Association of bovine leukemia virus and Mycobacterium avium subsp paratuberculosis with shedding of Shiga toxin-producing Escherichia coli (STEC)

Authors

  • C. Venegas-Vargas Department Large Animal Clinical Sciences, Michigan State University, East Lansing, MI 48824
  • P. Bartlett Department Large Animal Clinical Sciences, Michigan State University, East Lansing, MI 48824
  • P. Coussens Department Animal Sciences, Michigan State University, East Lansing, MI 48824
  • S. D. Manning Department Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824
  • D. Grooms Department Large Animal Clinical Sciences, Michigan State University, East Lansing, MI 48824

DOI:

https://doi.org/10.21423/aabppro20133818

Keywords:

Shiga-toxin, E. coli, hemolytic uremic syndrome, Bovine leukemia virus, BLV, lymphocytosis, lymphosarcoma, Johnes' disease, chronic disease, contamination

Abstract

Cattle are a reservoir of Shiga toxin-producing Escherichia coli (STEC), which is an important cause of foodborne illness and hemolytic uremic syndrome (HUS) in children. Bovine leukemia virus (BLV) is a retrovirus that causes enzootic bovine leukosis. Most animals infected with BLV never develop clinical signs, but 30% of BLV carriers will develop a persistent lymphocytosis, and< 5% will develop malignant lymphosarcoma. Johnes' disease (JD) is caused by Mycobacterium avium subsp paratuberculosis (MAP), and cattle generally become infected with MAP at a very early age ( < 30 days old), although clinical disease does not typically manifest itself until 3-5 years of age. Recent studies have estimated the herd prevalence of BLV and JD in Michigan dairy herds to be approximately 85% and 50%, respectively. Both diseases are chronic in nature and can have a negative impact on the health and productivity of cattle from both clinical and subclinical effects. Because of their chronic and potentially debilitating nature, secondary health issues are often associated with BLV and JD. Our hypothesis was that cattle infected with BLV and JD were more likely to shed STEC than were uninfected cattle. Our rationale for this hypothesis was that BLV affects the immune system of cattle, which might favor the colonization and shedding of STEC. In the case of JD, the alteration of normal intestinal function and structure could potentially favor the colonization and shedding of STEC in infected cattle. Our objective was to determine whether cattle that test positive for JD and BLV could be a potential target population for the implementation of control strategies to reduce STEC contamination in the human food chain.

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Published

2013-09-19

Issue

Section

Research Summaries 2

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