Serotype IV and invasive group B Streptococcus disease in neonates, Minnesota, USA, 2000-2010

Abstract

Group B Streptococcus (GBS) is a major cause of invasive disease in neonates in the United States. Surveillance of invasive GBS disease in Minnesota, USA, during 2000-2010 yielded 449 isolates from 449 infants; 257 had early-onset (EO) disease (by age 6 days) and 192 late-onset (LO) disease (180 at age 7-89 days, 12 at age 90-180 days). Isolates were characterized by capsular polysaccharide serotype and surface-protein profile; types III and Ia predominated. However, because previously uncommon serotype IV constitutes 5/31 EO isolates in 2010, twelve type IV isolates collected during 2000-2010 were studied further. By pulsed-field gel electrophoresis, they were classified into 3 profiles; by multilocus sequence typing, representative isolates included new sequence type 468. Resistance to clindamycin or erythromycin was detected in 4/5 serotype IV isolates. Emergence of serotype IV GBS in Minnesota highlights the need for serotype prevalence monitoring to detect trends that could affect prevention strategies.

Keywords: CPS; GBS; Minnesota; United States; antimicrobial resistance; bacteria; capsular polysaccharide; clindamycin resistance; early-onset GBS disease; group B Streptococcus; invasive GBS disease; late-onset GBS disease; neonatal GBS disease; neonates; prophylaxis; serotype; serotype IV; streptococci.

Figure 1

Distribution of early-onset and late-onset invasive group B Streptococcus disease in infants, by year, Minnesota, USA, 2000–2010. Bars indicate isolates of all capsular polysaccharide serotypes (CPS); line indicates all serotype IV isolates. A total of 257 infants had early-onset and 192 infants late-onset disease; 12 infants had type IV infection.

Figure 2

Incidence of early-onset and late-onset group B Streptococcus disease per 1,000 live births, by year, Minnesota, USA, 2000–2010.

Figure 3

DNA macrorestriction profiles for serotype IV isolates from invasive group B Streptococcus (GBS) disease in infants, Minnesota. Isolates were studied by SmaI digestion and pulsed-field gel electrophoresis (PFGE) analysis and were designated as expressing C-protein α (C-α) or group B protective surface protein (BPS). Lane number is at the top and PFGE profile number at the bottom of each lane. A) Lane 2, λ molecular size standard; lanes 3 and 4, serotype IV/C-α GBS isolates from early-onset disease; lanes 5–7, prototypes of PFGE profile groups 39 (IV/C-α), 38 (IV/C-α), and 37 (IV/C-α and BPS); lane 8, internal standard 89-022 (Ib/C-α and C-β). B) Lane 1, λ molecular size standard; lane 2, PFGE profile 37 prototype (IV/C-α and BPS); lanes 3–6, isolates from late-onset disease; lanes 7–9, isolates from early-onset disease; lane 10, internal standard 89-022. Protein profile of isolates in lanes 2–4, C-α and BPS; lanes 5–8, BPS only. The isolate in lane 9 did not express any of the proteins studied.