📋 Key Information Summary
- Acute skin eruptions in Australian primary care require a systematic diagnostic approach using morphology, distribution, onset timing, and associated symptoms to narrow the differential.
- Urticaria affects ~20% of Australians in their lifetime; acute urticaria (<6 weeks) is most commonly idiopathic or drug/food-related and responds to second-generation H₁ antihistamines as first-line therapy.
- Drug eruptions account for ~2–3% of all dermatology consultations; the most common pattern is a widespread morbilliform (exanthematous) eruption appearing 7–14 days after drug initiation.
- Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening emergencies (mortality 10–50%) requiring immediate cessation of the causative drug and transfer to a burns/ICU unit.
- Key high-risk medications for SJS/TEN in Australia include carbamazepine, allopurinol, sulfonamides, lamotrigine, and NSAIDs; HLA-B*5701 and HLA-B*1502 testing is available on Medicare (MBS item 71157).
- Fixed drug eruptions recur at the same anatomical site on re-exposure and typically present as a solitary dusky erythematous plaque; common culprits include paracetamol, NSAIDs, tetracyclines, and trimethoprim-sulfamethoxazole.
- Pityriasis rosea is a self-limiting eruption often preceded by a herald patch; it follows skin lines in a "Christmas-tree" pattern on the trunk and resolves spontaneously within 6–8 weeks.
- Guttate psoriasis presents as numerous small (0.5–1.5 cm) salmon-pink scaly papules, typically 1–3 weeks after streptococcal pharyngitis; throat swab and antistreptolysin O titre (ASOT) should be performed.
- Secondary syphilis must be considered in any widespread papulosquamous or palmoplantar eruption, especially in men who have sex with men (MSM), Aboriginal and Torres Strait Islander communities in remote areas, and people with HIV.
- The "great imitator" — secondary syphilis can mimic pityriasis rosea, guttate psoriasis, drug eruption, and viral exanthem; always order syphilis serology (RPR/VDRL + TPPA/TPHA) in unexplained widespread eruptions.
- Primary HIV eruption (acute retroviral syndrome) presents 2–4 weeks post-exposure with a diffuse maculopapular rash, fever, lymphadenopathy, pharyngitis, and mucosal ulcers; fourth-generation HIV Ag/Ab test is essential in at-risk patients.
- Aboriginal and Torres Strait Islander populations have significantly higher rates of syphilis (especially in northern and central Australia); the Australian Syphilis Action Plan mandates opportunistic testing in antenatal and sexual health settings.
- All patients with suspected drug eruptions should be documented on the Australian Adverse Drug Reaction Reporting System (via TGA) and flagged in My Health Record.
Introduction & Australian Epidemiology
Acute skin eruptions are among the most common presentations in Australian general practice, accounting for approximately 10–15% of all consultations. They span a broad differential — from benign self-limiting conditions such as pityriasis rosea to life-threatening emergencies such as Stevens–Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) and acute HIV seroconversion. Accurate diagnosis hinges on a structured approach integrating lesion morphology, distribution, timeline of onset, systemic features, and exposure history.
In Australia, several epidemiological factors shape the landscape of acute skin eruptions:
- Polypharmacy and an ageing population: The prevalence of adverse drug reactions increases with the number of concurrent medications. Older Australians (≥65 years) take a median of five prescription medications, placing them at elevated risk for drug eruptions.
- High UV exposure: Australia has the highest rate of skin cancer globally; while this primarily drives melanoma and non-melanoma skin cancer, UV-triggered eruptions (polymorphic light eruption, photoallergic drug reactions) are also prevalent.
- Infectious disease burden: Syphilis notifications have increased markedly since 2010, particularly among Aboriginal and Torres Strait Islander communities in northern Australia and among MSM nationally. The 2017–2024 syphilis outbreak prompted a national action plan.
- Immunisation landscape: Widespread MMR vaccination has reduced measles and rubella exanthems, but vaccine-related rashes (e.g., MMR at 7–12 days post-vaccine) remain relevant.
- HLA pharmacogenomics: Australia has pioneered HLA-B*5701 screening for abacavir hypersensitivity and HLA-B*1502 screening for carbamazepine-related SJS/TEN; both are available on the Medicare Benefits Schedule.
This article provides a systematic framework for evaluating and managing acute skin eruptions in Australian primary and secondary care, with emphasis on conditions most commonly encountered: urticaria, drug eruptions, pityriasis rosea, guttate psoriasis, secondary syphilis, and primary HIV eruption.
Acute Skin Eruptions Diagnostic Model
A structured diagnostic approach is essential when evaluating acute skin eruptions. The following mnemonic — MORPH–DASH — provides a systematic framework for Australian clinicians.
| Pattern | Key Morphology | Typical Distribution | Timing | Top Differential |
|---|---|---|---|---|
| Transient wheals | Erythematous, raised, pruritic, each lasting <24 h | Any site; often generalised | Minutes to hours | Urticaria |
| Morbilliform | Confluent macules/papules, blanching | Trunk → limbs; spares palms/soles | 7–14 days after drug | Drug eruption, viral exanthem |
| Herald patch + secondary | Oval scaly plaques following skin lines | Trunk ("Christmas tree") | Days to weeks | Pityriasis rosea |
| Small scaly papules | Salmon-pink, 0.5–1.5 cm, fine scale | Trunk, proximal limbs | 1–3 weeks post-pharyngitis | Guttate psoriasis |
| Papulosquamous + palmoplantar | Copper-coloured papules/plaques | Palms, soles, trunk, mucous patches | Weeks–months post-primary chancre | Secondary syphilis |
| Target lesions + blistering | Atypical targets, flaccid blisters, positive Nikolsky | Trunk → generalised; mucosae | 7–21 days after drug | SJS / TEN |
Urticaria & Drug Reactions
Urticaria
Urticaria affects approximately 20% of the Australian population at some point in their lifetime. Acute urticaria (duration <6 weeks) is characterised by transient, pruritic wheals (<24 hours per individual lesion) and is most commonly triggered by infections, medications (especially NSAIDs and antibiotics), food allergens, or physical stimuli. Chronic urticaria (≥6 weeks) has a point prevalence of ~1% and may be spontaneous or inducible.
First-Line Management — Acute Urticaria
Refractory Acute / Chronic Urticaria
If symptom control is inadequate after 2–4 weeks at licensed dose, up-dose to 4× the standard dose of the chosen second-generation antihistamine (as per ASCIA/EAACI guidelines). Add short course of prednisolone (0.5–1 mg/kg/day, maximum 50 mg, for 3–7 days) for severe acute flares. For chronic spontaneous urticaria (CSU) refractory to high-dose antihistamines, refer to an immunologist/allergist for consideration of omalizumab (Xolair®), which is available on the PBS via authority prescription for CSU.
Drug Eruptions
Adverse cutaneous drug reactions (ACDR) occur in 2–3% of hospitalised patients and are one of the most frequent reasons for dermatology referral. The pattern of drug eruption is determined by the medication, the patient's immune response, and pharmacogenomic risk factors.
High-Risk Medications for SJS/TEN in Australia
| Medication | HLA Association | Screening Available | MBS Item |
|---|---|---|---|
| Carbamazepine | HLA-B*1502 (Southeast Asian, Han Chinese) | Yes — pre-treatment recommended in at-risk populations | 71157 |
| Allopurinol | HLA-B*5801 (Korean, Han Chinese, Thai, European) | Yes — recommended in high-risk populations | 71157 |
| Abacavir | HLA-B*5701 | Yes — mandatory before initiation | 71157 |
| Lamotrigine | HLA-B*1502 (Southeast Asian) | Yes — recommended in at-risk populations | 71157 |
| Sulfonamides (incl. cotrimoxazole) | No specific HLA association | N/A | N/A |
| Nevirapine | HLA-DRB1*0101 | Yes — CD4 count and HLA testing recommended | 71157 |
Stevens–Johnson Syndrome / Toxic Epidermal Necrolysis — Emergency Management
Fixed Drug Eruption
Fixed drug eruption (FDE) presents as one or a few well-circumscribed, dusky erythematous to violaceous plaques that recur at the exact same anatomical site upon re-exposure to the causative agent. Post-inflammatory hyperpigmentation is characteristic. Commonly affected sites include the lips, genitalia, hands, and feet. Oral mucosal involvement is possible (non-pigmenting FDE variant).
- Common culprits: Paracetamol (increasingly recognised in Australia), NSAIDs (especially ibuprofen), trimethoprim-sulfamethoxazole, tetracyclines (especially doxycycline), metronidazole, and pseudoephedrine.
- Diagnosis: Clinical — based on history of recurrence at same site. Skin biopsy (if needed) shows interface dermatitis with dyskeratotic keratinocytes, pigment incontinence.
- Management: Identify and cease the causative agent. Acute episodes respond to topical corticosteroids (e.g., mometasone furoate 0.1% once daily). Extensive/mucosal FDE may require short course of prednisolone (0.5 mg/kg/day for 5–7 days). Provide written documentation of the causative drug for the patient's records and flag in My Health Record.
DRESS Syndrome
Drug reaction with eosinophilia and systemic symptoms (DRESS), also known as drug-induced hypersensitivity syndrome (DIHS), is a severe, potentially life-threatening drug reaction characterised by a prolonged latency period (2–6 weeks), widespread eruption, facial oedema, lymphadenopathy, haematological abnormalities (eosinophilia or atypical lymphocytes), and organ involvement (hepatitis most common, followed by nephritis, pneumonitis, and myocarditis).
- Common causative agents: Carbamazepine, phenytoin, allopurinol, dapsone, sulfonamides, minocycline, vancomycin, and nevirapine.
- RegiSCAR scoring: Use to confirm diagnosis (fever, lymphadenopathy, eosinophilia, atypical lymphocytes, skin involvement, organ involvement, resolution time, biopsy findings).
- Management: Discontinue causative drug. Systemic corticosteroids (prednisolone 1 mg/kg/day) with slow taper over 6–8 weeks to prevent relapse. Monitor liver function (LFTs every 48–72 h), renal function, and thyroid function (autoimmune thyroiditis may develop 1–3 months post-recovery). Referral to dermatology and immunology. Report to TGA.
- Herpesvirus reactivation: HHV-6, HHV-7, EBV, and CMV reactivation is common in DRESS and may drive flares. Consider viral PCR if clinical deterioration occurs.
Toxic Erythema (Toxic Erythema of Chemotherapy)
Toxic erythema of chemotherapy (TEC), previously termed "palmoplantar erythrodysesthesia" or "chemotherapy-related acral erythema," is a distinct cutaneous reaction to various chemotherapeutic agents. It presents with painful erythema, oedema, and desquamation affecting the palms, soles, and intertriginous areas. Common causative agents include cytarabine, doxorubicin, capecitabine, and 5-fluorouracil. Management involves dose reduction, cooling compresses, emollients, topical corticosteroids, and supportive analgesia.
Pityriasis Rosea & Guttate Psoriasis
Pityriasis Rosea
Pityriasis rosea (PR) is a common, self-limiting papulosquamous eruption that typically affects adolescents and young adults (peak incidence 10–35 years). It is believed to be triggered by reactivation of human herpesvirus 6 (HHV-6) or HHV-7. The condition is characteristically preceded by a prodromal illness in ~50% of cases.
Clinical Features
- Herald patch: A single, oval, salmon-pink, scaly plaque (2–5 cm) appearing 1–2 weeks before the generalised eruption. Often misdiagnosed as a ringworm lesion (tinea corporis).
- Secondary eruption: Numerous smaller (0.5–2 cm) oval papules and plaques with a peripheral "collarette" of scale. Distribution follows skin tension lines on the trunk in a characteristic "Christmas-tree" pattern.
- Atypical variants: Inverse PR (face, flexures, acral sites), papular PR (in children and darker skin types — higher risk of post-inflammatory hyperpigmentation), purpuric PR, and giant PR.
- Duration: Self-resolves within 6–8 weeks (range 2–12 weeks). Recurrence rate ~2–3%.
- Pruritus: Variable; often mild, but can be moderate–severe in some patients.
Differential Diagnosis
| Condition | Key Distinguishing Features | Investigation |
|---|---|---|
| Secondary syphilis | Copper-coloured, palm/sole involvement, mucous patches, lymphadenopathy, condylomata lata | RPR/VDRL + TPPA/TPHA |
| Guttate psoriasis | Salmon-pink with thicker scale, often preceded by streptococcal infection, family history of psoriasis | Throat swab, ASOT |
| Tinea corporis | Annular with active scaly border, KOH positive | KOH mount, fungal culture |
| Nummular eczema | Coin-shaped, more eczematous (oozing/crusting), intensely pruritic | Clinical |
| Drug eruption | Temporal relation to medication, less patterned distribution | Drug history, biopsy if needed |
Management
- Reassurance and observation: The mainstay of treatment. PR is self-limiting. Explain the expected course (6–8 weeks) and provide written information.
- Pruritus management: Emollients, topical corticosteroids (e.g., triamcinolone acetonide 0.1% once daily to pruritic areas), and/or second-generation antihistamines (cetirizine 10 mg PO once daily).
- UV therapy: Natural sunlight exposure or narrowband UVB phototherapy (3–5 sessions/week for 2–3 weeks) may accelerate resolution. Refer to dermatology for phototherapy in persistent or severe cases.
- Oral erythromycin: Some evidence for efficacy (250 mg QID for 2 weeks) in shortening disease duration. Use only in selected, severe cases.
- Avoid: Fragranced products, harsh soaps, and hot water which may exacerbate pruritus.
Guttate Psoriasis
Guttate psoriasis ("gutta" = drop) is an acute form of psoriasis characterised by numerous small (0.5–1.5 cm), salmon-pink, scaly papules predominantly affecting the trunk and proximal extremities. It accounts for approximately 2% of all psoriasis and is the most common form of psoriasis in children and young adults. A strong association exists with preceding streptococcal pharyngitis (reported in 56–97% of cases).
Pathogenesis
Beta-haemolytic Streptococcus pyogenes (Group A Streptococcus, GAS) pharyngeal infection triggers a cross-reactive immune response involving streptococcal M-protein epitopes, which activate T cells and cytokine cascades (IL-17, IL-23, TNF-α) that drive epidermal hyperproliferation in genetically susceptible individuals. Up to one-third of patients with guttate psoriasis will later develop chronic plaque psoriasis.
Investigations
- Throat swab: Culture for GAS (available via standard pathology providers; results 24–48 hours).
- Antistreptolysin O titre (ASOT): Evidence of recent streptococcal infection (rises 1–3 weeks post-infection, peaks at 3–6 weeks). Medicare-rebatable (MBS item 65750).
- Anti-DNase B: Complementary to ASOT, particularly useful when presentation is delayed >6 weeks.
- Syphilis serology: As per pityriasis rosea — RPR/VDRL + TPPA/TPHA to exclude secondary syphilis.
- Skin biopsy (rarely needed): If diagnosis uncertain — shows regular acanthosis, parakeratosis, Munro microabscesses, dilated capillaries in dermal papillae.
Management
- Treat streptococcal infection: If throat swab positive or ASOT elevated, treat with penicillin V (phenoxymethylpenicillin) 500 mg PO BD for 10 days (adults) or 250 mg PO BD for 10 days (children). Alternative: amoxicillin 500 mg PO TDS for 10 days. For penicillin allergy: azithromycin 500 mg PO day 1, then 250 mg PO days 2–5.
- Topical therapy: Emollients + moderate-potency topical corticosteroids (e.g., betamethasone dipropionate 0.05% once daily for 2–4 weeks) for symptomatic control. Vitamin D analogues (calcipotriol 50 mcg/g) as adjunct or steroid-sparing agent.
- UV phototherapy: Narrowband UVB for widespread or persistent disease. Refer to dermatology.
- Reassurance: Approximately 60–70% of cases resolve spontaneously within 2–3 months. Recurrence can occur with subsequent streptococcal infections.
Secondary Syphilis & Primary HIV Eruption
Secondary Syphilis
Syphilis, caused by the spirochaete Treponema pallidum, has experienced a dramatic resurgence in Australia. Notifications have increased approximately 5-fold since 2010. The 2017–2024 syphilis outbreak disproportionately affected Aboriginal and Torres Strait Islander populations in northern, central, and Western Australia, as well as MSM nationally. Secondary syphilis occurs 4–10 weeks after the primary chancre and represents disseminated infection.
Clinical Features of Secondary Syphilis
- Rash: Generalised, symmetric, non-pruritic, copper-coloured (or "ruddy") macules and papules. Involves the trunk, limbs, palms, and soles (palmoplantar involvement is a hallmark feature and should always prompt syphilis testing).
- Mucous patches: Painless, grey-white erosions on oral, genital, or rectal mucosa. Highly infectious.
- Condylomata lata: Flat, moist, grey-white papules/plaques in warm, moist skin folds (groin, axillae, intergluteal). Highly infectious. Differentiated from condylomata acuminata (genital warts) by their flat, smooth surface.
- Generalised lymphadenopathy: Non-tender, rubbery, mobile nodes. Often bilateral inguinal, cervical, and epitrochlear.
- Constitutional symptoms: Malaise, low-grade fever, headache, sore throat, patchy alopecia ("moth-eaten" pattern), and weight loss.
- Systemic involvement: Hepatitis (raised transaminases), nephropathy (membranous glomerulonephritis), osteitis, uveitis, meningitis.
Investigations
Treatment — Secondary Syphilis
Follow-Up & Serological Monitoring
Non-treponemal titres (RPR/VDRL) should be checked at 3, 6, and 12 months post-treatment. A four-fold decline in RPR titre (e.g., 1:32 → 1:8) indicates adequate treatment response. Failure of titres to fall four-fold by 12 months constitutes treatment failure and requires re-treatment (with benzathine penicillin 1.8 g IM weekly × 3) and lumbar puncture to exclude neurosyphilis. Patients must be counselled to avoid sexual contact until lesions have fully resolved and to notify all sexual partners (partner notification is a legal requirement in most Australian states/territories under public health legislation).
Primary HIV Eruption (Acute Retroviral Syndrome)
Acute HIV seroconversion illness (acute retroviral syndrome, ARS) occurs in 40–90% of newly infected individuals, typically 2–4 weeks after exposure. The cutaneous eruption is one of the most consistent features and is often the presenting complaint in primary care. ARS is a critical diagnostic opportunity — identifying HIV infection during this phase allows early antiretroviral therapy (ART) initiation, which improves long-term outcomes and reduces onward transmission.
Clinical Features of ARS
- Rash: Generalised, symmetric, erythematous, non-pruritic maculopapular eruption. Involves the face, trunk, and limbs (including palms and soles in ~50%). Can resemble a viral exanthem or drug eruption. Lasts 5–10 days.
- Fever: The most common symptom (~90%). Typically 38.5–40°C.
- Pharyngitis: Non-exudative pharyngitis (distinguishable from GAS pharyngitis).
- Lymphadenopathy: Generalised, non-tender, particularly posterior cervical, axillary, and epitrochlear.
- Mucocutaneous ulcers: Painless oral, oesophageal, or genital ulcers (differentiated from syphilis chancres which are painless but non-ulcerative in many cases).
- Other features: Myalgia/arthralgia, headache, weight loss, diarrhoea, hepatosplenomegaly.
Investigations
Management
- Immediate referral: Referral to a specialist HIV service (s100 prescriber) for confirmation, baseline investigations, and ART initiation. Current Australian guidelines recommend initiating ART as soon as possible after diagnosis, including during ARS.
- Symptomatic management of eruption: Emollients, topical corticosteroids for pruritus, paracetamol for fever/myalgia.
- PrEP cascade: Assess recent sexual contacts for post-exposure prophylaxis (PEP) if within 72 hours of exposure, or pre-exposure prophylaxis (PrEP) for ongoing risk.
- Public health notification: HIV is a notifiable disease in all Australian states and territories. Notification to the state/territory public health unit is mandatory.
- Patient support: Referral to community organisations (e.g., ACON, Thorne Harbour Health, NAPWHA) for peer support, counselling, and care coordination.
Monitoring
| Condition | Follow-Up Schedule | Key Monitoring Parameters | Treatment Failure Criteria |
|---|---|---|---|
| Acute urticaria | 2–4 weeks; then PRN | Symptom control, medication side effects | Persistence >6 weeks → reclassify as chronic; refer to immunology |
| Drug eruption (morbilliform) | 1 week after drug cessation | Rash resolution, LFTs if hepatitic features | Failure to resolve by 2 weeks — consider alternative diagnosis |
| DRESS syndrome | Weekly for 4 weeks, then 2-weekly for 2 months, then monthly for 6 months | FBC, LFTs, UEC every visit. Thyroid function (TSH, fT4) at 2 and 6 months post-recovery. | Organ function deterioration → escalate to immunology/dermatology |
| SJS / TEN | Continuous inpatient (burns/ICU). Follow-up at 2, 6, and 12 weeks post-discharge. | BSA, SCORTEN, infection markers, ophthalmology review, mucosal assessment | Persistent epidermal sloughing, secondary sepsis, ocular scarring |
| Pityriasis rosea | 2–4 weeks (optional); PRN if not resolving | Rash resolution, pruritus control | Persistence >12 weeks — reconsider diagnosis (biopsy, syphilis serology) |
| Guttate psoriasis | 4–6 weeks post-treatment; 3-monthly for 12 months | Rash clearance, ASOT decline, plaque psoriasis development | Persistent/worsening disease → dermatology referral for systemic therapy |
| Secondary syphilis | 3, 6, and 12 months post-treatment | Quantitative RPR titre — expect 4-fold decline by 6 months | <4-fold decline by 12 months or rising titre — re-treat + LP for neurosyphilis |
| Acute HIV (ARS) | 2–4 weeks post-ART initiation, then 3-monthly until viral suppression, then 6-monthly | HIV viral load, CD4 count, LFTs, renal function, lipid profile, adherence assessment | Detectable viral load at 24 weeks — assess adherence, resistance testing |
Special Populations
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Australians experience a significantly higher burden of sexually transmitted infections, including syphilis, compared to non-Indigenous Australians. The ongoing syphilis outbreak, which began in 2011 in northern Australia, has disproportionately affected Indigenous communities. Additionally, skin conditions such as scabies, impetigo, and post-streptococcal glomerulonephritis are more prevalent, reflecting broader social determinants of health including overcrowded housing, limited access to healthcare, and the effects of systemic disadvantage.
Key Considerations
Quick Reference — First-Line Treatment Summary
📚 References
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