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LAIM: Respiratory > Equine - Respiratory Dz > Flashcards

Equine - Respiratory Dz Flashcards

1
Q

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

A

Equine influenza.

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2
Q

Describe the equine influenza virus (EIV).

A
  • Family: Orthomyxoviridae.
  • Genera: Influenza A virus.
  • Segmented, single-stranded RNA virus.
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3
Q

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

A
  • 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.
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4
Q

What three countries are free of EIV?

A

Australia, New Zealand and Iceland.

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5
Q

What are risk factors for development of EIV infection?

A
  • Age: 1-5yo or foals if naive population.
  • Low serum EI specific ABs.
  • Frequent contact with a large number of horses.
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6
Q

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

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

Describe the pathophysiology of EIV infection.

A
  • 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.
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8
Q

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

A
  • 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.
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9
Q

What clinical signs are demonstrated by horses infected with EIV?

A
  • 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).
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10
Q

What complications can occur following EIV infection?

A
  • Secondary bacterial pneumonia.
  • Myositis.
  • Myocarditis.
  • Limb oedema.
  • Potentially may predispose to IAD, RAO, EIPH.
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11
Q

Outline recommended strategies to prevent/control EIV infection.

A
  • 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.
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12
Q

Describe the equine arteritis virus (EAV).

A
  • 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.
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13
Q

Describe the epidemiology of EAV infection.

A
  • 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.
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14
Q

Describe the pathophysiology of EAV infection.

A
  • 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.
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15
Q

List the clinical signs associated with EAV infection.

A
  • 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.
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16
Q

List necropsy findings in foals that die following EAV infection.

A
  • Interstitial pneumonia.
  • Lymphocytic arteritis.
  • Renal tubular necrosis.
  • Tunica media necrosis.
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17
Q

How is EAV infection diagnosed in horses?

A
  • 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.
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18
Q

Outline recommended strategies to prevent/control EAV infection.

A
  • 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
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19
Q

Describe the equine rhinitis virus.

A
  • Family: Picornaviridae (same as FMDV!)
  • Non-enveloped RNA viruses.
  • 4 serotypes: ERAV, ERBV1, ERBV2, ERBV3.
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20
Q

Describe the epidemiology of equine rhinitis virus.

A
  • 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.
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21
Q

List the clinical signs associated with equine rhinitis virus infections.

A
  • 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
Q

How is equine rhinitis virus infection prevented?

A

No vaccine available.

23
Q

How is equine rhinitis virus infection diagnosed?

A
  • Serology: 4 fold increase 2 wks apart.

- RT-PCR/virus isolation: nasal or nasopharyngeal swab.

24
Q

Describe the equine adenovirus (EAdV).

A
  • Family: Adenoviridae.
  • Non-enveloped, icosahedral DNA virus.
  • Two serotypes: EAdV-1 (resp) and EAdV-2 (enteric, foals).
25
Q

Describe the epidemiology of EAdV infection.

A
  • 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
Q

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

A
  • 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
Q

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

A
  • 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
Q

How is equine adenovirus infection prevented?

A

No vaccine available.

29
Q

How is equine adenovirus infection diagnosed?

A
  • 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
Q

Describe the Hendra virus.

A
  • Family: paramyxoviridae.
  • Genus: henipavirus.
  • Enveloped RNA virus.
31
Q

Describe the epidemiology and pathophysiology of Hendra virus infection.

A
  • Bats –> horses –> humans (+ dogs?)
  • Horse-to-horse transmission very rare but has occurred.
  • Majority of cases June-Aug (fruit bat birthing season) in QLD and northern NSW.
  • Incubation period 5-16d, CSx ~2d pre-death, 25% horses may survive if they weren’t all euthanised.
  • HeV uses cell surface membrane bound ephrin-B2 (wide dist inc vascular endothelial cells) and ephrin-B3 (CNS) as receptors.
32
Q

What clinical signs are seen in horses with HeV infection?

A
  • Wide variety incl resp, neuro, colic, shifting-limb lameness, oedema, death.
  • NB shed from prior to onset of CSx in all secretions; shedding inc as dz progresses.
33
Q

How is Hendra virus diagnosed?

A
  • PCR: early clinical course of dz, turnaround is 24-48hrs.
  • ELISA: indirectly detects the presence of HeV antibodies in a sample; screening test – negaive sample is a reliable indicator a horse has not been infected but positive is not always a reliable indicator that a horse has been infected. Therefore ELISA positive require additional testing.
  • Virus neutralisation test: detects the presence of HeV antibodies in a sample; must be conducted under high-level biocontainment as involves mixing the blood sample with live virus; takes up to 2weeks.
34
Q

How is Hendra virus prevented/controlled?

A
  • Vaccine.

- Strict biosecurity.

35
Q

Describe herpesviruses.

A
  • Family: Herpesviridae.
  • Double-stranded DNA viruses.
  • Two subfamilies: alpha and gamma.
36
Q

List the alpha herpesviruses that infect equids and the diseases they cause.

A
  • EHV-1: resp dz, abortions, myeloencephalopathy, neonatal death, chorioretinopathy; horses, donkeys, mules, cattle, camelids and deer can be infected.
  • EHV-3: equine coital exanthema.
  • EHV-4: resp dz, sometimes abortions.
  • ASHV-1: similar to EHV-3.
  • ASH-3: similar to EHV 1 and 4.
37
Q

List the gamma herpesviruses that infect equids and the diseases they cause.

A
  • EHV-2: no CSx (ubiquitous ‘cytomegalovirus’), keratoconjunctivitis.
  • EHV-5: Equine Multinodular Pulmonary Fibrosis.
  • ASHV-2.
  • ASHV-4.
  • ASHV-5: interstitial pneumonia in donkeys; pyogranulomatous pneumonia in one mare.
  • ASHV-6.
  • Zebra HV-1.
38
Q

Describe the epidemiology of EHV-1 and EHV-4 infections.

A
  • Ubiquitous; most horses are infected in the first weeks/months of life –> latent infections –> shedding with stress –> dz in host and infection of other horses.
  • EHV-1: outbreaks of resp dz, abortions, myeloencephalopathy, neonatal death, chorioretinopathy.
  • EHV-4: outbreaks of resp dz; indv abortions, EHM, neonatal death.
  • Resp dz particularly of importance in young performance horses.
39
Q

Describe the pathophysiology of EHV-1 and EHV-4 respiratory disease in horses.

A
  • Infection via inhalation –> EHV-4 mainly stays in resp tract; –> resp LNs –> lymphocyte-associated viraemia (EHV-1) –> delivery of virus to other tissues e.g. uterus.
  • Viraemia persists up to 21d, nasal shedding 4-7d.
  • At secondary sites virus spreads to endothelial cells –> vasculitis +/- haemorrhage, thrombosis, ischaemia, necrosis.
40
Q

Describe the immune response to EHV-1 and EHV-4 infection in horses.

A
  • Protective IR is short-lived post-infection; high titres of VN AB dec shedding but do not prevent infection/CSx –> rapid intracellular translocation of the virus?
  • Intracellular virus is susceptable to cytotoxic C-lymphocytes (lyse infected cell) –> CD8+ lymphocytes very imp in preventing/minimising infection.
  • Immunoevasion strategies of EHV-1 modulation of cytokine responses and T/B cell responses, interference with antigen presentation by down regulation of MHC-1 expression, alteration of NK-cell lysis, dec efficient chemoattraction of antigen presenting cells.
41
Q

Describe the clinical signs of EHV-1/EHV-4 respiratory infection in horses.

A
  • Bi-phasic fever (24-48h then 4-8d if viraemic).
  • Lethargy.
  • Anorexia.
  • Nasal discharge (serous to mucopurulent d5-7).
  • +/- conjunctivitis, lymphadenitis, oedema/vasculitis in distal limbs.
42
Q

How can EHV respiratory disease be prevented?

A
  • EHV-1 vaccines protect against EHV-4; none against EHM.
  • Inactivated vacc (low and high antigen load) can limit resp signs, nasal shedding and incidence of abortion storms.
  • MLV –> limited EHV-specific cellular immunity.
  • Vacc q6mo; preg mares 5th, 7th, 9th mo gestation.
43
Q

Describe the pathophysiology of Multinodular Pulmonary Fibrosis caused by EHV-5 infection and other interstitial lung diseases in horses.

A
  • Inciting agent damages pulmonary epithelial or endothelial cells –> alveolar necrosis.
  • Acute/exudative stage: pulmonary congestion, interstitial oedema, erythrocyte extravasation, alveolar flooding. Fibrin, protein rich fluid, cellular debris and inflammatory cells form hyaline membranes.
  • Proliferative stage: type II pneumocytes replace damaged type I pneumocytes. Interlobar septae widen due to proliferation of fibroblast and inflammatory cell infiltration.
  • Chronic disease: fibrosis of alveolar walls and accumulation of mononuclear cells in the interstitium. Granulomas and smooth muscle hyperplasia may form.
  • EHV-5 has tropism for lungs and skin and potential sites of latency in lymphocytes, mononuclear cells, macrophages, dendritic cells, conjunctiva.
  • EHV-2 and EHV-5 share a common isotope, therefore must dx via PCR/virus isolation not serology.
44
Q

List the clinical signs of EMPF.

A
  • CSx greater than 1 week duration; lack of response to prior treatment for bacterial pneumonia or IAD.
  • Fever.
  • Lethargy.
  • Weight loss.
  • Cough.
  • Tachypnoea.
  • Respiratory distress.
  • Nasal discharge.
45
Q

List clinicopathologic findings in horses with EMPF.

A
  • CBC: leukocytosis, neutrophilia; +/- lymphopaenia, monocytosis, anaemia, hyperfibrinogenaemia.
  • MBA: in some cases elevated liver enzymes reported.
  • Blood gas: hypoxaemia.
  • TTW/BAL analysis: predominance of non-degenerate neutrophils > lymphocytes and monocytes; intranuclear eosinophilic inclusions bodies may be seen in BALF.
46
Q

List diagnostic imaging findings in horses with EMPF.

A
  • Radiographs: severe, diffuse, nodular interstitial pattern, either uniformy distrubuted OR mid-ventral to CV; may transition from interstitial to more nodular pattern over time.
  • Ultrasound: bilateral, diffuse roughening of the plural surface; multiple, superficial, discrete nodules.
47
Q

Describe histopathologic findings in the lungs of horses with EMPF.

A
  • Marked interstitial expansion by well-organised mature collagen, infiltration of the interstium by inflammatory cells (lymphocytes > macrophages and neutrophils > eosinophils) and preservation of ‘alveolar-like’ architecture.
  • Alveolar luminal infiltrates may be present, predominately neutrophils and macrophages.
  • Alveoli are lined by hyperplastic cuboidal epithelial cells (type II pneumocytes).
  • Large macrophages with abundant eosinophilic cytoplasm and intranuclear viral inclusion bodies occasionally observed in the alveolar lumen.
48
Q

Describe gross findings in the lungs of horses with EMPF on post mortem exams.

A
  • Lungs do not collapse on opening thorax.
  • All lung regions affected.
  • Multiple firm pale tan-white nodules with a discrete borders. Nodules are uniformly coloured and foci of fibrosis bulge from surrounding tissue.
  • Bronchial LNs enlarged in 50% of cases.
  • Two forms described:
    i) Coalescing: multiple coalescing nodules, 1-5cm diameter, little unaffected lung; more common form.
    ii) Multiple discrete nodules: larger nodules (up to 10cm diameter), same appearance as coalescing form, larger areas of normal lung tissue in between nodules.
49
Q

List components of treatment in horses with EMPF.

A
  • Corticosteroids.
  • Broad-spectrum antibiotics.
  • Anti-virals (valacyclovir better bioavail than acyclovir).
  • NSAIDs.
  • InO2.
  • Fluid and nutritional support.
50
Q

What is the prognosis for horses with EMPF?

A

Guarded to poor.

51
Q

List causes of interstitial lung disease in horses.

A
  • Viral e.g. EHV-5.
  • Bacterial: R. equi in older foals. P. carinii in immunocompromised horses, Mycoplasma spp.
  • Parasitic: parascaris equorum migration.
  • Ingested chemicals e.g. PAs, Crofton weed, Perilla mint.
  • Inhaled chemicals e.g. smoke, oxygen toxicity, agrichemicals e.g. paraquat, silicates.
  • Hypersensitivity reactions e.g. inhalation of fungi and chicken dust.
  • Endogenous metabolic and toxic conditions –> ALI and ARDS e.g. acute uraemia, shock, trauma, burns.

LAIM: Respiratory (5 decks)

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