Scientists from the University of Glasgow in Scotland are reporting they have found a way to treat E. coli O157 infections without causing serious side effects.
The study, published in Infection and Immunity, looks at how the aurodox was able to block E. coli O157 infections. The medication could be used as an anti-virulence therapy for the treatment of these infections.
The compound reduced the ability of E. coli O157 to bind to human cells and, unlike the use of traditional antibiotics in E. coli O157 patients, did not cause the release of toxins. The team showed it did not induce expression of a protein called RecA, which is essential for production of Shiga toxin.
Scotland has one of the highest incidences of E. coli O157 and almost half of such cases in the country are in children less than 16 years old.
Professor Andrew Roe, professor of molecular microbiology and lead author of the paper, said aurodox prevented the E. coli bacteria from binding to human cells and acted as a disease-blocking compound.
“E. coli O157 is a potentially fatal bacteria bug that currently is not recommended for treatment with antibiotics. Our results are encouraging and suggest that this compound could be used as a promising anti-virulence therapy for the treatment of these infections,” he said in the paper.
Researchers characterized the effect of aurodox on the Type Three Secretion System (T3SS) in Enterohaemorrhagic E. coli (EHEC) O157:H7, Enteropathogenic E. coli (EPEC) O127:H6 and Citrobacter rodentium demonstrating the effects are independent of growth.
E. coli O157:H7 is transmitted to humans primarily through contaminated foods such as raw or undercooked ground meats and raw milk. Symptoms include abdominal cramps and diarrhea. The incubation period can range from three to eight days and most people recover within 10 days.
Aurodox is a specialized metabolite of streptomyces goldiniensis discovered in 1973.
T3SSs play a central role in the pathogenesis of many bacterial species. The team found that Aurodox resulted in a concentration dependent inhibition of T3S in EPEC, EHEC and C. rodentium and at the concentrations used (highest of 5 µg/ml) there were no effects on bacterial growth rate or viability in the species tested.
Researchers suggested a model in which aurodox acts upstream of Ler and not directly on the T3SS itself. The T3SS of EHEC and EPEC is encoded by the Locus of Enterocyte Effacement (LEE) Island. This pathogenicity island is regulated by the master regulator, Ler.
The work was funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and done collaboratively with the University of Strathclyde.
Source: Food Safety News