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Dietary ergot alkaloids as a possible cause of tail necrosis in rabbits
This study describes the association between tail necrosis in rabbits and mycotoxins in rabbit feed. Clinical cases of tail necrosis were observed in 14 out of 103 rabbits kept in an outdoor group housing, fed with hay and a commercial pelleted feed. The observed clinical symptoms, alopecia, erosion...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202174/ https://www.ncbi.nlm.nih.gov/pubmed/25234267 http://dx.doi.org/10.1007/s12550-014-0208-0 |
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author | Korn, A. K. Gross, M. Usleber, E. Thom, N. Köhler, K. Erhardt, G. |
author_facet | Korn, A. K. Gross, M. Usleber, E. Thom, N. Köhler, K. Erhardt, G. |
author_sort | Korn, A. K. |
collection | PubMed |
description | This study describes the association between tail necrosis in rabbits and mycotoxins in rabbit feed. Clinical cases of tail necrosis were observed in 14 out of 103 rabbits kept in an outdoor group housing, fed with hay and a commercial pelleted feed. The observed clinical symptoms, alopecia, erosions, crusts and necrosis were restricted to the tail area and exclusively occurred in young rabbits aged 113 ± 20 days. Dermatological examination suggested that ischemia had caused necrosis. Analysis of blood samples showed an elevated level of creatine kinase. No weight loss occurred in affected rabbits. Trauma caused by injuries or technopathic lesions was also excluded. Histopathologically, the lesions were characterized by acute muscle fibre degeneration and chronic active dermatitis with granulation tissue formation. Necropsy of one rabbit revealed hepatocellular degeneration and necrosis as remarkable findings. Feed analysis for ergot alkaloids by enzyme immunoassays yielded a mean and maximum ergot alkaloid content of 410 ± 250 μg/kg and 1,700 μg/kg, respectively. Faeces of affected rabbits contained ergot alkaloids at levels up to 200 μg/kg. The mean and maximum dietary intake of total ergot alkaloids were 17 and 71 μg/kg bodyweight, respectively. Fusarium toxins (trichothecenes, zearalenone, fumonisins) were also found in the feed, but at levels which did not explain the observed effects. The results indicate that ergot alkaloids may have been the cause of tail necrosis, which is supported by literature data showing that rabbits are especially sensitive towards these toxins. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12550-014-0208-0) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4202174 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-42021742014-10-23 Dietary ergot alkaloids as a possible cause of tail necrosis in rabbits Korn, A. K. Gross, M. Usleber, E. Thom, N. Köhler, K. Erhardt, G. Mycotoxin Res Original Paper This study describes the association between tail necrosis in rabbits and mycotoxins in rabbit feed. Clinical cases of tail necrosis were observed in 14 out of 103 rabbits kept in an outdoor group housing, fed with hay and a commercial pelleted feed. The observed clinical symptoms, alopecia, erosions, crusts and necrosis were restricted to the tail area and exclusively occurred in young rabbits aged 113 ± 20 days. Dermatological examination suggested that ischemia had caused necrosis. Analysis of blood samples showed an elevated level of creatine kinase. No weight loss occurred in affected rabbits. Trauma caused by injuries or technopathic lesions was also excluded. Histopathologically, the lesions were characterized by acute muscle fibre degeneration and chronic active dermatitis with granulation tissue formation. Necropsy of one rabbit revealed hepatocellular degeneration and necrosis as remarkable findings. Feed analysis for ergot alkaloids by enzyme immunoassays yielded a mean and maximum ergot alkaloid content of 410 ± 250 μg/kg and 1,700 μg/kg, respectively. Faeces of affected rabbits contained ergot alkaloids at levels up to 200 μg/kg. The mean and maximum dietary intake of total ergot alkaloids were 17 and 71 μg/kg bodyweight, respectively. Fusarium toxins (trichothecenes, zearalenone, fumonisins) were also found in the feed, but at levels which did not explain the observed effects. The results indicate that ergot alkaloids may have been the cause of tail necrosis, which is supported by literature data showing that rabbits are especially sensitive towards these toxins. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12550-014-0208-0) contains supplementary material, which is available to authorized users. Springer Berlin Heidelberg 2014-09-19 2014 /pmc/articles/PMC4202174/ /pubmed/25234267 http://dx.doi.org/10.1007/s12550-014-0208-0 Text en © The Author(s) 2014 https://creativecommons.org/licenses/by/4.0/ Open Access This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. |
spellingShingle | Original Paper Korn, A. K. Gross, M. Usleber, E. Thom, N. Köhler, K. Erhardt, G. Dietary ergot alkaloids as a possible cause of tail necrosis in rabbits |
title | Dietary ergot alkaloids as a possible cause of tail necrosis in rabbits |
title_full | Dietary ergot alkaloids as a possible cause of tail necrosis in rabbits |
title_fullStr | Dietary ergot alkaloids as a possible cause of tail necrosis in rabbits |
title_full_unstemmed | Dietary ergot alkaloids as a possible cause of tail necrosis in rabbits |
title_short | Dietary ergot alkaloids as a possible cause of tail necrosis in rabbits |
title_sort | dietary ergot alkaloids as a possible cause of tail necrosis in rabbits |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202174/ https://www.ncbi.nlm.nih.gov/pubmed/25234267 http://dx.doi.org/10.1007/s12550-014-0208-0 |
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