| 1. |
- Hultin Jäderlund, Karin, et al.
(author)
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Cerebrospinal Fluid PCR and Antibody Concentrations against Anaplasma phagocytophilum and Borrelia burgdorferi sensu lato in Dogs with Neurological Signs
- 2009
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In: Journal of Veterinary Internal Medicine. - : Wiley. - 0891-6640 .- 1939-1676. ; 23, s. 669-672
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Journal article (peer-reviewed)abstract
- The tick-borne bacteria Borrelia burgdorferi sensu lato (sl) and Anaplasma phagocytophilum have been suspected to cause neurological signs in dogs. Diagnosis often has been made based on positive antibody titers in serum of dogs with neurological signs, but a high seroprevalence in dogs in at-risk populations makes diagnosis difficult.To determine if the neurological signs in dogs examined were caused by any of these bacteria.Fifty-four dogs presented to a board-certified neurologist.Prospective study. We divided dogs into 2 groups: those with inflammatory diseases of the central nervous system (CNS) and those with neurological signs from other diseases. Blood and cerebrospinal fluid (CSF) from all dogs were analyzed.Dogs with inflammatory CNS diseases showed no serum antibodies against any of the agents. Among dogs with neurological signs from other diseases, 10.3% had serum antibodies for B. burgdorferi sl and 20.5% for A. phagocytophilum. All blood samples analyzed for bacterial deoxyribonucleic acid (DNA) and all CSF analyzed for antibodies and bacterial DNA for the 2 agents were negative.Based on this study, these bacteria are unlikely causes of neurologic disease in dogs and the presence of serum antibodies alone does not document or establish a definitive diagnosis of CNS disease caused by these organisms. Dogs that have neurologic disease and corresponding serum antibodies against these agents should have additional tests performed to assess for other potential etiologies of the signs.
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| 2. |
- Baranowska, Izabella, et al.
(author)
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Sensory ataxic neuropathy in golden retriever dogs is caused by a deletion in the mitochondrial tRNATyr gene
- 2009
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In: PLoS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 5:5, s. e1000499-
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Journal article (peer-reviewed)abstract
- Sensory ataxic neuropathy (SAN) is a recently identified neurological disorder in golden retrievers. Pedigree analysis revealed that all affected dogs belong to one maternal lineage, and a statistical analysis showed that the disorder has a mitochondrial origin. A one base pair deletion in the mitochondrial tRNA(Tyr) gene was identified at position 5304 in affected dogs after re-sequencing the complete mitochondrial genome of seven individuals. The deletion was not found among dogs representing 18 different breeds or in six wolves, ruling out this as a common polymorphism. The mutation could be traced back to a common ancestor of all affected dogs that lived in the 1970s. We used a quantitative oligonucleotide ligation assay to establish the degree of heteroplasmy in blood and tissue samples from affected dogs and controls. Affected dogs and their first to fourth degree relatives had 0-11% wild-type (wt) sequence, while more distant relatives ranged between 5% and 60% wt sequence and all unrelated golden retrievers had 100% wt sequence. Northern blot analysis showed that tRNA(Tyr) had a 10-fold lower steady-state level in affected dogs compared with controls. Four out of five affected dogs showed decreases in mitochondrial ATP production rates and respiratory chain enzyme activities together with morphological alterations in muscle tissue, resembling the changes reported in human mitochondrial pathology. Altogether, these results provide conclusive evidence that the deletion in the mitochondrial tRNA(Tyr) gene is the causative mutation for SAN.
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| 3. |
- Baranowska Körberg, Izabella, et al.
(author)
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Clinical characteristics of epilepsy of unknown origin in the Rottweiler breed
- 2015
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In: Acta Veterinaria Scandinavica. - : Springer Science and Business Media LLC. - 0044-605X .- 1751-0147. ; 57
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Journal article (peer-reviewed)abstract
- Background: Epilepsy is one of the most common neurological conditions in dogs. Despite that epilepsy appears to be common in the Rottweiler breed, published literature about the phenotype of epilepsy in this breed is lacking. The aim of this questionnaire-based study was to describe the clinical characteristics of epilepsy in the Rottweiler breed including; signalment, pedigree, housing conditions and information about the seizures such as age at onset, seizure type, duration, and progression, as well as number of seizure days (24 h), effect and side effects of anti-epileptic drugs, and potential comorbidities. The diagnosis for epilepsy of unknown origin was based on the following inclusion criteria: >= 2 seizure days, starting between 6 months and 7 years of age, no known history of poisoning or serious head trauma, and (when available), pre-study routine serum biochemical parameters were within the reference intervals.Results: A total of 37 cases (23 females and 14 males) were included in the study. The median age at onset of seizures was 36 months (range 8-84 months). The dogs suffered from generalized tonic-clonic seizures, and more than 50 % of the dogs had experienced cluster seizures (>1 seizure in 24 h). The dogs commonly started to seizure while resting (23/36) and/or sleeping (20/36). Only 3 of the 36 dogs experienced seizures during activities such as walking or training. All of the 24/37 (64.9 %) dogs on antiepileptic drugs received phenobarbital. Five dogs needed addon treatment (n = 5), and of these: one dog was on 3 drugs (phenobarbital, potassium bromid and levetiracetam) (n = 1), three dogs were on phenobarbital and potassium bromide (n = 3), and one dog received phenobarbital and imepitoin (n = 1). Seizure frequency did not necessarily improve following antiepileptic treatment, and for six of 21 (28.6 %) of the dogs, seizure frequency increased. All of the Rottweilers in this study had relatives with epilepsy reported.Conclusions: The Rottweilers suffering from epilepsy in this study presented with generalized tonic-clonic seizures, and their response to antiepileptic treatment was variable. More than 50 % of the dogs had experienced cluster seizures (>1 seizure in 24 h).
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| 4. |
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| 5. |
- Drögemüller, Cord, et al.
(author)
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A deletion in the N-myc downstream regulated gene 1 (NDRG1) gene in Greyhounds with polyneuropathy
- 2010
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In: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 5:6, s. e11258-
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Journal article (peer-reviewed)abstract
- The polyneuropathy of juvenile Greyhound show dogs shows clinical similarities to the genetically heterogeneous Charcot-Marie-Tooth (CMT) disease in humans. The pedigrees containing affected dogs suggest monogenic autosomal recessive inheritance and all affected dogs trace back to a single male. Here, we studied the neuropathology of this disease and identified a candidate causative mutation. Peripheral nerve biopsies from affected dogs were examined using semi-thin histology, nerve fibre teasing and electron microscopy. A severe chronic progressive mixed polyneuropathy was observed. Seven affected and 17 related control dogs were genotyped on the 50k canine SNP chip. This allowed us to localize the causative mutation to a 19.5 Mb interval on chromosome 13 by homozygosity mapping. The NDRG1 gene is located within this interval and NDRG1 mutations have been shown to cause hereditary motor and sensory neuropathy-Lom in humans (CMT4D). Therefore, we considered NDRG1 a positional and functional candidate gene and performed mutation analysis in affected and control Greyhounds. A 10 bp deletion in canine NDRG1 exon 15 (c.1080_1089delTCGCCTGGAC) was perfectly associated with the polyneuropathy phenotype of Greyhound show dogs. The deletion causes a frame shift (p.Arg361SerfsX60) which alters several amino acids before a stop codon is encountered. A reduced level of NDRG1 transcript could be detected by RT-PCR. Western blot analysis demonstrated an absence of NDRG1 protein in peripheral nerve biopsy of an affected Greyhound. We thus have identified a candidate causative mutation for polyneuropathy in Greyhounds and identified the first genetically characterized canine CMT model which offers an opportunity to gain further insights into the pathobiology and therapy of human NDRG1 associated CMT disease. Selection against this mutation can now be used to eliminate polyneuropathy from Greyhound show dogs.
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| 6. |
- Hultin Jäderlund, Karin, et al.
(author)
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A cohort study of epilepsy among 665,000 insured dogs : Incidence, mortality and survival after diagnosis
- 2014
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In: Veterinary Journal. - : Elsevier BV. - 1090-0233 .- 1532-2971. ; 202, s. 471-476
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Journal article (peer-reviewed)abstract
- 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.
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| 7. |
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| 8. |
- Hultin Jäderlund, Karin
(author)
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New aspects of hereditary ataxia in smooth-haired fox terriers
- 2010
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In: Veterinary Record. - : Wiley. - 0042-4900 .- 2042-7670. ; 166, s. 557-560
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Journal article (peer-reviewed)abstract
- 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.
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| 9. |
- Hultin Jäderlund, Karin, et al.
(author)
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Re-emergence of hereditary polyneuropathy in Scandinavian Alaskan malamute dogs-old enemy or new entity? A case series
- 2017
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In: Acta Veterinaria Scandinavica. - : Springer Science and Business Media LLC. - 0044-605X .- 1751-0147. ; 59
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Journal article (peer-reviewed)abstract
- A homozygous mutation has been identified in the N-myc downstream-regulated gene 1 (NDRG1) in recent cases of polyneuropathy in Alaskan malamute dogs from the Nordic countries and USA. The objective of the present study was to determine if cases diagnosed 30-40 years ago with polyneuropathy in the Alaskan malamute breed in Norway had the same hereditary disease as the recent cases. Fourteen historical cases and 12 recently diagnosed Alaskan malamute dogs with hereditary polyneuropathy, and their parents and littermates (n = 88) were included in this study (total n = 114). After phenotyping of historical and recent cases, NDRG1 genotyping was performed using DNA extracted from archived material from five Norwegian dogs affected by the disease in the late 1970s and 1980s. In addition, pedigrees were analysed. Our study concluded that historical and recent phenotypic polyneuropathy cases were carrying the same NDRG1-mutation. The pedigree analysis showed that all affected Alaskan malamute cases with polyneuropathy could be traced back to one common ancestor of North American origin. By this study, a well-documented example of the silent transmission of recessive disease-causing alleles through many generations is provided, demonstrated by the re-emergence of a phenotypically and genetically uniform entity in the Scandinavian Alaskan malamute population.
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| 10. |
- Johansson Wensman, Jonas, et al.
(author)
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Bornavirus Infection
- 2023
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In: Greene's Infectious Diseases of the Dog and Cat : Fifth Edition. - 9780323509343 ; , s. 501-506
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Book chapter (peer-reviewed)abstract
- • First Described: Staggering disease was first described in the 1970s in Sweden (Kronevi et al., 1974). It was linked to BoDV infection in 1995 in Sweden (Lundgren et al., 1995)• Causes: Borna disease virus (BoDV) (species Mammalian 1 orthobornavirus), family Bornaviridae.• Affected Hosts: Mammalian 1 orthobornavirus mainly affects horses and sheep, but also cats, dogs, other equids, and ungulates.• Geographic Distribution: Europe (endemic in horses and sheep in Central Europe; in cats mainly reported in Sweden), worldwide serologic evidence of exposure in various species.• Primary Mode of Transmission: Not entirely known. Reservoirs (small mammals) have been suggested.• Major Clinical Signs: Gait disturbances and behavioral changes.• Differential Diagnoses: Other feline encephalitides and neoplastic diseases affecting the CNS.• Human Health Significance: A variant bornavirus (Mammalian 2 orthobornavirus) has been associated with three cases of fatal encephalitis in breeders of variegated squirrels. Also, at least eight cases of BoDV-1 in humans have been described further emphasizing the zoonotic potential for BoDV-1, especially in endemic regions. Suggested association of BoDV and neuropsychiatric disorders in humans is however still highly controversial.
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