scholarly journals Effect of Oxidizing Disinfectants (Chlorine, Monochloramine, and Ozone) on Helicobacter pylori

2002 ◽  
Vol 68 (2) ◽  
pp. 981-984 ◽  
Author(s):  
Katherine H. Baker ◽  
John P. Hegarty ◽  
Brady Redmond ◽  
Nathan A. Reed ◽  
Diane S. Herson
Keyword(s):  
Escherichia Coli ◽  
Helicobacter Pylori ◽  
Distribution Systems ◽  
E Coli ◽  
H Pylori

ABSTRACT The susceptibility of Helicobacter pylori to disinfectants was compared to that of Escherichia coli. H. pylori is more resistant than E. coli to chlorine and ozone but not monochloramine. H. pylori may be able to tolerate disinfectants in distribution systems and, therefore, may be transmitted by a waterborne route.

scholarly journals Antibacterial Activity of Geraniol in Combination with Standard Antibiotics against Staphylococcus aureus, Escherichia coli and Helicobacter pylori

2018 ◽  
Vol 13 (7) ◽  
pp. 1934578X1801300 ◽  
Author(s):  
Subrat Kumar Bhattamisra ◽  
Chew Hui Kuean ◽  
Lee Boon Chieh ◽  
Vivian Lee Yean Yan ◽  
Chin Koh Lee ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Staphylococcus Aureus ◽  
Helicobacter Pylori ◽  
Antibacterial Activity ◽  
Synergistic Effect ◽  
Inhibitory Concentration ◽  
Therapeutic Potential ◽  
E Coli ◽  
Checkerboard Assay ◽  
H Pylori

The antibacterial activity of geraniol and its effect in combination with ampicillin, amoxicillin and clarithromycin against Staphylococcus aureus, Escherichia coli and Helicobacter pylori was tested. The minimum inhibitory concentrations (MICs) and combinatory effects of geraniol against the bacteria were assessed by using the modified broth microdilution and checkerboard assay, respectively. The combinatory effect is expressed as fractional inhibitory concentration index (FICI). The MIC of geraniol against S. aureus, E. coli and H. pylori was found to be 11200, 5600, and 7325 μg/mL, respectively. A significant synergistic effect was observed with geraniol and ampicillin against S. aureus with FICI in the range 0.19 to 0.32. Geraniol and ampicillin exhibited a partial synergistic effect against E. coli. A similar effect was observed with geraniol and clarithromycin against S. aureus. A partial synergistic effect was observed with clarithromycin and geraniol against H. pylori with the FICI value in the range 0.86 to 0.89. An additive effect was observed with geraniol and amoxicillin combination against H. pylori. However, the amoxicillin and clarithromycin dose was reduced by thirty-two fold when combined with geraniol against H. pylori. The anti- H. pylori effect of geraniol with clarithromycin and amoxicillin could be of potential interest in the treatment of H. pylori infection and associated ulcers in humans. Further, geraniol, in combination with other antibiotics, has substantial therapeutic potential against S. aureus and E.coli infection.

scholarly journals Bacterial killing in gastric juice – effect of pH and pepsin on Escherichia coli and Helicobacter pylori

2006 ◽  
Vol 55 (9) ◽  
pp. 1265-1270 ◽  
Author(s):  
H. Zhu ◽  
C. A. Hart ◽  
D. Sales ◽  
N. B. Roberts
Keyword(s):  
Escherichia Coli ◽  
Helicobacter Pylori ◽  
Gastric Juice ◽  
Bacterial Killing ◽  
E Coli ◽  
Test Organisms ◽  
H Pylori ◽  
Ph Range ◽  
K 12 ◽  
Rough Mutant

The susceptibility of Escherichia coli and Helicobacter pylori to pH and the effect of pepsin-mediated proteolysis were investigated. This was to establish the relative importance of their bacterial killing properties in gastric juice. Solutions in the pH range 1.5–7.4 with or without pig pepsin A were used, together with seven gastric juice samples obtained from patients undergoing routine gastric collection. Escherichia coli C690 (a capsulate strain), E. coli K-12 (a rough mutant) and Helicobacter pylori E5 were selected as the test organisms. Suspensions of bacteria (1×106 E. coli ml−1 and 1×108 H. pylori ml−1) were pre-incubated with test solutions at 37 °C for up to 2 h, and then cultured to establish the effect on subsequent growth. Survival of bacteria was diminished at pHs of less than 3.5, whereas killing required a pH of less than 2.5. Pre-incubation with pig pepsin at 0.5, 1.0 and 2.0 mg ml−1 at pH 3.5 reduced viable counts by 100 % for E. coli 690 and E. coli K-12 after 100 min incubation. With H. pylori, the viable counts decreased to 50 % of the control after 20 min incubation in 1 mg pepsin ml−1 at pH 2.5, 3.0 and 3.5. The gastric juices showed bactericidal activity at pH 3.5, and the rate of killing was juice dependent, with complete death of E. coli 690 occurring between 5 and 40 min post-incubation. Thus, killing of E. coli and H. pylori occurs optimally at pHs of less than 2.5. At pH 3.5, little effect is observed, whereas addition of pepsin alone or in gastric juice causes a marked increase in bacterial susceptibility, suggesting an important role for proteolysis in the killing of bacteria.

scholarly journals 16S rRNA Mutations That Confer Tetracycline Resistance in Helicobacter pylori Decrease Drug Binding in Escherichia coli Ribosomes

2005 ◽  
Vol 187 (11) ◽  
pp. 3708-3712 ◽  
Author(s):  
Lisa Nonaka ◽  
Sean R. Connell ◽  
Diane E. Taylor
Keyword(s):  
Escherichia Coli ◽  
Helicobacter Pylori ◽  
16S Rrna ◽  
Binding Site ◽  
Tetracycline Resistance ◽  
Drug Binding ◽  
Multicopy Plasmid ◽  
Wild Type ◽  
E Coli ◽  
H Pylori

ABSTRACT Tetracycline resistance in clinical isolates of Helicobacter pylori has been associated with nucleotide substitutions at positions 965 to 967 in the 16S rRNA. We constructed mutants which had different sequences at 965 to 967 in the 16S rRNA gene present on a multicopy plasmid in Escherichia coli strain TA527, in which all seven rrn genes were deleted. The MICs for tetracycline of all mutants having single, double, or triple substitutions at the 965 to 967 region that were previously found in highly resistant H. pylori isolates were higher than that of the mutant exhibiting the wild-type sequence of tetracycline-susceptible H. pylori. The MIC of the mutant with the 965TTC967 triple substitution was 32 times higher than that of the E. coli mutant with the 965AGA967 substitution present in wild-type H. pylori. The ribosomes extracted from the tetracycline-resistant E. coli 965TTC967 variant bound less tetracycline than E. coli with the wild-type H. pylori sequence at this region. The concentration of tetracycline bound to the ribosome was 40% that of the wild type. The results of this study suggest that tetracycline binding to the primary binding site (Tet-1) of the ribosome at positions 965 to 967 is influenced by its sequence patterns, which form the primary binding site for tetracycline.

scholarly journals Effect of Host Species on RecG Phenotypes in Helicobacter pylori and Escherichia coli

2004 ◽  
Vol 186 (22) ◽  
pp. 7704-7713 ◽  
Author(s):  
Josephine Kang ◽  
Don Tavakoli ◽  
Ariane Tschumi ◽  
Rahul A. Aras ◽  
Martin J. Blaser
Keyword(s):  
Escherichia Coli ◽  
Helicobacter Pylori ◽  
Replication Forks ◽  
E Coli ◽  
Repeat Sequences ◽  
Dna Repeat ◽  
H Pylori ◽  
Dna Repeat Sequences ◽  
Prokaryotic Evolution ◽  
Fundamental Mechanism

ABSTRACT Recombination is a fundamental mechanism for the generation of genetic variation. Helicobacter pylori strains have different frequencies of intragenomic recombination, arising from deletions and duplications between DNA repeat sequences, as well as intergenomic recombination, facilitated by their natural competence. We identified a gene, hp1523, that influences recombination frequencies in this highly diverse bacterium and demonstrate its importance in maintaining genomic integrity by limiting recombination events. HP1523 shows homology to RecG, an ATP-dependent helicase that in Escherichia coli allows repair of damaged replication forks to proceed without recourse to potentially mutagenic recombination. Cross-species studies done show that hp1523 can complement E. coli recG mutants in trans to the same extent as E. coli recG can, indicating that hp1523 has recG function. The E. coli recG gene only partially complements the hp1523 mutation in H. pylori. Unlike other recG homologs, hp1523 is not involved in DNA repair in H. pylori, although it has the ability to repair DNA when expressed in E. coli. Therefore, host context appears critical in defining the function of recG. The fact that in E. coli recG phenotypes are not constant in other species indicates the diverse roles for conserved recombination genes in prokaryotic evolution.

scholarly journals Helicobacter pylori DnaB helicase can bypass Escherichia coli DnaC function in vivo

2005 ◽  
Vol 389 (2) ◽  
pp. 541-548 ◽  
Author(s):  
Rajesh K. Soni ◽  
Parul Mehra ◽  
Gauranga Mukhopadhyay ◽  
Suman Kumar Dhar
Keyword(s):  
Escherichia Coli ◽  
Helicobacter Pylori ◽  
Temperature Sensitive ◽  
Chromosomal Dna ◽  
E Coli ◽  
Dnab Helicase ◽  
H Pylori

In Escherichia coli, DnaC is essential for loading DnaB helicase at oriC (the origin of chromosomal DNA replication). The question arises as to whether this model can be generalized to other species, since many eubacterial species fail to possess dnaC in their genomes. Previously, we have reported the characterization of HpDnaB (Helicobacter pylori DnaB) both in vitro and in vivo. Interestingly, H. pylori does not have a DnaC homologue. Using two different E. coli dnaC (EcdnaC) temperature-sensitive mutant strains, we report here the complementation of EcDnaC function by HpDnaB in vivo. These observations strongly suggest that HpDnaB can bypass EcDnaC activity in vivo.

Activation of Helicobacter pylori ureA promoter by a hybrid Escherichia coli–H. pylori rpoD gene in E. coli

Gene ◽  
1999 ◽  
Vol 239 (2) ◽  
pp. 351-359 ◽  
Author(s):  
Mutsunori Shirai ◽  
Ryutaro Fujinaga ◽  
Junko K Akada ◽  
Teruko Nakazawa
Keyword(s):  
Escherichia Coli ◽  
Helicobacter Pylori ◽  
E Coli ◽  
Rpod Gene ◽  
H Pylori

scholarly journals Cloning, Expression, and Catalytic Activity ofHelicobacter hepaticus Urease

2001 ◽  
Vol 69 (9) ◽  
pp. 5914-5920 ◽  
Author(s):  
Catherine S. Beckwith ◽  
David J. McGee ◽  
Harry L. T. Mobley ◽  
Lela K. Riley
Keyword(s):  
Escherichia Coli ◽  
Helicobacter Pylori ◽  
Intestinal Tract ◽  
Acidic Environment ◽  
Helicobacter Hepaticus ◽  
Transporter Gene ◽  
Urea Transporter ◽  
E Coli ◽  
Urease Gene ◽  
H Pylori

ABSTRACT Helicobacter hepaticus causes disease in the liver and lower intestinal tract of mice. It is strongly urease positive, although it does not live in an acidic environment. The H. hepaticus urease gene cluster was expressed in Escherichia coli with and without coexpression of the Helicobacter pylori nickel transporter NixA. As for H. pylori, it was difficult to obtain enzymatic activity from recombinant H. hepaticus urease; special conditions including NiCl2supplementation were required. The H. hepaticus urease cluster contains a homolog of each gene in the H. pyloriurease cluster, including the urea transporter gene ureI. Downstream genes were homologs of the nik nickel transport operon of E. coli. Nongastric H. hepaticusproduces urease similar to that of H. pylori.

scholarly journals Development of an Internal Control for Evaluation and Standardization of a Quantitative PCR Assay for Detection of Helicobacter pylori in Drinking Water

2007 ◽  
Vol 73 (22) ◽  
pp. 7380-7387 ◽  
Author(s):  
Keya Sen ◽  
Nancy A. Schable ◽  
Dennis J. Lye
Keyword(s):  
Helicobacter Pylori ◽  
Drinking Water ◽  
Quantitative Pcr ◽  
Water Samples ◽  
Sodium Thiosulfate ◽  
Qpcr Assay ◽  
E Coli ◽  
H Pylori ◽  
Labeled Probe ◽  
Treated Drinking Water

ABSTRACT Due to metabolic and morphological changes that can prevent Helicobacter pylori cells in water from growing on conventional media, an H. pylori-specific TaqMan quantitative PCR (qPCR) assay was developed that uses a 6-carboxyfluorescein-labeled probe (A. E. McDaniels, L. Wymer, C. Rankin, and R. Haugland, Water Res. 39:4808-4816, 2005). However, proper internal controls are needed to provide an accurate estimate of low numbers of H. pylori in drinking water. In this study, the 135-bp amplicon described by McDaniels et al. was modified at the probe binding region, using PCR mutagenesis. The fragment was incorporated into a single-copy plasmid to serve as a PCR-positive control and cloned into Escherichia coli to serve as a matrix spike. It was shown to have a detection limit of five copies, using a VIC dye-labeled probe. A DNA extraction kit was optimized that allowed sampling of an entire liter of water. Water samples spiked with the recombinant E. coli cells were shown to behave like H. pylori cells in the qPCR assay. The recombinant E. coli cells were optimized to be used at 10 cells/liter of water, where they were shown not to compete with 5 to 3,000 cells of H. pylori in a duplex qPCR assay. Four treated drinking water samples spiked with H. pylori (100 cells) demonstrated similar cycle threshold values if the chlorine disinfectant was first neutralized by sodium thiosulfate.

Protection against Helicobacter pylori infection in mice by intragastric vaccination with H. pylori antigens is achieved using a non-toxic mutant of E. coli heat-labile enterotoxin (LT) as adjuvant

Vaccine ◽  
1998 ◽  
Vol 16 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Marta Marchetti ◽  
Michela Rossi ◽  
Valentina Giannelli ◽  
Marzia M Giuliani ◽  
Mariagrazia Pizza ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Helicobacter Pylori Infection ◽  
E Coli ◽  
Heat Labile ◽  
H Pylori

scholarly journals Evaluation of Select Sensors for Real-Time Monitoring of Escherichia coli in Water Distribution Systems

2011 ◽  
Vol 77 (8) ◽  
pp. 2813-2816 ◽  
Author(s):  
Syreeta L. Miles ◽  
Ryan G. Sinclair ◽  
Mark R. Riley ◽  
Ian L. Pepper
Keyword(s):  
Escherichia Coli ◽  
Real Time ◽  
Distribution Systems ◽  
Water Distribution ◽  
Water Distribution Systems ◽  
Warning System ◽  
Quality Changes ◽  
Microbial Water Quality ◽  
Content Type ◽  
E Coli

ABSTRACTThis study evaluated real-time sensing ofEscherichia colias a microbial contaminant in water distribution systems. Most sensors responded to increasedE. coliconcentrations, showing that select sensors can detect microbial water quality changes and be utilized as part of a contaminant warning system.

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