Good new approaches are available to prevent resistance. In particular, calculated enzyme flexibility is very seldom so high that a simultaneous attack on several pathways does not have a good chance of success [44, 45]. The evolutionary flexibility of pathogens can be estimated by considering genetic mechanisms for immune escape and new mutations available: Are there specific antigen-shifting mechanisms? What about recombination, resistance plasmids, genome instability, transposons? - to name just some of the more common mechanisms. Interestingly, this list shows that meticulous genome annotation (see above) is in fact quite important in determining and assessing pathogen flexibility in this genetic respect.
Another important consideration takes account of the typical resistance mechanisms against antibiotics. Fortunately, similar mechanisms for this are used in many pathogens: resistance is often achieved by (a) inactivation of the attacking antibiotic, (b) modification of the antibiotic target within the bacterial cell, (c) increased transport of antibiotic out of the cell, or (d) prevention of antibiotic uptake. Combined strategies, fighting with both a standard antibiotic and resensi-tization by blocking such typical resistance mechanisms against antibiotics, are thus quite promising and a bioinformatic prediction about the capabilities in regard to these four mechanisms can be made for the pathogen in question.
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