Cardiotoxic and Lethal Effects of Listeria monocytogenes Hemolysin

G C Kingdon1, C P Sword

  • 1Department of Microbiology, The University of Kansas, Lawrence, Kansas 66044.

Insights

Listeria monocytogenes hemolysin causes rapid death in mice by damaging heart muscle. This cardiotoxicity, indicated by altered heart rhythms and elevated creatine phosphokinase, can be prevented by inactivating the hemolysin.

Area of Science:

  • Microbiology
  • Toxicology
  • Cardiology

Background:

  • Listeria monocytogenes produces hemolysin, a toxin with known cytotoxic effects.
  • The specific cardiotoxic mechanisms and lethal outcomes of this hemolysin require further elucidation.

Purpose of the Study:

  • To investigate the cardiotoxic and lethal effects of Listeria monocytogenes hemolysin in a murine model.
  • To elucidate the potential mechanisms underlying hemolysin-induced mortality.

Main Methods:

  • CD-1 mice were intravenously injected with varying doses of purified Listeria monocytogenes hemolysin.
  • Lethality, plasma creatine phosphokinase levels, electrocardiograms (ECG), and plasma potassium levels were monitored.
  • Mice were pretreated with adrenergic blocking agents, antihistamines, or hemolysin was incubated with cholesterol, heat-treated, or cysteine-inactivated prior to injection.

Main Results:

  • Intravenous injection of 100 complete hemolytic units (CHU) resulted in 100% mortality within 4-5 minutes.
  • Doses of 40-50 CHU caused approximately 50% mortality.
  • Increased plasma creatine phosphokinase and ECG alterations indicated myocardial damage and rhythm disturbances.
  • Adrenergic blocking agents and antihistamines did not prevent lethality.
  • Cardiotoxic effects were prevented by pre-incubation with cholesterol, heating, or failure to reactivate with cysteine.

Conclusions:

  • Listeria monocytogenes hemolysin exhibits potent cardiotoxicity and lethality in mice, likely through direct damage to cardiac muscle and pacemaker tissues.
  • The mechanism of death appears to involve functional cardiac impairment and electrical arrest, rather than the release of vasoactive agents.
  • Inactivation of hemolysin through cholesterol binding, heat, or cysteine dependency neutralizes its lethal and cardiotoxic properties.

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