PostScript
Enteroviral meningoencephalitis in an infant: an increasingly recognised infection A baby boy was delivered at 37 weeks gestation following induction for maternal illness with abdominal pain and an elevated C-reactive protein (CRP). The baby was born in good condition and weighed 3.2 kg. His newborn examination was normal apart from mild jaundice for which he received phototherapy on day 2. Four-hourly observations were normal and he was discharged the next day. During the next 3 days he fed less well and by day 7 appeared listless and was brought back to hospital. Initial assessment recorded weight 2.9 kg, moderate jaundice, reduced responsiveness, poor perfusion and irregular breathing but no fever or rash. Initial blood tests were normal other than a CRP of 12 mg/dL. A capillary blood sample revealed a mild respiratory acidosis. Chest X-ray, abdominal ultrasound scan and brain MRI were normal. Cerebrospinal fluid (CSF) contained 10 polymorphs and 180 lymphocytes, protein 2.2 and glucose 2.3 (blood 4.3) mmol/L. Initial management included fluid resuscitation, humidified heated high-flow oxygen, intravenous antibiotics and acyclovir. His condition, deteriorated rapidly, necessitating ventilation and inotropic support for worsening cardiac output associated with high creatine kinase levels (2173 iu/L). He also received fresh frozen plasma, vitamin K and platelets for progressive disseminated intravascular coagulation. Despite intensive care, he suffered a cardiac arrest and died within 18 h of admission. Following his death, CSF was reported enterovirus (EV) RNA positive, typed as Coxsackie B serotype 2. Postmortem findings confirmed meningoencephalitis, focal myocardial necrosis, acute renal tubular necrosis and pneumonitis with all tissues testing positive for the same virus. Over the past decade, molecular testing in the UK has led to a 7-fold increase in 208
laboratory-confirmed episodes of enteroviral meningoencephalits with the highest incidence in
Enteroviral meningoencephalitis in an infant: an increasingly recognised infection A baby boy was delivered at 37 weeks gestation following induction for maternal illness with abdominal pain and an elevated C-reactive protein (CRP). The baby was born in good condition and weighed 3.2 kg. His newborn examination was normal apart from mild jaundice for which he received phototherapy on day 2. Four-hourly observations were normal and he was discharged the next day. During the next 3 days he fed less well and by day 7 appeared listless and was brought back to hospital. Initial assessment recorded weight 2.9 kg, moderate jaundice, reduced responsiveness, poor perfusion and irregular breathing but no fever or rash. Initial blood tests were normal other than a CRP of 12 mg/dL. A capillary blood sample revealed a mild respiratory acidosis. Chest X-ray, abdominal ultrasound scan and brain MRI were normal. Cerebrospinal fluid (CSF) contained 10 polymorphs and 180 lymphocytes, protein 2.2 and glucose 2.3 (blood 4.3) mmol/L. Initial management included fluid resuscitation, humidified heated high-flow oxygen, intravenous antibiotics and acyclovir. His condition, deteriorated rapidly, necessitating ventilation and inotropic support for worsening cardiac output associated with high creatine kinase levels (2173 iu/L). He also received fresh frozen plasma, vitamin K and platelets for progressive disseminated intravascular coagulation. Despite intensive care, he suffered a cardiac arrest and died within 18 h of admission. Following his death, CSF was reported enterovirus (EV) RNA positive, typed as Coxsackie B serotype 2. Postmortem findings confirmed meningoencephalitis, focal myocardial necrosis, acute renal tubular necrosis and pneumonitis with all tissues testing positive for the same virus. Over the past decade, molecular testing in the UK has led to a 7-fold increase in 208
laboratory-confirmed episodes of enteroviral meningoencephalits with the highest incidence in
