Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 191, Issue 12, Pages 2082-2089Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/430349
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Funding
- NIAID NIH HHS [R01 AI24145] Funding Source: Medline
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Campylobacter fetus causes gastrointestinal and systemic infections in humans. Although relapse is common despite antibiotic treatment, the mechanisms are not well understood. The surface-layer proteins (SLPs) of C. fetus, which are critical in virulence, undergo high-frequency phenotypic switching due to recombination of sap homologues, resulting in antigenic variation. To investigate the mechanisms involved in relapsing C. fetus infections, we compared SLP variation in 4 pairs of C. fetus strains that infect humans; initial and follow-up isolations were performed 20 days to 34 months apart. Of the 4 pairs of strains, 2 had antigenic variation, and another provided evidence for selection for SLP-positive populations. Southern hybridization indicated recombination underlying the SLP variation and up-regulation. The fourth pair had the same SLP antigenic profile and sap homologue hybridization pattern, which is consistent with latency of the original strain in a privileged locus. In total, these findings indicate that relapse may reflect at least 3 differing pathogenetic pathways.
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