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Updated: Aug 8, 2026

Immunolabelling Myofiber Degeneration in Muscle Biopsies
Published on: December 5, 2019
Group A streptococcal myonecrosis: increased vimentin expression after skeletal-muscle injury mediates the binding of
Amy E Bryant1, Clifford R Bayer, Jeremy D Huntington
1Veterans Affairs Medical Center, Boise, Idaho 83702, USA. amy.bryant@mindspring.com
Abstract:
Necrotizing fasciitis and myonecrosis caused by invasive infection with group A streptococci (GAS) are life-threatening conditions that have reemerged worldwide. Half of all GAS myonecrosis cases have no known portal of entry; yet, for unknown reasons, infection becomes established precisely at the site of a prior, nonpenetrating minor injury, such as a muscle strain. We hypothesized that GAS establishes infection by binding to surface molecules that are up-regulated on injured skeletal-muscle cells. Here, we isolated and identified vimentin as the major skeletal-muscle GAS-binding protein. Furthermore, we found that vimentin expression was up-regulated on injured skeletal-muscle cells in vitro and was expressed in muscle tissues from a patient with GAS myonecrosis who died of streptococcal toxic shock syndrome. These findings provide a molecular mechanism to explain the development of severe GAS soft-tissue infections at the sites of prior minor muscle trauma. This understanding may provide a basis for novel preventive strategies or therapies for patients with this devastating infection.
Insights
Group A Streptococcus (GAS) causes severe myonecrosis by binding to vimentin, a protein upregulated on injured muscle cells. This explains how GAS infections develop at minor injury sites, paving the way for new therapies.
Area of Science:
- Microbiology
- Cell Biology
- Pathology
Background:
- Invasive group A streptococci (GAS) infections, including necrotizing fasciitis and myonecrosis, are life-threatening and reemerging globally.
- A significant proportion of GAS myonecrosis cases lack a clear entry point, with infections often establishing at sites of prior minor trauma.
Purpose of the Study:
- To investigate the molecular mechanisms by which GAS establishes infection at sites of minor muscle injury.
- To identify specific skeletal muscle cell surface molecules that GAS binds to during infection.
Main Methods:
- Isolation and identification of GAS-binding proteins from skeletal muscle cells.
- In vitro assessment of vimentin expression on injured skeletal muscle cells.
- Analysis of vimentin expression in muscle tissue from a patient with fatal GAS myonecrosis.
Main Results:
- Vimentin was identified as the primary protein on skeletal muscle cells to which GAS binds.
- Vimentin expression was significantly increased on injured skeletal muscle cells in vitro.
- Vimentin was present in muscle tissue from a patient who succumbed to GAS myonecrosis and streptococcal toxic shock syndrome.
Conclusions:
- GAS utilizes vimentin, upregulated on injured muscle, as a key binding protein to initiate infection.
- This molecular interaction provides a mechanism explaining GAS soft-tissue infections at sites of prior minor muscle trauma.
- Understanding this pathway may lead to novel preventive strategies and treatments for severe GAS infections.
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