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Infection and Immunity, September 2001, p. 5471-5476, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5471-5476.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Salmonella enterica Serovar Gallinarum Requires the Salmonella Pathogenicity Island 2 Type III Secretion System but Not the Salmonella Pathogenicity Island 1 Type III Secretion System for Virulence in Chickens

Michael A. Jones,* Paul Wigley,dagger Kerrie L. Page, Scott D. Hulme, and Paul A. Barrow

Institute for Animal Health, Compton, Berkshire RG20 7NN, United Kingdom

Received 30 March 2001/Returned for modification 2 May 2001/Accepted 15 June 2001

Salmonella enterica serovar Gallinarum is a host-specific serotype that causes the severe systemic disease fowl typhoid in domestic poultry and a narrow range of other avian species but rarely causes disease in mammalian hosts. Specificity of the disease is primarily at the level of the reticuloendothelial system, but few virulence factors have been described other than the requirement for an 85-kb virulence plasmid. In this work, by making functional mutations in the type III secretion systems (TTSS) encoded by Salmonella pathogenicity island 1 (SPI-1) and SPI-2, we investigated the role of these pathogenicity islands in interactions between Salmonella serovar Gallinarum and avian cells in vitro and the role of these pathogenicity islands in virulence in chickens. The SPI-1 mutant showed decreased invasiveness into avian cells in vitro but was unaffected in its ability to persist within chicken macrophages. In contrast the SPI-2 mutant was fully invasive in nonphagocytic cells but failed to persist in macrophages. In chicken infections the SPI-2 mutant was attenuated while the SPI-1 mutant showed full virulence. In oral infections the SPI-2 mutant was not observed in the spleen or liver, and following intravenous inoculation it was cleared rapidly from these sites. SPI-2 function is required by Salmonella serovar Gallinarum for virulence, primarily through promoting survival within macrophages allowing multiplication within the reticuloendothelial system, but this does not preclude the involvement of SPI-2 in uptake from the gut to the spleen and liver. SPI-1 appears to have little effect on virulence and survival of Salmonella serovar Gallinarum in the host.

* Corresponding author. Mailing address: Institute for Animal Health, Compton, Berkshire RG20 7NN, United Kingdom. Phone: (44)1635 578411. Fax: (44)1635 577243. E-mail: majones{at}bbsrc.ac.uk.

dagger Present address: School of Pharmacy and Pharmaceutical Sciences, De Montfort University, The Gateway, Leicester LE1 9BH, United Kingdom.

Infection and Immunity, September 2001, p. 5471-5476, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5471-5476.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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