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N. James MacLachlan
Researcher at University of California, Davis
Publications - 93
Citations - 4705
N. James MacLachlan is an academic researcher from University of California, Davis. The author has contributed to research in topics: Virus & Equine viral arteritis. The author has an hindex of 37, co-authored 93 publications receiving 4422 citations. Previous affiliations of N. James MacLachlan include University of Pretoria & University of California.
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Rift Valley fever virus
TL;DR: R Rift Valley fever epizootics and epidemics can rapidly overwhelm the capacities of the public health and veterinary medical communities to provide rapid diagnostic testing and adequate medical care for affected humans and other animals, which can number in the tens of thousands.
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Bluetongue virus: virology, pathogenesis and immunity.
Isabelle Schwartz-Cornil,Peter P. C. Mertens,Vanessa Contreras,Behzad Hemati,Florentina Pascale,Emmanuel Bréard,Philip S. Mellor,N. James MacLachlan,Stéphan Zientara +8 more
TL;DR: The bluetongue virus, an orbivirus of the Reoviridae family encompassing 24 known serotypes, is transmitted to ruminants via certain species of biting midges (Culicoides spp.) and causes thrombohemorrhagic fevers mainly in sheep as mentioned in this paper.
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Re-emergence of bluetongue, African horse sickness, and other Orbivirus diseases
TL;DR: Although climate change has been incriminated in the emergence of BTV infection of ungulates, the precise role of anthropogenic factors and the like is less certain and it is not yet clear what the future holds in terms of these diseases, nor of other potentially important but poorly characterized Orbiviruses.
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Vaccines against bluetongue in Europe
TL;DR: After the incursion of bluetongue virus (BTV) into European Mediterranean countries in 1998, vaccination was used in an effort to minimize direct economic losses to animal production, reduce virus circulation and allow safe movements of animals from endemic areas.
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Bluetongue: history, global epidemiology, and pathogenesis.
TL;DR: Bluetongue disease results from vascular injury, likely through a process analogous to that of human hemorrhagic viral fevers in which production of vasoactive mediators from virus-infected macrophages and dendritic cells results in enhanced endothelial paracellular permeability with subsequent vascular leakage and hypovolemic shock.