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PATHOLOGY Based on the autopsies performed on patients who died within two weeks after the onset of illness, the histopathological findings shows that these patients mainly had disseminated microinfarctions of the central nervous system results from the vasculitis-induced thrombosis. Autopsies on patients who died more than a month after infection shows massive intracerebral and intraventricular hemorrhage with severely increased intracranial pressure. Residual parenchymal inflammation and vasculitis were also evident from the autopsy. The hemorrhage was attributed to vascular fragility resulting from vasculitis. There are also presence of delayed-onset disease with encephalitis but no evidence of vasculitis or microinfarction. (Khean et al, 2000)Samples collected from patient’s autopsy with positive results of cultures for Nipah virus showed histologic findings of endothelial damage and vasculitis, mainly in arterioles, capillaries, and venules. Beside brain which was the most severely affected organ, the lungs, the heart, and the kidneys, can also be affected. Vessel-wall necrosis, thrombosis, and inflammatory cell infiltration of neutrophils and mononuclear cells are the caharcteristics of vasculitis of blood vessels. Syncytial cell formation was seen in the endothelium of affected blood vessels in the brain and lungs and in the Bowman’s capsule of the glomerulus. Zones of microinfarction and ischemia were commonly found surrounding or adjacent to vasculitic blood vessels. As is seen in other paramyxovirus infections, many neurons had eosinophilic cytoplasmic and nuclear viral inclusions showed in the brain. (Kaw Bing Chua, Sai Kit Lam, 2002)

LABORATORY DIAGNOSIS Nipah virus is classified internationally as a biosecurity level (BSL) 4 agent. Laboratory diagnosis of Nipah virus include :- serology, – histopathology, – PCR and – virus isolation. Serum Neutralization Test, ELISA, and RT-PCR are used for laboratory confirmation. Laboratory Investigations : – Thrombocytopenia found in 30 percent of patients – Leukopenia found in 11 percent of patient. – Elevated levels of alanine aminotransferase were found in 33 percent of patients, – Elevated levels of aspartate aminotransferase were found in 42 percent of patients. – Abnormal chest radiographs in 6 percent of patients with increased focal markings over the lung fields and – Mild basal atelectasis. All of these patients had primarily neurologic features at presentation.MRI of the brain during the acute phase of the illness shows widespread focal lesions in the subcortical and deep white matter and, to a lesser extent, in the gray matter. Electroencephalographic findings are usually correlated with the severity of the disease. Electroencephalograms mainly shows abnormalities such as : -diffuse slow waves with focal sharp waves, and- continuous, diffuse, irregular slow waves, and intermittent, diffuse slow waves. (Khean et al, 2000)

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TREATMENTAs for now, there is no effective treatment for Nipah virus disease, but ribavarin was administered to some patients to alleviate symptoms of nausea, vomiting, and convulsions which treatment mostly focused on managing the fever and neurological symptoms. Severely affected patients may require intensive care with ventilation support. (Thomas G. Ksiazek, 2018) 

CONCLUSION  Nipah virus is a zoonotic pathogen that causes severe febrile encephalitis giving a mortality rate of nearly 40%. Nipah virus is considered a biosafety level-4 pathogen and is listed as a select agent with high risk for public health and security due to its high mortality rate in human. The natural reservoir for Nipah virus is the fruit bats of the genus Pteropus. Research reviewed in this paper suggests that changes in ecological conditions and anthropogenic driven ecological changes were the underlying causes of its emergence. Treatment are still under development. Half the patients required mechanical ventilatory support. Ribavirin, an antiviral is used as to alleviate certain symptoms.CLINICAL FEATURES The clinical features of Nipah virus infection are different from the Hendra virus, to which Nipah is antigenically related. Affected patients mean age are of 37 years old, and the male patients are most likely to be affected than the female patients with ratio of 4.5:1. Ninety-three percent of the patients who had direct contact with pigs, usually have onset of illness within 2-3 weeks. The main features of presentation were :- fever, – headache, – dizziness, and – vomiting. – Half of the patient may had a reduced level of consciousness and prominent brain stem dysfunction. Distinctive clinical signs included : – segmental myoclonus, – areflexia, – hypotonia, – abnormal doll’s eye reflex – hypertension, and – tachycardia. This suggests that the brain stem and the upper cervical spinal cord were involved. With their condition rapidly deteriorated, it can causes fatality. Patients may recovered fully but can have persistent neurologic deficits. The onset of symptoms during relapses was rapid and the symptoms and signs :- fever, – headache, – focal neurologic signs, – seizure, dizziness, – reduced consciousness, and – myoclonus. Clinical relapse was seen in some of the surviving patients, which results in either neurologic symptoms reappeared after an initial illness, or there was a long latency period between the initial finding of seropositivity after exposure to the virus and the development of neurologic symptoms. (Kaw Bing Chua, Sai Kit Lam, 2002)Nipah virus also causes severe acute febrile encephalitis with virus in?ltrating most major organs and endothelial cells. (Wong et al, 2002)

ETIOLOGY  The etiologic agent of Nipah virus is an enveloped, negative-sense, single-stranded RNA virus. The virus is closely related to Hendra virus and is assumed to have been introduced into the swine population from several species of Pteropus found with antibodies during research on the outbreak. This suggested that the virus occur in areas are within the range of this genus of bats. In Malaysia, genetic analysis of virus from human and swine clinical materials strongly supported a single introduction of the virus with spread through the commercial swine population. There was evidence of infection among several other species of domestic animals, including dogs, cats, and horses. (Thomas G. Ksiazek, 2018) Studies indicated that Nipah virus is highly pathogenic to chicken embryos which represent a useful model for studying the vascular and neuronal tropisms of Nipah virus. The virus also grows well in many of the mammalian cells but the rate of growth and patterns of cytopathic effect (CPE) produced in all culture varies with the type of mammalian cells used. (Tanimura et al, 2006), (Kulkarni et al, 2013)       TRANSMISSION AND PATHOGENESIS Infected bats are assumed to shed virus if they get stressed and hungry or their immune system gets weaker, in their excretion such as saliva, urine, and semen but they are symptomless carriers. The Nipah virus (NiV) is highly contagious among pigs, which can even spread through coughing. Infection in pigs is assumed to have been a transfer from the reservoir bat species to pigs. Once the virus was introduced into, serologic tests suggested that nearly all pigs on an affected premise can be infected. In South Asia, infection of people appears to occur indirectly by means from the reservoir bats, contamination of sap collected in pots on palm trees, contact with trees contaminated by bats or person-to-person transmission, although no evident of occurence in Malaysia. Direct contact with infected pigs was also identified as the predominant mode of transmission in humans (Thomas G. Ksiazek, 2018) 

EPIDEMIOLOGY  In late September 1998, an outbreak of severe febrile encephalitis with high fatality occurred among pig farmers in the suburb of state of Perak, Malaysia. Initially, the deaths were thought to be due to Japanese encephalitis (JE), a disease that is endemic in Malaysia because 4 serum samples from 28 patients in this outbreak area tested positive for JE-specific IgM. However, the epidemiologic characteristics of the disease were different from those of JE. JE virus, which is mosquito-borne, is most common among young children and has no association with a particular occupation, whereas Nipah virus mostly occurred in men who worked with pigs. Early control measures, mosquito control (mosquito fogging) and JE virus vaccination programs did not affect the course of the outbreak. The possibility that JE virus was the cause were eliminated as there are illnesses and deaths among infected pigs. By February 1999, similar diseases arised in pigs and humans in other states in Malaysia, result by the movement of infected pigs into the new outbreak areas. In March 1999, a cluster of 11 cases of respiratory illnesses and encephalitis was noted in Singapore among pig farmers. The outbreak in Singapore ended when importation of pigs from Malaysia was prohibited, and the outbreak in Malaysia ceased when >1 million pigs were culled from the outbreak area. (Kaw Bing Chua, Sai Kit Lam, 2002)Isolation of the Nipah virus from the cerebrospinal fluid (CSF) of an outbreak victim (from Sungai Nipah village) brought acknowledgement that the infection was indeed caused by an agent unknown to science. This was done by a medical virologist at the University of Malaya in early March 1999. It was shown that Nipah virus and Hendra virus shared epitopes for Hendra virus antigens to be used in a prototype serological test for Nipah virus antibodies. This helped tremendously in the subsequent screening and diagnosis of Nipah virus infection. Prohibition of importation of pigs from Malaysia ended the outbreak in Singapore and the outbreak in Malaysia ceased culling of over a million pigs. 265 cases of acute Nipah virus encephalitis with 105 deaths had been recorded in Malaysia, giving a mortality rate of nearly 40%. (Lai Meng Looi, Kaw Bing Chua, 2007) 

INTRODUCTION Nipah virus is a disease of swine and human associated infection with a novel paramyxovirus named Nipah virus. Nipah virus belongs to the family Paramyxoviridae and it is now recognised as a new genus, Henipavirus (Hendra + Nipah), making it closely related to Hendra virus which emerged in the northern part of Peninsular Malaysia in 1998 and 1999. Nipah virus is a zoonotic type of disease, which means it passes from animals to humans. In Malaysia, Nipah virus outbreak occurred in pigs and humans from September 1998 to April 1999 resulted in death of 105 persons and 265 infected people. Fruit bats of the genus Pteropid (also known as flying foxes) appear to be the natural hosts of the virus. People can be infected by this virus from infected bats, pigs or even infected human. Nipah virus can causes systemic infections mostly in humans and pigs. However, this virus can also infect other mammal. Nipah virus caused an outbreak of severe febrile encephalitis in humans with a high mortality rate, as it was linked to severe encephalitis among people exposed to infected pigs, mostly in Malaysia and Singapore. Whereas, in pigs and other mammals, it causes encephalitis and respiratory diseases with a relatively low mortality rate. Characteristic of the disease are recognized by histopathological and radiological findings. (Kaw Bing Chua, 2003)    Nipah virus infection is an emerging infectious disease in the South-East Asia region. Evidence suggested that the emergence of Nipah virus is believed to be due to changes in ecological conditions, such as climatic and anthropogenic driven ecological changes, such as urbanization, deforestation and drought which resulting in shortage of resources for bat populations. This could have compelled bats to move to agricultural areas from their natural habitats. Other factors that contributed to the disease emergence is the establishment of pig farms within the range of natural host that led to the initial introduction of virus into the pig population. Rapid dissemination of the infection within local pig populations are led by the maintenance of high densities of pigs. The rapid spread of disease in pigs, especially in southern Malaysia and Singapore are led by the transportion of pigs to other geographic areas for commerce. The presence of high density, amplifying host population result in facilitated transmission to humans. The outbreak in humans may also be due to direct contact with bats or indirectly by contact with material contaminated by bats. The medical and veterinary professionals should also increase the awareness of the disease particularly hosts or reservoir of the virus and mode of transmission of the virus. The disease was eradicated from the national commercial swine population by control efforts. (Kulkarni et al, 2013)

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