Arbo viral diseases

Arbo viral Diseases
Dr. Sujatha Sathananthan MD.,DPH.,
Assistant Professor
Department of Community Medicine
Chengalpattu Medical College

Arthropod-Borne Viruses
Arthropod Borne Viruses (Arbo Viruses)
are viruses that can be transmitted to
man by arthropod vectors.
12 May 2018 2Chengalpattu Medical College

Arbovirus – Clinical Syndromes
Febrile Group Haemorrhagic
Group
Encephalitis
Group
Chikungunya,
Dengue
Chikungunya
Dengue
KFD
Yellow Fever
ZIKA (NEWLY
EMERGING)
JE

Arboviruses in India1
COMMON :
 Dengue V
 Japanese Encephalitis
V
 Chikungunya V
 Kyasunur Forest
Disease V
Group A (Alpha virus)
- Chikungunya
- Sindibis
Group B (Flavi virus)
- Dengue
- JE
- KFD
- West Nile Fever

Virus Reservoir Vector Disease
Chikungunya Monkeys Mosquito Chikungunya fever
Dengue Monkeys, Man Mosquito Dengue haemorrhagic
fever
Japanese B
encephalitis
Wild birds, pigs Mosquito Encephalitis
Kyasanur forest
disease
Forest birds,
animals
Tick Haemorrhagic fever
Arboviruses prevalent in India

Dengue
Dengue is a acute febrile illness caused by arboviruses
4 antigenically distinct serotypes (DENV 1,2,3,4),
transmitted by Aedes mosquitoes (Aedes aegypti)
Aedes mosquito also transmits chikungunya, yellow
fever and Zika infection
May present as
1. “Classical” Dengue fever or
2. DHF without shock or
3. DHF with shock also called as Dengue Shock
Syndrome (DSS).

Problem statement
2.5 billion people are at risk of the disease in the
tropical and subtropical countries
50 million dengue infections occur worldwide
annually
5lakh people with DHF require hospitalization
each year
Approximately 90% of them are children <5
years and about 2.5% of these will die.

Categories based on endemicity-
South East Asian Region
Category A – India, Bangladesh , Indonesia ,
Maldives, Myanmar , Srilanka , Thailand and
Timor-Leste
1. Major public health problem
2. Leading cause of Hospitalization and death
among children
3. Hyper endemicity with all 4 serotypes
circulating in urban areas
4. Spreading to rural areas

Categories based on endemicity
Category B: Bhutan , Nepal
Endemicity uncertain
Category C : DPR Korea
No evidence of endemicity

Dengue on the Globe
Highly endemic Recently acquired12 May 2018 10Chengalpattu Medical College

Dengue on the
Globe- 2015
Philippines- 1,08,263 cases
with 317 deaths
Malaysia- 96,222 cases of with 263 deaths
Singapore- 7,815 cases
China - 1917 cases
Australia - 1,393 cases
The Island of Hawaii, United States of America, was
affected by an outbreak with 181 cases reported in
2015 and ongoing transmission in 2016.
Source- WHO

DENGUE - INDIA
The risk of dengue increases in recent years due
to
1. rapid urbanization
2. life style changes and
3.deficient water management including water
storage practices in urban, peri-urban and rural
areas
This all leads to proliferation of mosquitoes
breeding sites

Dengue cases double in 2015 (INDIA)
 2014- 10,097, with 37 deaths
 2015- 19,704 cases with 41 deaths
CITIES
 Delhi- 1259 cases
 Bengaluru- 1139 cases
 Mumbai – 306 cases
 Kolkata – 187 cases
 Delhi- dengue has become a hyper-endemic due to co-
circulation of different subtypes. There have been cases
of the same person being infected by two different
serotypes.

Dengue cases in Tamil Nadu, 2015
Dengue cases double this year in Tamil Nadu
Total - 2,357 cases with 5 deaths
Of which 80 cases from Chennai (Adyar,
Kodambakkam and Alandur zones)
High risk districts - Tirupur, Trichy, Theni, Salem,
Dharmapuri and Krishnagiri districts
In 2014 - 1,146 cases
Tamil Nadu takes 2nd place in dengue numbers
after Maharashtra

Dengue cases in India 2016 (till oct 18)
State :
West Bengal- 6933 cases (25 deaths)
Orissa - 6963 cases (11 deaths)
Kerala - 5988 cases (10 deaths)
Karnataka- 4556 cases (8 deaths)
Maharashtra – 4033 cases (4 deaths)
Delhi – 2122 cases (4 deaths)
Tamil Nadu – 1752 cases (4 deaths)
Source- NVBDCP

Dengue cases in Tamil Nadu, 2016
Total – 1752 cases and 4 deaths
Thiruvallur
Coimbatore
Kanchipuram
Thiruporur

Epidemiological Triad
The Host
The Agent(Virus) The Environment
Interaction

The Agent
Dengue Virus

The Dengue Virus
Flavivirus
Single stranded RNA virus
40 to 50 nanometers
Arthropod borne
Four sero-sub types
- DENV-1, DENV- 2, DENV-3,
DENV-4

The Vector
Aedes aegypti
(Infected Female Mosquito)
(also Aedes albopictus)

AEDES MOSQUITO
 Tiger mosquito – White stripes on black body
 It is a day biting mosquito when normally coils, repellents,
nets etc are not used
 It breads in fresh water around homes
 Lays eggs preferentially in manmade containers water jars,
coconut shells, old tires, cement tanks, overhead tanks,
discarded containers, etc, in which water stagnates for more
than a week
 Can transmit trans-ovarially the infection in mosquitoes.
 It is an urban vector

BREEDING SOURCES

Breeding Sources

Breeding sources

Peculiarities of A.aegypti
Highly domesticated,
Strongly anthropophilic,
Nervous feeder - it bites more than one host to
complete one blood meal
Discordant species - it needs more than one feed
for completion of gonotropic cycle
 This habit results in the generation of multiple
cases.

Peculiarities of
A.albopictus
 Aedes albopictus partly
invades peripheral areas
of urban cities.
 It is aggressive feeder
 Concordant species - the species can complete its
blood meal in one person and also does not require a
second blood meal for completion of gonotropic cycle)

Host factors
 All ages and sexes are affected
 Children usually suffer from
a milder illnesss when compared to adults
 Males suffer more often

Environmental factors
 The population of A.aegypti fluctuates with rainfall and
water storage
 Relative humidity - 60 to 80%
 Temperature - between 16 to 30 deg C

Dengue virus
•A factor complicating eradication of the vector mosquito is that the Ae.
Aegypti eggs can withstand long periods of desiccations (dry environments),
sometimes for more than a year.
Dengue virus elimination is
not possible
Mosquito transmit dengue virus
(transovarian) in to the eggs
so next generation of mosquito
by birth
are infected with virus
Mosquito eradication is difficultEggs survive
more than 1 year period

• Mosquito once
infected, it remains
infective for its life,
transmitting the
virus to susceptible
individuals.
Dengue virus Sources
Mosquito infective for its life
Dengue Life Cycle

Spectrum of disease

Criteria for clinical Diagnosis
Dengue Fever:
Probable Diagnosis:
Acute febrile illness with 2 or more of the following’
 Headache
 Retro orbital pain
 Myalgia
 Arthralgia/bonepain
 Rash
 Hemorrhagic manifestations
 Leucopenia (WBC <= 5000 cells /cubic mm)
 Thrombocytopenia (platelet count <150000cells/cubic mm)
 Raising Hematocrit (5-10%)
And atleast one of the following:
 Supportive serology on single serum sample : Titre >= 1280 with Haemagglutination
Inhibition Test, comparable IgG titre with ELISA assay or test positive in IgM antibody
test
 Occurence at the same location and time as confirmed cases of Dengue fever

Confirmed Diagnosis- Dengue Fever
Probable case with at least one of the following:
 Isolation of Dengue virus from serum, CSF, autopsy
sample
 Fourfold or greater increase in serum IgG by
(Haemagglutination inhibition test) or increase in
antibody specific to Dengue virus
 Detection of dengue virus or antigen in tissue , serum or
CSF by immuno histo chemistry, immunofluorescence or
ELISA
 Detection of dengue virus genomic sequences by RT -
PCR

Dengue Hemorrhagic Fever
All of following:
 Acute onset of Fever of 2 to 7 days duration
 Haemorrhagic manifestations, shown by any of the following :
 Positive torniquet test
 petechiae,
 ecchymoses or purpura or
 bleeding from mucosa,GIT,injection sites
 Platelet count <= 100000cells/cubic mm
 Objective evidence of plasma leakage due to increased
vascular permeability shown by any of the following :
 Raising haematocrit / haemoconcentration >= 20% from
baseline or
 evidence of plasma leakage such as pleural effusion, ascites
or hypo proteinaemia / albuminaemia

Dengue Shock Syndrome
Criteria for Dengue haemorrhagic Fever with signs of
shock including:
 Tachycardia, cool extremities , delayed capillary
refill,weak pulse , lethargy or restlessness, which may be
a sign of reduced brain perfusion
 Pulse pressure <=20 mmHg with increased diastolic
pressure
 Hypotension by age , defined as systolic pressure <80
mmHg for those aged <5 years or 80-90 mmHg for older
children and adults

Laboratory Diagnosis
1.Virus Isolation :
• Specimen taken with in 6 days of illness and processed without
delay
• Acute phase serum , plasma or washed buffy coat from the
patient , autopsy tissue (liver , spleen , LN and thymus) and
mosquitoes collected from the affected areas.
2.Viral Nucleic acid detection:
RT-PCR assay
3.Immunological Response and Serological tests:
• HIA (Haemagglutination Inhibition Assay)
• Complement Fixation
• Neutralization test
• IgM Capture ELISA
• Indirect IgG ELISA and IgM/IgG ratio

Laboratory Diagnosis
4.Viral Antigen Detection:
 ELISA and Dot Blot Assays - envelope/ Membrane
antigens
 Non Structural Protein 1 (NS1) – can be detected up to 6
days after the onset of illness
• It donot differentiates between the serotypes
• Early diagnostic marker for clinical management.
5. RDT : serological test kits for anti dengue IgM and IgG
antibodies , results with in 15 minutes .
6. Analysis of Haematological parameters:
 Platelet count
 Haematocrit values

WARNING SIGNS
No clinical improvement or worsening of the situation just
before or during the
transition to afebrile phase or as the disease progresses.
Persistent vomiting, not drinking.
Severe abdominal pain.
Lethargy and/or restlessness, sudden behavioural changes.
 Bleeding: Epistaxis, black stool, haematemesis, excessive
menstrual bleeding, darkcoloured
urine (haemoglobinuria) or haematuria.
Giddiness.
 Pale, cold and clammy hands and feet.
•Less/no urine output for 4–6 hours.

Home care advise for the patient
 Adequate bed rest
 Adequate fluid intake (>5 glasses for average-sized adults or
accordingly in Children) Milk, fruit juice, ORS
 Take paracetamol
 Tepid sponging
 Look for Mosquito breeding places in and around the Home
and eliminate them.
 Educate them on the warning symptoms.

Admit the patient
 Existing warning signs
 Plasma leakage with shock and / or fluid accumulation with
respiratory distress
 Bleeding manifestations like epistaxis, hemetemesis, malena,
increased menstrual bleeding, haematuria, bleeding gums
 Coexisting conditions such as pregnancy, infancy, Children, Old
age, diabetes, mellitus, renal failure, COPD, immune supressed

Treatment protocol?
 Control temperature
 Oral fluids or intra venous fluids
 platelet transfusion / red cell transfusion
 Other supportive therapy

Discharge Criteria
 Clinical – No fever for 48 hours
Improvement in clinical status
(general well-being, appetite,
haemodynamic status, urine
output, no respiratory distress)
 Laboratory – Increasing trend of platelet
count (> 50000/cubic mm).
Stable haematocrit
without intravenous fluids

Control
 Vector control- Removal of Breeding sources , anti larval
and anti adult measures
 Management of roof tops , porticos and sunshades , proper
covering of stored water , observation of weekly dry day
 Vaccination- no satisfactory measure available in India
 DENGAVAXIA – Sonafi –Pasteur –French company , vaccine
approved – 11 countries: indonesia , thailand , singapore ,
mexico , philippines,brazil ,peru , el salvador, costa rica ,
paraguay , guatemala.
 Individual protection- wearing full sleeves, full pants ,
repellant creams , coils , mosquito nets

Chikungunya fever

Chickungunya fever
 Group A virus
 Aedes agypte mosquitoes
 First isolated – Tanzania Epidemic – 1952
 Doubling up
 2006 – India , 1.39 million cases
 occurs in rainy season

Cycle of Infection

Chickungunya fever
Incubation period :4-7 days
Clinical features:
 fever , chills, cephalagia, anorexia, lumbago and CONJUNCTIVITIS
 Adenopathy , Morbilliform rash (60-80%), occasionally purpura, on
the trunk and limbs
 Cutaneous eruptions recur every 3 to 7 days.
 Coffee coloured vomiting, epistaxis and petechiae
 Arthropathy- pain ,swelling , stiffness
 Metacarpophalengeal , wrist ,elbow, shoulder , knee , ankle and
metatarsal joints
 Appears between 3rd and 5th day after the onset of clinical
symptoms
 Persists for many months and even years.
 No deaths have been attributed to chikungunya

Chickungunya fever
Diagnosis :
Serological diagnosis – most commonly
used
ELISA – to detect IgM
RT-PCR

Chickungunya fever
Treatment:
 Usually self limiting
 Only supportive treatment
 Analgesics , Anti Pyretics ,fluid supplementation
 Aspirin and steroids to be avoided
 No Vaccine

Chickungunya fever
Vector Control:
 Aedes mosquito- eliminate the breeding places
 Abate – larvicide,prevents breeding upto 3 months
 Anti adult measures: aerosol spray of Ultra low volume
(ULV) quantities of Malathion or Sumithion (250 ml /
hectare)- effective in interrupting the transmission and
stops the Epidemic of DHF
 Tiny droplets kill mosquitoes in air as well as in water.
 2 ULV treatments 10 days apart – reduces mosquito
density >98% for several weeks

Japanese
EncephalitisJapanese
Encephalitis

Japanese encephalitis(JE) is a mosquito-borne
encephalitis caused by group B arbovirus (Flavivirus)
It is a zoonotic disease, the reservior being pigs and
cattle,transmitted accidentally to human beings,by
the bite of infective,female,culex mosquito.
INTRODUCTION

Japanese Encephalitis is an Public health importance,
because of its epidemic potential, high case fatality
rate, permanent sequelae, no treatment and it is
preventable.
J.E. is primarily a disease of rural,semi urban, agricultural
areas where vector mosquitoes proliferate in close association
with pigs and other animal reservoirs.
Recent estimated 68,000 cases of JE occur globally each
year,with 20,400 deaths .

JE ENDEMIC AREAS IN INDIA
57
JE affected areas
• Andhra Pradesh
• Assam
• Bihar
• Haryana
• Kerala
• Karnataka
• Maharashtra
• Manipur
• Tamil Nadu
• Uttar Pradesh
• West Bengal
12 May 2018 Chengalpattu Medical College

AREA OF HIGH OCCURRENCE
The three southern states of Tamil Nadu (TN),
Andhra Pradesh, Karnataka were reporting
higher incidence.
JE is emerging as a public health problem in
Kerala
 In a few villages of Cuddalore district of Tamil
Nadu, a known JE-endemic area (Chidambaram,
Virudhachalam, Thittakudi)

TAMILNADU
In the early cases were reported from Tamilnadu in
the following revenue districts Tiruvannamalai,
Dharmapuri, Namakkal, Trichirapalli, Dindigul,
Theni, Madurai,Virdhunagar, Tirinelveli, and
Tuticorin.
However for the past 5 years sporadic cases are
reported from Villupuram, Cuddalore,and
Perambalur districts only.

60
Tamilnadu Japanese Encephalitis –Endemic Districts

Agent Factor
Agent :Arbo virus(JE virus) belong
to family Flavo-virus.
It is a ss RNA virus,positive
sense,non-segmented,envelped
virus.
It has three proteins
A) Envelope glycoprotein
B) Core protein and
C) Membrane lipid protein.
It is an an neurotropic virus.

Natural host and Reservior
 Chief reservior-Animals(pigs and cattle) and water birds.
 Pigs are called as ‘Amplifier host’ because infected pigs
do not manifest any symptoms but circulate the virus so
that mosquitoes get infected and can transmit the virus
to man.They help only in multiplication of virus.
 Cattle –neither suffer nor act as amplifier host.They are
only the next attractants.
 Horse-the only animal which develop manifestation of
encephalitis.
 Birds – ardeid birds,pond-herons and poultry ducks

Human Reservior
 They are the only active clinical cases and subclinical
cases.
 Even the cases do not act as source of infection because
of short period of viraemia and low level of circulating
viruses.
 For symptomatic JE case, there are likely to be about
300 – 1000 people infected with JE virus but without any
clinical manifestation.

Host Factor
Affects all age groups mostly children below 15
years.
Males are mostly affected than females.
Mostly affects the low socio – economic group
People live in close association with animals are
vulnerable.

Environmental Factor
 Atmospheric temperature of about 20 deg.C and relative
humidity 70 percent are favourable.
 Rice cultivation
 Pig rearing.
 Duck rearing.
 Availability of ponds and lakes.
 Movement of migratory birds.

 Seasonality of the disease: The Japanese encephalitis virus
is transmitted seasonally. In temperate regions, it is
transmitted during the summer and early fall, approximately
from May to September.
 In subtropical and tropical areas, seasonal patterns of viral
transmission are correlated with the abundance of vector
mosquitoes and of vertebrate-amplifying hosts. These, in
turn, fluctuate with rainfall, with the rainy season, and with
migratory patterns of avian-amplifying hosts.

Culex tritaeniorhynchus

Bionomics-Culex
 Breeds in water polluted with organic material (refuse,
excreta ) such as soak pits, septic tanks, pit latrines, shallow
ditches and clean water in irrigated rice fields
 Biting habit They are mainly zoophilic and not
anthrophilic (i.e.they feed mainly on blood of animals and
not human beings
 Bite through out the night
 Rest indoors in dark corners of rooms, shelters and hanging
clothes outdoors (exophilic) on vegetation, tree holes and
underneath culverts.

Culex
Extrinsic incubation period- 10 to 12 days.
Once mosquito become infective,it remain
infective throughout its life.
Average life span-20 days.
It can fly for 1 to 3 km.

Clinical features
Incubation period-5 to 15 days
 Prodromal Stage
 Acute encephalitic Stage and
 Late stage

Prodromal Stage : is characterised
by
 Sudden onset of Fever
 Rigors
 Headache
 Nausea and
 Vomiting
The duration of this stage usually
lasts for 1 to 3 days.

Acute Encephalitic Stage:
Begins by the third to fifth day.
The symptoms include:
 High grade fever(38-40.7 deg.C)
 Neck rigidity
 Convulsion
 Altered sensorium
 Disorientation
 Progressing in many cases to coma and
 death

Late stage and sequelae
More than 50 percent of them develop neurological and
psychological defecits
Characterized by:
 Amnesia
 Abnormal movements,ataxia
 Personality changes
 Emotional disability
 Paralysis
CFR varies between 20-40 per cent ,but it may reaches 80
per cent during an epidemic
The average period between onset of illness and death is
about 9 days

JE Case Classification
 Suspect: a case that is compatible with the clinical
description
 Probable: a suspect case with presumptive laboratory
results
 Confirmed: a suspected case that is laboratory confirmed

Differential Diagnosis
Meningitis
Febrile Convulsions
Rey’s Syndrome
Rabies
Toxic Encephalopathy

Control and preventive
measures

CONTROL AND PREVENTION
Vector control
-Eliminate mosquito breeding areas
-Adult and larval control
-Personal protective measures
Vaccination
-Equine and swine
-Humans
Control of Amplifying host

Vector Control
Adults Larvae
Indoor
Residual
Spray
Thermal
Fogging
Operation
• Certain improvised
Agricultural practice
• Using Neem coated
urea.

Larval control measures
 Physical method- improvement of sanitation(source
reduction) by means of deweeding of ponds,removal of
submerged grasses and using herbicides(shell weed
killer-D)
 Chemical method-spraying larvicides such as abate in
concentration of 1 ppm in the breeding places
 Biological method-using larvivorous fish such as
gambusia fish
 Biocide method-using bacilus sphaericus which infect
larvae and kill them

Reduction of Breeding Source for
Larvae
 They are water management system with intermittent
irrigation system.Its a strategy of alternate drying and
wetting water management system in the rice fields.
 Incorporation of neem products in rice fields

Adult control measures
Consist of indoor and outdoor spraying with
insecicides such as 5% malathion or
fenitrothion.
All the infected villages and uninfected villages
within the radius of 3 km are covered
Indoor spray: Malathion is sprayed in the
pigsites,catlle-shed and inside the houses,once
in a fortnight for three fortnights

Adult control measures
 Outdoor spray: This consist of a technique called ULV-
fogging,wherein the insecticide malathion is heated to
vapour at high temperature in a special machine
 The vapour after coming out,comes in contact with the
moisture of cooler air and forms a fine fog,which when
comes in contact with the mosquitoes,destroy them.It is
called ‘Dry fogging’.
 Methods : 1.Ground level application technique
2.Aerial application technique

Ground level application technique:
 The special machine is employed called TIFA machine.It
is fitted to the open jeep vehicle.
 When malathion is heated and vapours start coming
out,
 the vehicle carrying the machine is driven slowly at a
speed of 5 to 6 km per hour on the roads of the villages.
 The favorable time for fogging is early morning or late
evening,because the air is cool and form fine fog.
 The ideal atmospherc temperature is about 20 deg.C
 The output of the vehicle is about 130 litres of
malathion per hour

TIFA(TODD Insecticide Fog Applicator)

Aerial application technique
This is done by using a special single
engine,single seated monoplane air craft called
‘Basant Agriculture Air Craft’,which is used for
ULV-fogging over the paddy fields
It flies about 40 meters above the ground
level,at a stretch of about one and half hours
Three such applications,on 1,3 and 12 day
respectively,are necessary for satisfactory
control of mosquitoes

Prevention of Mosquito Bites
87
Avoid going to rural area during dusk and
dawn when the mosquitoes are most active
Wear light-coloured, long-sleeved clothing
and trousers
Apply DEET-containing mosquito-repellents
over exposed parts of the body and clothes
every 4 to 6 hours
For DEET products used by children, its
concentration should be less than 10%

Prevention of Mosquito Bites
88
 mosquito nets
 hang mosquito screens around
your bed, use insecticides or coils
to repel mosquitoes
Install mosquito nets to doors
and windows so that mosquitoes
can’t get in

Control of amplifying host
 Pig control has been attempted in 3ways: segregation,
slaughtering or vaccination.
 Segregation is not practical in many settings.
 Slaughtering has a high economic impact and affects
the livelihood of many families.
 Vaccination of pigs is costly, difficult and very time
consuming.

Vaccine availability
Currently, there are three types of JE vaccines in
large-scale use:
 Mouse brain-derived, purified and inactivated vaccine
 Cell culture-derived, inactivated JE vaccine based on
the Beijing P-3 strain (only available in China and
being replaced by live attenuated vaccine).
 Cell culture-derived, live attenuated vaccine based on
the SA 14-14-2 strain of the JE virus.

Vaccine
Live attenuated SA-14-14-2 JE vaccine, Freeze dried and to
be mixed with diluents supplied with the vaccine. Changes
to transparent pink/orange after dilution.
Manufacturer Chengdu Institute of Biological Products (CDIBP), China
Storage +2 to +8º C
Dose Single dose (0.5ml) with AD syringe for every child.
Route Injection - Subcutaneous
Site Upper arm
Target
1 – 15 years age group
(i.e. more than 12 months till 15 years)
SA-14-14-2 JE vaccine:

JE Vaccination
Target beneficiaries : 1-15 year age group in
identified districts following prioritization
Routine immunization to target children

KYASANUR FOREST DISEASE

History
 KFD was first recognized in 1957 in Shimoga district of
Karnataka State in South India.
 Local inhabitants called the disease "monkey disease"
because of its association with dead monkeys.
 The disease was later named after the locality-
Kyasanur Forest - from where the virus was first
isolated.
 Restricted to four districts (Shimoga, North Kannada,
South Kannada and Chikamagaloor) in Karnataka

Agent
 Member of group B togaviruses (flaviviruses)- tick borne
virus
 Antigenically related to other tick-borne flaviviruses.
particularly the Eastern tick-borne encephalitis and
Ormsk haemorrhagic fever.
 Unlike in many other arbovirus infections. KFD has a
prolonged viremia:10 days or more.

Natural hosts & reservoirs
 Small mammals particularly rats and squirrels -main
reservoirs of the virus .
 Birds and bats are less important
 Amplifying hosts: monkeys
– Not effective maintenance hosts because most of
them die from KFD infection.
 Cattle:
– Provide Haemaphysalis ticks with a plentiful source
of blood
– Thus cattle are very important in maintaining tick
population but play no part in virus maintenance .
 Humans: incidental or dead-end host,

Vector
 The virus has a complex life cycle involving a wide
variety of tick species
 At least 15 species of hard ticks of species
Haemaphysalis, particularly H. spinigera and H. turtura
 Also isolated from soft ticks (not in India)
 Monkey infections occur during drier months, from
January to June.
-This period coincides with the peak nymphal activity
of ticks.

Host factors
 Age:
-Majority of cases affected were between 20 & 40 years
 Sex : Attack rate was greater in males
 Occupation :
-Cultivators who visit forests accompanying cattle
-Wood cutters
 Human activity :
-The epidemic correlates well with the period of greatest
human activity in the forest, i.e., from January until
the onset of rains, in June

Transmission
The transmission cycle involves mainly monkeys
The disease is transmitted by the bite of
infective ticks especially nymphal stages.
There is no evidence of human to human
transmission.

Clinical features
 Incubation period: 3 to 8 days
 Sudden onset of fever, headache and severe myalgia, with
prostration
 Acute phase: lasts for about 2 weeks
 Severe cases:
-Gastrointestinal disturbances
-Hemorrhages from gums, stomach and intestine ,
 Second phase:
-Mild meningoencephalitis after an afebrile period of 7 to 21 days
-Return of fever, severe head ache, followed by neck stiffness,
coarse tremors, abnormal reflexes and mental disturbances.
 Case fatality rate: 5 to 10 per cent
 Diagnosis :Isolation of the virus in the blood and/or
serological evidence.

Control
Control of ticks:
 For control of ticks in forests,
-application can be made by power equipment or by
aircraft-mounted equipment to dispense carbaryl,
fenthion, naled or propoxur at2.24 kg of active
ingredient per hectare
-The spraying must be carried out in "hot spots i.e.,
in areas where monkey deaths have been
reported.
-50 metres around the spot of the monkey deaths,
besides : endemic foci.
Restriction of roaming cattle in forests
 Vaccination: Killed KFD vaccine
 Personal protection: repellents like dimethyl phthalate,
DEET; adequate clothing; examine the body for tick and
remove them;habit of sitting or lying down on the ground
shoud be discouraged12 May 2018 102Chengalpattu Medical College

Zika Virus
An arthropod-borne virus (arbovirus).
A member of the Flavivirus genus in the
family Flaviviridae.
It is related to other pathogenic vector borne
flaviviruses including
Dengue,
Yellow fever
West Nile
Japanese encephalitis viruses.

Name origin
 It owes its name from Zika Forest of
Uganda, where it was first isolated in
1947.
 The infection, known as Zika Fever.
 In humans it was first identified in
1952 in Uganda and United Republic of
Tanzania and the virus was first
isolated in Nigeria in 1968.
 The sporadic cases of infection were
reported in Southeast Asia and Sub-
Saharan Africa.

Systematic Classification of Zika
Virus
Group IV ((+)ssRNA)Group
FlaviviridaeFamily
FlavivirusGenus
Zika virusSpecies

Zika virus
 Zika virus was first isolated in 1947 from the blood of a
Rhesus monkey in Zika forest, in Uganda
 Subsequently, the virus was recovered from humans and
mosquitoes in Uganda, Senegal, Nigeria, Ivory Coast, the
Central African Republic and Malaysia.
 An outbreak of Zika virus was reported in 2007 on Yap
Island of Micronesia
 Another outbreak in the Pacific was reported in French
Polynesia in 2013 and later spread to New Caledonia
 In 2015, Zika virus emerged in South America with further
spread across the Americas.

Recent outbreak
 ZIKA virus moved out of Asia and Africa and caused
an epidemic in YAP islands of Micronesia (2007) and
French Polynesia, New Caledonia, The Cook Islands
and in Easter Islands in 2013 and 2014.
 In 2015 there has been an upsurge in ZIKA infection
dramatically in America with Brazil being most
affected; 444,000 to 1.3 million cases reported
through December 2015.
 It has been reported that ZIKA infection has spread to
23 countries across America.

ZIKA
Aedes albopictus was identified as the
primary vector for ZIKA transmission during
2007 Gabon outbreak
Sexually transmitted

Pathogenesis
Mosquito-borne flaviviruses are thought to
replicate initially in dendritic cells near the site of
inoculation.
Then spread to lymph nodes and the
bloodstream.
Although flaviviral replication is thought to occur
in cellular cytoplasm, one study suggested that
Zika Virus antigens could be found in infected cell
nuclei.

Alerts are being issued warning of the Aedes aegypti
mosquito, carrier of the Zika virus which might cause
microcephaly and Guillain-Barré syndrome, a condition
that causes the immune system to attack one’s own
nerves.

Diagnosis of zika virus
Polymersase Chain Reaction :Nucleic acid detection by
reverse transcriptase-polymerase chain reaction (RT-PCR).
Nucleic Acid Amplification Test :Nucleic acid amplification
test (NAT) for detection of viral RNA can also be
performed.
Plaque Reduction Neutralization Assay The Plaque
reduction neutralization assay generally has improved
specificity over immunoassays, but may still yield cross-
reactive results in secondary flavivirus infections.

Diagnosis of zika virus (cont.,)
• Serological Tests :
• An ELISA has been developed to detect IgM
to ZIKV only after five days.
• NS1 antigen can be detected by ELISA in
acute phase specimens
Important Note !!!!!!
• IgM antibodies against Zika virus, dengue
viruses, and other flaviviruses have strong
cross-reactivity which may generate false
positive results in serological tests.

Prevention and control of zika virus
 Avoid travel to areas with an active
infestation.
 Reducing mosquito populations through
source reduction (removal and modification
of breeding sites)
 Reducing contact between mosquitoes and
people through:
• wearing clothes (preferably light-coloured)
that cover as much of the body as possible
• using physical barriers such as window
screens
• closed doors and windows
• sleeping under mosquito nets
• Using repellents
 Safer sexual practices

World Health
Organization has
declared the Zika
outbreak a global
health emergency

Disease Background
 First account of
sickness diagnosed as
YF occurred in 1648.
 Causative agent: genus
Flavivirus.
 Vector: Aedes aegypti
(mosquito).
 Nonhuman primates
maintain disease.

Global Distribution
In 45 countries of Africa
& Latin America.
More than 900 million
people are at risk.
200,000 cases & 30,000
deaths worldwide each
year.

EPIDEMIOLOGY
Flavivirus Fibricus
Man (>240 C and
>60% Humidity)
YELLOWFEVER

Agent
 Flavivirus Fibricus
 Group B Arbovirus

Reservoir & Vector
• Monkey
• Aedes Mosquito

Host Factor
All ages & both sexes
Persons in contact with
forests.
Wood cutters, Hunters.
Immunity- One attack of
yellow fever gives
lifelong immunity.

Environmental Factor
Climate
Tropical with a relative
humidity.
Endemic presence of disease
in the jungle.
Social Factors
Urbanization,
More Populated,
Forest.

INCUBATION PERIOD – 3-6 days
PERIOD OF COMMUNICABILITY - Blood of patients is
infective during the first 3-4days of illness

Cycles of YF Transmission
MOSQUITO
MONKEY
HUMAN,
MONKEY
MOSQUITO
HUMAN HUMAN
MOSQUITO MOSQUITO
MOSQUITO MOSQUITO
Jungle Village Urban
www.who.int12 May 2018 129Chengalpattu Medical College

Clinical features
Similar to viral haemorrhagic fevers
More severe hepatic and renal
Involvement
Jaundice, haemorrhagic manifestations
(black vomit, epistaxis, melena)
Albuminuria or anuria
Shock , stupor, coma
CFR : 80% in severe cases
Survivors exhibit : life long Immunity

Diagnosis & Management
Serological Tests
Supportive Treatment
IV Fluids
Antipyretics
Vector control measures
Use of Mosquito-net or
mosquito repellents.

Prevention & Control
 17D Vaccine , live attenuated vaccine.
 Subcutaneously 0.5ml,
 Immunity begins to appear on the7th day & lasts for
more than 35 years.
 Surveillance : Aedes aegypti index <1 (house
index)
 International Certificates- validity begins 10 days
after vaccination and extends up to 10 years

West Nile Fever
 Acute febrile illness – group B arbovirus.
 Endemic in India , middle east and south west asia ,
africa .
 Culex mosquitoes
 IP :2-14 days
 Sudden onset of fever, severe headache and malaise
for several days.
 In children , maculopapular rash appears .
 Less than one percent cause neuro invasive disease.
 Fatal meningoencephalitis is more common in older
people.

Pathogenic Pathway
West Nile Virus
Mosquito bite  virus injected into blood
 Virus replicates in lymphocytes
 Fever, myalgia
 Virus spreads to the brain (neurons):
encephalitis, headache, confusion
 Slow recovery
 Immunity to the virus (One Serotype)

Diagnosis and Management
Diagnosis :
• Real time PCR
• IgM and IgG ELISA
• Complement fixation tests
Treatment:
Supportive Therapy

SAND FLY FEVER

SANDFLY FEVER
Also known as Phlebotomus fever
Insect borne disease caused by bunyavirus of
Phlebovirus genus
Transmitted by female sandfly – Phlebotomus
papatsii
Transovarian transmission occurs
Infection is common among children in endemic
areas.

SANDFLY FEVER
 Pathogenesis: bite itchy papules viremia
 CF: headache, malaise, nausea, fever,
photophobia, stiffness of neck and back,
abdominal pain
 All patients recover.
 No specific treatment
 Prevention: using insect repellent at night and
residual insecticides.

THANK YOU

Arbo viral diseases

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Arbo viral diseases

Similar to Arbo viral diseases (20)

More from sujatha sathananthan

More from sujatha sathananthan (13)

Recently uploaded

Recently uploaded (20)

Arbo viral diseases