The association between Campylobacter jejuni infection and Guillain-Barr6 syndrome was investigated serologically in a retrospective study of 56 patients admitted to this hospital over four years. Evidence of preceding C jejuni infection was found in 21 (38%) of these patients, indicating that C jejuni was the most common single identifiable pathogen precipitating the disease. Among those patients who had presented with preceding diarrhoea the serum antibody response was similar to that in uncomplicated C jejuni enteritis. Patients with serological evidence of preceding C jejuni infection manifested a significantly more severe form of the disease. In cerebrospinal fluid the predominant specific antibody class was IgG, and this was closely related to the serum titres of specific IgG. IgA and IgM specific antibodies were found only in the cerebrospinal fluid of patients with recent C jejuni infection.These findings support the possibility that humoral immune factors are responsible for the neural damage and demyelination seen in Guillain-Barre syndrome.

Antibody response to Campylobacter pylori was measured in ethnic groups of Vietnamese, El Salvadorean and Ethiopian origin. The results were compared with the previously reported antibody titres found in sera of culture positive and culture negative patients, patients suffering from duodenal ulcer, white Australian blood donors and Australian Aboriginals. While in Vietnamese the prevalence of serologically positive sera was found to be similar to the white Australian population, numbers of serologically positive sera in El Salvadorean and Ethiopian ethnic groups was found to be very high. The high incidence of serologically positive sera in the Ethiopians correlated with the reported high incidence of duodenal ulcer in this population.

No abstract

A solid-phase enzyme immunoassay method for the measurement of total and class-specific serum antibodies to Campylobacterjejuni was developed. The test was found to be both sensitive and specific. Immunoglobulin M, G, and A antibodies were detected in about 90% of sera collected from patients recovering from Campylobacter enteritis, with the pattern of appearance and decline of these antibodies conforming to that usually seen in an acute infection. A poor antibody response was noted in patients with intermittent or prolonged enteritis. The clinical implications and diagnostic value of this test are discussed.

The association between duodenal ulcer, gastritis and gastroduodenal colonization with Campylobacter pylori suggests a causal role for this newly described bacterium. In an attempt to challenge the verity of this association we studied a group of people in whom duodenal ulcer is apparently absent. Serological evidence of infection was sought with a sensitive, specific ELISA assay for C. pylori specific IgG and was compared with results from control sera from teenagers referred for respiratory viral serology, volunteer blood bank donors, patients with duodenal ulcers and patients in whom the presence or absence of C. pylori had been determined by histological and microbiological examination of gastric tissue. A relatively isolated group of Australian Aborigines in whom peptic ulceration is virtually unknown, was observed to possess age-specific mean C. pylori antibody levels comparable those found in a group of white Australian dyspeptic patients without microbiological evidence of infection with this organism. The antibody levels of Aborigines were lower than those found in an aged-matched group of 'healthy' white Australians, both of these groups having levels which were significantly lower than the levels found in culture positive white Australian dyspeptic patients. It was found that 21/144 'healthy' white Australians (14.6%) had antibody levels greater than or equal to the lower 99% confidence interval of the mean level found in culture positive patients, while only 2/274 Aborigines (0.7%) had such elevated levels. By contrast, 89/142 (62.7%) patients with endoscopically proven duodenal ulcer had similarly elevated specific antibody levels. These differences were highly significant. We consider these findings to be consistent with the hypothesis that C. pylori is important in the pathogenesis of duodenal ulcer.