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Clinical Pathology > Skin and soft tissue infections > Flashcards

Skin and soft tissue infections Flashcards

1
Q

What organisms constitute the normal skin flora?

A

Coagulase-negative staphylococci

Staph. aureus

Propionibacterium,

Corynebacterium spp.

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2
Q

What is the pathogenesis of localised skin infections?

A

Penetration of skin with a contaminated object

  • Accidental, e.g. tooth, rusty nail, knife etc.
  • Deliberate, e.g. surgical procedure, therapeutic injection, injection drug use etc.

Contamination of pre-existing breach in the skin surface
- e.g. abrasion, athletes foot lesion etc.

Neuronal migration in herpes simplex

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3
Q

Which systemic/generalised infections have skin complications?

A

Chicken pox

Meningococcal sepsis

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4
Q

Which viruses can cause skin disease?

A

Herpes viruses
- Herpes simplex virus (HSV)
Varicella zoster virus (VZV)

Molluscum contagiosum

Human papilloma virus (HPV)

Orf

Cowpox

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5
Q

What is 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 dorsal root ganglion

In latent infection viral DNA exists as “episomes” and no virus-coded proteins are present to stimulate an immune response

In reactivation it is believed that virus particles migrate outwards to sensory nerve endings and cause clinical manifestations of infection

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6
Q

What are the triggers for Herpes simplex?

A

Infection or stress

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7
Q

What would you find on examination in a primary infection of HSV?

A

Extensive, painful lesions
Inside mouth

Peri-oral ulcer (or genital)
Weeping, vesicular

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8
Q

What is the treatment for herpes?

A

Cold sores
- Topical acyclovir

Genital herpes, immunosuppressed patient
- Oral acyclovir

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9
Q

What is shingles?

A

Reactivation of varicella zoster virus in a single dermatome

Triggered by physical or emotional stress

Preceded by pain, tingling and/or numbness

Weeping vesicular rash with dermatomal distribution.

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10
Q

What is the treatment for shingles?

A

Oral acicolvir/valaciclovir

IV aciclovir
- Depending on age of patient, immune status and severity of shingles

Seek specialist advice
- Severe/widespread rash, severe immunosuppression or multiple dermatomes involved

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11
Q

What is molluscum contagiosum?

A

Caused by poxvirus - molluscum contagiosum

Raised, pearly lesions up to 3 mm, Umbilicated

Clinical diagnosis

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12
Q

What is the treatment for molluscum contagiosum?

A

Treatment

  • None – lesions usually disappear in 6-18 months
  • Various topical preparations
  • Physical treatments (cryotyherapy, diathermy, laser therapy)
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13
Q

What are the causative agents of most bacterial skin infections?

A

Mainly Staph. aureus and group A β-haemolytic streptococci (S. pyogenes)

A few others e.g. Haemophilus influenzae, Pasteurella multocida, enteric organisms and rarities

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14
Q

What are the features of S.aureus?

A

Gram-positive cocci in clusters, catalase-positive

Normal nasal flora in approx. 30% of pop’n

Large number of virulence factors e.g. DNAse, coagulase, teichoic acid

Exotoxin production

  • epidermolytic toxins A & B (ETA & ETB)
  • toxic shock syndrome toxin (TSST-1)
  • Panton-Valentine leukocidin (PVL)
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15
Q

What are the features of S.pyogenes?

A

Gram-positive cocci in chains, catalase-negative
Express many virulence factors e.g.
- Adhesins
- M proteins (antiphagocytic)
- Hyaluronic acid capsule (antiphagocytic)
- Hyaluronidase (facilitates interstitial spread)
- C5a peptidase (anticomplementary)
- Streptolysins-O and -S (lysis of red & white blood cells)
- Pyrogenic exotoxins

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16
Q

What is Impetigo?

A

Infection of epidermis (superficial)

Causative agent
- S. aureus, S. pyogenes or both

History
- Often occurs at a site of skin damage: Cut, graze, insect bite, chickenpox, molluscum contagiosum lesion

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17
Q

What is the appearance of impetigo?

A

Plaque-like lesions

Yellowish exudate

Thick scabs
- “Honey crusted lesions”

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18
Q

How is impetigo diagnosed?

A

Clinical diagnosis

Bacterial culture
- Sensitivity testing may be useful

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19
Q

What are the possible complications of impetigo?

A

Epidermolytic toxin production (ETA & ETB)

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20
Q

What are the manifestations of Epidermolytic toxin production (ETA & ETB)

A

Localised: Bullous impetigo

Generalised: Staphylococcal scalded skin syndrome (SSSS)

21
Q

What is the pathogenesis of Epidermolytic toxin production (ETA & ETB)?

A

Desmosomal glycoprotein desmoglein-1

  • Required for cell-to-cell adhesion in the superficial epidermis
  • Inactivated by ETA & ETB
22
Q

What is erysipelas?

A

Infection of dermis

Causative agent
- S. pyogenes

History

  • Often occurs at a site of skin damage
  • Predominantly face or shin
  • Preceded by pain & tenderness
23
Q

What would you find on examination in erysipelas?

A

Fever & malaise

Well-demarcated inflamed lesion
- Red, swollen, painful and hot

Lymph node enlargement

Clinical diagnosis

24
Q

What is cellulitis?

A

Infection of skin and subcutaneous tissues

Causative agents include:

  • S. aureus
  • S. pyogenes
  • Pasteurella multocida (animal bites)
  • Haemophilus influenzae
25
What is the presentation of cellulitis?
Fever & malaise Diffuse inflamed lesion - Erythema, swelling, tenderness, heat
26
How would you perform a microbiological diagnosis of cellulitis?
Lesion swabs - Positive in 85% of cases - Swab if lesion is ulcerated Lesion aspirates and skin biopsy - Positive in 10-20% of cases - Not recommended routinely Blood cultures - Positive in only 2-4% of cases - Use if severe sepsis or systemic signs of infection
27
What are the differential diagnoses for cellulitis?
Stasis dermatitis - Absence of pain or fever; circumferential; bilateral Acute arthritis - Involvement of joint; pain on movement Pyoderma gangrenosum - Ulcerations on the legs; history of inflammatory bowel disease Hypersensitivity - Exposure to allergen or drug; pruritus; absence of fever; absence of fever or pain DVT - Absence of skin changes or fever Necrotising fasciitis - Severe pain, swelling and fever; rapid progression; pain out of proportion; systemic toxicity; skin crepitus; necrosis; ecchymosis
28
What is anthrax?
Bacillus anthracis - Spore-forming aerobic Gram-positive bacillus Acquired from imported wool, hair and animal hides Inoculation through breaks in the skin - “Malignant pustule” = “eschar” - May become “septicaemic” Patterns of disease - Cutaneous anthrax - readily treated (mortality 20%) - Pulmonary anthrax (mortality 80%)
29
What is the epidemiology of anthrax?
Epidemiology - Traditionally “Woolsorters’ disease” - Contemporary risk factors are exposure to imported (West African) drum skins and injecting drug use
30
What is necrotising fasciitis (NF)?
Infection of skin and subcutaneous tissues - specifically fascia Causative agents - Type 1: Polymicrobial Enteric Gram-negative bacilli Anaerobes - Type 2: Streptococcus pyogenes
31
What is peripheral NF sometimes called?
Fournier’s or synergistic gangrene
32
What is found on history and examination in NF?
History - Spontaneous or at site of skin penetration - Any part of body Examination - Fever & malaise - Dark, rapidly spreading, necrotic lesion
33
How is NF diagnosed?
Microscopy and culture - Debrided material - Blood
34
How is NF treated?
Treatment - Intravenous antibiotics - Surgical debridement
35
Why are anaerobic infections of the skin uncommon?
Because O2 is readily available
36
What is the common name given to anaerobic infections of the skin?
Gas gangrene
37
What are the features of gas gangrene?
Clinically similar to “synergistic gangrene” (polymicrobial necrotising fasciitis) Palpable subcutaneous gas Usually post-operative surgical site infection - “Dirty” lower GI procedures - Devitalised tissue (e.g. amputation) Causative organism is Clostridium perfringens (anaerobic Gram-positive bacillus) Treatment - Intravenous antibiotics - Surgical debridement
38
For bacterial infections, how do you decide treatment route?
Depends on disease severity Topical therapy used for superficial infections only (e.g. impetigo, infected grazes etc.) Severe infections (cellulitis, necrotising fasciitis etc.) treated with IV antibiotics
39
What empiric therapy would you use in S.aureus or S.pyogenes infections?
Flucloxacillin (fusidic acid or mupirocin for impetigo) Penicillin allergy: erythromycin/clarithromycin, vancomycin, linezolid
40
What empiric therapy would you use in NF?
Necrotising fasciitis – need to cover anaerobes, Enterobacteriaceae, streptococci and staphylococci - Meropenem + clindamycin
41
What empiric therapy would you use in anaerobic infections?
Include anti-anaerobic agents (e.g. metronidazole)
42
What empiric therapy would you use in infections high risk for MRSA (prev. MRSA etc.)
Vancomycin | Linezolid
43
What are dermatophyte infections?
Skin - Tinea corporis - Tinea pedis (athletes foot) - Tinea cruris Nails - Onychomycosis Scalp - Tinea capitis (scalp ringworm, kerion)
44
What are the causative agents in dermatophyte infections?
Tricophyton spp. (e.g. T. rubrum) Microsporum spp. (e.g. M. canis)
45
What is the pathogenesis of dermatophyte infections?
Dermatophytes use keratin as nutritional substrate Usually restricted to stratum corneum Rarely penetrate the living cells of the epidermis
46
How does one perform diagnoses of dermatophyte infections?
Skin scrapings - microscopy & culture | - Exclude other conditions e.g. psoriasis
47
What is the treatment for dermatophyte infections?
Topical or systemic antifungal agents | - Depending on site & extent of infection
48
What is the treatment for fungal skin infections?
Topical antifungal therapy | - Clotrimazole, terbinafine
49
What is the treatment for fungal scalp and nail infections?
Systemic antifungal therapy | - Terbinafine, itraconazole, griseofulvin

Clinical Pathology (65 decks)

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