an indication of antidiuretic hormone activity. Polyuria and polydipsia were abolished by oral chlorpropamide therapy, which was indirect evidence for partial deficiency of antidiuretic hormone.     

Pyruvate kinase deficiency in a Somali cat in Australia

A 7-year-old neutered male Somali cat, bred in Western Australia, was presented for investigation of jaundice and severe anaemia. Splenomegaly and hepatomegaly were evident on physical examination. Severe anaemia, along with leukopenia and increased liver enzymes, were present on laboratory evaluation. Clinical investigation identified cholangitis and treatment for this resolved the jaundice but failed to resolve the anaemia. Treatment for Mycoplamsa haemofelis was administered concurrently. Genetic testing was then performed and pyruvate kinase deficiency was identified, the first time this has been reported in an Australian cat. Treatment with immunosuppressive medication was not successful.     

Degenerative myelopathy associated with cobalamin deficiency in a cat

A severe myelopathy was observed in a 9-year-old neutered male cat with a clinical history of chronic pancreatitis associated with deficiency of serum cobalamin and folates concentrations, and progressive spinal ataxia. The spinal cord lesions mainly involved the dorsal columns of the caudal cervical and cervico-thoracic segments, and were characterized by diffuse vacuolated myelin sheaths and axonal degeneration, marked gliosis, fibrosis and presence of gitter cells. The pancreas showed severe atrophy of the exocrine tissue, periductular fibrosis and infiltration of inflammatory cells, consistent with chronic interstitial pancreatitis. This condition can be accountable for cobalamin deficiency, as the pancreas is the only source of intrinsic factor in cats. The spinal cord lesions in the cat of this report resembled the subacute combined degeneration of the spinal cord described in human beings with cobalamin deficiency and hence a similar pathogenetic mechanism is hypothesized.     

Congenital factor XI deficiency in a domestic shorthair cat

A 6-month-old, female, domestic shorthair cat was examined after onychectomy and ovariohysterectomy because of bleeding from the paws. Prolonged activated partial thromboplastin time was discovered, Coagulation factor analyses revealed deficiency of factor XI coagulant activity. Plasma mixing studies indicated factor deficiency or dysfunction rather than factor inhibition. Feline factor XI deficiency in one adult cat has been previously reported but was attributed to factor XI inhibitors. The signalment, lack of primary disease, and the finding of persistent factor XI deficiency in the absence of coagulation inhibitors were considered compatible with congenital factor XI deficiency in the cat of this report.     

Cobalamin deficiency associated with methylmalonic acidemia in a cat.

A 9-month-old sexually intact male longhair cat was examined because of lethargy, anorexia, cold intolerance, and failure to thrive since acquisition at an early age. Clinical signs of disease were less pronounced when the cat was fed a low-protein diet. Anemia, hypoglycemia, low total CO2 content, and hyperammonemia were detected. The cat was euthanatized. Urine obtained immediately before euthanasia contained a large amount of methylmalonic acid. Total serum cobalamin concentration was low. Hepatic methylmalonic-CoA mutase activity, with and without the addition of coenzyme adenosylcobalamin, was consistent with a cobalamin deficiency. Methylmalonic acidemia secondary to a putative defect in cobalamin absorption was diagnosed.     

Organic acidemia in a young cat associated with cobalamin deficiency

Objective: To describe a case of severe metabolic acidosis and encephalopathy secondary to cobalamin (Cbl) deficiency in a young cat. Case summary: A 4‐year‐old spayed female domestic short hair cat weighing 2.5 kg, presented with a 2‐day history of neurological signs referable to the cerebrum. The cat was evaluated for similar episodes twice before, however, no definitive diagnosis was made for either visit. On presentation the cat was minimally responsive and had a metabolic acidosis and ketonuria with no apparent reason, such as lactic acidosis or diabetic ketoacidosis. The patient was diagnosed postmortem with an organic acidemia secondary to low Cbl levels. New or unique information provided: The purpose of this report is to alert emergency clinicians to be suspicious of an organic acidemia in any case of metabolic acidosis and ketonuria that cannot be explained. Early identification of inherited organic acidemias in domestic animals may allow prompt and appropriate treatment of these conditions.     

A suspected case of ornithine transcarbamylase deficiency in a cat

An 18 month-old, intact female American Shorthair cat was presented for evaluation of stunted growth and postprandial depression. Fasting serum ammonia and serum bile acid concentrations were above reference ranges at 396 microg/dl and 6.5 micromol/ l and their postprandial concentrations were 785 microg/dl and 9.5 micromol/l, respectively. The initial tentative diagnosis of a portosystemic shunt was excluded by mesenteric portography and histopathology of the liver. The cat was then suspected of a urea cycle enzyme deficiency and its urine was analyzed by gas chromatography-mass spectrometry. A presumptive diagnosis of ornithine transcarbamylase deficiency was made on the basis of the detection of orotic acid and uracil.     

Taurine deficiency in dogs with dilated cardiomyopathy: 12 cases (1997-2001)

OBJECTIVE: To determine signalment, history, clinical signs, blood and plasma taurine concentrations, electrocardiographic and echocardiographic findings, treatment, and outcome of dogs with low blood or plasma taurine concentrations and dilated cardiomyopathy (DCM). DESIGN: Retrospective study. ANIMALS: 12 client-owned dogs with low blood or plasma taurine concentrations and DCM. PROCEDURE: Medical records were reviewed, and clinical data were obtained. RESULTS: All 12 dogs were being fed a commercial dry diet containing lamb meal, rice, or both as primary ingredients. Cardiac function and plasma taurine concentration improved with treatment and taurine supplementation. Seven of the 12 dogs that were still alive at the time of the study were receiving no cardiac medications except taurine. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that consumption of certain commercial diets may be associated with low blood or plasma taurine concentrations and DCM in dogs. Taurine supplementation may result in prolonged survival times in these dogs, which is not typical for dogs with DCM. Samples should be submitted for measurement of blood and plasma taurine concentrations in dogs with DCM, and taurine supplementation is recommended while results of these analyses are pending.