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Gastrointestinal endoscopy is an important tool for the indentification and treatment of disorders of the gastrointestinal tract. However, nosocomial infections of Helicobacter pylori have been linked to the use of contaminated endoscopes. Disinfectants such as glutaraldehyde, ortho-phthalaldehyde and peracetic acid are generally used in the reprocesssing of endoscopes, but these chemicals are hazardous to human health. Thus, safer reprocessing and disinfecion methods are needed. In this study, we applied a dielectric barrier discharge (DBD) plasma torch for inactivation of H. pylori to investigate a potential new methodology to disinfect endoscopes. Suspensions of H. pylori in 10% glycerol were subjected to the DBD plasma torch, which reduced the viable cell count to undetectable levels after 2 min of treatment. Furthermore, urease activity of H. pylori was eliminated after 2 min-plasma treatment, while plasma-treatment reduced the intact DNA of H. pylori in a time-dependent manner. Next, we examined several potential bactericidal factors produced by the DBD plasma torch. Two min-plasma treatment resulted in a small temperature rise (4 °C), ultraviolet radiation (UV) generation, and the production of hydrogen peroxide. H. pylori samples were then exposed to equivalent levels of each of these factors in turn. Our results showed that treatment with heat and hydrogen peroxide at the levels produced after 2-min of plasma treatment did not efficiently inactivate H. pylori, whereas exposure to UV had a significant bactericidal effect. Taken together, UV generated by the plasma torch may be crucial for efficient inactivation of H. pylori by damaging the bacterial DNA., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

We investigated whether near-ultraviolet light emitted from light-emitting diodes (LEDs) effects Helicobacter pylori viability and whether this new method can potentially apply to eradication therapy. Three H. pylori strains were used for near-ultraviolet (UV) LED irradiation experiments. Viability of isolates exposed to near-UV light was compared with controls by counting colony forming units. A time-dependent bactericidal effect of near-UV light was definitely observed. LED irradiation with near-UV light showed effective bactericidal activity against H. pylori strains. Eradication therapy with LED might provide a new avenue of treatment in patients refractory to eradication due to antibiotic resistance and/or adverse effects of antibiotics.

Three strains of Helicobacter pylori were exposed to UV light from a low-pressure source to determine log inactivation versus applied fluence. Results indicate that H. pylori is readily inactivated at UV fluences typically used in water treatment regimens. Greater than 4-log(10) inactivation was demonstrated on all three strains at fluences of less than 8 mJ cm(-2).

Helicobacter pylori persists in the human stomach where it may encounter a variety of DNA-damaging conditions, including gastric acidity. To determine whether the nucleotide excision repair (NER) pathway contributes to the repair of acid-induced DNA damage, we have cloned the putative H. pylori NER gene, uvrB. Degenerate oligonucleotide primers based on conserved amino acid residues of bacterial UvrB proteins were used in PCR with genomic DNA from H. pylori strain 84-183, and the 1.3-kb PCR product from this reaction was used as a probe to clone uvrB from an H. pylori genomic library. This plasmid clone had a 5.5-kb insert containing a 2.0-kb ORF whose predicted product (658 amino acids; 75.9 kDa) exhibited 69.5% similarity to E. coli UvrB. We constructed an isogenic H. pylori uvrB mutant by inserting a kanamycin-resistance cassette into uvrB and verified its proper placement by Southern hybridization. As with uvrB mutants of other bacteria, the H. pylori uvrB mutant showed a greatly increased sensitivity to the DNA-damaging agents methylmethane sulfonate and ultraviolet radiation. The uvrB mutant also was significantly more sensitive than the wild-type strain to killing by low pH, suggesting that the H. pylori nucleotide excision repair (NER) pathway is involved in the repair of acid-induced DNA damage.