Nipah virus encephalitis: serial MR study of an emerging disease.
ABSTRACT To report the serial magnetic resonance (MR) imaging findings of the Nipah virus.
Twelve patients underwent serial MR imaging. Eight patients were examined at the outbreak; 11, at 1 month; and seven, at 6 months. Contrast material-enhanced MR images, diffusion-weighted images, and single-voxel proton MR spectroscopic images were reviewed. Clinical and neurologic assessment, as well as analysis of the size, location, and appearance of brain lesions on MR images, were performed.
During the outbreak, all eight patients had multiple small foci of high signal intensity within the white matter on T2-weighted images. In six patients, cortical and brain stem lesions were also detected, and five patients had diffusion-weighted MR imaging-depicted hyperintensities. One month after the outbreak, five patients had widespread tiny foci of high signal intensity on T1-weighted images, particularly in the cerebral cortex. Diffusion-weighted images showed decreased prominence or disappearance of lesions over time. There was no evidence of progression or relapse of the lesions at 6-month follow-up. MR spectroscopy depicted reduction in N-acetylaspartate-to-creatine ratio and elevation of choline-to-creatine ratios.
The Nipah virus has findings unlike other viral encephalitides: small lesions that are primarily within the white matter, with transient punctate cortical hyperintensities on T1-weighted images.
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ABSTRACT: We studied the type and frequency of differences between data presented in conference abstracts and subsequent published papers in the fields of infectious diseases and microbiology. We reviewed all abstracts from the first session of 7 of 15 major research categories presented in the 1999 and 2000 Interscience Conference on Antimicrobial Agents and Chemotherapy. For each selected pair of abstract and related published paper, two independent investigators performed a detailed data comparison. From 190 abstracts reviewed, 68 (36%) were subsequently published as full papers by March 2004. Fifty-two pairs referred to the same study population and period. Differences were found in 30 of 51 pairs, which were further analyzed (point estimate=59%, 95% C.I.: 45-73%). The identified differences were related to both the aims and conclusions of the study (3/30), the study conclusions only (2/30), numbers and/or rates of the studied patients (10/30), numbers or rates of microbiological isolates (9/30), MIC values or K(i) values (5/30), other pharmacological properties of antibiotics (2/30), odds ratio (1/30), and duration of observation (1/30). Some differences were considered major. In bivariable associations, time to publication (from presentation in the conference to publication of the full paper) was associated with identifiable differences between the conference abstract and the full paper (OR=1.76, 95% CI 0.95-3.24/year of delay, P=0.07). It is reassuring that although we identified several reportable differences, only a very small proportion of studies exhibited differences in their aims and/or conclusions. Researchers may benefit from the above findings in improving the accuracy of presented data.The FASEB Journal 06/2005; 19(7):673-80. DOI:10.1096/fj.04-3140lfe · 5.48 Impact Factor
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ABSTRACT: Zoonoses as causes of human infections have been increasingly reported, and many of these are viruses that cause central nervous system infections. This paper focuses on the henipaviruses (family Paramyxoviridae, genus henipavirus) that have recently emerged to cause severe encephalitis and systemic infection in humans and animals in the Asia-Pacific region. The pathological features in the human infections comprise vasculopathy (vasculitis, endothelial multinucleated syncytia, thrombosis, etc.) and parenchymal cell infection in the central nervous system, lung, kidney, and other major organs. Most animals naturally or experimentally infected show more or less similar features confirming the dual pathogenetic mechanism of vasculopathy-associated microinfarction and direct extravascular parenchymal cell infection as causes of tissue injury. The most promising animal models include the hamster, ferret, squirrel monkey, and African green monkey. With increasing evidence of infection in the natural hosts, the pteropid bats and, hence, probable future outbreaks in many more countries, a greater awareness of henipavirus infection in both humans and animals is imperative.09/2011; 2011:567248. DOI:10.4061/2011/567248
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ABSTRACT: Objective Nipah virus (NiV) is an emerging zoonosis. Central nervous system disease frequently results in high case-fatality. Long-term neurological assessments of survivors are limited. We assessed long-term neurologic and functional outcomes of 22 patients surviving NiV illness in Bangladesh.Methods During August 2005 and May 2006, we administered a questionnaire on persistent symptoms and functional difficulties to 22 previously identified NiV infection survivors. We performed neurologic evaluations and brain magnetic resonance imaging (MRI).ResultsTwelve (55%) subjects were male; median age was 14.5 years (range 6–50). Seventeen (77%) survived encephalitis, and 5 survived febrile illness. All but 1 subject had disabling fatigue, with a median duration of 5 months (range, 8 days–8 months). Seven encephalitis patients (32% overall), but none with febrile illness had persistent neurologic dysfunction, including static encephalopathy (n = 4), ocular motor palsies (2), cervical dystonia (2), focal weakness (2), and facial paralysis (1). Four cases had delayed-onset neurologic abnormalities months after acute illness. Behavioral abnormalities were reported by caregivers of over 50% of subjects under age 16. MRI abnormalities were present in 15, and included multifocal hyperintensities, cerebral atrophy, and confluent cortical and subcortical signal changes.InterpretationAlthough delayed progression to neurologic illness following Nipah fever was not observed, persistent fatigue and functional impairment was frequent. Neurologic sequelae were frequent following Nipah encephalitis. Neurologic dysfunction may persist for years after acute infection, and new neurologic dysfunction may develop after acute illness. Survivors of NiV infection may experience substantial long-term neurologic and functional morbidity. Ann Neurol 2007Annals of Neurology 09/2007; 62(3):235 - 242. DOI:10.1002/ana.21178 · 11.91 Impact Factor