Pathogenesis ofCampylobacter fetus

Campylobacter fetus has been recognized as a significant pathogen of livestock for nearly a century. The genome sequence of C. fetus subsp. fetus strain 82-40 has recently been determined. Analysis of this sequence has confirmed and extended previous observations and has also provided new insights into C. fetus metabolism, physiology, and pathogenesis. The majority of the C. fetus N-linked general glycosylation pathway genes are also found in C. fetus, although unlike in C. jejuni, the genes are arranged in multiple clusters. The major pathogenesis-related difference of C. fetus compared with C. jejuni is the presence of the C. fetus S-layer. Surface array protein, type A (SapA) lacked an amino-terminal signal sequence that would direct its secretion to the cell surface. Before this, the only surface-layer protein (SLP) that lacked a signal sequence was that of C. crescentus. Observations made during the cloning of the sapA genes were important toward understanding the mechanisms by which the expression and antigenic variation of the encoded proteins are controlled. To investigate the role of the S-layer proteins in ovine abortion, an in vivo model was developed that used pregnant ewes subcutaneously challenged with C. fetus subsp. fetus strain 23D. The outcome of the infection in terms of effects on the fetus is dependent on the interaction between the pathogen and the host response. This model also provides a context to understand the role of S-layer proteins as virulence factors in human infections.