Sensitivity and specificity of serology in determining recent acute Campylobacter infection

Publisher Website
Google Scholar
Abstract
Background : The measurement of serum antibodies to Campylobacter spp. has been used to investigate links between prior Campylobacter infections and the development of Guillain−Barre syndrome and its variants. Little is known of the serum antibody response to acute infections in the short‐ or long‐term. Aims : The aims of the present study were to investigate the normal serum response to an acute Campylobacter infection and the sensitivity and specificity of anti‐Campylobacter antibodies in determining recent Campylo­bacter infection. Methods : An enzyme‐linked immunosorbent assay (ELISA) method was used to measure serum anti‐Campylobacter immunoglobulin G (IgG), IgA and IgM antibodies. Controls consisted of 420 blood donors without recent gastroenteritis, 25 patients with other gastrointestinal infections, 24 patients with neurological conditions not affecting the peripheral nerves and 19 patients with autoimmune disorders. Three patient groups were assessed: 99 patients with acute Campy­lo­bacter infections, all of whom were tested 3 weeks post‐infection; 69 of these patients tested 3−6 months later; and 74 additional patients tested>20 months post‐­infection. Western blot analysis was performed on controls and patients with high titre anti‐Campylobacter anti­bodies to assess for cross‐reactivity and specificity. Results : Following acute infections, all antibody classes rose in the majority of but not in all patients, followed by decreasing titres that did not return to baseline levels. Sixteen per cent of enteritis cases did not demonstrate a rise in titres and 9% of cases had significant levels of antibodies>20 months post‐infection. The ELISA used was shown to be highly specific for the detection of Campylobacter antibodies. Conclusion : The use of Campylobacter‐specific antibody levels as the sole marker of prior infection is an unreli­able method of determining the association between Campylobacter infection and neurological disease. (Intern Med J 2004; 34: 250−258)