Arboviruses - 2013 (FN) [Compatibility Mode].pdf
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Transcript of Arboviruses - 2013 (FN) [Compatibility Mode].pdf
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Arbo viruses
Dr Faseeha NoordeenDepartment of Microbiology
University of Peradeniya
May 2013
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Modes of transmission and the pathogenesis of
ARBO viral infections / diseases in humans
Clinical features of ARBO viral infections / diseases
Principles of diagnosis, management and prevention
ARBO viral infections / diseases
Learning outcomes
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Introduction
Transmission:
Haematogenous arthropods andmammalian hosts
Viraemic mammals Arthropods
Mammals
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Important arboviral infections in SL Japanese encephalitis (JE)
Dengue fever (DF)
Dengue haemorrhagic fever (DHF) Chikungunya fever (CHIK fever)
Other arboviral infections of global importance California encephalitis, Sand fly fever, yellow
fever, Colorado tick fever, Carimean-Congo
haemorrhaigic fever
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Japanese encephalitis (JE) Aetiology: JE virus
Flaviviridae,
Mosquito borne RNA virus
Transmission: MosquitoesCulex tritaeniorhynchus
Culex gelidus
Distribution: South and Southeast Asia
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Epidemiology of JE
Migrant birds & pigs are infected with virus
Infection seen in pigs 2-3 weeks prior to
human infection Changing patterns of JE with climatic
conditions
Epidemics mosquito density is high
JEV replicates in salivary gland of
mosquitoes
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Epidemiology of JE
Humans
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Pathogenesis of JE in humans
Inoculation of virus through mosquito bite
Viraemia Early non-specific symptoms
Blood
Brain
Neurological symptoms
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Clinical manifestations JE in humans
1 in 50-1000 results in typical encephalitis
IP is 6-16 days
Disease begins with a non-specificprodrome, abrupt onset of high feverchills, severe headache, nausea, vomiting,abdominal pain, dizziness and
Progress to neurological signs hyperexcitability, stupor, disorientation, coma,tremors, paralysis (generalised) and lossof co-ordination
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Children with JE
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Epidemiology of JE in Sri Lanka
Endemic: North central & western provinces
Pig farming is popular in these areas
Pigs act as the amplifier host
Migrant birds are infected with the virus
Large areas of wetland habitats mosquitoes
Epidemics: Vector density is high
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Diagnosis1. History + clinical symptoms
2. Epidemiological data
3. Laboratory:
a. JEV antigen or RNA detection in CSF
b. Antibody detection in serum (IgM)
c. Detection of 4-fold rise in antibody titre in acute:
convalescent sera
d. CSF picture for viral infection (lymphocytosis)
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Treatment No specific treatment
Supportive therapy until recovery
Outcome
Case fatality is 20 - 50%
70 % survivors - mental retardation,
psychiatric complains + paralysis
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Prevention
1. Vaccination in humans killed and live
attenuated JE vaccines
2. Vaccination in pigs
3. Vector management - intermittent drying of
paddy fields to kill mosquito larvae
4. Minimizing vector density - chemicals5. Monitoring infection rates using sentinel pigs
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DF/DHF
Aetiology: Dengue virus (4serotypes)
Flaviviridae,
Mosquito borne RNA virus
Transmission: MosquitoesAedes aegypti
Aedes albopictus
Distribution: South and Southeast Asiaincluding SL
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Clinical manifestationsof DF/DHF
Inoculation of virus through mosquito bite
Viraemia
Early non-specific symptoms
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Clinical manifestations of DHFViraemia Early non-specific symptoms
Purpuric rash, bleeding fromthe mucosae (vomitous + faeces)
Drop in platelets
Extravasation of fluid from thevascular compartment
Hypovoleaemia, hypotension,tachycardia, apathy and shock
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Pathogenesis of DF/DHFDengue viral infections are asymptomatic in many
DF primarily occurs in non-immune adults and children
Symptoms begin after 5-10-days of incubation period
DHF/DSS usually occurs during a second dengue virus infection in
persons with pre-existing immunity to a heterologous dengue virus
serotype
Illness begins abruptly within 2-4 days of infection and rapiddeterioration
Increased vascular permeability and bleeding may be mediated by
circulating dengue antigen-antibody complexes, activation of
complement and release of vaso-active cytokines
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Epidemiology of DF/DHF in SL Endemic: Many parts of the Island
First DHF: 1965 in SL
No non-human hosts
Man Mosquitoes Man
Clean water habitats/households mosquitoes
Epidemics: Vector density is high
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Diagnosis
1. History + clinical symptoms + Epidemiology
2. Laboratory: Detection of dengue virus RNAduring the acute phase
Detection of serum antibodiesfrom the 5th day
Analysis acute and convalescentsera Confirmatory
Monitoring the PCV + Platelets
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Treatment No specific treatment Supportive therapy until recovery
Early recognition of DHF is important
1. Vector management Removal ofAedes
mosquito breeding sites
2. Minimising vector density chemicals
3. Prevention of mosquito bites (nets and
repellents)
Control
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Chikungunya fever
Spread by the bite of infected mosquitoes
Resembles DF and is characterized bysevere, sometimes persistent, joint pain
(arthritis), as well as fever and rash
It is non-life-threatening, widespreadoccurrence of diseases causes morbidity
and economic loss
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Chikungunya fever in IndiaIn October 2006, 151 districts of India have been
affected by chikungunya fever with >1.25
million cases
Attack rates have reached up to 45%
SL experienced an outbreak in 2006/07
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1. History + clinical symptoms + Epidemiology
2. Laboratory: Detection of CHIK virus RNAduring the acute phase
Detection of CHIK antibodies in
acute and convalescent sera
Detection of CHIK virus specificIgM in the acute phase serum
Diagnosis
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Symptomatic treatment for pain and fever
using anti-inflammatory drugs
Recovery from CHIK is the expected outcome,
convalescence can be prolonged for years
Persistent arthralgia may require analgesic andlong-term anti-inflammatory therapy
Treatment
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Prevention/controlNo vaccine is available
Prevention is entirely dependent on takingsteps to avoid mosquito bites and
elimination of mosquito breeding sites
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