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small animal final year > Non-Notifiable Viral Disease > Flashcards

Non-Notifiable Viral Disease Flashcards

1
Q

Name 2 viruses which may occur to viral infection of fetus in utero (3)

A
  • Pestiviruses – bovine viral diarrhoea, Border disease, classical swine fever
  • Parvovirus - feline panleukopenia
  • Bunyavirus – Schmallenberg virus
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2
Q

Other than neuro signs, name other signs

A

–Recumbency

–Ataxia

–Blindness

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3
Q

When do calves need to be infected with BVDV to show neuro signs?

A

day 100-200 of gestation

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4
Q

Name signs of border disease

A

–EED and abortion

–Lambs born with hairy fleece and involuntary tremor

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5
Q

What causes border disease?

A

Pestivirus

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6
Q

A) What does border disease cause?

B) What does it result from?

C) What infection do animals get?

A

A) Demyelination of nerve fibres in CNS

B) Infection in early gestation

C) Persistent infection

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7
Q

How can we diagnose pestiviruses?

A
  • History of abortion etc in flock/herd
  • Clinical signs may be suggestive
  • Detection of serum/milk antibody suggests exposure (or vaccination!)
  • Detection of virus

–ELISA for virus antigen , RT-PCR, virus isolation

–Pooled blood samples, ear tag samples

•Post mortem

–Even if the animal is culled, diagnosis should be discussed due to the potential impact of the virus to herd health

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8
Q

Feline parvovirus:

A) What is the transmission route?

B) What is infected?

C) What is needed to propagate?

D) Who is susceptible?

A

A) Faecal-oral

B) Infects lymph nodes of naso- and oro-pharynx, then spreads to other tissues

C) Rapidly dividing cells

D) Kittens and unvaccinated cats

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9
Q

What is the pathogeneis with Parvovirus and:

A) Panleukopenia?

B) Enteritis?

C) Cerebellar hypoplasia?

A

A) Decreased white blood cell count, killing of lymphoid and myeloid stem cells

B) Killing of stem cells in crypts

C) Infection in neonatal kittens [in utero or <2 wks birth]

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10
Q

What is the difference here?

A

Top - normal

Bottom - infected

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11
Q

How can we diagnose feline parvovirus?

A

Clinical signs, history, MRI, PME

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12
Q

How can we control FPV?

A

Maternally derived antibody wanes after about 8 weeks

  1. Vaccinate : attenuated live and inactivated virus vaccines available [boost every 1 to 3 yrs]. Don’t use attenuated live virus vaccines in pregnant queens!
  2. Management : Prevent exposure of kittens to

FPV in environment (if prior outbreak on premises)

  1. Important to use effective disinfectant, maintain quarantine in veterinary practice (bleach diluted 1:32).
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13
Q

Schmallenberd Virus:

A) What causes it?

B) How is it transmitted?

C) Name signs

D) What causes neuro signs?

A

A) Orthobunyavirus

B) By insect vectors (mainly Culicoides)

C) Stillbirths, abortion, congenital deformities

D) Due to hydranencephaly, poliomyelitis

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14
Q

How can we diagnose Schmallenberg Virus?

A

•Serology (ELISA) to detect antiviral antibody.

–Paired samples collected 2-3 wk interval to demonstrate rising titre

–Single sample to show exposure

–Bulk milk sample

  • RT-PCR to detect virus in tissues at PM
  • RT-PCR on blood (EDTA) to detect virus in acute phase of infection (NB difficult as prior to clinical signs!)
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15
Q

How can we prevent schmallenberg virus?

A
  • Vaccination theoretically possible in event of re-emergence
  • MSD Zoetis Zulvac & Merial SBVvax
  • Inactivated virus vaccines, alum adjuvanted
  • Use in non pregnant animals
  • Duration of immunity not yet determined
  • Vaccine availability uncertain
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16
Q

Name 2 tick borne encephalitides (3)

A

–Louping ill

–Spanish sheep encephalitis

–Turkish sheep encephalitis/Greek goat encephalitis

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17
Q

What is the morphology of Borna virus?

A

Enveloped negative sense, single RNA

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18
Q

Where does borna disease infect?

A

•Infects neurons; cellular immune response leads to tissue destruction (meningitis, encephalomyelitis)

19
Q

Borna disease:

A) Name signs

B) How do we diagnose?

A

A) Pyrexia, ataxia, pharyngeal paralysis, hyperaesthesia

–Frequently fatal (within several weeks)

B) histopathology, RT-PCR

20
Q

Tick borne encephalitis:

A) What causes it?

B) What type of virus is it?

C) How is it transmitted?

A

A) Caused by flaviviruses

B) Enveloped +ve sense ss RNA virus

C) Transmitted by ticks (Ixodes ricinus)

21
Q

Who does louping ill effect?

A

•Neurological disease in sheep, red grouse (cattle, deer, horses, humans)

22
Q

Louping ill:

A) When are ticks infected?

B) Where does the virus replicate?

C) What maintains virus in developing ticks?

A

A) When feed on viraemic animal (or from tick to tick spread in same area when feeding)

B) In gut and salivary glands of ticks

C) Transtadial transmission

23
Q

How long does tick maturation take?

A

up to 3 years

24
Q

How does louping ill cause disease?

A
  • Virus infection of lymph nodes then spreads to other lymphoid tissue +/- CNS
  • Neurological signs incl. tremors, exaggerated gait, death.
  • Immunosuppression

–Anaplasma (Ehrlichia) phagocytophila worsens prognosis

–Staphylococcus aureus pyaemia

25
Q

How can you diagnose louping ill?

A

•Diagnosis confirmed by serology

–Haemagglutination inhibition assay

–Anti-viral IgM

•Confirmation by PM examination

–Non-suppurative polioencephalomyelitis

–Medullary, cerebellar, pons, thalamic lesions

–Demonstrate virus Ag in lesions by Ab staining

26
Q

How can you control louping ill?

A

–vaccination - which sheep, when?

•currently vaccine shortage - until 2019!

–vector control e.g. “tick mops”

–host management?

27
Q

Canine distemper:

A) What causes it?

B) How is it transmitted?

C) Where does the virus replicate?

A

A) Morbillivirus (Paramyxovirus)

B) Direct

C) URT

28
Q

Where does canine distemper spread?

A
  • Spread to tonsils/lymph nodes
  • Viraemia and systemic spread to epithelia +/- CNS
29
Q

Name clinical signs of distemper

A
  • Pyrexia, depression
  • Ocular and nasal discharge
  • Cough
  • Vomiting, diarrhoea
  • Hyperkeratosis of nose/pads (“hardpad”)
30
Q

If an animal has a good immune response and they are infected with distemper what happens?

A

Recovers

31
Q

What happens if a dog has a poor immune response and is infected with distemper?

A

Development of neurological signs

32
Q

Wha are the neurological signs of distemper?

A
  • Circling, head tilt, nystagmus
  • Paralysis
  • Convulsions, involuntary “chewing”
  • Associated with demyelination lesions
  • Viral inclusion bodies in CNS (skin, GI tract, bronchi, etc)
  • Death in 2-4 weeks
33
Q

What are some consequences of long term distemper?

A
  • Enamel hypoplasia
  • Old dog encephalitis

–Dementia, blindness, circling

–Often in distemper vaccinated dogs

–CSF often normal

34
Q

How can we diagnose distemper?

A
  • Virus isolation
  • Immunofluorescence

–e.g. using Ab to detect viral antigen in ocular/nasal smears

  • RT-PCR
  • Serology

–IgM

–Rising titre of IgG

  • Histopathology
  • Inclusion bodies on blood/conjunctival smears
35
Q

How do we treat distemper?

A

•Supportive treatment

–Fluid therapy

–Antibiotics (secondary infections)

–Treatment with anticonvulsants?

36
Q

How can we prevent canine distemper?

A

–Vaccination

–Usually modified live vaccines

37
Q

Feline infectious peritonitis:

A) What causes it?

B) Where is it most common?

A

A) Coronavirus

B) Purebreeds

38
Q

What are the signs of wet FIP?

A

ascites

pleural effusion

fever, anorexia, depression

39
Q

What are the sign of dry FIP?

A

signs may be vague

fever, anorexia, depression

ocular lesions (uveitis)

neurological signs

40
Q

What do neuro signns depend on?

What signs are seen?

A

•Variable – depends on site of inflammatory lesion(s)

–cranial, cerebellar, spinal cord

•Paresis, ataxia, hyperaesthesia, convulsions, behavioural changes

41
Q

Why does FIP arise?

A

•Probable mutation of virus

–recombination or spontaneous?

  • Stress?
  • Viral load?
  • “Inappropriate” immune response

–Poor cellular immune response

42
Q

How can we diagnose FIP?

A
  • History and clinical signs may be suggestive
  • Histopathology shows characteristic lesions (rarely available ante-mortem)
  • Peritoneal/Pleural fluid

–High protein content (elevated gamma globulins)

–Viscous, yellow, may clot

•FCoV antibody titre

–Titre of 0 makes FIP unlikely (but effusive forms?)

–Merely indicates infection with FCoV

–A healthy cat with a titre to FCoV does not have FIP!!

•Albumin:globulin ratio

–Serum A:G < 0.4 is suggestive (> 0.8 rules out)

•Alpha 1 acid glycoprotein (AGP)

–>1500 ug/ml is suggestive

•Haematology

–anaemia, neutrophilia (left shift), lymphopenia

•Wet FIP – also fluid analysis

43
Q

How can we control FIP?

A

•Maintain FeCV free catteries

–Isolation

–Use seronegative stud males

•Manage catteries effectively

–Early weaning of kittens from infected dams (at 5 wk before MDA wanes)

•Vaccinate??

–Not available in UK

44
Q

How can we treat FIP?

A
  • Generally palliative
  • Treat secondary bacterial infections
  • Corticosteroids may reduce clinical signs
  • Interferon?

–feline interferon omega

•Polyprenyl immunostimulant?

small animal final year (317 decks)

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