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Therapeutic Nanostructures in Antitubercular Therapy
Published in Bhaskar Mazumder, Subhabrata Ray, Paulami Pal, Yashwant Pathak, Nanotechnology, 2019
Paulami Pal, Subhabrata Ray, Anup Kumar Das, Bhaskar Mazumder
However, antibiotic resistance has been a difficult problem at hand for several years, now reaching a state of crisis whereby certain strains of M. tuberculosis are resistant to the two most powerful drugs, namely isoniazid and rifampicin. These strains lead to a disease condition which can be referred to as MDR-TB. To make the situation even worse, the development of resistance by other strains leads to inadequate management of TB. These MDR strains are also resistant to isoniazid and rifampin, as well as being resistant to at least one of the quinolones, capreomycin, kanamycin, or amikacin. The disease caused by such strains is known as extensively drug-resistant TB (XDR-TB).
Mechanism of Drug Resistance in Staphylococcus aureus and Future Drug Discovery
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Felipe Wakasuqui, Ana Leticia Gori Lusa, Sven Falke, Christian Betzel, Carsten Wrenger
Rifampicin is a semi synthetic broad-spectrum bactericidal antibiotic that binds in the B subunit of the DNA-dependent RNA polymerase, inhibiting RNA synthesis (Campbell et al., 2001). Resistance is associated with mutations of the rpoB gene (Aubry-Damon et al., 1998). Rifampicin should not be used in a monotherapy due to expected rapid development of resistance (Auwaerter, 2018).
Macrophage Targeting: A Promising Strategy for Delivery of Chemotherapeutics in Leishmaniasis and Other Visceral Diseases
Published in Sarwar Beg, Mahfoozur Rahman, Md. Abul Barkat, Farhan J. Ahmad, Nanomedicine for the Treatment of Disease, 2019
Jaya Gopal Meher, Pankaj K. Singh, Yuvraj Singh, Mohini Chaurasia, Anita Singh, Manish K. Chourasia
Chemotherapy in any disease has its limitations and associated adverse effects. In case of leishmaniasis the existing chemotherapeutics have comparatively greater challenges: severe adverse effect, low cure rate as well as the most frightening, drug resistance. Whether it is antimonials, amphotericin B or orally active miltefosine, all reported antileishmanial drugs cause musculoskeletal pain, gastrointestinal disturbances, hypersensitivity, cardiotoxicity, renal failure etc. Long non-ambulatory administrative procedures pose additional discomfort to patients who are already distressed by unwanted adverse effects. Treatment failure is also sometimes encountered. In some parts of Asian countries like India, up to 65% of human treatment cases are found to be unresponsive to antimonials (Sundar, 2001). Investigational reports on such matters suggest a number of reasons viz. expression of multidrug resistance and efflux transporters, down-regulation of aquaporins, overproduction of thiol metabolizing enzyme. Recently, aberrant alteration in the sterol profiles of Leishmania parasite has been noticed where the cholesta–5,7,24-trien–3-ol is observed to be in membrane of parasite instead of ergosterol. This has significantly diminished selectivity of the gold standard drug amphotericin B. Miltefosine, is also on the verge of drug resistance, the reasons for which might be attributed to its long half-life as well as mutations in P-glycoprotein-LdRos3 and LdMT that are directly related to uptake of drug. Drug resistance is also reported for paromomycin, where parasites are observed to develop changes such as up-regulation of glycolytic enzymes and ATP-Binding cassette transporters. These modifications in parasites are acquired progressively with multiple stimulatory factors like inadequate treatment, partial or incomplete treatment as well as long term therapeutic interventions (Yasinzai et al., 2013). Infectious disease tuberculosis requires simultaneous treatment with multiple drugs viz. rifampicin, isoniazid, ethambutol, pyrazinamide, streptomycin, fluoroquinolones, kanamycin, capreomycin, amikacin, viomycinetc for long periods of time. All these drugs are reported to cause an array of adverse drug reactions. Apart from the side effects, the causative organism Mycobacterium has either acquired full or is on the verge of acquiring resistance to most of the listed drugs. Mutation in various genes is known to be responsible for drug resistance in M. tuberculosis. So chemotherapy with the current therapeutics is a challenge. Furthermore role of efflux pumps and porins are also caused drug resistance (Köser et al., 2015). In all of the infectious diseases, co-infection with HIV is reported to aggravate the case and treatment becomes more challenging. In such situations the duration of therapy increases multiple times and the socio-economic conditions of patients, their homelessness, poverty, non-compliance to therapeutic schedule remain the main reason for failure in therapy and development of drug resistance. Often the bioavailability of these drugs at the target site is also uncertain. Conventional therapy underperforms in other visceral diseases like hepatic diseases and cardiovascular diseases too (Acevedo, 2015).
Identification of microbes from textile dye wastewater and its antibiotic resistance from local textile factory
Published in Bioremediation Journal, 2023
Nur Hanis Mohamad Hanapi, Hadieh Monajemi, Azimah Ismail, Zarizal Suhaili, Hafizan Juahir
Streptomycin, an antibiotic that has similar characteristics with streptothricin, derived from Streptomyces and shown to have same activity as streptothricin, to against E.coli, B. subtilis, A. aerogenes, and P. vulgaris while less active to against S. aureus and few certain strains of Salmonella, and showed much more activity toward B. mycoides, B.cereus, Mycobacterium phlei, Serratia marcescens, Ps. aeruginosa, Ps. Fluorescens, and Cl. Butylicum. It possesses strong bactericidal properties, soluble in water and has selective activities against gram-positive and gram-negative bacteria (Schatz et al. 2005). Rifampicin, an antibiotic has been reported to be effective against tuberculosis which is caused by Mycobacterium tuberculosis (Hughes and Brandis 2013; Grumbach, Canetti, and Le Lirzin 1969; Maggi et al. 1966). Rand, Houck, and Silverman (2007) stated in the study of the mechanism of rifampicin that rifampicin acts by entering the cell cytoplasm, and inhibiting the transcription process by binding to RNA polymerase (rpoβ). The act of resistance to rifampicin is usually because of the substitutions of amino acid clusters in the three known resistance clusters in the rifampicin-binding site of rpoβ (Campbell et al. 2001). Luna et al. (2007) in their study reported that a few species of Bacillus; B. anthracis, B. thuringiensis, B. cereus, B. mycoides and B. pseudomycoides showed a susceptible activity toward rifampicin. The last antibiotic used in the study is gentamicin. Gentamicin as reported by Jao and Jackson (1964) is isolated from culture filtrates from species of Micromonospora, a bacterium and has shown the clinical efficacy toward Pseudomonas and Proteus organisms of gram-negative bacilli which inhibition process were active and as well as to staphylococci, Aerobacter and coliform bacteria. Gentamicin inhibits the activity of bacteria by interrupting the protein synthesis through irreversible binding of 30S of subunit of bacteria ribosome. Kauffman et al. (1978) reported that gentamicin-resistant includes gram-negative bacilli such as Pseudomonas and Klebsiella though no gram-positive bacilli were mentioned. However, based on the results obtained, it can be deduced that all the isolates (C1, C3K and C3W) showed an intermediate response toward gentamicin.