Route of infection alters virulence of neonatal septicemia Escherichia coli clinical isolates

Abstract

Escherichia 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.

Antibiotic resistance and molecular characterization of bacteremia Escherichia coli isolates from newborns in the United States

“…These studies are relevant because differences in specific molecular traits among neonatal E . coli strains likely determine at least in part the virulence phenotype of these isolates, as we have shown in our studies in vitro and in animal models [60]. Despite the limitations of our study, we believe that the data provide new and relevant information on contemporary resistance rates to several antibiotics in E .…”

Maternal activation of the EGFR prevents translocation of gut-residing pathogenic Escherichia coli in a model of late-onset neonatal sepsis

“…Combining the previous studies with the observation that the enteric route of entry has been shown to contribute to virulence and disease when compared to i.p. injection (43), ACF represents a physiologic route for bacterial translocation. ACF and colonization offer a minimally invasive model of dissemination without pharmacological manipulation or physical breach of the intestinal or skin barriers.…”

cjrABC-senB hinders survival of extraintestinal pathogenic E. coli in the bloodstream through triggering complement-mediated killing

“…To investigate whether cjrABC-senB plays a role in ExPEC bacteremia, we utilized the archetypal K1 bacteremia E. coli strain RS218 [ 14 ], which harbors a copy of cjrABC-senB encoded in the plasmid pRS218 [ 6 ]. Equal numbers of the wild-type RS218 (WT-RS218) and a cjrABC-senB deletion mutant of RS218 (∆ cjr -RS218) were independently inoculated into mice through intraperitoneal injection.…”

“…Bacterial strains and plasmids E. coli K1 strain RS218 (O18:K1:H7) is a bacteremia clinical isolates which is isolated from the cerebrospinal fluid (CSF) from a neonate with meningitis [13][14][15][16]. The spontaneous streptomycin-resistant derivative of RS218 and its derivatives were used in this study ( Table 1).…”