Gram positive cocci Flashcards

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1
Q

What is the first step in differentiating gram positive cocci?

A

Catalase +: Staph

Catalase -: Strep

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2
Q

If a gram+ cocci is catalase +, what is the next step in differentiating?

A

Coag+: Staph aureus

Coag-: S. epidermis, S. saprophyticus

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3
Q

If a gram+ cocci is catalase + and coag -, what is the next step in differentiating?

A

Novobiocin sensitive: S. epidermis

Novobiocin resistant: S. saprophyticus

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4
Q

What are the main protective factors of Staph Aureus

A

Coagulase: allows fibrin clot formation around organism
Protein A: binds Fc-IgG, preventing opsonization and phagocytosis.
Also: hemolysins, leukocidins, penicillinase

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5
Q

What are the tissue-destroying proteins of Staph Aureus?

A
  1. hyaluronidase (breaks down connective tissue)
  2. Staphylkinase (lyses formed clots)
  3. lipase (breaks down fats)
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6
Q

By what three mechanisms does Staph Aureus cause toxin-mediated disease?

A
  1. Exfoliatin (scalded skin syndrome)
  2. Enterotoxin (food poisoning)
  3. Toxin-Shock-Syndrome-Toxin 1 (TSST): toxic shock syndrome
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7
Q

What does staph aureus exfoliatin toxin cause?

A

Staph scalded skin syndrome.
Exfoliative toxin A and B can diffuse far from local infection site, cause cleavage of middle epidermis, with fine sheets of skin peeling to reveal moist red skin beneath.

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8
Q

How does staph aureus enterotoxin work?

A

Pre-formed heat stable toxin, causes rapid-onset (2-6hrs) food poisoning with non-bloody diarrhea and vomiting < 24 hrs.

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9
Q

How does staph aureus TSST1 toxin work?

A

Superantigen that binds to MHC II and t-cell receptor, resulting in polyclonal t-cell activation by stimulation of TNF and IL-1.

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10
Q

What is the presentation of toxic shock syndrome? What is it associated with?

A

fever, vomiting, rash, desquamation, shock, end-organ failure.
Associated with prolonged tampon use/nasal packing.

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11
Q

Where does staph aureus cause disease by direct invasion?

A

Pretty much everywhere:
Skin infections, organ abscesses, meningitis, pneumonia, endocarditis, septic arthritis, osteomyelitis, bacteremia/sepsis, etc…

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12
Q

What differentiates MRSA from MSSA?

A

Methicillin-resistant staph aureus has altered penicillin binding protein, and community acquired MRSA has a mean Panton-Valentine Leukocidin that forms abscesses.

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13
Q

Where is S. epidermis found?

A

Normal skin flora.

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14
Q

What is the virulence factor of S. epidermis?

A

Forms adherent biofilms.

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15
Q

What is a biofilm again?

A

extracellular polysaccaride network that forms scaffold around organism. Very difficult for abx to penetrate.

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16
Q

What infections are associated with S. epidermis?

A

Infects prosthetic devices - hip implant, heart valve and IV catheters.

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17
Q

What is S. saprophyticus associated with?

A

Second most common cause of UTI in young women. (first is E coli).

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18
Q

If a gram+ cocci is catalase negative, what is the next step in differentiation?

A

Hemolysis:
Alpha (partial): S. Pneumo or S. Viridans
Beta (complete): Group A (s pyogenes) or Group B (galactic)
Gamma (not): Group D (enterococcus or not)

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19
Q

If a gram + cocci is catalase negative and alpha hemolytic, what is the next step in differentiation:

A

S. pneumo: optochinin sensitive, +capsule, +bile lyses.

S. viridans: optochinin resistant, - capsule, - bile lyses

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20
Q

What is significant about strep pneumo’s capsule? What shape are strep pneumo?

A

Shape: lancet shaped. Capsule: Highly varied. 83 serotypes. Vaccinations contain 13/23 most common. No virulence without capsule.

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21
Q

What does pneumolysin (S. pneumo) do?

A

Binds to cholesterol in host-cell membranes.

22
Q

What are the clinical presentations of S. pneumo infections?

A
Meningitis
Otitis media (in children)
Pneumonia (rusty sputum)
Sinusitis
Sepsis in Sickle Cell
23
Q

Where does the viridans group of Streptococci live?

A

Normal flora of the oropharynx.

24
Q

How are viridans distinguished from S. pneumo?

A

Optochinin resistant.

25
Q

What are dental caries caused by?

A

Strep mutans (mutilates the teeth)

26
Q

What is subacute bacterial endocarditis caused by?

A

S. sanguinis (blood in heart)

27
Q

How does S. sanguinis cause subacute bacterial endocarditis?

A

Makes extracellular dextrans, which bind to fibrin-platelet aggregates on previously damaged heart valves.

28
Q

What sub-group of S. viridans causes brain of liver abscesses?

A

Strep intermedius group.

29
Q

If a gram+ cocci is catalase negative, and beta-hemolytic, what is the next step in differentiating?

A

Bacitracin sensitive: Group A (s pyogenes)

Bacitracin resistant: Group B (s. agalactiae).

30
Q

What is the significant of streptolysin O of S. pyogenes?

A

It is one of the enzymes that destroys RBCs and facilitates hemolysis; it is antigenic and can be detected on ASO titer.

31
Q

What is the significance of the M protein of S. pyogenes?

A

70 types. Adherence factor on capsule, antigenic, induces antibodies which can lead to subsequent antibody-mediated disease.

32
Q

What is pyrogenic toxin of S. pyogenes responsible for?

A

Pharyngitis, Skin infections (Cellulitis, Impetigo, Erysipelas),

33
Q

What is exotoxin A of S. pyogenes responsible for?

A

TSST-1-like toxin creats toxic shock syndrome, scarlet fever, necrotizing fasciitis.

34
Q

What are the immunologic-mediated complicates of S. pyogenes?

A

Rheumatic fever

Post-streptococcal glomerulonephritis

35
Q

What is the disease presenting as rash with sandpaper-like texture, strawberry tongue, circumoral pallor, and desquamation?

A

Scarlet fever.

36
Q

What are the sx of acute rheumatic fever?

A
Joint pain
<3 carditis
Nodules (subQ)
Erythema marginatum
Syndenham chorea
37
Q

How does acute post-strep glomerulonephritis present?

A

Tea-colored urine weeks following skin/pharynx infection.

38
Q

Is impetigo more likely to precede glomerulonephritis or rhuematic fever?

A

Glomerulonephritis.

39
Q

Does S. pyogenes also have a bunch of tissue invading toxins?

A

Yes. Hyaluronidase, DNAase, anti-C5a peptidase, etc.

40
Q

If a gram positive cocci is catalase negative, beta hemolytic, but not bacitracin sensitive, what is it

A

Group B strep - agalactiae.

41
Q

Where does Group B strep colonize?

A

Vagina

42
Q

What diseases does Group B Strep cause?

A

Neonatal meningitis, pneumonia, sepsis.

43
Q

What factor does Group B strep create?

A

CAMP factor (not same as cylic AMP). Enlarges area of hemolysis around S. aureus

44
Q

What other test is Group B positive on?

A

Hippurate test +.

45
Q

When should pregnant women be screened for GBS?

A

35-37weeks. If+, intrapartum penicillin ppx.

46
Q

What group do catalase negative, non-hemolytic gram+ cocci belong to? How to differentiate?

A

Group D strep. Both grow in bile.
Grows in 6.5% NaCl: Enterococcus CAN BE ALPHA HEMOLYTIC
Doesn’t grow in 6.5% NaCl: S. bovis, also called gallolyticus (or equinus)

47
Q

Where are E. faecalis and E. faecium found?

A

Normal colonic flora.

48
Q

What disease can enterococcus be associated with?

A
  1. subacute endocarditis (dextrans) following GI/GU procedures.
  2. biliary tract infections
  3. UTIs
49
Q

Are enterococci susceptible to penicillin?

A

No. Treat w/ ampicillin.

Vancomycin-Resistant-Enterococcus = badness. (linezolid, dapto)

50
Q

What is S. bovis associated with?

A
  1. bacteremia/subacute endocarditis

2. Colon cancer.