NIPAH EPIDEMIC - THE UH Team Interview

Interview by Dr Muruga Vadivale with Prof Dr C T Tan, Assoc Prof Dr Adeeba Kamarulzaman and Dr Goh Khean Jin

Q.1 When did you first suspect that the present outbreak was not JE and why?

We saw first patient on the 26/2/99 and subsequently, 96 patients were admitted to University Hospital, KL from the outbreak area viz. Bt Pelanduk, Sg Nipah and Sepang. There were atypical features from JE that struck us even before a new virus was confirmed &ndash the age group affected were adults (mean age 37 years) as opposed to JE, which mainly affects children. A majority of patients had had prior vaccination against JE (at least twice of three times) and should have been protected to certain extent. Furthermore there has been clustering of the cases amongst family members and workers of the same farm suggesting that the infection rate was much higher that that of JE (usually 1:300 to 1:1000). In addition, these are mainly adult men who were working directly with pigs. We have had instances where the family members who worked with pigs came down with the illness while the sole member who stayed in the house remained well suggesting that this disease may not be mosquito borne.

An important point was that the patients admitted to the fact their pigs fell sick around Chinese New Year with respiratory illness in which many died. Pigs are not sick in JE.

Q.2 From your experience, what are the signs and symptoms of a typical case?

Most patient present with an encephalitic illness with fever, headaches, dizziness and reduction in conscious level. Some patients remain relatively stable with mild obtundation while others become deeply comatose with/without seizures and focal neurological signs.

Q.3 What is the mortality and morbidity of this viral encephalitis?

If the patient becomes deeply comatose, have focal neurological signs and seizures then the prognosis worsens. Our mortality rate is about 30%. We still have patients in the ward who are in long-term coma and may require prolonged care.

Q.4. Were there any distinguishing features between Nipah and JE in relation to clinical, biochemical, histo-pathological, pathological,CSF, and MRI picture?

Clinically, on the whole all encephalitis appear similar. In Nipah infection however we were taken but certain typical features in patients who were more severely affected. There was a prominence of focal signs viz. segmental myoclonus affecting the diaphragm, limbs, cerebellar signs as well as abnormal Doll&rsquos and pupillary reflexes. Some patients showed delayed recovery of limbs which remained flaccid while cognition improved.

CSF feme has been variable although the majority had evidence for an encephalitic process. Some very ill patients had relatively normal CSF on admission.

Histopathologically, we are told that there is evidence of a vasculitis causing thrombosis of the small and medium arteries with microinfarction. Neuronal invasion was also seen when immunohistochemistry was done

Q.5 What is the long term prognosis of this disease. Is it too early to tell? Will these patients be followed-up?

Its probably too early to tell. We have had two patients readmitted with worsening conscious level after having been sent home while another patient was readmitted with a III nerve palsy. We think these are related to the disease

Q.6. How did you'll manage the patients?

Treatment is essentially supportive - careful monitoring, treat epileptic seizures and concomitant sepsis, intensive care support (including ventilation) for deeply comatose patients. We were fortunate that the intensive care physicians provided us with excellent support for the patients. The hospital admin was pro-active and managed to organise all the parties &ndash doctors, nurses, labs etc. concerned to work together. A temporary ICU was also established in the new OT recovery area at the height of the outbreak. An important reason for the relatively fewer deaths at UH was probably because of the intensive care management

We gave almost all patients aspirin, trental and later the antiviral ribavirin. The former drugs were because the histopathological studies showed perivascular inflammation with evidence of microthrombi and infacts.

Q.7. Is there a role for ribavarine in the management of these disease.

We feel that it has made some difference however full analysis needs to be made.

 

Q.8 How infectious is Nipah virus in term of animal to human transmission? Any evidence of human to human transmission?

Thus far we are told that there has been no nosocomial spread of the disease. There has been no evidence of any human-human spread in other context as well. Our patients epidemiological have had close contact with pigs and this suggests that infected secretions may be a mode of transmission. The incubation period is variable, most of our patients have had contact about a week or two before illness but we have had one or two patients with last contact more than a month ago.

 

Q.9 In your expert opinion are we dealing with a JE outbreak or a Nipah encephalitis outbreak?

On the whole, this was probably nipah viral encephalitis outbreak.

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Last Updated 9th May 2005.

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