Displaying publications 41 - 60 of 68 in total

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  1. Emerging and re-emerging diseases in Malaysia
    Lam SK
    Asia Pac J Public Health, 2002;14(1):6-8.
    PMID: 12597511 DOI: 10.1177/101053950201400103
    Emerging and re-emerging infectious diseases have become a major global problem. Malaysia appears to be an epicenter for such infections and in recent years, several outbreaks have occurred resulting in loss of lives and economic hardships. In this paper, we discussed the outbreaks of leptospirosis, enterovirus 71 encephalitis, chikungunya polyarthritis and Nipah encephalitis and how a developing country such as Malaysia managed the situation with the help of international agencies and organisations. Many valuable lessons were learned and by sharing our experience, it is hoped that we will be in a better position to handle future outbreaks and prevent their spread to countries in the region.
    Matched MeSH terms: Encephalitis, Viral/epidemiology
  2. Neurovirulence of four encephalitogenic dengue 3 virus strains isolated in Malaysia (1992-1994) is not attributed to their envelope protein
    Fong MY, Yusup R, Yusof R, Lam SK
    Trans R Soc Trop Med Hyg, 2004 Jun;98(6):379-81.
    PMID: 15099995
    The amino acid sequences of the envelope (E) protein of four encephalitogenic and five non-encephalitogenic dengue 3 virus strains isolated in Malaysia were determined and compared. Multiple sequence alignment revealed a high degree of similarity in the E protein of the strains suggesting that neurovirulence of these four encephalitogenic strains is not attributed to this protein.
    Matched MeSH terms: Encephalitis, Viral/virology*
  3. Understanding Enterovirus 71 Neuropathogenesis and Its Impact on Other Neurotropic Enteroviruses
    Ong KC, Wong KT
    Brain Pathol, 2015 Sep;25(5):614-24.
    PMID: 26276025 DOI: 10.1111/bpa.12279
    Enterovirus A71 (EV-A71) belongs to the species group A in the Enterovirus genus within the Picornaviridae family. EV-A71 usually causes self-limiting hand, foot and mouth disease or herpangina but rarely causes severe neurological complications such as acute flaccid paralysis and encephalomyelitis. The pathology and neuropathogenesis of these neurological syndromes is beginning to be understood. EV-A71 neurotropism for motor neurons in the spinal cord and brainstem, and other neurons, is mainly responsible for central nervous system damage. This review on the general aspects, recent developments and advances of EV-A71 infection will focus on neuropathogenesis and its implications on other neurotropic enteroviruses, such as poliovirus and the newly emergent Enterovirus D68. With the imminent eradication of poliovirus, EV-A71 is likely to replace it as an important neurotropic enterovirus of worldwide importance.
    Matched MeSH terms: Encephalitis, Viral/pathology*
  4. COVID-19 and its effects on neurological functions
    Yew MMT, Lip JQ, Ling APK
    Trop Biomed, 2021 Sep 01;38(3):435-445.
    PMID: 34608117 DOI: 10.47665/tb.38.3.086
    Ever since the first reported case series on SARS-CoV-2-induced neurological manifestation in Wuhan, China in April 2020, various studies reporting similar as well as diverse symptoms of COVID-19 infection relating to the nervous system were published. Since then, scientists started to uncover the mechanism as well as pathophysiological impacts it has on the current understanding of the disease. SARS-CoV-2 binds to the ACE2 receptor which is present in certain parts of the body which are responsible for regulating blood pressure and inflammation in a healthy system. Presence of the receptor in the nasal and oral cavity, brain, and blood allows entry of the virus into the body and cause neurological complications. The peripheral and central nervous system could also be invaded directly in the neurogenic or hematogenous pathways, or indirectly through overstimulation of the immune system by cytokines which may lead to autoimmune diseases. Other neurological implications such as hypoxia, anosmia, dysgeusia, meningitis, encephalitis, and seizures are important symptoms presented clinically in COVID-19 patients with or without the common symptoms of the disease. Further, patients with higher severity of the SARS-CoV-2 infection are also at risk of retaining some neurological complications in the long-run. Treatment of such severe hyperinflammatory conditions will also be discussed, as well as the risks they may pose to the progression of the disease. For this review, articles pertaining information on the neurological manifestation of SARS-CoV-2 infection were gathered from PubMed and Google Scholar using the search keywords "SARS-CoV-2", "COVID-19", and "neurological dysfunction". The findings of the search were filtered, and relevant information were included.
    Matched MeSH terms: Encephalitis, Viral/virology
  5. Fulltext The Nipah virus outbreak--a reminder
    Tambyah PA
    Singapore Med J, 1999 May;40(5):329-30.
    PMID: 10489488
    Matched MeSH terms: Encephalitis, Viral/epidemiology*
  6. Fulltext Detailed analysis of the pathologic hallmarks of Nipah virus (Malaysia) disease in the African green monkey infected by the intratracheal route
    Cline C, Bell TM, Facemire P, Zeng X, Briese T, Lipkin WI, et al.
    PLoS One, 2022;17(2):e0263834.
    PMID: 35143571 DOI: 10.1371/journal.pone.0263834
    Disease associated with Nipah virus infection causes a devastating and often fatal spectrum of syndromes predominated by both respiratory and neurologic conditions. Additionally, neurologic sequelae may manifest months to years later after virus exposure or apparent recovery. In the two decades since this disease emerged, much work has been completed in an attempt to understand the pathogenesis and facilitate development of medical countermeasures. Here we provide detailed organ system-specific pathologic findings following exposure of four African green monkeys to 2.41×105 pfu of the Malaysian strain of Nipah virus. Our results further substantiate the African green monkey as a model of human Nipah virus disease, by demonstrating both the respiratory and neurologic components of disease. Additionally, we demonstrate that a chronic phase of disease exists in this model, that may provide an important opportunity to study the enigmatic late onset and relapse encephalitis as it is described in human disease.
    Matched MeSH terms: Encephalitis, Viral/pathology*
  7. Clinical and pathological manifestations of human henipavirus infection
    Wong KT, Tan CT
    Curr. Top. Microbiol. Immunol., 2012;359:95-104.
    PMID: 22427144 DOI: 10.1007/82_2012_205
    The clinicopathological features of human Nipah virus and Hendra virus infections appear to be similar. The clinical manifestations may be mild, but if severe, includes acute encephalitic and pulmonary syndromes with a high mortality. The pathological features in human acute henipavirus infections comprise vasculopathy (vasculitis, endothelial multinucleated syncytia, thrombosis), microinfarcts and parenchymal cell infection in the central nervous system, lung, kidney and other major organs. Viral inclusions, antigens, nucleocapsids and RNA are readily demonstrated in blood vessel wall and numerous types of parenchymal cells. Relapsing henipavirus encephalitis is a rare complication reported in less than 10% of survivors of the acute infection and appears to be distinct from the acute encephalitic syndrome. Pathological evidence suggests viral recrudescence confined to the central nervous system as the cause.
    Matched MeSH terms: Encephalitis, Viral/complications; Encephalitis, Viral/mortality; Encephalitis, Viral/pathology*; Encephalitis, Viral/virology
  8. In enterovirus 71 encephalitis with cardio-respiratory compromise, elevated interleukin 1β, interleukin 1 receptor antagonist, and granulocyte colony-stimulating factor levels are markers of poor prognosis
    Griffiths MJ, Ooi MH, Wong SC, Mohan A, Podin Y, Perera D, et al.
    J Infect Dis, 2012 Sep 15;206(6):881-92.
    PMID: 22829643 DOI: 10.1093/infdis/jis446
    BACKGROUND: Enterovirus 71 (EV71) causes large outbreaks of hand, foot, and mouth disease (HFMD), with severe neurological complications and cardio-respiratory compromise, but the pathogenesis is poorly understood.

    METHODS: We measured levels of 30 chemokines and cytokines in serum and cerebrospinal fluid (CSF) samples from Malaysian children hospitalized with EV71 infection (n = 88), comprising uncomplicated HFMD (n = 47), meningitis (n = 8), acute flaccid paralysis (n = 1), encephalitis (n = 21), and encephalitis with cardiorespiratory compromise (n = 11). Four of the latter patients died.

    RESULTS: Both pro-inflammatory and anti-inflammatory mediator levels were elevated, with different patterns of mediator abundance in the CSF and vascular compartments. Serum concentrations of interleukin 1β (IL-1β), interleukin 1 receptor antagonist (IL-1Ra), and granulocyte colony-stimulating factor (G-CSF) were raised significantly in patients who developed cardio-respiratory compromise (P = .013, P = .004, and P < .001, respectively). Serum IL-1Ra and G-CSF levels were also significantly elevated in patients who died, with a serum G-CSF to interleukin 5 ratio of >100 at admission being the most accurate prognostic marker for death (P < .001; accuracy, 85.5%; sensitivity, 100%; specificity, 84.7%).

    CONCLUSIONS: Given that IL-1β has a negative inotropic action on the heart, and that both its natural antagonist, IL-1Ra, and G-CSF are being assessed as treatments for acute cardiac impairment, the findings suggest we have identified functional markers of EV71-related cardiac dysfunction and potential treatment options.

    Matched MeSH terms: Encephalitis, Viral/blood; Encephalitis, Viral/cerebrospinal fluid; Encephalitis, Viral/etiology*; Encephalitis, Viral/epidemiology
  9. Fulltext Agricultural intensification, priming for persistence and the emergence of Nipah virus: a lethal bat-borne zoonosis
    Pulliam JR, Epstein JH, Dushoff J, Rahman SA, Bunning M, Jamaluddin AA, et al.
    J R Soc Interface, 2012 Jan 7;9(66):89-101.
    PMID: 21632614 DOI: 10.1098/rsif.2011.0223
    Emerging zoonoses threaten global health, yet the processes by which they emerge are complex and poorly understood. Nipah virus (NiV) is an important threat owing to its broad host and geographical range, high case fatality, potential for human-to-human transmission and lack of effective prevention or therapies. Here, we investigate the origin of the first identified outbreak of NiV encephalitis in Malaysia and Singapore. We analyse data on livestock production from the index site (a commercial pig farm in Malaysia) prior to and during the outbreak, on Malaysian agricultural production, and from surveys of NiV's wildlife reservoir (flying foxes). Our analyses suggest that repeated introduction of NiV from wildlife changed infection dynamics in pigs. Initial viral introduction produced an explosive epizootic that drove itself to extinction but primed the population for enzootic persistence upon reintroduction of the virus. The resultant within-farm persistence permitted regional spread and increased the number of human infections. This study refutes an earlier hypothesis that anomalous El Niño Southern Oscillation-related climatic conditions drove emergence and suggests that priming for persistence drove the emergence of a novel zoonotic pathogen. Thus, we provide empirical evidence for a causative mechanism previously proposed as a precursor to widespread infection with H5N1 avian influenza and other emerging pathogens.
    Matched MeSH terms: Encephalitis, Viral/epidemiology*; Encephalitis, Viral/transmission
  10. Organ- and endotheliotropism of Nipah virus infections in vivo and in vitro
    Maisner A, Neufeld J, Weingartl H
    Thromb. Haemost., 2009 Dec;102(6):1014-23.
    PMID: 19967130 DOI: 10.1160/TH09-05-0310
    Nipah virus (NiV) is a highly pathogenic paramyxovirus that was first isolated in 1999 during an outbreak in Malaysia. In contrast to other paramyxoviruses NiV infects many mammalian species. Because of its zoonotic potential, the high pathogenicity and the lack of therapeutic treatment, NiV was classified as a biosafety level 4 pathogen. In humans NiV causes a severe acute encephalitis whereas in some animal hosts respiratory symptoms are predominantly observed. Despite the differences in the clinical outcome, microvascular endothelial cell damage predominantly underlies the pathological changes in NiV infections in all susceptible host species. NiV generally induces a pronounced vasculitis which is primarily characterised by endothelial cell necrosis and inflammatory cell infiltration. For future developments of specific antiviral therapies or vaccines, a detailed understanding of the molecular basis of NiV pathogenesis is required. This article reviews the current knowledge about natural and experimental infections in different mammals, focusing on the main organ and cell tropism in vivo, and summarises some recent studies in cell culture on the role of ephrin-B2 and -B3 receptors in NiV infection of endothelial cells.
    Matched MeSH terms: Encephalitis, Viral/etiology; Encephalitis, Viral/virology
  11. Dengue encephalitis: a true entity?
    Lum LC, Lam SK, Choy YS, George R, Harun F
    Am J Trop Med Hyg, 1996 Mar;54(3):256-9.
    PMID: 8600761 DOI: 10.4269/ajtmh.1996.54.256
    Involvement of the central nervous system in dengue fever and dengue hemorrhagic fever has always been thought to be secondary to vasculitis with resultant fluid extravasation, cerebral edema, hypoperfusion, hyponatremia, liver failure, and/or renal failure. Thus, the condition has been referred to as dengue encephalopathy. Encephalitis or direct involvement of the brain by the virus was thought to be unlikely. This paper reports on six children who were seen over a period of two years presenting on the second or third day of illness with dengue encephalitis. The diagnosis was based upon a clinical picture of encephalitis and confirmed by cerebrospinal fluid (CSF) microscopy and electroencephalography changes. All six cases were confirmed dengue infections. Dengue 3 virus was isolated from the CSF of four cases and in one case, dengue 2 was detected by the polymerase chain reaction in both the CSF and blood. In the sixth case, virologic evidence was negative but dengue immunoglobulin M was detected in the CSF and blood. Since the onset of encephalitis appears early in the course of illness coinciding with the viremic phase, we postulate that the virus crosses the blood-brain barrier and directly invades the brain causing encephalitis. This study provides strong evidence that dengue 2 and 3 viruses have neurovirulent properties and behave similarly to other members of the Flaviviridae.
    Matched MeSH terms: Encephalitis, Viral/cerebrospinal fluid; Encephalitis, Viral/virology*
  12. Nipah virus: an emergent paramyxovirus causing severe encephalitis in humans
    Bellini WJ, Harcourt BH, Bowden N, Rota PA
    J Neurovirol, 2005 Oct;11(5):481-7.
    PMID: 16287690
    Nipah virus is a recently emergent paramyxovirus that is capable of causing severe disease in both humans and animals. The first outbreak of Nipah virus occurred in Malaysia and Singapore in 1999 and, more recently, outbreaks were detected in Bangladesh. In humans, Nipah virus causes febrile encephalitis with respiratory syndrome that has a high mortality rate. The reservoir for Nipah virus is believed to be fruit bats, and humans are infected by contact with infected bats or by contact with an intermediate animal host such as pigs. Person to person spread of the virus has also been described. Nipah virus retains many of the genetic and biologic properties found in other paramyxoviruses, though it also has several unique characteristics. However, the virologic characteristics that allow the virus to cause severe disease over a broad host range, and the epidemiologic, environmental and virologic features that favor transmission to humans are unknown. This review summarizes what is known about the virology, epidemiology, pathology, diagnosis and control of this novel pathogen.
    Matched MeSH terms: Encephalitis, Viral/diagnosis*; Encephalitis, Viral/epidemiology*
  13. Nipah viral encephalitis or Japanese encephalitis? MR findings in a new zoonotic disease
    Lim CC, Sitoh YY, Hui F, Lee KE, Ang BS, Lim E, et al.
    AJNR Am J Neuroradiol, 2000 Mar;21(3):455-61.
    PMID: 10730635
    BACKGROUND AND PURPOSE: An epidemic of suspected Japanese encephalitis occurred in Malaysia in 1998-1999 among pig farmers. In neighboring Singapore, an outbreak occurred among pig slaughterhouse workers. It was subsequently established that the causative agent in the outbreak was not the Japanese encephalitis virus but a previously unknown Hendra-like paramyxovirus named Nipah virus.

    METHODS: The brain MR images of eight patients with Nipah virus infection were reviewed. All patients tested negative for acute Japanese encephalitis virus. Seven patients had contrast-enhanced studies and six had diffusion-weighted examinations.

    RESULTS: All patients had multiple small bilateral foci of T2 prolongation within the subcortical and deep white matter. The periventricular region and corpus callosum were also involved. In addition to white matter disease, five patients had cortical lesions, three had brain stem involvement, and a single thalamic lesion was detected in one patient. All lesions were less than 1 cm in maximum diameter. In five patients, diffusion-weighted images showed increased signal. Four patients had leptomeningeal enhancement and four had enhancement of parenchymal lesions.

    CONCLUSION: The brain MR findings in patients infected with the newly discovered Nipah paramyxovirus are different from those of patients with Japanese encephalitis. In a zoonotic epidemic, this striking difference in the appearance and distribution of lesions is useful in differentiating these diseases. Diffusion-weighted imaging was advantageous in increasing lesion conspicuity.

    Matched MeSH terms: Encephalitis, Viral/diagnosis*; Encephalitis, Viral/epidemiology
  14. Fulltext Encephalitis followed by optic neuritis: a case report and review of literature
    Hasan S, B Basri H, P Hin L, Stanslas J
    Pak J Med Sci, 2013 May;29(3):859-62.
    PMID: 24353644
    Encephalitis has been included in the causes of optic neuritis, but post encephalitic optic neuritis has been rarely reported. Majority of the cases of optic neuritis are either idiopathic or associated with multiple sclerosis, especially in western countries. This is very important in the Asian population where the incidence and prevalence of multiple sclerosis is not as high as in the Western countries. Although post infectious optic neuritis is more common in children, it can also be found in adults and is usually seen one to three weeks after a symptomatic infective prodrome. Here, we present a case of a 48 year-old-male who developed optic neuritis following viral encephalitis. His first presentation was with severe headache of two weeks duration. Viral encephalitis was diagnosed and treated. The patient presented again three weeks later with right eye pain and other features typical of optic neuritis. Corticosteroid therapy facilitated prompt recovery. Optic neuritis is an uncommon manifestation of encephalitis. It is important that both doctors and patients remain aware of post infectious cause of optic neuritis, which would enable a timely diagnosis and treatment of this reversible cause of vision loss.
    Matched MeSH terms: Encephalitis, Viral
  15. Human Hendra virus infection causes acute and relapsing encephalitis
    Wong KT, Robertson T, Ong BB, Chong JW, Yaiw KC, Wang LF, et al.
    Neuropathol. Appl. Neurobiol., 2009 Jun;35(3):296-305.
    PMID: 19473296 DOI: 10.1111/j.1365-2990.2008.00991.x
    To study the pathology of two cases of human Hendra virus infection, one with no clinical encephalitis and one with relapsing encephalitis.
    Matched MeSH terms: Encephalitis, Viral/immunology; Encephalitis, Viral/pathology*; Encephalitis, Viral/virology
  16. Nipah virus outbreak in Malaysia
    Chua KB
    J Clin Virol, 2003 Apr;26(3):265-75.
    PMID: 12637075
    Nipah virus, a novel paramyxovirus, closely related to Hendra virus emerged in northern part of Peninsular Malaysia in 1998. The virus caused an outbreak of severe febrile encephalitis in humans with a high mortality rate, whereas, in pigs, encephalitis and respiratory diseases but with a relatively low mortality rate. The outbreak subsequently spread to various regions of the country and Singapore in the south due to the movement of infected pigs. Nipah virus caused systemic infections in humans, pigs and other mammals. Histopathological and radiological findings were characteristic of the disease. Fruitbats of Pteropid species were identified as the natural reservoir hosts. Evidence suggested that climatic and anthropogenic driven ecological changes coupled with the location of piggeries in orchard and the design of pigsties allowed the spill-over of this novel paramyxovirus from its reservoir host into the domestic pigs and ultimately to humans and other animals.
    Matched MeSH terms: Encephalitis, Viral/mortality; Encephalitis, Viral/epidemiology*; Encephalitis, Viral/virology
  17. Fulltext Nipah virus encephalitis — a review
    Tan, C.T., Chua, K.B., Wong, K.T.
    ASM Science Journal, 2009;3(1):91-96.
    MyJurnal
    The Nipah virus was first discovered in 1999, following a severe outbreak of viral encephalitis among pig farm workers in Malaysia. The virus was thought to have spread from Pteropus bats to pigs, then from infected pigs to humans by close contact. Mortality of the disease was high at about 40%. The main necropsy finding was disseminated microinfarction associated with vasculitis and direct neuronal involvement. Relapsed encephalitis was seen in approximately 10% of those who survived the initial illness. Since its first recorded emergence in peninsular Malaysia, 10 outbreaks of Nipah virus encephalitis have been reported in Bangladesh and West Bengal in India. The outbreaks occurred from January to May, with Pteropus giganteus as the reservoir of the virus. In Bangladesh, evidence indicated that the virus transmitted directly from bats to human, with human to human transmission as an important mode of spread. The mortality of the illness was higher in Bangladesh which stood at around 70%. This was likely to be due to genetic variation of the virus.
    Matched MeSH terms: Encephalitis, Viral
  18. Risk factors for Nipah virus infection among abattoir workers in Singapore
    Chew MH, Arguin PM, Shay DK, Goh KT, Rollin PE, Shieh WJ, et al.
    J Infect Dis, 2000 May;181(5):1760-3.
    PMID: 10823780
    During 10-19 March 1999, 11 workers in 1 of 2 Singaporean abattoirs developed Nipah-virus associated encephalitis or pneumonia, resulting in 1 fatality. A case-control study was conducted to determine occupational risk factors for infection. Case patients were abattoir A workers who had anti-Nipah IgM antibodies; control subjects were randomly selected abattoir A workers who tested negative for anti-Nipah IgM. All 13 case patients versus 26 (63%) of 41 control subjects reported contact with live pigs (P=.01). Swine importation from Malaysian states concurrently experiencing a Nipah virus outbreak was banned on 3 March 1999; on 19 March 1999, importation of Malaysian pigs was banned, and abattoirs were closed. No unusual illnesses among pigs processed during February-March were reported. Contact with live pigs appeared to be the most important risk factor for human Nipah virus infection. Direct contact with live, potentially infected pigs should be minimized to prevent transmission of this potentially fatal zoonosis to humans.
    Matched MeSH terms: Encephalitis, Viral/diagnosis; Encephalitis, Viral/epidemiology*; Encephalitis, Viral/transmission
  19. Case-control study of risk factors for human infection with a new zoonotic paramyxovirus, Nipah virus, during a 1998-1999 outbreak of severe encephalitis in Malaysia
    Parashar UD, Sunn LM, Ong F, Mounts AW, Arif MT, Ksiazek TG, et al.
    J Infect Dis, 2000 May;181(5):1755-9.
    PMID: 10823779
    An outbreak of encephalitis affecting 265 patients (105 fatally) occurred during 1998-1999 in Malaysia and was linked to a new paramyxovirus, Nipah, that infected pigs, humans, dogs, and cats. Most patients were pig farmers. Clinically undetected Nipah infection was noted in 10 (6%) of 166 community-farm controls (persons from farms without reported encephalitis patients) and 20 (11%) of 178 case-farm controls (persons from farms with encephalitis patients). Case patients (persons with Nipah infection) were more likely than community-farm controls to report increased numbers of sick/dying pigs on the farm (59% vs. 24%, P=.001) and were more likely than case-farm controls to perform activities requiring direct contact with pigs (86% vs. 50%, P=.005). Only 8% of case patients reported no contact with pigs. The outbreak stopped after pigs in the affected areas were slaughtered and buried. Direct, close contact with pigs was the primary source of human Nipah infection, but other sources, such as infected dogs and cats, cannot be excluded.
    Matched MeSH terms: Encephalitis, Viral/epidemiology; Encephalitis, Viral/transmission; Encephalitis, Viral/virology*
  20. Fulltext Risk factors, prevention and communication strategy during Nipah virus outbreak in Malaysia
    Chua KB
    Malays J Pathol, 2010 Dec;32(2):75-80.
    PMID: 21329177 MyJurnal
    An outbreak of acute febrile encephalitis affecting pig-farm workers and owners was recognized in peninsular Malaysia as early as September 1998. The outbreak was initially thought to be due to Japanese encephalitis (JE) virus and thus very intensive prevention, control and communication strategies directed at JE virus were undertaken by the Ministry of Health and Ministry of Agriculture of Malaysia. There was an immediate change in the prevention, control and communication strategies with focus and strategies on infected pigs as the source of infections for humans and other animals following the discovery of Nipah virus. Information and understanding the risks of Nipah virus infections and modes of transmission strengthened the directions of prevention, control and communication strategies. A number of epidemiological surveillances and field investigations which were broadly divided into 3 groups covering human health sector, animal health sector and reservoir hosts were carried out as forms of risk assessment to determine and assess the factors and degree of risk of infections by the virus. Data showed that there was significant association between Nipah virus infection and performing activities involving close contact with pigs, such as processing of piglets, administering injection or medication to pigs, assisting in the birth of piglets, assisting in pig breeding, and handling of dead pigs in the affected farms. A complex process of anthropogenic driven deforestation, climatic changes brought on by El Niño-related drought, forest fire and severe haze, and ecological factors of mixed agro-pig farming practices and design of pig-sties led to the spillovers of the virus from its wildlife reservoir into pig population.
    Matched MeSH terms: Encephalitis, Viral/prevention & control*
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