Enzymes and Toxins of Staphylococci
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p207-208
2025-08-23
470
Enzymes and Toxins
Staphylococci can produce disease both through their ability to multiply and spread widely in tissues and through their production of many extracellular substances. Some of these substances are enzymes; others are considered to be toxins, although they may function as enzymes. Many of the toxins are under the genetic control of plasmids; some may be under both chromosomal and extrachromosomal control; and for others, the mechanism of genetic control is not well defined.
A. Catalase
Staphylococci produce catalase, which converts hydrogen peroxide into water and oxygen. The catalase test differentiates the staphylococci, which are positive, from the streptococci, which are negative.
B. Coagulase and Clumping Factor
S. aureus produces an extracellular coagulase, an enzyme like protein that clots oxalated or citrated plasma. Coagulase binds to prothrombin; together they become enzymatically active and initiate fibrin polymerization. Coagulase may deposit fibrin on the surface of staphylococci, perhaps altering their ingestion by phagocytic cells or their destruction within such cells. Coagulase production is considered syn onymous with invasive pathogenic potential.
Clumping factor is cell wall bound and is another example of an MSCRAMM (see earlier) that is responsible for adherence of the organisms to fibrinogen and fibrin. When mixed with plasma, S. aureus forms clumps. Clumping factor is distinct from coagulase. Because clumping factor induces a strong immunogenic response in the host, it has been the focus of vaccine efforts. However, no human vaccines against this factor are available to date.
C. Other Enzymes
Other enzymes produced by staphylococci include a hyaluronidase, or spreading factor—a staphylokinase resulting in fibrinolysis but acting much more slowly than streptokinase, proteinases, lipases, and β-lactamase.
D. Hemolysins
S. aureus possesses four hemolysins that are regulated by agr (see Regulation of Virulence Determinants). α-Hemolysin is a heterogeneous protein that acts on a broad spectrum of eukaryotic cell membranes. The β-toxin degrades sphingomyelin and therefore is toxic for many kinds of cells, including human red blood cells. The δ-toxin is heterogeneous and dissociates into subunits in nonionic detergents. It disrupts biologic membranes and may have a role in S. aureus diarrheal diseases. The γ-hemolysin is a leukocidin that lyses white blood cells and is composed of two proteins designated S and F. γ-Hemolysin can interact with the two proteins comprising the Panton–Valentine leukocidin (PVL; see later discussion) to form six potential two-component toxins. All six of these protein toxins are capable of efficiently lysing white blood cells by causing pore formation in the cellular membranes that increase cation permeability. This leads to massive release of inflammatory mediators such as IL-8, leu kotriene, and histamine, which are responsible for necrosis and severe inflammation.
E. Panton–Valentine Leukocidin
This toxin of S. aureus has two components, and unlike the chromosomally encoded hemolysins above, PVL is encoded on a mobile phage. It can kill white blood cells of humans and rabbits. The two components designated as S and F act synergistically on the white blood cell membrane as described for γ-toxin. This toxin is an important virulence factor in CA MRSA infections.
F. Exfoliative Toxins
These epidermolytic toxins of S. aureus are two distinct proteins of the same molecular weight. Exfoliative toxin A is encoded by eta located on a phage and is heat stable (resists boiling for 20 minutes). Exfoliative toxin B is plasmid mediated and heat labile. These epidermolytic toxins yield the generalized desquamation of the staphylococcal scalded skin syndrome by dissolving the mucopolysaccharide matrix of the epidermis. The toxins are superantigens.
G. Toxic Shock Syndrome Toxin
Most S. aureus strains isolated from patients with toxic shock syndrome produce a toxin called toxic shock syndrome toxin-1 (TSST-1), which is the same as enterotoxin F. TSST-1 is the prototypical superantigen. TSST-1 binds to major histocompatibility class (MHC) class II molecules, yielding T-cell stimulation, which promotes the protean manifestations of the toxic shock syndrome. The toxin is associated with fever, shock, and multisystem involvement, including a desquamative skin rash. The gene for TSST-1 is found in about 20% of S. aureus isolates, including MRSA.
H. Enterotoxins
There are 15 enterotoxins (A–E, G–P) that, similar to TSST 1, are superantigens. Approximately 50% of S. aureus strains can produce one or more of them. The enterotoxins are heat stable and resistant to the action of gut enzymes. Important causes of food poisoning, enterotoxins are produced when S. aureus grows in carbohydrate and protein foods. Ingestion of 25 µg of enterotoxin B results in vomiting and diarrhea. The emetic effect of enterotoxin is probably the result of central nervous system stimulation (vomiting center) after the toxin acts on neural receptors in the gut.
The exfoliative toxins, TSST-1, and the enterotoxin genes are on a chromosomal element called a pathogenicity island. It interacts with accessory genetic elements—bacteriophages— to produce the toxins.
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