H. pylori is one crazy bug.
It lives in one of the most hostile environments in the body: the highly acidic stomach. In fact, it not only lives there, it seems to thrive! It has managed to colonize over half of the world’s population. It’s a nasty bug too, at least in some ways: it causes gastritis, gastric ulcer, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. How does it manage to do all these things and still look pretty?
H. pylori has a ton of cool features that allow it to survive in the stomach and cause disease there. Here’s a short list:
1. Urease. This is one of the most important features of H. pylori; without it, the bug could not survive in the stomach. Urease is an enzyme that breaks urea (an abundant substance in the body) into carbon dioxide and ammonia. The carbon dioxide gets blown off, but the ammonia stays and surrounds the bug, raising the pH and allowing the bug to sit comfortably in this otherwise deadly environment.
2. Mucinase. Here’s another cool enzyme in H. pylori‘s arsenal. Mucinase does just what the name suggests: it busts apart the thick mucin layer that normally overlies the gastric epithelium, allowing H. pylori to walk on through this layer of protection and get right onto the surface of the epithelial cells.
3. Corkscrew motility. H. pylori is curved, and it has a few nice flagellae at one end. So it sort of corkscrews itself down through the mucin to reach the epithelial layer. Much more effective than a regular old straight rod trying to push its way through.
4. CagA. This is a virulence factor that does a ton of stuff, including disrupting cell junctions, affecting cell proliferation and differentiation, and inducing inflammation. Patients who have cagA positive strains generally have more severe gastritis, and a significantly increased risk of developing ulcers and carcinoma.
5. VacA. This is another virulence factor that does a ton of stuff, including making vacuoles, inducing apoptosis, disrupting cell pathways, inducing inflammation, and modulating the immune system (it allows H. pylori bugs to live in macrophages, and also inhibits T-cell production by decreasing IL-2 production). Nasty. Patients with vacA positive strains also have an increased risk of severe gastritis, ulcers and carcinoma.
- Kristine said No that makes absolute sense! If the likelihood of PE is low, then you do a D-dimer to rule it out (...
- Fatima said As the hemoglobin drops, you need to make more reticulocytes to get up to the normal range of 0.5 –...
- praveen pandey said I read in Harrison 18ed fig 300-3 algorithm. It says we do a d-dimer for low likelihood of PE. For h...
- Md.Abu Jar said thanks a lot my loving teacher….kristine krafts
- sama said Amazing
- vijaya said Thanks
- Sandeep Jain said As always, fantastic explanation! The delay in maturation time with decreasing Hgb is good to know!
- Baraniko Eromanga said Thanks for discussing this, it’s confusing me for long time, now I understand the differences.
- Kristine said Thanks, Raffi. No – the concept of shift reticulocytes is not the same as polychromasia. Polyc...
- Raffi said Thanks for the post. By chance, is the “shift reticulocyte” the same as polychromasia? I...
- vetstudent said u make things a lot of easier! tq
- Kristine said Sure – you just multiply the percentages by the total white blood cell count. For example: the...