The Incidence of<i>Helicobacter pylori</i>Acquisition in Children of a Canadian First Nations Community and the Potential for Parent‐to‐Child Transmission

Sinha, Samir K.; Martin, Bruce D.; Gold, Benjamin D.; Song, Qunsheng; Sargent, Michael; Bernstein, Çharles N.

doi:10.1111/j.1083-4389.2004.00199.x

Cited by 51 publications

(30 citation statements)

References 59 publications

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“…In addition, results of studies using PCR based on the primers studied here reporting the detection of H. pylori in environmental samples should be viewed with caution since even multiples of these primer sets produced a very high rate of false-positive results (i.e., 54% in saliva samples). Possibly, the accuracy and specificity could be improved by using magnetic beads or other techniques to separate the organism coupled with primers designed to detect H. pylori-specific proteins unrelated to urease (13,19,23) or possibly to have positive results with multiple potentially H. pylori-specific virulence genes (e.g., cagA or vacA) (40,46,54). The Human Microbiome Project should enrich the GenBank with many as-yet-uncultured human microbes such that searches should help eliminate primer pairs that cross-react with non-H. pylori bacteria and cause false-positive PCR results.…”

Section: Discussionmentioning

confidence: 99%

Unreliability of Results of PCR Detection of Helicobacter pylori in Clinical or Environmental Samples

Sugimoto

Abudayyeh

et al. 2009

J Clin Microbiol

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The aim of this study was to compare published Helicobacter pylori primer pairs for their ability to reliably detect H. pylori in gastric biopsy specimens and salivary samples. Detection limits of the 26 PCR primer pairs previously described for detection of H. pylori DNA in clinical samples were determined. Sensitivity and specificity were determined using primers with detection limits of <100 CFU/ml using 50 H. pylori-positive and -negative (by concordance by culture and histology) coded gastric biopsy specimens. These results were then confirmed with gastric biopsy specimens and saliva from patients with confirmed H. pylori status. Five of the twenty-six previously reported primer pairs (HP64-f/HP64-r, HP1/HP2, EHC-U/EHC-L, VAG-F/VAG-R, and ICT37/ICT38) had detection limits of <100 CFU/ml in the presence of gastric tissue. None had 100% specificity or sensitivity; all produced false-positive results. The HP64-f/HP64-r for ureA and HP1/HP2 for 16S rRNA individually had sensitivities and specificities of >90% with gastric biopsy specimens. No combinations of primer pairs improved the results. Using these five primer pairs, 54% of the positive saliva samples were determined to be false positive; both the HP64-f/HP64-r and the HP1/HP2 sets produced false positives with saliva. We conclude that clinicians should not rely on results using current PCR primers alone to decide the H. pylori status of an individual patient or as a basis for treatment decisions. The results of studies based on PCR identification of H. pylori in environmental samples should be viewed with caution. Possibly, specific primers sets can be identified based on the presence of multiple putative virulence factor genes.

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Section: Discussionmentioning

confidence: 99%

Unreliability of Results of PCR Detection of Helicobacter pylori in Clinical or Environmental Samples

Sugimoto

Abudayyeh

et al. 2009

J Clin Microbiol

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“…Evidence that H. pylori might be transmitted by saliva comes from a study by Megraud et al (13), who found a higher risk of H. pylori associated with the custom of the premastication of food when mothers feed their children in western Africa. Recently, Sinha et al (19) demonstrated H. pylori positive PCR in maternal saliva and in the water in which children's soothers (pacifiers) were stored suggesting a plausible route of mother-to-child oral transmission.…”

Section: Discussionmentioning

confidence: 99%

Five-Year Follow-Up Study of Mother-to-Child Transmission ofHelicobacter pyloriInfection Detected by a Random Amplified Polymorphic DNA Fingerprinting Method

et al. 2005

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Recent studies have speculated on the possible role of the mother in transmitting Helicobacter pylori infection to their children. In an attempt to either prove or disprove this supposition, we investigated the rates of infection of children born to H. pylori-positive mothers from birth to 5 years of age using serology and the stool antigen test. When infection of the children did occur, the strains from the children were compared to those of their mothers using DNA analysis. Sixty-nine of the 350 pregnant mothers (19.7%) had a positive serology for H. pylori. Fifty-one children underwent serological examinations and stool antigen tests at 4 to 6 days after birth, followed by 1, 3, and 6 months. They were continuously given the stool antigen test at 4-to 6-month intervals until the age of 5 years. Gastric juice samples were collected from the infected children and their mothers for culture and DNA analyses using a random amplified polymorphic DNA fingerprinting method. None of the 51 children acquired H. pylori infection during the first year of life. Of the 44 children enrolled in a 5-year follow-up study, five (11%) acquired H. pylori infection. They acquired the infection at the age of 1 year 2 months, 1 year 3 months, 1 year 6 months, 1 year 8 months, and 4 years 4 months. Random amplified polymorphic DNA fingerprinting confirmed that the strains of the five children exhibited DNA fingerprinting patterns identical to those of their mothers. These findings suggest that mother-to-child transmission is the most probable cause of intrafamilial spread of H. pylori.

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“…As conclusive evidence for zoonotic transmission of H. pylori is not yet available (195), new infections are thought to occur as a consequence of direct human-to-human transmission, via either an oral-oral or fecaloral route or both. H. pylori has been detected in saliva, vomitus, gastric refluxate, and feces (10,177,178,298,361,492,569), but there is no conclusive evidence for predominant transmission via any of these products. This may be due to the fact that most research on transmission has focused on adults.…”

Section: Transmission and Sources Of Infectionmentioning

confidence: 99%

Pathogenesis ofHelicobacter pyloriInfection

2006

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SUMMARY Helicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world's population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Disease outcome is the result of the complex interplay between the host and the bacterium. Host immune gene polymorphisms and gastric acid secretion largely determine the bacterium's ability to colonize a specific gastric niche. Bacterial virulence factors such as the cytotoxin-associated gene pathogenicity island-encoded protein CagA and the vacuolating cytotoxin VacA aid in this colonization of the gastric mucosa and subsequently seem to modulate the host's immune system. This review focuses on the microbiological, clinical, immunological, and biochemical aspects of the pathogenesis of H. pylori.

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The Incidence ofHelicobacter pyloriAcquisition in Children of a Canadian First Nations Community and the Potential for Parent‐to‐Child Transmission

Cited by 51 publications

References 59 publications

Unreliability of Results of PCR Detection of Helicobacter pylori in Clinical or Environmental Samples

Unreliability of Results of PCR Detection of Helicobacter pylori in Clinical or Environmental Samples

Five-Year Follow-Up Study of Mother-to-Child Transmission ofHelicobacter pyloriInfection Detected by a Random Amplified Polymorphic DNA Fingerprinting Method

Pathogenesis ofHelicobacter pyloriInfection

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