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DVM2 > Virology > Flashcards

Virology Flashcards

1
Q

What are the normal routes of transmission for poxviruses?

A

Aerosol droplets
Mechanical transmission by arthropod vector (not an arbovirus!!)
Contact

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2
Q

How are poxviruses usually diagnosed?

A

On the basis of clinical signs

If needed, electron microscopy and histopathology

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3
Q

African swine fever is the only member of what family? It is the only DNA virus that….?

A

Asfarviridae

Can be regarded as an arbovirus

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4
Q

How is African swine fever (family: asfarviridae) transmitted?

A

By soft ticks (ornithodoros). Ticks become infected when they feed off viraemic warthogs. Infection within the tick population is by sexual, transovarial and transstadial transmission.

Infection is also transmitted from pig to pig by contact and aerosol

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5
Q

Is African Swine Fever single or double stranded rna/DNA?

A

ds DNA

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6
Q

Are viruses of Reoviridae enveloped or not? What important diseases of this family did we learn about?

A

Non-enveloped

Genus orbivirus:
African horse sickness
Bluetongue virus

Genus rotavirus (general)

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7
Q

What is the general pathogenesisof orbiviruses (family reoviridae)?

A

Transmitted via a blood feeding insect-> primary replication in regional lymph nodes-> spread to the spleen, thymus and other lymph nodes-> viral replication in endothelial cells-> endothelial cell damage and vascular injury -> capillary leakage, haemorrhage and intravascular coagulopathies

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8
Q

What is Bluetongue and what animals does it effect? What vector is important for its transmission?

A

A non-contagious disease (orbivirus) of sheep, cattle, goats and deer which is spread by biting insects (culicoides midges)

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9
Q

What are some characteristic signs of bluetongue? Which animals are most severely affected and what is the incubation period?

A

Fever
Hyperaemia
Vascular congestion
Oedema

Sheep (and deer)

Up to 10 days

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10
Q

What is the outcome for sheep with Bluetongue?

A

Most recover although convalescence is prolonged.

Foetal death, abortions etc may arise if pregnant ewes are infected

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11
Q

Describe briefly the epidemiology of Bluetongue.

A

Dependent on host-agent-environment interactions. Outbreaks are most commonly seen in late summer (in tropical and sub tropical climates) when the density of culicoides is greatest (warm conditions with high humidity).

The female midge remains infected for life!

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12
Q

How is Bluetongue diagnosed? How might it be controlled?

A

On basis of clinical signs.
Can use PCR, ELISAs etc.

Vaccinations in endemic countries (but these need to be polyvalent to enable cross-protection between serotypes).
Larvicides?

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13
Q

Where is African horse sickness endemic? What is the incubation period?
What is the main vector species?

A

Tropical and subtropical Africa
Up to 7 days
Culicoides imicola

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14
Q

What are the four clinically recognised forms of African Horse Sickness?

A
  1. Pulmonary form= peracute, high fever, depression, nasal discharge, severe respiratory distress, dyspnoea, coughing, pulmonary oedema and pleaural effusion (predominant feature). More than 95% affected will die.
  2. Cardiac form= subacute, fever, conjunctivitis, abdominal pain and progressive dyspnoea. Subcut oedema of head and neck (supraorbital fossa, palpebral conjuncytiva and intermandibular space). Hydropericardium is a consistent PM finding
  3. Mild= seen in zebras and donkeys. Low grade fever with occasional clinical signs such as congested mucous membranes.
  4. Mixed= signs of both pulmonary and cardiac form. Diagnosed at PM
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15
Q

What are reservoir hosts for African Horse Sickness?

A

Zebras (donkeys and mules may also play a role)

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16
Q

How might African Horse Sickness be controlled?

A

Movement restriction, quarantine, vector control (insect screens, pesticides). Vaccines are available

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17
Q

Are rotaviruses enveloped or not? What do they cause and in what animals?

A

Non-enveloped. Cause serious diarrhoea in intensively raised do,enticing animals worldwide. Particularly calves and foals

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18
Q

Rotaviruses:
What is their incubation period?
What is their pathogenesis?

A

Less than 24 hours

Faeco-oral route. Viruses passes through stomach and infects enterocytes at apical tips of villi➡️ villi shortening/fusion, inflammatory cell infiltration and viral replication.

Infected cells lyse and are replaced by immature cuboidal cells which have decreased absorptive capacity and surface area. This leads to osmotic diarrhoea and increased undigested disaccharides in intestinal lumen

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19
Q

How is NSP4 important in rotavirus infections?

A

Enterotoxin that causes inflammatory and secretory diarrhoea

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20
Q

What are some clinical signs of rotavirus infection?

A

Depression, anorexia, light-coloured semi-liquid faeces

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21
Q

Why is isolation of rotavirus not a common diagnostic method?
Why is vaccination of neonates problematic?

A

Because they are difficult to grow in cell culture.

Bc gut immunity is needed which requires oral exposure
Live oral vaccines are neutralised by maternal antibodies. Therefore should vaccinate dam to increase lactogenic immunity

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22
Q

What are the three forms of equine encephalitis virus (family togaviridae)? What are the reservoir hosts and which form is most severe?

A

Eastern>Venezuelan>Western

Passerines are reservoirs

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23
Q

What are some clinical signs associated with equine encephalitis?

A

Photophobia, inability to swallow, low carriage of the head, depression, blindness, wide base stance…

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24
Q

What is the vector species responsible for spread of eastern equine encephalitis? How about for western and Venezuelan?

A

Eastern= culiseta melanura (ornithophilic) mosquitoes transmit it between birds. Aedes transmit it from birds to mammals.
Venezuelan and wester= culex spp.

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25
Q

What is the incubation period for bovine coronavirus? How is it maintained in a population? What may it cause in adults?

A

1-2 days
Affects 3-21 day old calves
Most adults are seropositive therefore maintained endemically
May. Cause winter dysentery in adults.

26
Q

How does infectious bronchitis virus of fowl cause disease?

A

Aerosol and faeco-oral route. Primary virus replication is in lungs and trachea. It then causes viraemia and replicates in lymphoid tissue, ovaries, oviducts and kidneys.

27
Q

Are coronaviruses enveloped? How do they bond to host cells?

A

Yep!

Bind via S protein (determines target cell specificity). It’s cleaved during infection

28
Q

What is the incubation period for transmissible gastroenteritis virus in pigs? What about the pathogenically similar porcine epidemic diarrhoea virus?

A

28-72hrs

Longer in PEDV

29
Q

For equine encephalitides (family togaviridae) how long may the incubation be? How is the virus transmitted?

A

Up to 9 days

By mosquitoes

30
Q

West Nile virus is an arbovirus transmitted by ________ species of mosquitoes. Amplifying hosts include ________ which is important because_________. Dead end or incidental hosts include _________.

A

Culex
Birds
Because it allows migratory birds to move the virus long distances
Horses and humans (and other mammals)

31
Q

Japanese encephalitis virus is the most important cause of viral encephalitis in what parts of the world?
Reservoir hosts include __________. Amplifying hosts of the disease include _________ whilst dead end or incidental hosts include __________.

A

Eastern and Southern Asia
Water birds
Pigs
Humans and horses

32
Q

Bovine viral diarrhoea virus (family flavivirus genus pestivirus) causes two forms of disease including:

a) ___
b) ___ (most severe)

Which animals may serve as reservoir hosts?

A

Acute (diarrhoea)
Chronic (mucosal disease)

Sheep, deer and pigs

33
Q

Describe how transplacental spread of bovine viral diarrhoea virus may affect the foetus.

A

If infected early in gestation (ie. <80days old) then the foetus May be aborted, be mummified, die or be resorbed.

If infected between 80 and 125 days old, effects will differ depending on the strain. A cytopathic strain will cause foetal lesions or weak/dead calves. A non-cytopathic strain will lead to tolerance and recognition of the virus as self. These animals will be infected for life.

If infected late (after 125 days) the foetus will mount an active immune response with Ab production

34
Q

What are the clinical signs of classical swine fever and how may it be transmitted? Why has it been hard to eradicate in Europe?

A

We see:

  • fever
  • leukopenia
  • diarrhoea
  • depression
  • conjunctivitis
  • paralysis, convulsions, death

Contact between pigs. Also persists in long time in frozen meat so can be transmitted via swill feeding.

Wild boar appear to be an ongoing source of infection for domestic pigs

35
Q

What is the impact of equine viral arteritis virus? How is it spread?

A

It occurs worldwide but most infections are asymptomatic. In some outbreaks we will see abortions, infections in foals leading to interstitial pneumonia or enteritis, leukopenia in adults, as well as ventral limb oedema and urticaria.

Spread horizontally by respiratory and venereal routes, as well as vertically across the placenta

36
Q

With what disease could we see cyanosis ears and vulva in pigs?
What is the significance of this disease? How is it transmitted and why is this particularly important? How is it shed?

A

Porcine respiratory and reproductive syndrome
Causes reproductive failure and inappetance (decrease growth rate)
Respiratory route (it has a tropism for alveolar macrophages). Important because airborne transmission can allow infection across farms. Airborne spread has been recorded for up 3km
Shed in semen, urine, saliva and faeces

37
Q

What family does infectious bursa disease belong to? What is it’s pathogenesis?

What is it’s morbidity and mortality like?

What does it cause?

A

Birnaviridae
Contracted via oral route. Virus replicates in m@crophages and gut-associated lymphoid tissue. It then causes viraemia via the portal circulation and enters the bursa of fabricious. Here it replicates again ing a secondary viraemia and infecting other tissues. It is shed in faeces.

100% morbidity 20-30% mortality.

Causes depression, diarrhoea, anorexia, ruffled feathers. Also causes permanent immunosuppressive due to destruction of part of B-cell repertoire.

38
Q

Feline Calicivirus:
How is it spread?
What does it cause?
What is it’s incubation period?

A

Respiratory tract (aerosols) or contact with forties or contaminated handlers.

Fever, anorexia, conjunctivitis, rhinitis, tracheitis, pneumonia, vesiculation/ulceration of tongue and oral mucosa, shifting lameness

5 days

39
Q

Why is vaccination against feline calicivirus an “imperfect solution”?

A

Because although there is only one serotype, there is extensive antigenic heterogeneity among virus strains.

40
Q

Rabbit haemorrhaging disease virus (calicivirus) leads to sudden death after 6-24 hours. How? In what age group is it seen?

A

Infections occurs via faeco-oral route. Virus replicates in mononuclear phagocytic cells and leads to acute hepatic necrosis and disseminated intravascular dissemination.
Seen in rabbits over 2 months of age

*Use inactivated vaccine to control

41
Q

Why is diagnosis of vesicular exantema of swine particularly important?
How may it be avoided?
What does it cause?
What are possible reservoir hosts?

A

Bc it’s clinically indistinguishable from foot and mouth disease.

Don’t feed swill

Acute febrile disease with vesicles on snout, tongue, oral cavity, feet and teats. +/- encephalitis, myocarditis and diarrhoea.

Marine mammals

42
Q

What is important about the structure of paramyxoviruses?

A

The envelope is covered in 2 major glycoprotein peplomers:
Haemagglutinin and neuraminidase.
Protective Abs are directed against these peplomers as well as against the Fusion (F) protein. Cleavage of the F protein is essential for infectivity.

43
Q

What is Newcastle disease and what is it’s pathogenesis?

A

A highly contagious disease of chickens (and other galliformes) that varies in its clinical presentation depending on the strain infectivity.

It is contracted by inhalation of aerosols or ingestion. The virus replicates in the epithelium of the GIT and respiratory tract leading to a viraemia. It spreads to spleen and bone marrow where it undergoes further replication before causing a secondary viraemia. It then spreads to the lungs and CNS.

44
Q

How do the different isolates of Newcastle disease differ in their disease presentation?

A
  1. Viscerotropic velogenic isolates: 90-100% mortality. Sudden. Depression, increased resp rate, anorexia, prostration, bright green diarrhoea, haemorrhaging intestinal lesions
  2. Neurotrophic velogenic isolates: 10-20% mortality. Tachypnoea, gasping, takes, oedema, tremors, paralysis, torticollis
  3. Mesogenic isolates: 10% mortality (young birds). Coughing, weight loss, decreased egg production. +/- neurological signs.
  4. Lentogenic strains: mainly subclinical. +/- mild resp signs and decreased egg production
45
Q

What factors of rinderpest virus made it able to be eradicated?

A 
It only had 1 serotype
1 vaccine confers lifelong immunity
There were no carriers of the disease and no reservoir host
Had good diagnostic tests
Were able to control movement
46
Q

What is Peste de Petit Ruminant virus?

A

A paramyxovirus of small ruminants that is closely related to rinderpest. (Presumably causes similar disease i.e. pyre is, infl and necrosis of mm, profuse haemorrhaging diarrhoea).

47
Q

What is arguably the most important viral disease of dogs? What is it’s pathogenesis?

A

Canine distemper virus (paramyxovirus).

Contracted by inhalation. Replicates in URT or conjunctiva then subsequently in the lymph nodes. Causes a viraemia and is carried in lymphocytes to the reticuloendothelial system. Causes secondary viraemia and then localises in mucosal epithelium of GIT and resp tract and CNS. Causes interstitial pneumonia, gastroenteritis and immunosuppression

48
Q

What are the two chronic sequelae of canine distemper?

A

Progressive loss of neurological function

Hyperkeratosis of foot pads and nose

49
Q

How is distemper best diagnosed?

A

Virus is difficult to isolate in cell culture so Immunohistochemistry is best to show Ag in impression smears of the conjunctiva or peripheral blood lymphocytes.

50
Q

What is a Nipah virus?

A

Virus closely related to Hendra that causes encephalitis in humans. Also spread by bats.

51
Q

What is winter dysentery?

A

A sporadic, acute disease of adult housed cattle. Clinical signs include explosive, often bloody diarrhoea, accompanied by reduced milk production, depression and anorexia.

Can be caused by bovine coronavirus

Some animals may also show respiratory signs such as nasolacrimal discharge and coughing.

52
Q

Describe the pathogenesis of bovine coronavirus.

A

Similar to rotavirus enteritis. Transmission via face oral route. Replicates in villous enterocytes in the small intestine and colon and causes cell lysis. Leads to decreased absorptive area and capacity. Osmotic diarrhoea results. Crypto cells are not affected.

53
Q

What is transmissible gastroenteritis virus and why is it of importance?

A

Porcine coronavirus. Highly contagious.

Causes high mortalities in newborn piglets, there is no effective or practical treatment, and available vaccines aren’t very effective. High level biosecurity is needed to prevent entry

54
Q

How can the association between age and severity of disease be explained for transmissible gastroenteritis virus?

A

Slower rate of replacement of enterocytes in newborns as well as specialisation of villous absorptive cells in newborns that are not present in adults

55
Q

How is porcine respiratory coronavirus related to transmissa Le gastroenteritis virus?

A

PRCoV is a deletion mutant of TGEV that infects respiratory epithelial cells and alveolar macrophages. The deletion occurs in the S (spike) protein.

56
Q

Why is the agent that causes scrapie unusual? (8)

A 
No nucleic acid identified
Too small to encode a protein
No vision-like structures
Highly resistant to inactivation
Infectivity destroyed by protein disruption
Infectivity is lipid associated
Filterable
Scrapie associated fibrils
57
Q

Why are transmissible spongiform encephalopathies unusual?

A

Long incubation period
No apparent immune response
No apparent inflammatory response
Adapts to host species
Incubation period decreases with increased dose
Strain characteristics
Influenced by a single gene (encodes PrP protein in scrapie associated fibrils)

58
Q

What is the incubation period and pathogenesis of rabies?

A

14-90 days
Bite from rabid animal-viral rep in muscle tissue-binds to Ach receptors at NMJ-travels up peripheral nerves to CNS (retrograde axonal transport)-viral rep in neurones-continued spread in CNS- shed in saliva

59
Q

What clinical signs might we see with rabies?

A

Initially we might see a change in behaviour:
Infection of limbic system leads to reduced cortical control of behaviour leading to furious rabies. Infection of neocortex leads to decreased CNS function presenting as Dumb rabies.

In late stage we might see convulsions, coma, respiratory arrest and death.

60
Q

What is 3 day sickness?

How is it transmitted and what clinical signs might we expect?

A

Bovine ephemeral fever

Transmitted by culicoides and mosquitoes.

Sudden fever, decreased milk yield, depression, lameness and stiffness, reluctance to stand. Neutrophilia and polyserositis

61
Q

Tell me about Akabane.

A

It’s a bunyavirus that affects ruminants. It is an arbovirus transmitted by culicoides brevitarsis.

If an unexposed dam is bitten by an infected midge, it will cross the placenta and infect foetus. No signs are seen in the dam. Clinical signs in foetus depend on gestational stage. (Developing brain- hydrancephaly, spinal cord- failure of motor neurone development and impaired muscle development- arthrogryposis)

DVM2 (13 decks)

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