Mycobacterium tuberculosis infection resistance

This process was undoubtedly developed for the manufacture of pyrazinamide (Zinamide, etc.),1696 a second-line drug for Mycobacterium tuberculosis infections, resistant to more effective and less toxic agents. Thus a mixture of 2-methyl-pyrazine (323), ammonia, oxygen, and steam is passed (at 400°C) over an alumina- or pumice-supported catalyst comprising one to three oxides of Ce, Cr, Mo, Mn, P, Sb, Ti, or (most importantly) V the main product (in up to 90% yield) is 2-pyrazinecarbonitrile (324), easily converted into 2-pyrazinecarboxamide... 

Beck-Sague C, Dooley SW, Hutton MD, et al. Hospital outbreak of multidmg-resistant Mycobacterium tuberculosis infections Eactors in transmission to staff and HIV-infected patients. JAMA 1992 268 1280-1286. 

Flynn JL, Goldstein MM, Triebold KJ, Sypek J, Wolf S, Bloom BR. lL-12 increases resistance of BALB/c mice to Mycobacterium tuberculosis infection. J Immunol 1995 155(5) 2515-2524. 

R = R = H) are intermediate, and gentamicin and tobramycin are most susceptible (66). Resistance to streptomycin is widespread, and its use is currently confined primarily to infections caused by Mycobacterium tuberculosis Yersiniapestis and Francisella tularensis. 

Mycobacterium tuberculosis is the causal organism of tuberculosis in humans. Allied strains cause infections in animals, e.g. bovine tuberculosis and tuberculosis in rodents. Due to the waxy nature of the cell wall this organism will resist desiccation and will survive in sputum. Tuberculosis has been largely eliminated by immunization and chemotherapy. 

The advent of multidrug resistant strains of Mycobacterium tuberculosis (MDR-TB) has led to increased fears of untreatable infections by serious pathogens. Rifampicin, streptomycin and, occasionally, the quinolones are drugs used in the treatment of mycobacterial infections and resistance to those agents is as described previously. There... 

Soro O, Pesce A, Raggi M, Debbia EA, Schito GC Selection of rifampicin-resistant Mycobacterium tuberculosis does not occur in the presence of low concentrations of rifaximin. Clin Microbiol Infect 1997 3 147-151. 

Mycobacteria are also killed in vitro, as expected from an antibiotic sharing the properties of the rifamycin family [24], In a study by Soro et al. [25], the MIC of rifaximin was determined for five Mycobacterium tuberculosis isolates from patients with tuberculosis. MIC concentrations were studied at 6, 20, 90 and 270 pg/ml, respectively. No resistant organisms were found. Growing M. tuberculosis in the presence of varying doses of rifaximin did not induce the occurrence of rifampicin-resistant strains [25]. In addition to this, experimental tubercular infection in the guinea pig was found not to be affected by an oral treatment course with rifaximin, therefore confirming the lack of absorption of the molecule after oral administration [26],... 

Reiling, N., et al., Cutting edge Toll-like receptor (TLR)2- and TLR4-mediated pathogen recognition in resistance to airborne infection with Mycobacterium tuberculosis,. /. Immunol. 169, 7, 3480, 2002. 

Intended for use concomitantly with other antituberculosis agents in pulmonary infections caused by capreomycin-susceptible strains of Mycobacterium tuberculosis, when the primary agents (eg, isoniazid, rifampin) have been ineffective or cannot be used because of toxicity or the presence of resistant tubercle bacilli. Administration and Dosage... 

Shi, R. et al. Temperature-mediated heteroduplex analysis for the detection of drug-resistant gene mutations in clinical isolates of Mycobacterium tuberculosis by denaturing HPLC, SURVEYOR nuclease. Microb. Infect. 2006, 8, 128-135. 

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