Treatment of HELICOBACTER PYLORI
HELICOBACTER PYLORI

Previously named Campylobacter pyloridis, is a Gram-negative, microaerophilic bacterium found in the stomach.

In 1982 Barry Marshall and Robin Warren, found that it was present in patients with chronic gastritis and gastric ulcers.

MORPHOLOGY

Helix-shaped (curved rod, not spirochaete), About 3 micrometres long, diameter-0.5 micrometres.

Microaerophilic; requires oxygen,  It contains a hydrogenase which can be used to obtain energy by oxidizing molecular hydrogen (H2) produced by intestinal bacteria, It produces oxidase, catalase, and urease. It is capable of forming biofilms and can convert from spiral to a coccoid form.

Scanning electron micrograph of H. pylori

PATHOPHYSIOLOGY OF H.pylori INFECTION

H. pylori  survives the acidic pH of the  stomach lumen,  Uses its flagella to burrow into the mucus of stomach to reach its microenvironment, close to the stomach's epithelial cell layer.

H. pylori senses the pH gradient within the mucus layer by chemotaxis.

It swims towards the more neutral pH environment of epithelial cell surface.

H. pylori produces large amounts of the enzyme urease, urease breaks down urea (which is normally secreted into the stomach) to carbon dioxide and ammonia. The ammonia is converted to ammonium by accepting a proton (H+), which neutralizes gastric acid.

Colonization of the stomach by H. pylori results in chronic gastritis.

The inflammatory response to the bacteria induces G cells in the antrum to secrete the hormone gastrin. Gastrin stimulates the parietal cells to secrete even more acid.

The number of parietal cells to also increase, further escalating the amount of acid secreted. The increased acid load damages the duodenum, and ulceration may eventually result.

LABORATORY DIAGNOSIS

Blood antibody test, Stool antigen test, Carbon urea breath test (in which the patient drinks 14C- or 13C-labelled urea, which the bacterium metabolizes, producing labelled carbon dioxide that can be detected in the breath), Rapid urease test:  A biopsy of mucosa is taken from the antrum, and is placed into a medium containing urea and an indicator such as phenol red. The urease produced by H. pylori hydrolyzes urea to ammonia, which raises the pH of the medium, and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE), Histological examination,  Microbial culture, Urine ELISA.

TREATMENT

The normal procedure is to eradicate H.pylori  and allow the ulcer to heal

First line treatment consists of one standard dose of proton pump inhibitor and two antibiotics 7-14days. This is called ‘tripple theray’

Second line treatment done for Individuals harbouring antibiotic-resistant bacteria, require alternative strategies, such as a ‘quadruple therapy’, which adds a bismuth colloid.

Amoxicillin could be replaced with metronidazole for people who are allergic to penicillin

Bismuth compounds have direct antimicrobial activity against H.pylori.

Examples-  bismuth subsalicylate, bismuth subcitrate potassium.