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Infection and Immunity, March 2000, p. 1687-1691, Vol. 68, No. 3
0019-9567/00/$04.00+0

Roles of the Surface Layer Proteins of Campylobacter fetus subsp. fetus in Ovine Abortion

R. Grogono-Thomas,1,dagger J. Dworkin,2 M. J. Blaser,2 and D. G. Newell1,3,*

Department of Farm Animal and Equine Medicine and Surgery, Royal Veterinary College, Hertfordshire,1 and Veterinary Laboratories Agency (Weybridge), New Haw, Surrey,3 United Kingdom, and Vanderbilt University School of Medicine and VA Medical Center, Nashville, Tennessee2

Received 4 October 1999/Returned for modification 10 November 1999/Accepted 7 December 1999

The role of the surface (S)-layer proteins of Campylobacter fetus subsp. fetus has been investigated using an ovine model of abortion. Wild-type strain 23D induced abortion in up to 90% of pregnant ewes challenged subcutaneously. Isolates recovered from both dams and fetuses expressed S-layer proteins with variable molecular masses. The spontaneous S-layer-negative variant, strain 23B, neither colonized nor caused abortions in pregnant ewes. A series of isogenic sapA and recA mutants, derived from 23D, also were investigated in this model. A mutant (501 [sapA recA+]) caused abortion in one of five challenged animals and was recovered from the placenta of a second animal. Another mutant (502 [sapA recA]) with no S-layer protein expression caused no colonization or abortions in challenged animals but caused abortion when administered intraplacentally. Mutants 600(2) and 600(4), both recA, had fixed expression of 97- and 127-kDa S-layer proteins, respectively. Two of the six animals challenged with mutant 600(4) were colonized, but there were no abortions. As expected, all five strains recovered expressed a 127-kDa S-layer protein. In contrast, mutant 600(2) was recovered from the placentas of all five challenged animals and caused abortion in two. Unexpectedly, one of the 16 isolates expressed a 127-kDa rather than a 97-kDa S-layer protein. Thus, these studies indicate that S-layer proteins appear essential for colonization and/or translocation to the placenta but are not required to mediate fetal injury and that S-layer variation may occur in a recA strain.

* Corresponding author. Mailing address: Veterinary Laboratories Agency (Weybridge), New Haw, Surrey KT15 3NB, United Kingdom. Phone: (44) 1932357547. Fax: (44) 1932357595. E-mail: dnewell.cvl.wood{at}gtnet.gov.uk.

dagger Present address: Department of Clinical Veterinary Science, Bristol University, Langford, Bristol, B540 5DU United Kingdom.

Infection and Immunity, March 2000, p. 1687-1691, Vol. 68, No. 3
0019-9567/00/$04.00+0


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