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A case of Japanese B encephalitis imported into the United Kingdom
Journal of Infection (I983) 6, ~61-265
CASE REPORT A case of Japanese B encephalitis imported into the United Kingdom M. R. Rose, S. M. Hughes* a n d B. J. Gatus
Department of Infectious Diseases and *Department of Anaesthesia, Northwick Park Hospital, Watford Road, Harrow, Middlesex H A I 3 Uff Summary A case of acute encephalomyelitis, serologically proven to be due to Japanese B encephalitis virus, is reported. The patient, a 35-year-old woman, contracted the disease whilst in Hong Kong but presented in the United Kingdom. She required ventilatory support and was given high-dose steroids. She recovered from the illness but died after a period of four months from respiratory/cardiac arrest.
Introduction Japanese B encephalitis (JBE) is the result of infection b y an R N A flavivirus which exists enzootically, infecting various animals, particularly pigs, 1 and is transmitted b e t w e e n hosts b y mosquitoes of the Culex species. M a n is an accidental host. T h e disease is endemic in the Far East, with late s u m m e r epidemics and sporadic outbreaks. 2, 3 J B E has caused significant problems in military personnel serving in the F a r East during the Second W o r l d , 4 K o r e a n 5 and Vietnamese ~, 7 wars. I m p o r t e d cases have been reported from Australia 8 and the U . S . A . 9 b u t as far as we are aware no such case has previously been reported from the U . K .
Case report A 35-year-old British-born female w h o had resided in H o n g K o n g for the past 22 years arrived b y air in the U . K . from H o n g K o n g on 7 July x982. A week previously she had developed a severe frontal headache accompanied by pain in the neck, p h o t o p h o b i a and general malaise. T h e s e s y m p t o m s had lasted five days, b u t with some i m p r o v e m e n t in the headache on the fourth day during which she m a n a g e d to fulfil a social engagement despite the general malaise. O n arrival in L o n d o n after the I 6 - h o u r flight she was unable to disembark from the aircraft due to unsteadiness of gait and paresis of b o t h arms, particularly the right. O n admission to hospital (directly from the airport) she had a t e m p e r a t u r e of 4o °C and was d r o w s y b u t able to give a history. Examination of the cardiovascular, respiratory and gastrointestinal systems was u n r e m a r k able. T h e r e was neck stiffness b u t Kernig's sign was negative. Cranial nerve functions were normal apart from some weakness of the sternomastoid muscles. F u n d a l examination was normal. T h e r e was flaccid paresis of b o t h arms more evident proximally and m o r e marked on the right with absent arm reflexes. T o n e and p o w e r were normal in the legs b u t the reflexes were symmetrically oi63-4453/83/o3oz6I + o5 $o2.oo/o
O I983 The British Society for the Study of Infection
262
M . R . ROSE, S. M. H U G H E S AND B. J. GATUS
Table I
Virus serology (reciprocal titres) Poliomyelitis virus: neutralising antibodies Serotypes
Date
i
2
3
7 July 1982 20 July 1982 6 August 1982 6 September 1982
15oo lO24 15oo --
64 128 64 --
512 512 256 --
Japanese B encephalitis virus: haemagglutination-inhibition antibodies*
IO 16o-32o 4o 2o
No poliomyelitis type I virus-specific IgM antibody was detected by a neutralisation technique in any of the sera after sucrose density fractionation. * Sera were also tested for other togavirus antibodies (including dengue and West Nile virus antibodies) with negative results.
brisk. T h e plantar responses were flexor. T h e r e was reduced sensation to pin-pricks in the right arm and over the right side of the body, conforming to a C4 to D IZ dermatomal distribution.
Investigations Haemoglobin I4"9 g/dl with normal indices, peripheral leucocyte count 8"1 x IO9/1 with a normal differential count, erythrocyte sedimentation rate (Westergren) 9 m m / h o u r rising to 56 m m / h o u r six weeks after admission. Blood urea, electrolytes, glucose and liver function tests (except bilirubin I9 #tool/l) normal. Mid stream urine showed no growth of organisms, blood cultures were sterile, throat swab showed normal bacterial flora, with no virus isolated. V D R L and T P H A were negative. Urinary porphyrins were also negative. X-rays of the chest, skull and cervical spine were normal. Myelography did not demonstrate a spinal block. Computerised tomography of the brain showed mild cerebral oedema with no space-occupying lesion and no areas of infarction. T h e cerebrospinal fluid (CSF) was clear and colourless with a pressure of 13 cm water and showed a free rise and fall. T h e CSF glucose and protein were normal, there were 117 leucocytes/mm3 (5o per cent polymorphonuclear cells and 5o per cent lymphocytes). No virus was isolated from the CSF and bacterial culture was sterile. Seven hours after admission there was complete paralysis of the right arm with further weakness of the left arm. T h e r e was now complete loss of sensation to all modalities in the right arm and a mild sensory deficit to pin-prick in the left hand. Signs in the legs were unchanged. Twelve hours after admission the patient complained of diplopia and became very confused and increasingly drowsy. Upper motor neurone weakness was now apparent in the legs with bilateral extensor plantar responses. Twenty-four hours after admission palatal weakness, ptosis and dysphagia developed with an absent gag reflex and a feeble cough response. Progressive respiratory impairment with central cyanosis and peripheral circulatory collapse ensued so the patient was intubated and mechanically ventilated. Despite this she became semicomatose with lower
Case of ffapanese B encephalitis
263
motor neurone paralysis of both arms, upper motor neurone paralysis of the legs and multiple bulbar palsies. During this period the pulse and blood pressure fluctuated markedly suggesting autonomic dysfunction, and urinary incontinence developed necessitating catheterisation. Intravenous methylprednisolone was started on the second day following admission. Four grams were given on the first day then 2oo mg daily for nine days, the dose then being tailed off over a further six days. Steroid-induced glucose intolerance developed which required the continuous intravenous infusion of soluble insulin. Intravenous cimetidine was given during the period of steroid administration and nasogastric feeding commenced. Her level of consciousness remained depressed for three days with response to pain only. On the fourth day there was marked improvement in conscious level and cranial nerve functions gradually returned. Power returned to the legs but the flaccid paresis of the arms (particularly the right) and sensory loss remained. T h e patient tired easily when off the ventilator but despite this she was alert and very much aware of her surroundings but had a short attention span. T h e temperature finally settled on the fifth day after admission and bladder sensation returned on the ninth day. Tracheostomy was performed on the eighth day after admission and it was not until the fourth week that the patient was gradually weaned off the ventilator. At four weeks she displayed symptoms of a psychosis with paranoid delusions which responded to thioridazine. T h e tracheostomy was closed after seven weeks but 48 hours following the closure she developed acute respiratory distress which required ventilation again. She was finally removed from ventilation three weeks later. Whilst on the ventilator she required various courses of antibiotics for respiratory infections. T h r e e weeks into the illness there was evidence of left lower lobe collapse and bilateral basal shadowing radiologically. Bronchoscopy was performed; this showed an inflamed bronchial tree but no sputum retention, and samples obtained yielded no virus nor bacteria. Histological studies on the samples showed no evidence of Pneumocystis carinii infection. T h e radiological abnormalities cleared without further treatment. T h r e e months after her initial presentation she was transferred to another hospital for long-term rehabilitation. At this time she was breathing spontaneously through a tracheostomy. Residual neurological impairment was confined to the arms. T h e right arm was grossly wasted and paretic with minimal finger movement only, and sensory loss to all modalities was present in the right hand. T h e muscle wasting also involved the right-sided intercostal muscles. T h e left arm was only mildly wasted but movement was confined to the elbow and below, the shoulder being immobile. T h e r e was no sensory deficit in the left arm. Nocturnal apnoea attacks were troublesome and the patient suffered at least two episodes of respiratory arrest. While these attacks, almost certainly central in origin, were being characterised unfortunately she suffered another respiratory/cardiac arrest and did not survive. Discussion
T h e diagnosis of JBE is based on epidemiological and clinical features together with results of serological testing. A fourfold rise in antibody titre to JBE using
264
M. R. ROSE, S. M. HUGHES AND B. J. GATUS
the haemagglutination inhibition (HI) and c o m p l e m e n t fixation (CF) techniques between acute and convalescent serum samples is diagnostic. 8 In this patient the rise in H I antibodies was not sustained and was u n d o u b t e d l y modified by steroid administration. I m a m and H a m m o n TM showed that the antibody response to JBE virus in infected hamsters was b l u n t e d w h e n cortisone was administered. In u r b a n areas of the Far East, pigs act as amplifier hosts for JBE virus and infection is readily transmitted to m a n via mosquitoes of the C u l e x species. Coincidentally, in the week that this patient left H o n g K o n g an article appeared in the local S o u t h C h i n a P o s t newspaper highlighting the political problems involved in attempting to reduce the huge u r b a n pig population. T w o t h o u s a n d pigs were said to live in the area where this patient resided.n Certain features of this patient's illness deserve c o m m e n t . Confusion associated with p r e d o m i n a n t l y u p p e r limb paresis and sensory changes mainly confined to the arms are characteristic of JBE. T h e onset of coma indicates severe m o r b i d i t y or fatality as shown by this patient. 7 Sternomastoid muscle weakness is present in virtually all cases b u t cranial nerve palsies are u n c o m m o n . Psychosis in the post-febrile period and patchy p n e u m o n i c shadows radiologically are part of the illness, s, 12 Fatality rates of between five and 50 per cent appear to be related to the availability and quality of medical care. s, 12 T h e value o f steroids in the t r e a t m e n t o f this disease has not been d e t e r m i n e d as no controlled trial has been reported. T h e decision to use high-dose m e t h y l prednisolone in this case was based on the gravity of the patient's condition and the hope that any immunologically m e d i a t e d central nervous system damage would be ameliorated. W i t h the rapidity of air travel the possibility of unfamiliar i m p o r t e d diseases m u s t always be borne in mind. T h e incubation period of J B E ranges from six to I6 clays but m a y be sufficiently prolonged to p e r m i t manifestations of the disease as late as three weeks after arrival from an endemic area. 13 (We thank Dr Hillas Smith for permission to publish details of this patient who was admitted under his care. We are indebted to the doctors and staff of the Intensive Therapy Unit at Northwick Park Hospital for their management of this patient, to Dr E. T. W. Bowen at the Public Health Laboratory Service, Porton Down, Salisbury for performing JBE virus serological studies, to Dr M. Roebuck at Colindale Public Health Service for performing poliomyelitis virus serology testing and to Dr P. Rudge for neurological advice.) References i. Theiler M, Downs WG. The arthropod-borne viruses of vertebrates. New Haven and London; Yale University Press, I973: I83-I85. 2. Work TH, Shah KU. Serological diagnosis of Japanese B type encephalitis in North Arcot District, Madras State, India with epidemiologic notes. Ind ff Med Sci I965; Io: 582-592. 3. Hale JH, Lira KA, Chee PH. Japanese B encephalitis in Malaya. Ann Trop Med I952; 46: 220-226. 4. Sabin AB. Epidemic encephalitis in military personnel; isolation of Japanese B virus on Okinawa in I945. Serological diagnosis, clinical manifestations, epidemiologic aspects and use of mouse brain vaccine. J A M A I947; I33: 281-293. 5. Sabin AB, Schlesinger RW, Ginder DR, Matumoto M. Japanese B encephalitis in American soldiers in Korea. Am J Hyg I947; 46:356-375 • 6. Russell PK, Rodgers WO, Lennon PA, Raftery JR. A serological survey for arbovirus and leptospiral infections in Australian soldiers in the Republic of Vietnam, Annual Progress Report I966-x967: 219.
Case of ffapanese B encephalitis
265
7. Ketel WB, Ognibene AJ. Japanese B encephalitis in Vietnam. A m ff Med S d I97I ; 26x(5) : 271-279. 8. Fleming K. Japanese B encephalitis in an Australian soldier returned from Vietnam. Med ff Aust I975; 2 : I 9 - 2 3 . 9. Pina FP, Merikangas UR. Japanese B encephalitis in an American soldier returned from Korea. New Englff Med 1953; 249: 531-532. IO. Imam ZEI, Hammon W M c D . Immunologic response and pathogenesis of Japanese B infection in peripherally inoculated normal and cortisone treated hamsters. Proc Soc Exp Biol Med I957; 95: 12-16. I I . South China Post. 9 July I982. 12. Dickerson RB, Newton JR, Hansen JE. Diagnosis and immediate prognosis of Japanese B encephalitis. Observations based on more than 20o patients with detailed analysis of 65 serologically confirmed cases. A m J Med 1952; I2(3): 277-288. 13. Aidem NiP, Garagusi VF. Japanese B encephalitis. A case report from New York and a brief review of the literature. Ann Int Med I 9 6 I ; 55(2): 324-327.
CASE REPORT A case of Japanese B encephalitis imported into the United Kingdom M. R. Rose, S. M. Hughes* a n d B. J. Gatus
Department of Infectious Diseases and *Department of Anaesthesia, Northwick Park Hospital, Watford Road, Harrow, Middlesex H A I 3 Uff Summary A case of acute encephalomyelitis, serologically proven to be due to Japanese B encephalitis virus, is reported. The patient, a 35-year-old woman, contracted the disease whilst in Hong Kong but presented in the United Kingdom. She required ventilatory support and was given high-dose steroids. She recovered from the illness but died after a period of four months from respiratory/cardiac arrest.
Introduction Japanese B encephalitis (JBE) is the result of infection b y an R N A flavivirus which exists enzootically, infecting various animals, particularly pigs, 1 and is transmitted b e t w e e n hosts b y mosquitoes of the Culex species. M a n is an accidental host. T h e disease is endemic in the Far East, with late s u m m e r epidemics and sporadic outbreaks. 2, 3 J B E has caused significant problems in military personnel serving in the F a r East during the Second W o r l d , 4 K o r e a n 5 and Vietnamese ~, 7 wars. I m p o r t e d cases have been reported from Australia 8 and the U . S . A . 9 b u t as far as we are aware no such case has previously been reported from the U . K .
Case report A 35-year-old British-born female w h o had resided in H o n g K o n g for the past 22 years arrived b y air in the U . K . from H o n g K o n g on 7 July x982. A week previously she had developed a severe frontal headache accompanied by pain in the neck, p h o t o p h o b i a and general malaise. T h e s e s y m p t o m s had lasted five days, b u t with some i m p r o v e m e n t in the headache on the fourth day during which she m a n a g e d to fulfil a social engagement despite the general malaise. O n arrival in L o n d o n after the I 6 - h o u r flight she was unable to disembark from the aircraft due to unsteadiness of gait and paresis of b o t h arms, particularly the right. O n admission to hospital (directly from the airport) she had a t e m p e r a t u r e of 4o °C and was d r o w s y b u t able to give a history. Examination of the cardiovascular, respiratory and gastrointestinal systems was u n r e m a r k able. T h e r e was neck stiffness b u t Kernig's sign was negative. Cranial nerve functions were normal apart from some weakness of the sternomastoid muscles. F u n d a l examination was normal. T h e r e was flaccid paresis of b o t h arms more evident proximally and m o r e marked on the right with absent arm reflexes. T o n e and p o w e r were normal in the legs b u t the reflexes were symmetrically oi63-4453/83/o3oz6I + o5 $o2.oo/o
O I983 The British Society for the Study of Infection
262
M . R . ROSE, S. M. H U G H E S AND B. J. GATUS
Table I
Virus serology (reciprocal titres) Poliomyelitis virus: neutralising antibodies Serotypes
Date
i
2
3
7 July 1982 20 July 1982 6 August 1982 6 September 1982
15oo lO24 15oo --
64 128 64 --
512 512 256 --
Japanese B encephalitis virus: haemagglutination-inhibition antibodies*
IO 16o-32o 4o 2o
No poliomyelitis type I virus-specific IgM antibody was detected by a neutralisation technique in any of the sera after sucrose density fractionation. * Sera were also tested for other togavirus antibodies (including dengue and West Nile virus antibodies) with negative results.
brisk. T h e plantar responses were flexor. T h e r e was reduced sensation to pin-pricks in the right arm and over the right side of the body, conforming to a C4 to D IZ dermatomal distribution.
Investigations Haemoglobin I4"9 g/dl with normal indices, peripheral leucocyte count 8"1 x IO9/1 with a normal differential count, erythrocyte sedimentation rate (Westergren) 9 m m / h o u r rising to 56 m m / h o u r six weeks after admission. Blood urea, electrolytes, glucose and liver function tests (except bilirubin I9 #tool/l) normal. Mid stream urine showed no growth of organisms, blood cultures were sterile, throat swab showed normal bacterial flora, with no virus isolated. V D R L and T P H A were negative. Urinary porphyrins were also negative. X-rays of the chest, skull and cervical spine were normal. Myelography did not demonstrate a spinal block. Computerised tomography of the brain showed mild cerebral oedema with no space-occupying lesion and no areas of infarction. T h e cerebrospinal fluid (CSF) was clear and colourless with a pressure of 13 cm water and showed a free rise and fall. T h e CSF glucose and protein were normal, there were 117 leucocytes/mm3 (5o per cent polymorphonuclear cells and 5o per cent lymphocytes). No virus was isolated from the CSF and bacterial culture was sterile. Seven hours after admission there was complete paralysis of the right arm with further weakness of the left arm. T h e r e was now complete loss of sensation to all modalities in the right arm and a mild sensory deficit to pin-prick in the left hand. Signs in the legs were unchanged. Twelve hours after admission the patient complained of diplopia and became very confused and increasingly drowsy. Upper motor neurone weakness was now apparent in the legs with bilateral extensor plantar responses. Twenty-four hours after admission palatal weakness, ptosis and dysphagia developed with an absent gag reflex and a feeble cough response. Progressive respiratory impairment with central cyanosis and peripheral circulatory collapse ensued so the patient was intubated and mechanically ventilated. Despite this she became semicomatose with lower
Case of ffapanese B encephalitis
263
motor neurone paralysis of both arms, upper motor neurone paralysis of the legs and multiple bulbar palsies. During this period the pulse and blood pressure fluctuated markedly suggesting autonomic dysfunction, and urinary incontinence developed necessitating catheterisation. Intravenous methylprednisolone was started on the second day following admission. Four grams were given on the first day then 2oo mg daily for nine days, the dose then being tailed off over a further six days. Steroid-induced glucose intolerance developed which required the continuous intravenous infusion of soluble insulin. Intravenous cimetidine was given during the period of steroid administration and nasogastric feeding commenced. Her level of consciousness remained depressed for three days with response to pain only. On the fourth day there was marked improvement in conscious level and cranial nerve functions gradually returned. Power returned to the legs but the flaccid paresis of the arms (particularly the right) and sensory loss remained. T h e patient tired easily when off the ventilator but despite this she was alert and very much aware of her surroundings but had a short attention span. T h e temperature finally settled on the fifth day after admission and bladder sensation returned on the ninth day. Tracheostomy was performed on the eighth day after admission and it was not until the fourth week that the patient was gradually weaned off the ventilator. At four weeks she displayed symptoms of a psychosis with paranoid delusions which responded to thioridazine. T h e tracheostomy was closed after seven weeks but 48 hours following the closure she developed acute respiratory distress which required ventilation again. She was finally removed from ventilation three weeks later. Whilst on the ventilator she required various courses of antibiotics for respiratory infections. T h r e e weeks into the illness there was evidence of left lower lobe collapse and bilateral basal shadowing radiologically. Bronchoscopy was performed; this showed an inflamed bronchial tree but no sputum retention, and samples obtained yielded no virus nor bacteria. Histological studies on the samples showed no evidence of Pneumocystis carinii infection. T h e radiological abnormalities cleared without further treatment. T h r e e months after her initial presentation she was transferred to another hospital for long-term rehabilitation. At this time she was breathing spontaneously through a tracheostomy. Residual neurological impairment was confined to the arms. T h e right arm was grossly wasted and paretic with minimal finger movement only, and sensory loss to all modalities was present in the right hand. T h e muscle wasting also involved the right-sided intercostal muscles. T h e left arm was only mildly wasted but movement was confined to the elbow and below, the shoulder being immobile. T h e r e was no sensory deficit in the left arm. Nocturnal apnoea attacks were troublesome and the patient suffered at least two episodes of respiratory arrest. While these attacks, almost certainly central in origin, were being characterised unfortunately she suffered another respiratory/cardiac arrest and did not survive. Discussion
T h e diagnosis of JBE is based on epidemiological and clinical features together with results of serological testing. A fourfold rise in antibody titre to JBE using
264
M. R. ROSE, S. M. HUGHES AND B. J. GATUS
the haemagglutination inhibition (HI) and c o m p l e m e n t fixation (CF) techniques between acute and convalescent serum samples is diagnostic. 8 In this patient the rise in H I antibodies was not sustained and was u n d o u b t e d l y modified by steroid administration. I m a m and H a m m o n TM showed that the antibody response to JBE virus in infected hamsters was b l u n t e d w h e n cortisone was administered. In u r b a n areas of the Far East, pigs act as amplifier hosts for JBE virus and infection is readily transmitted to m a n via mosquitoes of the C u l e x species. Coincidentally, in the week that this patient left H o n g K o n g an article appeared in the local S o u t h C h i n a P o s t newspaper highlighting the political problems involved in attempting to reduce the huge u r b a n pig population. T w o t h o u s a n d pigs were said to live in the area where this patient resided.n Certain features of this patient's illness deserve c o m m e n t . Confusion associated with p r e d o m i n a n t l y u p p e r limb paresis and sensory changes mainly confined to the arms are characteristic of JBE. T h e onset of coma indicates severe m o r b i d i t y or fatality as shown by this patient. 7 Sternomastoid muscle weakness is present in virtually all cases b u t cranial nerve palsies are u n c o m m o n . Psychosis in the post-febrile period and patchy p n e u m o n i c shadows radiologically are part of the illness, s, 12 Fatality rates of between five and 50 per cent appear to be related to the availability and quality of medical care. s, 12 T h e value o f steroids in the t r e a t m e n t o f this disease has not been d e t e r m i n e d as no controlled trial has been reported. T h e decision to use high-dose m e t h y l prednisolone in this case was based on the gravity of the patient's condition and the hope that any immunologically m e d i a t e d central nervous system damage would be ameliorated. W i t h the rapidity of air travel the possibility of unfamiliar i m p o r t e d diseases m u s t always be borne in mind. T h e incubation period of J B E ranges from six to I6 clays but m a y be sufficiently prolonged to p e r m i t manifestations of the disease as late as three weeks after arrival from an endemic area. 13 (We thank Dr Hillas Smith for permission to publish details of this patient who was admitted under his care. We are indebted to the doctors and staff of the Intensive Therapy Unit at Northwick Park Hospital for their management of this patient, to Dr E. T. W. Bowen at the Public Health Laboratory Service, Porton Down, Salisbury for performing JBE virus serological studies, to Dr M. Roebuck at Colindale Public Health Service for performing poliomyelitis virus serology testing and to Dr P. Rudge for neurological advice.) References i. Theiler M, Downs WG. The arthropod-borne viruses of vertebrates. New Haven and London; Yale University Press, I973: I83-I85. 2. Work TH, Shah KU. Serological diagnosis of Japanese B type encephalitis in North Arcot District, Madras State, India with epidemiologic notes. Ind ff Med Sci I965; Io: 582-592. 3. Hale JH, Lira KA, Chee PH. Japanese B encephalitis in Malaya. Ann Trop Med I952; 46: 220-226. 4. Sabin AB. Epidemic encephalitis in military personnel; isolation of Japanese B virus on Okinawa in I945. Serological diagnosis, clinical manifestations, epidemiologic aspects and use of mouse brain vaccine. J A M A I947; I33: 281-293. 5. Sabin AB, Schlesinger RW, Ginder DR, Matumoto M. Japanese B encephalitis in American soldiers in Korea. Am J Hyg I947; 46:356-375 • 6. Russell PK, Rodgers WO, Lennon PA, Raftery JR. A serological survey for arbovirus and leptospiral infections in Australian soldiers in the Republic of Vietnam, Annual Progress Report I966-x967: 219.
Case of ffapanese B encephalitis
265
7. Ketel WB, Ognibene AJ. Japanese B encephalitis in Vietnam. A m ff Med S d I97I ; 26x(5) : 271-279. 8. Fleming K. Japanese B encephalitis in an Australian soldier returned from Vietnam. Med ff Aust I975; 2 : I 9 - 2 3 . 9. Pina FP, Merikangas UR. Japanese B encephalitis in an American soldier returned from Korea. New Englff Med 1953; 249: 531-532. IO. Imam ZEI, Hammon W M c D . Immunologic response and pathogenesis of Japanese B infection in peripherally inoculated normal and cortisone treated hamsters. Proc Soc Exp Biol Med I957; 95: 12-16. I I . South China Post. 9 July I982. 12. Dickerson RB, Newton JR, Hansen JE. Diagnosis and immediate prognosis of Japanese B encephalitis. Observations based on more than 20o patients with detailed analysis of 65 serologically confirmed cases. A m J Med 1952; I2(3): 277-288. 13. Aidem NiP, Garagusi VF. Japanese B encephalitis. A case report from New York and a brief review of the literature. Ann Int Med I 9 6 I ; 55(2): 324-327.