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Year : 2019  |  Volume : 21  |  Issue : 2  |  Page : 104-107

A case of West Nile virus and tuberculosis coinfection

Department of Medicine, Government Medical College, Calicut, Kerala, India

Date of Submission20-Apr-2019
Date of Decision03-Jun-2019
Date of Acceptance19-Jun-2019
Date of Web Publication13-Dec-2019

Correspondence Address:
Dr. P V Shiji
Department of Medicine, Government Medical College, Calicut, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jomt.jomt_13_19

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Tuberculous meningitis is a common differential diagnosis in tropical countries when a patient presents with prolonged fever, headache, and cranial nerve palsies. But here is a patient who presented with a short duration history but other clinical features and investigations strongly supported the diagnosis of tuberculous meningitis. What makes the case all the more interesting is that her blood investigations revealed a strongly positive test for West Nile virus infection. So the patient has tuberculous meningoencephaltis with West Nile virus coinfection, which has been rarely reported till date.

Keywords: fever; headache, tuberculousmeningitis, westnile virus co-infection

How to cite this article:
Shiji P V. A case of West Nile virus and tuberculosis coinfection. J Med Trop 2019;21:104-7

How to cite this URL:
Shiji P V. A case of West Nile virus and tuberculosis coinfection. J Med Trop [serial online] 2019 [cited 2023 Feb 6];21:104-7. Available from:

  Introduction Top

West Nile Virus infection is a rare infection in this part of the world. It can present in various clinical forms ranging from meningoencephalitis to multiple cranial palsies and quadriparesis. Tuberculous meningitis is one of the commonest differential diagnosis of a patient with prolonged fever, headache and cranial nerve palsies.

  Case report Top

A 24-year-old female, housewife with no known comorbidities, presented with a history of headache and neck pain followed by high-grade fever and recurrent episodes of tonic posturing with frothing from mouth that was present for the previous 7 days. Her sensorium progressively deteriorated from day 1 of fever, and at presentation, she was bedridden. She used to have about two episodes of seizures per day and had status epilepticus on the day of admission. After 2 to 3 days of fever, she developed drooping of right eye followed by other in 3 days. She was unable to open her eyes at presentation to our hospital. She also had multiple episodes of vomiting.

She had no history of any respiratory or gastrointestinal symptoms. There was no recent travel history outside Kerala. There was no history suggestive of connective tissue disorder, no similar illness in neighborhood, and no significant past and menstrual history. She belonged to low socioeconomic class. Her father had died of tuberculosis 3 years before.

On reaching the casualty, she was drowsy with a glassgow coma scale (GCS) of E1V2M5, blood pressure of 140/90 mmHg, and pulse rate (PR) of 120/’ regular; on auscultation, chest had bilateral conducted sounds and cardiovascular system was within normal limit. She had bilateral ptosis and her pupils were equally dilated, not reacting to light. She had one episode of ongoing focal seizure of left upper limb. Neck stiffness and Kernig sign were present. All four limbs were hypotonic and hyporeflexic. Plantar was bilaterally flexor.

Differential diagnosis thought at this point were acute meningoencephalitis, either viral or bacterial, tubercular meningitis, cerebral malaria, and remote possibility of brain abscess.

She was started on ceftriaxone, vancomycin, acyclovir, antiedema measures, and other supportive measures after lumbar puncture (LP) study. Meanwhile, a computed tomography (CT) of the head was done that showed hyperdense area with surrounding hypodense area with increased vascularity in right frontoparietal lobe [Figure 1].
Figure 1: CT head showing hyperdense area with surrounding hypodense area with increased vascularity in right frontoparietal lobe. CT, computed tomography.

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Her routine complete blood count, renal and liver function tests were normal except for an elevated Erythrocyte Sedimentation Rate of 66 mm/hr ([Table 1]). Her cerebrospinal fluid examination revealed a high protein of 390 mg/dl and a low sugar level of 12 mg% (corresponding blood sugar was 25 mg%). CSF adenosisine deaminase levels was 9.8U (normal-<11U). The CSF cell revealed no cells.
Table 1: Blood Investigations

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Considering the history and examination findings and investigations revealing a high CSF protein with lymphocytic predominance, and CT study of head revealing a hyperdense lesion, the patient was started on empirical antituberculous treatment with steroids strongly suspecting the possibility of tuberculosis due to its high prevalence in our country, although the presentation was acute. A magnetic resonance imaging of the brain was also done that showed tuberculous meningitis with vasculitis and secondary hemorrhagic cortical infarct [Figure 2].
Figure 2: MRI brain with tuberculous meningitis with secondary hemorrhagic infarct. MRI, magnetic resonance imaging.

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Her Mantoux test was negative. She was also screened for collagen vascular diseases and antiphospholipid antibodies rapid malarial antigen that were all negative. Blood and urine culture and sensitivity came out to be sterile.

Disseminated tuberculosis was primarily ruled out with a normal chest X-ray and ultrasound of the abdomen.

At the same time, her CSF viral panel report arrived from Central Institute of Virology, Pune. Her serum was positive for plaque reduction neutralization test for West Nile virus (WNV) infection that was repeated twice.

She was continued on antituberculous treatment (ATT) and acyclovir and steroids. She gradually regained consciousness with reduced tachycardia, but her pupils were bilaterally dilated and nonreacting and she also had complete ophthalmoplegia. Other cranial nerves were normal. Her limbs remained to be hypotonic with grade 4/5 power in upper limbs and lower limbs, deep tendon reflexes sluggish, and plantar bilateral flexor. Fundus examination showed no evidence of papilledema.

A repeat LP was done on day 15 that showed a total cells of 270, 100% lymphocytes, and a high protein (900 mg%), low sugar (42 mg%), and a high adenosine deaminase (36); CSF GeneXpert was negative for Mycobacterium tuberculosis. But GeneXpert is low sensitive in CSF, hence the patient was continued on antituberculous treatment in view of the strong clinical suspicion.

By day 21 she became conscious and afebrile. She had started taking oral feeds.

As the clinical picture was strongly in favor of tuberculous meningitis and since WNV infection has no definitive treatment, she was continued on ATT and steroids. She was under constant follow-up and 2 months later, her ptosis disappeared and she was asymptomatic. Hence, the final diagnosis was tuberculous meningitis with WNV coinfection.

  Discussion Top

Tuberculous meningitis is very common in developing countries like India and it mimics any other chronic meningoencephalitis with its wide variety of clinical presentations. Rapid diagnosis and treatment is crucial in tuberculous meningitis. Diagnosis is mainly clinical with corroborative findings on CSF examination as well as imaging of brain. Here the clinical presentation was that of an acute meningoencephaltis but the clinical findings and CSF and imaging findings were in favor of tuberculous meningitis.[1]

WNV is a mosquito-borne disease. WNV is commonly found in Africa, Europe, Middle East, North America, and West Asia. The virus belongs to Flavi virus genus. Human infection is from infected mosquitos who get infected when they feed on infected birds. Members of the crow family are particularly susceptible.[2] They are mainly maintained in a mosquito–bird–mosquito cycle and human infections are dead ends. Culex mosquitos mainly spread the infection. Most WNV infections are symptomless. The incubation period is 12 to 14 days. One in 150 infected patients will develop a fatal infection and encephalitis.[3] WNV encephalitis presents as high-grade fever followed by signs of meningitis and encephalitis. Rare neurological manifestations include myelitis, optic neuritia, and polyradiculitis. The clinical picture of our patient although initially mimicked encephalitis, the bilateral ptosis, the CSF picture with high protein, and the magnetic resonance imaging were all favouring tuberculous meningitis. The patient initially received 2 weeks of antiviral therapy (acyclovir) and antibiotics along with antituberculous medication and steroids. The patient showed dramatic improvement and ptosis improved completely after 2 months of ATT.

A positive plaque reduction neutralization test is considered to be a gold standard for acute WNV infection. The plaque reduction neutralization test is used to quantify the titer of neutralizing antibody for a virus. The concentration of serum to reduce the number of plaques by 50% compared to the serum-free virus gives the measure of how much antibody is present or how effective it is.[4] Hence, the patient definitely had WNV infection but as the rest of the clinical picture was suggestive of tuberculous meningitis, the final conclusion was that the patient was having tuberculous meningitis with WNV coinfections.[5] WNV was considered to be the cause of acute encephalitis syndrome in Assam as early as 2006. A West Nile encephalitis outbreak leading to three deaths occurred in Alappuzha district of Kerala in 2017.[6] So far, no case has been reported from this part of Kerala. So probably this is the first reported case from Kozhikode district. More surveillance has to be done to find out asymptomatic infections in the community. Henceforth, WNV infection has to be one of the differential diagnosis in all cases of acute encephalitis syndromes from this part of Kerala.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Thwaites GE, Tran TH. Tuberculous meningitis: many questions, too few answers. Lancet Neurol 2005;4:160-70.  Back to cited text no. 1
Tsai TF, Popovici F, Cernescu C, Campbell GL, Nedelcu NI, for the Investigative Team. West Nile encephalitis epidemic in southeastern Romania. Lancet 1998;352:767-71.  Back to cited text no. 2
O’Leary DR, Marfin AA, Montgomery SP, Kipp AM, Lehman JA, Biggerstaff BJ et al. The epidemic of West Nile virus in the United States, 2002. Vector Borne Zoonotic Dis 2004;4:61-70.  Back to cited text no. 3
Schmidt NJ, Dennis J, Lennette EH. Plaque reduction neutralization test for human cytomegalovirus based upon enhanced uptake of neutral red by virus-infected cells. J Clin Microbiol 1976;4:61-6.  Back to cited text no. 4
Mackenzie JS, Gubler DJ, Petersen LR. Emerging flaviviruses: the spread and resurgence of Japanese encephalitis, West Nile and dengue viruses. Nat Med 2004;10(12s):S98-109.  Back to cited text no. 5
Khan SA, Dutta P, Khan AM, Chowdhury P, Borah J, Doloi P et al. West Nile virus infection, Assam, India. Emerg Infect Dis 2011;17:947-8.  Back to cited text no. 6


  [Figure 1], [Figure 2]

  [Table 1]


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