Abstract
The principal virulence factor of Shiga toxin (Stx)-producing Escherichia coli (STEC), the eponymous Stx, modulates cellular immune responses in cattle, the primary STEC reservoir. We examined whether immunization with genetically inactivated recombinant Shiga toxoids (rStx1MUT/rStx2MUT) influences STEC shedding in a calf cohort. A group of 24 calves was passively (colostrum from immunized cows) and actively (intra-muscularly at 5th and 8th week) vaccinated. Twenty-four calves served as unvaccinated controls (fed with low anti-Stx colostrum, placebo injected). Each group was divided according to the vitamin E concentration they received by milk replacer (moderate and high supplemented). The effective transfer of Stx-neutralizing antibodies from dams to calves via colostrum was confirmed by Vero cell assay. Serum antibody titers in calves differed significantly between the vaccinated and the control group until the 16th week of life. Using the expression of activation marker CD25 on CD4+CD45RO+ cells and CD8αhiCD45RO+ cells as flow cytometry based read-out, cells from vaccinated animals responded more pronounced than those of control calves to lysates of STEC and E. coli strains isolated from the farm as well as to rStx2MUT in the 16th week. Summarized for the entire observation period, less fecal samples from vaccinated calves were stx1 and/or stx2 positive than samples from control animals when calves were fed a moderate amount of vitamin E. This study provides first evidence, that transfer to and induction in young calves of Stx-neutralizing antibodies by Shiga toxoid vaccination offers the opportunity to reduce the incidence of stx-positive fecal samples in a calf cohort.
Highlights
Enterohemorrhagic Escherichia coli (EHEC), a subset of Shiga toxin-producing E. coli (STEC), is a food-borne pathogen that can evoke life-threatening diseases in humans such as hemorrhagic colitis and hemolytic-uremic syndrome
The nStx2Ab titer in 21 of 24 VAC− animals even remained below the detection limit
In the VAC− group, nStx1Ab titers dropped below the detection limit in the 11th week
Summary
Enterohemorrhagic Escherichia coli (EHEC), a subset of Shiga toxin-producing E. coli (STEC), is a food-borne pathogen that can evoke life-threatening diseases in humans such as hemorrhagic colitis and hemolytic-uremic syndrome. The only virulence marker common to all STEC serotypes is the possession of a gene. Long-term studies on anti-Stx antibody titers in serum and fecal STEC shedding by cattle unveiled significantly delayed humoral immune responses following experimental STEC infection [17] and natural exposure [12]. Delayed adaptive cellular immune responses was shown after experimental STEC infection [17]. The principal STEC virulence factor, the eponymous Stx, modulates cellular immune responses in cattle [18,19,20,21]. Current knowledge of STEC shedding dynamics and influences of Stx on immune responses suggests, that Stx may hinder the development of an effective immune response by hitherto immunologically naïve animals upon first STEC contact at early calves’ ages
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