NIPAH VIRUS ENCEPHALITIS
A SCIENTIFIC SEMINAR
PROGRAM AND ABSTRACTS OF SCIENTIFIC PAPERS
Chairperson : Prof. C.C. Lang Deputy Dean
Date : Monday 26 July 1999
Place : Lecture Hall 2 and Lecture Hall 3
University of Malaya
- Arrival of invited guests
- Welcome by Chairperson of Seminar
- Opening Remarks by the Dean, Faculty of Medicine,
University of Malaya
- Session 1
- Epidemiological Characteristics of the Nipah Virus Encephalitis Outbreak Cases Seen at the University of Malaya Medical Centre (UMMC)
- Clinical Features of Nipah Virus Encephalitis : The UMMC Experience
- Nipah Virus Encephalitis : Imaging Features
- Pathological Changes in Nipah Virus Infection
- Nipah Virus Encephalitis : Tracking a Killer Virus
- Coffee Break
- Session 2
- Nipah Virus Outbreak: Clinical Management at the UMMC
- Viral Encephalitis : A Recent Neuro-Intensive Care Experience.
- Nursing Care of Patients with Nipah Virus Encephalitis.
- Future Directions
- Question and Answer Session
Epidemiological Characteristics of the Nipah Virus Encephalitis Outbreak Cases Seen At The University of Malaya Medical Centre (UMMC)
Arokiasamy JT, Teoh ST
Department of Social and Preventive Medicine
Epidemiological investigations are an integral component of any infectious disease outbreak. The comprehensive scope of investigations during an outbreak is outlined so as to appreciate the actual scope of the investigations that was carried out in a hospital setting. Preliminary results of the analysis of the data on the University Hospital cases are presented, and wherever possible compared to available national data. The age, sex, and ethnic distribution of the University of Malaya Medical Centre cases are described along with the outcome of the cases based on data currently available. A brief outline of actual field epidemiological studies currently being carried out is also described.
Clinical Features of Nipah Virus Encephalitis: The UMMC Experience
Goh KJ, Tan CT, Tan PSK, Kamarulzaman A, Chew NK, Tan KS, Delikan AE*
Department of Medicine and * Anaesthesiology and Intensive Care.
From February to April 1999, 96 patients were admitted to the University of Malaya Medical Centre (UMMC) from the Nipah virus encephalitis outbreak areas. Ninety-one patients were found to have the disease based on clinical findings and on cerebrospinal fluid (CSF) examination. The male: female ratio was 5.1: 1. Age range was 13-58 years (mean 36.5). The ethnic breakdown was 82.4% Chinese, 14.3% Indian, 1.1% Malay and 2.2% others. The majority (95.6%) had direct contact with pigs. Main presenting symptoms were fever, headache, nausea/vomiting, and drowsiness. Focal neurological signs observed included segmental myoclonus, cerebellar signs, tremors, ptosis and tendon aflexia. Seizures occurred in 22%. 59.3% of patients had deterioration of consciousness. Forty four (48.4%) were ventilated. CSF was abnormal in 77.5% of patients 33.7% CSF lymphocytosis, raised protein and 43.8% raised protein only. Hendra serology was positive 73.4% and equivocal in 2.2%. Electroencephalograph (EEG) shows diffuse slow waves with/without bitemporal independent sharp waves. 28 (30.8%) patients died, 52 (57.1%) discharged while 11 (12.1%) remained in hospital. Poor prognostic factors included low Glasgow coma scale score at nadir, high maximum heart rate and blood pressure, seizures, segmental myoclonus, small pin-point pupils and abnormal dolls eye reflex and sharp waves on EEG. Flaccid tetraplegia during recovery was observed in some cases. Four cases had neurological relapse.
Conclusion: The Nipah virus causes a febrile encephalitic illness. Severe cases were characterised by reduced conscious level, seizures, focal neurological signs and signs of brain-stem dysfunction. Neurological relapse may occur.
Nipah Virus Encephalitis : Imaging Features
Sarji SA, Abdullah BJJ, Goh KJ*, Kamarulzaman A*.
Departments of Radiology and *Medicine.
This study describes the findings on imaging in 26 patients who were admitted into the UMMC with clinical features of encephalitis and were from the outbreak areas. Their brains were imaged by computed tomography (CT) or magnetic resonance imaging (MRI). There were no abnormalities found in those who were imaged by CT, but MRI demonstrated abnormalities in the brains of all 26 patients. In both the acute and later phases of encephalitis, the main MRI finding was the presence of multiple, small, asymmetrically distributed focal lesions in the subcortical and deep white matter, likely areas of infarcts. In patients who had neurological relapse or worsening of neurological symptoms, diffuse continuous involvement of the cortical gray matter was demonstrated and this extended into the deep white matter on follow-up imaging. Widespread cerebral vasculopathy resulting in areas of demyelination or a direct attach on the neurons by the virus may be the underlying cause.
In conclusion, MRI was found to be a sensitive and useful imaging process for diagnosing Nipah encephalitis and for following the progression of the disease in the brain. The MRI features appear distinct from MRI descriptions of other viral encephalitides.
Pathological Changes In Nipah Virus Infection
Wong KT, Looi LM
Department of Pathology
This study describes the pathological changes in tissues of patients who died of the Nipah virus infection, and postulates on its pathogenesis. Eighteen autopsy brains and 4 sets of other organs were examined after formalin fixation, routine processing and H&E staining. Material gathered from 14 autopsies performed in the Ministry of Health and 4 performed in the UMMC. All the patients had direct contact with pigs and presented with clinical features typical of Nipah virus encephalitis. Sixteen had anti-Hendra antibodies either in the serum and/or CSF. In addition 4 cases had virus isolated from the CSF. The main pathological change was vasculitis in small blood vessels (venules, capillaries, arterioles, and muscular arteries), particularly in the brain. Other organs involved included the lung, heart and kidney. Vasculitis-induced thrombosis appeared to cause widespread, focal infarction/ischaemia. Occasionally, endothelial syncytia formation was noted. Syncytial formation was also noted in the Bowmans capsule. Neuronal inclusions, presumably viral, were observed in the brain. The pathogenesis of Nipah virus infection appears to be primarily due to endothelial damage resulting in vasculitis, thromboses and infarction which is especially severe in the brain but direct neuronal infection may also play an important role.
Nipah Virus Encephalitis : Tracking A Killer Virus
Chua KB, Lam SK
Department of Medical Microbiology
The outbreak of viral encephalitis started in Perak in late September 1998 and spread to Negeri Sembilan by late February 1999. We received cerebrospinal fluid specimens from Seremban Hospital on 1st March and worked on a fast track to isolate and identify the killer virus.
Although we confirmed several cases of Japanese encephalitis infection serologically, epidemiological evidence suggested the existence of another virus. Specimens were inoculated into a variety of host systems and within five days, we detected a virus which caused syncytial formation in Vero cells. Electron microscopy revealed pleomorphic viral particles ranging in size from 160 300 nm, making us suspect that it is a member of the paramyxovirus family.
At CDC, Fort Collins, arborviruses were ruled out and electron microscopy confirmed our own observation. Further studies at CDC, Atlanta, revealed that the virus was related antigenically to the Australian Hendra virus. Since it is obviously a new virus, it was named Nipah virus after the locality of the outbreak.
After confirming that Nipah virus is a paramyxovirus, we advised the Ministry of Health on relevant control measures, which included the avoidance of direct contact with infected pigs and the liberal use of disinfectants in pig farms. Based on our suggestion, ribavarin was used in the management of infected patients showing early symptoms. We also established that throat gargles and urine from patients contained the virus and the information was used to prevent nosocomial infections.
Tracking this killer virus, from isolation to identification, took exactly 17 days.
Nipah Virus Outbreak : Clinical Management At The UMMC
Kamarulzaman A, Goh KJ, Tan PSK, Delikan AE, Imran ZA, Tan CT
Departments of Medicine and Anaesthesiology
The Nipah virus outbreak and the identification of a new causative agent whose properties were largely unknown at the onset of the outbreak provided an enormous challenge to those involved in the clinical care of patients.
A multidisciplinary approach involving neurologists, infectious disease physician, intensivists, nurses and physiotherapists was essential in the overall management. Supportive care was the mainstay of treatment which included intensive care monitoring and the initiation of mechanical ventilation as needed for airway protection with the onset of neurological deterioration.
With the recognition that arterial thrombosis may play an important role in the pathology of the disease anti-thrombotic agents aspirin and pentoxyfyline were used in all patients.
Ribavarin, a nucleoside analogue which has in vitro activity against Hendra was used in an open labeled nonrandomised trial in 73 patients admitted to UMMC. The results of its clinical activity in Nipah encephalitis will be discussed.
Given the limited treatment options and high case fatality rate of Nipah encephalitis, prevention of the disease particularly in the health-care setting was paramount, infection control measures involving standard and droplet precautions were employed in the outbreak as soon as the identification of a new potentially highly infectious agent was recognised.
Viral Encephalitis A Recent Neuro-Intensive Care Experience
Delikan AE, Tan P, Tan CT, Goh KJ, Kamarulzaman A, Ong G
Departments of Anaesthesiology and Medicine
The basic criterion for admission into an intensive care unit is when a patient has a failing vital system or systems, (Central Nervous System, Respiratory System, Cardiovascular System, Hepatic/Renal Systems) needing artificial support (drugs, mechanical and monitoring equipment, specialised dedicated nursing) without which the patient would die. The underlying pathology should hopefully be reversible and quality of neurological salvage should hopefully be acceptable.
In Neuro-Intensive Care cerebral protection is important particularly when the underlying (eg encephalitis) pathology depresses central nervous system function producing falling levels of consciousness and possibly secondary sequelae which can increase intracranial pressure and reduce cerebral perfusion and blood flow to the brain. Deteriorating levels of consciousness should be taken as a warning sign to warrant neuro-intensive care and close monitoring of the adequacy of respiratory function and the related protective reflexes. The decision to ventilate and protect the patient should be made before respiratory arrest occurs. Once vital system support has been established this should be continued with cerebral protection while the underlying pathology is treated positively (if there is a specific therapy); or the neuro-intensive care support should continue while the underlying pathology, hopefully, runs its course. The management illustrates and exemplifies the critical care team concept involving Anaesthesiologists, Neurologists, Infection Control Physicians and Dedicated Intensive Nursing.
The data on the patients involved and the outcome are presented.
Nursing Care Of Patients With Nipah Virus Encephalitis
Nursing Sister, Intensive Care Unit 48
The care of this group of patients employed a multidisciplinary team approach and each member of the team (nurses, doctors and relatives) played a vital role.
The nursing care was directed towards achieving the objectives of preventing potential complications, especially under these conditions where the mode of transmission was still uncertain. Patients with viral encephalitis were nursed in isolation to avoid the spread of infection and cross infection to other patients and other health care staff. Universal precautions were practiced.
Nursing care started from the time the patient was admitted to the medical ward and the patients were observed intensely with regard to their general condition, complaints, and most importantly, all their neurological changes, vital signs, change of behaviour and any deterioration in their condition.
Above all , total patient care was initiated to ensure comfort and to maintain hygiene at all times. Therefore, to maintain a constant standard of nursing care, a sufficient number of nurses were needed. This was especially so when there was an outbreak and the number of patients increased tremendously which warranted an expansion of the unit to accommodate them.
The problems and difficulties faced by all the nurses will be highlighted together with their willingness to accept the challenges and how they overcame the stress at work, deaths of patients and their grieving relatives.
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