Vector-borne diseases-Malaria, Filariasis, Dengue, JE, YF, Chikungunya, KFD, Leishmaniasis and the national program against vector-borne diseases NVBDCP.

1. MALARIA

2. What is Malaria?
• You know it. Well done.
• And for those who think they know little
about malaria, follow us for next 35
minutes and go through your book at
home.

3. MALARIA
THE PARASITE

4. • Plasmodium falciparum
• Plasmodium vivax
• Plasmodium ovale
– Tropical Africa
• Plasmodium malariae
– Karnataka

6. MALARIA
THE VECTOR

7. Some species
• An. culicifacies
• An. fluviatilis
• An. stephensi
• An. minimus
• An. philippinensis
• An. sundaicus
• An. maculatus

8. Factors which determine vectorial
importance of mosquitoes
• DENSITY
– Critical density- below which effective
transmission cannot be maintained in a
community
• An. culicifacies- high density
• An. fluviatilis- low density
• LIFE SPAN

9. • CHOICE OF HOST
– Anthrophilic species like An. fluviatilis are better
vectors of malaria than zoophilic species
• RESTING HABITS
– Endophily
– Exophily
• BREEDING HABITS
• TIME OF BITING
• RESISTANCE TO INSECTICIDES

10. MALARIA
THE DISEASE

11. Reservoir of infection
• Human reservoir
– Harbors the sexual forms (gametocytes) of
the parasite
• P. malariae
– Chimpanzees in tropical Africa

12. • A patient can be a carrier of several
plasmodia species at the same time
• Children are more likely to be gametocyte
carriers than adults. The child is thus
epidemiologically a better reservoir than the
adult.

13. Conditions that must be met before a
person can serve as a reservoir
• Both male and female gametocytes are
present in blood
• Gametocytes are mature
• Gametocytes are viable
• Gametocytes are present in sufficient density
to infect mosquitoes (at least 12/cumm of
blood)

14. Period of communicability
• As long as mature, viable gametocytes exist
in circulating blood in sufficient density

15. Mode of transmission
• Vector transmission
• Direct transmission
• Congenital malaria

16. Incubation period
• Falciparum
– 12 (9-14)
• Vivax
– 14 (8-17)
• Ovale
– 17 (16-18)
• Malariae
– 28 (18-40)

17. Clinical features
• Signs and symptoms
• Complications
– Cerebral malaria – Dehydration
– ARF – Collapse
– Liver damage – Anemia
– GI symptoms – Blackwater fever

18. • Anemia
• Splenomegaly
• Enlargement of liver
• Herpes
• Renal complications

19. MALARIA
GLOBAL SCENARIO

26. Every minute 2 people die of malaria. By
the time we will finish this lecture
malaria would have killed180 more
people.

27. MALARIA
SOUTH-EAST ASIA REGION

33. MALARIA
PREVENTION & CONTROL

34. A. Malaria Vector Control
• Integrated Vector Management (IVM)
• Indoor Residual Spraying (IRS)
Integrated vector management (IVM) is a
•rational decision-making process for the
Insecticide Treated Nets (ITNs)
•optimal use of resources in the management
Other methods
of – Larviciding
vector populations, so as to reduce or
– Environmental management approaches to
interrupt transmission of vector-borne vector
control
diseases.
– Personal protection measures (includes ITNs)
– Fogging or area spraying

35. INSECTICIDES
Organo-Chlorines DDT
Organo- Malathion,Abate, Fent
Phosphates hion, Chlorpyrifos
Carbamates Propoxur, Carbaryl
Synthetic Tetramethrin, Resmeth
pyrethroids rin, Allethrin

36. B. Diagnosis
• Direct Microscopy
• RDTs (Rapid diagnostic tests)

37. • Histidine-rich protein-2 (HRP2)
• Parasite-specific lactate dehydrogenase
(pLDH)

40. C. Treatment
CQ Chloroquine 25 mg/Kg over 3days
PLUS
Sensitive
Primaquine 0.25 mg/kg BW daily for 14 days
Vivax
CQ ACT
PLUS
Resistant Primaquine 0.25 mg/kg BW daily for 14 days
ACT
Falciparum PLUS
Primaquine 0.75 mg/kg BW single dose
Severe Parenteral Artemesinin Followed by full
Malaria derivatives/Quinine course of ACT

41. • Plasmodium vivax cases
– Day 0: T. Chl 10 mg/kg BW (600 mg
adult dose)
– Day 1: T. Chl 10 mg/kg BW (600 mg
adult dose)
– Day 2: T. Chl 5 mg/kg BW (300 mg
adult dose)
PLUS
T. Primaquin 0.25 mg/kg BW daily for
14 days

42. ACT (Artesunate Combination Therapy)
T. Artesunate 4mg/kg BW daily X 3days
PLUS
T. Sulphadoxine 25 mg/kg BW and T.
Pyrimethamin 1.25 mg/kg BW on the first day
Resistance to Chloroquine and ACT
Oral Quinine 10 mg/kg BW and T.
Doxycycline 100 mg daily for 3 days
THEREAFTER T. Primaquin 0.75 mg/kg BW
single dose

43. 1.Artesunate 2.4 mg/Kg BW IV or IM at
0, 12 & 24 hrs, then daily
2.Artemether 3.2 mg/Kg BW at 0, then
1.6 mg.Kg BW per day
3.Quinine 20 mg salt/Kg BW at 0 (IV
infusion), then 10 mg/Kg BW every 8
hrs

44. D. Intermittent Preventive
Treatment

47. E. Malaria vaccines

48. • Pre-erythrocytic vaccines
• Blood-stage vaccines
• Transmission-blocking vaccines
– Pfs25
• Cocktail vaccines
– SPf66

49. F. Chemoprophylaxis
• Travelers from non-endemic areas
• Soldiers serving in highly endemic areas
• Migrant labourers
• Should be complemented by personal
protection and environmental measures
• Intermittent preventive treatment in
pregnancy

50. • For short-term prophylaxis (< 6 weeks)
– Doxycycline 100 mg X OD in adults or 1.5 mg/kg BW for children >8
years old.
– Started 2 days before travel and continued for 4 weeks after leaving
the malarious area.
– Contraindicated in pregnant females and children <8 years.
• For long-term prophylaxis (>6 weeks)
– Mefloquine 5 mg/kg BW (upto 250 mg) weekly
– Started 2 weeks before travel and continued till 4 weeks of leaving the
malarious area.
– Contraindicated in cases with H/O convulsions, neuropsychiatric
problems and cardiac conditions.

51. MALARIA
INDICATORS

52. • Eradication era
– Annual parasite incidence (API)
– Annual blood examination rate (ABER)
– Annual falciparum incidence (AFI)
– Slide positivity rate (SPR)
– Slide falciparum rate (SFR)

53. LYMPHATIC FILARIASIS

54. • The term “lymphatic filariasis” covers
infection with three closely related nematode
worms
– Wuchereria bancrofti
– Brugia malayi
– Brugia timori

55. • Transmitted to man by the bites of infective
mosquitoes.
• Adult worms live in the lymphatic vessels;
their offspring-the microfilariae-circulate in
peripheral blood and are available to infect
mosquito vectors when they come to feed.

56. FILARIA ENDEMIC DISTRICTS
250 Endemic districts in 20 States/UTs
Population: 600 Million

57. Agent factors
Organism Vectors
W. bancrofti Culex
B. malayi Mansonia, Aedes
B. timori Anopheles

58. • The Mf display nocturnal periodicity. They
appear in large numbers at night and retreat
from the blood stream during the day.
• The maximum density of Mf in blood is
reported between 10 pm and 2 am.

59. Mf W. bancrofti Mf B. malayi
General Graceful, Crinkled,
appearance sweeping curves secondary curves
Length 244 to 296 µ 177 to 230 µ
Excretory pore Not prominent Prominent
Caudal end Uniformly Kinkled and two
tapering to a terminal nuclei
delicate point; present
no terminal
nuclei present
Nuclear column Nuclei discrete Smudged

60. The typical vector for Brugia malayi filariasis are mosquito species from the
genera Mansonia and Aedes. During a blood meal, an infected mosquito
introduces third-stage filarial larvae onto the skin of the human host, where
they penetrate into the bite wound . They develop into adults that
commonly reside in the lymphatics . The adult worms resemble those of
Wuchereria bancrofti but are smaller. Female worms measure 43 to 55 mm
in length by 130 to 170 μm in width, and males measure 13 to 23 mm in
length by 70 to 80 μm in width. Adults produce microfilariae, measuring
177 to 230 μm in length and 5 to 7 μm in width, which are sheathed and
have nocturnal periodicity. The microfilariae migrate into lymph and enter
the blood stream reaching the peripheral blood . A mosquito ingests the
microfilariae during a blood meal . After ingestion, the microfilariae lose
their sheaths and work their way through the wall of the proventriculus and
cardiac portion of the midgut to reach the thoracic muscles . There the
microfilariae develop into first-stage larvae and subsequently into third-
stage larvae . The third-stage larvae migrate through the hemocoel to the
mosquito's prosbocis and can infect another human when the mosquito
takes a blood meal .

62. • Reservoir of infection:
– There is no evidence that W. bancrofti has
animal reservoirs in India
– Animal reservoirs of Brugia are present in
monkeys, cats and dogs
• Source of infection:
– A person with circulating Mf in peripheral
blood
– In late obstructive stages Mf are not
present in the blood

63. Vectors of lymphatic filariasis
• Main vectors in India are:
– C. quinquefasciatus for Bancroftian
filariasis
– Mansonia mosquitoes for Brugian filariasis

64. • Modes of transmission:
– Bite of infected vector mosquitoes
• Incubation period:
– 8-16 months

65. Clinical manifestations
• Asymptomatic microfilaraemia
• Acute adenolymphangitis (ADL)
• Chronic lymphoedema/Elephentiasis
• Tropical pulmonary eosinophilia (TPE)

66. Diagnosis
• Demonstration of Mf in peripheral blood
– Blood collected between 8:30 pm to 12:00 am
• DEC provocation test
– Blood examined one hour after administration of
100 mg DEC given orally

67. • Antigen detection assays
• Serological assays to detect antibodies to Mf
and adults using IF and CF techniques
– Do not distinguish between past and present
infection

68. Parasitological parameters
• Microfilaria rate
– % of persons showing Mf in their peripheral
blood
• Filarial endemicity rate
– % of persons examined showing Mf in their
blood, or clinical manifestations, or both
• Microfilarial density
– Number of Mf per unit volume (20cumm) of
blood
• Average infestation rate
– Average number of Mf per positive slide

69. Control measures
• Chemotherapy
– DEC (Diethylcarbamazine)
• Selective treatment (6 mg/kg X 12 days)
• Mass therapy (MDA)
– Ivermectin
• Vector control

70. DENGUE
(Breakbone fever)

71. WHAT IS DENGUE?
• Viral disease (Flavivirus)- four serotypes
• Transmitted by the infective bite of Aedes
aegypti/Aedes albopictus
• Man develops disease after 5-6 days of being
bitten by an infective mosquito
• Occurs in two forms
– Dengue Fever and
– Dengue Haemorrhagic Fever(DHF)

72. World-wide dengue distribution, 2006. Red: Epidemic dengue.
Blue: Aedes aegypti

73. DISTRIBUTION OF DENGUE/DHF IN INDIA

74. • Disease is prevalent throughout India in most
of the metropolitan cities and towns
• Outbreaks have also been reported from rural
areas of Haryana, Maharashtra & Karnataka

75. CASES
DEATHS

76. TRANSMISSION CYCLE OF DENGUE
Man-Mosquito-Man

77. VECTOR OF DENGUE/DENGUE
HAEMORRHAGIC FEVER
• Aedes aegypti
• Extrinsic IP= about 7 to 8 days
• Feeding Habit
– Day biter
– Mainly feeds on human beings in domestic and
peridomestic situations
– Bites repeatedly

78. • RESTING HABIT
– Rests in the domestic and peridomestic situations
– Rests in the dark corners of the houses, on
hanging objects like clothes, umbrella, etc. or
under the furniture
• BREEDING HABITS
– Aedes aegypti mosquito breeds in any type of
man made containers or storage containers
having even a small quantity of water
– Eggs of Aedes aegypti can live without water for
more then one year

79. • FAVOURED BREEDING PLACES
– Desert coolers, Drums, Jars, Pots, Buckets, Flower
vases, Plant
saucers, Tanks, Cisterns, Bottles, Tins, Tyres, Roof
gutters, Refrigerator drip pans, Cement
blocks, Cemetery urns, Bamboo stumps, Coconut
shells, Tree holes and many more places where
rainwater collects or is stored

80. • PERIOD OF COMMUNICABILITY
– Infected person with Dengue becomes infective to
mosquitoes 6 to 12 hours before the onset of the
disease and remains so upto 3 to 5 days
• AGE & SEX GROUP AFFECTED
– All age groups & both sexes are affected
– Deaths are more in children during DHF outbreak

81. SIGNS & SYMPTOMS OF DENGUE
FEVER
• Abrupt onset of high fever
• Severe frontal headache
• Pain behind the eyes which worsens with eye
movement
• Muscle and joint pains
• Loss of sense of taste and appetite
• Measles-like rash over chest and upper limbs
• Nausea and vomiting

82. SIGNS & SYMPTOMS OF DENGUE
HAEMORRHAGIC FEVER AND
SHOCK SYNDROME
• Symptoms similar to dengue fever
• Severe continuous stomach pains
• Skin becomes pale, cold or clammy
• Bleeding from nose, mouth & gums and skin
rashes

83. • Frequent vomiting with or without blood
• Sleepiness and restlessness
• Patient feels thirsty and mouth becomes dry
• Rapid weak pulse
• Difficulty in breathing

84. DIAGNOSIS
• Tourniquet test (look for the petechiae)
• Low platelet count (<100,000/mm3)
• Hemoconcentration (Hematocrit increased by
20% or more of the baseline value)

85. MANAGEMENT OF DENGUE CASE
• Early reporting
• Management of dengue fever is symptomatic
& supportive
• In dengue shock syndrome, the following
treatment is recommended:
– Replacement of plasma losses
– Correction of electrolyte and metabolic
disturbances
– Blood transfusion

86. Control of Dengue/ DHF
• No drug/vaccine available
• Control of Aedes aegypti only method of
choice

87. • Vector control measures:
– Environmental management & source reduction
– Biological control
– Chemical control
– Personal protection measures
– Health education
– Community participation

88. DO’S AND DON’TS
• Remove water from coolers and other small
containers at least once in a week
• Use aerosol during day time to prevent the
bites of mosquitoes
• Do not wear clothes that expose arms and
legs
• Children should not be allowed to play in
shorts and half sleeved clothes
• Use mosquito nets or mosquito repellents
while sleeping during day time

89. JAPANESE ENCEPHALITIS
(JE)

90. What is Japanese Encephalitis?
• A viral disease- Flavivirus
• Transmitted by infective bites of female
mosquitoes mainly belonging to Culex
tritaeniorhynchus, Culex vishnui and Culex
pseudovishnui group
• JE virus is primarily zoonotic in its natural
cycle and man is an accidental host
• JE virus is neurotorpic and arbovirus and
primarily affects central nervous system

91. PROBLEM STATEMENT
• Leading cause of viral encephalitis in Asia
with 30-50,000 cases reported annually
• Fewer than 1 case/year is reported in U.S.
civilians and military personnel traveling to
and living in Asia

92. • Countries which have had major epidemics in
the past, but which have controlled the
disease primarily by vaccination
• China Korea
• Japan Taiwan
• Thailand
• Countries that still have periodic epidemics
• Viet Nam Cambodia
• Myanmar India
• Nepal Malaysia

93. JE endemic areas

94. Extent of problem of JE in India
• JE viral activity has been widespread in India.
The first evidence of presence of JE virus dates
back to 1952.
• First case was reported in 1955
• Outbreaks have been reported from different
parts of the country.
• During recent past (1998-2004), 15 states and
Union Territories have reported JE incidence

95. 7000
6000
Number of cases
5000
4000
6061
3000
3024
1124 3003
2000
2320
1030
1000
0
2003 2004 2005 2006 2007 2008
AP Assam Bihar Haryana Karnataka Kerala Maharashtra TN UP WB

96. 1800
1600
1400
Number of deaths
1200
1000
1500
800
645
600 237
400 528 536
228
200
0
2003 2004 2005 2006 2007 2008
AP Assam Bihar Haryana Karnataka Kerala Maharashtra TN UP WB

97. JE affected districts in India

98. TRANSMISSION CYCLE
•Culex- Vector
•Pigs- Amplifier host
•Ardeid birds (Cattle egret, Pond heron)- Natural
hosts
•Man- Dead end (Mosquitoes do not get infection
from JE patient)

100. CATTLE EGRET
POND HERON
Reintroduction
of infected
mosquitoes or
TRITAENORHYNCUS
vertebrates PIG
Viral
CULEX
amplification
Vertical transmission
Infected vertebrate
reservoir

101. • Japanese encephalitis outbreaks are usually
circumscribed and do not cover large areas
• They usually do not last more than a couple
of months, dying out after the majority of the
pig amplifying hosts have become infected

102. Epidemiological features
• Incubation period:
– Usually 5 to 15 days
• Mortality rate:
– Case-fatality rates range from 0.3% to 60%
(Usually 20-40%)

103. • Who is at risk for getting Japanese
encephalitis?
– Residents of rural areas in endemic locations
– Active duty military deployed to endemic areas
– Expatriates who visit rural areas
• Japanese encephalitis does not usually occur
in urban areas

104. Clinical features
• Febrile illness of variable severity associated
with neurological symptoms ranging from
headache to meningitis or encephalitis
• Ratio of overt disease to inapparent infection
varies from 1:300 to 1:1000
• Headache, fever, meningeal
signs, stupor, disorientation, coma, tremors, paralysis
(generalized), hypertonia, loss of coordination

105. • Prodromal stage:
– Abrupt (1-6 hours)
– Acute (6-24 hours)
– Subacute (2-5 days)- more common
– Fever, headache, malaise

106. • Acute encephalitic stage:
– Usually lasts for a week
– Convulsions
– Alteration of sensorium
– Behavioural changes
– Motor paralysis
– Involuntary movement
– Focal neurological deficit

107. • Convalescent phase:
– Prolonged; may vary from a few weeks to several
months
– Those who survive may fully recover through
steady improvement or suffer with residual
neurological deficit
• JE virus infection presents classical symptoms
similar to any other virus causing encephalitis.
Clinically it is difficult to differentiate between
JE and other viral encephalitis

108. Diagnosis
• Clinical
• Laboratory
– Antibody detection
• HI, CF, ELISA for IgG (paired) and IgM (MAC) antibodies
– Antigen Detection
• RPHA, IFA
• Immunoperoxidase
• Genome Detection – RTPCR
• Isolation – Tissue culture, Infant mice, etc
• In view of the limitations associated with various
tests, IgM ELISA is the method of choice provided
samples are collected 3-5 days after the infection

109. Prevention and control
• Vector control:
– reducing the vector density
– role of insecticides is limited
– reduction in mosquito breeding (eco-
management; source reduction)
– personal protection against mosquito bites
– using insecticide treated mosquito nets

110. • Vaccination:
Three types of vaccines available
– Mouse brain-derived, purified and
inactivated, freeze dried vaccine
(Nakayama strain)
– Cell culture-derived inactivated vaccine
(Beijing strain)
– Cell culture-derived live attenuated vaccine
(SA 14-14-2 strain)

111. Mouse brain-derived inactivated
vaccine
• Has been used globally • Multiple doses ( 3 Primary
successfully to control + Booster)
JE • High cost
• Safe, efficacious • Low availability
• Limited duration of induced
• Manufactured in India protection
and used in many • CRI may also close down
states since 70s the production

112. • Immunization schedule
– 2 primary doses 4 weeks apart
– Booster after 1 year
– Subsequent boosters every 3 years till 10-15 years
of age
• Route of administration
– SUBCUTANEOUS
• Dose
– 0.5ml (<3 years)
– 1 ml (>3 years)

113. SA14-14-2 Live attenuated JE Vaccine
• Has been used since 1988 in China
• Over 200 million children vaccinated
• Safe and efficacious
• High immunogenicity following single dose (booster after 1
year)
• Licensed in Nepal and South Korea and Thailand
– Following this the vaccine has been licensed in India for
use in public health programs and is in the final stages of
licensing in Sri Lanka
• Special cost of vaccine for public program in GAVI eligible
countries
– Approximately 13 children could be vaccinated with the
SA14-14-2 vaccine with the cost of vaccinating one child
with the inactivated m-b derived vaccine

114. “A proven immunization strategy for JE
control seems to be to initiate a preventive
campaign in high risk areas and age groups
followed by introduction of vaccine into the
routine EPI programme”

115. JE Vaccination Strategy for India
• Vaccinate all children between the age
group of 1-15 years with a single dose of
live attenuated SA14-14-2 JE vaccine in a
one time campaign
• Integration into the routine immunization
in the district to cover the new cohort of 1-
2 years

116. • Control of piggeries:
– Vaccination of swine
– Live/killed vaccines available
– Maintaining vaccination coverage is difficult
because their population is renewed very rapidly
– Piggeries may be kept away (4-5 kms) from
human dwellings

117. CHIKUNGUNYA FEVER

118. • Dengue like disease
• Flavivirus
• Aedes aegypti (Culex?, Mansonia?)
• Sub- Saharan Africa, India, Asia
• 151 districts in 8 states/UTs have reported
cases between Feb 2006 & Oct 2006
• South & central India
• Karnataka & Maharashtra

119. • Incubation period:
– 4-7 days
• Clinical features:
– Fever, chills, headache, backache
– Adenopathy
– Rash on trunk and limbs
– Arthropathy
• Adults
• Metacarpophalangeal, wrists, elbow, shoulder, knee, an
kle, metatarsal
• Can persist for months or even years

120. • No deaths have been reported
• Diagnosis by serology (ELISA to detect IgM)
• No vaccine available
• No specific treatment
• Control
– Vector control

121. VIRAL HEMORRHAGIC FEVERS

122. • Arenaviridae
– Lassa fever
• Filoviridae
– Marburg hemorrhagic fever, Ebola HF
• Flaviviridae
– Dengue HF, Yellow fever, KFD
• Bunyaviridae
– HF with renal syndrome (Hantaan virus), Rift valley
fever

123. YELLOW FEVER

124. • Zoonotic disease caused by an arbovirus
(Flavivirus, ssRNA)
• Viral hemorrhagic fever
• Tropical & subtropical regions of Africa &
Americas
• Historically, accompanied travelers during
European colonial period

125. Problem Statement

126. • ETHIOPA
– 1 lakh cases, 30000 deaths
• GAMBIA
– 2.5% prevalence of severe infection, with a CFR of
19%
• NIGERIA
– 18735 cases, 4522 deaths

127. • No cases reported from Asia where Dengue, a
closely related disease is endemic
• Dengue immunity ? Cross-protection against
yellow fever- Yellow fever immunization does
not protect against dengue
• INDIA
– Population unvaccinated & susceptible to YF
– Aedes aegypti is abundant
– Climatic conditions are favorable for transmission
– Indian monkey (Macacus) is susceptible to YF
– ? Missing link-Virus is not present in India

128. Agent factors
• AGENT
– Flavivirus, ssRNA
• RESERVOIR OF INFECTION
– Forest areas- Monkeys, Forest mosquitoes
– Urban areas- Man, Aedes aegypti
• PERIOD OF COMMUNICABILITY
– Man- 1st 3-4 days of illness
– Mosquitoes- 8-12 days Extrinsic IP
– Transovarian transmission documented

129. Host factors
• AGE & SEX
– All ages & both sexes susceptible
• OCCUPATION
– Contact with forests (wood cutters, hunters)
• IMMUNITY
– One attack gives life-long immunity

130. Environmental factors
• CLIMATE
– >24⁰C, 60% RH- required fro multiplication of virus
in the mosquito
• SOCIAL FACTORS
– Urbanization
– Forest encroachment
– Expanding population
– Travel- frequency and speed

131. Modes of transmission
Three types of transmission cycle for
yellow fever
• Sylvatic (or Jungle) yellow fever
– Monkeys
• Intermediate yellow fever
– Monkeys & humans
• Urban yellow fever
– Humans

132. • Sylvatic (or Jungle) yellow fever- Africa &
America
– Occurs in monkeys infected by wild mosquitoes
(Haemagogus in America; Aedes africanus in Africa) in
tropical rainforests
– Infected monkeys pass the virus to mosquitoes during
feeding
– Infected wild mosquitoes bite humans entering the
rainforest (accidental infection)- Sporadic cases
– The majority of cases are young men working in the
forest (logging, etc)
– On occasion, the virus spreads beyond the affected
individual

133. • Intermediate yellow fever- Africa
– Small-scale epidemics that occur in humid or
semi-humid grasslands of Africa
– Separate villages experience simultaneous
infections transmitted by semi-domestic
mosquitoes that infect both monkey and human
hosts
– Most common type of outbreak in Africa
– It can shift to a more severe urban-type epidemic
if the infection is carried into a suitable
environment (with the presence of domestic
mosquitoes and unvaccinated humans)

134. • Urban yellow fever- Africa & America
– Large epidemics occurring when the virus is
introduced into high human population areas by
migrants
– Domestic mosquitoes of one species (Aedes
aegypti) transmit the virus from person to
person
– Monkeys are not involved in transmission
– Outbreaks spread from one source to cover a wide
area

135. Incubation period
• 3-6 days
• SIX days recognized for International Health
Regulations

136. Clinical features
• Mild, undifferentiated fever to severe illness
• Hemorrhagic, hepatic & renal manifestations
predominate
• Jaundice- develops after 4-6 days of illness
• Renal Tubular Necrosis- during 2nd week
• Albuminuria, Anuria
• Hemoptysis, Melena, Epistaxis
• Death between 5th & 10th day of illness

137. Prevention & Control
1. Treatment
– No specific treatment for yellow fever
– ORS and paracetamol for dehydration and fever
– An appropriate antibiotic(s) for any superimposed
bacterial infection
– Intensive supportive care may improve the
outcome for seriously ill patients, but is rarely
available in poorer, developing countries

138. 2. Vaccination
– Type of vaccine
• Live attenuated freeze dried chick embryo
• 17D vaccine
– Dose
• One dose of 0.5 ml subcutaneously
– Schedule
• Routine immunization with measles vaccine at
nine months of age

139. – Booster
• International health regulations require a
booster every 10 years
– Contraindications
• Egg allergy
• Immune deficiency from medication or disease
• Symptomatic HIV infection
• Hypersensitivity to previous dose
• Pregnancy*

140. – Special pecautions
• Do not give before six months of age
• Avoid during pregnancy
• Cholera & YF vaccines should be given at least
3 weeks apart
– Adverse effects
• Hypersensitivity to egg
• Rarely, encephalitis in the very young
• Hepatic failure
• Yellow fever vaccine-associated viscerotropic
disease; among older recipients

141. – Storage
• Between +5 & -30 deg C, preferably
below ZERO deg C
• Saline diluent
• Discarded if not used within half an hour
of dilution
• Kept on ice away from sunlight

142. – Validity
• The validity of yellow fever vaccination
certificate begins 10 days after the date
of vaccination and extends up to 10 years
– India requires vaccination of infants too

143. 3. Vector control
– Anti-adult measures
– Anti-larval measures
– “Source reduction”- Elimination of breeding
places
– Personal protection
– Health education- for community involvement

144. 4. Surveillance
– Clinical
– Serological
– Histopathological
– Entomological
– “Aedes aegypti Index”
• The percentage of houses & their premises, in a
limited well-defined area, showing actual breeding of
Aedes aegypti larvae
• This index should not be more than 1% in towns &
seaports in endemic areas

145. 5. International measures
– “Yellow fever receptive area”- An area in which
YF is does not exist, but where conditions would
permit its development if introduced
– Valid international YF vaccination certificate for
travelers to endemic areas or traveling through
such areas
– If not present, QUARANTINE for 6 days
– Aerosol spraying of ships & aircraft from
endemic areas
– AEI kept below 1% at airports & seaports (kept
free from breeding places over 400 m area
around their perimeters)

146. KAYASANUR FOREST DISEASE
(KFD)

147. • Viral hemorrhagic fever
• Arboviral; Flavivirus
• Transmitted to man by bite of infective ticks
(Haemaphysalis)
• Karnataka in 1957
• 2167 cases & 69 deaths in 1983-84
• 306 cases & 11 deaths in 2003

148. Epidemiological determinants
• AGENT
– Tick-borne flavivirus
• NATURAL HOSTS & RESERVOIR
– Main reservoirs- Rats & squirrels
– Amplifying host- Monkeys
– Man is an incidental or dead-end host
– Cattle- Provide blood meals for ticks; important in
maintaining tick populations

149. • VECTORS
– Haemaphysalis spinigera, H turtura
– Nymph stages
– January to June- Highest number of infections;
peak nymphal activity of ticks
• HOST FACTORS
– Age- 20-40 years
– Sex- Males>Females
– Occupation- involving forest visits
– Human activity- Forest activity; Jan to June

150. • MODE OF TRANSMISSION
– Transmission cycle involves monkeys and ticks
– No evidence of man to man transmission
• INCUBATION PERIOD
– 3-8 days

151. Clinical features
• Sudden onset fever, headache and severe
myalgia
• Acute phase for 2 weeks
• GI disturbances and hemorrahges
• SECOND PHASE
– Mild meningoencephalitis after an afebrile period
of 7-21 days
• CFR= 5-10%

152. Diagnosis
• Presence of virus in blood
• Serology

153. CONTROL
• CONTROL OF TICKS
– Carbaryl/Fenthion/Propoxur
– Carried out in “hot spots” ( areas where monkey
deaths have been reported)
– Restriction of cattle movement

154. • PERSONAL PROTECTION
– Adequate clothing
– Insect repellents (DEET)
– Remove ticks from body and clothing at the end of
the day
– Discourage lying down or sitting on ground
• VACCINATION
– Killed vaccine

155. Leishmaniasis

156. • A group of protozoal diseases caused by
parasites of the genus Leishmania, and
transmitted to man by the bite of female
phlebotomine sandfly
• Majority of leishmaniasis are zoonoses
involving wild or domestic mammals
(rodents, canines)
• Indian kala-azar is considered to be a non-
zoonotic infection

157. • Visceral leishmaniasis (VL)
• Cutaneous leishmaniasis (CL)/Oriental sore
• Muco-cutaneous leishmaniasis (MCL)

158. Problem statement
• Visceral leishmaniasis
Bangladesh India
Brazil Sudan
• Cutaneous leishmaniasis
Afghanistan Iran
Brazil Peru
Saudia Arabia Syria
• Muco-cutaneous leishmaniasis
Brazil Bolivia
Peru

160. • Endemic in 88 countries
• Co-infection of VL & AIDS is emerging due to
spread of the AIDS pandemic particularly in
southern Europe, where 25-70% of adult VL
cases are related to HIV infection, & 1.5-9% of
AIDS patients suffer from newly acquired or
reactivated VL

161. Indian scenario
• Kala-azar (VL)
Bihar Jharkhand
West Bengal Uttar Pradesh (eastern)
• Cutaneouos Leishmaniasis
North-western India (Rajasthan)

162. • Both cutaneous and visceral diseases occur in
India
• Kala-azar is the most important leishmaniasis
in India

163. Epidemiological determinants
• AGENT:
– VL (Kala-azar)
• Leishmania donovani
– CL (Oriental sore)
• L. tropica
• L. major
– MCL
• L. braziliensis

164. • Sandfly injects the promastigote stage into
skin
• Promastigotes transform into amastigotes
(LD bodies) inside the macrophages (human)
• Sandfly ingests amastigotes
• Amastigotes transform into promastigote
stage inside the sandfly midgut, divide &
migrate to proboscis

166. • RESERVOIRS OF INFECTION:
– Rodents, dogs, jackals, foxes etc
– Indian kala-azar is considered to be a non-
zoonotic infection with man as the only reservoir

167. • HOST FACTORS:
– Kala-azar can occur in all age groups. Peak age
in India is 5-9 years
– Males are affected twice as often as females
– Population movement can result in spread of
infection from non-endemic to endemic areas
– Lower socio-economic class
– Farming practices, forestry, mining, fishing etc
are risk occupations

168. • ENVIRONMENTAL FACTORS:
– Kala-azar is mostly confined to the planes;
does not occur in altitudes over 2000 feet
– Generally there is a high prevalence during &
after rains
– Generally confined to rural areas
– Overcrowding
– Ill-ventilation
– Accumulation of organic matter in the
environment

169. Vector
• Kala-azar
– Phlebotomus argentipes
• CL
– P. papatasi
– P. sergenti
• New world
– Lutzomyia species

170. • Sandflies breed in cracks and crevices in the
soil & buildings, tree holes, caves etc
• They have nocturnal habits
• Only females bites

171. Mode of transmission
• Bite of the female phlebotomine sandfly (P.
argentipes/papatasi/sergenti)
• By contact when the insect is crushed during
the act of feeding
• Extrinsic IP = 6-9 days
• Transmission of kala-azar has also been
recorded by blood transfusion

172. Incubation period
• 1 to 4 months (10 days to 2 years)

173. Clinical features
• Kala-azar:
– Fever
– Splenomegaly
– Hepatomegaly
– Anaemia
– Weight loss
– Darkening of skin (face, hands, feet, abdomen)

174. • PKDL (Post-kala-azar Dermal Leishmaniasis):
– Common in India
– Occurs one to several months after apparent cure
of kala-azar
– Multiple nodular infiltrations of the skin
– Numerous parasites in the skin lesions;
important in disease transmission

175. • Cutaneous leishmaniasis:
– Painful ulcers in areas of skin exposed to sandfly
bite (legs, arms, face)
• Muco-cutaneous leishmaniasis:
– Ulcers around mouth & nose
– Can mutilate the face

177. Laboratory diagnosis
• Demonstration of the parasite LD bodies
(Leishman-Donovan body) in the aspirates of
spleen, liver, bone marrow, LNs, or in the skin
(in CL)

178. • Napier’s Aldehyde test
– 1-2 ml of serum + 40% formalin
– White opacity within 2-20 min = strongly positive
– Becomes positive 2-3 months after onset of
disease, & reverts to negative 6 months after
cure
– Non-specific
• Serology
– ELISA

179. • Leishmanin test (Montenegro test)
– Leishmanin is a prepration of 106 per ml washed
promastigotes of leishmania suspended in 0.5%
phenol
– An intradermal injection of 0.1 ml on the flexor
aspect of forearm is given and examined after 48-
72 hours

180. – An induration of 5 mm or more is considered
positive
– The test is usually positive 4-6 weeks after onset in
case of CL and MCL
– Usually negative in the active phases of kala-azar &
becomes positive in 75% cases within one year of
recovery

181. • Haematological findings:
– Leucopenia
– Anaemia
– Reversal of A:G ratio
– Decreased WBC:RBC ratio (1:1500 or more)
– Increased ESR

182. Control measures
• Control of reservoir
• Sandfly control
• Personal protection

183. Control of reservoir
• Man
– Active & passive case detection
– Treatment of those found to be infected
(including PKDL)
• Sodium stibogluconate
– 20mg/kg (max 850 mg) IM/IV X 20 days
• Pentamidine
– (3mg/kg) IV X 10 days
• Amphotericin B
• Miltefosine

184. Sandfly control
• Insecticides
– DDT
– Spraying should be undertaken in human
dwellings, animal shelters, & all other resting
places up to a height of 6 feet from floor level

185. • Sanitation measures
– Elimination of breeding places (cracks in mud or
stone walls, rodent burrows, removal of
firewood, rubbish around the house)
– Location of cattle sheds & poultry at a fair
distance from human dwellings
– Improvement of housing & general sanitation

186. Personal protection
• Avoiding sleeping on floor
• Using fine-mesh nets around the bed
• Insect repellents
• Health education
• There are no drugs for personal prophylaxis

187. NVBDCP (National Vector Borne
Diseases Control Program)

188. • Malaria
• Filariasis
• Kala-azar
• Japanese encephalitis
• Dengue
• Chikungunya

189. Three pronged strategy:
• Disease management
– Early case detection and complete treatment
– Strengthening of referral services
– Epidemic preparedness and rapid response

190. • Integrated vector management
– Indoor residual spraying
– Insecticide treated bed nets
– Larvivorous fish
– Source reduction and minor environmental
engineering

191. • Supportive interventions
– Behavior change communication
– Public private partnership & intersectoral
convergence
– Human resource development
– Operational research
– Monitoring and evaluation

192. MALARIA

193. • National Malaria Control Program – 1953
• National Malaria Eradication Program – 1958
• Modified Plan of Operations (MPO) – 1977
• National Anti-Malaria Program – 1999

194. • Objectives of MPO:
– Consolidation of the achievements already made
in the containment of malaria
– Prevention of malaria mortality and reduction of
malaria morbidity
– Maintenance of agricultural and industrial
productivity by intensive operations in the labor-
intensive endemic areas

195. • Organization and implementation:
– Integration of the malaria organization with the
state health system
– Reinforcement
• District Malaria Officer
• Malaria laboratory in every PHC
• Fever Treatment Depots (FDT) - (Smear+Drugs)
• Drug Distribution Centers (DDC) - Drugs

196. • Operational details:
– For API 2 or more areas
• Regular insecticidal spraying
– 2 DDT (1g/sq m) OR 3 Malathion (2 g/sq m) OR 2 Synthetic
pyrethroids (0.25g/sq m)
• Entomological assessment
• Surveillance (active & passive)
• Treatment of cases

197. – For API less than 2 areas
• Focal spraying around Pf cases detected
• Surveillance
• Treatment
• Follow-up
• Epidemiological investigation

198. • Area-based initiatives:
– Enhanced Malaria Control Project (EMCP)
• Tribal population
• 100 districts in 8 states
• 100% assistance through World Bank support
• 1997 – 2005
• 48 districts achieved an API of less than 2

199. – Intensified Malaria Control Project
• Launched in 2005 with assistance from ‘Global Fund
for AIDS, Tuberculosis, and Malaria’
• Increase access to rapid diagnosis & treatment
through community participation
• Use of ITNs
• Vector control by larvivorous fish
• NGO & private sector participation

200. – Assistance to NE states
• 100% central assistance to NE states

201. • Activity-based initiatives:
– Indoor Residual Spraying
– Insecticide-treated bed-nets
– Larvivorous fish use
– Case detection and treatment

202. • Present strategies for prevention and control
of malaria
1. Early case Detection and Prompt Treatment
(EDPT)
2. Vector control
3. Community Participation
4. Environmental Management & Source
Reduction Methods
5. Monitoring and Evaluation of the program

203. • Annual parasite incidence (API)
• Annual blood examination rate (ABER)
• Annual falciparum incidence (AFI)
• Slide positivity rate (SPR)
• Slide falciparum rate (SFR)

204. MALARIA CONTROL

205. Two different approaches to
malaria control
• Management of malaria cases in the
community
• Active intervention to control or interrupt
malaria transmission with community
participation

206. Management of malaria cases in
the community
• Case detection
• Treatment
– Uncomplicated malaria
• Plasmodium vivax
• Plasmodium falciparum
– Severe and complicated malaria
• Chemoprophylaxis

207. Case detection
• Active and passive case detection
• Fever cases presumed to be suffering to be
suffering from malaria, unless proved
otherwise
• In case laboratory diagnosis is not
immediately available, differential diagnosis
on clinical grounds should be made

208. Treatment
• Any fever in endemic areas during transmission
season without any other obvious cause should
be considered as malaria and investigated and
treated accordingly
• Drug resistance are present in country, but
chloroquine is still safe and effective
• The best approach in malaria control is diagnosis
and treatment on the same day

209. Treatment: Uncomplicated malaria
• Plasmodium vivax cases
– Day 0: T. Chl 10 mg/kg BW (600 mg adult dose)
– Day 1: T. Chl 10 mg/kg BW (600 mg adult dose)
– Day 2: T. Chl 5 mg/kg BW (300 mg adult dose)
PLUS
T. Primaquin 0.25 mg/kg BW daily for 14 days
• Plasmodium falciparum cases
• Chloroquin sensitive areas
– Day 0: T. Chl 10 mg/kg BW (600 mg adult dose)
– Day 1: T. Chl 10 mg/kg BW (600 mg adult dose)
– Day 2: T. Chl 5 mg/kg BW (300 mg adult dose)
THEREAFTER
T. Primaquin 0.75 mg/kg BW single dose

210. Treatment: Uncomplicated malaria
• Plasmodium falciparum cases
• Chloroquin resistant areas
• Give ACT (Artesunate Combination Therapy)
• T. Artesunate 4mg/kg BW daily X 3days
PLUS
• T. Sulphadoxine 25 mg/kg BW and T. Pyrimethamin 1.25 mg/kg
BW on the first day (Contraindicated in pregnant females)
THEREAFTER
T. Primaquin 0.75 mg/kg BW single dose
• Resistance to Chloroquine and ACT
• Oral Quinine 10 mg/kg BW and T. Doxycycline 100 mg daily for 3
days THEREAFTER T. Primaquin 0.75 mg/kg BW single dose

211. Treatment: In severe and
complicated malaria
• Cases should be hospitalized for treatment
– Quinine
– Artesunate
Followed by full
– Artemether
course of ACT
– Artether
– Use of Mefloquin alone or in combination with
artesunate should be avoided in cerebral malaria
due to neuro-psychiatric complications
associated with it.

212. Chemoprophylaxis
• Travelers from non-endemic areas
• Soldiers serving in highly endemic areas
• Migrant labourers
• Should be complemented by personal
protection and environmental measures
• Intermittent preventive treatment in
pregnancy

213. Chemoprophylaxis
• For short-term prophylaxis (< 6 weeks)
– Doxycycline 100 mg X OD in adults or 1.5 mg/kg BW for children >8
years old.
– Started 2 days before travel and continued for 4 weeks after leaving
the malarious area.
– Contraindicated in pregnant females and children <8 years.
• For long-term prophylaxis (>6 weeks)
– Mefloquine 5 mg/kg BW (upto 250 mg) weekly
– Started 2 weeks before travel and continued till 4 weeks of leaving the
malarious area.
– Contraindicated in cases with H/O convulsions, neuropsychiatric
problems and cardiac conditions.

214. Active intervention measures
• Stratification of the problem
• Vector control strategies
– Anti-adult measures
– Anti-larval measures
• Malaria vaccines

215. Stratification of the problem
• For planning and development of a sound
control strategy to maximize the utilization of
available resources
• Stratification is based on API
– Areas with API<2
– Areas with API>2

216. Vector control strategies
• Anti-adult measures
– Residual spraying
– Personal protection measures
• ITN
• LLITN
• Repellents
• Protective clothing
• Screening of houses

217. • Anti-larval measures
– Source reduction
– Larvicides
• Oils
• Paris green
• Insecticides (Temephos)
– Integrated control

218. Malaria vaccines
• Pre-erythrocytic vaccines
• Blood-stage vaccines
• Transmission-blocking vaccines
– Pfs25
• Cocktail vaccines
– SPf66

220. FILARIASIS

221. • National Filaria Control Program – 1955
– Implemented through
• Filaria control units
Endemic
• Filaria clinics
urban towns
• Survey units
• Though PHc system in rural areas
– Filaria control strategy
• Vector control
• Detection & treatment of microfilaria carriers
• Morbidity management
• IEC

222. • WHA resolution of 1997 – global elimination
of lymphatic filariasis
• Elimination of filariasis by 2015
– Revised filaria control strategy
• Annual MDA
– Single dose DEC (6mg/kgBW) for 5 years or more to ‘at risk
population’ excluding pregnant females, children <2 years of
age, seriously ill patients
• Case management
• Capacity building
• Social mobilization

223. Kala-azar

224. • Strategies for Kala-azar elimination are:
– Enhanced case detection and complete
treatment (including rapid diagnostic
kits, miltefosine)
– Vector control
– BCC and intersectoral convergence
– Capacity building
– Monitoring, supervision and evaluation
– Research

225. • In may 2005, a tripartite MoU between
India, Nepal & Bangladesh; to reduce the
annual incidence of Kala-azar to <1/10000
population at sub-district level by 2015.
• National Health Policy envisages Kala-azar
elimination by 2010.

226. Dengue and Chikungunya

227. • Case management
– Health personnel training- upgrading clinical skills and diagnostic
competence
• Health education
– Community is informed on the characteristic features of the disease
and the facilities available for their clinical management
• Vector control
– Elimination of vector breeding sites
– Disposing of all the junk material that collects water & encourages
vector breeding
– Keeping all water containers and storage facilities tightly covered
– Cleaning the water coolers at least once a week before refilling
• Monitoring and surveillance

228. JAPANESE ENCEPHALITIS

229. • Operational strategy:
– Early case detection and prompt management
– Vector density reduction by adulticidal and
larvicidal measures
– IEC campaigning for community participation
– Immunization of high-risk population groups

230. 233