Download to read offline
More Related Content
Similar to 2 STREPTOCOCCI1 - ne.ppt
2 STREPTOCOCCI1 - ne.ppt
- 1.
- 3.
- 4.
- 5. 5 Structure Streptococci are Gram-positive, Nonmotile, Non spore forming, Catalase-negative cocci that occur in pairs or chains
- 6. 6 Catalase test • Addhydrogen peroxide to culture material
- 7. 7 Classification of Streptococcibased on : Hemolysis on blood agar They are divided into three groups by the type of : beta-hemolytic (clear, complete lysis of red cells). alpha hemolytic (incomplete, green hemolysis), gamma hemolytic (no hemolysis). Serologic grouping is based on antigenic differences in cell wall carbohydrates (Lancfield group Streptococcus A to V), in cell wall pili- associated protein, and in the polysaccharide capsule in group B streptococci.
- 8. Classification of Streptococci •Strep: gram positive, catalase negative –Nutritionally fastidious –Facultative anaerobes but don’t use oxygen metabolically (create lactic acid) • Initial classification based on hemolysis on sheep blood agar plates –α (partial, reduction), β (complete), and γ (none)
- 9. Hemolysis • β-hemolysis – Redblood cells (RBCs) are completely lysed, resulting in a clear area around the colony. • Α-hemolysis – RBCs are partially lysed, resulting in a greening of the area around the colony. • α’ Hemolysis has intact zone of RBCs with hemolysis around them • γ-hemolysis (nonhemolytic) – RBCs are not lysed, so there is no change in agar color. Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 10. 10 hemolysis reaction -sheep blood agar • α (alpha) – partial hemolysis – green color • β (beta) – complete clearing • γ (gamma) - no lysis White colonies
- 11. Hemolysis Patterns ofStreptococci
- 12. Types of Hemolysis(Cont.) Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 13. Hemolysis on BloodAgar Hemolysis on BA – -hemolysis Partial hemolysis Green discoloration around colonies e.g. S. pneumoniae & S. viridans – -hemolysis Complete hemolysis Clear zone of hemolysis around colonies e.g. Lancefield Group A & B (S. pyogenes & S. agalactiae) – -hemolysis No hemolysis e.g. Group D (Enterococcus sp.) • Acute glomerulonephritis • Scarlet fever
- 15. 15 Rebecca Craighill Lancefield(1895-1981)
- 16. Classification of Strepfrom Humans Species Lancefield Hemolytic Comments S. pyogenes A β S. agalactiae B β Group B Strep S. dysgalactiae subsp. equisimilis C, G β Formerly S. equisimilis; pyogenic; respiratory, SSTI S. pneumoniae None α S. bovis species group D α, γ Viridans; associated with colon cancer; IE S. mutans group not useful α, γ, rarely β Viridans; dental caries and IE S. salivarius group not useful α, γ Viridans; opportunistic S. mitis group not useful α Viridans; IE, opportunistic S. anginosus group A, C, F, G, or no detectable α, β, γ Viridans; formerly known as S. milleri; 3 species S. anginosus, S. constellatus, and S. intermedius; purulent infxns
- 17. Lancefield Groups • MembraneAg • Groups A-H, K-V – Group A • Strep. pyogenes – Group B • Strep. agalactiae – Group C, F, G • Strep equisimilis • Strep zooepidemicus • Strep anguinosus – Group D • E. faecalis • Strep bovis • Strep equines – Group K • Strep salivarius – Viridans • Strep mutans • Strep mitis • Strep sanguis – Pneumococci
- 18. MEDICAL IMPORTANT SPECIES 1.S.Pyogenes. 2. S.agalacticae 3. S.pneumoniae 4. S.Viridans 18
- 19. S. pyogenes (GroupA) Virulence Factors • M protein – Essential for virulence – Resistance to infection is related to M protein antibody production. • Fibronectin- binding protein (Protein F) • Lipoteichoic acid – Mediate attachment to host cells • Capsule prevents opsonized phagocytosis. Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 20. S. pyogenes (GroupA) Virulence Factors (Cont.) • Streptolysin O – Responsible for hemolysis on blood agar plate (BAP) • Oxygen labile: only active under anaerobic conditions – Destroys white blood cells (WBCs), platelets, RBCs, and other tissues • Streptolysin S – Oxygen stable • Can lyse RBCs and WBCs Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 21. S. pyogenes (GroupA) Virulence Factors (Cont.) • DNases A-D – Help destroy foreign DNA by excreting it into surrounding area • Hyaluronidase (spreading factor) – Breakdown of connective tissue • Streptococcal pyrogenic exotoxins (SPEs) – Formerly erythrogenic toxin – Causes a red spreading rash Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 22.
- 23. S. pyogenes (GroupA) Clinical Infections • Pharyngitis – Strep throat • Scarlet fever – Streptococcal pyrogenic exotoxins cause rash. – Rash appears on the chest and spreads to the trunk and limbs. Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 24.
- 25.
- 26. S. pyogenes (GroupA) Clinical Infections (Cont.) • Skin or pyodermal infections • Through bites or abrasions to the skin – Impetigo • Usually in very young children – Erysipelas • Skin infection with a spreading red rash with a demarcated but irregular edge – Mostly elderly – Cellulitis • Deep invasion of GAS leading to necrosis and gangrene • Sepsis Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 27.
- 28.
- 29.
- 30.
- 31. S. pyogenes (GroupA) Clinical Infections (Cont.) • Necrotizing fasciitis – Invasive infection characterized by a rapidly progressing inflammation and necrosis of the skin, subcutaneous fat, and fascia • Described as “flesh-eating disease” – Life-threatening infection Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 32. Necrotizing Fascilitis (flesheating strept): •
- 33. S. pyogenes (GroupA) Clinical Infections (Cont.) • Streptococcal toxic shock syndrome – Rare but results from the toxin associated with scarlet fever Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 34. Post-Streptococcal Sequelae • Rheumaticfever – Occurs after pharyngitis – Inflammation of the joints, heart, blood vessels, and subcutaneous tissues – Can cause serious damage to the heart valves • Acute glomerulonephritis (AGN) – Can occur after pharyngitis or cutaneous infection – Immunologic mechanisms lead to antigen antibody complexes, resulting in damage to the kidneys Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 35. Laboratory Diagnosis • Specimencollection – Swab rubbed over the posterior pharynx and each tonsillar area • If exudate is present, it should also be touched with the swab. – Avoid contamination by tongue and uvula – Recovery • Sheep blood agar (SBA) plate is inoculated and streaked for isolation. • Observe after 24 hours for the presence of β-hemolytic colonies – If none, incubate for an additional 24 hours Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 36. Laboratory Diagnosis (Cont.) Copyright© 2015 by Saunders, an imprint of Elsevier Inc. Key Tests Throat cultures: bacitracin, pyrrolidonyl aminopeptidase (PYR), Lancefield typing Other specimens: hippurate hydrolysis, Christie Atkins Munch-Petersen (CAMP) test, bile esculin test, 6.5% sodium chloride (NaCl) broth
- 37. Strep pyogenes diseasessummary • Pharyngitis • Scarlet Fever (rash) • Skin – Pyoderma – Impetigo – Erysipelas – Cellulitis • Strep TSS • Necrotizing fasciitis • Immune Mediated – Rheumatic fever – Glomerulonephritis
- 38. PATHOGENESIS • Human areonly reservoir. • Transmission is through ,contact ,droplets, food , fomites • Port of entry is through skin or pharynx. • Children are predominant group affected for cutaneous and throat infections. • Systemic infections and progressive diseases may occur if untreated. 38
- 39. SIGNS AND SYMPTOMS •Pharyngitis… > horse of muffled voice , difficult in swallowing. • Pyoderma…. > redness of skin( resemble to spider bites ), • Acute rhematic fever …>tenderness in joints , fever. • Acute glomerulonephritis …>. Tiredness , loss of appetite , dry skin. 39
- 40. Streptococcus agalactiae (GroupB Streptococcus) • Capsule is most significant virulence factor • Colonizes genital and lower GI tracts of 10- 40% of women; also found in oropharynx, upper GI • Pass to baby during birth
- 41. Streptococcus agalactiae (GroupB Streptococcus) Pathogenicity S. agalactiae (Lancefield Group B), it forms part of the normal microbial flora of the female genital tract. causes septic abortion and puerperal or gynaecological sepsis, and occasionally urinary tract infection. Occasionally it causes neonatal septicaemia and meningitis (rare in most developing countries).
- 42. Streptococcus agalactiae (GroupB Streptococcus) LABORATORY FEATURES • Specimens: Include cerebrospinal fluid and blood for culture from neonates. • High vaginal swab is required from women with suspected sepsis.
- 43. Laboratory Diagnosis Copyright ©2015 by Saunders, an imprint of Elsevier Inc. β-hemolysis Bacitracin, Hippurate hydrolysis, and CAMP test
- 44. S. agalactiae (GroupB) Virulence Factors • Capsule: preventing phagocytosis • Sialic acid appears to be important factor in inhibiting alternative pathway of complement. • Hemolysin • DNases • Hyaluronidase • Protease Treatment – Ampicillin Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 45. S. agalactiae (Group B)Infections (Cont.) • Detection of group B strep – Collect vaginal and rectal material between 35 and 37 weeks gestation – Inoculate to select broth, – All positive women should be treated to reduce the risk to infant. Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 46.
- 47. Cont.. • S.pneumoniae isa frequent colonizer of human nasopharynx Pathogenicity • S. pneumoniae causes lobar pneumonia, bronchitis (often with H. influenzae), meningitis, bacteraemia, otitis media, sinusitis and conjunctivitis. • Severe infections can occur in the elderly and those already in poor health or immunosuppressed. 47
- 48.
- 49. Pathogenesis • S.pneumoniae isa normal member of the respiratory tract flora invasion results in pneumonia .The best virulence factor is polysaccharide capsule which protect the bacterium phagocytosis. 49
- 50. HOST DEFFENCE • Protectionagainst infection depends on a normal mucocilary barrier and intact phagocytic and T-independent immune response type specific anti-capsule antibody is protective 50
- 51. EPIDEMIOLOGY • Pneumococcal pneumoniaeis most common elderly debilitated or immunosuppressed individuals . • The disease often sets in after a preceding viral infection damages the respiratory ciliated epithelium , incidence there fore peaks in the winter. 51
- 52. Diseases • Pneumonia • Meningitis •Sinusitis • Otitis media 52
- 53.
- 54. Viridans Streptococci • Normalflora of URT, female genital tract, and gastrointestinal (GI) tract • Many show α hemolysis • Fastidious, with some requiring CO2 • Viridans streptococci have five groups – S. mitis group – S. mutans group – S. salivarius group – S. bovis group – S. anginosus group Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 55. Viridans Streptococci ClinicalInfections • Generally opportunistic pathogens – Oropharyngeal commensals • Most common cause of bacterial endocarditis – More common in children than adults in patients with hematologic malignancies • Other diseases – Tooth decay • Most penicillin susceptible Copyright © 2015 by Saunders, an imprint of Elsevier Inc.
- 56. Enterococcus • Part ofStreptococcus until 1984. • Can grow in 6.5% NaCl and from 10°-45°C; hydrolyze esculin in presence of 40% bile salts • Most infections from E. faecalis or E. faecium; leading cause of nosocomial infxns • Colonize GI tract; selected for by abx
- 57. Enterococcus: Clinical Manifestations Epidemiology: Foundin intestinal tract , female genital tract ,less in oral cavity ( infrequent brushers) Disease caused: Infection in urinary tract Septicemia Ocassionally endocarditis or Meningitis