Helicobacter pylori is a bacterium that grows in the digestive tract. H. pylori is a microaerophilic, gram-negative, and urease-producing microbe. It is a spiral-shaped bacterium in its normal living form. Buts the coccoid form can also cause lesions. About half of the world population have the bacterium. Unless treated, colonization remains a lifetime (Ansari & Yamaoka, 2018).
The genus Helicobacter belongs to the subdivision of the Proteobacteria, order Campylobacterales, family Helicobacteraceae (Camilo, Sugiyama & Touati, 2017). The genus Helicobacter contains over 20 species with the number projected to rise as some species are awaiting formal recognition. Helicobacter species has two major classifications: gastric Helicobacter species and enterohepatic (nongastric) species.
The first report reported case of H. pylori was in 1906 where it was suggested to be an association between a spiral organism and gastric carcinoma (Kao, Sheu, & Wu, 2016). A report in 1938 indicated that at least 40% of human stomachs contained spiral organisms (Ansari & Yamaoka, 2018). In 1940, researchers reported the therapeutic effect of bismuth in patients with peptic ulcers induced by spiral organisms. In 1982, interest in the microbe resurfaced after Marshall and Warren discovered it; they first named it Campylobacter pylori, later Helicobacter pylori. As of 2000, the complete genome (1590 genes) of H. pylori had been unmasked (Kao, Sheu, & Wu, 2016).
- pylori is a gram-negative bacterium, measuring 2 to 4 μm in length and 0.5 to 1 μm in width (Camilo, Sugiyama & Touati, 2017). The size of the two sequenced H. pylori genomes is approximately 1.7Mbp with a G+C content of 35 to 40%. The H. pylori strain contains about 1587 genes. Although the bacterium is usually spiral-shaped, it may be rod- or coccoid-shaped, with coccoid shapes appearing after prolonged in vitro or antibiotic treatment. The spiral morphology and flagellar motility assists in penetrating the viscous mucus layer, where the neutral pH conditions allow the growth of the species. H. pylori feature of microaerophilicity is key in its growth, with optimal growth at O2 levels of 2-5% and additional need of 5-10% CO2 and high humidity (Camilo, Sugiyama & Touati, 2017). H. pylori thrive well in the harsh acidic environment of the stomach. The bacteria can reduce their acidity to ensure survival.
Disease Mechanisms
Clinical features of H. pylori range from asymptomatic gastritis to gastrointestinal malignancy (Diaconu et al., 2017). Studies show that the incidence of gastric cancer is higher in countries with a higher prevalence of infection (Diaconu et al., 2017). The microbe colonizes the stomach of man where it induced various mucosal inflammations and a local and systematic immune response. It can change its membrane potential at external pH from 3.0 to 7.0 to maintain a neutral internal (Kao, Sheu, & Wu, 2016). H. pylori strains differ and not all are pathogenic.
Available research evidence suggests H. pylori be considered as a healthcare issue as it is linked to infections such as ulcers and gastric cancer (Choi et al., 2018). Humans infected with H. pylori develop gastritis including children and adolescents. In most cases, gastritis is the first manifestation of H. pylori infection. An acute form of gastritis develops immediately after infection, characterized by hypochlorydia that later evolves into chronic active gastritis affecting the antrum, the corpus or both (Diaconu et al., 2017). H. pylori gastritis lead to a mixture of acute and chronic inflammatory reaction that stimulates both neutrophils and eosinophils, and mast and dendritic cells. Gastric adenocarcinoma from H. pylori infection develops via a series of gastritis (atrophy- intestinal metaplasia-dysplasia-carcinoma) (Diaconu et al., 2017).
Peptic ulcer disease is a leading cause of morbidity and distal gastric adenocarcinoma (Ansari & Yamaoka, 2018). However, only a small percentage of people infected present peptic ulcer disease, the majority remain symptoms free throughout their lifetime. The lifetime risk of developing peptic ulcer disease is 15% and the likelihood of developing gastric neoplasms including lymphoma and adenocarcinoma is even smaller. Generally, 92% of children with duodenal ulcers have H. pylori and 25% of those with gastric ulcers (Kao, Sheu, & Wu, 2016). Contraction of H. pylori infection is primarily in childhood, with children infected having a higher risk of carcinogenesis later in their life.
However, although H. pylori may be the main microbial trigger for various gastric diseases, it is not the only one, other microorganisms may play a role in the development of complications in H. pylori-related gastritis (Ansari & Yamaoka, 2018).
Body Reaction
Variability in the host response to H. pylori-associated symptoms is a factor that contributes to the heterogenecity of the microbe. Patients with H. pylori have reduced duodenal bicarbonate secretion which returns to normal once the microbe is eradicated (Kao, Sheu, & Wu, 2016). Generally, H. pylori infection in children is asymptomatic and not linked to particular gastrointestinal symptoms. In the absence of duodenal ulcer, H. pylori gastritis does not appear to be linked to specific symptoms (Ansari & Yamaoka, 2018). Based on initial symptoms, it is not possible to distinguish children with H. pylori from non-infected children.
The prevalence of H. pylori in adults with gastroesophageal reflux disease is significantly lower. Although the role of H. pylori in duodenogastric reflux is unclear, researchers suggest that a reduction in mean acid output in subjects with H. pylori could explain the inverse relationship between reflux and H. pylori (Kao, Sheu, & Wu, 2016). H. pylori-infected patients have a higher likelihood of experiencing heartburn and epigastric pain.
In adults, H. pylori is linked to an increased incidence of gastrointestinal cancer (Choi et al., 2018). Despite the acquisition of H. pylori in infancy being considered a significant factor to develop gastric carcinoma, the rarity of gastric ulcer in the black African population suggests otherwise (Kao, Sheu, & Wu, 2016). Diseases associated with H. pylori infection include hematologic diseases such as idiopathic iron deficiency, ITP, anemia, and B12 deficiency (Diaconu et al., 2017).
Like any other chronic inflammatory condition, H. pylori is associated with reduced growth, but socioeconomic status confounds the issue (Diaconu et al., 2017). Tumor necrosis factor-alpha, which is inversely correlated with growth, increases with H. pylori infection. H. pylori is also associated with extra digestive diseases such as functional vascular diseases and skin and endocrine autoimmune diseases (Ansari & Yamaoka, 2018).
Medical Responses
Available test to detect H. pylori includes antibody tests, stool antigen tests, urea breath tests, and endoscopic biopsies (Diaconu et al., 2017). Blood tests are useful in detecting the presence of antibodies of H. pylori. However, the persistence of blood antibodies years after the eradication of the bacteria makes it difficult to determine successful eradication. The urea breath test (UBT) accurately tests the presence of H. pylori in the stomach. Endoscopy is an accurate test for the diagnosis of the infection, the inflammation, and ulcers (Diaconu et al., 2017). Stool test determines the presence of H. pylori in the stomach and can be used to determine if treatment has been effective in eradicating the bacteria.
Treatment aims at eradicating H. pylori and prevents the return of ulcers and ulcer complications, However, prevention of stomach cancer by treating H. pylori is still controversial (Diaconu et al., 2017). Treatment should only be offered to patients with a positive H. pylori test. H. pylori is difficult to treat as it offers resistance. The resistance varies regionally. As a result, two or more antibiotics are usually prescribed together with PPI or bismuth-containing compounds for eradication.
Recurrence in the form of recrudesces or reinfection of the H. pylori after eradication therapy is a concerning issue (Diaconu et al., 2017). Reinfection refers to an infection by a new strain of H. pylori after the confirmation of a successful eradication. Recrudescence is defined as the reactivation of the same strains which reduced to undetectable levels after eradication therapy.
Patients who seek medical attention in the early stages of the disease mostly experience a complete remission with antibacterial treatment while those with a more extensive disease (lymphadenopathy, invasion throughout the wall, nodular submucosal mass lesions, or ulcerations) requiring standard lymphoma therapy (Diaconu et al., 2017).
Other Unique Microbe Characteristics
All strains of H. pylori contain some virulence factors such as urease and flagella, which are necessary for pathogenesis and colonization. Flagella plays a central role in persistent gastric colonization with the gene F1bA needed for flagellar expression (Kao, Sheu, & Wu, 2016). H. pylori produces enzymes with mostly metabolic, antioxidant and toxic properties.
Urease is located in intra and extracellular and id required to establish infection. It a nickel-containing cytoplasmic enzyme consisting of UreA and UreaB structural units whose main function is to hydrolyze urea to bicarbonate and ammonia leading to a net increase in the ambient pH. The bacteria utilize ammonia as a nutrient resulting in the development of lesions along the gastric epithelium through various mechanisms (Ansari & Yamaoka, 2018). Although surface urease protects against acid exposure, it not clear why bacteria deep underneath gastric mucus contain the compound, where the pH is thought to be neutral. Ureasest imulates the release a set of inflammatory cytokines including tumor necrosis factor-alfa, interleukin-6, interleukin-beta, and chemokines such as interleukin-8 (Kao, Sheu, & Wu, 2016). Various phospholipases produced by H. pylori weaken the hydrophobicity of the gastric mucous and mucosa and can also generate ulcer ogenic substances.