Interventions for Tuberculosis Control and Elimination
Next
Previous
First
Last
While it is desirable to treat patients with multidrug-resistant tuberculosis as early as possible, the tools to diagnose it are not widely available. In most low-income countries, treatment failure must be diagnosed based on sputum smear microscopy as culture followed by suscpetibility testing takes too long time to act and is not commonly available. Direct tests to simultaneously identify M tuberculosis and determining its susceptibility pattern are being developed but before they mature into an ubiquitously available and inexpensive, sustainable tool are not currently reality.
Sputum smear microscopy as a tool to assess true treatment failure has drawbacks as non-viable bacilli might also be stained. Before the introduction of rifampicin, the presence of stainable bacilli during treatment virtually always predicted vialbe bacilli. With the introduction of rifampicin throughout the treatment, increasingly staining bacilli are no more viable and thus suggest failure where there is actually none.
The explanation for this discordance that is offered most frequently is that isoniazid acts by interference with mycolic acids which are a necessary component of the mycobacterial cell wall and if the cell wall cannot be built properly, bacilli can also no more be stained. In contrast, rifampicin acts by interfering at the ribosomal level, acts more swiftly than isoniazid and bacilli may still have stainable cell walls but can no more replicate. They will thus stain but can no more be cultivated.
