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Microbiology test 3 > Bacterial Skin Infections > Flashcards

Bacterial Skin Infections Flashcards

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1
Q

Characteristics & excreted chemicalsof INTACT EPIDERMIS

A 
acidic pH
low moisture
salty sweat
low surface temperature
EXCRETES: sebum (fatty acids), high salt
Normal flora
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2
Q

Langerhans Cells: what, where

A

motile dendritic cell of epidermis

capture, transport & present antigens to T-cells

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3
Q

3 common bacterial skin & soft tissue pathogens, what do they cause

A

Propionibacterium acnes: acne vulgaris
Staphylococcus aureus: localized abscesses
Streptococcus pyogenes: spreading infections

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4
Q

Other common bacterial skin and soft tissue pathogens (5)

A

Pseudomonas, Acinetobacter, Vibrio, Pasteurella, Clostridium perfringens

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5
Q

Locations & routes of infection for skin/soft tissue (3)

A

Exogenous: disrupted integrity of skin barrier
Endogenous: seeded into tissues from blood or lymph
Toxin induced: made at dinstant site, cause pathogenesis in/near (Staphylococcal scaled skin syndrome, staphylococcal & streptococcal toxic shock syndrome {TSS &STSS}

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6
Q

Macules

A

flat, non-palpable lesions

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7
Q

Papules

A

palpable lesions

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8
Q

Vesicles

A

palpable, fluid-filled lesions

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9
Q

Pustules

A

palpable & contain pus

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10
Q

Acne vulgaris etiology & description

A 
Propionibacterium acnes
GRAM-POSITIVE
ANAEROBIC, nonmotile, pleomorphic rod
normal skin flora
commonly colonizes skin, esp. sebaceous glands
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11
Q

4 contributing factors to acne vulgaris

A
  1. GENETICS
  2. FOLLICULAR EPIDERMAL HYPERPROLIFERATION-due to androgen hormones (may be initial trigger)
  3. EXCESS SEBUM PRODUCTION: regulated by variety of hormones (androgens, growth hormone, insulin-like growth hormone)
  4. PROPIONBACTERIUM ACNES: produces lipase (sebum) initiates an immune response,
    results in INFLAMMATION
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12
Q

Progression of Acne from Micromedo to Nodule: 6 steps

A 
0- Hair follicle
1-closed comedo or whitehead
2- open comedo or blackhead
3- papule
4- pustule
5- nodule/cyst
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13
Q

Noninflammatory acne vulgaris description

A

formation of a MICROMEDO

FOLLICLD OPENING partially OBSTRUCTED, SEBUM, KERATINOCYTES, HAIR

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14
Q

Closed Comedos description

A

WHITEHEDS, enlarged/plugged hair follicle beneath skin

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15
Q

OPEN comedos description

A 
BLACKHEADS, contents closed-comedo reaches surface of skin
contents protrude
compacted melanin (cells)-black appearance
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16
Q

inflammatory acne vulgaris description

A

develops when FOLLICULAR CONTENTS rupture into DERMIS causing formation of:
PAPULES: mildest form, small firm pink bump
PUSTULE: clearly inflamed & contain visible pus
NODULE: large, painful, inflamed, pus-filled lesions lodged deep within the skin
NODULE IS MOST SEVERE FORM OF ACNE
CYST: contents harden

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17
Q

Folliculitis general description/presentation

A
  1. Superficial: multiple small papules & pustules on erythematous base, pierced by a central hair
  2. Deep: lesions manifest as erythematous, often fluctant nodules
    [note: the bacterium involved distinguishes acne from folliculitis]
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18
Q

Superficial Folliculitis: 2 primary pathogens, gram stain

A
  1. Staphylococcus aureus: majority of abcess-type infections, GRAM POSITIVE; coagulase-positive cocci in clusters
  2. Pseudomonas aeruginosa: GRAM-NEGATIVE bacilli, opportunistic pathogen, ubiquitous, PYOCYANIN/PYOVERDIN-blue (pus) & green (fluorescent) pigments
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19
Q

Staphylococcus aureus: skin dz manifestation

A

Superficial Folluculitis
IMPETIGO OF BOCKHART-BARBER’s ITCH: bearded area (upper lip near nose), erythematous follicular-based papules or pustules: rupture & leave yellow crust, common carriers nasal staph
STY (hordeolum)-folliculitis of eyelid (can be front or back of eyelid)

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20
Q

Pseudomonas aeruginosa: skin dz manifestion

A

Wetsuit, “hot tub” folliculitis
appears 8-48 h after exposure, contaminated water (inadequate chlorine)
typical signs in areas occluded by swimwear
SYSTEMIC COMPONENT: Fever, HE, sore throat, malaise, GI distress, LPS or Exotoxin
self-limiting infection

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21
Q

Furuncles

A

(aka “boils”) larger abscesses: enlarged folliculitis, extend into dermis and subcutaneous tissue
-on neck, thighs, buttocks & face

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22
Q

Carbuncles

A

massive inflammation involving SEVERAL HARI FOLLICLES
extend into DERMIS & SUBCUTANEOUS TISSUE
(C) on back of neck, back & thighs

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23
Q

Nonbullous Impetigo etiology

A 
#1 S. aureus
other: Streptococcus pyogenes, possible coinfection GAS or GABHS=group A beta-hemolytic strep gram POSITIVE cocci-chains
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24
Q

Non bullous impetigo a/w and/or not a/w

A

can be associated w/ ACUTE GLOMERULONEPHRITIS (tropics)

but NOT rheumatic fever

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25
Q

Nonbullous impetigo epidemiology

A

frequently EPIDEMIC among PRESCHOOL-AGED CHILDREN (1-5 years of age)
EXPOSED AREAS of body (begins on face, then spread to arms through self-inoculation)
prevalent during WARM/MOIST WEATHER
impetigo STREP strains, not pharyngitis strains

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26
Q

Nonbullous impetigo: clinical manifestations

A

infectious INTRAEPIDERMAL VESICLES, may be painful, filled w/serous exudate
forms THICK AMBER-COLORED & ADHESIVE CRUSTS
CONTAGIOUS!!-vesicles contain pathogen, easily transmitted (can spread by fomites-towels), self-infecting: spread to arms, legs, face from focus

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27
Q

NONbullous impetigo strain(s)

A

S. aureus/GAS

28
Q

Bullous impetigo strain(s)

A

S. aureus ONLY

29
Q

Bullous impetigo etiology

A

Staphylococcus aures
infections are RARE
bullae localized action of Exfoliatin Toxin (ET)
ET digests epidermal intercellular connections

30
Q

Bullous Impetigo: clinical manifestations

A

bullae: large superficial, think-walled blisters
bullae rupture, crust forms over area
CONTAGIOUS!!
BOTH S. aureus & ET TOXIN in bullae
ET-NOT systemic (as in staphylococcal scalded syndrome)

31
Q

Cellulitis etiology

A

S. aureus and/or S. pyogenes (GAS)

>90% cases

32
Q

other cellulitis pathogens (4) and they are a/w

A

other cellulitis pathogens account for <10% cases

  1. Acinetobacter baumannii: pleomorph, HA SSTI (emerging infection), a/s PREVIOUS TRAUMA/SURGERY
  2. Pasteurella multocida: coccobacillus a/w CAT or dog but
  3. Aeromonas hydrophilia: bacillus a/w fresh water injuries
  4. Vibrio vulnificus: Vibrio a/w salt water injuries
33
Q

Acinetobacter baumannii

A

other cellulitis pathogen
pleomorph, HA SSTI (emerging infection)
a/w previous trauma/surgery

34
Q

Pasteurella multocida

A

other cellulitis pathogen

coccobacillus a/w CAT or dog bite

35
Q

Aeromonas hydrophilia

A

other cellulitis pathogen

bacillus a/w fresh water injuries

36
Q

Vibrio vulnificus

A

other cellulitis pathogen

vibrio a/w salt water injuries

37
Q

Cellulitis clinical manifestations

A

HEET: heat, erythema, edema, & tenderness
-results from infected skin break, endogenous seeding
-may not be an evident wound
-acute inflammation of SUBCUTANEOUS CONNECTIVE TISSUE, extends up into lower part of DERMIS
FEW MICROBES present
may progress into necrotizing fasciitis or gangrene (myonecrosis)

38
Q

Cellulitis Hallmarks

A

“HEET”: areas of heat, erythema, edema & tenderness

39
Q

Cellulitis looks like

A

localized “sunburn” (HEET)

BORDERS BLEND in elevation and color to surrounding tissue

40
Q

What are cellulitis sxs due to

A

bacterial toxins

inflammatory response

41
Q

Cellulitis dx

A

NO lab workup IF: minimal pain & confined to small area, no signs of systemic infection, no RISK FACTORS for more serious illness
(risk factors: skin lesions (incl. varicella), immunocompromise or immunodeficiency & chronic steroid use)
REQUIRED LAB WORKUP if: spreading or large area of involvement, must confirm cellulitis, NOT necrotizing fasciitis (NF) or myonecrosis

42
Q

Cellulitis: basic definition

A

infection of subcutaneous connective tissue

43
Q

Cellulitis lab work includes

A
  • cultures of blood, pus or bullae-more usedful than leading edge aspiration or punch biopsy
  • MRI, CT, Ultrasound or X-ray examination (rule out NF or myonecrosis)
44
Q

Cellulitis tx

A

elevation of affected area-drainage of edema (predisposing conditions: tinea pedis, lymphedema, chronic venous insufficiency)
antibiotics-vary w/microbe & susceptibility
AVOID NSAIDS!!!

45
Q

NSAIDS in cellulitis

A

AVOID NSAIDS b/c they:

  1. may mask indicators (pain) of worsening dx, necrotizing fasciitis/myonecrosis
  2. Affect host immune response: inhibit PMN responses, interfere w/CYTOKINE release
46
Q

Necrotizing fasciitis type 1 etiology

A

polymicrobic: at least 1 facultative aerobe & 1 anaerobic bacterium
ex: anaerobes-bacteroids, clostridium (facultative aerobes are PESSKEY strains)

47
Q

Necrotizing fasciitis type 1 risk factors

A

diabetes, surgery, immune compromise

48
Q

Necrotizing fasciitis type 1 forms

A

cervical-odontogenic infection
surgical wound infection
Fournier’s gangrene: male or female genetalia

49
Q

Necrotizing fasciitis type 2 description and etiology

A

“Flesh-eating bacteria”
group A Streptococcus pyogenes (monomicrobic)
EXPOSURE often NOT FOUND
can follow: blunt trauma, bug bite, chickenpox, IVDU, surgical procedure, strep throat

50
Q

necrotizing fasciitis type 2 risk factors

A

IMMUNE COMPETENT
NO significant past medical history
any age group

51
Q

Necrotizing fasciitis overview of spread

A
  • infection of deeper tissues (destruction of muscle fascia & overlying subQ)
  • spreads along muscle fascia-poor blood supply
  • initially overlying tissue appears unaffected
  • muscle tissue spared-generous blood supply
52
Q

Necrotizing fasciitis clinical manifestations

A

(U) acute onset: affected area HEET & shiny,
PAIN OUT OF PROPORTION TO PE
RAPID PROGRESSION OVER SEVERAL DAYS
SKIN CHANGES COLOR-red-purple to patches of blue-gray
3-5 days after onset: skin breakdown w/bullae, thick pink/purple fluid, cutaneous gangrene visible, no longer tender-cutaneoua anesthesia-b vessels & nervew
CLUE: NF if cutaneous anesthesia precedes skin necrosis

53
Q

CLUE to NECROTIZING FASCIITIS

A

NF if cutaneoues anesthesia precedes skin necrosis

54
Q

Advanced necrotizing fasciitis clinical manifestations

A

fever, tachycardia & systemic toxicity
systemic toxicity: behavior appears as confused & in an altered mental state
other sxs: malaise, myalgia, diarrhea & anorexia, hypotension (initially or develops)
PUTRID ODOR ONLY w/ANAEROBIC PATHOGEN

55
Q

does necrotizing fasciitis have an odor

A

ONLY w/ANAEROBIC pathogen (type I)

56
Q

Necrotizing fasciitis tissue appearance during surgery/debridement

A

fascia: SWOLLEN & DULL GRAY, no true pus anywhere, only THIN BROWNISH EXUDATE
- EXTENSIVE UNDERMINING of surrounding tissue evident
- necrotic tissue separates along fascial planes

57
Q

Necrotizing fasciitis antibiotic therapy

A

NF fails to respond to antibiotic therapy

-differentiates NF from cellulitis, which would respond in 24-48hrs

58
Q

Necrotizing Fasciitis dx

A

-SURGERY is only way to CONFIRM PRESENCE & EXTENT of NF
-Gram stain & culture (tissue biopsies=best source cultures; stain exudate=poly- or monomicrobic)
-Initial extent of infection (detection by MRI, CT, ultrasound or x-ray)
type 2: RAPID STREP TEST for streptococcus pyogenes (GAS); PCR genes for Spe proteins-Streptococcal Pyrogenic Exotoxins)

59
Q

Necrotizing fasciitis tx (4)

A
  1. surgical debridement-expose extent of damage
  2. antibiotic tx
  3. hyperbaric oxygen therapy (HBO): follows debridement (extremities), kill anaerobes, enhance antibiotics
  4. Maggot therapy: used to promote healing in nonhealing wounds
60
Q

Myonecrosis etiology

A 
gangrene (necrosis large area-no blood flow)
Clostridial myonecrosis (Gas gangrene): Clostridium perfringens type A- spore-forming, GRAM-POSITIVE anaerobic bacillus
61
Q

Myonecrosis aka/virulence factor(s)

A

aka: Gas Gangrene
VF: alpha-toxin=phospholipase C: lechithinase, cytotoxic, destructive to membranes
-primarily responsible for clostridial myonecrosis sxs: lyses RBCs, myocytes, fibroblasts, platelets, leukocytes

62
Q

Myonecrosis pathogenesis

A
  1. introduction of anaerobic CELLS or SPORES
  2. reduced oxygen tension-trauma & other bacteria (circulatory failure, necrotic tissue, foreign bodies, presence of oxygen utilizing bacteria)
  3. production of exotoxin(s) & insoluble H2 gas-invasion of nearby tissue
63
Q

Myonecrosis clinical manifeststions

A

(aka gas gangrene) is a MEDICAL EMERGENCY
-rapid onset of sxs toxin mediated ischemia
Skin: initially pale-at site of infection
-readily develops a BRONZE appearance
-becomes tense (edema), intensely tender & crepitant (H2 gas)
-overlying bullae: clear, red, blue or purple
-can be similar in presentation to necrotizing fasciitis
EXUDATE: sweet or mousy smell (cut hay)->Clostridium perfringens
If foul odor: nonclostridial anaerobe or polymicrobic
SYSTEMIC EFFECTS: fever, tachycardia & altered consciousness

64
Q

Myonecrosis diagnosis

A

TISSUE BIOPSY is CRITERION STANDARD for rapid dx (frozen section=results in 15 mins)
gram stain of biopsy shows: MUSCLE NECROSIS, GRAM-VARIABLE rods w NO PMNs->dx for Clostridia myonecrosis
imaging to visualize the extent of gas packets

65
Q

Myenecrosis tx (4)

A
  1. Debridement & opening of infected tissues to OXYGEN
  2. HBO kills anaerobes
  3. ANTIBIOTICS: same as necrotizing fasciitis
  4. Maggot therapy used on some cases
66
Q

Clostridium perfingens descriptions

A

gram POSITIVE bacillus spore former

Microbiology test 3 (8 decks)

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