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Flashcards in Equine - Respiratory Dz Deck (51)
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1

What is the most frequently reported viral respiratory disease in horses?

Equine influenza.

2

Describe the equine influenza virus (EIV).

- Family: Orthomyxoviridae.
- Genera: Influenza A virus.
- Segmented, single-stranded RNA virus.

3

What are the two subtypes of EIV and what is the basis of this subdivision.

- H7N7 (not isolated since 1980s) and H3N8 (several variants, Eurasian and American lineages).
- Two surface antigens determine subtype:
-- Haemagglutinin: glycoprotein, viral receptor binding protein.
- Neuraminidase: once HA glycoprotein binds sialic acid in host cell, NA facilitates movement of virion into host cell.

4

What three countries are free of EIV?

Australia, New Zealand and Iceland.

5

What are risk factors for development of EIV infection?

- Age: 1-5yo or foals if naive population.
- Low serum EI specific ABs.
- Frequent contact with a large number of horses.

6

What is the mode of transmission, incubation period and duration of shedding of EIV?

- Aerosol (explosive cough), fomites, nose-to-nose.
- Incubation period: 1-5 days.
- Shedding: 6-7 days.

7

Describe the pathophysiology of EIV infection.

- NA alters efficiency of mucociliary apparatus.
- HA attaches to sialic-acid containing cell surface receptors on epithelial cells in the nasal mucosa, trachea and bronchi.
- Epi cells internalise virus and surround it with an endosome.
- Viral replication --> host cell death --> loss of ciliated resp epi and exposure of irritant receptors --> hypersecretion of submucosal serous glands, damage to MCA, inflammation, lymphocytic infiltration, oedema; predisposes to secondary bacterial infection.
- Foals can get fatal bronchointerstitial pneumonia.
- Recovery of epi damage begins in 3-5d; takes 3-6wk.

8

Describe the immune response in horses infected with EIV and defences of the virus to the immune response.

- Humoral IR targets HA and NA therefore changes in surface antigens can block host immune response.
- Local IgA (nasal secretions) blocks viral penetration, systemic IgGa, IgGb (serum) enhance phagocytosis.
- Natural exposure induces protective immunity against homologous strain for 8mo, partial immunity for 12+mo.
- Virus defences: antigenic drift, anti-interferon activity of NS1 protein, alveolar macrophages are destroyed by PB1-F2 protein.

9

What clinical signs are demonstrated by horses infected with EIV?

- Onset usually within 48 hours.
- Rarely fatal unless neonates.
- Pyrexia (1-2d), serous to mucopurulent nasal discharge (2-4d), dry hacking cough (up to 3wk), anorexia (1-2d).

10

What complications can occur following EIV infection?

- Secondary bacterial pneumonia.
- Myositis.
- Myocarditis.
- Limb oedema.
- Potentially may predispose to IAD, RAO, EIPH.

11

Outline recommended strategies to prevent/control EIV infection.

- Basic biosecurity.
- OIE recommends vacc should contain FL Clade 1 and Clade 2 strains, but none do yet.
- Inactivated vaccines: ~6mo, 7mo, 10mo then yearly.
- MLV: intranasal, single dose at 6mo, 12mo then yearly; should not be given pre-foaling or to foals.
- Canary pox vector: 2 boosters then yearly.
- If high risk horse give boosters q6mo vs q12mo.

12

Describe the equine arteritis virus (EAV).

- Family: Arteriviridae (same family as PRRSV).
- Order: Nidovirales.
- Enveloped, positive-stranded RNA virus.
- Major viral envelope proteins: M and GPS.
- One serotype, two clades.
- Extensive variation in virulence of different isolates.
- Readily inactivated by sunlight, high temps, lipid solvents, disinfectants; survives -0 C temperatures.

13

Describe the epidemiology of EAV infection.

- Spread by respiratory and venereal routes.
- 30-70% infected stallions become carriers; virus persists in ampulla of vas deferens (testosterone dependent).
- 85-100% mares bred by stallions/fomites become infected --> spread via resp route to others on farm.
- Infection --> immunity for several years.
- Colostral ABs last until 2-6mo.
- Seroprevalence varies b/w breeds: SB>TB.
- Variation in host's genome (CD3+T) and outcome.

14

Describe the pathophysiology of EAV infection.

- Invades resp epi cells then bronchial and alveolar macrophages --> bronchial and other regional LNs (2-3d) --> viraemia --> replication in adrenals, thyroid, liver, testes.
- Virus remains in buffy coat 2-21d, plasma 7-9d, elim 28d.
- Virus replicated in endothelial cells --> damage to endo cells and adj muscularis media --> vascularis charac by fibrinoid necrosis of small muscular aa, leukocyte infiltrations, perivascular haemorrhage and oedema.

15

List the clinical signs associated with EAV infection.

- Majority of infections are subclinical.
- Occasional outbreaks of resp dz and abortions.
- Incubation period: 2-14d (resp), 6-8d (venereal).
- Mild (fever, leukopaenia) to severe (death).
- Fever (1-5d), anorexia, nasal discharge (serous to mucoid), conjunctivitis +/- cough, +/- urticaria, oedema.
- Stallions: transient dec in sperm quality (16wk).
- Mare: abortions, 2-10mo gestation, no premonitory signs.
- Foals: severe resp signs, high mortality.

16

List necropsy findings in foals that die following EAV infection.

- Interstitial pneumonia.
- Lymphocytic arteritis.
- Renal tubular necrosis.
- Tunica media necrosis.

17

How is EAV infection diagnosed in horses?

- Paired serologic titres 3-4 wks apart; complement-enhanced virus neutralization test most reliable.
- In the absence of a certified vacc hx, stallions with a serum neutralizing antibody titer ≥1:4 should be considered potential carriers until proven otherwise, based on an absence of detectable EAV in their semen.
- PCR/virus isolation: nasopharyngeal swabs, conjunctival swabs, whole blood, placenta, semen.

18

Outline recommended strategies to prevent/control EAV infection.

- MLV (non-preg) --> complete or partial protection up to 2y against CSx but virus can still replicate.
- Killed vaccine (pregnant mares).
- Control prog aimed at dec risk of abortion and foal infections: vacc all breeding colts

19

Describe the equine rhinitis virus.

- Family: Picornaviridae (same as FMDV!)
- Non-enveloped RNA viruses.
- 4 serotypes: ERAV, ERBV1, ERBV2, ERBV3.

20

Describe the epidemiology of equine rhinitis virus.

- Worldwide distribution.
- Horses usually infected at 1-2yo.
- Survives well in the environment.
- ERAV: increased risk with co-mingling, stress, concurrent dz, Winter/Spring.
- ERBV: clinical significance unclear.

21

List the clinical signs associated with equine rhinitis virus infections.

- Subclinical infection can occur; horses may shed for a long time in urine and faeces.
- Fever, anorexia, nasal discharge, pharyngitis, lymphadenitis.
- Rarely laryngitis or mild bronchitis.
- Viraemia 4-5d --> long lasting antibodies.

22

How is equine rhinitis virus infection prevented?

No vaccine available.

23

How is equine rhinitis virus infection diagnosed?

- Serology: 4 fold increase 2 wks apart.
- RT-PCR/virus isolation: nasal or nasopharyngeal swab.

24

Describe the equine adenovirus (EAdV).

- Family: Adenoviridae.
- Non-enveloped, icosahedral DNA virus.
- Two serotypes: EAdV-1 (resp) and EAdV-2 (enteric, foals).

25

Describe the epidemiology of EAdV infection.

- Worldwide distribution
- Unknown if clinical signs in adults; causes dz in foals.
- Transmission via direct contact or fomites.
- Virus persists in URT of adults (reservoir) and enviro (1yr at 4 C).

26

Describe the clinical signs and necropsy findings of EAdV infections in immunocompetent yearlings and foals.

- Yearlings: nasal discharge (4-12d), serum ABs peak at 13d and decrease by 2mo.
- Foals (10-35do): incubation period 3-5d, pyrexia, nasal and ocular discharge, tachypnoea, cough, dxa (25%) --> recover by day 10.
- PM: atelectasis, suppurative bronchopneumonia, swelling and hyperplasia resp epi, intranuclear inclusion bodies.

27

Describe the clinical signs and necropsy findings of EAdV infections in immunocompetent foals with SCID.

- Rapid clinical decline and death.
- PM: conjunctivitis, rhinitis, tracheitis, bronchopneumonia, pancreatitis, sialodenitis; intranuclear inclusion bodies in resp epi and pancreatic acinar and ductal cells.

28

How is equine adenovirus infection prevented?

No vaccine available.

29

How is equine adenovirus infection diagnosed?

- Virus isolation from nasopharyngeal and conjunctival swabs during the acute phase of infection is possible but not frequently reported or from lung at necropsy.
- Adenovirus can also be detected in fecal samples by electron microscopy.
- Seroconversion can be detected by serum neutralisation of haemagglutination inhibition (HI) of paired samples collected 10-14 days apart.

30

Describe the Hendra virus.

- Family: paramyxoviridae.
- Genus: henipavirus.
- Enveloped RNA virus.