Helicobacter
In 1983 Spiral gram negative rods resembling campylobacters were found in patients with gastritis, They originally classified as campylobacters, Reclassified as a new genus Helicobacter, Helicobacters have been isolated from many other mammals.Figure 2. Helicobacter pylori ATCC 43579. Electron micrograph
HelicobacterH pylori is associated with Antral gastritis, Duodenal (peptic) ulcer disease, Gastric ulcers, Gastric adenocarcinoma, Ggastric mucosa-associated lymphoid tissue (MALT) lymphomas.
Helicobacter
Helicobacter are curved or spiral organisms They have a rapid, corkscrew motility resulting from multiple polar flagella, Microaerophilic, and produces urease, Unusual in their ability to colonize the stomach, where low pH normally protects against bacterial infection, It is oxidase positive and catalase positive, has a characteristic morphology, is motile, and is a strong producer of Urease.Helicobacter
32 species have been characterized:- Helicobacter pylori, Helicobacter cinaedi, Helicobacter fennelliae, Curved gram negative rods, Highly motile, Catalase and oxidase positive, Do not ferment or oxidize carbohydrates, Require a complex medium with blood, serum, charcoal or starch.Helicobacter Under Electron Microscopes
Pathogenesis and PathologyHelicobacter pylori grows optimally at a pH of 6.0–7.0 and would be killed or not grow at the pH within the gastric lumen,Gastric mucus is relatively impermeable to acid and has a strong buffering capacity,On the lumen side of the mucus, the Ph is low (1.0–2.0); on the epithelial side, the pH is about 7.4,Helicobacter pylori is found deep in the mucous layer near the epithelial surface where physiologic pH is present.Helicobacter pylori also produces a protease that modifies the gastric mucus and further reduces the ability of acid to diffuse through the mucus.
Pathogenesis and Pathology
Helicobacter pylori produces potent urease activity, which yields production of ammonia and further buffering of acid, Helicobacter pylori is quite motile, even in mucus, and is able to find its way to the epithelial surface.
Pathogenesis and Pathology
The mechanisms by which H pylori causes mucosal inflammation and damage involve both bacterial and host factors. The bacteria invade the epithelial cell surface to a limited degree. Toxins and lipopolysaccharide may damage the mucosal cells, and the ammonia produced by the urease activity may also directly damage the cells.Histologically, gastritis is characterized by acute and chronic inflammation. Polymorphonuclear and mononuclear cell infiltrates are seen within the epithelium and lamina propria. Vacuoles within cells are often pronounced. Destruction of the epithelium is common, and glandular atrophy may occur. H pylori thus is a major risk factor for gastric cancer.
Pathogenesis and Pathology
Transmission of Helicobacter pylori is thought to be from person to person, because the organism has not been isolated from food or water. The organism survives in the mucus layer that coats the epithelium and causes chronic inflammation of the mucosa Urease released by Helicobacter pylori produces ammonia ions that neutralize stomach acid in the vicinity of the organism, favoring bacterial multiplication. Ammonia may also both cause injury and potentiate the effects of a cytotoxin produced by Helicobacter pylori.
Pathogenesis and Pathology
Pathogenesis and Pathology
Pathogenesis and PathologyThe Helicobacter pylori LPS antigens can mimic human Lewis antigens may help Helicobacter pylori to evade the immune response and thus enhance bacterial adherence to gastric epithelium
Pathogenesis and Pathology
Helicobacter
Prevalence is high in developing countries 90%, 40% in developed countries, 70-100% of patients with gastritis, gastric or duodenal ulcers are infected with Helicobacter pylori, Humans are the primary reservoir for Helicobacter pylori, Transmission is most likely via the fecal-oral route,Helicobacter-Diseases
Gastritis (infiltration of neutrophils and mononuclear cells into the gastric mucosa). Feeling of fullness, nausea, vomiting and hypochlorhydria, Evolve to chronic gastritis, with disease confined to the gastric antrum (where few acid-secreting parietal cells are present) in individuals with normal acid secretion involve the entire stomach (pangastritis) if acid secretion is suppressedHelicobacter-Diseases
Approximately 10% to 15% of patients with chronic gastritis will progress to develop peptic ulcers, The ulcers develop at the sites of intense inflammation, Commonly involving the junction between the corpus and antrum (gastric ulcer) or the proximal duodenum (duodenal ulcer), Helicobacter pylori is responsible for 85% of gastric ulcers and 95% of duodenal ulcers.Helicobacter-Diseases
Chronic gastritis leads to replacement of the normal gastric mucosa with fibrosis and proliferation of intestinal-type epithelium, Infection is also associated with infiltration of lymphoid tissue into the gastric mucosa,In a small number of patients, a monoclonal population of B cells may develop and evolve into a MALT (Mucosa Assocıated Lymphoid Tissue) lymphoma.Diagnostic Laboratory Tests
1. Specimens Gastric biopsy specimens can be used for histologic examination or minced in saline and used for culture. Blood is collected for determination of serum antibodies. Stool samples may be collected for H pylori antigen detection. 2. Smears The diagnosis of gastritis and H pylori infection can be made histologically. A gastroscopy procedure with biopsy is required. Routine stains demonstrate gastritis, and Giemsa or special silver stains can show the curved or spiral-shaped organisms.Diagnostic Laboratory Tests
3. CultureCulture sensitivity can be limited, contamination with other mucosal bacteria.H pylori grows in 3–6 days when incubated at 37°C in a microaerophilic environment.The media for primary isolation include Skirrow’s medium with vancomycin, polymyxin B, and trimethoprim, chocolate medium,The other selective media with antibiotics (eg, vancomycin, nalidixic acid, amphotericin). The colonies are translucent and 1–2 mm in diameter.Diagnostic Laboratory Tests
4. Antibodies Several assays have been developed to detect serum antibodies specific for Helicobacter pylori. The serum antibodies persist even if the Helicobacter pylori infection is eradicated, and the role of antibody tests in diagnosing active infection or after therapy is therefore limited.