Microbiologic Etiology and Infant Factors Associated with Early Onset Neonatal Bacteremia at the Mount Sinai Hospital

Background/Rationale: Early-onset neonatal sepsis (EOS) is often acquired through vertical transmission and is an important cause of morbidity and mortality in infants. The etiology of neonatal sepsis has changed over time, and the intrapartum management of women at risk for infection has been shown to improve neonatal outcomes. Hypothesis or Research Question: To identify the microbiologic etiology of organisms causing EOS and evaluate the impact of maternal illness, labor and delivery practices, and postnatal factors on EOS rates at Mount Sinai Hospital (MSH). Study Design/Methods: An IRB approved descriptive retrospective chart review of cases of EOS in infants less than 7 days of age at MSH from 2015–2018 was conducted. A total of 41 infants were identified. Clinical charts were reviewed and classified into two groups based on age at time of presentation: very early onset sepsis (VEOS) (age days 0–2) and delayed early onset sepsis (DEOS) (age days 3–7). Corresponding maternal charts were also reviewed to identify obstetric risk factors and whether at-risk mothers received appropriate intrapartum prophylaxis. Results: In the VEOS group, 41% of cases were caused by Group B Streptococcus (GBS), 30% by E.coli, and 18% by other Streptococci. In the DEOS group, 33% of cases were coagulase-negative Staphylococci, 27% E.coli, and 20% S. aureus. There were no cases of GBS among the DEOS group. On average, VEOS occurred in term infants (37.40 ± 4.41 weeks) with a normal weight (2840 ± 88g), while DEOS occurred in preterm infants (30.74 ± 6.08 weeks) with a low birth weight (1550 ± 104g). 36.4% of GBS isolates demonstrated resistance to clindamycin. E.coli isolates demonstrated resistance to ampicillin/sulbactam (66.7%), co-trimoxazole (41.7%), and gentamicin (35%). No extended spectrum beta-lactamase-producing E.coli isolates were found in the VEOS or DEOS groups. Within the GBS EOS cases, 63.6% of infants who developed GBS EOS were born to women with a documented GBS negative screening test. Conclusions/Future Plans: The microbiologic etiology of VEOS and DEOS varied, with GBS only identified in the VEOS group and E.coli common in both the VEOS and DEOS groups. The failure to identify GBS colonization in women who give birth to infants that develop GBS EOS requires further exploration. Our study demonstrates the need for both strategies to reduce the risk of E.coli EOS among preterm, low birth weight neonates, as well as further investigation into E.coli EOS resistance patterns.