What is the basic structure of the Paramyxoviridae?
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
What are the two major peplomers found on the envelope of Paramyxoviridae?
Haemagglutinin and Neuraminidase protein
Nucleocapsid phosphoprotein and Neuraminidase protein
Hernagglutinin and Neuraminidase protein
Haemagglutinin and Nucleocapsid phosphoprotein
Why is the Fusion (F) protein essential?
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
What are important features of Newcastle disease?
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
What is the incubation period of Newcastle disease?
~ 5 days
~ 10 days
~ 9 days
~ 15 days
~ 2 days
Clinical presentation of Newcastle disease relates to?
Virulence of the virus strain
Tissue tropism
Age of chicken
Immune status
Temperature
❌ = high virulence. Produce sudden high mortality (~100%)
❌ = intermediate virulence. Cause mild disease with mortality confined to young birds
❌ = low virulence. Cause mild disease or inapparent infection
❌= a virus that has a preference for the viscera (organs)
❌= a virus that is able to infect nerve cells
What is virulence associated with in Paramyxoviridae?
“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
What are the clinical signs of a virus that is Viscerotropic velogenic?
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
What are the clinical signs of a virus that is Lentogenic?
What are the clinical signs of a virus that is Mesogenic?
What are the clinical signs of a virus that is Neurotropic velogenic?
Where does Newcastle disease replicate?
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
What is true of the epidemiology of Newcastles disease?
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)
How might you control Newcastles disease?
Antivirals
ND free countries use test and slaughter
ND endemic countries use attenuated live vaccine strains (such as the V4 strain that is an endemic Australian strain)
Sentry chickens
When was Rinderpest eradicated?
2011
1998
1972
2001
2014
What is Rinderpest characterised by?
Pyrexia, inflammation and necrosis of the mucous membranes
Diarrhoea and fever
Abortion and reproductive failure
Neurological symptoms (encephalitis)
Rinderpest has?
High morbidity and high mortality
High morbidity and low mortality
Low morbidity and high mortality
Low morbidity and low mortality
How long is the incubation period of Rinderpest?
3 – 5 days
6 – 9 days
1 – 2 days
1 – 4 days
What are the clinical signs of Rinderpest?
Mucopurulent nasal and ocular discharge
Necrotic foci (ulcers and erosions)
Profuse haemorrhagic diarrhoea
Dehydration, wasting and secondary infection
How long until death occurs in an animal infected with Rinderpest?
Within 12 days
Within 2 days
Within 5 days
Within 9 days
What is the pathogenesis of Rinderpest?
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
What is the epidemiology of Rinderpest?
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
How was Rinderpest eradicated?
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
What other disease does the Rinderpest vaccine control?
Pest de Petit Ruminants
Newcastles disease
Bovine vascular disease
Canine Distemper
Outline the epidemiology of Canine Distemper?
Virus shed in expired air, faeces, urine, other secretions
Requires direct contact or close aerosol transmission
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)
How long is the incubation period of Canine Distemper?
3- 6 days
5- 9 days
1- 2 days
9- 10 days
What is true of the clinical signs of Canine Distemper?
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
What is the pathogenesis of Canine Distemper?
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How is Canine Distemper controlled?
Maternal antibodies and vaccination
Test and kill
Vaccinate to kill
What is the reservoir for Hendra virus?
Wild birds
Flying foxes (Fruit bats)
Rodents
Arthropods
In what year was the initial Hendra outbreak?
1994
1995
1991
What are the clinical signs of Hendra virus?
Congested, firm, fluid filled lungs, with dilated lymphatics. Thick, foamy, haemorrhagic exudate in airways
Liver necrosis
Diarrhoea
Encephalitis
What virus is closely related to Hendra virus?
Nipah virus
African Horse Sickness
Japanese Encephalitis
What is the basic structure of Orthomyxoviridae?
Enveloped, segmented, ss, - sense RNA
Non-enveloped, segmented, ss, - sense RNA
Non-enveloped, segmented, ds, - sense RNA
Enveloped, segmented, ss, + sense RNA
Which of the below are genera of Orthomyxoviridae?
Orbivirus
Thogotovirus
Quaranjavirus
Isavirus
Influenzavirus B
Influenzavirus A
Which genera of Orthomyxoviridae ismainly responsible for epidemics and pandemics in the susceptible populations?
Influenzavirus C
Orthomyxoviridae are labile in the environment, sensitive to high temperatures and acid pH
How many subtypes of inflenza A are there?
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
What subtypes of influenza A commonly infect swine?
H1N1
H1N2
H3N2
H5N1
H7N9
What subtype of influenza A is associated with Equine influenza currently?
H7H7
H3N8
H2N3
How long does it take influenza A virus to spread through the respiratory tract?
1-3 days
5-7 days
7-9 days
4-5 days
What clinical signs are often associated with influenza A?
Fever (up to 41°C)
Coughing
Sneezing and oranasal discharge
Fatigue and anorexia
Lymphadenopathy
Diarrhoea and vomiting
How many times has equine influenza been found in Australia?
Twice
Once
Three times
It is endemic to Australia
How long does it take a horse with equine influenza to recover?
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
What is the difference between Low pathogenicity avian influenza (LPAI) and High pathogenicity avian influenza (HPAI)
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
What is the function of HA (haemagglutin)?
Attachment, Fusion and Antigenicity
Attachment, Fusion and Disattachment
Attachment, Fusion and Exclusion
What is the function of Neuraminidase?
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
❌- 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.
❌- results in the emergence of a NEW SUBTYPE within a population, and this is usually is an abrupt change.
What is the basic structure of Picornaviridae?
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
Which of the below genera of Picornaviridae are of veterinary importance?
Hepatovirus
Rhinovirus
Enterovirus
Cardiovirus
Erbovirus
Aphthovirus
Parechovirus
Which disease of economic importance is found within the genera Aphthovirus (family Picornaviridae)?
Foot and Mouth Disease
Encephalomyocarditis virus
Equine Rhinitis A virus
Porcine enterovirus 1
Poliomyelitis
Swine vesicular disease virus
What is the biggest disadvantage of FMD?
High mortality
Dramatic reduction in production
Infertility
What are the main features of FMD?
Carrier state
Rapid replication
Virus shedding before clinical signs
Small infective dose
Multiple serotypes
Multiple modes of transmission
Multiple host species
Persistent infection
Why is FMD such an issue in dairy cattle?
Lost milk production for remainder of lactation and subsequent lactations - mastitis 25% loss of milk
Reduced growth rate
Reproductive dysfunction
How long is the FMD incubation?
2 – 8 days
9 – 12 days
What species of animal does FMD infect?
Infects cloven hoofed animals
Infects birds (eg. chickens)
Infects horses
Infects carnivores
What clinical symptoms are associated with FMD?
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
What is the main route of infection for FMD?
Via the respiratory tract- Inhalation of aerosolised droplets
Via the skin (broken or damaged skin, direct contact)
Venereal transmission
Vector transmission
Faecal-oral route
Where does FMD virus replication occur?
Pharyngeal mucosa and draining lymph nodes
The GIT
The LRT
Which is the amplifier host for FMD infection?
Birds
Cattle
Sheep
Goats
Horses
Pigs
What is important in the epidemics of FMD?
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
How many serotypes of FMD are there?
7
3
4
2
9
What are outbreaks of FMD associated with?
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
Where can FMD remain infective?
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
FMD is clinically indistinguishable from other vesicular diseases of livestock
How is FMD controlled in FMD endemic countries?
Eradication campaign with blanket vaccination
Ring vaccination, +/- slaughter, blanket vaccination
Serological test & slaughter (positive and in contact animals)
How is FMD controlled in FMD free countries if an outbreak were to occur?
Which of the below are clinically indistinguishable from FMD?
Vesicular exanthema of swine
Swine Vesicular Disease
Swine influenza
Swine coronavirus
Equine rhinitis A virus is?
An upper respiratory tract disease in horses
A reproductive disease in horses
A GIT disease in horses
A lower respiratory tract disease in horses
Encephalomyocarditis virus is a disease of what species?
Swine
Porcine encephalomyelitis (Porcine enterovirus 1) is an important exotic disease of pigs causing?
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
How long can Porcine encephalomyelitis (Porcine enterovirus 1) survive in the environment?
4 weeks
3 days
6 months
2 weeks
4 months
Porcine encephalomyelitis (Porcine enterovirus 1) is highly contagious, how is it transmitted?
Faecal – oral route of transmission
Respiratory droplets
Vertical transmission
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