Regulation of PI-2b Pilus Expression in Hypervirulent Streptococcus agalactiae ST-17 BM110

Périchon, Bruno; Szili, Noémi; Merle, Laurence du; Rosinski‐Chupin, Isabelle; Gominet, Myriam; Bellais, Samuel; Poyart, Claire; Trieu-Cuot, Patrick; Dramsi, Shaynoor

doi:10.1371/journal.pone.0169840

Cited by 22 publications

(25 citation statements)

References 30 publications

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“…We suggest that each human-associated CC has maintained these genes following zoonotic transfer [Botelho, et al, 2018]. This is in hypervirulence have also been identified in this analysis including the Pi-IIb locus [Périchon et al, 2017], part of which is represented by the CC17-associated genes gcc1732, lepB, inlA_2, gcc1733 (Table S3), supporting the validity of this analysis.…”

Section: S Agalactiae Isolated From Human and Animal Sources Is Charsupporting

confidence: 79%

Pan-GWAS of Streptococcus agalactiae highlights lineage-specific genes associated with virulence and niche adaptation

Gori

Harrison

Mlia

et al. 2019

Preprint

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Streptococcus agalactiae (Group B streptococcus, GBS) is a coloniser of the gastrointestinal and urogenital tracts in adults, and an opportunistic pathogen of infants and adults. The worldwide population of GBS is characterised by a series of Clonal Complexes (CCs) with different invasive potentials. CC17 for example is commonly associated with neonatal sepsis and meningitis, while CC1 often causes invasive disease in adults with co-morbidities. The genetic basis of GBS virulence and to what extent different CCs have adapted to different host environments remain uncertain. We have therefore applied a pan-genome wide association study approach to 1988 GBS strains isolated from different hosts and countries, to identify the genes responsible for the phenotypic differences between clonal complexes.Our results show 279 CC-specific genes belonging to metabolic pathways that appear to explain the differential virulence potential of particular CCs, including CC17. Moreover, our analysis leads us to suggest that human-associated GBS CCs have largely evolved in animal hosts before crossing to the human host and then spreading clonally.

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Section: S Agalactiae Isolated From Human and Animal Sources Is Charsupporting

confidence: 79%

Pan-GWAS of Streptococcus agalactiae highlights lineage-specific genes associated with virulence and niche adaptation

Gori

Harrison

Mlia

et al. 2019

Preprint

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“…57 Strains vary in their expression of virulence factors, many of which are highly regulated by 2-component regulatory systems. [58][59][60][61][62] The hypervirulent serotype III multilocus sequence type 17 (ST17), for example, is commonly found in cases of GBS meningitis. 6,23…”

Section: Gbs Virulencementioning

confidence: 99%

Management of Infants at Risk for Group B Streptococcal Disease

et al. 2019

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Group B streptococcal (GBS) infection remains the most common cause of neonatal early-onset sepsis and a significant cause of late-onset sepsis among young infants. Administration of intrapartum antibiotic prophylaxis is the only currently available effective strategy for the prevention of perinatal GBS earlyonset disease, and there is no effective approach for the prevention of late-onset disease. The American Academy of Pediatrics joins with the American College of Obstetricians and Gynecologists to reaffirm the use of universal antenatal microbiologic-based testing for the detection of maternal GBS colonization to facilitate appropriate administration of intrapartum antibiotic prophylaxis. The purpose of this clinical report is to provide neonatal clinicians with updated information regarding the epidemiology of GBS disease as well current recommendations for the evaluation of newborn infants at risk for GBS disease and for treatment of those with confirmed GBS infection. This clinical report is endorsed by the American College of Obstetricians and Gynecologists (ACOG), July 2019, and should be construed as ACOG clinical guidance. The Centers for Disease Control and Prevention (CDC) first published consensus guidelines on the prevention of perinatal group B streptococcal (GBS) disease in 1996. These guidelines were developed in collaboration with the American Academy of Pediatrics (AAP), the American College of Obstetricians and Gynecologists (ACOG), the American College of Nurse-Midwives, the American Academy of Family Physicians, and other stakeholder organizations 1 on the basis of available evidence as well as expert opinion. The 1996 consensus guidelines recommended either an antenatal culture-based or risk factor-based approach for the administration of intrapartum antibiotic prophylaxis (IAP) to prevent invasive neonatal GBS early-onset disease (EOD). 1 The guidelines were updated in 2002 primarily on the basis of new data from a CDC multistate retrospective cohort study in which authors found universal screening for group B streptococci (Streptococcus agalactiae) was .50% more effective at preventing the disease compared to a risk-based approach. 2,3 In 2010,

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“…23 GBS A909 capsular serotype Ia sequence type (ST)-9 (GBSIa) and GBS BM110 capsular serotype III ST17 (GBSIII), both well-characterized isolates from human with invasive infections, were killed as previously described. 19,23 This killing process using formaldehyde allows bacterial inactivationpreventing active infection and toxicitywhile preserving most GBS components, as shown in other animal models of immunization. 24,25 A total of 32 time-pregnant primiparous Lewis rats (Charles River Laboratories) were randomized into three groups and injected intraperitoneally every 12 h (8 am/pm) from gestational day (G) G19 to G22 with 100 µl of either: (Group 1) sterile 0.9% saline (control; CTL, number [n] = 8 dams), (Group 2) GBSIa (10 9 CFU suspended in saline, n = 8 dams) or (Group 3) GBSIII (10 9 CFU suspended in saline, n = 16 dams).…”

Section: Experimental Designmentioning

confidence: 99%

“…17 GBSIII is documented as more virulent than GBSIa, and is associated with worse clinical outcomes. [18][19][20] Using rat models of end-gestational active GBSIa infection and inactivated GBS-induced inflammation, we previously reported sex dichotomous effects in maternofetal inflammatory responses, chorioamnionitis and subsequent forebrain injuries as well as time-specific neurobehavioral impairments. [21][22][23] We hypothesized that end-gestational exposure to GBSIII will cause IUGR and CP-like neurobehavioral features.…”

Section: Introductionmentioning

confidence: 99%

Causal role of group B Streptococcus-induced acute chorioamnionitis in intrauterine growth retardation and cerebral palsy-like impairments

Allard

Brochu

Bergeron

et al. 2019

J Dev Orig Health Dis

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Chorioamnionitis and intrauterine growth retardation (IUGR) are risk factors for cerebral palsy (CP). Common bacteria isolated in chorioamnionitis include group B Streptococcus (GBS) serotypes Ia and III. Little is known about the impact of placental inflammation induced by different bacteria, including different GBS strains. We aimed to test the impact of chorioamnionitis induced by two common GBS serotypes (GBSIa and GBSIII) on growth and neuromotor outcomes in the progeny. Dams were exposed at the end of gestation to either saline, inactivated GBSIa or GBSIII. Inactivated GBS bacteria invaded placentas and triggered a chorioamnionitis featured by massive polymorphonuclear cell infiltrations. Offspring exposed to GBSIII – but not to GBSIa – developed IUGR, persisting beyond adolescent age. Male rats in utero exposed to GBSIII traveled a lower distance in the Open Field test, which was correlating with their level of IUGR. GBSIII-exposed rats presented decreased startle responses to acoustic stimuli beyond adolescent age. GBS-exposed rats displayed a dysmyelinated white matter in the corpus callosum adjacent to thinner primary motor cortices. A decreased density of microglial cells was detected in the mature corpus callosum of GBSIII-exposed males – but not females – which was correlating positively with the primary motor cortex thickness. Altogether, our results demonstrate a causal link between pathogen-induced acute chorioamnionitis and (1) IUGR, (2) serotype- and sex-specific neuromotor impairments and (3) abnormal development of primary motor cortices, dysmyelinated white matter and decreased density of microglial cells.

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Regulation of PI-2b Pilus Expression in Hypervirulent Streptococcus agalactiae ST-17 BM110

Cited by 22 publications

References 30 publications

Pan-GWAS of Streptococcus agalactiae highlights lineage-specific genes associated with virulence and niche adaptation

Pan-GWAS of Streptococcus agalactiae highlights lineage-specific genes associated with virulence and niche adaptation

Management of Infants at Risk for Group B Streptococcal Disease

Causal role of group B Streptococcus-induced acute chorioamnionitis in intrauterine growth retardation and cerebral palsy-like impairments

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