Flashcards in Equine - Respiratory Dz Deck (51)
What is the most frequently reported viral respiratory disease in horses?
Describe the equine influenza virus (EIV).
- Family: Orthomyxoviridae.
- Genera: Influenza A virus.
- Segmented, single-stranded RNA virus.
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.
What three countries are free of EIV?
Australia, New Zealand and Iceland.
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.
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.
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.
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.
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).
What complications can occur following EIV infection?
- Secondary bacterial pneumonia.
- Limb oedema.
- Potentially may predispose to IAD, RAO, EIPH.
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.
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.
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.
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.
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.
List necropsy findings in foals that die following EAV infection.
- Interstitial pneumonia.
- Lymphocytic arteritis.
- Renal tubular necrosis.
- Tunica media necrosis.
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.
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
Describe the equine rhinitis virus.
- Family: Picornaviridae (same as FMDV!)
- Non-enveloped RNA viruses.
- 4 serotypes: ERAV, ERBV1, ERBV2, ERBV3.
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.
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.
How is equine rhinitis virus infection prevented?
No vaccine available.
How is equine rhinitis virus infection diagnosed?
- Serology: 4 fold increase 2 wks apart.
- RT-PCR/virus isolation: nasal or nasopharyngeal swab.
Describe the equine adenovirus (EAdV).
- Family: Adenoviridae.
- Non-enveloped, icosahedral DNA virus.
- Two serotypes: EAdV-1 (resp) and EAdV-2 (enteric, foals).
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).
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.
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.
How is equine adenovirus infection prevented?
No vaccine available.
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.