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Polysaccharides and virulence of Burkholderia pseudomallei

M Sarkar-Tyson1, J E Thwaite1, S V Harding1

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

Journal of Medical Microbiology
|July 24, 2007
PubMed

Insights

New polysaccharide gene clusters in Burkholderia pseudomallei (the cause of melioidosis) were identified. Mutants lacking these polysaccharides showed increased survival in mice, highlighting their role in virulence and potential for vaccine development.

Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Burkholderia pseudomallei causes melioidosis, a significant human and animal infectious disease.
  • Previous research identified gene clusters for capsular polysaccharide (type I O-PS) and lipopolysaccharide (LPS, type II O-PS), both crucial for virulence.

Purpose of the Study:

  • To identify and characterize novel polysaccharide gene clusters in B. pseudomallei.
  • To investigate the role of these newly identified polysaccharides (type III O-PS and type IV O-PS) in bacterial virulence.
  • To assess the potential of these polysaccharides in developing protective immunity against melioidosis.

Main Methods:

  • Identification of two new putative polysaccharide gene clusters (type III O-PS and type IV O-PS) in B. pseudomallei.
  • Generation of B. pseudomallei mutants lacking specific O-PS or capsular polysaccharide gene clusters.
  • Virulence assessment by challenging mice with wild-type and mutant strains.
  • Immunization studies using killed bacterial cells of wild-type and mutant strains followed by challenge with wild-type B. pseudomallei.

Main Results:

  • Mice infected with type III O-PS or type IV O-PS mutants exhibited significantly longer survival times compared to those infected with wild-type B. pseudomallei.
  • Immunization with all tested polysaccharide mutant strains delayed mortality in mice challenged with wild-type B. pseudomallei.
  • Different degrees of protection were observed following immunization with distinct polysaccharide mutant strains, indicating their varied immunological significance.

Conclusions:

  • The identified type III O-PS and type IV O-PS gene clusters contribute to B. pseudomallei virulence.
  • Surface polysaccharides of B. pseudomallei play a critical role in the host immune response.
  • Targeting these polysaccharide clusters holds promise for developing effective vaccines against melioidosis.

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