&lt;i&gt;Helicobacter pylori&lt;/i&gt; in the Oral Cavity Reflects Handling of Contaminants but Not Gastric Infection

Doré-Davin, C.; Heitz, M.; Yang, Haw‐Ching; Herranz, Mercedes Berlanga; Corthésy–Theulaz, Irène

doi:10.1159/000007659

Cited by 33 publications

(21 citation statements)

References 18 publications

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“…Furthermore, the detection of H. pylori DNA does not reflect the presence of living bacteria and, thus, does not necessarily equate to a real infection. Other groups have obtained supporting hints that detection of H. pylori DNA might reflect contact with H. pylori rather than an infection [26].…”

Section: Discussionmentioning

confidence: 94%

Real-time quantitative PCR assay for the detection of Helicobacter pylori: no association with sudden infant death syndrome

et al. 2005

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Helicobacter pylori infection is known to be one of the most common chronic infectious diseases in humans. Recently, a hypothesis was proposed that H. pylori infection could be a frequent cause for sudden infant death syndrome (SIDS). We have investigated this postulated association by examining formalin-fixed paraffin-embedded gastric tissues of a retrospective cohort of 94 SIDS cases: The presence of H. pylori was inferred from a newly developed real-time quantitative PCR assay with SYBR Green I detection. This assay is based on the amplification of the single-copy H. pylori-specific glmM gene. Accuracy and precision were verified using a plasmid containing a 977-bp fragment of this glmM gene. The assay was very sensitive, and as few as 30 template copies per PCR reaction could be detected even in the presence of excess human DNA. The assay was validated on mucosal biopsy samples of patients with known H. pylori infections. Interfering effects due to SIDS gastric tissue were excluded. Only two (2.1%) of the SIDS samples yielded H. pylori DNA copy numbers and only beyond the lowest standard concentration. These results could be confirmed independently by immunohistochemistry using an H. pylori-specific antibody. Thus, an infection by H. pylori is very rare in cases of SIDS, and thus the postulated association of H. pylori infection and SIDS cannot be confirmed.

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Section: Discussionmentioning

confidence: 94%

Real-time quantitative PCR assay for the detection of Helicobacter pylori: no association with sudden infant death syndrome

et al. 2005

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“…If there were a relationship between oral and gastric H. pylori infection, one would expect older people, living in developing countries and having gastric symptoms to have higher oral H. pylori prevalence. Using conventional PCR, no clear association between age, country, periodontal disease and gastric symptoms with prevalence of oral H. pylori was observed in various studies (4,6,7,9,14,20,23,32). Therefore, comparisons of the prevalence and quantity of oral H. pylori between subjects with and without gastric symptoms, with and without periodontal disease, and in developing and developed countries could be the subjects of future research using a realtime PCR.…”

Section: Discussionmentioning

confidence: 99%

Absence of Helicobacter pylori in the oral cavity of 10 non‐dyspeptic subjects demonstrated by real‐time polymerase chain reaction

Martínez-Gomis¹,

Diouf²,

Lakhssassi³

et al. 2006

Oral Microbiology and Immunology

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Helicobacter pylori is a gram-negative, curved, microaerophilic organism that has been implicated in the aetiology of gastritis, in the process of gastric and duodenal ulcer formation, and in gastric cancer (15,17). Approximately 10% of individuals are affected by gastritis and/or gastric ulcer during their lifetime and over 50% of the world's population carries this infection (7). The prevalence of gastric H. pylori infection depends on age and varies strongly between developing and developed countries, and according to ethnicity, place of birth and socioeconomic factors among people living in the same country Background/aims: Helicobacter pylori plays a significant role in gastric disease. However, the presence of this bacterium in the oral cavity remains controversial. The aim of the present study was to detect and quantify H. pylori in 29 different sites of the oral cavity in non-dyspeptic subjects by means of real-time polymerase chain reactions (PCR). Methods: Ten subjects without gastric symptoms were studied. Samples from unstimulated saliva, three sites of the tongue, oral mucosa, and 12 sites of both supragingival and subgingival plaque were collected from each subject. DNA was extracted from the oral samples and analysed for the presence of H. pylori by real-time PCR (LightCycler Ò ) using JW23/22 primers which targeted the 16S rRNA gene. DNA from H. pylori DSM 4867 was used as a positive control. Relative quantification with external standards was performed by calculating the target to reference ratio. Results: Amplification efficiency for the LightCycler Ò 2.0 runs ranged from 1.8 to 2.4. Melting curve analysis identified all the positive control capillaries, which contained H. pylori reference DNA, as a single and narrow peak at a melting temperature between 84.5 and 84.9°C. All the negative control capillaries with no template control and the 29 oral samples from each subject showed either no melting peaks or broad melting peaks below 80°C, which were considered as primer dimers. Therefore, H. pylori was not detected from any of the 290 oral samples. Conclusion: Helicobacter pylori seems not to be permanently present in the oral cavity of a non-dyspeptic population.

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“…ysis of the DNA, they were typically different, suggesting that either different H. pylori strains exist in the stomach and saliva in same patient or that there was misidentification of the spiral-shaped, urease-positive organisms obtained from the mouth (10). It seems likely, given that more than 300 recognized taxa have been identified in the oral cavity, many spiral bacteria are as yet uncultivated.…”

Section: Discussionmentioning

confidence: 99%

“…We evaluated the 26 primer pairs previously reported for detection of H. pylori in clinical samples and included 2 primer pairs for the ureA gene, 2 for the 860-bp DNA gene, 3 for the16S rRNA gene, 1 for the 26K species-specific antigen gene, 8 for the vacA gene, 6 for the cagA gene, 3 for the glmM gene, and 1 for the adhesin gene. We used PCR conditions exactly matching those described by the authors reporting their use (7,10,16,20,26,27,29,32,34,40,43,47,48,55).…”

Section: Methodsmentioning

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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<i>Helicobacter pylori</i> in the Oral Cavity Reflects Handling of Contaminants but Not Gastric Infection

Cited by 33 publications

References 18 publications

Real-time quantitative PCR assay for the detection of Helicobacter pylori: no association with sudden infant death syndrome

Real-time quantitative PCR assay for the detection of Helicobacter pylori: no association with sudden infant death syndrome

Absence of Helicobacter pylori in the oral cavity of 10 non‐dyspeptic subjects demonstrated by real‐time polymerase chain reaction

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

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