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Helicobacter pylori (H. pylori), a Gram-negative bacterium, is one of the most common infections worldwide, affecting one-third of the population in developed countries and more than two-thirds in developing countries .
Mainly transmitted intrafamilially, it colonizes the human gastric mucosa, leading to conditions ranging from chronic gastritis to gastric cancer.
Advances in understanding the pathogenesis of H. pylori have enabled the development of effective treatments, although antibiotic resistance today represents a major challenge in the management of this infection.
In 1983, spiral-shaped organisms resembling Campylobacter spp. were isolated from the human stomach; these organisms were named Campylobacter pylori.
Based on many studies, the genus Helicobacter was established in 1989 and C. pylori was renamed Helicobacter pylori. Approximately 32 species are included in this genus, the majority of which colonize mammalian stomachs or intestines.
The genus Helicobacter consists of curved, microaerophilic, gram-negative rods, the majority of species exhibiting urease activity. Humans isolates include H. pylori, H. cinaedi, H. fennelliae, H. heilmannii (formerly known as Gastrospirillum hominis), H. westmeadii, H. canis, H. canadensis sp. nov., H. pullorum, and “H. rappini” (formerly known as “Flexispira rappini”).
The primary habitat of H. pylori 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.
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. Although H. pylori is noninvasive, untreated colonization persists despite the host's immune response.
Helicobacter 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.
H pylori has many characteristics in common with campylobacters. It has multiple flagella at one pole and is actively motile.
Culture sensitivity can be limited by prior therapy, contamination with other mucosal bacteria, and other factors. H pylori grows in 3-6 days when incubated at 37°C in a microaerophilic environment, as for C jejuni.
The media for primary isolation include Skirrow's medium with vancomycin, polymyxin B, and trimethoprim, chocolate medium, and other selective media with antibiotics (eg, vancomycin, nalidixic acid, amphotericin). The colonies are translucent and 1-2 mm in diameter.
Ultrasound is often used as the first imaging modality to evaluate the kidneys and urinary tract. It can detect the presence of kidney or bladder stones, urinary obstructions, kidney cysts, or dilatations of the urinary tract.
Computed tomography (CT) and MRI are less commonly used than ultrasound, but they can be useful in certain cases.
H pylori is oxidase positive and catalase positive, has a characteristic morphology, is motile, and is a strong producer of urease.
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.
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.
As above. Culture is performed when patients are not responding to treatment, and there is a need to assess susceptibility patterns.
Several assays have been developed to detect serum antibodies specific for H pylori. The serum antibodies persist even if the H pylori infection is eradicated, and the role of antibody tests in diagnosing active infection or after therapy is therefore limited.
Rapid tests to detect urease activity are widely used for presumptive identification of H pylori in specimens. Gastric biopsy material can be placed onto a urea-containing medium with a color indicator. If H pylori is present, the urease rapidly splits the urea (1-2 hours), and the resulting shift in pH yields a color change in the medium.
In vivo tests for urease activity can be done also. In urea breath tests, 13C- or 14C-labeled urea is ingested by the patient. If H pylori is present, the urease activity generates labeled CO2 that can be detected in the patient's exhaled breath.
Detection of H pylori antigen in stool specimens is appropriate as a test of cure for patients with known H pylori infection who have been treated.
Except for metronidazole and clarithromycin, most laboratory susceptibility assays are unsuccessful in predicting clinical outcome. Routine testing of H. pylori isolates' susceptibility to metronidazole is recommended using the E-test and agar or broth dilution methods.
Therapy for H. pylori infection is problematic. H. pylori readily becomes resistant when metronidazole, clarithromycin, azithromycin, rifampin, or ciprofloxacin is prescribed as a single agent. Current regimens recommend triple-drug therapy including metronidazole, a bismuth salt, and either amoxicillin or tetracycline.
An alternative and simple regimen for patients with metronidazole resistant strains includes omeprazole or lansoprazole (proton pump inhibitors cause rapid symptom relief while working synergistically with the antibiotics) and amoxicillin or clarithromycin. Relapses occur often. Helicobacter spp. associated with enteritis and proctitis may respond to quinolones; however, appropriate therapy has not been established.
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