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Ultraviolet and Light Absorption Spectrometry
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Zoltan M. Dinya, Ferenc J. Sztaricskai
The representatives of the viomycin antibiotics are hexapeptides consisting of a peptide ring and a basic amino side chain. They show strong specific absorption at 266—268 nm, which is shifted to 290 nm in alkaline solution. Some of these antibiotics [such as viomycin and capreomycin (36)] gained limited clinical application in the chemotheraphy of tuberculosis [113].
Viomycin
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
Viomycin is a cyclic polypeptide antibiotic that is no longer in clinical use because safer and more effective drugs are available. For this reason, only a brief outline of this drug is included. The chemical structure of viomycin is shown in Figure 136.1.
Ototoxicity
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
Good evidence for the ototoxicity of many of the other drugs listed in Table 59.1 is relatively sparse. Vancomycin has been reported to cause transient hearing loss and/or tinnitus but many of these clinical reports derive from cases in which it has been used in combination with other potentially ototoxic drugs. The few experimental studies which have been performed suggest no loss of hair cells or permanent hearing impairment from systemic administration of polypeptide antibiotics even at very high doses.204 Viomycin has been reported to be predominantly vestibulotoxic following chronic treatment regimes,205,206 and animal studies have confirmed that, after repeated systemic injections of relatively high doses, viomycin causes hair cell death in the vestibular sensory organs in a pattern similar to that seen with aminoglycosides.207 Chloramphenicol has been shown to cause irreversible hearing loss following infusion into the middle ear cavity in animals,208 presumably gaining access to the perilymph following uptake across the round window membrane, but clinical reports of hearing loss following use of chloramphenicol are rare. Polymyxin B when perfused through the perilymphatic spaces caused an almost immediate decline in cochlear microphonic (CM) potential followed shortly after by a decline in EP, suggesting separate effects on both the organ of Corti and the SV.209 However, the rarity of clinical reports in which an ototoxic effect can be attributed directly to polymyxin B suggests the use of this antibiotic does not present a significant risk to the inner ear. Desferrioxamine (deferoxamine mesylate (DFO)) binds iron and is used in patients with b-thalassaemia to remove excess iron from the serum. In cultured explants of inner ear sensory epithelia DFO attenuates aminoglycoside-induced hair cell loss.112 However, repeated high-dose systemic administration of DFO to patients has been reported to cause high-frequency hearing loss in about 20–40% of those receiving long-term therapy.210–212 On the other hand, other clinical studies failed to identify a direct ototoxic effect of DFO213,214 and experimental studies with a mammalian model (chinchilla) could find no effects on cochlear physiology following long-term systemic treatment.215 The reasons for these apparent discrepancies have not been resolved. Differences between experimental models may derive from the differences in susceptibility between species, known to be the case for aminoglycosides (above), and differing treatment regimes and/or patient groups may account for differences in clinical reports.211,216
The molecular patterns of resistance to anti-tuberculosis drugs: an analysis from Istanbul, Turkey
Published in Journal of Chemotherapy, 2020
Hatice Yazisiz, Derya Hircin Cenger, Nilay Uçarman, Sedat Altin
GenoType MTBDRsl version 1.0, a DNA strip assay, can detect resistance to fluoroquinolones (FLQ; e.g. ofloxacin and moxifloxacin), aminoglycosides/cyclic peptides (AG/CP; injectable antibiotics, such as kanamycin, amikacin, capreomycin, and viomycin) and ethambutol (EMB), allowing for the diagnosis of extensively drug-resistant TB (XDR‐TB) among MDR‐TB patients. In the meta-analysis, the sensitivity of MTBDRsl assays was found as 0.874–0.869, 0.826–0.868, 0.820–0.879, 0.444–0.501, and 0.679–0.686, with the specificity at 0.971–0.973, 0.995–0.998, 0.973–0.970, 0.993–0.991, and 0.799–0.871, for FLQ, amikacin, capreomycin, kanamycin, and EMB, respectively.12,13
Mechanistic investigation of resistance via drug-inactivating enzymes in Mycobacterium tuberculosis
Published in Drug Metabolism Reviews, 2018
Aanchal Kashyap, Pankaj Kumar Singh, Om Silakari
Various enzymes have also been reported that result in the modification of the targets of ani TB drugs and their subsequent resistance. Rrs tlyA enzyme belongs to the class of methyltransferases and is responsible for conferring capreomycin and viomycin resistance. Rrs Tlya genes encode for 2′-O-methyltransferase that methylates rRNA and modifies the target at the binding site of capreomycin and veomycin at ribosome subunit interface (Johansen et al. 2006).
Potential of dry powder inhalers for tuberculosis therapy: facts, fidelity and future
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Piyush Mehta, C. Bothiraja, Shivajirao Kadam, Atmaram Pawar
At present, available chemotherapy contains first-line drugs such as isoniazid, rifampicin, pyrazinamide and ethambutol; second-line drugs such as injectable drugs (streptomycin, amikacin, kanamycin, viomycin and capreomycin), fluoroquinolones (levofloxacin, ofloxacin, moxifloxacin and gatifloxacin) and other oral drugs (cycloserine, ethionamide, prothionamide, para-amino salicylic acid and terizidone) [5]. WHO suggests that TB therapy needs large doses of antibiotics in combination to be taken orally continuously for at least 6 months. Usually, during the initial phase patients receive 3–4 first-line drugs daily for 2 months for a quick amelioration of clinical signs. In the maintenance period, 2–3 drugs are given regularly for 4–7 months to eradicate remaining Mtb cells and control the relapse rate [6]. The second-line drugs are utilized when therapy with first-line drugs not succeed or in occurrence of MDR-TB cases. These molecules are more toxic and unavailable in many growing countries because of high cost. There are several new agents presently in development phase and in clinical trials and recently two new molecules (bedaquiline and delamanid) have been approved for the treatment of MDR-TB, when other alternatives are not available [5]. But both these molecules have been conditionally approved due to severe side effects (hERG toxicity concerns and multiple ADME problems because of their high lipophilicity) have been noted [2]. In addition to above-mentioned restrictions, administration routes possess few serious challenges. The oral route is the most suitable and least expensive; however, extended administration of high doses is required and sub-therapeutic levels of anti-TB drugs reach the site of action because of the hepatic first-pass metabolism, slower onset of action and harsh gastrointestinal environment. The oral route is also coupled with adverse effects as a result of high systemic exposure. Compared to oral route, pulmonary and parenteral routes have highest bioavailability and are not issue to first-pass metabolism [5]. But, preventing repeated painful intramuscular injections mandatory for parenteral drugs is evenly important, especially for small children with little muscle mass and wasted adults. Furthermore, it also necessitates the presence of healthcare workers [7]. In this context, direct lung delivery of anti-TB drugs using pulmonary route could be more advantageous [5,7].