855. Evolution of Group B Streptococcal Capsular Type V Invasive Infections in Neonates and Young Infants: A Whole Genome Sequencing Study

Abstract

Background

Since 1970 group B Streptococcus (GBS) has been a frequent cause of sepsis or meningitis in young infants. Capsular polysaccharide type V was first recognized in 1990 and has increased to the point where it now causes ~15% of GBS infections. GBS type V strains are almost entirely sequence type 1 (ST1) in adult infections. To understand the emergence of type V GBS, we compared infant strains before 1990 to more contemporary isolates from young infants and adults.

Methods

Thirty-five strains isolated from blood or CSF of infants <90 days of age (Houston, 1979–1996) were compared with the following previously sequenced type V, ST1 strains: (1) 14 from infant blood or CSF from Center for Disease Control and Prevention (CDC) (2015–2017), (2) 193 blood ST1 isolates from adults (Houston, 1992–2013), and (3) 516 invasive isolates from the CDC (2015–2017). Isolates were sequenced using an Illumina MiSeq instrument followed by molecular typing, antimicrobial resistance gene determination, and phylogenetic analysis. Antimicrobial susceptibility testing (AST) was performed using disk diffusion and E-test.

Results

The majority (29/35) of Houston young infant strains were ST1. Type V GBS strains isolated prior to 1990 were more likely to be of ST-2 or ST-26 (5/10) compared with those from 1990 or later (24/25 and 14/14 CDC infant invasive type V). Tetracycline resistance was identified in 83% (29/35) while macrolide resistance (MR) occurred in only 23% (8/35) of the strains. Compared with early neonatal isolates, MR was significantly more frequent among contemporary neonatal (12/14, 86%, P < 0.0001) and adult (502/710, 71%, P < 0.0001) ST1 GBS. Phylogenetic analysis showed two distinct clades defined, in part, by MR. A high-frequency MR (340/360, 94%) clade was defined by the presence of erm(B) on Tn3872 while the low-frequency MR clade (159/350, 45%) was more diverse in mobile elements contributing to MR. The majority (27/29) of early neonatal ST1 GBS strains were observed in the low-frequency MR clade.

Conclusion

Infant invasive disease due to type V GBS before 1990 consisted of more diverse STs but is now almost exclusively ST1. Differences in the frequency of MR between early neonatal and contemporary type V ST1 GBS suggest MR may, at least in part, have driven the expansion of type V ST1 GBS.

Disclosures

All Authors: No reported Disclosures.