Herpes simplex infection in children

Overview & Definition

Picture an eighteen-month-old brought to the emergency department with a fever, drooling, and a mouth so painful she has not drunk for a day. Inside her lips and on her gums are clusters of shallow grey ulcers on inflamed bases, and her cervical nodes are enlarged and tender. This is primary herpetic gingivostomatitis — the commonest first encounter with herpes simplex virus in childhood — and recognising it instantly sets two priorities: relieve the pain and protect the hydration, and remember that this child now carries the virus for life. [10] [9]

Herpes simplex virus types 1 and 2 are neurotropic double-stranded DNA human herpesviruses. HSV-1 is transmitted mainly through oral secretions and causes most orolabial and central nervous system disease in childhood; HSV-2 is transmitted mainly sexually and causes most genital and neonatal disease. After primary infection the virus travels up sensory nerves to a ganglion — the trigeminal for orolabial disease, the sacral for genital — and establishes lifelong latency. Reactivation sends it back down the same nerve to the same dermatome, producing recurrent lesions at the original site. [1] [3]

For most children the encounter is a self-limiting mucocutaneous illness. The clinician's job has two halves, and the second is what the fellowship examiner tests. The acute half is to recognise the syndrome, gauge the host-risk tier, treat with the right strength of aciclovir, and protect hydration and vision. The preventive half is to understand that the same virus can devastate a neonate or a temporal lobe, and to run the maternal-neonatal prevention pathway that stops that happening. [1] [2]