MMI-Exam 2-Lecture 11: Staphylococcus

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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
    Beta/Non-hemolytic
  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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