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the biofilm’s characteristics ..

24/04/1998 · Antimicrobial resistance to disinfectants in ..

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resistance to disinfectants in biofilms ..

This analysis of options suggests that the development of a universal antibiofilm therapy, possibly on the basis of targeting of persister proteins, is a long-term project, yet a possible simple solution to biofilm infection follows directly from the dynamics of in vitro biofilm eradication. The rationale is to administer a cidal antibiotic, then withdraw it, and then add it again. The first application of antibiotic will eradicate the bulk of biofilm cells, leaving persisters. In a realistic example, ofloxacin decreases the size of a P. aeruginosa biofilm from 108 cells to 105 persisters (). Withdrawal of the antibiotic will allow this persister population to start growing. Assume that after two divisions the persistence phenotype is lost. At this point, the new population of 4 × 105 cells will produce 40 persisters. A second application of antibiotic should then completely eradicate the biofilm. This type of a simple cyclical antibiotic regimen was proposed previously by Bigger () for eradication of staphylococcal persisters. This approach might work in topical applications, in which the delivery of antibiotics can be well controlled. For example, biofilm infections are common in urinary catheters, into which a desired solution can be instilled. P. aeruginosa biofilm infections of cystic fibrosis patients provide another example in which this approach might work well. Antibiotics can be delivered topically to cystic fibrosis patients as aerosols. The popular medication Tobra (PathoGenesis/Chiron) is a tobramycin aerosol. This antibiotic is very effective in eradicating planktonic cells, which explains the clinical usefulness of the preparation. However, as discussed above, biofilms are resistant to tobramycin. In a cyclical application, one would deliver an aerosol of a fluoroquinolone antibiotic like ciprofloxacin, which would penetrate the biofilm and kill the cells. A second antibiotic application after a minimal period of time that would be necessary for survivors to start growing and loose their persister phenotype could then eradicate the biofilm. The feasibility of a cyclical biofilm eradication approach will depend on the rate with which persisters lose resistance to killing and regenerate new persisters and on the ability to manipulate the antibiotic concentration. Development of resistance in a situation in which the antibiotic concentration is allowed to drop is a concern, but cycling of two different antibiotics could largely eliminate this problem. If this approach works for topical applications, it will encourage an inquiry into the possible use of cyclical treatment of systemic biofilms as well. It is entirely possible that successful cases of antimicrobial therapy of biofilm infections result from a fortuitous optimal cycling of an antibiotic concentration that eliminated first the bulk of the biofilm and then the progeny of the persisters that began to divide.

CHARACTERISTICS OF ANTIBIOTICS WASTES - …
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Biofilms are enclosed within an exopolymer matrix that can restrict the diffusion of substances and bind antimicrobials. This will provide effective resistance for biofilm cells against large molecules such as antimicrobial proteins lysozyme and complement. The diffusion barrier is also probably effective against smaller antimicrobial peptides—the numerous defensins and their analogs. The negatively charged exopolysaccharide is very effective in protecting cells from positively charged aminoglycoside antibiotics by restricting their permeation, possibly through binding (, ).

22/12/2017 · CHARACTERISTICS OF A..

mechanisms of biofilm resistance to antibiotics
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Abstract:
Biofilms are three-dimensional structures that contains billions of genetically identical bacteria submerged in a self-produced extracellular matrix, which protect bacteria from antibiotics and the human immunological defenses. More than 85 % of chronic and/or recurrent human infections are linked to bacterial biofilms. In addition, spore-forming pathogenic bacteria represent an additional community threat because of their intrinsic refractory behavior against antibiotics, phagocytes and their easy utilization in bioterrorist attacks. Therefore, every day the available microbicide arsenal against biofilms and spores becomes scarcer. Accordingly, nano-material biotechnology emerges as a promising alternative for reducing the detrimental effects of microbial-related diseases. Here we describe the development of novel nanostructured coating systems with improved photocatalytic and antibacterial activities. These systems comprise, in one case, layers of SiO2 followed by layers of mesoporous or dense TiO2-anatase, and doping with silver nanoparticles (Ag NPs). In the other case, we developed Copper NPs and its oxides by a chemical method based on a bottom up approach and its stabilization using aminosilanes as surface modifiers. The activity of CuNPs and AgNPs (MNPs) was measured against spores and vegetative (planktonic and sessile) forms of the relevant human pathogens Enterohemorrhagic Escherichia coli (etiological agent of Hemolytic Uremic Syndrome), Listeria monocytogenes (etiological agent of septic abortion), Bacillus anthracis (etiological agent of Anthrax), Clostridium perfringens (etiological agent of food-associated diarrhea and Gas Gangrene), cystic-fibrosis related Pseudomona aeruginosa and methicillin-resistant Staphylococcus aureus ( etiological agent of sepsis and myocardiopathies). The planktonic and sessile growth (measured as the final cellular yield at 600 nm and crystal violet staining, respectively) of each pathogen, as well as the sporocide effect on C. perfringens and B. anthracis spores, was very significant at submillimolar concentrations of MNPs (95 % of vegetative growth inhibition and sporocide effect, p

Abstract:
Biofilms are three-dimensional structures that contains billions of genetically identical bacteria submerged in a self-produced extracellular matrix, which protect bacteria from antibiotics and the human immunological defenses. More than 85 % of chronic and/or recurrent human infections are linked to bacterial biofilms. In addition, spore-forming pathogenic bacteria represent an additional community threat because of their intrinsic refractory behavior against antibiotics, phagocytes and their easy utilization in bioterrorist attacks. Therefore, every day the available microbicide arsenal against biofilms and spores becomes scarcer. Accordingly, nano-material biotechnology emerges as a promising alternative for reducing the detrimental effects of microbial-related diseases. Here we describe the development of novel nanostructured coating systems with improved photocatalytic and antibacterial activities. These systems comprise, in one case, layers of SiO2 followed by layers of mesoporous or dense TiO2-anatase, and doping with silver nanoparticles (Ag NPs). In the other case, we developed Copper NPs and its oxides by a chemical method based on a bottom up approach and its stabilization using aminosilanes as surface modifiers. The activity of CuNPs and AgNPs (MNPs) was measured against spores and vegetative (planktonic and sessile) forms of the relevant human pathogens Enterohemorrhagic Escherichia coli (etiological agent of Hemolytic Uremic Syndrome), Listeria monocytogenes (etiological agent of septic abortion), Bacillus anthracis (etiological agent of Anthrax), Clostridium perfringens (etiological agent of food-associated diarrhea and Gas Gangrene), cystic-fibrosis related Pseudomona aeruginosa and methicillin-resistant Staphylococcus aureus ( etiological agent of sepsis and myocardiopathies). The planktonic and sessile growth (measured as the final cellular yield at 600 nm and crystal violet staining, respectively) of each pathogen, as well as the sporocide effect on C. perfringens and B. anthracis spores, was very significant at submillimolar concentrations of MNPs (95 % of vegetative growth inhibition and sporocide effect, p

kanamycin were effective against biofilm ..

Micro Ch 10 Flashcards | Quizlet
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In conclusions, a thorough study of bacterial biofilm is required to better understand bacterial cells behaviour in biofilm, and also to understand bacterial resistance to multiple drugs. An elaborate molecular study is further needed to understand various gene expression/repression during biofilm formation [-]. These various molecular mechinisms can be targetd to control or inhibit biofilm formation. As biofilms show multiple drug resistance due to less penetration of antibiotics, therefore new therapeutic strategies are mandatory such as new agents are needed that can disrupt the biofilms to reach bacteria residing deep down in the biofilms. Main approaches for controlling these infections include the use of inhibitors of quorum sensing to prevent bacterial biofilm formation and disintegrate synthesis of polysaccharides [-].

Another mechanism of resistance is the synthesis proteins that may protect the ribosomes against the antibiotic action. These antibiotics inhibit protein synthesis on bacterial ribosomes and act against 30S subunits (Tc and GAs) or 50S (CAP and macrolides) [].

resistance occurring through ..
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    antibiotics against ..

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Foods | An Open Access Food Science Journal from MDPI

: Streptogramins are antibiotics that are a combination of two types: streptogramins A and B. Streptogramins B share the same site of action as macrolides and lincosamides, while streptogramins A act at a separate site on the ribosome that enhances the effect of the streptogramins A (). The original agent in the class, pristinamycin, has been available as an oral medication in France for many years. More recently, a semisynthetic injectable streptogramin combination, quinupristin-dalfopristin, has been developed particularly aimed at the treatment of multi-resistant Gram-positive infections. The advantage of these agents is that activity is usually retained against staphylococci and other gram-positives that are resistant to macrolides and lincosamides (,), and thus all forms of MRSA. Resistance to quinupristin-dalfopristin is currently very rare (,).

Foods, an international, peer-reviewed Open Access journal.

A similar targeted search for persister (tolerance) genes was performed with S. pneumoniae (). The same dual test that Moyed and colleagues used was applied to screen for mutants, saving those with increased resistance to killing by penicillin and those with unchanged susceptibility to growth inhibition by penicillin. One of the 17 mutants obtained in this screen appeared to have a mutation in a new sensory kinase, which was named VncS. vncS mutants were reported to be resistant not only to cell wall inhibitors but also to aminoglycosides and quinolones. At the same time, growth of the vncS mutant was inhibited by antibiotics as effectively as growth of the wild type, showing that antibiotics were able to act normally against their targets in vncS mutant cells. In S. pneumoniae, an autolysin (LytA) is responsible for autolysis, and lytA mutants are resistant to killing by cell wall inhibitors like penicillin () (antibiotics that are not cell wall inhibitors were not tested with the lytA mutant). LytA was normally expressed in the vncS strain. Apparently, VncS does not control the synthesis of LytA but, rather, regulates expression of an unknown factor that activates LytA in response to an antibiotic's action (). VncS is activated at least in part by an extracellular peptide pheromone ().

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