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Phenotypic characteristics and pathogenic ability across distinct morphotypes of Burkholderia pseudomallei DT

Yao-Shen Chen1, Hsi-Hsun Lin, Chih-Chang Hung

  • 1Section of Infectious Disease, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.

Microbiology and Immunology
|March 24, 2009
PubMed

Insights

Burkholderia pseudomallei exhibits six colony morphotypes. Types I and III cause higher mortality and liver damage in mice, despite similar bacterial loads across morphotypes.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Infectious Diseases

Background:

  • Burkholderia pseudomallei is an opportunistic bacterial pathogen.
  • This bacterium displays significant colony morphotype variation.
  • Understanding morphotype-specific virulence is crucial for disease management.

Purpose of the Study:

  • To investigate the differential virulence and behavior of six distinct Burkholderia pseudomallei morphotypes.
  • To correlate colony morphotype with host-pathogen interactions and disease outcomes.

Main Methods:

  • Infection of mice with six distinct Burkholderia pseudomallei morphotypes.
  • Assessment of bacterial motility, bacterial association with host cells, bacterial loads in organs, mortality rates, and liver pathology.
  • Observation of morphotype switching in vivo.

Main Results:

  • Distinct morphotypes exhibited varied motility (Types III and V stronger) and host cell association (Type VI highest).
  • No significant difference in organ bacterial loads across morphotypes.
  • Types I and III infections led to significantly higher mortality (100% and 89%) and liver damage compared to other morphotypes.
  • Morphotype switching to a mucoid type was observed in vivo, but not the reverse.

Conclusions:

  • Colony morphotype is a critical factor influencing Burkholderia pseudomallei virulence and host response.
  • Specific morphotypes (I and III) are associated with increased mortality and tissue damage.
  • The observed unidirectional morphotype switching suggests a potential adaptation mechanism during infection.

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