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Mothers a common source of infection in late-onset GBS
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Premature infants had a high rate of group B streptococcus infections, and many likely acquired this illness from their mothers, according to results of a recent study.
Alberto Berardi, MD, of the Azienda Osspedaliero-Universitaria Proclinico in Italy, and colleagues evaluated group B streptococcus (GBS) late-onset disease in about 100 infants between 2003 and 2010. The researchers also collected cultures from the mothers’ breast milk and rectovaginal cultures to determine whether infected breast milk may have contributed to the babies’ GBS disease.
The rate of GBS late-onset disease in full-term neonates was 0.32 per 1,000 live births. The most common presentation of the late-onset disease was meningitis, sepsis or focal infection. Sixty-four percent of 47 mothers were positive for GBS at the rectovaginal site, and 6% of 53 mothers had GBS mastitis, according to the study researchers. In some cases, the milk was infected even when the mother did not have mastitis.
“Intrapartum antibiotic exposure was significantly associated with mild (12 of 22) rather than severe (11 of 45; P=.03) [late-onset disease],” they wrote.
Alberto Berardi, MD, can be reached at berardi.alberto@policlinico.mo.it.
Disclosure: Berardi reports no relevant financial disclosures.
Perspective
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Morven S. Edwards, MD
A prospective cohort study from the GBS Prevention Working Group in Emilia-Romagna, Italy, provides contemporary data helpful in understanding the pathogenesis of late-onset GBS disease. One hundred late-onset disease (LOD) cases were identified over an 8-year period (2003-2010). First, the role of maternal colonization in LOD acquisition was confirmed. Mothers of affected neonates were more likely to have rectovaginal colonization with GBS at the time of the LOD diagnosis (30 of 47 cases) than at the time of antenatal screening (13 of 40 cases; P<.01), supporting the importance of a maternal source for some LOD acquisition.
Next, insight regarding the impact of intrapartum antibiotic prophylaxis (IAP) upon LOD presentation was provided. Infants with IAP for any length of time were older at presentation (mean age, 43.6 days; median 40 days) than those without IAP exposure (mean age, 29 days; median 24 days; P<.01). This is an interesting association but one that that lacks a biological explanation, as does that indicating that neonates born to women receiving IAP were significantly more likely to have a mild (12 of 22), rather than a severe (11 of 45 infants), clinical presentation (P=.03).
Finally, a subset (6%) of mothers had GBS mastitis at the time of LOD presentation, supporting the premise that ingestion of contaminated breast milk can be a route of LOD transmission. However, it is also possible that women with antenatal negative GBS cultures were colonized at delivery, vertically transmitted the GBS to the neonatal upper airway, and the mother’s milk ducts were colonized by the baby.
The overall LOD incidence of 0.32 per 1,000 live births supports the ongoing need for LOD prevention, the promising method being GBS vaccine development. The authors’ finding that 68% of cases occurred among term and another 9% in near-term infants suggests that a GBS glycoconjugate vaccine would prevent most LOD, regardless of mode of acquisition and clinical presentation.
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