Multidrug-resistant tuberculosis MDRTB

In the treatment of tuberculosis, resistant strains of M. tuberculosis (multidrug-resistant tuberculosis, MDRTB) present a growing problem, so that new antituber-culotic agents are required which act according to a different mechanism to that of standard agents such as isoniazid, rifampicin, pyrazinamide, and ethambutol. The more modern fluoroquinolones are of particular interest, and in particular moxifloxacin, which has powerful in vitro and in vivo activity and, in contrast to sparfloxacin and clinafloxacin, is not photo toxic [191]. 

Amaral et al. [3] prepared a review providing cogent evidence that both intracellular multidrug-resistant tuberculosis (MDRTB) and intracellular methicillin-resistant Staphylococcus aureus (MRSA) can be killed by concentrations of thioridazine in the medium that is below that present in the plasma of the patients treated with this agent. Although thioridazine has been claimed to cause arrhythmias and even sudden death, the frequencies of those episodes are rare and, when present, they are related to a patient s underlying cardiac status, as opposed to the direct effect of the agent itself. 

Multidrug-resistant M. tuberculosis (MDRTB) strains have become a problem. As pointed out previously, the mycobacterial cell wall presents a major barrier to the entry of chemotherapeutic drugs. Possible solutions are (i) to design drugs of increasing hydrophobicity that will pass through the cell wall, as with isoniazid derivatives [89, 90], (ii) to use a second antibiotic in combination with a known inhibitor of arabinogalactan or mycolic acid biosynthesis [238]. 

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