Question 1
Question
What is the basic structure of the Paramyxoviridae?
Answer
-
Enveloped, ss – sense, RNA viruses
-
Non-enveloped, ss – sense, RNA viruses
-
Enveloped, ss + sense, RNA viruses
-
Enveloped, ds – sense, RNA viruses
-
Non-nveloped, ss + sense, RNA viruses
Question 2
Question
What are the two major peplomers found on the envelope of Paramyxoviridae?
Answer
-
Haemagglutinin and Neuraminidase protein
-
Nucleocapsid phosphoprotein and Neuraminidase protein
-
Hernagglutinin and Neuraminidase protein
-
Haemagglutinin and Nucleocapsid phosphoprotein
Question 3
Question
Why is the Fusion (F) protein essential?
Answer
-
Cleavage of F protein is essential for infectivity
-
Cleavage of F protein is essential for entering the host cell
-
Cleavage of F protein is essential for leaving the host cell
Question 4
Question
What are important features of Newcastle disease?
Answer
-
Characterised by respiratory, gastrointestinal, circulatory and nervous signs
-
Virulence varies between strains
-
Important disease of poultry worldwide
-
Highly contagious
-
Spreads rapidly among susceptible birds
-
Zoonotic
-
Latent infection
Question 5
Question
What is the incubation period of Newcastle disease?
Answer
-
~ 5 days
-
~ 10 days
-
~ 9 days
-
~ 15 days
-
~ 2 days
Question 6
Question
Clinical presentation of Newcastle disease relates to?
Question 7
Question
[blank_start]Velogenic[blank_end] = high virulence. Produce sudden high mortality (~100%)
[blank_start]Mesogenic[blank_end] = intermediate virulence. Cause mild disease with mortality confined to young birds
[blank_start]Lentogenic[blank_end] = low virulence. Cause mild disease or inapparent infection
[blank_start]Viscerotropic[blank_end]= a virus that has a preference for the viscera (organs)
[blank_start]Neurotropic[blank_end]= a virus that is able to infect nerve cells
Answer
-
Velogenic
-
Mesogenic
-
Lentogenic
-
Viscerotropic
-
Neurotropic
Question 8
Question
What is virulence associated with in Paramyxoviridae?
Answer
-
“cleavability” and activation of the F protein
-
“cleavability” and activation of the Haemagglutinin protein
-
“cleavability” and activation of the Neuraminidase protein
-
“cleavability” and activation of the Haemagglutinin/Neuraminidase protein
Question 9
Question
What are the clinical signs of a virus that is Viscerotropic velogenic?
Answer
-
Severe fatal disease with haemorrhagic intestinal lesions and bright green diarrhoea (mortality 90-100%)
-
Respiratory signs: tachypnoea, gasping, rales, oedema of head/neck. Progresses to nervous signs: tremors, paralysis, torticollis (mortality 10-20% in adults)
-
Coughing, weight loss, reduced egg production (mortality ~10% - usually young birds)
-
Mainly subclinical
Question 10
Question
What are the clinical signs of a virus that is Lentogenic?
Answer
-
Mainly subclinical
-
Coughing, weight loss, reduced egg production (mortality ~10% - usually young birds)
-
Respiratory signs: tachypnoea, gasping, rales, oedema of head/neck. Progresses to nervous signs: tremors, paralysis, torticollis (mortality 10-20% in adults)
-
Severe fatal disease with haemorrhagic intestinal lesions and bright green diarrhoea (mortality 90-100%)
Question 11
Question
What are the clinical signs of a virus that is Mesogenic?
Answer
-
Coughing, weight loss, reduced egg production (mortality ~10% - usually young birds)
-
Mainly subclinical
-
Respiratory signs: tachypnoea, gasping, rales, oedema of head/neck. Progresses to nervous signs: tremors, paralysis, torticollis (mortality 10-20% in adults)
-
Severe fatal disease with haemorrhagic intestinal lesions and bright green diarrhoea (mortality 90-100%)
Question 12
Question
What are the clinical signs of a virus that is Neurotropic velogenic?
Answer
-
Mainly subclinical
-
Coughing, weight loss, reduced egg production (mortality ~10% - usually young birds)
-
Respiratory signs: tachypnoea, gasping, rales, oedema of head/neck. Progresses to nervous signs: tremors, paralysis, torticollis (mortality 10-20% in adults)
-
Severe fatal disease with haemorrhagic intestinal lesions and bright green diarrhoea (mortality 90-100%)
Question 13
Question
Where does Newcastle disease replicate?
Answer
-
Virus replication in epithelia of respiratory and gastrointestinal tracts
-
Secondary viraemia - infection of lung, intestine, CNS
-
Haematogenous spread - spleen and bone marrow (viraemia)
-
Arthropod vector transmission replicates at localised site initially
Question 14
Question
What is true of the epidemiology of Newcastles disease?
Answer
-
Wide range of avian species are susceptible
chickens, turkeys, ducks, geese, pheasants, pigeons…
-
Wild birds may act as reservoir – mutation at cleavage
-
Virus is excreted in faeces, from respiratory tract and survives in environment and in carcasses for weeks
-
Transmission by inhalation of aerosols or ingestion of contaminated food or water
-
Transmission by arthropods (mosquitos)
Question 15
Question
How might you control Newcastles disease?
Question 16
Question
When was Rinderpest eradicated?
Question 17
Question
What is Rinderpest characterised by?
Answer
-
Pyrexia, inflammation and necrosis of the mucous membranes
-
Diarrhoea and fever
-
Abortion and reproductive failure
-
Neurological symptoms (encephalitis)
Question 18
Answer
-
High morbidity and high mortality
-
High morbidity and low mortality
-
Low morbidity and high mortality
-
Low morbidity and low mortality
Question 19
Question
How long is the incubation period of Rinderpest?
Answer
-
3 – 5 days
-
6 – 9 days
-
1 – 2 days
-
1 – 4 days
Question 20
Question
What are the clinical signs of Rinderpest?
Answer
-
Mucopurulent nasal and ocular discharge
-
Necrotic foci (ulcers and erosions)
-
Profuse haemorrhagic diarrhoea
-
Dehydration, wasting and secondary infection
-
Abortion and reproductive failure
Question 21
Question
How long until death occurs in an animal infected with Rinderpest?
Answer
-
Within 12 days
-
Within 2 days
-
Within 5 days
-
Within 9 days
Question 22
Question
What is the pathogenesis of Rinderpest?
Answer
-
Leucopaenia due to destruction/necrosis of lymphoid tissue
-
Transmission by inhalation
-
Viraemia: spread of virus to other lymphoid tissue and mucosae of respiratory and gastrointestinal tracts
-
Replication in tonsils and local URT lymph nodes
Question 23
Question
What is the epidemiology of Rinderpest?
Answer
-
One serotype, but different strains recognised
-
No carrier state (young animals affected in endemic areas)
-
Virus is labile in environment
-
Infection requires close contact
-
Shedding before obvious clinical signs
-
Virus shed in faeces, urine, respiratory secretions etc
-
Can survive in the environment for weeks
-
Carrier states exist
Question 24
Question
How was Rinderpest eradicated?
Answer
-
Vaccination: attenuated vaccine (eradication planned by 2010, achieved 2011)
-
Lasting immunity to vaccine, no carriers, no animal reservoir, good
diagnostic tests
-
Quarantine
-
Rinderpest spreads slowly
Question 25
Question
What other disease does the Rinderpest vaccine control?
Answer
-
Pest de Petit Ruminants
-
Newcastles disease
-
Bovine vascular disease
-
Canine Distemper
Question 26
Question
Outline the epidemiology of Canine Distemper?
Answer
-
Virus shed in expired air, faeces, urine, other secretions
-
Requires direct contact or close aerosol transmission
-
Virus is labile in environment
-
Outbreaks recorded in dogs, foxes, skunks, racoons, ferrets and lions
-
Higjly contagious
-
Urban dogs: infection spreads rapidly among young dogs as maternal antibody wanes (3-6months)
-
Rural dogs: lower population pressure, more susceptible, unvaccinated dogs. Outbreaks in dogs of varying ages
-
Urban dogs: lower population pressure, more susceptible, unvaccinated dogs. Outbreaks in dogs of varying ages
-
Rural dogs: infection spreads rapidly among young dogs as maternal antibody wanes (3-6months)
Question 27
Question
How long is the incubation period of Canine Distemper?
Answer
-
3- 6 days
-
5- 9 days
-
1- 2 days
-
9- 10 days
Question 28
Question
What is true of the clinical signs of Canine Distemper?
Answer
-
Hyperkeratosis of nose and footpads
-
Skin rash and pustules may develop
-
Variable duration and severity of illness
-
Biphasic pyrexia: Second peak = onset of oculonasal discharge, pharyngitis, tonsillar enlargement
-
Old dog encephalitis: persistence in brain, motor and behavioural deterioration, invariably fatal
-
Acute disease is followed by recovery and life-long immunity, or progresses to CNS disease
-
Neurological signs include myoclonic contractions,
ataxia, paresis, seizures and death-- Grave prognosis for dogs with neurological signs
-
Animals develop cough, vomiting, diarrhoea
-
Usually asymptomatic
Question 29
Question
What is the pathogenesis of Canine Distemper?
Question 30
Question
How is Canine Distemper controlled?
Question 31
Question
What is the reservoir for Hendra virus?
Question 32
Question
In what year was the initial Hendra outbreak?
Question 33
Question
What are the clinical signs of Hendra virus?
Answer
-
Congested, firm, fluid filled lungs, with dilated lymphatics. Thick, foamy, haemorrhagic exudate in airways
-
Liver necrosis
-
Diarrhoea
-
Encephalitis
Question 34
Question
What virus is closely related to Hendra virus?
Answer
-
Nipah virus
-
African Horse Sickness
-
Japanese Encephalitis
Question 35
Question
What is the basic structure of Orthomyxoviridae?
Answer
-
Enveloped, segmented, ss, - sense RNA
-
Non-enveloped, segmented, ss, - sense RNA
-
Non-enveloped, segmented, ds, - sense RNA
-
Enveloped, segmented, ss, + sense RNA
Question 36
Question
Which of the below are genera of Orthomyxoviridae?
Answer
-
Orbivirus
-
Thogotovirus
-
Quaranjavirus
-
Isavirus
-
Influenzavirus B
-
Influenzavirus A
Question 37
Question
Which genera of Orthomyxoviridae ismainly responsible for epidemics and pandemics in the susceptible populations?
Answer
-
Orbivirus
-
Influenzavirus B
-
Thogotovirus
-
Quaranjavirus
-
Isavirus
-
Influenzavirus A
-
Influenzavirus C
Question 38
Question
Orthomyxoviridae are labile in the environment, sensitive to high temperatures and acid pH
Question 39
Question
How many subtypes of inflenza A are there?
Answer
-
17 HA subtypes and 9 NA subtypes
-
7 HA subtypes and 5 NA subtypes
-
17 HA subtypes and 4 NA subtypes
-
9 HA subtypes and 17 NA subtypes
Question 40
Question
What subtypes of influenza A commonly infect swine?
Question 41
Question
What subtype of influenza A is associated with Equine influenza currently?
Question 42
Question
How long does it take influenza A virus to spread through the respiratory tract?
Answer
-
1-3 days
-
5-7 days
-
7-9 days
-
4-5 days
Question 43
Question
What clinical signs are often associated with influenza A?
Question 44
Question
How many times has equine influenza been found in Australia?
Question 45
Question
How long does it take a horse with equine influenza to recover?
Answer
-
2-3 weeks for well-rested, mildly affected horses and up to 6 months in the
most severe cases
-
2-3 months for well-rested, mildly affected horses and up to 6 months in the
most severe cases
-
2-3 weeks for well-rested, mildly affected horses and up to 3 months in the
most severe cases
-
2-3 months for well-rested, mildly affected horses and up to 9 months in the
most severe cases
Question 46
Question
What is the difference between Low pathogenicity avian influenza (LPAI) and High pathogenicity avian influenza (HPAI)
Answer
-
Mortality rates in HPAI are nearly 100% compared to 3-15% iin LPAI
-
Mortality rates in HPAI are nearly 100% compared to 40% iin LPAI
-
Mortality rates in HPAI are nearly 100% compared to 30-50% iin LPAI
Question 47
Question
What is the function of HA (haemagglutin)?
Answer
-
Attachment, Fusion and Antigenicity
-
Attachment, Fusion and Disattachment
-
Attachment, Fusion and Exclusion
Question 48
Question
What is the function of Neuraminidase?
Answer
-
cleaves sialic acid (also known as neuraminic acid) from glycoproteins and glycolipids and removes sialic acid from newly formed virions to prevent their aggregation and promote their release from infected cells
-
Attachment of the virion to the host cell
-
Breakdown of the host cell so that the new virions can leave
Question 49
Question
[blank_start]Antigenic DRIFT[blank_end]- occurs WITHIN a subtype and describes the gradual accumulation of mutations in the HA or NA sequence and appearance of new strains of the same subtype.
[blank_start]Antigenic SHIFT[blank_end]- results in the emergence of a NEW SUBTYPE within a population, and this is usually is an abrupt change.
Answer
-
Antigenic DRIFT
-
Antigenic SHIFT
Question 50
Question
What is the basic structure of Picornaviridae?
Answer
-
Non-enveloped, Icosahedral ss + sense RNA
-
Enveloped, Icosahedral ss + sense RNA
-
Non-enveloped, Icosahedral ds - sense RNA
-
Non-enveloped, Icosahedral ss - sense RNA
-
Enveloped, Icosahedral ss - sense RNA
Question 51
Question
Which of the below genera of Picornaviridae are of veterinary importance?
Answer
-
Hepatovirus
-
Rhinovirus
-
Enterovirus
-
Cardiovirus
-
Erbovirus
-
Aphthovirus
-
Parechovirus
Question 52
Question
Which disease of economic importance is found within the genera Aphthovirus (family Picornaviridae)?
Question 53
Question
What is the biggest disadvantage of FMD?
Question 54
Question
What are the main features of FMD?
Question 55
Question
Why is FMD such an issue in dairy cattle?
Question 56
Question
How long is the FMD incubation?
Answer
-
2 – 8 days
-
1 – 2 days
-
9 – 12 days
Question 57
Question
What species of animal does FMD infect?
Question 58
Question
What clinical symptoms are associated with FMD?
Answer
-
Fever, inappetence, depression
-
Vesicles on tongue and oral mucosa-->Excessive salivation
-
Reduced milk production
-
Vesicles in interdigital region and coronary bands
-
Vesicles on teats, nasal mucosa, muzzle
-
Ulceration (ruptured vesicles)
-
Myocarditis which result in sudden death in young piglets and calves
-
Pulmonary oedema
-
Reproductive failure
-
Abortions
Question 59
Question
What is the main route of infection for FMD?
Answer
-
Via the respiratory tract- Inhalation of aerosolised droplets
-
Via the skin (broken or damaged skin, direct contact)
-
Venereal transmission
-
Vector transmission
-
Faecal-oral route
Question 60
Question
Where does FMD virus replication occur?
Question 61
Question
Which is the amplifier host for FMD infection?
Answer
-
Birds
-
Cattle
-
Sheep
-
Goats
-
Horses
-
Pigs
Question 62
Question
What is important in the epidemics of FMD?
Answer
-
Virus excretion ceases 4-6 days after vesicle appearance (when circulating antibodies develop)
-
Virus shed longer from hoof vesicles than oral
-
Virus shed in milk (23 days) and semen (56 days)
-
Vaccinated animals are protected, but can become carriers
-
80% of ruminants become persistently infected (pharyngeal and upper oesophageal tissues)
-
Latent infection can occur
Question 63
Question
How many serotypes of FMD are there?
Question 64
Question
What are outbreaks of FMD associated with?
Answer
-
Oral infection of pigs (swill feeding)
-
Aerosol spread to a susceptible population (10km over land and 250km over water)
-
Direct contact with sub-clinical / carrier animals or contaminated material
-
Changes in climate/weather causing an increase in athropods
-
Mutation of the virus
Question 65
Question
Where can FMD remain infective?
Answer
-
FMDV is acid labile (pH < 4 or > 11)
-
Virus can remain infective in uncooked, salted meats, improperly fermented salami, cheese etc
-
Virus can remain infective in faeces, urine and soil
-
Virus can remain infective on fomites for several weeks
Question 66
Question
FMD is clinically indistinguishable from other vesicular diseases of livestock
Question 67
Question
How is FMD controlled in FMD endemic countries?
Answer
-
Eradication campaign with blanket vaccination
-
Ring vaccination, +/- slaughter, blanket vaccination
-
Serological test & slaughter (positive and in contact animals)
Question 68
Question
How is FMD controlled in FMD free countries if an outbreak were to occur?
Answer
-
Serological test & slaughter (positive and in contact animals)
-
Ring vaccination, +/- slaughter, blanket vaccination
-
Eradication campaign with blanket vaccination
Question 69
Question
Which of the below are clinically indistinguishable from FMD?
Question 70
Question
Equine rhinitis A virus is?
Answer
-
An upper respiratory tract disease in horses
-
A reproductive disease in horses
-
A GIT disease in horses
-
A lower respiratory tract disease in horses
Question 71
Question
Encephalomyocarditis virus is a disease of what species?
Answer
-
Swine
-
Cattle
-
Horses
-
Sheep
Question 72
Question
Porcine encephalomyelitis (Porcine enterovirus 1) is an important exotic disease of pigs causing?
Answer
-
Fever, depression, anorexia followed by tremors and ataxia, the hind limbs show neurological
signs first, progressing to paralysis, convulsions, coma and death
-
Odd behaviour (tongue lolling, salivation, head bobbing) which returns to normal when the virus is cleared
-
Pulmonary and myocardial oedema
Question 73
Question
How long can Porcine encephalomyelitis (Porcine enterovirus 1) survive in the environment?
Answer
-
4 weeks
-
3 days
-
6 months
-
2 weeks
-
4 months
Question 74
Question
Porcine encephalomyelitis (Porcine enterovirus 1) is highly contagious, how is it transmitted?