Ulcer-associated dyspepsia is caused by infection with Helicobacter pylori. H. pylori is linked to a majority of peptic ulcers. Antibiotic treatment does not always inhibit or kill H. pylori with potential for antibiotic resistance. The objective of this study was to determine the potential for using phenolic phytochemical extracts to inhibit H. pylori in a laboratory medium. Our approach involved the development of a specific phenolic profile with optimization of different ratios of extract mixtures from oregano and cranberry. Subsequently, antimicrobial activity and antimicrobial-linked urease inhibition ability were evaluated. The results indicated that the antimicrobial activity was greater in extract mixtures than in individual extracts of each species. The results also indicate that the synergistic contribution of oregano and cranberry phenolics may be more important for inhibition than any species-specific phenolic concentration. Further, based on plate assay, the likely mode of action may be through urease inhibition and disruption of energy production by inhibition of proline dehydrogenase at the plasma membrane.Dyspepsia and related problems with peptic ulcers linked to Helicobacter pylori are major problems in many parts of the world (37). H. pylori is a gram-negative, spiral-shaped bacterium that lives in the stomach and duodenum. By releasing an enzyme called "urease," H. pylori is able to survive in the stomach. Urease converts urea into ammonia, which then counters the stomach acid. This creates a neutralizing environment for protecting H. pylori from the acid in the stomach. Gastric infection with H. pylori may lead to the onset of various gastric-related diseases (13). Most patients specifically with duodenal ulcer can be cured by killing H. pylori with antibiotics and proton pump inhibitors (22, 29). In recent studies, H. pylori infection was also suspected to be associated with coronary artery and ischemic heart disease (4, 9, 21, 23). Many antibiotic-linked treatments have been recommended for eradication of H. pylori, but the emergence of antibiotic resistance makes the treatments more complicated, and the infection is sustained at higher levels when the drug treatment is stopped (12,29). Two common antibiotics used for treatment of H. pylori infection are metronidazole and clarithromycin. Several triple-or quadruple-antibiotic therapies with proton pump inhibitors have been shown to be effective in eradication of H. pylori (14), but no single treatment regimen is considered the final treatment of choice.Research has indicated that urease of H. pylori is located in the cytoplasm in freshly prepared cultures and in the outer membrane in older cultures (15). In addition to pathogenicity from H. pylori, evidence indicates that ammonia generated by urease can cause injury to the gastroduodenal mucosa (33, 42). Specific inhibition of urease activity has been proposed as a possible strategy to inhibit this microorganism (25). It has been demonstrated that a urease-negative mutant does not cause ga...

No abstract

No abstract

Optimized phenolics from oregano and cranberry extracts were evaluated for antimicrobial activity against Listeria monocytogenes in laboratory media and in beef and fish. The antimicrobial activity increased when oregano and cranberry extracts were mixed at a ratio of 75% oregano and 25% cranberry (wt/wt) with 0.1 mg of phenolic per disk or ml, and the efficacy was further enhanced by lactic acid. The inhibition by phytochemical and lactic acid synergies was most effective when beef and fish slices were stored at 4°C.

Clostridium perfringens is a leading cause of bacterial food-borne illness in countries where consumption of meat and poultry is high. For example, each year in the United States, this organism is the second or third most common cause of confirmed cases of food-borne illness. Surveys of the incidence of this organism in retail foods were done in the 1960s without regard to whether isolates were enterotoxigenic. It is now known that not all strains of this organism possess the enterotoxin gene responsible for illness. We examined the incidence of this organism in 131 food samples from retail food stores in an area of the northeastern United States. Forty isolates were obtained by using the iron milk method at 45°C, with confirmation by use of motility nitrate and lactose gelatin media. The presence of the C. perfringens enterotoxin (cpe) and alpha toxin (cpa) genes was determined by PCR using previously published primer sequences. All isolates possessed cpa. None of the isolates were identified as carrying the cpe gene by this method or by another method using a digoxigeninlabeled gene probe. Consistent with these results, none of the sporulating-cell extracts contained enterotoxin as determined by reverse passive latex hemagglutination. Pulsed-field gel electrophoresis was used to determine the genetic relatedness of the isolates. About 5% of the isolates were considered to be closely related (2-to 3-band difference). The others were considered to be unrelated to one another. The results demonstrate the rarity of cpe ؉ strains in retail foods and the genetic diversity among nonoutbreak strains.