Rhombencephalitis and Coxsackievirus A16

References 1. Udo EE, Pearman JW, Grubb WB. Genetic analysis of community isolates of methicillin-resistant Staphylococcus au-reus in Western Australia. between Staphylococcus aureus strains carrying gene for Panton-Valentine leu-kocidin and highly lethal necrotising pneumonia in young immunocompetent patients. Spread of a methicillin-resistant Staphylococcus aureus ST80-IV clone in a Danish community. Eijkelkamp BA, et al. Multiple cases of fa-milial transmission of community-acquired methicillin-resistant Staphylococcus au-reus.tour-clamped homogeneous electric field electrophoresis of Staphylococcus aureus. al. Control of methicillin-resistant Staphylococcus aureus (MRSA) in an Australian metropolitan teaching hospital complex. To the Editor: Hand, foot, and mouth disease (HFMD) is a common illness in children and is mainly caused by coxsackievirus A16 (CA16) and enterovirus 71 (EV71). Although its clinical course is usually uneventful and most patients experience a full recovery, serious neurologic complications , including encephalitis, can occur secondarily to HFMD caused by EV71. Such neurological complications occurred during an epidemic in Taiwan in 1998 (1). Encephalitis caused by EV71 is characterized by rhombencephalitis, which is a combination of brainstem encephalitis and cerebellitis. Signs and symptoms of rhombencephalitis are irritability, myoclonus, ataxia, and cranial nerve involvement (1). In contrast to EV71, HFMD caused by CA16 is associated with few neurologic complications with the exception of infrequent asep-tic meningitis (2). We report a case of rhombencephalitis that developed in an infant as a complication of HFMD caused by CA16. HFMD was diagnosed in a 23-month-old girl on the basis of high fever (>40°C, 3 d duration), stomati-tis, and multiple papules on her palms, soles, and buttocks. Her illness occurred in the summer of 2007, when sentinel surveillance in the region indicated an epidemic of HFMD caused by both CA16 and EV71. She was admitted to our hospital in Fukoka, Ja-pan, on day 4 of illness because of abnormal eye movement, irritability, and inability to stand. She had intermittent to-and-fro, horizontal oscillations of the eyes (ocular flutter). She also had truncal and limb ataxia and myoclonus in her head and limbs. Brain magnetic resonance imaging (MRI) showed T1-low and T2-high bulbopontine and cerebellar lesions around the fourth ventricle (Figure). Peripheral blood showed a mild leukocytosis (13.13 × 10 9 /L) and a C-reactive protein level within reference range (0.9 mg/L). Blood chemistry results were unre-markable. Cerebrospinal fluid (CSF) examination showed mononuclear pleocytosis (74/µL) with normal protein and glucose levels. CA16 was isolated from her stool specimen on day 4 of illness. Based on reverse transcription–PCR, CSF …