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Growth of Staphylococcus aureus in Diprivan and Intralipid: implications on the pathogenesis of infections

P B Langevin1, N Gravenstein, T J Doyle

  • 1Department of Anesthesiology, University of Florida College of Medicine, Gainesville, USA. anita@anest2.anest.ufl.edu

Anesthesiology
|November 7, 1999
PubMed
Abstract

Insights

Intralipid and Diprivan may increase infection risk through mechanisms beyond bacterial growth. Studies show Staphylococcus aureus replicates poorly in these agents, suggesting other factors contribute to infection.

Area of Science:

  • Microbiology
  • Immunology
  • Pharmacology

Background:

  • Intralipid and Diprivan administration is linked to increased infection incidence and severity.
  • Intralipid may suppress host immunity by inhibiting the reticuloendothelial system.
  • Diprivan is suspected to promote infection by supporting bacterial growth and increasing inoculum size.

Purpose of the Study:

  • To investigate if bacterial replication in Intralipid and Diprivan adequately explains increased infection risk.
  • To explore potential alternative mechanisms contributing to infection risk with these agents.

Main Methods:

  • Cultured Staphylococcus aureus in Intralipid and Diprivan under clinical conditions.
  • Assessed bacterial growth in Intralipid with and without EDTA.
  • Injected rabbits with S. aureus and Intralipid to evaluate infection development and bacterial load in tissues.

Main Results:

  • Staphylococcus aureus did not grow in Diprivan or Intralipid with EDTA.
  • Bacterial growth in plain Intralipid was delayed and slow, occurring after media conditioning.
  • Intralipid administration significantly increased S. aureus recovery in rabbit kidneys.

Conclusions:

  • Diprivan and Intralipid appear to be poor growth media for Staphylococcus aureus.
  • Mechanisms other than increased bacterial inoculum size likely contribute to the infection risk associated with Diprivan and Intralipid.

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