Skin and Soft Tissue Infections Flashcards
1
Q
What are the normal microbiota of the skin?
A
- Coagulase-negative Staphylococci
- Staphylococcus epidermis
- Staphylococcus aureus
- Streptococcus pyogenes
- Propionibacterium acnes
- Corynebacterium sp.
- Candida sp.
2
Q
What are the possible routes of infection (breaches of skin integrity)?
A
-
Skin
- Pores
- Hair follicles
-
Wounds
- Scratches
- Cuts
- Burns
-
Bites
- Insects
- Animals
3
Q
Where do these common skin infections occur:
- Ringworm?
- Impetigo?
- Folliculitis?
- Cellulitis?
- Necrotising fasciitis?
- Gas gangrene?
A
- Ringworm - keratinised epithelium
- Impetigo - epidermis
- Folliculitis - hair follicles
- Cellulitis - subcutaenous layers
- Necrotising fasciitis - multi-layer
- Gas gangrene - muscle
4
Q
What is a furuncle?
A
A deep inflammatory lesion progressing from a folliculitis.
5
Q
What is a carbuncle?
A
Carbuncles extend into the subcutaneous layer. Multiple abscesses develop, separated by connective tissue septs.
Essentially a collection of boils.
6
Q
What is folliculitis?
A
A folliculitis is a pyoderma of the hair follicle
7
Q
What is ecthyma?
How does it spread?
A
- Rupturing vesicles leading to erythematous lesions and dried crusts
- Spreads into the dermis
8
Q
Where does erysipelas spread?
A
Spreads into the deeper dermis.
9
Q
What is cellulitis?
How does it spread?
A
- Erythematous inflammation affecting deeper dermis and subcutaneous fat.
- Spreads laterally into the subcutaneous layer of the skin.
10
Q
What is a pyoderma?
A
Pus-forming skin infection; cutaneous abscess.
11
Q
What is impetigo?
A
Vesicles developing into rupturing pustules then forming dried crusts.
- Picture - impetigo (contagiosa / non-bullous).
12
Q
What is erysipelas?
A
Erythema and inflammation of superficial dermis.
13
Q
What is dehiscence?
A
Wound rupture along a surgical suture.
14
Q
Describe non-bullous impetigo.
A
- Thin-walled vesicles or pustules. Associated exudate: characteristic golden / brown crust. Once crusts have dried they separate leaving mild erythema which then fades. Heals spontaneously without scarring within 2-3 weeks.
- Found anywhere on the body.
- Satellite lesions may develop following autoinoculation.
- Non-bullous impetigo is usually asymptomatic but may be mildly itchy.
- Systemic features are uncommon but in severe cases regional lymphadenopathy and fever may occur.
15
Q
Describe bullous impetigo.
A
- Lesions appear as flaccid fluid-filled vesicles and blisters (that can persist for 2-3 days). Blisters rupture leaving a thin, flat yellow-brown crust.
- Healing usually occurs within 2-3 weeks without scarring.
- Lesions can occur anywhere on the body but are most common in the flexures, face, trunk and limbs.
- Systemic features may occur if large areas of skin are affected and include fever, lymphadenopathy, diarrhoea and weakness.
16
Q
What should be asked in the history when ?impetigo?
A
- Onset, evolution, duration and location of lesions.
- Contacts with a similar rash.
- PMHx noting skin conditions such as eczema or immunosuppression.
- Skin trauma or abrasions or insect bites.
- Previous treatment including antimicrobial therapy.
- Systemic features such as fever.
17
Q
Describe the management of impetigo.
A
- Referral rarely needed unless:
- Part of an outbreak
- Diagnostic uncertainty
- Resistant to maximal treatment
- Complications e.g. acute glomerulonephritis
- Advise hygiene measures help to aid healing and stop infection spreading:
- Wash affected areas with soap and water
- Wash their hands regularly, in particular after touching a patch of impetigo
- Avoid scratching affected areas
- Avoid sharing towels etc.
18
Q
Describe staphylococcal scalded skin syndrome.
A
- Characterised by red blistering skin that looks like a burn or scald.
- Caused by the release of toxins from S. aureus.
- Also known as Ritter’s disease.
- Occurs in newborns.
- Syndrome of acute exfoliation followed by an erythematous cellulitis.
-
Clinical findings:
- Localised S. aureus infection of the skin or URT, although this may go unnoticed.
- Fever and irritability but patients do not appear overly unwell.
- Macular erythema is followed by diffuse, confluent erythema with bullae, which rupture easily.
- Marked epidermal exfoliation with the skin peeling off in sheets leaving exposed most, bright-red tender areas.
- The Nikolsky sign (gentle stroking of he skin causes the skin to separate at the epidermis) is positive.
- SSSS differs from the more severe, and generally drug-induced, toxic epidermal necrolysis (TEN), in that the cleavage site in SSSS is intraepidermal, as opposed to TEN, which involves necrosis of the entire epidermis.
19
Q
Describe toxic shock syndrome.
A
- Rare but potentially fatal illness - but can be treated.
- Associated with tampon use - when they are left in / poor hygiene.
- Caused by bacterial toxins - superantigens most commonly from S. aureus and S pyogenes.
- Symptoms include:
- High fever
- Low BP
- Malaise
- Confusion
- Characteristic rash:
- Resembles sunburn
- Affects any region of the body
- Desquamates 10-14 days later
20
Q
Describe the management of SSSS.
A
- SSSS requires prompt recognition and treatment. Same day contact should be made with the on-call dermatologist as hospital admission will almost certainly be required.
- Parenteral ABx to cover S. aureus.
- Topical therapies, such as fusidic acid and / or muppirocin, are sometimes used as adjuncts to parenteral ABx.
- Supportive treatment.
- Children generally revocer ell and healing is usually complete within 5-7 days of starting treatment.
- The mortality rate from SSSS in children is very low (1-5%), unless associated with sepsis or an underlying serious medical condition exists.
- Mortality rate in adults is higher (as high as 50-60%).
- SSSS is an infection control issue and there may be a carrier in care home or nursery.
21
Q
Why are diabetic patients particularly susceptible to infections?
A
- High blood glucose can alter the normal microbiota.
- Reduced blood flow in the vasculature may result in problems in mobilising the immune system effectively.
- Neuropathy, particularly in the extremities, may result in increased injury.
- Injection with insulin provides a portal of entry.
22
Q
What questions should be asked in the hx when ?cellulitis?
Describe the examination.
A
- HX of PC with a focus on emerging sensitivity.
- What co-morbidities are present?
- What predisposition is present e.g. foreign travel or salt-water exposure?
- Is there trauma, bite, burn or potential foreign body?
-
Examination
- Describe and delineate the infection carefully (draw a line)
- Fever, nausea, rigors
- Skin break
- Blisters
- Crepitus
- Concomitant skin conditions e.g. eczema
- Identify underlying risk factors (such as lymphoedema and leg oedema).
- Exclude other diagnoses: erysipelas, contact allergic dermatitis, DVT and cutaneous abscess.
23
Q
How do you classify cellulitis?
A
- Class 1 - there are no signs of systemic toxicity and the person has no uncontrolled comorbidities.
- Class 2 - the person is either systemically unwell or systemically well but with a comorbidity (e.g. peripheral arterial disease, chronic venous isufficiency, or morbid obesity) which may complicate or delay resolution of infection.
- Class 3 - the person has significant systemic upset, such as tachycardia, tachypnoea, hypotension or unstable comorbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromise.
- Class 4 - the person has sepsis or a severe life-threatening infection, such as necrotising fasciitis.
24
Q
What are the criteria for hospital admission in a patient with cellulitis?
A
- Has class IV cellulitis (sepsis or severe life-threatening infection such as necrotising fasciitis).
- Has class III cellulitis (significant systemic upset, such as acute confusion, tachycardia, tachypnoea, hypotension or unstable comorbidities, or a limb-threatening infection due to vascular compromise).
- Has severe or rapidly-deteriorating cellulitis (e.g. extensive areas of skin).
- Is very young (<1) or frail.
- Is immunocompromised.
- Has significant lymphoedema.
- Has facial cellulitis (unless very mild).
- Has suspected orbital or periorbital cellulitis (admit to ophthalmology).
- Has class II cellulitis (systemically unwell or systemically well but with a comorbidity).
- Admission may not be necessary if the facilities and expertise are available in the community to give IV ABx and monitor the person.
25
How is cellulitis managed in primary care?
* Class 1 cellulitis - draw a line around the lesion, prescribe high-dose oral ABx according to local guidelines.
* Pain relief and elevation.
* Deal with concomitant skin lesions.
* Provide patient information on cellulitis.
* Refer patients with recurrent cellulitis.
* Review in 48 hours.
26
Describe the clinical features, diagnosis and treatment of erysipelas.
* S. pyogenes infection usually face, shin, dorsum of foot.
* Aching, throbbing and tenderness.
* Indurated, hot and tender.
* Clear boundary with normal skin.
* Moderate fever and rise in WBC.
* Diagnosis is clinical.
* Treatment is as for cellulitis.
27
Describe necrotising fasciitis.
* Starts as a localised infection. Cellulitis rapidly develops and spreads into deeper fascia and muscles.
* Often associated with fever, severe pain and systemic toxicity.
* Effects of toxins - may lead to loss of limb, toxic shock and death.
* Cause - **streptococcus pyogenes** or **mixed infection** (gram negative anaerobes, facultative anaerobes, anaerobic and facultative anaerobic cocci).
* **Early symptoms**
* ****Intense and severe pain which may seem out of proportion to any external signs of infection on the skin.
* A small but painful cut or scratch on the skin.
* Fever and flu-like symptoms.
* **Advanced symptoms (usually within 3-4 days)**
* ****Swelling of the painful area, accompanied by a rash.
* D&V
* Large dark blotches, that will turn into blisters and fill up with fluid
* Critical symptoms (usually within 4-5 days) include:
* Severe fall in BP
* Shock unconsciousness as the body weakens
28
What are coagulase-negative staphylococci?
* Coagulase = enzyme that causes clot formation.
* We can use this characteristic when culturing to aid in identification.
* Coagulase negatives are part of our normal microbiota and are usually, in a healthy host, of low virulence.
* This class of bacteria are becoming increasingly recognised as a clinically important cause of infection.
* Examples:
* S. aureus
* P. aeruginosa
29
What is erythema granulosum?
* Ulcerative form of impetigo
* Vesicle has ruptured
* Further breach of defensive structures
30
What are the fungal infections of the skin?
* Fungal infections = mycoses.
* **Dermatophytes** (fungus that requires keratin for growth)
* ****Tinea spp., for example:
* Tinea pedis
* Tinea corporis
* Tinea cruris
* **Yeasts**
* ****Candida albicans
* Malassezia furfur
31
Describe tinea corporis.
* **Ringworm of the body**
* Ring-like, red, scaly rash.
* Highly infectious.
32
Describe tinea pedis.
* **Athlete's foot**
* Causes scaling, flaking, itching of the foot.
* Loves a warm, moist environment to incubate such as the inside of a sweaty trainer.
* May spread to other 'moist' areas of the skin.
* ~15% of the population affected.
33
What is tinea cruris?
* **Ringworm of the groin**
* 'Jock itch'
34
Describe HPV.
* Group of viruses.
* Affect the skin and the moist membranes lining the body (cervix, anus, mouth and throat).
* Changes to cells within the cervix can lead to cervical cancer.
* Also responsible for verrucas.
* Also found on genital areas, hands and conjunctiva.
* Different types of warts - plantar, pedunculated, sessile.
35
Describe HSV.
* **Cold sores and genital warts.**
* Genital warts are spread through vaginal, anal and oral intercourse.
* \>90% of adults are antibody positive for HSV1.
* They can also be passed on to infants during childbirth.
36
Describe varicella zoster virus.
* **Chicken pox and shingles.**
* Once infected, the virus is not eliminated and remains latent in dorsal root ganglia or cranial nerve without causing any symptoms.
* It may later recrudesce and spread along nerves of an affected segment and infect the corresponding dermatome.
* Hence, note the localisation of the shingles.
37
Describe Coxsackie A virus.
* **Hand, foot and mouth disease**
* Usually in children
* Cold-like symptoms
* Non-itchy rash with vesicles in te locations shown
* Usually self-limiting
38
Describe the effect of sarcoptes scabei (mite) on the skin.
* **Causes** **scabies**
* Mite burrows into the skin
* Female lays eggs
* Infection is asymptomatic
* Hypersensitivity may occur
* May lead to superinfection
39
Describe the infection risk associated with animal bites.
* **Cats**
* ****Deep puncture wound
* Little superficial damage
* **Dogs**
* ****Extensive superficial injury
* Crush injury +++
* Human response:
* Clenched fist
* Deep infection common
* BBV
* HIV
* HBV
* HCV
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