Helicobacter pylori infection in an Australian regional city: prevalence and risk factors

Hedley G Peach, Dora C Pearce and Stephen J Farish
Med J Aust 1997; 167 (6): 310-313.
Published online: 15 September 1997

Helicobacter pylori infection in an Australian regional city: prevalence and risk factors

Hedley G Peach, Dora C Pearce and Stephen J Farish

Readers may print a single copy for personal use. No further reproduction or distribution of the articles should proceed without the permission of the publisher. For permission, contact the Australasian Medical Publishing Company
Journalists are welcome to write news stories based on what they read here, but should acknowledge their source as "an article published on the Internet by The Medical Journal of Australia <>".

Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details

- - ©MJA1997



Objective: To investigate the prevalence of Helicobacter pylori infection and potential risk factors for infection in an adult Australian population.
Design: Cross-sectional study.
Setting: Ballarat, a major regional city in Victoria (population, 78 000; 92% born in Australia), November 1994 to July 1995.
Participants: 217 adults randomly selected from the electoral roll.
Main outcome measures: H. pylori IgG antibody status by enzyme immunoassay; amount of dental plaque; sociodemographic and other potential risk factors; odds ratios for risk factors determined by logistic regression analysis.
Results: Age-standardised prevalence of H. pylori infection was 30.6%. After adjustment for age, sex and socioeconomic index, positive H. pylori status was significantly associated with increasing number of tooth surfaces with a high plaque score (odds ratio [OR], 1.7; 95% confidence interval [CI], 1.1-2.7), increasing number of years in a job with public contact (OR, 1.7; 95% CI, 1.3-2.3), blood group B antigen (OR, 3.1; 95% CI, 1.1-9.1), and having lived in a household with more than six members during childhood (OR, 2.5; 95% CI, 1.1-5.5). Negative H. pylori status was significantly associated with increasing education, having ever lived on a farm, and having teeth scaled less than once a year.
Conclusions: H. pylori infection is common. Dental plaque may be a reservoir for H. pylori, which is probably transmitted by person-to-person contact, and blood group B antigen may predispose to infection. Community education about effective oral hygiene and adoption of good hygiene practices by those with regular public contact may be important to prevent acquisition and transmission of H. pylori .

MJA 1997; 167: 310-313  


The presence of Helicobacter pylori in humans is now recognised as a chronic infection which in most cases persists indefinitely and is involved in the development of several serious diseases, including peptic ulcer, gastric cancer, and possibly cardiovascular disease.1 It is uncertain from where and how H. pylori is acquired, but most investigators seem to favour person-to-person transmission.1

In developed countries, including Australia, the prevalence of H. pylori infection increases with age at the rate of about 1% per annum, to reach 40% or more at age 60 years.2 In contrast, in developing countries prevalence is 40% or more at age 10 years.2 Seroconversion in childhood also seems more likely in particular populations in developed countries; it was found to occur among people of lower socioeconomic background in Northern Ireland3 and England 4 and in a rural town in Western Australia.5

Suspected childhood risk factors for H. pylori infection in developed countries include having a single parent, lower parental social class, greater housing density or proportion of rented housing in school catchment area, overcrowding, bed-sharing, and absence of a fixed hot water supply.6 In adults, previously investigated risk factors include race-ethnicity, socioeconomic status, education, dental prosthesis and irregular dental treatment, public contact, working with animals, smoking status, alcohol consumption, homosexuality, sexually transmitted diseases, and having an infected child or partner.1,2,7-10

To assess the importance of these and other risk factors for H. pylori infection in Australia, we investigated the H. pylori status and risk factors of a sample of adults in Ballarat, a regional city in Victoria.  



Setting and population

Ballarat is a major regional city in Victoria (population, 78 000; with 92% of residents born in Australia according to the 1991 census).11 The study population was drawn from the population sample used in a 1992 survey of cardiovascular disease risk factors. This survey used the procedures of the National Heart Foundation for its surveys of Australian capital cities.12 A sample of 501 adults randomly selected from the electoral roll was invited to attend a screening clinic; 338 (68%) attended and gave informed consent. Between November 1994 and July 1995, 217 of the 262 participants who were still contactable (83%) participated in our study of risk factors for H. pylori infection, after again giving informed consent.

The study was approved by the Ballarat Base Hospital Ethics Committee.  


Plasma samples were tested for H. pylori IgG antibodies with the Pyloriset EIA-G Kit (Pyloriset, Orion Corporation, Orion Diagnostica, Espoo, Finland). This kit uses one of the two original Marshall and Warren strains of H. pylori13 for antigen preparation. A cut-off antibody titre of 500 was used to classify subjects as positive or negative, as recommended by the manufacturer (sensitivity, 92.5%; specificity, 84.3%).14

Dental plaque was also assessed for the 156 dentate subjects. The mouth was rinsed with water before and after fluorescein application, and plaque score was recorded on a modified Dental Health Services of Victoria treatment chart.15 Research personnel were blind to the H. pylori status of each subject. A high plaque score (≥2) was defined as a clear line of plaque along the gingival margin or a larger coverage of the tooth surface with plaque.15 After examination, the subject was given toothpaste and a toothbrush to remove residual fluorescein.

A questionnaire on socio demographic and potential risk factors was administered by one of three trained research personnel. Job title and duties were used to classify jobs held over a subject's lifetime, without knowledge of his or her H. pylori status, as mainly involving contact with the general public or otherwise. Subjects identified the 1991 Census Collector's District in which they lived from a map of Ballarat; this was classified according to socioeconomic index.16 Blood group was determined if unknown.  

Statistical analyses

The sample-based estimate of the prevalence of H. pylori infection was standardised to the age distribution of Ballarat's population.12 This accounted for any imbalances between respondents and the general population caused by under-representation of younger or more mobile residents in the electoral rolls or differential response rate by age.

Odds ratios (ORs) and 95% confidence intervals (CIs) for suspected risk factors for H. pylori infection were produced by logistic regression analyses. Collinearity was first assessed through a series of multiple linear regression analyses, using each predictor variable in turn as the dependent variable and all others as independent variables. Dependent variables with an R2 greater than 0.95 were excluded. All remaining variables were entered into the logistic regression model, and then excluded manually in a stepwise manner if they were not significantly associated with H. pylori status and had an OR in the range 0.95-1.05. Edentate subjects were assigned the mean plaque score of subjects with teeth, as recommended by Thompson.17 This avoided having to analyse edentate and dentate subjects separately, with the inevitable loss in precision when estimating risk associated with other variables.

The effect of response to the study on ORs was assessed by the method of Criqui.18 The associations found using H. pylori status as a dichotomous variable, based on a cut-off antibody titre of 500, were confirmed using H. pylori antibody titres (logarithmically transformed) as a continuous variable in a multiple linear regression model.  


The prevalence of H. pylori infection in Ballarat was estimated as 30.6% after standardising to the age distribution of the city's population. The proportion of subjects who were H. pylori-negative in the H. pylori study (66.8%) was similar to that in the original cardiovascular study (69.6%). H. pylori-positive subjects in the H. pylori study had similar age, sex distribution, education and median antibody titres to those in the original cardiovascular study. H. pylori-negative subjects in the two populations were also similar for these variables. Therefore, the ORs for suspected risk factors were unlikely to be affected by the response rate.18

The association between positive H. pylori antibody status and possible risk factors in the final logistic regression model is shown in the Box. In the final model, which adjusted for age, sex and socioeconomic index of residence, the following were significantly associated with positive H. pylori status: increasing number of buccal and lingual tooth surfaces with a plaque score ≥2 (adjusting for the absence of natural teeth and number of teeth), increasing years in a job with public contact, presence of blood group B antigen, and having lived in a household of six or more people during the first 16 years of life. Washing of hands only sometimes or rarely after using the toilet and visiting a dentist less than once a year had a large but not statistically significant association with positive H. pylori status.

Negative H. pylori status was significantly associated with increasing education, having ever lived on a farm, and having teeth scaled less than once a year. Univariate analysis showed that dentate subjects who visited a dentist at least annually had a significantly lower prevalence of H. pylori infection if they had their teeth scaled less than once a year (three out of 25) compared with more often (20 out of 56) (chi-squared = 4.78; P = 0.03; 1 degree of freedom). In addition, among those who had their teeth scaled less than once a year, visiting a dentist at least annually was protective (three infected out of 25) compared with visiting a dentist less often (27 infected out of 78) (chi-squared = 4.69; P = 0.03; 1 degree of freedom).

The following variables were initially included in the logistic regression model, but excluded from the final model because of lack of a significant association with H. pylori status: dentures, history of gum infections, frequency of sharing toothbrush or cup, travel to high prevalence countries, smoking status, lifetime alcohol consumption, vegetarian diet, eating unwashed home-grown vegetables, washing hands before eating, years with occupational or recreational contact with animals, having visited farms, marital status, height, weight, and variation between interviewer/oral health observers.

The results of multiple regression analysis confirmed those of the logistic regression analysis for all variables except increasing education, which was negatively, but not significantly, associated with H. pylori titre.  


To our knowledge, this is the first time in Australia that the prevalence of H. pylori infection has been determined in a random sample of the adult population. Our crude age-specific prevalences were among the lowest of such figures published for European countries and white Americans.19 Nevertheless, the considerable proportions of gastroduodenal ulcers, peptic ulcer bleeds and gastric cancers attributable to H. pylori make an infection rate of 30.6% an important public health issue.20

The cost-benefit ratio for eradicating H. pylori infection with antibiotics in asymptomatic adults will not be known for some time.20 It is therefore important to identify factors associated with the acquisition and transmission of H. pylori. This is the first time that

  • Public contact through employment;
  • Moderate or heavy accumulation of dental plaque;
  • Frequent scaling of teeth;
  • Only rarely or sometimes washing hands after using the toilet; and
  • Having blood group B antigen
have been found to be positively associated with H. pylori infection. Further, it is the first time that having lived on a farm, as a third of our sample had done, has been identified to be protective against H. pylori infection. We confirmed that living in an overcrowded household during childhood and visiting a dentist less than once a year are positively associated with H. pylori infection in Australia, although the latter association was not significant.

The association between H. pylori infection and public contact through employment was not surprising, as overcrowding in childhood has led to speculation that close personal contact may promote transmission of the organism.7 The protective effect of having lived on a farm in our study may be a consequence of low population density in rural areas. Rural China has a significantly lower prevalence of H. pylori infection, despite poorer standards of hygiene, compared with urban China.2,21

There is other evidence to corroborate our finding that moderate or heavy accumulation of dental plaque is significantly associated with H. pylori infection. H. pylori has been cultured from dental plaque, and identical H. pylori ribotypes were found in the mouth and gastric antrum of ulcer patients.22,23 Moreover, H. pylori has been detected by reverse transcription polymerase chain reaction in only moderate to heavy accumulations of plaque.22

Our finding that visiting the dentist less than once a year increased the risk of H. pylori infection is consistent with the protective effect of regular dental treatment found by Gasbarrini et al.10 If H. pylori inhabits plaque, scaling may lead to ingestion of the organism and inoculation of the stomach. A decreased risk of H. pylori infection from having teeth scaled less than once a year is therefore plausible.

In agreement with other studies, we found no significant association between H. pylori infection and alcohol consumption. We also found no significant association with smoking, although 52% of our sample were current or ex-smokers. Others have found significantly more smokers among patients with no abnormalities on endoscopy who had H. pylori infection,8 and the difference could be caused by confounding by oral hygiene. Smokers have poor oral hygiene and visit their dentist and brush their teeth less often than non-smokers.24 Further, in our study, dentate subjects who had ever smoked had a significantly larger mean number of tooth surfaces with a high plaque score than non-smokers, after adjusting for number of teeth (P = 0.02).

Although the risk of H. pylori infection was increased for people who washed their hands only sometimes or never after using the toilet, because of the small number of these subjects the odds ratio had a wide confidence interval and the association was not significant. Faecal-oral spread of the organism is known to occur, but our data imply that it is relatively uncommon between adults, as others have suggested.1 Nevertheless, this result underlines the importance of good hygiene practices and the provision of handwashing facilities both indoors and out-of-doors. Eating from communal bowls has been postulated as a mechanism of H. pylori transmission in China.21 Our study found that sharing of cups and cooking utensils was not common in Ballarat and not a risk factor.

Genetic effects have been found to influence the acquisition of H. pylori.1 However, the importance of the association we found between the presence of blood group B antigen and H. pylori infection must await further research into the mechanisms of genetic susceptibility to H. pylori infection.

Our results imply that good hygiene practices are essential for those in frequent contact with the public to prevent H. pylori transmission. As moderate to heavy dental plaque emerged as a clear risk factor, reducing plaque may have an important role in preventing acquisition of H. pylori. This is another reason for educating the public, adults and children about effective tooth-brushing and other oral hygiene techniques. Regular dental treatment may need to be encouraged, while avoiding the ingestion of plaque debris which could occur during tooth scaling. In view of these potentially important public health implications, confirmatory evidence of our results should be sought.  


We thank Mrs Wendy Ross and Mrs Cheryl Potter for assistance with the interviews and oral examinations, Dr John Williams for advice on the examinations, Mr Christopher Pearce (Dorevitch Pathology, Ballarat Base Hospital) for technical assistance, State Data Centre, Ballarat, for mapping the Census Collector's Districts, Colgate for toothbrushes and toothpaste, and Chiron Diagnostics for serological advice. The study was funded by the Shepherd Foundation, Melbourne, VIC.  


  1. Hunt RH. Helicobacter pylori : from theory to practice. Am J Med 1996; 100: 1S-64S.
  2. Taylor DN, Blaser MJ. The epidemiology of Helicobacter pylori infection. Epidemiol Rev 1991; 13: 42-59.
  3. McCallion WA, Ardill JES, Bamford KB, et al. Age dependent hypergastrinaemia in children with Helicobacter pylori gastritis -- evidence of early acquisition of infection. Gut 1995; 37: 35-38.
  4. Banatvala N, Mayo K, Megraud F, et al. The cohort effect and Helicobacter pylori . J Infect Dis 1993; 168: 219-221.
  5. Cullen DJE, Collins BJ, Christiansen KJ, et al. When is Helicobacter pylori infection acquired? Gut 1993; 34: 1681-1682.
  6. Patel P, Mendall MA, Khulusi S, et al. Helicobacter pylori infection in childhood: risk factors and effect on growth. BMJ 1994; 309: 1119-1123.
  7. Whitaker CJ, Dubiel AJ, Galpin OP. Social and geographical risk factors in Helicobacter pylori infection. Epidemiol Infect 1993; 111: 63-70.
  8. Bateson MC. Cigarette smoking and Helicobacter pylori infection. Postgrad Med J 1993; 69: 41-44.
  9. Aceti A, Attanasio R, Pennica A, et al. Campylobacter pylori infection in homosexuals. Lancet 1987; 2: 154-155.
  10. Gasbarrini G, Pretolani S, Bonvicini F, et al. A population based study of Helicobacter pylori infection in a European country: the San Marino Study. Relations with gastrointestinal diseases. Gut 1995; 36: 838-844.
  11. HealthWIZ [computer file]: national social health database. Canberra: Department of Health and Family Services.
  12. National Heart Foundation. Risk factor prevalence survey. Canberra: National Heart Foundation, 1989: 133-136.
  13. Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984; 1: 1311-1314.
  14. Pearce DC, Peach HG, Farish SJ. Helicobacter pylori antibody titres in serum, plasma and successively thawed specimens: implications for epidemiological and clinical studies. J Clin Pathol 1996; 49: 1017-1019.
  15. Muhlemann HR. Introduction to oral preventive medicine. Carol Stream, Ill: Quintessance Publishing Company, 1976: 124.
  16. Ross R, Farish S, Plunkett M. Indicators of socio-economic disadvantage for Australian schools. Geelong: Deakin Institute for Studies in Education, 1988.
  17. Thompson WD. Statistical analysis of case-control studies. Epidemiol Rev 1994; 16: 33-50.
  18. Criqui MH. Response bias and risk ratios in epidemiologic studies. Am J Epidemiol 1979; 109: 394-399.
  19. Goodman KJ, Correa P. The transmission of Helicobacter pylori . A critical review of the evidence. Int J Epidemiol 1995; 24: 875-887.
  20. Axon A, Forman D. Helicobacter gastroduodenitis: a serious infectious disease. BMJ 1997; 314: 1430-1431.
  21. Mitchell HM, Li YY, Hu PJ, et al. Epidemiology of Helicobacter pylori in Southern China: identification of early childhood as the critical period for acquisition. J Infect Dis 1992; 166: 149-153.
  22. Nguyen A-MH, Engstrand L, Genta RM, et al. Detection of Helicobacter pylori in dental plaque by reverse transcription-polymerase chain reaction. J Clin Microbiol 1993; 31: 783-787.
  23. Khandaker K, Palmer KR, Eastwood MA. DNA fingerprints of Helicobacter pylori from mouth and antrum of patients with chronic ulcer dyspepsia. Lancet 1993; 342: 751.
  24. Hardo PG, Tugnait A, Hassan F, et al. Helicobacter pylori infection and dental care. Gut 1995; 37: 44-46.

(Received 18 Feb, accepted 21 Jul, 1997)

Authors' details

Department of Public Health and Community Medicine, University of Melbourne, Ballarat Health Services Base Hospital, Ballarat, VIC.
Hedley G Peach, PhD, FFPHM, Professor;
Dora C Pearce, BAppSc(Biol), Research Fellow.

Epidemiology and Biostatistics Unit, Department of Public Health and Community Medicine, University of Melbourne, VIC.
Stephen J Farish, MEd, Senior Lecturer.

Reprints: Professor H G Peach, Department of Public Health and Community Medicine, University of Melbourne, Ballarat Health Services Base Hospital, PO Box 577, Ballarat, VIC 3353.
E-mail: a.temperley AT

©MJA 1997

<URL:> © 1997 Medical Journal of Australia.

Received 2 July 2022, accepted 2 July 2022

  • Hedley G Peach
  • Dora C Pearce
  • Stephen J Farish



remove_circle_outline Delete Author
add_circle_outline Add Author

Do you have any competing interests to declare? *

I/we agree to assign copyright to the Medical Journal of Australia and agree to the Conditions of publication *
I/we agree to the Terms of use of the Medical Journal of Australia *
Email me when people comment on this article

Online responses are no longer available. Please refer to our instructions for authors page for more information.