• 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.

Virulence factors

• 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.

Infection

• 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).

Summary Illustration:

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.

Treatment

Because chronic gastritis can lead to severe consequences, treatment is important.

• Macrolides, Beta-lactams, and proton-pump inhibitors.

Enterohepatic helicobacters

Helicobacter cinaedi and Helicobacter fenneliae

• Invade the intestines and liver, and can cause gastroenteritis and bacteremia, particularly in immunocompromised individuals.