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Staphylococcus Eva L. Dizon, M.D.,FPPS,FPIDSP
Staphylococcus Staphyle- Bunch of grapes 0.5 to 1 um Non motile Aerobic or Facultative Anaerobic Catalase positive Grow in media containing 10% NaCl at temp 18 to 40 C Present on the skin and mucuos membrane
Species S. aureus S. epidermidis S. saphrophyticus S. capitis S. haemolyticus Micrococcus sp Stomatococcus mucilaginosus Alloiococcus otitidis
Physiology and Structure
Structure
 
Structure CAPSULE - loose fitting polysaccharide layer  (slime layer) - protects bacteria by inhibiting  chemotaxis and phagocytosis - facilitates adherence of bacteria to  catheters and synthetic materials PEPTIDOGLYCAN - half of the cell wall - consist of layers of glycan chains with  alternating subunits of N –acetylmuramic  acid and N- acetylglucosamine - has endotoxin like activity
Structure TEICHOIC ACID-  phosphate containing polymers  bound to peptidoglycan layer or to  cytplasmic membrane - mediates the attachment of  staphylococcus to mucosal surfaces S. aureus  Ribitol teichoic acid with N-acetylglucosamine  ( Polysaccharide A)  S. epidermidis  glycerol  teichoic acid with glucosyl residues (polysaccharide B)-
PROTEIN A-  covalentlylinked to peptidoglycan   - has affinity to Fc receptor of Ig  - blocks opsonization and phagocytosis
Structure CYTOPLASMIC MEMBRANE-  osmotic barrier for the  cell and provides an anchorage for the  biosynthetic and respiratory enzyme COAGULASE and other SURFACE PROTEIN -Clumping factor or Bound coagulase  binds fibrinogen convert to insoluble  fibrin causing staphylococcus to  clump - collagen , elastin and fibronectin binding  protein
Toxins A.  5 Cytolytic or membrane damage toxin Alpha Beta Gamma Delta Panton Valentine  B.  2 Exfoliative toxin C.  8 Enterotoxin D.  Toxic Shock Syndrome Toxin(TSST 1)
Cytotoxins Lyse neutrophils    release of lysosomal enzymes    damage sorrounding tissues Alpha toxin  – disrupts the smooth muscle in blood      vessels    - toxic to erythrocytes, hepatocytes,      platelets, cultivated cells   - integrates to host cell membrane         pores    efflux of K and influx of Na,Ca        osmotic swelling    cell lysis - septic shock
Cytotoxin Beta Toxin  -  Sphingomyelinase C   - specific for sphingomyelin and      lysophosphatidylcholine   - toxic to RBC, WBC,Macrophage and fibroblast   - catalyze hydrolysis of  membrane phospholipids in    susceptible cells   - tissue destruction and abscess formation Delta toxin-  disrupts cell membrane   - toxic to variety of cells
Cytotoxin Gamma toxin and Panton Valentine -both damage membrane of susceptible cells - lyze nuetrophils and macrophages - cell lysis is mediated by pore formation Cause necrotizing skin infection  -PVL -potent leukotoxicity
Exfoliative toxin ETA - heat stable ETB – heat labile Serine protease  Exposure    splitting of desmosomes or intercellular bridges in the stratum granulosum epidermis Common in neonates – ETA and ETB binds to GM4 like glycolipids present in neonates
Enterotoxin A-E, G-I Stable to heating , resistant to hydrolysis Enterotoxin A – most commonly associated with disease Enterotoxin C and D- contaminated milk products Enterotoxin B- Pseudomembranous colitis Superantigens
 
TSST-1 Formerly pyrogenic exotoxin C and entertoxin F Induce cytokine release from macrophage and T lymphocytes Increase sensitivity to endotoxin Produce leakage of endothelial cells Penetrate mucosal barrier
Staphylococcal enzymes convert fibrinogen   react with globulin    plasma factor    insoluble fibrin to form  staphylothrombin   Clumping Cause formation of fibrin layer  around abscess protecting staphylococcus from phagocytosis Coagulase Bound  Free
Staphylococcal enzymes Catalase - catalyze the conversion of toxic hydrogen peroxide to water and oxygen Hyalurodinase - hydrolyzes hyaluronic acid in acellular matrix of connective tissue    spread
Staphylococcal enzymes Fibrinolysin- staphylokinase . Dissolve fibrin clot- aid in bacterial spreading Lipases hydrolyse lipid to ensure survival in sebaceous areas of the body Nuclease  Penicillinase- plasmid Fatty acid modifying enzyme (FAME)- antibacterial lipid- prolonged bacterial survival
Epidemiology Transient colonizer of skin Nasal carriage – anterior nasopharynx Persistent carrier – hospital personnel Killed by high temperature and disinfectant Direct contact, fomites Handwashing
Sites of infection
Ritters disease or SSSS Perioral erythema   spread    body   bullous   desquamation Nikolsky sign Bullous impetigo – localized form of SSSS - localized blister   - culture positive
SSSS most commonly in children and neonates. Starts abruptly with perioral (around the mouth) erythema with sunburn-like rash rapidly turning bright red spreading to bullae (large vesicle appearing as a circumscribed area) in 2-3 days and desquamating (peeling) within 5 days.
Staphylococcal food poisoning Ham , salted pork, custard, potato sald, ice cream Hands, Nasal carriage I.P. – 4 hrs Vomiting, diarrhea, abd. pain
Toxic shock syndrome Growth of organism in vagina or wound   release of TSST-1 Fever, macular erythematous rashes, hypotension, multiorgan involvement, desquamation of palm and sole
TSS
Cutaneous infection Impetigo Folliculitis Furuncle Carbuncle Wound infection
Folliculitis - superficial folliculitis is essentially a staphylococcal  impetigo in which a small area of erythema develops around a hair follicle and subsequently becomes a dome-shaped pustule. Carbuncle - a deep-seated pyogenic infection of the skin and subcutaneous tissues.
Impetigo - a contagious superficial pyoderma, caused by S. aureus and Streptococcus pyogenes, that begins with a superficial flaccid vesicle which  ruptures and forms a thick yellowish crust, most commonly occurring in the face.
Others  Bacteremia Endocarditis  Pneumonia Empyema Osteomyelitis Septic arthritis
Pneumonia
S.Epidermidis and CNS Endocarditis- native or artificial valves Catheter and shunt infection Prosthetic joint infection UTI
Laboratory diagnosis Microscopy Culture Grow rapidly within 24 hours Large, golden, smooth colonies Blood Agar- hemolysis Selective media- add NaCl 7.5% Mannitol – fermented by S. aureus Serology Insensitive  Antibody against teichoic acid Bacteremia. Endocarditis  After 2 weeks
Culture – S. aureus
S. epidermidis  S. saphrophyticus
Coagulase test Showing positive (upper tube) and negative (lower tube) coagulase tests.
Mannitol Salt Agar test
Identification Biochemical testing Coagulase  Heat stable  nuclease Alkaline phospatase Mannitol fermentation test
Treatment and Prevention Semisynthetic penicillinase resistant penicillin Resistance ( mecgene A –codes for PBP 2’)
 
 
Thank You

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Staphylococcus (1)

  • 1. Staphylococcus Eva L. Dizon, M.D.,FPPS,FPIDSP
  • 2. Staphylococcus Staphyle- Bunch of grapes 0.5 to 1 um Non motile Aerobic or Facultative Anaerobic Catalase positive Grow in media containing 10% NaCl at temp 18 to 40 C Present on the skin and mucuos membrane
  • 3. Species S. aureus S. epidermidis S. saphrophyticus S. capitis S. haemolyticus Micrococcus sp Stomatococcus mucilaginosus Alloiococcus otitidis
  • 6.  
  • 7. Structure CAPSULE - loose fitting polysaccharide layer (slime layer) - protects bacteria by inhibiting chemotaxis and phagocytosis - facilitates adherence of bacteria to catheters and synthetic materials PEPTIDOGLYCAN - half of the cell wall - consist of layers of glycan chains with alternating subunits of N –acetylmuramic acid and N- acetylglucosamine - has endotoxin like activity
  • 8. Structure TEICHOIC ACID- phosphate containing polymers bound to peptidoglycan layer or to cytplasmic membrane - mediates the attachment of staphylococcus to mucosal surfaces S. aureus Ribitol teichoic acid with N-acetylglucosamine ( Polysaccharide A) S. epidermidis glycerol teichoic acid with glucosyl residues (polysaccharide B)-
  • 9. PROTEIN A- covalentlylinked to peptidoglycan - has affinity to Fc receptor of Ig - blocks opsonization and phagocytosis
  • 10. Structure CYTOPLASMIC MEMBRANE- osmotic barrier for the cell and provides an anchorage for the biosynthetic and respiratory enzyme COAGULASE and other SURFACE PROTEIN -Clumping factor or Bound coagulase binds fibrinogen convert to insoluble fibrin causing staphylococcus to clump - collagen , elastin and fibronectin binding protein
  • 11. Toxins A. 5 Cytolytic or membrane damage toxin Alpha Beta Gamma Delta Panton Valentine B. 2 Exfoliative toxin C. 8 Enterotoxin D. Toxic Shock Syndrome Toxin(TSST 1)
  • 12. Cytotoxins Lyse neutrophils  release of lysosomal enzymes  damage sorrounding tissues Alpha toxin – disrupts the smooth muscle in blood vessels - toxic to erythrocytes, hepatocytes, platelets, cultivated cells - integrates to host cell membrane  pores  efflux of K and influx of Na,Ca  osmotic swelling  cell lysis - septic shock
  • 13. Cytotoxin Beta Toxin - Sphingomyelinase C - specific for sphingomyelin and lysophosphatidylcholine - toxic to RBC, WBC,Macrophage and fibroblast - catalyze hydrolysis of membrane phospholipids in susceptible cells - tissue destruction and abscess formation Delta toxin- disrupts cell membrane - toxic to variety of cells
  • 14. Cytotoxin Gamma toxin and Panton Valentine -both damage membrane of susceptible cells - lyze nuetrophils and macrophages - cell lysis is mediated by pore formation Cause necrotizing skin infection -PVL -potent leukotoxicity
  • 15. Exfoliative toxin ETA - heat stable ETB – heat labile Serine protease Exposure  splitting of desmosomes or intercellular bridges in the stratum granulosum epidermis Common in neonates – ETA and ETB binds to GM4 like glycolipids present in neonates
  • 16. Enterotoxin A-E, G-I Stable to heating , resistant to hydrolysis Enterotoxin A – most commonly associated with disease Enterotoxin C and D- contaminated milk products Enterotoxin B- Pseudomembranous colitis Superantigens
  • 17.  
  • 18. TSST-1 Formerly pyrogenic exotoxin C and entertoxin F Induce cytokine release from macrophage and T lymphocytes Increase sensitivity to endotoxin Produce leakage of endothelial cells Penetrate mucosal barrier
  • 19. Staphylococcal enzymes convert fibrinogen react with globulin plasma factor insoluble fibrin to form staphylothrombin Clumping Cause formation of fibrin layer around abscess protecting staphylococcus from phagocytosis Coagulase Bound Free
  • 20. Staphylococcal enzymes Catalase - catalyze the conversion of toxic hydrogen peroxide to water and oxygen Hyalurodinase - hydrolyzes hyaluronic acid in acellular matrix of connective tissue  spread
  • 21. Staphylococcal enzymes Fibrinolysin- staphylokinase . Dissolve fibrin clot- aid in bacterial spreading Lipases hydrolyse lipid to ensure survival in sebaceous areas of the body Nuclease Penicillinase- plasmid Fatty acid modifying enzyme (FAME)- antibacterial lipid- prolonged bacterial survival
  • 22. Epidemiology Transient colonizer of skin Nasal carriage – anterior nasopharynx Persistent carrier – hospital personnel Killed by high temperature and disinfectant Direct contact, fomites Handwashing
  • 24. Ritters disease or SSSS Perioral erythema  spread  body  bullous  desquamation Nikolsky sign Bullous impetigo – localized form of SSSS - localized blister - culture positive
  • 25. SSSS most commonly in children and neonates. Starts abruptly with perioral (around the mouth) erythema with sunburn-like rash rapidly turning bright red spreading to bullae (large vesicle appearing as a circumscribed area) in 2-3 days and desquamating (peeling) within 5 days.
  • 26. Staphylococcal food poisoning Ham , salted pork, custard, potato sald, ice cream Hands, Nasal carriage I.P. – 4 hrs Vomiting, diarrhea, abd. pain
  • 27. Toxic shock syndrome Growth of organism in vagina or wound  release of TSST-1 Fever, macular erythematous rashes, hypotension, multiorgan involvement, desquamation of palm and sole
  • 28. TSS
  • 29. Cutaneous infection Impetigo Folliculitis Furuncle Carbuncle Wound infection
  • 30. Folliculitis - superficial folliculitis is essentially a staphylococcal impetigo in which a small area of erythema develops around a hair follicle and subsequently becomes a dome-shaped pustule. Carbuncle - a deep-seated pyogenic infection of the skin and subcutaneous tissues.
  • 31. Impetigo - a contagious superficial pyoderma, caused by S. aureus and Streptococcus pyogenes, that begins with a superficial flaccid vesicle which ruptures and forms a thick yellowish crust, most commonly occurring in the face.
  • 32. Others Bacteremia Endocarditis Pneumonia Empyema Osteomyelitis Septic arthritis
  • 34. S.Epidermidis and CNS Endocarditis- native or artificial valves Catheter and shunt infection Prosthetic joint infection UTI
  • 35. Laboratory diagnosis Microscopy Culture Grow rapidly within 24 hours Large, golden, smooth colonies Blood Agar- hemolysis Selective media- add NaCl 7.5% Mannitol – fermented by S. aureus Serology Insensitive Antibody against teichoic acid Bacteremia. Endocarditis After 2 weeks
  • 36. Culture – S. aureus
  • 37. S. epidermidis S. saphrophyticus
  • 38. Coagulase test Showing positive (upper tube) and negative (lower tube) coagulase tests.
  • 40. Identification Biochemical testing Coagulase Heat stable nuclease Alkaline phospatase Mannitol fermentation test
  • 41. Treatment and Prevention Semisynthetic penicillinase resistant penicillin Resistance ( mecgene A –codes for PBP 2’)
  • 42.  
  • 43.