Biofilms and planktonic cells of Pseudomonas aeruginosa have similar resistance to killing by antimicrobials

Biofilms are considered to be highly resistant to antimicrobial agents. Str ictly speaking, this is not the case-biofilms do not grow in the presence o f antimicrobials any better than do planktonic cells. Biofilms are indeed h ighly resistant to killing by bactericidal antimicrobials, compared to loga rithmic-phase planktonic cells, and therefore exhibit tolerance. It is assu med that biofilms are also significantly more tolerant than stationary-phas e planktonic cells. A detailed comparative examination of tolerance of biof ilms versus stationary- and logarithmic-phase planktonic cells with four di fferent antimicrobial agents was performed in this study. Carbenicillin app eared to be completely ineffective against both stationary-phase cells and biofilms. Killing by this beta -lactam antibiotic depends on rapid growth, and this result confirms the notion of slow-growing biofilms resembling the stationary state. Ofloxacin is a fluoroquinolone antibiotic that kills non growing cells, and biofilms and stationary-phase cells were comparably tole rant to this antibiotic. The majority of cells in both populations were era dicated at low levels of ofloxacin, leaving a fraction of essentially invul nerable persisters. The bulk of the population in both biofilm and stationa ry- phase cultures was tolerant to tobramycin. At very high tobramycin conc entrations, a fraction of persister cells became apparent in stationary-pha se culture. Stationary-phase cells were more tolerant to the biocide perace tic acid than were biofilms. In general, stationary-phase cells were somewh at more tolerant than biofilms in all of the cases examined. We concluded t hat, at least for Pseudomonas aeruginosa, one of the model organisms for bi ofilm studies, the notion that biofilms have greater resistance than do pla nktonic cells is unwarranted. We further suggest that tolerance to antibiot ics in stationary-phase or biofilm cultures is largely dependent on the pre sence of persister cells.