69 Matching Annotations
  1. May 2017
  2. Apr 2017
    1. he most common mechanism employed by pathogens, including GBS, to resist AMPs is to decrease the charge on their cell surface [133]. Since AMPs are positively charged and the bacterial cell surface is negatively charged, the initial interaction between them is electrostatic.

      Avoidance

    2. These interactions often involve the initial binding of GBS to ECM proteins such as fibrinogen, fibronectin and laminin, which facilitate subsequent interactions with host-cell surface integrins and entry into the host cell

      Attachment mechanism (brief, check article for more detail).

    3. Pathogen resistance to host-encoded ROS is integral to host immune evasion. Apart from pigment (see section on β-H/C), GBS encodes a Mn2+ cofactored superoxide dismutase, SodA, for resistance to ROS and immune evasion. Superoxide dismutases convert singlet oxygen or superoxide anions (O2−) to molecular oxygen (O2) and H2O2, which are subsequently metabolized by catalases or peroxidases. Consequently, these enzymes enable pathogenic bacteria to resist oxidative stress during infection.

      More immune evasion, by use of enzyme to resist oxidative stress during infection.

    4. GBS are encapsulated by a sialic acid-rich CPS belonging to one of the ten capsular serotypes: Ia, Ib or II-IX. The CPS of GBS exemplifies a classical example of molecular mimicry. Since the CPS of GBS is decorated with sialic acid, a family of nine carbon sugars also commonly present on glycans of vertebrate cells, the host fails to recognize GBS as nonself.

      One of the means of immune evasion

    1. The current gold standard after inoculation is to use selective enrichment broth (that is, Lim Broth, TransVag Broth or Carrot Broth) and incubate for 18 to 24 hours. That is followed by a subculture using selective media for another 18 to 24 hours. If colonies are present, they undergo extraction to determine if Group A or B streptococcus is present and, if necessary, susceptibility testing for antibiotics (another 12 to 24 hours).

      Lab Test for GBS

    1. To study the effect of the environmental pH on GBS binding to ECM, we evaluated the adherence of strain 2603 to ECM proteins at acidic and neutral pHs. GBS binding to immobilized fibrinogen and fibronectin was greater at a neutral pH than at an acidic pH (Fig. 3B). In contrast, binding to laminin was similar at pH 7.4 and pH 5.0

      pH

    1. Asymptomatic carriage in gastrointestinal and genital tracts is common. Intrapartum transmission via ascending spread from the vagina occurs. Mode of transmission of disease in non-pregnant adults is unknown.
    1. GBS hyaluronidase degrades pro-inflammatory hyaluronan (HA) fragments to disaccharides•HA disaccharides block TLR2/4 signaling by both HA fragments and TLR2/4 agonists•Hyaluronidases secreted by Gram-positive pathogens promote immune evasion•HA disaccharides and GBS hyaluronidase inhibit inflammation in a lung injury model

      Immune evasion

    1. Procedures for collecting clinical specimens for culture of group B Streptococcus (GBS) at 35–37 weeks’ gestation[1 page](https://www.cdc.gov/groupbstrep/guidelines/downloads/procedure-collecting.pdf). Procedures for processing clinical specimens for culture of group B Streptococcus (GBS)[1 page](https://www.cdc.gov/groupbstrep/guidelines/downloads/procedure-specimen.pdf).
    1. GBS grows readily on blood agar plates as microbial colonies surrounded by a narrow zone of β-haemolysis. GBS is characterized by the presence in the cell wall of the group B antigen of the Lancefield classification (Lancefield grouping) that can be detected directly in intact bacteria using latex agglutination tests. [9] The CAMP test is also another important test for the identification of GBS. The CAMP factor acts synergistically with the staphylococcal β-haemolysin inducing enhanced haemolysis of sheep or bovine erythrocytes. [9]

      Various tests of diagnosis

    1. However,monomicrobial necrotizing fasciitis caused by GBS innon-pregnant adults is extremely rare, with just over tencases being reported in the English-language medicalliterature to date

      GBS necrotizing fasciitis is very rare

    2. Five patients with monomicrobial necrotizing fasciitiscaused by GBS were identified during this time period. Allpatients were female, with ages ranging from 38 to 66years. Diabetes mellitus was a frequent association andwas noted in four of the patients.

      Cases seen in Singapore of GBS were common to females and had an association with diabetes

    1. high index of suspicion should be present when abdominal radiographs demonstrate subcutaneous emphysema in a patient with skin lesions [4]. On CT, free air with evidence of soft tissue invasion is consistent with the diagnosis [2].

      Gas formation under the skin.

    1. previously healthy 50-year-old man was admitted to the hospital with fever, severe pain and swelling of the right shoulder and arm, 1 week after moderate trauma.

      No sign of a laceration--- can occur in vivo, Group B may not have to enter the body from a wound site

    2. reminiscent of a disease course more common-ly associated with group A streptococci or Staphylococcus aureus

      Group B streptococcus cases causing necrptozomg fasciitis have originally emerged, more common type is Group A