Helicobacter pylori’s primary habitat is the human gastric mucosa. The organism is distributed worldwide. Although acquired early in life in underdeveloped countries, the exact mode of transmission is unknown. An oral-oral, fecal-oral, and a common environmental source have been proposed as possible routes of transmission, with familial transmission associated with H. pylori infections. Research studies suggest mother-to-child transmission as the most probable cause of intrafamilial spread. In industrialized nations, antibody surveys indicate that approximately 50% of adults >60 years of age are infected by H. pylori. Gastritis incidence increases with age. H. pylori has occasionally been cultured from feces and dental plaque, thereby suggesting a fecal-oral or oral-oral transmission.

The habitat for H. cinaedi and H. fennelliae appears to be the human gastrointestinal tract, and the organisms may be normal flora; hamsters have also been proposed as a reservoir for H. cinaedi. Although the epidemiology of these organisms is not clearly delineated, these two bacterial agents have been associated with sexual trans mission among homosexual men.

H. pylori is capable of colonizing the mucous layer of the antrum and fundus of the stomach but fails to invade the epithelium. Motility allows H. pylori to escape the acidity of the stomach and burrow through and colonize the gastric mucosa in close association with the epithelium. In addition, the organism produces urease that hydrolyzes urea-forming ammonia (NH3) significantly increasing the pH around the site of infection. The change in pH protects the organism from the acidic environment produced by gastric secretions. H. pylori also produces a protein called CagA and injects the protein into the gastric epithelial cells. The protein subsequently affects host cell gene expression inducing cytokine release and altering cell structure, and interactions with neighboring cells enabling H. pylori to successfully invade the gastric epithelium. Individuals who demonstrate positive antibody response to cag protein are at increased risk of developing both peptic ulcer disease and gastric carcinoma. Other possible virulence factors include adhesins for colonization of mucosal surfaces, mediators of inflammation, and a cytotoxin capable of causing damage to host cells (Table 1). Although H. pylori is noninvasive, untreated colonization persists despite the host’s immune response.

Table1. Genes and Their Possible Role in Enhancing  Virulence of H. pylori

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دراسة حديثة تكشف ما تفعله الشاشات بـ"قلوب الأطفال" !

متلازمة المبنى المريض.. هكذا يتحول تكييف الهواء إلى خطر صحي ؟؟

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كيف تتعامل مع حرارة الطقس أثناء القيادة؟

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COXIELLA

Ehrlichia and Anaplasma

Rickettsia