Serology has been used worldwide to detect Helicobacter pylori infection. Using an immunoblot assay with an antigen from strain ATCC 43579, we sought to determine the antibodies which were good markers of colonization and the antibody patterns associated with ulcers or atrophy. Out of 98 dyspeptic patients, 41 were colonized byH. pylori, based on a positive culture or on positive results of both a urease test and direct examination. These 41 patients were seropositive by an enzyme immunoassay, and 12 of them had ulcers and 29 had evidence of atrophy. Fifty-seven of the 98 patients were noncolonized. Twenty-five of the 57 had evidence of gastric atrophy, and 10 were seropositive; 5 of these 10 had ulcers. By Western blot analysis, 12 antibodies were significantly more frequent in sera from colonized patients, and they produced immunoreactive bands at 125, 87, 74, 66, 54, 48, 46, 42, 35, 30, 16 and 14 kDa. The presence of at least one band at 54, 35, or 42 kDa was the best marker of infection (sensitivity, 95%; specificity, 82%). In the group of colonized patients, none of the antibody patterns were correlated to gastric atrophy. Conversely, the presence of a band at 125, 87, or 35 kDa was statistically associated with the presence of an ulcer. The simultaneous presence of bands at 87 and 35 kDa predicted the risk of ulcers with 83% sensitivity and 69% specificity. By using CagA-positive and VacA-positive strains and CagA-negative and VacA-negative isogenic mutants, the antigens corresponding to the bands at 125 and 87 kDa were shown to be CagA and VacA, respectively. On the other hand, the 35-kDa antigen is a novel uncharacterized component ofH. pylori. These results may help to optimize the composition of antigenic preparations for serologic detection ofH. pylori colonization. Immunoblot assay would be useful for screening patients at high risk of ulcers.

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The aim of this study was to evaluate the performance of three antigenic preparations for serological diagnosis of Helicobacter pylori infection: (i) native antigens from Helicobacter pylori strain N6 or its aflagellated isogenic mutant N6flbA-, or an acellular extract (antigen AgFA) from a pool of six clinical strains; (ii) recombinant antigens consisting of CagA fused to MS2 polymerase and HspA or recombinant UreA and UreB fused to the maltose-binding protein, and (iii) the preparations provided with two commercial kits, the Cobas Core (Roche Diagnostic Systems, France) and the Pylori Stat (BioWhittaker, Belgium). All preparations were used in an enzyme immunoassay to test 92 sera from dyspeptic patients for whom the status of Helicobacter infection was established. Sensitivities were higher (90 to 100%) for the native antigens and the commercial kits than for the recombinant antigens. Specificities were higher than 90%, except with UreA + UreB (42%). The most useful antigens were those extracted from strains N6 and N6flbA-.

An enterotoxigenic strain of Bacteroides fragilis was the sole organism isolated from the cerebrospinal fluid of a two-and-a-half-month neonate who had a medullary-colonic fistula as part of a complex congenital malformation, but no brain abscess. A rapid latex particle agglutination test for detection of bacterial antigen was positive for Haemophilus influenzae type b, suggesting that Bacteroides fragilis and Haemophilus influenzae type b might share some capsular antigens. In order to determine the role of the enterotoxin with respect to virulence of the strain, antibodies to a 20 kDa protein were sought in the patient's serum, but Western blot of the culture supernatant revealed only antibodies to a 45 kDa bacterial protein. The patient was successfully treated with metronidazole and imipenem.