Related Experiment Video
Updated: Aug 9, 2026

Assessing Bacterial Invasion of Cardiac Cells in Culture and Heart Colonization in Infected Mice Using Listeria monocytogenes
Published on: May 27, 2015
Cardiotoxic and Lethal Effects of Listeria monocytogenes Hemolysin
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.
Abstract:
Cardiotoxic and lethal effects of Listeria monocytogenes hemolysin were studied in CD-1 mice injected with varying doses of hemolysin. Intravenous injection of 100 complete hemolytic units (CHU) caused 100% lethality within 4 to 5 min. Doses ranging from 40 to 50 CHU caused death of approximately 50% of the animals. Adrenergic blocking agents and antihistamine failed to protect mice against lethality and thereby suggested that death was not due to release of vasoactive agents by hemolysin. Plasma levels of creatine phosphokinase increased after intravenous administration of hemolysin and suggested myopathy, possibly of the myocardium. Electrocardiograms from hemolysin-treated mice indicated serious alterations in heart rate and rhythm, suggesting damage to contractile and pacemaker cardiac tissue. In addition, there were indications of increased potassium levels influencing the heart. Presumably, death was due to functional damage to heart muscle and electrical arrest. The cardiotoxic and lethal effects could be prevented by prior incubation of hemolysin with cholesterol, heating, or failure to reactivate the preparation with cysteine.
Related Concept Videos
Hypersensitivity Reactions: Cytolytic Reactions
Cellular Injury IV: Necrosis
Myocarditis I: Introduction
Bacterial Toxins
Inhalation Anthrax
Bacterial Gastroenteritis

