-
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 +
-
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
-
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)
-
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
-
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)
-
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
-
Tissue Destroying Enzymes
- Destroy Everything
- -Hyaluronidase
- -Lipase
- -Nuclease
- -
-
Fibrinolysin
- -Fibrinolysin (Staphylokinase)
- -Immune evasion enzymes/binding proteins -Staphylokinase: Activates plasminogen to form plasmin, digest fibrin clots
- -Disrupt fibrin meshwork
-
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
-
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
-
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)
-
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
-
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.
-
Hemolytic Nature of S. aureus
Beta/Non-hemolytic
-
S. aureus can do what to Neutrophils
They can lyse them from within
-
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)
-
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
-
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
-
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
-
S. aureus Clinical Isolates show what type of capsule
Type 5 or 8
-
Diseases Caused by Pathogenic S. aureus
- -Toxic diseases
- -Cutaneous diseases
- -Pneumonia
- -Endocarditas
- -Osteomyeltis
- -Wound infections
- -Often induces copious pus production=pyogenic pathogen
-
Diseases Caused by Pathogenic S. epidermidis
- -Infections of prosthetic devices
- -Infections of catheters
-
Diseases Caused by Pathogenic S. saprophyticus
-Urinary tract infection of young women
-
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
-
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
-
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
-
Skin and Tissue infection
Impetigo, Folliculitis, Furuncles/Boils, Carbuncles, Wound infection
-
Impetigo
- -Caused by group A streptococci (S. pyogenes)
- -Involves formation of multiple pustules on skin
- -Rupture and form crusty legions
-
Folliculitis
- -Pus-filled (pyogenic) infections of hair follicles
- -Folliculitis of eyelash is a stye
-
Furuncles/boils
-Progression of folliculitis where large reddened nodule develop
-
Carbuncles
- -Groups of furuncles join together
- -Connect through sinuses, involve deeper subcutaneous tissue
- -May result in bacteremia, spread to other tissues may occur
-
Wound Infections
-Can result from exposure of deeper tissues to Staphylococci -Stiches, surgery, splinters, traumatic wounds
-
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
-
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
-
Osteomyelitis (S. aureus)
- -Trauma leading to spread of S. aureus to long bones
- -May require surgery to drain and debride the infected tissue
-
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
-
Staphylococcus saprophyticus
- -Coagulase(-) staphylococci
- -Common cause of urinary tract
- infection (cystitis) in young women
-
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
|
|