Mechanisms underlying Campylobacter fetus pathogenesis in humans: Surface-layer protein variation in relapsing infections

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Abstract

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. © 2005 by the Infectious Diseases Society of America. All rights reserved.

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APA

Tu, Z. C., Gaudreau, C., & Blaser, M. J. (2005). Mechanisms underlying Campylobacter fetus pathogenesis in humans: Surface-layer protein variation in relapsing infections. Journal of Infectious Diseases, 191(12), 2082–2089. https://doi.org/10.1086/430349

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