Detection of West Nile virus sequences in cerebrospinal fluid

The Lancet ◽  
2000 ◽  
Vol 355 (9215) ◽  
pp. 1614-1615 ◽  
Author(s):  
Thomas Briese ◽  
William G Glass ◽  
W lan Lipkin
2021 ◽  
pp. 247412642097925
Author(s):  
Kareem Moussa ◽  
Karen W. Jeng-Miller ◽  
Leo A. Kim ◽  
Dean Eliott

Purpose: This work aims to evaluate the utility of nucleic acid amplification testing (NAAT) and serology in confirming West Nile Virus (WNV) infection in patients with suspected WNV chorioretinitis. Methods: A retrospective cross-sectional study was conducted of a cluster of patients who presented to the Retina Service of Massachusetts Eye and Ear between September and October 2018. Results: Three patients were identified with classic WNV chorioretinitis lesions with negative cerebrospinal fluid NAAT and positive serum serology findings. The diagnosis of WNV chorioretinitis was made based on the appearance of the fundus lesions and the presence of characteristic findings on fluorescein angiography as previously described in the literature. Conclusions: This report highlights 3 unique cases of WNV chorioretinitis in which NAAT of cerebrospinal fluid failed to identify WNV as the inciting agent. These cases stress the importance of serum serologic testing in diagnosing WNV infection.


2010 ◽  
Vol 15 (16) ◽  
Author(s):  
P Angelini ◽  
M Tamba ◽  
A C Finarelli ◽  
R Bellini ◽  
A Albieri ◽  
...  

Following a large West Nile virus (WNV) epidemic in northeastern Italy in 2008, human and animal surveillance activities were implemented in Emilia Romagna. Human surveillance was performed by serology or genome detection on blood and cerebrospinal fluid for all suspected cases suffering from acute meningoencephalitis in the regional territory. Animal surveillance consisted of passive and active surveillance of horses and active surveillance of wild birds and mosquitoes. Between 15 June and 31 October 2009, nine of 78 possible cases of West Nile neuroinvasive disease were confirmed (three fatal). From May to October, 26 cases of neurological West Nile disease were confirmed among 46 horses. The overall incidence of seroconversion among horses in 2009 was 13%. In 2009, 44 of 1,218 wild birds yielded positive PCR results for WNV infection. The planned veterinary and entomological surveillance actions detected WNV activity from the end of July 2009, about 2-3 weeks before the onset of the first human neurological case. Passive surveillance of horses seems to be an early and suitable tool for the detection of WNV activity, but it will be less sensitive in the future, because an intensive programme of horse vaccination started in June 2009.


2004 ◽  
Vol 31 (4) ◽  
pp. 289-291 ◽  
Author(s):  
Hema Kapoor ◽  
Kimberly Signs ◽  
Patricia Somsel ◽  
Frances P. Downes ◽  
Patricia A. Clark ◽  
...  

2016 ◽  
Vol 17 (3) ◽  
pp. 803-808 ◽  
Author(s):  
M. R. Wilson ◽  
L. L. Zimmermann ◽  
E. D. Crawford ◽  
H. A. Sample ◽  
P. R. Soni ◽  
...  

2004 ◽  
Vol 11 (4) ◽  
pp. 651-657 ◽  
Author(s):  
A. Scott Muerhoff ◽  
George J. Dawson ◽  
Bruce Dille ◽  
Robin Gutierrez ◽  
Thomas P. Leary ◽  
...  

ABSTRACT Humans infected with West Nile virus (WNV) develop immunoglobulin M (IgM) antibodies soon after infection. The microtiter-based assays for WNV IgM antibody detection used by most state public health and reference laboratories utilize WNV antigen isolated from infected Vero cells or recombinant envelope protein produced in COS-1 cells. Recombinant antigen produced in COS-1 cells was used to develop a WNV IgM capture enzyme immunoassay (EIA). A supplementary EIA using WNV envelope protein expressed in Drosophila melanogaster S2 cells was also developed. Both assays detected WNV IgM in the sera of experimentally infected rhesus monkeys within approximately 10 days postinfection. Human sera previously tested for WNV IgM at a state public health laboratory (SPHL) were evaluated using both EIAs. Among the sera from 20 individuals with laboratory-confirmed WNV infection (i.e., IgM-positive cerebrospinal fluid [CSF]) that were categorized as equivocal for WNV IgM at the SPHL, 19 were IgM positive and one was negative by the new EIAs. Of the 19 IgM-positive patients, 15 were diagnosed with meningitis or encephalitis; the IgM-negative patient was not diagnosed with neurological disease. There was 100% agreement between the EIAs for the detection of WNV IgM. CSF samples from 21 individuals tested equivocal for WNV IgM at the SPHL; all 21 were positive in both bead assays, and 16 of these patients were diagnosed with neurological disease. These findings demonstrate that the new EIAs accurately identify WNV infection in individuals with confirmed WNV encephalitis and that they exhibit enhanced sensitivity over that of the microtiter assay format.


2009 ◽  
Vol 41 (1) ◽  
pp. 42-49 ◽  
Author(s):  
A. Petzold ◽  
M. Groves ◽  
A.A. Leis ◽  
F. Scaravilli ◽  
D.S. Stokic

2021 ◽  
pp. 177-180
Author(s):  
Michel Toledano

A 62-year-old woman sought care in late summer for a 4-day history of upper respiratory tract symptoms, intermittent fevers, headache, and a 1-day history of disorientation, word-finding difficulties, and unsteady gait. Upon arrival to the emergency department, she had a witnessed seizure and was intubated because of increased lethargy. Her temperature was 39.4 °C, but she was otherwise hemodynamically stable. She had normal ophthalmoscopic examination findings and antigravity strength in all 4 extremities. Her deep tendon reflexes were brisk, but plantar responses were flexor. She had no rash. Cerebrospinal fluid analysis showed a normal glucose value, protein concentration of 82 mg/dL, and mixed pleocytosis. She had been hiking recently, but her family reported that there were no tick exposures or mosquito bites. Brain magnetic resonance imaging showed areas of T2 fluid-attenuated inversion recovery hyperintensity involving primarily the left thalamus and basal ganglia without definitive gadolinium enhancement. Both serum and cerebrospinal fluid were positive for immunoglobulin M antibodies to West Nile virus. The patient was diagnosed with West Nile virus encephalitis. After the seizure, the patient was treated with levetiracetam, and empiric antimicrobials were started for acute meningoencephalitis, along with adjunctive dexamethasone. Continuous electroencephalography was obtained because of the persistent encephalopathy and showed no evidence of subclinical seizures. The dexamethasone was stopped after 2 doses because of low suspicion for pneumococcal meningitis, and the antibiotics were discontinued after results of serum and cerebrospinal fluid cultures were negative for bacteria (48 hours). Acyclovir was stopped after the polymerase chain reaction results were negative for herpes simplex virus and varicella-zoster virus.


2015 ◽  
Vol 53 (8) ◽  
pp. 2749-2752 ◽  
Author(s):  
Adam J. Gomez ◽  
Jesse J. Waggoner ◽  
Megumi Itoh ◽  
Seth A. Hollander ◽  
Kathleen M. Gutierrez ◽  
...  

The diagnosis of encephalitis is particularly challenging in immunocompromised patients. We report here a case of fatal West Nile virus encephalitis confounded by the presence of budding yeast in the cerebrospinal fluid (CSF) from a patient who had undergone heart transplantation for dilated cardiomyopathy 11 months prior to presentation of neurologic symptoms.


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