Long-Term Trends in the Epidemiology of Neonatal Sepsis and Antibiotic Susceptibility of Causative Agents

Agnes van den Hoogen, Leo J. Gerards, Malgorzata A. Verboon‐Maciolek, André Fleer, Tannette G. Krediet

Neonatology · 2009 · 200 citations · 24 references

Concepts

Abstract

BACKGROUND: In an era with increased maternal antibiotic use, patterns in early- and late-onset sepsis and antibiotic susceptibility may have changed. OBJECTIVES: To identify longitudinal trends in causative microorganisms for neonatal sepsis and analyze antibiotic susceptibility of all blood isolates of infants with sepsis. METHODS: Early- and late-onset sepsis cases from 29 years (1978-2006) were studied retrospectively, in five clusters of 5 years (period I-V) and one cluster of 4 years (period VI), including antibiotic susceptibility profiles of blood isolates during the years 1999-2006. RESULTS: The incidence of early-onset sepsis decreased (p < 0.01) from 4% during period I (1978-1982) to 1.2% during period VI (2003-2006). 78% of the infants with group B streptococcal (GBS) sepsis were premature during period I, compared to 47% during period VI (p < 0.05). The incidence of early-onset Gram-negative infections remained low during all periods. The incidence of late-onset sepsis, predominantly caused by coagulase-negative staphylococci (CONS) and Staphylococcus aureus, increased since period III from 7.1 to 13.9% in period VI (p < 0.01). Infections due to fungi or yeasts were rare (incidence <0.3%). The majority of CONS blood isolates were oxacillin-resistant, but vancomycin-susceptible. 95% of CONS blood isolates were susceptible for first-generation cephalosporins. Amoxicillin/clavulanic acid-resistant Escherichia coli were infrequent causes of infection. CONCLUSIONS: The incidence of early-onset sepsis mainly caused by GBS decreased. In contrast, the incidence of late-onset sepsis, predominantly caused by CONS, increased significantly. The incidence of fungal and yeast infections remained low. The majority of CONS blood isolates were susceptible for first-generation cephalosporins.

References

24