Morphology and cultural characteristics
Bacteria of the genus Streptococcus have the shape of slightly elongated spherical cells, 0.5–2.0 µm in size. They are non-motile (lack flagella), do not form spores, but many strains possess a capsule. The cell wall is three-layered and consists of peptidoglycan, polysaccharide, and a protein layer. An important feature is the ability to form cell-wall-deficient L-forms.
By type of respiration, they are facultative anaerobes (capnophiles are also encountered). Optimal growth conditions: temperature 35–37 °C and pH 7.2–7.4. These microorganisms are fastidious regarding nutrient media, thus they are cultivated with the addition of blood, serum, and carbohydrates.
On solid media, they form small, grayish-translucent colonies. The appearance of the colonies correlates with virulence: matt colonies contain numerous filamentous protrusions (M protein) and are more aggressive, whereas glossy colonies are less virulent. Biochemically, the pathogen ferments glucose, lactose, and other sugars to produce lactic acid, is not lysed in bile, and does not reduce nitrates.
Pathogenicity factors of serogroup A
The aggressiveness of S. pyogenes is due to the production of more than 20 extracellular substances, as well as the structural features of the cell wall.
Surface factors:
- Capsule and M protein: provide antiphagocytic activity (protection against the immune system).
- Lipoteichoic acids: are responsible for adhesion (attachment) to the epithelium.
Enzymes of aggression and invasion:
- Streptokinase (fibrinolysin): converts plasminogen to plasmin, destroying fibrin and dissolving blood clots, which helps bacteria spread.
- Hyaluronidase: a "spreading factor" that breaks down the connective tissue matrix.
- Streptodornase (DNase): liquefies pus.
- C5a peptidase: inhibits the migration of phagocytes to the focus of infection.
Exotoxins:
- Pyogenic exotoxin (erythrogenic toxin): produced by lysogenic strains, acts as a superantigen. Causes scarlet fever and toxic shock syndrome.
- Streptolysin O: oxygen-labile, destroys blood cells, highly immunogenic.
- Streptolysin S: oxygen-stable, cytotoxic, but does not induce antibody production.
Pathogenesis and clinical manifestations
Streptococcus affects any tissues (lacks organ tropism). The infection spreads via lymphatic (causing lymphadenitis) or hematogenic routes, which can lead to septicopyemia. Pathogenesis consists of three leading syndromes:
- Infectious: local inflammation (purulent, serous, necrotic) due to invasion.
- Toxic: fever, delirium, vomiting due to the action of exotoxins.
- Allergic: development of hypersensitivity to bacterial components.
It is specific sensitization (allergic syndrome) that triggers diffuse connective tissue diseases, such as acute glomerulonephritis and rheumatic fever. Chronicity of the process (chronic tonsillitis, recurrent erysipelas) is associated with the ability of bacteria to persist as L-forms.
Diagnostics and treatment
The main method of microbiological diagnostics is bacteriological. The specimen (pus, blood, sputum) is inoculated onto blood agar, followed by identification of the Lancefield serogroup and biochemical testing. Bacterioscopy is only of orientational value.
Serological methods—determining the titer of antibodies to toxins—play an important role. The main marker is Antistreptolysin O (ASO).
Treatment involves antibiotics (penicillins, macrolides, chloramphenicol), to which most strains are highly susceptible. The main therapeutic challenge lies not in pathogen resistance, but in the development of severe immunopathological disorders that require correction of the immune response (especially in rheumatic fever).
Briefly: answers to topical questions
What protein type-specific cell wall antigens does Streptococcus pyogenes possess?
Streptococcus pyogenes has two main protein type-specific cell wall antigens, upon the specificity of which the intragroup division into serovars is based. Surface proteins include:
- M protein — a thermolabile protein forming filamentous protrusions. It provides antiphagocytic activity, while strains with its high content form matt colonies and possess greater virulence.
- F protein — a fibronectin-binding protein.
What pyogenic inflammatory diseases of the skin and soft tissues does Streptococcus pyogenes cause?
Streptococcus pyogenes causes the following pyogenic inflammatory diseases of the skin and soft tissues:
- Pyoderma.
- Contagious impetigo — infection of the superficial layers of the skin; etiology is often mixed — S. pyogenes and S. aureus.
- Erysipelas — acute or chronic inflammation, hyperergic inflammation and relapses are possible.
- Phlegmon — diffuse purulent inflammation of connective tissue.
What rapid diagnostic methods exist for group A streptococcus in a throat swab?
For the rapid diagnosis of group A beta-hemolytic streptococcus in a throat swab, immunochromatographic determination of Streptococcus pyogenes antigen is used. If the rapid test is negative in patients older than 3 years, as well as in children and adolescents with suspected GAS pharyngitis, the result should be confirmed by a cultural (bacteriological) examination of throat discharge.
Invasion enzymes can be remembered by their destructive targets: Kinase dissolves blood clots (Blood), DNase liquefies pus, Hyaluronidase destroys connective tissue.
Class and exam questions
What is the difference between streptolysin O and streptolysin S?
Streptolysin O is oxygen-labile and stimulates antibody production (ASO), which is important for diagnostics. Streptolysin S is oxygen-stable, causes surface hemolysis on agar, but does not induce antibody production in the body.
What is the high virulence of streptococcal matt colonies associated with?
Matt colonies contain a large amount of M protein on their surface. This protein, in the form of filamentous protrusions, protects the bacterium from phagocytosis.
What is the main mechanism of development of rheumatic fever following streptococcal infection?
Rheumatic fever develops as part of the allergic syndrome. Hypersensitivity to bacterial components is formed, leading to immunopathological damage to the body's own tissues (heart, joints).
What else to study on this topic
- Structure and role of M protein and F protein
- Mechanism of action of pyogenic exotoxin (superantigen)
- Principles of streptococcal classification by R. Lancefield
- Process of formation and persistence of L-forms
- Features of the immune response and hypersensitivity in scarlet fever
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