CASE REPORT |
https://doi.org/10.5005/jp-journals-10081-1466 |
A Pediatric Case of Chandipura Virus Encephalitis: Clinical Presentation and Management during an Outbreak
1–4,6Department of Pediatrics, GMERS Medical College, Gandhinagar, Gujarat, India
5Department of Microbiology, BJ Medical College and Civil Hospital, Ahmedabad, Gujarat, India
Corresponding Author: Devesh N Joshi, Department of Pediatrics, GMERS Medical College, Gandhinagar, Gujarat, India, Phone: +91 9428388867, e-mail: dr.deveshjoshi91@gmail.com
Received: 28 August 2024; Accepted: 31 December 2024; Published on: 20 March 2025
ABSTRACT
Introduction: Chandipura virus (CHPV) is an emerging but underrecognized cause of acute encephalitis syndrome (AES), primarily affecting children in the Indian subcontinent. Typically, CHPV presents as a severe disease with high mortality, with nearly two-thirds of cases resulting in death.
Case description: This report highlights an atypical presentation of CHPV encephalitis in an 18-month-old male during a recent outbreak. The child presented with symptoms including high-grade fever, generalized pustular rash, abnormal behavior, and a single episode of generalized tonic-clonic seizures (GTCS). This case is particularly significant due to its mild course and the involvement of skin manifestations, which are uncommon in CHPV infections. Initial investigations revealed normal organ function and normal cerebrospinal fluid (CSF) analysis. The diagnosis was confirmed by positive CHPV serology in serum samples. The patient responded well to supportive care and was discharged after 12 days without further complications.
Discussion and conclusion: During the outbreak, six additional cases of suspected CHPV encephalitis were managed, with outcomes ranging from full recovery to fatal multiorgan failure, underscoring the virus’s typical severity. The unique presentation of this case contrasts with the usually fatal course of CHPV, emphasizing the variability in clinical manifestations and the importance of early diagnosis and management. This case highlights the need for awareness of CHPV, especially in regions where it is endemic, and calls for further research into the virus’s pathogenesis and clinical spectrum.
Keywords: Case report, Chandipura virus, Emerging infection, Viral encephalitis
How to cite this article: Joshi DN, Dantaliya U, Gandhi S, et al. A Pediatric Case of Chandipura Virus Encephalitis: Clinical Presentation and Management during an Outbreak. Pediatr Inf Dis 2025;7(2):65–67.
Source of support: Nil
Conflict of interest: None
Patient consent statement: The author(s) have obtained written informed consent from the patient’s parents/legal guardians for publication of the case report details and related images.
INTRODUCTION
Acute encephalitis syndrome (AES) is a clinical condition characterized by the rapid onset of fever and altered mental status, often accompanied by seizures.1 Despite extensive diagnostic efforts, the etiology of AES remains unidentified in the majority of cases.2 Among the known causative agents, the Chandipura virus (CHPV) has emerged as a significant yet underrecognized pathogen. Discovered in India in 1965, CHPV has not been as thoroughly studied as other viral agents, leaving many aspects of its epidemiology, pathogenesis, and clinical manifestations poorly understood.3
Chandipura virus has been implicated in numerous outbreaks and sporadic cases of acute encephalitis, primarily affecting children in the Indian subcontinent. The virus has also been detected in neighboring regions such as Bhutan, Nepal, and Sri Lanka, as well as parts of Africa. Significant outbreaks have been recorded in various Indian states, including Andhra Pradesh (2004, 2005, 2007, 2008), Gujarat (2005, 2009–2012), the Vidarbha region of Maharashtra (2007, 2009–2012), and Odisha (2015).3,5 Despite the high mortality rates associated with these outbreaks—ranging from 50 to 70% among affected children6—the CHPV remains relatively underexplored, with limited coverage in standard medical texts and a scarcity of scientific literature.
The concentration of CHPV outbreaks in specific geographic regions, coupled with its severe impact on pediatric populations, underscores the urgent need for further research and public health awareness. This case report presents a detailed account of a Chandipura serology-positive patient, along with a discussion of other suspected cases encountered during a recent outbreak, to contribute to the growing body of knowledge on this elusive pathogen.
CASE DESCRIPTION
An 18-month-old male child presented at a tertiary care center in the capital city of Gujarat, Gandhinagar, with a 2-day history of fever and skin rashes, followed by abnormal behavior for 1 day and convulsions. The fever was high-grade and intermittent. The skin lesions, which appeared as pustules, began on the 1st day of illness and were generalized, though few in number, affecting both the central part and the limbs.
One day prior to admission, the child exhibited abnormal behavior, irritability, and self-biting. The child experienced one episode of generalized tonic-clonic seizure (GTCS) lasting for 30 minutes and was brought to our hospital in status epilepticus. Immediate medical management was initiated.
On investigation, the child had a normal white cell count of 8,600 with 22% polymorphs and 66% lymphocytes. The child was anemic with a hemoglobin level of 8.8 gm/dL and a mean corpuscular volume (MCV) of 68 fL, suggestive of nutritional iron deficiency anemia. The platelet count was 2.54 lakhs/µL. Other organ function tests were normal, with serum glutamic pyruvic transaminase (SGPT) of 8.3 U/L, creatinine of 0.38 mg/dL, and urea of 20.7 mg/dL. Electrolytes were within normal range, with sodium at 134 mEq/L and potassium at 4.9 mEq/L.
The child was admitted to the pediatric intensive care unit (ICU) and started on antiepileptic drugs, ceftriaxone, and other supportive medical management. Cerebrospinal fluid (CSF) analysis done on the same day of admission revealed a glucose level of 59.5 mg/dL, protein of 62.8 mg/dL, and three cells (two lymphocytes and one neutrophil). The child was diagnosed with viral encephalitis and started on intravenous acyclovir. Other viral etiologies were investigated, including dengue, malaria, and chikungunya, all of which were negative.
Although the child had fever and rash, the history did not support a diagnosis of varicella. Consequently, CSF and serum samples, which were preserved, were sent to the National Virology Laboratory in Pune for detailed etiological and molecular studies. The results returned positive for CHPV serology with IgM positivity and negative for other serologies, including Japanese encephalitis (JE), herpes simplex virus (HSV), and polymerase chain reaction (PCR) of all pathogens, including JE, Chandipura, enterovirus, and HSV. Reverse transcription polymerase chain reaction (RT-PCR) for all viruses, including Chandipura, HSV, JE, and enterovirus, was negative.
The child improved with medical management. No further convulsions occurred after admission, although the fever persisted for 2 more days (a total of 4 days). On the 4th day of admission, despite the absence of classical signs of raised intracranial pressure (ICP), the child was started on intravenous mannitol due to persistent irritability and responded well, so it was continued and later stopped before discharge.
Magnetic resonance imaging (MRI) of the brain revealed hyperintensity in the bilateral frontoparietal and temporal lobes, as well as in the bilateral head of the caudate nucleus, without significant hypointensity on apparent diffusion coefficient (ADC) imaging, suggestive of viral encephalitis (Fig. 1).
Fig. 1: Altered signal intensity DWI hyperintensity involving bilateral frontoparietal and temporal lobes and head of bilateral caudate nucleus without any significant hypointensity on ADC
Considering the clinical and investigative findings, the absence of other possible etiological factors, and the positive Chandipura IgM in the context of an ongoing Chandipura encephalitis outbreak, the case was diagnosed as Chandipura encephalitis. The child was asymptomatic and discharged home after 12 days of admission.
Similar Cases
During the recent outbreak of Chandipura encephalitis in the Gujarat state, we managed a total of seven cases of AES over 2 weeks. The case reported above was one of these. Another patient in this series tested positive for dengue with NS1 and IgM and was managed as dengue encephalitis, unfortunately resulting in central nervous system (CNS) sequelae.
The remaining five patients were clinically diagnosed with viral encephalitis, but without laboratory evidence for dengue, malaria, or HSV. Bacterial cultures were negative, ruling out partially treated or atypical bacterial infections. Due to technical issues and financial constraints, enterovirus and JE screening were not performed in these cases. However, given the outbreak conditions and the positive Chandipura serology in the index case, these five cases were considered suspected Chandipura encephalitis.
Among these five, two patients had a grievous outcome. They presented on the same day of illness with high-grade fever, loose motions, and convulsions. Within 24 hours of symptom onset, both patients developed elevated SGPT levels, raised international normalized ratio (INR), prothrombin time (PT), and activated partial thromboplastin time (APTT), indicative of fulminant hepatic failure, and succumbed within 36 hours of illness onset.
Another two patients were mildly symptomatic and responded to supportive care, including mannitol for subtle signs of raised intracranial tension (ICT), and showed improvement within 2 days. However, one patient, who was admitted 48 hours after the onset of symptoms, deteriorated rapidly and died due to multiorgan failure on the 3rd day of admission and the 5th day of illness.
This cluster of cases highlights the variability in the clinical course of Chandipura encephalitis, ranging from mild, responsive cases to fulminant, rapidly fatal ones. The early identification and management of symptoms, along with supportive care, play crucial roles in improving patient outcomes. Additionally, the outbreak underscores the need for timely and comprehensive diagnostic resources to confirm etiological agents, which can be challenging during epidemic situations, particularly in resource-limited settings.
DISCUSSION
The reported case of an 18-month-old male presenting with fever, rash, abnormal behavior, and convulsions, leading to a diagnosis of CHPV encephalitis, provides valuable insights into the clinical presentation and challenges associated with this viral infection. CHPV, a member of the Rhabdoviridae family, has been recognized as a significant cause of AES outbreaks in various parts of India.3 The case aligns with the established clinical pattern observed in previous outbreaks, including high-grade fever, altered sensorium, and seizures.
In our case, the child presented with high-grade, intermittent fever lasting for 2 days, followed by abnormal behavior and convulsions, consistent with other reported cases where fever typically preceded neurological symptoms by 1–2 days. Similarly, in a study by Rao et al., 21 out of 104 suspected CHPV encephalitis cases exhibited high-grade fever lasting 2–3 days, with neurological manifestations developing shortly thereafter.7 Skin changes, observed as pustules in our patient, were noted in 12.5% of cases in Rao’s study, typically presenting as papular urticaria, predominantly on exposed parts of the body.
The diagnosis of Chandipura encephalitis was supported by positive CHPV serology in serum samples. This finding is consistent with earlier studies where serological and molecular assays, such as IgM ELISA and PCR, have been pivotal in confirming the diagnosis during outbreaks.3 In the study by Tandale et al., the diagnosis of Chandipura encephalitis in 25 out of 52 cases was confirmed either through virus isolation or serology, further highlighting the utility of these diagnostic tools during outbreaks.8
Our case report also mirrors the clinical variability and outcomes seen in CHPV infections. The index case and others in our series experienced a range of symptoms from mild to fulminant, with rapid progression in some patients leading to fatal outcomes. This variability is well-documented in the literature, with CHPV encephalitis showing a spectrum from mild illness to severe, rapidly fatal cases, as seen in previous outbreaks in Telangana and Andhra Pradesh.7,8
The presence of vesicular eruptions in our case also finds a parallel in the Gujarat outbreak, where similar lesions were reported, developing into hyperpigmentation upon healing.9 This underscores the importance of recognizing the diverse cutaneous manifestations that may accompany CHPV infections.
The seroprevalence of CHPV varies significantly across different regions in India, with studies reporting rates from 6% to as high as 89%.10 This raises questions about whether IgM seropositivity in some cases reflects true infection or merely underlying seroprevalence in the population. However, the acute clinical presentation, coupled with positive serology in the context of an ongoing outbreak, strongly supports the diagnosis of CHPV encephalitis in our reported cases.
CONCLUSION
This case report highlights the critical importance of recognizing CHPV as a potential cause of AES, particularly in regions where outbreaks have been previously documented. The reported case underscores the diverse clinical presentations, ranging from mild symptoms to rapidly fatal outcomes, associated with this viral infection. Early diagnosis and prompt initiation of supportive care are essential to improve patient outcomes. Additionally, the findings emphasize the need for robust public health surveillance and timely access to advanced diagnostic tools during outbreak situations to facilitate accurate identification and effective management of this underrecognized pathogen.
ORCID
Devesh N Joshi https://orcid.org/0000-0003-4375-4294
REFERENCES
1. Tandale BV, Narang R, Kumar GV, et al. Infectious causes of acute encephalitis syndrome India—decadal change and the way forwardin. Indian Pediatr 2023;60(9):709–713. DOI: 10.1016/j.jcv.2022.105194
2. Glaser CA, Honarmand S, Anderson LJ, et al. Beyond viruses: clinical profiles and etiologies associated with encephalitis. Clin Infect Dis 2006;43(12):1565–1577. DOI: 10.1086/509330
3. Sapkal GN, Sawant PM, Mourya DT. Chandipura viral encephalitis: a brief review. Open Virol J 2018;12:44–51. DOI: 10.2174/1874357901812010044
4. Ba Y, Trouillet J, Thonnon J, et al. Phlébotomes du Sénégal: inventaire de la faune de la région de Kédougou: isolements d’arbovirus. Bull Soc Pathol Exot 1999;92(2):131–135. DOI: 10.1371/journal.pone.0014773
5. Kemp GE. Viruses other than arenaviruses from West African wild mammals. Factors affecting transmission to man and domestic animals. Bull World Health Organ 1975;52(4–6):615–620. PMID: 1085217.
6. Acute encephalitis syndrome due to Chandipura virus—India. WHO. 2024. Available from: https://www.who.int/emergencies/disease-outbreak-news/item/2024-DON529.
7. Rao SN, Wairagkar NS, Mohan VM, et al. Brainstem encephalitis associated with Chandipura in Andhra Pradesh outbreak. J Trop Pediatr 2008;54(1):25–30. DOI: 10.1093/tropej/fmm078
8. Tandale BV, Tikute SS, Arankalle VA, et al. Chandipura virus: a major cause of acute encephalitis in children in North Telangana, Andhra Pradesh, India. J Med Virol 2008;80(1):118–124. DOI: 10.1002/jmv.21041
9. Chadha MS, Arankalle VA, Jadi RS, et al. An outbreak of Chandipura virus encephalitis in the eastern districts of Gujarat state, India. Am J Trop Med Hyg 2005;73(3):566–570. PMID: 16172482.
10. Sudeep AB, Gurav YK, Bondre VP. Changing clinical scenario in Chandipura virus infection. Indian J Med Res 2016;143(6):712–721. DOI: 10.4103/0971-5916.191929
________________________
© The Author(s). 2025 Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and non-commercial reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.