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SUMMARY One hundred and three gastroscopic biopsies from 80 patients were cultured for Campylobacter pyloridis and studied histologically. Active chronic gastritis, as shown by the presence of polymorphonuclear leucocytes, was diagnosed in 51 biopsies and C pyloridis was found in 47. Sixteen gastric biopsies showed normal histology (no inflammation); C pyloridis was detected in only one of these, and a second biopsy taken from this patient at the same time showed active gastritis. Biopsies could be kept at 4°C for five hours without loss of viability of C pyloridis. An inoculum made by grinding the biopsy in a ground glass grinder consistently gave a much heavier growth of C pyloridis than one made by mincing the specimen. The campylobacter supplement ferrous sulphate, sodium metabisulphite, sodium pyruvate (FBP) (Oxoid) was inhibitory for some isolates; the inhibitory component was found to be sodium metabisulphite. Contaminants, but not C pyloridis, were inhibited by the incorporation of vancomycin 6 mg/l, nalidixic acid 20 mg/l, and amphotericin 2 mg/I, but higher concentrations inhibited C pyloridis. Undried plates kept in a plastic container at room temperature for up to two weeks were as satisfactory as freshly poured plates for the isolation of C pyloridis.

SUMMARY One hundred patients with duodenal ulceration and Campylobacter pylori in their stomach were entered into a double blind placebo controlled prospective study. Treatment schedules were cimetidine and placebo, or cimetidine and tinidazole, or colloidal bismuth subcitrate (CBS) and placebo, or CBS and tinidazole. Seventeen per cent of isolates of C pylori obtained at the first endoscopy were resistant to tinidazole and 70% of the second isolates from patients given cimetidine and tinidazole became tinidazole resistant. Suspensions of nitroimidazole sensitive cultures of C pylori showed that three of 22 isolates had a nitroimidazole resistant subpopulation. In patients who healed and remained free of C pylori after treatment ulcers recurred less often than in patients who healed but retained C pylori (23% v 73% over 12 months, p < 0-001).The spiral bacteria first cultured from the gastric mucosa of patients with histologically confirmed gastritis at Royal Perth Hospital in 1982' were originally named Campylobacter pyloridis,2 but the revised name is now Campylobacter pylori.3 Cpylori is highly susceptible to many antibiotics.245 We recently concluded a double blind, placebo controlled, prospective study ofpatients with duodenal ulceration and C pylori in their stomach, which included the nitroimidazole drug (tinidazole), given in addition to standard prophylaxis. We report the development of tinidazole resistance in a high proportion of the patients given tinidazole and cimetidine; the full clinical details of the study will be reported elsewhere. Some patients remained unhealed after 10 weeks of treatment and were then entered into an open study of various antibacterial regimens. Colloidal bismuth subcitrate (CBS) has a powerful bactericidal action against C pylori; the minimum inhibitory concentration of bismuth of C pylori is 8 mg/I,5 and ultrastructural studies of the gastric mucosa 75 minutes after administration of CBS have shown that most bacteria seem to have been killed.

Antibody to Campylobacter pyloridis was measured by ELISA in the sera of 160 patients from whom gastric biopsy specimens were also obtained. The antigen was an acid-glycine extract of C. pyloridis, and titers ranged from 80 to 22,000 ELISA units (EU). Of 117 patients in whom C. pyloridis was detected microbiologically or histologically, 87 (74%) had a titer greater than or equal to 300 EU, and only one had a titer less than 150 EU. Of 43 patients in whom C. pyloridis was not detected, only two (5%) had a titer greater than 300 EU. Thus, for a titer of 300 EU the ELISA test had a specificity of 97% and a sensitivity of 81%. At 150 EU the specificity was 78%, and the sensitivity was 99%. Histological diagnosis of active chronic gastritis was associated with a high median ELISA titer (485 E), chronic gastritis with a much lower titer (150 EU), and normal histology with a titer of 110 EU. Discriminating use of this serological test could be of assistance to detect C. pyloridis in the gastric mucosa.

The minimum inhibitory and bactericidal concentrations of twenty-two antibiotics, in liquid and solid media, and three anti-peptic ulcer drugs in liquid media were determined against twenty isolates of Campylobacter pyloridis. Camp. pyloridis was very susceptible to most antibiotics, more so than Camp. jejuni and Camp. fetus, but was resistant to nalidixic acid. The MIC90 of cimetidine against Camp. pyloridis was 512 mg/l, and of ranitidine was 6400 mg/l. The difference in susceptibility patterns between Camp. pyloridis and other campylobacters may indicate that Camp. pyloridis is not a member of the Campylobacter genus.