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Premium member Presentation Transcript Group A Streptococcus Streptococcus pyogenes: Group A Streptococcus Streptococcus pyogenes Dr.T.V.Rao MD Dr.T.V.Rao MD 1Preliminary Grouping of Gram Positive Cocci: 2 Preliminary Grouping of Gram 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?PowerPoint Presentation: 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 infectionsPowerPoint Presentation: Group A S treptococcal infection and Health C are 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 4Group A streptococcal infection and health care: 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 5Group A Streptococcal infection and health care: 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 6Rebecca Lancefield Classifies Streptococcus: Rebecca Lancefield C lassifies Streptococcus Dr.T.V.Rao MD 7CHARACTERISTICS: 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 8LANCEFIELD CLASSIFICATION: 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 9Classification - Lancefield: 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 originClassification - Lancefield: 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 S treptococcus & 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 11Lancefield Capillary Precipitation: 12 Lancefield Capillary Precipitation Antibody against a 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 ExtractStreptococcus spp: 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 13Streptococcus pyogenes: Microscopic appearance & Colonial morphology: Streptococcus pyogenes: Microscopic appearance & Colonial morphology Dr.T.V.Rao MD 14Structure of Streptococci: Structure of Streptococci Dr.T.V.Rao MD 15PowerPoint Presentation: Dr.T.V.Rao MD 16 Classification Based on O 2 requirement Aerobes Anaerobes Peptostreptococci Growth on BA α h emolysis β h emolysis γ h emolysis Incomplete h emolysis (green color) Complete h emolysis α / β / no h emolysis 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 typesCLASSIFICATION TABLE: CLASSIFICATION TABLE SEROLOGIC BIOCHEMICAL HEMOLYTIC 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 17PRESUMPTIVE IDENTIFICATION OF STREPTOCOCCI: PRESUMPTIVE IDENTIFICATION OF STREPTOCOCCI Organism Susceptibility 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 18Group A Streptococcus (S. pyogenes): 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 19Streptococcus pyogenes: 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 20VIRULENCE FACTORS: VIRULENCE FACTORS Capsule – non-immunogenic M protein – hair-like projections on the cell wall - major virulence factor - promotes adherence - antiphagocytic - anticomplement - type specific Dr.T.V.Rao MD 21Virulence Factors of b-Hemolytic S. Pyogenes: 22 Virulence Factors of b -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 MDVirulence Factors: 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 10 5 -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 23PowerPoint Presentation: Dr.T.V.Rao MD 24 Streptococcus pyogenes – 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) / HyalarunidaseVirulence Factors of b-Hemolytic S. Pyogenes: Virulence Factors of b -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 MDVirulence Factors of b-Hemolytic S. Pyogenes: Virulence Factors of b -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 26Virulence Factors of b-Hemolytic S. Pyogenes: Virulence Factors of b -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 27Virulence Factors of b-Hemolytic S. Pyogenes: Virulence Factors of b -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 28Infections caused by Streptococcus pyogenes (GAS): Infections caused by Streptococcus pyogenes (GAS) Superficial diseases pharyngitis, skin & soft tissue inf n , erysipelas, impetigo, vaginitis, post-partum inf n Deep infections bacteraemia, necrotising fasciitis, deep soft tissue inf n , 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 29Group A streptococcal infection Overall disease burden: Group A streptococcal infection 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 30CLINICAL SYNDROMES: CLINICAL SYNDROMES A . 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 31Pharyngitis the Prominent and common Infection: Pharyngitis the Prominent and common Infection Dr.T.V.Rao MD 32Pharyngitis and tonsillitis: Pharyngitis and tonsillitis 33 Dr.T.V.Rao MDInfection of Tonsils: Infection of Tonsils Dr.T.V.Rao MD 34URI continues to be common presentation: URI continues to be common presentation Dr.T.V.Rao MD 35Skin lesions: Skin lesions Dr.T.V.Rao MD 36CLINICAL SYNDROMES: 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 37CLINICAL SYNDROMES: CLINICAL SYNDROMES Pneumonia – rapidly progressive & severe most commonly a sequela to viral infections like influenza or measles Dr.T.V.Rao MD 38PowerPoint Presentation: Erysipelas Dr.T.V.Rao MD 39Streptococcus pyogenes Necrotizing Fasciitis: 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 40Rheumatic Heart disease is leading cause of Morbidity: Rheumatic Heart disease is leading cause of Morbidity Dr.T.V.Rao MD 41Streptococcus pyogenes Sequellae to strep throat: 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 42Post streptococcal diseases: 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 43CLINICAL SYNDROMES: CLINICAL SYNDROMES B. 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 44Rheumatic Fever: 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 45Lesions in the Heart: Lesions in the Heart Dr.T.V.Rao MD 46Rheumatic Fever: 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 47Streptococcus 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 Streptococcus pyogenes Sequellae to strep throat or Skin Infections Dr.T.V.Rao MD 48Glomerulonephritis: 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 49Glomerulonephritis: 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 50DIAGNOSIS: DIAGNOSIS Microscopy Culture – Bacitracin Test (Taxo-A) Antigen detection tests – Enzyme-linked immunosorbent assay (ELISA) or agglutination tests Antibody detection ASO titer – for respiratory disease antiDNAse & antihyaluronidase – for skin infections Dr.T.V.Rao MD 51Diagnosis and treatment of Strep Throat: 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 52Lab diagnosis – Strep. pyogenes: Dr.T.V.Rao MD 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 Bacitracin sensitive Penicillin sensitive ASO titre / DNAase B test B BDIAGNOSIS: DIAGNOSIS Microscopy Culture – Bacitracin Test (Taxo-A) Antigen detection tests – Enzyme-linked immunosorbent assay (ELISA) or agglutination tests Antibody detection ASO titer – for respiratory disease antiDNAse & antihyaluronidase – for skin infections Dr.T.V.Rao MD 54Streptococci grown Blood agar: Streptococci grown Blood agar Dr.T.V.Rao MD 55TREATMENT: TREATMENT Penicillin G – drug of choice 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 56PowerPoint Presentation: Programme created by Dr.T.V.Rao MD for Medical and Paramedical Students in the Developing World Email email@example.com Dr.T.V.Rao MD 57 You do not have the permission to view this presentation. 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