Childhood exanthems are characterised by fever and widespread rash.
Maternal antibodies protect for the first 6 to 12 months. Although the inci- dence of exanthems has diminished as a result of vaccination, incomplete uptake results in infections in later life.
Measles
The WHO has set the objective of eradicating measles, but vaccination of 95% of a population is required to prevent outbreaks. Natural illness pro- duces lifelong immunity.
Clinical features
Infection is by respiratory droplets with an incubation period of 6–19 days to onset of rash. A prodromal illness occurs 1 to 3 days before the rash, with upper respiratory symptoms, conjunctivitis and the presence of ‘Koplik’s spots’ (small white spots surrounded by erythema) on the internal buccal mucosa (Fig. 5.1). As natural antibodies develop, the maculopapular rash appears (Fig. 5.2), spreading from face to extremities. Lymphadenopathy and diarrhoea are common.
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Fig. 5.1 Koplik’s spots (arrows) seen on buccal mucosa in the early stages of clinical measles.
Fig. 5.2 Typical measles rash.
Complications include:
• Otitis media. • Bacterial pneumonia. • Encephalitis/convulsions. • Subacute sclerosing panencephalitis (rare, late and serious).
Management
In the immunocompetent, measles is self- limiting; however, severity and complications are increased in the malnourished and immuno- suppressed. Disease is attenuated in the immunocompromised and in nonimmune pregnant women by immunoglobulin treatment. All children aged 12 to 15 months should receive measles vaccination as a com- bined vaccine with mumps and rubella, with a further dose at age 4 years.
Rubella (German measles)
Rubella is transmitted by respiratory droplets, with infectivity from up to 10 days before to 2 weeks after the onset of the rash. The incubation period is 15 to 20 days. Most childhood cases are subclinical, although disease can present with fever, lymphadenopathy and a maculopapular rash that spreads from the face to the trunk. Complications include arthralgia, throm- bocytopenia, hepatitis and rarely encephalitis.
If transplacental infection takes place in the first trimester or later, viral persistence is likely, and severe congenital disease may result. Following exposure during pregnancy, confirmation of infection is provided either by rubella IgM antibodies in serum or by IgG seroconversion. In an exposed pregnant woman, absence of rubella IgG confirms the potential for con- genital infection. All children should be immunised with MMR to prevent rubella. Prepregnancy MMR is now considered the best way of protecting pregnant women.
Parvovirus B19
This air- borne virus causes mild or subclinical infection in normal hosts.
Around 50% of children and 60% to 90% of adults are seropositive. In addition to the clinical manifestations summarised in Box 5.13, there may be a transient block in erythropoiesis, which is insignificant unless haemo- globinopathy or haemolysis is also present. Parvovirus B19 DNA may be detected in the serum by PCR; however, as illness is usually mild or sub- clinical and self- limiting, confirmatory blood tests are not always required.
If infection occurs during pregnancy, the fetus should be monitored closely for signs of hydrops.
Human herpesvirus 6 and 7
These viruses are associated with a benign febrile illness of children with a maculopapular erythematous rash: ‘exanthem subitum’. In the immu- nocompromised, they cause an infectious mononucleosis- like syndrome.
Around 95% of children are infected by age 2 years.
Chickenpox
Varicella zoster virus (VZV) is a dermotropic and neurotropic virus causing primary infection, usually in childhood, which may reactivate in later life. It
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is spread by aerosol and direct contact and is highly infectious. Disease in children is usually better tolerated than in adults, pregnant women and the immunocompromised.
The incubation period is 11 to 20 days, after which a vesicular eruption begins (Fig. 5.4), often on mucosal surfaces first, followed by rapid dissemi- nation in a centripetal fashion. New lesions occur in crops every 2 to 4 days, accompanied by fever. The rash progresses within 24 hours from small pink macules to vesicles and pustules, which then crust. Infectivity lasts from 2 to 4 days before the rash appears until the last crusts separate. Diagnosis is clinical but may be confirmed by PCR of vesicular fluid.
Complications include:
• Secondary bacterial infection of rash (caused by scratching). • Self- limiting cerebellar ataxia. • Congenital abnormalities if maternal disease is contracted in the first trimester. • Pneumonitis, which may be fatal.
Antiviral agents such as aciclovir and famciclovir are not required for uncomplicated childhood chickenpox. They are used in adults when patients present within 24 to 48 hours of vesicle onset, and in all patients with complications, pregnant women and the immunosuppressed. More severe cases require prolonged treatment, initially parenteral. Human VZV immunoglobulin may attenuate infection in highly susceptible contacts of chickenpox sufferers such as the immunosuppressed and pregnant women. VZV vaccine, now in use in the United States, offers effective protection.
5.13 Clinical features of parvovirus B19 infection Syndrome/affected age group Clinical manifestations Fifth disease (erythema infectiosum)
Small children Three clinical stages: a ‘slapped cheek’
appearance (Fig. 5.3), reticulate eruption on the body and limbs then resolution.
Often the child is quite well throughout Gloves and socks syndrome
Young adults Fever and an acral purpuric eruption with
a clear margin at the wrists and ankles.
Mucosal involvement also occurs Arthropathies
Adults, occasionally children Polyarthropathy of small joints. In chil- dren it tends to involve the larger joints in an asymmetrical distribution
Impaired erythropoiesis Adults, those with haematological disease, the immunosuppressed
Can cause a mild anaemia, but in an individual with underlying haemato- logical abnormality can precipitate an aplastic crisis
Hydrops fetalis
Transplacental fetal infection
Asymptomatic or symptomatic maternal infection can cause fetal anaemia with aplastic crisis leading to nonimmune hydrops fetalis and spontaneous abortion
Fig. 5.3 Slapped cheek syndrome. The typical facial rash of human parvovirus B19 infection.
Fig. 5.4 Chickenpox.
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Shingles (herpes zoster)
This is produced by reactivation of latent VZV from the dorsal root ganglion of sensory nerves, and most commonly involves the thoracic dermatomes (Fig. 5.5) and the ophthalmic division of the trigeminal nerve.
Burning discomfort develops in the affected dermatome, followed 3 to 4 days later by a vesicular rash. There may be viraemia and distant ‘satel- lite’ lesions. Severe, extensive or prolonged disease suggests underlying immunosuppression, for example, HIV. Chickenpox may be caught from shingles, but not vice versa.
Complications
• Ophthalmic trigeminal involvement: may lead to corneal ulceration, and requires ophthalmology review. • Ramsay Hunt syndrome: facial palsy, ipsi- lateral loss of taste and buccal ulceration and a rash in the external auditory canal. • Postherpetic neuralgia: can be difficult to treat, but may respond to amitriptyline or gabapentin. • Myelitis/encephalitis: rare.
Early therapy with aciclovir helps to limit early- and late- onset pain and to prevent the development of postherpetic neuralgia. VZV vaccination is now offered to patients aged 70 and 78 years in the UK to prevent shingles.