Flaviviridae, Togaviridae, Reoviridae Flashcards
1
Q
Flaviviridae
A
- positive sense ssRNA
- enveloped; labile in environment
- vectors (arthropods) important in transmission
2
Q
Flaviviridae is separated in 2 generas
A
- Flavivirus
2. Pestivirus
3
Q
Significant Flavivirus
A
- Japanese encephalitis (JE) virus
- Louping ill virus
- West Nile Virus (WNV
- Kunjin Virus (KUN)
4
Q
Epidemiology of Flavivirus
A
- Arboviruses; transmitted by arthropods- infects a range of vertebrate species, mammals, bird
5
Q
Pathogenesis of flavivirus
A
- Arthropod bites
- replicates in LN at site of inoculation
- virameia
- Dissemination (other organs, tissues, and brain)
- replication–> disease
6
Q
Enveloped viruses need what responses?
A
Humoral AND cell mediated responses
7
Q
Flavivirus immunity
A
- Neutralises antibodies to envelop proteins; recovery and long term immunity
- non-structural viral proteins induce cytotoxic T cell response
8
Q
Japanese encephalitis (JE)
A
- most important mosqito-borne pathogen
- mosquito-pig-mosuito transmission cycle
9
Q
Main reservoir host of JE
A
Waterfowl- also amplifying host
Pigs are also important amplifying host
10
Q
JE in humans and horses
A
- severe and fatal encephalitis
- dead end (horses and humans cant infect mosquito)
11
Q
JE control
A
- horses must be vaccinated prior to travelling to aus
- ectoparasite control
12
Q
West Nile virus
A
- human, horse and birds
- lethargy, depression, fever
- threat to AUS
- mosquito vector
13
Q
West Nile Virus control
A
- reduce vector numbers; drain standing water to prevent breeding mosquitos
- reduce risk of exposure to vectors; reduce dawn dusk outdoor activities when mosquitoes are active- keep horse in stable at the time, insect repellant
- vaccination
14
Q
Pestiviruses
A
- classic swine fever virus (hog cholera)
- Bovine Viral Diarrhea virus (BVDV)
15
Q
Hog cholera
A
Pestivirus exotic to aus.
- oral/respiratory
- replication in tonsil–> viraemia00> haemorrhagic disease–> vomiting, diarrhoea, coughing, tremor
16
Q
BVDV
A
2 syndromes:
- Bovine viral diarrhoea
- Mucosal disease
17
Q
Pathogenesis of BVDV
A
- oral/nasal route
1. replication in oronasal mucosa
2; viraemia; immunosuppression, transplacental spread
3. attacks rapidly dividing enterocytes of intestinal crypts
4. diarrhoea and intestinal haemorrhage
18
Q
Transmission BVDV
A
- contagious secretions
- mutations compromise herd immunity
- rare indirect spread bc environmentally labile
- no arthropod vectors
19
Q
BVDV in non-pregnant cattle
A
- drop milk yield
- 2 degree bacterial infection
20
Q
BVDV pregnant cow
A
- biggest problem
- transplacental spread to fetus
- fetal death <125 days
- > 125 days; develop neutralizing antibody, eliminates virus
21
Q
Consequences of early pregnancy (80-125 days) transplacental transmission BVDV
A
- cow and fetus infected w non-cytopathic BVDV in early pregnancy
- cow becomes immune. Fetus becomes tolerant and unable to make antibody
- Calf remains infected w virus for life
- mutation of virus to cytopathic form may occur
- superinfection of this and other viremic animals w cytopathic virus causes fatal mucosal disease
22
Q
BVDV diagnosis
A
- muscosal; chronic
- bovine viral diarrhea; acute
- detect virus using cell culture virus isolation; faeces, blood, immunohistochemistry, RT PCR
23
Q
BVDV control
A
- killed vaccine- limited success
- live vaccines; may cause severe mucosal disease in persistenyl infected animal
- immunotolerant animals are biggest source of virus
- faecal screening for viral antigen or RNA of progeny
- eliminate positive
- biosecurity
- change clothing, disinfect
24
Q
Togaviridae
A
+ssRNA, enveloped
25
Togaviridae genus Alphavirus
- Arboviruses
- picked up from blood meals from animals
- non-cytopathic in insect vector
- replication in salivary gland
- transmission by biting other animals
- mechanical biological vector
26
Significant togaviruses
- Eastern equine encephalitis (EEE)
- Western equine encephalitis (WEE)
- Venezuelan encephalitis (VEE0
- Ross river (RR)
- Getah virus
27
Basic pathogenesis of togavirus disease
1. animal is bitten by infected insect
2. virus enters bloodstream, taken up by mononuclear cell and viraemia occurs
3. replication occurs in spleen and lymph nodes
4. cell associated secondary virameina which results in clinical signs
5. If sufficient, virus is produced during secondary phase to escape immune protection and to reach critical target tissues--> severe systemic disease and encephalitis
28
RR and Getah virus do not
produce encephalitis in horses
29
WEE and EE epidemioloy
Reservoir hosts: birds and small mammals (mortality and disease in these hosts)
vectors: mosquito
human horses: dead end
30
Epidemioogy of VEE
- in rainforests
- cycles between mosquitoes and forest rodents; reservoir hosts
- produces high viraemiea in horse- mosquito cycle
31
Signs of WEE and EE in horse
- fever, hypersensitivity, aimless walking, circling, death after 4 days
32
signs of VEE
- similar encephalitis signs of WEE and EEE
33
WEE EEE VEE diagnosis
- ELISA, haemaglutination, Viral isolation
34
WEE EEE VEE control
reduce insect vector conc; drain standing water, pesticide, clothing, repellent
35
Reoviridae
- dsRNA
| - non-enveloped
36
Significant reoviruses
- Rotaviruses; cause enteritis and diarrhoea in all domestic animals
- stable over wide range of pH and survives month in faecal contaminated env and long periods in water
37
Diagnosis reoviruses
- Faecal/intestinal contents
| - EM, direct ELISA, RT-PCR, difficult to culture
38
Treatment control Reoviruses
Treatment: supportive therapy, replace milk w water and electrolytes
control: reduce exposure to virus; young animals, clearning, disinfecting, vaccinate pregnant dams, ensure adequate colostrum, minimise stress
39
Bluetongue virue
An orbivirus mainly in sheep and other ruminants
Host factors: age and breed of sheep
Environmental factors: nutritional status and exposure to sunlight
40
Culicoids spp (midges)
1. female midges infected when feeding on infected animal
2. virus replicates in their tissues
3. transmite via saliva and is infectious for life
- movement via environmental conditions; wind, seasonal, climate change
41
Pathogenesis of bluetongue
1. replication in regional LN from site of inoculation and carried in blood to lymphocytes for further replication
2. Localization and multiplies in endothelium of small blood vessels
3. Viraemia
42
Clinical signs of blue tongue
- fever, depression, lameness, ulcers, oedemin in lips and tongue, fleece loss
43
Bluetonge diagnosis
- clinical findings, post mortem
- viral isolation LN, spleen
- RT PCR
- ELISA
44
Bluetonge control
- ectoparasite control
| - killed vaccine
