Common Childhood Infectious Diseases

Last updated 1 Jun 2026 · Paediatrics / Infectious Disease

📋 Key Information Summary

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Varicella (chickenpox) is caused by varicella-zoster virus (VZV); the varicella vaccine (Varilrix®) is funded on the NIP at 18 months (as MMRV) and for catch-up in susceptible adolescents/adults. Most cases are self-limiting but neonatal varicella and immunocompromised hosts carry significant mortality.
Aciclovir (oral or IV) is indicated for varicella in immunocompromised children, neonates, adolescents > 14 years, and those on salicylates or corticosteroids; oral aciclovir within 24 hours of rash onset may shorten illness in otherwise healthy children.
Rubella is usually mild in children but poses catastrophic risk to the fetus (congenital rubella syndrome). Australia aims for elimination; MMR vaccination at 12 months and MMRV at 18 months on the NIP is critical.
Roseola (exanthem subitum) caused by HHV-6 is characterised by high fever (39–40°C) for 3–5 days followed by a maculopapular rash upon defervescence; febrile seizures occur in 6–15% of cases. Treatment is supportive.
Parvovirus B19 (erythema infectiosum / "slapped cheek") causes a self-limiting exanthem in children but is dangerous in pregnancy (hydrops fetalis) and in patients with chronic haemolytic anaemia (aplastic crisis).
Scarlet fever is a Group A streptococcal (GAS) exotoxin-mediated illness requiring antibiotic treatment with phenoxymethylpenicillin (or amoxicillin) for 10 days to prevent acute rheumatic fever (ARF) and post-streptococcal glomerulonephritis.
Mumps has re-emerged in Australia in under-vaccinated cohorts; orchitis occurs in ~30% of post-pubertal males. MMR/MMRV vaccination remains the only effective prevention.
Hand-foot-and-mouth disease (HFMD) is caused by coxsackievirus A16 or enterovirus 71; it is self-limiting but enterovirus 71 can cause fatal encephalitis and pulmonary oedema in young children. Supportive care only.
Kawasaki disease is the leading cause of acquired heart disease in Australian children; early IVIG (within 10 days of fever onset) and aspirin reduce coronary artery aneurysm risk from ~25% to < 5%.
Kawasaki disease diagnostic criteria: fever ≥ 5 days plus ≥ 4 of 5 clinical features (bilateral conjunctival injection, oral mucosal changes, cervical lymphadenopathy ≥ 1.5 cm, polymorphous rash, extremity changes). Incomplete Kawasaki disease requires a high index of suspicion in infants < 12 months.
Aboriginal and Torres Strait Islander children experience higher rates of ARF, rheumatic heart disease, and invasive GAS infection; rheumatic fever prophylaxis and culturally safe health service engagement are priorities.
Exclusion periods for schools and childcare vary by disease; compliance with state/territory public health notification requirements is mandatory for rubella, varicella, and mumps.

Introduction & Australian Epidemiology

Childhood exanthems — febrile illnesses accompanied by rash — remain a common reason for primary care and emergency department presentations across Australia. While the introduction of universal vaccination programmes has dramatically reduced the incidence of several vaccine-preventable diseases (measles, rubella, varicella), non-vaccine exanthems such as roseola, parvovirus B19, hand-foot-and-mouth disease, and scarlet fever continue to circulate widely in Australian childcare and school settings.

Kawasaki disease, although not infectious in aetiology, frequently presents in a similar age group with fever and rash and must be considered in the differential diagnosis of any prolonged febrile illness in a child under 5 years. It accounts for approximately 9 per 100,000 children aged < 5 years in Australia, with higher rates observed in children of East Asian descent.

Accurate diagnosis is essential — both to guide targeted therapy and to implement appropriate public health measures including exclusion from school or childcare, notification to state/territory health authorities, and post-exposure prophylaxis for vulnerable contacts.

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Differential diagnosis matters: The clinical overlap between childhood exanthems is significant. A child with fever and rash may have a self-limiting viral illness or a life-threatening condition such as meningococcal disease or toxic shock syndrome. Maintain a low threshold for sepsis workup in any toxic-appearing child.

Disease	Pathogen	Peak Age	Incidence (Australia)	Vaccine Available
Varicella	VZV (HHV-3)	1–9 years	Significant decline post-NIP (2005); ~1,000–2,000 notifications/year	Yes — NIP (MMRV at 18 months)
Rubella	Rubella virus	5–15 years	Near-eliminated; < 50 cases/year	Yes — NIP (MMR 12 mo, MMRV 18 mo)
Roseola	HHV-6 (rarely HHV-7)	6 months – 2 years	Very common; not notifiable, no surveillance data	No
Erythema infectiosum	Parvovirus B19	5–15 years	Common; endemic, periodic outbreaks	No
Scarlet fever	Group A Streptococcus	3–10 years	Increasing trend since 2014; notifiable in some states	No
Mumps	Mumps virus	5–15 years	Resurgent in young adults; ~100–300 cases/year	Yes — NIP (MMR/MMRV)
HFMD	Coxsackievirus A16 / EV-A71	< 5 years	Very common; cyclic epidemics, not notifiable	No (EV-A71 vaccine available in China only)
Kawasaki disease	Unknown (immune-mediated)	6 months – 5 years	~9/100,000 < 5 years	N/A

Varicella (Chickenpox) & Complications

Aetiology & Transmission

Varicella is caused by varicella-zoster virus (VZV), a highly contagious human herpesvirus. Transmission occurs via respiratory droplets and direct contact with vesicular fluid. The infectious period extends from 1–2 days before the rash onset until all lesions have crusted (typically 5–7 days). The incubation period is 10–21 days (average 14 days). Secondary household attack rates exceed 80% in unvaccinated individuals.

Clinical Features

Prodromal low-grade fever, malaise, and anorexia precede the rash by 1–2 days. The hallmark rash is a centripetal distribution (trunk > face > limbs) vesicular eruption on an erythematous base, described as a "dewdrop on a rose petal." Lesions appear in crops and progress through macule → papule → vesicle → crust over 24–48 hours, with all stages visible simultaneously. Pruritus is prominent. The rash may involve the oropharynx, conjunctivae, and perineum.

Complications

Mild

Uncomplicated Varicella

Low-grade fever, < 300 lesions, pruritus, secondary bacterial skin infection (Staphylococcus aureus, GAS) in ~5%.

Setting: GP / home management

Moderate

Varicella with Significant Complications

Varicella pneumonia (most common severe complication in adolescents/adults), cerebellar ataxia, hepatitis, thrombocytopenia, secondary invasive bacterial infection.

Setting: Hospital admission, IV aciclovir

Severe

Life-Threatening Varicella

Disseminated VZV in immunocompromised, neonatal varicella (maternal onset 5 days before to 2 days after delivery — mortality up to 30%), VZV encephalitis, necrotising fasciitis, toxic shock syndrome.

Setting: PICU / tertiary centre, IV aciclovir ± VZIG

Management

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Avoid aspirin in children with varicella: Aspirin use during varicella is associated with Reye syndrome, a rare but potentially fatal hepatocerebral disorder. Use paracetamol (15 mg/kg PO QID PRN) for fever/pain. Avoid ibuprofen in acute varicella due to reports of increased risk of invasive Group A streptococcal soft tissue infection.

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Aciclovir (oral)

Zovirax® · Generic available · Antiviral (nucleoside analogue)

Indication Consider in all children > 12 years, immunocompromised, chronic skin/lung disease, salicylate therapy; ideally within 24 h of rash onset

Paediatric dose 20 mg/kg (max 800 mg) PO QDS for 5 days

Adult dose 800 mg PO QDS for 5 days

Renal adjustment eGFR 10–25 mL/min: reduce frequency to TDS; eGFR < 10: halve dose, increase interval

PBS status ✔ PBS General Benefit

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Aciclovir (IV)

Zovirax IV® · Antiviral (nucleoside analogue)

Indication Immunocompromised, disseminated varicella, neonatal varicella, varicella pneumonia, encephalitis

Paediatric dose 500 mg/m² IV TDS (or 10–20 mg/kg QDS for infants); duration 7–10 days

Adult dose 10 mg/kg IV TDS

Renal adjustment Reduce dose and extend interval as per eGFR; consult pharmacy

PBS status ✔ PBS Authority Required

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Varicella Vaccine (Varilrix®)

Varilrix® · Live attenuated VZV vaccine

Schedule NIP-funded: MMRV (Priorix-Tetra®) at 18 months; catch-up for susceptible individuals > 14 years requires 2 doses (0, 4–8 weeks apart)

Contraindications Immunosuppression, pregnancy, anaphylaxis to vaccine components

PBS status ✔ NIP-funded for children; PBS Authority for catch-up ≥ 14 years

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Varicella-Zoster Immunoglobulin (VZIG)

Zoster Immunoglobulin-VF® · Passive immunisation

Indication Post-exposure prophylaxis for: immunocompromised susceptible contacts, susceptible pregnant women, neonates (maternal varicella onset 5 days before to 2 days after delivery), premature infants < 28 weeks or < 1000 g regardless of maternal immunity

Dose ≥ 40 IU/kg IM (max 625 IU); within 96 hours of exposure (may extend to 10 days)

Availability Through the Australian Red Cross Lifeblood; contact state blood bank

PBS status ⚪ Not PBS-listed; funded via state/territory programmes

Exclusion & Public Health

Exclude from school/childcare until all vesicles have crusted (typically 5–7 days after rash onset). Varicella is notifiable in all Australian states and territories. Contacts who are immunocompromised, pregnant, or neonates should receive VZIG within 96 hours of exposure.

Rubella, Roseola & Parvovirus B19

Rubella (German Measles)

Rubella is a mild, self-limiting viral illness caused by the rubella virus. It is characterised by a fine, pink, maculopapular rash (face → trunk → limbs, fading within 3 days), post-auricular and suboccipital lymphadenopathy, and low-grade fever. Up to 50% of infections are subclinical. The clinical significance of rubella lies entirely in its teratogenic potential: maternal infection in the first trimester causes congenital rubella syndrome (CRS) — sensorineural deafness, cataracts, cardiac defects (PDA, pulmonary artery stenosis), hepatosplenomegaly, and intellectual disability.

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Congenital rubella syndrome (CRS) is preventable. Ensure all women of childbearing age have documented immunity (rubella IgG positive). Rubella is notifiable. Susceptible pregnant contacts should be counselled by an infectious disease specialist; post-exposure immunoglobulin does not reliably prevent CRS.

Exclusion: Exclude from school/childcare for at least 4 days after rash onset. Notifiable in all Australian jurisdictions.

Roseola (Exanthem Subitum / Sixth Disease)

Roseola is caused predominantly by human herpesvirus 6 (HHV-6), occasionally HHV-7. It is one of the most common infections of infancy, with nearly universal seroconversion by age 2 years. Transmission is via respiratory secretions; the incubation period is 9–10 days.

Clinical pattern:

Febrile phase (days 1–3/5): Abrupt onset of high fever (39.5–40.5°C), often the only sign. The child may appear paradoxically well between fever spikes.
Rash phase: Defervescence coincides with appearance of a blanching, maculopapular rash, predominantly on the trunk and neck, spreading to the limbs. The rash fades within 1–2 days.

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Febrile seizures in roseola: HHV-6 is the most common infectious trigger of febrile seizures in children aged 6–24 months (6–15% of cases). Seizures are typically brief and generalised. Manage per standard febrile seizure guidelines; consider EEG if recurrent or focal features present.

Management: Entirely supportive. Paracetamol (15 mg/kg PO QID PRN) and/or ibuprofen (10 mg/kg PO TDS PRN, if > 3 months) for fever. Adequate hydration. No antiviral therapy is indicated in immunocompetent children. In immunocompromised children with HHV-6 reactivation, ganciclovir or foscarnet may be considered under specialist guidance.

Parvovirus B19 (Erythema Infectiosum / Fifth Disease)

Parvovirus B19 is a non-enveloped DNA virus transmitted via respiratory droplets. The incubation period is 4–14 days (up to 21 days for aplastic crisis). The illness classically progresses through several phases:

Phase 1 (days 1–3): Non-specific febrile illness, coryza, headache. Peak viraemia and highest contagion.
Phase 2 (days 4–7): Characteristic "slapped cheek" appearance — intense erythema of both cheeks with circumoral pallor.
Phase 3 (days 4–14+): Reticular, lacy, erythematous maculopapular rash on the trunk and extremities (particularly extensor surfaces). Rash may wax and wane for weeks, exacerbated by heat, sunlight, or exercise.

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Parvovirus B19 in pregnancy: Maternal infection in the first 20 weeks carries a ~10% risk of hydrops fetalis and fetal death. All pregnant women with suspected or confirmed parvovirus B19 exposure should be tested (B19 IgM/IgG) and referred for serial ultrasound surveillance (MCA Doppler) for 8–12 weeks. Refer to maternal-fetal medicine.

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Aplastic crisis in chronic haemolytic anaemia: Parvovirus B19 causes transient aplastic crisis in children with sickle cell disease, hereditary spherocytosis, thalassaemia, and other chronic haemolytic conditions. Reticulocyte count drops to near zero; haemoglobin nadir occurs at day 10–14. Urgent transfusion and haematology referral may be required.

Management: Supportive in immunocompetent children. Not notifiable. Exclusion from school is not required once the rash appears (children are no longer contagious at this stage). Educate families that the rash may persist or recur for weeks.

Scarlet Fever, Mumps & Hand-Foot-and-Mouth Disease

Scarlet Fever

Scarlet fever is a toxin-mediated manifestation of Group A Streptococcal (GAS / Streptococcus pyogenes) pharyngitis. It is caused by erythrogenic toxin production by specific GAS strains (M protein serotypes). Incidence in Australia has been rising since 2014, particularly in children aged 3–10 years.

Clinical features:

Sore throat, fever (≥ 38.3°C), tonsillar exudates, palatal petechiae
Rash: diffuse, erythematous, sandpaper-textured (rough) maculopapular eruption, beginning on the trunk and spreading centrifugally. Accentuated in skin creases (axillae, groin) — Pastia lines
Tongue: initially white-coated with red papillae ("white strawberry tongue"), progressing to erythematous ("strawberry tongue") by day 3–4
Circumoral pallor
Desquamation of palms and soles occurs 1–3 weeks after rash onset (late but characteristic sign)

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Treat scarlet fever to prevent ARF: Although acute rheumatic fever (ARF) is rare following scarlet fever in non-Indigenous Australian populations, it remains a significant risk in Aboriginal and Torres Strait Islander children. All cases of scarlet fever require a full 10-day course of oral penicillin. Do not shorten the course even if the child appears well.

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Phenoxymethylpenicillin (Penicillin V)

Cilicaine VK® · Generic available · Beta-lactam antibiotic

Paediatric dose < 20 kg: 250 mg PO BD or TDS; ≥ 20 kg: 500 mg PO BD or TDS — for 10 days

Adult dose 500 mg PO BD for 10 days

Notes First-line for GAS pharyngitis/scarlet fever. No renal adjustment required. Consider amoxicillin if adherence to QDS is a concern.

PBS status ✔ PBS General Benefit

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Amoxicillin

Amoxil® · Generic available · Aminopenicillin

Paediatric dose 25–50 mg/kg/day PO in 2–3 divided doses for 10 days (max 500 mg TDS)

Notes Acceptable alternative to penicillin V; better palatability (suspension). Some guidelines prefer penicillin V for GAS as first-line to preserve amoxicillin spectrum.

PBS status ✔ PBS General Benefit

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Cefalexin

Keflex® · Generic available · First-generation cephalosporin

Paediatric dose 25–50 mg/kg/day PO in 2–3 divided doses for 10 days (max 500 mg TDS)

Notes For penicillin-allergic patients (non-anaphylaxis). Cross-reactivity risk with true penicillin allergy is low (< 2%). Avoid in anaphylaxis to penicillin — use azithromycin instead.

PBS status ✔ PBS General Benefit

Exclusion: Exclude from school/childcare until 24 hours after commencing antibiotics. Notify to state/territory health authority (requirements vary by jurisdiction).

Mumps

Mumps is caused by the mumps virus (Paramyxoviridae family). Transmission is via respiratory droplets. The incubation period is 12–25 days (average 16–18 days). Infectious period extends from 2 days before to 5 days after parotid swelling.

Clinical features: Unilateral or bilateral parotid gland swelling (70–80% of symptomatic cases) with tenderness, trismus, earache, and fever. Approximately 30% of infections are asymptomatic.

Complications:

Orchitis: Occurs in ~30% of post-pubertal males (unilateral in 80%); rarely causes sterility (bilateral orchitis < 1%)
Oophoritis: ~5% of post-pubertal females; benign course
Aseptic meningitis: ~10% of cases; usually self-limiting
Mumps encephalitis: Rare (~1:6,000 cases)
Sensorineural deafness: Rare, typically unilateral, may be permanent
Pancreatitis: Rare

Management: Supportive. Analgesia with paracetamol. Cold compresses to parotid region. No specific antiviral therapy. MMR vaccination (NIP: 12 months and 18 months as MMRV) is the primary prevention. Cases are notifiable in all Australian jurisdictions. Exclude from school/childcare for 5 days after onset of parotid swelling.

Hand-Foot-and-Mouth Disease (HFMD)

HFMD is a common enteroviral infection most frequently caused by coxsackievirus A16, with enterovirus A71 (EV-A71) responsible for more severe outbreaks. It predominantly affects children < 5 years. Transmission is via the faecal-oral route, respiratory droplets, and direct contact with vesicular fluid. The incubation period is 3–6 days.

Clinical features:

Prodrome: low-grade fever, malaise, poor appetite (1–2 days)
Oral lesions: painful vesicles and shallow ulcers on the buccal mucosa, tongue, soft palate, and gums — often the most distressing symptom, causing drooling and refusal to eat/drink
Skin lesions: 2–10 mm vesicles or papules on the palms, soles, and interdigital areas; may also involve knees, elbows, and buttocks. Lesions are typically non-pruritic and resolve within 7–10 days

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EV-A71 neurological complications: Enterovirus A71 outbreaks (notably in the Asia-Pacific region including Australia) can cause severe neurological complications: brainstem encephalitis, acute flaccid paralysis, neurogenic pulmonary oedema, and cardiopulmonary failure. Monitor for red flags: persistent vomiting, myoclonic jerks, ataxia, lethargy, and tachycardia out of proportion to fever. Urgent hospital assessment is required.

Management: Supportive. Oral fluids to prevent dehydration (offer cold, bland fluids; avoid citrus and salty foods). Paracetamol for pain and fever. Topical oral anaesthetic gel (lidocaine 2% gel — available OTC) for oral ulcer pain; apply before meals. No specific antiviral therapy exists. Not notifiable. No exclusion from school/childcare once vesicles have dried — though outbreaks in childcare may require public health guidance.

Kawasaki Disease

Overview

Kawasaki disease (KD) is an acute, self-limited systemic vasculitis predominantly affecting medium-sized arteries, with a particular predilection for the coronary arteries. It is the most common cause of acquired heart disease in children in developed countries. In Australia, the incidence is approximately 9 per 100,000 children aged < 5 years, with higher rates in children of East Asian or Pacific Islander descent and in males (M:F ratio 1.5:1). Peak incidence is between 6 months and 2 years of age.

The aetiology remains unknown. An infectious trigger in a genetically susceptible host is the prevailing hypothesis. No single pathogen has been identified. Seasonal variation (winter–spring) and epidemic patterns support an infectious aetiology.

Diagnostic Criteria

Classical (complete) Kawasaki disease requires:

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Fever ≥ 5 days (mandatory criterion) PLUS ≥ 4 of the following 5 features:

1. Bilateral non-exudative conjunctival injection — limbic-sparing, painless
2. Oral mucosal changes — strawberry tongue, erythema/fissuring of lips, diffuse oropharyngeal erythema
3. Cervical lymphadenopathy — usually unilateral, ≥ 1.5 cm diameter
4. Polymorphous rash — maculopapular, erythroderma, or erythema multiforme-like (NOT vesicular or bullous)
5. Extremity changes — erythema and/or oedema of hands and feet (acute); periungual peeling (subacute, typically weeks 2–3)

Incomplete Kawasaki Disease

Incomplete KD accounts for 15–20% of cases and is more common in infants < 12 months, who are at the HIGHEST risk of coronary artery abnormalities. Suspect incomplete KD in any child with fever ≥ 5 days and 2–3 clinical criteria, OR fever ≥ 5 days with unexplained systemic inflammation (CRP ≥ 30 mg/L or ESR ≥ 40 mm/hr).

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Infants < 12 months are at greatest risk for coronary artery aneurysms but are the LEAST likely to present with classical features. Have a low threshold for investigation (echocardiography, inflammatory markers) in any infant with prolonged unexplained fever.

Risk Stratification

Low Risk

Standard Risk

Age 1–5 years, no coronary changes on baseline echo, responds to first-line IVIG (defervescence within 36 h), normal ALT/albumin, Na > 133 mmol/L.

Risk of coronary aneurysm: < 5% with treatment

Moderate Risk

IVIG Non-Responder

Persistent/recrudescent fever ≥ 36 h after IVIG completion (occurs in ~15% of cases). Risk factors: age < 1 year, day of illness ≤ 5, high CRP, low albumin, high ALT, low sodium, male sex.

Requires second-line therapy; ~25% coronary risk

High Risk

Kawasaki Disease Shock Syndrome / Coronary Aneurysm

Haemodynamic instability (KDSS in ~7%), giant coronary artery aneurysms (z-score ≥ 10), myocarditis, valvular regurgitation. Requires intensive care and multidisciplinary management.

PICU admission; rheumatology + cardiology + infectious diseases input

Treatment

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Time-critical: IVIG should be administered within the first 10 days of illness (ideally days 5–7) to maximise reduction in coronary artery aneurysm risk. Delays beyond day 10 reduce IVIG efficacy. Every day of persistent fever beyond day 5 is an opportunity to initiate treatment — do not wait for all criteria to be met.

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Intravenous Immunoglobulin (IVIG)

Intragam P® / various brands · Immunoglobulin

Dose 2 g/kg as a single infusion over 8–12 hours

Timing Within 10 days of fever onset; ideally days 5–7. If diagnosed after day 10, still administer if fever is ongoing or CRP remains elevated.

Response ~85% defervesce within 36 h. Non-response (persistent/recrudescent fever) requires second-line therapy.

Caution Hypotension risk (infuse slowly initially); aseptic meningitis (rare); haemolytic anaemia in non-group O recipients; fluid overload. Check IgA level before administration — IgA deficiency increases anaphylaxis risk (use IgA-depleted product).

PBS status ⚪ Authority Required — Hospital Authority

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Aspirin (Acetylsalicylic acid)

Aspro Clear® / Generic · NSAID / Antiplatelet

Acute phase dose 30–50 mg/kg/day PO in 3–4 divided doses (high-dose). Continue until afebrile for ≥ 48 h or up to day 14 of illness.

Subacute phase dose 3–5 mg/kg PO once daily (low-dose antiplatelet). Continue for ≥ 6–8 weeks if no coronary abnormalities. If coronary changes present, continue indefinitely (dose adjusted by cardiology).

Notes The evidence base for high-dose aspirin in the acute phase is debated. Some centres use only low-dose aspirin from the outset. Follow local hospital protocol. Avoid ibuprofen (may antagonise antiplatelet effect of aspirin).

PBS status ✔ PBS General Benefit

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Corticosteroids (Methylprednisolone)

Solu-Medrol® · Glucocorticoid

Indication Second-line for IVIG non-responders. Also considered as primary adjunctive therapy in high-risk patients (z-score ≥ 2.5, KDSS, age < 6 months).

Dose (primary adjunctive) IV methylprednisolone 30 mg/kg (max 1 g) over 2–3 h daily for 1–3 days, then oral prednisolone 2 mg/kg/day (taper over 2–3 weeks)

Notes Increasing evidence supports primary adjunctive corticosteroid use in high-risk KD. Current Australian/RAISE registry data show improved coronary outcomes. Consult paediatric rheumatology.

PBS status ✔ PBS Authority Required (hospital use)

Investigations

Essential Transthoracic echocardiography Baseline at diagnosis (before IVIG), then at 1–2 weeks and 6–8 weeks. Assess coronary artery dimensions (z-scores per Dallaire/Dahdah), LV function, valvular regurgitation, pericardial effusion.

Essential FBC, CRP, ESR, LFTs, albumin, sodium, urinalysis CRP typically markedly elevated (> 30 mg/L). Normocytic normochromic anaemia, thrombocytosis (peaks week 2–3, may exceed 1,000 × 10⁹/L), hypoalbuminaemia, elevated ALT. Sterile pyuria in ~33%.

Available Troponin, BNP/NT-proBNP Myocardial injury markers; BNP helps differentiate KD from other febrile illnesses.

Available Blood cultures To exclude bacterial sepsis (mandatory in differential workup).

Long-Term Follow-Up

Patients with no coronary abnormalities can be discharged from cardiology follow-up after 6–8 weeks, provided repeat echo is normal. Patients with persistent coronary artery changes require lifelong cardiology follow-up, antiplatelet/anticoagulation therapy (managed by paediatric cardiology), and serial echocardiography. Annual influenza vaccination is recommended as aspirin is contraindicated in Reye syndrome.

Exclusion Periods & Public Health Notifications

Compliance with exclusion periods and notification requirements is essential for outbreak control. The following table summarises the recommended exclusion from schools and childcare centres for the diseases covered in this guideline.

Disease	Exclusion Period	Notifiable	Notes
Varicella	Until all vesicles have crusted (≥ 5 days after rash onset)	Yes (all states/territories)	Immunocompromised contacts require VZIG
Rubella	Until ≥ 4 days after rash onset	Yes (all states/territories)	Exclude pregnant contacts; advise bloods
Roseola	None required (infectious before rash appears)	No	Exclude while febrile as a general measure
Parvovirus B19	None (not contagious once rash appears)	No (routine)	Notify if pregnant contact exposed
Scarlet fever	Until 24 h after commencing antibiotics	Varies by jurisdiction	Complete 10-day antibiotic course
Mumps	Until 5 days after onset of parotid swelling	Yes (all states/territories)	MMR vaccination for susceptible contacts
HFMD	Until vesicles have dried (varies by jurisdiction)	No (routine)	Hand hygiene paramount
Kawasaki disease	Not applicable (non-infectious)	No	Hospital admission required for IVIG

Special Populations

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Pregnancy

Varicella

Maternal varicella in the first 20 weeks may cause congenital varicella syndrome (limb hypoplasia, cicatricial skin scarring, cortical atrophy, microcephaly). Risk is low (~1–2%) but referral to maternal-fetal medicine is essential. Varicella at term (5 days before to 2 days after delivery) carries ~30% neonatal mortality — administer VZIG to the neonate immediately.

Rubella

CRS risk is highest in the first trimester (up to 85% at < 8 weeks gestation). All women should have documented rubella immunity pre-conception. Rubella vaccine (MMR) is contraindicated in pregnancy; avoid conception for 28 days post-vaccination.

Parvovirus B19

~10% risk of hydrops fetalis if maternal infection occurs before 20 weeks. All exposed pregnant women need serology (IgM/IgG) and if seronegative: serial MCA Doppler ultrasound for 8–12 weeks. Consider intrauterine transfusion if hydrops develops.

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Neonates & Infants

Neonatal varicella

Highly lethal if untreated. IV aciclovir 20 mg/kg QDS for 10 days + VZIG for the neonate. Aciclovir should commence within 24 h of first vesicle eruption. Monitor for visceral dissemination (hepatitis, pneumonitis).

Kawasaki disease in infants < 6 months

At highest risk of coronary artery aneurysms but least likely to meet classic criteria. A high index of suspicion is required. Any infant with unexplained fever ≥ 5 days should have CRP, ESR, echo, and a thorough examination for mucocutaneous features.

Roseola in infants < 6 months

Maternal antibodies provide passive immunity until ~6 months. First infection thereafter may be severe (very high fever, febrile seizures). HHV-6 can rarely cause hepatitis, encephalitis, or haemophagocytic lymphohistiocytosis in neonates.

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Immunocompromised

Varicella

Disseminated VZV carries significant mortality (7–30%). All immunocompromised children with varicella or significant exposure require IV aciclovir and/or VZIG. Live varicella vaccine is contraindicated; use VZIG for post-exposure prophylaxis.

HHV-6 (Roseola)

Reactivation of HHV-6 post-transplant (especially HSCT) can cause encephalitis, myelosuppression, and graft rejection. Treat with ganciclovir (5 mg/kg IV BD) or foscarnet (60–90 mg/kg IV BD) under specialist guidance.

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Renal Impairment

Aciclovir

Renally cleared. Reduce dose and extend interval for eGFR < 50 mL/min. Ensure adequate hydration to prevent crystalline nephropathy. IV aciclovir: consult pharmacy for renal dosing tables.

Phenoxymethylpenicillin

No dose adjustment required in renal impairment.

IVIG in Kawasaki disease

Fluid load risk in renal impairment. Monitor renal function, electrolytes, and fluid balance closely. Consult nephrology if eGFR < 30 mL/min.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander children experience a disproportionate burden of infectious disease, driven by social determinants of health including overcrowded housing, reduced access to primary health care in remote communities, delayed presentation, and lower immunisation coverage in some regions (although the Indigenous childhood immunisation rate has improved significantly and now exceeds the non-Indigenous rate for many vaccines on the NIP).

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Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) remain a national crisis for Aboriginal and Torres Strait Islander communities. Incidence rates in Northern Territory Aboriginal children are among the highest in the world (up to 400 per 100,000 per year in the 5–14 year age group). Any GAS infection (including scarlet fever) must be treated promptly and completely. Suspicion of ARF requires urgent referral per the 2020 Australian RHD guidelines.

Immunisation access

Remote community access to MMR/MMRV and varicella vaccines has improved. However, some communities experience delayed catch-up schedules. Mobile immunisation clinics and Aboriginal Community Controlled Health Organisations (ACCHOs) play a vital role in closing the gap.

Scarlet fever / GAS

GAS skin infections and pharyngitis are highly prevalent in remote Aboriginal communities (skin sores affect up to 50% of children in some communities). Prompt treatment with intramuscular benzathine penicillin G (Bicillin L-A®) is preferred over oral therapy in communities where adherence to 10-day oral courses is unreliable. Secondary prophylaxis for ARF with 4-weekly Bicillin L-A is critical.

Kawasaki disease recognition

Kawasaki disease may be underdiagnosed in remote communities due to limited access to paediatric echocardiography and specialist services. Telehealth and retrieval services are essential. Any child in a remote community with unexplained fever ≥ 5 days should be assessed for KD features and evacuated if suspected.

Cultural safety

Health services must engage with families in a culturally safe manner. Use of Aboriginal Health Workers and Practitioners, access to interpreters where English is not the first language, respect for family decision-making, and understanding of sorry business obligations are all essential to ensuring engagement with treatment and follow-up.

Overcrowded housing

Overcrowded housing in remote communities facilitates rapid spread of highly contagious infections such as varicella, rubella, and mumps. Environmental health interventions (improved housing, water supply, hygiene infrastructure) are as important as clinical interventions for disease prevention.

📚 References

1. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health. Canberra: DoH; 2024. Available from: immunisationhandbook.health.gov.au.
2. GBD 2019 Diseases and Injuries Collaborators. Global burden of 369 diseases and injuries in 204 countries and territories, 1990–2019. Lancet. 2020;396(10258):1204–1222.
3. McCrindle BW, Rowley AH, Newburger JW, et al. Diagnosis, treatment, and long-term management of Kawasaki disease: a scientific statement from the American Heart Association. Circulation. 2017;135(17):e927–e999.
4. Burns JC, Glodé MP. Kawasaki syndrome. Lancet. 2004;364(9433):533–544.
5. Australian Institute of Health and Welfare (AIHW). Acute rheumatic fever and rheumatic heart disease in Australia. AIHW; 2023. Cat. No. CVD 88.
6. RHDAustralia (ARF/RHD writing group). National guidelines for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
7. Heuchan AM, Isaacs D. The management of neonatal varicella. J Paediatr Child Health. 2001;37(2):111–115.
8. Heymann DL, editor. Control of Communicable Diseases Manual. 21st ed. Washington, DC: APHA Press; 2022.
9. de Melker HE, Berbers GA, Hahné SJ, et al. The epidemiology of varicella and herpes zoster in the Netherlands: implications for varicella zoster virus vaccination. Vaccine. 2006;24(18):3946–3952.
10. Centers for Disease Control and Prevention (CDC). Epidemiology and Prevention of Vaccine-Preventable Diseases. 14th ed. Washington, DC: Public Health Foundation; 2021. Chapter: Varicella.
11. NSW Health. Control Guideline for Public Health Units: Varicella (Chickenpox). Sydney: NSW Ministry of Health; 2020.
12. Perry RT, Halsey NA. The clinical significance of measles: a review. J Infect Dis. 2004;189(Suppl 1):S4–S16. [Cross-reference for exanthem differential.]
13. Yoto Y, Kutsuzawa T, Saito H, et al. Parvovirus B19 infection and severe complications. Lancet Infect Dis. 2011;11(4):291.
14. Centers for Disease Control and Prevention (CDC). Hand, foot, and mouth disease: clinical overview. Centers for Disease Control and Prevention; 2023.
15. > National Health and Medical Research Council (NHMRC). Australian guidelines for the prevention and control of infection in healthcare. Canberra: NHMRC; 2019 (updated 2024).
16. Australian Bureau of Statistics (ABS). Estimates of Aboriginal and Torres Strait Islander Australians. ABS; 2024. Cat. No. 3238.0.55.001. [Demographic data for ATSI section.]

for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).