Questions

Equine encephalitis viruses: Questions

Study questions about Equine encephalitis viruses: multiple-choice, clinical scenarios, short-answer and exam-style.

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Sit this set one question at a time. Multiple-choice questions mark themselves; written questions reveal a tickable mark scheme so you can score your own answer. You get a combined score at the end.

15 questions: 15 MCQ, 0 written.

Diagnosis rests on serology, with virus-specific IgM in serum and cerebrospinal fluid and a rising IgG on paired sera, because the viraemia is usually past by the time encephalitis appears; reverse-transcription PCR helps early, especially in Venezuelan infection.

Agar culture, urinary antigen, electroencephalography alone and skin biopsy are not the approach.

Western equine encephalitis is generally mild in adults but can be severe in infants, with seizures and a substantial risk of permanent brain damage in survivors.

The other groups are at lower risk.

Madariaga virus is the species into which the South American strains formerly called Eastern equine encephalitis virus were reclassified, and it is generally much less virulent in people.

It is not a vaccine strain, not tick-borne, not the most virulent member, and not Western virus.

Eastern equine encephalitis virus cycles between passerine birds and the mosquito Culiseta melanura in freshwater hardwood swamps of eastern North America, with less host-specific bridge vectors carrying it to people and horses.

The rodent cycle belongs to Venezuelan virus, and the other pairings are wrong.

The incubation period is about two to ten days, varying by virus, followed by a febrile prodrome that may progress to encephalitis.

The other intervals are far too short or too long.

Most people with Venezuelan equine encephalitis have a self-limited influenza-like febrile illness, and only a minority, mainly children, develop encephalitis.

It is not usually fatal, arthritic, haemorrhagic, or silent in everyone.

Epidemics arise when mutation of an enzootic strain produces a variant that replicates to high titre in horses, which then amplify the virus for floodwater mosquitoes to spread.

It is not spread person-to-person, through water, by ticks, or between birds.

The equine encephalitis viruses are New World agents not found in South Africa, so their relevance is as an imported differential in a traveller returning from the Americas.

The locally important alphaviruses are instead Sindbis, Middelburg and Ndumu; these viruses are not endemic, tick-borne, or locally eliminated.

Eastern equine encephalitis has the highest case-fatality, of the order of 30% or more, with frequent severe neurological sequelae in survivors, especially children.

The others are considerably less lethal.

Western equine encephalitis virus arose by recombination, its genome descended from an Eastern-equine-encephalitis-like ancestor with the structural genes of a Sindbis-like virus.

The others are not recombinants.

Western equine encephalitis virus, isolated from horse brains in California in 1930, was the first alphavirus ever grown in culture.

The three viruses were recovered from encephalitic horses in the Americas during the 1930s, not from African birds, not after 2000, and not before 1900.

Human Western equine encephalitis has all but vanished, with no North American case for many years, for reasons that appear ecological rather than a loss of virulence.

Its vector is Culex tarsalis, not Culiseta melanura; it is a New World, mosquito-borne virus.

LDLRAD3, a low-density lipoprotein receptor-related protein, is a key entry receptor for Venezuelan equine encephalitis virus.

MXRA8 serves the arthritogenic Old World alphaviruses, and the others are not its receptor.

All three viruses are neurotropic, invading the brain and infecting neurons, and Eastern equine encephalitis virus is the most neurovirulent.

Susceptibility to fatal disease is highest at the extremes of age, and neuroinvasion can occur by several routes, not only along nerves.

There is no licensed human vaccine; veterinary vaccines protect horses, and Venezuelan equine encephalitis virus is highly infectious by aerosol and a recognised biothreat.

Human vaccines remain investigational, the laboratory-aerosol hazard is real, and equine vaccination is central to outbreak control.

MCQ
How are the equine encephalitis viruses usually diagnosed in a patient with encephalitis?
- A. Blood culture on standard bacteriological agar plates
- B. Antigen testing of a urine sample
- C. Serology, with IgM in serum and cerebrospinal fluid
- D. Electroencephalography on its own
- E. Skin biopsy of a rash
Show answer
Correct answer: C
Diagnosis rests on serology, with virus-specific IgM in serum and cerebrospinal fluid and a rising IgG on paired sera, because the viraemia is usually past by the time encephalitis appears; reverse-transcription PCR helps early, especially in Venezuelan infection.

Agar culture, urinary antigen, electroencephalography alone and skin biopsy are not the approach.
What should be corrected?Credit me as (optional)
MCQ
In Western equine encephalitis, severe disease is most likely in:
- A. Healthy young adults
- B. Infants
- C. Adolescents
- D. Middle-aged women
- E. People with prior immunity
Show answer
Correct answer: B
Western equine encephalitis is generally mild in adults but can be severe in infants, with seizures and a substantial risk of permanent brain damage in survivors.

The other groups are at lower risk.
What should be corrected?Credit me as (optional)
MCQ
Madariaga virus is best described as:
- A. The live-attenuated laboratory-worker vaccine strain of Venezuelan virus
- B. A tick-borne relative within the group
- C. The reclassified South American Eastern virus, usually milder
- D. The single most virulent member of the complex
- E. Another name for Western equine encephalitis virus
Show answer
Correct answer: C
Madariaga virus is the species into which the South American strains formerly called Eastern equine encephalitis virus were reclassified, and it is generally much less virulent in people.

It is not a vaccine strain, not tick-borne, not the most virulent member, and not Western virus.
What should be corrected?Credit me as (optional)
MCQ
The enzootic cycle of Eastern equine encephalitis virus involves:
- A. Passerine birds and Culiseta melanura in freshwater swamps
- B. Forest rodents and Culex (Melanoconion) mosquitoes in tropical swamps
- C. Horses and Psorophora floodwater mosquitoes
- D. Humans and Aedes aegypti in cities
- E. Ticks and swamp-dwelling deer
Show answer
Correct answer: A
Eastern equine encephalitis virus cycles between passerine birds and the mosquito Culiseta melanura in freshwater hardwood swamps of eastern North America, with less host-specific bridge vectors carrying it to people and horses.

The rodent cycle belongs to Venezuelan virus, and the other pairings are wrong.
What should be corrected?Credit me as (optional)
MCQ
The incubation period of the equine encephalitis viruses is on the order of:
- A. Several hours
- B. 4 to 8 weeks
- C. 2 to 3 months
- D. 2 to 10 days
- E. Over 3 months
Show answer
Correct answer: D
The incubation period is about two to ten days, varying by virus, followed by a febrile prodrome that may progress to encephalitis.

The other intervals are far too short or too long.
What should be corrected?Credit me as (optional)
MCQ
The typical presentation of Venezuelan equine encephalitis in humans is:
- A. A self-limited influenza-like illness, encephalitis in a minority
- B. An almost invariably fatal necrotising encephalitis
- C. A chronic destructive polyarthritis
- D. A viral haemorrhagic fever with heavy bleeding and circulatory shock
- E. An entirely asymptomatic infection in everyone
Show answer
Correct answer: A
Most people with Venezuelan equine encephalitis have a self-limited influenza-like febrile illness, and only a minority, mainly children, develop encephalitis.

It is not usually fatal, arthritic, haemorrhagic, or silent in everyone.
What should be corrected?Credit me as (optional)
MCQ
What drives large epidemics of Venezuelan equine encephalitis?
- A. Direct person-to-person respiratory droplet spread
- B. Amplification of an epizootic strain in horses
- C. Contaminated municipal water supplies
- D. The bite of forest-dwelling ticks
- E. Airborne spread between wild birds
Show answer
Correct answer: B
Epidemics arise when mutation of an enzootic strain produces a variant that replicates to high titre in horses, which then amplify the virus for floodwater mosquitoes to spread.

It is not spread person-to-person, through water, by ticks, or between birds.
What should be corrected?Credit me as (optional)
MCQ
What is the relevance of the equine encephalitis viruses to South African practice?
- A. They are a common cause of locally acquired viral encephalitis
- B. They are endemic across the central and interior plateau of the whole country
- C. They are transmitted by hard ticks found across South Africa
- D. They were eliminated locally by routine vaccination
- E. An imported differential in a traveller returning from the Americas
Show answer
Correct answer: E
The equine encephalitis viruses are New World agents not found in South Africa, so their relevance is as an imported differential in a traveller returning from the Americas.

The locally important alphaviruses are instead Sindbis, Middelburg and Ndumu; these viruses are not endemic, tick-borne, or locally eliminated.
What should be corrected?Credit me as (optional)
MCQ
Which arboviral encephalitis carries the highest case-fatality in the Americas?
- A. Western equine encephalitis
- B. Venezuelan equine encephalitis
- C. West Nile encephalitis
- D. St Louis encephalitis
- E. Eastern equine encephalitis
Show answer
Correct answer: E
Eastern equine encephalitis has the highest case-fatality, of the order of 30% or more, with frequent severe neurological sequelae in survivors, especially children.

The others are considerably less lethal.
What should be corrected?Credit me as (optional)
MCQ
Which equine encephalitis virus is a natural recombinant?
- A. Eastern equine encephalitis virus
- B. Western equine encephalitis virus
- C. Venezuelan equine encephalitis virus
- D. Madariaga virus
- E. None of them is a recombinant
Show answer
Correct answer: B
Western equine encephalitis virus arose by recombination, its genome descended from an Eastern-equine-encephalitis-like ancestor with the structural genes of a Sindbis-like virus.

The others are not recombinants.
What should be corrected?Credit me as (optional)
MCQ
Which is true of the discovery of the equine encephalitis viruses?
- A. Western equine encephalitis virus was the first alphavirus cultured, in 1930
- B. They were first isolated from wild migratory birds trapped across Africa
- C. All three were first discovered after the year 2000
- D. They were first recovered from human cerebrospinal fluid samples
- E. Eastern equine encephalitis virus was fully characterised before the year 1900
Show answer
Correct answer: A
Western equine encephalitis virus, isolated from horse brains in California in 1930, was the first alphavirus ever grown in culture.

The three viruses were recovered from encephalitic horses in the Americas during the 1930s, not from African birds, not after 2000, and not before 1900.
What should be corrected?Credit me as (optional)
MCQ
Which is true of Western equine encephalitis?
- A. It remains the commonest arboviral encephalitis across the Americas
- B. It is transmitted mainly by Culiseta melanura
- C. Human disease has all but disappeared in North America
- D. It occurs only on the African continent
- E. It is spread by the bite of an infected tick
Show answer
Correct answer: C
Human Western equine encephalitis has all but vanished, with no North American case for many years, for reasons that appear ecological rather than a loss of virulence.

Its vector is Culex tarsalis, not Culiseta melanura; it is a New World, mosquito-borne virus.
What should be corrected?Credit me as (optional)
MCQ
Which molecule is a key entry receptor for Venezuelan equine encephalitis virus?
- A. Heparan sulfate acting on its own
- B. The neuronal acetylcholine receptor
- C. MXRA8
- D. LDLRAD3
- E. The transferrin receptor
Show answer
Correct answer: D
LDLRAD3, a low-density lipoprotein receptor-related protein, is a key entry receptor for Venezuelan equine encephalitis virus.

MXRA8 serves the arthritogenic Old World alphaviruses, and the others are not its receptor.
What should be corrected?Credit me as (optional)
MCQ
Which statement about equine encephalitis virus pathogenesis is correct?
- A. The viruses do not infect central-nervous-system neurons
- B. Disease severity bears no relation to the age of the host
- C. Western virus is by far the most neurovirulent of the three
- D. They reach the brain only by travelling slowly along the peripheral nerves
- E. All three are neurotropic, and Eastern virus is the most neurovirulent
Show answer
Correct answer: E
All three viruses are neurotropic, invading the brain and infecting neurons, and Eastern equine encephalitis virus is the most neurovirulent.

Susceptibility to fatal disease is highest at the extremes of age, and neuroinvasion can occur by several routes, not only along nerves.
What should be corrected?Credit me as (optional)
MCQ
Which statement about preventing equine encephalitis is correct?
- A. A safe licensed human vaccine is in widespread routine clinical use worldwide
- B. Venezuelan virus poses no laboratory-aerosol hazard at all
- C. Only antiviral prophylaxis is effective against these viruses
- D. No licensed human vaccine exists; Venezuelan virus is an aerosol biothreat
- E. Vaccinating horses plays no part in outbreak control
Show answer
Correct answer: D
There is no licensed human vaccine; veterinary vaccines protect horses, and Venezuelan equine encephalitis virus is highly infectious by aerosol and a recognised biothreat.

Human vaccines remain investigational, the laboratory-aerosol hazard is real, and equine vaccination is central to outbreak control.
What should be corrected?Credit me as (optional)