Abstract
We characterised Lancefield group B streptococcal (GBS) isolates causing invasive disease among non-pregnant adults in Portugal between 2009 and 2015. All isolates (n = 555) were serotyped, assigned to clonal complexes (CCs) by multilocus sequence typing and characterised by surface protein and pilus island gene profiling. Antimicrobial susceptibility was tested by disk diffusion and resistance genotypes identified by PCR. Overall, serotype Ia was most frequent in the population (31%), followed by serotypes Ib (24%) and V (18%). Serotype Ib increased significantly throughout the study period (p < 0.001) to become the most frequent serotype after 2013. More than 40% of isolates clustered in the CC1/alp3/PI-1+PI-2a genetic lineage, including most isolates of serotypes Ib (n = 110) and V (n = 65). Erythromycin and clindamycin resistance rates were 35% and 34%, respectively, both increasing from 2009 to 2015 (p < 0.010) and associated with CC1 and serotype Ib (p < 0.001). The Ib/CC1 lineage probably resulted from acquisition of the type Ib capsular operon in a single recombination event by a representative of the V/CC1 macrolide-resistant lineage. Expansion of the new serotype Ib/CC1 lineage resulted in increased macrolide resistance in GBS, causing invasive disease among adults in Portugal. The presence of this clone elsewhere may predict more widespread increase in resistance.
Highlights
Streptococcus agalactiae, or Lancefield group B streptococci (GBS), are recognised as part of the human microbiota and a leading cause of neonatal infections [1]
There was a higher frequency of GBS invasive disease among older than younger adults (overall incidence rate ratio (IRR) = 6.32; 95% confidence intervals (CI): 5.32–7.73)
We have identified a significant increase in the number of GBS infections in older adults in recent years in Portugal, similar to what has been reported elsewhere [3,4,28]
Summary
Streptococcus agalactiae, or Lancefield group B streptococci (GBS), are recognised as part of the human microbiota and a leading cause of neonatal infections [1]. In the past decade, significant increases in macrolide and lincosamide resistance rates in both neonatal and adult invasive infections were reported worldwide [3,4,6]. GBS infections are mostly caused by a limited number of genetic lineages and serotypes. Particular serotype/genotype combinations were identified as leading causes of invasive GBS disease worldwide, namely the serotype III hypervirulent lineage among neonates, represented by clonal complex (CC) 17 [9]. Despite the clonality observed within GBS populations causing invasive disease, increasing diversity within these homogenous genetic lineages reveals some extent of serotype exchange.
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