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Mouldy feed, mycotoxins and Shiga toxin - producing Escherichia coli colonization associated with Jejunal Hemorrhage Syndrome in beef cattle

BACKGROUND: Both O157 and non-O157 Shiga toxin - producing Escherichia coli (STECs) cause serious human disease outbreaks through the consumption of contaminated foods. Cattle are considered the main reservoir but it is unclear how STECs affect mature animals. Neonatal calves are the susceptible age...

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Autores principales: Baines, Danica, Erb, Stephanie, Turkington, Kelly, Kuldau, Gretchen, Juba, Jean, Masson, Luke, Mazza, Alberto, Roberts, Ray
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135542/
https://www.ncbi.nlm.nih.gov/pubmed/21639911
http://dx.doi.org/10.1186/1746-6148-7-24
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author Baines, Danica
Erb, Stephanie
Turkington, Kelly
Kuldau, Gretchen
Juba, Jean
Masson, Luke
Mazza, Alberto
Roberts, Ray
author_facet Baines, Danica
Erb, Stephanie
Turkington, Kelly
Kuldau, Gretchen
Juba, Jean
Masson, Luke
Mazza, Alberto
Roberts, Ray
author_sort Baines, Danica
collection PubMed
description BACKGROUND: Both O157 and non-O157 Shiga toxin - producing Escherichia coli (STECs) cause serious human disease outbreaks through the consumption of contaminated foods. Cattle are considered the main reservoir but it is unclear how STECs affect mature animals. Neonatal calves are the susceptible age class for STEC infections causing severe enteritis. In an earlier study, we determined that mycotoxins and STECs were part of the disease complex for dairy cattle with Jejunal Hemorrhage Syndrome (JHS). For STECs to play a role in the development of JHS, we hypothesized that STEC colonization should also be evident in beef cattle with JHS. Aggressive medical and surgical therapies are effective for JHS, but rely on early recognition of clinical signs for optimal outcomes suggesting that novel approaches must be developed for managing this disease. The main objective of this study was to confirm that mouldy feeds, mycotoxins and STEC colonization were associated with the development of JHS in beef cattle. RESULTS: Beef cattle developed JHS after consuming feed containing several types of mycotoxigenic fungi including Fusarium poae, F. verticillioides, F. sporotrichioides, Penicillium roqueforti and Aspergillus fumigatus. Mixtures of STECs colonized the mucosa in the hemorrhaged tissues of the cattle and no other pathogen was identified. The STECs expressed Stx1 and Stx2, but more significantly, Stxs were also present in the blood collected from the lumen of the hemorrhaged jejunum. Feed extracts containing mycotoxins were toxic to enterocytes and 0.1% of a prebiotic, Celmanax Trademark, removed the cytotoxicity in vitro. The inclusion of a prebiotic in the care program for symptomatic beef calves was associated with 69% recovery. CONCLUSIONS: The current study confirmed that STECs and mycotoxins are part of the disease complex for JHS in beef cattle. Mycotoxigenic fungi are only relevant in that they produce the mycotoxins deposited in the feed. A prebiotic, Celmanax Trademark, acted as a mycotoxin binder in vitro and interfered with the progression of disease.
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spelling pubmed-31355422011-07-14 Mouldy feed, mycotoxins and Shiga toxin - producing Escherichia coli colonization associated with Jejunal Hemorrhage Syndrome in beef cattle Baines, Danica Erb, Stephanie Turkington, Kelly Kuldau, Gretchen Juba, Jean Masson, Luke Mazza, Alberto Roberts, Ray BMC Vet Res Research Article BACKGROUND: Both O157 and non-O157 Shiga toxin - producing Escherichia coli (STECs) cause serious human disease outbreaks through the consumption of contaminated foods. Cattle are considered the main reservoir but it is unclear how STECs affect mature animals. Neonatal calves are the susceptible age class for STEC infections causing severe enteritis. In an earlier study, we determined that mycotoxins and STECs were part of the disease complex for dairy cattle with Jejunal Hemorrhage Syndrome (JHS). For STECs to play a role in the development of JHS, we hypothesized that STEC colonization should also be evident in beef cattle with JHS. Aggressive medical and surgical therapies are effective for JHS, but rely on early recognition of clinical signs for optimal outcomes suggesting that novel approaches must be developed for managing this disease. The main objective of this study was to confirm that mouldy feeds, mycotoxins and STEC colonization were associated with the development of JHS in beef cattle. RESULTS: Beef cattle developed JHS after consuming feed containing several types of mycotoxigenic fungi including Fusarium poae, F. verticillioides, F. sporotrichioides, Penicillium roqueforti and Aspergillus fumigatus. Mixtures of STECs colonized the mucosa in the hemorrhaged tissues of the cattle and no other pathogen was identified. The STECs expressed Stx1 and Stx2, but more significantly, Stxs were also present in the blood collected from the lumen of the hemorrhaged jejunum. Feed extracts containing mycotoxins were toxic to enterocytes and 0.1% of a prebiotic, Celmanax Trademark, removed the cytotoxicity in vitro. The inclusion of a prebiotic in the care program for symptomatic beef calves was associated with 69% recovery. CONCLUSIONS: The current study confirmed that STECs and mycotoxins are part of the disease complex for JHS in beef cattle. Mycotoxigenic fungi are only relevant in that they produce the mycotoxins deposited in the feed. A prebiotic, Celmanax Trademark, acted as a mycotoxin binder in vitro and interfered with the progression of disease. BioMed Central 2011-06-03 /pmc/articles/PMC3135542/ /pubmed/21639911 http://dx.doi.org/10.1186/1746-6148-7-24 Text en Copyright ©2011 Baines et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Baines, Danica
Erb, Stephanie
Turkington, Kelly
Kuldau, Gretchen
Juba, Jean
Masson, Luke
Mazza, Alberto
Roberts, Ray
Mouldy feed, mycotoxins and Shiga toxin - producing Escherichia coli colonization associated with Jejunal Hemorrhage Syndrome in beef cattle
title Mouldy feed, mycotoxins and Shiga toxin - producing Escherichia coli colonization associated with Jejunal Hemorrhage Syndrome in beef cattle
title_full Mouldy feed, mycotoxins and Shiga toxin - producing Escherichia coli colonization associated with Jejunal Hemorrhage Syndrome in beef cattle
title_fullStr Mouldy feed, mycotoxins and Shiga toxin - producing Escherichia coli colonization associated with Jejunal Hemorrhage Syndrome in beef cattle
title_full_unstemmed Mouldy feed, mycotoxins and Shiga toxin - producing Escherichia coli colonization associated with Jejunal Hemorrhage Syndrome in beef cattle
title_short Mouldy feed, mycotoxins and Shiga toxin - producing Escherichia coli colonization associated with Jejunal Hemorrhage Syndrome in beef cattle
title_sort mouldy feed, mycotoxins and shiga toxin - producing escherichia coli colonization associated with jejunal hemorrhage syndrome in beef cattle
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135542/
https://www.ncbi.nlm.nih.gov/pubmed/21639911
http://dx.doi.org/10.1186/1746-6148-7-24
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