In C/M-R2 strain the morphology was conserved in about half of the analyzed bacteria (Figure 2F), whereas ~ 40% of cells showed granular cytoplasm and ~ 35% altered outer membrane. Flagella were observed and vesicles were present in C/M-R2 strain only (Table 3). As far as the strains assayed with metronidazole are concerned, CCUG 17874 strain was characterised by organisms with severely altered shape and peculiar detachments

between membrane and cytoplasm that often appeared fragmented (Figure 2G); Hydroxychloroquine flagella and vesicles were not observed in the sample (Table 3). C/M-R2 strain did not show any peculiar ultrastructural alterations after metronidazole treatment (Figure 2H). In the samples treated with both polysorbate 80 and clarithromycin, the shape was altered in both bacterial strains and the synergic effect of the two compounds was evident (Figures 2I, 2J). The examination of CCUG 17874 strain revealed swollen cells, granular cytoplasm and

altered outer membrane, typical alterations induced by polysorbate 80, together with detachment of the inner membrane from the cytoplasm and “holes” in the cytoplasm, typical effect of clarithromycin (Table 3). Flagella and rare vesicles were observed. C/M-R2 strain showed swollen bacteria with cytoplasm that gradually had lost its homogeneity; numerous vesicles and rare fragments of flagella were present check details (Table 3). The examination of CCUG 17874 strain treated with polysorbate 80 and metronidazole (Figure 2K) showed swollen bacteria with non-homogeneous cytoplasm, presence of vesicles (typical features of polysorbate 80 treatment) concomitant with peculiar detachments of the membrane from cytoplasm that often appeared fragmented (typical alterations caused by metronidazole).

Vesicles were only present, flagella were not observed (Table 3). C/M-R2 strain showed swollen bacteria with granular cytoplasm and the presence of vesicles (Figure 2L), all characteristics typical of polysorbate 80 treatment (Table 3); no flagella were found. Discussion Chemoresistances are the main cause of therapeutic failure of H. pylori infection [18]. The occurrence of acquired resistances in such species is very high, because of certain characteristics that make H. pylori hypermutable [19]. Mutation rates in H. pylori are in fact 10–700 fold higher than that observed in other species, for instance Escherichia coli; in addition, the mechanisms of acquired chemoresistance in H. pylori include its significant genetic competence (i.e. the ability to recombine exogenous DNA) [19].