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Scanning electron micrograph of Helicobacter bacteria.
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Epsilon Proteobacteria
Order: Campylobacterales
Family: Helicobacteraceae
Genus: Helicobacter
Goodwin et al. 1989

H. acinonychis
H. anseris
H. aurati
H. bilis
H. bizzozeronii
H. brantae
H. canadensis
H. canis
H. cholecystus
H. cinaedi
H. cynogastricus
H. felis
H. fennelliae
H. ganmani
H. hepaticus
H. mesocricetorum
H. marmotae
H. muridarum
H. mustelae
H. pametensis
H. pullorum
H. pylori
H. rappini
H. rodentium
H. salomonis
H. trogontum
H. typhlonius
H. winghamensis

Helicobacter is a genus of Gram-negative bacteria possessing a characteristic helix shape. They were initially considered to be members of the Campylobacter genus, but since 1989 they have been grouped in their own genus.[1][2]

Some species have been found living in the lining of the upper gastrointestinal tract, as well as the liver of mammals and some birds.[3]. The most widely known species of the genus is H. pylori. Some strains of this bacterium are pathogenic to humans as it is strongly associated with peptic ulcers, chronic gastritis, duodenitis, and stomach cancer. It also serves as the type species of the genus.

Helicobacter spp. are able to thrive in the very acidic mammalian stomach by producing large quantities of the enzyme urease, which locally raises the pH from ~2 to a more biocompatible range of 6 to 7.[4] Bacteria belonging to this genus are usually susceptible to antibiotics such as penicillin, are microaerophilic (require small amounts of oxygen), and are fast-moving with their flagella.[5]


Helicobacter Facts.[6]

Curved cells discovered in 1979 in stomach biopsied specimens.

Causes 90% of stomach & duodenal ulcers.

People with type O blood have a 1.5-2X higher rate of ulcers.

Produces large amounts of urease.

Infection common especially in lower socioeconomic class/developing nations.

Humans primary reservoir.

Person-to-person spread via fecal-oral route.

Ubiquitous, no seasonal incidence.

Gastric and Lymphoid Cancers

In 1994, the World Health Organization’s International Agency for Research on Cancer (IARC) classified H. pylori as a Group 1 carcinogen. This decision was based on the results of numerous studies that confirmed the association between H. pylori infection and gastric adenocarcinoma. H. pylori infection also significantly increases the risk of gastric lymphoma of mucosa-associated lymphoid tissue (MALT) (Suerbaum, 2002).


H. pylori infection can be confirmed by invasive or noninvasive methods. Invasive tests require upper esophagogastroduodenal (EGD) endoscopy, which is considered the reference method of diagnosis. During endoscopy, biopsy specimens of the stomach and duodenum are obtained, and the diagnosis of H. pylori can be made by urease testing, histology and/or culture. If possible, noninvasive testing is done before tissue testing.

H. pylori stool antigen (HpSA) testing is based on monoclonal antibody immunochromatography of stool samples. This testing method identifies active infection and can be used to detect eradication after treatment. A sensitivity and specificity range of 92–98% is reported in the literature for stool antigen testing.

Serological assays (blood serum) measure specific H. pylori immunoglobulin G (IgG) antibodies that can determine if an individual has been infected. The sensitivity and specificity of these assays range from 80–95%, depending on the assay used. Serological testing has been the mainstay of H. pylori diagnosis, particularly in primary care, due to the accessibility, rapid results and low cost of this testing method.

Urease test, Urease Breath Test (UBT) (positive in as little as 2 hours) [7]


Therapy with tetracycline, metronidazole, azithromycine, bismuth (Peptobismol).


  1. ^ Goodwin CS, Armstrong JA, Chilvers T, et al (1989). "Transfer of Campylobacter pylori and Campylobacter mustelae to Helicobacter gen. nov. as Helicobacter pylori comb. nov. and Helicobacter mustelae comb. nov., respectively.". Int. J. Syst. Bacteriol. 39: 397–405.
  2. ^ Vandamme P, Falsen E, Rossaq R, et al (1991). "Revision of Campylobacter, Helicobacter, and Wolinella taxonomy: emendation of generic descriptions and proposal of Arcobacter gen. nov.". Int. J. Syst. Bacteriol. 41: 88–103.
  3. ^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill. ISBN 0-8385-8529-9. 
  4. ^ Dunn BE, Cohen H, Blaser MJ (1997). "Helicobacter pylori.". Clin Microbiol Rev. 10: 720–741.
  5. ^ Hua JS, Zheng PY, Ho B (1999). "Species differentiation and identification in the genus of Helicobacter.". World Journal of Gastroenterology. 5 (1): 7–9.
  6. ^ Kathleen Park Talaro (2006). Foundations in Microbiology, 6th ed., McGraw Hill. ISBN 0072994959. 
  7. ^ Robert P H Logan, Marjorie M Walker (2001). "Epidemiology and diagnosis of Helicobacter pylori infection .". BMJ 2001;323:920-922 ( 20 October ): –741.

See also

This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Helicobacter". A list of authors is available in Wikipedia.
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