Staphylococcus aureus (S. aureus) causes a broad range of infections. This variety is related to a number of virulence factors that allow it to adhere to surface, invade or avoid the immune system, and cause harmful toxic effects to the host.
Why is S. aureus capable of producing wound infections?
To cause infection, a bacteria needs to first gain access to the host. This is preceded by attaching to the host cells or tissues. S. aureus has numerous surface proteins that promote attachment to host proteins such as laminin and fibronectin that form part of the extracellular matrix.
Fibronectin is also present on epithelial and endothelial surfaces and is also a part of blood clots. The bacteria have a fibrinogen/fibrin binding protein that helps them to attach to blood clots and traumatized tissue. This is the reason why S. aureus is capable of producing wound infections and post-surgery infections.
The virulence factors of Staphylococcus aureus include antigens, enzymes and toxins like:
- α –Toxin
- β –Toxin
- P-V Leukocidin
- Exfoliative Toxin
- Toxic Shock Syndrome Toxin
Adherence factors (surface proteins and antigens)
Attachment of S. aureus to the host cell surface is mediated by several adhesins. One major class of S. aureus adhesins comprises of proteins covalently anchored to cell peptidoglycans. These molecules recognize the most prominent components of the extracellular matrix or blood plasma, including fibrinogen, fibronectin, and collagens.
Typical members of the family of adhesins called MSCRAMM are staphylococcal protein A (SpA), fibronectin-binding proteins A and B (FnbpA and FnbpB), collagen-binding protein, and clumping factor (Clf) A and B proteins.
Exoproteins (enzymes, toxins and surface proteins)
These are a group of exoproteins such as exotoxins and enzymes, including nucleases, proteases, lipases, hyaluronidase, and collagenase. These proteins convert local host tissue into nutrients required for bacterial growth.
The proteins cause breakdown of the host cells and are thus said to be cytolytic. Cytolytic toxins form pores of holes called β-barrel pores in the plasma membrane. This leads to leakage of the cell’s content and lysis of the target cell.
Other toxins include α-hemolysin, β-hemolysin, γ-hemolysin, leukocidin, and Panton-Valentine leukocidin (PVL). PVL inserts itself into the host’s plasma membrane and forms a pore of a hole. PVL exhibits a high affinity toward leukocytes or white blood cells, while other toxins, γ-hemolysin and leukocidin, are cytotoxic toward erythrocytes or red blood cells and WBCs, respectively.
S. aureus produces additional group of toxins called the toxic shock syndrome toxin-1 (TSST-1). It also secretes staphylococcal enterotoxins (SEA, SEB, SECn, SED, SEE, SEG, SEH, and SEI) and the exfoliative toxins A and B (ETA and ETB). Of these TSST-1 and the staphylococcal enterotoxins are fever inducing or are called pyrogenic toxin superantigens (PTSAgs). These stimulate the proliferation of T-lymphocytes. These toxins cause toxic shock syndrome and food poisoning. Further ETA and ETB are involved in staphylococcal scalded skin syndrome (SSSS).
Effect of S. aureus on host immunity
S. aureus secretes several proteins to protect itself from the host’s innate and adaptive immune system. Some of these proteins include:
- chemotaxis inhibitory protein of S. aureus (CHIPS)
- staphylococcal complement inhibitor (SCIN)
- extracellular fibrinogen binding protein (Efb)
- staphylokinase (SAK)
- formyl peptide receptor-like-1 inhibitory protein (FLIPr)
- extracellular adherence protein (Eap)
Virulence of S. aureus
The virulence of S. aureus is multifactorial and due to the combined action of several virulence determinants. This is except toxic syndromes such as toxic shock syndrome, SSSS, and staphylococcal food poisoning, which are caused by toxic shock syndrome toxin, exfoliative toxins A and B, and different staphylococcal enterotoxins, respectively.
The virulence of the bacteria is further regulated by extracellular and cell wall components that are expressed during different stages of infection for example during avoidance of host defense, growth and cell division, and spread of the bacteria.