Dear Editor,

Attending the XXXVth Workshop of the European Helicobacter & Microbiotica Study Group in Glasgow, I enjoyed the high standard of research and the progress in understanding Helicobacter pylori (Hp). Listening to and looking at the presentations, I got the impression that there exists just one strain from the bacterium and one aim: how best to get rid of the bug. Aside from countless genetic variations there are at least three clearly different main strains of Hp. These strains are defined by the two different antigens CagA and VacA and can easily be diagnosed by an immunoassay. In our outpatients’ clinic, we found 56% of the patients to be Hp negative and 44% Hp positive. Of the Hp positive patients were:

66% CagA positive/VacA negative

20% CagA positive/VacA positive

14% CagA negative/VacA negative.

In our unit, the decision for eradication of Hp was not made by the mere detection of the bacterium but only by the gastric history or the histological findings. I am aware that many patients are at danger from Hp in the stomach, the duodenum and by toxins via the vagus nerve in the brain. However, I am convinced that others may benefit from the bacterium. E.g. certain strains of Staphylococcus and E.coli can cause severe life threatening disease. Nonetheless, numerous strains of Staphylococcus and E.coli within the human microbiome are peaceful residents producing vitamin K1,2. Helicobacter induces an immune response in the lung protecting against Asthma and it produces spermidine an important biogenic amine3,4. Just as nobody claims that only a dead Staphylococcus is a good Staphylococcus and only a dead E.coli is a good E.coli, the dictum that only a dead Helicobacter is a good Helicobacter should be “eradicated”.

In our patients with ulcers and acute, chronic or atrophic gastritis we found CagA and VacA in many patients; however, we also saw patients with extremely high antibody titers of CagA and VacA who never had any gastric disease or noticeable histology. It is the immune response of the patient that shows us what to do. Why use a dual antibiotic treatment when the patient does not need it, increasing the risk of antibiotic resistance. And if one is afraid that the “benign” histologic finding may later decline, why not do a control 5 to 10 years later?

The author of this letter is 83 years old. He never had gastric symptoms except for an occasional bout of reflux from a small hiatus hernia. For the last 37 years, he knows of his stomach resident Hp. (CagA negative/VagA negative). His histology (Figure 1) shows a mild gastritis without metaplasia or intraepithelial lymphocytosis. Maybe he benefits from the production of spermidine from his microbial resident.

May this little note stimulate research about the pathological effects of the different Hp strains and their immune reactions?