Nanodiamonds facilitate killing of intracellular uropathogenic E. coli in an in vitro model of urinary tract infection pathogenesis

Background. Diabetic patients are more susceptible to urinary tract infection compared to nondiabetic patients, Escherichia coli being the most common uropathogen causing UTI. Unreasonable and incorrect antibiotic prescription for UTI in these patients may induce the development of antibiotic-resistant urinary pathogens resulting in delayed recovery and longer hospitalization. In addition to these, biofilm forming capacity of the pathogen may worsen the problem. The main aim of this cross-sectional study (conducted from March to September 2015) is to detect the biofilm forming capacity of UTI causing micro-organisms and compare the antibiotic resistance pattern of Escherichia coli, the most common cause of UTI, which will help the physician in choosing the best antibiotic. Method. Total of 1,099 clean-catch mid stream urine (CCMSU) was processed by standard microbiological technique; 182 were from the diabetic group and 917 nondiabetic. Following identification, all isolates were subjected to antibiotic susceptibility testing using modified Kirby-Bauer disc diffusion method. In-vitro biofilm forming capacity of the isolates were detected by Microtitre plate method. The data were analyzed using SPSS software 16. Result. Urinary tract infection was found to be significantly higher in diabetic patients (42.9%) compared to nondiabetic patients (17.4%) with Escherichia coli as the most common uropathogen in both diabetic and nondiabetic groups. Similarly, UTI was more common in elderly population (29.5%). Imipenem, nitrofurantoin and amikacin were found to be the most effective drug for uropathogenic E. coli in both diabetic and nondiabetic patients, whereas amoxicillin, ciprofloxacin, and cotrimoxazole were least effective. Of the total bacterial isolates, 43.3% showed positive results for in-vitro biofilm production by the Microtitre plate method. A significantly higher resistance rate was observed among biofilm producing E. coli for quinolones, cotrimoxazole, and third generation cephalosporin ceftriaxone. Most of the biofilm producers (79.5%) were found to be MDR (p-value 0.015). Conclusion. Elderly populations with diabetes are at a higher risk of UTI. Higher biofilm production and resistance to in-use antimicrobial agents in this study render its inefficacy for empirical treatment and point out the importance of biofilm screening to ensure the effective management of infection.

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In vitro inhibition of Escherichia coli from women with urinary tract infection by cranberry hydroalcoholic extract

Revista Fitos ◽

10.32712/2446-4775.2019.792 ◽

2019 ◽

Vol 13 (4) ◽

pp. 278-288

Author(s):

Mariê Scotegagna Chiavini ◽

Jane Mary Lafayette Neves Gelinski ◽

Claudriana Locatelli ◽

Pâmela Aparecida da Costa ◽

Vânia Aparecida Vicente

Keyword(s):

Escherichia Coli ◽

Urinary Tract Infection ◽

Urinary Tract ◽

Tract Infection ◽

Direct Action ◽

E Coli ◽

Antimicrobial Potential ◽

Diffusion Assay

The antimicrobial potential of cranberry hydro alcoholic extracts (CrE) was evaluated against Escherichia coli isolated from women with urinary tract infection (UTI). CrE was diluted based on the percentage of proanthocyanidins (PACs) in extract powder for final concentrations: 1.26%; 2.52%; 3.35%, 5.03% and 10.06%. CrE antimicrobial potential was evaluated by disk and well diffusion assays, and by in vitro direct action against E. coli. Antibacterial action was observed for all performed tests: minimal inhibitory concentration (MIC) was 1.26% PACs per disk diffusion assay and 2.52% of PACs by well diffusion assay. The in vitro antimicrobial direct action against E. coli resulted 3.8 Log10 cycles reduction for a concentration of 5.03% of PACs. One of the isolates showed multi resistance to antibiotics. But it was also inhibited more than any of the antibiotic tested in well diffusion assay. Only for concentrations 1.26%, 2.52% and 3.45% the inhibition of Escherichia coli by cranberry extract was dose-dependent, i.e directly proportional to the concentration of PACs. The results indicate a inhibitory action high potential of CrE. However, more in vitro and in vivo analysis can be performed to fix which the best concentration of CrE capable of causing a real beneficial effect on UTI´s.

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Urinary tract infection in iNOS-deficient mice with focus on bacterial sensitivity to nitric oxide

AJP Renal Physiology ◽

10.1152/ajprenal.00101.2002 ◽

2003 ◽

Vol 284 (1) ◽

pp. F22-F31 ◽

Cited By ~ 24

Author(s):

Mirjana Poljakovic ◽

Katarina Persson

Keyword(s):

Nitric Oxide ◽

Urinary Tract Infection ◽

Urinary Tract ◽

Tract Infection ◽

Inflammatory Cells ◽

E Coli ◽

Bacterial Sensitivity ◽

Oxide Synthase ◽

Deficient Mice

Inducible nitric oxide synthase (iNOS)-deficient mice were used to examine the role of iNOS in Escherichia coli-induced urinary tract infection (UTI). The toxicity of nitric oxide (NO)/peroxynitrite to bacteria and host was also investigated. The nitrite levels in urine of iNOS+/+but not iNOS−/−mice increased after infection. No differences in bacterial clearance or persistence were noted between the genotypes. In vitro, the uropathogenic E. coli 1177 was sensitive to 3-morpholinosydnonimine, whereas the avirulent E. coli HB101 was sensitive to both NO and 3-morpholinosydnonimine. E. coli HB101 was statistically ( P < 0.05) more sensitive to peroxynitrite than E. coli 1177. Nitrotyrosine immunoreactivity was observed in infected bladders of both genotypes and in infected kidneys of iNOS+/+mice. Myeloperoxidase, neuronal (n)NOS, and endothelial (e)NOS immunoreactivity was observed in inflammatory cells of both genotypes. Our results indicate that iNOS−/−and iNOS+/+mice are equally susceptible to E. coli-induced UTI and that the toxicity of NO to E. colidepends on bacterial virulence. Furthermore, myeloperoxidase and nNOS/eNOS may contribute to nitrotyrosine formation in the absence of iNOS.

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Evaluation of direct in-vitro effect of Vaccinium macrocarpon against E. coli in urinary tract infection patients

International Journal of Biosciences (IJB) ◽

10.12692/ijb/9.6.440-445 ◽

2016 ◽

Vol 9 (6) ◽

pp. 440-445

Keyword(s):

Urinary Tract Infection ◽

Urinary Tract ◽

Tract Infection ◽

Vaccinium Macrocarpon ◽

E Coli ◽

Vitro Effect

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Antimicrobial Activity Evaluation of Tebipenem (SPR859), an Orally Available Carbapenem, against a Global Set of Enterobacteriaceae Isolates, Including a Challenge Set of Organisms

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.02618-18 ◽

2019 ◽

Vol 63 (6) ◽

Cited By ~ 3

Author(s):

S. J. Ryan Arends ◽

Paul R. Rhomberg ◽

Nicole Cotroneo ◽

Aileen Rubio ◽

Robert K. Flamm ◽

...

Keyword(s):

Escherichia Coli ◽

Antimicrobial Activity ◽

Urinary Tract Infection ◽

Urinary Tract ◽

Tract Infection ◽

Broth Microdilution ◽

Wild Type ◽

Content Type ◽

E Coli

ABSTRACT The antimicrobial activity of tebipenem and other carbapenem agents were tested in vitro against a set of recent clinical isolates responsible for urinary tract infection (UTI), as well as against a challenge set. Isolates were tested by reference broth microdilution and included Escherichia coli (101 isolates), Klebsiella pneumoniae (208 isolates), and Proteus mirabilis (103 isolates) species. Within each species tested, tebipenem showed equivalent MIC50/90 values to those of meropenem (E. coli MIC50/90, ≤0.015/0.03 mg/liter; K. pneumoniae MIC50/90, 0.03/0.06 mg/liter; and P. mirabilis MIC50/90, 0.06/0.12 mg/liter) and consistently displayed MIC90 values 8-fold lower than imipenem. Tebipenem and meropenem (MIC50, 0.03 mg/liter) showed equivalent MIC50 results against wild-type, AmpC-, and/or extended-spectrum β-lactamase (ESBL)-producing isolates. Tebipenem also displayed MIC50/90 values 4- to 8-fold lower than imipenem against the challenge set. All carbapenem agents were less active (MIC50, ≥8 mg/liter) against isolates carrying carbapenemase genes. These data confirm the in vitro activity of the orally available agent tebipenem against prevalent UTI Enterobacteriaceae species, including those producing ESBLs and/or plasmid AmpC enzymes.

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Effect of Inactivation of the Global Oxidative Stress Regulator oxyR on the Colonization Ability of Escherichia coli O1:K1:H7 in a Mouse Model of Ascending Urinary Tract Infection

Infection and Immunity ◽

10.1128/iai.74.1.461-468.2006 ◽

2006 ◽

Vol 74 (1) ◽

pp. 461-468 ◽

Cited By ~ 34

Author(s):

James R. Johnson ◽

Connie Clabots ◽

Henry Rosen

Keyword(s):

Escherichia Coli ◽

Urinary Tract Infection ◽

Urinary Tract ◽

Tract Infection ◽

Wild Type ◽

In Vitro Susceptibility ◽

E Coli ◽

C57bl Mice ◽

The Impact

ABSTRACT To survive within the host urinary tract, Escherichia coli strains that cause urinary tract infection (UTI) presumably must overcome powerful oxidant stresses, including the oxygen-dependent killing mechanisms of neutrophils. Accordingly, we assessed the global oxygen stress regulator OxyR of Escherichia coli as a possible virulence factor in UTI by determining the impact of oxyR inactivation on experimental urovirulence in CBA/J and C57BL (both wild-type and p47phox−/−) mice. The oxyR and oxyS genes of wild-type E. coli strain Ec1a (O1:K1:H7) were replaced with a kanamycin resistance cassette to produce an oxyRS mutant. During in vitro growth in broth or human urine, the oxyRS mutant exhibited the same log-phase growth rate (broth) and plateau density (broth and urine) as Ec1a, despite its prolonged lag phase (broth) or initial decrease in concentration (urine). The mutant, and oxyRS mutants of other wild-type ExPEC strains, exhibited significantly increased in vitro susceptibility to inhibition by H2O2, which, like the altered growth kinetics observed with oxyRS inactivation, were reversed by restoration of oxyR on a multiple-copy-number plasmid. In CBA/J mice, Ec1a significantly outcompeted its oxyRS mutant (by >1 log10) in urine, bladder, and kidney cultures harvested 48 h after perurethral inoculation of mice, whereas an oxyR-complemented mutant exhibited equal or greater colonizing ability than that of the parent. Although C57BL mice were less susceptible to experimental UTI than CBA/J mice, wild-type and p47phox−/− C57BL mice were similarly susceptible, and the oxyR mutant of Ec1a was similarly attenuated in C57BL mice, regardless of the p47phox genotype, as in CBA/J mice. Within the E. coli Reference collection, 94% of strains were positive for oxyR. These findings fulfill the second and third of Koch's molecular postulates for oxyR as a candidate virulence-facilitating factor in E. coli and indicate that oxyR is a broadly prevalent potential target for future preventive interventions against UTI due to E. coli. They also suggest that neutrophil phagocyte oxidase is not critical for defense against E. coli UTI and that the major oxidative stresses against which OxyR protects E. coli within the host milieu are not phagocyte derived.

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