JE & Filariasis

1. Japanese Encephalitis
&
Filariasis
Dr. Rahul Netragaonkar
Professor
Dept. Of Community Medicine
Zydus Medical College,
Dahod

2. 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

3. History
• 1871 Japanese Encephalitis
Described In Japan.
• 1934 Japanese Encephalitis Virus
Was Isolated.

4. 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.

6. 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.

8. 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

9. Agent
Je Virus
Flavivirus
Ss-RNA
Enveloped
Icosahedral
Epidemological Aspects

10. NATURAL CYCLE OF JE VIRUS

11. 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.

13. 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 receptive areas.
 Occupation
Mostly A Rural Disease ,
Closely Related To Agricultural Practises.

14. 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.

15. VECTOR OF JE
Culicine Mosquitoes.
(C.Tritaeniorhynchus,c.Vishnui,
C.Gelidus)
Some Anophelines.
C.Tritaeniorhynchus Has Been
Implicated As Important Vector
In South India.

16. 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.

17. 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

18. PATHOGENESIS OF JE
LYMPH NODE

19. 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

20. CLINICAL FEATURES
• Divided into three stages:
1. Prodromal stage
2. Encephalitic stage
3. Late stage

21. 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 BRAIN FEVER

22. 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

23. DURING OUTBREAK

24. HOSPITILISATION

25. • 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.

26. 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

27. 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.

28. Management of J E
Only symptomatic treatment
• Maintenance of airway
• Fluid and electrolyte balance
• Control of convulsions,
raised Intra Cranial Pressure,
temperature

29. FILARIASIS
• INTRODUCTION
Worldwide prevalent, arthropod borne,
causing
permanent, long term disability &
disfigurement &
associated with social & economic
stigma.
It causes-Isolation
-Psychological stress
-Family discord
-Impair employment
-Impair mobility & domestic
activities

30. FILARIASIS
FILARIASIS
LYMPHATIC
Wuchereria
bancrofti
Brugia
malayi
Brugia timori
NON-
LYMPHATIC
Sub-
cutaneous
Onchocerca
volvulus
Loa loa
Mansonella
streptocerca
Serous
Mansonella
ozardi
Mansonella
perstans

31. Lymphatic filariasis
• Caused by W.Bancrofti
B.Malayi
B.Timori
History:
600 BC-SUSHRUTA described ELEPHENTANOID LEG.
1709 ad-the term malabar leg was applied by clarke.
1866 ad-Wucherer demonstrated mf in chylous urine.
1876 ad-bancroft described female adult worm.
1878 ad-manson identified culex as the vector &
Described periodicity.
This was the first discovery of insect transmission of a
Human disease.

32. PROBLEM STATEMENT
• Widely distributed in tropics & sub-tropics-ASIA,
AFRICA, WESTERN PACIFIC, SOUTH
AMERICA.
• Most seriously affected areas are INDIA, SOUTH
EAST ASIA, CHINA, EAST COAST of AFRICA &
NEW GUINEA.
• Affecting 120 million people in 83 countries.
• 40% of the affected people are in INDIA, 33% in
AFRICA.

33. LOA LOA (LOAIASIS)
• Confined to Africa.
• Vector Chrysops flies. They live in the rainy forest.
• Monkeys are the reservoir hosts.
ONCHOCERCA VOLVULUS (RIVER
BLINDNESS)
 Distributed in Africa & South America.
 Endemic in West Africa, Equatorial & East Africa &
Sudan.
 Vector - black fly = Simulum damnosum.

34. • W.bancrofti widely distributed throughout the tropics &
sub tropics which account for nearly 90% of the
lymphatic filariasis.
• Brugia malayi has only been recognized in ASIA &
localized to INDONESIA, MALAYSIA, PHILIPPINES,
THAILAND, VIETNAM, CHINA, SOUTH KOREA,
INDIA.
• Brugia timori is prevalent in islands of TIMOR &
FLORES. First described in 1964 from the island of
TIMOR of INDONESIA.
LYMPHATIC FILARIASIS

36. • IN INDIA
Only W.bancrofti & B.malayi are seen.
Endemic along coastal states – increasing
every year. Heavily infected areas are
found in U.P, Bihar, Jharkhand, A.P.,
Orissa, T.N., Kerala & Gujarat.
B.malayi – KERALA - largest endemic
area. ASSAM, ORISSA, M.P., W.B
-epidemic pockets.

38. • SYMPTOM PREVALENCE -
27 million - GENITALFILARIASIS
16 million - ELEPHANTIASIS of LEG

39. EPIDEMIOLOGY
AGENTS
W.BANCROFTI
B.MALAYI
B.TIMORI
Definite host is MAN.
Intermediate host is
MOSQUITO.
Adult worms live in LYMPHATIC
SYSTEM remain coiled together.
Male 2.5-4cm. &
Female 8-10cm.
Mf are seen in
blood, lung (capillaries), kidney
(glomerular tufts).

41. HUMANS - is a person with circulating Mf in
peripheral blood.
ANIMALS - no animal reservoir for Wb & Bt.Bm -
dogs, cats, monkeys, wild carnivores & rodents.
Reservoir

43. MAN is a natural host.
Age: all ages are susceptible. infectious rate rises with
age up to 20-30yrs.
Sex :higher in men.
Migration: causes extension of filariasis into areas
previously non endemic.
Immunity: resistance to infection after many years of
exposure.
HOST FACTORS

44. • A) Climate: is an imp. Factor in the epidemiology
of filariasis.it influences
1)Mosquito-longevity & breeding
2)determines the development of parasite in
the vector
Max. prevalence observed at temp.22-38°C
humidity-70%
B) Town planning: rapid urbanization in INDIA
causing inadequate sewage disposal –
aggravating the problem.
C) Drainage: mosq. breed profusely in polluted
water.
ENVIRONMENTAL FACTORS

45. 1)Major leading cause of disability in the world.
2)Associated with urbanization, industrialization,
migration,
poverty, illiteracy, poor sanitation.
3)Serious impact on health & economic status of
people.
4)Costs billions of dollars across the world.
SOCIO ECONOMIC FACTORS

46. INCUBATION PERIOD
IP
INTRINSIC(MAN)
PRE PATENT CLINICAL
EXTRINSIC(MOSQ)
Inoculation of
infective larva to the
first appearance of
detectable Mf.
Inoculation of infective
larva to the
development of clinical
manifestations-8-
16mon. or longer.
Entry of Mf to
the
appearance
of inf.
Larvae-10-14
days.
NB.Mf does not multiply in the mosq.

47. • VECTORS
Wb - Culex quinquefaciatus(fatigans) in urban & semi-
urban areas.
- Anopheles in rural areas of Africa
- Aedes in Pacific islands
Bm - Mansonia annulifers & M.uniformis
COMMON BREEDING HABITS
1)CULEX-cess pools, soakage pits, ill maintained drains,
septic tanks, open ditches, burrow pits,etc.
2)MANSONIA-confined to areas where PISTIA plants are
there.

48. SEPTIC PITS & DRAINS CONTAINING
STAGNANT WATER.

49. PISTIA PLANTS

50. • MODE OF
TRANSMISSION
By the bite of infected
vector mosq.
Transmission depends
upon the man -
mosq.contact (eg.infective
biting rate).
NOTE - as many as 15,000
bites are necessary to
produce infection.

51. 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”

52. • Life history of MOSQUITO:

53. • 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.

54. • 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.

55. 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.

56. • 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.
ANTI-ADULT MEASURES-

57. • 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”

58. Anatomy

59. 1–2 days
5–7 days
1–2 days
2–3 days

60. Eggs
Anopheles
Mansonia
Aedes
Culex

61. Culex larvae & pupa

62. Anopheles adult

63. Culex adult

64. Aedes adult

65. Mansonia adult

66. Integrated Approach
• Anti-larval:
• Environmental control: source reduction
• Chemical control: mineral oil, paris green, synthetic
• Biological control: Gamusia affinis, Lebister reticularis
• Anti-adult:
• Residual spray: DDT, Lindane, Malathion
• Space spray: Pyrethrum, Fenitrothion
• Genetic control: sterile male, cytoplasmic incompatibility,
chromosomal translocations
• Personal protective measures:
• Mosquito net: size of pore < 0.0475 inch
• Screening: windows
• Repellents: Diethyltoluamide (DEET), Indalone

67. Thanks