Bacterium Helicobacter pylori Essay Example

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    Biology
  • Document type:
    Essay
  • Level:
    Masters
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    2
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    1249

Immunity and Microbiology – Bacterium Helicobacter pylori

Introduction

Bacterium Helicobacter pylori is a widespread bacterial infections among humans. Fifty percent of the world’s population has been infected by the Bacterium Helicobacter pylori (H. pylori) (1). The bacterium is posited to be a significant risk factor for developing gastric mucosa-associated lymphoid tissue lymphoma and gastric cancer. It is associated with stomach ulcers due to the carcinogen-producing nature of the bacterium. The Center for Digestive Diseases (2) classifies the bacteria as Class 1 carcinogen based on declarations from the World Health Organization. This is because the bacteria’s invasion of the mucous lining in the stomach contributes to 75 percent of gastric ulcers, 95 percent of the duodenal cancer, lymphoma, and gastric cancer (2). This paper assesses the role of H. pylori in causing gastric disease, action mechanism in the stomach and the pathogenesis of the bacteria.

Immunity and Microbiology

Role in Gastric Disease

H. pylori is strongly associated with gastric disease. Two Australian scientists confirmed the bacterium’s existence in the stomach in the 1970s. In 1982, they posited that the bacterium increased the possibility of developing gastric disease and stomach ulcers (3). A study on the genetics of Helicobacter species concurred that H. pylori was a gastric helicobacter and posed a risk factor for gastric conditions similar to H. centorum (including H. felis and H. salomonis), H. baculiformis and H suis (4). H. pylori bacterium contributes to gastric disease by altering the gastric lining into a pre-cancerous form (2). The bacterium modifies the surface component of the lining called lipopolysaccharide (LPS) thereby making it undetectable by the immune system components (such as the white blood cells) and increasing resistance to antimicrobial compounds which are secreted by the gastric mucus cells (5,6,7). This resistance from the immune response in the host allows the bacterium to continue infecting the gastric mucosa thereby causing chronic gastric disease.

Stomach

The bacterium affects the stomach by inducing an active and chronic inflammation. According to the Iron Disorders Institute (3), H. pylori burrow into the thick mucus lining in the stomach and obtain its nourishment from hemoglobin. Access to hemoglobin allows the bacterium to absorb iron for nourishment. H. pylori absorb iron from the heme and from lactoferrine, which is obtained from human secretions. The secretions include tears, saliva, gastrointestinal fluids, seminal fluids, and vaginal fluids. H. pylori infect the stomach lining through its burrowing and release the urease enzyme for protection. The enzyme produces ammonia and bicarbonate, which neutralize stomach acid and protect the bacterium from white blood cells. As more white blood cells continue to attack the bacterium’s protective cover, they proliferate and die off leaving free radicals in the stomach (3, p.4). The host then experiences gastritis symptoms such as headaches, stomach pain, nausea, belching and acid reflux (8).

Progression and Pathogenesis

Research by the Center for Digestive Diseases (2) asserts that there has been extensive research on the spread of the bacterium. However, research on the transmission mode remains unclear. Furthermore, there is evidence showing that the bacterium can be transmitted from one person to another through fecal-oral interactions. There is also evidence showing that H. pylori can be transmitted through oral-to-oral methods. In addition, infection rates of H. pylori are significantly higher among populations who live in crowded conditions or have poor personal hygiene, water supply, or sanitation (2).

H. pylori infections are common in males and females. The infections are usually asymptomatic in majority of the infected people. Only ten percent or less develop symptoms such as indigestion, burping, vomiting, loss of appetite and burning pain in upper abdomen area (2). These symptoms are associated with gastric cancer, lymphoma or peptic ulcer disease. The pathogenesis of the bacterium is determined by the interactions between host cells and the bacterial aspects (1).

It is important to diagnose H. pylori to prevent the development of gastric disease and cancer. The bacterium may be diagnosed in two ways: invasive or non-invasive. Invasive methods include gastroscopy and serology while non-invasive techniques include urea breath tests (2, 9). Gastroscopy involves the insertion of an endoscope through the mouth of a sedated patient. The gastroenterologist then collects a sample of the tissue (biopsy) to conduct pathological tests or H. pylori. The pathological tests usually reveal the condition of the stomach lining to help the gastroenterologist determine whether the infection is chronic or acute gastritis, metaplasia, lymphoma, or Barrett’s esophagus. The bacterium cultures could also be tested for sensitivity to antibiotics to improve the accuracy of the diagnosis. Alternatively, the gastroenterologist may screen the patient’s blood for antibodies. The urea breath test provides a non-invasive option for detecting active H. pylori infection (2).

Treatment prevents further development of H. pylori infections by 75 percent (2). First-line treatment would use combinations of acid suppressors with antibiotics to kill bacteria (such as amoxicillin) and stomach protectors (9). The level of treatment depends on the patient’s sensitivity to antibiotics and level of antibiotic resistance of the H. pylori. Second-line treatment would involve customizing antibiotic combinations to increase the patient’s success rate (10).

Conclusion

H. pylori is a risk factor for the development of gastric disease in humans. It alters the gastric lining into a pre-cancerous form. The bacterium infects the stomach by inducing an active and chronic inflammation. H. pylorus burrows in the stomach lining and releases an enzyme, which protects the bacterium from attacks from the host’s immune response. This infection is asymptomatic in majority of the population but causes symptoms associated with gastric disease and lymphoma in about 10 percent of the population. Gastroscopy, serology, and urea breath tests would help physicians to diagnose the bacterium and initiate treatment to reduce the malignancy of the infection.

References

  1. Jinxiong W, Jennifer N, Elena Z, Judith R, Pelayo C, Wael E, Richard P, Alexander Z. Pathogenic bacterium Helicobacter pylori alters the expression profile of p53 protein isoforms and p53 response to cellular stress. Proceedings of the National Academy of Sciences [Internet]. 2012 Apr [cited 2014 Aug 28]; 109(38): E2543-2550. Available from: http://www.pnas.org/content/109/38/E2543.full

  2. Centre for Digestive Diseases. Helicobacter pylori [Internet]. [New South Wales: CDD, 2009 [cited 2014 Aug 28]. Available from: http://www.cdd.com.au/pages/disease_info/ heliobacter_pylori.html

  3. Iron Disorders Institute. Helicobacter: H. pylori. A common bacterium often overlooked by physicians. ID Insight [Internet]. 2002 Spring [cited 2014 Aug 28]. Available from: http://www.irondisorders.org/Websites/idi/files/Content/854291/hpylori.pdf

  4. Yoshan M, Bodo L, Robert B, Martin N, Himla S, Carina MS, et al. Age of the association between Helicobacter pylori and man. PLos Pathog [Internet]. 2012 May [cited 2014 Aug 28]; 8(5): e1002693. Available from: 10.1371/journal.ppat.1002693

  5. Thomas C, David KG, Lindsey W, Chantal E, Ivo GB, Stephen T. Helicobacter pylori versus the host: Remodeling of the bacteria membrane is required for survival in the Gastric mucosa. PLos Pathog [Internet]. 2011 December [cited 2014 Aug 28]; 7(12):e1002454. Available from: 10.1371/journal.ppat.1002454

  6. E Fosso-Kankeum, Du, PH, Jagals, P. Health implications of lipopolysaccharide endotoxins in domestic container water used by rural households in South Africa. Journal of Water & Health, 2010; 8(4): 601-610.

  7. Raetz C, Whitfield C Lipopolysaccharide endotoxins. Annu Rev Biochem. 2002; 71: 635-700.

  8. Nina RS, Mara LH, Anne M. Life in the human stomach: Persistence strategies of the bacterial pathogen Helicobacter pylori. Nature Reviews Microbiology [Internet]. 2013 [cited 2014 Aug 28]; 11(6): 385-399. Available from: doi:10.1038/nrmicro3016

  9. Richard MP. Helicobacter pylori infection and disease: From humans to animal models. Dis Models Mech [Internet]. 2008 Jul-Aug [cited 2014 Aug 28]; 1:50-55. Available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2561984/

  10. Robin M, Massimo R. Pathogenesis of Helicobacter pylori infection. Helicobacter [Internet]. 2012 Sep [cited 2014 Aug 28]; 17(S1): 9-15. Available from: 10.1111/j.1523-5378.2012.00976.x