Helicobacter pylori
Table of Contents
- What is Helicobacter pylori? (H. pylori)
- How is H. pylori infection diagnosed?
- How is infection with H. pylori treated?
- H. pylori infection among Alaska Natives
- Projects in Progress
- Future Plans
- References
What is Helicobacter pylori?
H. pylori is a spiral-shaped gram negative bacterium that can live in the stomach and in the duodenum which is the section of intestine below the stomach. It is the most common cause of ulcers of the stomach and duodenum, accounting for up to 90% of duodenal ulcers and up to 80% of gastric ulcers. Ulcers can also be caused by some medications or too much stomach acid, but the most common cause is H. pylori infection. Infection with H. pylori also causes gastritis, and infected persons also have a 2- to 6-fold increased risk of developing mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer compared with uninfected counterparts.
H. pylori infection is common in the United States and is most often found in persons from lower income groups and older adults. About 20% of persons less than 40 years of age and about 50% of persons over 60 years of age are infected. Most infected people do not have symptoms and only a small percentage go on to develop disease.
How H. pylori is passed from one person to another is not known at this time. How people get infected with H. pylori is not known. The germs have been found in saliva, dental plaque and in the stools of children. Overcrowding and close contact with others in households may increase the spread of infection.
How is H. pylori infection diagnosed?
- Endoscopy
- Small samples of the lining of the stomach are taken through a tube that is passed through the mouth into the stomach. The samples are tested for H. pylori. The histology test, considered the gold standard of diagnostic tests for H. pylori, can be performed on the tissue sample. The culture test, performed in very few laboratories, is important when we wish to know if a person's H. pylori will be killed by certain antibiotics.
- Urea Breath Test (UBT)
- H. pylori infection can be detected in the exhaled breath using this special test. This test is positive only if the person has a current infection. Sensitivity and specificity of this test ranges from 94-98%.
- Serologic test (IgG antibody)
- A blood test that shows if a person has ever been infected. This test remains positive for years after infection and also for several months after H. pylori has been successfully treated. Sensitivity and specificity of this test ranges from 80-95% depending on the type of assay used.
How is infection with H. pylori treated?
At the present time, national guidelines recommend that H. pylori infection be treated only in persons who have ulcers, low-grade gastric MALT lymphoma, or in persons following removal of early gastric cancer. It is difficult to kill the H. pylori germs because the place where they live in the lining of the stomach helps protect them from antibiotics. To be sure the infection is cleared, at least two effective antibiotics plus either an acid-lowering agent (proton-pump inhibitor or histamine H2 receptor blocker) or bismuth subsalicylate (Pepto-Bismol) are taken. These medicines are all taken at the same time, either 2 to 4 times a day (depending on the regimen) for 1-2 weeks. Currently, there is no conclusive evidence of treatment benefit to H. pylori infected persons with non-ulcer dyspepsia (stomach upset without an ulcer).
H. pylori infection among Alaska Natives
Attention was focused on H. pylori among Alaska Natives when it was discovered that anemia caused by blood loss in the stool appeared to be associated with H. pylori. High rates of iron deficiency anemia had been observed among Alaska Natives dating back to the 1950s, despite adequate intake of nutrients offering optimum iron nutrition [Petersen, et al. 1996]. Therefore, gastrointestinal blood loss was examined as a cause of anemia. This led to the discovery that 99% of those with increased fecal blood loss had chronic active gastritis caused by H. pylori [Yip, et al. 1997].
To determine the prevalence of H. pylori in Alaska Natives, over 2000 serum samples collected in the 1980s in Alaska Native communities were assessed for H. pylori IgG antibodies. Overall, 75% were positive for H. pylori. Rates increased from 32% among 0 to 4 year olds up to 86% in those 20 years or older. There were difference in the rates by region of the state, which was most pronounced among the youngest children (0-4 years), where rates ranged from 5% in south-central (Anchorage vicinity) to 65% in interior Alaska. Ferritin determinations on the same samples supported an association between H. pylori infection and iron deficiency, especially in those under 20 years of age [Parkinson, et al. 1997].
CDC's Arctic Investigations Program (AIP) coordinates laboratory-based surveillance for H. pylori infections in Alaska Natives. Four regional hospitals and 2 tertiary care centers now participate in this system. Biopsies from patients undergoing diagnostic EGDs are cultured for H. pylori. Antimicrobial susceptibilities (clarithromycin, metronidazole, tetracyline, amoxicillin) are measured by agar dilution. To date 1,765 biopsies have been cultured; 916 (52%) have tested culture positive. Of isolates tested for antimicrobial susceptibilities by agar dilution 33% are resistant to clarithromycin (MICs ≥ 1.0 ug/ml), 48% are resistant to metronidazole (>8ug/ml), 2% are resistant to amoxicillin (MICs > 1.0 ug/ml) and 1 culture isolate was resistant to tetracycline (MIC = 2 ug/ml). A high proportion of H. pylori isolates recovered from Alaska Native patients are resistant to commonly used antibiotics in this population [Bruce, et al. 2002].
In 1996, the H. pylori Village Impact Survey was undertaken in persons ≥ 7 years of age. Residents of five rural villages (467 persons) and Anchorage (243 persons) participated. Serology and UBT were performed and a questionnaire for risk factors was done. Eighty-one percent of participants had a positive UBT, indicating current infection. For Anchorage residents, 60% of participants had a positive UBT. Antibodies to H. pylori were found in 73% of participants, with a lower proportion among Anchorage residents. Evidence of H. pylori infection among non-Natives was less common; 17% had positive UBT and 23% had antibodies to H. pylori. Gastrointestinal symptoms were not more common among persons with H. pylori infection compared with uninfected persons. Evidence of H. pylori infection by presence of antibodies or by a positive UBT were more common among rural participants, among those who reported sharing chewing gum, went hunting, or who had a child in the household less than 2 years of age. These data indicate that H. pylori infections are more common among Alaska Natives than non-Natives and more common among rural compared with urban Alaska Native residents.
In 1997, a study looking at the risk of H. pylori infection among 203 non-Native educators living in rural Alaska was performed. Blood was collected for serologic testing, and a questionnaire for risk factors was done. Twenty-four percent of non-Native participants had antibodies to H. pylori, indicating infection. The mean age of infected participants (48 years) was significantly higher (p < .001) than those who were not infected (42 years). Participants who had lived ≥ 6 months in rural Alaska were more likely to be infected than those who had not (RR 2.1, 95% CI 1.3-3.6) [Lynn, et al. 1998].
In 1997, the H. pylori Reinfection Study was started to see how often persons become reinfected with H. pylori after being treated for the infection. Three groups are included:
- H. pylori infected Alaska Natives living in Anchorage (N=100),
- H. pylori infected Alaska Natives living in rural Alaska (N=50), and
- H. pylori infected non-Natives living in Anchorage (N=50) in whom H. pylori had been treated .
Preliminary results from the group of Alaska Natives living in Anchorage shows an overall treatment failure rate of 23% with H. pylori showing high levels of resistance to clarithromycin (30%), metronidazole (66%), or to both of these antibiotics (23%). To see if prior use of antibiotics is linked to antibiotic resistance, records of 126 patients were reviewed. There was a significant relationship between the use of any macrolide antibiotic and H. pylori resistance to clarithromycin (OR 8.6, p < 0.001). Prior use of metronidazole was also found to predict subsequent Hp resistance to metronidazole (OR 14.4, p < 0.001). Among persons with clarithromycin-resistant isolates who were treated with clarithromycin, only 23% cleared the infection (RR treatment failure 6.2, p < 0.001). Among persons with metronidazole resistant isolates who were treated with metronidazole, 89% cleared the infection (RR treatment failure 1.4, p > .05). [McMahon, et al. 2002].
Projects in Progress
- Study to examine the reinfection rate after successful eradication of Helicobacter pylori infection in Alaska Natives living in Anchorage (to be finished Winter 2002).
- Study to examine the reinfection rate after successful eradication of Helicobacter pylori infection in non-Natives living in Anchorage (to be finished Summer 2005).
- Study to examine the reinfection rate after successful eradication of Helicobacter pylori infection in Alaska Natives living in rural Alaska (to be finished Spring 2006).
- Study looking at the risk of H. pylori infection among 203 non-Native educators living in rural Alaska (to be published in Winter 2003).
- Laboratory-based surveillance for H. pylori infections in Alaska Natives at 3 regional hospitals and a tertiary care center.
Future Plans
Because of the high rates of gastric cancer in Alaska Natives, and its current association with H. pylori infection (class 1 carcinogen), the Arctic Investigations Program and Native Health Corporations are in the process of developing studies to better understand gastric cancer in the Alaska Native population and determine if it is associated with H. pylori infection in this population. Another goal is to look for factors that might predict which of the many persons with Hp infection will go on to develop more severe problems such as ulcers or cancer.
References
Petersen KM, Parkinson AJ, Nobmann ED, Bulkow L, Yip R, Mokdad A. Iron deficiency anemia among Alaska Natives may be due to fecal loss rather than inadequate intake. Journal Nutrition 1996;126:2774- 2783.
Yip R, Limburg PJ, Ahlquist DA, Carpenter HA, et al. Pervasive occult gastrointestinal bleeding in an Alaska Native population with prevalent iron deficiency: role of Helicobacter pylori gastritis. Journal of the American Medical Association 1997;277:1135-1139.
Parkinson AJ, Gold BD, Bulkow L, Wainwright RB, et al. High prevalence of Helicobacter pylori in the Alaska native population and association with low serum ferritin levels in young adults. Clin Diagn Lab Immunol. 2000 Nov;7(6):885-8.
Bruce MG, McMahon BJ, et al. High Frequency of Metronidazole and Clarithromycin Resistance (by Agar Dilution) in Helicobacter pylori Isolates from Alaska Natives. Presented at the International Conference on Emerging Infectious Diseases, Atlanta, Georgia, 2002.
Lynn TV, Landen M, et al. Risk of Helicobacter pylori Infection Among Non-Native Educators in Alaska. Presented at the 47th Annual Epidemic Intelligence Service (EIS) Conference, Atlanta Georgia, 1998.
McMahon BJ, Hennessy T, et al. Antimicrobial Resistance in Patients with Helicobacter pylori Infection: Relationship to Prior Antimicrobial Use and Outcome after Treatment. Presented at the Digestive Disease Week Meeting, San Francisco, California, 2002.
