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DVM 2 - 1 > Virology 1 > Flashcards

Virology 1 Flashcards

1
Q

Family Poxviridae what is the main sub-family and characteristics

A

Chordopoxvirinae

- pox viruses of vertebrates

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2
Q

Poxviridae pathogenesis of the lesion and where find

A

Typical “pock” lesion

1) Begins as a raised, reddened macule
2) Progresses to form a papule
3) Becomes a fluid filled vesicle
4) Ruptures to form a crater (pock)
5) Scarring - if survive life-long
- Clinical signs referrable to skin lesions in localised disease, or to organ damage in generalised disease (such as sheeppox)

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3
Q

Poxviridae features in environment, carriers, duration of immunity

A
  • Pox viruses are very resistant in the environment - envelope but large and sturdy envelope
  • Infectious virus survives for years in infected material (scabs)
  • Surviving animals are NOT long term carriers
  • Duration of immunity < life span of recovered animal - possible for life with new research
    ○ Generally older animals are protected as exposed as young animals, so mainly see in younger animals as the environment becomes a carrier
  • Reinfection possible
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4
Q

Poxvirus transmission between animals may be, list the 3 types

A

1) Via abraded skin - skin lesions
2) Respiratory route by droplets - in outbreak situation in close proximity
3) Mechanical transmission - vectors, skin lesions

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5
Q

Orthopoxvirus what is the family within and List 4 viruses within

A

Poxvirus -> Chordopoxvirinae -> Orthopoxvirus

1) Smallpox virus - major cause of human morbidity and mortality
2) Vaccinia virus
3) Cowpox virus
4) Monkeypox

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6
Q

Monkeypox what type of virus what are the hosts involved, what type of disease

A

Poxviridae

  • transmitted through primates including humans, rodents are also hosts
  • Is an emerging disease, wasn’t such an issue when the smallpox vaccination was circulated as some cross-protection, now herd immunity is low so monkey pox is attacking mainly younger children and generations
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7
Q

Capripoxvirus what type of virus, what are the 3 diseases

A

Poxviridae
• Sheeppox
• Lumpy skin disease
• Goat pox

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8
Q

Sheeppox, goatpox, lympy skin disease what type of virus, where present, what type of spread

A

Capripoxvirus

  • Endemic in SE Europe, Middle East, Africa and Asia
  • Endemic: generalised disease and mortality uncommon
  • In outbreaks can get respiratory spread, systemic disease - more serious clinical signs
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9
Q

Sheeppox, goatpox, lympy skin disease what type of virus and pathogenesis

A
  • Virus shed from skin lesions and nasal/ocular discharge
    ○ Infection via skin abrasions or inhalation of aerosols
  • Replicates locally in skin
  • Replicates in lungs following inhalation
  • Spread to regional lymph nodes
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10
Q

Sheeppox, goatpox, lympy skin disease what type of virus clinical signs and mortality

A 
Capripoxvirus
Clinical Signs
- Incubation period ~ 1 week
- Fever, oedema of eyelids, conjunctivitis and nasal discharge
- Skin lesions
- (Lung consolidation and haemorrhage - with larger outbreaks and repsiratory transmission 
Mortality:
- Up to 50% in indigenous breeds
- Up to 100% in European breeds
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11
Q

Molluscipoxvirus and

Avipoxvirus what type of virus and importance

A
  • Molluscipoxvirus - significantly zoonotic

* Avipoxvirus - Fowlpox virus and other avian pox viruses- Used as a vector for vaccines such as equine influenza

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12
Q

Fowl pox what type of virus and the 3 transmission

A

1) Mechanical transmission by mosquitoes
2) Physical touch - skin abrasion - remain infectious in scab material for a long time
3) Aerosol transmission

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13
Q

Parapoxvirus what type of virus, what are the 3 also calld

A

Poxviridae -> Chordopoxvirinae

1) Orf virus (scabby mouth)
2) pseufocowpox virus
3) bovine papular stomatits virus

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14
Q

Orf (Scabby Mouth) where occur, what does it lead to and transmission

A 
• Occurs worldwide
• (Contagious pustular dermatitis)
• (Contagious ecthyma)
Pathogenesis
• Epitheliotropic virus
• Proliferative wart‐like lesions
Replicates in epidermal keratinocytes
• Papular lesions progress to vesicles, pustules and then scabs
• Lesions heal within 4 weeks (if no secondary bacterial infection)
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15
Q

Orf (Scabby Mouth) epidemiology and control

A

Epidemiology
• Transmission via abrasions
• Primarily a disease of young sheep
• Maintained in flocks by chronic carriers
• Lesions on lips and muzzle (feet, genitalia and teats)
• Can be zoonotic
Control
• Virulent vaccination
• Scarification of axilla of ewe prior to lambing - scratch into skin

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16
Q

What is the main virus in Leporipoxviruses, host and disease

A

Myxomatosis
• Poxvirus disease of rabbits
• Causes benign fibromas in wild rabbits but severe generalised disease in european rabbits - highly fatal 90% often within 48 hours
•

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17
Q

Was the biological control of Myxomatosis a success or fail

A

Success - dramatic decrease in numbers of rabbits and maintained at this lower level, also still killing rabbits today
Fail - getting increased genetic resistance and now using calicivirus instead

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18
Q

Family Asfarviridae what type of genome, features, how long survive and the main disease

A

• Complex double stranded DNA virus
• Enveloped
• Stable in environment over wide range of temperatures (4‐20oC) and wide range of pH
• May persist for months in meat of infected pigs
African swine fever virus

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19
Q

African swine fever virus within what family, what infect, mortality and control

A

Family Asfarviridae
• Infect only Suidae (all members tested) and soft ticks
Mortality/control
• Die of extensive haemorrhages due to platelet damage and complement activation ‐haemorrhage in all organs, lymph nodes resemble blood clots
• Survivors may be normal or chronically ill ‐ all are carriers
• No neutralizing antibody produced
• No vaccine
• Risks of international spread ‐ live pigs, pig meat, food scraps

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20
Q

Herpesviruses common characteristics, what length of infection

A

• Enveloped double stranded DNA
• Labile in environment - FRAGILE
○ Easily inactivated by heat,
○ detergents, pH, drying
• Close or mucosal contact for transmission (droplet)
• Lifelong latent infection, remain dormant

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21
Q

What does the envelope on the virus initiate

A

Envelope - doesn’t provide protection

  • Does provide glycoproteins needed to initiate infection and disease
  • Also attachment - start of the virus life-cycle
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22
Q

Describe the latency of Herpesviruses

A

• Persistent infection with continuous or periodic shedding
• Copies DNA in infected cells (often neurons)
• No viral gene expression
○ Generally doesn’t cause large amounts of disease unless immunocompromised • Reactivation during periods of stress leads to shedding (source of virus)
○ May be sub‐clinical - due to pathogen host relationship
○ Recrudescent disease - rival of the infection and disease

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23
Q

What are the 3 sub-families of herpesviridae and which is the one with horses

A

1) Alphaherpesvirinae
2) Betaherpesvirinae
3) Gammaherpesvirinae - equine herpes virus 1 and 2

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24
Q

Bovine herpesvirus 1 what are the 7 general clinical disease it leads to

A

1) rhinotracheitis
2) vulvovaginitis
3) balanoposthitis
4) conjunctivitis
5) abortion
6) enteritis
7) generalised disease of newborn calves

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25
Q

Rhinotracheitis clinical signs list 5, how long to recover and major issue

A 
• Nasal discharge
• Hyperaemic nasal mucosa
• Dyspnoea
• Coughing
• Recover within 5‐10 days
PROBLEM - Predispose to other bacterial secondary infections
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26
Q

Vulvovaginitis Clinical signs list 4 and how spread

A 
• Frequent micturition
• Swollen vulval labia
• ± vulval discharge
• Hyperaemic vestibular mucosa with pustules
CAN GET SPREAD VIA GENITAL ROUTE as well
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27
Q

Bovine herpesvirus 2 what also called and two forms of clinical diseases

A

Bovine mammillitis virus (Pseudo‐lumpy skin disease virus)

  • Causes a two forms of clinical diseases
    1. Mammillitis. Lesions localised to the teats.
    2. Generalised skin lesions. Nodules & necrosis of the superficial epidermis
  • Looks like lumpy skin which is an important trade disease
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28
Q

Bovine herpesvirus 5 what also called and what does it called

A

Bovine encephalitis virus
- Causes fatal meningoencephalitis in calves thought to be due to direct neural spread from nasopharynx via trigeminal nerve

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29
Q

Equine herpesvirus 1 EHV1 how is it present in the population, what animals most at risk, general disease, infection via

A
  • Most important viral cause of abortion in horses worldwide - group at risk are pregnant mares
  • Endemic in all horse populations - not going to prevent infection of foals just want to prevent pregnant mares from having the activation of latent or getting activated virus
  • Causes respiratory disease, abortion and neurological disease
  • Infection via respiratory tract
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30
Q

EHV1 abortions what signs, when occur and what are the 2 causes

A
  • No premonitory signs
  • Usually late gestation - last trimester
  • Most commonly a single abortion
  • Outbreaks occur when index case is poorly managed
    Caused by: 1. Mare gets infected from other mare 2. latent infection in mare becomes active leading to abortion
  • The aborted foetus has extremely high levels of virus, need to keep other horses away
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31
Q

List 2 control mehtods to minimise risk of EHV1 abortions

A

1) Pregnant mares be kept separate from other horses - can have in other horses not high risk
2) Small groups based on foaling date - decrease risk of abortion via exposure to virus
○ If one mare aborts separate down into smaller groups to further decrease risk of exposure if possible

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32
Q

EHV1 Epidemiology how long is aborting mare infectious

A
  • Aborting mare is infectious for 1‐2 days from reproductive tract and up to 2 weeks from the respiratory tract - need to separate from every other horse
    ○ Latent infection (as are many others in the herd) - if wasn’t already infected (likely)
    ○ Breed again on first oestrus after foal heat)
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33
Q

What are the spreads of disease in EHV1

A
  1. Mare to foal spread - pre-weaning
    ○ Colostrum or aerosols
  2. Foal to foal spread - pre-weaning
  3. Foal to foal spread - post-weaning
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34
Q

Equine herpesvirus 4 what also called, what disease, cause, what age most susceptible and control

A

Equine rhinopneumonitis
- Causes acute respiratory disease characterised by nasal discharge and lymphadenopathy
- Foals infected early in life
- Weanlings and yearlings show most severe clinical signs
Combined EHV1 and EHV4 vaccine available

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35
Q

Feline herpesvirus 1 what also called, what disease cause, when seen and control

A
  • Causes acute respiratory disease characterised by nasal discharge, ocular discharge, sneezing, dyspnoea and occasional oral ulcers
  • Seen most frequently in multi‐cat households and catteries
    ○ Infected by activated virus within a latent adult, kittens haven’t developed immunity yet
  • Inactivated and live attenuated vaccines available
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36
Q

Gallid herpesvirus 1 what also called, host, what leads to

A

Infectious laryngotracheitis (ILT)

  • Most common in young chickens (although all ages susceptible)
  • Causes acute respiratory disease characterised by nasal and ocular discharge, sneezing, dyspnoea, loud gasping and coughing
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37
Q

Family Adenoviridae what type of disease, what type of virus and host range

A
  • Respiratory and gastroenteric disease
  • Mild or sub-clinical in most cases
  • dsDNA viruses
  • Non-enveloped - more stable in environment
  • Narrow host range
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38
Q

What is the main genera in family adenoviridae

A

1) Mastadenovirus -

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39
Q

Canine adenovirus 1 what also called and the 3 general clinical signs

A
  1. Peracute disease: pup found dead, often with short lived (3-4 hours) or no apparent illness
  2. Acute disease: may be fatal. Fever, vomiting, bloody diarrhoea, sudden collapse, petechial haemorrhages of gums, pale mucous membranes, abdominal pain
  3. Mild or unapparent disease
40
Q

Fowl aviadenovirus what type of virus and what are the main lesions

A

Adenovirus

  • When infect cells go into nucleus leads to internuclear inclusion bodies
  • Inclusion body hepatitis
41
Q

Canine adenovirus 2 what also called, disease it leads to, clinical signs and control

A

Infectious canine tracheobronchitis (makes up kennel cough)

  • CAV2 causes localised respiratory disease (part of kennel cough complex)
  • Bronchitis and bronchiolitis
  • No systemic infection
  • CAV2 provides complete homologous protection and cross protection against disease caused by CAV1 without side effects
42
Q

Equine adenovirus 1 and 2 where isolated from, disease cause in what animals

A
  • Isolated worldwide
  • Equine adenovirus 1 isolated from young horses with and without respiratory disease
  • Equine adenovirus 2 isolated from lymph nodes and faeces of foals with respiratory disease and diarrhoea
  • Mostly asymptomatic or mild disease associated with these viruses
    ○ Except for arabian foals with genetically-based primary severe combined immunodeficiency
43
Q

Family Papillomaviridae how does infection occur and clinical presentation

A
  • Infection through skin abrasions
    ○ Move up the skin and then shed into the environment
  • Papillomas (warts) - usually regress after several weeks
  • Carcinomas in cattle (bracken fern) or rabbits
44
Q

Bovine Papillomaviruses what are the 2 main forms of transmission and clinical presentation

A

Transmission
- Fomite transfer (equipment and facilities)
- Sexual transmission venereal warts is likely (not by AI)
Clinical presentation
- Fibropapillomas (warts) on udder, teat, head and neck and genitalia
- Papillomas (lesions with less fibrous tissue)
- Bovine papillomavirus and Bracken fern poisoning (enzootic haematuria)
○ Neoplastic transformation
- BoPV4 is associated with lesions in the alimentary tract, some of which progress to squamous cell carcinoma (Bracken fern)

45
Q

Equine Papillomaviruses what does it cause, where on the body and what happens

A

Cause aural plaques and cutaneous papillomas

- Generally occur around the muzzle of young horses
- Regress of 1-9 months
46
Q

Fibrosarcome what is it, what causes, features and transmission

A
  • Most common skin tumour of horses, mules and donkeys (single or multiple)
  • Bovine papillomavirus implicated (replication?)
  • More common <4 years of age
  • Head, ventral abdomen and limbs affected most commonly.
  • Sites of previous injury or scarring
  • Locally aggressive, does not metastasize
  • Superficial ulceration and secondary trauma are common
    Transmission: fomites, flies?
47
Q

Parvoviruses what are the main features

A
  • Small non‐enveloped single stranded DNA viruses
  • Replicate in nucleus
  • Require rapidly dividing cells (S‐phase) to replicate within
  • Very stable in the environment
  • Very resistant to detergents, drying, heat, solvents, pH changes, disinfectants
48
Q

What are the 3 main parvoviruses of veterinary significance, how contagious and what does it cause

A

1) Feline Panleukopaenia virus
- Highly contagious, systemic and enteric disease of cats
- Bone marrow suppression, GIT signs, cerebellar hypoplasia (foetus)
2) Canine Parvovirus 2
- Highly contagious, enteric disease of dogs
- Haemorrhagic gastroenteritis, myocarditis (rare)
3) Porcine Parvovirus
- Reproductive disease

49
Q

Feline panleukopaenia virus how many serotypes, distribution, what ages susceptible and the infection transmission

A
  • one serotype -> only need one type of vaccination
  • Worldwide distribution
  • Endemic disease in unvaccinated cat populations: young cats
    affected
  • Cats of all ages susceptible
    ○ Primarily see disease in kittens as maternal antibody wanes
  • Trans‐placental infection in susceptible queens (unneutered female cat - foetus is rapidly dividing)
  • Virus excretion in faeces (several weeks after clinical recovery), also in saliva, urine vomit (acute stages)
50
Q

Feline panleukopaenia virus incubation period, stages of the disease and what occurs after infection

A
  • Incubation period ~5 days
  • Onset of disease associated with profound panleukopaenia + fever
  • Severe cases die in peracute stage
  • Acute cases progress to vomiting, (bloody) diarrhoea, dehydration
  • Strong long‐lasting immunity
51
Q

Feline panleukopaenia virus where replicate and what can utero infection cause

A
  • Perinatal, or in utero infection can cause cerebellar (part of the brain that leaves to fine motor control) hypoplasia/atrophy
    Pathogenesis
  • Virus enters via oropharynx, replicates in pharyngeal lymphoid tissue
  • Distributed by free and cell associated viraemia
  • Mitotically active cells (S‐phase)
    • Intestinal crypt cells
    • Lymphopoietic cells of bone marrow
    • Foetal cells (cerebellum, retina, death)
52
Q

Feline panleukopaenia virus prevention and treatment

A
  • No specific treatment
  • Supportive therapy:
    • Fluid therapy
    • Blood / plasma transfusion
    • Broad spectrum antibiotics
  • Vaccination
    • Inactivated and live‐virus vaccines available
    ○ If outdoor cat in contact with other cats probably need multiple vaccines however if indoor, only 1 cat household and vaccinated once, probably doesn’t need another vaccine
  • Catteries: strict hygiene, quarantine and disinfection required
53
Q

Canine parvovirus 2 mortality and morbidity, how stable in environment, route of infection and most susceptible ages

A
  • High morbidity and mortality in initial outbreak situation (all ages)
  • Faeco‐oral route of infection following exposure to virus contaminated faeces
  • Very stable virus in environment
  • Severe disease in pups between 6 weeks and 6 months of age (waning maternal immunity) - if not vaccinated
54
Q

Canine parvovirus 2 clinical signs and where replicate

A
  • Disease may be mild or sub‐clinical if sufficient immunity
  • Haemorrhagic gastroenteritis and vomiting
  • Myocarditis (uncommon) in pups infected late gestation or first 2 weeks of age due to rapid proliferation of myocytes in the perinatal period - young working dogs that haven’t been exposed
  • Rapidly dividing cells in intestinal crypts are infected
    ○ Crypt cells are progenitors to entire intestinal mucosa
    ○ Mucosal collapse with contraction and fusion of villi of small intestine
    ○ Maldigestion and malabsorption and often severe haemorrhage (foetid smell - blood, intestinal mucosa, faeces)
    ○ Severely affected animals die
55
Q

List 4 diagnosis techniques for Canine parvovirus 2, prevention and treatment

A

1) Presumptive diagnosis based on sudden onset of foul smelling haemorrhagic diarrhoea
2) Faecal immunoassays (virus shedding is transient: 3‐7 days after infection
3) Haemagglutination
4) PCR assays
Prevention and treatment
- No specific treatment
- Supportive therapy:
• Fluid therapy
• Blood / plasma transfusion
• Broad spectrum antibiotics
- Vaccination
• Inactivated and live‐virus vaccines available
- Kennels and shelters: strict hygiene, quarantine and disinfection required

56
Q

List 4 core canine vaccines

A
  • Canine Distemper Virus (CDV) Vaccine (I)
  • Canine Parvovirus Type 2 (CPV‐2) Vaccine (I)
  • Canine Adenovirus Type 2 (CAV‐2 Vaccine (prevents CAV‐1, ICH) (I)
  • Rabies Virus (RV) Vaccine (NI)
57
Q

Vaccination intervals

A
  • CDV, CPV-2, CAV-2: administer initial puppy series start no earlier than 6 to 8 weeks (due to maternal immunity), end at not less than 14 to 16 weeks of age, again at 1 yr. of age (or 1 yr. after last puppy vaccination). Adult revaccination not more often than every 3 years.
  • Rabies Virus: administer at 3-6 months, at 1 year (or 1 year later), followed by adult revaccination every 3 yrs. – State or country regulations
58
Q

Why are multiple doses of infectious vaccines to puppies

A 
Need to give as early as possible as don't know which are still protected from mum and which aren't, those that are protected won't mount immune response on first exposure therefore have to give multiple exposures over a small period to ensure get animals that lose protection as early as possible and still get them
Early - 40% protected 
8,9,10 - 75% 
11-12,13 age - 90%
14-15,16 - 98%
59
Q

Porcine parvovirus what are the 4 clinical signs where present and features

A 
S.M.E.D.I.
· Stillbirth
· Mummification
· Embryonic Death
· Infertility
- Single serotype
- Enzootic in many herds
- Morbidity reduced by vaccination
- Virus stable in environment for months
60
Q

Porcine parvovirus clinical signs, transmission and replication

A
  • Clinical signs referable to reproductive failure
    ○ First clinical sign is often increased number of young sows returning to oestrus ○ 3‐8 weeks after breeding
    Some sows remain “endocrinologically pregnant” and don’t come back into oestrus until expected farrowing date
    § Production loss
  • Infection of sow via oronasal route
  • Local replication in tonsillar lymphoid tissue precedes viraemia and trans‐placental
61
Q

Porcine parvovirus how long does it take to reach foetus and what occurs <30, 30-70 and >70 days

A
  • Takes ~ 15 days for virus to reach foetus after infection
    • <30 days gestation: foetal death and resorption
    • 30‐70 days gestation: foetus fail to develop (mummification/stillbirth)
    • >70 days gestation: stillbirth or normal piglet (depends on immune response)
62
Q

Porcine parvovirus list 4 ways to diagnose

A

Diagnosis

  • Infected foeti contain high levels of virus - source of infection and contamination of environment
  • Haemagglutination assays
  • PCR assays
  • Serology limited usefulness
63
Q

circoviridae what are the 2 main viruses within

A

1) Psittacine - beak and feather disease

2) Porcine circovirus 2

64
Q

Family circoviridae features, how resistant, where replicate and what lead to

A
  • Non‐enveloped
  • Single stranded DNA
  • Very stable in environment
    • Resistant to heating at 60oC, 30 minutes - substitutional
    • Resistant to disinfectants - very containment environment
    • Stable at pH 3‐9
  • Require actively dividing cells
  • Persistent infections
65
Q

Psittacine beak and feather disease what bird does it affect, age and what lead to

A
  • Disease in cockatoos, parrots and budgerigars
  • Birds under 5 years at greater risk
  • Feather loss, feather deformities
    • Pin feathers (constricted, stunted)
    • Adult feathers (retention of sheaths, blood in shaft, fracture of rachis)
  • Beak and claw deformities
    • Broken
    • Overgrown and shiny
    • Delaminations
    • Palatine necrosis
66
Q

Psittacine beak and feather disease where replicate, what lead to in wild birds and diagnosis and control

A
  • Virus replicates in basal epithelial layer of feather follicles, beak and claws
  • In wild birds, malformed feathers and beak lead to difficulty feeding and death. In care, these birds can live for months/years if fed
    Diagnosis
    1) clinical signs, histolofy
    2) PCR assay
    Control
    1) strict hygiene
    2) experimental vaccine
67
Q

Porcine circovirus 2 what lead to at what age

A
  • Progressive wasting disease 6 week old pigs present with weight loss, enlarged lymph nodes and dyspnoea
68
Q

Family Reoviridae what type of virus and feature

A
  • DSRNA virus

- non-enveloped

69
Q

Family Reoviridae what are the two genus of veterinary importance and diseases within

A

1) Orbivirus -> bluetongue, african horse sickness, equine encephalosis
2) Rotavirus -> host-specific

70
Q

Bluetongue what family of virus, what are the 5 main clinical signs

A

Family Reoviridae

  1. Hyperaemia of oral and buccal cavities (salivation / frothy mouth)
  2. Nasal discharge (serous – mucopurulent – blood flecked)
  3. Cyanosis of the tongue
  4. Hyperaemia of the coronary bands - lameness as can slough off
  5. Oedema (head and neck)
71
Q

Bluetongue what family of virus, what variety in disease presentation and post mortem findings

A

Family Reoviridae
- sub-clinical to death - depends on virulence of strain
- goats not as bad as sheep, death most commonly 2-8%
- Ewes affected during pregnancy may either abort or produce lambs with congenital abnormalities (hydranencephaly)
Post mortem findings:
- Consistent with vasculitis/vascular fragility
- Haemorrhage and oedematous lungs, congestion
- Sub serosal haemorrhage - LOTS OF HAEMORRHAGE

72
Q

Bluetongue what family of virus, genus incubation time, where replcate, how long infectious, how transmitted and number of serotypes

A

Family Reoviridae, orbivirus
- Incubation period ~ 1 week
- Replicates in regional lymphoid tissue, other lymphoid tissue and endothelial cells (vascular occlusion, stasis and exudation)
- Viraemia lasts 14-28 days (cows up to 10 weeks - infectious to the insect for a long time - prolonged outbreak)
- transmitted via Culicoides (Arbovirus) (dependent on climate -> late summer greater density, females shed in saliva
>25 serotypes -> harder to vaccinate

73
Q

Bluetongue what family, genus of virus, 3 ways to diagnose and 2 ways to control

A

Family Reoviridae, orbivirus
Diagnosis:
1) Presumptive (clinical signs and post mortem findings)
2) Isolation (washed blood cells), PCR
3) Serology (ELISA, neutralisation assay
Control
1. Vaccination programmes
- Live attenuated vaccines are available and used overseas
2. Monitoring schemes: Vector and host surveillance
- National arbovirus monitoring programme
○ Monitor where the vectors are present in Australia

74
Q

Bluetongue what family,genus of virus, is it present in australia

A

Family Reoviridae, orbivirus
Vectors in northern Australia, in these places sheep aren’t found therefore sheep in Australia are bluetongue free as not in contact with the vector
○ Important in terms of production and trade

75
Q

African Horse Sickness what family, hosts and the 3 main groups of clinical signs

A 
Family Reoviridae
Disease of equidae: horses > mules > donkeys > zebras
Clinical signs 
1) peracute pulmonary form 
2) subacute cardiac form 
3) mild or sub- clinical
76
Q

African Horse Sickness what occurs with peracute pulmonary form

A
  • Nasal discharge progressing to respiratory distress and often 100% mortality
    ○ Collapse and die within 4 – 24 hours
    • High fever (>41 degrees)
    • Sudden onset of clinical signs
    ○ Increasing dyspnoea
    ○ Rapid abdominal breathing
    ○ Paroxysmal coughing (dry progressing to frothy discharge from nostrils)
    ○ Pulmonary oedema obvious on auscultation
    ○ Saw-horse stance
77
Q

African Horse Sickness what occurs with subacute cardiac form and/or mild or sub-clinical

A

Subacute cardiac form:
○ Conjunctivitis, abdominal pain and progressive dyspnoea
○ Subcutaneous oedema with swelling of head and neck (supraorbital fossae, palpebral conjunctiva and intra-mandibular space)
3. Mild or sub-clinical
- “Horse sickness fever” – donkeys and zebras

78
Q

African Horse Sickness family, genus list the main 5 general findings, underlying pathology, how transmitted and what associated wtih

A

Family Reoviridae, orbivirus
Generalised - Oedema, vasculitis, exudate, haemorrhages, effusions
UNDERLYING PATHOLOGY
- Vasculitis/vascular fragility
Arbovirus: transmitted by Culicoides spp.
- Associated with red blood cells and leukocytes -> onset of fever

79
Q

African Horse Sickness family, genus serotypes, incubation period, replicated where

A

Family Reoviridae, orbivirus

  • 9 serotypes of AHSV (need to be immune to all 9 to be protected)
  • Incubation period ~ 1 week (4 – 9 days)
  • Replicates primarily in regional lymphoid tissue, with secondary replication in other lymphoid tissues, heart, brain and lungs and endothelial cells
80
Q

African Horse Sickness family, genus diagnosis and control methods

A

Family Reoviridae. orbivurs
1. Presumptive diagnosis – based on clinical signs, rapid death, typical lesions and seasonal prevalence of a competent vector
2. Virus isolation or RT-PCR from washed red cells
3. Antigen capture ELISA
4. Immunofluorescence
Control
Is it a threat to horse in Australia?
- Yes but only inside the horse - we don’t import horses from those areas
1. Vaccination available - vaccine contains 7 of the 9 serotypes (live virus attenuated)
2) Regionalisation and vaccination programme in South Africa

81
Q

Rotavirus what type of virus, what major cause of, feature of virus and important mlecule, incubation period

A

Family Reoviridae

  • Major cause of diarrhoea in many domestic species (humans)
  • Non-enveloped viruses
  • Tough outer capsid – VP4 cleaved by chymotrypsin in small intestine which greatly increases infectivity]
  • If going to culture needs to put chymotrypsin to increase activity
  • Short incubation period (12-24 hours)
82
Q

Rotavirus clinical signs and mortality and what age generally see

A
  • Profuse watery diarrhoea (white scours)
  • Inappetence, depression, dehydration
  • May stop suckling
  • Low mortality, often associated with dehydration or secondary bacterial infection - need to put on fluids
  • Disease usually seen in animals 1-8 weeks old
  • Not in first week (colostrum) UNLESS
    § Reduced colostrum intake, overcrowding, poor hygiene, chilling
83
Q

Rotavirus transmission, infectious dose, where replicate and what lead to

A
  • Transmission by ingestion of contaminated food, water or fomites
  • Very high concentrations are shed in faeces of infected animals - where can get infection
  • Infectious dose is small
    Replicate
  • Intestinal epithelial cell destruction (apical cells) - in the proximal small intestine
    Reduce capacity to absorb water, high amount of sugar (from the milk - neonate) - pulling water into the lumen resulting in OSMOTIC DIARRHOEA
  • Fluid accumulation in gut lumen - secretory diarrhoea
84
Q

List 3 control strategies and treatment

A

Control
1) Improved hygiene (unlikely to control on its own)
2) Antibody in colostrum
- Crosses lumen of neonate gut and becomes systemic IgG - in circulatory system
3) Antibody in milk (lactogenic immunity)
- Vaccination of dam
Treatment - Dehydration and electrolyte imbalances are the major cause of death in rotavirus cases (fluid therapy and no milk)

85
Q

Coronaviridae what are the two genus and general diseases

A

1) Coronavirus - respiratory disease

2) Torovirus - cause of diarrhoea

86
Q

Coronaviridae

List 2 main enteric diseases, 2 respiratory, 1 immunopathological and 2 neurological

A 
Enteric 
1. bovine/feline/canine coronavirus diarrhoea 
2. transmissible gastroenteritis
Respiratory 
1. infectious bronchitis 
2. porcine respiratory coronavirus 
Immunopathlogical 
1. feline infectious peritonitis
Neurological 
1. Porcine hemagglutinating  
2. Encephalomyelitis
87
Q

Family Coronaviridae features, spread, are they contagious

A

Enveloped
Spread: Inhalation and ingestion - faecal oral route or via aerosol
Contagious?: Variable, some are: infectious bronchitis, FIP, bovine coronavirus

88
Q

Bovine Coronavirus Diarrhoea what does it lead to, where replicate (what then lead to), what age most susceptible and transmission

A
  • Second most common cause of diarrhoea in calves (after rotavirus)
  • Replicates in mature small intestinal epithelial cells
    ○ fluid absorption and digestion of disaccharides reduced from the small intestines - leads to OSMOTIC DIARRHOEA
  • Less than 2 weeks old – diarrhoea lasts 4-5 days
  • Faecal – oral route of transmission
89
Q

List the 4 porcine coronaviruses

A

1) transmissible gastroenteritis virus
2) porcine repiratory coronavirus
3) porcine epidemic diarrhoea
4) porcine hemagglutinating encephalomyelitis

90
Q

what occurs in normal animals with FIPV and the two times when cats get infected

A

1) exposure -> replication in macrophages -> effective CMI -> eliminated
2) Young cats defective CMI -> Immune-mediated vasculitis -> moderate or severe disease (progressive fatal in months)
3) Older animals no longer mount an appropriate immune response and may or may not get the disease due to decreased CMI over different exposures (decreased CMI)

91
Q

What are the 2 feline coronaviruses and what generay lead to

A

1) Feline enteric coronaviruses (FECV) -> mild or inappernt enteritis
2) feline infectious peritonitis virus (FIPV) -> sporadic, fatal disease of young cats

92
Q

FIPV what type of virus, where shed, how transmitted, how long infected

A

Coronavirus
- FIPV shed in faeces and oronasal secretions
- Transmission by inhalation, or ingestion
○ Kittens infected from mother, or adult cats
- In infected households ~ 15% of cats are persistently infected and shedding the virus
- Most cats are transiently infected (eliminate virus)

93
Q

Infectious bronchitis why important, where replicate, transmission, how long incubation

A
  • Highly contagious, economically important disease of chickens worldwide
  • Respiratory system is the site of primary replication
  • Viraemia within 1-2 days of exposure
  • Respiratory transmission by aerosol (most important route)
  • Shed from respiratory tract for several weeks
  • 48 hour incubation
94
Q

Infectious bronchitis clinical signs, diagnosis and treatment

A
  • Most severe in young birds
    ○ <3weeks – gasping, nasal exudate mortality from occluded bronchi
  • Older birds – rales and gasping
    ○ Reduced egg production for about 7 days in individuals
    Diagnosis:
  • Virus isolation (egg inoculation)
  • Serology (neutralisation, ELISA, HI)
    Treatment:
  • No specific treatment
  • Live and killed vaccines available
    ○ have led to outbreaks of disease with reversion of virulence
95
Q

What are the two results in disease from feline infectious peritonitis virus

A

1) Dry FIP - moderate - pyogranulomatous lesions
2) Wet FIP - severe - marked vascular permeability
ALL progressive fatal disease within months

DVM 2 - 1 (31 decks)

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