Sci. STKE, 14 September 2004
MICROBIOLOGY Bacterial Persistence and Antibiotic Resistance
The inherent persistence of bacterial populations after exposure to antibiotics or other stress is well known but little understood. Such persistence is distinct from acquired antibiotic resistance and, on regrowth, such bacteria are still antibiotic sensitive (see the Perspective by Levin). Balaban et al. investigated the growth dynamics of various mutant and wild-type Escherichia coli using a microfluidic device to track individual organisms. At least three different phenotypes were revealed. Those with a normal growth rate were killed. Type I persisters exited stationary phase very slowly--hours rather than minutes after nutrients were restored. Type II persisters arose by a spontaneous switch from the normal growth rate to grow consistently more slowly, regardless of growth conditions, and, rarely, could switch back to the normal growth rate. Many pathogens have become resistant to the β-lactam antibiotics, like penicillin, by a variety of mechanisms, including mutation of penicillin-binding protein genes, destruction of the antibiotic by β-lactamases, or inhibition of uptake by the bacterial cells. Miller et al. (see the Perspective by Levin) describe another mechanism for avoiding the lethal effects of antibiotics. Damage to penicillin binding protein 3 activates the DpiBA two-component signal transduction cascade and eventually triggers the SOS DNA repair response. When SOS kicks in, cell division pauses, and the bacteria escape lethal damage, at least from short-term antibiotic exposure, because synthesis of new cell walls shuts down.
C. Miller, L. E. Thomsen, C. Gaggero, R. Mosseri, H. Ingmer, S. N. Cohen, SOS response induction by ß-lactams and bacterial defense against antibiotic lethality. Science 305, 1629-1631 (2004). [Abstract] [Full Text]
Citation: Bacterial Persistence and Antibiotic Resistance. Sci. STKE 2004, tw331 (2004).
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