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Jonathan D. K. Trager, MD
Department of Pediatrics Children's Hospital of Pittsburgh Pittsburgh, PA 15213-2583

Judith M. Martin, MD; Karen Barbadora, MT(ASCP); Michael Green, MD, MPH; Ellen R. Wald, MD
Pittsburgh

Arch Pediatr Adolesc Med. 1996;150(7):766-768.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The leading life-threatening neonatal pathogen in North America is group B Streptococcus (GBS).¹ While early-onset disease has been shown to occur through vertical transmission of GBS from mother to infant, the mode of transmission in late-onset infection has not been clearly defined.^1,2 Over the last 2 decades, studies of infants in newborn nurseries and neonatal intensive care units have demonstrated that horizontal (nosocomial) transmission of GBS occurs between infants and is responsible for the acquisition of GBS in some cases of late-onset disease. These studies provided epidemiologic data^3-5 and microbiologic evidence of the identity of GBS isolated from different patients.^6-10

Knowledge regarding the natural history of colonization with GBS in the infant and child and the role of community acquisition of GBS in the pathogenesis of late-onset disease is incomplete.^1,4,11,12 We describe a case of late-onset GBS sepsis in a 2-month-old infant. The organism was . . . [Full Text PDF of this Article]

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