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PubMed | Institute of Diagnostic Virology Friedrich Loeffler Institute, James Cook University, Marches Veterinary Group, University of Surrey and 2 more.
Type: Journal Article | Journal: Veterinary microbiology | Year: 2014

An outbreak of neurological disease in grower pigs characterised by ataxia and paraparesis was investigated in this study. The outbreak occurred 3-4 weeks post weaning in grower pigs which displayed signs of spinal cord damage progressing to recumbency. Pathology in the affected spinal cords and to a lesser extent in the brainstem was characterised by pronounced inflammation and neuronophagia in the grey matter. Molecular investigation using a pan-virus microarray identified a virus related to porcine sapelovirus (PSV) in the spinal cord of the two affected pigs examined. Analysis of 802 nucleotides of the virus polymerase gene showed the highest homology with those of viruses in the genus Sapelovirus of Picornaviridae. This PSV, strain G5, shared 91-93%, 67-69% and 63% nucleotide homology with porcine, simian and avian sapeloviruses, respectively. The nucleotide homology to other members of the Picornaviridae ranged from 41% to 62%. Furthermore, viral antigen was detected and co-localised in the spinal cord lesions of affected animals by an antibody known to react with PSV. In conclusion, clinical and laboratory observations of the diseased pigs in this outbreak are consistent with PSV-G5 being the causative agent. To the best of the authors knowledge, this is the first unequivocal report of polioencephalomyelitis in pigs by a neuroinvasive PSV in the United Kingdom.


Dagleish M.P.,Moredun Research Institute | Martin S.,Animal Health and Veterinary Laboratories Agency Lasswade | Steele P.,Moredun Research Institute | Finlayson J.,Moredun Research Institute | And 13 more authors.
PLoS ONE | Year: 2015

European red deer (Cervus elaphus elaphus) are susceptible to the agent of bovine spongiform encephalopathy, one of the transmissible spongiform encephalopathies, when challenged intracerebrally but their susceptibility to alimentary challenge, the presumed natural route of transmission, is unknown. To determine this, eighteen deer were challenged via stomach tube with a large dose of the bovine spongiform encephalopathy agent and clinical signs, gross and histological lesions, presence and distribution of abnormal prion protein and the attack rate recorded. Only a single animal developed clinical disease, and this was acute with both neurological and respiratory signs, at 1726 days post challenge although there was significant (27.6%) weight loss in the preceding 141 days. The clinically affected animal had histological lesions of vacuolation in the neuronal perikaryon and neuropil, typical of transmissible spongiform encephalopathies. Abnormal prion protein, the diagnostic marker of transmissible encephalopathies, was primarily restricted to the central and peripheral nervous systems although a very small amount was present in tingible body macrophages in the lymphoid patches of the caecum and colon. Serial protein misfolding cyclical amplification, an in vitro ultra-sensitive diagnostic technique, was positive for neurological tissue from the single clinically diseased deer. All other alimentary challenged deer failed to develop clinical disease and were negative for all other investigations. These findings show that transmission of bovine spongiform encephalopathy to European red deer via the alimentary route is possible but the transmission rate is low. Additionally, when deer carcases are subjected to the same regulations that ruminants in Europe with respect to the removal of specified offal from the human food chain, the zoonotic risk of bovine spongiform encephalopathy, the cause of variant Creutzfeldt-Jakob disease, from consumption of venison is probably very low. © 2015 Dagleish et al.


Laming E.,Moredun Research Institute | Melzi E.,Moredun Research Institute | Scholes S.F.,Animal Health and Veterinary Laboratories Agency Lasswade | Connelly M.,Moredun Research Institute | And 5 more authors.
BMC Research Notes | Year: 2012

Background: Bovine neonatal pancytopenia (BNP) is a syndrome characterised by thrombocytopenia associated with marked bone marrow destruction in calves, widely reported since 2007 in several European countries and since 2011 in New Zealand. The disease is epidemiologically associated with the use of an inactivated bovine virus diarrhoea (BVD) vaccine and is currently considered to be caused by absorption of colostral antibody produced by some vaccinated cows ("BNP dams"). Alloantibodies capable of binding to the leukocyte surface have been detected in BNP dams and antibodies recognising bovine MHC class I and β-2-microglobulin have been detected in vaccinated cattle. In this study, calves were challenged with pooled colostrum collected from BNP dams or from non-BNP dams and their bone marrow hematopoietic progenitor cells (HPC) cultured in vitro from sternal biopsies taken at 24 hours and 6 days post-challenge. Results: Clonogenic assay demonstrated that CFU-GEMM (colony forming unit-granulocyte/erythroid/macrophage/megakaryocyte; pluripotential progenitor cell) colony development was compromised from HPCs harvested as early as 24 hour post-challenge. By 6 days post challenge, HPCs harvested from challenged calves failed to develop CFU-E (erythroid) colonies and the development of both CFU-GEMM and CFU-GM (granulocyte/macrophage) was markedly reduced. Conclusion: This study suggests that the bone marrow pathology and clinical signs associated with BNP are related to an insult which compromises the pluripotential progenitor cell within the first 24 hours of life but that this does not initially include all cell types. © 2012 Laming et al.; licensee BioMed Central Ltd.

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