Aflatoxin, Fumonisin and Shiga Toxin-Producing Escherichia coli Infections in Calves and the Effectiveness of Celmanax®/Dairyman’s Choice™ Applications to Eliminate Morbidity and Mortality Losses

Danica Baines,Mark Sumarah,Gretchen Kuldau,Alberto Mazza,Jean Juba,Luke Masson

doi:10.3390/toxins5101872

Abstract

Mycotoxin mixtures are associated with Shiga toxin-producing Escherichia coli (STEC) infections in mature cattle. STEC are considered commensal bacteria in mature cattle suggesting that mycotoxins provide a mechanism that converts this bacterium to an opportunistic pathogen. In this study, we assessed the mycotoxin content of hemorrhaged mucosa in dairy calves during natural disease outbreaks, compared the virulence genes of the STECs, evaluated the effect of the mucosal mycotoxins on STEC toxin expression and evaluated a Celmanax®/Dairyman’s Choice™ application to alleviate disease. As for human infections, the OI-122 encoded nleB gene was common to STEC genotypes eliciting serious disease. Low levels of aflatoxin (1–3 ppb) and fumonisin (50–350 ppb) were detected in the hemorrhaged mucosa. Growth of the STECs with the mycotoxins altered the secreted protein concentration with a corresponding increase in cytotoxicity. Changes in intracellular calcium indicated that the mycotoxins increased enterotoxin and pore-forming toxin activity. A prebiotic/probiotic application eliminated the morbidity and mortality losses associated with the STEC infections. Our study demonstrates: the same STEC disease complex exists for immature and mature cattle; the significance of the OI-122 pathogenicity island to virulence; the significance of mycotoxins to STEC toxin activity; and, finally, provides further evidence that prebiotic/probiotic applications alleviate STEC shedding and mycotoxin/STEC interactions that lead to disease.

Highlights

Shiga toxin-producing Escherichia coli (STEC) challenges result in hemorrhagic enteritis (HE) in calves and Jejunal Hemorrhage Syndrome (JHS) in weaned to mature cattle [1,2,3,4]
Recordings were performed at 37 °C and the experiment was repeated twice. To validate this as a cytotoxin effect, we examined whether exposure to aflatoxin increased the amount of proteins produced by the STECs under the different growth conditions and applied the proteins to a lawn of bovine colonic cells to evaluate any changes in cytotoxicity in vitro (Table 4)
The current study determined that STEC co-infections are associated with HE cases in calves less than one month old

Summary

Introduction

STEC challenges result in hemorrhagic enteritis (HE) in calves and Jejunal Hemorrhage Syndrome (JHS) in weaned to mature cattle [1,2,3,4]. Stx suppresses the activation and proliferation of intraepithelial lymphocytes and macrophages from the mucosa of cattle [6,10], while Stx increases STEC colonization of bovine colonic cells in vitro [11]. This suggests that there is a role for Stxs in enhancing the expression of HE through an impairment of the intestinal defense system and increasing the ability of STEC to colonize the intestinal tract. The composition of STEC infections in natural disease outbreaks support a role for co-infections in the development of serious disease in immature and mature cattle [1,2], but the role of virulence genes in promoting co-infection is unclear. Understanding the composition and genetic nature of STEC infections in cattle is critical to developing a solution for breaking the transmission chain to food products

Results

Discussion

Conclusion