Mode of Spread:

Transmission of Nipah virus takes place through direct contact with infected bats, pigs, or from other NiV-infected people (Figures 2 & 3).

When Nipah Virus was First Identified?:

Nipah virus was first identified in Kampong Sungai Nipah, Malaysia in 1998.

Nipah Virus first Incidence:

a. In India, Nipah Virus affected the humans without any involvement of pigs. The first outbreak was observed in Siliguri, West Bengal in 2001.

b. The second incident recorded in Nadia district at West Bengal in 2007, India.

c. According to WHO the virus claimed over 300 lives across Malaysia, Singapore, Bangladesh and India between 1998 and 2008 (Figure 4).

Nipah Virus Infection across the Globe!

a. According to a 2013 ICMR.

b. Bangladesh recorded several Nipah outbreaks in humans almost every year from 2001 to 2013.

c. The virus has been detected in Cambodia, Thailand, Indonesia and Madagascar in Southern Africa and Ghana in West Africa on fruit bats or bats seropositive to NiV antibodies.^[2]

Figure No 4: Nipah virus outbreaks in the world.

Figure No 5: sample of cerebrospinal fluid from an infected patient.

1) HISTORICAL BACKGROUND:

The first incidence of the NiV was recorded simultaneously in humans and pigs in Malaysia in 1998–1999. has presented a detailed account of the initial Nipah outbreak in Malaysia, where several human cases of viral encephalitis occurred over a 35-week period from September 1998 to May 1999. On the basis of clinical signs and association of pigs, the disease was considered to be already circulating Japanese encephalitis among pig farmers, creating considerable anxiety and fear throughout the country.^[3]Total 265 cases were reported of which 105 died. The outbreak started in the pig farmers near Ipoh in the Kinta District of Perak, some 200 km north of Kuala Lumpur and spread to three other major pig-rearing areas (the largest in Southeast Asia) in Negeri Sembilan and SungeiBuloh in Selangor. The disease was named after Kampung Sungai Nipah (Nipah River Village), where the first viral isolate was obtained and therefore named as NiV. Retrospective investigations conducted later had suggested that NiV was responsible for sporadic disease in pigs in Peninsular Malaysia since late 1996, but was not recognized because the clinical signs were not markedly different from those of several endemic pig diseases, and because morbidity and mortality were not remarkable. Singapore recorded the subsequent outbreak in 1999 in slaughterhouse persons due to infected pigs brought from Malaysia. In India, the disease was recorded in humans without any involvement of pigs. There were two outbreaks, major one occurred in 2001 in Siliguri in West Bengal and an isolated incidence in Nadia also in West Bengal in 2007. Bangladesh recorded several Nipah outbreaks in human beings covering several districts almost every year during 2001–2013.^[4]

The disease was eradicated from Malaysia in 1999 and the last of the two recognized outbreaks from India was in 2007 but the clinical expression of the disease in human being with very high case fatality has been continued in Bangladesh. Nevertheless, in addition to these countries, the virus has been detected in fruit bats or the bats were seropsitive to NiV antibodies from Cambodia, Thailand, Indonesia, India, Madagascar in Southern Africa and Ghana in West Africa P. giganteus is the only Pteropusspecies present in Bangladesh. In the Naogaon (Bangladesh) investigation, 2 of 19 P. giganteus specimens had antibody against NiV. None of 31 other animals from various species had Nipah Antibodies.^[5]

In the initial Malaysian outbreaks, concurrent respiratory ailment, encephalitis with mortality in pigs was recorded. It was also revealed that majority of the human cases comprised of occupationally related to the pigs and having the history of direct contact with live pigs. It was also revealed that the disease spread to Negeri Sembilan through the sale and movement of infected pigs. Preliminary characterization of an isolate from a human case at the Centers for Disease Control and Prevention (CDC) in Fort Collins and Atlanta, USA, showed the primary causative agent in the outbreak to be a previously undescribed virus of the family Paramyxoviridae. These investigations showed the new virus, named NiV, was closely related to (already known since 1994) Hendra virus.

During the Malaysian NiV outbreak, two Indonesian farm workers who returned home to Indonesia from Malaysian pig farm were also succumbed to infection. The outbreak also spread to neighboring Singapore during March 1999 where 11 abattoir workers handling pigs from infected farms in Malaysia developed the disease with one fatality. In addition to these 11 cases in Singapore, there were two apparently asymptomatic case patients among workers in this abattoir.

NiV in Malaysia emerged in 1998 during an outbreak of infectious respiratory and neurologic disease in commercially farmed pigs, presumably after virus spillover from Malaysian flying foxes. Pigs were the source of infection for farm and abattoir workers, resulting in awide spread outbreak of severe febrile encephalitic disease among humans. NiV infection has not been detected in Malaysia or Singapore after 1999, but recurring (almost annual) human cases of Nipah encephalitis with very high case fatalities in Bangladesh and sporadic outbreaks in India since 2001.^[6]

The detailed account of the first NiV outbreak in India (Siliguri, West Bengal) during 2001 has been published in two reports. An outbreak of acute encephalitis occurred in Siliguri (West Bengal) town of India between January 31 and February 23, 2001. A total of 66 probable human cases and 45 deaths were reported. Later, the clinical material obtained during the Siliguri out break was retrospectively analyzed for evidence of NiV infection. Analysis of the limited sequence data suggested that the NiV strains associated with the outbreak were more closely related to NiV isolated in Bangladesh than to NiVisolated in Malaysia.^[7]

In the Malaysian outbreak, pigs were the intermediate hosts. NiV was isolated from fruit bats in Malaysia. Fruit bats with antibodies to NiV were captured in the outbreak areas of Bangladesh but no intermediate animal host was identified. In Bangladesh, NiV might have been transmitted to humans by direct contact with bats or indirectly by contact with material contaminated by bats. Person-to-person spread was also noted during the 2004 NiV outbreak in Faridpur, Bangladesh. The range of Pteropus giganteus, one of the flying foxes commonly found in South Asia includes West Bengal. Therefore, the range of the proposed natural reservoir for NiV extends into northeastern India. Since the geographical features ofWest Bengal are similar to those of Bangladesh, environmental circumstances that favor transmission of NiV to humans would also likely be same in West Bengal. Many of the epidemiologic features of the outbreak in Siliguri were similar to those of the recent NiV outbreaks in Bangladesh.

Analysis of the limited sequence data suggested that the NiV strains associated with the outbreak were more closely related to NiV isolated in Bangladesh than to NiV isolated in Malaysia. These data extend the previous observation that viruses circulating in different areas have unique genetic signatures and suggest that these strains may have co-evolved within local natural reservoirs. After 2001, the second NiV outbreak was reported in West Bengal in India in 2007. Between 11 and 28 April 2007, reported 30 cases of fever with acute respiratory distress and/or neurological symptoms from Nadia district of West Bengal in India. The cases presented mainly with fever, headache and body ache with a few cases having episodes of vomiting, disorientation, respiratory distress.^[8]Five cases ended fatally within 3–10 days of onset. However, investigated the same outbreak and stated that similar other cases had not been reported from the village or the surrounding area, thus showed case fatality (5/5) as 100%. They also amplified full-genome sequence of NiV (18252 nt) from lung tissue that showed 99.2% nucleotide and 99.8% amino acid identity with the Bangladesh-2004 isolate, suggesting a common source of the virus. discussed the relationship between Henipa viruses and fruit bats.^[9]

Epidemiological studies have shown that the virus could be transmitted from bat to human and from human to human. Wildlife studies have also shown that the virus was widely distributed in at least 10 genera and 23 species of bats in a large part of Asia and Africa. As bats are long distant flying, gregarious animals living in large colonies which could exchange novel viruses from one species to another, it is not unexpected that the seroprevalence of Henipavirus among bat colonies are relatively high.^[10]also commented that due to widespread distribution of both the Henipavirus and its hosts, the virus will remain an important cause of zoonotic disease.

2) STRUCTURE OF NIPAH VIRUS:

Figure No 6: Structure of Nipah Virus.

Nipah virus is a highly pathogenic paramyxovirus causing deadly encephalitis in humans. Single stranded negative sense RNA, 18246 bp (Malaysian isolate) and 18252 bp (bangladesh isolate) Genome has six transcriptional unit that has six structural proteins. They are nucleo capsid (N), phosphor protein (P), matrix protein (M), fusion protein (F), glycoprotein (G) and polymerase (L) Protein associated with genome: large (L) protein, phospoprotein (P) Viral proteins: fusion protein (F) and attachment glycoprotein protein (G) Phosphoprotein (P): it role as a polymerase cofactor, enhancing polymerase processivity and allowing the encapsidation of the newly synthesized viral genomes and antigenomes. Phosphorotein of Nipah virus has an additional role in immunosuppression: blocking interferon signaling by binding host STAT-1.

It’s replication requires a constant supply of unassembled nucleoprotein (NO) in complex with its viral chaperone, the phosphor protein. Host attachment is achieved by the viral G protein that binds to the host cell surface receptors ephrin B2 or B3. Next, the cellular and viral membranes fuse and the capsid disassembles to deliver the viral genome into the cell. Once in the cytoplasm, the viral messenger and genomic RNAs are synthesized and translated to generate viral proteins. Successful infection requires evasion of the interferon (IFN)-α/β response (a key component of the innate immune response to virus infection). Four Nipah-encoded proteins (P, V, W, and C, all encoded by the P gene) participate in overcoming the innate immune response.^[11]

Nipah virus (NiV) is a RNA virus belongs to family Paramyxoviradae and genus Henipavirus.

Size: 40-600nm

Shape: pleuromorphic

nvelope: present

3) THE TRANSMISSION ROUTE OF NIPAH VIRUS:

The direct contact with pigs or fresh pig products was responsible for NiV transmission to humans, confirming preliminary observations by health workers. The Malaysian experience showed that the disease spread rapidly among pigs in the infected farm that was attributed to direct contact with excretions and secretions such as urine, saliva, pharyngeal and respiratory secretions of infected pigs. The findings in the pig’s respiratory system could explain the severe pulmonary symptoms in these animals and provide support for the suggestion that aerosol spread of NiV from pig to human represents an important mode of transmission.^[12]Widespread surveillance of pig populations to detect infected pigs, and culling of sick pigs stopped the epidemic. Urine exposure may also be associated with transmission as NiV antigen has been demonstrated in the renal tubules of pigs and a concurrent outbreak of NiV among abbatoir workers in Singapore also showed the associated ness of infected pig urine and exposure to the workers.^[13]The possible mechanical transmission by repetitive use of same needles or equipment without further sterilization after each use for health intervention and artificial insemination and sharing of boar semen within a farm were also implicated. The possible role of transmission by infected dogs and cats found in the affected farm could not be excluded. Several outbreaks of NiV have been reported in human beings in Bangladesh from 2001 to 2013 and two outbreaks in India, but none had showed any involvement of pigs.^[14]

Investigation of different Nipah outbreaks in Bangladesh have identified different routes of transmission including climbing trees (probably contaminated with infected date palm sap), contact with sick persons, and contact with sick animals. Another way of NiV getting transmitted from P. giganteus to humans recorded in Bangladesh is food-borne. Fruit bats (P. giganteus) are a nuisance to date palm sap collectors because the bats drink the sap at night from the clay pots used to collect the sap. The investigations by suggested that NiV was transmitted from P. giganteus to persons through drinking fresh date palm sap.^[15]Date palm sap is a national delicacy that is enjoyed by millions of Bangladeshis each winter. However, the sap is occasionally contaminated with NiV-infected bat urine or saliva that contains a sufficient dose of NiV to be fatal to humans. In India, in a bat sample survey, NiV RNA was detected in a liver homogenate of P. giganteus captured in Myanaguri, West Bengal (Figs. 7,8,9) In Siliguri, India, transmission of the virus was also reported within a health-care setting, where 75% of cases occurred among hospital staff or visitors. Nipah cases tend to occur in a cluster or as an outbreak, although 18% of cases in Bangladesh were isolated. Strong evidence indicative of human-to-human transmission of NiV was found in Siliguri (India) in 2001 and in Bangladesh in 2004. Approximately one-half of recognized Nipah case patients in Bangladesh developed their disease following person-to-person transmission of the virus further confirmed human-to-human transmission during Bangladesh outbreak in 2010 while studying 16 case-patients.^[16]

Figure No 7: The date palm trees are scratched to collect sap through a bamboo channel

Figure No 8: An earthen pot is tied for collection of the sap.

Figure No 9: A bat (P. giganteus) colony in Malda town in West Bengal.

4) MODE OF TRANSMISSION:

It was discovered that the main carrier of the virus are four species off fruit bats. The virus was found in the urine and saliva of infected flying foxes (bats) and pigs consuming food contaminated by these secretions can be infected. This occurs specially when the pig farms are located close to fruit orchards or fruit trees that attracted flying foxes. It can be transmitted to humans from animals such as bats, pigs etc via intake of fruits bitten by bats or contaminated by the sick animals urine^[17]. Nipah virus also spread to Pigs, cows, horses, cats, sheep, goat etc through bats. It can also spread from humans to humans through body fluids. Transmission of infection occurs via respiratory droplets, contact with both the body fluids and tissues of a sick animals. Niv virus is highly contagious among pigs and is spread by coughing. As per some epidemiological study reports bats excrete these virus when they are in stress and when they are pregnant. Incidents of human-to-human transmission have also been reported, with these being the major route of infection for the Bangladeshi strains.

Figure No10. Mode of transmission of Nipah Virus.

5) SOURCES OF VIRUS:

Nipah virus has been found in urine and uterine fluids of wild pteropid bats, experimentally isolated from urine, kidney and uterus of infected bats. Virus may be found in fruit or juice (e.g. unpasteurised date palm sap) contaminated with bat saliva or urine. Other sources for infection are contaminated drinking water and aborted bat foet uses or other fluids/tissues of parturition. Infected pigs shed Nipah virus in respiratory secretions, saliva and urine. Role of other animals as a source of virus in outbreaks is less clear though virus has been isolated from feline respiratory secretions, urine, placenta and embryonic fluids.^[18]

6) PROGNOSIS, SEQUELAE AND COMPLICATION:

Poor prognostic factors for acute NiV encephalitis included brain stem involvement, presence of virus in the CSF and diabetes mellitus. Although the mortality of acute NiV encephalitis was high, most of the patients who recovered did not suffer any serious sequelae. In one rare case of acute encephalitis, the patient recovered from a coma to be able to walk and communicate but later developed a fatal intracerebral hemorrhage while still in the ward. Most unexpectedly, a small number of patients suffered a second or even a third neurologic episode following what appeared to be complete recovery. These relapsed NiV encephalitis patients constitute about 8% of the total number of survivors.^[19]Symptoms appeared after an average of about 8 months following viral exposure. In addition, about 3% who were either asymptomatic or only had mild non-encephaliticillness initially also developed similar neurologic episodes (late-onset NiV encephalitis) for the first time several months later. Clinical, radiologic and pathologic findings suggested that, essentially, relapsed and late-onset NiV encephalitis was the same disease process that was distinct from acute NiV encephalitis.^[20]The sequelae and complications of acute NiV infection are summarized in Fig. 10. The presence of neuronal viral antigen in brains of fatal cases suggested that relapsed and late-onset NiV encephalitis were due to recurrent infections rather than Fig 11.

Figure No. 11. Sequelae and complications of acute Nipah virus infection

Post infectious demyelination seen following acute measles or other viral infections. Relapsed NiV encephalitis appeared analogous to the single human case of HeV encephalitis in which the patient developed fatal encephalitis 13 months after meningitis associated with drowsiness. HeV antigen was demonstrated in the brain. However, in both relapsed/late-onset NiV encephalitis and HeV encephalitis, the respective viruses have so far not been isolated.

Late-onset NiV encephalitis appears in some ways to resemble subacute sclerosingpanencephalitis (SSPE), an infection due to measles virus, in that in both diseases the initial infection is non-encephalitic and neurologic complications appear late. However, in contrast to SSPE which is relentless, some patients with late-onset NiV encephalitis may recover, although the long-term prognosis remains unknown.^[21]

The factors that determine the occurrence of relapsed and late-onset NiV encephalitis are still unknown. Possibilities include viral genomic mutations in, and alteration in host’s immune response to, residual foci of viruses. In the case of SSPE, pathogenesis is associated with viral genomic mutations. Since measles infection could be associated with immunosuppression^[22]NiV could conceivably also have this effect on the host, but its contribution to disease severity and pathogenesis of acute and relapse/late-onset NiV encephalitis is unknown.

7) SIGNS AND SYMPTOMS:

a) Humans:

The incubation period generally varies from four days to 2 weeks, but may be extended up to 45 - 60 days. The clinical course is characterized by high fever followed by seizure and death due to encephalitis or respiratory disease. Human infections range from asymptomatic infection to fatal encephalitis. Infected people initially develop influenza-like symptoms of high fever, headache, myalgia, sore throat and weakness. This can be followed by impairment in spatial perception and stability, feeling abnormally sleepy, altered consciousness, and neurological signs, sometimes accompanied by nausea and vomiting, that indicate acute encephalitis.^[23]Some patients infected with NiV Bangladesh strain can also experience atypical pneumonia and severe respiratory problems, including acute respiratory distress. Seriously affected patients can develop septicaemia, gastrointestinal bleeding, and renal impairment. Encephalitis and seizures occur in severe cases, progressing to coma within 24 to 48 hours. The case fatality rate estimates remain ~40- 100% during sporadic outbreaks. Most people who survive acute encephalitis make a full recovery, but around 20% are left with residual neurological consequences such as persistent convulsions and personality changes. A limited number of recovered patients may experience encephalitic relapse up to years later and sub clinically infected individuals may show central nervous signs up to 4 years later.^[24]

b) Nipah virus in domestic animals:

Nipah outbreaks in pigs and other domestic animals (horses, goats, sheep, cats and dogs) were first reported during the initial Malaysian outbreak in 1999. Many pigs had no symptoms, but others developed acute febrile illness, laboured breathing, and neurological symptoms such as trembling, twitching and muscle spasms.^[25]

c) Swine:

Nipah virus is highly contagious in pigs. Pigs are infectious during the incubation period, which lasts from 4 to 14 days. Generally, mortality was low except in young piglets. Available observations of clinical signs in swine would suggest a respiratory and neurologic involvement. Clinical manifestations are associated with age groups.^[26] Suckling pigs and piglets (<1 month old): laboured breathing and muscle tremors with limb weakness. Mortality in piglets can be high (40%). Young swine (1 to 6 months old): begins as an acute fever with respiratory signs, laboured breathing, nasal discharge and loud nonproductive cough (“barking pig syndrome” and “one-mile cough”). Accompanying neurologic signs: muscular fasciculation, myoclonus, limb weakness, and spastic paresis, and in some cases, lateral recumbency with paddling and tetanic spasms. Disease presentation can be mild to fulminant with high morbidity and low mortality (<5%). Older animals (>6 months old): acute febrile course with marked neurologic signs. Central nervous system involvement: nystagmus, bruxism, head pressing, aggressive behaviour, tetanic spasms and seizures. Respiratory signs may include open-mouthed breathing, nasal discharge and sialorrhea (possibly due to pharyngeal paralysis). Sudden death in this age group with few signs has been reported. Abortions during the first trimester have also been reported. Morbidity in confined animals approaches 100%.^[27]

d) Other species:

Limited clinical information exists for other species. In dogs, distemper-like syndrome was described with pyrexia, depression, dyspnea and conjunctivitis with purulent ocular-nasal discharge. Severe disease with mortality was also reported. NiV infection was confirmed by immune histo chemical examination of 1 dead and 1 dying dog from the epidemic area in Malaysia. Both showed histologic evidence of severe disease^[28]. Morbidity in dogs during outbreaks in Malaysia was interestingly high, with a zero pre valence from 15% up to 46%. Nipah affected cats were observed on farms during outbreaks in Malaysia and some of these resulted in death. Experimental intranasal and oral inoculation of cats produced clinical disease characterized by acute febrile course with respiratory complications. Fruit bats show no serious signs of infection.

e) Lesions:

In humans: different pathological features have been observed, primarily at the level of central nervous system. Confirmed NiV patients showed marked vasculitis with endothelial damage, up to cellular lyses, in the arterioles, venules, and capillaries of various organs. The brain was the most severely affected organ. In one study, evaluation at autopsy of microscopic features in the CNS showed necrotic lesions, perivascular cuffing, thrombosis, and vasculitis in 80% to 90% of the 30 cases examined; endothelial syncytia were present in 27% and meningitis in 57% of the patients. The severity of the CNS pathology was demonstrated also by Magnetic Resonance Imaging (MRI) analysis of encephalitis patients in the Malaysian outbreak.^[29] Investigations by MRI revealed a pattern similar to is chaemic infarction caused by obstruction of small cerebral blood vessels. Patients had multiple small (less than 1cm in maximum diameter) bilateral abnormalities within the subcortical and deep white matter; in some patients, the cortex, brainstem, and corpus callosum were also involved. However, relapse and late-onset cases in Malaysia, and other outbreaks of Nipah virus in Bangladesh, showed a different pattern of predominantly confluent cortical lesions.

Other affected organs were the kidney, lung, and heart. The respiratory disease was reported in up to 63% of confirmed case during the outbreaks in Bangladesh. In the lung, vasculitis was seen in 62% of cases and fibrinoid necrosis was found in 59% of cases. Fibrinoid necrosis often involved several adjacent alveoli and was frequently associated with small vessel vasculitis. Multinucleated giant cells with intra nuclear inclusions were occasionally noted in alveolar spaces adjacent to necrotic areas. Alveolar hemorrhage, pulmonary edema, and aspiration pneumonia were often encountered. Histopathological changes of bronchiolar epithelium were uncommon. In the kidney, focal glomerular fibrinoid necrosis was seen in 34% of cases. In some cases, the glomeruli were totally destroyed by inflammation. Vasculitis, thrombosis, and interstitial inflammation were occasionally seen. Syncytial formation involving the periphery of the glomerulus and tubular epithelium was rarely seen. In the heart, vasculitis was noted in 31% of cases. A large myocardial infarction associated with vasculitis was found in a patient comatose for >2 weeks. In another patient who survived more than a month, focal myocardial fibrosis associated with vasculitis was noted. ^[30]

f) In animals:

Principal gross and microscopic lesions associated with Nipah in swine are found in lungs and/or central nervous system. Lung lesions may vary from mild to severe pulmonary consolidation with petechial or ecchymotichaemorrhages and distended interlobular septa. Trachea and bronchi may be filled with frothy exudate which varies in appearance from clear to blood-tinged. Meningeal oedema with congestion of the cerebral blood vessels has been observed in the brain. Some cortical renal congestion may be evident.

Histologically, epithelia of all the major respiratory pathways are affected with presence of syncytial multinucleated cells in vascular endothelium. A mononuclear vasculitis with fibrinoid necrosis is often observed associated with thrombosis. Principal histologic changes in the brain, if present, are perivascular cuffs and gliosis. General is edvasculitis in cats and non-suppurative meningitis in horses have been also reported.

Reported lesions from experimentally infected animals resemble the lethal disease observed in humans, increasing the information on pathogenesis and representing suitable models to develop new immunotherapeutic approaches using antiviral drug testing and vaccine development against acute NiV infection. For example, golden hamsters develop systemic vasculitis, pulmonary disease, and encephalitis. Ferrets develop severe respiratory and neurological disease.^[31]NiV is similar to HeV infection in cats except there is more involvement of the upper and lower respiratory tract. Cats may be a suitable model for the respiratory aspects of NiV, but they are not useful for studying the encephalitic form. NiV is highly pathogenic to chicken embryos, a useful animal model for studying NiV and the effects on the vascular endothelium or neurons. Where as allantoic inoculation of NiV results in considerable variation and only partial mortality, yolk sac inoculation results in generalized fatal disease of chicken embryos, with gross lesions of petechial to ecchymotic hemorrhages and congestion in the kidneys. Mice are not a suitable model of NiV disease. Swiss mice inoculated either by the intranasal or the intra peritoneal routes do not develop clinical signs, but NiV antibodies can be produced after repeated infection. However, NiV can be lethal if administered intra cranially into suckling mice.^[32]

8) DIAGNOSIS:

Nipah virus infection can be diagnosed by a number of different tests. Since Nipah is classified as a biosafety level 4 (BSL4) agent, special precautions must be undertaken in the collection, submission and processing of samples. Biosafety considerations require that this work be carried out only in a physical containment level 4 (PC4) facilities. Various strategies have been developed to reduce the risk of laboratory sera, including gamma-irradiation or sera dilution and heat-inactivation. Henipa virus antigens derived from tissue culture for use in ELISA can be irradiated with 6 kilo Greys prior to use, with negligible effect on antigen titer.^[33]

9) PREVENTION AND CONTROL:

There is no effective treatment for Nipah virus disease, but ribavarin may alleviate the symptoms of nausea, vomiting, and convulsions. Treatment is mostly focused on managing fever and the neurological symptoms. Severely ill individuals need to be hospitalized and may require the use of a ventilator. Human-to-human transmission of NiV has been reported in recent outbreaks demonstrating a risk of transmission of the virus from infected patients to healthcare workers through contact with infected secretions, excretions, blood or tissues. Healthcare workers caring for patients with suspected or confirmed NiV should implement Standard Precautions when caring for patients and handling specimens from them.^[34]

A vaccine is being developed. A recombinant sub-unit vaccine formulation protects against lethal Nipah virus challenge in cats. ALVAC Canarypox vectored Nipah F and G vaccine appears to be a promising vaccine for swine and has potential as a vaccine for humans.^[35]The main strategy is to prevent NiV in humans. Establishing appropriate surveillance systems will be necessary so that NiV outbreaks can be detected quickly and appropriate control measures initiated. The close contact among infected people can be avided. Regular hand washing should be carried out after caring for or visiting sick people.

CONCLUSION:

According to WHO R&D list Nipah is a high priority disease but there is no current treatment or vaccine; therefore disease can be avoided only by taking preventive measures against it. The social awareness regarding the disease is very less so there is need to educate people regarding its preventive measures for avoiding transmission and progression of disease by human to human contact or human to animal contact by any way. This review can help people to get the information regarding disease and possible risk factors. The preventive measures discussed in this review can also be helpful in future when there is a risk of transmission of disease by coming close contact with diseased person or animal. The most of recent outbreaks are originated from bat so there is need to focus and study about it. If this situation cannot taken seriously then there is possibility of more such outbreaks in future which can affect human life greatly.

REFERENCE:

1. BS Web Team. (2018)

2. https://timesofindia.indiatimes.com/city/kozhikode/keralarecord.

3. MMWR. Outbreak of Hendra-like virus-Malaysia & Singapore 1998–1999.Morb Mortal Weekly Report.1999; 48: 265–269.

4. World Health Organization Nipah virus outbreaks in the WHO South-East Asia Region, Communicable Diseases Department, Disease Surveillance and Epidemiology. Update 1 May 2012.

5. Drexler JF, Corman VM, Gloza-Rausch F, Seebens A, Annan A, Ipsen A, Kruppa T, Mu¨ller MA, Kalko EK, Adu-Sarkodie Y, Oppong S, Drosten C. Henipavirus RNA in African bats. PLoS ONE. 2009;4(7):63-67.

6. Hsu VP, Hossain MH, Parashar UD, Ali MM, Ksiazek TG, Kuzmin I, Niezgoda M, Rupprecht C, Bresee J, Breiman RF. Nipah virus encephalitis reemergence, Bangladesh. Emerg Infect Dis. 2004;10: 2082–7.

7. Institute of Epidemiology, Disease Control and Research (IEDCR). Nipah Infection in 2013—Update on 5 Feb, 2013.

8. International Centre for Diarrheal Disease Research, Bangladesh (ICDDRB). Nipah outbreak in Faridpur District, Bangladesh.Health Sci Bull. 2010;8: 6–11.

9. World Health Organization Global Early Warning System for Major Animal Diseases, including Zoonoses. Zoonoses& Vet Pub Hlth. 2007.

10. International Centre for Diarrheal Disease Research, Bangladesh (ICDDRB). Person-to-person transmission of Nipah virus during outbreak in Faridpur District.Health Sci Bull. 2004; 2:5–9.

11. Nipah virus outbreak in kerala: Times now digital. may 23.2018.www.timesnownews.com › Health.

12. Arankalle VA, Bandyopadhyay BT, Ramdasi AY, Jadi R, Patil DR, Rahman M, Majumdar M, Banerjee PS, Hati AK, Goswami RP, Neogi DK, Mishra AC. Genomic characterization of Nipah virus, West Bengal, India. Emerg Infect Dis. 2011;17: 907–9.

13. Institute of Epidemiology, Disease Control and Research (IEDCR). Nipah Infection in 2013.

14. World Health Organization Global Early Warning System for Major Animal Diseases, including Zoonoses. Zoonoses& Vet Pub Hlth. 2007.

15. Chadha MS, Comer JA, Lowe L, Rota PA, Rollin PE, Bellini WJ, Ksiazek TG, Mishra A. Nipah virus-associated encephalitis outbreak, Siliguri, India. Emerg Infect Dis. 2006;12(2):235–40.

16. International Centre for Diarrheal Disease Research, Bangladesh (ICDDRB). Outbreaks of encephalitis due to Nipah/Hendra-like viruses. Western Bangladesh. Health Sci Bull. 2003; 1:1–9.

17. Neethu C. Sharma. What is Nipah virus and how is it transmitted? May 23 2018. 12.

18. WorldOrganisation for Animal Health (Office International des Épizooties: OIE) Nipah (virus encephalitis). Technical Disease Cards, OIE, Paris. (2009)

19. Chong HT, Tan CT, Goh KJ, et al Occupational exposure, age, diabetes mellitus and out come of acute Nipah encephalitis. Neurol J Southeast Asia (2001) 6:7

20. Tan CT, Goh KJ, Wong KT, et al. Relapse and late-onset Nipah encephalitis. Ann Neuro (2002) l51:703

21. Wong KT, Shieh WJ, Kumar S, et al (in press) Nipah virus infection: Pathology and pathogenesis of an emerging paramyxoviral zoonosis. Confirmed to be accepted for publication by the American J of Pathology.

22. Griffin DE, Bellini WJ Measles virus. In: Fields B et al (eds) Field’s virology. Lippincott-Raven, Philadelphia, pp 1267–131244. (1996) Sarji SA, Abdullah BJJ, Goh KJ, et al Magnetic resonance imaging features of Nipah encephalitis. AJR (2000) 175:437.

23. Wahed F, Kader SA, Akhtarunnessa, Mahamud MM Nipah Virus: An Emergent Deadly Paramyxovirus Infection In Bangladesh. J Bangladesh Soc Physiol. (2011) 6: 134-139.

24. Chong HT, Tan CT. Relapsed and late-onset Nipah encephalitis, a report of three cases. Neurol J Southeast Asia (2003) 8: 109-112.

25. Uppal PK, Emergence of Nipah virus in Malaysia. Ann N Y Acad Sci (2000) 916: 354-357.

26. World Organisation for Animal Health (Office International des Épizooties: OIE) Nipah (virus encephalitis). Technical Disease Cards, OIE, (2009) Paris.

27. Mohd Nor MN, Gan CH, Ong BL Nipah virus infection of pigs in peninsular Malaysia. Rev Sci Tech (2000) 19: 160-165.

28. Middleton DJ, Westbury HA, Morrissy CJ, van der Heide BM, Russell GM, et al. Experimental Nipah virus infection in pigs and cats. J Comp Pathol (2002) 126: 124-136.

29. Tanimura N, Imada T, Kashiwazaki Y, Sharifah SH Distribution of viral antigens and development of lesions in chicken embryos inoculated with nipah virus. J Comp Pathol (2006) 135: 74-82.

30. Bossart KN, McEachern JA, Hickey AC, Choudhry V, Dimitrov DS, et al. Neutralization assays for differential henipavirus serology using Bio-Plex protein array systems. J Virol Methods (2007) 142: 29-40.

31. Middleton DJ, Westbury HA, Morrissy CJ, van der Heide BM, Russell GM, et al. Experimental Nipah virus infection in pigs and cats. J Comp Pathol (2002) 126: 124-136

32. Mungall BA, Middleton D, Crameri G, Bingham J, Halpin K, et al. Feline model of acute nipah virus infection and protection with a soluble glycoprotein-based subunit vaccine. J Virol (2006) 80: 12293-12302.

33. WorldOrganisation for Animal Health (Office International des Épizooties: OIE) Manual of Diagnostic Tests and Vaccines for Terrestrial Animals, OIE, Paris, Hendra and Nipah virus diseases, (2010) 2.9.(6). 3-9.

34. McEachern JA, Bingham J, Crameri G, Green DJ, Hancock TJ, Middleton D, et al. A recombinant subunit vaccine formulation protects against lethal Nipah virus challenge in cats. Vaccine. Volume 26, Issue 31, 2008:3842-3852.

35. Weingartl et al. Recombinant Nipah virus vaccines protect pigs against challenge. Journal of Virology 80, 2006: 7929-38.

Received on 18.08.2020 Modified on 12.10.2020

Res. J. Pharma. Dosage Forms and Tech.2021; 13(1):31-40.

DOI: 10.5958/0975-4377.2021.00007.0