Abstract
Persisters are a small proportion of a bacterial population that exists in a physiological state permitting survival despite the lethal activity of antibiotics. To explain this phenomenon, it has been suggested
that persisters are bacteria repairing spontaneous errors of DNA synthesis. To verify this assumption,
Escherichia coli
AB 1157 and its
lexA3
derivative were exposed to a dose 6× MIC
of various antibiotics representative of different molecular mechanisms of action (ampicillin, ceftriaxone, meropenem, amikacin, ciprofloxacin). Bacterial cell counts, after 24 hr of exposure to the antimicrobials,
revealed a reduction of about 90% of viable organisms in the
lexA3
strains in comparison to the lexA
+
. In several cases, the number of colony-forming units decreased below the limit of
assay. This behavior was noted with all antibiotics used, alone or in combination (amikacin plus ceftriaxone and amikacin plus ciprofloxacin). The same experiments were repeated using
E. coli
AB1157
cultured in the presence of mitomycin C (0.25× MIC), and the number of survivors exceeded by about 90% the values found in the nonexposed control. In contrast, in the
sulA
background, mitomycin
C reacted synergically with all the antibiotics tested causing a strong reduction of the survivors in comparison with the control. The addition of chloramphenicol (0.125× MIC), on the contrary, caused
a reduction of the number of survivors of about 90%. These findings indicate that, when DNA repair is active (a mechanism known to block cell division), the number of survivors is greater than that observed
with
lexA3
. Thus, in addition to other possible explanations, persisters might be a fraction of bacteria that during antibiotic treatment are not growing because they are repairing spontaneous errors
of DNA synthesis.