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Virology > Viruses > Flashcards

Viruses Flashcards

1
Q

Describe the generalised pathology of poxviruses

A
  • cytoplasmic inclusion bodies
  • pustular lesions in mammals
  • proliferative lesions in birds
  • sometimes with generalised disease
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2
Q

Briefly describe the importance of smallpox

A
  • First disease to be innoculated against (using cowpox)
  • First disease for vaccine development (using vaccinia)
  • First disease to be globally eradicated (1977)
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3
Q

Why was eradication against smallpox possible?

A

Production of a highly immunogenic (efficacious) vaccine

Vaccine was heat-stable and easy to store and distribute

There was only one serotype of the virus (not rapidly evolving)

No persistent infection → death, or recovery + cessation of shedding

International and interpersonal cooperation (no anti-vaxxers)

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4
Q

Discuss important factors about vaccina

A
  • used in smallpox vaccinations
  • ability to affect a wide host range (cattle, horses, pigs)
  • appears to have become established in buffalo (buffalopox)
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5
Q

Describe the pathology of buffalopox

A
  • lesions on teats and udders of buffalo
  • rarely, severe generalised disease in calves
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6
Q

Describe the host range for cowpox

A

Reservoir hosts: rodents

Infects cows, people, cats, zoo animals

Probably exotic to Australia

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7
Q

Describe the pathology of cowpox in cows

A

Pox leasions on the teats of cows

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8
Q

Describe the pathology of cowpox in cats

A

Esp immunosuppressed cats.

  • widespread skin lesions
  • occassional severe disease

+/- pneumonia and 2ndary bacterial infection

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9
Q

Describe the pathology of sheeppox/goatpox

A

Severe, systemic disease

High case fatality rate

Widely distributed cutaneous pox lesions including nodules on skin, mouth, trachea

Consolidated areas in lungs

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10
Q

Describe the control of sheeppox/goatpox

A

Live attenuated and inactivated vaccines in endemic countries

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11
Q

Describe the host range of lumpy skin disease

A

Cattle, buffalo

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12
Q

Is lumpy skin disease endemic to Australia?

A

No - Africa, Middle East, Eastern Europe

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13
Q

Describe the pathology of lumpy skin disease

A

Widespread cutaneous pox lesions - may become necrotic

Generalised infection

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14
Q

What family of viruses does lumpy skin disease belong to?

A

Poxviridae

related to sheeppox

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15
Q

What family of viruses does scabby mouth belong to?

A

Parapox viruses

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16
Q

Describe the host range of Scabby Mouth disease

A

Sheep

Zoonotic = “Orf” (self-limiting, human -> human transmission)

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17
Q

Describe the pathology of scabby mouth

A

Pox lesions on mouth, muzzles and udders of sheep

Severe disease in lambs, impairs feeding

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18
Q

Describe the diagnosis of scabby mouth

A

EM diagnosis

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19
Q

Describe the control of scabby mouth

A

LIVE vaccine - scarified on inner thigh or shoulder of sheep. Only does not produce disease due to the location of vaccination

Spread by fomites that penetrate the skin around the mouth or teats

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20
Q

What familiy does pseudocowpox/papular stomitis belong to?

A

Parapox

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21
Q

Describe the host range of pseudocowpox/papular stomatitis

A

Cows

zoonotic = “milkers nodule” (by contact)

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22
Q

Describe the pathology of pseudocowpox/papular stomitis

A

Pseudocowpox = teat lesions

Predispostion to mastitis

Papular stomatitis = mouth lesions

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23
Q

Describe the transmission of pigpox

A

Direct contact; associated with lice

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24
Q

Describe the pathology of pigpox

A

Widespread cutaneous lesions, especially young pigs

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25
Q

Describe the host range of myxoma virus

A

Myxamatosis

Wild rabbits in Americas = mild disease

European rabbits = generalised disease

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26
Q

Describe the transmission of the myxoma virus

A

Mechanical transmission by insect vectors

Released as a form of population control

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27
Q

Describe the control of myxoma virus

A

Attenuated myxoma vaccine

Vaccination with rabbit fibroma virus

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28
Q

Describe the pathology of myxoma virus

A

Conjunctivitis

Gelatinous swellings

Severe generalised disease

No typical pox lesions

(Localised benign fibroma in American wild rabbits)

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29
Q

Which family of viruses does myxoma belong to?

A

Poxviridae

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30
Q

Describe the host range of fowlpox

A

Chickens

(Most bird species have their own pox virus, e.g. pidgeonpox, turkeypox)

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31
Q

Describe the transmission of fowlpox

A

mechanical transmission by insects

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32
Q

Describe the pathology of fowlpox

A

Severe disease with proliferative lesions in young birds

Pox lesions on comb, wattle, feet, vent, +/- respiratory tract

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33
Q

Describe the control of fowlpox

A

Attenuted fowlpox or pigeonpox vaccines

Vector control

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34
Q

Describe the pathology of human adenoviruses

A

Upper respiratory tract infection

Conjunctivitis

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35
Q

Describe the pathology of bovine adenoviruses

A

Some serotypes: Upper respiratory tract infections; pneumonia

Some serotypes: keratoconjunctivitis

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36
Q

Describe the pathology of porcine adenoviruses

A

Some can cause respiratory disease (experimental innoculation)

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37
Q

Describe the pathology of equine adenoviruses

A

Subclinical or mild respiratory disease

Severe disease in young Arab SCID foals: fatal pneumonia

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38
Q

Describe the pathology of avian adenoviruses

A

Most apathogenic.

Respriatory disease (may resemble mild infectious laryngeotrachetis)

Decreased egg production

Immunosuppressed birds (infectious bursal disease): 
Inclusion body hepatitis, moderate mortality \<10% in 5-10w.o chicks

Haemmorhagic enteritis in turkeys

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39
Q

What family of viruses does infectious canine hepatitis virus belong to?

A

Adenovirus

(Canine adenovirus 1)

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40
Q

Describe the host range of infectious canine hepatitis

A

Dogs, foxes

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41
Q

Describe the pathology of infectious canine hepatitis in foxes

A

Encephalitis

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42
Q

Describe the pathology of infectious canine hepatitis in dogs

A
  • hepatitis/hepatic necrosis
  • upper respiratory tract infection
  • chronic interstitial & glomerulo- nephritis
  • vascular damage, petechial haemorrhage, oedma
  • “blue eye” = corneal odema (AB-AG complexes)
  • inclusion bodies

Mortality may reach 100%

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43
Q

Describe the detection of the canine infectious hepatitis virus

A
  • present in secretions during acute phase
  • present in urine > 6 months
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44
Q

Describe the transmission of canine infectious hepatitis

A
  • shed in urine >6m (and secretions, acute phase)
  • persists in environment at least a week

Close contact and possible ingestion usual method of infection

Rarely, aerosols (respiratory disase)

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45
Q

Describe the control of infectious canine hepatitis

A
  • attenuated canine adenovirus 2 vaccine
  • inactivated canine adenovirus 1 vaccine
  • immunity is cross-protective
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46
Q

Describe the pathology of canine infectious laryngotracheitis

A

Mild respiratory disease

+/- fatal bronchopneumonia

Role in Kennel Cough

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47
Q

Describe the replication of papillomaviruses

A
  • Virus gains entry to basal cells (stratum basale) - only DNA present
  • causes proliferation of intermediate cell layers (stratum granulosum) -> papilloma lesions (“warts”)
  • virus particles shed in exfoliated keratinised cells (stratum corneum)
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48
Q

Describe the pathology of human papillomaviruses

A

Most benign

Some associated with carcinomas (cervical, laryngeal, skin)

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49
Q

Describe the pathology of equine papillomavirus

A

Papillomas on nose and face of young horses

Spontaneous regression with immunity

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50
Q

Describe the pathology of canine papillomaviruses

A

Oral papallomas. Usually benign, some evidence of neoplastic transformation

Also on feet of greyhounds

Spontaneous regression

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51
Q

Describe the pathology of ovine papillomas

A

Lesions most common on ears, face, vulva. May undergo neoplastic transformation

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52
Q

Describe the pathology of caprine papillomas

A

Lesions usually on udder, genital skin. Some neoplastic transformation

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53
Q

Describe the pathology of bovine papillomas in cattle

A

1,2,3,5,6: cutaneous papillomas, may be extensive and coalescing (esp young animals)

Papillomas on penis of bulls

5, 6: Papillomas and fibropapillomas on teats of cows

4: Papillomas of alimentary tract

Neoplastic transformation associated with grazing brachenfern

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54
Q

Describe the pathology of bovine papilloma in horses

A

Equine sarcoids

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55
Q

Describe the control of papillomaviruses

A

Inactivated autogenous vaccines

But spontaneous regression common, so difficult to evaluate worth

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56
Q

Describe the host range of feline panleucopenia virus

A
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57
Q

Describe the transmission of feline panleucopenia virus

A

Infection possible via any route, especially ingestion

Virus in blood in acute phase, may be spread by biting insects

Virus excreted in urine, faeces, saliva, and in utero for many months

Highly contagious

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58
Q

Describe the pathology of panleucopenia virus

A

Affinity for rapidly dividing cells (foetal, GIT, bone marrow)

enteritis, diarrhoea, leucopenia

Foetal death/cerebellar hypoplasia

Secondary bacterial infection probably important in pathogenesis

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59
Q

Describe the control of feline panleucopenia virus

A

Attenuated and inactivated vaccines

Attenuated vaccines should not be used on pregnant cats

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60
Q

Describe the pathology of canine parvovirus

A

severe haemorrhagic enteritis, leucopenia, (myocarditis)

especially young dogs

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61
Q

Describe the transmission of canine parvovirus

A

Transmission via fecal-oral route

Shed for 1-2 weeks

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62
Q

Is canine parvovirus a good candidate for eradication? Why/why not?

A

No

  • Virus extremely resistant in environment, including to a range of pH, temperatures
  • Virus shed in very large quantities
  • Low infective dose (only a few virus particles needed for infection)
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63
Q

Describe the diagnosis of canine parvovirus

A

Tentative diagnosis based on clinical signs

Rapid, commercially available serological tests to confirm presence of antigen (robust, due to large number of viral particles shed)

PCR limited availability

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64
Q

Describe the control of canine parvovirus

A

Attenuated or inactivated vaccines

Inactivated vaccine used in pregnant bitches

Cross-react between subtypes, strongly immunogenic -> solid immunity

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65
Q

Describe the pathology of porcine parvovirus

A

Not pathenogenic for young or adult pigs

Spread across placenta, variety of breeding abnormalities: death, mummifcation, malformation, stilllbirths

Disease occurs in gilts seronegative at the time of first mating

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66
Q

Describe the diagnosis of porcine parvovirus

A

Antigen detection in foetal tissue

(Antibody detection of little value because disease is widespread)

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67
Q

Describe the control of porcine parvovirus

A

Attenuated and inactivated vaccines

Gilts can be purposely infected prior to pregnancy

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68
Q

What family does psittacine beak and feather disease belong to?

A

Circoviridae

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69
Q

Describe the pathology of psittacine beak and feather disease

A

In parrots: species variability

Cockatoos suceptible, lorikeets resistant

abonormalities of feathering, beak and feet

hepatitis

diarrhoea

immunosuppression

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70
Q

What family does chicken anaemia virus belong to?

A

Circoviridae

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71
Q

Describe the transmission of chicken anaemia virus

A

Horizontal and vertical transmission

Breeders infected during lay produce infected eggs for ~6 weeks

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72
Q

Describe the pathology of chicken anaemia virus

A

Vertically infected chicks become diseased at about 10 days old

~60% mortality

Stunted growth, anemia, immunosuppression

Secondary skin infections, especially fungal

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73
Q

Describe the control of chicken anaemia virus

A

Virulent vaccine in drinking water

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74
Q

Describe the pathology of porcine circovirus 1

A

apathogenic

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75
Q

Describe the pathology of porcine circovirus 2

A

Post-weaning multisystemic wasting syndrome (~6w.o)

Case fatality 10%

Respiratory disease

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76
Q

Describe the control of porcine circovirus 2

A

Good husbandry (environmental factors important in pathogenesis)

Removal of affected animals

Elimination of infectious agents

PCV2 vaccine

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77
Q

Describe the pathology of canine circovirus

A

Recently discovered in dogs in the US

vasculitis, histocytic inflamation, thrombocytopenia

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78
Q

Describe the transmission of herpesviruses

A

Close contact, venerial, short-distance droplets in production systems

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79
Q

Describe the resistance of herpesvirus in the environment

A

relatively fragile

Except Mareks, very resistant

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80
Q

Describe the clinical pattern of infection in herpesviruses

A

Characteristically produce latent infections

Virus undergoes retrograde transport along peripheral nerves to ganglia

During latent phase, viral DNA is found in the ganglia

Factors (e.g. stress, fever, UV, corticosteroid therapy) trigger the reactivation of the virus, which undergoes anterograde transport along peripheral nerves

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81
Q

Are herpesviruses good candidates for eradication? Why/why not?

A

Yes

  • can screen population using antibody detection tests (relatively cheap)
  • remove carriers (AB+)
  • fragile virus with no long-term environmental reservoirs
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82
Q

What family does infectious bovine rhinotracheitis belong to?

A

Herpesvirdiae

(Bovine herpesvirus 1)

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83
Q

Describe the pathology of infectious bovine rhinotracheitis

A

respiratory disease

conjunctivitis

genital disease (infectious pustular vulvovaginitis)

Exotic strain causes abortion

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84
Q

Describe the aetiology of bovine respiratory disease

A

Multifactorial

Pathogen exposure to >4 viruses and >3 bacteria

Bovine herpesvirus 1
Bovine viral diarrhoea virus
Bovine respiratory syncytial virus
Bovine coronavirus
Bovine adenovirus
Bovine parainfluenza virus 3

Environmental factors
Stress, climate, transport, food, density, etc
Peak incidence of disease 21 days after being moved to a new feedlot

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85
Q

Describe control of infectious bovine rhinotracheitis

A
  • live attenuated bovine herpesvirus 1 vaccine
  • detection and removal of infected animals
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86
Q

Describe the pathology of bovine herpesvirus 5

A

fatal neurological disease in calves

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87
Q

Describe the pathology of bovine herpes mamillitis

A

(Bovine herpesvirus 2)

Vesicles on teats and udder

predispostion to mastitis

loss of production

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88
Q

Describe the pathology of malignant catarrhal fever

A
  • generalised disease, invariably fatal
  • erosive lesions of GIT
  • respiratory lesions
  • mucopurulent naso-occular discharge
  • lymphoproliferation and lymphocyte infiltration
  • vasculitis
  • corneal opacity
  • neurological sins
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89
Q

Describe the epidemiology of malignant catarrhal fever

A

Carried asymptomatically by wildebeast and sheep

Sporadic transmission to cattle, deer via contact or infected pastures

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90
Q

Describe the diagnosis of malignant catarrhal fever

A

PCR

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91
Q

Describe the control of malignant catarrhal fever

A

No vaccine available

Control contact with wildbeast/sheep/infected pasture?

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92
Q

Which herpesviruses are exotic to Australia?

A

Type 1.1 and 1.2a Infectious bovine rhinotracheitis (Type 2b endemic)

Porcine herpesvirus 1 (Aujeszky’s disease)

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93
Q

Which family does Aujeszky’s disease belong to?

A

Herpeviridae

(Porcine herpesvirus 1)

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94
Q

Describe the pathology of Porcine herpesvirus 1 in pigs

A
  • subclinical/mild respiratory disease in adult pigs
  • abortion
  • generalised fatal disease in piglets (100% mortality)
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95
Q

Describe the pathology of porcine herpesvirus 1 in non-pig hosts

A

fatal meningioencephaltis and pruritis in sheep, cattle, dogs, cats (pseudorabies, “mad itch”)

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96
Q

What family of viruses does equine coital exanthema belong to?

A

Herpeviridiae

(Equine herpesvirus 3)

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97
Q

Describe the pathology of equine coital exanthema

A

Ulcerative lesions on penis/vulva

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98
Q

Which family does equine rhinopneumatitis virus belong to?

A

Herpeviridae

(Equine herpesvirus 4)

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99
Q

Describe the pathology of equine rhinopneumatitis virus

A

respiratory disease, especially in young foals

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100
Q

Which family does equine abortion virus belong to?

A

Herpeviridae

(Equine herpesvirus 1)

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101
Q

Describe the pathology of equine abortion virus

A

abortion

respiratory disease

fatal generalised disease in neonates

encephalomyelitis

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102
Q

Describe the control of equine abortion virus

A

Killed/recombinant vaccine

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103
Q

Describe the pathology of equine cytomegaloviruses

A

Mostly apathogenic

possible immunosuppression

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104
Q

Which family does feline rhinotracheitis virus belong to?

A

Herpeviridae

(Feline herpesvirus 1)

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105
Q

Describe the pathology of feline rhinotracheitis virus

A

upper respiratory tract disease

responsible for 40% of cat flu

rhinitis

oculo-nasal discharge

inappetance

confjunctivitis

keratatis

+/- secondary bacterial pneumonia

generalised disease in neonates

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106
Q

Describe the control of feline rhinotracheitis virus

A

Live attenuated vaccine

not 100% protective

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107
Q

Describe the treatment of feline rhinotracheitis virus

A

management of clincal signs

reduce stress

prevent/treat secondary bacterial infections

nucleotide analogues (famcyclovir)

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108
Q

Describe the pathology of elephant endotheliotropic herpesvirus

A

1&2: fatal disease in young (1-7 y.o)

lethargy and inappetance

death may occur <24 hours

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109
Q

Describe the pathology of canine herpesvirus 1

A

generalised, severe disease in neonatal pups (fading puppy syndrome)

multifocal necrosis in multiple organs

can die in 24-48 hours

Unlikely after 4w.o -> mature thermoregulation

occasional vesicular lesions on external genetalia of adults

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110
Q

Describe the pathology of infectious laryngeotracheitis virus

A

In chickens, esp 4-18m.o

respiratory tract disease (coughing, sneezing, naso-ocular discharge, dyspnoea, haemorrhagic trachetis)

up to 70% mortality

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111
Q

Describe the control of infectious laryngeotracheitis virus

A

Live attenuated vaccine

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112
Q

What family does infectious laryngeotracheitis belong to, and what species does it affect?

A

Herpeviridae

Chickens

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113
Q

Describe the pathology of Marek’s disease 1

A

esp. 12-24w.o

neoplastic transformation of T cells

lympho-proliferative lesions

tumours in nerve tissue, spleen, liver

neurological signs

paresis/paralysis

high case fatality

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114
Q

Describe the pathology of Mareks Disease 2

A

Non-pathogenic in chickens

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115
Q

Describe the pathology of Mareks Disease virus 3

A

Non-pathogenic herpesvirus in turkeys

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116
Q

Describe the control of Mareks disease

A

Cross-protective

attentuated Mareks disease vaccine or turkey herpesvirus

Imperfect (“leaky”) vaccine -> evolution of virulence

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117
Q

Describe the transmission of Mareks disease

A

Shedd in of enveloped, infectious particles from feather follicles into environment

Highly resistant in environment

Infection via inhalation

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118
Q

Describe the pathology of herpes simplex 1

A

stomatitis, cold sores

occasional encephalitis

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119
Q

Describe the pathology of herpes simplex 2

A

genital lesions

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120
Q

Describe the pathology of Epstein Barr virus

A

infectious mononucleosis (glandular fever)

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121
Q

Describe the pathology of varicella zoster

A

Chickenpox (initial infection)

Shingles (recurring infection)

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122
Q

Describe the host range of Aujeszky’s disease

A

Rodents, pigs

Dead-end hosts: sheept, cattle, cats, dogs

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123
Q

Describe the transmission of Aujeszky’s disease

A

Pigs infected through oral and nasal mucosa

Excrete virus for ~13 weeks

Other animals infected through abrasions in skin, contact with infected pigs or rats

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124
Q

Describe the control of Aujeszky’s virus

A

Attenutated vaccine

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125
Q

Discuss the transmission of retroviruses

A

Very fragile in environment, transmission by close contact with body fluids

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126
Q

Describe the clincial timecourse of retroviruses

A

Produce persistent, progressive lifelong infections

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127
Q

Describe the diagnosis of retroviruses

A

Detection of antibodies

Virus not detectable until ~disease period

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128
Q

Describe the mechanisms of oncogenic retroviruses

A
  1. possess viral oncogene -> rapid oncogenesis
    replication deficient virus requires “helper virus” for replication
  2. affect cellular oncogene -> slow oncogenesis
    e. g. activation or increased transcription of cellular oncogenes if inserted in genome near an oncogene (occurs by chance)
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129
Q

What family does avian lymphoid leucosis belong to?

A

Retroviruses (oncovirus)

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130
Q

Describe transmission of avian lymphoid leucosis

A
  • horizontal or vertical

Vertical: chick is persistently viremic but antibody negative
Sporadic development of tumours > 4mo

Horizontal: adults mount immune response, clear tumour. EXCEPTION to lifelong infection

Horizonally infected chicks may become carriers

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131
Q

Describe the control of avian lymphoid leucosis

A

Genetic resistance

Avian leucosis-free flocks

No vaccine available

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132
Q

Compare and contrast avian lymphoid leucosis with Marek’s disease

A
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133
Q

Which family does feline leukaemia virus belong to?

A

Retrovirus (oncovirus)

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134
Q

Discuss the prognosis of feline leukaemia virus

A

Depends on age and dose

Older cats: usually clear infection (immune response)

Young cats: persistent viremea, development of clinical signs, Px 2-3 years

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135
Q

Discuss the pathology of feline leukaemia virus

A

Older cats: clinically unaffected

Persistently viremic (esp young) cats: (FeLV-A + …)

  • *FeLV-B**
  • lymphoid and myeloid leukaemia
  • lymphosarcoma
  • *FeLV-C**
  • bone marrow aplasia and anaemia
  • *FeLV-T**
  • immunosuppression

less commonly,

  • reproductive failure
  • glomerulonephritis
  • osteosclerosis (abnormal hardening of bone)
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136
Q

Discuss the transmission of feline leukaemia virus

A

Shed in saliva and other excretions/secretions

Infection by prolonged close contact (e.g. sharing bowls, mutual grooming), via ingestion

Prevalence highest in multi-cat households and catteries

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137
Q

Describe diagnosis of feline leukaemia virus

A

Detection of FeLV antigen
Immunofluoresence, ELISA, rapid antigen detection tests

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138
Q

Describe control of feline leukaemia virus

A

Recombinant vaccine

Cats should be tested to ensure antibody-negative prior to vaccination

Test & remove effective in catteries

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139
Q

What family does enzootic bovine leucosis belong to?

A

Retrovirus (oncovirus)

(Bovine leukaemia virus)

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140
Q

Describe the pathology of enzootic bovine leucosis

A

Persistant lymphocytosis

Non-regenerative anaemia

Infiltration of lymphoblastic lymphocytes producing diffuse or nodular enlargement of many organs

Small proportion: lymphosarcoma

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141
Q

Describe transmission of enzootic bovine leucosis

A

Blood transfer between animals

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142
Q

Describe control of enzootic bovine leucosis

A

Antibody test (gel diffusion test) and culling of AB+ animals

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143
Q

Describe the pathology of avian lymphoid leucosis

A

Often no clincial signs

May be decreased egg laying and hatchability

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144
Q

Describe the pathology of reticuloendotheliosis virus

A

In chickens

reticuloendothelial tumours

runting

feathering defects

immunodepression

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145
Q

Which oncoviruses (retroviruses) are exotic to Australia?

A

Pulmonary adenomatosis (Jaagsiekte)

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146
Q

Why do lentiviruses (retroviruses) cause lifelong, slowly progressive disease?

A
  • viral genome inserted into host DNA, hidden from immune system
  • high mutagenic rate (no proofreading), difficult for immune system to eliminate
  • infect lymphocytes and monocytes, leading to immune dysfunction
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147
Q

Describe the timecourse of lentigenic disease

A
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148
Q

Which lentiviruses are exotic to Australia?

A

Visna-maedi

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149
Q

Describe the pathology of human immunodeficiency virus

A

Destruction of CD4+ T (helper) cells leading to severe immunosuppression and opportunistic infection

Progression to AIDS

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150
Q

Describe the pathology of Maedi-visna virus

A

Maedi: slowly progressive pnuemonia
Visna: slowly progressive demyelination

Death

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151
Q

Which family does caprine arthritis encephalitis virus belong to?

A

Retrovirus (Lentivirus)

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152
Q

Describe the pathology of caprine arthritis encephalitis virus

A

Chronic lesion in mammary gland, lung, brain, and joints

Cachexia

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153
Q

What family does equine infectious anaemia belong to?

A

Retroviruses (lentivirus)

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154
Q

Describe the pathology of equine anaemia virus

A

fever, anaemia, abnormal iron metabolism, gammaglobulin immunosuppression, cachexia

acute death (unusual for lentiviruses) or recurrent periods of disease with progressive debilitation

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155
Q

Describe the transmission of equine anaemia virus

A

mechanimal transmission by biting insects (flies, mosquitos)

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156
Q

Describe the pathology of feline immunodeficiency virus

A

immunosuppression, opportunisitic infections

anaemia

lymphadenopathy

lethargy

febrile episdes

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157
Q

Describe the prevalence of feline immunodeficiency virus

A

transmitted via biting/fighting

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158
Q

Describe control of feline immunodeficiency virus

A

Killed vaccine

Keeping cats indoors

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159
Q

Describe diagnosis of feline immunodeficiency virus

A

detection of antibodies in serum

vaccine causes AB+ response, PCR for detection of pro-virus-DNA in blood samples now available

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160
Q

Describe the prognosis of feline immunodeficiency virus

A

Many cats live long lives

Only a small percentage develop AIDS (poor prognosis)

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161
Q

Are retroviruses good candiates for eradication? Why/why not

A

Yes

  • fragile in environment, no reservoir
  • testing for antibodies detects carriers, can be culled
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162
Q
A
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163
Q

Discuss the role of arthropod vectors in transmission of viral disease

A
  • mechanical (no replication in arthropod) or biological (replication in arthropod host; arboviruses)
  • both have replication in vertebrate host
  • some arboviruses can only be transmitted by arthropod host; some can also be transmitted by direct contact between vertebrate hosts
164
Q

Discuss endemic and epidemic cycles in terms of arboviruses

A

Endemic cycle: between arthropod and maintenence vertebrate host; no disease in either species; usually restricted to a geographic location

Epidemic cycle: spillover into “unusual” vertebrate host; disease; usually associated with high numbers of arthropod vectors

165
Q

Discuss the host range of equine encephalitis viruses

A

Arthropod host: mosquitoes

Eastern, Western EE: maintenence host = birds

Venezualan EE: maintenence host = mammals

Dead end host = horses and humans

166
Q

Which togaviruses can infect people?

A

Eastern, western, venuzualan equine encephalitis

167
Q

Which togaviruses are exotic to Australia?

A

Eastern, Western, Venuzualan equine encephalitis

168
Q

Discuss the control of equine encephalitis

A

Vaccination of horses

Control of mosquito populations

169
Q

Describe the host range of Japanese B encephalitis

A

Endemic: mosquito-bird

Amplifying host: pigs

Unusual hosts: horses, people

170
Q

Describe the pathology of Japanese B encephalitis

A

encephalitis in horses, people

reproductive problems (stillbirths, abortion) in pigs

171
Q

Which flaviviruses are exotic to Australia?

A

Yellow fever

Japanese B encephalitis

West Nile virus

172
Q

Which flaviviruses can cause infection in humans?

A

Japanese B Encephalitis

Murray Valley Encephalitis

Dengue

West Nile virus

West Nile-Kunjin virus

173
Q

Describe the host range of Murray Valley encephalitis

A

Endemic: bird-mosquito

Unusual hosts: horses, peole, domestic animals

174
Q

Describe the pathology of Murray Valley encephalitis

A

Encephalitis in horse and people

175
Q

Describe the host range of Dengue

A

Endemic: mosquito - non-human primates

Now: mosquito - human (millions of cases annually)

176
Q

Describe the pathogenesis of Dengue

A

Bite by infected mosquitos

Complicated pathogenesis

4 serotypes, not cross-protective

Infection with >1 serotype facilitates disease

177
Q

Describe the pathology of Dengue

A

Rash, arthragia, haemorrhagic fever

178
Q

Describe the host range of West Nile virus

A

Endemic: mosquito-bird

Causes disease in humans, horses, some bird species

Seroconversion with no disease in many species

179
Q

Describe the pathology of West Nile virus

A

rash, arthralgia, (rarely) encephalitis in people

encephalitis in horses and some bird species

180
Q

Describe the host range of West Nile virus-Kunjin virus

A

Endemic: mosquito-bird

Mutated strain: causes disease in horses and people

181
Q

Describe the pathology of WNV-Kunjin virus

A

Encephalitis in horses and people caused by mutated strain with additional virulence factors

182
Q

List three syndromes caused by Bovine Virus Diarrhoea virus

A
  1. Virus diarrhoea
  2. Reproductive problems
  3. Mucosal disease
183
Q

List the two biotypes of Bovine Virus Diarrhoea virus

A

Cytopathic

Non-cytopathic

184
Q

Describe the pathology of virus diarrhoea syndrome

A

Mild GIT erosions

diarrhoea

immunosuppression

respiratory disease

May be mild or subclinical

185
Q

Describe the pathogenesis and epidemiology of virus diarrhoea

A

Infection with cytopathic or non-pathogenic Bovine Virus Diarrhoea Virus

Acute disease

High incidence rate but low case fatality rate

186
Q

Describe the pathology of reproductive syndrome caused by bovine virus diarrhoea virus

A

Reproductive problems in naive dams infected with cytopathic or non-pathogenic strains

embryonic death, abortion, calves with cerebellar hypoplasia

+/- Bovine virus diarrhoea

187
Q

Describe the pathology of mucosal disease

A

Severe erosion of the GIT and digits

Depression, fever, profuse diarrhoea

188
Q

Describe the pathogenesis and epidemiology of mucosal disease

A

Specific pattern of infection with bovine virus diarrhoea virus

Low incidence, but invariably fatal

Naive dam infected with non-pathogenic strain at 40-120 days of gestation

Foetus becomes immunotolerant (does not recognise as non-self)

Persistent infection, AB -ve

Infection with exogenous cytopathic strain, or mutation of non-cytopathic strain -> cytopathic 6-18 m.o

Mucosal disease

189
Q

Describe the pathogenesis of bovine virus diarrhoea virus when infecting foetuses at varying stages of gestation

A

If infected at (day) of gestation

Day 0-40: embryonic loss

Day 40-120: Persistently infected, immunotolerent calf (Ag +ve, AB -ve) -> Mucosal disease 6-18mo

Day 90- 160: Congenital abnormalities (Ag, AB variable)

Day 140-280: clinically normal, or small weak calf (Ag -ve, AB +ve)

190
Q

Describe the pathology of Border disease virus

A

abortion

developmental abnormalities (hairy shaker lamb)

neurological signs in lambs

altered birth coat

191
Q

Describe the epidemiology of hog cholera

A

Highly contagious, high incidence, high case fatality -> explosive

Strains vary from mild to severe

192
Q

Describe the pathology of hog cholera (swine fever virus)

A

leucopenia

immunosuppression

haemorrhages (petichiae, ecchymoses)and skin discolouration

vomiting, diarrhoea

neurological signs, encephalitis

abortion, congenital defects

193
Q

Describe the control of mucosal disease

A

Serological testing (skin or blood samples) for Ag +ve, AB =ve (persitently infected animals)

Killed or attenuated live vaccines in some countries

194
Q

Which pestiviruses are exotic to Australia?

A

Swine fever (hog cholera)

195
Q

Describe the control of swine fever (hog cholera)

A

Detection of viral antigen (immunofluorescence, antige ELISA)

Slaughter

196
Q

Is African Swine Fever Virus endemic to Australia?

A

No - Africa, Europe, Asia

197
Q

Describe the transmission of African swine fever virus

A

Endemic cycle: ticks - warthogs and native pigs

Disease in domestic pigs

Biological transmission by ticks; direct contact

198
Q

Describe the pathology of African swine fever virus

A

Warthogs, wild pigs: no disease

Domestic pigs: fever, haemorrhages, dystentery, death

199
Q

Describe the transmission of swine fever (hog cholera)

A

Infection by oral or respiratory route

200
Q

Discuss why influenza viruses are difficult to control with vaccination

A

2 types of peplomers (H, N); 8 segments of RNA

Virus undergoes antigenic drift: small spontanous mutations reduce Ag-AB binding, decreased immune response and efficacy of vaccine

Virus also undergoes antigenic shift: genetic reassortment of RNA fragments between viruses -> change in RNA for H or N -> new subtype; results in epidemics, ABs do not recognise new subtype

201
Q

How do new human influenza subtypes emerge?

A

H binds to SA (sialic acid) receptors on tracheal epithelium

  • Avians express SA-alpha2,3
  • Humans express SA-alpha2,6
  • Pigs express both in 1:1 ratio
  • Pigs infected by two subtypes -> genetic shift (reassortment) -> new subtype that can affect humans

Recent concern that some avian influenzas can directly affect humans, bypassing pig

202
Q

Describe the pathology of Influenza A(H1N1(pdm09)) in people

A

children, pregnant women, some chronic conditions most at risk

severe disease and death from viral pneumonia

203
Q

Discuss the pathogenesis of Avian influenza in birds

A
  • all subtypes present
  • range from asymptomatic to severe (fowl plague)
  • species differences in pathogenicity
204
Q

Describe the pathology of Fowl Plague

A

respiratory distress, cyanosis, nervous signs, diarrhoea, haemorrhage, rapid death

205
Q

Describe the control of human influenza

A

Killed vaccine containing current strain, protective 6-9 months

206
Q

Which influenza subtypes are exotic to Australia

A

H7N7(equi 1)

H1N1 Swine flu (has been isolated in Aus, but no disease)

H5N1 Avian influenza

207
Q

Discuss the control of zoonotic Avian influenza

A

Control avian disease with quarentine, culling, vaccination

Vaccination of humans for human strains

Protection of people at high risk with PPE and antivirals

Mass culling probably not a solution due to economic and production importance of poultry in many countries

208
Q

Discuss the pathology of equine influenza

A

fever, naso-ocular discharge, cough

+/- secondary bacterial infection, pneumonia

209
Q

Describe the control of equine influenza

A

vaccination:

inactivated bivalent vaccine (both subtypes)

recombinant canarypox vaccine (no booster required)

subunit vaccine containing H & N

Not fully protective, boosters 6-9 months

210
Q

Describe the epidemiology of equine influenza

A

highly contagious, spreads rapidly, self-limiting

211
Q

Describe the pathology of canine influenza

A

respiratory disease ranging from mild, to severe + pneumonia; fever, cough.

212
Q

Describe the epidemiology of canine influenza

A

H3N8 equine influnza virus tranmitted to dogs, become host adapted in USA

Probably multiple transmission events from horses to dogs

Dog-Dog transmission still in question (no evidence in UK or Aus)

213
Q

Describe the pathology of swine influenza in pigs

A

respiratory disease and distress, cough, pyrexia, anorexia and emaciation

+/- secondary bacterial infection

Mortality highest in piglets from non-immune sows

214
Q

Describe the pathology of parainfluenza virus 3

A

Shipping fever + calf pneumonia in cattle

summer pneumonia in sheep

+/- secondary bacterial infection

Possibly apathogenic in pigs, horses, dogs

215
Q

Describe the pathology of parainfluenza virus 2

A

Upper respiratory tract infection

Role in kennel cough in dogs

216
Q

Describe the pathology of respiratory syncytial virus

A

calf pneumonia and respiratory disease in feedlots

217
Q

Which paramyxoviruses are exotic to Australia?

A

Rinderpest (globally eradicated, 2011)

Velogenic Newcastle disease (but outbreaks from mutated lentogenic strains in 1990s)

Nipah virus (AB/virus detected, but no disease)

218
Q

Describe the epidemiology of rinderpest

A

severe disease, high incidence, high case fatality in cattle

Mild disease in cattle, buffalo, game animals, sheep, goats

219
Q

Describe the pathology of rinderpest

A

inflammation, haemorrhage, erosions, necorsis of digestive mucosal membranes, diarrhoea, death

220
Q

Describe the host range of canine distemper virus

A

canids (dog, foxes), racoon, panda, ferrets, minks, large felids, red panda, civits, hyena

221
Q

Describe the pathology of canine distemper

A

pyrexia, repiratory disease (pneumonia, bronchitis), conjunctivitis, gastroenteritis, encephalitis

+/- secondary bacterial infection

222
Q

Describe the sequelae of canine distemper

A

Demyelinating encephalitis: within months of recovery (autoimmune)

“Old dog” encephalitis: years after recovery (slow, persistent viral replication)

Neurological signs, loss of proprioception

223
Q

Which family does rinderpest belong to?

A

Paramyxovirus

224
Q

Which family does canine distemper belong to?

A

Paramyxovirus (Morbillivirus)

225
Q

Describe the pathogenesis of canine distemper

A

aerosol infection > viremia, infection of lymphoid tissue, fever > virus in connective tissue

If AB response insufficient > infection of epithelial cells (respiratory, conjunctiva, GIT) > Death

OR > Recovery > late sequelae > demyelinating encephalitis or old dog encephalitis

226
Q

Discuss control of canine distemper

A

Very effective, live attenuated vaccine

Usually combined with parvovirus & canine adenovirus 2 +/- parainfluenza virus 2 & B. bronchiseptica

in some countries, attenuated measles vaccine used to avoid MAB interference

Vaccination of other species (fox, lion)

227
Q

Describe the pathology of Newcastle disease

A

severe, generalised disease (sometimes confused with fowl plague)

in chickens, turkeys, pigeons, parrots, +/- other avians

respiratory, intestinal, nervous signs

haemorrhagic enteritis and tracheitis, encephalitis, hepatic necrosis and haemorrhage

228
Q

What family does Newcastle disease belong to?

A

Paramyxovirus (Morbillivirus)

229
Q

Describe the subcategories of newcastle disease

A

Only one serotype, BUT

Lentogenic: can only replicate in epithelial cell, no disease

Mesogenic: moderate disease

Velogenic: can replicate in many cell types - severe disease, high case fatality, highly virulent. Varies by 2 amino acids from lentogenic strain

Viscerotropic: prediliction for GIT

Pneumotropic: prediliction for resp. tract

230
Q

Describe control of Newcastle disease

A

In endemic countries, vaccination with lentogenic strain (selected for heat stability)

In exotic locations, slaughter

231
Q

Describe the pathogenesis of canine distemper

A

pathogenesis depends on AB response

infection via droplets

severe pathology with secondary bacterial infection

232
Q

Describe the transmission of Newcastle disease

A

Respirtory route

233
Q

What family does Hendra virus belong to?

A

Paramyxovirus (Henipavirus)

234
Q

Describe the host range of Hendra virus

A

Reservoir host: fruit bats (no disease)

>50 spillover events into horses

Occasional spillover into humans

235
Q

Describe the epidemiology of Hendra virus

A

Reservoir host in bats

Requires coordinted set of events for spillover to horses; bats rarely shed virus;

does not last long in environment

To date, zoonotic transmission from horses-> humans; no evidence of transmission from bats -> humans

236
Q

Describe the pathology of Hendra virus

A

Bats: no disease

Horses: acute onset, pyrexia, severe respiratory signs, pulmonary oedema, neurological signs

Humans: respiratory and neurological signs; 4/7 deaths

237
Q

Describe control agains Hendra

A

Limit horses grazing under fruit trees

Horse vaccination (recombinant with Nipah): 2 initial doses 21 days appart, yearly boosters

238
Q

Describe diagnosis of Hendra

A

PCR. New variant recently discovered, not detected by current PCR -> updating assays

239
Q

What family does Nipah virus belong to?

A

Paramyxovirus (Henipavirus)

240
Q

Describe the host range of Nipah virus

A

Fruit bats

Pigs

Humans

241
Q

Describe the pathology of Nipah virus

A

Bats: no disease

Pigs: encephalitis, respiratory signs

Humans: 75% fatality

242
Q

Describe the transmission of Nipah virus

A

Infected eating fruit or palm juice contaminated with urine or saliva of infected bats

human-human transmission

243
Q

What family does rabies belong to?

A

Rhabdovirus (Lyssavirus)

244
Q

Describe the host range of rabies

A

Non-specific: broad host range affecting warm-blooded animals

245
Q

Describe the pathogenesis of rabies

A

Transmission by bite, break in skin, rarely by aerosol > replication in muscle fibres > enters nerve and slowly migrates to CNS (incubation period weeks - 6 months) > fatal encephalitis and neurological signs (disease course ~1 week) > travels down nerves to saliva > shedding of virus in saliva

246
Q

Describe the two main types of rabies

A

Paralytic rabies: usually herbivores

Furious rabies: usually carnivores

247
Q

Which rhabdoviruses are exotic to Australia?

A

Rabies

Vesicular stomatitis

248
Q

Describe the epidemiological features of rabies

A

Urban rabies maintained in domestic dog populations (Africa, Asian, Latin America). Transmitted between dogs, then to people

Sylvatic rabies maintained in wild animal (fox, skunk, raccoon, mongoose) species: Europe, north and south America. Transmitted between bats and wild species. Human infection is known to come from bats. Other species questionable human transmission

Different species with slightly different genetic differences

249
Q

Describe the diagnosis of rabies

A

Histological staining for Negri (intracytoplasmic) inclusion bodies. Essentially pathognomonic, but such a serious disease, confirmed with other tests

Immunofluorescent staining of brain section using labelled anti-rabies antibodies (conclusive)

PCR and sequencing to determine origin/stain

250
Q

Describe control of rabies

A
  1. vaccinate domestic animals, esp. dogs, cats
  2. Kill/vaccinate wildlife vectors (requires resources; cultural implications e.g. culling in Buddhist countries)
  3. Control stray feral dog and cat populations (requires resources)
  4. Surveillance programs to monitor incidence and distribution
  5. Public education regarding pet vaccinations and interactions with wild animals
251
Q

What type of vaccination is used for rabies

A

Developing countries - vaccine dervived from neural tissue, can cause allergic (often fatal) encephalitis

Live attenutated or inactivated diploid vaccines for domestic animals and people

Live recombinant vaccina virus/vaccine baits used to vaccinate wildlife in some countries

252
Q

Describe the prophylactic and post-exposure therapy for rabies

A

Prophylactic vaccination for at-risk people, domestic animals, wildlife

Post exposure: wash and disinfect wound

Vaccinated people: series of 2 doses vaccination

Unvaccinated people: antiserum (1/2 dose given at wound site) + series of 5 vaccinations

253
Q

Describe the pathology of rabies in humans

A

Early: may be vague, non-descript symptoms

Later: Shaking, speech difficulties, severe anxiety, vomiting, agitiation, muscle tremors, paralysis, encephalitis

254
Q

What family does Australian bat lyssavirus belong to?

A

Rhabdovirus (Lyssavirus)

255
Q

Describe the pathology of rabies in animals

A

Prodromal phase

Paralysis of pharyngeal muscles impacting deglutition -> appearing to cause excessive salivation

Paralytic (herbivores)

Aggression, loss of fear response in carnivores

Fatal encephalitis

Disease is often fatal even in bats

256
Q

Describe the host range of Australian Bat Lyssavirus

A

Causes disease in fruit bats and insectivorous bats, also caused disease in some horses and can be zoonotic

Does not appear to cause infection or disease in other species

257
Q

Describe the pathology of Australian bat lyssavirus

A

Bats: paresis/paralysis, aggression, self-mutilation, other CNS signs, often found moribund or dead

Horses: neurological signs, progressive ataxia, pyrexia

258
Q

Describe control of Australian bat lyssavirus

A

Rabies vaccination and post-exposure protocol (96% shared DNA)

259
Q

What family does vesicular stomiatitis belong to?

A

Rhabdovirus

260
Q

Describe the pathology of vesicular stomatitis virus

A

Similar to FMD: causes vescicular lesions on mouth, snout, feet; rupture to leave ulcerative areas

261
Q

Describe the host range of vesicular stomatitis

A

pigs, horses, cattle, zoonotic

262
Q

Describe the transmission of vesicular stomatitis virus

A

Arthropod vectors (probably mechanical)

263
Q

Which family does bovine ephemeral fever belong to?

A

Rhabdoviruses

264
Q

Compare and contrast vesicular diseases

A
265
Q

Describe transmission of bovine ephemeral fever

A

Biological transmission by mosquitos and culicoides species

266
Q

Describe the pathology of bovine ephemeral fever

A

fever, depression, odema, lameness, decreased milk yield, recumbency, abortion

related to immune response: better immune system -> more signs

Usually spontaneous regression in days (<2 weeks)

2% mortality

267
Q

Describe the control of bovine ephemeral fever

A

Attenuated live and inactivated vaccines available, but not often used as only lasts 6-12 months and disease course is acute with low morbidity

268
Q

Which poxviruses are exotic to Australia

A

Smallpox - globally eradicated

Buffalopox

Cowpox

Sheepox/Goatpox

Lumpy skin disease

269
Q

Which family does infectious bronchitis belong to?

A

Coronavirus (in chickens)

270
Q

Describe the pathology of infectious bronchitis

A

Young birds (1-4w.o): gasping, coughing, nasal exudates, respiratory distress, mortality 25-30(-70)%

Older birds: milder signs, drop in egg production, lay abnormal eggs

Post mortem: mucosal thickening, exudate in nasal passages, trachea, bronchi

271
Q

Describe the control of infectious bronchitis

A

live attenuated vaccines in water, by spray, or by eyedrops

Vaccine failure from emergence of new antigenic varients

272
Q

Describe the diagnosis of infectious bronchitis

A

detection of viral antigens or RNA in tracheal tissue

virus culture in eggs -> dwarfed, curled embryos

273
Q

Which family does transmissible gastroenteritis belong to?

A

Coronavirus

274
Q

Describe the pathology of transmissible gastroenteritis

A

In pigs:

villous atrophy, profuse diarrhoea, vomiting, dehydration, death

Most severe in piglets < 3w.o

<=100% mortality

275
Q

Which coronaviruses are exotic to Australia?

A

Transmissible gastroenteritis

Porcine epidemic diarrhoea

276
Q

Describe the diagnosis of transmissible gastroenteritis

A

detection of viral antigen or RNA in intestinal tissue

Pathology -> villous atrophy

277
Q

Describe the control of transmissible gastroenteritis

A

Live attenuated vaccines

Vaccination of pregnant sows confers MAB to piglets

278
Q

Describe the pathology of porcine epidemic diarrhoea

A

watery diarrhoea, sometimes vomiting,

mortality in piglets <3w.o <=100%

Adult pigs with mild or no signs

279
Q

Describe control of porcine epidemic diarrhoea

A

Vaccination in some countries

280
Q

Describe the pathology of porcine haemagluttinating encephalomyelitis

A

Only affects young pigs

depression, incoordination, hyperaesthesia vomiting, anorexia, wasting

mortality <=100%

281
Q

Describe control of porcine haemagglutinating encephalomyelitis

A

No vaccine

Disease not usually seen in endemic herds -> piglets protected by MAB

282
Q

Which family does porcine epidemic diarrhoea belong to?

A

Coronavirus

283
Q

Which family does porcine haemagglutinating encephalomyelitis belong to?

A

Coronavirus

284
Q

Which family does feline infectious peritonitis belong to?

A

Coronavirus

285
Q

Describe the pathology of feline infectious peritonitis

A

effusions in peritoneal and pleural cavities

granulomas and necrosis in visceral organs

immunosuppression

usually in cats < 2yo

usually fatal

286
Q

Describe the pathogenesis of feline infectious peritonitis

A

Complex pathogenesis:

host to feline enteric coronavirus -> quasispecies variant with tropism changed from enteric epithelium to macrophages

immunological basis: defective cell-mediated immunity -> uncontrolled viral replication -> production of non-protective AB -> immune mediated vasculitis

287
Q

Describe the control of feline infectious peritonitis

A

Vaccine available, BUT

Experimental infection of immunocompetent cats -> no disease

So questionable efficacy. May have higher disease rates if vaccinated

Cross-reacts serologically with feline enteric coronavirus, so antigen detection tests of questionable usefullness

288
Q

Describe the pathology of canine coronavirus

A

enteric and respiratory coronaviruses

Gastroenteritis, may be subclinical

In young pups: Severe clinical signs - vomiting, anorexia, depression, diarrhoea

Low case fatality rate

289
Q

Describe the diagnosis of canine parvovirus

A

Rapid antigen detection tests, sometimes combined with tests for canine parvovirus

Some labs have developed PCR tests

290
Q

Describe control of canine coronavirus

A

Inactivated vaccine, questionable efficacy

291
Q

Describe the pathology of bovine coronavirus

A

Neonatal diarrhoea < 3w.o

Winter dysentery and respiratory disease in cows

292
Q

Describe the control of bovine coronavirus

A

Neonatal calves most at risk -> vaccinate dams, ensure sufficient colostrum intake

293
Q

Describe the pathology of severe acute respiratory distress syndrome

A

fever, cough, pneumonia, diarrhoea

10% mortality (>750 deaths/8100 cases)

294
Q

Which family does severe acute respiratory distress syndrome belong to?

A

Coronavirus

295
Q

Describe the epidemiology of severe acute respiratory distress syndrome

A

Epidemiological associations with wildlife meats

Chinese rufous horseshoe bats natural reservoir

296
Q

Describe the pathology of Middle East Respiratory syndrome

A

Severe respiratory disease, 40% mortality (>800 deaths/>2000 cases)

297
Q

Which family does Middle East respiratory syndrome belong to?

A

Coronavirus

298
Q

Describe the host range of Middle East respiratory syndrome

A

Dromedary camels reservoir host

Isolated in bats from Hong Kong

Humans

299
Q

Describe the mortality rate of COVID-19

A

More than 2.5 million deaths worldwide

2% case fatality rate

300
Q

What leads to the “spillover” events of coronaviruses?

A
  • change in virus with expanded host range and increased virulence (but viruses have been mutating forever)
  • disruption to ecosystems, changing behaviours or mixing of species
  • Changes in wildlife trade, e.g. market structure, use of wild animals
301
Q
A
302
Q

Write brief notes on vesicular exanthema

A

Disease seen in pigs in USA between 1932-1956 (now eradicted)

Vesicular disease, similar to FMD

Same as San Miguel sea lion virus

Probably resulted from feeding pigs marine mammals

303
Q

Which family does vesicular exanthema belong to?

A

Calcivirus

304
Q

Describe the pathology of feline calcivirus

A

Upper respiratory tract infection (rhinitis, fever, conjunctivitis)

ulcerative glossitis

Sometimes pneumonia and death, esp. kittens

Some virulent strains cause systemic infections with facial and limb oedema, alopecia, and ulceration of feet (rare)

305
Q

List the pathogens involved in cat flu

A

Feline calcivirus (40%)

Feline herpesvirus (40%)

Chlamydia (20%)

306
Q

Is feline calcivirus a good candidate for eradication? Why/why not?

A

No

  • Many serotypes, leading to vaccination failure
  • Shed from oropharynx for >1y after recovery (carrier animals)
  • Resistant in environment
307
Q

Describe the control of feline calicvirus

A

Attenuated vaccines available, but vaccination failures not uncommon (many serotypes)

308
Q

Describe the pathology of rabbit haemorrhagic disease

A

hepatic necrosis, disseminated intravascular coagulopathy, lung congestion and oedema, enlarged spleen, peracute death (6-24hr)

Only occurs in rabbits >2mo. Innate property of young rabbits, immature hepatocytes and enzymes do not support viral replication, possible altered clotting factors. May die from starvation if dam dies. If survive, no disease, AB+ve

309
Q

Describe the control of rabbit haemorrhagic disease

A

killed vaccine used to protect pets, farmed, and lab rabbits

Used as a form of biological control in some countries

Accidentally released into Australia after trials on neighbouring islands, illegally released in NZ -> reduced impact, needed to be released out of breeding season to prevent persistance in young rabbits. Effective in more arid regions

310
Q

Which family does foot and mouth disease belong to?

A

Picornavirus (Apthovirus)

311
Q

Describe the host range of foot and mouth disease

A

Cloven-hoofed animals including cattle, deer, sheep, goats, pigs

rarely, humans

312
Q

Describe pathology of foot and mouth disease

A

Cows, pigs: fever, depression, loss of production

vesicles on tongue, gums, snout, feet, teats

Sheep and goats with mild or subclincal infections

313
Q

Discuss the economic factors involved in foot and mouth disease

A

Loss of production, but less significant in endemic areas

Significant impacts on international trade

314
Q

Discuss transmission of foot and mouth disease

A
  • short incubation period
  • high concentrations of virus shed in aerosols, esp. pigs; can be transmitted long distances on wind;
  • infection via respiratory route
  • virus can be shed before clinical signs observed
  • small infectious dose
315
Q

Is foot and mouth disease a good candidate for eradication? Why/why not?

A
  • large amounts of virus shed into environment, can travel long distances on wind
  • can be shed before clinical signs observed
  • rapid replication cycle (short incubation period)
  • small infective dose
  • many serotypes & subtypes, short-lived immunity -> vaccination problems
  • extremely resistant in environment at neutral pH (resistant to detergents and dessication)
316
Q

Discuss the serotypes of foot and mouth disease

A
  • 7 serotypes: A, O, C, SAT1, SAT2, SAT3, Asia1
  • Many subtypes per serotype (> 80 total)
  • Immunity to one serotype does not protect against others
  • Immunity to one subtype may or may not protect against others
  • Need correct subtype in inactivated vaccines to protect against local strains
  • short-lived immunity, boosters required /6m
317
Q

Describe the control of foot and mouth disease in exotic countries

A
  • strict control for importation of animal products/swill feeding to pigs
  • strict quarantine measures
  • slaughter of affected animals
  • +/- ring vaccination
  • alert authorities if suspect vesicular disease
  • monitoring/surveillence
318
Q

Describe the host range of swine vesicular disease

A

Pigs only

319
Q

Describe the pathology of swine vesicular disease

A

foot lesions; snout lesions uncommon

320
Q

Which family does swine vesicular disease belong to?

A

Picornavirus

321
Q

Which family do porcine enteroviruses belong to?

A

Picornavirus

322
Q

Describe the pathology of porcine enteroviruses

A

13 strains, variable in pathological effects:

  • asymptomatic
  • neurological disease comparible to polio in humans (encephalmyelitis, tremors, convulsions, ataxia, paralysis)
  • reproductive problems in naive pregnant animals (stillbirts, mummification, embryonic death, infertility)
  • pneumonia, myocarditis, pericarditis
323
Q

Which family does avian infectious encephalomyelitis belong to?

A

Picornavirus

324
Q

Describe the pathology of avian infectious encephalomyelitis

A

Paralysis and death in young chickens (2-3wo)

drop in egg production in adult birds

325
Q

Describe the transmission of avian infectious encephalomyelitis

A

horizontal or vertical transmission

326
Q

Describe the control of avian infectious encephalomyelitis

A

Vaccination of pullets (before lay)

  • > No vertical transmission
  • > Chicks protected by maternal antibodies
327
Q

Describe the host range of rhinoviruses

A

cattle, horses, people

328
Q

Describe the pathology of rhinoviruses

A

upper respiratory tract disease (common cold)

329
Q

List the host range of encephalomyocarditis virus

A

maintained in rodents

pigs

+ other species including monkeys, kangaroos

330
Q

Describe the pathology of encephalomyocarditis virus

A

Pigs: acute myocarditis and sudden death (mortality <=100% in young pigs)

Sudden death in monkeys, kangaroos

331
Q

Which family does encephalomyocarditis virus belong to?

A

Picornavirus

332
Q

Name the three genera of Reoviruses

A

Orthoreovirus

Orbivirus

Rotavirus

333
Q

What family does bluetongue belong to?

A

Reovirus (Orbivirus)

334
Q

Describe transmission of bluetongue

A

arbovirus (biological transmission by Culicoides)

Multifactorial: age, stress, rough terrain; sheep vs cattle proportions (preferred host = cattle)

Non-contagious between sheep; severity depends on strain of virus and breed of sheep

Cattle important amplifying hosts (viremia ~4 months)

335
Q

Describe the pathology of bluetongue in sheep

A

Can be prolonged, progressive disease

Variability in clinical signs
- catarrhal (mm) inflammation of digestive and respiratory tracts with erosions)

  • fever, swollen lymph nodes
  • mucopurulent nasal discharge; swelling of nose and mouth
  • damage to small blood vessels
  • odema, cyanosis, haemorrhage
  • distension of tongue
  • coronitis (hyperaemia, red->purple swelling of coronary band)
  • muscle degeneration, loss of condition, emaciation
  • congenital abnormalities
  • Postmortem: yellow/gelatinous/haemorrhagic SQ, thoracic, abdominal oedema

-

336
Q

Describe the pathology of bluetongue in cattle

A

Usually asymptomatic or mild disease

congenital defects from in utero infection

337
Q

Describe some of the major attributes of bluetongue

A

arbovirus

>20 serotypes, not cross protective

11 strains present in Aus; mostly low virulence; this may be changed with changing climactic factors and spread of cattle into sheep areas

338
Q

Discuss the control of bluetongue

A

Live attenuated or killed vaccines used in some countries (need to know local serotype of prevelance)

Attenuated viruses can cause congenital defects

Concerns about genetic reassortment of vaccine and field strains (killed vaccines may be safer, but less effective)

339
Q

Discuss the pathology of African Horse Sickness

A

peracute - acute, very severe, often fatal disease of horses, donkeys, mules

acute dyspnoa, pulmonary oedema, haemorrhage, profuse nasal discharge; may be confused with Hendra

340
Q

Which family does African horse sickness belong to?

A

Reovirus (Orbivirus)

341
Q

Describe the transmission of African horse sickness

A

Arbovirus (culicoides)

342
Q

Describe control of African horse sickness

A

9 serotypes -> polyvalent vaccine

343
Q

Describe the diagnosis of foot and mouth disease

A

-Detection of viral antigen (complement fixation test, ELISA) or viral RNA (PCR) in samples of vesicular fluid or tissues

344
Q

Which reoviruses are exotic to Australia?

A

Some strains of Bluetongue

African horse sickness

345
Q

Which family do rotaviruses belong to?

A

Reovirus

346
Q

Discuss the pathology of rotaviruses

A

diarrhoea in neonatal animals, depression

dehydration or secondary bacterial infection

347
Q

List the host range of rotaviruses

A

piglets, calves, foals, lambs, mice, babies

348
Q

Describe the epidemiology of rotaviruses

A

large amounts shed in excretions

highly stable in environment

349
Q

Describe the control of rotaviruses

A

detection of viral antigen in faeces (serological assays)

detection of viral RNA in PCR

350
Q

Describe the control of rotaviruses

A

Ensure sufficient colostrum intake

killed vaccines for dams (sows and cows)

351
Q

Which family does infectious bursal disease (Gumboro’s disease) belong to?

A

Birnavirus

(Bi = 2, (ds)RNA, virus)

352
Q

Discuss the pathology of infectious bursal disease

A

Viral replication in Bursa of Fabricius (decreased size) -> immunosuppression

decreased response to pathogens and vaccination

depression, ruffled feathers, diarrhoea, trembling, muscular, renal and intestinal lesions; esp chicks 2-6 wo

353
Q

Discuss the control of infectious bursal disease

A

Live attenuated and killed vaccines

Outbreak of virulent strains in some countries not effectively controlled by vaccination -> serious economic losses

354
Q

Which family does Akabane belong to?

A

Bunyaviruses

355
Q

Discuss the transmission of Akabane

A

Arbovirus (Cullicoides)

356
Q

Describe the pathology of Akabane

A

No disease in adult hosts

Foetal abnormalities: Arthrogryposis (fixed flexion or extension of joints), hydroencephaly, encephalitis

357
Q

Describe the host range of Akabane

A

Mosquitos -> Cattle, sheep, goats

358
Q

Discuss the presence of Akabane in Australia

A

Endemic to QLD, disease rarely seen (dams infected prior to pregnancies)

Outbreak into naive populations in NSW

359
Q

Describe the detection of akabane

A

detection of AB in pre-colostral sera of neonate; or rising titre levels in dam

Detection of virus or components not viable, because foetus clears virus prior to birth

360
Q

Which family does Schmallenberg virus belong to?

A

Bunyavirus

361
Q

Describe the transmission of Schmallenberg virus

A

arbovirus (culicoides)

362
Q

Describe the host range of Schmallenberg virus

A

cattle, sheep, other ruminants

363
Q

Describe the pathology of Schmallenberg virus

A

congenital abnormalites, stillbirths, production losses

364
Q

Which family does Rift Valley fever belong to?

A

Bunyavirus

365
Q

Describe transmission of Rift Valley fever

A

Arbovirus (mosquitoes) with transovarial transmission

Humans infected via mosquito or contaminated blood (e.g. autopsy, slaughter)

366
Q

Describe the host range of Rift Valley fever

A

Mosquitos -> cattle, sheep, goats, most domestic animals, zoonotic

367
Q

Describe the pathology of Rift Valley fever

A

hepatitis, encephalitis, abortion

disease and death in humans

368
Q

Which bunyaviruses are exotic to Australia?

A

Schamallenberg virus

Rift Valley fever

369
Q

Describe the pathology of equine viral arteritis

A

Range of signs

  • asymptomatic
  • fever, oedema, respiratory signs, abortion, necrosis of small arteries
370
Q

Describe the transmission of equine viral arteritis

A

aerosols, semen

371
Q

Describe the control of equine viral arteritis

A

removal of carrier stallions, vaccinations

virus present in Australia, but no disease seen (non-virulent strain)

372
Q

Which family does porcine respiratory and reproductive syndrome belong to?

A

Arteriviruses

373
Q

Which arteriviruses are exotic to Australia

A

Porcine respiratory and reproductive syndrome

Equine viral arteritis is present in Australia, but does not cause disease

374
Q

Describe the pathology of porcine respiratory and reproductive syndrome

A

abortion, neonatal deaths, respiratory disease in young piglets

375
Q

Describe the control of porcine respiratory and reproductive syndrome

A

Killed and live attenuated vaccines in endemic countries

376
Q

Describe the common features of prion disease

A

long incubation period (years)

slowly progressive, fatal disease caused by an unconvential agent

minimal inflammatory response and no immune response

brain lesions including deposition of amyloid-like material, vacuolation of neurons

377
Q

Describe the differences of PrPSc as compared to PrPc

A

PrPc = normal protein of unknown function, formed by alpha-helicies

PrPSc = abnormal protein; beta-pleated sheets; less soluable; resistant to proteases; extremely resistant and difficult to inactivate; stable at a wide range of pH, after boiling, standard autoclaving, most disinfectants, formalin fixation, UV irradiation, ether/alcohol treatment

378
Q

Describe the recommended inactivation protocol for prions

A
  • autoclaving at 132ºC for 90 min
  • hot solutions of sodium hydroxide
  • high concentrations of sodium hypochlorite

(NOT a guarentee of inactivation)

379
Q

Describe the mechanisms of prion disease

A

Externally aquired:
Ingestion of PrPSc -> absorbed through intestines, into lymph nodes

  • *Internally aquired:**
    1. Mutation of gene encoding PrPC -> PrPSc
    2. Spontaneous incorrect folding of protein

all processes lead to PrPSc in the brain

Conversion
PrPSc induces conversion of PrPC to PrPSc -> exponential accumulation -> aggregation of deposits and fibrils -> disruption of brain function

380
Q

Discuss the host barrier as it relates to prion disease

A

Host species may be resistant to prions of some species, but not others

Species barrier depends on amino acid sequence and shape of proteins

381
Q

Discuss the classification of prions

A

Depends on molecular and biological properties

  1. amino acid sequence (reflective of host species)
  2. banding pattern on Western blot
  3. Bioassays: intracerebral innoculation of mice
    - incubation period and mortality pattern
    - distribution of brain lesions
    - infectivity titre
382
Q

Which family does Scrapie belong to?

A

None - Prion

383
Q

Describe the host range of scrapie

A

Sheep, goats

More common in sheep

384
Q

Describe the pathology of scrapie

A

pruritis, decreased wool quality

progressive neurological disease: ataxia, tremors, apprehension, increased excitability, paralysis

emaciation, death

385
Q

What is the incubation period of scrapie?

A

1-5 years

386
Q

Which prion diseases are exotic to Australia?

A

Scrapie

Bovine spongiform encephalopathy

Transmissible mink encephalopathy

Creuztfeld-Jacob disease

Kuru

387
Q

Describe the transmission of scrapie

A

Usually by oral route; possibly in neonatal period by exposure to foetal fluids and contaminanted milk

Pastures may remain contaminated for years (forever?)

Susceptibility associated with certain PrP alleles

388
Q

Describe the diagnosis of scrapie

A

histopathology of brain (vacuolation, degeneration of neurons)

EM for fibrils

immunoblotting

(no detectable serological response)

389
Q

Which family does bovine spongiform encephalopathy belong to?

A

None: prion

390
Q

Describe the host range of bovine spongiform encephalopathy

A

Cows

-> CJD in humans

391
Q

Describe the pathology of bovine spongiform encephalopathy

A

progressive neurological disease: hindlimb incoordination, locomotory disturbances, abnormal gait and carriage of head

Marked behavioural changes: temperment changes, aggression, loss of herd heirarchy, erratic behaviour and abnormal responses

emaciation, death

392
Q

What is the incubation period of bovine spongiform encephalopathy?

A

2-5 years

393
Q

Discuss the epidemiology of bovine spongiform encephalopathy

A

significant association with eating meat and bone meal, following changes to the processing regie: dose dependent

horizontal transmission does not appear to occur, maternal transmission considered minimally important

394
Q

Describe the Australian response to bovine spongiform encephalopathy

A
  1. National surveillance: targeted sampling of 400 cows and 450 sheep per year
  2. ruminant feed ban: ban on feeding restricted animal material, including blood, bone, meat, fish, poultry, feathermeals to ruminants
  3. Quarantine measures: importation of meat and bone meal, cattle, sheep = prohibitied

4, Be prepared: preparedness and response capability

395
Q

Which family does chronic wasting disease of deer and elk belong to?

A

None: prion

396
Q

Describe the pathology of chronic wasting disease of deer and elk

A

severe wasting, trembling, ataxia

397
Q

Describe the transmission of chronic wasting disease of deer and elk

A

Horizontal transmission occurs through prion in saliva

398
Q

Which family does Kuru belong to?

A

None: prion

399
Q

Describe the host range and incidence of Kuru

A

Occurs in humans, PNG, as a result of cannabalistic rituals involving consumption of human brains . Transmission via ingestion.

Decline in incidence since cannibalism abandoned

400
Q

List the two types of Cruetzfeld-Jakob disease

A
  1. Sporadic CJD
  2. New variant CJD
401
Q

Discuss the host range of sporadic Cruetzfeld-Jakob disease

A

Humans of all nationalities and ethnic groups, usually > 50 years old

402
Q

Discuss the mechanism of sporadic Cruetzfeld-Jakob disease

A

Mutation of PrPC gene to produce PrPSc protein

Spontaneous misfolding

Transmission by:
Iatrogenic transmission
Corneal transplants
Growth hormones harvested from cadavers

403
Q

Describe the pathology of sporadic Cruetzfeld-Jakob disease

A

Neurological signs: sensory disturbance, sleeping disorders, dementia, motor disturbances, coma, death

404
Q

What are the differences with new variant Cruetzfeld-Jakob disease compared to sporadic CJD?

A

Symptoms: psychiatric (e.g. depression/anxiety) cf neurological

Pathology: lesions more florid (elaborate)

Age of affected people: 19-45 y.o (cf >50)

Epidemiology: likely associated with eating BVD-contaminanted tissues (rather than spontaneous mutation or misfolding)

405
Q

Why is it thought that new variant Cruetzfeld-Jakob disease is related to bovine spongiform encephalopathy

A

Presents in a different demographic and with different clinical signs to sporadic CJD

Began ~10 years after BSE described

Bioassays show similarities to BSE

-> removal of neural tissue now mandated before entering food chain

Virology (4 decks)

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