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Q1: What is Helicobacter heilmannii?
Helicobacter heilmannii was first described in 1987 as a Gram negative urease producing tightly coiled bacillus, morphologically distinct to Helicobacter pylori and labelled Gastrospirillum hominis.1 It has been reclassified as a non-pylori Helicobacterspp and found to have a 90% homology in the 16s RNA nucleotide sequence to H pylori.2Following the description of a large series of patients by a German pathologist in 1991 the organism has been renamed H heilmannii.3 It is now recognised as the commonest non-pylori species in humans with an average incidence in a civilised human population of 0.3%.3 Culture of this bacillus is difficult and its method of detection varies world wide and as such its prevalence varies geographically.4 H heilmannii shows little variation but reported numbers in clinical series are small.2 It bears a close genotypic profile to Helicobacter felis, which is usually found in the gastric mucosa of cats and dogs, and this has prompted theories of zoonotic transmission. Seventy per cent of patients with H heilmannii infection have contact with pets.5
Q2: What does it do?
H heilmannii has been shown to cause a neutrophilic inflammatory response in the gastric mucosa and in some reports mucosal atrophy, metaplasia, and dysplasia. The degree of inflammation seen is to a lesser extent than that seen withH pylori. There have been suggestions of a synergistic relationship with H pylori, although other studies show a protective effect ofH heilmannii against H pylori.6 7
Q3: What is the clinical significance?
Heilman in 1991 showed an association between infection and gastrointestinal disease in humans.2 Further reports support an association with predominantly superficial gastritis.2 7 There are a few case reports of an association with peptic ulcer disease and gastric cancer.2 8
Q4: Does it require treatment?
H heilmannii has been shown to spontaneously disappear together with total resolution of inflammatory change.2 7 However, chronicity has been described and there is evidence to suggest susceptibility to H pylori eradication therapy.2 8 Whether it is a true pathogen remains an open question.
In this case, as the man was symptomatic, it was decided to treat him with H pylori eradication therapy and to continue on a proton pump inhibitor. He became asymptomatic after the initial eradication treatment and is now in the process of stopping all treatment.
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