The growth of Gardnerella vaginalis and Lactobacillus acidophilus in Sorbarod biofilms

Muli, F. W.; Struthers, J. K.

doi:10.1099/00222615-47-5-401

Cited by 19 publications

(27 citation statements)

References 11 publications

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“…In E. coli, increasing concentrations of ciprofloxacin or imipenem caused an initial 100-to 1,000-fold decrease in live cells of a biofilm, while the remaining small population was essentially insensitive to further increases in drug concentration (4). This pattern was also observed with amoxicillin and clindamycin in Lactobacillus acidophilus and with erythromycin and metronidazole in the case of Gardnera vaginalis biofilms, where initial rapid killing was followed by a plateau of resistant cells (66). It appears that biofilm survival can be largely explained by the increased production of persistor cells.…”

Section: Death and Survival In Biofilmsmentioning

confidence: 49%

Programmed Death in Bacteria

Lewis

2000

Microbiol Mol Biol Rev

543

411

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SUMMARY Programmed cell death (PCD) in bacteria plays an important role in developmental processes, such as lysis of the mother cell during sporulation of Bacillus subtilis and lysis of vegetative cells in fruiting body formation of Myxococcus xanthus. The signal transduction pathway leading to autolysis of the mother cell includes the terminal sporulation sigma factor EςK, which induces the synthesis of autolysins CwlC and CwlH. An activator of autolysin in this and other PCD processes is yet to be identified. Autolysis plays a role in genetic exchange in Streptococcus pneumoniae, and the gene for the major autolysin, lytA, is located in the same operon with recA. DNA from lysed cells is picked up by their neighbors and recombined into the chromosome by RecA. LytA requires an unknown activator controlled by a sensory kinase, VncS. Deletion of vncS inhibits autolysis and also decreases killing by unrelated antibiotics. This observation suggests that PCD in bacteria serves to eliminate damaged cells, similar to apoptosis of defective cells in metazoa. The presence of genes affecting survival without changing growth sensitivity to antibiotics (vncS, lytA, hipAB, sulA, and mar) indicates that bacteria are able to control their fate. Elimination of defective cells could limit the spread of a viral infection and donate nutrients to healthy kin cells. An altruistic suicide would be challenged by the appearance of asocial mutants without PCD and by the possibility of maladaptive total suicide in response to a uniformly present lethal factor or nutrient depletion. It is proposed that a low rate of mutation serves to decrease the probability that asocial mutants without PCD will take over the population. It is suggested that PCD is disabled in persistors, rare cells that are resistant to killing, to ensure population survival. It is suggested that lack of nutrients leads to the stringent response that suppresses PCD, producing a state of tolerance to antibiotics, allowing cells to discriminate between nutrient deprivation and unrepairable damage. High levels of persistors are apparently responsible for the extraordinary survival properties of bacterial biofilms, and genes affecting persistence appear to be promising targets for development of drugs aimed at eradicating recalcitrant infections. PCD in unicellular eukaryotes is also considered, including aging in Saccharomyces cerevisiae. Apoptosis-like elimination of defective cells in S. cerevisiae and protozoa suggests that all unicellular life forms evolved altruistic programmed death that serves a variety of useful functions.

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Section: Death and Survival In Biofilmsmentioning

confidence: 49%

Programmed Death in Bacteria

Lewis

2000

Microbiol Mol Biol Rev

543

411

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“…For example, in E. coli, increasing concentrations of ciprofloxacin or imipenem caused an initial decrease in the number of live cells of a biofilm by 2 to 3 orders of magnitude, while the remaining small population was essentially insensitive to a further increase in the drug concentration (4). This pattern was also observed with amoxicillin and clindamycin in Lactobacillus acidophilus and with erythromycin and metronidazole in the case of Gardnerella vaginalis biofilms, in which initial rapid killing was followed by a plateau of resistant cells (43).…”

Section: Unusual Suspectsmentioning

confidence: 64%

Riddle of Biofilm Resistance

Lewis

2001

Antimicrob Agents Chemother

1,719

1,248

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“…In E. coli, increasing concentrations of ciprofloxacin or imipenem caused an initial decrease in live cells of a biofilm by 2 to 3 orders of magnitude, while the remaining small population was essentially insensitive to a further increase in drug concentration (3). This pattern was also observed with amoxicillin and clindamycin in Lactobacillus acidophilus, and with erythromycin and metronidazole in the case of Gardnerella vaginalis biofilms, where initial rapid killing was followed by a plateau of resistant cells (28). To our knowledge, the phenom- FIG.…”

Section: Discussionmentioning

confidence: 86%

A Dose-Response Study of Antibiotic Resistance in Pseudomonas aeruginosa Biofilms

Brooun

Liu

Lewis

2000

Antimicrob Agents Chemother

432

313

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Bacterial biofilms show enormous levels of antibiotic resistance, but little is known about the underlying molecular mechanisms. Multidrug resistance pumps (MDRs) are responsible for the extrusion of chemically unrelated antimicrobials from the bacterial cell. Contribution of the MDR-mediated efflux to antibiotic resistance of Pseudomonas aeruginosa biofilms was examined by using strains overexpressing and lacking the MexAB-OprM pump. Resistance of P. aeruginosa biofilms to ofloxacin was dependent on the expression of MexAB-OprM but only in the low concentration range. Unexpectedly, biofilm resistance to ciprofloxacin, another substrate of MexAB-OprM, did not depend on the presence of this pump. Dose-dependent killing indicated the presence of a small "superresistant" cell fraction. This fraction was primarily responsible for very high resistance of P. aeruginosa biofilms to quinolones. Bacterial cells recovered from a biofilm and tested under nongrowing conditions with tobramycin exhibited higher resistance levels than planktonic cells but lower levels than cells of an intact biofilm.

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The growth of Gardnerella vaginalis and Lactobacillus acidophilus in Sorbarod biofilms

Cited by 19 publications

References 11 publications

Programmed Death in Bacteria

Programmed Death in Bacteria

Riddle of Biofilm Resistance

A Dose-Response Study of Antibiotic Resistance in Pseudomonas aeruginosa Biofilms

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