The human pathogen Helicobacter pylori is associated with gastritis, peptic ulcer disease, and gastric cancer. The pathogenesis of H. pylori infection in vivo was studied by adapting fresh clinical isolates of bacteria to colonize the stomachs of mice. A gastric pathology resembling human disease was observed in infections with cytotoxin-producing strains but not with noncytotoxic strains. Oral immunization with purified H. pylori antigens protected mice from bacterial infection. This mouse model will allow the development of therapeutic agents and vaccines against H. pylori infection in humans.

Colonization of the mucosa of the stomach and the duodenum by Helicobacter pylori is the major cause of acute and chronic gastroduodenal pathologies in humans. Duodenal ulcer formation strongly correlates with the expression of an antigen (CagA) that is usually coexpressed with the vacuolating cytotoxin (VacA), a protein that causes ulceration in the stomach of mice. However, the relationship between these two virulence factors is unknown. To define whether CagA and VacA are coexpressed in all clinical isolates and their relationships, we collected 43 clinical isolates of H. pylori and studied their genetic and phenotypic properties. Based on this analysis, most of the strains could be classified into two major types. Type I bacteria had the gene coding for CagA and expressed the CagA protein and the vacuolating cytotoxin. Type II bacteria did not have the gene coding for CagA and did not express either the CagA protein or the vacuolating cytotoxin. Type I and type II bacteria represented 56 and 16%, respectively, of the 43 clinical isolates, while the remaining 28% had an intermediate phenotype, expressing CagA independently of VacA or vice versa. This finding shows that although it is present in most cytotoxic strains, CagA is not necessary for the expression of the vacuolating cytotoxin.

A total of 66.6% of Campylobacter pylori strains isolated from patients with peptic ulcers produced a cytotoxin active against mammalian cells in vitro, versus 30.1 % of strains isolated from patients with chronic gastritis of various degrees of severity only. This difference was statistically significant and suggests that the toxic substance could be involved in the development of peptic ulcers.

In a 1-year period (January to December 1984), Aeromonas strains were isolated from feces of 21 of 561 (3.7%) children with gastroenteritis and from 12 of 576 (2.1%) children without intestinal disturbances (controls). The difference between the two isolation rates was not significant (X2 = 2.2; P > 0.05). In five cases of illness other intestinal pathogens were isolated together with Aeromonas in the same stool sample. A total of 39 Aeromonas strains were detected since in some cases aeromonads with different biochemical characteristics were obtained from the same stool sample. Of the 39 Aeromonas isolates, 6 strains (5 from patients) were Aeromonas hydrophila, 5 strains (3 from patients) were Aeromonas sobria, and 26 strains (18 from patients) were Aeromonas caviae; 2 strains isolated from controls did not ferment sucrose and were considered a distinct group of Aeromonas. We found no significant difference between the prevalence of each of these species from patients and the prevalence from controls. We found no significant difference in the prevalence of enterotoxinproducing strains (suckling mouse model), cytotoxin-producing strains (HEp-2 cell model), or hemolysinproducing strains (rabbit erythrocyte model) between patients and controls. In our geographical region there is no evidence that Aeromonas species are primary intestinal pathogens in children.

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