Equine - Respiratory Dz Flashcards
1
Q
What is the most frequently reported viral respiratory disease in horses?
A
Equine influenza.
2
Q
Describe the equine influenza virus (EIV).
A
- Family: Orthomyxoviridae.
- Genera: Influenza A virus.
- Segmented, single-stranded RNA virus.
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.
4
Q
What three countries are free of EIV?
A
Australia, New Zealand and Iceland.
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.
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.
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.
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.
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).
10
Q
What complications can occur following EIV infection?
A
- Secondary bacterial pneumonia.
- Myositis.
- Myocarditis.
- Limb oedema.
- Potentially may predispose to IAD, RAO, EIPH.
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.
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.
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.
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.
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.
16
Q
List necropsy findings in foals that die following EAV infection.
A
- Interstitial pneumonia.
- Lymphocytic arteritis.
- Renal tubular necrosis.
- Tunica media necrosis.
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.
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
19
Q
Describe the equine rhinitis virus.
A
- Family: Picornaviridae (same as FMDV!)
- Non-enveloped RNA viruses.
- 4 serotypes: ERAV, ERBV1, ERBV2, ERBV3.
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.
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.
