Download to read offline
More Related Content
Similar to Streptococci.pdf
Streptococci.pdf
- 1.
- 2. Cocci arrangein chain were first seen and describe by Billorth in purulent exudates from erysipelas and infection who gave the name streptococci. Streptos meaning winded or twisted. Rosenbach gave the name Streptococcus pyogenes to cocci arranged in chain which is isolated from human suppurative lesions.
- 3. CLASSIFICATION Based onoxygen requirement: Aerobes Facultative anaerobes Obligate anaerobes Based on hemolysis on blood agar: Alpha (α) hemolytic Beta (β) hemolytic Gamma (γ) hemolytic
- 4. CLASSIFICATION Based oncarbohydrate (C) antigen: Lancefield groups – A to V (without I and J) Based on M proteins: Griffith typing – 80 types of S. pyogenes
- 7. STREPTOCOCCUS PYOGENES - GroupA streptococci MORPHOLOGY Cocci, spherical or oval, 0.5–1.0 μm in diameter Arranged in chains Chain formation – cocci divide in one plane, daughter cells fail to separate completely.
- 8. GROWTH CHARACTERISTICS Aerobesand facultative anaerobe. Fastidious in nutritive requirement, growth occur only in enriched media containing blood or serum. Blood agar – colonies small, semitransparent, circular with a clear zone of hemolysis around them. Liquid media – glucose or serum broth, granular turbidity with a powdery deposit.
- 9. Blood agar: S.pyogenesshowing beta hemolysis
- 10. BIOCHEMICAL REACTIONS Catalasenegative (unlike staphylococci) Not soluble in 10% bile (unlike pneumococci) PYR test positive Ferment several sugars producing acid but no gas.
- 11. RESISTANCE Easily destroyedby heat (54°C for 30 min) Rapidly inactivated by antiseptics Resistant to crystal violet Selective media – crystal violet, nalidixic acid, colistin sulphate Does not develop resistance to drugs Sensitivity to bacitracin – S. pyogenes
- 12. ANTIGENIC STRUCTURE Capsule– Group A streptococci are capsulated, made up of hyluronic acid. • Capsule is antiphagocytic but no antigenic. Cell wall: Outer layer – protein and lipoteichoic acid (helps in adhesion) Middle layer – c carbohydrate antigen. Inner layer – peptidoglycan Peptidoglycan is responsible for cell wall rigidity. Serological grouping depends on the C carbohydrate antigen. (integral part of cell wall)
- 13. On thebasis of carbohydrate C antigen, S.pyogenes – Lancefield group A Outer layer protein layer consist of M, T and R proteins. Antigenic relationships have been Demonstrated between: Capsular hyaluronic acid and human synovial fluid Cell wall proteins and myocardium Group A carbohydrates and cardiac valves Cytoplasmic membrane antigens and vascular intima Peptidoglycans and skin antigens
- 15. TOXINS AND VIRULENCEFACTORS ➢ S. pyogenes forms several exotoxins and enzymes ➢ M protein act as virulence factor by inhibiting phagocytosis ➢ C polysaccharide – toxic effect ➢ Hemolysins
- 16. ➢ Hemolysins: Streptococciproduce two hemolysins, streptolysin O and S. Streptolysin O : oxygen labile, antigenic Anti streptolysin O appears in sera following streptococcal infection. ASO test is standard test for diagnosis of streptococcal infection. ASO titer in more than 200 units is considered significant and suggests either recent or recurrent infection. ASO titer is more in rheumatic fever . Streptolysin S : oxygen stable, not anigenic. Protein but not antigenic, responsible for haemolysis around colonies on the blood agar plates.
- 17. STREPTOKINASE (fibrinolysin) Promoteslysis of human fibrin clots by activating plasma precursor – plasminogen. Streptokinase is given IV in treatment of early myocardial infection & thromboembolic disorders. DEOXYRIBONUCLEASES (streptodornase DNAase) Pyogenic exudates contain large amounts of DNA Streptodornase causes depolymerisation of DNA and helps liquefy the thick pus May be responsible for the thin serous character of the streptococcal exudates Useful in diagnosis of S.pyogenes infection, particularly in skin lesions, where ASO titer is low.
- 18. HYALURONIDASE Breaks downhyaluronic acid of tissues This may favour spread of infection along intracellular spaces The enzyme is antigenic and specific antibodies appear in convalescent sera.
- 19. PATHOGENICITY Disease –suppurative or non- suppurative (including sequelae to post-streptococcal infections) S. pyogenes produces pyogenic lesions with a tendency to spread locally along lymphatics and through blood stream. SUPPURATIVE 1) Respiratory infections 2) Skin and soft tissue infections 3) Genital infections NON-SUPPURATIVE (post-streptococcal sequelae) 1) Acute rheumatic fever 2) Acute glomerulonephritis
- 20. SUPPARATIVE COMPLICATION : RESPIRATORYINFECTIONS Primary site of invasion – throat Sore throat – most common Localised – tonsillitis Diffuse – pharyngitis SKIN AND SOFT TISSUE INFECTION Two typical streptococcal infections: ▪ Erysipelas Diffuse infection involving the superficial lymphatics Affected skin red, swollen and indurated,sharply demarcated from surrounding healthy area Seen in older patients
- 21. ▪ Impetigo • Impetigoand streptococcal infection of scabies lesions are the main causes of acute glomerulonephritis in children in the tropics S. pyogenes causes a variety of suppurative infections of wounds or burns, with a predilection to produce lymphangitis and cellulitis Subcutaneous infections – range from cellulitis to necrotising fasciitis Necrotising fasciitis – more common, caused by mixed aerobic and anaerobic bacterial infection S. pyogenes M types 1 and 3 forming pyrogenic exotoxin A – may alone be responsible – ‘flesh eating bacteria
- 23. Necrotising fasciitis Extensivenecrosis of subcutaneous and muscular tissue and adjacent fascia associated with a severe systemic illness – a toxic shock–like syndrome, with disseminated intravascular coagulation and multisystem failure. GENITAL INFECTIONS Aerobic and anaerobic streptococci – normal inhabitants of female genital tract S. pyogenes cause puerperal sepsis
- 24. Non suppurative complications: Non-suppurative post-streptococcal sequelae: two important sequelae Acute rheumatic fever Acute glomerulonephritis Complications – 1 to 3 weeks after the acute infection
- 25. EPIDEMIOLOGY Streptococcal infections– respiratory tract -frequent in children at 5–8 years of age More common in winter in the temperate countries No seasonal distribution in the tropics Crowding – important factor in transmission of infection Outbreaks in closed communities – boarding schools or army camps
- 26. LABORATORY DIAGNOSIS Acuteinfections – diagnosis established by culture Non-suppurative complications – diagnosis based on demonstration of antibodies.
- 27. Specimen Throat swab,pus or exudates In rheumatic fever and glomerulonephritis –serum sample Microscopy Gram-stained films from pus – presumptive information Smears from throat – no value – streptococci form part of normal resident flora
- 29. Culture Sample eitherplated immediately or transported in Pike’s medium (blood agar with crystal violet and sodium azide) Specimen plated on sheep blood agar – incubated at 37°C under 5–10% CO2 or anaerobically Identification Hemolytic streptococci – grouped by Lancefield technique – specific antisera Rapid diagnostic tests – streptococcal group A antigen Bacitracin sensitivity – S.pyogenes
- 30. Serology Rheumatic feverand glomerulonephritis – retrospective diagnosis Antistreptolysin O titration (ASO titre) higher than 200 indicative of prior streptococcal infection Antideoxyribonuclease B (anti-DNAase B) higher than 300 – significant Streptozyme test – sensitive and specific screening test
- 31. TREATMENT All betahemolytic Group A streptococci are sensitive to penicillin G In patients allergic to penicillin, erythromycin or cephalexin may be used Tetracyclines and sulphonamides are not recommended Antimicrobial drugs have no effect on established glomerulonephritis and rheumatic fever
- 32. OTHER HEMOLYTIC STREPTOCOCCI Besides S. pyogenes, streptococci belonging to groups B, C, D, F, G and rarely H, K, O and R may also cause human infection Of these B, C and G are more common GROUP B STREPTOCOCCI : Important pathogens of cattle, producing bovine mastitis Streptococcus agalactiae – important human pathogen responsible for: Neonatal infections Adult infections Identified by CAMP reaction.