BackgroundMelioidosis is a serious, and potentially fatal community-acquired infection endemic to northern Australia and Southeast Asia, including Sarawak, Malaysia. The disease, caused by the usually intrinsically aminoglycoside-resistant Burkholderia pseudomallei, most commonly affects adults with predisposing risk factors. There are limited data on pediatric melioidosis in Sarawak.MethodsA part prospective, part retrospective study of children aged <15 years with culture-confirmed melioidosis was conducted in the 3 major public hospitals in Central Sarawak between 2009 and 2014. We examined epidemiological, clinical and microbiological characteristics.FindingsForty-two patients were recruited during the 6-year study period. The overall annual incidence was estimated to be 4.1 per 100,000 children <15 years, with marked variation between districts. No children had pre-existing medical conditions. Twenty-three (55%) had disseminated disease, 10 (43%) of whom died. The commonest site of infection was the lungs, which occurred in 21 (50%) children. Other important sites of infection included lymph nodes, spleen, joints and lacrimal glands. Seven (17%) children had bacteremia with no overt focus of infection. Delays in diagnosis and in melioidosis-appropriate antibiotic treatment were observed in nearly 90% of children. Of the clinical isolates tested, 35/36 (97%) were susceptible to gentamicin. Of these, all 11 isolates that were genotyped were of a single multi-locus sequence type, ST881, and possessed the putative B. pseudomallei virulence determinants bimABp, fhaB3, and the YLF gene cluster.ConclusionsCentral Sarawak has a very high incidence of pediatric melioidosis, caused predominantly by gentamicin-susceptible B. pseudomallei strains. Children frequently presented with disseminated disease and had an alarmingly high death rate, despite the absence of any apparent predisposing risk factor.

Acute necrotizing encephalopathy (ANE) in childhood is a rare clinico-radiological syndrome with distinctive bilateral thalamic lesions. The diagnosis is often based on the criteria proposed by Mizuguchi et al. 1 It comprises a spectrum of virus-associated encephalopathy, 2 often but not exclusively associated with influenza infection and a familial and a relapsing form have been reported. The mortality rates are varied, ranging from 0% to 43% and survivors often have severe disabilities. [3][4][5][6][7][8] Whilst there is no clear consensus for ANE treatment, 9 the key therapeutic strategy is the early initiation of firstline immunotherapy, particularly of corticosteroids. 4,9 More C