Helicobacter pylori

Gastric helicobacter because it colonizes the stomach. Transmission is human to human; exact mechanisms uncertain. Life-long colonization; infection typically occurs during childhood and produces symptoms during adulthood. Gatalase, oxidase, and urease positive. Spiral, Gram-negative rods that can appear as coccoid in older cultures. Microaerobic: Grow in conditions of reduced oxygen and increased carbon dioxide. Helicobacter pylori has several adaptations that allow it to survive the acidic environment of the human stomach and persist for decades. Urease converts urea to ammonia and bicarbonate to neutralize gastric acids. Multiple flagella provide corkscrew motility. Mucinase production allows the bacteria migrate through the viscous mucus that covers the surface of the stomach. Infection triggers host production of IL-8, which is a pro-inflammatory cytokine that recruits neutrophils that release harmful molecules and damage host tissues. The bacteria protect themselves from these harmful molecules by producing superoxide dismutase and catalase, which detoxify reactive oxygen species. Lipopolysaccharide endotoxin; however, as compared with many other Gram-negative bacteria, its endotoxin has low toxicity. Vacuolating cytotoxin A promotes pore formation, disrupts cell signaling, and induces apoptosis and necrosis of host cells. Cytotoxin-associated gene A (cagA) product promotes proliferation and morphological changes in host tissues, and induces T-cell apoptosis. Type IV secretion systems inject the cagA effector protein into host cells. Gastritis is inflammation of the stomach lining with infiltration of neutrophils and mononuclear cells; T-1 helper cells are also implicated. Some individuals are asymptomatic, and others experience an acute phase of nausea, bloating, and vomiting. Inflammation can be localized to one area, usually the pyloric antrum, or widespread In a subset of patients, gastritis progresses to more serious conditions. Peptic ulcers 10-20% of patients with gastritis will develop peptic ulcers, in which inflammation erodes the stomach tissues. Ulcers can be located in the stomach, or they can be in the duodenum, which is the first portion of the small intestine. Gastric adenocarcinoma In approximately 1-2%, chronic inflammation will lead to gastric adenocarcinoma. This occurs when inflammation leads to metaplasia; over time, the gastric mucosa is replaced by fibrotic tissue, and can become neoplastic. Reduced gastric acid secretion is associated with a higher risk of adenocarcinoma. Gastric-associated lymphoid tissue B-cell lymphomas In response to Helicobacter pylori infection, lymphoid tissues infiltrate the stomach; in some cases, monoclonal B cells proliferate and form MALT lymphomas (MALT = Mucosa-Associated Lymphoid Tissue). We draw the stomach, esophagus, and duodenum. Gastritis can be localized in the pyloric antrum, and indicate that this is associated with increased acid production and formation of duodenal ulcers. Multifocal inflammation, as in pangastritis, is associated with atrophy and reduced acid production; this is associated with gastric metaplasia and cancer. Helicobacter pylori infection causes destruction of the mucosa, which allows acids and toxins, as well as the microbes themselves, access to deeper tissues.

• Ulceration leads to bleeding, perforation, and, in severe cases, metaplasia.

Because chronic gastritis can lead to severe consequences, treatment is important. Macrolides, Beta-lactams, and proton-pump inhibitors. Helicobacter cinaedi and Helicobacter fenneliae Invade the intestines and liver, and can cause gastroenteritis and bacteremia, particularly in immunocompromised individuals.