Evaluation of the Virulence Factor Profile of Avian Pathogenic Escherichia Coli in Clinical Isolates of Avian Samples in Caloto, Cauca, Colombia

Abstract

Avian pathogenic E. coli (APEC), produces an extraintestinal infection in chickens, turkeys, and other types of birds, called colibacillosis, and is considered one of the main causes of economic losses due to morbidity, mortality, and the disposal of poultry carcasses. The objective of the present study was to characterize the genetic profile of the virulence factors of different isolates of avian E. coli in Caloto, Cauca, Colombia. Materials and methods: E. coli was isolated and identified by biochemical tests, from 47 clinical isolates. Subsequently, the DNA was extracted using Chelex. Three multiplex PCRs were designed to amplify 13 virulence factors (iroN, hlyF, iss, iutA, frz, vat, sitA, KpsM, sitD, fimH, pstB, sopB, and uvrY), using primers previously reported for each. The amplification products were verified on agarose gels. Each isolate was classified according to the number of virulence factors: group A (between 10 and 13), group B (between 5 and 9), and group C (4 or less). Conclusion: we were able to identify the presence of a group of virulence factors in clinical isolates of APEC, which allows us to demonstrate that both the frequency and the profile of virulence factors in the isolated strains showed a different profile than the reported by other authors. The virulence genes pstB and fimH were detected in all of our samples, and the iss gene was the one with the lowest frequency. And according to the number of virulence factors, the group A was the most frequent.

Enterococcus faecalisOG1RF Evolution at Low pH Selects Fusidate-sensitive Mutants in Elongation Factor G and at High pH Selects Defects in Phosphate Transport

“…Mutations in fusA may confer resistance to fusidic acid (35, 36); but our fusA mutants show a tradeoff of fusidate sensitivity. The pts loci are associated with virulence (37, 38). In our biofilm-evolved strains, base-selected mutations in pstABC and in pyrR (pyrimidine biosynthesis regulator) led to small-colony growth, a class of phenotype associated with virulence in clinical strains (39, 40).…”