Tuberculosis rifampicin

Mycobacterium tuberculosis Rifampicin + isoniazid + ethambutol + pyrazinamide ... 

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... 

Saline Rifaximin (60 mg/kg daily) Rifampicin (30 mg/kg daily) 54.11 extensive tuberculosis 54.47 extensive tuberculosis 11.00 very limited infection... 

The lack of absorption and, consequently, the lack of systemic therapeutic activity was also demonstrated in a model of experimental tuberculosis in the guinea pig [75], Here again, oral rifampicin but not oral rifaximin did protect the animals from the development of the infection (table 3) [76],... 

A study in the guinea pig with experimentally induced tuberculosis [44] did show that sensitivity to both rifampicin and rifaximin of the Mycobacterium (H37RY strain) remained unchanged after 3 months of drug administration, the MIC values being virtually the same before and after treatment. The development of resistance to rifaximin of different strains of M. tuberculosis, isolated from patients with pulmonary and renal tuberculosis, was studied under extremely stringent conditions [45]. 

Malvisi Stracciari J, Venturini AP, Anfossi P, Marchi E, Stracciari GL Sensitivity to rifaximin and rifampicin of Mycobacterium tuberculosis isolated from guinea pigs treated orally with rifaximin. Chemioterapia (Florence) 1987 6 82-84. 

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],... 

Rifampicin appears to be particularly promising in the treatment of tuberculosis, especially in combination with isoniazid. The prolonged high blood levels attainable with a single daily dose should simplify therapy. 

Rifampicin is highly active with respect to Mycobacterium tuberculosis. Among atypical mycobacteria, it is active with respect to M. kansasii, M. marinum, and to most types... 

Rifampicin is the most effective drng for treating pnlmonary and non-pulmonary forms of tuberculosis, including tnbercnlosis meningitis. It shonld always be used in combination with other drngs. Synonyms of this drng are rifadin, rimactan, rifapiam, rimactazide, and others. 

Previous guidelines specifically stated that rifampicin was contraindicated for patients who were taking any PI or NNRTI. New data indicate that rifampicin can be used for the treatment of tuberculosis in three situations ... 

Treatment of latent tuberculosis infection (LTBI) with isoniazid (INH) is very effective in preventing persons infected with M. tuberculosis from developing tuberculosis, regardless of HIV-1 serostatus. Several recent studies have shown that rifampicin and pyrazinamide taken for 2 months is as effective as 6-12 months of INH for the prevention of active TBC in HIV-1 seropositive persons although more hepatotoxicity is seen. 

The rifamycins, a class of antibacterials isolated from Streptomyces mediterranei, contain a macrocyclic ring bridging across two nonadjacent positions on an aromatic system. Rifampicin (9.96), a semisynthetic derivative of rifamycin, is a drug of choice in the treatment of tuberculosis as well as leprosy, either alone or in combination with other drugs. Rifampicin is much safer than other antituberculotics since it inhibits DNA-directed RNA polymerase in bacteria but not in mammals. Another rifamycin, rifabutin (9.97), is a spiroimidazopiperidyl derivative of the rifamycin. 

It is similar to rifampicin and shows significant activity against M. tuberculosis, M. avium complex and M. fortuitum. Rifabutin is both substrate and cytochrome 450 enzyme inducer. Because it is less potent inducer, rifabutin is used (in place of rifampicin) for the treatment of tuberculosis in HIV-infected patients, who are on concurrent antiretroviral therapy with a protease inhibitor. It is used alone or in combination with pyrazi-namide. 

It is an analog of rifampicin active against M. tuberculosis and M. avium. It inhibits bacterial RNA polymerase and it is a potent inducer of cytochrome P450 enz5mies. 

It is indicated in the treatment of tuberculosis caused by rifampicin susceptible strains. 

Suarez, S., O hara, P., Kazantseva, M., et al. (2001a). Respirable PLGA microspheres containing rifampicin for the treatment of tuberculosis Screening in an infectious disease model. Pharmaceut. Res., 18, 1315-1319. 

Detection of Rifampicin-Resistant Strains of Tuberculosis Rifampicin is an important antibiotic used to treat tuberculosis, as well as other mycobacterial diseases. 

Some strains of Mycobacterium tuberculosis, the causative agent of tuberculosis, are resistant to rifampicin. These strains become resistant through mutations that alter the rpoB gene, which encodes the /3 subunit of the RNA polymerase. Rifampicin cannot bind to the mutant RNA polymerase and so is unable to block the initiation of transcription. DNA sequences from a large number of rifampicin-resistant M. tuberculosis strains have been found to have mutations in a specific 69 bp region of rpoB. One well-characterized strain with rifampicin resistance has a single base pair alteration in rpoB that results in a single amino acid substitution in the J3 subunit a His residue is replaced by an Asp residue. 

Streptomycin (Boxes 20-B, 20-H) was introduced into clinical use against tuberculosis in about 1943. However, resistant mutants always survived until newer drugs were developed. Isonicotinylhydrazide (isoniazid) is especially effective in combinations with suitable antibiotics and other drugs.8 The four-drug combination isoniazid, rifampicin (Box 28-A), pyrazinamide, and ethambutol is often used. Nevertheless, bacteria resistant to all of these have developed. 

A 62-year-old man with recurrent non-Hodgkin s lymphoma developed pulmonary tuberculosis, for which he received rifampicin. Within 2 weeks, his thyrotropin (TSH) concentration increased to 170 mU/1 and the serum concentrations of thyroxine (T4) and triiodothyronine (T3) fell to 24 pg/l and 180 ng/1 respectively. He was given thyroxine. After the course of rifampicin therapy had been completed, thyroxine was withdrawn and he remained euthyroid for 4 years. 

The combination of rifampicin and isoniazid reduces serum concentrations of 25-hydroxy cholecalciferol. Rifampicin acts by induction of an enzyme that promotes conversion of 25-hydroxycholecalciferol to an inactive metabolite, and isoniazid acts by inhibiting 25-hydroxyla-tion and 1-hydroxylation (SEDA-14, 258). Children or pregnant women with tuberculosis have increased calcium requirements independent of rifampicin administration... 

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