57 ARBOVIRUSES new fr allied.health science ppt

PrabhuPrabhu89 95 views 73 slides Jun 29, 2024
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About This Presentation

ARBOVIRUSES new fr allied.health science ppt


Slide Content

Arboviruses

Introduction
•Arthopod–borne viruses
•A group of RNA viruses that are transmitted by blood
sucking arthropods (insect vectors) from one vertebrate
host to another.
•The viruses must multiply inside the insects and should
establish a lifelong harm less infection to them.

•The viruses produce viremia in the
vertebrate host.
•Multiply in the tissues of arthropod host.
•Passed on to the new vertebrate host by the
bite of arthropod.
(after a period of extrinsic incubation).

•1.Togaviridae.
•2.Flaviviridae
•3.Bunyaviridae
•4.Reoviridae.
•5.Rhabdoviridae.
Classification

1. Chikungunya
2. O’nyong-nyong
3. Semliki forest
4. Sindbis
5. Ross river
6. Eastern equine encephalitis
7. Western equine Encephalitis
8. Venezuelan equine Encephlalitis.
Family –Togaviridae
Genus -Alphaviruses

1. Japanese encephalitis.
2. West nile encephalitis
3. Yellow fever
4. Dengue fever
5. Kyasanur forest disease
6. RussianSpringSummerEncephalitis
7. Omsk haemorrhagic fever.
8. Murray valley encephalitis
Family -Flaviviridae
Genus -Flaviviruses

•California encephalitis.
•Oropouche
•Turlock
Genus -2.Phlebovirus
•Sand fly fever
•Rift valley fever
Family -Bunyaviridae.
Genus-1.Bunyavirus

•Genus -3.Nairo virus
•Crimean Congo haemorrhagic fever
•Nairobi sheep disease
•Ganjam virus.
•Genus -4.Hanta virus
•Hantan,
•Seoul,Puumala
•Prospect hill
•Sin nombre virus.

•African horse sickness
•Colorado tick fever
•Blue tongue viruses.
•Vesicular stomatitis virus.
•Chandipura virus.
Family -Reoviridae
Genus -Orbiviruses
Family –Rhabdoviridae
Genus -vesiculo virus

General introduction/properties
1.Arboviruses belong to various taxonomical
familiesToga, Bunya, Reo,
Rhabdoviridae
2.They have wide host range many
animals and birds.
3.Important vectors are mosquitoes,
Phlebotomous(sand fly ),Ticks.

4. Cubical,helical or bullet shaped viruses.
5. Size–40-170 nm , enveloped, single stranded
RNA genome.
6. Inactivated by ether, bile salt or other lipid
solvents
7. Mice are commonly used laboratory
animals.
Intra cerebral inoculation into suckling
mice.

Key features: Epidemiology
•Zoonotic: Many are Endemic in animals, few are
human pathogens (100)
•Transmission cycle: maintained in nature between
animals and insect vectors.
•Humans are accidental hosts.
•Arthropod vectors: Mosquitoes (Aedes, Culex,).
Ticks, and rarely sand fly.
•Climatic variation: More prevalent in tropics than
temperate climate.
•Geographical distribution: Depends on climatic
conditions presence of vector.

•The virus enters the body through bite of
infected insect vector
•multiplies in the RE system
•Viremia transported to target organs
CNS -Encephalitis.
Liver -in YF
Capillary endothelium –
haemorrhagicfevers.
Common Pathogenesis

Arboviruses found in INDIA
•Common: Dengue, Chikungunya, Japanese B
Encephalitis.
•Rare: Kyasanurforest disease, West Nile,
Crimean Congo hemorrhagic fever, Ganjam,
Chandipura, and sandflyfevers are rare.

1.Fever with or without rash , arthralgia
group.
2.Encephalitis group.
3.Hemorrhagic fever group.
Clinical syndrome : Classification

•Virus identification from
•Insect vector
•Reservoir animal
•Avian species also helps in the diagnosis.

Alpha virus: Fever-Arthritis group
•Chinkungunya virus
•Onyong-nyongvirus (ONN)
•Mayarovirus
•Ross River Virus
•SindbisVirus
•All causes Chinkungunya like illness
characterized by arthralgia and rash.

Alpha virus –Encephalitis group
•Eastern-EEE, Western -WEE, and Venezuelan
Equine EncepahlitisViruses -VEE.
•EEE and WEE confined to North America.
•VEE –Confined to South and Central America.
•Causes Encephalitis in horses and Humans.
•Vaccine are available for all.

Flaviviriade
Mosquito transmitted Flaviviruses
•Encephalitis group :-
•JapanesB EncepahlitisVirus :
•West Nile Virus:
•Murray Valley Encephalitis Viruses.
•St.LouisEncepahlitisViruses.
•RacioEncepahlitisViruses.

FlaviVirus : Hemorrhagic fever Group
•Dengue Viruses.
•Yellow fever Viruses.

Tick transmitted Faviviruses:
-Encephalitis group:
Tick Borne Encephalitis viruses –TBE
Central European encephalitis virus
Western Siberian encephalitis virus
Russian spring summer encephalitis virus.
Powassanencephalitis virus.
Louping-ill Virus

Tick transmitted Faviviruses:
Hemorrhagic fever group
•KyasanurForest Disease Virus –KFD.
•Omsk Hemorrhagic fever Virus

ARBOVIRUSES IN INDIA
•Chikungunyavirus
•Japanese B encephalitis
•Dengue fever
•Kyasanurforest disease

•Virus isolation
•Serology.
•Virus isolation
In the acute phase of the disease
•Specimen
a) blood b) CSF c) brain tissue
•Inoculated intra cerebrally into
suckling mice, chick embryo , tissue
culture.
Laboratory diagnosis

8. Culture –
Egg -Yolk sac, CAM of chick embryo.
Tissue culture
-vero cell lines, He La ,
-chick embryo fibroblast cell lines.
9. Haemagglutination -
-can agglutinate RBC of goose
& one day old chick cells.
-No elution.

•Haemagglutination
•Compliment Fixation test.
•Gel precipitation
•Immunofluorescence
•Immunochromatography
•Neutralization
•ELISA
•Rise in specific antibody titer.
Isolates are identified by
Serology

•First isolated from Tanzania -1952 .
•Chikungunya meaning doubled up/ due to
severe joint pains .
•1963 –outbreaks at irregular intervals along the
east coast of India and Maharashtra till 1973., since
then the virus has been quiescent.
Chikungunya virus:

CHIKUNGUNYA VIRUS
•Family Togaviridae
•Genua Alpha viruses
•First appeared in India in 1963 --extensive
epidemics in Kolkata, Chennai and along East
coast of India. In Maharastra prevailed till 1973,
thereafter quiescent

1. Sudden onset of fever, biphasic type.
2. Joint pains.
3. Lymphadenopathy.
4. Conjunctivitis
5. Maculopapular rash , rarely haemorrhages.
6. No animal reservoir
7. Vector -Aedes aegypti.
8. No vaccine is available at present.

O’ nyong–nyongvirus:
•Isolated from Uganda 1942.
•Aedesmosquitoes are vectors.
Sindbisvirus:
•Isolated from Egypt 1952.
•Subsequently recovered from other parts of the
world
•Africa ,India, Philippines and Australia.
•Febrile illness transmitted by culexmosquitoes.

•Flavus= Yellow / Latin word.
•a.Mosquito borne,
•b. Tick borne.
Flaviviruses

Mosquitoborngroup Encephalitis viruses
•1.St Louis encephalitis virus:
North and central America.
Culex tarsalis is the vector.
•2.Ilheus-
South and Central America.
•3.West Nile virus:
Uganda, 1937.
Reported from India
Reservoir hosts wild birds.
Vector -culex.
Febrile illness ,encephalitis
reported from Rajasthan Karnataka.

•4. Murray valley encephalitis virus:
Australia -1951.
New Guinea.
Wild birds –reservoir.
Culexmosquito –vector.
•5. Japanese encephalitis:
Culex–vector.
Herons -wild birds & pigs are reservoir hosts.

•6. Yellow fever :
Mainly reported from
Africa ,Cuba &Panama
Aedesaegyptiis the vector for human cycle.
Forest or sylvaticcycle
Forest mosquitoes Haemogogusspecies are
vectors for wild monkeys .
•7.Dengue fever:
Break bone fever .
Reported from Tropics , sub tropics , S E Asia ,
Thailand , Hawaii , New Guinea Philippines & India.

•1. Encephalitis. RSSE.
•2.Haemorrhagic fever .
•A) Kyasanur forest disease: KFD.
Haemophysalis ticks are vectors, forest birds, small
mammals are reservoir hosts , monkeys are amplifier
hosts.
•B) Omsk haemorrhagic fever:
USSR, Rumania.
Dermocentor ticks are vectors.
Tick borne group :

•Phlebotomus fever or sand fly fever .
Reported from North west India.
Self limited non fatal fever.
Phlebotomus papatasi is the vector.
•Rift valley fever :
•Kenya, Africa.
Bunyaviruses

•Nairo viruses :
1.Nairobi sheep disease virus.
2. Crimean congo haemorrhagic fever.
Africa ,Central America, Congo –Zaire.
Hyalomma ticks are vectors.
Cattle ,sheep, goats and other domestic animals.
3.Ganjam virus :
Isolated from ticks in India., Orissa state.
closely related to Nairobi sheep disease virus,
Isolated from sheep &goats.

•Genus -Hanta virus:
Haemorrhagic fever with renal syndrome .
Epidemic or endemic nephrosonephritis 
mild epidemic nephritis or severe epidemic
haemorrhagic fever.
Reported from Korea, Scandinavia , Russia &
China.
1. Hanta virus-severe HFRS -Fareast.
2.Seol virus-mild disease.
3.Pumala virus-nephropathia epidemica –
North &Eastern Europe.
4.Prospect hill virus–USA ,Voles .no human
illness.

1.Natural pathogens of rodents.
2.Field mice -Apodemusagrarius.
3.Rats -Rattusrattus.
4.Viremia in rats, virus is shed in feces, saliva .
5.Transmission from rodent to rodent.,
6.Rodent to human .
7.Aerosols inhalation of virus contained in dried
excreta Mites can transmit the infection.
8.Laboratory diagnosis: Demonstration of IgM antibody
by ELISA.
9.Haemagglutinatingantibodies in paired serum
samples.

•Hanta virus pulmonary syndrome:
•South west USA 1993.
•Fever ,malaise ,myalgia, GIT symptoms.3-4 days.
•Pulmonary edema ,tachypnea, tachycardia,
hypotension, hypoxia & death, in severe cases.

•Sin Nombre virus : newly identified virus.
•Associated with Deer mouse and other rodents.
•No arthropod has been linked with transmission of
virus.
•Infection occurs inhalation of virus aerosols
dried rodent feces.

•Reo viridae :
•Genus -Orbivirus
•Double stranded RNA genome.
•Colorado tick fever :
•Western USA -mild fever without rash,
–tick acts as the vector and reservoir.
•Natural infection in rodents.

•African horse sickness virus:
•Culicoidesvector. extensive disease in
horses and mules in India.
•Palyam,Kasba& Vellore viruses belong
to Orbivirus group, isolated from
mosquitoes in India.
•Rhabdoviridae:
•Chandipuravirus : vesiculovirus group.
isolated in1967 from blood of a patient .
•Virus is isolated from Sand fly & Aedes.

•Ungrouped arbo viruses:
•Wanowri virusHyalommaticks are vectors.
•Isolated from India, Srilanka., from the brain of a
girl died after 2 days fever.
•Bhanja virus: Haemophysalis ticks from goats in
Ganjam district, Orissa state.
•West Africa ,S. E .Europe, Yugoslavia.

Japanese encephalitis
•Recognized in Japan since 1871.
•Isolated in 1935 epidemic.
•Epidemics show seasonal incidence summer-
autumn in temperate regions. Not evident in
tropical countries.
•The virus is isolated from Korea, Japan, India,
Malaysiaalong the orient.
•Culex tritianorhynchus is the mosquito vector.

Clinical disease
•Abrupt onset of fever-continuous
•high fever, head ache, vomiting .
•After 1-6 days signs of encephalitis, nuchal
rigidity, convulsions, altered sensorium&
coma.
•Neutrophilleukocytosis+ in peripheral
blood.
•Slightly raised protein, sugar in CSF.
•Mortality rate is high in epidemics up to 50 %
convalescence takes many weeks. Residual
damage is seen.

•1000 asymptomatic cases occur for every one
clinical case .In 1955 JE occurred in India .Isolated
from mosquitoes of culexvishnuicomplex –Tamil
nadu. ,A.P.
•1973-West Bengal.
•1976-Many parts of India, Assam ,U.P., Goa,
Karnataka, T.N. & Pondicherry.

•Natural cycle:
•Herons-reservoir hosts.
•Pigs-Amplifier hosts
•Human infection is a tangential dead end.
•Bird to bird transmission +
•Ducks, pigeons, sparrows are involved.
•Cattle ,buffaloes, pigs –vertebrate hosts.
•Culex tritianorhynchus has a predilection for
cattle and bites them in preference to human
or pigs.
•High cattle pig ratio in India has been
suggested as a factor limiting human
infection.

Vaccines
•1.Formalin inactivated mouse brain vaccine
using Nakayama strain.
•Two doses at 2 wks interval , booster 6-12
months later.
•2.Live attenuated vaccine-developed in
China. J. E. strain SA14-14-2.
•Vaccine is produced in primary baby hamster
kidney cells, passed through weanling mice.
•Administered in 2 doses, one year apart.
•Very effective in preventing the clinical
disease.

•Vaccination for pigs has been proposed , not
practicable.
•During epidemics slaughter of pigs as a
containment measure.

Dengue fever/break bone fever
•Distributed through out tropics and sub
tropics .
•Caused by Dengue virus.
•Clinical manifestations similar to
Chikungunya, O’ nyong -nyong .
•4types
•Dengue 1 Hawaii -1944.
•Dengue 2 New Guinea1944.
•Dengue 3-4 Philippines 1956.
•Aedes aegypti is the vector mosquito.

•I.P. is 2-8 days.
•Fever, head ache, retro bulbar pain ,
pain in the back and limbs.
•Fever –sudden onset, biphasic or saddle back
lasts for 5-7 days.
•Severe forms –
•haemorrhagic manifestations,
•shock syndrome.
•Common in previously healthy children in indigenous
population of endemic areas.

Dengue fever
•Affects older children and adults
•Benign with biphasic fever (saddle back),
headache, bone and muscle pains
•Incubation period is 5-8 days
•Maculopapularrash after 2-3 days
•Fever till 10 days
•Recovery is complete

•4 serotypes: 1, 2, 3 & 4 are presen
•Transmitted by insect vector Aedes aegyptii
•Though antigenically related with Yellow fever no
cross immunity
•2 types of clinical presentations
-Dengue fever
-Dengue haemorrhagic fever & Dengue shock
syndrome

•Hypersensitivity response to sequential
dengue virus infection in persons already
sensitized by prior exposure to other
serotypes of the virus.
•Haemorrhagic Dengue is rare in India .
•No vertebrate host other than human
beings.
•No vaccine.
•All types of dengue virus are present in
India .

Dengue haemorrhagic fever
•Affects 5-10 yr age group
•Initial symptoms are present with serious hemorrhage and
shock due to hyper Immune reaction by multiple virus
serotypes in those who are infected in the past (virus-
antibody complex)
•Mortality is 5-10%
•Deaths due to DHF and DSS

•Circulating Ig M antibody estimation by
Capture ELISAwith in 2-5 days of the onset of
illness ,persists for 1-3 months
•Rapid diagnosis –strip Immuno chromatographic
test Ig M.
•Alive attenuated vaccine under field trials in
Thailand .
•Protective against all 4 types of the virus.

•Virus isolation is difficult
•Serology is useful by demonstration of specific IgM
antibodies in serum by ELISA early in disease i.e. 2-5
days and persists for 1-3 months
•Immunochromatographicstrip test for IgM is a rapid
method for diagnosis
•Prophylaxis is by mosquito extermination measures
•No effective vaccine is available but a live attenuated
vaccine of all 4 serotypes is under trial

Tick borne encephalitis
•Russian spring summer encephalitis: (RSSE )
In Scotland –Louping illPrimarily in sheep with leaping
gait.
human cases are reported –mild aseptic meningitis.
Seen in Central Europe and Russia -
Biphasic meningo encephalitis .
Serious form , high rate of case fatality permanent
paralytic sequelae in survivors.

•Transmitted by the bite of Ixodid ticks.
•Transovarial transmission is seen in ticks .
•They serve as vectors and also as reservoir
hosts.
•Wild rodents other migrating birds act as
reservoir hosts.
•Biphasic meningo encephalitis transmitted by
drinking milk of infected goats is also
reported.
•Formalin inactivated RSSE vaccine is useful.

Tick borne haemorrhagic fever
•Kyasanur forest disease: KFD.
•Haemorrhagic fever in Kyasanur forest in Shimoga
district of Karnataka.
•Sudden onset of fever, head ache, conjunctivitis ,
myalgia, severe prostration.
•Haemorrhages into skin, mucosa and viscera.

•Haemophysalis spinigera is the vector tick,
monkey is the amplifier host ,forest birds small
rodents are reservoir hosts.
•Trans ovarialtransmission + in ticks.
•Killed KFD vaccine under field trial.
•Antigenically related to RSSE complex.

Yellow fever
•The disease is a native of Africa, transported
to Europe and America.
•Aedesaegyptiis the vector mosquito
Extrinsic incubation period is 12 days.
•Clinical features :
•I.P. 3-6 days. Fever, chills, head ache,
nausea ,vomiting, high temperature,
•Lowered pulse rate, jaundice, albuminuria,
•haemorhagicmanifestations
•hepatic & renal failure.

•Histology of liver cloudy and fatty degeneration
necrosis, necrosed cells coalase and hyalinised
leading to the formation of eosinophilic masses
known as cuncilman bodies.
•Acidophilic intranuclear inclusion bodies Torres
bodies + in infected liver cells in early stages.

•Urban cycle :
•Human –natural reservoir and definitive host.
•Aedes aegypti is the vector.
•Sylvatic or forest cycle :
•Wild monkey forest mosquito Aedes
africanus, Haemogogus spegazini Human
cases occur when trespass into forest or monkeys
raid over villages near forest.

•Vaccines -French neurotropicvaccine -
Dakar vaccine, produced from infected
mouse brain, administered by scarification.
High risk of producing encephalitis in
children, not used now.
•Safe, effective 17 D vaccine:
•Passing Asibistrainserially in mouse embryo
whole chick embryo tissue and then chick
embryo tissue from which CN tissue has
been removed.

•17 D vaccine is thermo labile.
•Given as subcutaneous injection.
•Vaccination is mandatory for travel to and from
endemic areas, valid for 10 years, beginning 10
days after vaccination.
•In India manufactured at Central Research
Institute, Kasauli.

•Yellow fever does not exist in India.
•India offers a receptive area with large
population of aedesaegypti, non immune
humans,
•Viral interference:
•stray virus inoculated may have been kept
out due to the prevalence of Dengue virus in
the Aedesaegyptimosquitoes.
•Another reason In Africa Yellow fever was
mainly in the west ,in India aedeswere
along the east coast. So, even stray virus by
sea may not have found suitable vector.

KYASANUR FOREST DISEASE
•First occurred a epizootic haemorrhagic disease in 1957
in Kyasanur forest of Karnataka among monkeys, and
as severe prostrating illness among some villagers there
•In National Institute of Virology, Pune, from the cases
and dead monkeys the virus is isolated and named as
KFD virus
•This virus is antigenically related to RSSE virus

•Birds, small mammals & ticks are reservoir hosts
•Transmission is transovarially by tick-bite
(Haemophysalis spinegera)
•As monkeys die with disease, they are amplifier hosts
rather than reservoirs
•Incubation period is 3-7 days
•Sudden fever with headache, vomiting, conjunctivitis,
myalgia and severe prostration leading to massive
haemorrage in GIT, chest and epistaxis in some
•Mortality rate is 5%

•For many years since 1957 it is confined to areas in &
around Sagar, Sorab and Shikarpur taluks of Shimoga
district of Karnataka
•1972-1975 in North Karnataka, a few more foci in
adjacent areas occured
•In 1982 in South Karnataka, an epizootic and epidemic
occurred in Belthangadi taluk
•In October 1982 an outbreak known as ‘monkey fever’
led to deaths of monkeys on a large scale
•In December 1982, first human case was reported, in
next 5 months 1142 human cases with 104 deaths was
reported, subsided in June due to monsoon, reappeared
in December due to ecological imbalance created by
felliing of the forest which activated the silent enzootic

•Prophylaxis is by
Control of ticks
Vaccination by killed KFD vaccine
Personal protection by
protective clothing
insect repellents