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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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