Helicobacter pylori is a sneaky bacteria that lives in the abdomen of about half of the world’s population. It was discovered by Marshall and Warren in 1982; they also received the Nobel Prize in physiology for their work on H. pylori. The transmission mode is from the human feces-oral, possibly saliva, or through vomitus, mostly from one infected person to another. 

Seroepidemiological studies show that H. pylori occur worldwide. Nonexclusive contamination of the population evolves infections from childhood, and it can reach 100% in adults, specifically in locations with poor hygiene. In industrialized countries, the average contamination level is 50% in older adults as it spreads through the fecal-oral route. 

According to an extensive research topic, humans are the primary reservoir of the spread of H. pylori infections. Low social class, high-density or crowded living conditions, and inadequate sanitation practices are oriented to a higher commonness of H. pylori infections.  

Some studies identify sheep as a possible source of transmission. H. pylori is foremost to prevent its spread and may help determine high-risk populations, especially in sectors with high rates of gastric lymphoma, ulcer, and cancer.

Scientific classification:  

Kingdom: Bacteria 

Phylum: Proteobacteria 

Class: Epsilonproteobacteria  

Order: Campylobacterales  

Family: Helicobacteraceae  

Genus: Helicobacter  

Species: Helicobacter pylori  

Structure: 

• Helicobacter pylori, also known as Campylobacter pylori, gram-negative bacterium usually found in the stomach. Its spiral shape (in which helicobacter expresses the genus name) can be evolved by focusing on penetrating the stomach’s mucoid lining and thereby administrating infection. 
• The shape and motility of the bacteria are specifically adapted to survive in the gastric mucus. H. Pylori requires optimum conditions to grow as it is microaerophilic. 
• Helicobacter pylori have a spiral or helical shape with 6-8 flagella at one end. The organism’s size measures 2-4 um x 0.5-1.0. In very acidic conditions, H. pylori thrive to grow well at a pH of 2.0 or less. 
• The chromosome of the organism contains genes that encode the cytotoxins and urease gene cluster in the membrane, 
• Some comparisons of the 16S ribosomal RNA showed that H. pylori were quite different from Campylobacter but like Wolinella succinogenes, by which its GC range was 42% to 49%. 

Helicobacter pylori are known to have several antigenic types, which are determined by the variation in the expression of its surface antigens. The most well-known antigenic types are: 

• CagA is a highly immunogenic protein encoded by the cagA gene located on the pathogenicity island of H. pylori. It is associated with increased virulence and developing peptic ulcers and gastric cancer. 
• VacA is another highly immunogenic protein encoded by the vacA gene located on the pathogenicity island of H. pylori. It is associated with forming vacuoles in host cells and developing peptic ulcers. 
• Blood group antigen-binding adhesin (BabA) is a protein that binds to Lewis b blood group antigens on the surface of gastric epithelial cells, allowing H. pylori to colonize the stomach. It is associated with increased adhesion and increased risk of gastric cancer. 
• Outer inflammatory protein (OipA) is a protein that is involved in the adhesion of H. pylori to host cells and the induction of inflammation. It is associated with increased virulence and the development of gastric cancer. 
• Heat shock proteins (HSP) are a family of highly conserved proteins involved in protecting cells against stress. HspB is an antigenic type of H. pylori-associated with increased adhesion and colonization of the stomach. 

Helicobacter pylori infect the epithelial layer of the stomach and are most acquired through interpersonal contact. 

Virulence factors of H. pylori: 

•  H. pylori has virulence strength of factors that supports pathogens to survive inside gastric mucosal layers. 
• These factors include cytotoxin-correlated gene A (CagA), vacuolating cytotoxin A (VacA), and outer inflammatory protein (OipA). CagA and VacA are meant to cause gastric epithelial damage in host cells. OiPA enhances the risk of gastric cancer and peptic ulcer disease.  
• However, a complex interplay of adhesion, inflammation, motility, and virulence factors helps the bacterium survive and colonize in the gastric mucosa, finally leading to successive pathogenesis of H. pylori. The above mechanism identifications have boosted the prevention of H. pylori-associated diseases and various strategies for treatment. 

The alpha 1,4-linked N-acetyl glucosamine is present in the stomach’s deeper mucosa lining, which strongly inhibits the growth of H. pylori. It becomes immobile, loses its shape, and eventually dies. 

The cell-growth immobilizing effect is like antibiotics, which lyse or dissolve the cell wall of H. pylori. The O-glycans combined with alpha 1,4-linked N-acetylglucosamine blocks H. pylori’s capability in cholesterol synthesis. Hence this naturally occurring cholesterol can cure stomach ulcers.  

Helicobacter pylori cause inflammation, peptic ulcers, duodenal ulcers, gastric ulcers, and even cancer in the duodenum and stomach. 

H. pylori some significant diseases,

• Chronic gastritis (stomach lining inflammation) 
• Lymphomas (lymphoid tissue cancers) 
• Gastric Mucosa Associated Lymphoid Tissue (MALT)lymphoma. 
• Non-cardia gastric cancer  

Most people with H. pylori infection are with no symptoms. In infection of H. pylori, symptoms start if it causes gastritis or peptic ulcers.  

These symptoms can be non-specific and may include the following: 

• Abdominal pain (specifically upper abdomen) 
• Nausea and Vomiting 
• Stomach bloating and irritation. 
• Low blood count (anemia) 
• Red-colored stools (indicates intestinal bleeding. 

Diagnostic testing methods available for H. pylori include non-invasive and invasive techniques include the following: 

• To detect H. pylori easily, Non-invasive techniques include breath testing, urea, stool antigen detection, and serology test. 
• Invasive techniques include the endoscopy method to collect gastric biopsies, including culture, histology, and rapid urease test. 
• H. pylori infection can be tested by low-grade MALT lymphoma test, early gastric cancer (EGC), or a history of endoscopic resection can help for detection. 
• Some guidelines recommend that patients with a history of PUD treated for H. pylori undergo eradication testing with a fecal antigen test or urea breath test. 
• Nonendoscopic testing should be considered for patients below 60 years of age with non-investigated dyspepsia and without alarm features; for patients who have undergone upper endoscopy and dyspepsia, gastric biopsy tissue testing should be carried out.

The ACG Clinical Guideline recommends that patients be tested after treatment to ensure the eradication of the infection. The test method includes a urea breath test, biopsy origin test, fecal antigen test, or at least 3-4 weeks after antibiotic therapy. After that, Protein pump inhibitors (PPI) therapy should not be given for at least 1 to 2 weeks. 

• Wash your hands regularly with water & soap. 
• Ensure proper sanitary practices are followed when handling food. 
• Strictly avoid sharing coffee cups, utensils, and personal hygiene equipment with others. 
• Maintain a healthy diet and exercise periodically to strengthen your immune system. 
• Cook your food thoroughly, especially poultry and meat. 
• Avoid ingesting milk products and unpasteurized milk.  
• Sexually transmitted infections that increase the high-risk factor of H. pylori infection can be avoided by safe sex practices. 
• Avoid drinking untreated water, especially when roaming in areas with poor hygiene. 
• Avoid smoking and alcohol consumption. 

https://en.wikipedia.org/wiki/Helicobacter_pylori  
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