scholarly journals Anti-Biofilm Effect of Octenidine and Polyhexanide on Uropathogenic Biofilm-Producing Bacteria

2021 ◽  
pp. 1-7
Author(s):  
Maria Loose ◽  
Kurt G. Naber ◽  
Larry Purcell ◽  
Manfred P. Wirth ◽  
Florian M.E. Wagenlehner

<b><i>Background:</i></b> A catheter allowing a release of antibacterial substances such as antiseptics into the bladder could be a new way of preventing biofilm formation and subsequent catheter-associated urinary tract infections. <b><i>Methods:</i></b> Minimal inhibitory and bactericidal concentration (MIC/MBC) determinations in cation-adjusted Mueller-Hinton broth and artificial urine were performed for 4 antiseptics against 3 uropathogenic biofilm producers, <i>Escherichia coli</i>, <i>Pseudomonas aeruginosa</i>, and <i>Proteus mirabilis</i>. Furthermore, effects of octenidine and polyhexanide against catheter biofilm formation were determined by quantification of biofilm-producing bacteria. <b><i>Results:</i></b> Sodium hypochlorite showed MIC/MBC values between 200 and 800 mg/L for all strains tested. Triclosan was efficient against <i>E. coli</i> and <i>P. mirabilis</i> (MIC ≤2.98 mg/L) but ineffective against <i>P. aeruginosa</i>. Octenidine and polyhexanide showed antibacterial activity against all 3 species tested (MIC 1.95–7.8 and 3.9–31.25 mg/L). Both octenidine and polyhexanide were able to prevent biofilm formation on catheter segments in a concentration dependent manner. Furthermore, adding 250 mg/L of each biocide disrupted biofilms formed by <i>E. coli</i> and <i>P. mirabilis</i>, whereas even 500 mg/L was not sufficient to completely destroy <i>P. aeruginosa</i> biofilms. <b><i>Conclusion:</i></b> Octenidine- and polyhexanide-containing antiseptics showed a broad effect against typical uropathogenic biofilm producers even in high dilutions. This study provides a basis for further investigation of the potential of octenidine and polyhexanide as prophylaxis or treatment of catheter biofilms.

2019 ◽  
Vol 11 (01) ◽  
pp. 017-022 ◽  
Author(s):  
Rashmi M. Karigoudar ◽  
Mahesh H. Karigoudar ◽  
Sanjay M. Wavare ◽  
Smita S. Mangalgi

Abstract BACKGROUND: Escherichia coli accounts for 70%–95% of urinary tract infections (UTIs). UTI is a serious health problem with respect to antibiotic resistance and biofilms formation being the prime cause for the antibiotic resistance. Biofilm can restrict the diffusion of substances and binding of antimicrobials. In this context, the present study is aimed to perform in vitro detection of biofilm formation among E. coli strains isolated from urine and to correlate their susceptibility pattern with biofilm formation. MATERIALS AND METHODS: A total of 100 E. coli strains isolated from patients suffering from UTI were included in the study. The identification of E. coli was performed by colony morphology, Gram staining, and standard biochemical tests. The detection of biofilm was carried out by Congo Red Agar (CRA) method, tube method (TM), and tissue culture plate (TCP) method. Antimicrobial sensitivity testing was performed by Kirby–Bauer disc diffusion method on Muller–Hinton agar plate. RESULTS: Of the 100 E. coli strains, 49 (49%) and 51 (51%) were from catheterized and noncatheterized patients, respectively. Biofilm production was positive by CRA, TM, and TCP method were 49 (49%), 55 (55%), and 69 (69%), respectively. Biofilm producers showed maximum resistance to co-trimoxazole (73.9%), gentamicin (94.2%), and imipenem (11.6%) when compared to nonbiofilm producers. Significant association was seen between resistance to antibiotic and biofilm formation with a P = 0.01 (<0.05). CONCLUSION: A greater understanding of biofilm detection in E. coli will help in the development of newer and more effective treatment. The detection of biofilm formation and antibiotic susceptibility pattern helps in choosing the correct antibiotic therapy.


2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S287-S287
Author(s):  
Geoffrey Cheminet ◽  
Patrice Nordmann ◽  
Francoise Chau ◽  
Nicolas Kieffer ◽  
Katell Peoc’h ◽  
...  

Abstract Background A strategy used by bacterial strains to resist β-lactam antibiotics is the expression of metallo-β-lactamases (MBL) requiring zinc for activity. The use of a zinc chelator may restore carbapenem activity against MBL-producing Enterobacteriaceae. DMSA is a heavy metal chelator approved in humans with a satisfactory safety record. Our objective was to evaluate the activity of DMSA in combination with carbapenems, in vitro and in a fatal murine peritonitis model, against MBL-producing Escherichia coli. Methods Isogenic derivatives of wild-type E. coli CFT073 producing the MBL NDM-1, VIM-2, IMP-1, and the serine carbapenemases OXA-48 and KPC-3 were constructed. Minimum inhibitory concentrations (MICs) of imipenem, meropenem, and ertapenem were determined against each strain alone or in combination with DMSA. Mice were infected with E. coli CFT073 or NDM-1 and treated intraperitoneally for 24 hours with imipenem 100 mg/kg every 4 hours, DMSA 200 mg/kg every 4 hours, or both. Mice survival rates and bacterial counts in peritoneal fluid (PF) and spleen were assessed at 24 hours. Results In vitro, DMSA in combination with each carbapenem permitted a significant decrease of the MICs against all MBL-producing strains, in a concentration-dependent manner. The maximum effect was found for the NDM-1 strain with a 6- to 8-fold MIC reduction, depending on the carbapenem used. NDM-1 strain became susceptible to carbapenems with concentrations of DMSA ≥6 mM. Increasing zinc concentrations above 1 mg/L (average human plasma concentration) did not alter this effect. No benefit of DMSA was observed against non-MBL strains. In vivo, when used alone, the DMSA regimen was not toxic in uninfected mice and ineffective against NDM-1-infected mice (100% mortality). Combination of imipenem and DMSA significantly reduced bacterial counts in PF and spleen as compared with imipenem alone (P < 0.001), and reduced mortality, although not significantly (11% vs. 37%, respectively, P = 0.12). No benefit of the combination was observed against CFT073. Conclusion DMSA is highly effective in vitro in reducing carbapenems MICs against MBL-producing E. coli and appears as a promising strategy in combination with carbapenems for the treatment of NDM-1-related infections. Disclosures All authors: No reported disclosures.


2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 296-297 ◽  
Author(s):  
Claudio Arzola ◽  
Elizabeth Latham ◽  
Robin Anderson ◽  
Jaime Salinas-Chavira ◽  
Yamicela Castillo ◽  
...  

Abstract The influence of ferulic acid (FA) and sodium chlorate (SC) was evaluated in two trials on the growth of Escherichia coli F18 and K88 (F18 and K88) incubated with porcine fecal bacteria. Treatments were 2 levels of FA (0 and 5 mg/mL) and 2 levels of SC (0 and 10 mM/mL). In trial one, ½-strength Mueller Hinton broth mixed with porcine feces (0.5% w/v) was inoculated with a novobiocin and naladixic acid resistant F18-strain. This fecal suspension was transferred to tubes (3/treatment) and anaerobically incubated at 39 oC for enumeration at 0, 6 and 24 h using MacConkey agar supplemented with novobiocin and naladixic acid with aerobic incubation at 37 oC. An interaction (FA x SC) at 6 and 24 h was observed (P &lt; 0.01). At 6 h of incubation, SC alone or combined with FA had the lowest counts (P &lt; 0.05); FA alone was lower than control but higher than SC or SC+FA (P &lt; 0.05). At 24 h, FA alone or combined with SC had the lowest counts (P &lt; 0.05); SC was lower than control but higher than FA or SC+FA (P &lt; 0.05). In trial 2 were used the same procedures of trial 1, except that K88 was used. There was an interaction at 6 h (P &lt; 0.01) where the lowest counts were in FA+SC (P &lt; 0.05). SC alone or FA alone were lower than control but higher than SC+FA (P &lt; 0.05). There was no interaction at 24 h (P = 0.16), where FA reduced the K88 counts (P &lt; 0.01), however it was not affected by SC (P = 0.12). In conclusion, SC reduced E. coli counts; however, at 24 h of incubation greater reductions were observed when FA alone or combined with SC was added into the incubation fluid with porcine feces.


2004 ◽  
Vol 72 (8) ◽  
pp. 4570-4578 ◽  
Author(s):  
Robert Blomgran ◽  
Limin Zheng ◽  
Olle Stendahl

ABSTRACT Type 1 fimbriae are the most commonly expressed virulence factor on uropathogenic Escherichia coli. In addition to promoting avid bacterial adherence to the uroepithelium and enabling colonization, type 1 fimbriae recruit neutrophils to the urinary tract as an early inflammatory response. Using clinical isolates of type 1 fimbriated E. coli and an isogenic type 1 fimbria-negative mutant (CN1016) lacking the FimH adhesin, we investigated if these strains could modulate apoptosis in human neutrophils. We found that E. coli expressing type 1 fimbriae interacted with neutrophils in a mannose- and lipopolysaccharide (LPS)-dependent manner, leading to apoptosis which was triggered by the intracellular generation of reactive oxygen species. This induced neutrophil apoptosis was abolished by blocking FimH-mediated attachment, by inhibiting NADPH oxidase activation, or by neutralizing LPS. In contrast, CN1016, which did not adhere to or activate the respiratory burst of neutrophils, delayed the spontaneous apoptosis in an LPS-dependent manner. This delayed apoptosis could be mimicked by adding purified LPS and was also observed by using fimbriated bacteria in the presence of d-mannose. These results suggest that LPS is required for E. coli to exert both pro- and antiapoptotic effects on neutrophils and that the difference in LPS presentation (i.e., with or without fimbriae) determines the outcome. The present study showed that there is a fine-tuned balance between type 1 fimbria-induced and LPS-mediated delay of apoptosis in human neutrophils, in which altered fimbrial expression on uropathogenic E. coli determines the neutrophil survival and the subsequent inflammation during urinary tract infections.


Microbiology ◽  
2005 ◽  
Vol 151 (7) ◽  
pp. 2487-2497 ◽  
Author(s):  
Anne Vianney ◽  
Grégory Jubelin ◽  
Sophie Renault ◽  
Corine Dorel ◽  
Philippe Lejeune ◽  
...  

Curli are necessary for the adherence of Escherichia coli to surfaces, and to each other, during biofilm formation, and the csgBA and csgDEFG operons are both required for their synthesis. A recent survey of gene expression in Pseudomonas aeruginosa biofilms has identified tolA as a gene activated in biofilms. The tol genes play a fundamental role in maintaining the outer-membrane integrity of Gram-negative bacteria. RcsC, the sensor of the RcsBCD phosphorelay, is involved, together with RcsA, in colanic acid capsule synthesis, and also modulates the expression of tolQRA and csgDEFG. In addition, the RcsBCD phosphorelay is activated in tol mutants or when Tol proteins are overexpressed. These results led the authors to investigate the role of the tol genes in biofilm formation in laboratory and clinical isolates of E. coli. It was shown that the adherence of cells was lowered in the tol mutants. This could be the result of a drastic decrease in the expression of the csgBA operon, even though the expression of csgDEFG was slightly increased under such conditions. It was also shown that the Rcs system negatively controls the expression of the two csg operons in an RcsA-dependent manner. In the tol mutants, activation of csgDEFG occurred via OmpR and was dominant upon repression by RcsB and RcsA, while these two regulatory proteins repressed csgBA through a dominant effect on the activator protein CsgD, thus affecting curli synthesis. The results demonstrate that the Rcs system, previously known to control the synthesis of the capsule and the flagella, is an additional component involved in the regulation of curli. Furthermore, it is shown that the defect in cell motility observed in the tol mutants depends on RcsB and RcsA.


Author(s):  
Gaurab Risal ◽  
Aayush Shrestha ◽  
Saroj Kunwar ◽  
Gajal Paudel ◽  
Rameshwor Dhital ◽  
...  

Background: In urinary tract infections, an important role is played by bacterial biofilms which are responsible for persistence infections together with the antimicrobial resistance. Higher resistance can be seen in biofilm forming uropathogens in comparison with free-floating bacteria. So, the present study was performed with a goal to find the prevalence of biofilm formation and also the antimicrobial resistant pattern of uropathogens.Methods: A descriptive method was conducted at Modern Technical College, Sanepa, Lalitpur in samples isolated from UTI suspected patients. The overall duration of this study was approximately 3 months. Total of 50 isolated E. coli was tested for biofilm formation and antimicrobial susceptibility testing was done by Kirby-Bauer disc diffusion method on Mueller Hinton agar as per CLSI guidelines.Results: From the 50 isolates of E. coli, 32 were biofilm producers (3 strong and 29 moderate) and 18 were weak/non-biofilm producers. Among the biofilm producers, cefotaxime was more resistant in 20 of the isolates followed by ceftriaxone in 16 and amoxyclav in 13, whereas amikacin was least resistant in 2 of the isolates.Conclusions: Among the isolated E. coli, biofilm-forming isolates showed higher antimicrobial resistance as compared to the non-biofilm producer. Thus, uropathogen should be routinely screened for biofilm formation. 


2020 ◽  
Vol 75 (12) ◽  
pp. 3593-3600 ◽  
Author(s):  
G Cheminet ◽  
V de Lastours ◽  
L Poirel ◽  
F Chau ◽  
K Peoc’h ◽  
...  

Abstract Background Carbapenemase-producing Enterobacterales represent a major therapeutic challenge. MBLs, requiring zinc at their catalytic site, could be inhibited by meso-dimercaptosuccinic acid (DMSA), a heavy metal chelator already widely used for treating lead intoxication. Objectives To evaluate the activity of carbapenems alone or combined with DMSA against MBL-producing Escherichia coli in a severe murine peritonitis model. Methods Isogenic strains of wild-type E. coli CFT073 producing the MBLs NDM-1, VIM-2 and IMP-1, and the control serine carbapenemases OXA-48 and KPC-3 were constructed. MIC determinations and time–kill assays were performed for imipenem, meropenem and ertapenem alone or in combination with DMSA. Infected mice were treated intraperitoneally for 24 h with imipenem, DMSA or their combination. Bacterial counts in peritoneal fluid and spleen were assessed at 24 h. Results DMSA in combination with each carbapenem caused a significant decrease in the MICs for all MBL-producing strains, in a concentration-dependent manner, but did not provide benefit against non-MBL strains. In mice infected with the NDM-1-producing strain, the combination of imipenem and DMSA significantly reduced bacterial counts in peritoneal fluid (P = 0.0006) and spleen (P &lt; 0.0001), as compared with imipenem alone, with no benefit against the KPC-3-producing and CFT073 strains. DMSA concentrations in plasma of mice were comparable to those obtained in humans with a standard oral dose. Conclusions DMSA restores the activity of carbapenems against MBL-producing strains, and its combination with carbapenems appears to be a promising strategy for the treatment of NDM-producing E. coli infections.


QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Eman Adel El-Haddad ◽  
Soha Abdel Rahman El-Hady ◽  
Amira Esmail Abdel Hamid ◽  
Hisham Abdel Majeed Fahim

Abstract Introduction Bacteria in most environments exist as communities of sessile cells in a selfproduced polymeric matrix known as biofilms. Biofilms are responsible for more than 80% of infections, including urinary tract infections (UTI). UTI is the most common hospital acquired infection, caused mainly by Escherichia coli (E.coli). E. coli can readily form biofilm in such infections, specially in the presence of indwelling urinary catheter. It’s difficult to eradicate bacteria in biofilms, since they are shielded from the host defense mechanisms as phagocytes and antibodies, as well as antibiotics. Searching for alternative or adjuvant substances for prevention and eradication of biofilm associated infections are therefore urgently needed. Aim of the work Studying the efficacy of the trans-cinnamaldehyde (TC) for preventing E. coli biofilm formation. Materials and methods Thirty isolates of E.coli were obtained from urine samples. To test the effect of TC on E.coli biofilm formation and preformed biofilms, microtitre plates (MTP) were inoculated with the isolated E.coli and were treated with different concentrations of TC and incubated at 37° C. A colorimetric assay was used to assess biofilm inhibition and inactivation and optical densities (OD) were compared before and after adding different TC concentrations. Results The mean OD of the isolated E.coli biofilms was 1.3 and significantly decreased when mixed with TC different concentrations. TC had high activity in inhibition of preformed E.coli biofilms, where no biofilm was detected on MTP treated with 1.25% and 1.5% TC. Conclusion TC inhibited the biofilm forming ability of E.coli isolates could fully inactivate formed biofilms, suggesting its possibility to be used as an anti-biofilm agent or adjuvant in preventing and treating UTI caused by biofilm producing E.coli.


Pathogens ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 885
Author(s):  
Mariarita Stirpe ◽  
Benedetta Brugnoli ◽  
Gianfranco Donelli ◽  
Iolanda Francolini ◽  
Claudia Vuotto

Poloxamers are nontoxic, amphiphilic copolymers used in different formulations. Due to its surfactant properties, Poloxamer 338 (P388) is herein proposed as a strategy to avoid biofilm formation often causing recalcitrant catheter-associated urinary tract infections (CAUTI). The aim is to evaluate the ability of P388 coatings to affect the adhesion of Ec5FSL and Ec9FSL Escherichia coli strains on silicone urinary catheters. Attenuated total reflection infrared spectroscopy, atomic force microscopy, and static water contact angle measurement were employed to characterize the P388-coated silicone catheter in terms of amount of P388 layered, coating thickness, homogeneity, and hydrophilicity. In static conditions, the antifouling power of P388 was defined by comparing the E. coli cells adherent on a hydrophilic P388-adsorbed catheter segment with those on an uncoated one. A P388-coated catheter, having a homogeneous coverage of 35 nm in thickness, reduced of 0.83 log10 and 0.51 log10 the biofilm of Ec5FSL and Ec9FSL, respectively. In dynamic conditions, the percentage of cell adhesion on P388-adsorbed silicone channels was investigated by a microfluidic system, simulating the in vivo conditions of catheterized patients. As a result, both E. coli isolates were undetected. The strong and stable antifouling property against E. coli biofilm lead us to consider P388 as a promising anti-biofilm agent for CAUTIs control.


1992 ◽  
Vol 70 (1) ◽  
pp. 43-48 ◽  
Author(s):  
S. S. Ghosh ◽  
Richard C. Franson

Autoclaved Escherichia coli labelled with [1-14C]oleate in the 2-acyl position have been used extensively to measure phospholipase A2 activity in vitro. The present study demonstrates that this membranous substrate is also useful for the measurement of in vitro phospholipase D activity. Phospholipase D from Streptomyces chromofuscus catalyzed the hydrolysis of [1-14C]oleate labelled, autoclaved E. coli optimally at pH 7.0–8.0 to generate [14C]phosphatidic acid in the presence of 5 mM added Ca2+. Other divalent cations would not substitute for Ca2+. Activity was linear with time and protein up to 30% of the hydrolysis of substrate. Phospholipase D activity was stimulated in a dose-dependent manner by the addition of Triton X-100. The activity was increased 5.5-fold with 0.05% Triton, a concentration that totally inhibited hydrolysis of E. coli by human synovial fluid phospholipase A2. Accumulation of [14C]diglyceride was observed after 10 min of incubation. This accumulation was inhibited by NaF (IC50 = 18 μM) or propanolol (IC50 = 180 μM) suggesting the S. chromofuscus phospholipase D was contaminated with phosphatidate phosphohydrolase. Phosphatidic acid released by the action of cabbage phospholipase D was converted to phosphatidylethanol in an ethanol concentration dependent manner. These results demonstrate that [1-14C]oleate labelled, autoclaved E. coli can be used to measure phospholipase D activity by monitoring accumulation of either [14C]phosphatidic acid or [14C]phosphatidylethanol.Key words: Escherichia coli, substrate, phospholipase D, Streptomyces chromofuscus, sodium fluoride, propranolol.


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