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RGUHS Nat. J. Pub. Heal. Sci Vol: 15  Issue: 4 eISSN:  pISSN

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Review Article
P S Shankar*,1,

1Dr. P S Shankar, Editor-in-Chief: RJMS, Emeritus Professor of Medicine, Rajiv Gandhi University of Health Sciences, Bengaluru and Distinguished Professor, KBN University, Kalaburagi, Karnataka, India.

*Corresponding Author:

Dr. P S Shankar, Editor-in-Chief: RJMS, Emeritus Professor of Medicine, Rajiv Gandhi University of Health Sciences, Bengaluru and Distinguished Professor, KBN University, Kalaburagi, Karnataka, India., Email: drpsshankar@gmail.com
Received Date: 2025-06-25,
Accepted Date: 2025-08-25,
Published Date: 2025-10-31
Year: 2025, Volume: 15, Issue: 4, Page no. 213-215, DOI: 10.26463/rjms.15_4_12
Views: 77, Downloads: 1
Licensing Information:
CC BY NC 4.0 ICON
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0.
Abstract

West Nile virus infection may present as encephalitis and is transmitted through the bite of an infected mosquito. Clinically, it is often indistinguishable from other causes of acute encephalitis syndrome. Since the condition is predominantly encountered in Kerala, where Japanese encephalitis and Nipah virus infections are also common, laboratory testing should include a viral panel for acute encephalitis syndrome. West Nile virus does not replicate in humans and is therefore not transmitted to other insects, birds, or persons.

<p><span style="font-size: 12.0pt; line-height: 115%; font-family: 'Calibri',sans-serif; mso-ascii-theme-font: minor-latin; mso-fareast-font-family: Calibri; mso-fareast-theme-font: minor-latin; mso-hansi-theme-font: minor-latin; mso-bidi-font-family: 'Times New Roman'; mso-bidi-theme-font: minor-bidi; mso-ansi-language: EN-US; mso-fareast-language: EN-US; mso-bidi-language: AR-SA;">West Nile virus infection may present as encephalitis and is transmitted through the bite of an infected mosquito. Clinically, it is often indistinguishable from other causes of acute encephalitis syndrome. Since the condition is predominantly encountered in Kerala, where Japanese encephalitis and Nipah virus infections are also common, laboratory testing should include a viral panel for acute encephalitis syndrome. West Nile virus does not replicate in humans and is therefore not transmitted to other insects, birds, or persons.</span></p>
Keywords
West Nile virus infection, Zoonotic flavivirus, Neuroinvasive disease, Acute encephalitis syndrome
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Introduction

Ten cases of West Nile Virus (WNV), a vector-borne disease, were reported from the districts of Kozhikode, Malappuram, Thrissur, and Ernakulum in Kerala, India, during the first week of May 2024. One death was reported in a 79-year-old man.1

Over a 12-year period from 2011 to 2023, 102 cases of WNV infection were reported in Kerala, with six deaths. The majority of cases occurred in 2011 (86 cases). The overall case fatality rate was 5.1%, with the highest rate observed in 2022 (33%).2

Aetiopathology

The disease is transmitted through the bites of Culex species mosquitoes carrying a zoonotic flavivirus. The virus is a single-stranded RNA virus and belongs to the Japanese encephalitis antigenic complex of the family Flaviviridae. Birds are the natural hosts, and mosquitoes become infected when they feed on infected birds. The virus is maintained in nature through a transmission cycle between birds and mosquitoes. West Nile Virus has been isolated from Culex vishnui mosquitoes in Andhra Pradesh and Tamil Nadu, from Culex quinquefasciatus mosquitoes in Maharashtra, and from humans in Karnataka.

Mosquitoes can transmit the virus to humans and horses accidentally. Climate change is one of many factors influencing the distribution and prevalence of vector-borne diseases. The virus does not spread through human-to-human contact. Infections are more common during the summer.

WNV was first reported in 1937 in a woman in the West Nile province of Uganda. Smithburn and colleagues recognized the neurotropic virus and named it as West Nile virus after the region of origin.3 It was detected in birds such as crows, doves, and pigeons in the Nile Delta region, in 1953. Subsequently, infections were reported in Africa, Middle East, North America, Australia, Venezuela, and West Asia. Notably, outbreaks have often occurred along major migratory bird routes. WNV fever made its appearance in Alappuzha district, Kerala, in 2011.4,5 In 2019, a six-year-old boy from Malappuram died of the infection, followed by the death of a 47-year-old man from Thrissur district in 2022. In 1952, Banker D in Mumbai (then Bombay) reported the presence of antibodies in patients against certain viruses, including West Nile Virus.6 Risbud and colleagues, in a post-epidemic serological survey for Japanese encephalitis (JE) virus antibodies conducted in South Arcot district of Tamil Nadu in 1991, also noted the presence of antibodies against WNV.7 Subsequent studies proved that WNV circulates in different parts of India.8,9 Virus activity has been documented across southern, central, and western parts of the country. In Kerala, the virus was first identified in Alappuzha in 2006 and later in Ernakulam in 2011. Balakrishnan and colleagues demonstrated a seroprevalence of Japanese encephalitis and West Nile virus of 37% in Alappuzha district, Kerala. In neighboring Karnataka and Tamil Nadu, serological studies revealed an incidence of nearly 50% for both viruses.10

The presence of WNV-neutralizing antibodies have been demonstrated in 20-30% human sera collected from the states of Tamil Nadu, Karnataka, Andhra Pradesh, Maharashtra, Gujarat, Madhya Pradesh, Odisha and Rajasthan.11

Clinical Features

WNV infection typically presents as a mild, self-limiting febrile illness. Most patients remain asymptomatic or exhibit a mild, flu-like illness characterized by fever, headache, muscular aches, anorexia, vomiting, diarrhoea, itching, arthralgia, dizziness, and impaired memory. A maculopapular rash on the trunk and lymphadenopathy may also occur. It should be noted that these symptoms are not observed in all patients. Generally, the symptoms begin after an incubation period of 3 and 14 days. Most individuals recover completely, although fatigue and weakness may persist for weeks or months in some cases. Rarely encephalitis may develop, resulting in unconsciousness and in some cases, death.12

The symptoms of WNV infection are similar to those of Japanese encephalitis (JE), although they are milder. In JE, symptoms are more severe, and death rate is high. JE primarily affects children, whereas WNV more commonly affects adults. Nearly 80% of infected persons remain asymptomatic, while about 20% develop fever and other flu-like symptoms. A small proportion may develop severe neuroinvasive disease, such as encephalitis, meningitis, or meningoencephalitis, presenting with headache, high fever, neck stiffness, stupor, disorientation, convulsions, muscular weakness, paralysis, and coma. These complications can lead to death or long-term disability.

Investigations

The diagnosis is confirmed by the demonstration of IgM antibodies in serum and cerebrospinal fluid (CSF). CSF examination may reveal elevated protein levels, and lymphocytic pleocytosis.13 Risk factors for the development of neurological disease include old age and immunosuppressive conditions such as solid organ transplantation or malignancy.12,13

Treatment

Treatment for WNV infection essentially focuses on alleviating symptoms and is primarily supportive, as no specific antiviral therapy is currently available. Supportive care includes adequate hydration and pain management. No vaccine exists at present. Preventive measures are therefore crucial. These include wearing protective clothing, application of mosquito repellants containing permethrin, and sleeping under mosquito nets. Care should be taken to keep the home and its surroundings clean and free from stagnant water. Mosquito control measures include eliminating breeding sites and applying larvicidal insecticides or pesticides to stagnant water. Picaridin-based insecticides can be applied to the skin and clothing.

Conclusion

WNF infection has emerged as a public health concern in Kerala. Outbreaks have been reported since 2011. The tropical climate, biodiversity hotspots of the Western ghats, extensive forest cover, multiple water bodies, and bird sanctuaries in Kerala provide ideal conditions for vector breeding and transmission of the virus. Strengthening vector control measures is essential to prevent further transmission.

Conflict of Interest

Nil

Financial Assistance

Nil

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References

1. West Nile fever cases detected in Kerala: What is the disease, how can it be prevented? The Indian Express. 2024 May 10 [cited 2024 Oct 5]. Available from: https://www.indianexpress.com

2. Directorate of Health Service, Kerala. Data on communicable diseases [Internet]. [cited 2024 Oct 5]. Available from: https://dhs.kerala.gov.in/en/ data-on-communicable-diseases/

3. Smithburn KC, Hughes TP, Burke AW, et al. A neurotropic virus isolated from the blood of a native of Uganda. Am J Trop Med Hyg 1940;20:471-492.

4. Anukumar B, Sapkal GN, Tandale BV, et al. West Nile encephalitis outbreak in Kerala, India 2011. J Clin Virol 2014;61:152-5.

5. Balakrishnan A, Butte DK, Jadhav SM. Complete genome sequence of West Nile virus isolated from Alappuzha district, Kerala, India. Genome Announc 2013;1(13):e00230-13.

6. Banker D. Preliminary observation on antibody patterns against certain viruses among inhabitants of Bombay City. Indian J Med Res 1952;6:733-746.

7. Risbud AR, Sharma V, Rao CV, et al. Post-epidemic serological survey for JE virus antibodies in South Arcot district (Tamil Nadu). Indian J Med Res 1991;93:1-5.

8. Gulati BR, Gupta AK, Kadian SK. West Nile virus infection among animals and humans in India. Adv Anim Vet Sci 2014;2(4S):17-23.

9. Khatun T, Chatterjee S. Emergence of West Nile virus in West Bengal, India: a new report. Trans R Soc Trop Med Hyg 2017;111(4):178-184.

10. Balakrishnan A, Thekkekare J, Sapkal J, et al. Seroprevalence of Japanese encephalitis virus & West Nile virus in Alappuzha district, Kerala. Indian J Med Res 2017;148(Suppl 1):S70-S76.

11. Paramasivan R, Muniaraj M, Kumar A. West Nile virus in India: An update on its genetic lineages. J Vector Borne Dis 2023;60(3):225-237.

12. Mostashari F, Bunning ML, Kitsutani PT, et al. Epidemic West Nile encephalitis, New York, 1999: results of a household-based seroepidemiological survey. Lancet 2001;358(9278):261-4.

13. Rea WJ, Patel KD. Reversibility of chronic disease and hypersensitivity. Volume 5. Treatment options of chemical sensitivity. Boca Raton: CRC Press; 2017. p. 699-700

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