Antigenic materials were extracted from Campylobacter fetus subsp. jejuni strains by heating bacterial suspensions in saline at 1000C and by exposure to ethylenediaminetetraacetic acid. The antigens were heat stable at 1000C, capable of sensitizing sheep erytnrocytes for agglutination in antisera, and able to elicit production of specific antibody in rabbits; they occurred with different immunological specificities in 23 strains. Antisera against the 23 strains could be used for discriminating among isolates of the species when the passive hemagglutination technique was used for serotyping. Three serotypes were more common than others among a collection of human isolates.

Hippurate hydrolysis tests performed on the serotype reference strains of the serotyping scheme based on thermostable antigens under development for Campylobacter jejuni showed that 42 strains were Campylobacter jejuni and 17 were Campylobacter coli. Moreover, only four (0.2%) of 2025 hippurate positive Campylobacter jejuni isolates reacted in Campylobacter coli antisera and 12 (4.3%) of the 282 Campylobacter coli reacted in Campylobacter jejuni antisera. Evidently each species has its own array of antigenic specificities. Separate schemes for serotyping Campylobacter jejuni and Campylobacter coli are advocated.

Lipopolysaccharides from phenol-water extraction of cells of Campylobacter jejuni serotype O:19 were separated into a water-soluble gel of low M(r) and a water-soluble component of high M(r). Acetic acid hydrolysis of the ketosidic linkages to lipid A furnished respectively a core oligosaccharide, the structure of which is reported herein, and an O antigenic polysaccharide. Structural investigations were performed on the O-deacetylated lipopolysaccharide of low M(r), the liberated core oligosaccharide and the various products from removal of neuraminic acid and phosphate residues, and from the Smith degradation. It is concluded that the lipopolysaccharide from the serostrain has a core region with two types of closely related oligosaccharide chains showing striking homologies with gangliosides, the first with a single N-acetylneuraminic acid residue in an outer chain resembling GM1 and the second with two N-acetyl-neuraminic acid residues with a terminal region resembling GD1a. Similar experiments were carried out on lipopolysaccharides of low M(r) from bacterial isolates OH 4384 and OH 4382 serotyped as O:19 that had been obtained from two patients who subsequently developed the Guillain-Barré syndrome. The core oligosaccharide region of lipopolysaccharide from the former isolate differed only slightly from that of the serostrain, whereas that from the latter isolate was distinctly shorter.

Complete structures, including the location of N-acetylneuraminic acid (NeuSAc) residues, were assigned for the core regions of Campylobacter jejuni serotypes 0:1, 0:4, and 0:23 and 0 : 3 6 lipopolysaccharides (LPS). In continuation of earlier studies, structure determinations of liberated oligosaccharides and, where necessary, of intact LPS, were by 'H-NMR spectroscopy, Smith degradation, chromium trioxide and enzymic degradations, in conjunction with methylation studies supported by fast-atom-bombardment mass spectrometry and linkage analyses by gas chromatography/ mass spectrometry. It was concluded on the basis of the following structures, in which each was linked 1-5 to a terminal 3-deoxy-~-manno-octu~osonic acid residue, that the core regions with qualititatively similar sugar compositions showed serotypic differences in one or more of their sequences, linkage types, and anomeric configurations : PEtn

To examine possible sources of Campylobacter pylori and to determine the routes by which it is transmitted to the human stomach, samples of dental plaque and saliva from 71 patients undergoing endoscopy in addition to stomach biopsies were collected and cultured on selective noninhibitory Skirrow medium. A total of 29 (40.8%) of the stomach biopsies yielded C. pylori. None of the saliva samples and only one of the dental plaque samples was found positive for C. pylori, and thus neither saliva nor dental plaque could be implicated as a significant reservoir of this organism.