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
Describe the host range of myxoma virus
Myxamatosis Wild rabbits in Americas = mild disease European rabbits = generalised disease
26
Describe the transmission of the myxoma virus
Mechanical transmission by insect vectors Released as a form of population control
27
Describe the control of myxoma virus
Attenuated myxoma vaccine Vaccination with rabbit fibroma virus
28
Describe the pathology of myxoma virus
Conjunctivitis Gelatinous swellings Severe generalised disease **No typical pox lesions** (Localised benign fibroma in American wild rabbits)
29
Which family of viruses does myxoma belong to?
Poxviridae
30
Describe the host range of fowlpox
Chickens (Most bird species have their own pox virus, e.g. pidgeonpox, turkeypox)
31
Describe the transmission of fowlpox
mechanical transmission by insects
32
Describe the pathology of fowlpox
Severe disease with proliferative lesions in young birds Pox lesions on comb, wattle, feet, vent, +/- respiratory tract
33
Describe the control of fowlpox
Attenuted fowlpox or pigeonpox vaccines Vector control
34
Describe the pathology of human adenoviruses
Upper respiratory tract infection Conjunctivitis
35
Describe the pathology of bovine adenoviruses
Some serotypes: Upper respiratory tract infections; pneumonia Some serotypes: keratoconjunctivitis
36
Describe the pathology of porcine adenoviruses
Some can cause respiratory disease (experimental innoculation)
37
Describe the pathology of equine adenoviruses
Subclinical or mild respiratory disease Severe disease in young Arab SCID foals: fatal pneumonia
38
Describe the pathology of avian adenoviruses
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
39
What family of viruses does infectious canine hepatitis virus belong to?
Adenovirus | (Canine adenovirus 1)
40
Describe the host range of infectious canine hepatitis
Dogs, foxes
41
Describe the pathology of infectious canine hepatitis in foxes
Encephalitis
42
Describe the pathology of infectious canine hepatitis in dogs
- 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%
43
Describe the detection of the canine infectious hepatitis virus
- present in secretions during acute phase - present in urine \> 6 months
44
Describe the transmission of canine infectious hepatitis
- 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)
45
Describe the control of infectious canine hepatitis
- attenuated canine adenovirus 2 vaccine - inactivated canine adenovirus 1 vaccine - immunity is cross-protective
46
Describe the pathology of canine infectious laryngotracheitis
Mild respiratory disease +/- fatal bronchopneumonia Role in Kennel Cough
47
Describe the replication of papillomaviruses
- 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)
48
Describe the pathology of human papillomaviruses
Most benign Some associated with carcinomas (cervical, laryngeal, skin)
49
Describe the pathology of equine papillomavirus
Papillomas on nose and face of young horses Spontaneous regression with immunity
50
Describe the pathology of canine papillomaviruses
Oral papallomas. Usually benign, some evidence of neoplastic transformation Also on feet of greyhounds Spontaneous regression
51
Describe the pathology of ovine papillomas
Lesions most common on ears, face, vulva. May undergo neoplastic transformation
52
Describe the pathology of caprine papillomas
Lesions usually on udder, genital skin. Some neoplastic transformation
53
Describe the pathology of bovine papillomas in cattle
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
54
Describe the pathology of bovine papilloma in horses
Equine sarcoids
55
Describe the control of papillomaviruses
Inactivated autogenous vaccines But spontaneous regression common, so difficult to evaluate worth
56
Describe the host range of feline panleucopenia virus
57
Describe the transmission of feline panleucopenia virus
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
58
Describe the pathology of panleucopenia virus
Affinity for rapidly dividing cells (foetal, GIT, bone marrow) enteritis, diarrhoea, leucopenia Foetal death/cerebellar hypoplasia Secondary bacterial infection probably important in pathogenesis
59
Describe the control of feline panleucopenia virus
Attenuated and inactivated vaccines Attenuated vaccines should not be used on pregnant cats
60
Describe the pathology of canine parvovirus
severe haemorrhagic enteritis, leucopenia, (myocarditis) especially young dogs
61
Describe the transmission of canine parvovirus
Transmission via fecal-oral route Shed for 1-2 weeks
62
Is canine parvovirus a good candidate for eradication? Why/why not?
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)
63
Describe the diagnosis of canine parvovirus
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
64
Describe the control of canine parvovirus
Attenuated or inactivated vaccines Inactivated vaccine used in pregnant bitches Cross-react between subtypes, strongly immunogenic -\> solid immunity
65
Describe the pathology of porcine parvovirus
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
66
Describe the diagnosis of porcine parvovirus
Antigen detection in foetal tissue (Antibody detection of little value because disease is widespread)
67
Describe the control of porcine parvovirus
Attenuated and inactivated vaccines Gilts can be purposely infected prior to pregnancy
68
What family does psittacine beak and feather disease belong to?
Circoviridae
69
Describe the pathology of psittacine beak and feather disease
In parrots: species variability Cockatoos suceptible, lorikeets resistant abonormalities of feathering, beak and feet hepatitis diarrhoea immunosuppression
70
What family does chicken anaemia virus belong to?
Circoviridae
71
Describe the transmission of chicken anaemia virus
Horizontal and vertical transmission Breeders infected during lay produce infected eggs for ~6 weeks
72
Describe the pathology of chicken anaemia virus
Vertically infected chicks become diseased at about 10 days old ~60% mortality Stunted growth, anemia, immunosuppression Secondary skin infections, especially fungal
73
Describe the control of chicken anaemia virus
Virulent vaccine in drinking water
74
Describe the pathology of porcine circovirus 1
apathogenic
75
Describe the pathology of porcine circovirus 2
Post-weaning multisystemic wasting syndrome (~6w.o) Case fatality 10% Respiratory disease
76
Describe the control of porcine circovirus 2
Good husbandry (environmental factors important in pathogenesis) Removal of affected animals Elimination of infectious agents PCV2 vaccine
77
Describe the pathology of canine circovirus
Recently discovered in dogs in the US vasculitis, histocytic inflamation, thrombocytopenia
78
Describe the transmission of herpesviruses
Close contact, venerial, short-distance droplets in production systems
79
Describe the resistance of herpesvirus in the environment
relatively fragile Except Mareks, very resistant
80
Describe the clinical pattern of infection in herpesviruses
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
81
Are herpesviruses good candidates for eradication? Why/why not?
Yes - can screen population using antibody detection tests (relatively cheap) - remove carriers (AB+) - fragile virus with no long-term environmental reservoirs
82
What family does infectious bovine rhinotracheitis belong to?
Herpesvirdiae | (Bovine herpesvirus 1)
83
Describe the pathology of infectious bovine rhinotracheitis
respiratory disease conjunctivitis genital disease (infectious pustular vulvovaginitis) Exotic strain causes abortion
84
Describe the aetiology of bovine respiratory disease
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
85
Describe control of infectious bovine rhinotracheitis
- live attenuated bovine herpesvirus 1 vaccine - detection and removal of infected animals
86
Describe the pathology of bovine herpesvirus 5
fatal neurological disease in calves
87
Describe the pathology of bovine herpes mamillitis
(Bovine herpesvirus 2) Vesicles on teats and udder predispostion to mastitis loss of production
88
Describe the pathology of malignant catarrhal fever
- generalised disease, invariably fatal - erosive lesions of GIT - respiratory lesions - mucopurulent naso-occular discharge - lymphoproliferation and lymphocyte infiltration - vasculitis - corneal opacity - neurological sins
89
Describe the epidemiology of malignant catarrhal fever
Carried asymptomatically by wildebeast and sheep Sporadic transmission to cattle, deer via contact or infected pastures
90
Describe the diagnosis of malignant catarrhal fever
PCR
91
Describe the control of malignant catarrhal fever
No vaccine available Control contact with wildbeast/sheep/infected pasture?
92
Which herpesviruses are exotic to Australia?
Type 1.1 and 1.2a Infectious bovine rhinotracheitis (Type 2b endemic) Porcine herpesvirus 1 (Aujeszky's disease)
93
Which family does Aujeszky's disease belong to?
Herpeviridae | (Porcine herpesvirus 1)
94
Describe the pathology of Porcine herpesvirus 1 in pigs
- subclinical/mild respiratory disease in adult pigs - abortion - generalised fatal disease in piglets (100% mortality)
95
Describe the pathology of porcine herpesvirus 1 in non-pig hosts
fatal meningioencephaltis and pruritis in sheep, cattle, dogs, cats (pseudorabies, "mad itch")
96
What family of viruses does equine coital exanthema belong to?
Herpeviridiae | (Equine herpesvirus 3)
97
Describe the pathology of equine coital exanthema
Ulcerative lesions on penis/vulva
98
Which family does equine rhinopneumatitis virus belong to?
Herpeviridae | (Equine herpesvirus 4)
99
Describe the pathology of equine rhinopneumatitis virus
respiratory disease, especially in young foals
100
Which family does equine abortion virus belong to?
Herpeviridae | (Equine herpesvirus 1)
101
Describe the pathology of equine abortion virus
abortion respiratory disease fatal generalised disease in neonates encephalomyelitis
102
Describe the control of equine abortion virus
Killed/recombinant vaccine
103
Describe the pathology of equine cytomegaloviruses
Mostly apathogenic possible immunosuppression
104
Which family does feline rhinotracheitis virus belong to?
Herpeviridae | (Feline herpesvirus 1)
105
Describe the pathology of feline rhinotracheitis virus
upper respiratory tract disease responsible for 40% of cat flu rhinitis oculo-nasal discharge inappetance confjunctivitis keratatis +/- secondary bacterial pneumonia generalised disease in neonates
106
Describe the control of feline rhinotracheitis virus
Live attenuated vaccine not 100% protective
107
Describe the treatment of feline rhinotracheitis virus
management of clincal signs reduce stress prevent/treat secondary bacterial infections nucleotide analogues (famcyclovir)
108
Describe the pathology of elephant endotheliotropic herpesvirus
1&2: fatal disease in young (1-7 y.o) lethargy and inappetance death may occur \<24 hours
109
Describe the pathology of canine herpesvirus 1
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
110
Describe the pathology of infectious laryngeotracheitis virus
In chickens, esp 4-18m.o respiratory tract disease (coughing, sneezing, naso-ocular discharge, dyspnoea, haemorrhagic trachetis) up to 70% mortality
111
Describe the control of infectious laryngeotracheitis virus
Live attenuated vaccine
112
What family does infectious laryngeotracheitis belong to, and what species does it affect?
Herpeviridae Chickens
113
Describe the pathology of Marek's disease 1
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
114
Describe the pathology of Mareks Disease 2
Non-pathogenic in chickens
115
Describe the pathology of Mareks Disease virus 3
Non-pathogenic herpesvirus in turkeys
116
Describe the control of Mareks disease
Cross-protective attentuated Mareks disease vaccine or turkey herpesvirus Imperfect ("leaky") vaccine -\> evolution of virulence
117
Describe the transmission of Mareks disease
Shedd in of enveloped, infectious particles from feather follicles into environment Highly resistant in environment Infection via inhalation
118
Describe the pathology of herpes simplex 1
stomatitis, cold sores occasional encephalitis
119
Describe the pathology of herpes simplex 2
genital lesions
120
Describe the pathology of Epstein Barr virus
infectious mononucleosis (glandular fever)
121
Describe the pathology of varicella zoster
Chickenpox (initial infection) Shingles (recurring infection)
122
Describe the host range of Aujeszky's disease
Rodents, pigs Dead-end hosts: sheept, cattle, cats, dogs
123
Describe the transmission of Aujeszky's disease
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
124
Describe the control of Aujeszky's virus
Attenutated vaccine
125
Discuss the transmission of retroviruses
Very fragile in environment, transmission by close contact with body fluids
126
Describe the clincial timecourse of retroviruses
Produce persistent, progressive lifelong infections
127
Describe the diagnosis of retroviruses
Detection of antibodies Virus not detectable until ~disease period
128
Describe the mechanisms of oncogenic retroviruses
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)
129
What family does avian lymphoid leucosis belong to?
Retroviruses (oncovirus)
130
Describe transmission of avian lymphoid leucosis
- 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
131
Describe the control of avian lymphoid leucosis
Genetic resistance Avian leucosis-free flocks No vaccine available
132
Compare and contrast avian lymphoid leucosis with Marek's disease
133
Which family does feline leukaemia virus belong to?
Retrovirus (oncovirus)
134
Discuss the prognosis of feline leukaemia virus
Depends on age and dose Older cats: usually clear infection (immune response) Young cats: persistent viremea, development of clinical signs, Px 2-3 years
135
Discuss the pathology of feline leukaemia virus
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)
136
Discuss the transmission of feline leukaemia virus
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
137
Describe diagnosis of feline leukaemia virus
Detection of FeLV antigen Immunofluoresence, ELISA, rapid antigen detection tests
138
Describe control of feline leukaemia virus
Recombinant vaccine Cats should be tested to ensure antibody-negative prior to vaccination Test & remove effective in catteries
139
What family does enzootic bovine leucosis belong to?
Retrovirus (oncovirus) | (Bovine leukaemia virus)
140
Describe the pathology of enzootic bovine leucosis
Persistant lymphocytosis Non-regenerative anaemia Infiltration of lymphoblastic lymphocytes producing diffuse or nodular enlargement of many organs Small proportion: lymphosarcoma
141
Describe transmission of enzootic bovine leucosis
Blood transfer between animals
142
Describe control of enzootic bovine leucosis
Antibody test (gel diffusion test) and culling of AB+ animals
143
Describe the pathology of avian lymphoid leucosis
Often no clincial signs May be decreased egg laying and hatchability
144
Describe the pathology of reticuloendotheliosis virus
In chickens reticuloendothelial tumours runting feathering defects immunodepression
145
Which oncoviruses (retroviruses) are exotic to Australia?
Pulmonary adenomatosis (Jaagsiekte)
146
Why do lentiviruses (retroviruses) cause lifelong, slowly progressive disease?
- 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
147
Describe the timecourse of lentigenic disease
148
Which lentiviruses are exotic to Australia?
Visna-maedi
149
Describe the pathology of human immunodeficiency virus
Destruction of CD4+ T (helper) cells leading to severe immunosuppression and opportunistic infection Progression to AIDS
150
Describe the pathology of Maedi-visna virus
Maedi: slowly progressive pnuemonia Visna: slowly progressive demyelination Death
151
Which family does caprine arthritis encephalitis virus belong to?
Retrovirus (Lentivirus)
152
Describe the pathology of caprine arthritis encephalitis virus
Chronic lesion in mammary gland, lung, brain, and joints Cachexia
153
What family does equine infectious anaemia belong to?
Retroviruses (lentivirus)
154
Describe the pathology of equine anaemia virus
fever, anaemia, abnormal iron metabolism, gammaglobulin immunosuppression, cachexia acute death (unusual for lentiviruses) or recurrent periods of disease with progressive debilitation
155
Describe the transmission of equine anaemia virus
mechanimal transmission by biting insects (flies, mosquitos)
156
Describe the pathology of feline immunodeficiency virus
immunosuppression, opportunisitic infections anaemia lymphadenopathy lethargy febrile episdes
157
Describe the prevalence of feline immunodeficiency virus
transmitted via biting/fighting
158
Describe control of feline immunodeficiency virus
Killed vaccine Keeping cats indoors
159
Describe diagnosis of feline immunodeficiency virus
detection of antibodies in serum vaccine causes AB+ response, PCR for detection of pro-virus-DNA in blood samples now available
160
Describe the prognosis of feline immunodeficiency virus
Many cats live long lives Only a small percentage develop AIDS (poor prognosis)
161
Are retroviruses good candiates for eradication? Why/why not
Yes - fragile in environment, no reservoir - testing for antibodies detects carriers, can be culled
162
163
Discuss the role of arthropod vectors in transmission of viral disease
- 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
Discuss endemic and epidemic cycles in terms of arboviruses
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
Discuss the host range of equine encephalitis viruses
Arthropod host: mosquitoes Eastern, Western EE: maintenence host = birds Venezualan EE: maintenence host = mammals Dead end host = horses and **humans**
166
Which togaviruses can infect people?
Eastern, western, venuzualan equine encephalitis
167
Which togaviruses are exotic to Australia?
Eastern, Western, Venuzualan equine encephalitis
168
Discuss the control of equine encephalitis
Vaccination of horses Control of mosquito populations
169
Describe the host range of Japanese B encephalitis
Endemic: mosquito-bird Amplifying host: pigs Unusual hosts: horses, people
170
Describe the pathology of Japanese B encephalitis
encephalitis in horses, people reproductive problems (stillbirths, abortion) in pigs
171
Which flaviviruses are exotic to Australia?
Yellow fever Japanese B encephalitis West Nile virus
172
Which flaviviruses can cause infection in humans?
Japanese B Encephalitis Murray Valley Encephalitis Dengue West Nile virus West Nile-Kunjin virus
173
Describe the host range of Murray Valley encephalitis
Endemic: bird-mosquito Unusual hosts: horses, peole, domestic animals
174
Describe the pathology of Murray Valley encephalitis
Encephalitis in horse and people
175
Describe the host range of Dengue
Endemic: mosquito - non-human primates Now: mosquito - human (millions of cases annually)
176
Describe the pathogenesis of Dengue
Bite by infected mosquitos Complicated pathogenesis 4 serotypes, not cross-protective Infection with \>1 serotype facilitates disease
177
Describe the pathology of Dengue
Rash, arthragia, haemorrhagic fever
178
Describe the host range of West Nile virus
Endemic: mosquito-bird Causes disease in humans, horses, some bird species Seroconversion with no disease in many species
179
Describe the pathology of West Nile virus
rash, arthralgia, (rarely) encephalitis in people encephalitis in horses and some bird species
180
Describe the host range of West Nile virus-Kunjin virus
Endemic: mosquito-bird Mutated strain: causes disease in horses and people
181
Describe the pathology of WNV-Kunjin virus
Encephalitis in horses and people caused by mutated strain with additional virulence factors
182
List three syndromes caused by Bovine Virus Diarrhoea virus
1. Virus diarrhoea 2. Reproductive problems 3. Mucosal disease
183
List the two biotypes of Bovine Virus Diarrhoea virus
Cytopathic Non-cytopathic
184
Describe the pathology of virus diarrhoea syndrome
Mild GIT erosions diarrhoea immunosuppression respiratory disease May be mild or subclinical
185
Describe the pathogenesis and epidemiology of virus diarrhoea
Infection with cytopathic or non-pathogenic Bovine Virus Diarrhoea Virus Acute disease High incidence rate but low case fatality rate
186
Describe the pathology of reproductive syndrome caused by bovine virus diarrhoea virus
Reproductive problems in naive dams infected with cytopathic or non-pathogenic strains embryonic death, abortion, calves with cerebellar hypoplasia +/- Bovine virus diarrhoea
187
Describe the pathology of mucosal disease
Severe erosion of the GIT and digits Depression, fever, profuse diarrhoea
188
Describe the pathogenesis and epidemiology of mucosal disease
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
Describe the pathogenesis of bovine virus diarrhoea virus when infecting foetuses at varying stages of gestation
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
Describe the pathology of Border disease virus
abortion developmental abnormalities (hairy shaker lamb) neurological signs in lambs altered birth coat
191
Describe the epidemiology of hog cholera
Highly contagious, high incidence, high case fatality -\> explosive Strains vary from mild to severe
192
Describe the pathology of hog cholera (swine fever virus)
leucopenia immunosuppression haemorrhages (petichiae, ecchymoses)and skin discolouration vomiting, diarrhoea neurological signs, encephalitis abortion, congenital defects
193
Describe the control of mucosal disease
Serological testing (skin or blood samples) for Ag +ve, AB =ve (persitently infected animals) Killed or attenuated live vaccines in some countries
194
Which pestiviruses are exotic to Australia?
Swine fever (hog cholera)
195
Describe the control of swine fever (hog cholera)
Detection of viral antigen (immunofluorescence, antige ELISA) Slaughter
196
Is African Swine Fever Virus endemic to Australia?
No - Africa, Europe, Asia
197
Describe the transmission of African swine fever virus
Endemic cycle: ticks - warthogs and native pigs Disease in domestic pigs Biological transmission by ticks; direct contact
198
Describe the pathology of African swine fever virus
Warthogs, wild pigs: no disease Domestic pigs: fever, haemorrhages, dystentery, death
199
Describe the transmission of swine fever (hog cholera)
Infection by oral or respiratory route
200
Discuss why influenza viruses are difficult to control with vaccination
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
How do new human influenza subtypes emerge?
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
Describe the pathology of Influenza A(H1N1(pdm09)) in people
children, pregnant women, some chronic conditions most at risk severe disease and death from viral pneumonia
203
Discuss the pathogenesis of Avian influenza in birds
- all subtypes present - range from asymptomatic to severe (fowl plague) - species differences in pathogenicity
204
Describe the pathology of Fowl Plague
respiratory distress, cyanosis, nervous signs, diarrhoea, haemorrhage, rapid death
205
Describe the control of human influenza
Killed vaccine containing current strain, protective 6-9 months
206
Which influenza subtypes are exotic to Australia
H7N7(equi 1) H1N1 Swine flu (has been isolated in Aus, but no disease) H5N1 Avian influenza
207
Discuss the control of zoonotic Avian influenza
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
Discuss the pathology of equine influenza
fever, naso-ocular discharge, cough +/- secondary bacterial infection, pneumonia
209
Describe the control of equine influenza
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
Describe the epidemiology of equine influenza
highly contagious, spreads rapidly, self-limiting
211
Describe the pathology of canine influenza
respiratory disease ranging from mild, to severe + pneumonia; fever, cough.
212
Describe the epidemiology of canine influenza
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
Describe the pathology of swine influenza in pigs
respiratory disease and distress, cough, pyrexia, anorexia and emaciation +/- secondary bacterial infection Mortality highest in piglets from non-immune sows
214
Describe the pathology of parainfluenza virus 3
Shipping fever + calf pneumonia in cattle summer pneumonia in sheep +/- secondary bacterial infection Possibly apathogenic in pigs, horses, dogs
215
Describe the pathology of parainfluenza virus 2
Upper respiratory tract infection Role in kennel cough in dogs
216
Describe the pathology of respiratory syncytial virus
calf pneumonia and respiratory disease in feedlots
217
Which paramyxoviruses are exotic to Australia?
Rinderpest (globally eradicated, 2011) Velogenic Newcastle disease (but outbreaks from mutated lentogenic strains in 1990s) Nipah virus (AB/virus detected, but no disease)
218
Describe the epidemiology of rinderpest
severe disease, high incidence, high case fatality in cattle Mild disease in cattle, buffalo, game animals, sheep, goats
219
Describe the pathology of rinderpest
inflammation, haemorrhage, erosions, necorsis of digestive mucosal membranes, diarrhoea, death
220
Describe the host range of canine distemper virus
canids (dog, foxes), racoon, panda, ferrets, minks, large felids, red panda, civits, hyena
221
Describe the pathology of canine distemper
pyrexia, repiratory disease (pneumonia, bronchitis), conjunctivitis, gastroenteritis, encephalitis +/- secondary bacterial infection
222
Describe the sequelae of canine distemper
Demyelinating encephalitis: within months of recovery (autoimmune) "Old dog" encephalitis: years after recovery (slow, persistent viral replication) Neurological signs, loss of proprioception
223
Which family does rinderpest belong to?
Paramyxovirus
224
Which family does canine distemper belong to?
Paramyxovirus (Morbillivirus)
225
Describe the pathogenesis of canine distemper
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
Discuss control of canine distemper
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
Describe the pathology of Newcastle disease
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
What family does Newcastle disease belong to?
Paramyxovirus (Morbillivirus)
229
Describe the subcategories of newcastle disease
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
Describe control of Newcastle disease
In endemic countries, vaccination with lentogenic strain (selected for heat stability) In exotic locations, slaughter
231
Describe the pathogenesis of canine distemper
pathogenesis depends on AB response infection via droplets severe pathology with secondary bacterial infection
232
Describe the transmission of Newcastle disease
Respirtory route
233
What family does Hendra virus belong to?
Paramyxovirus (Henipavirus)
234
Describe the host range of Hendra virus
Reservoir host: fruit bats (no disease) \>50 spillover events into horses Occasional spillover into humans
235
Describe the epidemiology of Hendra virus
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
Describe the pathology of Hendra virus
Bats: no disease Horses: acute onset, pyrexia, severe respiratory signs, pulmonary oedema, neurological signs Humans: respiratory and neurological signs; 4/7 deaths
237
Describe control agains Hendra
Limit horses grazing under fruit trees Horse vaccination (recombinant with Nipah): 2 initial doses 21 days appart, yearly boosters
238
Describe diagnosis of Hendra
PCR. New variant recently discovered, not detected by current PCR -\> updating assays
239
What family does Nipah virus belong to?
Paramyxovirus (Henipavirus)
240
Describe the host range of Nipah virus
Fruit bats Pigs Humans
241
Describe the pathology of Nipah virus
Bats: no disease Pigs: encephalitis, respiratory signs Humans: 75% fatality
242
Describe the transmission of Nipah virus
Infected eating fruit or palm juice contaminated with urine or saliva of infected bats human-human transmission
243
What family does rabies belong to?
Rhabdovirus (Lyssavirus)
244
Describe the host range of rabies
Non-specific: broad host range affecting warm-blooded animals
245
Describe the pathogenesis of rabies
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
Describe the two main types of rabies
Paralytic rabies: usually herbivores Furious rabies: usually carnivores
247
Which rhabdoviruses are exotic to Australia?
Rabies Vesicular stomatitis
248
Describe the epidemiological features of rabies
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
Describe the diagnosis of rabies
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
Describe control of rabies
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
What type of vaccination is used for rabies
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
Describe the prophylactic and post-exposure therapy for rabies
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
Describe the pathology of rabies in humans
Early: may be vague, non-descript symptoms Later: Shaking, speech difficulties, severe anxiety, vomiting, agitiation, muscle tremors, paralysis, encephalitis
254
What family does Australian bat lyssavirus belong to?
Rhabdovirus (Lyssavirus)
255
Describe the pathology of rabies in animals
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
Describe the host range of Australian Bat Lyssavirus
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
Describe the pathology of Australian bat lyssavirus
Bats: paresis/paralysis, aggression, self-mutilation, other CNS signs, often found moribund or dead Horses: neurological signs, progressive ataxia, pyrexia
258
Describe control of Australian bat lyssavirus
Rabies vaccination and post-exposure protocol (96% shared DNA)
259
What family does vesicular stomiatitis belong to?
Rhabdovirus
260
Describe the pathology of vesicular stomatitis virus
Similar to FMD: causes vescicular lesions on mouth, snout, feet; rupture to leave ulcerative areas
261
Describe the host range of vesicular stomatitis
pigs, horses, cattle, zoonotic
262
Describe the transmission of vesicular stomatitis virus
Arthropod vectors (probably mechanical)
263
Which family does bovine ephemeral fever belong to?
Rhabdoviruses
264
Compare and contrast vesicular diseases
265
Describe transmission of bovine ephemeral fever
Biological transmission by mosquitos and culicoides species
266
Describe the pathology of bovine ephemeral fever
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
Describe the control of bovine ephemeral fever
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
Which poxviruses are exotic to Australia
Smallpox - globally eradicated Buffalopox Cowpox Sheepox/Goatpox Lumpy skin disease
269
Which family does infectious bronchitis belong to?
Coronavirus (in chickens)
270
Describe the pathology of infectious bronchitis
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
Describe the control of infectious bronchitis
live attenuated vaccines in water, by spray, or by eyedrops Vaccine failure from emergence of new antigenic varients
272
Describe the diagnosis of infectious bronchitis
detection of viral antigens or RNA in tracheal tissue virus culture in eggs -\> dwarfed, curled embryos
273
Which family does transmissible gastroenteritis belong to?
Coronavirus
274
Describe the pathology of transmissible gastroenteritis
In pigs: villous atrophy, profuse diarrhoea, vomiting, dehydration, death Most severe in piglets \< 3w.o \<=100% mortality
275
Which coronaviruses are exotic to Australia?
Transmissible gastroenteritis Porcine epidemic diarrhoea
276
Describe the diagnosis of transmissible gastroenteritis
detection of viral antigen or RNA in intestinal tissue Pathology -\> villous atrophy
277
Describe the control of transmissible gastroenteritis
Live attenuated vaccines Vaccination of pregnant sows confers MAB to piglets
278
Describe the pathology of porcine epidemic diarrhoea
watery diarrhoea, sometimes vomiting, mortality in piglets \<3w.o \<=100% Adult pigs with mild or no signs
279
Describe control of porcine epidemic diarrhoea
Vaccination in some countries
280
Describe the pathology of porcine haemagluttinating encephalomyelitis
Only affects young pigs depression, incoordination, hyperaesthesia vomiting, anorexia, wasting mortality \<=100%
281
Describe control of porcine haemagglutinating encephalomyelitis
No vaccine Disease not usually seen in endemic herds -\> piglets protected by MAB
282
Which family does porcine epidemic diarrhoea belong to?
Coronavirus
283
Which family does porcine haemagglutinating encephalomyelitis belong to?
Coronavirus
284
Which family does feline infectious peritonitis belong to?
Coronavirus
285
Describe the pathology of feline infectious peritonitis
effusions in peritoneal and pleural cavities granulomas and necrosis in visceral organs immunosuppression usually in cats \< 2yo usually fatal
286
Describe the pathogenesis of feline infectious peritonitis
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
Describe the control of feline infectious peritonitis
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
Describe the pathology of canine coronavirus
enteric and respiratory coronaviruses Gastroenteritis, may be subclinical In young pups: Severe clinical signs - vomiting, anorexia, depression, diarrhoea Low case fatality rate
289
Describe the diagnosis of canine parvovirus
Rapid antigen detection tests, sometimes combined with tests for canine parvovirus Some labs have developed PCR tests
290
Describe control of canine coronavirus
Inactivated vaccine, questionable efficacy
291
Describe the pathology of bovine coronavirus
Neonatal diarrhoea \< 3w.o Winter dysentery and respiratory disease in cows
292
Describe the control of bovine coronavirus
Neonatal calves most at risk -\> vaccinate dams, ensure sufficient colostrum intake
293
Describe the pathology of severe acute respiratory distress syndrome
fever, cough, pneumonia, diarrhoea 10% mortality (\>750 deaths/8100 cases)
294
Which family does severe acute respiratory distress syndrome belong to?
Coronavirus
295
Describe the epidemiology of severe acute respiratory distress syndrome
Epidemiological associations with wildlife meats Chinese rufous horseshoe bats natural reservoir
296
Describe the pathology of Middle East Respiratory syndrome
Severe respiratory disease, 40% mortality (\>800 deaths/\>2000 cases)
297
Which family does Middle East respiratory syndrome belong to?
Coronavirus
298
Describe the host range of Middle East respiratory syndrome
Dromedary camels reservoir host Isolated in bats from Hong Kong Humans
299
Describe the mortality rate of COVID-19
More than 2.5 million deaths worldwide 2% case fatality rate
300
What leads to the "spillover" events of coronaviruses?
- 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
302
Write brief notes on vesicular exanthema
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
Which family does vesicular exanthema belong to?
Calcivirus
304
Describe the pathology of feline calcivirus
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
List the pathogens involved in cat flu
Feline calcivirus (40%) Feline herpesvirus (40%) Chlamydia (20%)
306
Is feline calcivirus a good candidate for eradication? Why/why not?
No - Many serotypes, leading to vaccination failure - Shed from oropharynx for \>1y after recovery (carrier animals) - Resistant in environment
307
Describe the control of feline calicvirus
Attenuated vaccines available, but vaccination failures not uncommon (many serotypes)
308
Describe the pathology of rabbit haemorrhagic disease
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
Describe the control of rabbit haemorrhagic disease
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
Which family does foot and mouth disease belong to?
Picornavirus (Apthovirus)
311
Describe the host range of foot and mouth disease
Cloven-hoofed animals including cattle, deer, sheep, goats, pigs rarely, humans
312
Describe pathology of foot and mouth disease
Cows, pigs: fever, depression, loss of production vesicles on tongue, gums, snout, feet, teats Sheep and goats with mild or subclincal infections
313
Discuss the economic factors involved in foot and mouth disease
Loss of production, but less significant in endemic areas Significant impacts on international trade
314
Discuss transmission of foot and mouth disease
- 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
Is foot and mouth disease a good candidate for eradication? Why/why not?
- 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
Discuss the serotypes of foot and mouth disease
- 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
Describe the control of foot and mouth disease in exotic countries
- 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
Describe the host range of swine vesicular disease
Pigs only
319
Describe the pathology of swine vesicular disease
foot lesions; snout lesions uncommon
320
Which family does swine vesicular disease belong to?
Picornavirus
321
Which family do porcine enteroviruses belong to?
Picornavirus
322
Describe the pathology of porcine enteroviruses
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
Which family does avian infectious encephalomyelitis belong to?
Picornavirus
324
Describe the pathology of avian infectious encephalomyelitis
Paralysis and death in young chickens (2-3wo) drop in egg production in adult birds
325
Describe the transmission of avian infectious encephalomyelitis
horizontal or vertical transmission
326
Describe the control of avian infectious encephalomyelitis
Vaccination of pullets (before lay) - \> No vertical transmission - \> Chicks protected by maternal antibodies
327
Describe the host range of rhinoviruses
cattle, horses, people
328
Describe the pathology of rhinoviruses
upper respiratory tract disease (common cold)
329
List the host range of encephalomyocarditis virus
maintained in rodents pigs + other species including monkeys, kangaroos
330
Describe the pathology of encephalomyocarditis virus
Pigs: acute myocarditis and sudden death (mortality \<=100% in young pigs) Sudden death in monkeys, kangaroos
331
Which family does encephalomyocarditis virus belong to?
Picornavirus
332
Name the three genera of Reoviruses
Orthoreovirus Orbivirus Rotavirus
333
What family does bluetongue belong to?
Reovirus (Orbivirus)
334
Describe transmission of bluetongue
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
Describe the pathology of bluetongue in sheep
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
Describe the pathology of bluetongue in cattle
Usually asymptomatic or mild disease congenital defects from in utero infection
337
Describe some of the major attributes of bluetongue
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
Discuss the control of bluetongue
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
Discuss the pathology of African Horse Sickness
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
Which family does African horse sickness belong to?
Reovirus (Orbivirus)
341
Describe the transmission of African horse sickness
Arbovirus (culicoides)
342
Describe control of African horse sickness
9 serotypes -\> polyvalent vaccine
343
Describe the diagnosis of foot and mouth disease
-Detection of viral antigen (complement fixation test, ELISA) or viral RNA (PCR) in samples of vesicular fluid or tissues
344
Which reoviruses are exotic to Australia?
Some strains of Bluetongue African horse sickness
345
Which family do rotaviruses belong to?
Reovirus
346
Discuss the pathology of rotaviruses
diarrhoea in neonatal animals, depression dehydration or secondary bacterial infection
347
List the host range of rotaviruses
piglets, calves, foals, lambs, mice, babies
348
Describe the epidemiology of rotaviruses
large amounts shed in excretions highly stable in environment
349
Describe the control of rotaviruses
detection of viral antigen in faeces (serological assays) detection of viral RNA in PCR
350
Describe the control of rotaviruses
Ensure sufficient colostrum intake killed vaccines for dams (sows and cows)
351
Which family does infectious bursal disease (Gumboro's disease) belong to?
Birnavirus | (Bi = 2, (ds)RNA, virus)
352
Discuss the pathology of infectious bursal disease
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
Discuss the control of infectious bursal disease
Live attenuated and killed vaccines Outbreak of virulent strains in some countries not effectively controlled by vaccination -\> serious economic losses
354
Which family does Akabane belong to?
Bunyaviruses
355
Discuss the transmission of Akabane
Arbovirus (Cullicoides)
356
Describe the pathology of Akabane
No disease in adult hosts Foetal abnormalities: Arthrogryposis (fixed flexion or extension of joints), hydroencephaly, encephalitis
357
Describe the host range of Akabane
Mosquitos -\> Cattle, sheep, goats
358
Discuss the presence of Akabane in Australia
Endemic to QLD, disease rarely seen (dams infected prior to pregnancies) Outbreak into naive populations in NSW
359
Describe the detection of akabane
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
Which family does Schmallenberg virus belong to?
Bunyavirus
361
Describe the transmission of Schmallenberg virus
arbovirus (culicoides)
362
Describe the host range of Schmallenberg virus
cattle, sheep, other ruminants
363
Describe the pathology of Schmallenberg virus
congenital abnormalites, stillbirths, production losses
364
Which family does Rift Valley fever belong to?
Bunyavirus
365
Describe transmission of Rift Valley fever
Arbovirus (mosquitoes) with transovarial transmission Humans infected via mosquito or contaminated blood (e.g. autopsy, slaughter)
366
Describe the host range of Rift Valley fever
Mosquitos -\> cattle, sheep, goats, most domestic animals, **zoonotic**
367
Describe the pathology of Rift Valley fever
hepatitis, encephalitis, abortion disease and death in humans
368
Which bunyaviruses are exotic to Australia?
Schamallenberg virus Rift Valley fever
369
Describe the pathology of equine viral arteritis
Range of signs - asymptomatic - fever, oedema, respiratory signs, abortion, necrosis of small arteries
370
Describe the transmission of equine viral arteritis
aerosols, semen
371
Describe the control of equine viral arteritis
removal of carrier stallions, vaccinations virus present in Australia, but no disease seen (non-virulent strain)
372
Which family does porcine respiratory and reproductive syndrome belong to?
Arteriviruses
373
Which arteriviruses are exotic to Australia
Porcine respiratory and reproductive syndrome Equine viral arteritis is present in Australia, but does not cause disease
374
Describe the pathology of porcine respiratory and reproductive syndrome
abortion, neonatal deaths, respiratory disease in young piglets
375
Describe the control of porcine respiratory and reproductive syndrome
Killed and live attenuated vaccines in endemic countries
376
Describe the common features of prion disease
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
Describe the differences of PrPSc as compared to PrPc
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
Describe the recommended inactivation protocol for prions
- autoclaving at 132ºC for 90 min - hot solutions of sodium hydroxide - high concentrations of sodium hypochlorite (NOT a guarentee of inactivation)
379
Describe the mechanisms of prion disease
**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
Discuss the host barrier as it relates to prion disease
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
Discuss the classification of prions
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
Which family does Scrapie belong to?
None - Prion
383
Describe the host range of scrapie
Sheep, goats More common in sheep
384
Describe the pathology of scrapie
pruritis, decreased wool quality progressive neurological disease: ataxia, tremors, apprehension, increased excitability, paralysis emaciation, death
385
What is the incubation period of scrapie?
1-5 years
386
Which prion diseases are exotic to Australia?
Scrapie Bovine spongiform encephalopathy Transmissible mink encephalopathy Creuztfeld-Jacob disease Kuru
387
Describe the transmission of scrapie
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
Describe the diagnosis of scrapie
histopathology of brain (vacuolation, degeneration of neurons) EM for fibrils immunoblotting (no detectable serological response)
389
Which family does bovine spongiform encephalopathy belong to?
None: prion
390
Describe the host range of bovine spongiform encephalopathy
Cows -\> CJD in humans
391
Describe the pathology of bovine spongiform encephalopathy
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
What is the incubation period of bovine spongiform encephalopathy?
2-5 years
393
Discuss the epidemiology of bovine spongiform encephalopathy
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
Describe the Australian response to bovine spongiform encephalopathy
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
Which family does chronic wasting disease of deer and elk belong to?
None: prion
396
Describe the pathology of chronic wasting disease of deer and elk
severe wasting, trembling, ataxia
397
Describe the transmission of chronic wasting disease of deer and elk
Horizontal transmission occurs through prion in saliva
398
Which family does Kuru belong to?
None: prion
399
Describe the host range and incidence of Kuru
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
List the two types of Cruetzfeld-Jakob disease
1. Sporadic CJD 2. New variant CJD
401
Discuss the host range of sporadic Cruetzfeld-Jakob disease
Humans of all nationalities and ethnic groups, usually \> 50 years old
402
Discuss the mechanism of sporadic Cruetzfeld-Jakob disease
Mutation of PrPC gene to produce PrPSc protein Spontaneous misfolding Transmission by: Iatrogenic transmission Corneal transplants Growth hormones harvested from cadavers
403
Describe the pathology of sporadic Cruetzfeld-Jakob disease
Neurological signs: sensory disturbance, sleeping disorders, dementia, motor disturbances, coma, death
404
What are the differences with new variant Cruetzfeld-Jakob disease compared to sporadic CJD?
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
Why is it thought that new variant Cruetzfeld-Jakob disease is related to bovine spongiform encephalopathy
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