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-Hemolytic Streptococci

-Hemolytic Streptococci. Ali Somily MD,FRCPC,D(ABMM). G+ve cocci in chains and/or pairs Colonize MM(Resp.,GIT& GUT) Catalase –ve Ferment CHO lactic acid. Grouped by either A.phenotypic Hemolysis( ,ß or ) Lancefield antigen Cell wall CHO A,B,C,D,Fand G ect Or B.Genotypic.

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-Hemolytic Streptococci

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  1. -Hemolytic Streptococci Ali Somily MD,FRCPC,D(ABMM)

  2. G+ve cocci in chains and/or pairs Colonize MM(Resp.,GIT& GUT) Catalase –ve Ferment CHOlactic acid Grouped by either A.phenotypic Hemolysis(,ß or ) Lancefield antigen Cell wall CHO A,B,C,D,Fand G ect Or B.Genotypic Introduction

  3. &ß Hemolysis

  4. Lancefield Agglutination

  5. -Hemolytic Streptococci • Partial hemolysis of blood • Green zoon around the colony • Examples: • S.Pneumoniae • S.Viridans • S.Bovis

  6. STREPTOCOCCUS PNEUMONIAE

  7. VIRULANCE VACTORS Capsule Autolysin Pneumolysin CLINICAL PRESENTATION NF Resp.20-40%/pharynx Inhalation/droplets STREPTOCOCCUS PNEUMONIAE

  8. Primary infection CAPalveoli Blood Endocarditis Meningitis Localized Sinusitis O.M Secondary Infection Non-capsulated Opportunistic infection Lungs only Impair or poor ciliary activity Viral, Smoking, dust Risk factor Hyposplenism Splenectomy Asplenia Sickle Cell Diseases Liver disease Hypogammaglobinaemia Alcoholism Cigarette smoking Malnutrition CLINICAL PRESENTATION

  9. Blood,CSF,Sputum& swab/aspirate DIRECT SMEAR G+ve diplococci Lancet shape Capsulated halo (antiphagocytic)/pathogenic Diagnosis

  10. Quellung test(AB’s swelling of capsule) Diagnosis

  11. CULTURE BAP; 5-10%CO2 -hemolytic Mucoid (capsule)SR Concave (punched out/collapse) IDENTIFICATION Bile solubility (NaDC) Optochin S (disk 5g&6mmzoon>=14 mm) 80 serotype(vaccine) capsular structure STREPTOCOCCUS PNEUMONIAE

  12. Treatment &Prevention • TTT • Penicillin(↑R recently)PBP • Ceftriaxon +/-Vancomycin or Rifampicin • Vaccination • Polsaccharide capsule • Conjugate vaccine • Indication • Children • SCD • Splenectomised patient • HIV • Elderly • Cardiopulmonary and renal diseases

  13. VIRIDANS STREPTOCOCCI

  14. Mitis Mutans Salvarius Angionosis Grouping of viridans streptococci

  15. CLINCAL PRESENTATION NF (GIT,UGT&Oral cavity) Opportunistic organisms Dental caries Endocarditis VIRIDANS STREPTOCOCCI

  16. Formation of dental plaque by Streptococcus mutans bacteria adhere to the tooth by a protein on the cell surface, grow and synthesize a dextran capsule binds the bacteria to the enamel and forms a biofilm 300-500 cells of thickness bacteria can cleave sucrose to glucose + fructose glucose is polymerized into an extracellular dextran polymer that cements the bacteria to tooth enamel and becomes the matrix of plaque this dextran slime can be depolymerized to glucose for use as a carbon source, resulting in the production of lactic acid within the plaque that decalcifies the enamel and leads to dental caries Example of a biofilm

  17. Damage ,prosthetic valve Predisposing factor RHD CHD Mitral valve prolapse Degenerative H diseases PV Pathogenesis Dextran adhere to the damaged valve vegetation(fibrin,bacteria & platelets) Symptoms Fever Murmurs Immunological manifestations O,P,S SBE 2-5 Wks Diagnosis Blood culture ECHO Endocarditis

  18. Treatment

  19. DIRECT SMEAR G+ve cocci in chains CULTURE Can be  OR  rarely ß hemolytic Most lack distinct LA IDENTIFICATION Urea VP( acetoin production) Arginine hydrolysis Esculin hydrolysis CHO ferementation Microbiology

  20. Enterococcus

  21. Introduction • Fecal strep separated genus/by molecular • Harsh conditionAbiquitous/soil,water,plants, GIT, GU human • 15 Spp/E.faecalis80-90% of clinical isolate • Colonization/infection

  22. NC BACTEREMIA 1/3 NC UTI 16% WOUND ENDOCARDITIS CNS PNEUMONIA (rare) ELDERLY I’C TTT Vancomycin VRE (Van A,B&C ect) Plasmid/chromosomal High/low level VDE Direct smear Short chain/pairs/coccobaccilary CLINICAL PRESENTATION

  23. CULTURE Facultative anaerobs  OR  hemolysis Catalase weak +ve Group D IDENTIFICATION Growth B/W 10-42 Co 6.5% NaCl Esculin hydrolysis(40%)bile salt Pyrrolidonyl arylamidase(PYR)+ve Leucine arylamidase(LAP)+ve Motility ,Pigmentation,arabinose and methyl --D-glucopyranoside

  24. All Group D Enterococcus S.Bovis Bile esculin

  25. PYR/PYR-LAP

  26. Endocarditis

  27. BOVIS GROUPNew NameStreptococcus gallolyticus(Group D Streptococci)

  28. CLINICAL Human intestine and animals Endocarditic Septicemia Link to colon cancer Stool isolation Two biotypes I&II Mannitol and glucan I DIRECT SMEAR G+ve cocci in chains BOVIS GROUP

  29. CULTURE  OR  on BAP IDENTIFICATION LG group D Differed from viridans Growth in 40% bile salt Hydrolyze esculin

  30. S.bovis Unable to grow in 45 Co 6.5% salt @ 37dC PYR –ve S to penicillin and cephalosporins R to vancomycin(rare) Enterococcus Able to grow in 45 Co 6.5% salt @ 37Co PYR +ve S to ampicillin How you differentiate S. bovis from enterococcus?

  31. Summary

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