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Virulence of Burkholderia pseudomallei does not correlate with biofilm formation

Suwimol Taweechaisupapong1, Cherdchai Kaewpa, Channarong Arunyanart

  • 1Department of Oral Diagnosis, Faculty of Dentistry, Khon Kaen University, Khon Kaen, 40002, Thailand. suvi_taw@kku.ac.th

Microbial Pathogenesis
|August 9, 2005
PubMed

Insights

Burkholderia pseudomallei forms more biofilm than Burkholderia thailandensis, but biofilm quantity does not correlate with virulence in mice. Biofilm likely does not play a role in melioidosis pathogenesis.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Infectious Diseases

Background:

  • Burkholderia pseudomallei causes melioidosis, a disease with poorly understood pathogenesis.
  • Biofilm formation is a virulence factor in gram-negative bacteria, aiding evasion of host defenses.
  • Previous reports suggest B. pseudomallei can form biofilms.

Purpose of the Study:

  • To quantify and compare biofilm formation between B. pseudomallei and B. thailandensis.
  • To investigate the relationship between biofilm formation and virulence in B. pseudomallei.

Main Methods:

  • Quantification of biofilm formation using a modified microtiter-plate assay.
  • Comparison of biofilm production in 50 strains of B. pseudomallei and 50 strains of B. thailandensis.
  • Assessment of virulence through LD50 determination in BALB/c mice and analysis of biofilm mutants.

Main Results:

  • B. pseudomallei exhibited significantly higher biofilm formation (P<0.01) compared to B. thailandensis.
  • Transmission electron microscopy revealed dense extracellular matrix in high-biofilm B. pseudomallei strains.
  • No correlation was found between biofilm formation capacity and LD50 values in mice.

Conclusions:

  • Biofilm formation is significantly greater in B. pseudomallei than in B. thailandensis.
  • Despite increased biofilm production, virulence did not correlate with biofilm formation.
  • These findings suggest biofilm formation may not be a significant factor in B. pseudomallei pathogenesis.

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