by Cynthia Lewis
Helicobacter pylori (5)
Disease: Peptic Ulcer Disease, chronic superficial gastritis (CSG, stomach inflammation), and possibly gastric carcinoma and lymphoma (3).
Transmission: Unknown. Believed to be contagious via fecal-oral route or oral-oral route between people (2).
Reservoirs: Unknown. Possibly contaminated water sources. Via contaminated endoscopes has been documented (2). Seemingly humans are its major reservoir (3). Recent research suggests that cats are a possible animal reservoir (7).
Etiologic agent: Helicobacter pylori
Characteristics: A very motile, spiral or curved rod shaped Gram-negative bacterium with multiple flagella (3) that lives in the gastric mucous-coated lining and the gastric pits of the epithelial tissue of the stomach and/or duodenum. H. pylori are microaerophilic and do not produce endospores. H. pylori are not tissue invasive. Its average length is 3.5microm and its average width ranges from .5-1microm (3). More than 90% of duodenal ulcers and 80% of gastric ulcers result from infection (2). Chemically abundant in the enzyme urease, a product of the bacterium that buffers the acidic environment of the stomach by releasing ammonia (3). No growth if incubated below 30oC; premium growth on chocolate agar (mmmm…chocolate) and blood agar plates when incubated for 2-5 days (3).
I.D. Tests: Blood test: serological test for IgG antibodies specific to H. pylori; sensitivity and specificity range between 80-95%(2)
Breath test: patient is given radioactive-labeled urea to drink. H. pylori metabolizes the labeled urea very quickly. The radioactive carbon dioxide measured from the patient’s breath indicates the presence of H. pylori; sensitivity and specificity range from 94-98% (2 & 6).
Esophagogastroduodenal Endoscopy/biopsy: a small camera attached to a tube is inserted into the mouth to the stomach to find ulcers; a biopsy from the stomach wall lining can be performed during (1). Fresh smears using phase-contrast microscopy is used for detection (3).
Stains: Warthin-Starry silver stain (7); Gram (carbol fuchsin counterstain); Giemsa or acradine orange stains (3)
Culture: nonselective media such as chocolate agar, or antibiotic-containing selective media like Goodwin or Skirrow (3)
Signs and Symptoms: Most common: burning pain in the abdomen (1), heartburn, indigestion (7)
Less common: vomiting, nausea, loss of appetite, weight loss, bloody stools, and anemia (1 &7).
Chronic superficial gastritis (CSG) is usually asympotomatic (3).
History: For much of the 20th century, ulcers were believed to be the product of poor diet and stress. Lifestyle modifications were the main form of treatment. Even after scientists Robin Warren and Barry Marshall of Australia discovered the pathogenic link between ulcers and H. pylori in 1982, the medical community stubbornly insisted that stress and diet were ultimately responsible. Finally in 1994, at the National Institutes of Health Consensus Development Conference, the relationship between H. pylori and ulcers was acknowledged and antibiotics were recommended for treatment, but in 1995 only 5% of ulcer patients were being treated with antibiotics, while 75% were on antisecretory meds. The general public still believed that stress and diet were to blame. The FDA one year later in 1996 approved the first antibiotic specific for ulcer treatment. In 1997, its genome was sequenced which has helped scientists further understand the nature of this microbe. That year the CDC launched a national campaign to educate the medical community and the public about the relationship between H. pylori and ulcer disease. (8)
Microbial Virulence: “Probably the second most common infectious disease in the world, after dental caries” (4). 30-50% of people in the developed world become infected and only 15% of them suffer from ulcers (6). People in developing countries are more at risk for infection than people from developed countries (3). People with type O blood are more vulnerable to disease. In 3% of the infected, gastric cancer develops (6). A pH of 4 is fatal to H. pylori. It thrives in the mucus layer of the stomach wall where pH is around 7.4. Also, urease production aids in buffering the stomach’s acidity. H. pylori in the duodenum do not produce urease (7). Damage caused to tissue by the bacterium is not clearly understood; theories concerning possible exotoxins are being explored (3). H. pylori can persist for years despite the body’s immune defense (3). Virulence factors are: adhesin, urease, catalase, cytotoxin-associated gene, cytotoxin, acid-inhibitory protein, superoxide dismutase, flagella, mucinase, and vacuolating cytotoxin (7).
Treatment: 1-2 weeks of one or more antibiotics as well as a medicine that will reduce stomach acid (1). Several antibiotics used are amoxicillin, tetracycline, metronidazole, and clarithromycin; these are usually used in combination with ranitidine bismuth citrate, bismuth subsalicylate, or a proton pump inhibitor, responsible for acid reduction and relieving common side effects like abdominal pain and indigestion. Longer treatment plans have proved more effective. (2)
Prevention: Since the means of transmission are not clearly understood, prevention methods are also not clear. The CDC recommends frequent and thorough hand washing, and insuring the cleanliness of food and water consumed (2).
Local Outbreaks: In the U.S., 25 million people will suffer from peptic ulcer disease at some point in their lives. Adults of low socioeconomic status are more likely to be infected (2).
Global Outbreaks: Roughly 2/3 of the world’s population is infected with H. pylori, however many never suffer from symptoms (2). People in developing countries are more at risk for infection than people from developed countries (3). Roughly 1% of the adult population from developed countries will be infected a year (3).
“H. Pylori adhering to a cultured gastric cell.” (4)
“A gastric ulcer caused by H. pylori. From the Helicobacter Foundation.” (5)
1. Centers for Disease Control and Prevention. “Helicobacter pylori and Peptic Ulcer Disease.” Sept. 28, 2006. http://www.cdc.gov/ulcer/consumer.htm. May 3, 2007.
2. Centers for Disease Control and Prevention. “The Key to Cure.” Sept. 28, 2006. http://www.cdc.gov/ulcer/keytocure.htm. May 3, 2007.
3. Blaser, Martin J., Perez-perez, Guillermo I. “Campylobacter and Helicobacter.” 2001. http://www.gsbs.utmb.edu/microbook/ch023.htm. May 6, 2007.
4. Kelleher, Dermot. “Helicobacter pylori: camouflage and stealth.” 2000. http://www.irishscientist.ie/2000/contents.asp?contentxml=037Bs.xml&contentxsl=insight3.xsl. May 6, 2007.
5. MicrobeWiki. “Helicobacter.” August 16, 2006. http://microbewiki.kenyon.edu/index.php/Helicobacter. May 6, 2007.
6. Case, Funke, and Tortora. Microbiology: an introduction 9th ed. San Francisco: Pearson Education, Inc. 2007. p760.
7. Medical Microbiology and Infectious Disease. “Helicobacter pylori.” June 19, 2006. http://medinfo.ufl.edu/year2/mmid/bms5300/bugs/helico.html. May 6, 2006.
8. Centers for Disease Control and Prevention. “Helicobacter pylori and Peptic Ulcer Disease.” Sept. 28, 2006. http://www.cdc.gov/ulcer/history.htm. May 6, 2007.