Identification of the High-Virulence Clone of Group B Streptococci by Using a Probe Containing a Putative Aldolase Gene

Palacios, Gerardo C.; Timmons, Brenda C.; Eskew, Elizabeth K.; Solórzano, Fortino; Mattingly, S J

doi:10.1007/s00284-002-3957-5

Cited by 3 publications

(2 citation statements)

References 25 publications

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“…In addition, we detected the genes for virulence factors Lmb, CylE, and ScpB in all our isolates and other virulence genes in variable percentages, among them the major virulence adhesin coded by the hvgA gene. These findings suggest that GBS hypervirulent clones are circulating in the population studied, as previously described in a sample of GBS isolates from Mexico City [ 56 ]. Although we did not find evidence of GBS disease, it illustrates the importance of knowing the pathogenic characteristics of GBS populations circulating in different regions.…”

Section: Discussionsupporting

confidence: 78%

Genomic analysis of virulence factors and antimicrobial resistance of group B Streptococcus isolated from pregnant women in northeastern Mexico

et al. 2022

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Introduction Group B Streptococcus (GBS) causes infections in women during pregnancy and puerperium and invasive infections in newborns. The genes lmb, cylE, scpB, and hvgA are involved with increased virulence of GBS, and hypervirulent clones have been identified in different regions. In addition, increasing resistance of GBS to macrolides and lincosamides has been reported, so knowing the patterns of antibiotic resistance may be necessary to prevent and treat GBS infections. This study aimed to identify virulence genes and antibiotic resistance associated with GBS colonization in pregnant women from northeastern Mexico. Methods Pregnant women with 35–37 weeks of gestation underwent recto-vaginal swabbing. One swab was inoculated into Todd-Hewitt broth supplemented with gentamicin and nalidixic acid, a second swab was inoculated into LIM enrichment broth, and a third swab was submerged into a transport medium. All samples were subcultured onto blood agar. After overnight incubation, suggestive colonies with or without hemolysis were analyzed to confirm GBS identification by Gram staining, catalase test, hippurate hydrolysis, CAMP test, and incubation in a chromogenic medium. We used latex agglutination to confirm and serotype GBS isolates. Antibiotic resistance patterns were assessed by Vitek 2 and disk diffusion. Periumbilical, rectal and nasopharyngeal swabs were collected from some newborns of colonized mothers. All colonized women and their newborns were followed up for three months to assess the development of disease attributable to GBS. Draft genomes of all GBS isolates were obtained by whole-genome sequencing. In addition, bioinformatic analysis to identify genes encoding capsular polysaccharides and virulence factors was performed using BRIG, while antibiotic resistance genes were identified using the CARD database. Results We found 17 GBS colonized women out of 1154 pregnant women (1.47%). None of the six newborns sampled were colonized, and no complications due to GBS were detected in pregnant women or newborns. Three isolates were serotype I, 5 serotype II, 3 serotype III, 4 serotype IV, and 2 serotype V. Ten distinct virulence gene profiles were identified, being scpB, lmb, fbsA, acp, PI-1, PI-2a, cylE the most common (3/14, 21%). The virulence genes identified were scpB, lmb, cylE, PI-1, fbsA, PI-2a, acp, fbsB, PI-2b, and hvgA. We identified resistance to tetracycline in 65% (11/17) of the isolates, intermediate susceptibility to clindamycin in 41% (7/17), and reduced susceptibility to ampicillin in 23.5% (4/17). The tetM gene associated to tetracyclines resistance was found in 79% (11/14) and the mel and mefA genes associated to macrolides resistance in 7% (1/14). Conclusions The low prevalence of colonization and the non-occurrence of mother-to-child transmission suggest that the intentional search for GBS colonization in this population is not justified. Our results also suggest that risk factors should guide the use of intrapartum antibiotic prophylaxis. The detection of strains with genes coding virulence factors means that clones with pathogenic potential circulates in this region. On the other hand, the identification of decreased susceptibility to antibiotics from different antimicrobial categories shows the importance of adequately knowing the resistance patterns to prevent and to treat GBS perinatal infection.

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Section: Discussionsupporting

confidence: 78%

Genomic analysis of virulence factors and antimicrobial resistance of group B Streptococcus isolated from pregnant women in northeastern Mexico

et al. 2022

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“…Sudden temperature upshift may induce temporary growth inhibition of bacterial cells and rearrangement of gene expression directed towards survival, including for GBS strains (5,(14)(15)(16). The present study demonstrated that temperature changes may influence GBS survival within endothelial cells.…”

Section: Discussionmentioning

confidence: 74%

Fever temperature enhances mechanisms of survival of Streptococcus agalactiae within human endothelial cells

Lione

Santos²,

Carvalho³

et al. 2010

Int J Mol Med

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Abstract. Group B streptococci (GBS) are the most common cause of pneumonia and sepsis during the neonatal period. However, the pathogenesis of invasive infection is poorly understood. We investigated the ability of GBS grown at 37˚C and 40˚C to adhere and invade human umbilical vein endothelial cells (HUVECs) at different periods of incubation (0, 0.5, 1, 2, 18 and 24 h). All strains tested, except strain 88641-vagina survived for 24 h in the intracellular environment at 40˚C. For serotype III grown at 40˚C, both strains (80340-vagina and 90356-liquor) showed increased adherence and intracellular survival when compared to bacteria grown at 37˚C (P<0.01). GBS serotype V strains (88641-vagina and 90186-blood) showed ability to survive inside HUVECs until 2 and 24 h post-infection at 40˚C and 37˚C, respectively (P<0.01). Influence of growth temperature in bacterial interaction with endothelial cells was partially dependent of serotypes and the clinical origin of strains. Serotypes III and V strains grown at both temperatures remained viable within acidic endothelial vacuoles which acquired Rab7 and LAMP-1 endosomal markers. The data emphasize the influence of temperature on cellular events of phagocytosis and pathogenesis of GBS diseases.

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High-Virulence Clone of Group B Streptococci Unable to Grow at High Temperatures Is Present in Serotypes Other Than Type III

et al. 2007

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Highly virulent clonotypes of serotype III seem to cause much of the perinatal morbidity and mortality attributed to Streptococcus agalactiae (group B streptococci, GBS), One of these clonal types, designated the "high-virulence clone" (HVC), was identified by its inability to grow at 40 degrees C in a chemically defined medium. In the present study, this inability to grow at high temperatures was used as a marker to identify HVC in a sample of 286 Mexican GBS isolates. Forty-three isolates (15%) were identified as belonging to this clone: 15 were invasive isolates, 33 were serotype III (77%), and 10 were of serotypes other than type III (23%). These results demonstrate that HVC is more prevalent in Mexico than previously reported and that this clone is not restricted to serotype III isolates.

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Identification of the High-Virulence Clone of Group B Streptococci by Using a Probe Containing a Putative Aldolase Gene

Cited by 3 publications

References 25 publications

Genomic analysis of virulence factors and antimicrobial resistance of group B Streptococcus isolated from pregnant women in northeastern Mexico

Genomic analysis of virulence factors and antimicrobial resistance of group B Streptococcus isolated from pregnant women in northeastern Mexico

Fever temperature enhances mechanisms of survival of Streptococcus agalactiae within human endothelial cells

High-Virulence Clone of Group B Streptococci Unable to Grow at High Temperatures Is Present in Serotypes Other Than Type III

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