Bacterial Phenotype Variants in Group B Streptococcal Toxic Shock Syndrome1

Sendi, Parham; Johansson, Linda; Dahesh, Samira; Sorge, Nina M. van; Darenberg, Jessica; Norgren, Mari; Sjölin, Jan; Nizet, Victor; Norrby‐Teglund, Anna

doi:10.3201/eid1502.080990

Cited by 48 publications

(62 citation statements)

References 38 publications

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“…However, the results obtained in this study indicate the absence of Cov R/S maker from most isolates and this may because of high rate mutation of this gene in GBS as mentioned by Sendi [15] who found that mutation in Cov R may reduce the virulence of this bacteria.…”

Section: Detection Of Covr/s In All Isolates Of S Agalactiaecontrasting

confidence: 38%

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Study of Some Virulence Factor and Detection of Sortase Enzymes A and Cov R/S of Streptococcus Agalactiae by PCR

2018

QJPS

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Abstract:This study included 100 pregnant and non-pregnant patients infected with vaginitis who were attended the hospital of maternity and children in Babylon province from January to May 2016. Only 25 isolates of Streptococcus agalactiae (GBS) were isolates.Sortase A enzyme were detected by using specific primer for PCR techniques and also found that all GBS strain have sortase A enzyme, so this enzyme is consider as housekeeping enzyme.Moreover, specific PCR primers were used for detection of CovR/S enzymes. It was found that CovR/S was observed only in tow isolates of Group B streptococcus GBS strains.The isolates have been examined to chick their ability to produce colonization factor antigens type1 (CFA/I) . The finding showed that they revealed the ability to produce CFA/1 in the existence of Dmannose and Vancomysin. Also, the isolates, have the ability to produce CFA/1 in the existence of Dmannose without Vancomysin.The capability of GBS isolates to produce Hemolysin in the presence of Vancomysin were studied. It was found that there was no hemolysis in the presence of Vancomysin (except for one isolate), this will give good sign for this antibiotic to reduce the ability of this bacteria to obtain iron from environment.Physiology Classification QR1-502-75-9905

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Section: Detection Of Covr/s In All Isolates Of S Agalactiaecontrasting

confidence: 38%

“…Sendi [15] found that isolates of GBS bacteria recovered from patients with TSS (toxic shock syndrome) exhibited phenotypically hyper-hemolytic, which was caused by derepression of Cyl E due to CovR mutations. …”

Section: Detection Of Covr/s In All Isolates Of S Agalactiaementioning

confidence: 99%

Study of Some Virulence Factor and Detection of Sortase Enzymes A and Cov R/S of Streptococcus Agalactiae by PCR

2018

QJPS

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“…In addition, some pathogens actively exploit phagocytes to facilitate movement between host tissues, and it is possible that a related process may underlie S. agalactiae dissemination (8,9). It has been reported that some virulence factors and regulatory genes of S. agalactiae affect survival of the bacterium in professional phagocytes (13,40,41). The ability to sense the environment and mount an appropriate adaptive transcriptional response may be of crucial importance for S. agalactiae colonization and pathogenicity.…”

Section: Discussionmentioning

confidence: 99%

Two Novel Functions of Hyaluronidase from Streptococcus agalactiae Are Enhanced Intracellular Survival and Inhibition of Proinflammatory Cytokine Expression

Wang

Guo

et al. 2014

Infect Immun

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Streptococcus agalactiae is the causative agent of septicemia and meningitis in fish. Previous studies have shown that hyaluronidase (Hyl) is an important virulence factor in many Gram-positive bacteria. To investigate the role of S. agalactiae Hyl during interaction with macrophages, we inactivated the gene encoding extracellular hyaluronidase, hylB, in a clinical Hyl ؉ isolate. The isogenic hylb mutant (⌬hylb) displayed reduced survival in macrophages compared to the wild type and stimulated a significantly higher release of proinflammatory cytokines, such as interleukin-1␤ (IL-1␤), IL-6, and tumor necrosis factor alpha (TNF-␣), than the wild type in macrophages as well as in mice. Furthermore, only Hyl ؉ strains could grow utilizing hyaluronic acid (HA) as the sole carbon source, suggesting that Hyl permits the organism to utilize host HA as an energy source. Fifty percent lethal dose (LD 50 ) determinations in zebrafish demonstrated that the hylb mutant was highly attenuated relative to the wild-type strain. Experimental infection of BALB/c mice revealed that bacterial loads in the blood, spleen, and brain at 16 h postinfection were significantly reduced in the ⌬hylB mutant compared to those in wild-type-infected mice. In conclusion, hyaluronidase has a strong influence on the intracellular survival of S. agalactiae and proinflammatory cytokine expression, suggesting that it plays a key role in S. agalactiae pathogenicity.

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“…Pneumonia, sepsis, and meningitis are potential complications of GBS transmission to the neonate, reflecting an array of bacterial virulence factors that act to impede phagocytic clearance, resulting in host tissue injury (10). Much of what is known about GBS virulence has been defined in animal models of systemic infection (18,20,23,25,28,46,47). GBS has also been described in animal models of localized colonization and infection, including vaginal (7, 8), pulmonary (15, 19, 22), mammary (52), and orogastric (27) infection models.…”

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confidence: 99%

Immune Activation and Suppression by Group B Streptococcus in a Murine Model of Urinary Tract Infection

et al. 2011

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Group B streptococcus (GBS) is a common commensal of the gastrointestinal and vaginal mucosa and a leading cause of serious infections in newborns, the elderly, and immunocompromised populations. GBS also causes infections of the urinary tract. However, little is known about host responses to GBS urinary tract infection (UTI) or GBS virulence factors that participate in UTI. Here we describe a novel murine model of GBS UTI that may explain some features of GBS urinary tract association in the human host. We observed high titers and heightened histological signs of inflammation and leukocyte recruitment in the GBS-infected kidney. However, extensive inflammation and leukocyte recruitment were not observed in the bladder, suggesting that GBS may suppress bladder inflammation during cystitis. Acute GBS infection induced the localized expression of proinflammatory cytokines interleukin-1␣ (IL-1␣), macrophage inflammatory protein-1␣ (MIP-1␣), MIP-1␤, and IL-9, as well as IL-10, more commonly considered an anti-inflammatory cytokine. Using isogenic GBS strains with different capsule structures, we show that capsular sialic acid residues contribute to GBS urinary tract pathogenesis, while high levels of sialic acid O-acetylation attenuate GBS pathogenesis in the setting of UTI, particularly in direct competition experiments. In vitro studies demonstrated that GBS sialic acids participate in the suppression of murine polymorphonuclear leukocyte (PMN) bactericidal activities, in addition to reducing levels of IL-1␣, tumor necrosis factor alpha, IL-1␤, MIP-1␣, and KC produced by PMNs. These studies define several basic molecular and cellular events characterizing GBS UTI in an animal model, showing that GBS participates simultaneously in the activation and suppression of host immune responses in the urinary tract.Group B streptococcus (GBS) is the leading cause of bacterial sepsis and meningitis in human newborns and is increasingly associated with invasive infections in adult populations such as pregnant women, diabetics, and the elderly (11,16,48,65). GBS colonizes the gastrointestinal and vaginal mucosa of approximately 30% of individuals tested at a given time and nearly 2/3 of those tested at multiple intervals over a year (35). While GBS colonization occurs asymptomatically, localized infections of the skin, lungs, and urinary tract are associated with progression to serious systemic infections in individuals with a compromised or underdeveloped immune system (4,16,48,65). For example, vaginal colonization in late pregnancy is associated with vertical transmission of GBS in utero due to ascending amniotic infection or by aspiration of contaminated vaginal fluids during delivery. Pneumonia, sepsis, and meningitis are potential complications of GBS transmission to the neonate, reflecting an array of bacterial virulence factors that act to impede phagocytic clearance, resulting in host tissue injury (10). Much of what is known about GBS virulence has been defined in animal models of systemic infection (18,20,23,25,28,4...

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Bacterial Phenotype Variants in Group B Streptococcal Toxic Shock Syndrome1

Cited by 48 publications

References 38 publications

Study of Some Virulence Factor and Detection of Sortase Enzymes A and Cov R/S of Streptococcus Agalactiae by PCR

Study of Some Virulence Factor and Detection of Sortase Enzymes A and Cov R/S of Streptococcus Agalactiae by PCR

Two Novel Functions of Hyaluronidase from Streptococcus agalactiae Are Enhanced Intracellular Survival and Inhibition of Proinflammatory Cytokine Expression

Immune Activation and Suppression by Group B Streptococcus in a Murine Model of Urinary Tract Infection

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