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Group A Streptococcus.pptx
Group A Streptococcus, or Streptococcus pyogenes, is an important human pathogen. It is classified based on Lancefield grouping, which identifies the carbohydrate antigens present in the bacterial cell wall. S. pyogenes is in Lancefield Group A and causes a variety of infections through various virulence factors like M protein, streptolysin toxins, and extracellular enzymes. These virulence factors allow the bacteria to adhere to tissues, resist phagocytosis, damage host cells, and spread infection. Common infections include pharyngitis, impetigo, and potentially life-threatening illnesses like necrotizing fasciitis and toxic shock syndrome.
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Group A Streptococcus.pptx
- 1. Group A Streptococcus Streptococcus pyogenes Dr.T.V.RaoMD Dr.T.V.Rao MD 1
- 2. 2 Preliminary Grouping ofGram Positive Cocci Gram Positive Coccus Catalase Rothia Staphylococcus Micrococcus PYR + _ + “A Disk* chains _ S.pyogenes “GAS” *A disc contains bacitracin Enterococcus Streptococcus sp & other Group genera + Other Strep Group genera S R _ See “Staph” PP Note: SBA hemolysis as alt to PYR?
- 3. 18.05.09 Phase I/Module VII Dr Ekta 3 Overview of the Medically Important Gram Positive Cocci Family, Genus, species Characteristics Clinical manifestations Staphylococcaceae Cocci in cluster; catalase-positive Staphylococcus aureus Coagulase +ve, yellow-pigmented colonies Pyogenic infections, toxicoses S. epidermidis Coagulase -ve, whitish colonies, normal flora Foreign body infections Streptococcaceae Cocci in chains and in pairs, catalase-negative Streptococcus pyogenes Cocci in chains, Lancefield group A, β - hemolysis Tonsillitis, scarlet fever, skin infections S. pneumoniae Diplococci, α-hemolysis Pneumonia, otitis media, sinusitis S. agalactiae Chain-forming cocci, group antigen B, β- hemolysis Meningitis/sepsis in neonates S. viridans Cocci in chains, α-hemolysis Endocarditis, dental caries Enterococcaceae In chains & pairs, α, β, or γ-hemolysis, group antigen D, catalase -ve Flora of intestines of humans and animals Enterococcus faecalis Enterococcus faecium Aesculin-positive, growth in 6.5% NaCl, pH 9.6 Opportunistic infections
- 4. Group A Streptococcalinfection and Health Care Alexander Gordon (1752-1799) “... seized such women only as were visited, or delivered, by a practitioner or nurse, who had previously attended patients affected by the disease….a specific contagion, or infection.... …I could venture to foretell what women would be affected with the disease, upon hearing by what midwife they were to be delivered..” 1795 Dr.T.V.Rao MD 4
- 5. Group A streptococcalinfection and health care Ignaz Philipp Semmelweis (1818-1865) All students or doctors who enter the wards for the purpose of making an examination must wash their hands thoroughly in a solution of chlorinated lime which will be placed in convenient basins near the entrance of the wards. This disinfection will be considered sufficient for this visit. Between examinations the hands must be washed in soap and water. 1847 Dr.T.V.Rao MD 5
- 6. Group A Streptococcalinfection and health care Louis Pasteur (1822-1895) ”It is the nursing and medical staff who carry the microbe from an infected woman to a healthy one…. This water, this sponge, this lint with which you wash or cover a wound, may deposit germs which have the power of multiplying rapidly within the tissue.... If I had the honour of being a surgeon....not only would I use none but perfectly clean instruments, but I would clean my hands with the greatest care...” 1879 Dr.T.V.Rao MD 6
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- 8. CHARACTERISTICS Gram positivecocci, in pairs or chains Catalase negative Facultative anaerobes Complex nutritional requirements (blood or serum enriched medium) Ferment carbohydrates with formation of lactic acid Dr.T.V.Rao MD 8
- 9. LANCEFIELD CLASSIFICATION • Group A– rhamnose-N-acetylglucosamine • Group B – rhamnose-glucosamine polysaccharide • Group C –rhamnose-N-acetylglucosamine • Group D – glycerol teichoic acid containing alanine & glucose • Group F – glucopyrasonyl-N- acetylgalactosamine Dr.T.V.Rao MD 9
- 10. 10 Classification - Lancefield •Lancefield realized that all species in each “group” generally (and conveniently) shared clinically significant properties such as type of hemolysis, normal host, body system or tissue where indigenous, etc. For example: – Group A - S. pyogenes: human upper respiratory – Group B - S. agalactiae: human urogenital – Group C - S. zooepidemicus: from animal products – Group D - S. faecalis: bile-resistant, fecal origin
- 11. Classification - Lancefield •Lancefield identified many other antigens, and proposed several Lancefield groups. Groups A, B, C, D, F, and G were the primary groups likely from human infections • Lancefield later determined that viridans Streptococcus & pneumococci did NOT possess antigens that reacted with her antisera • More recently, a new species, S. milleri was found to carry A,C, F & G antigens, and display all 3 types of hemolysis. Dr.T.V.Rao MD 11
- 12. 12 Lancefield Capillary Precipitation Antibody againsta strep group antigen Strep Antigen Extract No Precipitate (Negative Test) Precipitate (Positive Test) Ag-Ab interface Ag-Ab interface Rabbit Anti- serum Rabbit Anti- serum Strep Antigen Extract
- 13. Streptococcus spp • Grampositive, facultatively- anaerobic • Catalase negative, no spores, nonmotile • Cell division: single plane ==> chains • Lancefield Grouping – species-specific CHO cell wall antigens – groups designated A-H, K-V – some not groupable Dr.T.V.Rao MD 13
- 14. Streptococcus pyogenes: Microscopic appearance& Colonial morphology Dr.T.V.Rao MD 14
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- 16. Dr.T.V.Rao MD 16 ClassificationBased on O2 requirement Aerobes Anaerobes Peptostreptococci Growth on BA α hemolysis β hemolysis γ hemolysis Incomplete hemolysis (green color) Complete hemolysis α / β / no hemolysis Strep. viridans Strep. pneumoniae Enterococcus fecalis Lancefield grouping specific C carbohydrate Ag on cell wall Group A – U (21 groups) Griffith typing of Group A on MTR proteins into > 100 types
- 17. CLASSIFICATION TABLE SEROLOGIC BIOCHEMICALHEMOLYTIC PATTERN A S. pyogenes Beta B S. agalactiae Beta, Alpha, Gamma C S. equimilis Beta D S. bovis S. faecalis Alpha, Gamma Alpha, Beta, Gamma F S. milleri Alpha, Beta, Gamma G S. milleri -do- - S. pneumoniae Alpha VIRIDANS S. salivarius, S. sanguis, etc Alpha, Gamma Dr.T.V.Rao MD 17
- 18. PRESUMPTIVE IDENTIFICATION OF STREPTOCOCCI OrganismSusceptibility A P Hydrolysis hippurate esculin Growth Bile NaCl Lysis bile S. pyogenes S R - - - - - S. agalactiae R R + - - + - Grp D S. faecalis S. bovis R R R R - + - - + + + - - - Viridans R R (var) - - - - - Pneumococcus R S - - - - + Dr.T.V.Rao MD 18
- 19. Group A Streptococcus (S.pyogenes) Structure: 1. Capsule – hyaluronic acid 2. Cell wall a. protein antigens M,T,R M protein major virulence factor T & R protein no role in the virulence b. group specific carbohydrates – rhamnose-N-acetylglucosamine 3. Pili consists partly of M protein & covered with lipoteichoic acid for attachment Dr.T.V.Rao MD 19
- 20. Streptococcus pyogenes • Streptococcuspyogenes is one of the most frequent pathogens of humans. It is estimated that between 5-15% of normal individuals harbor the bacterium, usually in the respiratory tract, without signs of disease. As normal flora, S. pyogenes can infect when defenses are compromised or when the organisms are able to penetrate the constitutive defenses. When the bacteria are introduced or transmitted to vulnerable tissues, a variety of types of suppurative infections can occur Dr.T.V.Rao MD 20
- 21. VIRULENCE FACTORS 1. Capsule– non-immunogenic 2. M protein – hair-like projections on the cell wall - major virulence factor - promotes adherence - antiphagocytic - anticomplement - type specific Dr.T.V.Rao MD 21
- 22. 22 Virulence Factors ofb-Hemolytic S. Pyogenes Produces surface antigens: – C-carbohydrates – protect against lysozyme – Fimbriae – adherence – M-protein – contributes to resistance to phagocytosis – Hyaluronic acid capsule – provokes no immune response –C5a protease hinders complement and neutrophil response Dr.T.V.Rao MD
- 23. Virulence Factors • StreptolysinO: thiol-activated toxin (Groups A,C,G) – damages membranes: RBCs, myocardial cells, PMNs – role in intracellular survival • Erythrogenic toxins: rash of scarlet fever – pyrogenicity, lethal shock – 105-fold increased sensitivity to endotoxin • Pyrogenic exotoxin A – contributes to streptococcal TSLS – stimulates cytokine production by T cells – endothelial cell damage, hypotensive shock, ischemia-based necrosis Dr.T.V.Rao MD 23
- 24. Dr.T.V.Rao MD 24 Streptococcuspyogenes – virulence factors Antigenic – produce ASLO Streptolysin S (SLS) Exotoxins Oxygen stable , non-antigenic Damage cardiac cells Streptolysin O (SLO) Oxygen labile Streptococcal Pyrogenic Exotoxin (SPEs) Manifestation of scarlet fever Exoenzymes Streptokinase (fibrinolysin) / Streptodornase (DNAase) / Hyalarunidase
- 25. Virulence Factors ofb-Hemolytic S. Pyogenes Extracellular enzymes 1 Streptokinase – digests fibrin clots 2 Hyaluronidase – breaks down connective tissue 3 DNase – hydrolyzes DNA 25 Dr.T.V.Rao MD
- 26. Virulence Factors ofb-Hemolytic S. Pyogenes 4. Lipoteichoic acid – for adherence 5. Erythrogenic toxin – pyrogenic exotoxins A,B,C - responsible for the rash of Scarlet fever 6. Streptolysin O – lyses WBC, platelets, RBC - immunogenic 7. Streptolysin S – non-immunogenic - responsible for the hemolytic zones around colonies Dr.T.V.Rao MD 26
- 27. Virulence Factors ofb-Hemolytic S. Pyogenes 8. Streptokinase (fibrinolysin) – lyze blood clots plasminogen plasmin digest fibrin & other proteins - facilitates spread of infection - used in the treatment of pulmonary emboli & coronary artery & venous thromboses Dr.T.V.Rao MD 27
- 28. Virulence Factors ofb-Hemolytic S. Pyogenes 9. DNAse (streptodornase) – depolymerizes cell-free DNA in purulent materials 10. Hyaluronidase – spreading factor - splits hyaluronic acid streptodornase & streptokinase used in enzymatic debridement liquefy exudates & facilitate removal of pus & necrotic tissue antibiotics gain better access Dr.T.V.Rao MD 28
- 29. Infections caused by Streptococcuspyogenes (GAS) • Superficial diseases pharyngitis, skin & soft tissue infn, erysipelas, impetigo, vaginitis, post-partum infn • Deep infections bacteraemia, necrotising fasciitis, deep soft tissue infn, cellulitis, myositis, puerperal sepsis, pericarditis, meningitis, pneumonia, septic arthritis • Toxin-mediated scarletina, toxic shock-like syndrome • Immunologically mediated rheumatic fever, post-streptococcal GN, reactive arthritis Dr.T.V.Rao MD 29
- 30. Group A streptococcalinfection Overall disease burden Each year • 1.8 million new cases of serious infection • at least 500,000 deaths • 110 million cases of soft tissue infection • 610 million cases of pharyngitis At least 18 million people suffer the consequences of serious GAS diseases Dr.T.V.Rao MD 30
- 31. CLINICAL SYNDROMES A. SuppurativeInfections 1. Skin Infections a. impetigo – superficial blisters covered with pus or honey–colored crust b. erysipelas – acute superficial cellulitis of the skin with lymphatic involvement Dr.T.V.Rao MD 31
- 32. Pharyngitis the Prominentand common Infection Dr.T.V.Rao MD 32
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- 35. URI continues tobe common presentation Dr.T.V.Rao MD 35
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- 37. CLINICAL SYNDROMES . Scarletfever – a complication of pharyngitis if the causative agent is capable of producing erythrogenic toxin initial symptoms of pharyngitis, diffuse erythematous rash with sparing of the palms & soles Circumoral pallor “strawberry tongue” Dr.T.V.Rao MD 37
- 38. CLINICAL SYNDROMES Pneumonia – rapidlyprogressive & severe most commonly a sequela to viral infections like influenza or measles Dr.T.V.Rao MD 38
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- 40. Streptococcus pyogenes Necrotizing Fasciitis •Invasive, nonTSLS disease – necrotizing fasciitis (“flesh-eating bacteria”) – rapid development of shock, multiple organ system failure – high fatality rate Dr.T.V.Rao MD 40
- 41. Rheumatic Heart diseaseis leading cause of Morbidity Dr.T.V.Rao MD 41
- 42. Streptococcus pyogenes Sequellae tostrep throat • Heart valve damage (rheumatic heart disease) – < 3% of people with strep throat, weeks after sore throat – migrating arthritis; heart valve damage (50%), some fatal – recurrences common, lifelong penicillin therapy – shared antigen: M protein, cardiac myosin – attack by T cells, Ab: inflammation, valve damage Dr.T.V.Rao MD 42
- 43. Post streptococcal diseases •Rheumatic Fever- autoimmune disease involving heart valves, joints, nervous system. Follows a strep throat • Acute glomerulonephritis or Bright’s Disease- inflammatory disease of renal glomeruli and structures involved in blood filter of kidney. Due to deposition of Ag/Ab complexes Dr.T.V.Rao MD 43
- 44. CLINICAL SYNDROMES B. Non-suppurativesequelae 1. Rheumatic fever – associated with M types causing URI & skin infections fever, malaise, migratory nonsuppurative polyarthritis, evidence of inflammation of the heart carditis leads to thickened & deformed valves & to small perivascular granulomas in the myocardium (Aschoff bodies) Dr.T.V.Rao MD 44
- 45. Rheumatic Fever • Mostcommon cause of permanent heart valve damage in children • Exact cause not yet known but there appears to be some antibody cross reactivity between the cell wall of S. pyogenes and heart muscle Dr.T.V.Rao MD 45
- 46. Lesions in theHeart Dr.T.V.Rao MD 46
- 47. Rheumatic Fever • Diagnosisis based on symptoms and is difficult • Occurs most frequently between ages of 6 and 15 • US it is about 0.05% of pop having strep infections • 100x more frequent in tropical countries Dr.T.V.Rao MD 47
- 48. • Glomerulonephritis – symptoms10 days after 1˚ infection: edema – decreased urination, hematuria, hypertension – Ag:Ab complexes accumulate, C’ activated – provoke inflammatory response, interferes with normal kidney function – young children: self-limiting – teenagers/adults: rare permanent kidney damage, chronic glomerulonephritis Streptococcus pyogenes Sequellae to strep throat or Skin Infections Dr.T.V.Rao MD 48
- 49. Glomerulonephritis 2. Acute Glomerulonephritis– associated with M types producing URI & skin infections particularly associated with types 12, 4, 2 & 49 which are nephritogenic initiated by ag-ab complexes on the glomerular basement membrane hematuria, proteinuria, edema & hypertension Dr.T.V.Rao MD 49
- 50. Glomerulonephritis • Diagnosis basedon history of Strep throat and clinical findings. • Symptoms include fever, malaise, edema, hypertension and blood or protein in urine • Occurs in 0.5% of those having strep throat. Dr.T.V.Rao MD 50
- 51. DIAGNOSIS 1. Microscopy 2. Culture– Bacitracin Test (Taxo-A) 3. Antigen detection tests – Enzyme-linked immunosorbent assay (ELISA) or agglutination tests 4. Antibody detection ASO titer – for respiratory disease antiDNAse & antihyaluronidase – for skin infections Dr.T.V.Rao MD 51
- 52. Diagnosis and treatmentof Strep Throat • Tell tale symptoms are slight fever associated with sore throat and visual of pus in back of throat • Quick diagnostic tests (Molecular) available but must be confirmed by throat swab and growth on blood agar (beta hemolysis) Dr.T.V.Rao MD 52
- 53. Dr.T.V.Rao MD 53 Labdiagnosis – Strep. pyogenes • Specimens: throat swab, pus, blood • Microscopy :Gram stain - GPC in chains • Culture: BA - beta hemolytic colonies • Identification tests - – Catalase Negative – Bacitracin sensitive – Penicillin sensitive – ASO titre / DNAase B test B B
- 54. DIAGNOSIS 1. Microscopy 2. Culture– Bacitracin Test (Taxo-A) 3. Antigen detection tests – Enzyme-linked immunosorbent assay (ELISA) or agglutination tests 4. Antibody detection ASO titer – for respiratory disease antiDNAse & antihyaluronidase – for skin infections Dr.T.V.Rao MD 54
- 55. Streptococci grown Bloodagar Dr.T.V.Rao MD 55
- 56. TREATMENT 1. Penicillin G– drug of choice 2. Erythromycin Antistreptococcal chemoprophylaxis in persons who have suffered an acute attack of rheumatic fever Penicillin G 1.2 M units IM every 3-4 weeks or daily oral penicillin or oral sulfonamide Dr.T.V.Rao MD 56
- 57. • Programme createdby Dr.T.V.Rao MD for Medical and Paramedical Students in the Developing World • Email • doctortvrao@gmail.com Dr.T.V.Rao MD 57