Group B streptococcus virulence factors associated with different clinical syndromes: Asymptomatic carriage in pregnant women and early-onset disease in the newborn

Abstract

BackgroundGroup B streptococcus (GBS) harbors many virulence factors but there is limited data regarding their importance in colonization in pregnancy and early-onset disease (EOD) in the newborn. We hypothesized that colonization and EOD are associated with different distribution and expression of virulence factors.MethodsWe studied 36 GBS EOD and 234 GBS isolates collected during routine screening. Virulence genes (pilus-like structures-PI-1, PI-2a, PI-2b; rib and hvgA) presence and expression were identified by PCR and qRT-PCR. Whole genome sequencing (WGS) and comparative genomic analyses were used to compare coding sequences (CDSs) of colonizing and EOD isolates.ResultsSerotype III (ST17) was significantly associated with EOD and serotype VI (ST1) with colonization. hvgA and rib genes were more prevalent among EOD isolates (58.3 and 77.8%, respectively; p < 0.01). The pilus loci PI-2b and PI-2a were more prevalent among EOD isolates (61.1%, p < 0.01), while the pilus loci PI-2a and PI-1 among colonizing isolates (89.7 and 93.1% vs. 55.6 and 69.4%, p < 0.01). qRT PCR analysis revealed that hvgA was barely expressed in colonizing isolates, even though the gene was detected. Expression of the rib gene and PI-2b was two-fold higher in EOD isolates compared to colonizing isolates. Transcription of PI-2a was three-fold higher in colonizing isolates compared to EOD isolates. ST17 isolates (associated with EOD) had a smaller genome size compared ST1 and the genome was more conserved relative to the reference strain and ST17 isolates. In a multivariate logistic regression analysis virulence factors independently associated with EOD were serotype 3, and PI-1 and PI-2a was protective.ConclusionThere was a significant difference in the distribution of hvg A, rib, and PI genes among EOD (serotype III/ST17) and colonizing (serotype VI/ST1) isolates suggesting an association between invasive disease and these virulence factors. Further study is needed to understand the contribution of these genes to GBS virulence.

Novel spore-forming species exhibiting intrinsic resistance to third- and fourth-generation cephalosporins and description of Tigheibacillus jepli gen. nov., sp. nov.

“…Our VF analysis of the Amphibacillaceae family revealed 17 human-associated VF gene homologs. Notably, the hasC gene homolog in C. terrae ’s genome is associated with biofilm formation and commonly found in pathogens like group B streptococci ( 43 ). The type IV secretion system effector BspE homolog in O. zhagkaii and the signal peptidase II encoding lspA homolog in O. scapharcae are associated with the human pathogens Brucella species and Rickettsia typhi, respectively ( 44 , 45 ), highlighting a diverse range of VF.…”

Vaginal microecological imbalance and expression of serum inflammatory factors in pregnant women with group B streptococcus infection and pregnancy outcome

“…Many literatures have reported the harm of GBS infection to pregnant women and newborns (18). In the 1990s, the Centers for Disease Control and Prevention of the United States issued guidelines for the prevention of GBS (19).…”

Interbacterial competition mediated by the type VIIb secretion system

“…In other strains of S. aureus as well as S. gallolyticus, esxA is co-transcribed with the rest of the T7SS structural genes, although RNAseq data show that S. aureus esxA transcript levels are much greater than for other T7SS genes [15,[33][34][35]. Some species carry two copies of esxA, the significance of which is not yet known [16,36]. Although frequently described as a T7SS substrate, EsxA is also required for secretion of all substrates so far tested, though its role in secretion is yet to be defined.…”

“…While many substrates and secretion factors are encoded at T7SSb loci directly downstream of the core machinery, T7-associated genes are also found at additional loci in some organisms. For example, the S. aureus LXG-substrate TspA, and the S. agalactiae T7-associated WXG100 protein SAG0230 are both encoded away from the T7SSb locus [36,53].…”