Skin & Soft Tissue Infection Flashcards

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1
Q

What are the microbiological components of normal skin flora? [6]

A
  1. Diphtheroid
  2. Corynebacteria
  3. Anaerobes
  4. (yeast)
  5. Staphylococci (S. aureus)
  6. Streptococci (A,B,C,G)
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2
Q

What can go wrong with skin flora? [4]

A
  1. Breach in the normal flora skin barrier invites pathogens to infect and they can spread throughout the deeper dermis and fat
  2. This causes the typical signs of inflammation locally at the side of the breach:
    • Oedema
    • Pain
    • Erythema
    • Warmth
  3. This local inflammation can be treated with oral antibiotics
  4. But it can progress into invasive disease → treated with IV antibiotics
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3
Q

What are the non-modifiable and modifiable general risk factors for cellulitis? [4]

A
  1. Non-modifiable:
    • pregnancy,
    • white Caucasian
  2. Modifiable:
    • venous insufficiency,
    • lymphoedema
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4
Q

What are the non-modifiable and modifiable local risk factors for cellulitis? [8]

A
  1. Non-modifiable:
    • trauma,
    • animal/insect bites,
    • tattoos
  2. Modifiable:
    • ulcers,
    • eczema,
    • athletes foot,
    • burns,
    • surgical
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5
Q

What features of cellulitis would warrant hospital admission? [7]

A
  1. Class III or IV
  2. Class II (Unless have OPAT facilities available)
  3. Severe or rapidly deteriorating cellulitis
  4. Very young (under 1 year of age) or frail
  5. Immunocompromised
  6. Facial cellulitis
  7. Suspected orbital or periorbital cellulitis (admit under ophthalmology)
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6
Q

List the differential diagnoses for cellulitis and the features of each differential [6]

A
  1. Stasis dermatitis
    • absence of pain
    • absence of fever
    • circumferential
    • bilateral
  2. Acute arthritis
    • joint involvement
    • pain on movement
  3. Pyoderma gangrenosum
    • ulcerations on legs
    • history of inflammatory bowel disease (IBD)
  4. Hypersensitivity/drug Rn
    • exposure to allergens/drug
    • pruritis
    • absence of fever and pain
  5. DVT
    • Absence of skin changes or fever
  6. Necrotising fasciitis
    • severe pain out of proportion
    • swelling
    • fever
    • rapid progression
    • systemic toxicity
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7
Q

How do you differentiate between cellulitis and necrotising fasciitis? [5]

A
  • Vital to rapidly differentiate from cellulitis:
    1. Initial PAIN, becoming PAINLESS
    2. RAPID spread
    3. SYSTEMICALLY unwell
    4. DUSKY skin and NECROSIS
    5. MAY have skin crepitus
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8
Q

What are the clinical manifestations of necrotising fasciitis? [8]

A
  1. Remarkably rapid progression
  2. Most common on the extremities e.g. legs
  3. Initially erythema and swelling without sharp margins
  4. Exquisite pain and tenderness
  5. Lymphatic involvement is rare
  6. Colour changes from red-purple to blue-grey
  7. Skin breakdown and bullae with development of anaesthesia
  8. Probing of the lesion reveals easy passage through the tissues
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9
Q

How is necrotising fasciitis managed? [7]

A
  1. Early suspicion + Surgical debridement
  2. 5 antibiotics used:
    • Penicillin
    • Flucloxacillin
    • Clindamycin
    • Gentamicin
    • Metronidazole
  3. SURGERY is essential
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10
Q

Describe the typical appearance of erysipelas [4]

A
  1. Involves the upper dermis and superficial lymphatics
  2. Raised lesions with clear line of demarcation
  3. Classically butterfly involvement of the face but now accounts for only about 20% of cases.
  4. The legs are affected in up to 80% of cases.
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11
Q

Who typically gets erysipelas? [2]

A

affects infants + elderly

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12
Q

What are the microbiological causes of erysipelas? [1]

A
  1. usually group A strep,
  2. rarely: B, C, G and Staph aureus
  3. Elevated ASOT 10 days
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13
Q

How do you differentiate between erysipelas from cellulitis? [1]

A

erysipelas involves the ear but cellulitis does not

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14
Q

What is impetigo? [1]

A

Staphylococcal infection of epidermis

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15
Q

What is the typical appearance of impetigo? [2]

A
  1. often peri-oral
  2. “Honey coloured” crust
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16
Q

Who typically gets affected by impetigo? [3]

A
  1. Affects primarily children or sports persons
  2. Transmissible
17
Q

How do you manage impetigo? [3]

A
  1. Remove crust gently
  2. Flucloxacillin
  3. Prevent secondary infection
18
Q

What is the cause/pathogenesis of scarlet fever? [2]

A
  1. Results from infection with a streptococcal strain that elaborates streptococcal pyrogenic exotoxins or erythrogenic toxins
  2. Usually post pharyngitis but may complicate wound infections and post-partum infections
19
Q

Describe the clinical presentation of scarlet fever [9]

A
  1. Diffuse red blush appears on the second day of infection, point of deeper red blanch on pressure
  2. Starts on the upper chest and spreads to the trunk, neck and extremities
  3. Occlusion of the sweat glands gives the skin a sandpapery touch
  4. Palms, soles and face are usually spared
  5. Circum-oral pallor
  6. White strawberry tongue, then red strawberry tongue
  7. Severe cases can be characterised by high fever and systemic toxicity
  8. Rash fades over the course of a week and desquamates over several weeks
  9. Mild eosinophilia in the early stages
20
Q

What antibiotics are used to treate pasteurella infection caused by animal bites? [5]

A
  1. Penicillins (flucloxicillin much less active)
  2. Cephalosporins
  3. Tetracyclines
  4. Quinolones
  5. Macrolides
21
Q

Describe soft tissue infections that occur following exposure to water including organisms [5], exposure cause [5] and features of the clinical syndrome [11] that each organism causes

A
  1. Aeromonas spp.
    • due to exposure to fresh water
    • clinical syndrome:
      • rapidly developing infection associated with fever and sepsis
  2. Edwardsiella tarda
    • due to exposure to fresh water
    • clinical syndrome:
      • cellulitis,
      • occasionally fulminant infection with bacteraemia
  3. Erysipelothrix rhusiopathiae
    • due to exposure to puncture wounds from crabs etc.
    • clinical syndrome:
      • indolent localised cutaneous eruption,
      • erysipeloid
  4. Vibrio vulnificus
    • due to exposure to salt or brackish water
    • clinical syndrome:
      • rapidly progressive necrotising infection,
      • bullous cellulitis,
      • sepsis
  5. Mycobacterium marinum
    • due to exposure to fresh or salt water incl. fish tanks
    • clinical syndrome:
      • indolent infection,
      • papules to ulcers,
      • ascending lesions may resemble sporotrichosis
22
Q

Define a burn [1]

A

damage to the skin (heat, chemical, radiation) causing protein denaturing

23
Q

Describe how burns are classified, including the features of each type of classification [4]

A
  1. Superficial (1st)
    • epidermis only
    • dry/red
    • blanches on pressure
    • painful
    • heals in 7 days
  2. Partial-thickness (2nd)
    • epidermis and dermis
    • superficial vs deep
    • blisters
    • typically painful
    • heal <21days +/- antibiotics/surgery/grafting
  3. Full thickness
    • to subcutaneous tissue
    • painless
    • non-blanching
    • treated by surgery
  4. Fourth Degree
    • reaching the fascia/muscle/bone
    • healing requires surgery
24
Q

Damage to skin due to burns compromises resistance to environment, hence this increases risk of…? [4]

A
  1. Infection
  2. Hypothermia
  3. Acid base abnormalities
  4. Dehydration
25
Q

How should infected burns be managed? [5]

A
  1. Cleaning
  2. Dressings
  3. Topical antimicrobials (Gauzes/ointments/creams)
    • (e.g. silver sulfadiazine, Bismuth-compounds, Chlorhexidine) — may impact healing
  4. Topical antibiotics (e.g. bacitracin)
  5. Systemic antibiotics, (directed by culture results), required in invasive infection
26
Q

What are the features of cutaneous anthrax? [9]

A
  1. Surrounded by extensive oedema
  2. Painless and non-tender
  3. Black eschar
  4. Progresses over 2-6 days through papular, vesicular and ulcerated stages before eschar appears
  5. Affects hands, forearms, face and neck. Site of injection
  6. Discharge of serous fluid
  7. Local erythema and induration
  8. Local lymphadenopathy
  9. Associated with systemic malaise including headache, chills and sore throat; but afebrile.
27
Q

What are the risk factors of cutaneous anthrax? [6]

A
  1. Working with animals or animal hides
  2. Making, owning or playing animal hide drums
  3. Drug use (particularly heroin use)
  4. Travel
  5. Working in postal sorting offices or handling large volumes of mail
  6. Received threatening letter or package containing white powder
28
Q

What antibiotics are used to treat cutaneous anthrax? [5]

A
  1. Penicillin
  2. Flucloxacillin
  3. Clindamycin
  4. Ciprofloxacin
  5. Metronidazole
29
Q

What is tinea? [2]

A
  1. Superficial dermatophyte infection characterized by scaly, inflammatory or non-inflammatory patches
  2. Generally limited to the epidermis and expands in a centrifugal pattern
30
Q

How is tinea transmitted? [1]

A

via direct skin-to-skin contact

31
Q

What are the symptoms of erythema infectiosum? [5]

A
  1. fever,
  2. headache,
  3. runny nose,
  4. followed by a pruritic rash on the face (“slapped cheek”), as well as the torso and extremities
32
Q

What is hand-foot-and-mouth disease, what is the viral cause and who typically gets it? [3]

A
  1. Viral illness with oral and distal-extremity lesions
  2. Coxsackie virus A16
  3. typically affects children and infants
33
Q

What are the symptoms of hand-foot-and-mouth disease? [6]

A
  1. fever
  2. rash
  3. headache
  4. sore throat
  5. oropharyngeal ulcers
  6. loss of appetite
34
Q

What are the 2 types of presentations of herpes simplex virus? [2]

A
  1. stomatitis “cold sore”
  2. genital herpes
35
Q

How do you treat herpes simplex virus (HSV)? [1]

A

acyclovir (topical, oral, IV)

36
Q

What is shingles and how does it present? [2]

A
  1. Reactivation of dormant varicella zoster virus (VSV) (dorsal root ganglia)
  2. Dermatomal distribution
37
Q

How do you treat shingles? [3]

A
  1. Treat only high-risk patients (immunocompromised, disseminated) with acyclovir
  2. Pain management:
    • NSAIDs,
    • gabapentin