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Enteric gram-negative bacilli bloodstream infections: 17 years' experience in a neonatal intensive care unit

      Abstract

      Objective

      To assess the occurrence of enteric gram-negative bacilli (EGNB) bloodstream infections (BSI) in a neonatal intensive care setting during a 17-year period in which a consistent antibiotic treatment program was in place. To document infections, outbreaks, or epidemics, emergence of antibiotic resistance, clinical correlates, and outcomes of the most prevalent EGNB (Escherichia coli, Klebsiella pneumoniae, and Enterobacter cloacae).

      Methods

      This study analyzed demographic, clinical, and bacteriologic information from 360 infants born 1986-2002 who developed 633 blood culture—proven BSI. A total of 121 EGNB were isolated (E coli, K pneumoniae, and E cloacae). Early-onset BSI were discovered within 48 hours from birth, and late-onset BSI were those that occurred thereafter. Suspected early-onset BSI were treated with ampicillin and gentamicin, suspected late-onset BSI with vancomycin and gentamicin. Antibiotics were changed on the basis of organism antimicrobial susceptibility.

      Results

      Early-onset BSI were noted in 52 of 21,336 (244/100,000) live births (1986-1991), 40 of 20,402 (196/100,000) live births (1992-1997), and 25 of 17,926 (139/100,000) live births (1998-2002). Of these cases, 39 were caused by E coli and 4 by K pneumoniae. Antibiograms for E coli isolated during the last 5 years of the study showed an increase in antibiotic resistance that coincided with obstetric group B streptococcus antepartum antibiotic prophylaxis. Group B streptococcus declined from 41 to 4 cases from the first to the last period. Late-onset BSI increased from 111 to 230 cases from the first to the second 6-year study period and declined modestly (171 cases) during the last. Fifteen percent (78 cases) of late-onset BSI were caused by EGNB, 5% by other gram-negative bacilli, 67% primarily by coagulase-negative staphylococcus, and 13% by fungus. Nonspecific clinical and hematologic signs of late-onset BSI were similar across EGNB species, but necrotizing enterocolitis was often associated with E coli, whereas pneumonia and prolonged thrombocytopenia characterized K pneumoniae infections. No outbreaks or epidemics were observed, and strains of EGNB with evidence of extended spectrum beta-lactamase production were never isolated.

      Conclusion

      Antepartum antibiotic prophylaxis may have increased antibiotic resistance in E coli isolates from early-onset BSI but has dramatically decreased group B streptococcus infections. Late-onset BSI caused by EGNB increased, but without changes in antibiotic susceptibility. In spite of medical advances, E coli, K pneumoniae, and E cloacae remain responsible for significant morbidity and mortality, especially in very low birth weight infants.
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