Arbovirus infections are caused by viruses transmitted through arthropod vectors such as mosquitoes and ticks. Diseases like dengue, Zika, chikungunya, and yellow fever pose global health risks. Prevention, surveillance, and nursing care are essential for outbreak control.
Introduction
Arboviruses, an acronym for arthropod-borne viruses, represent a diverse group of viruses transmitted primarily by blood-sucking arthropods such as mosquitoes and ticks. These viruses are responsible for significant morbidity and mortality across the globe, especially in tropical and subtropical regions. Arboviral infections are of particular public health concern due to their potential for causing outbreaks, their complex epidemiology, and the severe clinical manifestations they can induce, ranging from mild febrile illness to fatal encephalitis and haemorrhagic fevers.
Chikungunya
Pathogenesis
Chikungunya virus (CHIKV) is an alphavirus of the family Togaviridae, primarily transmitted by Aedes aegypti and Aedes albopictus mosquitoes. Upon entry via mosquito bite, the virus initially replicates locally in fibroblasts and endothelial cells before disseminating to the bloodstream (viraemia). It targets muscle, joint, and skin tissues, provoking a robust immune response. The pathogenesis involves both direct viral cytopathic effects and immune-mediated mechanisms, resulting in inflammation of joints and muscles, which accounts for the characteristic arthralgia.
Clinical Manifestations
The incubation period for Chikungunya ranges from 2 to 12 days. The disease typically presents with sudden onset of high fever, severe polyarthralgia (often symmetrical and affecting multiple joints), myalgia, headache, and rash. Arthralgia can be debilitating and may persist for weeks to months, occasionally leading to chronic arthritis. Other symptoms include nausea, vomiting, and conjunctivitis. Severe complications are rare but may occur in neonates, the elderly, and immunocompromised individuals.
Epidemiology
Chikungunya is endemic in Africa, Asia, and the Indian subcontinent, with periodic outbreaks reported in Europe and the Americas. The disease re-emerged in India in 2005 after a gap of over three decades, causing large-scale outbreaks. Factors such as urbanisation, increased travel, and vector adaptation have contributed to its resurgence. Outbreaks are more common during and after the monsoon season due to increased mosquito breeding sites.
Laboratory Diagnosis
Laboratory diagnosis of Chikungunya involves detection of viral RNA by reverse transcription polymerase chain reaction (RT-PCR) during the acute phase, or serological tests such as enzyme-linked immunosorbent assay (ELISA) to detect IgM and IgG antibodies in the convalescent phase. Virus isolation in cell culture is possible but not routinely performed due to biosafety concerns. Differential diagnosis includes dengue, Zika, and other febrile illnesses.
Kyasanur Forest Disease Virus (KFDV)
Pathogenesis
Kyasanur Forest Disease Virus is a member of the Flaviviridae family, transmitted primarily through the bite of infected hard ticks (Haemaphysalis spinigera). After entry, the virus replicates in dendritic cells and macrophages, disseminating to lymphoid tissues, liver, and bone marrow. The pathogenesis is characterised by direct viral cytopathic effects, vascular endothelial damage, and immune dysfunction, leading to haemorrhagic manifestations.
Clinical Manifestations
The incubation period is typically 3 to 8 days. KFD presents in two phases: the first phase is marked by high fever, severe headache, myalgia, vomiting, and gastrointestinal symptoms. Haemorrhagic features such as bleeding from the nose, gums, and gastrointestinal tract may develop. After a brief remission, a second phase may occur with neurological symptoms including mental confusion, tremors, and meningoencephalitis. Mortality rates range from 2% to 10%, with higher rates in untreated cases.
Epidemiology
KFD is endemic to the Western Ghats region of India, particularly in Karnataka, Kerala, Tamil Nadu, and Goa. The disease was first recognised in 1957 in Kyasanur Forest, Karnataka. Transmission occurs mainly during the dry season (January to May), coinciding with peak tick activity. Monkeys serve as amplifying hosts, and humans are accidental hosts, usually acquiring infection during forest activities.
Laboratory Diagnosis
Diagnosis is confirmed by RT-PCR for viral RNA or detection of specific IgM antibodies by ELISA. Virus isolation from blood is possible in specialised laboratories. Serological cross-reactivity with other flaviviruses can pose diagnostic challenges, making molecular methods preferable. Haematological findings may include leucopenia and thrombocytopenia.
Japanese B Encephalitis (JEV)
Pathogenesis
Japanese Encephalitis Virus, another member of the Flaviviridae family, is transmitted by Culex mosquitoes, particularly Culex tritaeniorhynchus. Following inoculation, the virus replicates in local tissues and regional lymph nodes before entering the bloodstream. It crosses the blood-brain barrier, causing neuronal infection, inflammation, and neuronal death, resulting in encephalitis. The host immune response contributes to both viral clearance and neuropathology.
Clinical Manifestations
The majority of JEV infections are asymptomatic. Symptomatic cases present after an incubation period of 5 to 15 days with non-specific febrile illness progressing to headache, vomiting, and signs of meningeal irritation. Severe cases develop altered sensorium, seizures, focal neurological deficits, and coma. Survivors may have persistent neurological sequelae. The case fatality rate ranges from 20% to 30% in symptomatic cases.
Epidemiology
JEV is endemic in South and Southeast Asia, including India, Nepal, Bangladesh, China, and Japan. Transmission peaks during the rainy season due to increased mosquito breeding. Pigs and water birds serve as amplifying and reservoir hosts, respectively, while humans are dead-end hosts. Large outbreaks are reported periodically, particularly in rural areas with paddy fields and pig farming.
Laboratory Diagnosis
Diagnosis is based on detection of JEV-specific IgM antibodies in serum or cerebrospinal fluid using ELISA. RT-PCR is useful in the early phase, though viraemia is often transient. Neuroimaging may show thalamic and basal ganglia involvement. Other causes of encephalitis must be excluded.
West Nile Encephalitis
Pathogenesis
West Nile Virus (WNV) is a flavivirus transmitted by Culex mosquitoes. Following infection, the virus replicates in dendritic cells and spreads to the bloodstream. In some individuals, WNV crosses the blood-brain barrier, leading to neuronal injury and inflammation. The pathogenesis is mediated by direct viral effects and immune-mediated mechanisms, resulting in encephalitis or meningitis.
Clinical Manifestations
Most WNV infections are asymptomatic. Around 20% of infected individuals develop West Nile fever, characterised by fever, headache, myalgia, arthralgia, and sometimes rash. Less than 1% progress to neuroinvasive disease, presenting with encephalitis, meningitis, acute flaccid paralysis, and, rarely, movement disorders. Elderly and immunocompromised individuals are at higher risk for severe disease and mortality.
Epidemiology
WNV is widely distributed in Africa, Europe, the Middle East, North America, and parts of Asia. The virus circulates in a bird-mosquito-bird cycle, with humans and horses as incidental hosts. Outbreaks are seasonal, peaking in late summer and early autumn. The emergence of WNV in North America in 1999 led to widespread epidemics and raised global awareness.
Laboratory Diagnosis
Diagnosis relies on detection of WNV-specific IgM antibodies in serum or cerebrospinal fluid by ELISA. RT-PCR can identify viral RNA during the acute phase. Cross-reactivity with other flaviviruses may complicate serological diagnosis. Neuroimaging and cerebrospinal fluid analysis support clinical diagnosis.
Yellow Fever
Pathogenesis
Yellow Fever Virus, a flavivirus, is transmitted by Aedes and Haemagogus mosquitoes. After inoculation, the virus replicates in lymph nodes and spreads to the liver, spleen, and bone marrow. Hepatocyte infection results in apoptosis, necrosis, and Councilman bodies on histology. The pathogenesis involves direct cytopathic effects, immune-mediated injury, and disruption of coagulation pathways, leading to jaundice and haemorrhagic manifestations.
Clinical Manifestations
Yellow fever has three phases: the initial phase with fever, chills, headache, myalgia, and nausea; the remission phase with transient improvement; and the toxic phase, which includes jaundice, renal dysfunction, bleeding, and shock. Haemorrhagic features such as epistaxis, gum bleeding, and gastrointestinal bleeding may occur. Case fatality rates can reach up to 50% in severe cases.
Epidemiology
Yellow fever is endemic in sub-Saharan Africa and tropical South America. Urban and sylvatic cycles involve different mosquito species and host animals. Outbreaks are associated with low vaccination coverage, increased vector populations, and movement of non-immune individuals into endemic areas. Effective vaccines have reduced the incidence but periodic outbreaks still occur.
Laboratory Diagnosis
Diagnosis is based on detection of viral RNA by RT-PCR or serological identification of specific IgM antibodies. Virus isolation is possible in specialised laboratories. Liver function tests reveal elevated transaminases and bilirubin. Differential diagnosis includes other causes of viral haemorrhagic fever and acute hepatitis.
Chikka Virus
Pathogenesis
Chikka Virus, though less widely recognised compared to other arboviruses, is believed to be transmitted by mosquitoes and follows a similar pathogenesis to other alphaviruses. Following inoculation, the virus replicates locally and then disseminates to various organs via the bloodstream. It primarily targets endothelial and immune cells, leading to inflammation and tissue injury.
Clinical Manifestations
Clinical presentation is characterised by fever, joint pain, rash, headache, and myalgia. The disease is generally self-limiting, but persistent arthralgia may occur in some cases. Severe complications are rare, but immunocompromised individuals may be at higher risk.
Epidemiology
Chikka Virus infection has been reported sporadically in certain regions of India and Southeast Asia. Outbreaks are often associated with monsoon seasons and increased vector density. The precise epidemiological patterns remain under investigation, and further research is needed to delineate its distribution and public health impact.
Laboratory Diagnosis
Laboratory confirmation is achieved through RT-PCR for viral RNA or serological detection of specific IgM antibodies. Cross-reactivity with other alphaviruses may complicate diagnosis. Virus isolation is not routinely performed due to biosafety concerns.
Key Differences and Similarities
| Infection | Family | Vector | Geographical Distribution | Key Clinical Features | Laboratory Diagnosis |
| Chikungunya | Togaviridae (Alphavirus) | Aedes mosquitoes | Asia, Africa, Americas | Fever, severe arthralgia, rash | RT-PCR, IgM/IgG ELISA |
| Kyasanur Forest Disease | Flaviviridae | Haemaphysalis ticks | India (Western Ghats) | Biphasic fever, haemorrhagic, neurological | RT-PCR, IgM ELISA |
| Japanese B Encephalitis | Flaviviridae | Culex mosquitoes | South, Southeast Asia | Encephalitis, seizures, coma | IgM ELISA, RT-PCR |
| West Nile Encephalitis | Flaviviridae | Culex mosquitoes | Worldwide | Fever, neuroinvasive disease | IgM ELISA, RT-PCR |
| Yellow Fever | Flaviviridae | Aedes, Haemagogus mosquitoes | Africa, South America | Jaundice, haemorrhage, renal failure | RT-PCR, IgM ELISA |
| Chikka Virus | Togaviridae (Alphavirus) | Mosquitoes | India, Southeast Asia (limited reports) | Fever, arthralgia, rash | RT-PCR, IgM ELISA |
Conclusion
Arboviral infections continue to pose significant challenges to public health systems, especially in tropical countries like India. Chikungunya, Kyasanur Forest Disease Virus, Japanese B Encephalitis, West Nile Encephalitis, Yellow Fever, and Chikka Virus each present unique clinical and epidemiological profiles, yet share commonalities in transmission dynamics and diagnostic approaches.
Early recognition, accurate laboratory diagnosis, and timely supportive care are critical for reducing morbidity and mortality. Vaccination programmes (available for Japanese Encephalitis and Yellow Fever), vector control strategies, and public health education remain the cornerstone of prevention. Ongoing research is essential to develop new diagnostics, therapeutics, and vaccines, and to understand the evolving epidemiology of these infections in the context of climate change and global mobility.
For clinicians and public health professionals, awareness of the distinguishing features and diagnostic challenges of arboviral infections is vital for effective management and outbreak control. Continued surveillance and investment in research infrastructure will be key to mitigating the impact of these formidable pathogens.
REFERENCES
- Apurba S Sastry, Essential Applied Microbiology for Nurses including Infection Control and Safety, First Edition 2022, Jaypee Publishers, ISBN: 978-9354659386
- Joanne Willey, Prescott’s Microbiology, 11th Edition, 2019, Innox Publishers, ASIN- B0FM8CVYL4.
- Anju Dhir, Textbook of Applied Microbiology including Infection Control and Safety, 2nd Edition, December 2022, CBS Publishers and Distributors, ISBN: 978-9390619450
- Gerard J. Tortora, Microbiology: An Introduction 13th Edition, 2019, Published by Pearson, ISBN: 978-0134688640
- Durrant RJ, Doig AK, Buxton RL, Fenn JP. Microbiology Education in Nursing Practice. J Microbiol Biol Educ. 2017 Sep 1;18(2):18.2.43. https://pmc.ncbi.nlm.nih.gov/articles/PMC5577971/
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