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Medical Forum / Diseases and Disorders / Sinusitis / January 2008Chelator-induced dispersal and killing of Pseudomonas aeruginosa cells in a biofilm.
Chelator-induced dispersal and killing of Pseudomonas aeruginosa cells in a biofilm. Banin E, Brady KM, Greenberg EP. Box 357242, Department of Microbiology, University of Washington School of Medicine, Seattle, WA 98195-7242, USA. Biofilms consist of groups of bacteria attached to surfaces and encased in a hydrated polymeric matrix. Bacteria in biofilms are more resistant to the immune system and to antibiotics than their free- living planktonic counterparts. Thus, biofilm-related infections are persistent and often show recurrent symptoms. The metal chelator EDTA is known to have activity against biofilms of gram-positive bacteria such as Staphylococcus aureus. EDTA can also kill planktonic cells of Proteobacteria like Pseudomonas aeruginosa. In this study we demonstrate that EDTA is a potent P. aeruginosa biofilm disrupter. In Tris buffer, EDTA treatment of P. aeruginosa biofilms results in 1,000- fold greater killing than treatment with the P. aeruginosa antibiotic gentamicin. Furthermore, a combination of EDTA and gentamicin results in complete killing of biofilm cells. P. aeruginosa biofilms can form structured mushroom-like entities when grown under flow on a glass surface. Time lapse confocal scanning laser microscopy shows that EDTA causes a dispersal of P. aeruginosa cells from biofilms and killing of biofilm cells within the mushroom-like structures. An examination of the influence of several divalent cations on the antibiofilm activity of EDTA indicates that magnesium, calcium, and iron protect P. aeruginosa biofilms against EDTA treatment. Our results are consistent with a mechanism whereby EDTA causes detachment and killing of biofilm cells. PMID: 16517655 [PubMed - indexed for MEDLINE] How do we get and use EDTA? Topically? Orally? Judy > Chelator-induced dispersal and killing of Pseudomonas aeruginosa cells > in a biofilm. [quoted text clipped - 27 lines] > > PMID: 16517655 [PubMed - indexed for MEDLINE] > How do we get and use EDTA? Topically? Orally? > Judy Common chemical. Ethylene Diamine Tetra Acetic Acid Use it along with ascorbic acid to take the scale out of boiler pipes. 600 mg capsules available over the internet. I am not familiar with the buffer that they used, but having used it in my own wash, it is pretty irritating and could use something to cut the edge. It is also used medically for Cleation therapy for lead and heavy element poisoning. Hi, I've just joined and have read all the mails about Pseudomonas a. with great interest. I'm just wondering if you can help me with a question that I have. My son picked up a pseudomonas a. infection whilst ventilated and was released with this infection. It, of course just got worse and worse and despite treatment with various antibiotics he didn't get rid of it. He had the infection for five months and needed oxygen.Eventually we started him on a dose of Cipro for a number of weeks and he tested negative for pseudo a. for four months and was still negative for this bacterium when hospitalised and intubated for a staph. epi infection. He was treated for the staph infection, which cleared well but after 3 weeks in hospital he again had a pseudo a. infection. We were told it was the same infection as before, as he had been colonized, but this pseudo infection was sensitive to gentamycin whilst the previous chronic infection had grown resistant. To me this could not have been the same infection, it had to be a new infection as surely a bacterium that was once sensitive to genta but then became resistant cannot be sensitive to genta again. Just wondering if I'm correct with this. My son was immunocompromised as he suffered chest infections due to Kyphoscoliosis. >Chelator-induced dispersal and killing of Pseudomonas aeruginosa cells >in a biofilm. [quoted text clipped - 27 lines] > >PMID: 16517655 [PubMed - indexed for MEDLINE] Hi, I've just joined and have read all the mails about Pseudomonas a. with great interest. I'm just wondering if you can help me with a question that I have. My son picked up a pseudomonas a. infection whilst ventilated and was released with this infection. It, of course just got worse and worse and despite treatment with various antibiotics he didn't get rid of it. He had the infection for five months and needed oxygen.Eventually we started him on a dose of Cipro for a number of weeks and he tested negative for pseudo a. for four months and was still negative for this bacterium when hospitalised and intubated for a staph. epi infection. He was treated for the staph infection, which cleared well but after 3 weeks in hospital he again had a pseudo a. infection. We were told it was the same infection as before, as he had been colonized, but this pseudo infection was sensitive to gentamycin whilst the previous chronic infection had grown resistant. To me this could not have been the same infection, it had to be a new infection as surely a bacterium that was once sensitive to genta but then became resistant cannot be sensitive to genta again. Just wondering if I'm correct with this. My son was immunocompromised as he suffered chest infections due to Kyphoscoliosis. >Chelator-induced dispersal and killing of Pseudomonas aeruginosa cells >in a biofilm. [quoted text clipped - 27 lines] > >PMID: 16517655 [PubMed - indexed for MEDLINE]
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