Development of resistance to chlorhexidine diacetate in Pseudomonas aeruginosa and the effect of a 'residual' concentration

Thomas, Louise; Maillard, Jean‐Yves; Lambert, R. H.; Russell, A. D.

doi:10.1053/jhin.2000.0851

Cited by 165 publications

(101 citation statements)

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“…Irrizary et al showed that chlorhexidine digluconate residues can have a selective effect on MRSA isolates (29). In another study, it was found that subinhibitory concentrations of chlorhexidine digluconate can cause a permanent increase in MIC values of P. aeruginosa isolates (30). These findings emphasize how important it is to clean surfaces first before disinfection occurs.…”

Section: Discussionmentioning

confidence: 96%

An investigation of the bactericidal activity of chlorhexidine digluconateagainst multidrug-resistant hospital isolates

Ekizoğlu¹,

Sağıroğlu²,

Kılıç³

et al. 2016

Turk J Med Sci

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Section: Discussionmentioning

confidence: 96%

An investigation of the bactericidal activity of chlorhexidine digluconateagainst multidrug-resistant hospital isolates

Ekizoğlu¹,

Sağıroğlu²,

Kılıç³

et al. 2016

Turk J Med Sci

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“…Thus routine use of antimicrobial oral health-care products could conceivably select for a population of bacteria with an intrinsic ability to resist antibiotic therapy, and consequently limit the effectiveness of antibiotic treatment following periodontal surgery. Development of resistance to chlorhexidine has been demonstrated in some Gram-negative bacteria including Pseudomonas aeruginosa (Thomas et al, 2000) and Klebsiella pneumoniae (Fang et al, 2002). With PDT, lethal photosensitization mediates bacterial killing via singlet oxygen and free radicals.…”

Section: Discussionmentioning

confidence: 99%

Susceptibility of microcosm subgingival dental plaques to lethal photosensitization

2007

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A B S T R A C TPhotodynamic therapy (PDT) offers potential as a non-invasive treatment of periodontal disease. In this study, microcosm biofilms were grown in vitro under conditions designed to mimic subgingival plaques typically found in patients with periodontitis. To investigate potential PDT modalities, biofilms were exposed to light from a helium/neon laser in conjunction with a photosensitizer, toluidine blue O (TBO), at varying output and concentration, respectively. To determine cytotoxic effects, viability profiling was undertaken on whole biofilms using standard plating methods, and on horizontal cross-sections of biofilms using confocal laser-scanning microscopy (CLSM) in conjunction with a differential viability stain. A light energy dose of 94.5 J in combination with 81.7 µM TBO was found to be optimal, achieving significant kills of over 97%. CLSM enabled visualization of the effects of PDT in three dimensions. Viability profiling of the CLSM images revealed that lethal photosensitization was most effective in the upper layers of biofilm. PDT was found to reduce the viability of subgingivally modelled plaques in vitro by a magnitude similar to that of chlorhexidine digluconate, which is commonly used to treat periodontal disease. The findings of this study indicate that PDT may be an effective alternative to conventional modalities in the treatment of periodontal disease.

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“…The results of Sørensen et al showed that the concentra-45 tion of hBD-3 increases within 4 days after sterile wounding [11]; therefore we assumed that 46 the bacteria are first exposed to CH for at least 3 days before the hBD-3 concentration on 47 skin increases. 48 49 It has been reported that different bacterial species are able to adapt to sub-lethal concentra-50 tions of CH [15][16][17][18][19][20] and that this adaptation affects the susceptibility to different biocides [21] 51 and antibiotics in Pseudomonas stutzeri [16,21,22]. Moore et al showed that different skin 52 bacteria were able to adapt to CH after repeated exposure [23].…”

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confidence: 99%

“…We found a significant decrease in hBD-3 susceptibility for both exposure times 261 only for S. capitis 19/2 and after 3h exposure to hBD-3 for S. warneri 16/1.In three cases 262 more CHG-exposed bacteria were killed by hBD-3 compared to non-exposed bacteria, al-263 though in one case the difference was less than 0.4 log-scales (Figures 1-5). Exposure to CH has been reported to result in adaptation, e.g., in skin bacteria [23], and 274 thus, changes susceptibility to different antibiotics and biocides [15][16][17][18][19][20][21][22]. Therefore an influ-275 ence of previous exposure to CHG on susceptibility to hBD-3 is possible due to the structural 276 properties of both substances and their comparable mode of action.…”

mentioning

confidence: 99%

“…A comparable 289 mechanism with a change in the bacterial surface charge to resist human beta-defensins is 290 also discussed for Gram-negative bacteria [31]. Therefore, a correlation between the mecha 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Reichel et al Bacterial response to human β-Defensin-3 after chlorhexidine exposure 15 nism of bacteria to circumvent the natural host defence of the skin caused by AMPs and the 292 mechanism for resistance to cationic antimicrobials, e.g. CH is likely.…”

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confidence: 99%

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Skin bacteria after chlorhexidine exposure—is there a difference in response to human β-Defensin-3?

Reichel

Heisig

et al. 2010

Eur J Clin Microbiol Infect Dis

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Purpose:We investigated whether exposure to sub-lethal concentrations of chlorhexidine digluconate (CH) changed the response of 5 Staphylococcus spp. to human β-Defensin-3. Methods:The change in response for each strain was determined in-vitro with time-kill-experiments in suspension by comparing the mean log10-reduction caused by hBD-3 at 1.5 and 3 h in exposed and non-exposed bacteria. Identity of staphylococcal species was verified by DNA sequence homology in the gyrA genes in comparison with reference strains.Results: Baseline sub-lethal concentrations allowing visible bacterial growth were between 0.0625 and 0.25 μg/ml. Sub-lethal CH concentrations increased within 3 days in two isolates. For Staphylococcus capitis 19/2, CH-exposed cells were less susceptible to 0.5 μg/ml hBD-3 (log10-reduction 0.78 versus 2.06 at 1.5 h; p <0.001; t-test). For Staphylococcus aureus, however, CH-exposed cells were more susceptible to 1 μg/ml hBD-3. The observed changes between CH-exposed and non-exposed cells did not indicate a general trend in response to hBD-3. Conclusions:Overall, we found no consistent evidence that 3 days of exposure to CHG changed the response of 5 Staphylococcus spp. to hBD-3. The use of CHG for skin antisepsis is, based on our data, unlikely to change the natural defence activity of hBD-3.Response to Reviewers: REVIEWER #1:Major points:Reviewer comment: Human beta-defensin-3 is a very sticky peptide. To minimize losses, cationic antimicrobial peptides are usually dissolved in weakly acidic solvents. The authors used water, which could influence losses of the peptide and thus might influence its concentration in the remaining solution.Response: We were aware that some studies were published with hBD-3 using acetic acid for dissolving the peptide, but the manufacturer (RELIATech) confirmed that their hBD-3 should be reconstituted in water, that it can also be diluted in water and that the use of water will not change the activity of the peptide which was used for the test. That was the reason why we used water (pH-value between 6.5 and 6.8).Reviewer comment: Did the authors pool the beta-defensin-3? If yes, did they use the material at exactly identical conditions (e.g. storage at ambient temperature or in the refrigerator after thawing). If not, one would expect variable results.Response: Whenever necessary, we pooled aliquots of the diluted peptide after thawing. We did not pool different batches because we only used one batch of the peptide. Nevertheless, we used cooled metal blocks for the storage of the peptide after thawing to ensure that the con-ditions did not change between tests.The part in the Methods section of the manuscript was amended to clarify the questions of the reviewer.Reviewer comment: Could the authors reproduce in independent experiments (with another peptide sample) the results they found in the four cases where hBD-3 killed significantly fewer bacteria?Response: It is a very interesting question if the decrease of the sensitivity of the strain to hBD-3 could also be ...

show abstract

Development of resistance to chlorhexidine diacetate in Pseudomonas aeruginosa and the effect of a 'residual' concentration

Cited by 165 publications

References 20 publications

An investigation of the bactericidal activity of chlorhexidine digluconateagainst multidrug-resistant hospital isolates

An investigation of the bactericidal activity of chlorhexidine digluconateagainst multidrug-resistant hospital isolates

Susceptibility of microcosm subgingival dental plaques to lethal photosensitization

Skin bacteria after chlorhexidine exposure—is there a difference in response to human β-Defensin-3?

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