47 research outputs found

    Seizure disorders in 43 cattle

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    BACKGROUND: Large animals have a relatively high seizure threshold, and in most cases seizures are acquired. No published case series have described this syndrome in cattle. OBJECTIVES: To describe clinical findings and outcomes in cattle referred to the Veterinary Teaching Hospital of the University of Turin (Italy) because of seizures. ANIMALS: Client‐owned cattle with documented evidence of seizures. METHODS: Medical records of cattle with episodes of seizures reported between January 2002 and February 2014 were reviewed. Evidence of seizures was identified based on the evaluation of seizure episodes by the referring veterinarian or 1 of the authors. Animals were recruited if physical and neurologic examinations were performed and if diagnostic laboratory test results were available. RESULTS: Forty‐three of 49 cases fulfilled the inclusion criteria. The mean age was 8 months. Thirty‐one animals were male and 12 were female. Piedmontese breed accounted for 39/43 (91%) animals. Seizures were etiologically classified as reactive in 30 patients (70%) and secondary or structural in 13 (30%). Thirty‐six animals survived, 2 died naturally, and 5 were euthanized for reasons of animal welfare. The definitive cause of reactive seizures was diagnosed as hypomagnesemia (n = 2), hypocalcemia (n = 12), and hypomagnesemia‐hypocalcemia (n = 16). The cause of structural seizures was diagnosed as cerebrocortical necrosis (n = 8), inflammatory diseases (n = 4), and lead (Pb) intoxication (n = 1). CONCLUSION AND CLINICAL IMPORTANCE: The study results indicate that seizures largely are reported in beef cattle and that the cause can be identified and successfully treated in most cases

    Morganella morganii septicemia and concurrent renal crassicaudiasis in a Cuvier’s beaked whale (Ziphius cavirostris) stranded in Italy

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    Information regarding bacterial diseases in Cuvier's beaked whale (CBW, Ziphius cavirostris) is scattered and mostly incomplete. This report describes a case of septicemia by Morganella morganii in a juvenile male CBW with concurrent renal crassicaudiasis. The animal stranded along the Ligurian coastline (Italy) and underwent a systematic post-mortem examination to determine the cause of death. Histopathology showed lesions consistent with a septicemic infection, severe meningoencephalitis, and renal crassicaudiasis. An M. morganii alpha-hemolytic strain was isolated in pure culture from liver, lung, prescapular lymph node, spleen, hepatic and renal abscesses, and central nervous system (CNS). The antimicrobial susceptibility profile of the strain was evaluated with the minimum inhibitory concentrations (MICs) method and reduced susceptibility to Trimethoprim-Sulfamethoxazole is reported. Crassicauda sp. nematodes were retrieved from both kidneys. No other pathogens were detected by immunohistochemistry, serology, or biomolecular analyses. Toxicological investigations detected high concentrations of immunosuppressant pollutants in the blubber. The chronic parasitic infestation and the toxic effects of xenobiotics likely compromised the animal's health, predisposing it to an opportunistic bacterial infection. To our knowledge, this is the first description of M. morganii septicemia with CNS involvement in a wild cetacean

    Genetic Predictions of Prion Disease Susceptibility in Carnivore Species Based on Variability of the Prion Gene Coding Region

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    Mammalian species vary widely in their apparent susceptibility to prion diseases. For example, several felid species developed prion disease (feline spongiform encephalopathy or FSE) during the bovine spongiform encephalopathy (BSE) epidemic in the United Kingdom, whereas no canine BSE cases were detected. Whether either of these or other groups of carnivore species can contract other prion diseases (e.g. chronic wasting disease or CWD) remains an open question. Variation in the host-encoded prion protein (PrP(C)) largely explains observed disease susceptibility patterns within ruminant species, and may explain interspecies differences in susceptibility as well. We sequenced and compared the open reading frame of the PRNP gene encoding PrP(C) protein from 609 animal samples comprising 29 species from 22 genera of the Order Carnivora; amongst these samples were 15 FSE cases. Our analysis revealed that FSE cases did not encode an identifiable disease-associated PrP polymorphism. However, all canid PrPs contained aspartic acid or glutamic acid at codon 163 which we propose provides a genetic basis for observed susceptibility differences between canids and felids. Among other carnivores studied, wolverine (Gulo gulo) and pine marten (Martes martes) were the only non-canid species to also express PrP-Asp163, which may impact on their prion diseases susceptibility. Populations of black bear (Ursus americanus) and mountain lion (Puma concolor) from Colorado showed little genetic variation in the PrP protein and no variants likely to be highly resistant to prions in general, suggesting that strain differences between BSE and CWD prions also may contribute to the limited apparent host range of the latter

    Discontools: Identifying gaps in controlling bovine spongiform encephalopathy.

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    This article summarizes the 2016 update of the DISCONTOOLS project gap analysis on bovine spongiform encephalopathy (BSE), which was based on a combination of literature review and expert knowledge. Uncertainty still exists in relation to the pathogenesis, immunology and epidemiology of BSE, but provided that infected material is prohibited from entering the animal feed chain, cases should continue to decline. BSE does not appear to spread between cattle, but if new strains with this ability appear then control would be considerably more difficult. Atypical types of BSE (L-BSE and H-BSE) have been identified, which have different molecular patterns and pathology, and do not display the same clinical signs as classical BSE. Laboratory transmission experiments indicate that the L-BSE agent has zoonotic potential. There is no satisfactory conclusion regarding the origin of the BSE epidemic. C-BSE case numbers declined rapidly following strict controls banning ruminant protein in animal feed, but occasional cases still occur. It is unclear whether these more recent cases indicate inadequate implementation of the bans, or the possibility that C-BSE might occur spontaneously, as has been postulated for H- and L-BSE. All of this will have implications once existing bans and levels of surveillance are both relaxed. Immunochemical tests can only be applied post-mortem. There is no immunological basis for diagnosis in the live animal. All aspects of disease control are expensive, particularly surveillance, specified risk material removal and feed controls. There is pressure to relax feed controls, and concurrent pressure from other sources to reduce surveillance. While the cost benefit argument can be applied successfully to either of these approaches, it would be necessary to maintain the ban on intraspecies recycling and some baseline surveillance. However, the potential risk is not limited to intraspecies recycling; recycling with cross-species transmission may be an ideal way to select or/and modify properties of transmissible spongiform encephalopathies agents in the future
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