Halitosis And Helicobacter Pylori - Antibiotic Cure Testimonial
Contributed by: Jimi Stein
HALITOSIS AND HELICOBACTER PYLORI : A CASE STUDY
Authors: Martin Atkinson-Barr, Ph.D., Barry J. Marshall, M.D.
Keywords: halitosis, Helicobacter pylori, breath, anaerobic bacteria, achlorhydria, gastritis, antibiotic therapy, tetracycline, metronidazole, bismuth, triple therapy.
Journal: Helicobacter Web. 1996; vol2:p1
Table of Contents
* Case Report
* Editor's Comments
We report a case study of a patient with chronic halitosis of > 60yrs duration that was resistant to all traditional therapies but was resolved following triple-therapy for Helicobacter pylori.
The causal relationship between Helicobacter pylori and upper gastrointestinal disease is now well established and published guidelines call for antimicrobials as first line therapy for ulcer patients (1). An early study by one of the authors reported on the symptomatic infection following ingestion of H. pylori (2) and one study has suggested that the disease may progress from an acute symptomatic phase to an asymptomatic infection with concomitant chronic gastritis (3). It was noted that the acute stage of infection was accompanied by fatigue, nausea, vomiting and bloating and that a family member reported that the subject had developed malodorous breath. Since then other authors have reported an apparent benefit when patients with halitosis have been treated for H. pylori(4,5).
Here we report on a case of chronic halitosis which was refractory to normal treatments. The patient was strongly seropositive for H. pylori and treatment was initiated with triple therapy which resolved the infection and the halitosis.
A very active non-smoking 76-year-old Caucasian woman of normal physique and living in Southern California presented with a 60-year history of halitosis. In the last ten years she reports some problem with gastro-esophageal reflux and a case of aggressively treated laryngitis in 1970 lead to dysphonia. In recent years she has experienced some age-onset diabetes. There is no history of peptic ulcer disease or dyspepsia.
She has clear memories from age 16 of her mother instructing her to improve her dental hygiene to eliminate the odor. She reported that the foul breath makes her social relationships difficult, particularly with her grandchildren, and she remembers that her husband had told her that it was of little use to repeatedly cleanse her teeth when the problem appeared to be coming from lower in the digestive system.
Over a period of many years she had sought an effective treatment for the halitosis from a number of dentists and in spite of fastidious care and frequent dental visits the problem continued. She does, however, enjoy enviable dentition with no loss of teeth and little evidence of caries. She reports that the odor is more severe on waking, as is commonly experienced and referred to as morning mouth.
An examination of the family history is strongly suggestive of H. pylori infection in at least one parent and siblings. One brother has a 20-year history of stomach ulcers and now suffers from coronary artery disease.
Antibody titers with specific ELISA were strongly positive for H. pylori and therapy was initiated with tetracycline/metronidazole/bismuth. Although the patient experienced some nausea she completed the prescribed treatment and it was noted that the halitosis had abated. In the ensuing months serological tests demonstrated a reduction in antibody titer though at six months it was clear that eradication had not been achieved and a second treatment was completed. The patient continues to be free of halitosis.
Bacterial anaerobic respiration produces foul smelling compounds which could cause halitosis under suitable conditions. There are two major problems with the hypothesis that H. pylori is the causative organism in this case of halitosis and that eradication of H. pylori led to the cessation of foul smelling breath:
H. pylori is very common infection affecting some 30% of the population. By contrast we know from normal experience that chronic halitosis is relatively uncommon. However since only 10% of the population ever develop peptic ulcer disease it is clear that the progression of the disease varies from subject to subject. Most other infections are self limiting and therefore such a long history indicates an unusual pathology which is supported by our knowledge of the nature of H. pylori within the gastric mucosa.
The combination of tetracycline and metronidazole is effective in the eradication of a wide spectrum of aerobes and anaerobes. Triple therapy will eradicate many possible candidate infections making it unclear whether the therapy was successful directly as a result of it's action on H. pylori or because another organism was eliminated. Over the 60 year period this patient had received a variety of antibiotic therapies for various medical problems without relief from halitosis.
The published guidelines call for routine antimicrobial treatment only in H. pylori infected subjects with ulcers and point out that, at the present time, there is no reason to consider the routine detection or treatment in the absence of ulcers. We await the conclusions of prospective studies on a related group, that is patients with non-ulcer dyspepsia. This case report identifies one patient who appears to have had halitosis as a result of the infection, without any symptoms that would indicate an ulcer and without a history of dyspepsia. More research is needed to establish the range and nature of the symptoms that exist in a non-ulcer H. pylori infected population. This large group has not previously been identified as a target for future research.
If H. pylori does cause halitosis then the mechanism might be that these people have intermittent achlorhydria and at times have residual food putrefying in the stomach. In a study in Brazil, we found that 25% of healthy males with HP were producing almost no acid. In this state food takes only a few hours to start to smell after being mixed with saliva and chewed to inoculate it with oral bacteria. If H. pylori and ammonia production (from urease) are present in the stomach of a person who only makes a small amount of acid, any residual acid is neutralized by the ammonia thus making the contents a perfect anaerobic culture medium. After eradication of HP, ammonia product stops and even a small amount of acid will be enough to keep the stomach sterile. Finally, even if the HP were not at fault, our two most effective HP antibiotics (clarithromycin and metronidazole) are secreted in saliva and are likely to eradicate any single pathogenic species, which could cause halitosis, and which might inhabit the mouth.
1. Helicobacter pylori in Peptic Ulcer Disease. NIH Consensus Statement 1994 Feb 7-9;12(1):
2. Marshall BJ, Armstrong JA, McGechie DB, Glancy RJ. Attempt to fulfil Koch's postulates for pyloric Campylobacter. Med J Aust 1985; 142:436-9
3. Dooley C, Cohen H, Fitzgibbons P, et al. Prevalence of Helicobacter pylori infection in histologic gastritis in asymptomatic persons. N Engl J Med 1989;321:1562-6
4. Norfleet, R.G. Helicobacter Halitosis (Letter). J.Clin.Gastroenterol. 16: 74, 1993.
5. Tiomny, E., Arber, N., Moshkowitz, M., Peled, Y., and Gilat, T. Halitosis and Helicobacter pylori. A possible link? J.Clin.Gastroenterol. 15:236-237, 1992.