Helicobacter pylori (H. pylori) infection is etiologically associated with gastric cancer and peptic ulcer diseases which are both important public health burdens which could be largely eliminated by H. pylori eradication. However, some investigators urge caution based on the hypothesis that eradication of H. pylori may result in an increase in the incidence of gastroesophageal reflux disease, esophageal adenocarcinoma, and childhood asthma. The ethnic Malays of northeastern Peninsular Malaysia have long had a low prevalence of H. pylori infection and, as expected, the incidence of gastric cancer and its precursor lesions is exceptionally low. The availability of a population with a low H. pylori prevalence and generally poor sanitation allows separation of H. pylori from the hygiene hypothesis and direct testing of whether absence of H. pylori is associated with untoward consequence. Contrary to predictions, in Malays, erosive esophagitis, Barrett's esophagus, distal esophageal cancers, and childhood asthma are all of low incidence. This suggests that H. pylori is not protective rather the presence of H. pylori infection is likely a surrogate for poor hygiene and not an important source of antigens involved in the hygiene hypothesis. Helicobacter pylori in Malays is related to transmission from H. pylori-infected non-Malay immigrants. The factors responsible for low H. pylori acquisition, transmission, and burden of H. pylori infection in Malays remain unclear and likely involves a combination of environmental, host (gene polymorphisms), and strain virulence factors. Based on evidence from this population, absence of H. pylori infection is more likely to be boon than a bane.
This review summarizes studies on the epidemiology and public health implications of Helicobacter pylori published in peer-reviewed journals from April 2010 through March 2011. Prevalence rates vary widely between different geographical regions and ethnic groups. An interesting study from the USA identified the degree of African ancestry as an independent predictor of H. pylori infection. Two studies have demonstrated early childhood as the period of transmission of infection and identified an infected sibling as an important risk factor. An oral-oral route of spread has been substantiated with several studies showing the presence of H. pylori in the oral cavity. Studies have shown the presence of H. pylori in drinking water and the role of poor living conditions and sanitation in H. pylori infection, supporting an oral-fecal route of spread. Screening for H. pylori as a gastric cancer pre-screening strategy has been described in Japan, and the importance of H. pylori eradication as a gastric cancer-prevention strategy has now been further emphasized in Japanese guidelines. Two studies have shown a decrease in the burden of dyspepsia and peptic ulcer disease with H. pylori eradication.
Observations of racial differences in the prevalence of Helicobacter pylori in Malaysia have been intriguing. The Indians and Chinese consistently have a higher prevalence compared to the Malays. The racial cohort theory has been proposed to explain these differences where transmission and perpetuation of infection takes place within a racial group rather than between races, races being separate owing to the low rate of interracial marriages. Studies have demonstrated distinctive bacterial strains between races. Phylogenetic studies have shown that H. pylori isolates amongst Chinese and Indians are distinctive while Malays have Indian and other strains suggesting a more recent acquisition of the bacterium from Indians. H. pylori is recognized as the major causative factor in peptic ulcer disease and gastric cancer. Despite the high prevalence of H. pylori, Indians have a relatively low prevalence of peptic ulcer disease and a low incidence of gastric cancer. This paradox with regards to gastric cancer has been termed the "Indian enigma". Bacterial strain differences between races may be putative but this observation may also indicate gastroprotective environmental factors or a lower genetic susceptibility to develop cancer in the Indians.
The Helicobacter pylori seroprevalence in a representative population of 328 Melbourne Chinese immigrants (162 men and 166 women) aged 25 years and older were studied. The population consisted of Chinese people born in China/Hong Kong (n = 110, 33.5%), Vietnam (n = 79, 24.1%), Malaysia/Singapore (n = 102, 31.1%), and elsewhere (n = 37, 11.3%). The overall seroprevalence of H. pylori was 59.5%; 60.5% in men and 58.4% in women. Gender specific analysis showed associations between higher seroprevalence and several socio-demographic factors; in men, age (P < 0.0001), lower education level (P < 0.002), cigarette smoking (P < 0.042), the use of antibiotics (P < 0.015) and chopsticks (P < 0.047), and in women, lower socioeconomical status [education level (P < 0.030), gross household income (P < 0.0001) and occupational status (P < 0.0001)] and use of chopsticks (P < 0.002). Seroprevalence differed between immigrants of various birthplaces (P < 0.001); those born in Malaysia/Singapore (43.1%) were lower than those born in China/Hong Kong (68.2%), Vietnam (68.4%), and elsewhere (59.5%). Immigrants of various birthplaces also differed in their pattern of socio-demographics. Multivariate analyses showed that risk factors for H. pylori infection within the Melbourne Chinese immigrants were, in men, age (B = 1.081) and birthplace (B = 1.769) and, in women, household income (B = 0.541) and use of chopsticks (B = 1.654). This study suggests person-to-person transmission of H. pylori via the oral-oral route with ethno-specific food practices an important risk factor.