Late-Onset Infection With CC17 GBS a Result of Mother-Infant Transmission

According to data published in Clinical Infectious Diseases, the high prevalence of CC17 group B Streptococcus (GBS) in cases of late-onset disease is likely a result of enhanced mother-to-infant postpartum transmission.

CC17 GBS is a hypervirulent clone responsible for late-onset disease; therefore, study investigators conducted a multicenter study in France to evaluate GBS colonization in 890 mother-baby pairs. Maternal vaginal samples and infant oral cavity and stool samples were analyzed at delivery and 21±7 days and 60±7 days postdelivery.

GBS colonized 7%, 21%, and 23% of the infants at birth, at day 21, and at day 60, respectively. Of these infants, CC17 GBS was identified in 10%, 11%, and 13% of the infants, at birth, day 21, and day 60, respectively. Concordance between maternal and infant GBS type was 96%.

The main risk factors for infant colonization with GBS at day 21 were simultaneous maternal colonization of the vagina (odds ratio [OR] 4.50; 95% CI, 1.69-15.61) and breast milk (OR, 7.93; 95% CI, 3.81-17.14). Of the infants colonized by CC17 GBS, 38% (95% CI, 23%-56%) appeared colonized for the first time at day 60, whereas the same was true for 18% of infants colonized by non-CC17 GBS. A multivariate analysis revealed a higher risk for de novo colonization at day 60 by CC17 than any other strain of GBS (OR, 2.45; 95% CI, 1.02-5.88).        

However, roughly one-third of participants did not complete follow-up, resulting in a loss of statistical power and the potential underestimation of the role of some variables. The study also did not include preterm infants, who represent up to 25% of cases of late-onset disease in France, as the aim was “to assess GBS colonization in infants without being biased by risk factors for infection.” The study investigators also conceded that the methods of GBS detection may suffer from a lack of sensitivity, and that the role of further environmental sources, such as colonization of other family members, was not investigated.

The researchers concluded that the results suggested that CC17 clones do not have increased colonization abilities, but rather, “the hypervirulent CC17 clone preferentially establishes or multiplies in the infant gut at a particular postdelivery time that coincides with that of [late-onset disease].” However, they noted that whether late-onset disease is a result of increased invasiveness or greater host susceptibility to infections at this point in development remains to be seen. Researchers further suggested that “these data need to be considered for the development of preventive strategies against GBS [late-onset disease], which is largely due to CC17 GBS,” and recommended future studies to determine, “whether specific management of infants born to CC17-colonized mothers could be indicated for [late-onset disease] prevention.”

Reference

Tazi A, Plainvert C, Anselem O, et al. Risk factors for infant colonization by hypervirulent CC17 Group B Streptococcus: Toward the understanding of late-onset disease [published online April 4, 2019]. Clin Infect Dis. doi:10.1093/cid/ciz033