1921
Volume 101, Issue 4
  • ISSN: 0002-9637
  • E-ISSN: 1476-1645
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Abstract

Abstract.

is a selective agent that causes septic melioidosis and exhibits a broad range of lethal doses in animals. Host cellular virulence and phagocytic resistance are pathologic keys of . We first proposed as the host cellular virulence model to mimic bacterial virulence against mammals and second established the resistance of to predation by as the phagocytosis model. The saprophytic sepsis–causing sp. (, , , and ) exhibited different virulence patterns in both simple models, but was the most toxic. Using both models, attenuated isolates of were selected from a transposon-mutant library and a panel of environmental isolates and reconfirmed by in vitro mouse peritoneal exudate cell association and invasion assays. The distinct pathological patterns of melioidosis were inducted by different selected isolates. Fatal melioidosis was induced by the isolates with high virulence in both simple models within 4–5 day, whereas the low-virulence isolates resulted in prolonged survival greater than 30 day. Infection with the isolates having high resistance to predation but a low killing effect led to 83% of mice with neurologic melioidosis. By contrast, infection with the isolates having low resistance to predation but high killing effect led to 20% cases with inflammation in the salivary glands. Our results indicated that individual isolates selected from simple biological models contribute differently to disease progression and/or tissue tropism.

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Supplemental Materials

  • Received : 16 Jan 2019
  • Accepted : 15 May 2019
  • Published online : 05 Aug 2019

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