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Fecal isolates of Clostridium difficile and its toxin B were followed prospectively in 50 preterm intensive care nursery (ICN) patients. The first stool specimen was obtained after 1 week of enteral feeding, at 15 ± 1 days of life, and 2 more specimens were collected at 2-week intervals, 24 ± 1 and 32 ± 2 days of life. The stools were cultured for C. difficile, and tested for C.difficile toxin B. In the first specimen 15% of stools grew C.difficile. In the second specimen C. difficile isolation rates increased to 33% and plateaued. Toxin B was detected in 71, 93 and 100% of culture-positive stools in the first, second, and third specimens, respectively. C.difficile colonization was not associated with a higher incidence of necrotizing enterocolitis or diarrhea, and using precollected, frozen human milk did not protect from C.difficile colonization.

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We undertook to determine Staphylococcus epidermidis colonization patterns and risks of sepsis in a cohort of 82 consecutive intensive care nursery admissions (birth weight 1,285 ± 57 g), with 24 infants weighing < 1,000 g at birth. Colonization was determined by skin and stool cultures collected at three time points. Multiple neonatal variables were classified into three intervals preceding the time of sample collection including the occurrence of S.epidermidis sepsis. 16 infants (20%) developed S.epidermidis sepsis. 81% of these episodes occurred in infants < 1,000 g. Skin colonization was nearly universal at all sampling points. Rectal colonization was 63.6% initially (10 ± 0.4 days), then declined to 32% by the third sample (37 ± 0.4 days). Neither prevalence of skin nor rectal colonization influenced the incidence of sepsis significantly. Statistically significant risk associations for sepsis for the entire intensive care nursery population included: low birth weight, gestational age, presence of a central line, and delayed feeding. For infants < 1,000 g the occurrence of sepsis during the second study time period (54% of the episodes) was associated with preceding steroid exposure. During the third study time period, birth weight and delayed attainment of full enteral feeds showed a statistically significant association with sepsis. We conclude that infants < 1,000 g are at an increased risk of S.epidermidis sepsis. Extreme immaturity, steroid therapy, and prolonged hyperalimentation are all significant risk associations.

Human neonates are immunologically immature, particularly in their humoral antibody responses to T cell-independent antigens, as exemplified by their increased susceptibility to infections with polysaccharide-encapsulated bacteria. To clarify the mechanism(s) underlying the unresponsiveness of neonates to polysaccharide antigens, we used an in vitro model with neonatal cord blood cells that has been shown to mimic surface Ig-dependent signaling in the adult by T cell-independent antigens. We studied the ability of cord blood human B cells to become activated after ligation of their surface Ig by unconjugated anti-Ig, dextran-conjugated anti-Ig, and Staphylococcus aureus Cowan A1, and compared their response with that of adult B cells. After the addition of nanogram concentrations of anti-Ig-dextran, neonatal cord blood B cells proliferated at levels comparable to that observed with adult B cells. The majority of cord blood B cells showed a marked rise in intracellular calcium, increased surface expression of human leukocyte antigen DR, and an increase in cell size. Direct activation of protein kinase C by phorbol esters in neonatal B cells led to cellular proliferation, and when combined with anti-Ig, a synergistic effect on proliferation was observed. These data suggest that the unresponsiveness of human neonates to polysaccharide antigens does not represent an inability of these antigens to induce early activation events in circulating B cells.