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Infection and Immunity, December 2006, p. 6907-6919, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.01116-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Mutation of the Maturase Lipoprotein Attenuates the Virulence of Streptococcus equi to a Greater Extent than Does Loss of General Lipoprotein Lipidation{triangledown}

Andrea Hamilton ,1,{dagger},{ddagger} Carl Robinson,2,{dagger} Iain C. Sutcliffe,1,3 Josh Slater,4 Duncan J. Maskell,5 Nick Davis-Poynter,2 Ken Smith,2 Andrew Waller,2 and Dean J. Harrington1,6*

University of Sunderland, SR1 3SD Tyne and Wear, United Kingdom,1 Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk CB8 7UU, United Kingdom,2 Northumbria University, Newcastle upon Tyne NE1 8ST, United Kingdom,3 Royal Veterinary College, Hertfordshire AL9 7TA, United Kingdom,4 Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, United Kingdom,5 University of Bradford, West Yorkshire BD7 1DP, United Kingdom6

Received 17 July 2006/ Returned for modification 30 August 2006/ Accepted 21 September 2006

Streptococcus equi is the causative agent of strangles, a prevalent and highly contagious disease of horses. Despite the animal suffering and economic burden associated with strangles, little is known about the molecular basis of S. equi virulence. Here we have investigated the contributions of a specific lipoprotein and the general lipoprotein processing pathway to the abilities of S. equi to colonize equine epithelial tissues in vitro and to cause disease in both a mouse model and the natural host in vivo. Colonization of air interface organ cultures after they were inoculated with a mutant strain deficient in the maturase lipoprotein ({Delta}prtM138-213, with a deletion of nucleotides 138 to 213) was significantly less than that for cultures infected with wild-type S. equi strain 4047 or a mutant strain that was unable to lipidate preprolipoproteins ({Delta}lgt190-685). Moreover, mucus production was significantly greater in both wild-type-infected and {Delta}lgt190-685-infected organ cultures. Both mutants were significantly attenuated compared with the wild-type strain in a mouse model of strangles, although 2 of 30 mice infected with the {Delta}lgt190-685 mutant did still exhibit signs of disease. In contrast, only the {Delta}prtM138-213 mutant was significantly attenuated in a pony infection study, with 0 of 5 infected ponies exhibiting pathological signs of strangles compared with 4 of 4 infected with the wild-type and 3 of 5 infected with the {Delta}lgt190-685 mutant. We believe that this is the first study to evaluate the contribution of lipoproteins to the virulence of a gram-positive pathogen in its natural host. These data suggest that the PrtM lipoprotein is a potential vaccine candidate, and further investigation of its activity and its substrate(s) are warranted.

* Corresponding author. Mailing address: University of Bradford, West Yorkshire BD7 1DP, United Kingdom. Phone: 44 1274 233571. Fax: 44 1274 309742. E-mail: d.harrington{at}bradford.ac.uk.

{triangledown} Published ahead of print on 2 October 2006.

Editor: J. N. Weiser

{dagger} These two authors contributed equally.

{ddagger} Present address: Enigma Diagnostics Ltd., Tetricus Science Park, Salisbury, Wiltshire SP4 0JQ, United Kingdom.

Infection and Immunity, December 2006, p. 6907-6919, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.01116-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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