BACKGROUND: Late-onset sepsis is a major problem in neonatology, but the habitat of the pathogens before bloodstream invasion occurs is not well established. METHODS: We examined prospectively collected stools from premature infants with sepsis to find pathogens that subsequently invaded their bloodstreams, and sought the same organisms in stools of infants without sepsis. Culture-based techniques were used to isolate stool bacteria that provisionally matched the bloodstream organisms, which were then genome sequenced to confirm or refute commonality. RESULTS: Of 11 children with late-onset neonatal bloodstream infections, 7 produced at least 1 stool that contained group B Streptococcus (GBS), Serratia marcescens, or Escherichia coli before their sepsis episode with provisionally matching organisms. Of 96 overlap comparison subjects without sepsis temporally associated with these cases, 4 were colonized with provisionally matching GBS or S. marcescens. Of 175 comparisons of stools from randomly selected infants without sepsis, 1 contained a GBS (this infant had also served as an overlap comparison subject and both specimens contained provisionally matching GBS). Genome sequencing confirmed common origin of provisionally matching fecal and blood isolates. The invasive E. coli were present in all presepticemic stools since birth, but gut colonization with GBS and S. marcescens occurred closer to time of bloodstream infection. CONCLUSIONS: The neonatal gut harbors sepsis-causing pathogens, but such organisms are not inevitable members of the normal microbiota. Surveillance microbiology, decolonization, and augmented hygiene might prevent dissemination of invasive bacteria between and within premature infants.
BACKGROUND: Late-onset sepsis is a major problem in neonatology, but the habitat of the pathogens before bloodstream invasion occurs is not well established. METHODS: We examined prospectively collected stools from premature infants with sepsis to find pathogens that subsequently invaded their bloodstreams, and sought the same organisms in stools of infants without sepsis. Culture-based techniques were used to isolate stool bacteria that provisionally matched the bloodstream organisms, which were then genome sequenced to confirm or refute commonality. RESULTS: Of 11 children with late-onset neonatal bloodstream infections, 7 produced at least 1 stool that contained group B Streptococcus (GBS), Serratia marcescens, or Escherichia coli before their sepsis episode with provisionally matching organisms. Of 96 overlap comparison subjects without sepsis temporally associated with these cases, 4 were colonized with provisionally matching GBS or S. marcescens. Of 175 comparisons of stools from randomly selected infants without sepsis, 1 contained a GBS (this infant had also served as an overlap comparison subject and both specimens contained provisionally matching GBS). Genome sequencing confirmed common origin of provisionally matching fecal and blood isolates. The invasive E. coli were present in all presepticemic stools since birth, but gut colonization with GBS and S. marcescens occurred closer to time of bloodstream infection. CONCLUSIONS: The neonatal gut harbors sepsis-causing pathogens, but such organisms are not inevitable members of the normal microbiota. Surveillance microbiology, decolonization, and augmented hygiene might prevent dissemination of invasive bacteria between and within premature infants.
Entities:
Keywords:
Escherichia coli; Serratia marcescens; group B streptococci; septicemia; whole-genome sequencing
Authors: Romina Libster; Kathryn M Edwards; Fatma Levent; Morven S Edwards; Marcia A Rench; Luis A Castagnini; Timothy Cooper; Robert C Sparks; Carol J Baker; Prachi E Shah Journal: Pediatrics Date: 2012-06-11 Impact factor: 7.124
Authors: Melissa S Bauserman; Matthew M Laughon; Christoph P Hornik; P Brian Smith; Daniel K Benjamin; Reese H Clark; Cyril Engmann; Michael Cohen-Wolkowiez Journal: Pediatr Infect Dis J Date: 2013-03 Impact factor: 2.129
Authors: Evan S Snitkin; Adrian M Zelazny; Pamela J Thomas; Frida Stock; David K Henderson; Tara N Palmore; Julia A Segre Journal: Sci Transl Med Date: 2012-08-22 Impact factor: 17.956
Authors: Norelle L Sherry; Jessica L Porter; Torsten Seemann; Andrew Watkins; Timothy P Stinear; Benjamin P Howden Journal: J Clin Microbiol Date: 2013-02-13 Impact factor: 5.948
Authors: Juliette C Madan; Richard Cowper Salari; Deepti Saxena; Lisa Davidson; George A O'Toole; Jason H Moore; Mitchell L Sogin; James A Foster; William H Edwards; Paul Palumbo; Patricia L Hibberd Journal: Arch Dis Child Fetal Neonatal Ed Date: 2012-05-06 Impact factor: 5.747
Authors: Claudio U Köser; Matthew T G Holden; Matthew J Ellington; Edward J P Cartwright; Nicholas M Brown; Amanda L Ogilvy-Stuart; Li Yang Hsu; Claire Chewapreecha; Nicholas J Croucher; Simon R Harris; Mandy Sanders; Mark C Enright; Gordon Dougan; Stephen D Bentley; Julian Parkhill; Louise J Fraser; Jason R Betley; Ole B Schulz-Trieglaff; Geoffrey P Smith; Sharon J Peacock Journal: N Engl J Med Date: 2012-06-14 Impact factor: 91.245
Authors: Simon R Harris; Edward J P Cartwright; M Estée Török; Matthew T G Holden; Nicholas M Brown; Amanda L Ogilvy-Stuart; Matthew J Ellington; Michael A Quail; Stephen D Bentley; Julian Parkhill; Sharon J Peacock Journal: Lancet Infect Dis Date: 2012-11-14 Impact factor: 25.071
Authors: Volker Mai; Roberto Murgas Torrazza; Maria Ukhanova; Xiaoyu Wang; Yijun Sun; Nan Li; Jonathan Shuster; Renu Sharma; Mark Lawrence Hudak; Josef Neu Journal: PLoS One Date: 2013-01-14 Impact factor: 3.240
Authors: Hannah M Rowe; Brett R Hanson; Donna L Runft; Qian Lin; Steve M Firestine; Melody N Neely Journal: Infect Immun Date: 2015-02-02 Impact factor: 3.441
Authors: Sukantha Chandrasekaran; Carey-Ann D Burnham; Barbara B Warner; Phillip I Tarr; Todd N Wylie Journal: Clin Infect Dis Date: 2018-07-02 Impact factor: 9.079
Authors: Benjamin D Reed; Kurt R Schibler; Hitesh Deshmukh; Namasivayam Ambalavanan; Ardythe L Morrow Journal: J Pediatr Date: 2018-03-16 Impact factor: 4.406