De novo acquisition of resistance to three antibiotics by XXXX .

@entity1987 @entity14116 @entity115 @entity39739 @entity74 @entity803 @entity526
The acquisition of resistance to @entity115 , @entity803 , and @entity14116 by @entity39739 was examined by exposing growing cells to constant or stepwise increasing concentrations of these compounds. The @entity1987 ( @entity1987 ) of @entity526 for @entity115 increased from 4-8 to 32    g/ml after growth in the presence of 1.25 or 2.5    g/ml. By stepwise increasing the exposure, an @entity1987 of 512    g/ml was reached. This high @entity1987 was maintained after removal of the antibiotics, whereas the lesser increase after exposure to low levels was reversed, indicating that the high @entity1987 was due to a @entity74 , but the lower one to phenotypic adaptation only. The @entity1987 for @entity803 increased from 2    g/ml to maximally 32    g/ml. The @entity1987 decreased to control levels in the absence of @entity803 , so no genetic changes seem to have occurred. The @entity1987 for @entity14116 increased from 0.25    g/ml to maximally 512    g/ml depending on the concentration during growth. These data mostly support the "radical-based" theory that bactericidal antibiotics induce a common mechanism that contributes to cell killing. Our findings indicate that exposure to low levels of antibiotics causes an increase in @entity1987 above the concentration that the cells were exposed to. The implication is that exposure to low levels of antibiotics should be prevented as much as possible, because this causes resistance far more than high concentrations that inhibit growth or kill the cell and thus prevent acquisition of resistance.
