Abstract
Introduction. Escherichia coli is a dominant cause of neonatal sepsis for which no prevention measures currently exist. Lactoferrin (LF) is an iron-sequestering antibacterial protein that has been noticed to decrease neonatal late-onset sepsis.Hypothesis/Gap Statement. LF's effect on in vitro growth of neonatal E. coli clinical isolates causing septicaemia is unknown. The prevalence of iron acquisition virulence genes which contribute to pathogenicity outcomes in these strains has also not been described in detail.Aim. To evaluate bovine lactoferrin's (bLF) effects on the in vitro growth of neonatal septicaemia E. coli isolates, and to determine the presence of iron acquisition virulence genes in these isolates.Methodology. E. coli clinical strains isolated from blood of septic neonates, including the archetypal RS218 strain, all representing prevalent phylogroups and multi-locus sequence types among neonatal invasive strains were studied. Strains were grown in batch growth with 0, 0.1, 1.0 and 10 mg ml(-1) bLF. OD measurements over time were used to generate growth curves, and the area under these curves was statistically compared using ANOVA or Kruskal-Wallis tests. Whole-genome sequencing (WGS) data were used to identify iron acquisition genes.Results. For all strains, growth decrease with 10 mg ml(-1) bLF compared to zero was highly significant (P<0.001), and with 1 mg ml(-1) for some strains (P≤0.02). WGS showed that all neonatal strains carried several iron acquisition virulence genes, including chuA, fyuA, irp2 and sitA. Additional siderophore genes were found in some strains.Conclusion. bLF is effective in impairing growth of neonatal sepsis-causing E. coli regardless of the presence of multiple iron acquisition virulence genes.