In this blog post I will talk about helicobacter pylori virulence factors and how this makes it a dangerous bacterium to encounter. I will also briefly cover the diagnosis and treatment of gastritis.
Helicobacter pylori Virulence Factors That Make it Better at Causing Disease
Helicobacter pylori is a highly motile gram-negative bacterium transmitted via the fecal-oral route (bacteria in faeces transmitted to mouth), and is responsible for causing the majority of peptic ulcers.
peptic ulcer is the breakdown/erosion in lining of the stomach or the first part of small intestine (duodenum). In the stomach it is known as a gastric ulcer and in the duodenum – duodenal ulcer.
pylori possesses several virulence factors (things that make it better at causing disease) that enable it to colonize and do damage to the lining of the stomach.
This includes producing protein that inhibits acid production by stomach cells, flagella that enables it to bore through the mucus lining and adhesins to help it bind to gastric cells. H. pylori also has enzymes that inhibit phagocytic killing.
When ingested, helicobacter pylori burrows through the stomach mucus to reach underlying epithelial cells where the bacteria can multiply.
The triggering of inflammation from the release of toxins and perhaps damage to mucus secreting cells causes mucus layer to become thin, allowing stomach gastric juice to ulcerate epithelial layer.
This in-turn allows pylori to gain access to underlying muscle tissue and blood vessels.
Phagocytosed bacteria may be able to survive by releasing catalase and super-oxide dismutase which are enzymes that neutralize part of a phagocytes killing mechanism.
pylori also actively produces a urease enzyme. This enzyme degrades urea found in gastric juice into ammonia, a highly alkaline chemical which can be used to neutralize stomach acid and increase gastric pH.
H. pylori also possesses adhesins that facilitate binding to gastric cells, and flagella to aid in its high level of motility.
Diagnosis and treatment of gastritis – main methods
Upper GI series of X rays following barium ingestion shows presence of ulcer. H. pylori can also be found in gram stained smears.
Urease test is effective in indicated presence of H. pylori in stomach specimen within 2 hours of culturing.
Urease test detects a micro-organisms ability to convert urea into co2 and ammonia. Ammonia makes phenol red (a type of pH indicator) turn from yellow to pink, indicating rise in pH.
Treatment is done with one or more antimicrobial (antibiotic (can also include antifungal, antiprotozoal etc)) drug in combination with drugs that inhibit acid production.
This generally resolves most ulcers in six to eight weeks.
Use of nonsteroidal anti-inflammatory medications such as ibuprofen and aspirin can exacerbate symptoms.
- Helicobacter pylori is a highly motile gram-negative bacterium transmitted via the fecal-oral route.
- It is the cause of most peptic ulcers.
- H.pylori has a range of virulence factors that enable it to colonize and damage stomach lining. This includes inhibiting phagocytic killing, being highly motile, ability to produce urease, and having adhesin molecules.
- pylori can be diagnosed using a range of tests including X-ray with radioactive marker, gram stain smear and rapid urease test.
- Treatment is usually handled with antimicrobial medication.
- Symptoms of peptic ulcer can be exacerbated by the use of nonsteroidal anti-inflammatory medication.
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