BMJ  2004;329:204-205 (24 July), doi:10.1136/bmj.329.7459.204

Paper

Acquisition of Helicobacter pylori infection after outbreaks of gastroenteritis: prospective cohort survey in institutionalised young people

¹ Inserm E9919-Université de Lille II JE 2225, Institut de Biologie de Lille, France, ² Centre Antoine de Saint-Exupéry, Vendin-le-Vieil, France, ³ Clinique de Pédiatrie, Hôpital Jeanne de Flandre, Lille, France

Introduction

The exact mode of spread of Helicobacter pylori is still unknown. Transmission during transit disorders of the gastrointestinal tract has been suggested, although there is no evidence to date of transmission during outbreaks of gastroenteritis.^1-3 We determined whether gastroenteritis in young people infected with H pylori can lead to acquisition of the bacterium by peers.

Participants, methods, and results

Our study took place in a French institution for neurologically handicapped children and adolescents. The young people had been institutionalised for several years and resided across five housing sections (A to E). We included all 112 residents in May 2001. H pylori infection present at the outset of the study was detected by using the non-invasive HpSA stool antigen test (Meridian; 91% sensitivity and 93% specificity).⁴ Stool samples were stored and transported at 4°C within 48 hours and then frozen. The residents were monitored for one year. Events and clinical data were recorded daily by nurses. Gastroenteritis was defined as a sudden outbreak of liquid stools in more than two residents concurrently. For each patient with H pylori infection, we defined one day of potentially infective diarrhoea or vomiting as that when at least one liquid stool or vomitus was emitted. Stool samples were collected every week for each resident who was free of infection at the study outset, and at the end of the study we compared the last sample with the first sample. When conversion was observed, we identified the oldest positive stool sample collected from that patient during follow up.

The prevalence of H pylori infection was high; 47 of the 112 residents (42%) were positive for H pylori at the study outset. Seven of the 65 residents who were initially negative for H pylori showed conversion during follow up (figure). Five of the seven young people lived in section E, and our records showed that the two other residents had frequent contacts with the infected patients from section E during physiotherapy and entertainment sessions. Vomitus was rare in all sections. The frequency of diarrhoeal stools from the infected patients varied across sections; residents of sections A and B had 475 and 338 person days of potentially infective diarrhoea over the year, respectively. Acute diarrhoea was rare in these sections, and no outbreaks of gastroenteritis were recorded. A lower frequency of diarrhoeal stools was observed in sections C, D, and E; 34, 104, and 164 person days of potentially infective diarrhoea over the year, respectively. The frequency was always low in sections C and D, where no outbreaks of gastroenteritis were observed, whereas in section E, four peaks of potentially infective diarrhoea occurred during outbreaks of gastroenteritis (figure). In all cases, conversion occurred three to 11 weeks after a peak of potentially infective diarrhoea.

View larger version (43K): [in this window] [in a new window]   Relation between new cases of Helicobacter pylori infection and exposure to infective diarrhoea and vomitus in housing section E

 

What is already known on this topic Diarrhoeal stools and vomitus from infected young people can contain viable Helicobacter pylori What this study adds New cases of H pylori infection can occur in cohabiting young people after acute diarrhoea or vomitus in infected peers

Comment

An association was found between gastroenteritis and subsequent acquisition of H pylori infection in cohabiting young people. Despite the limitations of the non-invasive test used to determine the presence of H pylori, time and space clustering shows that conversions were not observed by chance. This chronological link suggests that, under usual conditions of life, there might be a causal link between outbreaks of gastroenteritis and transmission of H pylori.⁵

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We thank Marie-Jeanne Capron, Christine Guillemant, and the nursing staff of Centre Antoine de Saint-Exupéry, Vendin-le-Vieil, for help during the study, Danielle Samaille, Institut Pasteur de Lille, for transport of samples, and M Simonet for critical reading of the manuscript.

Contributors: RL performed the literature search, data collection, and biological and epidemiological analysis and interpretation, and drafted the report. PV was the academic supervisor of RL. PV initiated the project, was responsible for funding and design, organised the collection of samples, helped interpret the results, and wrote and revised the report; he will act as guarantor for the paper. PhP and PP were responsible for the care of the patients and management of the institution. FG was involved in the design of the study and advised on medical issues and discrepancies during the study. All authors critically analysed the data and wrote the paper.

Funding: RL received a scholarship from Laboratoire Gallia.

Competing interests: None declared.

Ethical approval: This study was approved by the local ethics committee, Vendin-le-Vieil.

References

1. Thomas JE, Gibson GR, Darboe MK, Dale A, Weaver LT. Isolation of Helicobacter pylori from human faeces. Lancet 1992;340: 1194-5.[CrossRef][ISI][Medline]
2. Parsonnet J, Shmuely H, Haggerty T. Fecal and oral shedding of Helicobacter pylori from healthy infected adults. JAMA 1999;282: 2240-5.[Abstract/Free Full Text]
3. Leung WK, Siu KL, Kwok CK, Chan SY, Sung R, Sung JJ. Isolation of Helicobacter pylori from vomitus in children and its implication in gastro-oral transmission. Am J Gastroenterol 1999;94: 2881-4.[CrossRef][Medline]
4. Gisbert JP, Pajares JM. Diagnosis of Helicobacter pylori infection by stool antigen determination: a systematic review. Am J Gastroenterol 2001;96: 2829-38.[CrossRef][ISI][Medline]
5. Hill AB. The environment and disease: association and causation. Proc R Soc Med 1965;58: 295-300.[ISI][Medline]

(Accepted 16 April 2004)

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