West Nile Virus Encephalitis 16 Years Later - PubMed (original) (raw)

Review

West Nile Virus Encephalitis 16 Years Later

Bette K Kleinschmidt-DeMasters et al. Brain Pathol. 2015 Sep.

Abstract

Arboviruses (Arthropod-borne viruses) include several families of viruses (Flaviviridae, Togaviradae, Bunyaviradae, Reoviradae) that are spread by arthropod vectors, most commonly mosquitoes, ticks and sandflies. The RNA genome allows these viruses to rapidly adapt to ever-changing host and environmental conditions. Thus, these virus families are largely responsible for the recent expansion in geographic range of emerging viruses including West Nile virus (WNV), dengue virus and Chikungunya virus. This review will focus on WNV, especially as it has progressively spread westward in North America since its introduction in New York in 1999. By 2003, WNV infections in humans had reached almost all lower 48 contiguous United States (US) and since that time, fluctuations in outbreaks have occurred. Cases decreased between 2008 and 2011, followed by a dramatic flair in 2012, with the epicenter in the Dallas-Fort Worth region of Texas. The 2012 outbreak was associated with an increase in reported neuroinvasive cases. Neuroinvasive disease continues to be a problem particularly in the elderly and immunocompromised populations, although WNV infections also represented the second most frequent cause of pediatric encephalitis in these same years. Neuropathological features in cases from the 2012 epidemic highlight the extent of viral damage that can occur in the CNS.

Keywords: arbovirus; epidemic; infection; neuropathology.

© 2015 International Society of Neuropathology.

PubMed Disclaimer

Figures

Figure 1

Figure 1

A. Severe zonal cohesive necrosis occupying almost the entire substantia nigra (sub. nigra), with B, profuse microglial influx, and C, foci of necrosis; all cases were severely affected at this site; three different cases illustrated. Caudate (D) was often involved, with diffuse microgliosis and, in this case, profuse perivascular lymphocytic cuffing. Thalamus was usually severely affected along with brainstem and multifocal disease could be highlighted at lower power by

CD68

immunohistochemistry (E); acutely ischemic foci showed rarefaction, necrotic neurons, and sometimes minimal cellular response (F).

Figure 2

Figure 2

(A) Thalamus here shows necrotic foci with

CD68

positive macrophages. Cerebellum was often severely affected by Purkinje cell, but not granule cell, neuronal loss (B–D), microgliosis of the molecular layer (m) (B–D), neuronophagia (D, arrow). Red nucleus could manifest microglial clusters or overt pallor, vacuolization and necrosis, as seen here (E). Basis pontis was frequently severely affected and in this case, multifocal ovoid areas of necrosis contained dystrophic basophilic axonal mineralization (F, upper left); without the admixed macrophages (F, arrows) and more typical non‐mineralized foci elsewhere, this might be construed as pontine leukodystrophy.

Figure 3

Figure 3

The same anatomical

CNS

/

PNS

sites are involved in severely immunocompromised patients as in patients with less severe comorbidities, but they are simply of larger volume and more necrotic; however, occasionally additional sites can be affected such as lateral medullary tegmentum (A), inferior olivary nucleus (B, arrows on microglial clusters), or dorsal gray matter of spinal cord (c, cc = central canal, vs = ventral sulcus). Near‐total cross‐sectional diameter of anterior horn (C,D), with neuronal loss, microglial clusters and neuronophagia (E) can be seen. The extension of inflammation in continuity from dorsal gray matter to anterior horn cell region, with involvement of

C

larke's column nucleus (F) lends histological support to theories of possible spread from

PNS

nerve roots to

CNS

.

Figure 4

Figure 4

Dorsal nerve root of spinal cord (A) from the mid‐thoracic region shows neuritis, as was noted in the original cases of

WNVE

, but severely immunocompromised patients may also show cranial nerve neuritis (B). Extent of lymphocytic response is variable from patient to patient and sometimes even site to site, but at times can consist of very activated lymphocytes (E); however small cytologically bland lymphocytes (A,B) are the rule. Despite the very minimal involvement of cerebral cortical gray matter even in these severely affected patients, cerebral white matter can show microgliosis (D,E), the extent of which is highlighted by

CD68

immunohistochemistry on low power (D); myelin pallor, however, is usually minimal (F, Luxol fast blue‐periodic acid

S

chiff).

Similar articles

Cited by

References

    1. Ali M, Safriel Y, Sohi J, Llave A, Weathers S (2005) West Nile virus infection: MR imaging findings in the nervous system. AJNR Am J Neuroradiol 26:289–297. - PMC - PubMed
    1. Armah HB, Wang G, Omalu BI, Tesh RB, Gyure KA, Chute DJ et al (2007) Systemic distribution of West Nile virus infection: postmortem immunohistochemical study of six cases. Brain Pathol 17:354–362. - PMC - PubMed
    1. Bains HS, Jampol LM, Caughron MC, Parnell JR (2003) Vitritis and chorioretinitis in a patient with West Nile virus infection. Arch Ophthalmol 121:205–207. - PubMed
    1. Basavaraju SV, Kuehnert MJ, Zaki SR, Sejvar JJ (2014) Encephalitis caused by pathogens transmitted through organ transplants, United States, 2002–2013. Emerg Infect Dis 20:1443–1451. - PMC - PubMed
    1. Biggerstaff BJ, Peterson LR (2002) Estimated risk of West Nile virus transmission through blood transfusion during an epidemic in Queens, New York City. Transfusion 42:1019–1026. - PubMed

Publication types

MeSH terms

LinkOut - more resources