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NTD > Common arbovirus infections > Flashcards

Common arbovirus infections Flashcards

1
Q

What are arboviruses and the three virus families?

A

Arthropod-borne virus – virus of vertebrates
- Viruses maintained in nature through biological transmission between susceptible vertebrate hosts by blood feeding arthopods (mostly mosquitoes)
- Over 130 arboviruses known to cause disease in humans

Three virus families
- Togaviridae
- Flaviviridae
- Bunyavirida

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2
Q

What are the two transmission cycles?

A

Man – arthropod – man

Animal – arthropod – man

reservoir may either be in either man or arthopod vector e.g dengue, urban yellow fever

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3
Q

Viruses of medical interest in the Americas

A
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4
Q

Important arboviruses

A

Dengue has 4 different serotypes.

Dengue, zika and yellow fever flavivirus
chikungunya is alphavirus.

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5
Q

What are all of the arboviruses transmitted by?

A

Aedes mosquitos - albopictus and aegypti

Ageypti has white lyre shaped markings on its thorax

Albopictus has median longitudinal white stripe

aegyptic most commonly in tropical regions, can’t survive when too cold

albopictus can survive in north and south us and europe, mostly in summer months

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6
Q

Dengue infection classic

A

Short lived
High fever 40C (saddleback)
Severe muscle pains (break bone fever)
Erythematous rash followed by morbilliform rash starting on extremities
Generalised lymphadenopathy
Moderately enlarged liver
Profound leucopenia
May have protracted convalescence

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7
Q

Dengue haemorrhagic fever/ shock syndrome

A

2nd to 5th day of classic dengue

Associated with second or later infections

Increased capillary permeability – shock

Increased bleeding, petechial haemorrhages etc

Increase in haematocrit because plasma leaves circulation and goes to tissues, blood concentration increases, drop in platelets – increased risk in bleeding

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8
Q

Diagnosing dengue

A

Positive touniquet test

Spontaneous haemorrhages

Thrombocytopenia

Increase in haematocrit

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9
Q

Why does the haemtocrit increase in severe dengue?

A

When you centrifuge the elements of blood separate

Dense red cells at bottom, layer of white blood cells and platelets and then plasma on top

In severe dengue there is increase in capillary permeability, plasma leaves vessels and goes into tissues, such that you lose plasma and get increase in haemoconcentration – increase in RBC column

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10
Q

What is erythematous (blanching) and morbilliform rash?

A

Erythematous (blanching) rash - Put hand on someone with dengue and press, you get blanching

Morbilliform rash
Appears after erythematous rash
Start from extremities and move inwards

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11
Q

What is petechial haemorrhages?

A

Small bleeding patches get bleeding directly from capillaries in skin, causing small haemorrhages in the skin

Larger haemorrhages called purpura

Can get bleeding to gums too

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12
Q

Dengue vaccines and efficacy

A

Live attenuated tetravalent (Dengvaxia)
Three dose schedule (cost >US$200)

Vaccine efficacy
- 76% against seropositives prior to vaccination
- 39% against seronegatives
- Excess severe dengue among seronegatives

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13
Q

How is a tourniquet test done?

A

Inflating a blood pressure cuff to a point mid-way between systolic and diastolic pressures for five minutes

A test is considered positive when 10 or more petechiae per 2.5cm2 (1 inch) are observed.

In DHF the test usually gives a definite positive result ie. >20 petechiae.

The test may be negative or mildly positive during the phase of profound shock

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14
Q

How is dengue transmitted?

A

Bitten by dengue infected mosquito, dengue virus injected

Virus attaches to immune cells e.g DC sign on dendritic cells or attach through mannose type receptor on a macrophage

Infects various immune cells

Outcome of infection varies on number of factors

Can get dengue fever, DHF, or undifferentiated fever

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15
Q

What two groups are most at risk of severe dengue?

A

Infants with declining levels of maternal antibodies, low levels of circulating antibodies, more susceptible to severe outcomes

Children (often <10yrs) with previous infection

Due to antibody-dependent enhancement – antibodies can bind dengue virus in circulation but binding is not very strong because they’re from a different serotype – doesn’t give right signals, virus is taken up in cell, survives and replicates within cells, releasing more virus – more severe disease

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16
Q

Diagnosing dengue

A

Early diagnosis with onset of fever if there is virus circulating by doing molecular test e.g PCR, antigen test

Antibodies appear at time viremia start to fall, IgM antibodies around day 3-4 from onset of symptoms

Week later from symptoms you get IgG produced

17
Q

Treatment of dengue

A

Supportive

Paracetamol – no aspirin because these affect ability of platelets to enhance clotting, can increase bleeding tendency

Tepid sponging for fever

Fluid replacement where necessary etc – carefully to prevent fluid overload

18
Q

Prevention and control of dengue

A

Vaccine
- Tetravalent vaccine (Sanofi)

Vector control
- Insecticide spraying
- Mosquito nets/screens
- Wolbachia and GM mosquitos

19
Q

What does WHO recommend regarding dengue vaccination?

A

WHO recommends that countries should consider vaccination (Sanofi-pasteur) with the tetravalent dengue vaccine only if the risk of severe dengus in seronegative individuals can be minimized either through:

Pre-vaccination screening – blood test to see if they have antibodies, if they don’t have antibodies against dengue you don’t give vaccine

Recent documentation of high seroprevalence rates in the area (at least 80% by 9 years old)

20
Q

What are the limitations of WHO’s recommendation of vaccinating?

A

Cost >US200

Three dose schedule with doses spaced 6 months apart

Need for pre-vaccination screening with seroprevalence data for regions where it is to be used >70% seroprevalence

Age restriction, 9-45 years

Poor efficacy in preventing symptomatic infections with DENV-1 and DENV-2

21
Q

What is the takeda TAK 003 vaccine?

A

Tetravalent live attenuated

Currently being evaluated in trials in 8 countries

  • Efficacy against seronegatives
  • Robust antibody responses to all 4 serotypes lasting >4 years
  • 4-60 years
  • Prevents 62% classical dengue and 83% hospitalisations
22
Q

Chikungunya disease

A

Incubation 2-7 days
High fever >39c
Rash – itchy maculopapular rash, follows fever
(poly)-Arthralgia – arthritis
- 30-90% cases
- Joints of wrist, ankle, fingers and the back
- Characteristic ‘bent-over’ posture
- Exacerbation of existing arthritis
- Swelling of joints, interphalangeal joints

23
Q

How to diagnose chikungunya

A

A week after infection you get viraemia, coincides with fever, arthralgia

Skin rash after fever

During early stage you can pick up viraemia via PCR

After first week you get IgM antibodies appearing in circulation

24
Q

Treatment of chikungunya

A

Bed rest, fluid, paracetamol

No aspirin but ibuprofen and other NSAIDs can be used because there’s overlap in symptoms with dengue

Chloroquine for persistent joint pain

Acute illness generally lasts no more than a week

Arthralgia generally resolves within a year

25
Q

What is zika virus?

A

Single stranded RNA virus from family Flaviviridae

3 genotypes – W, E Africa and asia with relatively little nucleotide divergence

Closely related to other flaviviruses (dengue, YF, etc(

Virus with neural tropism

26
Q

How is zika transmitted?

A

Via a vector
Mainly aedes aegypti but also other Aedes species – albopictus etc
Might also be spread by Anopheles and Culex spp

Direct human to human
- In utero, perinatal including breastfeeding, transfusion, sexual

27
Q

Clinical presentation

A

Incubation period <7 days and illness lasts 7 days
Onset symptoms associated with viraemia
80% asymptomatic
Mild self limiting illness
- Mild fever <38C 65%
- Maculopapular and pruritic rash 90%
- Non-purulent conjunctivitis 55%
- Arthralgia 65%

28
Q

Clinical neurological complications of zika, guillain-barre syndrome

A

First noted in Polynesia (incidence <1 in 1000)
3 or so weeks after infection
Anti-ganglioside Ab negative
EPS-acute motor axonal neuropathy – can result in respiratory paralysis in severe cases

29
Q

Clinical neurological complication of zika microcephaly

A

Small head for gestational size, <2nd centile

Increase first noted in brazil and retrospectively in Polynesia

Highest risk probably during first trimester

Risk of microcephaly now estimated at 3-4% - cf rubella in 1st trimester causes 90% congenital abnormalities

Severe neurological development problems relating to how virus damages cerebral cortex

As brain develops, it pushes out developing skull, if you don’t get development of cortex you get a smaller skull because brain isn’t developing and pushing out skull

30
Q

Diagnosis of zika

A

Specific RT-PCR for RNA
- RNA detectable in blood for up to week after onset
- 10 days in urine
- weeks in semen

Specific IgM and IgG ELISAs
- IgM persists for several months, IgG for years
- Problem with cross-reactivity with other flaviviruses
(eg dengue)

Neutralization tests (PRNT) for 4-fold increase in
titers
- More specific than ELISA
- Costly and labour-intensive, specialised

31
Q

How to prevent zika

A

No treatment or vaccine

Repellents/screens/residual spraying/breeding sites

Postpone travel to endemic areas to not get infected

Postpone pregnancy

Safe sex

32
Q

Clinical presentation of yellow fever

A

Red eyes
Fever
Vomiting
Back pain
Headache
Bleeding
Jaundice
Muscle aches
Hepatomegaly

33
Q

Yellow fever clinical disease

A

Incubation 3-6 days
3-4 days of fever, headache, chills, back pain, muscle pain, nausea, vomiting
15% go on to develop more severe illness
- Recurring fever
- Jaundice and abdominal pain
- Bleeding and haematemesis
- Death 5% but 20-50% of those with jaundice

34
Q

Yellow fever vaccine

A

17D developed in 1937
Liver attenuated vaccine
Single dose, lifelong protection
Cases of reversion to virulence

35
Q

How can arbovirus infections be controlled?

A

Aedes aegypti domesticated vector that breeds around households
- Water containers, bottles, used tyres

Eggs resistant, can survive more than 6 months in desicated state
- Eggs need very little water to develop e.g teaspoon

Rapid urbanisation in overcrowded slums without drainage and rubbish disposal provide perfect environment for vectors

Personal and household protection
- Clothes, repellents, nets, window and door screens, covering water sources

Spraying
- Residual insecticides

community education

GM mosquitoes

Wolbachia

36
Q

Insecticides

A

Community campaigns and insecticides can be effective in mosquito control
- Synthetic insecticides can have adverse health and ecological effects

Insecticide resistance growing problem
- Pyrethroids have been replaced by malathion
- Malathion persists in clothes etc
- Abate (temephos) in water

Larval surveys important in surveillance - Needs to be done at regular intervals
- Resource intensive

NTD (11 decks)

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