Pathogenesis of Campylobacter fetus Infections

We developed a mouse model to compare the virulence of Campylobacter fetus strains with (S-plus) and without (Sminus) surface array protein (S-protein) capsules. In adult HA/ICR mice pretreated with ferric chloride, the LDF0 for S-plus strain 84-32 was 43.3 times lower than its spontaneous S-minus mutant 84-54. Seven strains of inbred mice were no more susceptible than the outbred strain. In contrast to the findings with Salmonella typhimurium by others, 3 X 107 CFU of strain 84-32 caused 90% mortality in C3H/HeN (LPS) mice and 40% mortality in C3H/HeJ (LPSd) mice. High-grade bacteremia in HA/ICR mice occurred after oral challenge with S-plus C. fetus strains and continued for at least 2 d, but was not present in any mice challenged with S-minus strains. Bacteremia at 30 min after challenge was 51.6-fold lower in mice pretreated with 10 ul of rabbit antiserum to purified S-protein than after pretreatment with normal rabbit serum. Challenge of mice with a mixture of S-minus strain 84-54 and free S-proteins at a concentration 31.1-fold higher than found in wildtype strain 84-32 caused 30% mortality, compared with 0% with strain 84-54 or S-protein alone. These findings in a mouse model point toward the central role of the S-protein in the pathogenesis of C. fetus infection. The S-protein is not toxic per se, but enhances virulence when present on the bacterial cell surface as a capsule. (J. Clin. Invest. 1990. 85:10361043.) surface array proteins C. fetus animal model * C. fetus infection * C. fetus bacteremia * C. fetus virulence factor