| 1. |
- Hultin Jäderlund, Karin, et al.
(författare)
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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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Ingår i: Journal of Veterinary Internal Medicine. - : Wiley. - 0891-6640 .- 1939-1676. ; 23, s. 669-672
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Tidskriftsartikel (refereegranskat)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.
(författare)
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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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Ingår i: PLoS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 5:5, s. e1000499-
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Tidskriftsartikel (refereegranskat)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.
(författare)
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Clinical characteristics of epilepsy of unknown origin in the Rottweiler breed
- 2015
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Ingår i: Acta Veterinaria Scandinavica. - : Springer Science and Business Media LLC. - 0044-605X .- 1751-0147. ; 57
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Tidskriftsartikel (refereegranskat)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.
(författare)
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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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Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 5:6, s. e11258-
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Tidskriftsartikel (refereegranskat)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.
(författare)
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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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Ingår i: Veterinary Journal. - : Elsevier BV. - 1090-0233 .- 1532-2971. ; 202, s. 471-476
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Tidskriftsartikel (refereegranskat)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
(författare)
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New aspects of hereditary ataxia in smooth-haired fox terriers
- 2010
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Ingår i: Veterinary Record. - : Wiley. - 0042-4900 .- 2042-7670. ; 166, s. 557-560
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Tidskriftsartikel (refereegranskat)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.
(författare)
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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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Ingår i: Acta Veterinaria Scandinavica. - : Springer Science and Business Media LLC. - 0044-605X .- 1751-0147. ; 59
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Tidskriftsartikel (refereegranskat)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.
(författare)
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Bornavirus Infection
- 2023
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Ingår i: Greene's Infectious Diseases of the Dog and Cat : Fifth Edition. - 9780323509343 ; , s. 501-506
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Bokkapitel (refereegranskat)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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| 11. |
- Johansson Wensman, Jonas, et al.
(författare)
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Expression of interferon gamma in the brain of cats with natural Borna disease virus infection
- 2011
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Ingår i: Veterinary Immunology and Immunopathology. - : Elsevier BV. - 0165-2427 .- 1873-2534. ; 141, s. 162-167
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Tidskriftsartikel (refereegranskat)abstract
- Borna disease virus (BDV) is a neurotropic, negative-stranded RNA virus, which causes a non-suppurative meningoencephalomyelitis in a wide range of animals. In cats, BDV infection leads to staggering disease. In spite of a vigorous immune response the virus persists in the central nervous system (CNS) in both experimentally and naturally infected animals. Since the CNS is vulnerable to cytotoxic effects mediated via NK-cells and cytotoxic T-cells, other non-cytolytic mechanisms such as the interferon (IFN) system is favourable for viral clearance. In this study, IFN-gamma expression in the brain of cats with clinical signs of staggering disease (N = 12) was compared to the expression in cats with no signs of this disease (N = 7) by quantitative RT-PCR. The IFN-gamma expression was normalised against the expression of three reference genes (HPRT, RPS7, YWHAZ). Cats with staggering disease had significantly higher expression of IFN-gamma compared to the control cats (p-value <= 0.001). There was no significant difference of the IFN-gamma expression in BDV-positive (N = 7) and negative (N = 5) cats having clinical signs of staggering disease. However, as BDV-RNA still could be detected, despite an intense IFN-gamma expression, BDV needs to have mechanisms to evade this antiviral immune response of the host, to be able to persist. (C) 2011 Elsevier B.V. All rights reserved.
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| 12. |
- Johansson Wensman, Jonas, et al.
(författare)
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Markers of Borna disease virus infection in cats with staggering disease
- 2012
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Ingår i: Journal of Feline Medicine and Surgery. - 1098-612X .- 1532-2750. ; 14, s. 573-582
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Tidskriftsartikel (refereegranskat)abstract
- Borna disease virus (BDV) is a RNA-virus causing neurological disorders in a wide range of mammals. In cats, BDV infection may cause staggering disease. Presently, staggering disease is a tentative clinical diagnosis, only confirmed at necropsy. In this study, cats with staggering disease were investigated to study markers of BDV infection aiming for improvement of current diagnostics. Nineteen cats fulfilled the inclusion criteria based on neurological signs and pathological findings. In 17/19 cats, BDV infection markers (BDV-specific antibodies and/or BDV-RNA) were found, and antibodies in serum (13/16, 81%) were the most common marker. BDV-RNA was found in 11/19 cats (58%). In a reference population without neurological signs, 4/25 cats were seropositive (16%). The clinical history and neurological signs in combination with presence of BDV infection markers, where serology and rRT-PCR on blood can be helpful tools, improve the diagnostic accuracy in the living cat.
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| 13. |
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| 14. |
- Rohdin, Cecilia, et al.
(författare)
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High prevalence of gait abnormalities in pugs
- 2018
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Ingår i: Veterinary Record. - : Wiley. - 0042-4900 .- 2042-7670. ; 182, s. 1-9
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Tidskriftsartikel (refereegranskat)abstract
- The objective of this prospective study was to determine the prevalence of gait abnormalities in a cohort of Swedish pugs by using an owner-based questionnaire targeting signs of gait abnormality and video footage showing the dog's gait. This study also evaluated associated conditions of abnormal gait, including other health disorders prevalent in the breed. Five hundred and fifty (550) pugs registered in the Swedish Kennel Club, of one, five and eight years of age, in 2015 and 2016, were included in the study. Gait abnormalities were reported in 30.7 per cent of the responses. In the majority of cases, the character of the described gait indicated a neurological cause for the gait abnormality. An association was observed between abnormal gait and age, with gait abnormalities being significantly more common in older pugs (P=0.004). An association was also found between abnormal gait and dyspnoea, with dyspnoea being significantly more common in pugs with gait abnormalities (P<0.0001). This study demonstrated that the prevalence of gait abnormalities was high in the Swedish pug breed and increased with age. Future studies on the mechanisms behind these gait abnormalities are warranted.
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| 15. |
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| 16. |
- Rohdin, Cecilia, et al.
(författare)
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Presence of thoracic and lumbar vertebral malformations in pugs with and without chronic neurological deficits
- 2018
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Ingår i: The Veterinary Journal. - : Elsevier BV. - 1090-0233 .- 1532-2971. ; 241, s. 24-30
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Tidskriftsartikel (refereegranskat)abstract
- Congenital vertebral malformations (CVMs) are common in brachycephalic dogs such as the pug, and are often considered incidental findings. However, specific CVMs have been suggested to be associated with neurological deficits in pugs. The objective of this study was to investigate the clinical importance of CVMs in the pug by comparing computed tomography studies of the thoracolumbar spine from pugs without neurological deficits with those from pugs with a confirmed T3-L3 spinal cord lesion and neurological deficits consistent with a chronic T3-L3 myelopathy. A total of 57 pugs were recruited into the study from Sweden (n=33), United Kingdom (n=21) and Norway (n = 3); 30 with neurological deficits and 27 without. Focal T3-L3 pathology was confirmed in all pugs with neurological deficits by magnetic resonance imaging (n = 29) and/or pathology (n = 15). Computed tomography studies of the thoracolumbar spine from pugs with and without neurological deficits were compared to investigate possible associations between presentation of neurological deficits consistent with chronic T3-L3 pathology and signalment variables, presence of CVMs and type of CVMs. Congenital vertebral malformations were as common in pugs with, as in pugs without, neurological deficits. Regardless of neurological status, the majority of pugs (96%) presented with one or more CVM. An association between presence, or type of CVM in the T1-L3 vertebral column, and neurological deficits consistent with T3-L3 pathology could not be confirmed.
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| 17. |
- Rohdin, Cecilia, et al.
(författare)
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TECPR2 Associated Neuroaxonal Dystrophy in Spanish Water Dogs
- 2015
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 10
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Tidskriftsartikel (refereegranskat)abstract
- Clinical, pathological and genetic examination revealed an as yet uncharacterized juvenile-onset neuroaxonal dystrophy (NAD) in Spanish water dogs. Affected dogs presented with various neurological deficits including gait abnormalities and behavioral deficits. Histopathology demonstrated spheroid formation accentuated in the grey matter of the cerebral hemispheres, the cerebellum, the brain stem and in the sensory pathways of the spinal cord. Iron accumulation was absent. Ultrastructurally spheroids contained predominantly closely packed vesicles with a double-layered membrane, which were characterized as autophagosomes using immunohistochemistry. The family history of the four affected dogs suggested an autosomal recessive inheritance. SNP genotyping showed a single genomic region of extended homozygosity of 4.5 Mb in the four cases on CFA 8. Linkage analysis revealed a maximal parametric LOD score of 2.5 at this region. By whole genome re-sequencing of one affected dog, a perfectly associated, single, non-synonymous coding variant in the canine tectonin beta-propeller repeat-containing protein 2 (TECPR2) gene affecting a highly conserved region was detected (c.4009C>T or p.R1337W). This canine NAD form displays etiologic parallels to an inherited TECPR2 associated type of human hereditary spastic paraparesis (HSP). In contrast to the canine NAD, the spinal cord lesions in most types of human HSP involve the sensory and the motor pathways. Furthermore, the canine NAD form reveals similarities to cases of human NAD defined by widespread spheroid formation without iron accumulation in the basal ganglia. Thus TECPR2 should also be considered as candidate gene for human NAD. Immunohistochemistry and the ultrastructural findings further support the assumption, that TECPR2 regulates autophagosome accumulation in the autophagic pathways. Consequently, this report provides the first genetic characterization of juvenile canine NAD, describes the histopathological features associated with the TECPR2 mutation and provides evidence to emphasize the association between failure of autophagy and neurodegeneration.
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| 18. |
- Rohdin, Cecilia, et al.
(författare)
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Thoracolumbar meningeal fibrosis in pugs
- 2020
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Ingår i: Journal of Veterinary Internal Medicine. - : WILEY. - 0891-6640 .- 1939-1676. ; 34:2, s. 797-807
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Tidskriftsartikel (refereegranskat)abstract
- Background Thoracolumbar myelopathies associated with spinal cord and vertebral column lesions, with a similar clinical phenotype, but different underlying etiologies, occur in pugs. Objectives To further characterize the clinical and neuropathological characteristics of pugs with longstanding thoracolumbar myelopathy. Animals Thirty client-owned pure-bred pugs with a history of more than a month of ataxia and paresis of the pelvic limbs, suggesting a myelopathy localized to the thoracolumbar spinal cord, were included in the study. Methods Prospective clinicopathological study. Included pugs underwent a complete neurological examination and gross and histopathologic postmortem studies with focus on the spinal cord. Computed tomography (n = 18), magnetic resonance imaging (n = 17), and cerebrospinal fluid analysis (n = 27) were performed before or immediately after death. Results Twenty male and 10 female pugs had a median age at clinical onset of 84 months (interquartile range, 66-96). Affected pugs presented with a progressive clinical course and 80% were incontinent. There was circumferential meningeal fibrosis with concomitant focal, malacic, destruction of the neuroparenchyma in the thoracolumbar spinal cord in 24/30 pugs. Vertebral lesions accompanied the focal spinal cord lesion, and there was lympho-histiocytic inflammation associated or not to the parenchymal lesion in 43% of the pugs. Conclusions and Clinical Importance Meningeal fibrosis with associated focal spinal cord destruction and neighboring vertebral column lesions were common findings in pugs with long-standing thoracolumbar myelopathy.
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| 19. |
- Sundstøl Eriksen, Gunnar, et al.
(författare)
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Poisoning of dogs with tremorgenic Penicillium toxins
- 2010
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Ingår i: Medical Mycology. - : Oxford University Press (OUP). - 1369-3786 .- 1460-2709. ; 48, s. 188-196
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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