Mycobacterium tuberculosis infection treatment

Bigbee CL, Gonchoroff DG, Vratsanos G, Nadler SG, Haggerty HG, Flynn JL. Abata-cept treatment does not exacerbate chronic Mycobacterium tuberculosis infection in mice. Arthritis Rheum 2007 56 2557-2565. 

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... 

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],... 

In an in vitro susceptibility study of 170 clinical isolates of Mycobacterium tuberculosis to fusidic acid, 19 isolates were resistant to at least one first-Une antituberculosis drug (21). In all, 1.8% of the isolates were resistant to fusidic acid. Fusidic acid can be a potential supplementary drug for the treatment of infections due to multidrug-resistant strains of M. tuberculosis. 

Reactivation of latent tuberculosis is a major concern with infliximab (SEDA-26, 402), and accounts for about one-third of infections in these patients. According to data from the manufacturers, 130 cases of active tuberculosis were notified up to October 2001. Many of the cases were disseminated or extrapulmonary tuberculosis, and several patients died. Several case reports have provided detailed information in at least seven other patients, including three who developed miliary tuberculosis and one who developed Mycobacterium tuberculosis enteritis (44-48). A detailed analysis of 70 cases of tuberculosis reported to the FDA has been published (49). Two-thirds of the cases were noted after three or fewer infusions and 57% of the patients had extrapulmonary disease. There were 64 cases from countries with a low incidence of tuberculosis. From these reports and the number of patients treated with infliximab, the estimated rate of tuberculosis in patients with rheumatoid arthritis treated with infliximab was four times higher than the background rate. Patients with evidence of active infection should not receive infliximab until the infection is under control all should be screened for tuberculosis before starting infliximab (50). From these and other data it has been estimated that the risk of tuberculosis in the first year of infliximab treatment is 0.035 in US citizens and 0.2% in non-US citizens. Further investigations, such as a chest X-ray and a Mantoux test, and prophylactic treatment with isoniazid, will show whether the incidence can be reduced in patients taking anti-TNF treatment (51). 

Not all mycobacterial infections are caused by Mycobacterium tuberculosis or Mycobacterium leprae. These atypical mycobacteria require treatment with secondary medications as well as other chemotherapeutic agents. For example, Mycobacterium marinum causes skin granulomas, and effective drugs in the treatment of the infection are rifampin or minocycline. Mycobacterium fortuitum causes skin ulcers, and the medications recommended for treatment are ethambutol, cycloserine, and rifampin in combination with amikacin. 

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