Clinical aspects of Japanese B encephalitis in North Vietnam

L e D u c Hinh*

Introduction

Although Japanese B encephalitis (J .B.E.) has been well known for some time ~,2 some prob- lems concerning diagnosis, therapy and preven- tion still remain to be solved, particularly with respect to Southeast Asian countries. Over the past three decades greater attention has conse- quently been devoted to J .B.E. under its so-called 'acute encephalitic syndrome' (A.E.S.) form in our environment 3. This viral disease often occurs as a seasonal epidemic and children are the most affected population 46 as well as some exposed foreigners who visit an endemic area. Both isolation of the causal virus and specific serological tests are very important for diagnosis 1~ Nevertheless because of a cer- tain delay of the laboratory findings, emphasis must be placed on clinical and epidemiological criteria for the early recognition of this affec- tion. The aim of this study is thus to delineate some outstanding characteristics of J .B.E. in our children based on recent outbreaks in North Vietnam.

Patients and methods

304 children with A.E.S. coming from different regions of North Vietnam were admitted to the Neurology Depar tment of Bach Mai Hospital during the years 1978 to 1980. In all patients

Summary

The author reports the retrospective study of 116 children suffering from Japanese B en- cephalitis in recent epidemics. This disease often appeared in summer and affected 2 to 7-year-old children. In the acute stage the clini- cal picture included meningeal signs, motor disorders, consciousness dysfunction and neurovegetative disturbances. 90.4% of cases presented abnormal features in CSF. Serologi- cal tests with Nakayama and H.N-60 strains were positive. B.M-79 Arbo virus was isolated from 1 case. Neuropathological examination revealed typical lesions in 16 cases. Sero-, viro- and anatomical correlations with clinical course confirmed the role of J.B.E. in outbreaks of 'acute encephalitic syndrome' in North Vietnam.

Key words: Japanese encephalitis, viral en- cephalitis, epidemic encephalitis.

determination of haemagglutination-inhibiting (H. I.) and complement-fixing (C.F.) antibodies with Nakayama and H.N.-60 stains 12 as well as virus-culture of CSF were systematically per- formed. In fatal cases post-mortem examination was done and autopsy brain tissues were immediately transferred to the virological laboratory for isolation of the virus.

* Department of Neurology, Bach Mai Hospital, Hanoi

Address for correspondence and reprint requests: Le Duc Hinh, Department of Neurology, Bach Mai Hospital, Hanoi, Vietnam

Accepted 28.1.86

Clin Neurol Neurosurg 1986. Vol. 88-3

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Serological tests, performed on paired serum specimens were positive in 51.9% of the incom- ing series; the remaining patients experienced encephalopaties/encephalitides from other aetiologies. An 18% mortality rate was calcu- lated for 3 epidemics (1978-1980) in our service. Thus 116 well documented out of 158 proven cases of J.B.E. form the basis of the present review.

R e s u l t s

Epidemiological data

The geographic distribution of J.B.E. was multifocal over much of the outskirts of Hanoi,especially in Ha Son Binh, Hai Hung, Ha Bac, Vinh Phu, Ha Nam Ninh and Bac Thai provinces. 93.1% of the cases appeared in May, June, and July with a peak (75%) in June. The number of patients was respectively 24 in 1978, 36 in 1979 and 56 in 1980. The group included 116 infants and children, namely 48 girls and 68 boys ranging from 8 months to 14 years of age. 83.6% were 2 to 7 years of age with 37.9% of 3-4 years of age.

Clinical manifestations

The onset of the illness (Table 1) was often abrupt without prodromes in previously healthy children, who had been immunized against J .B.E. Early symptoms were non specific with fever and vomiting. Headache might be detected in children of 4 years of age.

Progression to frank encephalitis occurred 1 or 2 days later. The clinical picture became much more complex with neurological signs, sensorium disorders (Table 2) and neurovegeta- tive disturbances (Table 3). On admission to our service 93.9% of patients presented fever be- tween 38 ~ and 40~ Meningeal irritation was often limited to stiff neck and Kernig's sign. Hypertonia, hemiparesis or tetraplegia, convul- sions, cranial nerve involvement, abnormal ten- don reflexes, and Babinski's sign were common. Disorders of sensorium were found in 87% of cases; mild lethargy could progress to confu- sion, stupor and coma.

The course of J.B.E. was frequently rapid and day-to-day fluctuations in symptoms were often

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Table 1. Symptoms of onset in 116 patients

Elevated temperature 100.0% Vomiting 56.8 Diarrhea 6.0 Abdominal pain 3.4 Cough 5.1 Headache 18.9 Tremer 2.5

Table 2. Neurological symptoms in acute stage

Stiffness of neck 89.6% Kernig's sign 71,5 Hypertonia 31.0 Motor deficit 42.2 Convulsions 73.2 Cranial nerve involvement 14.6 Abnormal tendon reflexes 50.0 Babinski's sign 55.1 Altered consciousness 87.0

Table 3. Neurovegetative signs in 116 patients

Fever higher than 38~ 93.9% Respiratory disturbances 55.1 Bronchial hypersecretion 23.2 Abdominal distension 13.7 Vomiting 9.4 Urinary retention 31.8

seen. Nevertheless the most critical phase was usually the 3rd to the 5th day. Hyperthermia, respiratory disturbances and urinary retention were outstanding features. Hypersecretion of the gastro-intestinal tract could lead to abdomi- nal distension with subsequent vomiting of blood. In cases of bronchial hypersecretion, if the patient was untreated, there was the risk of increasing respiratory distress, and apnea was imminent.

Our 116 patients might be classified into 4 groups according to clinical symptoms: - 74 cases developed the triad 'fever higher

than 38~ - convulsions and/or motor deficit - sensorium disorders';

- 27 cases presented 'high fever and sensorium disorders';

- 8 cases showed 'fever and motor deficit'; - 7 cases had only 'fever'.

Fatal outcome generally occurred by the third to the eighth day following the onset of the disease. This group included in this study 9 girls and 7 boys under the age of 6. Respiratory distress was the last manifestation.

In the absence of dramatic complications, consciousness gradually returned within 3 to 5 days. A decreased temperature lower than 38~ could be observed during the second week. This was followed by progressive improvement of other clinical features. However, extrapyrami- dal dysfunction as well as behavioural distur- bances sometimes developed at a later stage. Some early sequelae such as hemiparesis, seizures, emotional lability or psychomotor retardation could however be observed.

Laboratory findings

J.B.E. was confirmed by serological investiga- tions carried out in the acute and convalescent stages. In most cases these specific tests became positive during the second week. They demon- strated a minimum fourfold H.I.titer rise in specimens from convalescent patients which commonly varied between 1:640 and 1:11,280.

Lumbar CSF was clear but presented other abnormal features in 90.4% of cases: the leukocyte count ranged from 10 to 100 cells/mm 3 (80.8%) with lymphocyte predominance; pro- tein level ranged from 50 to 500 mg/100 ml (61.7%). Glucose and chloride were quite nor- mal. Virus cultures were negative.

Blood cultures were also negative. Polymorphonuclear leukocyte count was ele- vated with neutrophilia. Erythrocyte sedimen- tation rate was raised. Serum electrolytes were often normal. A slight degree of proteinuria was disclosed in some cases. Chest roentgenograms usually showed images of bronchitis and hilar adenopathy. Tuberculin skin tests were negative.

Histopathological changes were predomi- nantly seen in gray matter. Cardinal features of J.B.E. included perivascularitis, cellular nodules and rarefaction necrosis. Severe lesions were always present in thalamus and substantia nigra.

B.M-79 virus, the only one isolated during the three epidemics observed in our service, was recovered from autopsy brain tissue of a 3-year- old patient. Virological studies demonstrated that this strain high virulence (L.D.50 = 10 -65~ accrued to arboviruses of the Togavirus family 13.

Discussion

Despite its geographic name J.B.E. is widespread in Southeast Asia 14-2~ but the topographic distribution is mostly confined to coast lands 2,11,2~. In Vietnam this disease occurs in both sporadic and epidemic forms. The sporadic form has long been reported especially in South Vietnam 8,22 while the epidemic form has been annually recorded in North Vietnam 3. The occurrence of annual outbreaks usually coincides with summer, which is recognized as hospital admission time for A.E.S. in North Vietnam. From the study here presented and according to our previous in- vestigation 6 it may be assumed that J.B.E. plays an important role in these seasonal epidemics since specific serological tests have been posi- tive in 50-70% of A.E.S. cases.

As regards the morbidity rate, besides its cor- relation with population density attention must also be focused on possible reservoirs in the localities concerned. It is common knowledge that the most important vector in Vietnam is the rural mosquito Culex tritaeniorhynchus z2,23 and that wild birds are natural reservoirs of the J.B.E. virus 1,2~,24. Emphasis should however be placed on pigs in our ecological conditions as amplifying hosts during epidemics 25-27.

In this review the patient population con- sisted selectively of children, 83.6% of whom were between the second and seventh year of life. Both sexes were equally affected, as reported in a previous paper 6. Since children are the most exposed population it becomes neces- sary to evaluate the non-apparent rate. In Japan the annual contamination rate of children was estimated at about 10% and 500 to 1.000 non- apparent infections may occur for each case of clinically apparent disease 28,29. As no such survey has been carried out by us, we would like to refer to investigations carried out between 1964 and 1978 demonstrating that 30.35 to 82.94% of Vietnamese have specific antibodies against J .B.E?.

In our patients the most common signs of onset were fever, vomiting and headache, followed by the triad 'fever higher than 38~ convulsions and/or motor deficit-sensorium disorders'. Abnormal features of CSF with lymphocyte predominance in the leukocyte

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c o u n t a n d a m o d e r a t e l y e l e v a t e d p r o t e i n l eve l

w e r e f o u n d in 9 0 . 4 % o f cases . I t is a p p r o p r i a t e

to c o m p a r e t h e s e d a t a w i th t h o s e o f o u r p r e v i o u s

r e p o r t s 5,6 s ince o u r i n v e s t i g a t i o n s w e r e c a r r i e d

o u t in t h e s a m e p r o s p e c t i v e m a n n e r . T h u s it

cou ld be s h o w n tha t J . B . E . usua l ly p r e s e n t s

w i t h t h e a b o v e - m e n t i o n e d cha rac te r i s t i c s in o u r

c h i l d r e n . In fac t , c l in ica l s igns w e r e c o n f i r m e d

by s e r o l o g i c a l i nves t i ga t i ons . M o r e o v e r , r e c o v -

e r y o f B . M - 7 9 A r b o v i rus c o n t r i b u t e d to t he

s tudy o f e t i o l o g y , d u r i n g e p i d e m i c s in t he p e r i o d

1978-19803,1~ 11"

J . B . E . o f t e n p o s e s a d i a g n o s t i c c h a l l e n g e to

t h e c l in ic ian as it c an m i m i c m a n y n e u r o l o g i c a l

d i s o r d e r s p a r t i c u l a r l y in ch i ld n e u r o l o g y .

S e v e r a l i n f ec t i ous d i seases c l in ica l ly mas-

q u e r a d e so succes fu l ly as v i ra l e n c e p h a l i t i s t ha t

t h e y can be d i f f e r e n t i a t e d on ly by spec i f ic reac-

t ions . B e c a u s e o f this e x p e r i e n c e it is s t r o n g l y

r e c o m m e n d e d tha t s e r o l o g i c a l tes ts a r e pe r -

f o r m e d d u r i n g an e p i d e m i c p e r i o d o n all ch i ld-

r e n w i t h a susp ic ious h i s to ry and s u g g e s t i v e

s y m p t o m s . L u m b a r p u n c t u r e s w h e n a v a i l a b l e

a r e m a n d a t o r y . T o d a y , a l t h o u g h the c o n c e p t o f

v i ra l e n c e p h a l i t i s has b e e n e x p a n d e d b e y o n d

J . B . E . , i n f e c t i o n s d u e to J . B . E . v i ru ses a re still

c o n s i d e r e d t o be a m a j o r cause o f m o r t a l i t y a n d

h a n d i c a p s in o u r ch i ld r en . T h e d e v e l o p m e n t o f

p r o p h y l a c t i c m e a s u r e s thus c o n t i n u e s to be a

rea l i s t i c a p p r o a c h to r e c u r r i n g e p i d e m i c s

w o r l d w i d e .

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