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VETM 422 Virology > Lecture 11: Bovine Viruses 2 > Flashcards

Lecture 11: Bovine Viruses 2 Flashcards

1
Q

What is bovine respiratory disease complex? What animals are affected? Why is it important?

A
  • Multifactorial
  • 1st 40 days on feed – associated with winter (but summer pneumonia too)
  • Most important cause of economic loss
  • Metaphylactic antimicrobials = antimicrobial resistance issues
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2
Q

What are the viral agents that can cause BRDC

A
  • Many bacterial and viral causes

o Viruses: BHV1, PI3, PRSV, BVDV

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3
Q

What s the taxonomy of bovine respiratory syncytial virus

A

Bovine Respiratory Syncytial Virus (BRSV)
* Family: Paramyxoviridae
* Subfamily: Pneumovirinae
* Genera: Pneumovirus

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4
Q

What are the clinical signs of bovine syncytial virus? what does it depend on?

A
  • Clinically: severe dyspnea, excessive foam/mucus obstructing trachea
    o 2-3% to 20% mortality
    o Depend on age, immune status/immunosuppression, presence of Ig, route/dose of virus/strain virulence
    o High fever (>40C), depression, anorexia, increased respiratory rate (hypersalivation/orthopnia/grunting)/ cough
    o Mucopurulent nasal discharge/pulmonary emphysema/edema = crackles and wheezes
    o Interstitial pneumonia
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5
Q

Who/when does BRSV affect?

A
  • Target: cattle
    o Seasonality: fall/winter
    o More pathogenic in young calves (neonates less susceptible)
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6
Q

How is BRSV transmitted?

A
  • Transmit: direct contact, aerosol, humans as a passive vector
    o 70% calves infected <1yo
    o Excrete in nasal discharge
    o Not persistent infection – re-infection is common
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7
Q

What is the prevalence of BRSV in beef and dairy populations

A
  • Very common: 60% of epizootic respiratory disease – dairy (70% in beef)
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8
Q

What s the pathogenesis of BRSV

A
  • Path: polynucleated cell (syncytium) form – pathogenesis related to host response/immune
    o No cytopathology = minimal viral caused damage
    o Enter respiratory tract and migrate through mucus – invade via sialic acid residue epithelial cells and replicate
    o Host immune system causes damage – upregulate pro-inflam/mast cell degeneration
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9
Q

What is a concern with the BRSV vaccine

A
  • Vaccine can induce disease (modern vaccines are better and this is less of a risk)
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10
Q

What is BPI3

A

Bovine Parainfluenza 3 Virus (BPI3)

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11
Q

How is BPI3 transmitted? How prevalent is it?

A
  • Transmit: same as BRSV: direct contact, aerosol, humans as a passive vector
    o 70% calves infected <1yo
    o Excrete in nasal discharge
    o Not persistent infection – re-infection is common
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12
Q

What is the pathogenesis for BPI3

A
  • Path: same as BRSV
    o Enter respiratory tract and migrate through mucus – invade via sialic acid residue epithelial cells and replicate
    o Will replicate well. In pulmonary alveolar macrophages = immunosuppression
    o Host immune system causes damage – upregulate pro-inflam/mast cell degeneration
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13
Q

What ar the clinical consequences of BPI3

A
  • Clinically: severe dyspnea, excessive foam/mucus obstructing trachea
    o Depend on age, immune status/immunosuppression, presence of Ig, route/dose of virus/strain virulence
    o High fever (>40C), depression, anorexia, increased respiratory rate (hypersalivation/orthopnia/grunting)/ cough
    o Mucopurulent nasal discharge/pulmonary emphysema/edema = crackles and wheezes
    o Less severe than BRSV
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14
Q

What is BHV1

A

Bovine Herpesvirus 1 (BHV1/IBR)

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15
Q

What type of virus is BHV1

A
  • Large dsDNA
    o Environmentally resistant – better at survival in cold temp
  • 3 types of BHV: type 1 is main in NA
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16
Q

What animals does BHV1 target? and how is it transmitted?

A
  • Transmit: cattle and buffalo
    o Nose to nose contact, aerosol (short distance)
    o Excreted in nasal fluid or semen
    o Incubation: 2-6d
17
Q

What are the general clinical signs of BHV1 infection

A

o Infectious bovine rhinotracheitis: serous rhinitis + hyperemia/edema
 Tracheal lesions + purulent inflammation and ulceration
 Secondary infection common – resulting pneumonia
o Conjunctivitis
o Infectious pustular vulvovaginitis or balanopostitis
o Abortion
o High fever
o Anorexia/cough/hypersalivation/nasal discharge/inflamed nares/dyspnea
o BHV1.1 (main): respiratory tract infection and abortion

18
Q

What are the 3 main types of BHV in NA? What are the general clinical signs associated with each type?

A

o BHV1.1 (main): respiratory tract infection and abortion
o BHV1.2a: respiratory and infectious pustular vulvovaginitis or balanopostitis and abortion
o BHV1.2b: respiratory and infectious pustular vulvovaginitis or balanopostitis

19
Q

What is the prognosis of BHV1

A
  • Prognosis: w/o pneumonia = recover in 4-5d
    o 10% mortality and 100% morbidity
20
Q

What is the pathogenesis of BHV1

A
  • Pathogenesis: enter epithelial cells/nerves of upper airway > lysis of infected cells
    o Lysis of ciliate epithelium in trachea (mucociliary elevator impair)
    o Immunosuppressive: kill CD4 cells, reduce MHC1 and 2 expression, down regulate type 1 IFN
21
Q

How to control and prevent BHV1

A
  • Control: modified live or killed vaccine (intranasal – always modified live)
    o Prevent calving in early spring – but unable to vaccinate when they go to market because they are too young (maternal Ig interference)
    o Marker vaccines
22
Q

Can BHV1 be eradicated? If so how?

A

o Not very effective – Ro is >1 meaning the virus is able to transmit between individuals
 Transmission is lower in vaccinated herds
 Prevent mixing of vaccinated and unvaccinated herds – this is a mechanism to eradicate BHV (drive Ro to <1 of transmission between herds – not necessarily within herd)

23
Q

What is a concern when using BHV1 vaccines

A

o Vaccine manufacturing uses fetal bovine serum – if serum contaminated = can infect cows with live BHV

24
Q

What are the 2 types of herpes viruses that can affect cattle

A

Bovine Herpesvirus 1 (BHV1/IBR)

Ovine Herpesvirus 2

25
Q

How is ovine herpes virus 2 transmitted

A
  • Transmit: from sheep/wildebeest to cow (not between cattle)
26
Q

How does ovine herpes virus 2 clinically present

A
  • Clinically: malignant catarrhal fever
    o High fever (~41)
    o Catarrhal inflame: erosion/mucopurulent exudation – upper resp/eyes/oral mucosa
     Eye: panopthalmitis, hypopyon, corneal opacity/keratitis
    o Swollen lymph nodes
    o Lameness
    o CNS: depression/trembling/hyporersponsiveness/sstuporr/sggressive/convulsion
    o 100% mortality
27
Q

What are the primary diagnostics used to diagnose BRD

A
  • Respiratory panel: culture/PCR (look for BRSV/PI3/IBIR/M. bovis)
28
Q

What are the 2 common causative agents of scours

A
  • Agents: Bovine coronavirus
    o Bovine rotavirus (similar to porcine rotavirus)
29
Q

What is the pathology of bovine coronavirus

A
  • Agents: Bovine coronavirus
     Path: replicate in respiratory or GI tract
     Many types all from bats

acts similarly to the porcine coronavirus

30
Q

What is the taxonomy of bovine rotavirus

A

o Bovine rotavirus (similar to porcine rotavirus)
 Genus: rotavirus, Family: Reoviridae

 dsRNA, segmented, non-enveloped + multi-layer capsid

31
Q

What is the pathogenesis of bovine rotavirus

A

 pathogenicity factors in genome can be important
* replicate in epithelial cytoplasm
* due to viral enterotoxin NSP4 = destroy mature enterocytes

32
Q

What are the features of the virus: bovine rotavirus

A

 dsRNA, segmented, non-enveloped + multi-layer capsid
 tons of serotypes = not feasible to make vaccines

33
Q

What is the clinical presentation of bovine rotavirus

A

 Clinically: lots of diarrhea in calf (1-2wk old)
* Maldigested/malabsorptive diarrhea = rapid dehydration

34
Q

What is the transmission of bovine rotavirus like

A

 1-2d incubation
 5-7d of high viral shedding

35
Q

What 3 other pathogens can cause scours (not bovine coronavirus or rotavirus)

A

o Also E. coli, salmonella, coccidia

VETM 422 Virology (19 decks)

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