DefinitionThis section has been translated automatically.
The genus Streptococcus consists of numerous species of gram-positive cocci, which are stored in chains or pairs. It is composed of species that are mostly part of the normal flora of human skin and mucosa, and which predominantly have a beneficial effect on host physiology. Group A streptococci are common colonizers of the pharynx (in 15-20% of children), and group B streptococci frequently colonize the lower gastrointestinal tract.
Human pathologically significant are mainly groups A (Streptococcus pyogenes) and groups B (Streptococcus agalactiae) as well as groups C, F and G. The cell wall of beta-hemolytic streptococci shows the typical structure of gram-positive bacteria. Besides the C-substance (C=engl. carbohydrate), S. pyogenes has additional cell wall components that are necessary for its virulence:
- M-protein, a highly variable fibrillar surface protein. The M protein has a highly specific toxicity to granulocytes and platelets. Due to its different antigenicity, > 80 variants can be distinguished. The M protein has a sequence homology to keratin 17, which could play a role in streptococcal-induced infectious allergic dermatoses (e.g. in psoriasis vulgaris).
- Protein F may function as an adhesin.
- The bound C5a peptidase protects the microorganism from the immune system by cleaving opsonins.
- Hyaluronidase, streptodornase, streptokinase, pyrogenic proteases (Streptococcal pyrogenicexotoxin, SPE-A and SP-E), promote diffuse uninhibited progression of infection in tissues (e.g., in phlegmonous processes) as so-called "spreading factors".
- Erythrogenic toxins (ET -A, B, C): When colonized in wound cavities, foreign bodies, or on the skin, uninhibited formation of erythrogenic toxins (ET -A, B, C) may occur because the body's immune defenses cannot access them in this case. ET-A and ET-C lead to the classic exanthema in scarlet fever and streptococcal toxic shock syndrome (STSS).
General definitionThis section has been translated automatically.
The classification is based on different biochemical criteria:
Hemolysis behavior on blood agar (alpha, beta, gamma):
-
alpha-hemolysis (greening streptococci): incomplete hemolysis by reduction of hemoglobin to biliverdin-like substances. Among the alpha-hemolytic streptococci there are two clinically significant pathogens
:Streptococcus pneumoniae or pneumococci (diplococci!) and Streptococcus viridans (a representative of the viridans group is Streptococcus sanguinis, a facultative anaerobic germ of the oral flora)
. - beta-hemolysis: hemolysis yard around colonies (strepotococci secrete hemolysins that completely dissolve erythrocytes). Typical representative is Streptococcus pyogenes.
- gamma-hemolysis: no hemolysis activity.
Lancefield typing of beta-hemolytic stre ptococci: Beta-hemolytic streptococci are further subdivided according to the Lancefield classification. This classification, which dates back to biologist Rebecca C. Lancefield in 1933, distinguishes > 20 groups of streptococci. It is based on the serological detection of the different antigenicity of the C-substance, a cell wall polysaccharide in the bacterial wall. According to Lancefield, the individual serogroups are named with capital letters (groups A-T). Streptococci of serogroup A(Streptococcus pyogenes) occur in more than 80 variants due to the different antigenicity of the M protein. This classification does not apply to viridans streptococci ("oral streptococci"). They are predominantly α-hemolytic and usually lack the corresponding polysaccharides that act as antigens. Streptococcus agalactiae has the B antigen of the C substance. The bacteria are infectious agents in animals (udder infections in cows). In humans, this streptococcal species occurs as a colonizer of the intestinal tract and vagina. It can be transmitted perinatally and lead to invasive infections.
"Antibiotic susceptibility" is of great importance in the clinical evaluation of a streptococcal infection. Streptococci are (in Germany) mostly sensitive to penicillin G. Other common antibiotics for the treatment of streptococcal infections are aminopenicillins (ampicillin and amoxicillin), macrolides (e.g. erythromycin) and cephalosporins (e.g. ceftriaxone or cefuroxime).
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PathogenThis section has been translated automatically.
Gram-positive cocci growing in chains under aerobic and anaerobic conditions (facultative anaerobic). The grouping of beta-hemolytic streptococci according to the classification published and named by Rebecca Lancefield in 1933 was based on different specific carbohydrate antigens(C-substance - C= carboanhydrate) of the cell wall.
The genus Streptococcus is composed of numerous species, most of which belong to the normal flora of human skin and mucosa. Group A streptococci are frequent colonisation germs of the pharynx (in 15-20% of children), group B streptococci frequently colonise the lower gastrointestinal tract.
Human pathologically significant are mainly groups A (Streptococcus pyogenes) and groups B (Streptococcus agalactiae) as well as groups C, F and G. The cell wall of beta-hemolytic streptococci shows the typical structure of gram-positive bacteria.
In addition to the C substance, S. pyogenes has additional cell wall components that are necessary for its virulence:
- M-protein, a highly variable fibrillar surface protein. The M protein has a highly specific toxicity to granulocytes and platelets. Due to its different antigenicity, > 80 variants can be distinguished. The M protein has a sequence homology to keratin 17, which could play a role in streptococcal-induced infectious allergic dermatoses (e.g. in psoriasis vulgaris).
- Protein F may function as an adhesin.
- The bound C5a peptidase protects the microorganism from the immune system by cleavage of opsonins.
- Hyaluronidase, streptodornase, streptokinase, pyrogenic proteases (Streptococcal pyrogenicexotoxin , SPE-A and SP-E), as so-called "spreading factors" promote the diffuse uninhibited progression of the infection in the tissue (e.g. in phlegmonous processes).
- Erythrogenic toxins (ET -A, B, C): In case of colonisation in wound cavities, foreign bodies or on the skin, an uninhibited formation of erythrogenic toxins (ET -A, B, C) can occur, since the body's own immune defence has no access to them. ET-A and ET-C lead to the classic exanthema in scarlet fever and streptococcal toxic shock syndrome (STSS).
Clinical pictureThis section has been translated automatically.
- Diseases caused by streptococci:
- Subacute bacterial endocarditis
- Caries (Streptococcus mutans, see below Oral streptococci)
- Subungual splinter hemorrhages (as a sign of streptococcal sepsis)
- Osler's nodules
- Janeway's spots
- Impetigo contagiosa, small vesicular
- Streptococcal dermatitis, perianal
- Scarlet fe ver:scarlet angina caused by S. pyogenes strains producing a pyrogenic ("erythrogenic") exotoxin.
- Skin infections: Typical representative is erysipelas (group A), besides superficial skin infections such as pyoderma, e.g. impetigo contagiosa.
- Necrotizing fasciitis: infiltrating inflammation caused by S. pyogenes alone or together with other germs with rapidly progressive necrosis of skin, subcutis, adjacent fascia and muscles.
- Streptococcal toxicshocksyndrome s.a.: Caused by pyrogenic exotoxins produced by certain streptococci. Preceded by severe soft tissue infection. Clinical picture with severe pain, high fever and erythema, followed by hypotension, symptoms of shock and multiple organ symptoms.
- Pharyngitis, angina, tonsillitis...
- Urethritis, bacterial
- Streptococcal allergic secondary diseases:
- Vasculitis, leukocytoclastic (non-IgA-associated)
- Acute rheumatic fever (only after streptococcal pharyngitis or angina) with erythema marginatum rheumaticum
- erythema nodosum
- acute poststreptococcal glomerulonephritis.
DiagnosisThis section has been translated automatically.
Fact Sheet:
Defin: Large group of bacteria with human and animal pathogenic representatives. The classification is based on various biochemical criteria:
-
Hemolysis behavior on blood agar (alpha, beta, gamma):
- alpha-haemolysis (greening streptococci): incomplete haemolysis by reduction of haemoglobin to biliverdin-like substances.
- beta-haemolysis: haemolysis around colonies
- gamma-hemolysis: no hemolysis activity.
-
Lancefield typing (of beta-hemolytic streptococci):
- Beta-hemolytic streptococci are further subdivided according to the Lancefield classification. This goes back to the biologist Rebecca C. Lancefield in 1933. It distinguishes more than 20 groups of streptococci; based on serological evidence of differential antigenicity of C-substance, a cell wall polysaccharide in the bacterial wall.
- According to Lancefield, the individual serogroups are named with capital letters (groups A-T). Streptococci of serogroup A (Streptococcus pyogenes) occur in more than 80 variants due to the different antigenicity of the M-protein.
- This classification is not used for viridans streptococci ("oral streptococci"). They are predominantly α-hemolytic, usually lacking the corresponding polysaccharides that act as antigens.
- Streptococcus agalactiae has the B antigen of the C substance. The bacteria are infectious agents in animals (udder infections in cows). In humans, this streptococcal species occurs as a colonizer of the intestinal tract and vagina. It can be transmitted perinatally and lead to invasive infections.
- Clin:
- Diseases caused by streptococci:
- Impetigo contagiosa, small vesicular
- caries(oral streptococci especially S. mutans)
- Streptococcal dermatitis, perianal
- Scarlet fever: infection by S. pyogenes strains producing a pyrogenic ("erythrogenic") exotoxin.
- Skin infections: Typical representative is erysipelas (group A), besides superficial skin infections such as pyoderma, e.g. impetigo contagiosa.
- Necrotizing fasciitis: infiltrating inflammation caused by S. pyogenes alone or together with other germs with rapidly progressive necrosis of skin, subcutis, adjacent fascia and muscles.
- Streptococcal toxicshocksyndrome s.a.: Caused by pyrogenic exotoxins produced by certain streptococci. Preceded by severe soft tissue infection. Clinical picture with severe pain, high fever and erythema, followed by hypotension, symptoms of shock and multiple organ symptoms.
- Pharyngitis, angina, tonsillitis...
- Urethritis, bacterial
- Streptococcal allergic sequelae:
- Vasculitis, leukocytoclastic (non-IgA-associated)
- Acute rheumatic fever (only after streptococcal pharyngitis or angina)
- acute poststreptococcal glomerulonephritis
- erythema nodosum
- purpura fulminans
- vasculitis allergica
- Acute episode of psoriasis
- Diseases caused by streptococci:
TherapyThis section has been translated automatically.
Note(s)This section has been translated automatically.
In daily paxis, a classification based on hemolysis behavior, antigenic structure, and oxygen demand has proven useful: A distinction is made:
- Pyogenic haemolytic streptococci
- Oral streptococci
- Pneumococci
- Streptococcus agalactiae (B streptococci)
- other streptococci (Streptococcus dysgalactiae , Abiotropha, Grannuliacatella)
LiteratureThis section has been translated automatically.
- Angel CS et al (1994) Degradation of C3 by Streptococcus pneumoniae. J Infect Dis. 170:600-608.
- Barlow T (1883) Erythema marginatum. Br Med J 509
- Chockalingam A et al (2004) Rheumatic heart disease occurrence, patterns and clinical correlates in children aged less than five years. J Heart Valve Dis 13: 11-14
- Jedrzejas MJ (2004) Extracellular virulence factors of Streptococcus pneumoniae. Front Biosci 9:891-914. review.
- Kadavath S et al.(2015) Adult-onset Still's disease-pathogenesis, clinical manifestations, and new treatment options. Ann Med 47:6-14
- Lähteenmäki K et al (2001) Bacterial plasminogen activators and receptors. FEMS Microbiol Rev 25:531-552.
- Lehndorff H, Leiner C (1922) Erythema annulare. Z Kinderheilkd (Berlin) 32: 46
- Martin WJ et al (2015) Post-infectious group A streptococcal autoimmune syndromes and the heart.Autoimmune Rev 14:710-725.
- Nitsche-Schmitz DP et al (2007) Group G streptococcal IgG binding molecules FOG and protein G have different impacts on opsonization by C1q. J Biol Chem 282:17530-17536.
- Rullan E et al (2001) Rheumatic fever. Curr Rheumatol Rep 3: 445-452.
- Schäkel K et al (2016) Pathogenesis of psoriasis. Dermatologist 67: 422-432
- Timmer AM et al (2009) Streptolysin O promotes group A Streptococcus immune evasion by accelerated macrophage apoptosis. J Biol Chem 284:862-871.
- Walz B et al. (2015) Fever, skin changes, myalgia--from early symptom to diagnosis. Dtsch Med Wochenschr 140:1137-1144.
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