30 Matching Annotations
  1. Jun 2017
    1. genome

      Crimean-Congo Hemorrhagic Fever Virus is a negative-sense, single strand RNA virus, but HIV is a positive-sense single strand RNA virus.

    2. zoonotic transmission

      Both Crimean-Congo Hemorrhagic Fever Virus and HIV have non-human reservoirs.

    1. negative-sense, single-stranded RNA genome

      Crimean-Congo Hemorrhagic Fever Virus is a negative-sense, single strand RNA virus, but HIV is a positive-sense single strand RNA virus.

    2. ticks infected with CCHFV

      Both Crimean-Congo Hemorrhagic Fever Virus and HIV have non-human reservoirs.

  2. May 2017
    1. S. marcescens is typically found in showers, toilet bowls, and around wetted tiles.

      Some of the places Serratia can be found

    1. The resistance to Cm is known to be me-diated by the plasmid-located enzymes called chlo-ramphenicol acetyltransferases (CAT) (Cannon et al., 1990), or by the nonenzymatic chloramphenicol resistance gene cmlA (Dorman and Foster, 1982), that encodes an efflux pump.

      Resistance mechanism to Chloramphenicol of Sal. enterica.

    1. Oral antibiotics such as β-lactams are appropriate first-line therapy for most patients. A proportion of H. influenzae isolates produce β-lactamase (this varies markedly between different locations) and in this circumstance, extended spectrum cephalosporins, amoxicillin-clavulinic acid, trimethoprim-sulfamethoxazole, tetracyclines, quinolones and macrolide antibiotics are appropriate therapeutic choices.

      Antibiotic treatment of H. influenzae

    1. Their capsule allows them to resist phagocytosis and complement-mediated lysis in the nonimmune host.

      Type b polysaccharide capsule of H. influenzae resists phagocytosis (immune evasion)

    1. The organism enters the body through the nasopharynx. Organisms colonize the nasopharynx and may remain only transiently or for several months in the absence of symptoms (asymptomatic carrier).

      Where the bacteria lives.

    1. Themostcommonmechanismofhigh-levelfluoroquino-loneresistanceisduetomutationinoneormoreofthegenesthatencodetheprimaryandsecondarytargetsofthesedrugs,thetypeIItopoisomerases(gyrA,gyrB,parC,andparE).TheregionwheremutationsariseinthesegenesthatencodefluoroquinoloneresistanceisashortDNAsequenceknownasthequinoloneresistance-deter-miningregion(QRDR)[28,29].MutationsintheQRDRofthesegenes,resultinginaminoacidsubstitutions,alterthetargetproteinstructureandsubsequentlythefluoroquin-olone-bindingaffinityoftheenzyme,leadingtodrugresis-tance[30,31].

      Fluoroquinolone resistance.

    1. The ribosomal protection proteins have homology to elongation factors EF-Tu and EF-G (259, 292). The greatest homology is seen at the N-terminal area, which contains the GTP-binding domain. The Tet(M), Tet(O), and OtrA proteins reduce the susceptibility of ribosomes to the action of tetracyclines. The Streptomyces Otr(A) protein has greatest overall amino acid similarity to elongation factors.

      Resistance to tetracycline

    1. Neisseria (N.) gonorrhoeae, the bacteria that cause the STD gonorrhea, has developed resistance to nearly all of the antibiotics used for gonorrhea treatment:  sulfonilamides, penicillin, tetracycline, and fluoroquinolones, such as ciprofloxacin.

      Antibiotic resistances

    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."

  3. Apr 2017
    1. 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

    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

    5. 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. 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

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

      Some developing antibiotic resistances

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

      Formation of air pockets and necrosis of subcutaneous fat.

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

      Bubbly tissue, dusky coloration.

    3. edema of the fascial layer

      Another sign/symptom.

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

      Localized swelling and pain.

    1. fever, hypotension and multiple organ failure.

      Fever seems to be recurring among GBS nec fasc patients.

    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.