Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Microbiology test 3 > Bacterial Skin Infections > Flashcards

Bacterial Skin Infections Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Langerhans Cells: what, where

A

motile dendritic cell of epidermis

capture, transport & present antigens to T-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Other common bacterial skin and soft tissue pathogens (5)

A

Pseudomonas, Acinetobacter, Vibrio, Pasteurella, Clostridium perfringens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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}

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Macules

A

flat, non-palpable lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Papules

A

palpable lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Vesicles

A

palpable, fluid-filled lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pustules

A

palpable & contain pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acne vulgaris etiology & description

A 
Propionibacterium acnes
GRAM-POSITIVE
ANAEROBIC, nonmotile, pleomorphic rod
normal skin flora
commonly colonizes skin, esp. sebaceous glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Noninflammatory acne vulgaris description

A

formation of a MICROMEDO

FOLLICLD OPENING partially OBSTRUCTED, SEBUM, KERATINOCYTES, HAIR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Closed Comedos description

A

WHITEHEDS, enlarged/plugged hair follicle beneath skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

OPEN comedos description

A 
BLACKHEADS, contents closed-comedo reaches surface of skin
contents protrude
compacted melanin (cells)-black appearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Furuncles

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Carbuncles

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

can be associated w/ ACUTE GLOMERULONEPHRITIS (tropics)

but NOT rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Nonbullous impetigo epidemiology
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
26
Nonbullous impetigo: clinical manifestations
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
27
NONbullous impetigo strain(s)
S. aureus/GAS
28
Bullous impetigo strain(s)
S. aureus ONLY
29
Bullous impetigo etiology
Staphylococcus aures infections are RARE bullae localized action of Exfoliatin Toxin (ET) ET digests epidermal intercellular connections
30
Bullous Impetigo: clinical manifestations
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
Cellulitis etiology
S. aureus and/or S. pyogenes (GAS) | >90% cases
32
other cellulitis pathogens (4) and they are a/w
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
Acinetobacter baumannii
other cellulitis pathogen pleomorph, HA SSTI (emerging infection) a/w previous trauma/surgery
34
Pasteurella multocida
other cellulitis pathogen | coccobacillus a/w CAT or dog bite
35
Aeromonas hydrophilia
other cellulitis pathogen | bacillus a/w fresh water injuries
36
Vibrio vulnificus
other cellulitis pathogen | vibrio a/w salt water injuries
37
Cellulitis clinical manifestations
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
Cellulitis Hallmarks
"HEET": areas of heat, erythema, edema & tenderness
39
Cellulitis looks like
localized "sunburn" (HEET) | BORDERS BLEND in elevation and color to surrounding tissue
40
What are cellulitis sxs due to
bacterial toxins | inflammatory response
41
Cellulitis dx
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
Cellulitis: basic definition
infection of subcutaneous connective tissue
43
Cellulitis lab work includes
- 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
Cellulitis tx
elevation of affected area-drainage of edema (predisposing conditions: tinea pedis, lymphedema, chronic venous insufficiency) antibiotics-vary w/microbe & susceptibility AVOID NSAIDS!!!
45
NSAIDS in cellulitis
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
Necrotizing fasciitis type 1 etiology
polymicrobic: at least 1 facultative aerobe & 1 anaerobic bacterium ex: anaerobes-bacteroids, clostridium (facultative aerobes are PESSKEY strains)
47
Necrotizing fasciitis type 1 risk factors
diabetes, surgery, immune compromise
48
Necrotizing fasciitis type 1 forms
cervical-odontogenic infection surgical wound infection Fournier's gangrene: male or female genetalia
49
Necrotizing fasciitis type 2 description and etiology
"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
necrotizing fasciitis type 2 risk factors
IMMUNE COMPETENT NO significant past medical history any age group
51
Necrotizing fasciitis overview of spread
- 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
Necrotizing fasciitis clinical manifestations
(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
CLUE to NECROTIZING FASCIITIS
NF if cutaneoues anesthesia precedes skin necrosis
54
Advanced necrotizing fasciitis clinical manifestations
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
does necrotizing fasciitis have an odor
ONLY w/ANAEROBIC pathogen (type I)
56
Necrotizing fasciitis tissue appearance during surgery/debridement
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
Necrotizing fasciitis antibiotic therapy
NF fails to respond to antibiotic therapy | -differentiates NF from cellulitis, which would respond in 24-48hrs
58
Necrotizing Fasciitis dx
-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
Necrotizing fasciitis tx (4)
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
Myonecrosis etiology
``` gangrene (necrosis large area-no blood flow) Clostridial myonecrosis (Gas gangrene): Clostridium perfringens type A- spore-forming, GRAM-POSITIVE anaerobic bacillus ```
61
Myonecrosis aka/virulence factor(s)
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
Myonecrosis pathogenesis
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
Myonecrosis clinical manifeststions
(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
Myonecrosis diagnosis
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
Myenecrosis tx (4)
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
Clostridium perfingens descriptions
gram POSITIVE bacillus spore former

Microbiology test 3 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions