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Translation
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
This conclusion was strengthened first by the dipeptide assay when the translocation reaction was completely blocked, either by addition of antibiotics, such as fusidic acid, or by washing the ribosomes to remove EF-G factor (Lodish 1969a; Roufa and Leder 1971). Such systems formed only the first peptide bond of the viral proteins, since synthesis stopped after formation of the formyl-methionyl-aminoacyl-tRNA complex. Using the intact f2 RNA, the assay did show the first peptide bond fMet-Ala of the coat but not fMet-Ser of the replicase (Lodish 1969a). Second, using 32P-labeled phage RNA, the RNA sequences were determined, which were bound to the initiation complex, consisting of both ribosomal subunits, initiation factors, fMet-tRNA and phage RNA, and protected from the ribonuclease digestion (Steitz 1969a,b). Again, when the intact unfragmented R17 (Steitz 1969a,b) or f2 (Gupta et al. 1970) RNA was used, the site for initiation of coat synthesis, but not of replicase synthesis, was protected.
Fusidate Sodium
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
There are several mechanisms recognized that cause resistance to fusidic acid. One class, FusA, is associated with mutations in fusA that reduce the affinity of fusidic acid for its target elongation factor G (EF-G) on the ribosome (Hansson et al., 2005; Besier et al., 2007). Mutations in fusA causing fusidic acid resistance in S. aureus or in S. epidermidis were shown to result in considerable loss of fitness in such strains (Besier et al., 2005; Gustafsson et al., 2003). In S. aureus, however, fitness-compensating mutations readily occurred (Besier et al., 2005). Mutations in fusA can also cause resistance to fusidic acid in Salmonella spp. (Macvanin et al., 2004). The second class, FusB, until now the most prevalent, is associated with a 21-kB plasmid that carries the fusB gene (O’Brien et al., 2002). This gene encodes an inducible protein that somehow protects EF-G against fusidic acid. FusB has been found to be prevalent in epidemic fusidic acid–resistant S. aureus causing impetigo (O’Neill et al., 2004). In addition, fusC and fusD are two homologs of fusB that have been found on the chromosome of S. aureus and Staphylococcus saprophyticus (O’Neill et al., 2007b). So far, fusB and fusC appear to be the most common fusidic acid resistance determinants in both methicillin-resistant Staphylococcus aureus (MRSA) in Europe and in coagulase-negative staphylococci in China, in both cases indicative of wide horizontal spread of these genes among most staphylococcal species (McLaws et al., 2011; Hung et al., 2015). FusE refers to a fusidic acid–resistance mechanism in S. aureus that phenotypically results in the appearance of small colony variants. It is due to mutations in rplF encoding for ribosomal protein L6. These can be auxotrophic for either hemin or menandione and may also be selected by aminoglycosides, showing that other antibiotics can select for fusidic acid resistance (Norström et al., 2007). Another fusidic acid–resistance mechanism, FusF, was added to the list in 2015 (Chen et al., 2015). It was found in Staphylococcus cohnii subsp. cohnii and subsp. urealyticus, which have MICs of 0.125–4 mg/l and 4–16 mg/l for the two subspecies, respectively. Each of the two subspecies already contains the fusA gene, whereas the fusF element showed 50–71% nucleotide sequence similarity to fusB, and its fusidic acid interaction was proven by cloning experiments (Chen et al., 2015). It is therefore thought to interact with the FusB-family proteins and EF-G (Chen et al., 2015).
The pharmacology of antibiotic therapy in hidradenitis suppurativa
Published in Expert Review of Clinical Pharmacology, 2020
Claudio Marasca, Paolo Tranchini, Vincenzo Marino, Maria Carmela Annunziata, Maddalena Napolitano, Davide Fattore, Gabriella Fabbrocini
Fusidic acid is a selective antibiotic that inhibits protein synthesis by preventing the turnover of elongation factor G (EF-G) from the ribosome. Pharmacokinetic and pharmacodynamic studies have shown that fusidic acid reaches a high antimicrobial concentration in deep skin layers after topical application both on the intact or the damaged epidermis. In its different topical formulations, it showed to be very effective in managing skin infections, and it was reported a high bactericidal activity against many pathogens such as Staphylococcus aureus (including penicillin-resistant strains, methicillin, cloxacillin, and ampicillin), Streptococcus pyogenes, Staphylococcus epidermidis, Propionibacterium acnes, Clostridia, and Corynebacteria [85]. Although these features make fusidic acid specifically useful in the treatment of skin condition, in literature there is only few case report about its use in hidradenitis suppurativa. In a recent prospective study on 627 patients affected by axillary hidradenitis (stage I), a protocol based on frequent washing, antibacterial soaps, and 2% fusidic acid has been used as a conservative treatment: 73.5% of patients had complete healing within two weeks, 20.3% within three weeks,6.2% within four weeks. The recurrence rate was 5.9% in which all patients were retreated conservatively and had complete healing, none required surgical intervention [86]
A review of antibiotics and psoriasis: induction, exacerbation, and amelioration
Published in Expert Review of Clinical Pharmacology, 2019
By binding on the elongation factor G (EF-G) and preventing EF-G turnover, fusidic acid inhibits bacterial protein synthesis. It mainly has effect on gram-positive cocci. Plaque psoriasis: previous promising and opposite reports [25–28] of fusidic acid in psoriasis treatment had led to a double-blind controlled trial (n = 20). Patients with recently overt or hidden infections were all excluded. The result showed no significant difference of clearing psoriasis in active treated group compared with placebo [29].