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Encephalitis in racehorses in Malaya

HALE JH, WITHERINGTON DH

J Comp Pathol, 1953 Jul;63(3):195-8.
PMID: 13084794
Matched MeSH terms: Encephalomyelitis*; Encephalomyelitis, Equine/epidemiology*
Fatal enterovirus 71 encephalomyelitis

Lum LC, Wong KT, Lam SK, Chua KB, Goh AY, Lim WL, et al.

J Pediatr, 1998 Dec;133(6):795-8.
PMID: 9842048

During an outbreak of hand-foot-mouth disease caused by enterovirus 71 (EV-71) in 1997, 4 children presented with sudden cardiopulmonary collapse and minimal neurologic features. All children received cardiopulmonary resuscitation but died within a few hours of admission. Postmortem studies showed infection by EV-71 with extensive damage to the medulla and pons. We postulate an etiologic link between EV-71 and brainstem encephalomyelitis as the cause of pulmonary edema and death.

Matched MeSH terms: Encephalomyelitis/pathology; Encephalomyelitis/virology*
Acute disseminated encephalomyelitis complicating dengue infection with neuroimaging mimicking multiple sclerosis: A report of two cases

Viswanathan S, Botross N, Rusli BN, Riad A

Mult Scler Relat Disord, 2016 Nov;10:112-115.
PMID: 27919476 DOI: 10.1016/j.msard.2016.10.001

Acute disseminated encephalomyelitis (ADEM) complicating dengue infection is still exceedingly rare even in endemic countries such as Malaysia. Here we report two such cases, the first in an elderly female patient and the second in a young man. Both presented with encephalopathy, brainstem involvement and worsening upper and lower limb weakness. Initial magnetic resonance imaging (MRI) of the brain was normal in the first case. Serum for dengue Ig M and NS-1 was positive in both cases. Cerebrospinal fluid (CSF) showed pleocytosis in both with Dengue IgM and NS-1 positive in the second case but not done in the first. MRI brain showed changes of perpendicular subcortical palisading white matter, callosal and brainstem disease mimicking multiple sclerosis (MS) in both patients though in the former case there was a lag between the onset of clinical symptoms and MRI changes which was only clarified on reimaging. The temporal evolution and duration of the clinical symptoms, CSF changes and neuroimaging were more suggestive of Dengue ADEM rather than an encephalitis though initially the first case began as dengue encephalitis. Furthermore in dengue encephalitis neuroimaging is usually normal or rarely edema, haemorrhage, brainstem, thalamic or focal lesions are seen. Therefore, early recognition of ADEM as a sequelae of dengue infection with neuroimaging mimicking MS and repeat imaging helped in identifying these two cases. Treatment with intravenous steroids followed by maintenance oral steroids produced good outcome in both patients.

Matched MeSH terms: Encephalomyelitis, Acute Disseminated/cerebrospinal fluid; Encephalomyelitis, Acute Disseminated/complications*; Encephalomyelitis, Acute Disseminated/drug therapy
Fulltext Acute disseminated encephalomyelitis: a report of six cases

Thomas GST, Hussain IHMI

Med J Malaysia, 2004 Aug;59(3):342-51.
PMID: 15727380 MyJurnal

Six children with Acute Disseminated Encephalomyelitis (ADEM) were seen at the Penang Hospital over a two year period (July 1999-June 2001). Diagnosis was based upon typical clinical features and characteristic findings on neuroimaging. Cerebrospinal fluid examination and other investigations were done, where appropriate, to rule out other causes of central nervous system disease. Three children had a prodromal illness. The most common presenting symptoms were fever, seizures, ataxia, focal neurological deficits and labile mood. Two children presented with status epilepticus. All children had an abnormal neurological examination. Brain magnetic resonance imaging revealed hyperintense signals on T2-weighted and FLAIR sequences in the subcortical and deep white matter regions of the frontal, parietal, and temporal lobes, as well as in the thalami, cerebellum and brainstem. One child had multiphasic disseminated encephalomyelitis (three episodes). The child with multiphasic disease had only one treated episode, and has suffered mild disability. Three children were treated with either methylprednisolone or immunoglobulins, and remain well. One child received both treatments but expired as a result of severe gastrointestinal bleeding from the use of methylprednisolone. The child who was not treated has severe disability.

Matched MeSH terms: Encephalomyelitis, Acute Disseminated/complications; Encephalomyelitis, Acute Disseminated/diagnosis*; Encephalomyelitis, Acute Disseminated/therapy
Smallpox vaccination: complications and present role

Balasundram R

Med J Malaya, 1972 Dec;27(2):89-94.
PMID: 4145716
Matched MeSH terms: Encephalomyelitis, Acute Disseminated/etiology; Encephalomyelitis/etiology
Identification of enterovirus 71 isolates from an outbreak of hand, foot and mouth disease (HFMD) with fatal cases of encephalomyelitis in Malaysia

AbuBakar S, Chee HY, Al-Kobaisi MF, Xiaoshan J, Chua KB, Lam SK

Virus Res, 1999 May;61(1):1-9.
PMID: 10426204

Thirteen enterovirus 71 (EV71) isolates were obtained from both fatal and non-fatal infections of patients seen in Peninsula Malaysia and in Sarawak during an outbreak of hand, foot and mouth disease (HFMD) in Malaysia in 1997, with incidences of fatal brainstem encephalomyelitis. The isolates were identified using immunofluorescence staining, neutralization assays, and partial sequencing of the 5' untranslated regions (UTR). Assessment of the potential genetic relationships of the isolates using the partial 5'UTR sequences suggested clustering of the isolates into at least two main clusters. Isolates from Peninsula Malaysia were found in both clusters whereas Sarawak-derived isolates clustered only in cluster II. Isolates derived from fatal infections, however, occurred in both clusters and no distinctive nucleotide sequences could be attributed to the fatal isolates. Examination of the nucleotide sequences revealed at least 13 nucleotide positions in all the isolates which differ completely from the previously reported EV71 5'UTR sequences. In addition, at least 11 nucleotide position differences within the 5'UTR were noted which differentiated cluster I from cluster II. Predicted secondary RNA structures drawn using the nucleotide sequences also suggested differences between isolates from the two clusters. These findings suggest the presence of at least two potentially virulent EV71 co-circulating in Malaysia during the 1997 HFMD outbreak.

Matched MeSH terms: Encephalomyelitis/mortality; Encephalomyelitis/epidemiology; Encephalomyelitis/virology*
Fulltext Intravenous immunoglobulin in the treatment of acute disseminated encephalomyelitis

Kanaheswari Y, Baizura J, Zulfiqar A

Med J Malaysia, 2004 Mar;59(1):103-7.
PMID: 15535344

We describe a case of acute disseminated encephalomyelitis in a child. This case is unusual in that the illness was characterised by recurrent episodes rather than a monophasic course and that the choice of treatment was intravenous immunoglobulin over corticosteroids. The rapid and remarkable recovery is highlighted and a review of the treatment for this rare condition is discussed.

Matched MeSH terms: Encephalomyelitis, Acute Disseminated/diagnosis; Encephalomyelitis, Acute Disseminated/drug therapy*
Neurogenic pulmonary oedema and enterovirus 71 encephalomyelitis

Lum LC, Wong KT, Lam SK, Chua KB, Goh AY

Lancet, 1998 Oct 24;352(9137):1391.
PMID: 9802304
Matched MeSH terms: Encephalomyelitis/epidemiology; Encephalomyelitis/virology*
Japanese B encephalitis in a horse

Chong Sue Kheng, Teoh Kim Chee, Marchette NJ, Garcia R, Rudnick A, Coughlan RF

Aust. Vet. J., 1968 Jan;44(1):23-5.
PMID: 5689238
Matched MeSH terms: Encephalomyelitis, Equine/immunology; Encephalomyelitis, Equine/epidemiology*
Multiphasic disseminated encephalomyelitis followed by optic neuritis in a child with gluten sensitivity

Ching BH, Mohamed AR, Khoo TB, Ismail HI

Mult Scler, 2015 Aug;21(9):1209-11.
PMID: 26199345 DOI: 10.1177/1352458515593404

Multiphasic disseminated encephalomyelitis (MDEM) followed by optic neuritis (ON) has been described as a new entity in recent years. Gluten encephalopathy has also been recognized as a neurological manifestation of celiac disease. Accurate diagnosis of both is important due to the therapeutic implications. We report a girl presenting with recurrent encephalopathic polyfocal demyelinating episodes followed by optic neuritis, and a clinical history suggestive of gluten sensitivity. She had persistently high ESR, neutrophilia, and tested positive for anti-MOG (myelin oligodendrocyte glycoprotein) antibody. She responded well to methylprednisolone in each relapse, and achieved remission for a year after azathioprine was added.

Matched MeSH terms: Encephalomyelitis, Acute Disseminated/complications*; Encephalomyelitis, Acute Disseminated/pathology
Fulltext Mumps encephalomyelitis

Tan KK, Manickam WD, Cardosa MJ

Singapore Med J, 1992 Oct;33(5):525-6.
PMID: 1455285

A 7-year-old Indian girl developed complete paralysis of her lower limbs and acute urinary retention 10 days after suffering from mumps. Encephalomyelitis due to mumps was not suspected initially since it is a rare complication of mumps, although relatively well-documented. However, the preceding history of parotitis and the presence of mumps-specific IgM in both blood and cerebrospinal fluid led to the diagnosis. The initially severe acute neurological deficits resolved completely three months after onset of her illness. Serological investigations were helpful in diagnosing neurological complications of mumps in this case, and especially where there is no preceding parotitis.
Keywords: Mumps, encephalomyelitis, infection, Pulau Pinang, general hospital, Malaysia

Matched MeSH terms: Encephalomyelitis/etiology*; Encephalomyelitis/microbiology
A monoclonal antibody to ameliorate central nervous system infection and improve survival in a murine model of human Enterovirus-A71 encephalomyelitis

Tan SH, Ong KC, Perera D, Wong KT

Antiviral Res, 2016 Aug;132:196-203.
PMID: 27340013 DOI: 10.1016/j.antiviral.2016.04.015

BACKGROUND: Enterovirus A71 (EV-A71) encephalomyelitis is an often fatal disease for which there is no specific treatment available. Passive immunization with a specific monoclonal antibody to EV-A71 was used on a murine model of EV-A71 encephalomyelitis to evaluate its therapeutic effectiveness before and after established central nervous system (CNS) infection.
METHODS: Mice were intraperitoneally-infected with a mouse-adapted EV-A71 strain and treated with a dose of monoclonal antibody (MAb) daily for 3 days on day 1, 2 and 3 post-infection or for 3 days on 3, 4 and 5 post-infection. Treatment effectiveness was evaluated by signs of infection and survival rate. Histopathology and qPCR analyses were performed on mice sacrificed a day after completing treatment.
RESULTS: In mock-treated mice, CNS infection was established from day 3 post-infection. All mice treated before established CNS infection, survived and recovered completely without CNS infection. All mice treated after established CNS infection survived with mild paralysis, and viral load and antigens/RNA at day 6 post-infection were significantly reduced.
CONCLUSIONS: Passive immunization with our MAb could prevent CNS infection in mice if given early before the establishment of CNS infection. It could also ameliorate established CNS infection if optimal and repeated doses were given.

Matched MeSH terms: Encephalomyelitis/drug therapy; Encephalomyelitis/immunology; Encephalomyelitis/mortality; Encephalomyelitis/virology*
Fulltext AIM2 Inflammasome-Mediated Pyroptosis in Enterovirus A71-Infected Neuronal Cells Restricts Viral Replication

Yogarajah T, Ong KC, Perera D, Wong KT

Sci Rep, 2017 07 19;7(1):5845.
PMID: 28724943 DOI: 10.1038/s41598-017-05589-2

Encephalomyelitis is a well-known complication of hand, foot, and mouth disease (HFMD) due to Enterovirus 71 (EV71) infection. Viral RNA/antigens could be detected in the central nervous system (CNS) neurons in fatal encephalomyelitis but the mechanisms of neuronal cell death is not clearly understood. We investigated the role of absent in melanoma 2 (AIM2) inflammasome in neuronal cell death, and its relationship to viral replication. Our transcriptomic analysis, RT-qPCR, Western blot, immunofluorescence and flow cytometry studies consistently showed AIM2 gene up-regulation and protein expression in EV-A71-infected SK-N-SH cells. Downstream AIM2-induced genes, CARD16, caspase-1 and IL-1β were also up-regulated and caspase-1 was activated to form cleaved caspase-1 p20 subunits. As evidenced by 7-AAD positivity, pyroptosis was confirmed in infected cells. Overall, these findings have a strong correlation with decreases in viral titers, copy numbers and proteins, and reduced proportions of infected cells. AIM2 and viral antigens were detected by immunohistochemistry in infected neurons in inflamed areas of the CNS in EV-A71 encephalomyelitis. In infected AIM2-knockdown cells, AIM2 and related downstream gene expressions, and pyroptosis were suppressed, resulting in significantly increased virus infection. These results support the notion that AIM2 inflammasome-mediated pyroptosis is an important mechanism of neuronal cell death and it could play an important role in limiting EV-A71 replication.

Matched MeSH terms: Encephalomyelitis/pathology; Encephalomyelitis/virology
Echovirus 7 associated encephalomyelitis

Lum LC, Chua KB, McMinn PC, Goh AY, Muridan R, Sarji SA, et al.

J Clin Virol, 2002 Jan;23(3):153-60.
PMID: 11595594

Hand, foot, and mouth disease (HFMD) is endemic in Malaysia. In 1997, a large outbreak of enterovirus 71 (EV-71) associated HFMD resulted in 41 deaths due to severe left ventricular dysfunction and central nervous system infection with extensive damage to the medulla and pons. The clinical presentation in all these patients were rapid cardio-respiratory decompensation leading to cardiac arrest. Another large outbreak of HFMD with 55 fatal cases and a similar clinical picture was reported in Taiwan in 1998. In 2000, an outbreak of HFMD resulted in the deaths of three children who had rapid cardio-respiratory decompensation and one child who survived a central nervous system infection.

Matched MeSH terms: Encephalomyelitis/blood; Encephalomyelitis/diagnosis; Encephalomyelitis/virology*
Acute disseminated encephalomyelitis in dengue viral infection

Wan Sulaiman WA, Inche Mat LN, Hashim HZ, Hoo FK, Ching SM, Vasudevan R, et al.

J Clin Neurosci, 2017 Sep;43:25-31.
PMID: 28625589 DOI: 10.1016/j.jocn.2017.05.033

Dengue is the most common arboviral disease affecting many countries worldwide. An RNA virus from the flaviviridae family, dengue has four antigenically distinct serotypes (DEN-1-DEN-4). Neurological involvement in dengue can be classified into dengue encephalopathy immune-mediated syndromes, encephalitis, neuromuscular or dengue muscle dysfunction and neuro-ophthalmic involvement. Acute disseminated encephalomyelitis (ADEM) is an immune mediated acute demyelinating disorder of the central nervous system following recent infection or vaccination. This monophasic illness is characterised by multifocal white matter involvement. Many dengue studies and case reports have linked ADEM with dengue virus infection but the association is still not clear. Therefore, this article is to review and discuss concerning ADEM in dengue as an immune-medicated neurological complication; and the management strategy required based on recent literature.

Matched MeSH terms: Encephalomyelitis, Acute Disseminated
Adenovirus in EV71-associated hand, foot, and mouth disease

Lum LC, Wong KT, Lam SK, Chua KB, Goh AY

Lancet, 2000 Jan 08;355(9198):146-7.
PMID: 10675193
Matched MeSH terms: Encephalomyelitis/virology*
Fulltext Acute disseminated encephalomyelitis (ADEM) presenting with seizures secondary to anti-tetanus toxin vaccination

Hamidon BB, Raymond AA

Med J Malaysia, 2003 Dec;58(5):780-2.
PMID: 15190671

Acute disseminated encephalomyelitis (ADEM) is an inflammatory demyelinating disease of the central nervous system (CNS) that is known to occur spontaneously in association with specific and non-specific viral illnesses and after vaccination against various pathogens. Although it is often a self-limited monophasic illness, the fatality rate is estimated to be as high as 20%, and many patients suffer residual neurologic impairment 1. The diagnosis is mainly based on clinical and radiological findings. The clinical presentation varies from merely, an asymptomatic condition to loss of consciousness, seizures, ataxia, optic neuropathy, cranial nerve palsies, and motor dysfunction. MRI of the brain is the single most important diagnostic radiological investigation and can facilitate early diagnosis and prompt treatment. This case report describes a patient with ADEM presenting with only seizures after vaccination with anti-tetanus toxin.

Matched MeSH terms: Encephalomyelitis, Acute Disseminated/etiology*
Fulltext Formaldehyde-inactivated whole-virus vaccine protects a murine model of enterovirus 71 encephalomyelitis against disease

Ong KC, Devi S, Cardosa MJ, Wong KT

J Virol, 2010 Jan;84(1):661-5.
PMID: 19864378 DOI: 10.1128/JVI.00999-09

Enterovirus 71 (EV71) causes childhood hand, foot, and mouth disease and neurological complications, and no vaccines or therapeutic drugs are currently available. Formaldehyde-inactivated whole-virus vaccines derived from EV71 clinical isolates and a mouse-adapted virus (MAV) were tested in a mouse model of EV71 encephalomyelitis. After only two immunizations, given to mice at 1 and 7 days of age, the MAV vaccine protected mice at 14 days of age from disease. Tissues from immunized mice were negative for virus by viral culture, reverse transcriptase PCR, immunohistochemistry analysis, and in situ hybridization. Cross-neutralizing EV71 antibodies to strains with genotypes B3, B4, and C1 to C5 generated in immunized adult mice were able to passively protect 14-day-old mice from disease.

Matched MeSH terms: Encephalomyelitis/prevention & control*
Phosphorylated neurofilament H (pNF-H) as a potential diagnostic marker for neurological disorders in horses

Intan-Shameha AR, Divers TJ, Morrow JK, Graves A, Olsen E, Johnson AL, et al.

Res Vet Sci, 2017 Oct;114:401-405.
PMID: 28750210 DOI: 10.1016/j.rvsc.2017.07.020

The current study aimed at the investigating the potential use of phosphorylated neurofilament H (pNF-H) as a diagnostic biomarker for neurologic disorders in the horse. Paired serum and cerebrospinal fluid (CSF) samples (n=88) and serum only (n=30) were obtained from horses diagnosed with neurologic disorders and clinically healthy horses as control. The neurologic horses consisted of equine protozoal myeloencephalitis (EPM) (38 cases) and cervical vertebral malformation (CVM) (23 cases). Levels of pNF-H were determined using an ELISA. The correlation between CSF and serum concentrations of pNF-H was evaluated using Spearman's Rank test and the significance of the difference among the groups was assessed using a nonparametric test. Horses had higher pNF-H levels in the CSF than serum. Horses afflicted with EPM had significantly higher serum pNF-H levels in comparison to controls or CVM cases. The correlation between CSF and serum pNF-H levels was poor in both the whole study population and among subgroups of horses included in the study. There was significant association between the likelihood of EPM and the concentrations of pNF-H in either the serum or CSF. These data suggest that pNF-H could be detected in serum and CSF samples from neurologic and control horses. This study demonstrated that pNF-H levels in serum and CSF have the potential to provide objective information to help in the early diagnosis of horses afflicted with neurologic disorders.

Matched MeSH terms: Encephalomyelitis/blood; Encephalomyelitis/cerebrospinal fluid; Encephalomyelitis/diagnosis; Encephalomyelitis/veterinary
Fulltext Pathologic characterization of a murine model of human enterovirus 71 encephalomyelitis

Ong KC, Badmanathan M, Devi S, Leong KL, Cardosa MJ, Wong KT

J. Neuropathol. Exp. Neurol., 2008 Jun;67(6):532-42.
PMID: 18520772 DOI: 10.1097/NEN.0b013e31817713e7

We describe a model of Enterovirus 71 encephalomyelitis in 2-week-old mice that shares many features with the human central nervous system (CNS) disease. Mice were infected via oral and parenteral routes with a murine-adapted virus strain originally from a fatal human case. The mice succumbed to infection after 2 to 5 days. Vacuolated and normal-appearing CNS neurons showed viral RNA and antigens and virions by in situ hybridization, immunohistochemistry, and electron microscopy; inflammation was minimal. The most numerous infected neurons were in anterior horns, motor trigeminal nuclei, and brainstem reticular formation; fewer neurons in the red nucleus, lateral cerebellar nucleus, other cranial nerve nuclei, motor cortex, hypothalamus, and thalamus were infected. Other CNS regions, dorsal root, and autonomic ganglia were spared. Intramuscular-inoculated mice killed 24 to 36 hours postinfection had viral RNA and antigens in ipsilateral lumbar anterior horn cells and adjacent axons. Upper cord motor neurons, brainstem, and contralateral motor cortex neurons were infected from 48-72 hours. Viral RNA and antigens were abundant in skeletal muscle and adjacent tissues but not in other organs. The distinct, stereotypic viral distribution in this model suggests that the virus enters the CNS via peripheral motor nerves after skeletal muscle infection, and spread within the CNS involves motor and other neural pathways. This model may be useful for further studies on pathogenesis and for testing therapies.

Matched MeSH terms: Encephalomyelitis/pathology*; Encephalomyelitis/virology*

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