-Hemolytic Streptococci

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

2. Introduction • Grouped either by : • A.phenotypic • Hemolysis(,ß or ) • Lancefield antigen • Cell wall CHO • A,B,C,D,Fand G ect Or B.Genotypic

3. &ß Hemolysis

4. Lancefield Agglutination

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

6. STREPTOCOCCUS PNEUMONIAE • Aerobic extracellular • Feature : • Gram Positive cocci in pairs or short chains(Lancet shape) • Colony :Gray –white variable on BAP • Non motile • Capsule : Polysaccharidemore than 80 types • Note : No Glycocalyx , No Exotoxin

7. Virulence Factors • Capsule: Polysaccharide (resist phagocytosis • IgA Protease:Prevent Opsonization by IgA at Mucous Membrane • Adhesion: Mediates attachement of S.pneumoniae to Epithelial Cell • Autolysin/Pneumolysin

9. Quellung Test (AB’s swelling of capsule

10. BAP; 5-10%CO2 -hemolytic Mucoid (capsule) SR Concave (punched out/collapse) CULTURE

11. Laboratory Tests • Catalase : -ve • Hemolysis : Alpha • 6.5% Nacl : No growth • CAMP Test : -ve • Bile Esculin: -ve • Bile Solubility : +ve • Optochin :Sensitive • Lancefiield : None (CHO C)

12. Bile solubility (NaDC) Optochin S (disk 5g&6mmzoon>=14 mm) IDENTIFICATION

13. Source and Transmission • Normal Flora of Upper Respiratory Tract in 20-40% of people • Horizontal Transmission via Droplet and Inhalation • Pulmonary infection due failure of Muccocilliary action AlveoliLobe • Meningitis after Sinusitis , Otitis Media or Bacteremia through Choroid Plexus

14. Primary infection Community Acquired Pneumonia Bacteremia Endocarditis Meningitis Localized Sinusitis O.M Secondary Infection Non-capsulated Opportunistic infection Lungs only Impair or poor ciliary activity Viral, Smoking, dust Clinical

15. Adult and Sickle Cell Disease Fever , cough(sputum), Dull on Percussion Can be fatal, Abscesses Diagnosis: Sputum GS and Culture Risk factor Hyposplenism Splenectomy Asplenia Sickle Cell Diseases Liver disease Hypogammaglobinaemia Alcoholism Cigarette smoking Viral Infection Malnutrition Lober Pneumonia

17. Adult and Elderly Symptoms: fever, neck Pain,Neck rigidity Medical Emergency Lumbar Puncture PMNs , Protein, Glucose and Cloudy Direct Extension : Sinises,OM or Through Blood Meningitis

18. Sinusitis and O.M • Sinusitis : S.pneumoniae most common cause, follow allergy or viral infection • O.M : S.pneumoniae most common cause, follow allergy or viral infection which prevent eustachian tube drainage.

19. Host Defense and Immunity • IgG Antibodies : Type specific immunity • Classical Pathway Immunity: C1 activated by capsule: Antibody -dependent Opsonization • Alternative Pathway Complement Antibody -independent Opsonization • C5a complement : chemotaxis attract PMNs • Vaccine :Immunity for few years

20. Treatment and Prevention • Treatment • PenicillinG ↑ resistant recently due to PBP alternation • Ceftriaxone for meningitis • Ceftriaxone +/-Vancomycin and or Rifampicin • Vaccination • Polsaccharide capsule • Conjugate vaccine • Indication • Children • SCD • Splenectomised patient • HIV • Elderly • Cardiopulmonary and renal diseases

21. VIRIDANS STREPTOCOCCI • Streptococcus Viridans Group • Mitis • Mutans • Salvarius • Angionosis • Extracellular aerobic Gram positive cocci in chains and pairs • Gray-white variable colony on BAP • No exotoxin

22. Virulence Factors • Dextran exopolysaccharide glycocalx: • Provides means of adherence to defective hearts valves • May block the action of antibiotics • Lipoteichoic Acid (LTA): mediates adhesion to fibronectin in clots on defective heart valves • Glucan: Polysaccharides made by S.mutans from sucrosein the mouth , they provide a mean of attachement to teeth enamel. • Other Acids: Made by S.mutans from fermentation of sugars in the mouth contributed to tooth decay

23. 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

24. Laboratory tests • Catalase : -ve • Hemolysis: Alpha • 6.5% NaCl : No growth • Bile Esculin : -ve • Bile Solubility : -ve • Optochin : Resistant • CAMP Test : -ve • Lancefield ; Non (CHO C)

25. Clinical • Normal Flora in the Oropharynx ,GIT and GUT, enters blood after dental work or due to poor oral hygiene • Bacteremia : S.mutan . • Sub-acute Endocarditis: most common cause , after bacteremia due to dental work and infect maily abnormal valve or prosthetic valve , rarely normal valves. It is fatal if not treated. • Dental caries: see above. • Lysis of bacteria by serum enzyme and lysosomal enzyme. • No vaccine available

26. Treatment • Dental prophylaxis : One hour before procedure in case of abnormal valve with ampicillin • Ampicillin +/- aminoglycoside in case of endocarditis • Vancomycin in penicillin allergic patient

27. Treatment

28. Enterococcus • Fecal strep separated genus/by molecular • Enterococcus Faecalis and E.Faecium • Extracellular Aerobic Gram positive cocci single in chains or pairs • Gray –white or variable colony on BAP • Non Motile, Not capsulated, no Glycocalx and No Exotoxin • Adhesion to defective heart valves and urinary tract • Antibiotics resistant

29. Laboratory Tests • Catalase : -ve • Hemolysis: Alpha, Beta or Gamma • 6.5% NaCl : Growth • PYR : + ve and LAP : +ve • Growth at 45 oC • 40% Bile Salt: +ve • Bile Esculin : +ve • CAMP Test : -ve • Lancefield ; group D (CHO C)

30. Source and Transmission • Normal Flora in GIT in human • Harsh condition Abiquitous / soil,water,plants, GIT, GU human • 15 Spp/E.faecalis80-90% of clinical isolate • Bacteremia after urinary tract infection, Intra-abdominal route or via indwelling catheters • Exogenous acquisition in the hospital (nosocomial)

31. Clinical • Urinary tract infection (UTI) : Nosocomial, upper and lower UTI • Bacteremia: From UTI , Intra-abdominal infection or indwelling catheter ( Intravenous or hemodialysis) , common in I’C patients • Sub-Acute Endocarditis : After bacteremia, affects abnormal or prosthetic valves , it is fatal if not treated • Host defense and immunity is unknown

32. Treatment and prevention • Ampicillin in case of UTI by E.faecalis • Vancomycin in case of E.faecium • Ampicillin or Vancomycin + gentamicine in case of endocarditis • Streptogramin or Linazolid in case of Vancomycin Resistant Enterococcus (VRE) • Infection control measures in case of VRE outbreak • No vaccine available

33. Endocarditis

34. Streptococcus Bovis ( Streptococcus gallolyticus NEW NAME) • Group D streptococci • Aerobic extracellular Gram positive cocci in chains or pairs • Gray-white colony on BAP • Non-Motile, Non-Capsulated and Glycocalyx • No Valulant factors

35. Laboratory Tests • Catalase : -ve • Hemolysis: Alpha, Beta or Gamma • 6.5% NaCl : No growth (opposite to enterococcus) • PYR : -ve (opposite to enterococcus) • No Growth at 45 oC (opposite to enterococcus) • 40% Bile Salt: +ve (opposite to viridans) • Bile Esculin : +ve (opposite to viridans) • CAMP Test : -ve • Lancefield ; group D (CHO C) • Two biotypes I &II

36. Clinical • Normal Flora in GIT • Infection after diruption of GI epithelium in case of malignancy • Bacteremia from GIT • Endocarditis after bacteremia, fatal if not treated • Colonic cancer has strong association with S.bovis bacteremia • IgA, IgG and PMNs • Treatment penicillin or vancomycin( rarely resistant to vancomycin) • No vaccination available

37. Summary + - +