Antibiotic resistance is the most challenging clinical and public health problem. Despite of living in the era of novel technologies in biomedical research, many of untreatable infectious diseases are ranked as the main causes of human death worldwide. Increased antibiotic use in human and use in animal production are the two major causes of emergence of resistant bacteria in hospitals, human communities, and also animal farms. Current body of evidences is indicating that major factors that led to existing crisis on antibiotics worldwide are poor educational programs on hygiene and health, inappropriate prescription in addition to the overprescription in clinical settings (mainly in developing countries with easier access to the antibiotics) and lack of accurate diagnostic tools in laboratories in order to control the emergence of antibiotics against widely used drugs in community. It sounds using the antibodies against problematic bacteria in farms has more benefits than treating them with susceptible antibiotics. As best strategy, we pointed that the crisis of antibiotic resistance may be solved when all contributors be acknowledged to their responsibilities and duties to minimize this global problem threatening the human health. China and the USA as the two main antibiotics user in industrial scale should have taken new policy in meat industry. Currently, antibiotic resistance presents a growing health threat worldwide being the cause of many nosocomial and often deadly infections.

Helicobacter pylori (H. pylori) as gram-negative and spiral microorganism is responsible for colonization in the gastric microniche for more than 50% of world population. Recent studies have shown a critical role of H. pylori in the development of peptic ulcers, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer. Over the past decade, there has been a sharp interest to use noninvasive tests in diagnosis of the H. pylori infection. During the years after discovery by Marshall and Warren, it has been frequently declared that the rapid urease test (RUT) is one of the cheapest and rapid diagnostic approaches used in detecting the infection. Although the specificity and sensitivity are durable for this test, clinical experiences had shown that the ideal results are only achieved only if we take biopsies from both corpus and antrum at the same time. Given the diagnosis of the H. pylori in clinical samples, gastroenterologists are facing a long list of various molecular and nonmolecular tests. We need more in-depth researches and investigations to correctly generalize rapid and accurate molecular tests determining both bacterial identity and antibiotic resistance profile.

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Helicobacter pylori (H. pylori) is a Gram-negative and motile bacterium that colonizes the hostile microniche of the human stomach, then persists for the host’s entire life, if not effectively treated. Clinically, H. pylori plays a causative role in the development of a wide spectrum of diseases including chronic active gastritis, peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Due to the global distribution of H. pylori, it is no exaggeration to conclude that smart strategies are contributing to adaptation of the bacterium to its permanent host. Thirty-four years after the discovery of this bacterium, there are still many unanswered questions. For example, which strategies help the bacterium to survive in this inhospitable microniche? This question is slightly easier to answer if we presume the same clinical concept for both persistent infection and disease. Understanding the mechanisms governing H. pylori persistence will improve identification of the increased risk of diseases such as gastric cancer in patients infected with this bacterium. A well-defined and long-term equilibrium between the human host and H. pylori allows bacterial persistence in the gastric microniche; although this coexistence leads to a high risk of severe diseases such as gastric cancer. To escape the bactericidal activity of stomach acid, H. pylori secretes large amounts of surface-associated and cytosolic urease. The potential to avoid acidic conditions and immune evasion are discussed in order to explain the persistence of H. pylori colonization in the gastric mucosa, and data on bacterial genetic diversity are included. Information on the mechanisms related to H. pylori persistence can also provide the direction for future research concerning effective therapy and management of gastroduodenal disorders. The topics presented in the current review are important for elucidating the strategies used by H. pylori to help the bacterium persist in relation to the immune system and the many unfavorable features of living in the gastric microniche.

BackgroundInfection with Helicobacter pylori is associated with severe digestive diseases including chronic gastritis, peptic ulcer disease, and gastric cancer. Successful eradication of this common gastric pathogen in individual patients is known to prevent the occurrence of peptic ulcer disease and gastric cancer.DiscussionWith half of the world’s population being infected with H, pylori and only few antibiotics result in an effective eradication, a successful antibiotic driven worldwide eradication program seems unlikely. In addition, H. pylori eradication is not always beneficial as it has been described that eradication can be associated with an increased frequency of other disorders such as pediatric asthma, inflammatory bowel diseases and Barrett’s Esophagus. We have to accept that eradication of this infection is a two-edged sword that is both useful and harmful and we should therefore focus our H. pylori eradication policy toward selectively identify and destroy only the virulent strains.ConclusionIn order to still be able to effectively treat H. pylori infections in the future we need an alternative diagnostic/treatment algorithm. This would involve a shift towards more precise and enhanced disease predicting diagnosis that tries to identify patients with chance of developing severe diseases such as gastric cancer, rather than the current regime that is geared towards find and destroy all H. pylori.

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that is well known in the involvement of chronic inflammation in the gastric mucosa of the human stomach. Several studies have investigated the possible role of H. pylori presence in different gastroduodenal disorders with conflicting results. This study aimed to further investigate such a field. Helicobacter pylori strains were cultured from 160 patients (mean age of 42 years; range 15-75; 90 were male, and 70 were female) [40 gastric cancer (GC), 55 duodenal ulcer (DU) and 65 non-ulcer dyspepsia (NUD)]. In this study, allelic variants of iceA 1, iceA 2 and babA 2 were identified by polymerase chain reaction. The overall prevalence of babA 2 gene was 40.6% (65/160). The prevalence of babA 2 gene was 95% with gastric cancer, 18.1% with duodenal ulcer and 26.1% with non ulcer dyspepsia, respectively. The prevalence of babA 2 in GC patients was significantly higher as compared to either NUD or UD patients (P = 0.0004), while no statistical significance was found between the latter two patient groups. Our study finds that babA 2 and iceA 1 genes are more prevalent in GC compared to either NUD or DU patients in Iran.

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While several distinct virulence factors of Helicobacter pylori have been shown to be associated with different clinical outcomes, there is still much to learn about the role of different bacterial factors in gastric carcinogenesis. This study looked at the distribution of the cagA, homA, and homB genes in strains isolated from patients suffering from gastroduodenal diseases in Iran and assessed if there was any association between disease state and the presence of the aforementioned virulence factors. Genomic DNA from 138 H. pylori strains was isolated and genotyped via PCR. Strains were obtained from dyspeptic patients (35 from gastritis patients, 62 from peptic ulcer patients, and 41 from gastric cancer patients) at the Teaching Touba Clinic and Imam Hospital of the Mazandaran University of Medical Sciences in Sari, Iran. The overall prevalence rates of cagA, homA, and homB were 58%, 54%, and 43%, respectively. Stratification of patients showed a significant difference in the prevalence of H. pylori virulence genes across the disease states. The frequency of homB was statistically significantly higher in gastric cancer patients (78%) than in patients suffering from peptic ulcers (20%) or gastritis (43%) (P < 0.0001). The presence of homB was also associated with the presence of cagA (r ‫؍‬ 0.243). These data suggest that in this population the presence of homB may be a predictor of more virulent strains of H. pylori and influence the severity of disease manifestation.