Eczema herpeticum and infected eczema

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Morphology and sensation separate urgency. Eczema herpeticum lesions are remarkably uniform and painful, may look grey, purple or dark against deeply pigmented skin, and leave circular erosions. Impetiginised eczema is more variable, with pustules, honey-coloured crust and increasing ooze. Either can coexist, so cloudy vesicle fluid or worsening despite antiviral treatment may justify bacterial sampling and therapy.

A patient who is systemically well with modest crusting often improves through better eczema control without antibiotics. Use NICE NG190 to weigh extent, severity, complication risk and previous antibiotics. If systemically unwell, oral or intravenous choice follows severity; obtain culture after failure or frequent recurrence rather than swabbing every flare.

Eczema herpeticum and infected eczema care should combine visible inflammation with itch, pain, sleep, occupation and treatment burden. Agree where each product goes, how much is used and when response will be reviewed; explain urgent features separately so normal fluctuation is not confused with infection or treatment failure.

Key points

Eczema herpeticum causes a sudden painful eruption of monomorphic vesicles and punched-out erosions, often with fever or malaise; ordinary eczema is usually itch-dominant and polymorphic.
Start systemic aciclovir immediately when eczema herpeticum is suspected and arrange same-day specialist assessment; do not wait for HSV PCR.
Periocular lesions, painful red eye, photophobia or visual symptoms require urgent ophthalmology as well as antiviral treatment.
Bacterial infection is suggested by increasing pain, pustules, purulent exudate, rapidly worsening crust, cellulitis or systemic illness, but eczema often carries bacteria without invasion.
NICE advises against routinely offering an antibiotic to a systemically well patient with secondary bacterial infection of eczema because benefit may be limited over topical eczema treatment.
Continue emollient and appropriate topical corticosteroid for the underlying eczema during bacterial infection unless a specific clinical reason or specialist plan changes it.
For Eczema herpeticum and infected eczema, document body sites, severity, sleep and function, recent treatment, infection features and what the patient can realistically apply each day.
In Eczema herpeticum and infected eczema, reassess the diagnosis when a well-used, correctly potent regimen fails rather than repeatedly intensifying treatment without examining adherence, exposure and mimics.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Herpes simplex inoculation

HSV-1, and less often HSV-2, enters barrier-impaired eczematous skin after contact with an active or asymptomatic source and can disseminate rapidly.

Bacterial barrier infection

Staphylococcus aureus and Streptococcus pyogenes exploit fissured or excoriated eczema, causing impetiginisation, pustules, cellulitis or invasive disease.

Non-infectious flare mimics

Irritants, contact allergy, undertreatment and ordinary inflammation cause weeping and crusting, so visible exudate alone does not prove bacterial infection.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Viral cytolysis
HSV replicates within epidermal cells, producing crops of similar vesicles that rupture into sharply punched-out painful erosions.
2
Barrier-wide dissemination
Atopic barrier impairment and suppressed local immunity allow viral lesions to spread across eczematous and apparently normal skin.
3
Bacterial colonisation versus invasion
S aureus commonly colonises eczema; clinically important infection arises when bacterial proliferation produces increasing pain, pustules, cellulitis or systemic response.
4
Inflammation-infection feedback
Microbial injury amplifies cytokine inflammation and scratching, while uncontrolled eczema creates additional entry points for infection.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Monomorphic painful crop

Similar-sized vesicles or punched-out circular erosions appear rapidly and are painful or tender rather than merely itchy.

Herpetic systemic signalRed flag

Fever, malaise and lymphadenopathy accompanying monomorphic lesions support disseminated HSV and increase admission need.

Periocular threatRed flag

Lesions around an eye, red painful eye, photophobia or visual change require urgent ophthalmic assessment.

Bacterial pattern

Pustules, purulent ooze, rapidly worsening crust, spreading warmth and pain support clinically meaningful bacterial infection.

Non-infected flare

Increased itch, dryness and variable eczema without pain, pus, fever or rapid spread may be inflammatory rather than infectious.

Red flags requiring action

Eye pain, photophobia, periocular vesicles, fever, malaise, rapidly spreading painful erosions, systemic illness, immunosuppression, infant age or dehydration requires urgent hospital assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Immediate full skin and eye assessmentFirst step
Why
Identify monomorphic HSV, bacterial cellulitis, affected surface and ophthalmic threat.
Interpretation and limitations
Examine oral and periocular areas and physiology; subtle colour does not reduce urgency when pain and uniform erosions are present.
02
HSV PCR from fresh vesicle or erosion
Why
Confirm herpes simplex and distinguish varicella-zoster when morphology is uncertain.
Interpretation and limitations
Take before or soon after treatment when feasible, but never postpone systemic aciclovir for the result.
03
Bacterial swab after failure or severe recurrence
Why
Identify organism and susceptibility when culture can change antibiotic choice.
Interpretation and limitations
Do not routinely swab at initial presentation; colonisation is common and a positive result does not by itself prove invasive infection.
04
FBC, renal and organ assessment in significant illness
Why
Assess systemic infection, dehydration and aciclovir dosing safety.
Interpretation and limitations
Normal early blood results do not exclude eczema herpeticum; renal function and hydration affect aciclovir toxicity.
05
Blood culture and sepsis investigations
Why
Investigate a systemically unwell patient before antimicrobials when safe.
Interpretation and limitations
Cultures support later refinement but should not delay antiviral, antibiotic or resuscitation treatment in instability.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Ordinary eczema flare

Itch, variable excoriation and non-uniform lesions without pain or systemic illness favour inflammation rather than disseminated HSV.

Impetigo and bacterial infection

Honey crust, pustules, purulent ooze and spreading warmth support bacterial disease, though HSV and bacteria may coexist.

Varicella or zoster

Successive crops in different stages or a dermatomal unilateral eruption suggests varicella-zoster rather than monomorphic eczema herpeticum.

Contact dermatitis or treatment reaction

Sharp exposure geometry or deterioration after a new topical product can create weeping eczema that will not improve with unnecessary antibiotics.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Suspected eczema herpeticumGive antiviral and escalate todayFirst stepEscalationPainful monomorphic vesicles or punched-out erosions occur, particularly with fever, facial or eye involvement.

1Start systemic aciclovir immediately, take HSV PCR if this does not delay treatment and arrange same-day dermatology or paediatric advice.
2Admit infants, immunocompromised or systemically unwell patients and anyone unable to maintain hydration or oral treatment for intravenous therapy assessment.
3Seek urgent ophthalmology for periocular lesions or eye symptoms and assess bacterial co-infection when lesions become purulent or the patient deteriorates.

02Systemically well bacterial featuresOptimise eczema before reflex antibioticsCrust, ooze or pustules occur without fever, spreading cellulitis or high complication risk.

1Explain that not all weeping eczema benefits from antibiotics, continue emollient and topical corticosteroid and give clear deterioration advice.
2When an antibiotic is justified by extent, severity or risk, choose topical treatment only for very local disease and oral treatment for widespread or severe disease.
3Review response and take a swab if symptoms worsen or fail after the course, checking HSV and contact allergy as alternatives.

03Systemic bacterial illnessTreat cellulitis or sepsis promptlyFever, rapidly spreading warmth and pain, lymphangitis, hypotension or other systemic compromise accompanies eczema.

1Perform ABC assessment, obtain cultures where safe and begin systemic antibiotics according to severity, allergy and local antimicrobial guidance.
2Use oral flucloxacillin for suitable adults who can take oral therapy under NICE NG190, and admit for intravenous treatment when severely unwell.
3Reassess within the advised timeframe and continue barrier treatment while monitoring hydration, spread, pain and organ function.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Licensed oral HSV regimen that can be used for selected systemically well adults after immediate same-day eczema-herpeticum assessment; severe disease often needs intravenous therapy.

Aciclovir 200 mg tablets

For adult herpes-simplex skin infection take 200 mg orally five times daily at roughly four-hour intervals, omitting the night dose, for five days; extend severe initial infection under specialist care.

Start early, maintain hydration, reduce dose in significant renal impairment and review neurotoxicity; infants, pregnancy, immunocompromise, eye disease and severe infection need specialist decisions.

NICE first-choice oral antibiotic for clinically significant secondary bacterial eczema infection when the patient is not penicillin-allergic and oral care is appropriate.

Flucloxacillin oral therapy

For adults with secondary bacterial infection of eczema when oral antibiotic is indicated, use 500 mg orally four times daily for five to seven days according to NICE NG190.

Check immediate and severe delayed penicillin allergy, liver history, interactions and local resistance; systemic illness, treatment failure or recurrent infection requires reassessment and culture.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Keratitis and sight loss

Periocular eczema herpeticum can involve cornea, producing pain, photophobia, scarring and permanent visual impairment without rapid ophthalmic care.

Viral dissemination

Untreated HSV can cause extensive skin disease, dehydration, viraemia, encephalitis and multiorgan illness, especially in infants or immunocompromised patients.

Bacterial sepsis

Cellulitis can extend through damaged skin and occasionally cause bacteraemia or systemic shock in vulnerable patients.

Antimicrobial harm

Repeated antibiotics for colonised or non-infected flares drive resistance, adverse effects and misleading allergy labels without controlling eczema.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review suspected eczema herpeticum within hours to a day according to severity, documenting pain, new lesions, temperature, hydration and eye symptoms.
For bacterial infection, reassess promptly if symptoms worsen rapidly, the patient becomes unwell or improvement has not begun after two to three days.
After recovery, update the action plan so the patient recognises painful monomorphic recurrence and knows how to access same-day care.
At review of Eczema herpeticum and infected eczema, compare itch, sleep, fissuring or ooze, affected sites, function and treatment use with the agreed baseline.
For Eczema herpeticum and infected eczema, record adverse effects, new contact exposures and the safety-net for pain, fever, rapidly spreading disease, eye symptoms or systemic illness.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Pain outweighs crust colour

Eczema herpeticum is often painful before extensive vesicles appear, while ordinary bacterial colonisation may create crust without systemic threat.

Uniformity is a viral clue

A field of lesions at the same stage is more suggestive of HSV than the varied excoriations and vesicles of an eczema flare.

Antibiotics do not repair barrier

Even when bacterial treatment is justified, continuing appropriate emollient and anti-inflammatory care addresses the substrate for recurrence.

Eye risk changes referral

Facial disease alone needs urgency, but periocular lesions or ocular symptoms add immediate ophthalmology because keratitis can scar.

A swab cannot diagnose cellulitis

Surface organisms are common in eczema; spreading pain, warmth and systemic physiology define invasive concern.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for virology before starting aciclovir in a classic painful monomorphic eruption.
02
Treating every weeping eczema flare with antibiotics despite a well patient and no invasive features.
03
Stopping all topical eczema treatment during bacterial infection and prolonging barrier inflammation.
04
Missing eye symptoms because lesions are recorded only as facial.
05
Using oral aciclovir without renal, hydration and severity review in a frail or systemically unwell patient.