Herpes simplex infection in children — formative SAQs

SAQ 1 (10 marks)

A 12-day-old term infant presents with a one-day history of fever (38.4 °C), poor feeding and increasing lethargy. The mother had a first episode of genital herpes at 38 weeks gestation and delivered vaginally 48 hours after the lesions appeared. There is a small vesicle on the infant's scalp. [2]

Question: Outline your assessment and management of this infant, including the differential diagnosis, investigations, treatment and the rationale for the maternal-neonatal prevention pathway. (10 marks) [7]

Model answer

Differential diagnosis and risk framing (2 marks). A febrile, lethargic neonate has bacterial sepsis and meningitis as the immediate framework, but this infant has a high-risk HSV exposure: a maternal primary genital HSV at 38 weeks with vaginal delivery through active lesions is the highest-transmission scenario, because the mother has not yet made antibody to pass to the baby. The scalp vesicle makes neonatal HSV the leading diagnosis. The error to avoid is attributing the lethargy to bacterial sepsis and missing HSV, so HSV stays at the top of the differential alongside the septic workup. [2] [7]

Investigations (3 marks). Send the full neonatal HSV workup: surface PCR swabs from the conjunctiva, oropharynx, rectum and the scalp vesicle, blood PCR, and CSF for cell count, protein, glucose and HSV PCR. Add liver function tests and coagulation to detect hepatitis and disseminated intravascular coagulation, a full blood count, and a chest X-ray for pneumonitis. Run the bacterial septic workup in parallel — blood culture, urine culture and CSF culture — because bacterial sepsis remains on the differential. Do not delay treatment while waiting for results. [2] [8]

Treatment (3 marks). Start high-dose intravenous aciclovir empirically — aciclovir 20 mg/kg/dose every eight hours — without waiting for the PCR, because the outcome of neonatal HSV worsens with every hour of delay. Add empiric antibiotics for bacterial sepsis while cultures are pending. Maintain hydration carefully to protect against aciclovir-induced nephrotoxicity, monitor for hepatitis and coagulopathy, and admit to a monitored neonatal bed with paediatric intensive care involvement if the infant deteriorates. The duration is 14 days for skin-eye-mouth disease and 21 days for central nervous system or disseminated disease, determined by the disease class and the CSF findings. [8] [2]

Prevention pathway and rationale (2 marks). This case illustrates why the maternal-neonatal pathway exists. A primary maternal genital HSV near delivery carries the highest transmission risk because the mother lacks antibody to transfer. Prevention rests on maternal suppressive aciclovir from 36 weeks to reduce shedding, caesarean delivery when active genital lesions are present, and the structured assessment of the exposed neonate along the Kimberlin-Baley pathway. After neonatal central nervous system or disseminated disease, six months of oral aciclovir suppression improves neurodevelopmental outcome. The lesson is that recognition of the maternal history and the exposed-neonate pathway is what prevents this presentation. [7] [5]

SAQ 2 (10 marks)

Question: A previously well 8-year-old child is brought to the emergency department with a three-day history of fever, headache and progressive confusion, followed by a focal seizure involving the right arm. There is no rash. (a) What is the most important diagnosis to consider and why? (b) Outline the investigations and treatment. (c) What determines the prognosis, and what are the key pitfalls in management? (10 marks) [8]

Model answer

(a) The diagnosis to consider (2 marks). The most important diagnosis is herpes simplex encephalitis — the commonest sporadic viral encephalitis, and the one for which empirical treatment is given before confirmation because the cost of delay is permanent neurological injury. The combination of fever, headache, progressive confusion and a focal seizure localises to a cortical process, and the temporal-lobe tropism of HSV makes it the leading diagnosis. It must not be attributed to a viral prodrome or a febrile delirium. [8] [2]

(b) Investigations and treatment (5 marks). Send cerebrospinal fluid for cell count (expect a lymphocytic pleocytosis), protein (raised) and glucose (usually normal), and HSV PCR — the diagnostic test, recognising that a very early sample can be falsely negative and a repeat lumbar puncture is reasonable if the picture persists. Request magnetic resonance imaging, which shows focal temporal-lobe signal change, often with haemorrhage, and an electroencephalogram, which may show periodic lateralised epileptiform discharges over a temporal lobe. A computed tomography is done first only if raised intracranial pressure threatens herniation before the lumbar puncture. Start high-dose intravenous aciclovir — 20 mg/kg/dose every eight hours for 21 days — empirically before the PCR returns, because outcome worsens with every hour of delay. Control seizures with anticonvulsants, manage airway and raised intracranial pressure, and admit to the paediatric intensive care unit if the child is encephalopathic or seizing. [8] [2]

(c) Prognosis and pitfalls (3 marks). The prognosis depends on the level of consciousness at presentation and the delay to aciclovir — early treatment dramatically improves survival and neurological outcome, while delay leaves a legacy of cognitive, behavioural and seizure burden that often requires long-term rehabilitation. The key pitfalls are: delaying aciclovir while awaiting PCR; attributing behavioural change to a viral prodrome rather than focal temporal-lobe disease; failing to repeat a lumbar puncture when an early CSF PCR is negative but the clinical picture persists; and under-resourcing the rehabilitation and follow-up that the survivor needs. The stance is empirical aciclovir first, confirmation alongside. [8] [5]