A fluoroquinolone resistant variant of Salmonella Typhi has emerged that is likely to be widespread in the Indian subcontinent; therefore fluoroquinolones should not be recommended for empirical typhoid fever therapy in this setting.
Penetration of the fluoroquinolones in tuberculosis lesions is heterogeneous even in fully cellular areas, is driven by macrophage content and decreases as the distance from lesion outer rim increases.
The major evolutionary routes to drug resistance in Salmonella Typhi are associated with fitness benefits, not fitness costs, implying that prudent antimicrobial use will have no effect as a public health intervention in controlling typhoid fever.
Mutations in several components of a bacterial ribosome are shown to broadly decrease antibiotic and stress sensitivity, and readily accessible reversion mutations allow these ribosomal mutations to serve as stepping stones to high level antibiotic resistance.
Sequential therapy with only β-lactam antibiotics achieves surprisingly high potency by exploiting both low rates of spontaneous resistance emergence and low rates of spontaneous cross-resistance among the drugs in sequence.
Selection imposed by antibiotics may dominate evolutionary forces acting on opportunistic pathogens like Acinetobacter baumannii, yet chance effects and a prior history in biofilm may constrain resistance and impose collateral sensitivities.
Population-level antibiotic resistance correlates with the breadth of antibiotic use, that is, the proportion of people taking an antibiotic, better than with intensity of use the amount of use among users.