In mid-1997, several children died in Sarawak, Malaysia, during an epidemic of enterovirus-71 (EV71) hand, foot, and mouth disease. The children who died had a febrile illness that rapidly progressed to cardiopulmonary failure and the cause was not satisfactorily resolved. We describe the isolation and identification of a subgenus B adenovirus from the children who died.
Between February and April, 1999, an outbreak of viral encephalitis occurred among pig-farmers in Malaysia. We report findings for the first three patients who died.
Vomiting, drowsiness, metabolic acidosis, polymorphonuclear leucocytosis, and encephalopathy developed in thirteen infants within hours of ingestion of margosa oil. Liver biopsy of one infant and necropsy examination of ICR strain mice after experimentally induced margosa-oil poisoning demonstrated pronounced fatty infiltration of the liver and proximal renal tubules as well as cerebral oedema. Electron microscopy demonstrated mitochondrial damage. These findings indicate that margosa oil may be involved in the aetiology of Reye's syndrome among Indians in Malaysia.
The distribution in Thailand of antibody to a recently discovered variant of circumsporozoite proteins of Plasmodium vivax was determined by enzyme-linked immunosorbent assay (ELISA). The ELISA capture antigens were a synthetic peptide of the principal variant sequence ANGAGNQPG and a candidate P vivax vaccine that contained the predominant repeat sequence GDRAA/DGQPA. Serological evidence of recent inoculation with the variant was found throughout Thailand and in migrants from Cambodia, Malaysia, and Burma. IgG antibody to the two P vivax circumsporozoite proteins was detected in 217 of 804 test sera (27%). Within the regions studied the proportion of positive sera specific for the variant epitope ranged from 28% to 66%. A vaccine against the predominant repeat domain may rapidly select for the variant, which already appears to be widespread within Thailand.
An iodinator was fitted to the existing gravity-fed water-supply of a remote village in Sarawak, Malaysia, where goitre was endemic. Within nine months, the prevalence of goitre had been reduced from 61% to 30%, with 79% of goitres showing visible reduction in size. All subjects were clinically euthyroid before and nine months after the start of iodination, although pre-treatment serum thyroid-stimulating hormone (TSH) concentrations varied from normal up to 24 mU/l. Before treatment basal serum triiodothyronine (T3) and thyroxine (T4) concentrations were typical of endemic goitre with a low mean serum T4 (80 +/- 30 [SD] nmol/l) and a slightly raised mean serum T3 (2.3 +/- 0.7 nmol/l). After iodination, circulating TSH concentration was generally undetectable (less than 0.1 mU/l), mean T3 concentration was unchanged, but the mean T4 rose significantly to 109 +/- 41 nmol/l (p less than 0.01). Urinary iodine concentrations fluctuated; this largely reflected intermittent blockage of the iodinator, but concentrations became consistent with a return to the iodine-replete state. There was no evidence of the Jod Basedow effect in the group studied. Iodinated water was more convenient to distribute than iodised salt and is less likely to cause Jod Basedow phenomenon than are injections of iodised oil. Moreover, iodination of water is effective in killing most microorganisms and this additional benefit could contribute significantly to village health.