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Micro final > Lect 23 > Flashcards

Lect 23 Flashcards

1
Q

If foreign body is present (splinter, stitches), what happens to the infection dose

A

infection dose drops dramatically

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2
Q

What is acne vulgaris

A
  • disease of sebaceous follicles
  • a noninfectious form of folliculitis
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3
Q

Acne vulgaris affects what patient population? what may be initial trigger?

A
  • teens and young adults
  • androgen hormones
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4
Q

acne vulgaris is caused by what pathogen

A

propionibacterium acnes

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5
Q

propionibacterium acnes

  • gram status
  • shape
  • oxygen requirement
  • where is it normally found
A
  • gram +
  • anaerobic
  • rod
  • normal skin flora, colonizes in sebaceous glands
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6
Q

how do inflammatory acne vulgaris develop

A
  • when follicular contents rupture into the dermis
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7
Q

stages of inflammatory acne vulgaris

A
  1. papules
  2. pustule
  3. nodule: most severe form of acne
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8
Q

multiple small papules and pustules on erythematous base pierced by central hair

A

superficial folliculitis

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9
Q

two primary pathogens of superficial folliculitis is

A
  • staph aureus: majority of abscess-type infection
    • gram +
  • pseudomonas aeruginosa
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10
Q

pseudomonas aeruginosa

  • gram status
  • shape
  • interesting feature
A
  • gram -
  • rod
  • pyocyanin/pyoverdin
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11
Q

hot tub folliculitis is caused by what pathogen

A

pseudomonas aeruginosa

  • appars 8-48 hrs after exposure in contaminated water
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12
Q

abscess caused by S. aureus involving a hair follicle and surrounding tissue, often on neck, thichs, buttocks, and face

A

furuncles (boils)

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13
Q

clusters of furuncles with subcutaneous connections, extend into dermis and subcutaneous tissue. may be accompanied by fever. common locations: back of neck, back, and thighs

A

Carbuncles

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14
Q

Carbuncles and furuncles may affect healthy young persons but are much more common in

A
  • obese
  • immunocompromised
  • diabetic
  • eldery
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15
Q

when are abx given for furuncles and carbuncles

A
  • lesions > 5 mm
  • do not resolve with drainage
  • evidence of spreading
  • occur in immunocompromised
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16
Q

impetigo is a superficial skin infection with crusting or bullae and caused by

A
  • staphylococci
  • streptococci
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17
Q

what is ecthyma

A

ulcerative form of impetigo

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18
Q

risk factors for impetigo and ecthyma

A
  • moist environment
  • poor hygiene
  • chronic nasopharyngeal carriage of agents
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19
Q

what is nonbullous impetigo? cause of nonbullous impetigo?

A
  • clusters of vesicles that rupture and crust
  • S. aureus
    • MRSA 20%
    • possible co-infection with strep pyogenes
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20
Q

what is bullous impetigo

A
  • vesicles enlarge to form bacteria-colonized fluid-filled bullae created by exfoliative toxin
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21
Q

cause of bullous impetigo

A

specific strains of S. aureus exclusively

22
Q

What is staphylococcal scaleded skin syndrome (Ritter’s disease)

A
  • acute and extensive epidermolysis due to action of staphylococcal toxin (Exfoliatin) that splits the skin just beneath the granule cell layer
23
Q

do bullae in staphylococcal scaleded skin syndrome (Ritter’s disease) have bacteria or leukocytes?

A
  • no, Bullae are sterile
  • due to toxin
24
Q

what sign is positive in staphylococcal scaleded skin syndrome (Ritter’s disease)

A

Nikolsky’s sign: skin peels easily

25
what patient population is most affected with staphylococcal scaleded skin syndrome (Ritter's disease)
* infants * children \< 6
26
mortality rate for staphylococcal scaleded skin syndrome (Ritter's disease)
* low * often due to secondary infections
27
if affected area of skin is extensive in staphylococcal scaleded skin syndrome (Ritter's disease), treat as if for
burns
28
how is staphylococcal scaleded skin syndrome (Ritter's disease) diagnosed
biopsy
29
what is erysipelas
* superficial cellulitis with focal dermal lymphatic involvement
30
erysipelas is usually caused by
group A streptococci
31
pathogens that cause cellulitis
* S aureus * S. pyogens (GAS) * more likely to create diffuse swiftly spreading infections
32
hallmarks of cellulitis
* HEET * heat * erythema * edema * tenderness
33
symptoms of cellulitis are due to
* bacterial toxins * inflammatory response
34
how is cellulitis diagnosed
* clinical exam * be aware infections may be mixed etiology
35
what medications should be avoided in the tx of cellulitis
NSAIDs * may mask pain of developing myonecrosis and interfere with response to agent
36
What are classic signs of necrotizing fasciitis
1. infection of deeper tissues 2. **spreads along muscle fascia, muscle tissue spared** 3. **pain out of proportion to clinical signs**
37
type 1 or polymicrobic necrotizing fasciitis is caused by
* Group A strep and * anaerobes
38
risk factors for type 1 or polymicrobic necrotizing fasciitis
* diabetes * surgery * immunocompromised
39
type 2-"flesh eating bacteria" necrotizing fasciitis is caused by
* Group A streptococcus pyogens: monomicrobic)
40
clinical presentation * skin breakdown with bullae * thick pink/purple fluid * cutaneous gangrene visible * no longer tender - cutaneous anesthesia
necrotizing fasciitis
41
which responds to antibiotic therapy: necrotizing fasciitis or cellulitis
cellulitis
42
Myonecrosis of gas gangrene is caused by
clostridium perfringens type A
43
clostridium perfringens type A * gram status * spore? * oxygen? * shape
* gram + * anaerobic bacillus * spore forming
44
pathogenesis of gas gangrene
1. introduction of anaerobic cells or spores 2. reduced oxygen tension: trauma or other bacteria 3. production of exotoxins and insoluble H2 gas * promotes split and invasion of nearby tissue
45
clinical presentation * rapid onset * \< 24 hrs * sudden onset of pain * skin: bronze appearance * skin becomes tense, **crepitant** * overlying bullae
gas gangrene * crepitant due to H2 gas
46
how is gas gangrene diagnosed
tissue biopsy
47
toxic shock syndrome is caused by
* staph aureus * strep pyogenes
48
streptococcal toxic shock syndrome begins as
* soft tissue inflammation at site of skin infection * patients are usually bacteremic and have necrotizing fasciitis
49
antigens of streptococcal causing toxic shock syndrome
superantigens SpeA and SpeC
50
antigen causing toxic shock syndrome by staph aureus
enterotoxin type B superantigen
51
staph aureus toxic shock syndrome is associated with
tampon use and surgery

Micro final (7 decks)

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