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. 1997 May;65(5):1962–1966. doi: 10.1128/iai.65.5.1962-1966.1997

Infection of the ferret stomach by isogenic flagellar mutant strains of Helicobacter mustelae.

K A Andrutis 1, J G Fox 1, D B Schauer 1, R P Marini 1, X Li 1, L Yan 1, C Josenhans 1, S Suerbaum 1
PMCID: PMC175254  PMID: 9125590

Abstract

Helicobacter mustelae, like Helicobacter pylori, possesses two flagellin proteins, FlaA and FlaB. Isogenic mutant strains of H. mustelae have been constructed by disruption of the flaA or flaB gene with a kanamycin resistance cassette or by introduction of both a kanamycin and a chloramphenicol resistance gene to produce a double mutant. To determine whether one or both flagellin proteins are necessary for colonization and persistence of infection with H. mustelae, 19 ferrets, specific pathogen free for H. mustelae, were given either the HMF1 flaA::km (weakly motile), ATCC 43772 flaB::km (moderately motile), or HMF1 flaA::cat flaB::km (non-motile) mutant strain, the wild-type parent strains, or sterile broth. Gastric tissue samples were obtained during sequential gastric biopsies beginning at 3 weeks postinoculation and ending at necropsy at 3 months postinoculation. H. mustelae infection status was determined by culture, histology, and serology. The wild-type parent strains of H. mustelae infected all ferrets at all time points. The double-mutant strain was unable to colonize; the flaA and flaB single-mutant strains were able to initially colonize at a low level and establish persistent infection with increasing numbers of organisms over time. The severity of gastritis produced by infection with these strains of H. mustelae correlated with the number of organisms present in the gastric mucosa. Flagellar motility is an important virulence factor for colonization and pathogenesis in the H. mustelae ferret model.

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Selected References

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