Pathogenesis of Campylobacter fetus infections. Role of surface array proteins in virulence in a mouse model

Z. Pei, M. J. Blaser

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50 Scopus citations


We developed a mouse model to compare the virulence of Campylobacter fetus strains with (S-plus) and without (S-minus) surface array protein (S-protein) capsules. In adult HA/ICR mice pretreated with ferric chloride, the LD50 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(n)) mice and 40% mortality in C3H/HeJ (LPS(d)) 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 μl of rabbit antiserum to purified S-protein than after pretreatment with normal rabbit serum. Chalenge 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 wild-type 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.

Original languageEnglish (US)
Pages (from-to)1036-1043
Number of pages8
JournalJournal of Clinical Investigation
Issue number4
StatePublished - 1990
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Medicine(all)


  • C. fetus animal model
  • C. fetus bacteremia
  • C. fetus infection
  • C. fetus virulence factor
  • surface array proteins


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