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J Med Microbiol 56 (2007), 1005-1010; DOI: 10.1099/jmm.0.47043-0
© 2007 Society for General Microbiology
ISSN 1473-5644

Polysaccharides and virulence of Burkholderia pseudomallei

M. Sarkar-Tyson1, J. E. Thwaite1, S. V. Harding1, S. J. Smither1, P. C. F. Oyston1, T. P. Atkins1 and R. W. Titball1,2

1 Defence Science and Technology Laboratory, Porton Down, Salisbury SP4 0JQ, UK

2 Department of Infectious and Tropical Disease, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK

Correspondence
M. Sarkar-Tyson
mstyson{at}dstl.gov.uk

Received 1 November 2006
Accepted 6 March 2007

Burkholderia pseudomallei is the causative agent of melioidosis, an infectious disease of humans and animals. Gene clusters which encode capsular polysaccharide (type I O-PS) and LPS (type II O-PS), both of which play roles in virulence, have previously been identified. Here, the identification of two further putative clusters, type III O-PS and type IV O-PS, is reported. Mice challenged with type III O-PS or type IV O-PS mutants showed increased mean times to death (7.8 and 11.6 days) compared to those challenged with wild-type B. pseudomallei (3 days). To investigate the possible roles of polysaccharides in protection, mice were immunized with killed cells of wild-type B. pseudomallei or killed cells of B. pseudomallei with mutations in the O antigen, capsular polysaccharide, type III O-PS or type IV O-PS gene clusters. Immunization with all polysaccharide mutant strains resulted in delayed time to death compared to the naïve controls, following challenge with wild-type B. pseudomallei strain K96243. However, immunization with killed polysaccharide mutant strains conferred different degrees of protection, demonstrating the immunological importance of the polysaccharide clusters on the surface of B. pseudomallei.

Abbreviations: i.p., intraperitoneal; MTTD, mean time to death.






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