Diseases H. pylori causes gastritis and peptic ulcers. Infection with H. pylori is a risk factor for gastric carcinoma and is linked to mucosal-associated lymphoid tissue (MALT) lymphomas.
Important Properties
Helicobacters are curved gram-negative rods similar in appearance to campylobacters, but because they differ sufficiently in certain biochemical and flagellar characteristics, they are classified as a separate genus. In particular, helicobacters are strongly urease positive, whereas campylobacters are urease negative.
Pathogenesis & Epidemiology
H. pylori attaches to the mucus-secreting cells of the gastric mucosa. The production of large amounts of ammonia from urea by the organism’s urease, coupled with an inflammatory response, leads to damage of the mucosa. Loss of the protective mucus coating predisposes to gastritis and peptic ulcer (see Table 1). The ammonia also neutralizes stomach acid, allowing the organism to survive. Epidemiologically, most patients with these diseases show H. pylori in biopsy specimens of the gastric epithelium.
Table1. Important Features of Pathogenesis by Curved Gram-Negative Rods Affecting the Gastrointestinal Tract
The natural habitat of H. pylori is the human stomach, and it is probably acquired by ingestion. However, it has not been isolated from stool, food, water, or animals. Person-to-person transmission probably occurs because there is clustering of infection within families. The rate of infection with H. pylori in developing countries is very high—a finding that is in accord with the high rate of gastric carcinoma in those countries.
MALT lymphomas are B-cell tumors located typically in the stomach, but they occur elsewhere in the gastrointestinal tract as well. H. pylori is often found in the MALT lesion, and the chronic inflammation induced by the organism is thought to stimulate B-cell proliferation and eventually a B-cell lymphoma. Antibiotic treatment directed against the organism often causes the tumor to regress.
Clinical Findings
Gastritis and peptic ulcer are characterized by recurrent pain in the upper abdomen, frequently accompanied by bleeding into the gastrointestinal tract. No bacteremia or disseminated disease occurs.
Laboratory Diagnosis
The organism can be seen on Gram-stained smears of biopsy specimens of the gastric mucosa. It can be cultured on the same media as campylobacters. In contrast to C. jejuni, H. pylori is urease positive. Urease production is the basis for a noninvasive diagnostic test called the “urea breath” test. In this test, radio labeled urea is ingested. If the organism is present, urease will cleave the ingested urea, radiolabeled CO2 is evolved, and the radioactivity is detected in the breath.
A test for Helicobacter antigen in the stool can be used for diagnosis and for confirmation that treatment has eliminated the organism. The presence of immunoglobulin (Ig) G antibodies in the patient’s serum can also be used as evidence of infection.
Treatment & Prevention
The concept that underlies the choice of drugs to treat gastritis and peptic ulcer is to use antibiotics to eliminate Helicobacter plus a proton-pump inhibitor to reduce gastric acidity. Quadruple drug therapy is used because resistance, especially to metronidazole, has emerged. One regimen consists of a combination of tetracycline, bismuth, metronidazole (or tinidazole), and a proton pump inhibitor (PPI) such as omeprazole. Another regimen consists of amoxicillin, clarithromycin, metronidazole (or tinidazole), and a PPI.
There is evidence that treating Helicobacter gastritis with antibiotics can prevent gastric carcinoma. There is no vaccine against Helicobacter.
