An epidemio-meteorotropic analytical study of Selangor, in the Southwest coast of Peninsular Malaysia, examines the monthly incidence of dengue for the period 1973-1982 to assess possible quantitative association with the monthly rainfall. The relationships between rainfall, abundance of A. aegypti and dengue infection during 1982 in Jinjang, a dengue-prone area in Selangor, were also examined. A quantitative association between rainfall and the number of dengue cases was found during the first wet period. The lag time between the onset of heavy rain and dengue outbreak was about two to three months. A 120% increase in the number of dengue cases was observed when the monthly rainfall was 300 mm or more. Positive associations were seen between the incidence of dengue and the Aedes house index and the Breteau index in Jinjang. The relationships between these three variables and rainfall suggest that the latter might have exerted its effect on dengue infection partly through the creation of more breeding sites for A. aegypti. Assessment of the importance of A. aegypti in the transmission of dengue in this locality was not possible because of the lack of adjustment for A. albopictus, the other known vector of dengue in the state, and for social and other environmental factors influencing infection rates. In spite of this and the interpretational problems common in aggregate studies, the present analyses have provided relatively strong statistical evidence of an association between rainfall and dengue outbreaks in Selangor, thereby indicating that it is a factor worthy of careful surveillance and monitoring.
Spirometra larvae are etiological agents of human sparganosis. However, the systematics of spirometrid cestodes has long been controversial. In order to determine the current knowledge on the evolution and genetic structure of Spirometra, an exhaustive population diversity analysis of spirometrid cestodes using the mitochondrial gene: cytochrome c oxidase subunit 1 (cox1) was performed. All publicly available cox1 sequences available in the GenBank and 127 new sequencing genes from China were used as the dataset. The haplotype identify, network, genetic differentiation and phylogenetic analysis were conducted successively. A total of 488 sequences from 20 host species, representing four spirometrid tapeworms (S. decipiens, S. ranarum, S. erinaceieuropaei and Sparganum proliferum) and several unclassified American and African isolates from 113 geographical locations in 17 countries, identified 45 haplotypes. The genetic analysis revealed that there are four clades of spirometrid cestodes: Clade 1 (Brazil + USA) and Clade 2 (Argentina + Venezuela) included isolates from America, Clade 3 contained African isolates and one Korean sample, and the remainders from Asia and Australia belonged to Clade 4; unclassified Spirometra from America and Africa should be considered the separate species within the genus; and the taxonomy of two Korea isolates (S. erinaceieuropaei KJ599680 and S. decipiens KJ599679) was still ambiguous and needs to be further identified. In addition, the demographical analyses supported population expansion for the total spirometrid population. In summary, four lineages were found in the spirometrid tapeworm, and further investigation with deeper sampling is needed to elucidate the population structure.
From April through June 1997, 29 previously healthy children aged <6 years (median, 1.5 years) in Sarawak, Malaysia, died of rapidly progressive cardiorespiratory failure during an outbreak of hand, foot, and mouth disease caused primarily by enterovirus 71 (EV71). The case children were hospitalized after a short illness (median duration, 2 days) that usually included fever (in 100% of case children), oral ulcers (66%), and extremity rashes (62%). The illness rapidly progressed to include seizures (28%), flaccid limb weakness (17%), or cardiopulmonary symptoms (of 24 children, 17 had chest radiographs showing pulmonary edema, and 24 had echocardiograms showing left ventricular dysfunction), resulting in cardiopulmonary arrest soon after hospitalization (median time, 9 h). Cardiac tissue from 10 patients showed normal myocardium, but central nervous system tissue from 5 patients showed inflammatory changes. Brain-stem specimens from 2 patients were available, and both specimens showed extensive neuronal degeneration, inflammation, and necrosis, suggesting that a central nervous system infection was responsible for the disease, with the cardiopulmonary dysfunction being neurogenic in origin. EV71 and possibly an adenovirus, other enteroviruses, or unknown cofactors are likely responsible for this rapidly fatal disease.