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Streptococci have more than 20 soluble antigens, enzymes, and toxins that contribute in the pathogenesis of various stages of streptococcal diseases.
Streptococci produce a wide range of virulence factors respon-sible for the disease, which include the following (Table 24-2):
1. Cell wall associated proteins and polymers
These include capsule, teichoic acid, M protein, and F protein that contribute to pathogenesis of diseases in various ways as mentioned in Table 24-2.
Capsule: The cell wall of theStreptococcusis surrounded by acapsule. The capsule is nonantigenic and weakly antiphagocytic. It acts like a barrier between the complement proteins bound to the bacteria and the phagocytic cells, thereby preventing phagocytosis of the bacteria. Capsulated strains that are rich in M proteins are highly pathogenic.
Teichoic acid, M protein, and F protein: Lipoteichoic acid andF proteins mediate the binding of the cocci with fibronectin present on the host cell surface. M protein is an adhesin and antiphagocytic, which inactivates C3b—an important complement factor responsible for phagocytosis.
Streptokinase: This enzyme is produced byS. pyogenesas wellas by group C and G streptococci. Two types of streptokinase have been described—streptokinase A and B. Streptokinase activates plasminogen to form plasmin, which breaks down the fibrin barrier around the infected site, thereby facilitating the spread of the infection. This thrombolytic property is made good use of in medical management of myocardial infarction. Antibodies appear against streptokinase (A and B) during the course of infection and are diagnostic.
Deoxyribonucleases: Four types of deoxyribonucleases havebeen described—deoxyribonucleases A, B, C, and D. Most strains ofS. pyogenes produce these enzymes. The enzyme depolymerizes free DNA present in the pus, thereby reduces viscosity of pus and helps in spread of the infection. The enzymes are antigenic, and the demonstration of antideoxyribonuclease B antibody in serum is diagnostic of S. pyogenes infections, particularly of skin infections.
Hyaluronidase: The enzyme is produced byS. pyogenesas wellas by other groups like B, C, G streptococci, Streptococcus suis, Streptococcus anginosus, and S. pneumoniae. The enzyme splitshyaluronic acid present in host connective tissue, thereby facilitating spread of the bacteria through tissues. The enzyme is antigenic.
Serum opacity factor: This is a lipoproteinase produced bysome M types of S. pyogenes. This enzyme produces opacity when applied to agar gel containing swine or horse serum, hence is known as serum opacity factor (SOP). SOP is antigenic.
Other enzymes: These include neuraminidase, amylase,esterase, lipase, and beta-glucuronidase.
Streptococcal pyrogenic exotoxins (SPEs): Streptococcalpyogenic exotoxin, otherwise called erythrogenic toxins, are of three types: Spes A, Spes B, and Spes C.
· These toxins are antigenic, and their production is regulated by a temperate phage in their genome.
· These toxins act as superantigen and are responsible for scarlet fever and streptococcal toxic shock syndrome.
Dick test: The susceptibility of a person to these toxins isdetermined by performing a skin test known as Dick test. In this test, 0.2 mL of the diluted toxin is injected intradermally. In a positive test, a localized erythematous reaction, around 1 cm in diameter, develops within 12–24 hours. A positive test indicates absence of antibodies against the toxin and shows susceptibility to the toxin and thus to scarlet fever. No reaction takes place in a negative test, which indicates the presence of specific antibodies against erythrogenic toxin in the serum.
Schultz Charlton test: Intradermal injection of antitoxin in apatient with scarlet fever causes local blanching of the rash. This is due to neutralization of erythrogenic toxin. This test is known as Schultz Charlton test.
Hemolysins: Two types of hemolysins, oxygen-labile streptolysinO (SLO) and oxygen-stable and serum-soluble streptolysin S (SLS), are produced by S. pyogenes.
Streptolysin O: SLO is an oxygen-labile and heat-labile proteinwith a molecular weight of 50,000–75,000 Da. It causes beta-hemolysis only when colonies are grown under the surface of blood agar plate.
· It is antigenic, and antibodies (ASLO) against it develop in group A streptococcal infection.
· Demonstration of ASLO antibodies is important for the determination of a recent group A streptococcal infection and also the late complications of streptococcal infections after the organisms have been eliminated from the host.
The SLO cross-reacts with similar hemolysins produced by streptococci of groups C and G, pneumolysins of S. pneumoniae, tetanolysin of Clostridium tetani, theta toxin of Clostridium per-fringens, cereolysin of Bacillus cereus, and listeriolysin of Listeria monocytogenes.
Streptolysin S: SLS is a serum-soluble (hence named as S) andoxygen-stable protein. It is a small polypeptide of 20,000 Da and is nonantigenic. Hence, no antibodies against this toxin are demonstrated in serum. This toxin:
· Is responsible for hemolysis around the colonies grown on surface of the blood agar.
· Inhibits chemotaxis and is antiphagocytic.
Pyrogenic exotoxins: There are two types of exotoxins—exotoxin A and B.
· Pyrogenic exotoxin A is similar to that of staphylococ-cal toxic shock syndrome toxin (TSST). It has the same mode of action as staphylococcal TSST. It acts by releas-ing large amounts of cytokines from helper T cells and macrophages.
· Pyrogenic exotoxin B is a protease that rapidly destroys tissuesand is produced in large amount by S. pyogenes.
S. pyogenes produces suppurative as well as nonsuppurativestreptococcal diseases by following mechanisms:
1. Adherence: Adherence ofS. pyogenesto surface of hostcells is the first stage in pathogenesis of the disease. The cocci adhere to the epithelium of the pharynx with the help of pili, lipoteichoic acid, F proteins, and M proteins. Initially, adherence is mediated by a weak binding between lipoteichoic acid and fatty acid of the cocci with fibronec-tin of epithelial cells of the host. Subsequently, a strong binding is established by M protein, F protein, and other adhesins of the cocci.
2. Invasion by the cocci: S. pyogenesinvades into epithelialcells mediated by M protein, F protein, and other antigens of the cocci. Invasion of the cocci is suggested to be respon-sible for the persistence of infection, such as streptococ-cal pharyngitis, as well as for invasion into deep tissues.
3. Hyaluronic acid capsule, M protein, and C5a peptidase of S. pyogenes are antiphagocytic. These factors prevent opso-nization and phagocytosis of bacteria in many ways.
· The capsule prevents phagocytosis of the bacteria by acting as a barrier between bacteria and cell.
· The M protein inactivates C3b, an important comple-ment factor that mediates phagocytosis of bacteria.
· The M protein also binds to the fibrinogen and blocks the activation of complement by alternate pathway, thereby reducing the amount of C3b production.
· The C5a peptidase inactivates the complement compo-nent C5a, which mediates chemotaxis of neutrophils and phagocytes.
4. Production of toxins and enzymes: S. pyogenesthen pro-duces a wide variety of toxins and enzymes that contribute to pathogenesis of many streptococcal diseases.
Acquired immunity to streptococcal infection is based on the development of specific antibodies against the antiphagocytic epitopes of M protein. The acquired immunity against a particu-lar M type of streptococci lasts longer in untreated persons than in treated persons. Although such antibodies protect from infection against a homologous M protein type, they confer no immunity against other M serotypes.S. pyogenes is a highly communicable bacterium. It can cause disease in people of all ages who do not have type-specific immunity against the specific serotype.
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