Role of partner's infection in reinfection after Helicobacter pylori eradication

Gisbert, Javier P.; Arata, I. García; Boixeda, D; Barba, Mercedes Sánchez; Cantón, Rafael; Plaza, A García; Jm, Pajares García

doi:10.1097/00042737-200208000-00009

Cited by 40 publications

(32 citation statements)

References 35 publications

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“…As siblings rarely cohabit as adults and strains are rarely passed between spouses (43,44), this suggests that strains were acquired during childhood, as has been shown for other populations (41,42). This therefore implies that H. pylori strains possessing type s1/m1 vacA were acquired before the development of gastric atrophy and hypochlorhydria and suggests that the association between toxigenic strains and these conditions is likely to be causal.…”

Section: Discussionmentioning

confidence: 77%

Toxigenic Helicobacter pylori Infection Precedes Gastric Hypochlorhydria in Cancer Relatives, and H. pylori Virulence Evolves in These Families

Argent

Thomas

Avilés-Jiménez

et al. 2008

Clinical Cancer Research

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Purpose: Helicobacter pylori infection by virulent strains is associated with gastric adenocarcinoma. We aimed to determine whether infection with virulent H. pylori preceeded precancerous gastric hypochlorhydria and atrophy in gastric cancer relatives and quantify the extent of virulence factor evolution. Experimental Design: H. pylori strains from 51Scottish gastric cancer relatives were characterized by genetic fingerprinting and typing the vacuolating cytotoxin gene (vacA), the cytotoxinassociated gene (cagA), and housekeeping genes. We phenotyped strains by coculture with gastric epithelial cells and assessing vacuolation (microscopy), CagA tyrosine phosphorylation (immunoblot), and interleukin-8 secretion (ELISA). Results: Toxigenic (vacA type s1/m1) H. pylori was associated with precancerous gastric hypochlorhydria (P < 0.01). Adult family members with this type of H. pylori had the same strain as currently noncohabiting adult family members in 68 % cases, implying acquisition during childhood from each other or a common source.We analyzed different isolates of the same strain within families and showed that H. pylori commonly microevolved to change virulence: this occurred in 22% individuals and a striking 44% cases where the strain was shared within families. Microevolution in vacA occurred by extragenomic recombination and in cagA by this or duplication/deletion. Microevolution led to phenotypic changes in virulence. Passage of microevolved strains could be tracked within families. Conclusions:Toxigenic H. pylori infection precedes and so likely causes gastric hypochlorhydria, suggesting that virulent H. pylori increases cancer risk by causing this condition. Microevolution of virulence genes is common within families of gastric cancer patients and changes H. pylori virulence.

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Section: Discussionmentioning

confidence: 77%

Toxigenic Helicobacter pylori Infection Precedes Gastric Hypochlorhydria in Cancer Relatives, and H. pylori Virulence Evolves in These Families

Argent

Thomas

Avilés-Jiménez

et al. 2008

Clinical Cancer Research

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“…The number of children in the household has been proposed as a risk factor for infection in parents (21), and in childless couples transmission between spouses was not supported (27). Other rather small studies have found no association between the number of children and the parents' infection status (12,32).…”

Section: Discussionmentioning

confidence: 82%

Concordance ofHelicobacter pyloriStrains within Families

et al. 2003

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Helicobacter pylori infection is typically acquired in early childhood, and a predominantly intrafamilial transmission has been postulated. To what extent family members share the same strains is poorly documented. Our aim was to explore patterns of shared strains within families by using molecular typing. Family members of H. pylori-infected 10-to 12-year-old index children identified in a school survey were invited to undergo gastroscopy. Bacterial isolates were typed with random amplified polymorphic DNA and PCRrestriction fragment length polymorphism of the genes ureA-B, glmM, or flaA. The presence or absence of the cag pathogenicity island, a bacterial virulence factor, was determined by PCR. GelCompar II software, supplemented with visual inspection, was used in the cluster analysis. In 39 families, 104 individuals contributed 208 bacterial isolates from the antrum and corpus. A large proportion, 29 of 36 (81%) of the offspring in a sibship, harbored the same strain as at least one sibling. Mother-offspring strain concordance was detected in 10 of 18 (56%) of the families. Of 17 investigated father-offspring relations in eight families, none were strain concordant. Spouses were infected with the same strains in 5 of 23 (22%) of the couples. Different strains in the antrum and corpus were found in 8 of 104 (8%) of the subjects. Our family-based fingerprinting study demonstrates a high proportion of shared strains among siblings. Transmission between spouses seems to be appreciable. The data support mother-child and sib-sib transmission as the primary transmission pathways of H. pylori.Helicobacter pylori colonizes half of the world's population, and the infection is associated with chronic gastritis, peptic ulcer, gastric cancer, and gastric lymphoma. In-depth knowledge of the transmission patterns may constitute important information for future intervention strategies.In the absence of consistent and verified environmental reservoirs, a predominantly person-to-person transmission has been postulated. H. pylori infection is associated with poor living conditions, and possible transmission routes are fecaloral, oral-oral, or gastro-oral, but firm evidence is lacking (36). The infection clusters in families and is usually acquired in early childhood. A child's risk of being infected is largely determined by the presence or absence of infected family members. Having an infected mother has been suggested to be a more prominent risk factor than having an infected father (30,35). Indications of sib-sib transmission have been reported (14). Transmission between spouses occurs but its significance is unclear (5, 9, 19).Molecular typing of pathogens can corroborate and further characterize the transmission pathways suggested by epidemiologic data based on infection status. Shared strains among individuals indicate person-to-person transmission or acquisition from a common source. Unrelated individuals harbor distinct H. pylori isolates (1), while clonal lineages can be discerned within families (2,7,11,16,20,22,24,2...

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“…Our PubMed search yielded 10 studies of H. pylori recurrence conducted in developed countries [4][5][6][7][8][9][10][11][12][13], and 7 studies conducted in developing countries [14 -20] that used the 13 CUBT at eradication and follow-up and otherwise met our inclusion criteria. Table 1 summarizes the studies from the developed countries, and Table 2, the studies from the developing countries.…”

Section: Resultsmentioning

confidence: 99%

Helicobacter pylori Recurrence in Developed and Developing Countries: Meta‐Analysis of ¹³C‐Urea Breath Test Follow‐Up after Eradication

Niv

Hazazi

2008

Helicobacter

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Objective: Recurrence of Helicobacter pylori infection after eradication is rare in developed countries and more frequent in developing countries. Most recurrent cases are attributed to recrudescence (recolonization of the same strain within 12 months) rather than to reinfection (colonization with a new strain after more than 12 months). The aim of the study was to analyze recurrence rates in developed and developing countries and to deduce the relative roles of recrudescence and reinfection. Methods: The PubMed database was searched up to January 31, 2007 using the keywords " Helicobacter pylori " or " H. pylori " and "recurrence" or "recrudescence," or "reinfection." Only prospective case studies in adults that used the 13 C-urea breath test ( 13 CUBT) were included. Meta-analyses were performed with STATDIRECT Statistical software, version 2.6.1, StatsDirect Ltd, Chesire, UK. Results: The literature search yielded 10 studies of H. pylori recurrence in developed countries (3014 patients followed for 24-60 months) and 7 studies in developing countries (2071 patients followed for 12-60 months). The calculated annual recurrence rates were 2.67% and 13.00%, respectively. Nested metaanalysis of cases with a longer follow-up after eradication revealed an annual recurrence rate of 1.45% (RR 0.54) in developed countries and 12.00% (RR 0.92) in developing countries. Conclusions: The similarity of the annual recurrence rates during the first year after eradication and the annual recurrence rates in the second year after successful eradication in developing countries supports reinfection as the main cause in the second period. Therefore, a different approach for followup of H. pylori eradication may be needed between developed and developing countries. KeywordsHelicobacter pylori , eradication, recurrence, recrudescence, reinfection. Recurrence of Helicobacter pylori ( H. pylori ) infection after successful eradication is rare in developed countries and more frequent in developing countries [1]. Recrudescence (recolonization of the same strain) rather than reinfection (colonization with a new strain) is considered the more likely culprit in most cases [2]. However, this assumption is based on studies using heterogeneous testing methods and strategies, such as The aim of the present meta-analysis was to provide a more accurate assessment of H. pylori recurrence rates in developed and developing countries, and to deduce from these findings the relative roles of recrudescence and reinfection. To avoid the bias introduced by the different approaches used, we limited our database search to studies in adults in which the 13 CUBT was administered at completion of treatment, with a minimum follow-up of 12 months. We also performed a nested analysis of findings Reprint requests to

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Role of partner's infection in reinfection after Helicobacter pylori eradication

Cited by 40 publications

References 35 publications

Toxigenic Helicobacter pylori Infection Precedes Gastric Hypochlorhydria in Cancer Relatives, and H. pylori Virulence Evolves in These Families

Toxigenic Helicobacter pylori Infection Precedes Gastric Hypochlorhydria in Cancer Relatives, and H. pylori Virulence Evolves in These Families

Concordance ofHelicobacter pyloriStrains within Families

Helicobacter pylori Recurrence in Developed and Developing Countries: Meta‐Analysis of ¹³C‐Urea Breath Test Follow‐Up after Eradication

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Role of partner's infection in reinfection after Helicobacter pylori eradication

Cited by 40 publications

References 35 publications

Toxigenic Helicobacter pylori Infection Precedes Gastric Hypochlorhydria in Cancer Relatives, and H. pylori Virulence Evolves in These Families

Toxigenic Helicobacter pylori Infection Precedes Gastric Hypochlorhydria in Cancer Relatives, and H. pylori Virulence Evolves in These Families

Concordance ofHelicobacter pyloriStrains within Families

Helicobacter pylori Recurrence in Developed and Developing Countries: Meta‐Analysis of 13C‐Urea Breath Test Follow‐Up after Eradication

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Helicobacter pylori Recurrence in Developed and Developing Countries: Meta‐Analysis of ¹³C‐Urea Breath Test Follow‐Up after Eradication