Related Experiment Video
Updated: Sep 21, 2025

Analyzing Platelet Subpopulations by Multi-color Flow Cytometry
Published on: June 10, 2025
Group B Streptococcal Hemolytic Pigment Impairs Platelet Function in a Two-Step Process
Kristin Jahn1, Patience Shumba1, Phoenicia Quach2
1Center for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, Interfaculty Institute for Genetics and Functional Genomics, University of Greifswald, 17489 Greifswald, Germany.
Insights
Group B streptococci pigment activates and then kills human platelets, a key factor in severe infections. This finding reveals a novel mechanism for platelet destruction during GBS disease.
Area of Science:
- Microbiology and Immunology
- Hematology
Background:
- Group B streptococci (GBS) are increasingly implicated in invasive infections beyond maternal-fetal contexts, including sepsis and toxic shock syndrome.
- These severe GBS infections are frequently associated with coagulation disorders and low platelet counts (thrombocytopenia).
- GBS produce a pigment toxin with hemolytic, cytolytic, and coagulatory properties.
Purpose of the Study:
- To investigate the direct impact of the GBS pigment toxin on human platelets.
- To elucidate the mechanism by which GBS pigment affects platelet function and viability.
Main Methods:
- Exposure of human platelets to GBS expressing the pigment toxin.
- Assessment of platelet activation markers and cell death following GBS pigment interaction.
Main Results:
- Infection with pigmented GBS initially triggered activation of human platelets.
- Prolonged exposure led to necrotic cell death in the affected platelets.
- The GBS pigment toxin was identified as the causative agent for platelet demise.
Conclusions:
- The GBS pigment toxin plays a critical role in the pathogenesis of GBS-associated coagulopathies.
- GBS pigment directly induces platelet activation followed by necrotic cell death, contributing to thrombocytopenia.
- This study demonstrates that GBS pigment is a potent platelet-killing factor.
Abstract:
Group B streptococci (GBS) cause a range of invasive maternal-fetal diseases during pregnancy and post-partum. However, invasive infections in non-pregnant adults are constantly increasing. These include sepsis and streptococcal toxic shock syndrome, which are often complicated by systemic coagulation and thrombocytopenia. GBS express a hyper-hemolytic ornithine rhamnolipid pigment toxin with cytolytic and coagulatory activity. Here, we investigated the effects of GBS pigment on human platelets. Infections of platelets with pigmented GBS resulted initially in platelet activation, followed by necrotic cell death. Thus, this study shows that GBS pigment kills human platelets.
Related Concept Videos
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Structure and Function of Platelets
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
Introduction to Hemostasis
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized,...
Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
Disorders of Hemostasis
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Coagulation
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...

