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Epidemiology final Topic (1-102) > 53. Bovine viral diarrhoea. > Flashcards

53. Bovine viral diarrhoea. Flashcards

1
Q

Info?

A

BOVINE VIRAL DIARRHOEA

Flaviviridae family- Pestivirus genus

  • Classical swine fever virus (CSFV, Hog cholera virus)
  • Bovine viral diarrhoea virus (genotype BVD-1,-2) ʹ remember Immunotolerance!!
  • Border disease virus (BDV) ʹ Immunotolerance, foetopathy
  • Close genetic relationships
  • Antigenic relationships
  • Foetopathy
  • Characteristic
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2
Q

BVD occurrence?

A

Bovine viral diarrhoea

  • Febrile illness of the cattle with general signs, diarrhoea & rarely with erosions in the mucosal surfaces of
  • the digestive tract leading to IMMUNE SUPPRESSION
  • History
  • 1946, USA ʹ virus diarrhoea
  • 1953, description of Mucosal disease
  • 1961, the same causative agent

Occurrence

  • World-wide,
  • Frequent (Eradication program in Western Europe)
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3
Q

Causative agent?

A

Causative agent

  • Flaviviridae, Pestivirus, Bovine viral diarrhoea virus
  • Susceptibility: cattle, zebu, buffalo, wild Ru, sheep (~border disease), goat, swine (subclinical)
  • Very SLOW spreads - invisible practically
  • Moderate resistance
  • 60oC ʹ few minutes; sensitive to disinfectants
  • In faeces, mucous survives for few weeks
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4
Q

Genotypes?

A

Genotypes

  • BVDV 1: world-wide distributed
  • Subtypes 1A ʹ 1L, Wildtype & vaccine strains (Osloss, NADL, Oregon)
  • BVDV 2 - Originally in N. America
  • since in 2000s in europe far east S. america Russia too
  • Subtypes 2A- 2D , increased virulence
  • Biotypes/virulence variants
  • Non-cytopathic strains (n-Cp) ʹ more frequent
  • persistent (tolerated) infections,
  • NO symptoms! Cannot detect in culture
  • Cytopathic strains (Cp)
  • Rounding of the cells, vacuolisation
  • Higher virulence
  • Non-cytopathic ʹ cytopathic switch
  • Insertion from the host cell & from the virus, small & large duplications
  • Point mutations/deletions on NS3 gene
  • Mainly on the NS3 gene ʹ virulence markers
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5
Q

Antigenicity and epizootiology?

A

Antigenicity

  • 4 structural proteins,
  • 3 of them are envelope glycoprotein (gp 25, gp48, gp53)
  • Gp53 is the neutralising antigen strains

Epizootiology

  • Transmission within farms Transmission between farms
  • Sick or infected will shed (milk, fetus, semen, discharge)
  • Infection: PO, mating, AI, airborne
  • Tolerated infected carries
  • lifelong/persist shed (continuous/intermittent)
  • Semen can contain virus EVEN if not found in WBC
  • In enzootic herd, calves are protected by maternal immunity
  • until 3- 4 months, so see CS 4-18 months
  • Ovary follicle not infected! Not transmitted with sufficient embryo transfer
  • Mucosal disease is sporadic
  • slow invisible spread
  • Immunosuppressive virus: increase other viral/bacterial diseases, typically respiratory
  • Persistently (tolerated) infected, carrier cattle (with or no signs!) will continue shedding!
  • (If infected during pregnancy, the virus is present so the immune response recognises it as itself- so wont initiate immune response but will keep spreading/shedding the virus!)
  • Semen of tolerated/persistent infected bull
  • Other susceptible animals (domestic, wild RU, SU)
  • Faeces, contaminated vehicles
  • Iatrogenic (mass vax)
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6
Q

Pathogenesis?

A

Pathogenesis

  1. Per os infection ➝ primary virus multiplication in the enteric mucosa and in the lymphatic tissue
  2. Viraemia in 1-4 days: serum, lymphocytes ➝ visceral organs (digestive tract mucosa, lung, spleen, lymphatic tissue,

salivary gland)

  1. Blood vessels endothelia damage ➝ haemorrhages
  2. Mucosal epithel damage ➝ erosions
  3. Lymphatic tissue damage ➝ immunosuppression ➝ confections (PI-3 virus, BAdV, BHV-1, Mycoplasma, Pasteurella)

• Infection of pregnant cow

  • Most frequently in first pregnancy
  • Virus infects embryo/foetus
  • Consequences depend on the age of the foetus and on the virulence of the virus strain

• Infection during pregnancy

  • With CP strain ➝ diarrhoea or respiratory disease in cow

‣ Day 0-40: embryo death, infertility

‣ Day 40-180: abortion

‣ Day 180-Parturition: foetal damages, joint and cranial defects, CNS disorders (developmental disorders)

  • With NCP strain ➝ no signs in cow

‣ Day 0-40: embryo, death, infertility

‣ Day 40-120: immunotolerance

‣ Day 120-Parturition: seropositivity (immune response)

• Mucosal disease (MD)

  • Immunotolerant cattle, which is persistently infected with a NCP strain is super infected with a CP strain
  • Or the NCP strain mutates to CP in the animal ➝ severe, haemorrhagic enteritis, fibrin precipitation and erosions on the mucosal surfaces ➝ lethal
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7
Q

Clinical signs?

A

Clinical signs

  • Incubation: 7- 9 days
  • Signs depend on the biotype of the virus strain & the age & immunological status of the host
  • In calves:
  • Cp strain
  • Fever, salivation, diarrhoea, respiratory disease, signs of co-infections
  • (immunosuppression), central cataract
  • Usually recover within 1-2 weeks
  • Ncp strain
  • Subclinical (seroconversion), milder immunosuppression
  • Mucosal disease (rare)
  • High fever, haemorrhagic diarrhoea
  • Erosions on the mucosal surfaces: oral cavity, eyelids, hooves, legs
  • Weakness, exsiccosis, high mortality
  • In cows: infertility, weaker fertilisation index
  • Cp strain: abortions, weak, underdeveloped calves born
  • Aborted foetus/infected newborn calf (Cp strain)
  • Brachygnatia, hydrocephalus
  • Cerebellar hypoplasia ʹ ataxia, ankyloses
  • Eyesight disorders
  • In swine
  • Subclinical, sometimes permanent carrier & shedder ʹ seropositive
  • ƒ In pregnant sow foetal damages, delivery of weak piglets is possible
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8
Q

Pathology, Histopathology?

A

Pathology, histopathology

  • Mucosal disease
  • Sharp-edged, usually round/oval ulcers (FMD: red base, tattered edge)
  • Gums, palate, tongue, cheek, lips
  • Pharynx, oesophagus, rumen, reticulum
  • Hydroptic dystrophy , necrosis (st.sp) erosion ulceration
  • Inflamed enteric mucosa
  • Inflammation of the Peyer-patches, haemorrhagic ulceration
  • Croupous or diphteroid pseudomembranes
  • Haemorrhages under the serosal surfaces & on the kidney cortex
  • Intrauterine infections ʹ cerebellar hypoplasia, hydrocephalus, mictrophtalmia
  • Histopath: degenerated villi, submucosal inflammatory cell infiltration
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9
Q

Diagnosis?

A

Diagnosis

  • Clinical signs, pathology ʹ suspicion
  • Lab tests
  • Antigen-capture ELISA, IF, PLA
  • PCR, real-time PCR
  • Virus isolation, PLA should supplement isolation because cannot see CP strain
  • Detection of persistent, carrier calves: ear skin PCR
  • Serology: ELISA (Serum, milk), virus neutralisation test (with cp strain orNPLA)
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10
Q

Differential diagnosis?

A

Differential diagnosis

  1. FMD: vesicles, tattered-edge erosions, no diarrhoea
  2. Malignant catarrhal fever: head oedema, CNS signs
  3. (Rinderpest), bluetongue, Rift-valley fever, orthobunyaviruses
  4. Co-infections!!
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11
Q

Treatment?

A

Treatment

  • Symptomatic & supportive (fluid therapy)
  • Parenteral AB therapy against co-infecting bacteria
  • Calves: drinking milk instead of calf nutrition formulas
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12
Q

Prevention and control?

A

Prevention & control

  • Vaccination in infected herds
  • 1) Attenuated live vaccine
  • To block an epizootic or for preventative reasons, long immunity (~1 year)
  • Infects the foetus (may damage, induces immune response)
  • May induce MD (early & late)
  • Heifer, cow: 1 month before fertilisation & 3-5 weeks beforeparturition
  • Calf: in the age of 3-4 months (depending on the maternal Ab level)
  • 2) Inactivated vaccine
  • Repeated immunisations
  • Low anti-NS3 Ig titre ʹ marker vaccine
  • Subunit vaccines under development
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13
Q

Eradication?

A

Eradication

  • Economically justified (so much loss!)
  • In Scandinavia & in Western Europe successful approaches
  • Selection of immunotolerant animals
  • Immunisation of the herd & subsequent serological investigations
  • Viral investigations (ELISA, PCR) of the animals that remain seronegative
  • Selection of the carrier + immunisation
  • Linking with IBR eradication programme is practical
  • Qualifying tests of the pedigree sires (PBMC, semen PCR)
  • Maintenance of BVDV-free status
  • Closed farms, epizootiology rules
  • Purchase of controlled, BVDV-free semen or embryos
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Epidemiology final Topic (1-102) (102 decks)

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