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Published on: December 18, 2010
Neonatal sepsis due to glycopeptide resistant Enterococcus faecium from colonized maternal gut- rare case evidence
Supram Hosuru Subramanya1, Rajesh Amberpet2,3, Dinesh Chaudhary1
11Department of Medical Microbiology, Manipal College of Medical Sciences, Pokhara, Nepal.
Insights
Maternal gut colonization by vancomycin-resistant Enterococcus faecium (VRE) caused neonatal septicemia. This case highlights the need for maternal VRE screening to prevent infant infections.
Area of Science:
- Neonatal Intensive Care Unit (NICU) infections
- Antimicrobial resistance
- Infectious disease epidemiology
Background:
- Vancomycin-resistant enterococcal (VRE) infections pose a growing global threat, particularly in neonatal intensive care units (NICUs).
- This report details a case of neonatal septicemia caused by multidrug-resistant VRE originating from the mother's gut.
Observation:
- A newborn diagnosed with septicemia and bacteremia was found to be infected with multidrug-resistant VRE.
- Screening identified VRE in both the infant and the mother, with identical genetic profiles (antibiogram, vanA gene, PFGE).
Findings:
- Maternal gut colonization was confirmed as the source of neonatal VRE sepsis.
- The infant successfully responded to a one-week course of oral linezolid, with VRE eradication confirmed by repeat stool cultures.
Implications:
- Implementing optimal infection control measures in NICUs is essential.
- Developing guidelines for monitoring VRE colonization in pregnant women could help reduce neonatal sepsis cases.
Background:
Vancomycin-resistant enterococcal infections in the neonatal ICU are growing global problems. We report a case of neonatal septicemia by multidrug-resistant vancomycin-resistant Enterococcus faecium (VRE), the source of infection being the mother's gut.
Case Presentation:
A newborn male child admitted to the neonatal intensive care unit (NICU) was diagnosed to have mild meconium aspiration syndrome, early onset neonatal septicemia, and bacteremia by multidrug and vancomycin-resistant Enterococcus faecium. Screening of gut flora of the baby and the mother were carried out to trace the source of infection. Stool cultures of the mother and the baby yielded Vancomycin-Resistant Enterococcus faecium. All three isolates of Enterococcus faecium had similar antibiogram, harbored the vanA gene and similar pulsed-field gel electrophoresis pattern. Baby responded to the 1 week therapy with oral linezolid suspension 20 mg/kg/day, 1 ml/t.d.s. No VRE was isolated from baby on a repeat stool culture 1 week after the linezolid therapy. He was discharged with the advice for the continuance of linezolid for seven more days.
Conclusion:
Isolation of MDR-VRE from the blood culture of the baby and stool specimens of the mother and the baby with the same antibiogram profile and clonal similarities reveals that maternal gut colonization was responsible for neonatal sepsis. Optimal infection control measures and the development of guidelines for monitoring VRE colonization in pregnant women might be useful in reducing the occurrence of neonatal sepsis.
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