A cohort study of epilepsy among 665,000 insured dogs: incidence, mortality and survival after diagnosis.

The main objective of this study was to estimate the incidence and mortality rates of epilepsy in a large population of insured dogs and to evaluate the importance of a variety of risk factors. Survival time after a diagnosis of epilepsy was also investigated. The Swedish animal insurance database used in this study has previously been helpful in canine epidemiological investigations. More than 2,000,000 dog-years at-risk (DYAR) were available in the insurance database. In total, 5013 dogs had at least one veterinary care claim for epilepsy, and 2327 dogs were euthanased or died because of epilepsy. Based on veterinary care claims the incidence rate of epilepsy (including both idiopathic and symptomatic cases) was estimated to be 18 per 10,000 DYAR. Dogs were followed up until they were 10 (for life insurance claims) or 12 years of age (veterinary care claims). Among the 35 most common breeds in Sweden, the Boxer was at the highest risk of epilepsy with 60.3 cases per 10,000 DYAR, and also had the highest mortality rate of 46.7 per 10,000 DYAR (based on life insurance claims). Overall, males were at a higher risk than females (1.4:1). Median survival time (including euthanasia and death) after diagnosis was 1.5 years. In general, breeds kept solely for companionship lived longer after diagnosis than those kept for dual-purposes, such as hunting and shepherd and working breeds. The study demonstrates marked breed differences in incidence and mortality rates, which are assumed to reflect genetic predisposition to epilepsy.

Acquired equine polyneuropathy in Norway and Sweden: a clinical and epidemiological study.

REASONS FOR PERFORMING STUDY: Acquired equine polyneuropathy (AEP, also known as 'Scandinavian knuckling syndrome'), is a serious disease of unknown aetiology, which emerged clustering in horse farms in Sweden, Norway and Finland in the 1990s. Clinical and epidemiological data regarding the syndrome are scarce. OBJECTIVES: To describe the clinical and epidemiological findings and outcome in outbreaks of AEP and compare risk factors in affected and unaffected horses on affected farms in Norway and Sweden during 2007-2009. METHODS: Neurological examinations were performed and data collected regarding demography, usage, turning-out, feeding, prophylactic strategies and long-term outcome. RESULTS: Thirteen affected farms with 157 horses of various breeds, of which 42 were AEP cases, were studied. Typical digital extensor dysfunction and knuckling of pelvic limbs were noted in 34 definitive cases. Eight additional plausible cases had a severe, acute course of neurological disease. There were no signs of brain orcranial nerve dysfunction. Cases occurred from December to April, with new cases emerging within 100 days of the index case. Affected and unaffected horses were fed wrapped forage. Prevalence for AEP was 27% and case fatality 29%. The median duration of AEP in survivors was 4.4 months (1-17 months). Survivors returned to full work within 19 months (median 6.6 months). Acquired equine polyneuropathy was less prevalent in horses aged > 12 years and young horses had a higher chance of survival than older horses. Management factors did not differ between affected and unaffected horses. CONCLUSIONS: Acquired equine polyneuropathy is a potentially fatal neurological disease characterised by pelvic limb knuckling. Surviving horses returned to normal function after a long period of rest. Cases were clustered in farms during the winter/spring season. Wrapped forage was used in all farms. POTENTIAL RELEVANCE: The results provide valuable insights into the dinical examination, handling and prognosis of cases of AEP, an emerging neurological disease of unknown aetiology in horses.

New aspects of hereditary ataxia in smooth-haired fox terriers.

Hereditary ataxia was diagnosed in three smooth-haired fox terrier puppies from Sweden, 25 years after the previous known case in the breed. In addition to the characteristic spinal cord pathology, brain involvement was evident clinically, in the form of behavioural changes and bilaterally decreased menace responses, and histopathologically, with degenerative changes in the brainstem. The striking similarities to hereditary ataxia in the Jack Russell terrier suggest the same disease process in both breeds. A common ancestor, a female dog born in 1951 and considered a carrier of the disease at that time, was found in both the maternal and paternal lines of the three puppies.

Poisoning of dogs with tremorgenic Penicillium toxins.

Fungi in the genus Penicillium, particularly P. crustosum, produce tremorgenic mycotoxins, as well as suspected tremorgenic compounds. The accidental intoxication of six dogs with such toxins are reported. The clinical signs included vomiting, convulsions, tremors, ataxia, and tachycardia, all of which are indicators of intoxications affecting the nervous system. This symptomatology caused us to think that the dog poisoning was the result of tremorgenic mycotoxins. One dog was euthanized in the acute phase, while three others recovered completely within a few days. However, neurological symptoms were still observed four months after the poisoning of two of the dogs. One of these recovered completely within the next 2-3 months, while the other still suffers from ataxia three years later. Available samples of feed, stomach content and/or tissues from the intoxications were subjected to mycological and chemical analysis. Penitrem A was found in all reported poisonings and roquefortine C in all cases when this toxin was included in the analysis. The producer of these toxins, Penicillium crustosum, was detected in all cases where material suitable for mycological examinations (feed or vomit) was available. To our knowledge, this is the first report documenting the presence of penitrems and roquefortine C in organs from poisoned dogs. Furthermore, the report indicates that the recovery period after severe poisonings with P. crustosum may be protracted.

A neurologic syndrome in Golden Retrievers presenting as a sensory ataxic neuropathy.

BACKGROUND: A sensory ataxic neuropathy has been observed in Swedish Golden Retrievers recently. ANIMALS: Twenty-one affected Golden Retrievers. METHODS: Clinical and neurologic status, electrophysiologic, and pathologic status as well as pedigree analyses were evaluated. RESULTS: Clinical signs had an insidious onset between 2 and 8 months of age and a slowly progressive course. Affected dogs were ataxic and dysmetric. They had abnormal postural reactions and decreased spinal reflexes but no apparent muscle atrophy. Clinical pathology, radiography, and electrophysiology of motor systems were all within reference values. Sensory nerve conduction results of affected dogs were significantly different from those of a group of control dogs. Necropsy revealed a chronic progressive central and peripheral sensorimotor axonopathy; the proprioceptive pathways were most severely affected. CONCLUSIONS AND CLINICAL IMPORTANCE: This disease in these Golden Retrievers is distinct from other canine breed-related neurodegenerative diseases or hereditary neurodegenerative diseases described in humans. Pedigree analyses indicated a hereditary background, but the mode of inheritance could not be established.