Los mecanismos genéticos y moleculares de M. tuberculosis son diversos; en estos radica su virulencia, difícil diagnostico y tratamiento.
Algunos de estos mecanismos actúan sobre diversos fármacos como por ejemplo:
Algunos de estos mecanismos actúan sobre diversos fármacos como por ejemplo:
Resistencia a la isoniácida: Posee una potente acción bactericida y actúa únicamente contra bacterias en fase de replicación activa. Su mecanismo de acción es desconocido aunque parece estar mediado por la enzima catalasa-peroxidasa de M. Tuberculosis que lo transforma en el principio activo, el cual es el responsable de la alteración de la síntesis del ácido micólico.
Resistencia a estreptomicina: El mecanismo de acción de la estreptomicina es similar al de los otros aminoglucósidos, uniéndose al fragmento 16S del ARN ribosomal (rARN) provoca la inhibición de la síntesis proteica. La resistencia a este fármaco con actividad antitubercular se asocia a mutaciones en el gen rrs que codifica la síntesis del fragmento 16S del rARN y en el gen rpsL que codifica el fragmento 12S.
Resistencia a rifampicina: La rifampicina se usa en el tratamiento antituberculoso desde el inicio de los años 70. El fármaco se une a la ARN polimerasa e interfiere con la síntesis del ácido nucleico en el proceso de replicación bacteriana. La resistencia a la rifampicina se asocia a determinadas mutaciones en una región de 81 bp del gen rpoB que codifica la subunidad beta de la ARN polimerasa. En el 97% de cepas de M. tuberculosis rifampicina resistentes se han detectado mutaciones en este gen.
"La búsqueda de un mecanismo responsable de la multiresistencia de M. Tuberculosis no ha sido fructífero y la única explicación está relacionada con la acumulación de mutaciones adquiridas en el genoma bacteriano.
"La búsqueda de un mecanismo responsable de la multiresistencia de M. Tuberculosis no ha sido fructífero y la única explicación está relacionada con la acumulación de mutaciones adquiridas en el genoma bacteriano.
Las alteraciones genéticas no siempre son detectadas en cepas consideradas como resistentes con los métodos convencionales (antibiograma), por lo que se supone que deben existir mutaciones todavía no identificadas en el genoma micobacteriano responsables de dicho fenotipo."
Fuente Bibliográfica:
http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S0034-79732001000400006
http://scielo.isciii.es/scielo.php?pid=S1137-66272007000400006&script=sci_arttext
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