Lessons from the Nipah virus outbreak in Malaysia.
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The Nipah virus outbreak in Malaysia (September 1998 to May 1999) resulted in 265 cases of acute encephalitis with 105 deaths, and near collapse of the billion-dollar pig-farming industry. Because it was initially attributed to Japanese encephalitis, early control measures were ineffective, and the outbreak spread to other parts of Malaysia and nearby Singapore. The isolation of the novel aetiological agent, the Nipah virus (NiV), from the cerebrospinal fluid of an outbreak victim was the turning point which led to outbreak control 2 months later. Together with the Hendra virus, NiV is now recognised as a new genus, Henipavirus (Hendra + Nipah), in the Paramyxoviridae family. Efforts of the local and international scientific community have since elucidated the epidemiology, clinico-pathophysiology and pathogenesis of this new disease. Humans contracted the infection from close contact with infected pigs, and formed the basis for pig-culling that eventually stopped the outbreak. NiV targeted medium-sized and small blood vessels resulting in endothelial multinucleated syncytia and fibrinoid necrosis. Autopsies revealed disseminated cerebral microinfarctions resulting from vasculitis-induced thrombosis and direct neuronal involvement. The discovery of NiV in the urine and saliva of Malaysian Island flying foxes (Pteropus hypomelanus and Petropus vampyrus) implicated these as natural reservoir hosts of NiV. It is probable that initial transmission of NiV from bats to pigs occurred in late 1997/early 1998 through contamination of pig swill by bat excretions, as a result of migration of these forest fruitbats to cultivated orchards and pig-farms, driven by fruiting failure of forest trees during the El Nino-related drought and anthropogenic fires in Indonesia in 1997-1998. This outbreak emphasizes the need for sharing information of any unusual illnesses in animals and humans, an open-minded approach and close collaboration and co-ordination between the medical profession, veterinarians and wildlife specialists in the investigation of such illnesses. Environmental mismanagement (such as deforestation and haze) has far-reaching effects, including encroachment of wildlife into human habitats and the introduction of zoonotic infections into domestic animals and humans. (+info)
Ephrin-B2 expression critically influences Nipah virus infection independent of its cytoplasmic tail.
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In-depth assessment of an outbreak of Nipah encephalitis with person-to-person transmission in Bangladesh: implications for prevention and control strategies.
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Continued Nipah encephalitis outbreaks in Bangladesh highlight the need for preventative and control measures to reduce transmission from bats to humans and human-to-human spread. Qualitative research was conducted at the end of an encephalitis outbreak in Faridpur, Bangladesh in May 2004 and continued through December 2004. Methods included in-depth interviews with caretakers of cases, case survivors, neighbors of cases, and health providers. Results show contrasts between local and biomedical views on causal explanations and appropriate care. Social norms demanded that family members maintain physical contact with sick patients, potentially increasing the risk of human-to-human transmission. Initial treatment strategies by community members involved home remedies, and public health officials encouraged patient hospitalization. Over time, communities linked the outbreak to supernatural powers and sought care with spiritual healers. Differing popular and medical views of illness caused conflict and rejection of biomedical recommendations. Future investigators should consider local perceptions of disease and treatment when developing outbreak strategies. (+info)
Nipah virus edits its P gene at high frequency to express the V and W proteins.
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