69 Matching Annotations
  1. May 2017
    1. Viridans streptococci gram-positive cocci usually in chains, but not always. Notice that these cannot be differentiated from Streptococcus pyogenes by the Gram stain.

      Viridans group strep photo. "Usually in chains, but not always."

  2. Apr 2017
    1. group B streptococci (Streptococcus agalactiae) have been reported to cause necrotizing fasciitis in only 4 instances (2 involving neonates) over the past 4 decades


    2. We speculate that group B streptococcus has recently acquired an increased ability to cause necrotizing fasciitis

      Emerging cases of GBS causing nec fasc.

    1. Antibiotic-killing kinetics of group B streptococci.

      Kinetics of vancomysin--> Purchased to see that it is resistant 4hr group a 20-24 hrs group b

    1. Because of possible resistance with clindamycin, vancomycin remains the initial treatment of choice for group B streptococcal infection in patients who are allergic to penicillin
    1. rare entity that has been reported in only 9 patients—in 2 nonpregnant adults.

      GBS causing nec fasc in nonpregnant adults is very rare

    2. loss of tissue-plane resistance and necrosis of the subcutaneous fat

      Formation of air pockets and necrosis of subcutaneous fat.

    3. skin was dusky up to the knee, with bullae formation

      Bubbly tissue, dusky coloration.

    4. edema of the fascial layer

      Another sign/symptom.

    5. left-leg swelling; the overlying skin had a dusky appearance. Severe left-leg pain

      Localized swelling and pain.

    1. Necrotizing fasciitis type II is a relatively uncommon, severe infection caused primarily by group A b-hemolytic streptococcus (GAS)

      Nec fasc usually caused by group A strep

    2. We report the second case of group B streptococcus causing necrotizing fasciitis and toxic shock-like syndrome. A black woman, aged 52 years

      Emergin cases of GBS causing nec fasc.

    1. BS strains resistant to penicillin were found to contain spontaneous mutations that conferred amino-acid substitutions


    2. 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.


    3. can cleave and inactivate the human complement component C5a. Since C5a is important for the recruitment of neutrophils to the site of infection

      Persistence and immune evasion

    4. Regulation of virulence factor expression.

      Virulence factors here

    5. 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).

    6. 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.

    7. 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

    8. GBS encodes at least two pore-forming toxins, known as β-hemolysin/cytolysin (β-H/C) and Christie Atkins Munch Peterson (CAMP) factor.

      Contributing to toxicity/sepsis and tissue destruction.

    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


    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.
    2. Adults with chronic illnesses (e.g., diabetes mellitus, obesity, and cardiovascular disease), pregnant women, the fetus, and the newborn are at risk.

      Those at high risk for group b strep

    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. Algorithm for recommended laboratory testing for prenatal screening for group B streptococcal (GBS) colonization[1 page](https://www.cdc.gov/groupbstrep/guidelines/downloads/recommended-prenatal.pdf).
    2. 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

    2. As mentioned, S. agalactiae is a Gram-positive coccus with a tendency to form chains, beta-haemolytic, catalase-negative, and facultative anaerobe.
    1. Types of Infection and Symptoms


    2. These skin infections may also be accompanied by a fever


    3. Red Swollen or painful Warm to the touch Full of pus or other drainage

      similar to the case

    4. rates of serious group B strep infections are higher among newborns

      Risk of group B strep highest among newborns.

    5. invasive group B strep infection (infections where the bacteria have entered a part of the body that is normally not exposed to bacteria)

      Transmission: bacterial exposure to area ex: cut on the hand like case #1 patient

    6. Spread to Others

      Source of invasive GBS is unknown when it is not from pregnant women. Mode of transmission=? Host=humans

    1. Significance of organism is determined by colony count.

      colony count from urine sample can determine the bacteria

    2. Group B Strep

      aerobic and in pairs/chains

    1. chromogenic pigments for the detection of beta-hemolytic GBS using color detection

      beta-hemolytic?--> breakdown of red blood cells,

    2. TransVag broth may be supplemented with 5% defibrinated sheep blood to increase the recovery of GBS


    1. penicillin, ampicillin, and first-generation cephalosporins

      antibiotics used to fight GBS

    2. Relatively elevated MICs to cefazolin (1 μg/ml) also were reported among three (0.05%) of 5,631 invasive GBS isolates collected through CDC’s active surveillance during 1999–2005

      More potential antibiotic resistances

    3. However, an increasing number of isolates with reduced susceptibility to penicillin have been found in Japan

      Some developing antibiotic resistances

    1. Group B strep screening identifies the presence of the bacteria in the vaginal/rectal area of a pregnant woman.

      Screening for group b strep in pregnant women.

    1. fever, hypotension and multiple organ failure.

      Fever seems to be recurring among GBS nec fasc patients.

    2. 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

    3. 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.

    2. worsening abdominal pain over the past 2 weeks with associated fever, dysuria, nausea, and vomiting.

      Symptoms of Group B Strep nec fasc, caused by a decubitus ulcer.

    1. Adults who develop invasive GBS infection may develop

      Sepsis, soft tissue infection, bone infection, pneumonia, UTI, meningitis

    2. The exact source of the infection in nonpregnant adults is often not determined

      The source of GBS in for non pregnant people is not yet determined.

    3. diabetes, cardiovascular disease, obesity, and cancer.

      Vulnerable Populations: Neonates and those with diabetes, cardiovascular disease, obesity, and cancer.

    4. Group B strep (GBS) are bacteria found normally in the intestine, vagina, and rectal area in about 25% of all healthy adult and pregnant women.

      Reservoir "GBS can exists in most women without causing any symptoms"

    1. The rate of invasive GBS in nonpregnant adults is in-creasing, and most cases are found in elderly persons and those with underlying diseases (26)

      Most common cases of GBS

    2. 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

    3. 2 of the best characterized are its exopolysaccharide capsule and the surface-associat-ed toxin, β-hemolysin/cytolysin (β-h/c).

      Virulence factors associated with Group B

    4. 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