Infections of the Skin and Soft Tissues | Medibuddy
16th July 2026

Infections of the Skin and Soft Tissues

Bacterial Infections

Impetigo

Impetigo is a superficial bacterial skin infection that primarily affects young children, though it can occur at any age. It is highly contagious and spreads through direct skin-to-skin contact or contaminated surfaces. The most common causative organisms are Staphylococcus aureus and Streptococcus pyogenes (Group A Streptococcus). 

There are two main forms:

  • Non-bullous impetigo (more common): Starts as erythematous macules that evolve into vesicles and pustules, which rupture to form honey-coloured crusts. Lesions typically affect the face.
  • Bullous impetigo: Caused by exfoliative toxin-producing S. aureus. It presents with flaccid bullae which rupture, leaving shallow erosions.

Risk factors include poor hygiene, minor skin trauma (e.g. insect bites), eczema or other dermatoses, hot and humid climates, and nasal carriage of S. aureus.

Diagnosis

Diagnosis is clinical. Swabs for culture and sensitivities are reserved for:

  • Recurrent or resistant cases
  • Widespread infection or suspected MRSA
  • Outbreak settings

Management

  • Localised, non-bullous impetigo:
    • Hydrogen peroxide 1% cream (first-line)
    • Topical fusidic acid or mupirocin if needed
  • Extensive or bullous impetigo:
    • Oral flucloxacillin or clarithromycin

Children should also be excluded from school until lesions are crusted or 48h after antibiotics.

Erysipelas

Erysipelas is a superficial bacterial skin infection affecting the upper dermis and lymphatics. It is caused almost exclusively by Streptococcus pyogenes (Group A streptococcus)

It presents with sudden-onset fever, chills, and a well-demarcated, raised, bright red rash. The face and lower limbs are most commonly affected. Risk factors include breaks in the skin barrier, lymphoedema, obesity, and immunosuppression.

Diagnosis

Diagnosis is clinical. Blood cultures may be taken in systemic illness. Differential diagnoses include cellulitis, DVT, contact dermatitis, and drug reactions.

Management

  • Oral phenoxymethylpenicillin (or flucloxacillin) for mild cases
  • IV benzylpenicillin or flucloxacillin for systemic features
  • Clarithromycin if penicillin-allergic

Cellulitis

Cellulitis is an acute infection involving the deep dermis and subcutaneous tissues. It typically presents with localised pain, erythema, warmth, and swelling, often with systemic signs like fever.

The most common pathogens are Streptococcus pyogenes and Staphylococcus aureus. Risk factors include diabetes, peripheral vascular disease, venous insufficiency, tinea pedis, and obesity.

Diagnosis

Diagnosis is clinical. Imaging may be considered if an abscess or necrotising fasciitis is suspected. Differentials include DVT, contact dermatitis, erysipelas, and stasis dermatitis.

Management

  • Mild: oral flucloxacillin
  • Severe or systemically unwell: IV flucloxacillin, consider MRSA cover if risk factors present
  • Treat underlying risk factors

Necrotising Fasciitis

Necrotising fasciitis is a rapidly progressing infection of the fascia and subcutaneous tissues, causing tissue necrosis. It is a surgical emergency with high mortality.

There are two main types:

  • Type I (polymicrobial)
  • Type II (usually Group A Streptococcus)

Presentation includes extreme pain out of proportion to findings, systemic toxicity, skin discolouration, crepitus, and hypotension.

Diagnosis

CT or MRI may show fascial thickening and gas in soft tissues. Bloods show raised inflammatory markers. Surgical exploration is often diagnostic.

Management

  • Urgent surgical debridement
  • Broad-spectrum IV antibiotics: meropenem + clindamycin + vancomycin
  • Supportive care in ICU if required

Viral Infections

Herpes Simplex Virus

Herpes simplex virus (HSV) is a double-stranded DNA virus responsible for a range of mucocutaneous infections. HSV-1 primarily causes orolabial lesions, whereas HSV-2 more commonly affects the genital region. However, either strain can infect any anatomic site depending on exposure. Following primary infection, the virus establishes latency in sensory ganglia, with the potential for reactivation under conditions such as stress, immunosuppression, or febrile illness.

Primary infection may present with fever, malaise, lymphadenopathy, and grouped vesicles on an erythematous base. It can be severe, especially in immunocompromised hosts. Recurrent infections tend to be milder. Other presentations include:

  • Herpetic whitlow: painful vesicular lesions on the fingers, typically seen in healthcare workers or thumb-sucking children.
  • Eczema herpeticum: widespread HSV infection in patients with atopic dermatitis — a medical emergency due to potential systemic spread.

Diagnosis

Diagnosis is usually clinical. Confirmatory tests are used in atypical or severe cases:

  • PCR from vesicle fluid (most sensitive and specific)
  • Viral culture (less common)
  • Tzanck smear (obsolete)
  • Direct fluorescent antibody testing in some labs

Management

  • Mild to moderate: Oral aciclovir 400 mg TDS for 5 days (or valaciclovir/famciclovir)
  • Severe/disseminated (eczema herpeticum): IV aciclovir
  • Recurrent or frequent flares: Suppressive therapy (e.g. aciclovir 400 mg BD for 6–12 months)
  • Counselling on avoiding direct contact during active lesions to prevent transmission

Herpes Zoster Virus (HZV)

Herpes zoster (HZV; shingles) results from reactivation of latent varicella-zoster virus (VZV) — the agent responsible for chickenpox. Following resolution of primary infection, VZV remains dormant in dorsal root or cranial nerve ganglia, reactivating years later, particularly in the elderly or immunocompromised.

It presents as a painful, unilateral vesicular rash distributed along a single dermatome. Prodromal burning, tingling, or hyperesthesia often precedes the rash by 1–3 days. Common sites include thoracic dermatomes and the trigeminal distribution.

Complications include:

  • Postherpetic neuralgia (PHN) — persistent neuropathic pain lasting >3 months
  • Herpes zoster ophthalmicus — involving the V1 branch; requires urgent ophthalmology referral
  • Disseminated zoster in immunocompromised individuals

Diagnosis

Diagnosis is typically clinical. Consider PCR of vesicular fluid or skin biopsy in atypical presentations.

Management

  • Antiviral therapy (start within 72 hours of rash onset):
    • Aciclovir 800 mg 5 times daily for 7 days
    • Alternatives: valaciclovir or famciclovir (better oral bioavailability)
  • Analgesia:
    • Paracetamol/NSAIDs
    • Neuropathic agents for PHN (e.g. gabapentin, amitriptyline)
  • Zoster vaccine is recommended for adults >50 years and those at increased risk

Fungal Infections

Fungal infections of the skin, also known as superficial mycoses, affect the stratum corneum and adnexal structures like hair and nails. These infections are typically caused by dermatophytes (Trichophyton, Microsporum, Epidermophyton), Candida species, and Malassezia. Dermatophyte infections are grouped under the term ‘tinea’ and are named according to the site involved — for example, tinea corporis (body), tinea pedis (feet), and tinea capitis (scalp).

Clinical features

Tinea corporis typically presents as annular plaques with an advancing scaly edge and central clearing. Tinea pedis may manifest as interdigital maceration, moccasin-type scaling, or vesiculobullous eruptions. Tinea capitis often affects children and presents with patchy hair loss and black dot alopecia. Onychomycosis affects the nails and causes discolouration, thickening, and onycholysis.

Candidal infections involve intertriginous areas, such as under the breasts or in the groin, presenting with erythematous plaques and satellite pustules. Malassezia infections like pityriasis versicolor cause hypopigmented or hyperpigmented macules with fine scale, commonly on the trunk.

Diagnosis

Diagnosis is often clinical but can be supported by potassium hydroxide (KOH) microscopy, fungal culture, or Wood’s lamp examination (especially in tinea capitis or pityriasis versicolor). Dermoscopy is increasingly used as a non-invasive adjunct.

Management

Management involves topical antifungals such as clotrimazole, miconazole, or terbinafine for most localised infections. Systemic treatment (e.g., oral terbinafine, itraconazole, or fluconazole) is indicated for tinea capitis, onychomycosis, or extensive disease. Preventative strategies include avoiding shared towels, keeping the skin dry, and managing risk factors like diabetes or immunosuppression.

Scabies

Scabies is a highly contagious parasitic skin infestation caused by the mite *Sarcoptes scabiei* var. hominis. It is transmitted through prolonged skin-to-skin contact and is especially common in crowded living environments.

Clinical Features and Diagnosis

The hallmark symptom is intense pruritus, particularly at night. Characteristic lesions include burrows, papules, and vesicles located in the finger web spaces, wrists, anterior axillary folds, areolae, and genitalia. In infants, the scalp and soles may also be affected.

Diagnosis is clinical, but dermoscopy may reveal the ‘delta wing jet’ sign (mite in burrow). Microscopy of skin scrapings may also confirm the diagnosis by revealing mites, eggs, or faecal pellets.

Management

First-line treatment is topical permethrin 5%, applied to the entire body (including the scalp and face in infants), repeated after 7 days. All close contacts must be treated simultaneously, regardless of symptoms. Bedding and clothing should be washed at high temperatures. Oral ivermectin is reserved for crusted scabies or outbreaks in institutional settings.

A post-scabetic rash or persistent pruritus may last for weeks after successful treatment and does not indicate treatment failure. Antihistamines or mild topical corticosteroids can be used for symptomatic relief.

Lyme Disease

Lyme disease is a tick-borne infection caused by the spirochete *Borrelia burgdorferi*, transmitted by Ixodes ticks. It is most prevalent in temperate woodland areas in Europe and North America. The condition has three stages: early localised, early disseminated, and late disease.

Clinical Features and Diagnosis

The classic hallmark of early localised Lyme disease is erythema migrans — an expanding, painless erythematous rash with central clearing (‘bull’s-eye’ appearance) occurring at the site of the tick bite. Systemic symptoms may include malaise, fatigue, headache, fever, and myalgia.

Early disseminated disease may involve multiple erythema migrans lesions, cranial nerve palsies (especially facial nerve), meningitis, or carditis. Late manifestations include arthritis (especially of the knees) and peripheral neuropathy.

Diagnosis is clinical in the presence of erythema migrans. Serological testing (ELISA followed by Western blot) is used for confirmation in later disease or atypical presentations. False negatives can occur in early disease due to low antibody titres.

Management

Treatment of early disease includes oral doxycycline for 14–21 days. Alternatives include amoxicillin or cefuroxime in pregnant women or children under 8. Neurological or cardiac involvement may require intravenous ceftriaxone. There is no current vaccine in the UK, so prevention relies on protective clothing and tick checks.

References

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