PubMed · 15366166
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Nicole Fraser-Hurt, Denise Mabey. 2003. Trachoma.. https://pubmed.ncbi.nlm.nih.gov/15366166/
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Tachyplesin I is a cyclic beta-sheet antimicrobial peptide isolated from the hemocytes of Tachypleus tridentatus. The four cysteine residues in tachyplesin I play a structural role in imparting amphipathicity to the peptide which has been shown to be essential for its activity. We investigated the role of amphipathicity using an analogue of tachyplesin I (TP-I), CDT (KWFRVYRGIYRRR-NH(2)), in which all four cysteines were deleted. Like TP-I, CDT shows antimicrobial activity and disrupts Escherichia coli outer membrane and model membranes mimicking bacterial inner membranes at micromolar concentrations. The CDT peptide does not cause hemolysis up to 200 microg/mL while TP-I showed about 10% hemolysis at 100 microg/mL and about 25% hemolysis at 150 microg/mL. Peptide-into-lipid titrations under isothermal conditions reveal that the interaction of CDT with lipid membranes is an enthalpy-driven process. Binding assays performed using fluorometry demonstrate that the peptide CDT binds and inserts into only negatively charged membranes. The peptide-induced thermotropic phase transition of MLVs formed of DMPC and the DMPC/DMPG (7:3) mixture suggests specific lipid-peptide interactions. The circular dichroism study shows that the peptide exists as an unordered structure in an aqueous buffer and adopts a more ordered beta-structure upon binding to negatively charged membrane. The NMR data suggest that CDT binding to negatively charged bilayers induces a change in the lipid headgroup conformation with the lipid headgroup moving out of the bilayer surface toward the water phase, and therefore, a barrel stave mechanism of membrane disruption is unlikely as the peptide is located near the headgroup region of lipids. The lamellar phase (31)P chemical shift spectra observed at various concentrations of the peptide in bilayers suggest that the peptide may function neither via fragmentation of bilayers nor by promoting nonlamellar structures. NMR and fluorescence data suggest that the presence of cholesterol inhibits the peptide binding to the bilayers. These properties help to explain that cysteine residues may not contribute to antimicrobial activity and that the loss of hemolytic activity is due to lack of hydrophobicity and amphipathicity.
BACKGROUND: Considering the potentials of gatifloxacin and moxifloxacin in the treatment of tuberculosis, the present study was aimed to define resistance to both these drugs. METHODS: Fifty Mycobacterium tuberculosis isolates, consisting of 30 ofloxacin-susceptible and 20 ofloxacin-resistant strains, were tested for their susceptibility to gatifloxacin and moxifloxacin using different susceptibility testing methods, namely the absolute concentration method on Lowenstein-Jensen medium (LJ), the proportion susceptibility testing method (PST) on LJ and 7H11 agar media, and the BACTEC radiometric method. RESULT: The minimal inhibitory concentration (MIC) of gatifloxacin and moxifloxacin was 1 microg/ml by the absolute concentration method on LJ. In the PST method on LJ and 7H11, using a criterion of > or =1% growth as resistant, there was 100% agreement with the absolute concentration method at a concentration of 0.5 microg/ml for gatifloxacin, and 96% agreement with the BACTEC method at a concentration of 0.25 microg/ml. For moxifloxacin, results by the PST method showed 96% agreement with the absolute concentration method on LJ at a concentration of 1 microg/ml and 92% agreement at a concentration of 0.5 microg/ml for both the absolute concentration method on 7H11 and the BACTEC method. CONCLUSIONS: The MICs of gatifloxacin and moxifloxacin were much lower than the MICs of other quinolones like ofloxacin and ciprofloxacin. Additionally, these two drugs have shown a low mean MIC and low concentration as a definition of resistance, which might help in treating the patients with low levels of quinolone resistance.
The bactericidal and fungicidal activity of Akacid plus, a novel polymeric compound of the cationic family of disinfectants, was compared with chlorhexidine digluconate using quality control strains of Staphylococcus aureus, Enterococcus hirae, Escherichia coli, Pseudomonas aeruginosa, Candida albicans and Aspergillus niger. In vitro activity was determined using the quantitative suspension tests described by the European Committee for Standardization. These use concentrations of 0.01-0.5% against bacterial strains/C. albicans, with 0.5-4% against A. niger, and exposure times of 5, 15 and 60 min in the presence and absence of 0.3% bovine albumin and with dilution in distilled and hard water. In the basic quantitative suspension test, Akacid plus destroyed all bacterial pathogens at a concentration of 0.1% in < or =5 min. Chlorhexidine was also highly active against S. aureus, E. coli and P. aeruginosa, but failed to eliminate E. hirae within 5 min. A high organic load reduced the bactericidal activity of both disinfectants slightly. Akacid plus showed fungicidal activity against C. albicans within 15-60 min and eliminated A. niger at a concentration of 1% in 5 min of contact. Chlorhexidine was fungicidal against C. albicans, but not against A. niger.