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Long-Term Study of Re-Infection Following Successful Eradication of Helicobacter pylori Infection

E.A.B. Cameron; G.D. Bell; L. Baldwin; K.U. Powell; S.G.J. Williams

Authors and Disclosures

Posted: 04/20/2006; Alimentary Pharmacology & Therapeutics. 2006;23(9):1355-1358. © 2006 Blackwell Publishing

Background: ‘Re-infection‘ with Helicobacter pylori after eradication has been estimated to occur in 0-14% of patients, although most so-called ‘re-infections‘ occur within the first year following ‘eradication‘ and many may actually be due to recrudescence of a temporarily suppressed infection.

Aim: To study the true re-infection rate, we have studied re-infection rates after eradication therapy by excluding the first year‘s data, minimizing the possible confounding effect of recrudescence.

Methods: All patients tested for H. pylori infection following eradication therapy between 1987 and 2004 were evaluated. Testing was carried out by urea breath test and gastric biopsy. Patients were included if they were found to be negative for H. pylori infection by testing at least 1 year following eradication and underwent at least one further test for H. pylori.

Results: 1162 patients met the inclusion criteria with median post-eradication follow-up of 3 years (1.5-14) including 4668 tests; 3319 years of follow-up were analysed. Thirteen cases of re-infection occurred (re-infection rate 0.4% per year).

Conclusions: This large study of H. pylori re-infection avoided cases of recrudescence by excluding the first post-eradication year. True re-infection is probably less common than previously thought.


Since its discovery in 1982, a great deal has been learnt about Helicobacter pylori infection. It is known to cause a number of gastrointestinal diseases including peptic ulcers, gastric carcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma and has been implicated in a number of non-gastrointestinal diseases. It can be successfully eradicated using a number of drug regimens consisting of combinations of acid suppressants and antibacterial agents leading to a dramatic reduction in ulcer recurrence and associated complications.[1]

Reappearance of H. pylori is thought to occur via two distinct mechanisms, recrudescence and re-infection. Recrudescence reflects reappearance of the original strain of H. pylori following its temporary suppression rather than successful eradication. True re-infection occurs when, after successful eradication, a patient becomes infected with either the original strain or a new strain of H. pylori. To prove re-infection, genomic differences need to be demonstrated between the strains present before and after eradication therapy. This is clearly not possible for those infections diagnosed by indirect methods (such as with urea breath tests and serology).

Studies suggest a wide range of rates of re-infection[2-10] but follow-up is generally short and patient numbers are relatively small ( Table 1 ). It is probable that a sizeable proportion of cases of the early reappearance of H. pylori infection are due to recrudescence. Bell et al. previously described follow-up of 304 patients in whom H. pylori infection had been apparently successfully eradicated. Eighteen of the 19 cases of apparent re-infection occurred within the first year after eradication with higher rates in patients treated with less effective regimes.[2] This pattern has been seen in most other studies with 80-95% of re-infections occurring within the first year.[11] Comparison of strains of H. pylori following reappearance have shown that 38% are identical to the pre-treatment strain in the first 6 months and none are identical following 1 year.[12] A previous study from Australia excluding recurrence within the first year found an annual re-infection rate of only 0.4%.[13]

In Ipswich, we have studied H. pylori infection since shortly after its discovery including development of the 14C-urea breath test,[14] histological stains for identification of the organism[15] and routine culture and antibiotic sensitivity testing of the organism since 1991.[16] It has thus been possible to study the success of eradication and the rate of re-acquisition of infection following apparently effective treatment. We have evaluated re-infection rates in a large cohort of patients following eradication therapy over long follow-up periods.

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