japanese encephalitis

1. JAPANESE ENCEPHALITIS

2. EPIDEMOLOGY

3. INTRODUCTION
 MOSQUITO BORNE ENCEPHALITIS
CAUSED BY GROUP B ARBOVIRUS
(FLAVI VIRUS) AND
TRANSMITTED
BY CULICINE MOSQUITOES.
 ZOONOTIC DISEASE
(METAZOONOSES)
 RURAL DISAEASE
 ICEBERG DISEASE
 EXHIBITS CYCLICAL TREND

4. HISTORY
 1871 JAPANESE ENCEPHALITIS
DESCRIBED IN JAPAN.
 1934 JAPANESE ENCEPHALITIS
VIRUS
WAS ISOLATED.

5. WORLD SCENARIO
 50000 CASES OF JE OCCUR GLOBALLY EACH
YEAR WITH 11000 DE ATHS AND NEARLY
9000 DISABLED.
 SPORADIC CASES (Occasional cases, widely
distributed in time and place): are observed in
China, Japan, Taiwan, Korea, Philippines,
Indonesia, Malaysia, Singapore, Myanmar,
Bangladesh and Eastern areas of Russia.
 REGIONAL, SEASONAL OUTBREAKS :
Occurs in Thailand, parts of India and Sri lanka.

7. INDIAN SCENARIO
 JE first isolated in 1955 at Vellore, Tamil
Nadu.
 Subsequently, the outbreaks have occurred
in 25 States / Union Territories of India.
 JE virus infection is widespread and is
particularly very high in Southern States of
India viz., Andhra Pradesh (AP) Tamil Nadu
and some parts of Karnataka.

9. NB: Indian authorities have reported 6171 cases
nation-wide, including 5700 cases and 1315 deaths in
Uttar Pradesh alone.
YEAR CASES DEATHS
1998
1999
2000
2001
2002
2003
2004
2005
2120
3428
2593
2061
1765
2241
1695
6200
507
680
556
479
460
670
367
1315
INCIDENCE OF JE

10. AGENT
JE VIRUS
FLAVIVIRUS
SS-RNA
ENVELOPED
ICOSAHEDRA
L
EPIDEMOLOGICAL ASPECTS

11. NATURAL CYCLE OF
JE VIRUS

12. ANIMAL RESERVOIRS
 PIGS
MAJOR VERTEBRATE HOSTS
CONSIDERED AS ‘AMPLIFIERS’ OF VIRUS
 CATTLES/BUFFALOES
NOT NATURAL HOSTS OF JE VIRUS
ACT AS ’MOSQUITC ATTRACTANTS’
 BIRDS
POND HERONS,CATTLE
ERGETS,POULTRY,DUCKS
NB:HORSES ARE ONLY ANIMALS WHICH MANIFEST
JE VIRUS INFECTION.

14. HOST FACTORS
 AGE:
MAJORITY OF CASES ARE CHILDREN LESS THAN 15
YEARS (85%) OR OVER 60 YEARS (10%).
 SEX:
MALES ARE MORE AFFECTED THAN FEMALES.
 POPULATION MOBILITY
MIGRATION OF PEOPLE FROM ENDEMIC AREAS TO
RCEPTIVE AREAS.
 OCCUPATION
MOSTLY A RURAL DISEASE ,CLOSELY RELATED TO
AGRICULTURAL PRACTISES.

15. ENVIRONMENTAL
FACTORS
 SEASON
JE IS A SEASONAL DISEASE
PREVALENCE IS FROM MAY
TO OCTOBER ( RELATED TO
AGRICULTURAL PRACTICES).
 RAINFALL
INCREASES THE OPPORTUNITIES FOR
BREEDING OF MOSQUITOES.

16. VECTOR OF JE
 CULICINE MOSQUITOES.
(C.TRITAENIORHYNCHUS,C.VISHNUI,
C.GELIDUS)
 SOME ANOPHELINES.
 C.TRITAENIORHYNCHUS HAS BEEN
IMPLICATED AS IMPORTANT VECTOR
IN SOUTH INDIA.

17. HABITS
 BREEDING HABITS
BREED IN RICE FIELDS,
SHALLOW DITCHES
AND POOLS.
 CHOICE OF HOST
ZOOPHILIC,FEEDING PRIMARILY ON ANIMAL
HOSTS.
 TIME OF BITING
USUALLY AT NIGHTS.

18. MODES OF TRANSMISSION
 DISEASE IS TRANSMITTED TO MAN BY BITE OF
INFECTED MOSQUITOES.
 NO MAN TO MAN TRANSMISSION
 MAN IS INCIDENTAL “DEAD END” HOST.
 INCUBATION PERIOD
VARIES FROM 5-15 DAYS

19. PATHOGENESIS OF JE
LYMPH NODE

20. PATHOGENESIS
 Neurotransmitter receptors are involved in binding of JE
virus to cells in CNS.
 Sensitized T cells stimulate inflammatory
Response by activating macrophages, lymphocytes
Perivascular space and parenchyma to form glial nodules
CD4 T cells - CFS, parenchyma
B cells - perivascular space

21. CLINICAL FEATURES
 Divided into three stages:
1. Prodromal stage
2. Encephalitic stage
3. Late stage

22. CLINICAL FEATURES
 Incubation period-5 to 16 days
 Disease:asymptomatic infection=1:250 to 1:1000
 Represents tip of iceberg
 Disease depends on –severity of infection
susceptibility of host
location of agent
 It is characterized by CNS involvement
 Japanese encephalitis is also called BRAINFEVER

23. SYMPTOMS AND SIGNS
 PRODROMAL PHASE:-
High grade fever,
headache
malaise
Duration :6 days
 ENCEPHALITIC STAGE:-
High fever, severe head ache, nuchal rigidity, focal
CNS signs, seizures, altered sensorium, abnormal
doll’s eye moments, absent corneal reflex, pupillary
reflex, deviation of angle of mouth, loss of
consciousness etc.
 Symptoms and signs of raised ICT-headache, vomiting,
hemiplegia,bradycardia,irregular breathing.
 Signs and symptoms of meningeal irration-kernigs sign

24. DURING OUTBREAK

25. HOSPITILISATION

26.  LATE STAGE:- Begins when active inflammation
is at end i.e.temp. and ESR touch normal
Mental impairment
Increased deep tendon reflexes
Paresis of UMN lesion
- LMN lesion type
- Speech impairment
 COMPLICATIONS:-
Death 35 - 50% - short prodromal stage
- deep coma
- hypertonia
- tachypnea
NB:If patient survives, complications are as that of
late stage.
 JE is the disease in children with early mortality.

27. DIAGNOSIS
 Clinical signs and symptoms
 LAB DIAGNOSIS:-
CSF lymphocytic pleocytosis
Normal glucose level
 SEROLOGICAL TESTS:-
Detection of IgM antibodies –first week
 NEW SEROLOGICAL TEST:-
ELISA shows sensitivity of 88% -with sera
81% -with CSF

29. NEUROIMAGING:- MRI-hypo and hyper intense lesion in thalamus

32. CONFIRMATORY DIAGNOSIS
 Altered sensorium
 Worsening clinical status
 Signs of infection
 Asymmetrical brain damage
 CSF examination:-viral meningitis

33. DD IN ENDEMICS
 Other viral meningitis:- serological tests
- viral culture
 Tubercular meningitis:-reduced CSF
glucose,papilledema.
 Parasitic infections :- toxoplasmosis
 Active demyelinating disease.
 Bulbar poliomyelitis - history of having not
received polio vaccine.
 Cerebral malaria

34. Prevention &
Control

35. Principles of Control :
• No specific treatment per se.
• Vector control is the main mode of
prevention of an individual and
community as a whole.
• Control of amplifier hosts.
• Vaccination.

36. Management of J E
Only symptomatic treatment
• maintenance of airway
• fluid and electrolyte balance
• control of convulsions,
raised ICP, temperature

37. VECTOR CONTROL
VECTORS: C.tritaenorhynchus,C.gelidus C.vishnui.
Principles of arthropod control:
• Environmental control
• Chemical control
• Biological control
• Genetic control
• Newer methods
NB :”Integrated approach”

38. • Life history of MOSQUITO:

39. • Mosquito control measures:
1.Anti larval measures
2.Anti adult measures
3.Personal protection
ANTI LARVAL MEASURES
1.Environmental control :best approach as results
are more permanent.
a. Source reduction-elimination of cesspools,
ditches.
b. Intermittent irrigation
c. Filling and drainage operation
d. Provision of piped water supply
e. Proper disposal of refuse.

41. • 2.Chemical control:
Commonly used larvicides are
• a. Mineral oil –diesel oil, kerosene, mosquito
larvicidal oil, etc.
MOA :oil spreads and forms thin film which cuts
air supply to larvae .appl rate - 40to90 L/hectare
once a week.
• b. Paris Green -[copper acetoarsenite] Micro
crystalline powder insoluble in water.
MOA-stomach poison. good sample contains 50%
arsenious oxide. Appl-2% dust which is prepared
by adding 2kg of Paris green and 8kg of diluent
such as slaked lime in a rotary mixer. Its dusted
by hand, rotary blowers. Dosage 1kg/hectare of
water surface.

42. c. Synthetic Insecticides - Organophosphorus
compounds like FENTHION, CHLORPYRIFOS,
ABATE etc.
abate-very effective and least toxic.ccn.-1ppm.
Toxicant Dosage/ha]
Abate 56-112
Fenthion 22-112
Chloropyrifos 11-16
3.Biological control- Small fish like Gambusia,
lebister which feed on larvae can be use in
burrow pits, cesspools etc.

43. Gambusia affinis

44. • ANTI-ADULT MEASURES-
1. Residual sprays -DDT is the insecticide of choice.
Dosage 1-2g of pure DDT / sq.m applied 1-3 times a year
to walls and other surfaces. Malathion, propoxur- applied
where DDT resistance encountered.
Toxicant dosage[g/sqm] avg,durationof
effectiveness
DDT 1-2 6-12 months
Malathion 2 3 “
2. Space sprays- sprayed into the atmosphere in the
form of fog or mist using hand guns or power sprays
a. Pyrethrum extract- excellant spray from pyrethrum
flowers. Active principle-pyrethrin is a nerve poison dose -
1oz/1000 cft.
b. Residual insecticides- Malathion ,Fenitrothion for ULV
fogging.

45. The pyrethrum flower

46. .
• Space spraying and spray guns

47. • 3. Genetic control- sterile male
technique,cytoplasmic
incompatability,chromosomal translocation
• Newer methods -insect growth
regulators,chemosterilants etc.
PERSONAL PROTECTION
[i] Mosquito nets - size of the holes 0.0475”
no. of holes/sq inch 150
[ii] Screening of buildings –Cu or Bronze gauze with
16 meshes/inch
[iii] Mosquito repellants or culicifuges-used mainly
on skin. Ex. Deet all-purpose
repellant
“INTEGRATED APPROACH”

49. • Mosquito coils

50. VACCINATION
• Active Immunization -worldwide 3 JE vaccines are present.
1.Inactivated mouse brain killed vaccine
2. “ Primary Hamster kidney,
3.Live attenuated PHK
Passive Immunization Ig’s are not available.
INACTIVATED MOUSE BRAIN KILLED VACCINE
Central Research institute ,Kasauli has developed this
vaccine.
VIRAL STRAIN- Nakayama strain of JE virus isolated from
spinal fluid of a human case in 1935 and maintained by cont.
mouse brain passage.
DOSAGE AND ROA-
1st-------------2nd--------------3rd-----------booster
7-14 d 1mnth 3yrs
Adults – 1ml dose s.c.
Children[1-3yrs] – 0.5 ml s.c.

51. INDICATIONS:
a. Endemic areas-In rural areas of Asia where intense JE
virus transmission through enzootic life cycle leads to high
risk of exposure at an early age. In such areas UNIVERSAL
PRIMARY IMMUNIZATION is indicated for children[1-
2yrs].Also in areas agricultural developed like Thailand &
Japan. In these areas immunity should be maintained
up to 10 yrs of age.
b. Expatriates in areas of endemic.
c. Travelers
d. Researchers and LAB workers.
CONTRAINDICATIONS :people allergic to rodent derived
products.
ADVERSE EFFECTS: Swelling ,redness and tenderness in 20%
vaccinees. Low grade fever and Myalgia in 10- 30% and
Post vaccination neurologic deficits.
EFFICACY : 60-80%

52. Figure 11
JE Incidence In Relationship To Vaccine Distribution

53. Figure 10
Antibody Response After JE Vaccination

54. • Vaccination is not recommended as outbreak control
measure as it takes 1 month after the 2nd dose to develop
antibodies at protective levels and outbreaks are short lived
• CONTROL OF PIGS -As pigs are amplifier host, piggeries
should be 4-5 km away from human habitat.
Disposal of garbage and sewage should be done
appropriately so that breeding of pigs can be controlled.
LEVELS OF PREVENTION:
• PRIMARY PREVENTION:
• HEALTH PROMOTION:
EFFICIENT CONTROL OF MOSQUITO AND OTHER
AMPLIFIER HOSTS LIKE PIGS AND EGRETS.
HEALTH EDUCATION
• SPECIFIC PROTECTION:
DEVELOPMENT OF SAFE AND STANDARD VACCINE.
PERSONAL PROTECTION MEASURES AGAINST MOSQUITOS
• SECONDARY PREVENTION:
EARLY DIAGNOSIS: Its possible through surveillance

55. There are 3 types of surveillance
1. Sero-surveillance in high risk groups, animals and birds.
2. Vector surveillance for vector density and infection
3. Case surveillance
A. where no JE transmission is detected but vector is
present [acute CNS syndromes, fever clustering.]
b. where it is endemic or epidemic [weekly or monthly
reporting on suspected or probable or confirmed cases]
EARLY TREATMENT : its symptomatic.
TERTIARY PREVENTION :Rehabilitation of paralytic
patients by physiotherapy.
Technical support for surveillance, epidemiological monitoring
of the disease, for outbreak investigations and control is
provided by state health authorities.

56. Inspite of all these methods Control of JE is difficult
because-
• Outdoor habit of the vector.
• Scattered distribution of cases spread over large areas.
• Role of different reservoir hosts.
• Specific vectors for different geographical and ecological
areas.
• Immunization status of various population groups is not
known making it difficult to delineate vulnerable groups.

57. NVBDCP

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