Imaging clues for an early diagnosis of Nipah encephalitis, a new epidemic alert—2021

Smilu Mohanlal; Sujith Janardhanan; Satish Kumar; Manjula Anand; EK Suresh Kumar; KG Ramakrishnan

doi:10.4103/pedc.pedc_8_23

CASE REPORT

Year : 2022 | Volume : 1 | Issue : 3 | Page : 64-66

Imaging clues for an early diagnosis of Nipah encephalitis, a new epidemic alert—2021

Smilu Mohanlal¹, Sujith Janardhanan², Satish Kumar³, Manjula Anand³, EK Suresh Kumar³, KG Ramakrishnan²
¹ Department of Adult and Paediatric Neurosciences, Aster Malabar institute of Medical Sciences, Kozhikode, Kerala, India
² Department of Radiology, Aster Malabar institute of Medical Sciences, Kozhikode, Kerala, India
³ Department of Pediatrics, Aster Malabar institute of Medical Sciences, Kozhikode, Kerala, India

Date of Submission	12-Mar-2023
Date of Acceptance	27-Jun-2023
Date of Web Publication	29-Aug-2023

Correspondence Address:
Dr. Smilu Mohanlal
Department of Adult and Paediatric Neurosciences, Aster MIMS, Kozhikode 673016, Kerala
India

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pedc.pedc_8_23

Abstract

We report an interesting case of viral encephalitis where neuroimaging and a careful clinicoepidemiologic correlation led to the diagnosis, and we could alert the public health facilities to take measures to contain the spread. A 12-year-old boy presented with fever, headache, photophobia, seizures, and altered sensorium. Magnetic resonance imaging brain revealed T2 FLAIR hyperintensities in bilateral cerebral hemispheres. The differential diagnoses considered were viral/bacterial/rickettsia encephalitis/vasculitis. He also had myocarditis and acute respiratory distress syndrome (ARDS). On careful observation of this triad of encephalitis, myocarditis, ARDS, and previous experience of Nipah encephalitis in North Kerala (Kozhikode), cerebrospinal fluid for Nipah virus isolation was sent and that was positive. Though the boy succumbed to ARDS, health authorities took measures such as quarantine measures, careful disposal of the body, and lockdown measures in the locality to curb the spread. This case report highlights the importance of careful clinicoradiologic epidemiologic correlation in unexplained encephalitis.

Keywords: Epidemic, imaging, Nipah encephalitis

How to cite this article:
Mohanlal S, Janardhanan S, Kumar S, Anand M, Suresh Kumar E K, Ramakrishnan K G. Imaging clues for an early diagnosis of Nipah encephalitis, a new epidemic alert—2021. Pediatr Companion 2022;1:64-6

How to cite this URL:
Mohanlal S, Janardhanan S, Kumar S, Anand M, Suresh Kumar E K, Ramakrishnan K G. Imaging clues for an early diagnosis of Nipah encephalitis, a new epidemic alert—2021. Pediatr Companion [serial online] 2022 [cited 2023 Oct 5];1:64-6. Available from: http://www.pediatriccompanionkerala.in/text.asp?2022/1/3/64/384600

Background

Nipah is a novel virus from paramyxovirus family. “Nipah” was first isolated from Sungei Nipah village in Negeri Sembilan.^[1] In 2001, Bangladesh experienced its first outbreak, and there have been three outbreaks in India since then, the last in Kerala in 2019. Transmission is via bats to pigs, pigs to humans, and humans to humans.^[2] We would like to share our experience in being vigilant in the early diagnosis of this deadly infection and how that helped in its containment.

Case presentation

A 12-year-old boy presented with a history of high-grade fever, headache, photophobia for 5 days, and generalized tonic-clonic status epilepticus on the day of admission. He was developmentally appropriate for age with no history of adverse perinatal events and comorbidities. Examination revealed a Glasgow coma scale score of 3/15 with tachycardia (heart rate: 180/min and blood pressure: 100/60 mmg) with no organomegaly/rashes. He was intubated in view of poor sensorium. The clinical diagnosis considered was acute encephalitis secondary to infection, vasculitis, or autoimmune pathology. He was investigated with magnetic resonance imaging (MRI) that revealed T2 FLAIR enhancing subcortical white matter hyperintensities in bilateral cerebral hemispheres with blooming in one lesion [Figure 1]. The imaging was suggestive of an infectious encephalitis versus vasculitis. Cerebrospinal fluid analysis was normal with sugar of 70 mg/dL, protein of 75 mg/dL, and no cells. Electroencephalogram showed multifocal spike and slow wave discharges with ictal rhythms. He was started on Midazolam infusion at 10 mcg/kg/min. He had raised cardiac troponin I of 1 ng/mL (normal range: 0–0.04 ng/mL) with normal serum electrolytes, and liver and renal function tests.

Figure 1: (A–C) FLAIR image shows discrete subcortical white matter hyperintensities in bilateral cerebral hemispheres, FLAIR contrast image show disseminated discrete predominantly subcortical enhancing lesions in bilateral cerebral hemispheres, and SWI images show blooming in one of these lesions

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With the clinical picture of myocarditis, encephalitis, and high-grade fever, the probable infectious agents considered were Enterovirus, West Nile virus, Dengue virus, and Rickettsial infections. He was started on ceftriaxone, acyclovir, azithromycin, and oseltamivir. His dengue serology (IgM) was negative and his throat swab for H1N1 was negative. Considering the previous experiences with Nipah encephalitis in Kozhikode (Northern part of Kerala) and the clinicoradiological corelate, CSF for Nipah virus (NiV) polymerase chain reaction (PCR) was sent and that was positive.

Outcome

On the day of admission, three children had worsening respiratory symptoms, and he succumbed to acute respiratory distress syndrome (ARDS). Timely diagnosis alerted the public health facilities in North Kerala to contain the spread of this deadly infection within the community.

Discussion

Though there are prior reports on this novel virus, we want to highlight the fact that in a child with high-grade fever, encephalitis, and myocarditis, a strong suspicion of NiV must be considered as the virus has a high case fatality rate of 91.3% (in the previous experience from Kerala).^[2] In the previous Kerala outbreak, fruit bats were suspected to be the source of infection and ingestion of bat-bitten fruits followed by human-to-human transmission leading to the spread of infection, whereas in the Malaysian outbreak, direct contact with infected pigs was identified, but unfortunately, we could not trace a source in our case. Other modalities of the spread of NiV in Bangladesh epidemics 2001 and 2007 were infected domestic cow consumption of date palm sap contaminated by bat secretions and human-to-human transmission.^[3],[4] The clinical manifestations of NiV include high-grade fever, headache, altered sensorium, hypertension, tachycardia, and segmental myoclonus; however, seizures were reported less commonly. The previous Kerala epidemic had both respiratory and neurological complications, the Malaysian epidemic had predominant neurological, whereas our case had neurological to begin with followed by ARDS leading to death.^[5] MRI forms an important diagnostic tool, the lesions described by Sarji^[6] and Lim et al.^[7] are small (2–7 mm) discrete high-intensity signal lesions disseminated throughout the cerebral hemisphere in the subcortical and deep white matter without a mass effect or cerebral edema, and these were attributed to the small vessel microinfarctions.^[6],[7]

Thrombocytopenia and raised aminotransferases found in about 60% of affected patients were poor prognostic markers. CSF analysis showed mildly elevated protein, and total counts and normal CSF were reported in 25% of symptomatic patients.^[8],[9] In the early stages of the disease isolation of the virus/reverse transcriptase PCR from throat/nasal swabs, urine, and blood, CSF is recommended, and during the convalescent phase, IgM and IgG antibody testing is used. NiV isolation in CSF was associated with an increase in mortality.^[10]

The differential diagnoses are Japanese encephalitis, rabies, dengue, measles, scrub typhus, leptospirosis, etc.^[10] Treatment is largely supportive. In a Malaysian outbreak between 1998 and 1999, ribavarin was given to 140 patients, and 45 (32%) deaths were seen with a 36% of reduction in mortality; however, a better medical care led to a decrease in mortality than the drug per se.^[10] Three patients who survived in 2018–2019 Kerala epidemic had received ribavarin in the early stages of the disease.^[11] The monoclonal antibodies m102.4 were found to be effective in the treatment of NiV in nonhuman primates but are under research for human use and were considered in the Kerala epidemic but were not used. Using standard precautions, hand hygiene and personal protective equipments (PPEs) remain the mainstay in preventing spread.

Learning points

In cases with encephalitis, myocarditis, and ARDS, the important differentials to be considered are Nipah, Dengue, Rabies, Measles, and Rickettsial infections.

Knowing the epidemiology of the region is important in arriving at the diagnosis.

Standard precautions such as using gloves, PPE, and isolation are mandatory while treating suspected infectious encephalitis cases, and these measures did help us to contain the spread within the intensive care.

Acknowledgements

The authors would like to thank Dr. Ramalingam Trivikraman.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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