[Cerebellar cortical degeneration in an American Staffordshire terrier]. / Cerebellaire corticale degeneratie bij een Amerikaanse Staffordshire terriër.

Most diseases affecting the cerebellum are congenital and three groups can be distinguished on pathogenetic grounds. In the first group, diseases are caused by intrauterine or neonatal viral infections, in the second group by malformations of genetic or unknown origin, and in the third group by degenerative disease, or abiotrophies. Familial late-onset cerebellar abiotrophy has been reported in the Gordon Setter the Old English Sheepdog, the Brittany Spaniel and more recently the American Staffordshire Terrier. This case report describes the clinical, diagnostic and pathological changes in an American Staffordshire Terrier with cerebellar cortical degeneration. This is the first case diagnosed in the Netherlands.

Effect of acetic acid consumption on clinical laboratory values in the dog.

To investigate the influence of food enriched with acetic acid on the clinical, biochemical, electrolyte, blood gas, haematological and urinary variables in the dog, a cross-over study was carried out with periods of approximately 2 weeks involving six healthy, adult dogs. Another objective was to determine the maximum concentration of acetic acid that the dogs found to be palatable. The dogs were maintained on a commercial meat-based food with added acetic acid and/or glucose. The administered acetic acid was increased in stages. All dogs accepted the diet containing acetic acid at a level of 5% of metabolizable energy. Except for a decrease in plasma total protein, none of the variables were significantly affected by acetic acid consumption. Acetic acid feeding did not affect plasma acetate concentration and urinary acetate excretion, indicating that dogs efficiently metabolize ingested acetic acid.

Fibrocartilaginous embolism of the spinal cord (FCE) in juvenile Irish Wolfhounds.

This study describes the occurrence of fibrocartilaginous embolism of the spinal cord (FCE) in eight juvenile Irish Wolfhounds that were presented within a period of 16 months (1996-1997). The dogs, seven males and one female between eight and 13 weeks of age, were presented because of an acute onset of abnormal locomotion. Five dogs were euthanized and FCE was diagnosed by the histomorphological presence of focal myelomalacia and Alcian blue-positive-nucleus-pulposus material in the spinal cord vasculature. Three dogs, which were thought to have FCE because of their clinical symptoms, improved with partial or almost complete return to normal locomotion. Although the observed high incidence may be a coincidence, oral information from breeders and lay reports of similar cases in journals for dog breeders from various countries suggest that FCE is a common disorder in young Irish Wolfhounds.

Cerebellar cortical abiotrophy in two Portuguese Podenco littermates.

Cerebellar cortical abiotrophy in two Portuguese Podenco littermates is reported and discussed. The disease is characterized by progressive cerebellar ataxia with an early onset of two to three weeks. Extensive loss, degeneration, and necrosis of Purkinje cells particularly involved the cerebellar hemispheres. An autosomal recessive pattern of inheritance is suspected.

Salinomycin-induced polyneuropathy in cats: morphologic and epidemiologic data.

In April 1996, an outbreak of toxic polyneuropathy in cats occurred in the Netherlands. All cats had been fed one of two brands of dry cat food from one manufacturer. Chemical analyses of these foods, stomach contents, and liver and kidney of affected cats revealed contamination with the ionophor salinomycin. Epidemiologic and clinical data were collected from 823 cats, or about 1% of the cats at risk. In 21 affected cats, postmortem examination was performed. The affected cats had acute onset of lameness and paralysis of the hindlimbs followed by the forelimbs. Clinical and pathologic examination indicated a distal polyneuropathy involving both the sensory and motor nerves.

[Periodic muscle weakness and cervical ventroflexion caused by hypokalemia in a Burmese cat]. / Periodieke spierzwakte en cervicale ventroflexie ten gevolge van hypokaliëmie bij een Burmese kat.

A 2-year-old female Burmese cat was referred to the University Hospital of Companion Animals of Utrecht University because of periodic muscle weakness and cervical ventroflexion. Laboratory examinations revealed hypokalemia. The combination of breed, clinical signs and hypokalemia warranted the diagnosis of 'periodic hypokalemic myopathy', a homozygote recessive hereditary disease in Burmese cats. Potassium supplementation resulted in complete disappearance of the signs. Possible causes of hypokalemia in the cat are discussed.

A neuronal vacuolar disorder in young rottweiler dogs.

Four rottweiler pups from two litters developed severe progressive signs of spinal ataxia, cerebellar ataxia and tetraparesis/paralysis. The signs started with ataxia of the pelvic limbs at seven to eight weeks of age and progressed to tetraparesis and paralysis within three to five weeks. Postmortem, a vacuolar neuronal disorder was found in the cerebellum, brainstem and the spinal cord, associated with Wallerian type degeneration in the brainstem, cerebellar peduncles and the medullary cord. Electron microscopy revealed empty membrane-bound vacuoles. Immunohistochemistry for PrPSc was negative. The disorder differs clinically and pathologically from other neurological disorders in the breed and a new (familial) neurological disorder in the rottweiler is suspected.

Progressive neuronopathy in two Cairn terrier litter mates.

Clinical, histopathological, and EM findings are described for two Cairn terrier litter mates, an 18-months-old male and an 11-month-old female with progressive neuronopathy. The initial clinical signs were characterized by hind limb weakness and ataxia, which deteriorated with exercise. These signs progressed over several months to tetraparesis. Pathological examination revealed extensive chromatolytic degeneration of neurons and moderate secondary Wallerian-type degeneration in the spinal cord and brain stem. Progressive neuronopathy can be differentiated clinically from globoid cell leukodystrophy, another progressive neurological disorder in Cairn terriers, by the exercise-induced deterioration of the neurological signs. Progressive neuronopathy occurs only in Cairn terriers and because of the similarity in age of onset and the occurrence in one litter, an inherited disease is suspected.

[Epidemic of nutritional polyneuropathy in the cat. Final report of the investigational team]. / Epidemie van alimentaire polyneuropathie bij de kat. Eindverslag onderzoeksteam.

In June 1996 companion animal practitioners received a report prepared by the Faculty Investigative Team on the outbreak of polyneuropathy among cats, and at the end of August a 'definitive' bulletin was circulated by Spillers Petfoods. The coccidiostatic drug salinomycin, which was present in the vitamin premix supplied by a third party, was considered the cause of the neuropathy. The investigative team is of the opinion that all veterinary practitioners in the Netherlands should receive a conclusive report about the epidemic because of the unique nature of the epidemic, which despite its sudden outbreak could be well documented, and because aspects of the affair merit the attention of veterinary practitioners.

Acute idiopathic polyneuropathy in nine cats.

This report describes nine unrelated cats with acute idiopathic polyneuropathy. All cats presented with acutely developing tetraparesis or tetraparalysis and loss of spinal reflexes. Seven cats recovered completely within 4 to 6 weeks, without any medication. Two years after complete recovery, none of these cats had had a relapse. In the acute stage, two cats were euthanized because of respiratory complications. Postmortem examination was performed on one of these cats and revealed generalized peripheral motor polyneuropathy. The clinical signs in these cats were identical to those of the Guillain-Barré syndrome in humans.

Hereditary necrotising myelopathy in Kooiker dogs.

A retrospective clinicopathological study of a neurological disorder in 22 Kooiker dogs (Dutch decoy dog) was made. The disease was found to occur equally in both sexes and clinical signs began at three to 12 months old. Physical examination revealed a progressive paresis of the hindlimbs. Post mortem examination showed symmetrical areas of malacia in the ventral, lateral and dorsal white matter of the spinal cord. In one dog dorsal white matter was spared. Cervical segments C4 to C8 were involved in all subjects. Rostral and caudal to these areas, Wallerian degeneration was prominent. The disease has much in common with similar myelopathies in the Afghan hound and the rottweiler. Indications of heritability were the similarity in clinical and pathological findings, the age of onset of the disease, and the significantly higher inbreeding coefficient in the patients than in the breed population (P = 0.001). All patients were descended from one pair. Segregation analysis suggested inheritance involving a simple autosomal recessive trait.

Familial stomatocytosis--hypertrophic gastritis (FSHG), a newly recognised disease in the dog (Drentse patrijshond).

A newly recognised disease, which we have given the provisional name of familial stomatocytosis-hypertrophic gastritis (FSHG), is described in two families of dogs of the Drentse partrijshond breed. The affected dogs consisted of 3 females and 5 males, 3 to 19 (mean 9.5) months of age at admission. The main clinical problems were diarrhoea, icterus, and ataxia and paresis of the pelvic limbs. Laboratory evaluation revealed abnormal red cell shape (stomatocytosis), increased osmotic fragility, haemolytic anaemia, and increased liver enzymes and serum bilirubin. Gastroscopic and histopathologic examination of the gastric mucosa revealed hypertrophic gastritis resembling Ménétrier's disease in man. Histologic findings in the liver were suggestive of progressive liver disease. Cysts were found in the kidneys of the five oldest patients. Electroneurography in 2 dogs revealed polyneuropathy. In the parents of 2 patients (sister and brother), there were no clinical or laboratory abnormalities. An autosomal recessive hereditary defect of lipid metabolism is suspected.

[Medical decision analysis in veterinary practice. An introduction with reference to the problem: to operate or not in cryptorchism in dogs]. / Medische besliskunde in de diergeneeskundige praktijk. Een introductie aan de hand van het probleem: het al of niet opereren van de cryptorche hond.

In the present report, medical decision analysis in veterinary practice is introduced. Fundamentals such as decision tree, utility, and sensitivity analysis are explained using a clinical example. The decision-analytic approach is found to produce an interesting result. Finally, a prospect for the future is presented.

Pharmacokinetics of three formulations of diphenylhydantoin in the dog.

The pharmacokinetics of the sodium salt of diphenylhydantoin was studied in three healthy dogs, using three formulations, a capsule, a tablet and a suspension. The results were essentially the same for all three formulations. The serum half life after intravenous injection ranged from 3.1 to 3.6 hours before and 1.3 to 1.6 hours after a two-week period of oral treatment. The bioavailability of the formulations varied from 43 to 54 per cent. Serum levels likely to be required for canine therapy could not be maintained with any of the formulations used in this experiment.