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Backup 2 > 8 Staphylococcus Pathogenesis > Flashcards

8 Staphylococcus Pathogenesis Flashcards

1
Q

What are key symptoms of Schlievert’s story of Infectious Endocarditis?? (4)

A
  • 65 yrs
  • Persistent fever
  • Severe night sweats
  • Weight loss 30 lbs
  • Excessive fatigue
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2
Q

What are key signs of Schlievert’s story of Infectious Endocarditis? (4)

A
  • Elevated PMN’s
  • Abnormal heart sounds
  • Cultures show catalase-positive, coagulase-positive gram-positive cocci (S. Aureus)
  • Not in story but often: metastatic abscesses
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3
Q

What happens to the physician after hospitalization in Schlievert’s story? (4)

A
  • stroke left side, takes 2 yrs to recover movement and 1 yr to recover speech
  • Hospitalized 6 weeks w/ “suportive care”
  • Lost 60 lbs
  • Practices medicine today.
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4
Q

What are the common causes of infectious endocarditis? (3)

A
  • Staph aureus [45%] highly valve-destructive
  • Viridans streptococci [35%]
  • Enterococcus faecalis & faecium [15%]
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5
Q

What makes enterococcus faecalis & faecium so bad?

A

-highly antibiotic resistant, including to vancomycin. Can transfer this resistance to other gram-positives.

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6
Q

How do we treat infectious endocarditis? (4)

A
  • antibiotics
  • supportive care
  • valve replacement
  • manage complications (stroke)
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7
Q

What does staph aureus do to skin? (7) Important!!

A

Primary inflammation: boils (furuncles), carbuncles (multiple boils), pimples (folliculitis), paronychia (nail beds), impetigo, soft tissue abscesses, atopic dermatitis

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8
Q

What is staph aureus’s virulence key is skin?

A

walling off organism by cell surface virulence factors, then spreading by secreted virulence factors

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9
Q

What does staph aureus do to mucous membranes thru inflammation? (6)

A 
Primary inflammation (less inflammation than skin due to less alpha-toxin made by these strains):
sinusitis, chronic otitis media, bronchial pneumonia, urinary tract infection vaginal infection, enterocolitis
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10
Q

What does staph aureus do to mucous membranes when non-inflammatory? (3)

A
  • Scalded Skin syndrome
  • Toxic shock syndrome (TSS)!! (including menstrual)
  • Staphylococcal food poisoning (pre-formed toxins)
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11
Q

What is scalded skin syndrome?

A

-1-2 day old infant skin peeling due to exfoliative toxins (becomes very susceptible to secondary serious infections

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12
Q

What are symptoms of staph food poisoning?

A

vomiting, diarrhea 2-8 hrs after eating, lasts up to 48 hrs

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13
Q

What systemic infections does staph aureus cause? (5)

A
  • Septicemia
  • TSS
  • Endocarditis
  • Osteomyelitis
  • Necrotizing fasciitis/myositis
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14
Q

What is septicemia?

A

high fever, hypotension, DIC & metastatic abscesses

[sound familiar from earlier lecture]

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15
Q

What are necrotizing fasciitis/myositis symptoms?

A

fever, necrotizing tissue damage often with TSS

[sound familiar from earlier lecture]

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16
Q

T/F S. aureus usually remains localized?

A

T

17
Q

T/F S. aureus all give rise to systemic superantigens, and if so then which?

A

T, TSST-1, SEB, SEC

18
Q

TSS: What cytokines?

A

IL1-B (fever), TNF-alpha & beta (hypotension), IFN-gamma, IL-2 (rash 7 other symptoms)

19
Q

Menstrual TSS is most common in which type of tampon?

A

absorbent. (oxygen)

20
Q

What is TSS often a complication of?

A

influenza

[sound familiar?]

21
Q

How is TSS defined? (6)

A
  • Fever over 102 degrees
  • hypotension systolic under 90
  • rash (macular erythroderma)
  • peeling of skin if survive
  • 3 mulit-organ changes
  • Must rule out other causes
22
Q

What if some criteria for TSS are missing?

A
  • 1 missing: “Probable TSS”

- More missing: “Toxin-mediated disease”

23
Q

Name “other” systemic signs of staph infection (see photos) (3)

A
  • Kidney abscess
  • Splinter nails
  • gangrene (lack of perfusion from hypotension)
24
Q

How do we treat staph aureus skin or mucous membrane infections?

A

antibiotics, surgery to drain abscess/furuncle, remove infected hair/nails

25
Q

How do we treat more serious ones? (recall infectious carditis treatment earlier card)

A
  • antibiotics (MRSA!)
  • B.P. support
  • Debridement in necrotizing illness
  • IVIG
  • Activated protein C (drotrecogin-alpha if needed)
  • Remove affected object (tampon etc)
  • Influenze vaccine to prevent future post-influenze TSS
26
Q

how to do prevention in hospitals? (don’t memorize)

A

hand-wash, antibiotic sensitivity monitoring, dust low, monitor infected patients, monitor visitors

27
Q

Coagulase-negative staph group includes what 3 pathogens?

A
  • Staph epidermidis
  • Staph saprophyticus
  • Staph lugdenensis
28
Q

staph epidermidis causes what 2 problems?

A
  • Septicemia (number 1 cause) & endocarditis associated w/ catheterization biofilms. [due to PIA & cytolysins, rarely superantigen]
  • UTI (urinary tract infection) associated w/ catheterization
29
Q

Staph saprophyticus causes what problem?

A

UTI

30
Q

Staph lugdenensis causes what problem?

A

endocarditis

31
Q

How are the 3 coagulase-negative infections treated?

A

Same as S. aureus, except must decide if the primary infection is staph or if it only came from catheterization thru the skin

32
Q

Do more inflammatory strains of staph live on skin or mucous membranes?

A

skin

33
Q

How does a fununcle (boil) form? (3 basic steps)

A
  • staph inside skin.
  • Fc of Ab’s are binding to staph, but the cell surface virulence factors are secreted & clotting cascade walls it off in a furuncle.
  • Once high density of bacteria inside, cell surface virulence factors turn off. Secreted virulence factors turn on & now it spreads to other areas of skin.
34
Q

What is are the key differences in the way staph behaves when on mucosal surfaces? (2)

A
  • Not walling itself off w/ coagulase

- Doesn’t make much alpha toxin

35
Q

Clotting in nailbeds is a strong sign of? (2)

A
  • Endocarditis (staph or strep)

- staph sepsis

36
Q

Which type of endocarditis progresses most quickly to death in a couple days?

A

staph

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