The epidemiology of Helicobacter pylori infection in African refugee children resettled in Australia

Helicobacter pylori infection is usually acquired in childhood.1,2 Acute infection is often silent, with symptoms and disease manifesting later in life, as does an increased risk of H. pylori-related malignancy.

The prevalence of H. pylori infection is markedly increased in developing countries,3,4 and risk factors include increasing age, large family size and socioeconomic deprivation.5-7 Refugees resettled in developed countries generally come from regions of high H. pylori prevalence, whereas those who have grown up in industrialised nations have a lower prevalence of H. pylori infection.3,8 Increased prevalence is also found in migrants and indigenous populations; adverse socioeconomic conditions in these groups account for some of the excess risk.7,9,10

Western Australia resettles about 1300 humanitarian refugees annually, representing over 10% of Australia’s refugee intake.11 Currently, many families are African, and about half the refugees are children.12

In this study, we investigated the prevalence and epidemiological associations of H. pylori infection in a high-risk paediatric population. The main outcome measure was H. pylori infection diagnosed by monoclonal faecal antigen enzyme immunoassay testing (MFAT). The effects of age, sex, transit through refugee camps, comorbidities and treatment interventions were investigated.

We conducted a cross-sectional study at the Migrant Health Unit (MHU) in Perth, WA, the sole screening unit for humanitarian refugees resettled in WA. About 80% of targeted refugees in WA receive an initial health assessment at the MHU.12 African children (aged less than 16 years) who presented for initial health assessment between 1 February and 30 November 2006 were included. Blood samples were obtained for routine screening investigations at the first clinic visit as part of standard clinical care and stool samples were collected 1 week later. Children were excluded from our study if they had received antibiotics or proton-pump inhibitors in the preceding month, if they had an immunodeficiency or active tuberculosis. Ethical approval was obtained from the Women and Children’s Ethics Committee, Princess Margaret Hospital for Children. Informed consent was obtained in the presence of trained interpreters, as appropriate.

Data on age, sex, ethnicity, country of last transit, transit period, country of birth, type of dwelling in country of transit, and recent drug administration were obtained at the first visit by means of a structured questionnaire. Breastfeeding history was recorded for children under 2 years of age. Details of premigration antihelminthic and antimalarial treatment were obtained from accompanying International Office of Migration documentation.

Two-hundred and one African refugee children presenting for screening at the MHU were recruited consecutively, with a 100% response rate. Eight children were excluded (five received antibiotics before screening and three were of non-African ethnicity). Of the 193 eligible children, 100 (52%) were male. The mean age was 7.9 years (SD, 4.4 years). Box 1 shows the main demographic features of the cohort.

Eighteen children (9%) were breastfeeding at the time of enrolment (mean age of breastfeeding children, 11.3 months; SD, 5.2 months). There were 116 children (60%) who had lived in refugee camps, with the remainder living in urban dwellings (apartments or houses). Almost all children who transited through Tanzania or Kenya (96 of 97; 99%) had lived in refugee camps, while all 28 who transited through Egypt had lived in apartments. The overall median transit time before resettlement in WA was 5.5 years (interquartile range [IQR], 3.0–8.4). Protracted refugee stays (more than 5 years in transit) were common (98 of 193; 51%); the median transit time for these 98 children was 8.0 years (IQR, 6.5–10.0).

Our study shows a high prevalence of H. pylori infection in African refugee children, confirming that children from developing countries are at greater risk of infection.14 Our results support the observation that early childhood is the main period of acquisition of H. pylori infection in high-prevalence populations.1,2,4 H. pylori infection was present in 82% of this cohort, and the odds of infection increased significantly with age. In comparison, the prevalence of H. pylori infection in Australian children is low,8 although the prevalence in Australian Aboriginal children is significantly higher, especially in those from remote areas,9 reflecting differences in socioeconomic status.

The protective effect of antimalarial treatment on H. pylori infection is a potentially important and unexpected finding. In children who received empirical premigration antimalarial treatment, this was given about 6 weeks before study enrolment. This correlated with the median time between arrival in Australia and the MHU health screening (Dr A Thambiran, Medical Director, MHU, Perth, WA, personal communication). Empirical premigration antimalarial treatment was ceased in mid 2006 because of concerns about efficacy and coverage.15

The antimalarial therapy may have eradicated existing H. pylori infection. The period between administration of antimalarial drugs and collection of faecal samples was short, and so reacquisition of H. pylori infection during this intervening period is unlikely. The elimination half-lives of pyrimethamine and sulfadoxine are relatively long (3–4 and 6–9 days, respectively) and that of dihydroartemisinin, the active metabolite of artesunate, is less than 1 hour.16 Antimalarial therapy is unlikely to have affected MFAT performance. The effect of antimalarial therapy remained significant in our final regression analyses, and was independent of albendazole therapy. To our knowledge, this in-vivo association has not been previously reported, although artemisinins are known to have antibacterial properties.17 It has been postulated that artemisinin derivatives may interact with iron-dependent bacteria (such as H. pylori) and potentially provide a mechanism for targeted bacterial death.18 The possible therapeutic role of artemisinins, which are cheap and well tolerated, in H. pylori eradication warrants further investigation.

A limitation of our study is the lack of a traditional “gold standard” for the diagnosis of H. pylori infection. Methods based on endoscopy and biopsy, or urea breath testing, are neither practical nor ethical for population-based screening of children, particularly in non-English speaking and often traumatised families. Recent international guidelines now recommend MFAT as an alternative in both adult and paediatric populations.19,20

In this study, we investigated potential epidemiological risk factors that may predispose refugee children to H. pylori infection. Surprisingly, transit through refugee camps did not place children at increased risk of infection, despite harsh environmental and nutritional conditions. The ubiquitous deprivation and overcrowding that characterise urban refugee conditions (eg, Egyptian apartments) may instead contribute to the non-significant association between dwelling type and H. pylori infection.

Intrafamilial spread of H. pylori, particularly mother-to-child transmission2,21,22 or from infected older siblings,2,23 is a potentially important mechanism for acquisition. In our cohort, older siblings had odds of H. pylori infection three times higher than those of their youngest siblings, supporting this premise. Parental H. pylori infection was not assessed in this study, but a high prevalence would be expected, in keeping with analogous published results.22-24 Reliable data on family size could not be obtained, as many siblings and/or parents were displaced in transit.

The relationship between breastfeeding and infection was not found to be statistically significant; however, the number of children being breastfed at the time of enrolment was small. Our study did not address the phenomenon of transient H. pylori infections.25 Over 60% of children aged under 2 years had H. pylori infection, which is similar to other reports of African infants.4 Given the high levels of overall infection in this cohort, reinfection is likely even if there were cases of transient infection in infancy.

Clinicians should be aware of the high prevalence of H. pylori infection in resettled refugee children, including the potential development of chronic complications. Longitudinal studies of this population are warranted.