The humoral antibody response to Bacteroides fragilis infections in humans

The humoral antibody response to Bacteroides fragilis infections in humans, with particular reference to ss. fragilis, was studied using an enzyme immunosorbent assay (EIA). Phenol-water extracted polysaccharide fractions (PS) from B. fragilis ss. fragilis, ss. ovatus, ss. distasonis and ss. vulgatus were used as antigens. Antibody titer determinations were done on sera collected from 57 patients where B. fragilis had been cultured and from 50 controls. In patients with septicemia caused by B. fragilis ss. fragilis a significant titer increase (greater than or equal to doubling) against PS from strain 9343 was seen during the course of the illness. In sera from patients with appendicitis, and where B. fragilis was isolated from the appendix, a titer increase against B. fragilis ss. fragilis 9343 was observed for 6 of 17 patients. However, in sera from 9 of the 17 patients a titer increase against B. fragilis ss. ovatus was also seen. No titer increase was observed in sera from most of the patients with salpingitis where B. fragilis had been isolated. In sera from 10 patients with Crohn's disease the median antibody titer against all four B. fragilis antigens was slightly higher than in sera from the controls. The median antibody titer against B. fragilis ss. ovatus was, however, significantly higher. Our experience is that a humoral antibody response against B. fragilis ss. fragilis can be expected in patients where the organism is isolated from blood. In diseases like appendicitis and salpingitis titer increases are less common. When they occur they are not necessarily directed against ss. fragilis only but are as frequent against ss. ovatus. Titer increases against ss. vulgatus and ss. distasonis are also seen. This raises the question if the observed titer increases are a consequence of a specific pathogenic role of B. fragilis in these infections, or if they merely represent the result of an antigenic stimulus as a result of an increased permeability of the mucosal barriers caused by inflammation and/or surgical manipulation.