Route of infection alters virulence of neonatal septicemia Escherichia coli clinical isolates
AuthorCole, Bryan K.
Akins, Darrin R.
Dyer, David W.
AffiliationUniv Arizona, Dept Pediat
MetadataShow full item record
PublisherPUBLIC LIBRARY SCIENCE
CitationRoute of infection alters virulence of neonatal septicemia Escherichia coli clinical isolates 2017, 12 (12):e0189032 PLOS ONE
Rights© 2017 Cole et al. This is an open access article distributed under the terms of the Creative Commons Attribution License.
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AbstractEscherichia coli is the leading cause of Gram-negative neonatal septicemia in the United States. Invasion and passage across the neonatal gut after ingestion of maternal E. coli strains produce bacteremia. In this study, we compared the virulence properties of the neonatal E. coli bacteremia clinical isolate SCB34 with the archetypal neonatal E. coli meningitis strain RS218. Whole-genome sequencing data was used to compare the protein coding sequences among these clinical isolates and 33 other representative E. coli strains. Oral inoculation of newborn animals with either strain produced septicemia, whereas intraperitoneal injection caused septicemia only in pups infected with RS218 but not in those injected with SCB34. In addition to being virulent only through the oral route, SCB34 demonstrated significantly greater invasion and transcytosis of polarized intestinal epithelial cells in vitro as compared to RS218. Protein coding sequences comparisons highlighted the presence of known virulence factors that are shared among several of these isolates, and revealed the existence of proteins exclusively encoded in SCB34, many of which remain uncharacterized. Our study demonstrates that oral acquisition is crucial for the virulence properties of the neonatal bacteremia clinical isolate SCB34. This characteristic, along with its enhanced ability to invade and transcytose intestinal epithelium are likely determined by the specific virulence factors that predominate in this strain.
NoteOpen access journal.
VersionFinal published version
SponsorsOklahoma INBRE program from NIH/NIGMS [8P20GM103447]