(62) Skin and soft tissue infections Flashcards

1
Q

Name the 4 layers in all epidermis

A
  • stratum basale
  • stratum spinosum
  • stratum granulosum
  • stratum corneum
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2
Q

What are the functions of the skin?

A
  • physical barrier (chemical, UV, micro-organisms)
  • homeostasis (thermoregulation, prevention of desiccation electrolyte loss)
  • immunological function (Ag presentation and phagocytosis, Langerhans cells, lymphocytes, mononuclear phagocytic cells)
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3
Q

Which bacteria colonise the skin?

A
  • coagulase-negative staphylococci
  • staph. aureus
  • propionibacterium
  • corynebacterium spp.
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4
Q

Give an example of local infection by inoculation

A
  • penetration of skin with contaminated object (rusty nail, knife, surgical procedure, injection etc)
  • contamination of pre-existing breach in skin surface (abrasion, athletes foot lesion etc)
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5
Q

Give an example of how else a localised infection might be caused (other than inoculation)

A

Neuronal migration in herpes simplex

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6
Q

Give 2 examples of systemic/generalised infection

A
  • chickenpox

- meningococcal sepsis

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7
Q

Name viruses that can cause skin/soft tissue infections

A
  • herpes viruses (HSV and VZV)

- molluscum contagiosum

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8
Q

Describe the pathogenesis of herpes simplex

A
  • vesicle formation followed by ulceration and release of vesicle fluid containing infective particles
  • virus gains entry via sensory nerve endings and migrates along nerve to DRG
  • in latent infection, viral DNA exists as “episomes” and no virus-coded proteins are present to stimulate immune response
  • in reactivation, virus particles migrate outwards to sensory nerve endings and cause clinical manifestations of infection
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9
Q

Describe the history in herpes simplex infection

A
  • triggered by infection or stress etc

- preceded by tingling

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10
Q

Describe examination findings in herpes simplex infection

A
  • primary infection (infants) = extensive, painful lesion, inside mouth (HSV2 = mainly genital infections)
  • secondary infection (all ages) = peri-oral (genitals), weeping, vesicular
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11
Q

How is herpes simplex diagnosed?

A
  • clinical

- difficult cases: vesicle fluid (PCR for herpes virus DNA)

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12
Q

How is herpes simplex treated?

A
  • cold sores = topical acyclovir

- genital herpes, immunosuppressed patient = oral acyclovir

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13
Q

Describe the history in herpes zoster (shingles)

A
  • previous chicken pox (“latent” infection)

- triggered by physical or emotional insult (proceded by tingling and/or pain)

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14
Q

Describe the examination findings in herpes zoster (shingles)

A
  • weeping, vesicular rash

- dermatomal distribution

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15
Q

How is herpes zoster (shingles) diagnosed?

A
  • clinical

- difficult cases: vesicle fluid (PCR for herpes virus DNA)

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16
Q

How is herpes zoster (shingles) diagnosed?

A
  • oral aciclovir/valaciclovir
  • IV aciclovir (depending on age, immune status, severity of shingles)
  • specialist advice if severe/widespread rash, severe immunosuppression or multiple dermatomes involved
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17
Q

What is the causative agent in molluscum contagiosum?

A

Molluscum contagiosum virus (a DNA poxvirus)

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18
Q

What is seen on examination in molluscum contagiosum?

A
  • raised, pearly lesions up to 3mm

- umbilicate

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19
Q

How is molluscum contagiosum diagnosed?

A

Clinical

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20
Q

How is molluscum contagiosum treated?

A
  • none (lesions usually disappear in 6-18 months)
  • various topical preparations
  • physical treatments (cryotherapy, diathermy, laser therapy)
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21
Q

What is cryotherapy?

A

The application of extreme cold to destroy abnormal or diseased tissue - used to treat a number of diseases especially skin conditions like warts, moles, skin tags and solar keratoses

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22
Q

What is diathermy?

A

High-frequency electric current is delivered via shortwave, microwave, or ultrasound to generate deep heat in body tissue

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23
Q

Name 6 bacterial skin infections

A
  • impetigo
  • erysipelas
  • cellulitis
  • necrotising fasciitis
  • gas gangrene
  • anthrax
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24
Q

What are the causative agents in bacterial skin infections?

A
  • mainly staph. aureus and group A b-haemolytic streptococci (S. pyogenes)
  • a few others eg. haemophilus influenzae, pasteurella multocida, enteric organisms etc.
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25
Q

Describe the features of S. aureus

A
  • gram-positive cocci in clusters
  • catalase-positive
  • normal nasal flora in approx 30%
  • large number of virulence factors eg. DNase, coagulase, teichoic acid
  • exotoxin production
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26
Q

What are the exotoxins that S. aureus produces?

A
  • epidermolytic toxins A and B (ETA and ETB)
  • toxic shock syndrome toxin (TSST-1)
  • Panton-Valentin leukocidin (PVL)
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27
Q

Describe the features of S. pyogenes

A
  • gram-positive cocci in chains
  • catalase-negative
  • expresses many virulence factors
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28
Q

What are the virulence factors that S. pyogenes expresses?

A
  • adhesins
  • M proteins (antiphagocytic)
  • hyaluronic acid capsule (antiphagocytic)
  • hyaluronidase (facilitates interstitial spread)
  • C5a peptidase (anticomplementary)
  • streptolysins-O and -S (lysis of red and white blood cells)
  • pyrogenic exotoxins
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29
Q

What is impetigo?

A

Infection of epidermis (superficial) - a common and highly contagious skin infection that causes sores and blisters

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30
Q

What are the causative agents in impetigo?

A
  • S. aureus
  • S. pyogenes
  • both
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31
Q

Describe the history in impetigo

A
  • occurs at site of skin damage (cut, graze, insect bite, chicken pox, molluscum contagiosum lesion)
  • contacts
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32
Q

What is seen on examination in impetigo?

A
  • plaque-like lesions
  • yellowish exudate
  • thick scabs “honey crusted lesions”
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33
Q

How is impetigo diagnosed?

A
  • clinical

- bacterial culture (sensitivity testing may be useful)

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34
Q

What are the complications associated with impetigo?

A

Epidermolytic toxic production (ETA and ETB)

  • localised = bullous impetigo
  • generalised = staphylococcal scalded skin syndrome (SSSS)
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35
Q

A complication of impetigo is SSSS due to ETA and ETB production. Describe the pathogenesis

A

Desmosomal glycoprotein desmoglein-1 is required for cell-cell adhesion in the superficial epidermis

= inactivated by ETA and ETB

36
Q

What is erysipelas?

A

Infection of dermis - infection of the upper dermis and superficial lymphatics, usually caused by beta-hemolytic group A Streptococcus bacteria on scratches or otherwise infected areas - more superficial than cellulitis, and is typically more raised and demarcated

37
Q

What is causative agent of erysipelas?

A

S. pyogenes

38
Q

Describe the presenting history in erysipelas

A
  • often occurs at sites of skin damage
  • predominantly face or shin
  • proceded by pain and tenderness
39
Q

What is seen on examination in erysipelas?

A
  • fever and malaise
  • well-demaractaed inflamed lesion (red, swollen, painful, hot)
  • lymph node enlargement
40
Q

How is erysipelas diagnosed?

A
  • clinical

- culture rarely helpful

41
Q

What is cellulitis?

A

Infection of skin and subcutaneous tissue - specifically affects the dermis and subcutaneous fat - area of redness which increases in size over a couple of days. The borders of the area of redness are generally not sharp and the skin may be swollen

42
Q

What are the causative agents of cellulitis?

A
  • S. aureus
  • S. pyogenes
  • pasteurella multocida (animal bites)
  • haemophilus influenzae
43
Q

Describe the history in cellulitis

A
  • site of skin penetration (cut, graze, IV catheter, surgical instrument, bite etc)
  • any part of body
  • portal may not be apparent
44
Q

What is found on examination in cellulitis?

A
  • fever and malaise

- diffuse inflamed lesion (erythema, swelling, tenderness, heat)

45
Q

How is cellulitis diagnosed?

A
  • clinical
  • broad differential diagnosis
  • microbiology (lesion swabs, lesion aspirates and skin biopsy, blood cultures)
46
Q

List the features of microbiology diagnostic techniques in cellulitis

A

Lesion swabs = positive in 85% of cases, swab if lesion is ulcerated

Lesion aspirates and skin biopsy = positive in 10-20%, not recommended routinely

Blood cultures = positive in only 2-4% of cases, use if severe sepsis or systemic signs of infection

47
Q

What are the defining characteristics of stasis dermatitis (differential diagnosis from cellulitis)

A
  • absence of pain or fever
  • circumferential
  • bilateral
48
Q

What are the defining characteristics of acute arthritis (differential diagnosis from cellulitis)

A
  • involvement of joint

- pain on movement

49
Q

What are the defining characteristics of pyoderma gangrenosum (differential diagnosis from cellulitis)

A
  • ulcerations on legs

- history of IBD

50
Q

What are the defining characteristics of hypersensitivity reaction/drug reaction (differential diagnosis from cellulitis)

A
  • exposure to allergen/drug
  • pruritus
  • absence of fever
  • absence of fever or pain
51
Q

What are the defining characteristics of DVT (differential diagnosis from cellulitis)

A
  • absence of skin changes or fever
52
Q

What are the defining characteristics of necrotising fasciitis (differential diagnosis from cellulitis)

A
  • severe pain
  • swelling and fever
  • rapid progression
  • pain out of proportion
  • systemic toxicity
  • skin crepitus
  • necrosis
  • ecchymosis
53
Q

What is anthrax?

A

An infection caused by the bacterium Bacillus anthracis. The skin form presents with a small blister with surrounding swelling that often turns into a painless ulcer with a black center.

54
Q

Which bacteria causes anthrax?

A

Bacillus anthracis (spore-forming aerobic gram-positive bacillus)

55
Q

How is bacillus anthracis acquired?

A

From imported wool, hair and animal hides

56
Q

How is a person infected with bacillus anthracis?

A

Inoculation through breaks in the skin (malignant pustule-eschar, may become septicaemic)

57
Q

Describe the epidemiology of anthrax

A
  • traditionally “woolsorters’ disease”

- contemporary risk factors are exposure to imported (West African) drum skins, and injecting drug use

58
Q

Describe the patterns of disease in anthrax

A
  • cutaneous anthrax = readily treated (mortality less than 1%)
  • inhalational/septicaemic anthrax = high mortality (around 45%)
59
Q

What is necrotising fasciitis?

A

Infection of skin and subcutaneous tissues - commonly known as flesh-eating disease, is a rare infection of the deeper layers of skin and subcutaneous tissues, easily spreading across the fascial plane within the subcutaneous tissue

60
Q

What are the causative agents of necrotising fasciitis?

A
  • type 1 = polymicrobial (enteric gram-negative bacilli and anaerobes)
  • type 2 = streptococcus pyogenes
61
Q

Perineal NF is sometimes referred to as what?

A
  • Fournier’s

- synergistic gangrene

62
Q

Describe the history in necrotising fasciitis?

A
  • spontaneous or at site of skin penetration

- any part of body

63
Q

Describe examination findings in necrotising fasciitis

A
  • fever and malaise

- dark, rapidly spreading, necrotic lesion

64
Q

How is necrotising fasciitis diagnosed?

A
  • microscopy and culture of debrided material and blood
65
Q

How is necrotising fasciitis treated?

A
  • intravenous antibiotics

- surgical debridement

66
Q

Why are anaerobic infections of the skin uncommon?

A

Because of the ready availability of O2

67
Q

Name a skin infection that is caused by an anaerobic bacteria

A

Gas gangrene

68
Q

What is gas gangrene?

A

A bacterial infection that produces gas in tissues in gangrene - clinically similar to synergistic gangene (polymicorbial necrotising fasciitis)
- palpable subcutaneous gas

69
Q

Gas gangrene usually happens when?

A

Usually post-operative surgical site infection

  • ‘dirty’ lower GI procedures
  • devitalised tissue eg. amputation
70
Q

What is the causative organism in gas gangrene?

A

Clostridium perfringens (anaerobic gram-positive bacillus)

71
Q

How is gas gangrene treated?

A
  • intravenous antibiotics

- surgical debridement

72
Q

What route of treatment is used for bacterial infections?

A
  • depends on disease severity
  • topical therapy used for superficial infections only (eg. impetigo, infected grazes etc)
  • severe infections e.g cellulitis, necrotising fasciitis etc. are treated with IV antibiotics
73
Q

What empiric therapy is used for most infections (caused by staph. aureus, step. pyogenes)?

A
  • flucloxacillin (fusidic acid or mupirocin for impetigo)

- penicillin allergy: erythromycin/clarithromycin, vancomycin, linezolid

74
Q

What antibiotics are used for necrotising fasciitis?

A

(need to cover anaerobes, enterbacteriaceae, streptococci and staphylococci)
- meropenem and clindamycin

75
Q

Give an example of an anti-anaerobic agent

A

Metronidazole

76
Q

Targeted therapy depends on what?

A

Culture results

77
Q

What are dermatophytes?

A

Fungi that require keratin for growth - can cause superficial infections of the skin, hair, and nail

78
Q

What are the dermatophyte infections of the skin?

A
  • tinea corproris
  • tinea pedis (athlete’s foot)
  • tinea curis
79
Q

Name a dermatophyte infection of the nails

A

Onychomycosis

80
Q

Name a dermatophyte infection of the scalp

A

Tinea capitis (scalp ringworm, kerion)

81
Q

What are the causative agents of dermatophyte infections?

A

Dermatophyte fungi

  • tricophyton spp. (eg. T. rugrum)
  • microsporum spp. (eg. M. canis)
82
Q

Describe the pathogenesis in dermatophyte infections

A
  • dermatophytes use keratin as nutritional substrate
  • usually restricted to stratum corneum
  • rarely penetrate the living cells of the epidermis
83
Q

How are dermatophytes diagnosed?

A

Skin scrapings - microscopy and culture (exclude other conditions eg. psoriasis)

84
Q

How are dermatophyte infections treated?

A
  • topical or systemic antifungal agents (depending on site and extent of infection)
85
Q

Name two topical anti fungal therapies used in skin infections

A
  • clotrimazole

- terbinafine

86
Q

Name three systemic anti fungal therapies used in scalp and nail infections

A
  • terbinafine
  • itraconazole
  • griseofulvin