Serotype IV and Invasive Group B Streptococcus Disease in Neonates, Minnesota, USA, 2000–2010¹

Patricia Ferrieri

, Ruth Lynfield, Roberta Creti, and Aurea E. Flores

Author affiliations: University of Minnesota Medical School, Minneapolis, Minnesota, USA (P. Ferrieri, A.E. Flores); Minnesota Department of Health, St. Paul, Minnesota, USA (R. Lynfield); Istituto Superiore di Sanità, Rome, Italy (R. Creti)

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.

Streptococcus agalactiae, or group B Streptococcus (GBS), is one of the leading causes of invasive bacterial diseases, such as bacteremia, pneumonia, and meningitis, in newborns and infants in the first months of life in the United States (1,2) and in other parts of the world (3–6). In newborns birth through 6 days of age, invasive GBS disease is designated as early-onset (EO) and late-onset (LO) in infants 7 days to 3 months of age; some investigators report an ultra-late period extending well beyond 3 months of age (3).
During the past 20 years, prevention of EO and LO invasive GBS disease in the United States has been an area of interest for clinicians and public health officials. In the early 1990s, the overall rate of EO disease in the United States was 1.7/1,000 live-born infants (7,8) but differed from one part of the country to another: for example, 0.56 for Minneapolis/St. Paul, 1.3 for Houston (9), and 1.3 for Maryland (10). This high rate prompted the Centers for Disease Control and Prevention (CDC) to issue guidelines in 1996 for preventing EO disease by screening pregnant women at 35–37 weeks’ gestation for GBS colonization and administering antimicrobial drug prophylaxis to women at risk of transmitting the organism to the child (11). Although implementation of the prescribed measures reduced the rate of EO disease in the United States to 0.47/1,000 live births by 1999–2001, problems remained (e.g., risk-based vs. culture-based approaches to prevention, laboratory detection of colonized mothers, use of antimicrobial drugs in women with allergies to penicillin, use of secondary prevention among infants) (12); these factors required revision of the guidelines in 2002 (7) and again in 2010 (13). However, measures designed to prevent EO disease have had little effect on the rate of LO disease, which remained 0.4/1,000 live births throughout the 1990s, varying only slightly from year to year (8,12).
GBS isolates are characterized according to capsular polysaccharide (CPS) serotype, of which 9 are recognized: Ia, Ib, II–VIII (9, 14–16), and a recently proposed serotype IX (17). Results from earlier studies in various parts of the United States, including Minnesota, indicated that Ia, III, and V were the predominant serotypes in EO disease, whereas serotype III and Ia were predominant in LO disease (9,10,12,15).
Since 1995, our laboratory has collaborated with the Minnesota Department of Health (MDH) to serotype isolates from cases of EO and LO disease in Minnesota in conjunction with the CDC Emerging Infections Program (7). This collaboration has enabled us to follow for almost 2 decades changes in serotype distribution of GBS isolates that cause invasive disease in Minnesota. Here we report on the epidemiology of EO and LO GBS disease in Minnesota over 11 years, the recent emergence of invasive disease in infants with serotype IV GBS, and an increase in disease caused by this serotype in 2010 compared with our previous findings (15). We provide serotyping results of all isolates from EO and LO disease collected during 2000–2010 and present data from molecular characterization by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST) of serotype IV isolates from EO and LO disease.