Streptolysin S is a toxin produced by certain bacteria that can damage and destroy human cells. As a type of cytolysin, its actions are a primary contributor to the symptoms and severity of particular infections. The toxin’s ability to disrupt normal cellular function makes it a factor in how these diseases progress within a host.
The Bacterial Origin of Streptolysin S
The bacterium Streptococcus pyogenes, or Group A Streptococcus (GAS), produces Streptolysin S. This bacterium colonizes the skin and upper respiratory tract and is a common cause of human infections. While sometimes harmless, GAS is responsible for diseases ranging from mild conditions like strep throat (pharyngitis) and impetigo, a skin infection.
The ability of S. pyogenes to cause illness is driven by the virulence factors it produces. These are molecules that help the bacterium infect a host and evade the immune system. Streptolysin S is one of these secreted factors, contributing directly to the bacterium’s ability to cause disease.
Cellular Mechanism of Streptolysin S
Streptolysin S’s primary mechanism involves forming pores in the membranes of host cells. This damage compromises the cell’s integrity, leading to lysis, where the cell ruptures and dies. The toxin is indiscriminate in its targets and affects a broad spectrum of cell types.
The toxin targets red blood cells, a destructive process called hemolysis. It also targets various white blood cells (leukocytes), which are foundational to the immune system. By destroying these immune cells, the toxin hampers the body’s ability to mount an effective defense against the invading bacteria.
A feature of Streptolysin S is that it is non-antigenic, meaning it does not stimulate the host’s immune system to produce antibodies against it. This is due to its small size. This quality allows the toxin to continue its destructive activity without being neutralized by a specific immune response. The toxin can also act without direct bacterial attachment to the host cell.
Role in Streptococcal Diseases
The cellular damage caused by Streptolysin S leads to the symptoms of streptococcal diseases. The destruction of tissue and immune cells generates inflammation. In strep throat, for example, the toxin’s activity contributes to the sore throat, redness, and swelling by killing epithelial cells in the pharynx.
The damage caused by the toxin helps S. pyogenes multiply with less resistance from the immune system. This action is not confined to the initial site of infection. Streptolysin S facilitates the bacterium’s movement across epithelial barriers, allowing it to invade deeper tissues and enter the bloodstream, which can lead to systemic infections.
This capability is observed in invasive diseases such as necrotizing fasciitis and Streptococcal Toxic Shock Syndrome (STSS). In necrotizing fasciitis, also known as “flesh-eating disease,” the toxin’s destruction of soft tissue is part of the condition’s progression. In STSS, the systemic effects of the toxin contribute to shock and multi-organ failure.
Diagnostic and Clinical Relevance
The activity of Streptolysin S has practical applications in the clinical laboratory. Its ability to lyse red blood cells is used as a diagnostic marker to identify S. pyogenes. When the bacteria are grown on a blood agar plate, a petri dish with nutrient agar and sheep blood, they secrete the toxin. This destroys the red blood cells in the surrounding medium.
This destruction creates a clear zone around the bacterial colonies known as beta-hemolysis. This characteristic is a sign used by microbiologists to identify Group A Strep in a patient sample, like a throat swab. The visual confirmation of beta-hemolysis provides a clue for diagnosis and helps guide treatment decisions.
The non-antigenic nature of Streptolysin S has clinical implications. Unlike its counterpart, Streptolysin O, it does not elicit a measurable antibody response. For this reason, there is no standard blood test to detect antibodies against Streptolysin S, though tests exist for other streptococcal products. Treatment strategies focus on eradicating the source bacteria with antibiotics to halt toxin production, rather than neutralizing the toxin itself.