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We analyzed group B Streptococcus (GBS) neonatal invasive infections reported during 2007-2019 in France. The hypervirulent clonal complex (CC) 17 GBS was responsible for 66% (827/1,262) of cases. The role of CC17 GBS increased over time (p for trend = 0.0001), together with the emergence of a multidrug-resistant CC17 GBS sublineage. [ABSTRACT FROM AUTHOR]

Group B Streptococcus (GBS) is the leading cause of invasive bacterial neonatal infections. Late-onset diseases (LOD) occur between 7 and 89 days of life and are largely due to the CC17 GBS hypervirulent clone. We studied the impact of estradiol (E2) and progesterone (P4), which impregnate the fetus during pregnancy, on GBS neonatal infection in cellular and mouse models of hormonal exposure corresponding to concentrations found at birth (E2-P4 C0) and over 7 days old (E2-P4 C7). Using representative GBS isolates, we show that E2-P4 C7 concentrations specifically favor CC17 GBS meningitis following mice oral infection. CC17 GBS crosses the intestinal barrier through M cells. This process mediated by the CC17-specific surface protein Srr2 is enhanced by E2-P4 C7 concentrations which promote M cell differentiation and CC17 GBS invasiveness. Our findings provide an explanation for CC17 GBS responsibility in LOD in link with neonatal gastrointestinal tract maturation and hormonal imprint. [ABSTRACT FROM AUTHOR]

Streptococcus pyogenes, also known as group A Streptococcus, causes a wide variety of diseases ranging from mild noninvasive to severe invasive infections. To identify possible causes of colonization-to-invasive switches, we determined the genomic sequences of 10 isolates from five pairs each composed of an invasive strain and a carriage strain originating from five infectious clusters. Among them, one pair displayed a single-nucleotide difference in covS, encoding the sensor histidine kinase of the two-component CovRS system that controls the expression of 15% of the genome. In contrast to previously described cases where the invasive strains harbor nonfunctional CovS proteins, the carriage strain possessed the mutation covST115C, leading to the replacement of the tyrosine at position 39 by a histidine. The CovSY39H mutation affected the expression of the genes from the CovR regulon in a unique fashion. Genes usually overexpressed in covS mutant strains were underexpressed and vice versa. Furthermore, the covS mutant strain barely responded to the addition of the CovS-signaling compounds Mg2+ and LL-37. The variations in the accumulation of two virulence factors paralleled the transcription modifications. In addition, the covST115C mutant strain showed less survival than its wild-type counterpart in murine macrophages. Finally, in two murine models of infection, the covS mutant strain was less virulent than the wild-type strain. Our study suggests that the CovSY39H protein compromises CovS phosphatase activity and that this yields a noninvasive strain. [ABSTRACT FROM AUTHOR]

Group B S treptococcus (GBS) (Streptococcus agalactiae) is a pathogen of growing importance in adults. The objective of this study was to describe the features of invasive infections by GBS in non-pregnant adults. GBS infections were reported to the national reference centre for streptococci. Clinical information was abstracted from questionnaires. Capsular typing, identification of the hypervirulent CC-17 clone, and antibiotic susceptibility testing were performed for all GBS isolates. Multi-locus sequence typing and assignment to clonal complexes (CCs) was performed on a representative sample of 324 isolates. In total, 1960 GBS invasive infections were analysed from 2007 to 2019. The median age at onset was 71 years old (range 18–103). The main manifestation was bacteraemia without focus (54.5%). Meningitis was more frequent in patients under 40 (26/180, 14.4% versus 78/1780, 4.4%, p < 0.0001). Capsular types Ia, Ib, II, III and V accounted for 91.0% of the cases (1786/1960). CC-1, -10, -17, -19 and -23 accounted for 96.3% (312/324) of the cases. Capsular type III and CC-17 were overrepresented in meningitis (38/104, 36.5%, p < 0.001 and 22/104, 21.2%, p 0.01, respectively). All isolates were susceptible to β-lactam antibiotics. Resistance to erythromycin (32.7%) and clindamycin (26.3%) remained stable, whereas decreased susceptibility to fluoroquinolones increased, reaching 2.7% in 2019 (p for trend 0.002). This work highlights the susceptibility of the elderly to GBS infections and differences in the clinical manifestations according to the patients' age and GBS type. In agreement with worldwide reports on emerging multidrug-resistant GBS, it reinforces the need for a continued surveillance of GBS epidemiology. [ABSTRACT FROM AUTHOR]