Serum and stool samples were collected from 128 individuals: 96 diarrhea patients and 32 apparently healthy controls. Stool specimens were cultured for enteric bacterial pathogens, while sera were screened by enzyme-linked immunosorbent assay for Campylobacter jejuni-reactive antibodies. Of 28 diarrhea patients who demonstrated C. jejuni-reactive antibodies (titers, >100), 14 were culture positive for this organism. The 32 healthy controls showed significantly lower antibody titers (P < 0.05) with the exception of 10 subjects who were culture positive for C. jejuni and had reactive immunoglobulin M (IgM) (6 subjects) and IgG (7 subjects). IgA was not detected in those 10 individuals (asymptomatic). Avidity was expressed as the thiocyanate ion concentration required to inhibit 50% of the bound antibodies. The avidity was higher in symptomatic patients than asymptomatic healthy controls. IgG was less avid (0.92 M) compared to IgM (0.1 M) and IgA (1.1 M), with no correlation between antibody titer and avidity. However, the thiocyanate ion concentration required for the complete inhibition of IgG (5 M)-bound antibodies was higher than that of IgA (2 M) and IgM (3 M). This study also shows that C. jejuni antibodies were variably cross-reactive with Escherichia coli, Shigella flexneri, Shigella sonnei, and Neisseria meningitidis in addition to Campylobacter coli and Campylobacter rectus. Campylobacter jejuni is among the most common bacterial causes of acute diarrheal disease in the world (4). Sequelae of the disease may include lymphadenitis, cystitis, cholecystitis, pancreatitis, hepatitis, hemolytic uremic syndrome, peritonitis, erythema nodosum, septic arthritis, osteomyelitis, septic abortion, and Guillain-Barré syndrome (20). Several lines of evidence suggest that protective immunity can be developed against this pathogen. Spreeuwel et al. (26) and Blaser and Duncan (5) reported the presence of specific serum immunoglobulin M (IgM), IgG, and IgA in acute Campylobacter intestinal disease. Both IgM and IgG persisted for 3 months or more, whereas IgA remained elevated for 1 month or less. Healthy individuals with occupational exposure to C. jejuni produced IgM without overt disease (28). Although much information exists on the microbial characteristics of C. jejuni and disease transmission, little is known about the immune response to this infection. Blaser and coworkers (6) found IgG titers greater than 1:32 by the immunofluorescence technique in sera from convalescent subjects with positive stool cultures, whereas sera from healthy control individuals showed titers of 1:2 to 1:16. However, antibody elevation in a disease process may mediate a variety of effector mechanisms that are dependent on specificity, avidity, and affinity and may be determined largely by class or subclass and site of action (16). Many host defenses, including complement activation (25), immune elimination (2), and neutralization (3) are affected by the avidity of the participating antibody (8).