staphylococcus Flashcards
gram staining
§ Reflects a fundamental differentiation based on permeability, presence or absence of outer membrane and cell wall thickness
4 typical cell types, which are common with one another?
Gram (+) rods
Gram (+) cocci
Gram (-) rods
Gram (-) cocci
• Gram positive rods have more in common with gram positive cocci than with gram negative rods
Gram positive cocci types
staphylococcus and streptococcus
Staphylococci types
where found?
often associated with?
S. aureus; S. saprophyticus; S. epidermidis
§ Found in many body sites; primarily skin infections &wounds; carbuncles; abscesses; leading to life threatening deep tissue infections: osteomyelitis,
endocarditis
§ Severe intoxications; Food poisoning
Streptococci
groups?
O2 use?
§ Alpha or beta hemolysis
Alpha: S. pneumoniae
Beta: Groups A-T; Group A most prevalent in human disease
§ faculative anaerobes
Bacteroides fragilis
ü Most common organism in the human intestine.
ü Can cause serious disease when deposited into deep tissues.
(abscesses)
ü Can be also be found in gingival pockets
ü Very stinky
Staphylococcus aureus gram? shape? color? catalase?
Gram +
cocci
gold
catalase +
S. aureus cell wall
Variations in oxygen requirement and tolerance for S. aureus
Facualtive anaerobe
Virulence Factors of staphylococci (10 total)
catalase coagulase clumping factor protein A leukocidin digestive enzymes staphylokinase B-lactamase hemolysins secreted exotoxins
catalase
Reduces the potential of phagocytes to kill, conversion H2O2 to water and o2
coagulase
how does it relate to tissue invasive potential?
what strain is it in?
what action does it have?
The tissue-invasive potential of staphylococcal infections is directly proportional to coagulase production (S.aureus; not in other Staph. species).
coagulase binds prothrombin: fibrinogen is cleaved anti-phagocytic fibrin coating on bacteria
clumping factor
fibrinogen-binding protein: cell surface proteins that bind to foreign materials (like sutures) and to extracellular matrix.
protein A action
on what species?
Anti-phagocytic, competes with neutrophils for Fc portion of opsonizing IgGs
on cell surface of S.aureus but not on other staphylococcal strains
leukocidins
how they work
major factor in the formation of what?
secretion: inhibits phagocytosis by forming pores in
phagosomal membranes which kills phagocytes.
Major factor in pus formation.
digestive enzymes
proteases, DNase, nuclease, lipases, hyaluronidase (spreading factor: digests extracellular matrix)
staphylokinase functions
additional function?
converts plasminogen to plasmin, increasing invasion by digesting fibrin clots
also cleaves C3b and IgG to inhibit phagocytosis
β-lactamase
Enzymatic digestion of penicillins (90% strains have plasmid-based antibiotic resistance)
hemolysins
α-, β-, γ-, and δ-toxins are all hemolysins: lyse erythrocytes (lab phenomenon)
alpha hemolyisns
kill what cells?
destroy what strucutre?
paralysis?
α-hemolysins (pores) are hemolytic and leukocytic
will destroy skin, cause smooth muscle paralysis
beta hemolysins
β-hemolysins are cytolytic sphingomyelinases that destroy nerves
γ-hemolysins
lyse like related leukocidin on neutrophil lysosomal membranes
hemolysins seen in which species
S. aureus
impetigo
caused by what strain?
affects what tissues?
accumulation of?
caused by S. aureus
skin and deeper tissue infection, accumulation of pus due to cell death
Empyema:
Collection of pus in a naturally existing anatomical cavity e.g. lungs, may be due to impetigo
pyogenic infections:
pus-forming (massive amounts of neutrophils and other leukocytes are lysed by bacterial factors (e.g. leukocidin) and release their lysosomal contents in attempting phagocytic killing of the staphylococci
folliculitis progression
Secreted exo-toxins of staphylcocci
super Ag: enterotoxins and TSST
others: exfoliative toxin
enterotoxins
super Ag
Heat-stable (cooking doesnt help!)
cause of gastrointestinal upset typical of food poisoning
TSST
super Ag
mass activation of T cells leads to large production of inflammatory cytokines
exfoliative toxin
heat?
causes what disorder?
production local? effects?
exfoliative toxin (heat-stable, chromosomal), B (heat-labile, plasmid) : SSSS
(staphylococcal scalded-skin syndrome)
toxin is produced locally but is distributed and acts systemically
TSS: Toxic Shock Syndrome
Increased oxygenation of vagina by tampons, and foreign surface adhesion, caused massive growth
allow aureus to grow and produce toxins
SSSS, what agents cause this?
cause loss of?
resolved with?
Ø exfoliative toxins A, B cause loss of layers of the skin in SSSS
resolved with Neutralizing Ab, recover without scarring
Nosocomial Staphylococci, what is the common species? coagulase + or -?
surgery, implant & instrument risk
often coagulase-negative S.epidermidis
endocarditis, species involved?
dental risk?
- acute: 60% S.aureus
- if artificial heart valves: 80% S.epidermidis
S.epidermidis: dental extraction risk
most frequent cause of bacterial arthrirts
S. aureus in all age groups
Epidemiology of S. aureus
found?
surface survival/hospitals?
temp/salt resistance?
found on skin, mucosa and aerosols
good surface survival (hospitals= nosocomial)
high temp and salt resistant too
resistances found in S. aureus
β-lactamase (plasmid): >90% penicillin resistant
penicillin-binding protein 2a (chromosomal): causes Methicillin Resistance
50% of hospital strains are MRSA; 20% of community strains are MRSA
VRSA possible
coagulase - strains
cell walls/capsules?
secrete?
where they are a problem?
Other Staphylococci like S.epidermidis or S.saprophyticus
• Thick cell wall, slime capsule, (S.saprophyticus: urease secretion → acute cystitis
• Opportunistic hospital pathogens (instruments, catheters, heart valves)
