Morphology and culturing. Gram-positive cocci with a diameter of 1 im that form chains (Fig. 4.3a). Colonies on blood agar (Fig. 4.3b) show ß-hemo-lysis caused by streptolysins (see below).
Fine structure. The murein layer of the cell wall is followed by the sero-group A carbohydrate layer, which consists of C substance and is covalently bound to the murein. Long, twisted protein threads that extend outward are anchored in the cell wall murein: the M protein. A streptococci are classified in serovars with characteristic M protein chemistry. Like the hyaluronic acid capsules seen in some strains, the M protein has an antiphagocytic effect.
— Streptococcus Pyogenes
— Streptococcus Pyogenes
Extracellular toxins and enzymes. The most important in the context of pathogenicity are:
■ Streptolysin O, streptolysin S. Destroy the membranes of erythrocytes and other cells. Streptolysin O acts as an antigen. Past infections can be detected by measuring the antibodies to this toxin (antistreptolysin titer).
■ Pyrogenic streptococcal exotoxins (PSE) A, B, C. Responsible for fever, scarlet fever exanthem and enanthem, sepsis, and septic shock. The pyro-genic exotoxins are superantigens and therefore induce production of large amounts of cytokines (p. 77).
^m ■ Streptokinase. Dissolves fibrin; facilitates spread of streptococci in tis-4 sues.
■ Hyaluronidase. Breaks down a substance that cements tissues together.
■ DNases. Breakdown of DNA, producing runny pus.
Pathogenesis and clinical pictures. Streptococcal diseases can be classified as either acute, invasive infections or sequelae to them.
■ Invasive infections. The pathogens enter through traumas or microtraumas in the skin or mucosa and cause invasive local or generalized infections (Fig. 4.4). The rare cases of severe septic infection and necrotizing fasciitis occur in persons with a high-risk MHC II allotype. In these patients, the PSE superantigens (especially PSEA) induce large amounts of cytokine by binding at the same time to the MHC II complex and the b chain of the Tcell receptor. The excess cytokines thus produced are the cause of the symptoms.
■ Sequelae. Glomerulonephritis is an immune complex disease (p. 113) and acute rheumatic fever may be a type II immune disease (p. 109).
Diagnosis. What is involved in diagnosis is detection of the pathogen by means of microscopy and culturing. Group A antigen can be detected using particles coated with antibodies that precipitate agglutination (latex agglutination, coagglutination). Using these methods, direct detection of A streptococci in tonsillitis is feasible in the medical practice. However, this direct detection method is not as sensitive as the culture. Differentiation of A streptococci from other b-hemolytic streptococci can be realized in the laboratory with the bacitracin disk test, because A streptococci are more sensitive to bac-itracin than the other types.
Therapy. The agents of choice are penicillin G or V. Resistance is unknown. Alternatives are oral cephalosporins or macrolide antibiotics, although resistance to the latter can be expected. In treatment of septic shock, a polyvalent immunoglobulin is used to inactivate the PSE.
— Streptococcus pyogenes Infections -
S. pyogenes (M protein, PSE, other pathogenicity factors)
Invasion via skin or mucosa
impetigo, erysipelas, cellulitis, lymphangitis, sinusitis, otitis media, tonsillitis
Anti-PSE antibodies (-)
scarlet fever (tonsillitis)
Generalized invasive infection
Anti-PSE antibodies (-) and high-risk MHC II allotype
sepsis septic shock necrotizing fasciitis
Fig. 4.4 a Pathogenesis and clinical pictures of S. pyogenes infections (simplified scheme). b Erysipelas caused by S. pyogenes.
Epidemiology and prophylaxis. Infection frequency varies according to geographical area, season, and age. Humans are the only pathogen reservoir for S. pyogenes. Transmission is by direct contact (smear infection) or droplets. The incubation period is one to three days. The incidence of carriers among children is 10-20%, but can be much higher depending on the epidemiological situation. Carriers and infected persons are no longer contagious 24 hours after the start of antibiotic therapy. Microbiological follow-up checks of patients and first-degree contacts are not necessary (exception: rheumatic history).
In persons with recurring infections or with acute rheumatic fever in their medical histories, continuous penicillin prophylaxis with a long-term penicillin is appropriate (e.g., 1.2 million IU benzathine penicillin per month).
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