MMI-Exam 2-Lecture 11: Staphylococcus

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  1. Staphylococcus Morphology
    • Forms clumps, divide in alternating planes (x then y axis)
    • -Gram + cocci
    • -1 micrometer diameter
    • -Nonmotile
    • -Facultative anaerobe
    • -Non-spore forming
    • -Catalase +
    • -S. aureus is coagulase +
  2. Important Staphyococci
    • -Aureus
    • -Colonizes nasal cavity (anterior nares), and on skin
    • -Opportunistic pathogen
    • -Main pathogenic strain
    • -Epidermidis
    • -Inhabit skin (normal biota)
    • -Protect against incursion by other pathogens
    • -Saprophyticus
    • -Part of normal biota
    • -Implicated in urinary tract infections of young women
  3. Laboratory Growth
    • -Grown easily on BAP, at 37 degrees C, colonies form in 24 hrs
    • -Selective/Differential plate for Aureus
    • -Grow on plates containing 7.5% NaCl (selective)
    • -Ferments mannitol, turns medium to yellow
    • (selective)
  4. Staphylococci Diagnostic Enzymes: Coagulase
    • -most important for detection of aureus
    • -Converts fibrinogen to insoluble fibrin
    • -Bound:causes clumping
    • -Free: reacts wit globulin plasma to form staphylothrombin
    • -May form protective fibrin layer around staphylococcal abscess
    • -Found in S. aureus, but not in others
  5. Coagulase Test for Staphylococci
    • -Dilute
    • human plasma mixed with staph-cells
    • -If coagulase produces, clot is formed
    • -Differentiates S. epidermidis from S. saprophyticus
    • -S. saprophyticus is resistant to novobiocin (a DNA gyrase inhibitor)

  6. Catalase and Catalase Test
    • -Catalase: differentiates between staphy (+) and strep (-)
    • -CatalaseTest:
    • -Rapid test to differentiate staphylococci from streptococci
    • -Put a drop of hydrogen peroxide onto colony
    • -Positive reaction if bubbling
  7. Tissue Destroying Enzymes
    • Destroy Everything
    • -Hyaluronidase
    • -Lipase
    • -Nuclease
    • -
  8. Fibrinolysin
    • -Fibrinolysin (Staphylokinase)    
    • -Immune evasion enzymes/binding proteins     -Staphylokinase: Activates plasminogen to form plasmin, digest fibrin clots            
    • -Disrupt fibrin meshwork
  9. Protein A
    • -Binds Fc fragment of some classes of immunoglobulin
    • -This prevents the Ig from doing job (i.e. opsonization)
    •      -Fc fragments normally bind to phagocyte, can’t do that if bound to bacteria
    • -Binds receptors for TNF-alpha
    •       -Induces cytokines, leads to inflammation
    • -Binds von Willebrand factor
    •       -serum glycoprotein that mediates
    • platelet aggregation at sites of endothelial damage
    • -Binds to class of variable regions on B-cell surface IgM molecules                                       -Induces apoptosis and poor antibody response
    • -Aids bacteria cell aggregation                        -Forms biofilm
    • -Produced_commercially:                              -Can be coupled to  small beads  
    • -Antibody binds this (through Fc region)             
    • -Placed into complex mixture, allows antigen to be isolated
  10. Staphylococcus aureus Toxins: Alpha Toxin
    • Pore-forming Toxins
    • -Disrupt smooth muscle in blood vessels
    • -Toxic to many cell types
    • -Forms pores in host cell membrane
    •       -Results in an influx of ions/cell lysis
  11. Staphylococcus aureus Toxins: Beta Toxin
    • Sphingomyelinase C
    • -Catalyzes hydrolysis of membrane phospholipids (sphingomyelin)
    • -Believed to be responsible for tissue destruction/abscess formation (with A toxin)
  12. Staphylococcal Toxins: Panton-Valentine Leukocidin
    • -Made by <5% of S. aureus  strains, nearly all community-acquired MRSA strains
    • -Encoded by prophage (lysogenesis)
    • -Two different soluble proteins (LukS/LukF) combine on phagocytic cell membrane, form   pore on phagocytic cell membrane that leads to leukotoxicity
    • -Significance of PV leucocidin in pathogenesis in controversial
  13. Staphylococcal Toxins: Phenol-soluble Modulins (PSMs)
    • -Small surfactant peptides (20-25 AA)
    • -Produced by methylcillin-resistent S. aureus (MRSA)/some S. epidermidis strains
    • -Delta toxin is a PSM
    • -Can lyse neutrophils and erythrocytes at high concentration
    • -At low concentrations “modulin” activity is observed
    • -Stimulate neutrophils to produce
    • cytokines and to positively chemotax toward local inflammatory site.
  14. Hemolytic Nature of S. aureus
  15. S. aureus can do what to Neutrophils
    They can lyse them from within
  16. Staphylococcal Exotoxins: Exfoliation
    • -Disrupts intercellular junctions
    •       -Splits epidermal layers of skin
    •       -Results in desquamation of epidermis
    • -Carried by about 5% of S. aureus
    • -Cause clinical signs of staphylococcal scaled skin syndrome (SSSS)
  17. Staphylococcal Exotoxins: Toxic Shock Syndrome Toxin (TSST)
    • -Associated with TSS causing S. aureus strains
    • -Binds host cells, induces cytokine production -This leads to disease
    • -Evolutionarily related to enterotoxins
  18. Staphylococcal Enterotoxins
    • -Heat (100 degree C) and acid (stomach pH)-stable
    • -Produced in foods contaminated with staphylococci
    • -Infestation of only toxin (w/o bacteria) can cause illness
    • -Binding of toxin to host cells releases cytokines
    • -Are Superantigens
  19. Superantigens
    • -Super antigens bind MHCII complex of antigen presenting cell
    • -Where normal antigens would then bind
    • to TCR of a proper T cell to release cytokines/proliferate specialized T cells,
    • superantigens bind to every T cell
    • -Lots of cytokines, lots of useless T cells
    • -Results in shock
  20. S. aureus Clinical Isolates show what type of capsule
    Type 5 or 8
  21. Diseases Caused by Pathogenic S. aureus
    • -Toxic diseases
    • -Cutaneous diseases
    • -Pneumonia
    • -Endocarditas
    • -Osteomyeltis
    • -Wound infections                                         
    •      -Often induces copious pus production=pyogenic pathogen
  22. Diseases Caused by Pathogenic S. epidermidis
    • -Infections of prosthetic devices
    • -Infections of catheters
  23. Diseases Caused by Pathogenic S. saprophyticus
    -Urinary tract infection of young women
  24. Toxic Shock Syndrome (TSS)
    • -Localized infection in which staphylococci produce TSST-1 toxin
    • -Causes_systemic_disease                                                             -Sudden fever, hypotension, diffuse erythematous rash
    • -Left undiagnosed, can cause multiple organ failure
    • -Can recur if antibiotic not effective/patient doesn’t develop TSST-1 antibodies
    • -Wide-spread recognition of disease
    • alongside illness/death of women with hyper-absorbant tampons
  25. Staphylococcal Food Poisoning
    • -Occurs when human carrier of S. aureus inoculates improperly refrigerated food.
    • -Organism multiplies and produces enterotoxin in food
    • -Important to note that even if bacteria dies, heat/acid resistant toxin can live
    • -Manifests 4-12 hour after consumption
    • -Severe vomiting, diarrhea, abdominal pain, nausea
    • -Self-limiting disease, recovery in 24 hours usually
  26. Staphylococcal Scalded Skin Syndrome (SSSS)
    • -Occurs in small children
    • -Characterized by abrupt onset of erythema (skin inflammation)
    • -Starts at mouth, covers whole body
    • -Bullae (cutaneous blisters) develop,
    • filled with clear liquid, lack leukocytes/staphylococci
    • -Clears in 7-10 days, no lasting
    • scarring
    • -Results from production of
    • exofoliatin at local site, disseminates through body
    • -Bullous impetigo- localized blisters that are
    • positive for Staphylococci
  27. Skin and Tissue infection
    Impetigo, Folliculitis, Furuncles/Boils, Carbuncles, Wound infection
  28. Impetigo
    • -Caused by group A streptococci (S. pyogenes)
    • -Involves formation of multiple pustules on skin
    • -Rupture and form crusty legions
  29. Folliculitis
    • -Pus-filled (pyogenic) infections of hair follicles
    • -Folliculitis of eyelash is a stye
  30. Furuncles/boils
    -Progression of folliculitis where large reddened nodule develop
  31. Carbuncles
    • -Groups of furuncles join together
    • -Connect through sinuses, involve deeper subcutaneous tissue
    • -May result in bacteremia, spread to other tissues may occur
  32. Wound Infections
    -Can result from exposure of deeper tissues to Staphylococci                                                            -Stiches, surgery, splinters, traumatic wounds
  33. Bacteremia/endocarditis (S. aureus)
    • -S. aureus
    • one of common causes
    • -Often associated with indwelling catheters, use of ‘dirty’ needles
    • -Heart tissue infection is a serious example
  34. Pneumonia (S. aureus)
    • -Can result from aspiration of oral secretions, or spread by blood stream
    • -Can be life-threatening consequence of viral influenza/cystic fibrosis
  35. Osteomyelitis (S. aureus)
    • -Trauma leading to spread of S. aureus to long bones
    • -May require surgery to drain and debride the infected tissue
  36. Staphylococcus epidermidis Morphology
    • -Coagulase(-)  staphylococci
    • -Commonly responsible for infection of replacement heart valves (pig and artificial)
    • -Common cause of catheter and prosthetic joint infection
    • -Can attach to and grow on artificial materials used in medicine
  37. Staphylococcus saprophyticus
    • -Coagulase(-) staphylococci
    • -Common cause of urinary tract
    • infection (cystitis) in young women
  38. Nosocomial Infection
    • -Epidermidis/aureus are common hospital acquired pathogens
    • -Easily spread by hand contact
    • -Both can be resistant to many anti-biotics
    • -MRSA commonly treated with Vancomycin
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MMI-Exam 2-Lecture 11: Staphylococcus
2013-10-25 22:08:46

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