Charles Darwin

"The love for all living creatures is the most noble attribute of man." Charles Darwin

Thursday, January 29, 2015

Helicobacter pylori




Helicobacter pylori


The cause of stomach ulcers had long been attributed to stress, spicy foods, smoking, or other lifestyle habits.[1]

Conventional thinking was that no bacterium could live within the acidic environment of the stomach.

It was not until the early 1980's when the bacteria, Helicobacter pylori (H. pylori) was discovered in the stomachs of patients with gastritis and stomach ulcers that conventional thinking began to change...

... Began to change ... as in, the 'H. pylori - ulcer' connection being proposed by Dr. Barry Marshall and Dr. Robin Warren in the early 80's was initially met with strong resistance from colleagues adhering to the accepted theories of the day.

Unable to gain access to suitable test subjects (H. pylori affects only primates), Marshall decided to take matters into his own hands by drinking a solution H. pylori from the gut of an ailing patient. Shortly thereafter, he began to develop symptoms of gastritis, the precursor to an ulcer. Taking a biopsy from his own gut (as one does), he was able to culture H. pylori and show the bacteria to be the underlying cause of ulcers.[16]

In recognition of their discovery, Dr. Barry Marshall and Dr. Robin Warren were awarded the 2005 Nobel Prize in Physiology or Medicine.[12][13][14][15]




  • It is estimated that at least half the world's population is infected by the H. pylori bacterium, making it the most widespread infection in the world.[4]

  • Considering that statistic, it is indeed fortunate that up to 85% of people infected with H. pylori never experience symptoms or complications.[5]

  • On another positive note, the overall frequency of H. pylori infection appears to be on the decline.[2][6]

  • Most frequently acquired in early childhood,[2] H. pylori is contagious, although the exact route of transmission is not known.[8][9] 

  • It is believed H. pylori may be transmitted person-to-person via the oral-oral or fecal-oral route; oral transmission may also occur through the ingestion of waste-tainted water.[10][11]



COMPLICATIONS ASSOCIATED WITH H. PYLORI INFECTION: 


ULCERS

A benign gastric ulcer of a gastrectomy 
specimen.
A natural mucous barrier exists on the lining of the stomach to protect against its strong digestive acids. 

There is normally a balance between the amount of acid produced by the stomach and the mucous defense barrier.[1][2][3]

H. pylori can damage the protective lining of the stomach and small intestine, and disrupt this balance, allowing stomach acid to create an open sore (ulcer).

Individuals infected with H. pylori have a 10 to 20% lifetime risk of developing peptic ulcers.[2][30][31][34]


INFLAMMATION OF THE STOMACH LINING

By the same action as described above, H. pylori infection can cause inflammation of the stomach lining (gastritis). This may develop into an ulcer.[31]


CANCER

Endoscopic image of gastric ulcer, biopsy proven
to be gastric cancer.
In 1994, the International Agency for Research on Cancer classified H. pylori as a carcinogen, or cancer-causing agent, in humans.[34]

Infection with H. pylori is the primary identified cause of non-cardia gastric cancer (cancer found in all other areas of the stomach other than the top portion).[35-43]







A meta-analysis[33] conducted in 2009 concluded the eradication of H. pylori reduces gastric cancer risk in previously infected individuals. The analysis suggested the continued presence of H. pylori constitutes a relative risk factor of 65% for gastric cancers; in terms of absolute risk, the increase was from 1.1% to 1.7%.[2][31][32]

Although it is not known for certain how H. pylori infection increases the risk of non-cardia gastric cancer, some researchers speculate that the long-term presence of an inflammatory response predisposes cells in the stomach lining to become cancerous.[40][41]

Long-term follow-up of data from a randomized clinical trial carried out in Shandong, China—an area where rates of gastric cancer are very high—found that short-term treatment with antibiotics to eradicate H. pylori reduced the incidence of gastric cancer.

During a nearly 15-year period after treatment, gastric cancer incidence was reduced by almost 40%.[42]

When the results of this trial were pooled with those of several smaller trials examining the effects of H. pylori eradication on incidence of gastric cancer, a similar reduction was seen.[42]



SYMPTOMS   

Acute infection may appear as an acute gastritis (inflammation of the stomach lining) with abdominal pain or nausea.[17]

Where this develops into chronic gastritis, the symptoms may include stomach pains, nausea, bloating, belching, and sometimes vomiting or black stool.[18][19]


DIAGNOSIS[20][21]

H. pylori can be detected via:
  • A breath test
  • A stool antigen test
  • A blood test to detect the presence of H. pylori antibodies 
  • If a biopsy sample of the stomach’s lining has been taken during gastroscopy, it can be tested for H. pylori.

Immunohistochemical detection of H. pylori in
gastric biopsy



TREATMENT

  • H. pylori infections are usually treated with two varieties of antibiotics at once, to help prevent the bacteria from developing a resistance to one particular antibiotic; as well as an acid-suppressing drug, to help the stomach lining heal.[1]

  • Despite efforts to prevent resistance, it is perhaps not entirely surprising to hear that an increasing number of infected individuals are being found to harbor antibiotic-resistant bacteria.[7][22]

  • This results in initial treatment failure and requires additional rounds of antibiotic therapy or alternative strategies.[23][24][25] 

  • Supplementing diets with yogurt containing Lactobacillus and Bifidobacterium has improved the rates of eradication of H. pylori in humans.[26]

  • The substance sulforaphane, which occurs naturally in broccoli and  cauliflower, has also been proposed as a treatment.[27][28][29] 


GENOME

  • H. pylori is believed to have migrated out of Africa along with its human hosts around 60,000 years ago.[50][51]

  • There is a great deal of diversity among the various strains of H. pylori. The genomes of three have been completely sequenced.[43-47]


A 'PATHOGENICITY ISLAND' IS THE NAME GIVEN TO A COMMON GENE SEQUENCE BELIEVED TO BE RESPONSIBLE FOR PATHOGENESIS

  • The Cag PATHOGENICITY ISLAND (cag PAI) is usually absent from H. pylori strains isolated from asymptomatic human carriers of the bacteria.[48]

  • About 50–70% of H. pylori strains in Western countries carry the cag PAI.[49]

  • Western patients infected with strains carrying the cag PAI have been shown to have a stronger inflammatory response in the stomach and are at a greater risk of developing peptic ulcers or stomach cancer than those infected with strains lacking the island.[2]





***
FIN








REFERENCES:

[1] http://www.mayoclinic.org/diseases-conditions/h-pylori/basics/definition/con-20030903
[2] Kusters JG, van Vliet AH, Kuipers EJ (July 2006). "Pathogenesis ofHelicobacter pylori Infection". Clin Microbiol Rev 19 (3): 449–90.doi:10.1128/CMR.00054-05. PMC 1539101. PMID 16847081.
[3] Amieva MR, El-Omar EM (January 2008). "Host-bacterial interactions in Helicobacter pylori infection". Gastroenterology 134 (1): 306–23. doi:10.1053/j.gastro.2007.11.009.PMID 18166359.
[4] Pounder RE, Ng D (1995). "The prevalence of Helicobacter pylori infection in different countries". Aliment. Pharmacol. Ther. 9 (Suppl 2): 33–9. PMID 8547526.
[5] Bytzer P, Dahlerup JF, Eriksen JR, Jarbøl DE, Rosenstock S, Wildt S (April 2011)."Diagnosis and treatment of Helicobacter pylori infection". Dan Med Bull 58 (4): C4271.PMID 21466771.
[6] Malaty HM (2007). "Epidemiology of Helicobacter pylori infection". Best Pract Res Clin Gastroenterol 21 (2): 205–14. doi:10.1016/j.bpg.2006.10.005. PMID 17382273.
[7] Mégraud F (September 2004). "H pylori antibiotic resistance: prevalence, importance, and advances in testing". Gut 53 (9): 1374–84. doi:10.1136/gut.2003.022111.PMC 1774187. PMID 15306603.
[8] Mégraud F (1995). "Transmission of Helicobacter pylori: faecal–oral versus oral–oral route". Aliment. Pharmacol. Ther. 9 (Suppl 2): 85–91. PMID 8547533.
[9] Cave DR (May 1996). "Transmission and epidemiology of Helicobacter pylori". Am. J. Med. 100 (5A): 12S–17S; discussion 17S–18S. PMID 8644777.
[10] Brown LM (2000). "Helicobacter pylori: epidemiology and routes of transmission". Epidemiol Rev 22 (2): 283–97.doi:10.1093/oxfordjournals.epirev.a018040. PMID 11218379.
[11] Delport W, van der Merwe SW (2007). "The transmission of Helicobacter pylori: the effects of analysis method and study population on inference". Best Pract Res Clin Gastroenterol 21 (2): 215–36. doi:10.1016/j.bpg.2006.10.001. PMID 17382274.
[12] http://www.webmd.com/digestive-disorders/h-pylori-helicobacter-pylori?
[13] "The Nobel Prize in Physiology or Medicine 2005".
[14] Atwood IV KC (2004). "Bacteria, Ulcers, and Ostracism? H. pylori and the making of a myth"
[15] "Helicobacter pylori in peptic ulcer disease". NIH Consensus Statement Online Jan 7–9;12(1):1–23.
[16] http://discovermagazine.com/2010/mar/07-dr-drank-broth-gave-ulcer-solved-medical-mystery.
[17] Butcher, Graham P. (2003). Gastroenterology: An Illustrated Colour Text. Elsevier Health Sciences. p. 25. ISBN 0-443-06215-3.
[18] Butcher 2003, pp. 24–5
[19] Ryan, Kenneth (2010). Sherris Medical Microbiology. McGraw-Hill. pp. 573, 576.ISBN 978-0-07-160402-4.
[20] http://www.webmd.com/digestive-disorders/h-pylori-helicobacter-pylori?
[21] http://www.patient.co.uk/health/helicobacter-pylori-and-stomach-pain
[22] http://en.wikipedia.org/wiki/Helicobacter_pylori
[23] Stenström B, Mendis A, Marshall B (August 2008). "Helicobacter pylori—The latest in diagnosis and treatment". Aust Fam Physician 37 (8): 608–12. PMID 18704207.
[24] Fischbach L, Evans EL (August 2007). "Meta-analysis: the effect of antibiotic resistance status on the efficacy of triple and quadruple first-line therapies for Helicobacter pylori".Aliment. Pharmacol. Ther. 26 (3): 343–57. doi:10.1111/j.1365-2036.2007.03386.x.PMID 17635369.
[25] Graham DY, Shiotani A (June 2008). "Newer concepts regarding resistance in the treatment Helicobacter pylori infections". Nat Clin Pract Gastroenterol Hepatol 5 (6): 321–31. doi:10.1038/ncpgasthep1138. PMC 2841357. PMID 18446147.
[26] Wang KY, Li SN, Liu CS et al. (September 2004). "Effects of ingesting Lactobacillus- and Bifidobacterium-containing yogurt in subjects with colonized Helicobacter pylori". The American Journal of Clinical Nutrition 80 (3): 737–41. PMID 15321816.
[27] J. K. Moon, J. R. Kim et al: Analysis and anti-Helicobacter activity of sulforaphane and related compounds present in broccoli (Brassica oleracea L.) sprouts. In: Journal of Agricultural and Food Chemistry. Volume 58, Number 11, June 2010, pp 6672–6677,ISSN 1520-5118. doi:10.1021/jf1003573. PMID 20459098.
[28] J. W. Fahey, X. Haristoy et al: Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors. In: PNAS. Volume 99, Number 11, May 2002, pp 7610–7615, ISSN 0027-8424. doi:10.1073/pnas.112203099. PMID 12032331. PMC 124299.
[29] X. Haristoy, K. Angioi-Duprez u. a.: Efficacy of sulforaphane in eradicating Helicobacter pylori in human gastric xenografts implanted in nude mice. In: Antimicrobial agents and chemotherapy. Volume 47, Number 12, December 2003, pp 3982–3984, ISSN 0066-4804. PMID 14638516. PMC 296232.
[30] http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/peptic-ulcer/Pages/overview.aspx
[31] http://www.patient.co.uk/health/helicobacter-pylori-and-stomach-pain
[32] Fuccio, L; Zagari, RM; Eusebi, LH; Laterza, L; Cennamo, V; Ceroni, L; Grilli, D; Bazzoli, F (2009). "Meta-analysis: can Helicobacter pylori eradication treatment reduce the risk for gastric cancer?". Ann Intern Med 151 (2): 121–8. doi:10.7326/0003-4819-151-2-200907210-00009. PMID 19620164.
[33] Greenland S, O' Rourke K: Meta-Analysis. Page 652 in Modern Epidemiology, 3rd ed. Edited by Rothman KJ, Greenland S, Lash T. Lippincott Williams and Wilkins; 2008.
[34] http://www.cancer.gov/cancertopics/factsheet/Risk/h-pylori-cancer
[35] Forman D, Burley VJ. Gastric cancer: Global pattern of the disease and an overview of environmental risk factors. Best Practice & Research Clinical Gastroenterology 2006; 20(4):633–649.
[36] Brenner H, Rothenbacher D, Arndt V. Epidemiology of stomach cancer. Methods in Molecular Biology 2009; 472:467–477.
[37] Atherton JC. The pathogenesis of Helicobacter pylori-induced gastro-duodenal diseases. Annual Review of Pathology 2006; 1:63–96.
[38] Kusters JG, van Vliet AH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clinical Microbiology Reviews 2006; 19(3):449–490
[39] Helicobacter and Cancer Collaborative Group. Gastric cancer and Helicobacter pylori: A combined analysis of 12 case control studies nested within prospective cohorts. Gut 2001; 49(3):347–353.
[40] Parsonnet J, Friedman GD, Vandersteen DP, et al. Helicobacter pylori infection and the risk of gastric carcinoma. New England Journal of Medicine 1991; 325(16):1127–1131.
[41] Huang JQ, Sridhar S, Chen Y, Hunt RH. Meta-analysis of the relationship between Helicobacter pylori seropositivity and. Gastroenterology 1998; 114(6):1169–1179.
[42] Eslick GD, Lim LL, Byles JE, Xia HH, Talley NJ. Association of Helicobacter pylori infection with gastric carcinoma: A meta-analysis. American Journal of Gastroenterology 1999; 94(9):2373–2379.
[43] Uemura N, Okamoto S, Yamamoto S, et al. Helicobacter pylori infection and the development of gastric cancer. New England Journal of Medicine 2001; 345(11):784–789.
[44] Parsonnet, J, Hansen S, Rodriguez L, et al. Helicobacter pylori infection and gastric lymphoma.New England Journal of Medicine 1994; 330(18):1267–1271.
[45] Sagaert X, Van Cutsem E, De Hertogh G, Geboes K, Tousseyn T. Gastric MALT lymphoma: A model of chronic inflammation-induced tumor development. Nature Reviews Gastroenterology & Hepatology 2010; 7(6):336–346.
[46] Ma JL, Zhang L, Brown LM, et al. Fifteen-year effects of Helicobacter pylori, garlic, and vitamin treatments on gastric cancer incidence and mortality. Journal of the National Cancer Institute 2012; 104(6):488-492.
[47] Tomb JF, White O, Kerlavage AR et al. (August 1997). "The complete genome sequence of the gastric pathogen Helicobacter pylori". Nature 388 (6642): 539–47.doi:10.1038/41483. PMID 9252185.
[48] "Genome information for the H. pylori 26695 and J99 strains". Institut Pasteur. 2002.
[49] "Helicobacter pylori 26695, complete genome". National Center for Biotechnology Information.
[50] "Helicobacter pylori J99, complete genome". National Center for Biotechnology Information.
[51] Oh JD, Kling-Bäckhed H, Giannakis M et al. (June 2006). "The complete genome sequence of a chronic atrophic gastritis Helicobacter pylori strain: Evolution during disease progression". Proc Natl Acad Sci U.S.A. 103 (26): 9999–10004.doi:10.1073/pnas.0603784103. PMC 1480403. PMID 16788065.
[52] Baldwin DN, Shepherd B, Kraemer P et al. (February 2007). "Identification ofHelicobacter pylori Genes That Contribute to Stomach Colonization". Infect Immun 75(2): 1005–16. doi:10.1128/IAI.01176-06. PMC 1828534. PMID 17101654.
[53] Peek RM, Crabtree JE (January 2006). "Helicobacter infection and gastric neoplasia". J. Pathol. 208 (2): 233–48. doi:10.1002/path.1868. PMID 16362989.
[54] Correa P, Piazuelo MB (January 2012). "Evolutionary History of the Helicobacter pyloriGenome: Implications for Gastric Carcinogenesis". Gut Liver 6 (1): 21–8.doi:10.5009/gnl.2012.6.1.21. PMC 3286735. PMID 22375167.
[55] Linz B, Balloux F, Moodley Y et al. (February 2007). "An African origin for the intimate association between humans and Helicobacter pylori". Nature 445 (7130): 915–8.doi:10.1038/nature05562. PMC 1847463. PMID 17287725.



IMAGE CREDITS

"EMpylori" by Yutaka Tsutsumi, M.D.Professor Department of PathologyFujita Health University School of Medicine - Yutaka Tsutsumi, M.D.Professor Department of Pathology Fujita Health University School of Medicinehttp://info.fujita-hu.ac.jp/~tsutsumi/photo/photo002-6.htmhttp://info.fujita-hu.ac.jp/~tsutsumi/image/002/2-6.jpg. Licensed under Copyrighted free use via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:EMpylori.jpg#mediaviewer/File:EMpylori.jpg

"Ulcer-causing Bacterium (H.Pylori) Crossing Mucus Layer of Stomach" by Illustration Credit: Zina Deretsky, National Science Foundation - NSF Flickr photostream, http://www.flickr.com/photos/nsf_beta/4822021538/in/set-72157621768317570. Licensed under Public Domain via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Ulcer-causing_Bacterium_(H.Pylori)_Crossing_Mucus_Layer_of_Stomach.jpg#mediaviewer/File:Ulcer-causing_Bacterium_(H.Pylori)_Crossing_Mucus_Layer_of_Stomach.jpg

"Benign gastric ulcer 1" by Ed Uthman, MD - http://web2.airmail.net/uthman/specimens/index.html. Licensed under Public Domain via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Benign_gastric_ulcer_1.jpg#mediaviewer/File:Benign_gastric_ulcer_1.jpg
"Gastric ulcer 3" by Original uploader was Samir (The Scope) at en.wikipedia - Originally from en.wikipedia; description page is/was here.. Licensed under CC BY-SA 3.0 via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Gastric_ulcer_3.jpg#mediaviewer/File:Gastric_ulcer_3.jpg

"Immunohistochemical detection of Helicobacter (1) histopatholgy" by User:KGH - User:KGH. Licensed under CC BY-SA 3.0 via Wikimedia Commons - http://commons.wikimedia.org/wiki/File:Immunohistochemical_detection_of_Helicobacter_(1)_histopatholgy.jpg#mediaviewer/File:Immunohistochemical_detection_of_Helicobacter_(1)_histopatholgy.jpg








No comments:

Post a Comment