The Nipah virus, a new threat amid the COVID-19 outbreak has caused worry in the southern states of India as the zoonotic disease presents with similar symptoms. This article spells out the epidemiology, transmissibility, symptoms, investigation and treatment therapies for the Nipah virus.

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Recently a 12-year-old child afflicted with the Nipah virus died at a private hospital in Kozhikode. The child had encephalitis and myocarditis, which are both inflammations of the brain and heart muscles. In Kerala, the recent reappearance of the Nipah virus has added a new threat, since it follows on the heels of the COVID-19 epidemic, which is causing more than 60% of all new cases in the nation right now. However, the Nipah virus has already been identified in Kerala and elsewhere in India, and past outbreaks have stayed mainly localised and been controlled rather swiftly.

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What does the Nipah virus entail?

Nipah virus is a zoonotic disease that has spread across Asia-Pacific. This is a family of RNA viruses known as the Paramyxoviridae. They are classified under the name Henipavirus.

Nipah virus infection epidemiology

Nipah virus was first identified when it caused an epidemic of viral encephalitis among Malaysian pig breeders. The virus was called for the town in which the afflicted patient resided in Malaysia. Since then, numerous outbreaks of acute Nipah encephalitis have occurred in different areas across Bangladesh, in India's adjacent district of Siliguri, and in the southern Philippines. In May 2018, the Indian state of Kerala reported an epidemic.

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How is the Nipah virus transmitted?

Reservoir animals

1. The main reservoir animals for henipaviruses are bats of the genus Pteropus. Nipah virus infection has been detected in 23 bat species belonging to ten genera in China's Yunnan and Hainan Islands, Cambodia, Thailand, India, Madagascar, and Ghana in West Africa.
2. Other animals may act as a virus's intermediary host. In the Malaysian epidemic, for example, they were pigs. Transmission between pigs occurred most often through direct contact with contaminated fluids such as urine, saliva, pharyngeal, and bronchial secretions.
3. Domestic animals such as cats and dogs also tested positive for Nipah virus serology.
4. Horses were believed to be the intermediary hosts in the Philippines epidemic.
5. It is a zoonotic virus, which means it has spread from animals to humans. The disease is spread mostly via the eating of contaminated food. However, transfer from human to human is also believed plausible. The fruit bat, often known as the flying fox, is believed to be the virus's animal host reservoir. Fruit bats have been seen transmitting this virus to various species including pigs, dogs, cats, goats, horses, and sheep.

Humans get infected mostly via direct contact with these animals or by the ingestion of food contaminated with their saliva or urine. Although person-to-person transmission has not been proven conclusively, recent research concluded that past outbreaks in Bangladesh, the Philippines, and India indicated that- respiratory droplets of an infected individual may spread the virus. Previously, anyone in close touch with an infected person, mostly hospital personnel and caretakers, acquired the illness.

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Symptoms of Nipah virus infection 

1. The incubation period is between seven and forty days. The first presentation is non-specific, with symptoms such as fever, headache, myalgia, nausea, and vomiting occurring suddenly. Meningismus occurs in around a third of individuals, although severe nuchal stiffness and photophobia are rare.
2. Patients in the Kerala and Bangladesh epidemics also reported respiratory symptoms and abnormal chest radiographs. Myocardial involvement (as shown by ECG alterations), left ventricular hypokinesia and increased troponin I levels have also been observed in Kerala.
3. Nipah virus is mainly associated with an encephalitic condition associated with a high death rate. Malaysia had a death rate of about 30% to 40% while Bangladesh had a mortality rate of more than 70%. In 2018, an epidemic in Kerala, India, resulted in the identification of 23 cases, with just two people surviving (case fatality rate of 91%).
4. Around 60% of patients develop the illness quickly, with loss of consciousness progressing to coma within five to seven days. Around 20% of individuals have generalised seizures. Additionally, Nipah encephalitis is linked with segmental myoclonus (mostly affecting the diaphragm, upper limb, and neck muscles), cerebellar dysfunction, tremors, and areflexia.
5. Brainstem involvement is more common in severe instances and is associated with pinpoint, unresponsive pupils, aberrant doll's eye reaction, tachycardia, and hypertension.
6. Certain individuals were diagnosed with relapsing encephalitis, which manifested as repeated bouts of neurological impairment. Additionally, a small number of individuals who were initially asymptomatic or had moderate non-encephalitic illness acquired late-onset neurological diseases.
7. Fever, headache, convulsions, and focal neurological symptoms were observed in these individuals. 18% of participants died. MRI scans revealed significant patchy, confluent lesions that were not present at the time of the original diagnosis.
8. Persistent tiredness and daytime somnolence were often reported as debilitating symptoms in long-term survivorship studies. Additionally, functional neurologic impairment was prevalent.

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Investigations 

Nipah encephalitis often exhibits nonspecific laboratory abnormalities. Although leukocyte counts are often normal, mild thrombocytopenia may develop. Although liver transaminases were mild to moderately increased, clinical jaundice was not a symptom of the disease.

In the majority of cases, abnormalities in the cerebrospinal fluid (CSF) were detected. The majority showed an increased white blood cell count (ranging from 10 to 800 cells/mm3), with a lymphocyte predominance, and an elevated protein content (ranging from 50 to 250 mg/dL). The glucose level in the CSF was normal, and red blood cells were often absent.

Neuroimaging

Magnetic resonance imaging (MRI) is a helpful technique for diagnosing Nipah encephalitis, but it does not differentiate it from another viral encephalitis. Multiple, tiny (less than 5 mm), asymmetric focal lesions in the subcortical and deep white matter without surrounding oedema are the typical MRI abnormalities.

These lesions are most likely micro-infarction sites that have been identified on histology. There is no connection between the results of magnetic resonance imaging and localised neurological symptoms. The electroencephalogram (EEG) reveals continuous, diffuse slow waves with or without intermittent, abrupt, wave discharges that are seen in bitemporal locations.

The reference standard for diagnosing Nipah virus infection is the presence of serum neutralising antibodies against Nipah virus in the patient's serum. However, since Nipah virus is designated as a biosafety category 4 agent, viral isolation is not performed regularly.

As a result, other techniques such as serology or polymerase chain reaction are increasingly often used. The new approach of using neutralisation tests on pseudotyped viruses expressing Nipah virus glycoproteins may allow for the omission of live viruses.

Enzyme-linked immunoassay

An enzyme-linked immunoassay may be used to diagnose Nipah virus infection (ELISA). Both an IgM capture ELISA and an indirect IgG ELISA have a good diagnostic specificity. Rapid immunological plaque assays have been devised for the quantification of Hendra and Nipah viruses and for the detection of neutralising antibodies against both viruses.

Polymerase chain reaction (PCR) and sequencing techniques are becoming more accessible. Diagnostic polymerase chain reaction (PCR) tests are regularly employed at the Australian Animal Health Laboratory and the Centers for Disease Control and Prevention in the United States (CDC). These assays may be employed to identify viral sequences in fixed or fresh tissue or CSF diagnostic specimens, or as a complement to the fast characterisation of viral isolates from cell culture.

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Therapy and prophylaxis of Nipah virus infection 

1. The majority of treatment is supportive care, and individuals who are infected may need intensive care monitoring.
2. Mechanical ventilation for airway protection should begin as soon as neurologic impairment is detected.
3. There is no evidence that antiviral therapy is helpful against Nipah virus infection.
4. Ribavirin, a nucleoside analogue, has generated some attention. While ribavirin has been shown to be ineffective in animal models, preliminary human trials indicate that it may have some advantages. During the Malaysian epidemic, 140 patients who received ribavirin were compared to 54 patients who did not get ribavirin, and the treated patients died at a lower rate (32 vs 54 per cent). Two of the six patients who got ribavirin survived in a case series of 12 patients from Kerala, while the six patients who were not treated all died. The efficacy of ribavirin in the management of Nipah virus infection remains unknown until more data are available.
5. Educating at-risk people about illness transmission is one method of prevention. To minimise the danger of bat-human transmission, people should be encouraged to avoid raw palm sap that may be contaminated, although this may be challenging and needs respect to indigenous traditions and beliefs.
6. Individuals managing ill animals or their tissues should wear gloves and other protective gear, and prevent close unprotected physical contact with patients who have Nipah virus infection.
7. Medical professionals who deal with patients with suspected or known infection, or manage their specimens, should follow normal infection control measures, as well as contact and droplet prevention.
8. The development of a vaccine against Nipah virus infection is still in the preclinical stage.

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Is Nipah as contagious as COVID-19?

During the most recent epidemic in Kerala in 2018, 17 of the 18 confirmed cases of infection resulted in death. In Ernakulam in 2019, one case of Nipah virus infection was discovered, however quick treatment prevented further spread. The afflicted individual lived.

According to a study published in the April 2020 issue of the journal Viruses, a total of 265 people were infected during the 1999 Malaysian outbreak, with 105 deaths, according to a study titled 'Nipah Virus: Past Outbreaks and Future Containment' by researchers from Cochin University of Science and Technology. In contrast, the COVID-19 pandemic is anticipated to have a death rate of about 1%.

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Is it necessary for other states to be concerned about the spread of Nipah?

Until far, all Nipah virus outbreaks have been controlled swiftly, at least in contrast to the current COVID-19 epidemic. The initial epidemic in Malaysia occurred in September 1998, but it was not until March of the following year that scientists were able to establish that they were dealing with a novel virus.

By May, the epidemic had been controlled. In Bangladesh, the country with the most recurring Nipah outbreaks, transmissions ceased after a few months. One of the primary reasons for a relatively fast conclusion to an epidemic is that Nipah virus is much less infectious than, say, SARS-CoV-2. Human-to-human transmission is neither as simple nor as rapid as SARS-CoV-2 transmission. With COVID-19 guidelines currently in place, there is a greater understanding of viral illness transmission.

According to a recent study, the reproductive number (R0) in past Nipah virus epidemics was around 0.48. The R-value indicates the rate at which a virus spreads within a population. A number less than one indicates that less than one individual is being infected by an already infected individual. The epidemic is anticipated to subside rather soon in this situation.

Additionally, the research adds that since Nipah outbreaks have occurred mostly in sparsely inhabited areas, the virus's ability to spread to a large number of people has been limited. Additionally, the very high mortality rates contribute to the poor transmission rate.

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Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.

The author is a practising super specialist from New Delhi.