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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Research Project #430611

Research Project: Characterization of Colonization of Shiga Toxin-producing Escherichia coli (STEC) in Cattle and Strategies for Effective Preharvest Control

Location: Food Safety and Enteric Pathogens Research

2018 Annual Report


4. Accomplishments
1. Identified genetic features unique to super-shed Escherichia coli O157 (O157). Shiga-toxin producing Esherichia coli serotype 0157 causes intestinal disease in humans, but colonizes cattle intestines without causing disease. Cattle that shed O157 in numbers greater than or equal to 10(4) colony forming units per gram of feces are referred to as super-shedders. Super-shedding cattle can easily disseminate O157 within large herds, which may increase transmission to meat at slaughter. The super-shed O157 bacteria may possess unique genetic features contributing to their increased adherence and persistence in the bovine intestinal tract. In a recently completed study by ARS researchers in Ames, Iowa, the genomes of two super-shed O157 strains were sequenced, analyzed and compared to other previously characterized O157 strains. Super-shed O157 have unique, recently acquired, genetic features especially in genes associated with motility, adherence, and metabolism that could influence their persistent colonization of bovine intestines. The proteins encoded by these genes could be developed into blocking therapies aimed at preventing super-shed O157 colonization of cattle. Limiting shedding from cattle is important for maintaining a safe and secure global food supply.

2. Improved a killed whole-cell O157 vaccine formulation to enhance immune responses in cattle. Shiga-toxin producing Esherichia coli serotype 0157 results in foodborne disease in humans, but colonizes cattle intestines without causing disease. Vaccination of cattle is considered an important option for reducing O157 carriage and thereby reducing human illnesses. However most vaccines, especially killed or chemically-inactivated whole-cell bacterial vaccines, require adjuvants (immune response enhancer) for optimal response against vaccine antigens. ARS researchers in Ames, Iowa, performed a study in which cattle were vaccinated with two doses of a vaccine formulation prepared by combining a mutant strain of O157 and a commercially available adjuvant. The vaccine-adjuvant combination not only enhanced immunity against O157 but also efficacy. Specifically, fecal shedding of O157 was significantly reduced after experimental challenge in animals that received the adjuvant formulation. These findings show that vaccine formulations for STEC must be tailored for optimal immune activation and memory response to reduce O157 colonization and fecal shedding in cattle after exposure. Successful vaccination protocols can provide a mechanism for limiting food and environmental contamination, which are critical for reducing transmission of O157 bacteria to humans.


Review Publications
Katani, R., Cote, R., Kudva, I.T., DebRoy, C., Arthur, T.M., Kapur, V. 2017. Comparative genomics of two super-shedder isolates of Escherichia coli O157:H7. PLoS One. 12(8):e0182940. https://doi:10.1371/journal.pone.0182940.

Sharma, V.K., Schaut, R.G., Loving, C.L. 2018. Vaccination with killed whole-cells of Escherichia coli O157:H7 hha mutant emulsified with an adjuvant induced vaccine strain-specific serum antibodies and reduced E. coli O157:H7 fecal shedding in cattle. Veterinary Microbiology. 219:190-199. https://doi.10.1016/j.vetmic.2018.04.003.

Carter, M.Q., Brandl, M., Kudva, I.T., Katani, R., Moreau, M.R., Kapur, V. 2017. Conditional function of autoaggregative protein cah and common cah mutations in Shiga toxin-producing Escherichia coli. Applied and Environmental Microbiology. 84(1):e01739-17. https://doi.org/10.1128/AEM.01739-17.

Schaut, R.G., Loving, C.L., Sharma, V.K. 2018. Escherichia coli O157:H7 virulence factors differentially impact cattle and bison macrophage killing capacity. Microbial Pathogenesis. 118:251-256. https://doi.org/10.1016/j.micpath.2018.03.045.