30 Matching Annotations
  1. Jun 2017
  2. May 2017
    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. 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

  3. Apr 2017
    1. 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).

    2. 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.

    3. 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. 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.