Group a streptococcus


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Streptococcus Pyogenes
Group a streptococcus

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Group a streptococcus

  1. 1. Group AStreptococcus Streptococcus pyogenes Dr.T.V.Rao MD Dr.T.V.Rao MD 1
  2. 2. Preliminary Grouping of Gram Positive Cocci Gram Positive Coccus Note: SBA hemolysis as Catalase alt to PYR? + _ + chains _StaphylococcusMicrococcusRothia PYR _ Other StrepSee “Staph” PP + Group genera S “A Disk* R Streptococcus sp & other S.pyogenes Enterococcus Group genera “GAS” *A disc contains bacitracin 2
  3. 3. Overview of the Medically Important Gram Positive CocciFamily, Genus, species Characteristics Clinical manifestationsStaphylococcaceae Cocci in cluster; catalase-positiveStaphylococcus aureus Coagulase +ve, yellow-pigmented colonies Pyogenic infections, toxicosesS. epidermidis Coagulase -ve, whitish colonies, normal Foreign body infections floraStreptococcaceae Cocci in chains and in pairs, catalase-negativeStreptococcus pyogenes Cocci in chains, Lancefield group A, β - Tonsillitis, scarlet fever, hemolysis skin infectionsS. pneumoniae Diplococci, α-hemolysis Pneumonia, otitis media, sinusitisS. agalactiae Chain-forming cocci, group antigen B, β- Meningitis/sepsis in hemolysis neonatesS. viridans Cocci in chains, α-hemolysis Endocarditis, dental cariesEnterococcaceae In chains & pairs, α, β, or γ-hemolysis, Flora of intestines of group antigen D, catalase -ve humans and animalsEnterococcus faecalis Aesculin-positive, growth in 6.5% NaCl, pH Opportunistic infectionsEnterococcus faecium 18.05.09 9.6 Phase I/ Module VII Dr Ekta 3
  4. 4. Group A Streptococcal infection 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. 5. Group A streptococcal infection 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. 6. Group A Streptococcal infection 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
  7. 7. Rebecca Lancefield Classifies Streptococcus Dr.T.V.Rao MD 7
  8. 8. CHARACTERISTICS Gram positive cocci, 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. 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 10
  11. 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 Rabbit Anti- Ag-Ab Ag-Ab serum interface interfaceRabbit StrepAnti- Antigenserum ExtractAntibody No Precipitate Precipitate (Negative Test) (Positive Test)against a Strepstrep group Antigenantigen Extract 12
  13. 13. Streptococcus spp• Gram positive, 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. 14. Streptococcus pyogenes:Microscopic appearance & Colonial morphology Dr.T.V.Rao MD 14
  15. 15. Structure of Streptococci Dr.T.V.Rao MD 15
  16. 16. Classification Based on O2Aerobes requirement AnaerobesGrowth on BA Peptostreptococciα hemolysis β hemolysis γ hemolysisIncomplete hemolysis Complete hemolysis α / β / no hemolysis(green color) Lancefield grouping specificStrep. viridans Strep. C carbohydrate Ag on cell wall Enterococcus fecalispneumoniae Group A – U (21 groups) Griffith typing of Group A on MTR proteins into > 100 types Dr.T.V.Rao MD 16
  17. 17. CLASSIFICATION TABLESEROLOGIC BIOCHEMICAL HEMOLYTIC PATTERN A S. pyogenes Beta B S. agalactiae Beta, Alpha, Gamma C S. equimilis Beta D S. bovis Alpha, Gamma S. faecalis Alpha, Beta, Gamma F S. milleri Alpha, Beta, Gamma G S. milleri -do- - S. pneumoniae AlphaVIRIDANS S. salivarius, S. sanguis, etc Alpha, Gamma Dr.T.V.Rao MD 17
  18. 18. PRESUMPTIVE IDENTIFICATION OF STREPTOCOCCI Organism Susceptibility Hydrolysis Growth Lysis A P hippurate esculin Bile NaCl bileS. pyogenes S R - - - - -S. agalactiae R R + - - + -Grp DS. faecalis R R - + + + -S. bovis R R - - + - -Viridans R R - - - - - (var)Pneumococcus R S - - - - + Dr.T.V.Rao MD 18
  19. 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. 20. Streptococcus pyogenes• Streptococcus pyogenes 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. 21. VIRULENCE FACTORS1. Capsule – non-immunogenic2. 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 of b-Hemolytic S. PyogenesProduces 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 22
  23. 23. Virulence Factors• Streptolysin O: 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. 24. Streptococcus pyogenes – virulence factorsStreptolysin O (SLO) Oxygen labile Damage cardiac cells Antigenic – produce ASLOStreptolysin S (SLS) Oxygen stable , non-antigenicExotoxins Streptococcal Pyrogenic Exotoxin (SPEs) Manifestation of scarlet feverExoenzymes Streptokinase (fibrinolysin) / Streptodornase (DNAase) / Hyalarunidase Dr.T.V.Rao MD 24
  25. 25. Virulence Factors of b-Hemolytic S. PyogenesExtracellular enzymes 1 Streptokinase – digests fibrin clots 2 Hyaluronidase – breaks down connective tissue 3 DNase – hydrolyzes DNA Dr.T.V.Rao MD 25
  26. 26. Virulence Factors of b-Hemolytic S. Pyogenes4. Lipoteichoic acid – for adherence5. Erythrogenic toxin – pyrogenic exotoxins A,B,C - responsible for the rash of Scarlet fever6. Streptolysin O – lyses WBC, platelets, RBC - immunogenic7. Streptolysin S – non-immunogenic - responsible for the hemolytic zones around colonies Dr.T.V.Rao MD 26
  27. 27. Virulence Factors of b-Hemolytic S. Pyogenes8. 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. 28. Virulence Factors of b-Hemolytic S. Pyogenes9. DNAse (streptodornase) – depolymerizes cell-free DNA in purulent materials10. 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. 29. Infections caused byStreptococcus pyogenes (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. 30. Group A streptococcal infection Overall disease burdenEach year• 1.8 million new cases ofserious infection• at least 500,000 deaths• 110 million cases of soft tissueinfection• 610 million cases ofpharyngitisAt least 18 million people sufferthe consequences of seriousGAS diseases Dr.T.V.Rao MD 30
  31. 31. CLINICAL SYNDROMESA. Suppurative Infections 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. 32. Pharyngitis the Prominent and common Infection Dr.T.V.Rao MD 32
  33. 33. Pharyngitis and tonsillitis Dr.T.V.Rao MD 33
  34. 34. Infection of Tonsils Dr.T.V.Rao MD 34
  35. 35. URI continues to be common presentation Dr.T.V.Rao MD 35
  36. 36. Skin lesions Dr.T.V.Rao MD 36
  37. 37. CLINICAL SYNDROMES. Scarlet fever – 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. 38. CLINICAL SYNDROMES Pneumonia – rapidly progressive & severe most commonly a sequela to viral infections like influenza or measles Dr.T.V.Rao MD 38
  39. 39. Erysipelas Dr.T.V.Rao MD 39
  40. 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. 41. Rheumatic Heart disease is leading cause of Morbidity Dr.T.V.Rao MD 41
  42. 42. Streptococcus pyogenes Sequellae to strep 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. 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. 44. CLINICAL SYNDROMESB. Non-suppurative sequelae 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. 45. Rheumatic Fever• Most common 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. 46. Lesions in the Heart Dr.T.V.Rao MD 46
  47. 47. Rheumatic Fever• Diagnosis is 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. 48. Streptococcus pyogenes Sequellae to strep throat or Skin Infections• Glomerulonephritis – symptoms 10 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 Dr.T.V.Rao MD 48
  49. 49. Glomerulonephritis2. 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. 50. Glomerulonephritis• Diagnosis based on 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. 51. DIAGNOSIS1. Microscopy2. Culture – Bacitracin Test (Taxo-A)3. Antigen detection tests – Enzyme-linked immunosorbent assay (ELISA) or agglutination tests4. Antibody detection  ASO titer – for respiratory disease  antiDNAse & antihyaluronidase – for skin infections Dr.T.V.Rao MD 51
  52. 52. Diagnosis and treatment of 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. 53. Lab diagnosis – Strep. pyogenes• Specimens: throat swab, pus, blood• Microscopy :Gram stain - GPC in chains• Culture: BA - beta hemolytic colonies• Identification tests - – Catalase Negative B B – Bacitracin sensitive – Penicillin sensitive – ASO titre / DNAase B test Dr.T.V.Rao MD 53
  54. 54. DIAGNOSIS1. Microscopy2. Culture – Bacitracin Test (Taxo-A)3. Antigen detection tests – Enzyme-linked immunosorbent assay (ELISA) or agglutination tests4. Antibody detection  ASO titer – for respiratory disease  antiDNAse & antihyaluronidase – for skin infections Dr.T.V.Rao MD 54
  55. 55. Streptococci grown Blood agar Dr.T.V.Rao MD 55
  56. 56. TREATMENT1. Penicillin G – drug of choice2. 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. 57. • Programme created by Dr.T.V.Rao MDfor Medical and Paramedical Students in the Developing World • Email • Dr.T.V.Rao MD 57