Streptococcus pyogenes
| Streptococcus pyogenes | ||||||||||||
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Streptococcus pyogenes |
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| Scientific name | ||||||||||||
| Streptococcus pyogenes | ||||||||||||
| Rosenbach 1884 |
Streptococcus pyogenes (from Greek πύον pus - pus-causing streptococci ) is a common bacterium that can cause,among other things, scarlet fever and purulent tonsillitis or tonsillopharyngitis in humans.
properties
Streptococcus pyogenes is gram-positive , chain-forming, beta-hemolytic and pyrrolidonyl arylamidase- positive. S. pyogenes grows anaerobically but is aerotolerant; H. the bacteria grow in the presence of atmospheric oxygen, but do not need oxygen for their metabolism . The single, rounded cell has a size of 0.6 to 1 µm. S. pyogenes cannot move actively and does not form endospores . On blood agar , a nutrient medium containing blood , gray-white slimy colonies develop . According to the Lancefield scheme , which differentiates the Streptococcus species according to their C polysaccharide , S. pyogenes belongs to group A.
Pathogenesis and Diseases Caused
Streptococcus pyogenes has various virulence factors that enable the bacterium to evade the defensive reaction of the human immune system and trigger diseases. One of the most important virulence factors is the M protein , an antiphagocytotic surface protein . The hyaluronic acid capsule found in some strains has a similar effect . In addition, a C5a peptidase cleaves important signaling molecules in the complement system and thus prevents the activation of this part of the immune system.
The fibronectin- binding proteins F1 and SfbI serve the bacterium to attach to the endothelial cells and thus support its penetration into human tissue. Once there, the streptolysins O and S destroy red blood cells and other cells. The streptokinase dissolves fibrin . In addition, various enzymes such as DNAsen, proteases and hyaluronidases also help the bacterium to spread in the tissue. In order to assert itself against other bacteria, S. pyogenes also secretes bacterial toxins.
Streptococcus pyogenes causes both acute invasive infections and non-invasive sequelae. The acute infections are often accompanied by the formation of pus because of the many tissue-dissolving enzymes . One possible target is the upper respiratory tract, where tonsillitis or sore throat can develop . Impetigo , erysipelas or phlegmon can develop on the skin , depending on the depth of the infection and the immune system. If the immune system is poor, local infections can also turn into generalized infections ( sepsis ).
If the streptococcal bacterium has been infected by a virus, the prophage β, it can use the virus genome to produce a pyogenic streptococcal exotoxin (PSE). This PSE comes in three variants A, B and C, with A and C acting as superantigens . PSE B breaks down immunoglobulins . All three toxins can also cause the symptoms of scarlet fever . In an equipment of the immune system with high-risk MHCII - allotypes there may be a necrotizing fasciitis or streptococcal-induced Toxic Shock Syndrome (STSS) may occur. Around 30 percent of those suffering from the latter die of shock and multiple organ failure. Only an early diagnosis enables successful treatment.
The immunologically related secondary diseases of streptococcal infection are feared, especially acute glomerulonephritis and acute rheumatic fever . It is the acute glomerulonephritis, which occurs about three weeks after the actual infection, to be distinguished from the acute interstitial nephritis that occurs with the infection. This takes place in the context of an excessive, cell-mediated immune response as an abacterial inflammation of the kidney interstitium. In glomerulonephritis, the deposition of antigen - antibody complexes ( immune complex disease type III) causes damage to the kidneys . In acute rheumatic fever, cross-reactions between the antigens of the streptococci and the body's own structures, especially collagen IV, play a role. Inflammation occurs in the heart ( endocarditis , myocarditis , pericarditis ), in joints ( arthritis ), in the brain ( chorea minor ) and in the skin ( erythema ) or, in rare cases, in the muscles ( pyomyositis ). Nodules form in the subcutaneous tissue.
Diagnosis
Depending on the location of the disease, blood, punctures, biopsy material or pus swabs can be examined in the laboratory. The typical chains can already be recognized there under the microscope. In order to grow S. pyogenes , agar plates are used to which meat extract, blood or serum has been added. At 37 ° C and 5 to 10% carbon dioxide, colony formation can be expected within 16 to 24 hours .
To differentiate the C-polysaccharide (see above) commercially available test kits that work with antibodies can be used . The genes for the M protein (emm genes) are sometimes also examined for scientific purposes .
If a rheumatic fever caused by S. pyogenes is suspected , the patient can be tested for antibodies against streptolysin O (see above) and against DNAse.
therapy
Streptococci can be combated well with penicillins , in severe cases also combined with clindamycin . In the event of intolerance, macrolide antibiotics are used. Other alternatives are cephalosporins .
Epidemiology
S. pyogenes occurs worldwide. It only affects humans, but is one of the most common pathogens causing skin and respiratory diseases. It is noticeable that throat infections play the largest role in temperate climates, while skin infections tend to occur in tropical countries. The germs are transmitted through both droplet and smear infections. Although germs can also be detected in people who have not developed a disease, apparently sick people are more common as sources of infection.
Others
Two enzymes from S. pyogenes are used in medicine for therapeutic purposes: Streptokinase is used to dissolve blood clots , and DNases are used in wound treatment.
In the “fight” with macrophages , S. pyogenes uses cytolysins to attack not only their cell membranes, but also the mitochondria in a cascaded process .
The surgeon Friedrich Fehleisen (1854–1924) discovered this pathogen, formerly known as Streptococcus erysipelatos, as the cause of the erysipelas and used it to treat malignant tumors.
literature
- Helmut Hahn et al. (Ed.): Medical microbiology and infectious diseases. 5th fully updated edition. Springer Medizin Verlag, Heidelberg et al. 2005, ISBN 3-540-21971-4 .
- Fritz H. Kayser among others: Medical microbiology. Pocket textbook medical microbiology . 11th revised and expanded edition. Thieme, Stuttgart et al. 2005, ISBN 3-13-444811-4 .
- Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich, 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , p. 230 f.
Web links
Individual evidence
- ↑ Dr. Dorothea Ranft: voracious streptococci: long-term consequences of infection can be dramatic. In: Medical Tribune. July 19, 2018, accessed July 9, 2019 .
- ↑ Oliver Goldman et al .: Streptococcus pyogenes induces oncosis in macrophages through the activation of an inflammatory programmed cell death pathway. Cellular Microbiology Vol. 11, No. 1, pp. 138-155, doi: 10.1111 / j.1462-5822.2008.01245.x .
- ↑ Friedrich Fehleisen: The Aetiology of the Erysipelas. Berlin 1883 ( digitized - Internet Archive ).
- ↑ Werner Köhler : Fehleisen, Friedrich. In: Werner E. Gerabek , Bernhard D. Haage, Gundolf Keil , Wolfgang Wegner (eds.): Enzyklopädie Medizingeschichte. Walter de Gruyter, Berlin and New York 2005, ISBN 3-11-015714-4 , p. 394.