West Nile Virus (WNV) is a member of the Japanese Encephalitis antigenic complex and can lead to a wide range of clinical symptoms, from asymptomatic disease to severe meningitis and encephalitis.
West Nile Virus is the leading cause of mosquito-borne disease in the continental United States.2 This case report examines a case of headache, weakness, and gait ataxia in a 63-year-old male, with the resulting diagnosis being West Nile Virus encephalitis.
The presentation of West Nile Virus ranges from asymptomatic disease to severe meningitis or encephalitis and even death. Approximately 25% of individuals infected develop a fever, and only 1 in 150-2501 patients develops neuro-invasive disease. Risk factors for developing neurological manifestations include age, malignancy, organ transplantation, and other genetic factors.2 WNV is most commonly spread to people by a bite of an infected mosquito, with a peak of cases occurring in summer and autumn. According to the CDC, the majority of cases in the U.S. are reported in South Carolina, Virginia, Delaware, California, and Arizona. This case report is a 63-year-old male in Philadelphia who was presumed to have WNV encephalitis and was documented as the second case in this region during the 2020 season.1
A 63-year-old male with past medical history of HTN, HLD, and Type II DM presented to the ED for a 5-day history of headaches, fever (Tmax of 102°F), decreased oral intake, and unsteady gait. He did not experience falls, loss of consciousness, or known COVID-19 exposures. He lives at home with his wife and his granddaughter, both of whom are feeling well. Of note, he states he is an avid outdoorsman and enjoys camping, hiking, and doing work outside around his home, which he has been doing a lot of in the past few weeks. He smokes 1 PPD, denies alcohol use and other non-prescription drug use, or any high-risk sexual activity.
Upon arrival to the ED, vital signs were significant for tachycardia to 102, a mild fever of 100.7°F, oxygen saturation of 97% on room air, respiratory rate of 20, and a BP of 169/83. His physical exam revealed bilateral paraspinal tenderness, full ROM of the head and neck with mild pain, a positive Brudzinski sign, mild ataxia with an otherwise non-focal neurological examination, and a blanchable petechial rash on the bilateral hands and palms. The remainder of his physical exam was unremarkable.
EKG performed in the ED was normal sinus rhythm with no concerning ST changes or T-wave abnormalities. Chest x-ray showed no signs of acute processes. CT of the brain showed no hemorrhage or signs of ischemia. Initial laboratory studies were pertinent for a leukocytosis of 18.9 with a neutrophil predominance, a venous lactate of 2.6, and hyperglycemia to 226, but otherwise grossly unremarkable.
Due to concern for meningitis and encephalitis a lumbar puncture was performed. An opening pressure was unavailable but per emergency physician documentation tube #1 was grossly purulent and yellow with no signs of blood. Tube #4 had 9 RBCs, 184 WBCs – 57% segs, 28% lymphocytes, 5% monocytes, 0% eosinophils. Other remarkable studies were as follows: elevated CSF glucose of 115, elevated CSF protein of 84, CSF culture showing rare WBCs and no organisms.
The patient was started on broad spectrum antibiotics and antivirals including ceftriaxone, vancomycin and acyclovir. Due to the patient’s history and physical exam, which included outdoor activities, gait ataxia and other meningeal signs, in addition to a recent WNV case in Bucks County, Pennsylvania, WNV Ab IgM PCR was sent along with additional viral testing.
Throughout the hospital stay, infectious disease was consulted and discontinued ceftriaxone as they determined a bacterial cause was unlikely. In addition, they added Lyme antibodies IgM and IgG. COVID-19 PCR was negative and blood culture showed no growth. Over the next 4 days, the patient clinically improved. Lyme antibodies and HSV PCR were both negative, so the acyclovir was discontinued. The patient was discharged 4 days after admission with WNV studies pending. One day after discharge, the WNV Ab IgM resulted positive at 4.21 with a reference range of <0.90. The positive result was reported to the patient and to the Pennsylvania Department of Public Health and was documented as the second case of WNV encephalitis in the Philadelphia region of the 2020 season.
There have been case reports of West Nile Virus infection and its clinical syndromes since its first case in 1937;3 however, this case is rare for two reasons: the location of the patient that was infected and the symptoms that brought the patient to the Emergency Department.
Regarding location, Pennsylvania and Philadelphia in particular are not typical regions for WNV infection. Per the Pennsylvania Department of Public Health, there had only been one diagnosed human case of WNV in the Philadelphia area since tracking started in May 2020. This is either due to patient’s having asymptomatic disease and not seeking testing, having symptomatic disease that goes unrecognized, or safe practices when doing outdoor activities that would subject them to mosquito encounters and possible infection.
Our patient also had an atypical presentation of WNV encephalitis. He did present with the typical fever, headache, meningeal signs, and anorexia; however, the presenting symptom of unsteady gait is atypical of this disease, concerning for cerebellar involvement. Common neurological manifestations of disease include coarse tremor, myoclonus particularly in the upper extremities, and parkinsonian features such as rigidity, postural instability, and bradykinesia. Other common manifestations include acute flaccid paralysis resulting from disruption of anterior horn cells. Less common neurologic manifestations of WNV include cranial nerve palsies, vertigo, dysarthria, seizures, cerebellar ataxia, and dysphagia.
As discussed, WNV can present with a wide array of clinical signs and symptoms, some rarer than others. This case offers a few lessons for physicians. First, it is our job as Emergency Department physicians to be aware of all local and regional outbreaks of mosquito-borne or other insect-borne illnesses and consider this in patients presenting with fever and headache. This case also illustrates the importance of a broad differential diagnosis especially during the COVID-19 pandemic. The emergency physician had seen multiple patients presenting with symptoms of COVID-19 in their shift that day and initially favored COVID-19 as a diagnosis. The patient’s complaint of unsteady gait was concerning and prompted further evaluation for encephalitis, resulting in lumbar puncture and avoidance of premature closure bias. In the absence of an effective human vaccine, WNV disease prevention depends on community-level mosquito control and household and personal protection measures.4
- West Nile virus. (2020, June 3). Centers for Disease Control and Prevention. Centers for Disease Control and Prevention.
- Peterson, L. (2020, August 7). Clinical manifestations and diagnosis of West Nile virus infection. UpToDate.
- Peterson, L. (2020, February 24). Epidemiology and Pathogenesis of West Nile virus infection. UpToDate.
- Lindsey NP, Staples JE, Lehman JA, Fischer M; Centers for Disease Control and Prevention (CDC). Surveillance for human West Nile virus disease - United States, 1999-2008. MMWR Surveill Summ. 2010 Apr 2;59(2):1-17. Erratum in: MMWR Surveill Summ. 2010 Jun 18;59(23):720. PMID: 20360671.
- West Nile Virus - Health Statistics A to Z. (n.d.). Department of Health Data . Department of Health.