Abstract:Infections account for a major cause of death throughout the developing world. This is mainly due to the emergence of newer infectious agents and more specifically due to the appearance of antimicrobial resistance. With time, the bacteria have become smarter and along with it, massive imprudent usage of antibiotics in clinical practice has resulted in resistance of bacteria to antimicrobial agents. The antimicrobial resistance is recognized as a major problem in the treatment of microbial infections. The bioch… Show more
“…Although there were some minor increases in the zones of inhibition for the TE exposures, none of these treatments were significant enough to provide a change in susceptibility, indicating that the change in antibiotic susceptibility was due to the effects of the E-field and not to any induced heating. Although the different classes of antibiotics work on various cellular targets to inactivate bacteria (Li et al 2015;Kapoor et al 2017), the first step in the mechanism of action for all antibiotics is to traverse the cell membrane and enter the cytoplasm (James et al 2009;Krause et al 2016). Research conducted by Pillet et al (2016) showed scanning electron, transmission electron and atomic force microscopy results demonstrating the morphological, mechanical and physical damage to the cell wall of Bacillus pumilus from various strengths of µs electric pulses (Pillet et al 2016).…”
Cell suspensions of Escherichia coli and Lactobacillus acidophilus were exposed to 600-ns pulsed electric fields (nsPEFs) at varying amplitudes or High-23.5 kV cm −1 ) and pulse numbers (0 (sham), 1, 5, 10, 100 or 1000) at a 1 hertz (Hz) repetition rate. The induced temperature rise generated at these exposure parameters, hereafter termed thermal gradient, was measured and applied independently to cell suspensions in order to differentiate inactivation triggered by electric field (E-field) from heating. Treated cell suspensions were plated and cellular inactivation was quantified by colony counts after a 24-hour (h) incubation period. Additionally, cells from both exposure conditions were incubated with various antibiotic-soaked discs to determine if nsPEF exposure would induce changes in antibiotic susceptibility. Results indicate that, for both species, the total delivered energy (amplitude, pulse number and pulse duration) determined the magnitude of cell inactivation. Specifically, for 18.5 and 23.5 kV cm −1 exposures, L. acidophilus was more sensitive to the inactivation effects of nsPEF than E. coli, however, for the 13.5 kV cm −1 exposures E. coli was more sensitive, suggesting that L. acidophilus may need to meet an E-field threshold before significant inactivation can occur. Results also indicate that antibiotic susceptibility was enhanced by multiple nsPEF exposures, as observed by increased zones of growth inhibition. Moreover, for both species, a temperature increase of ≤ 20 °C (89% of exposures) was not sufficient to significantly alter cell inactivation, whereas none of the thermal equivalent exposures were sufficient to change antibiotic susceptibility categories.
“…Although there were some minor increases in the zones of inhibition for the TE exposures, none of these treatments were significant enough to provide a change in susceptibility, indicating that the change in antibiotic susceptibility was due to the effects of the E-field and not to any induced heating. Although the different classes of antibiotics work on various cellular targets to inactivate bacteria (Li et al 2015;Kapoor et al 2017), the first step in the mechanism of action for all antibiotics is to traverse the cell membrane and enter the cytoplasm (James et al 2009;Krause et al 2016). Research conducted by Pillet et al (2016) showed scanning electron, transmission electron and atomic force microscopy results demonstrating the morphological, mechanical and physical damage to the cell wall of Bacillus pumilus from various strengths of µs electric pulses (Pillet et al 2016).…”
Cell suspensions of Escherichia coli and Lactobacillus acidophilus were exposed to 600-ns pulsed electric fields (nsPEFs) at varying amplitudes or High-23.5 kV cm −1 ) and pulse numbers (0 (sham), 1, 5, 10, 100 or 1000) at a 1 hertz (Hz) repetition rate. The induced temperature rise generated at these exposure parameters, hereafter termed thermal gradient, was measured and applied independently to cell suspensions in order to differentiate inactivation triggered by electric field (E-field) from heating. Treated cell suspensions were plated and cellular inactivation was quantified by colony counts after a 24-hour (h) incubation period. Additionally, cells from both exposure conditions were incubated with various antibiotic-soaked discs to determine if nsPEF exposure would induce changes in antibiotic susceptibility. Results indicate that, for both species, the total delivered energy (amplitude, pulse number and pulse duration) determined the magnitude of cell inactivation. Specifically, for 18.5 and 23.5 kV cm −1 exposures, L. acidophilus was more sensitive to the inactivation effects of nsPEF than E. coli, however, for the 13.5 kV cm −1 exposures E. coli was more sensitive, suggesting that L. acidophilus may need to meet an E-field threshold before significant inactivation can occur. Results also indicate that antibiotic susceptibility was enhanced by multiple nsPEF exposures, as observed by increased zones of growth inhibition. Moreover, for both species, a temperature increase of ≤ 20 °C (89% of exposures) was not sufficient to significantly alter cell inactivation, whereas none of the thermal equivalent exposures were sufficient to change antibiotic susceptibility categories.
“…For years, antimicrobial photodynamic therapy (aPDT) has been used effectively in the eradication of gram-positive and gram-negative bacteria [6,7]. Various bacterial cells' structures and components are the targets for PDT in contrast to one major target in the case of antibiotics [8,9]. Thus, PDT reduces the risk of developing resistance of microorganisms exposed to it [10].…”
Photodynamic therapy (PDT) has been proven to kill different microbial cells. However, to our knowledge, none of the available reports describes the modulatory effect of this therapy on the antibacterial activity of antibiotics against Escherichia coli rods being the main causative agent of urinary tract infections (UTIs). Therefore, the aim of our study was to verify if the PDT can enhance the antibacterial activity of antibiotics recommended in the treatment of UTIs. An attempt to determine the optimal conditions of PDT to enhance the bactericidal activity of ciprofloxacin, amikacin, and colistin has been made. In order to find the optimal antimicrobial conditions, the efficacy of four protocols associated with the use of different energy doses (70 and 120 J/ cm 2 ) and chlorin e6 (Ce6) concentrations (50 and 100 μg/mL) has been verified. The antibacterial effect of combined PDT and antibiotics was assessed by the time-kill assay. The best results were achieved for Ce6 at a concentration of 100 μg/mL and the energy dose 120 J/cm 2 for bacterial suspensions treated with ciprofloxacin. Taken together, our results showed that PDT using Ce6 improves the antibacterial activity of antibiotics effectively inhibiting bacterial growth and being promising in the elimination of bacterial UTIs in humans.
“…Over time this leads to selection of resistant organism, the use of the antimicrobial resulting in 'selection pressure' for resistance. Although this may seem complicated, it is a simple Darwinian Table 6.3 Mechanisms of resistance in bacteria (Giedraitienė et al 2011;Kapoor et al 2017 selection occurring as a result of antimicrobial use. This is the reason why antimicrobials are fundamentally different to all other medicines; they have both an individual effect (curing the infection) and a population effect (selection for resistance), and sometimes these conflict (Sandoval-Motta and Aldana 2016).…”
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