MMI-Exam 2-Lecture 11: Staphylococcus

• 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 +

• -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

• -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)

• -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

• -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)
• 
  

• -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

• Destroy Everything
• -Hyaluronidase
• -Lipase
• -Nuclease
• -

• -Fibrinolysin (Staphylokinase)    
• -Immune evasion enzymes/binding proteins     -Staphylokinase: Activates plasminogen to form plasmin, digest fibrin clots            
• -Disrupt fibrin meshwork

• -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

• 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

• Sphingomyelinase C
• -Catalyzes hydrolysis of membrane phospholipids (sphingomyelin)
• -Believed to be responsible for tissue destruction/abscess formation (with A toxin)

• -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

• -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.

Beta/Non-hemolytic

They can lyse them from within

• -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)

• -Associated with TSS causing S. aureus strains
• -Binds host cells, induces cytokine production -This leads to disease
• -Evolutionarily related to 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

• -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

Type 5 or 8

• -Toxic diseases
• -Cutaneous diseases
• -Pneumonia
• -Endocarditas
• -Osteomyeltis
• -Wound infections                                         
•      -Often induces copious pus production=pyogenic pathogen

• -Infections of prosthetic devices
• -Infections of catheters

-Urinary tract infection of young women

• -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

• -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

• -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

Impetigo, Folliculitis, Furuncles/Boils, Carbuncles, Wound infection

• -Caused by group A streptococci (S. pyogenes)
• -Involves formation of multiple pustules on skin
• -Rupture and form crusty legions

• -Pus-filled (pyogenic) infections of hair follicles
• -Folliculitis of eyelash is a stye

-Progression of folliculitis where large reddened nodule develop

• -Groups of furuncles join together
• -Connect through sinuses, involve deeper subcutaneous tissue
• -May result in bacteremia, spread to other tissues may occur

-Can result from exposure of deeper tissues to Staphylococci                                                            -Stiches, surgery, splinters, traumatic wounds

• -S. aureus
• one of common causes
• -Often associated with indwelling catheters, use of ‘dirty’ needles
• -Heart tissue infection is a serious example

• -Can result from aspiration of oral secretions, or spread by blood stream
• -Can be life-threatening consequence of viral influenza/cystic fibrosis

• -Trauma leading to spread of S. aureus to long bones
• -May require surgery to drain and debride the infected tissue

• -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

• -Coagulase(-) staphylococci
• -Common cause of urinary tract
• infection (cystitis) in young women

• -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