staphylococcus Flashcards

1
Q

gram staining

A

§ Reflects a fundamental differentiation based on permeability, presence or absence of outer membrane and cell wall thickness

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2
Q

4 typical cell types, which are common with one another?

A

Gram (+) rods
Gram (+) cocci
Gram (-) rods
Gram (-) cocci

• Gram positive rods have more in common with gram positive cocci than with gram negative rods

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3
Q

Gram positive cocci types

A

staphylococcus and streptococcus

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4
Q

Staphylococci types
where found?
often associated with?

A

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

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5
Q

Streptococci
groups?
O2 use?

A

§ Alpha or beta hemolysis
Alpha: S. pneumoniae
Beta: Groups A-T; Group A most prevalent in human disease

§ faculative anaerobes

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6
Q

Bacteroides fragilis

A

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

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7
Q
Staphylococcus aureus 
gram?
shape?
color?
catalase?
A

Gram +
cocci
gold
catalase +

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8
Q

S. aureus cell wall

A
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9
Q

Variations in oxygen requirement and tolerance for S. aureus

A

Facualtive anaerobe

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10
Q

Virulence Factors of staphylococci (10 total)

A
catalase 
coagulase 
clumping factor 
protein A
leukocidin 
digestive enzymes
staphylokinase 
B-lactamase
hemolysins
secreted exotoxins
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11
Q

catalase

A

Reduces the potential of phagocytes to kill, conversion H2O2 to water and o2

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12
Q

coagulase
how does it relate to tissue invasive potential?
what strain is it in?
what action does it have?

A

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

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13
Q

clumping factor

A

fibrinogen-binding protein: cell surface proteins that bind to foreign materials (like sutures) and to extracellular matrix.

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14
Q

protein A action

on what species?

A

Anti-phagocytic, competes with neutrophils for Fc portion of opsonizing IgGs
on cell surface of S.aureus but not on other staphylococcal strains

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15
Q

leukocidins
how they work
major factor in the formation of what?

A

secretion: inhibits phagocytosis by forming pores in
phagosomal membranes which kills phagocytes.
Major factor in pus formation.

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16
Q

digestive enzymes

A

proteases, DNase, nuclease, lipases, hyaluronidase (spreading factor: digests extracellular matrix)

17
Q

staphylokinase functions

additional function?

A

converts plasminogen to plasmin, increasing invasion by digesting fibrin clots
also cleaves C3b and IgG to inhibit phagocytosis

18
Q

β-lactamase

A

Enzymatic digestion of penicillins (90% strains have plasmid-based antibiotic resistance)

19
Q

hemolysins

A

α-, β-, γ-, and δ-toxins are all hemolysins: lyse erythrocytes (lab phenomenon)

20
Q

alpha hemolyisns
kill what cells?
destroy what strucutre?
paralysis?

A

α-hemolysins (pores) are hemolytic and leukocytic

will destroy skin, cause smooth muscle paralysis

21
Q

beta hemolysins

A

β-hemolysins are cytolytic sphingomyelinases that destroy nerves

22
Q

γ-hemolysins

A

lyse like related leukocidin on neutrophil lysosomal membranes

23
Q

hemolysins seen in which species

24
Q

impetigo
caused by what strain?
affects what tissues?
accumulation of?

A

caused by S. aureus

skin and deeper tissue infection, accumulation of pus due to cell death

25
Empyema:
Collection of pus in a naturally existing anatomical cavity e.g. lungs, may be due to impetigo
26
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
27
folliculitis progression
28
Secreted exo-toxins of staphylcocci
super Ag: enterotoxins and TSST | others: exfoliative toxin
29
enterotoxins
super Ag Heat-stable (cooking doesnt help!) cause of gastrointestinal upset typical of food poisoning
30
TSST
super Ag | mass activation of T cells leads to large production of inflammatory cytokines
31
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
32
TSS: Toxic Shock Syndrome
Increased oxygenation of vagina by tampons, and foreign surface adhesion, caused massive growth allow aureus to grow and produce toxins
33
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
34
Nosocomial Staphylococci, what is the common species? coagulase + or -?
surgery, implant & instrument risk | often coagulase-negative S.epidermidis
35
endocarditis, species involved? | dental risk?
* acute: 60% S.aureus * if artificial heart valves: 80% S.epidermidis S.epidermidis: dental extraction risk
36
most frequent cause of bacterial arthrirts
S. aureus in all age groups
37
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
38
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
39
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)