The bacterium Helicobacter pylori is a common organism that colonizes the human stomach, capable of causing significant gastrointestinal disease. Its distinctive spiral or helical shape often leads to the question of whether it belongs to the group of bacteria known as spirochetes. Despite this resemblance, H. pylori is not a spirochete. This distinction is based on fundamental differences in cellular structure and genetic makeup.
H. pylori’s Correct Classification
Helicobacter pylori is classified as a Gram-negative bacterium belonging to the phylum Campylobacterota and the family Helicobacteraceae. Its name, derived from the Greek word “heliko” (spiral), describes its typical morphology as a curved rod, or sometimes an S-shape or a more pronounced helix. The initial confusion regarding its identity stems from its discovery in the 1980s, when it was temporarily named Campylobacter pyloridis. Subsequent genetic sequencing established the distinct genus Helicobacter in 1989. The organism’s true classification is based on differences in its ribosomal RNA sequence, unique flagellar structure, and fatty acid profile, all of which separate it from both Campylobacter and the true spirochetes.
Defining the Spirochetes
Spirochetes are a distinct phylum of bacteria characterized by a helical cell shape, including pathogens like Treponema pallidum and Borrelia burgdorferi. The defining feature that separates them from H. pylori is the location of their flagella, which are internal. These internal flagella, called endoflagella or axial filaments, are found within the periplasmic space. The rotation of these enclosed filaments causes the entire bacterial body to twist and flex, enabling a unique corkscrew-like movement.
Motility and Survival in the Stomach
The ability of H. pylori to survive and colonize the acidic environment of the stomach relies on two specialized mechanisms, beginning with its motility.
Motility
Instead of internal endoflagella, H. pylori is equipped with a tuft of four to six external, sheathed flagella located at one pole of the cell. The coordinated rotation of these external appendages allows the bacterium to propel itself with a corkscrew motion directly through the thick layer of gastric mucus.
Acid Neutralization
Once it penetrates the mucus, the bacterium uses its urease enzyme as a chemical shield against the surrounding acid. Urease catalyzes the breakdown of urea, a substance present in the stomach, into carbon dioxide and ammonia. The resulting ammonia acts as a base, locally neutralizing the stomach acid in the immediate vicinity of the bacterium, creating a habitable microenvironment that allows the organism to successfully colonize the gastric epithelial layer.
Clinical Effects of H. pylori Infection
The colonization of the stomach lining by H. pylori triggers a persistent inflammatory response, known as chronic gastritis. While most infected individuals remain asymptomatic, this inflammation can progress to serious health issues. The bacterium is a primary cause of peptic ulcer disease, leading to painful sores in the lining of the stomach (gastric ulcers) or the upper part of the small intestine (duodenal ulcers). Furthermore, the chronic inflammation and tissue damage classify H. pylori as a Group 1 carcinogen. Prolonged infection significantly increases the risk for developing two types of cancer: gastric mucosa-associated lymphoid tissue (MALT) lymphoma and gastric adenocarcinoma.