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Respiratory 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 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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5
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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6
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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7
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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8
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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9
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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10
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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11
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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12
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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13
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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14
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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15
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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16
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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17
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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18
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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19
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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20
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.
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21
Q

How is equine rhinitis virus infection diagnosed?

A
  • Serology: 4 fold increase 2 wks apart.- RT-PCR/virus isolation: nasal or nasopharyngeal swab.
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22
Q

Describe the equine adenovirus (EAdV).

A
  • Family: Adenoviridae.- Non-enveloped, icosahedral DNA virus.- Two serotypes: EAdV-1 (resp) and EAdV-2 (enteric, foals).
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23
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).
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24
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.
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25
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.
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26
Q

How is equine adenovirus infection prevented?

A

No vaccine available.

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27
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.
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28
Q

Describe the Hendra virus.

A
  • Family: paramyxoviridae.- Genus: henipavirus.- Enveloped RNA virus.
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29
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.
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30
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.
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31
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.
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32
Q

How is Hendra virus prevented/controlled?

A
  • Vaccine.- Strict biosecurity.
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33
Q

Describe herpesviruses.

A
  • Family: Herpesviridae.- Double-stranded DNA viruses.- Two subfamilies: alpha and gamma.
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34
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.
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35
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.
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36
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.
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37
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.
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38
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.
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39
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.
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40
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.
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41
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.
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42
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.
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43
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.
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44
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.
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45
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.
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46
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.
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47
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.
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48
Q

What is the prognosis for horses with EMPF?

A

Guarded to poor.

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49
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.
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50
Q

Describe the epidemiology of fungal rhinitis in cattle and common fungi implicated.

A
  • Rare.- No age/breed/sex predisposition.- More common in warm, wet climates.- Rhinosporidium, helminthosporidium, dreschslera rostrata, aspergillus, phycomycetes, stachybotrys, bipolaris; also nocardia bacteria.
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51
Q

List the clinical signs of fungal rhinitis in cattle.

A
  • Stridor.- Dyspnoea.- Mucopurulent nasal discharge.- +/- epistaxis.- +/- open-mouth breathing.
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52
Q

How is fungal rhinitis diagnosed in cattle?

A

Histo: granulation tissue with eosinophils, mononuclear cells, sporangia, hyphae, filamentous bacteria.

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53
Q

How is fungal rhinitis treated in cattle?

A
  • Surgical debulking.- Sodium iodide (NB overdose –> cough, scaly skin, excessive lacrimation).
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54
Q

Describe the pathophysiology of allergic rhinitis/Enzootic Nasal Granuloma of cattle and sheep.

A

Type I (IgE) hypersensitivity to pollen/fungi etc –> ongoing reaction exposure –> tissue damage by mast cell factors –> chronic epithelial, duct, goblet cell hyperplasia, mucus hypersecretion and granulomatous inflammation (type IV hypersensitivity).

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55
Q

Is there a breed or age predisposition for Enzootic Nasal Granuloma in cattle?

A
  • Channel island breeds (Guernsey, Jersey, Alderney) and Friesians. - 6mo to 2yo.
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56
Q

Describe the clinical signs of Enzootic Nasal Granuloma in cattle and sheep.

A
  • Sneezing.- Nasal pruritis.- Dyspnoea.- Stertor.- Profuse bilateral nasal discharge.- +/- facial swelling, tachypnoea, hyperpnoea, ulceration of nasal mucosa, lacrimation, chemosis.- Granulomas: multiple, firm, white, raised, 1-2mm.
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57
Q

How is Enzootic Nasal Granuloma in cattle and sheep diagnosed?

A
  • Endoscopy.- Biopsy.- Culture.- Antigen detection/serology to rule out bacterial, viral or fungal infection.- Inc eosinophils in nasal secretions.
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58
Q

Describe the treatment of Enzootic Nasal Granuloma in cattle and sheep.

A
  • Remove allergens.- Anti-histamines.- Meclofenamic acid.- Steroids.
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59
Q

List the neoplasias that have been reported to occur in the nasal passages of cattle.

A
  • Osteomas.- Osteosarcomas.- Squamous cell carcinomas.- Neuroblastomas.- Haemangiosarcomas.- Ethmoid adenocarcinoma: endemic pattern, 6-9yo, unilateral, viral origin? Mets in LN and lung.
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60
Q

List clinical signs of nasal neoplasia in cattle.

A
  • Inspiratory dyspnoea.- Stridor.- Nasal discharge.- Epistaxis.- Halitosis.- Decreased airflow through nares.- Open-mouth breathing.- Distortion of facial bones.- NB not typically treated.
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61
Q

Describe the lesion seen in congenital cystic nasal turbinate disease of cattle.

A

Nasal conchae lack communication with nasal cavity and fill with fluid.

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62
Q

Describe the clinical signs and diagnosis of congenital cystic nasal turbinates in cattle.

A
  • Stridor.- Tachypnoea.- Decreased air flow.- Exercise intolerance.- Open-mouth breathing.- Palpation.- Endoscopy.- Rads –> large, smooth, cystic ventral conchae.
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63
Q

Describe the treatment of congenital cystic nasal turbinates in cattle.

A
  • Sx: bilateral dorsal lateral nasal bone flaps.- Sx: transnasal removal with gigli wire.
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64
Q

Describe the signalment and aetiology of sinusitis in ruminants.

A
  • Cattle > sheep or goats.- Usually frontal (dehorning) or maxillary (tooth).- Other causes: injury, extension of actinomyces or nasal neoplasia, resp viruses (MCF, IBR, PI3), sinus cysts, lymphoma, oestrus ovis.
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65
Q

Describe the clinical signs of sinusitis in cattle.

A
  • Acute or chronic.- Anorexia.- Lethargy.- +/- fever.- Dehorning site discharging pus.- Unilateral or bilateral nasal discharge.- Stridor.- Foul breath.- Head held at an angle.- +/- frontal bone distortion, exophthalmus, neuro signs.
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66
Q

Describe the diagnosis of sinusitis in cattle.

A
  • Clinical signs and history.- Percussion (dull sounds or pain).- Radiographs.- Sinus centesis (Steinmann pin).
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67
Q

Describe treatment of sinusitis in cattle.

A
  • Sinus trephination (1 or 2 sites).- Lavage.- +/- remove tooth.- If systemic signs: NSAIDs, ABs (penicillin for Trueperella - dehorning, oxytet for pastuerella - not dehorning).
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68
Q

Describe the aetiology of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.

A
  • Trauma: balling gun, dose syringe, specula, stomach tube, rough stemmy feeds, grass awns, brias, FBs.- T. pyogenes, Actinobacillus, Pastuerella, Bordatella. Fusobacterium necrophorum, Streptococcus.
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69
Q

List the clinical signs of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.

A
  • Inspiratory dyspnoea with stertor.- Extended head and neck.- Ptyalism.- Quidding.- Pain or swelling.- Regurgitation through nostrils.- Mucopurulent to blood nasal discharge with fetid odour.- Cough.- Bloat.- Palpable swelling in the pharyngeal area.- If severe dz: depression, fever, anorexia, dehydration, forestomach stasis.
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70
Q

Describe the diagnosis of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.

A
  • Oral exam.- Endoscopy.- Rads.- CBC: neutrophilia, +/- metabolic acidosis due to saliva loss.
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71
Q

List the treatment of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.

A
  • Drain abscess into pharynx and lavage.- Drain externally.- ABs.- NSAIDs.- Tracheotomy.- IVFT.- Feed through rumenostomy.- Good Px.
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72
Q

Describe the epidemiology and pathophysiology of Necrotic Laryngitis (aka Calf Diphtheria).

A
  • Feedlot cattle.- Young (3-18mo); >30 days on feed.- URT infection –> laryngeal contact ulcers or H. somni infection –> damage to laryngeal mucosa –> invasion of F. necrophorum –> acute to chronic infection of laryngeal mucosa and cartilages.- Worldwide distribution, occur year-round but more common in Autumn and Winter.
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73
Q

Describe the clinical signs of Necrotic Laryngitis in cattle.

A
  • Acute onset moist, painful cough.- Severe inspiratory dyspnoea, stertor, head and neck extended.- Salivation/frequent swallowing or sipping water.- Anorexia, fever, hyperaemic MMs.- Bilateral fetid nasal discharge.- Un-treated die in 2-7d.- Recovered may become roarers, get aspiration pneumonia or be poor doers.
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74
Q

Describe the treatment and prognosis of Necrotic Laryngitis.

A
  • ABs: oxytetracycline, penicillin, TMPS.- NSAIDs (1 dose steroid if severe swelling).- +/- tracheotomy.- Nursing care.- Px good if dx early and aggressive tx, otherwise poor.
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75
Q

Describe lesions found at necropsy of cattle that have died from Necrotic Laryngitis.

A
  • Vocal processes and medial angles of arytenoids.- Acute: oedema, hyperaemia, swelling, discharge around necrotic ulcer.- Chronic: focus of necrotic cartilage surrounded by purulent exudate with tract to mucosal surface; arytenoid rotated into lumen or cavities.
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76
Q

Describe laryngeal papillomatosis of feedlot cattle.

A
  • Common disease.- Papovavirus enters via laryngeal ulcers.- CSx: sterterous respiration, cough.- Lesion: sessile to pedunculated, yellow, frond-like, 1-10mm growths on vocal processes or arytenoids.- Tx: usually not indicated; may remove surgically.
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77
Q

Describe the aetiology of tracheal collapse and stenosis in cattle.

A
  • Infrequently reported.- Unknown aetiology; potential causes incl trauma (roping, dystocia), tracheostomies, congenital defects.
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78
Q

Describe the clinical signs of tracheal collapse and stenosis in cattle.

A
  • BAR –> tachypnoea, tachycardia, mucosal hyperaemia, dyspnoea exacerbated by exercise/excitement, stertor, ‘honking’ cough.- Lack of response to tracheostomy, NSAIDs, ABs.
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79
Q

Describe the diagnosis of tracheal collapse and stenosis in cattle.

A
  • Endoscopy.- Rads: dorsoventral flattening in caudal cervical or cranial thoracic trachea most common; can be lateral.- Necropsy: dorsally or laterally flattened trachea.
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80
Q

Describe the treatment and prognosis of tracheal collapse and stenosis in cattle.

A
  • Px poor.- Surgery reported to enable survival to slaughter.
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81
Q

Describe the aetiology and pathogenesis of tracheal oedema syndrome (aka Honker Cattle) of feedlot cattle.

A
  • Extensive oedema and haemorrhage of dorsal wall of trachea.- Acute and chronic form; unknown if related.- Proposed aetiologies: URT viruses, bacteria e.g. P. multocida or H. somni, feedbunk trauma, fat, mycotoxins, hypersensitivity reaction.
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82
Q

Describe the clinical presentation of the acute form of tracheal oedema syndrome in cattle.

A
  • Heavy feedlot cattle in last 2/3 feeding period.- Summer.- Subclinical: sudden death.- Dyspnoea, guttural inspiratory sounds, open mouth breathing, extending head and neck, cyanosis, recumbency, death.
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83
Q

Describe the clinical presentation of the chronic form of tracheal oedema syndrome in cattle.

A
  • Lighter cattle (130-400kg).- +/- Hx of IBR/pneumonia.- Continuous deep, hacking cough.- +/- unthrifty.
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84
Q

Describe treatment and prognosis of tracheal oedema syndrome in cattle.

A
  • Acute: steroids, oxygen, decrease stress.- Chronic: no tx.- Px: poor.
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85
Q

Describe necropsy findings in cattle that have died from tracheal oedema syndrome.

A
  • Acute: dorsal oedema up to 5cm thick, caudal half of trachea; mucosal, submucosal and peritracheal oedema +/- haemorrhage.- Chronic: hyperaemia of mucosa in caudal third of trachea; +/- thin layer mucopurulent exudate; +/- fibre-like projections and polyps.
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86
Q

List the infectious pathogens which contribute to he Bovine Respiratory Disease Complex.

A
  • Bovine Herpesvirus-1 (BHV-1).- Bovine Respiratory Syncytial Virus (BRSV).- Bovine Viral Diarrhoea Virus (BVDV).- Bovine Parainfluenza 3 Virus (PI3).- Bovine Coronavirus (BCoV).- Adenovirus.- Viruses of unknown clinical sig: Bovine Rhinitis Virus, Bovine Reovirus, Calicivirus, Influenza.- Mannheimia haemolytica.- Pastuerella multicodia.- Histophilus somni.- Mycoplasma bovis.- Biberstenia trehalosi.- Trueperella pyogenes.- Bacteria w unknown clinical sig: Chlamydial organisms.
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87
Q

Describe the Bovine Herpesvirus-1 (BHV-1).

A
  • Family: Herpesviridae.- Subfamily: alpha.- Enveloped DNA virus.
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88
Q

List the diseases caused by BHV-1.

A
  • Infectious Bovine Rhinotracheitis (IBR).- Conjunctivitis.- Infectious pustular vulvovaginitis.- Balanoposthitis.- Encephalomyelitis.- Mastitis.
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89
Q

List the clinical signs of IBR in cattle.

A
  • Can be mild to severe (influence of type-1 interferon genotype??)- ‘Red nose’: hyperaemic muzzle.- Pustules on nasal mucosa –> diphtheritic membranes.- Conjunctivitis +/- corneal opacity.- Pyrexia.- Anorexia.- Dec milk prod.- Tachypnoea.- Ptyalism.- Cough.- Nasal discharge (serous to mucopurulent).- Harsh bronchovesicular sounds; referred tracheal noise.- +/- secondary bacterial pneumonia.- +/- abortion.
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90
Q

Describe the pathophysiology of IBR.

A
  • Transmitted via aerosol and direct contact.- BHV-1 surface glycoproteins interact w heparin sulfate proteoglycans and other host cell proteins –> enter resp epi cells and neighbouring epi cells via intracellular bridges.- Invade lymphocytes and monocytes –> extra-respiratory infections.- Latency in trigeminal ganglia and tonsils mediated by latency-related transcript (prevents apoptosis, re-activates shedding).- Disease mechanisms:i) Direct injury of infected URT/bronchial epi cells –> inflammation and susceptibility to secondary infection.ii) Immunosuppression: dysfunction of neuts, lymphs, macro incl dec neut chemotaxis, dec mitogen-induced blastogenesis of lymphocytes, dec expression of MHC-1 molecules, inc apoptosis of lymphs, mono.
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91
Q

Describe the epidemiology of IBR.

A
  • Widespread.- Adult cattle are reservoir.- Increased attack rate and fatality in feedlot cattle.- Historically first few weeks after entry, now seeing late outbreaks (mutation not covered by current vacc?).- Not important in epizootic pneumonia of calves.
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92
Q

Describe necropsy findings in animals that have died from IBR.

A
  • Rhinitis, laryngitis, tracheobronchitis.- Mucosa congested or haemorrhagic.- Pustular lesions –> plaques on resp. ocular, repro mucosa.- +/- oesophageal lesions.- Neonates: systemic dz w necrotic foci in all organs.- NB intranuclear inclusion bodies NOT common feature of BHV-1 infections.
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93
Q

How is IBR diagnosed in cattle?

A
  • Virus isolation, IFA, PCR from nasal and conj swabs.- Paired serology (Ab titre).
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94
Q

Describe treatment and prevention of IBR in cattle.

A
  • Decrease stress.- Ensure access to food and water.- +/- NSAIDs.- +/- ABs (if evidence of secondary infection).- +/- vaccination (outbreak).- IN/IM vaccines are widely available; protect from infection in challenge studies but few field trials; inactivated for preg cows and neonates, MLV others –> immunity in 2-3d therefore must induce CMI.- Management essential in prevention e.g. dec co-mingling, dec stress.
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95
Q

Describe the Bovine Respiratory Syncytial Virus (BRSV).

A
  • Family: Paramyxoviridae.- Subfamily: Pneumovirina.- Enveloped RNA virus.- Recent change in BRSV G glycoprotein reported in Europe, likely secondary to antigenic pressure from vaccination.
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96
Q

List the clinical signs of BRSV infection in cattle.

A
  • Inapparent to severe; CSx limited to resp tract.- Fever, depression, inappetence.- Tachypnoea.- Ptyalism.- Cough.- Nasal/lacrimal discharge.- Inc bronchovesicular sounds +/- wheezes/crackles in mid- to dorsocaudal lungfields.- +/- absent dorsal BV sounds (ruptured bullae).- Late infection: pronounced dyspnoea, inc expr effort, open-mouth breathing, +/- s/c emphysema.
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97
Q

Describe the epidemiology of BRSV infection in cattle.

A
  • 60-80% US cattle have Abs assoc w seroconversion.- High morbidity, low mortality (0-20%).- Adult cattle believed to be reservoir.- Tranmission: aerosol, direct contact, fomites.- Incubation period: 3-5 days.
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98
Q

Describe the pathogenesis of BRSV infection in cattle.

A
  • Infects cells of nasal, tracheal, bronchial epi +/- alveolar and circulating macrophages.- Epi cells fuse –> multinucleated cells (syncytia) –> slough into lumen –> phagocytosed by neut/alv macro.- Bronchitis, bronchiolitis, alveolitis +/- AIP.- Infected macro have dec function, dec phagocytosis, dec prod chemotactic factors.
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99
Q

Describe the role of the immune response in BRSV infection in cattle.

A
  • Severity of dz is related to humoral and CM immunity.- CSx most notable mast cell degran –> bronchoconstriction, pulmonary oedema.- Vaccine-enhanced dz is rare but is reported w inactivated and MLV vaccines (vacc is still recommended as rare).
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100
Q

Describe necropsy findings in cattle that have died from BRSV infection.

A
  • Neutrophilic to mononuclear bronchitis, broncheolitis, alveolitis +/- syncytial cells.- AIP –> dorsocaudal lungs heavy, rubbery, emphysema.- Histo: alveolar epi hyperplasia, hyaline membranes, interstitial inflamm cells, haemorrhage, oedema.
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101
Q

Outline diagnosis of BRSV in cattle.

A
  • Virus does not survive well, therefore not virus iso.- PCR, IHC, IFA of nasal swabs, TTW or BALF, lung tissue; less likely to be found 10-15d post-infection.- Seroconversion: ELISA or VN Abs.
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102
Q

Describe treatment and prevention of BRSV infection in cattle.

A
  • Goal: decrease resp inflamm and prevent secondary bacterial infection.- NSAIDs; steroids if severe resp distress/AIP.- Antibiotics.- InO2, furosemide if required.- IN/IM vaccines available.
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103
Q

Describe the Bovine Viral Diarrhoea Virus (BVDV).

A
  • Family: Flaviviridae.- Genus: Pestivirus.- Enveloped RNA virus.
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104
Q

Describe the respiratory disease causes by BVDV infection in cattle.

A
  • Some strains cause mild pneumonia.- Importance is as a co-infector in BRDC e.g. w M. haemolytica, M. bovis, BHV-1, BRSV.
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105
Q

Describe the pathogenesis of BVDV in BRDC infections.

A
  • Suppresses immune resp to co-infecting agents.- Suppresses immune resp to vacc against other BRDC pathogens.- Infects the resp tract and enhances pathogenicity of co-infectors.
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106
Q

Describe the Bovine Parainfluenza-3 Virus (PI3).

A
  • Family: Paramyxoviridae.- Subfamily: Paramyxovirinae.- Enveloped RNA virus.
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107
Q

List the clinical signs of PI3 infection in cattle.

A
  • Range from subclinical to mild.- Fever.- Cough.- Nasal and ocular discharge.- Tachypnoea.- Inc bronchovesicular sounds, wheezes.
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108
Q

Describe the epidemiology of PI3 infection in cattle.

A
  • Very widespread.- Often no clinical signs.- Important initiator of BRDC.- Incubation period 2d.
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109
Q

Describe the pathophysiology of PI3 infection in cattle.

A
  • CSx of URT and LRT infection.- Virus found in nasal, tracheal, broncheolar, alveolar epi cells.- Damages mucociliary apparatus, dec alveolar macro function (Fc receptor expression, phagocytosis, microbicidal action) –> predisposes to secondary infection.
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110
Q

Describe necropsy findings in cattle that have died from PI3 infection.

A
  • Rarely seen.- Experimental infection –> necropsy –> changes like mild BRSV.
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111
Q

Outline the diagnosis of PI3 infection in cattle.

A
  • Virus isolation.- PCR of nasal swabs.- Paired serology to demonstrate rising titre.
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112
Q

Describe methods for prevention of PI3 infection.

A
  • Inactivated and ML vaccines.- Registered for cattle only; off-label in sheep and goats.
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113
Q

Describe the Bovine Coronavirus (BoCV).

A
  • Family: Coronaviridae.- Group 2 Coronavirus.- Enveloped, single-stranded RNA virus.
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114
Q

List diseases caused by Bovine Coronavirus.

A
  • Calf diarrhoea.- Winter dysentary of adult cattle.- Respiratory disease (recent evidence).
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115
Q

Describe the contribute of BoCV to BRDC in cattle.

A
  • Important role identified in two Shipping Fever outbreaks.- Evidence vaccination –> less resp dz in feedlot cattle.- Other evidence suggests no role in BRDC.
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116
Q

Describe the Bovine Herpesvirus-4 Virus.

A
  • Family: Herpesviridae.- Subfamily: Gamma herpesviridae.- Enveloped DNA virus.
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117
Q

List the diseases caused by BHV-4.

A
  • Abortions.- Metritis.- Mammilitis.- Enteric dz.- Conflicting data whether or not causes respiratory dz.
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118
Q

Describe adenoviruses of ruminants.

A
  • Family: Adenoviridae.- Serotypes: Cattle - at least 10, sheep - at least 6, goats - 2.- Non-enveloped, double-stranded DNA viruses.
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119
Q

Describe presentation of Bovine Adenovirus infections.

A
  • Widespread.- Frequently subclinical, often assoc w other pathogens.- Assoc w pneumonia, enteritis, keratoconjunctivitis; weak calf syndrome?
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120
Q

Describe the bacteria Mannheimia haemolytica.

A
  • Family: Pasteurellaceae.- Gram negative aerobe, small rod.- At least 12 serotypes.- Cattle: A1, A6 most common pneumonic lungs, A2 normal flora in nasopharynx.- Sheep and goats: A2 most common pneumonic lungs; A7, A9 pathogenic.
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121
Q

Describe the epidemiology of Mannheimia haemolytica infection in cattle.

A
  • Most common bacterial isolate from feedlot cattle w fatal fibrinous pleuropneumonia.- Not commonly associated with outbreaks of pneumonia in dairy calves.
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122
Q

Describe the pathophysiology of Mannheimia haemolytica infection in cattle.

A
  • Infected v early in life -> n commensal org in nasopharynx.- Numbers inc w transport/URT viral infection –> opportunistic pathogen of LRT –> multiply in lungs –> severe, necrotising, fibrinous pleuropneumonia.- Virulence factors:– Leukotoxin: binds to cells via CD18, beta subunit of beta 2 integrins –> inc expression of LFA-1 by leukocytes –> apoptosis/cell lysis of platelets, lympho, macro, neut.– LPS: works synergistically w leukotoxin; v rapid resp –> initiation of complement and coag cascades, activation of endo cells, recruitments of neuts, activation of neuts and macro –> inc pro-inflam cytokines (IL-1b, IL-8, TNF-a); death of massive influx of neuts –> elastase, collagenase, reactive O2 –> necrosis/fibrinous exudation.– Polysaccharide capsule: aids attachment, prevents phagocytosis by neutrophils.– Iron-regulated outer membrane proteins: bind transferrin, alter neutrophil function.– Adhesins: mediate attachment to host cells.– Neuraminidase: dec viscosity of mucus, dec repellant negative charge on host cells.
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123
Q

List clinical signs of Mannheimia haemolytica infection in cattle.

A
  • Fever.- Tachypnoea.- Depression.- Dec appetite.- NB no cough during early disease.- +/- thoracic pain.- +/- endotoxaemia.- Harsh BV sounds over cranioventral lungs.- +/- death/chronic infection.- Usually secondary to viral dz.
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124
Q

Describe necropsy findings in cattle infected with Mannheimia haemolytica.

A
  • Fibrinopurulent bronchopneumonia or pleuropneumonia OR pulmonary consolidation w/out fibrin (dairy calves, sheep, goats).- Cranioventral lobes to whole lung.- May see infarcts, coagulative necrosis, swollen red LNs.
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125
Q

Outline diagnosis of Mannheimia haemolytica infection in cattle.

A
  • Culture and cytology.- TTW, BAL, thoracocentesis or lung tissue.
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126
Q

Outline treatment of Mannheimia haemolytica infection in cattle.

A
  • Many labelled antibiotics.- NSAIDs in cattle with SIRS.
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127
Q

Outline methods for prevention of Mannheimia haemolytica infection in cattle.

A
  • Antibiotic metaphylaxis e.g. tilmicosin, florfenicol just pre- or post-shipping.- Ensure no FPT.- Vaccination.- Minimise stressors: viral infection, co-mingling, long distance shipping, pre-conditioning.
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128
Q

Describe the bacteria Pasteurella multocida.

A
  • Family: Pasteurellaceae.- Gram negative aerobe.- 5 serogroups: A - most common resp infection, B+E - haemorrhagic septicaemia (Asia and Africa), D+F - resp infection in some regions (esp in sheep).
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129
Q

Describe the epidemiology of Pasteurella multocida infection in cattle.

A
  • Normal URT commensal in cattle, sheep and goats.- Debate if primary or only secondary lung pathogen.
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130
Q

Describe the pathophysiology of Pasteurella multocida infection in cattle.

A
  • Little known.- LPS.- Capsule: resists phagocytosis.- Iron-regulated outer membrane proteins: inc ability to proliferate in host.- Damage to resp epi (viruses, poor ventilation etc) –> chronic inhalation of small numbers of bacteria –> bronchopneumonia.- Possible cause of enzootic pneumonia of calves.
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131
Q

List clinical signs of Pasteurella multocida infection in cattle.

A
  • Fever.- Tachypnoea.- Depression.- Coughing.- Mucoid to mucopurulent nasal discharge.- Harsh BV sounds cranioventrally; crackles (fluid in large airways).- +/- endotoxaemia.- Generally milder CSx than M. haemolytica.- Calves > feedlot cattle.
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132
Q

Describe necropsy findings in cattle infected with Pasteurella multocida.

A
  • Purulent bronchopneumonia w plum-coloured CV consolidation and purulent exudate on cut section.- Fibrin possible.
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133
Q

Outline diagnosis of Pasteurella multocida infection in cattle.

A
  • Culture and cytology.- TTW, BAL or lung tissue.
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134
Q

Outline methods for treatment and prevention of Pasteurella multocida infection in cattle.

A
  • Many labelled antibiotics; as infections usually chronic may require 3-5d at labelled dose.- Dec exposure to viruses and environmental contributors.- Vaccines available but questionable efficacy.
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135
Q

Describe the bacteria Histophilus somni.

A
  • Family: Pasteurellaceae.- Gram negative aerobe.- NF of URT and genital mucosa of cattle, goats, sheep.- Different strains have different virulence.
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136
Q

Describe the epidemiology of Histophilus somni infection in cattle.

A
  • Exposure common.- Dz of feedlot cattle > calves.
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137
Q

Describe the pathophysiology of Histophilus somni infection in cattle.

A
  • Primary viral dz –> secondary bacterial infect of resp tr.- Virulence factors:– Outer membrane proteins: bind Fc region of Ab –> escape opsonisation, resist killing following phagocytosis.– Lipooligosaccharide: like LPS; interacts w P2X7 receptor on endo cells –> apoptosis –> vasculitis and thrombosis; induces IgE prod –> hypersens post-vacc/more severe dz.
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138
Q

List clinical signs of Histophilus somni respiratory infection in cattle.

A
  • Causes dz in multiple body systems: septicaemia, TEME, endometritis, abortion, infertility, pneumonia, pleuritis, laryngitis, otitis, conjunctivitis, myocarditis, mastitis, polyarthritis.- Mild to severe respiratory infections.- Fever.- Tachypnoea.- Cough.- Nasal discharge.- Depression.- Harsh BV sounds cranioventrally.- Pain (pleuritis).- +/- SIRS.
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139
Q

Describe necropsy findings in cattle infected with Histophilus somni.

A
  • Plum and brown consolidation CV lungs.- +/- abscesses.- Purulent material on cut section of lung tissue.- +/- fibrinous pleuritis.- +/- haemorrhage.
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140
Q

Outline diagnosis of Histophilus somni infection in cattle.

A
  • Culture: TTW, BAL, pleurocentesis, lung tissue; NB hard to grow in culture therefore trans immediately, pre-tx samples.- IHC lung tissue.- Paired titres.
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141
Q

Outline methods for treatment and prevention of Histophilus somni infection in cattle.

A
  • Several antibiotics.- Prophylaxis w oxytet does not result in improvement.- Killed whole bacterins –> IgE prod –> risk of anaphylaxis on subsequenc vacc therefore only vacc high risk cattle.- Enviro/stress management, dec viral infections.
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142
Q

Describe the bacteria Mycoplasma bovis.

A
  • Family: mycoplasma.- Small, pleomorphic organisms w/out cell wall.
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143
Q

Describe the epidemiology of Mycoplasma bovis infection in cattle.

A
  • Cattle; rare in sheep and goats.- Found in healthy and diseased cattle.- Spread by aerosol, direct contact, in milk.- Spreads rapidly in feedlots.- Found in dairy calves and feedlot cattle, partic w chronic resp dz.
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144
Q

Describe the pathophysiology of Mycoplasma bovis infection in cattle.

A
  • Little known.- General mycoplasma characteristics:– Variable surface proteins allow attachment to host cells.– Invasion of tissues e.g. can move b/w resp epi cells.– Evade host IR, impair neut activity, kill lymphocytes, induce inflammatory response.
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145
Q

List clinical signs of Mycoplasma bovis infection in cattle.

A
  • Fever.- Tachypnoea.- Inappetence.- +/- resp distress.- +/- cough.- +/- nasal discharge.- Outbreaks: some –> otitis (young calves), arthritis or polysynovitis (calves or weanlings).- Lack of response to therapy, chronic infections.- Ill-thrift.- Usually secondary but can cause primary resp dz.- Other dz: mastitis, otitis, arthritis, polysynovitis, sinusitis, myocarditis, pericarditis, reproductive failure.
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146
Q

Describe necropsy findings in cattle infected with Mycoplasma bovis.

A
  • Dark red, firm, consolidated CV lungs.- +/- raised white-yellow firm nodules = foci of caseous necrosis (eosinophilic coagulative necrosis).- +/- arthritis, tenosynovitis, otitis.
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147
Q

Outline diagnosis of Mycoplasma bovis infection in cattle.

A
  • PM: IHC or culture of organisms plus typical gross/histo lesions.
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148
Q

Outline methods for treatment and prevention of Mycoplasma bovis infection in cattle.

A
  • Poor response to ABs in many cases.- ABs labelled for M. bovis incl tulathromycin, florfenicol, enrofloxacin, gamithromycin; tx 7-10d+.- Success suggested to be based on early tx.- Vaccines: field trials lacking.- Predisposing factors unknown.
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149
Q

Does mycoplasma mycoides infection occur in cattle?

A

Exotic to North America but can cause bovine pneumonia.

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150
Q

Describe the bacteria Biberstenia trehalosi.

A
  • Family: Pasteurellaceae.- Gram negative, facultative anaerobe.
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151
Q

List clinical signs of Biberstenia trehalosi infection in ruminants.

A
  • Cattle/calves: severe acute/peracute bronchopneumonia –> death.- Sheep: pneumonia or systemic dz w multi-organ infection.
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152
Q

How can Biberstenia trehalosi infections be prevented in cattle?

A

Possible cross-protection from M. haemolytica vaccines.

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153
Q

Describe the bacteria Trueperella pyogenes.

A
  • Family: Actinomycetaceae.- Gram positive rod, facultative anaerobe.
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154
Q

What is the significance of Trueperella pyogenes in respiratory disease of cattle.

A
  • Secondary or tertiary invader in pneumonia –> lung abscesses.- Virulence factors incl pyolysin: cytolytic toxin; molecules that aid in adherence to host cells.- Tx primary dz to prevent chronic pneumonia and involvement of T. pyogenes.
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155
Q

Define the clinical presentation and list the necropsy findings in Acute Respiratory Distress Syndrome of cattle.

A
  • Acute onset (usually severe) dyspnoea and AIP.- Gross findings: lungs fail to collapse, heavy, firm, rubbery texture; usually interlobular or bullous emphysema; +/- oedema; +/- ‘patchwork’ appearance. - Histo: alveolar hyaline membranes, alveolar fibrin, interstitial oedema, type II pneumocyte proliferation; +/- haemorrhage, emphysema, inflam infiltrates.
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156
Q

Describe the definition and aetiology of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Definition: ARDs w change to lush green pastures in cattle >2yo; aka ‘Fog Fever’.- Aetiology: L-tryptophan in lush pasture –> rumen –> 3-methylindole (pneumotoxin).
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157
Q

Describe the epidemiology of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Seen in adult cattle; nursing calves not affected.- Autumn.- May be indv but usually outbreaks.- ~50% morbidity, 30% mortality.
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158
Q

Describe the pathophysiology of Acute Bovine Pulmonary Oedema and Emphysema.

A

L-tryptophan (lush forage) ingested –> ruminal micro-org convert to indole acetic acid –> 3-methylindole –> bloodstream –> metab by P-450 in Clara cells and type I pneumocytes –> reactive intermediates bind w intracellular proteins/macromolecules –> degen/necrosis/exfoliation of Clara cells and type I pneumocytes + oedema –> hyaline membrane formation, adenomatosis (type II pneumocyte prolif) and Clara cell proliferation.

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159
Q

List the clinical signs of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • CSx dev w/in 2wk of change to lush pasture.- Severe dyspnoea w expr grunt, tachypnoea, frothing at mouth, open-mouthed breathing, head/neck extended, nostril flaring.- +/- fever, tachycardia.- Lung sounds quiet +/- crackles.- Severe exercise intolerance.- Up to 30% mortality OR improve after 3d –> tachypnoea, harsh BV sounds, crackles, wheezes (esp caudal), +/- s/c emphysema.- Rpt episodes can –> pulmonary fibrosis and alveolitis.- NB no cough, sepsis, adventitious lung sounds.
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160
Q

Outline diagnosis of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Usually presumptive.- Can perform rads –> interstitial pneumonia.- Research: measure 3-MI in blood and urine.
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161
Q

Outline treatment of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Controversial; stress of handling/moving off pasture more dangerous than not tx?- Potential meds: furosemide, flunixin, dexamethasone.
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162
Q

Outline methods for prevention of Acute Bovine Pulmonary Oedema and Emphysema.

A
  • Limit access to lush pasture e.g. feed hay –> put out for 2h –> inc to 24h over 10d, put sheep/young cattle on lush pastures, strip-grazing, use after hard frost, mow.- Monensin, lasolacid: feed 1-6d prior to, and first 10d on, pasture.
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163
Q

Describe aetiology of Feedlot Acute Interstitial Pneumonia.

A
  • Unknown.- Proposed mechanisms: feed assoc pneumotoxins or factors related to protein metab, chronic bacterial pneumonia, gender/hormonal influences, chronic small airway injury, BRSV, heat or dust exposure, hypersensitivity reactions –> multifactorial?
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164
Q

Describe the epidemiology of Feedlot Acute Interstitial Pneumonia.

A
  • Second leading cause of death of feedlot cattle behind bronchopneumonia.- Most often cattle on feed >60d (vs 45d peak for Shipping Fever).- Inc risk in Summer and in heifers.
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165
Q

List the clinical signs of Feedlot Acute Interstitial Pneumonia.

A
  • Found dead.- Rapid onset expr dyspnoea +/- tachypnoea, open-mouth breathing, head and neck extended.- +/- froth from mouth.- +/- fever.- +/- cyanosis, tachycardia, s/c emphysema.- Ausc –> dull areas throughout lungs w some crackles.
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166
Q

Describe necropsy findings in cattle that die from Feedlot Acute Interstitial Pneumonia.

A
  • Petechial/eccymotic haemorrhages in larynx, trachea, bronchi; frothy fluid in airways.- Lungs fail to collapse, heavy, firm, rubbery texture; usually interlobular or bullous emphysema; +/- oedema; +/- ‘patchwork’ appearance. - Histo: alveolar hyaline membranes, alveolar fibrin, interstitial oedema, type II pneumocyte proliferation; +/- haemorrhage, emphysema, inflam infiltrates. - +/- changes related to chronic resp dz e.g. fibrin on pleura, peribronchiolar lymphoid cuffing or vascular fibrosis.
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167
Q

Outline treatment and prevention of Feedlot Acute Interstitial Pneumonia.

A
  • Furosemide, flunixin, dexamethasone, ABs (often concurrent bronchopneumonia).- Px guarded therefore consider slaughter.- No specific methods of prevention, dec infections and dust, monensin not effective.
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168
Q

Describe aetiology of Mouldy Sweet Potato Toxicity.

A

Ingestion of toxin produced by sweet potatoes (Ipomoea batatas) infected with Fusobacterium solani.

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169
Q

Describe the epidemiology of Mouldy Sweet Potato Toxicity in cattle.

A
  • Outbreaks when cattle fed mouldy sweet potatoes.- High morbidity and mortality.- Nursing calves not affected.
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170
Q

Describe the pathophysiology of Mouldy Sweet Potato Toxicity in cattle.

A
  • F. solani infects sweet potato –> sweet potato produces 4-hydroxymyoporone (hepatotoxic) –> fungus converts to pneumotoxins; most abundant is 4-ipomeanol.- 4-ipomeanol ingested –> bloodstream –> lungs –> metab by P-450 mixed oxidase system in Clara cells and type I pneumocytes –> reactive intermediates bind w intracellular proteins/macromolecules –> degen/necrosis/exfoliation of Clara cells and type I pneumocytes + oedema –> hyaline membrane formation, adenomatosis (type II pneumocyte prolif) and Clara cell proliferation.
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171
Q

List the clinical signs of Mouldy Sweet Potato Toxicity in cattle.

A
  • Acute onset tachypnoea, tachycardia, hyperpnoea, dyspnoea w expr grunt, extension of head/neck, flaring nostrils, frequent deep cough.- Ausc: crackles, harsh BV sounds.- CSx dev in 24h, death in 2-5d.
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172
Q

Describe necropsy findings in cattle with Mouldy Sweet Potato Toxicity.

A
  • Lungs wet, firm large, fail to collapse, haemorrhagic, gelatinous oedema fluid, emphysematous w bullae.- Histo: alveolar hyaline membranes, alveolar fibrin, interstitial oedema, type II pneumocyte proliferation; +/- haemorrhage, emphysema, inflam infiltrates.
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173
Q

Outline treatment and prevention of Mouldy Sweet Potato Toxicity in cattle.

A
  • Furosemide, flunixin, dexamethasone.- Do not feed mouldy sweet potatoes.
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174
Q

Describe aetiology of Perilla Ketone Toxicity.

A
  • Perilla/purple mint (Perilla frutescens) leaves and seeds contain a pneumotoxin.- Common weed in SE USA.- 2m high, square stem, serrated leaves, small white-purple flowers.
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175
Q

Describe the epidemiology of Perilla Ketone Toxicity in cattle.

A
  • Cattle, sheep and goats susceptible.- Adult cattle avoid plant, calves may prefer it.- Most toxic seed-flower stage (Aug-Oct).- Toxic in hay.
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176
Q

Describe the pathophysiology of Perilla Ketone Toxicity in cattle.

A
  • Volatile oils of P. frutescens contain furans.- Perilla ketone predominates in late growing season –> ingested –> absorbed from rumen into bloodstream –> lungs –> metab by P-450 mixed oxidase system in Clara cells and type I pneumocytes –> reactive intermediates bind w intracellular proteins/macromolecules –> degen/ necrosis/exfoliation of Clara cells and type I pneumocytes + oedema –> hyaline membrane formation, adenomatosis (type II pneumocyte prolif) and Clara cell prolif.
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177
Q

List the clinical signs of Perilla Ketone Toxicity.

A
  • Animals often found dead.- Sudden onset moderate to severe dyspnoea, wheezing, frothing at mouth, expr grunt.- Worse with exertion.- Death in 3-7 days.
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178
Q

Describe necropsy findings in cattle with Perilla Ketone Toxicity.

A
  • Lungs distended, fail to collapse, moist, heavy, oedematous, emphysematous.- Often bullae, pleural effusions, froth.- Histo: oedema, alveolar epi hyperplasia, emphysema, congestion.
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179
Q

Outline treatment and prevention of Perilla Ketone Toxicity in cattle.

A
  • Furosemide, flunixin, dexamethasone.- Eliminate perilla mint from pasture/take cattle off hay.
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180
Q

Describe the presentation of pulmonary disease in animals with pyrrolizidine alkaloid toxicity.

A
  • Animals w chronic liver dz from PA tox can also develop lung lesions.- PA toxin activated by P-450 mixed oxidase system in lungs –> oedema, congestion, haemorrhage, prolideration of bronchiolar and alveolar epi cells with megalocytosis, interstitial fibrosis and inflammatory infiltrates.
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181
Q

Describe the pathophysiology of toxic gas-induced lung injury in cattle.

A
  • Enviro gases/fumes/smoke.- Chronic low level exposure –> dec dz resistance, dec growth rate.- Exposure to higher levels –> lethargy, mild dyspnoea, anorexia, dec growth rate, excessive lacrimation or salivation.- Low incidence sudden death/stillbirths.- Acute, severe outbreaks of ARDs possible.
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182
Q

List sources of toxic gas exposure in ruminants.

A
  • Silos: nitrogen dioxide.- Cutting/welding galvanised pipes: zinc oxide.- Machinery exhausts/heaters: carbon monoxide.- Ag chemical spills: chlorine, formaldehyde, insecticides.- Manure: hydrogen sulphide, ammonia, methane, CO, CO2.
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183
Q

Describe the aetiology of Hypersensitivity Pneumonitis in cattle.

A

Exposure to dusk from mouldy hay/grain/plant matter containing actinomycete spores.

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184
Q

Describe clinical signs of Hypersensitivity Pneumonitis in cattle.

A
  • Similar to RAO in horses; coughing, inc expr effort/wheezes.- Dz of confined cattle (Winter).- Acute and chronic forms.
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185
Q

Describe necropsy findings in cattle with Hypersensitivity Pneumonitis.

A
  • Acute: lungs superficially normal but see small grey spots which represent interstitial and peribronchiolar acumm of lympho, in others see red centres of atelectasis surrounded by pink, inflated lung.- Chronic: similar findings plus intra-alveolar fibrosis and epithelial hyperplasia.
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186
Q

Describe treatment of cattle with Hypersensitivity Pneumonitis.

A
  • Environmental management key i.e. remove mouldy hay/grain/straw etc. from environment, improve ventilation, turnout if possible.- Steroids +/- bronchodilators.
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187
Q

Describe Dictyocaulus viviparus.

A

Trichostrongylid nematode that lives in the bovine trachea and bronchi; 8cm white worms.

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188
Q

Describe the lifecycle of Dictyocaulus viviparus.

A
  • Survives in temperate climates.- Adult worm in lungs lay eggs, mature to larvae –> coughed up and swallowed –> faeces –> L3 –> ingested –> migrated through intestines to mesenteric LNs –> L4 –> migrate through blood and lymph to lungs –> adult.
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189
Q

Describe clinical signs of Dictyocaulus viviparus infection in cattle.

A
  • CSx in eosinophilic exudate in small airways –> gradual cough and tachypnoea; if very severe infection may see death.ii) Patent phase (25-55d): adults, eggs, larvae in airway –> tracheitis, bronchitis, pneumonia w consolidation in caudodorsal lungs; cough, tachypnoea, dyspnoea, anorexia, wt loss, fever if secondary bacterial inf, harsh BV sounds, wheezes and crackles; may –> death.iii) Late patent phase (55-90d): CSx grad resolve, adults expelled, may –> worsening CSx/death with secondary infection/re-infection.
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190
Q

Outline diagnosis of Dictyocaulus viviparus infection in cattle.

A
  • Larvae ID from faeces or TTW via Baerman test: 390-450um, pointed end, dark granules in intestines.- CBC: eosinophilia.- Abs ID via ELISA of serum or milk.
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191
Q

Describe necropsy findings in cattle that died of Dictyocaulus viviparus infection.

A
  • Atelectic lung lobules –> consolidation in caudoventral lungs.- Larvae and worms in airways.- If re-infection occurred: pulmonary lymphoid nodules under pleura with eosinophilic parasitic debris, macrophages, multi-nucleated giant cells, hyperplastic bronchiolar epithelium, eosinophils, plasma cells.
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192
Q

Describe treatment and prevention of Dictyocaulus viviparus infection in cattle.

A
  • Azoles and mectins.- Only cough –> good Px, additional CSx –> guarded.- Rotational deworming and pasture management.
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193
Q

What parasitic organism can cause acute interstitial pneumonia in cattle co-grazing pastures with pigs?

A
  • Ascaris suum.- CSx: depression, anorexia, fever, tachycardia, tachypnoea, dyspnoea, coughing, ruminal stasis, bloat, inc BV sounds.- Dx: necropsy and demonstration of larvae.
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194
Q

What disease syndromes are associated with BVDV infection in camelids?

A
  • Diarrhoea.- Ill thrift.- Reproductive losses or congenital infection –> PI crias.- Disseminated disease.
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195
Q

What is the period of susceptibility of camelid foetuses for induction of BVDV PIs?

A

Unknown, as the gestation period of camelids is much longer than cattle.

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196
Q

What methods can be used to diagnose BVDV infection in camelids?

A
  • Virus isolation from LNs, blood, foetal tissues, placenta.- PCR from whole blood.- IHC on formalin fixed tissues.- NB antigen-capture ELISA used in cattle can give false positive results.- PI-specific assays used in cattle e.g. BVD viral antigen ELISAs on ear notches or serum have not been validated in camelids.
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197
Q

Is there a BVDV vaccine licensed for use in camelids?

A

No.Use of cattle vaccines is not recommended as this is not a widespread problem in camelids.

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198
Q

Adenovirus-associated pneumonia has been reported in four camelids. What type of virus is this? What clinical signs and necropsy findings were reported?

A
  • Double-stranded DNA virus.- Bronchopneumonia, fibrinous pleuritis and peritonitis, chronic wasting, nasal discharge and lethargy.- Inclusion bodies in liver and virus detected by fluorescent antibody testing in lungs.
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199
Q

What virus has been implicated (but not proven) to be the cause of acute respiratory syndrome in alpacas?

A
  • A group 1 coronavirus.- Mild to severe respiratory signs; interstitial pneumonia with lymphocytic infiltrates on post mortem exam.
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200
Q

List neoplasias that have been reported to occur in the nasal passages of sheep and goats.

A
  • Adenopapillomas.- Adenomas.- Adenocarcinomas.- Squamous cell carcinomas.- Ovine/caprine adenocarcinoma virus.
201
Q

Describe the type of virus, clinical signs and prognosis for small ruminants infected with the Ovine/Caprine Adenocarcinoma Virus.

A
  • Retrovirus.- Infected secretory epithelial cells of the nasal turbinates.- No breed/sex predilection.- Typically affects young adults.- Benign, locally invasive; eventually causes weight loss, asphyxia, secondary infection, death.- Dx: endoscopy, rads, PCR (serology not useful).- Surgical tx has been attempted but poor Px.
202
Q

Describe the lifecycle of oestrus ovis.

A
  • Infects sheep more frequently than goats; occ infects other animals –> conjunctivitis in people.- Adult female fly lays 1st instar larvae near the nose of sheep, migrates to nasal and ethmoid turbinates.- 2nd instar larvae develops and migrates to sinus.- 3rd instar larvae migrates to nasal passages.- Sneezed onto ground –> pupate –> adult flies (active in warm months and climates).
203
Q

Describe the clinical signs of oestrus ovis infection in sheep and goats.

A
  • Larvae irritate nasal passages/sinuses.- Mucoid-mucopurulent-blood-tinged nasal discharge.- Sneezing.- Nose rubbing.- Inspiratory stridor.- Adult flies annoy sheep, decrease productivity, predispose to secondary bacterial rhinitis, sinusitis, pneumonia.
204
Q

Describe treatment and prevention of oestrus ovis infection.

A
  • Ivermectin after a frost (when adults are dead).- Outside US: inj moxidectin and doramectin, pour on epinomectin.
205
Q

Are there breed and sex predilections for development of laryngeal abscesses in sheep?

A
  • Rams > ewes.- Texel and Southdown.
206
Q

Describe the aetiology of laryngeal abscesses in ruminants.

A

FB, trauma or congenital cavitation in cartilage –> infection with T. pyogenes.

207
Q

Describe the clinical signs and diagnosis of laryngeal abscesses in ruminants.

A
  • Alert, afebrile, eating well until terminal dyspnoea.- Tachypnoea.- Extension of head and neck.- Progressive dyspnoea.- Cyanosis.- Stertor.
208
Q

Describe the treatment and prognosis of laryngeal abscesses in ruminants.

A
  • Tracheostomy.- PPG.- NSAID.- Px: guarded.
209
Q

Ingestion of what plant by ewes can cause congenital tracheal stenosis in lambs?

A

Veratrum californicum at 31-33 days gestation –> rapid death of lambs after birth.

210
Q

Do herpesviruses cause respiratory disease in small ruminants?

A

Importance of ovine and caprine herpesviruses in respiratory disease is unknown.

211
Q

Do respiratory syncytial viruses cause respiratory disease in small ruminants?

A

Yes, there is an ovine respiratory syncytial virus and a caprine respiratory syncytial virus. No vacc available. CSx similar to cattle with BRSV.

212
Q

Describe presentation of Ovine Adenovirus infections.

A

Causes mild respiratory and enteric disease in lambs.

213
Q

What are the clinical signs of Mycoplasma mycoides ss mycoides (large colon type) infection in goats?

A
  • Adults: polyarthritis, mastitis, AIP +/- death.- Kids (2-8wks): high mortality:i) High fever, death in 12-24h.ii) CNS syndrome w opisthotonus and death in 24-72h.iii) Fever, swollen/painful joints, pneumonia, recumbency.
214
Q

Describe necropsy findings in goats that have died of Mycoplasma mycoides ss mycoides (large colon type) infection.

A
  • Fibrinopurulent polyarthritis.- Pneumonia: patchy to diffuse red consolidation, bronchointerstitial pneumonia +/- fibrinous exudate +/- pleural effusion.- +/- pericarditis, peritonitis, enlarged liver/spleen/kidneys.
215
Q

Describe diagnosis of Mycoplasma mycoides ss mycoides (large colon type) infection in goats.

A
  • Ear canal PCR identifies chronic carriers.- Culture of milk, joint fluid, blood, urine or tissue.
216
Q

Describe treatment and prevention of Mycoplasma mycoides ss mycoides (large colon type) infection in goats.

A
  • ABs almost always unsuccessful (tylosin, tetracycline).- Kids that survive –> arthritis; does –> carriers.- Prevention: maintain MmmLC free herd; purchase does w no hx of kid deaths from pneumonia or arthritis and neg bulk tank +/- indv milk cultures.- Control in an outbreak: feed pasteurised goat or cow colostrum, pasteurised milk to 1mo, pasteurised milk/replace till weaning; cull kids w swollen joints.
217
Q

<p>A horse presents for respiratory evaluation and chronic weight loss. The animal shares pasture with a mini donkey (Panchito), and the owner does not do any primary health care on Panchito since it is a donkey, and donkeys are tough. How would you diagnose the horses condition?</p>

A

<ul> <li>Presence of D. arnfieldilarvae in BAL or TTW</li> <li>Increase eosinophils in TTW or BAL</li></ul>

<p>Baerman usually false</p>

<p>Peripheral eosinophilia does not correlate.</p>

218
Q

<p>According to the 2016 Consensus Statement, define the IAD phenotype based on clinical presentation and dx tests.</p>

A

<p>Clinical presentation:</p>

<p>- any age but more common in young horses</p>

<p>- clinical signs include poor performance (non-respiratory causes should be ruled out if this is only clinical sign) and chronic (>3 weeks), occasional coughing.</p>

<p>Diagnostic confirmation:</p>

<p>- endoscopy revealing excess tracheol-bronchial mucus (>2/5 for racehorses; >3/5 for sports/pleasure horses).</p>

<p>Rule out other causes of poor perfromance OR</p>

<p>- BAL cytology characterised by mild increases in neutrophils, eosinophils and/or metachromatic cells</p>

<p>- further confirmed for research purposes by documenting pulmonary dysfunction based on evidence of lower airway obstruction, airway hyperresponsiveness or impaired blood gas exchange</p>

<p>Exclusion criteria:</p>

<p>- evidenced of systemic signs of infection (anorexia, lethargy, haematologic abnormalities compatible with infection)</p>

<p>- increased respiratory effort at rest (heaves)</p>

219
Q

<p>Action of macrophages in R. equi©</p>

A

<p>Activation of IFNg by CD4+</p>

220
Q

<p><b><span>Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) comprise a syndrome of severe pulmonary dysfunction and respiratory failure that affects foals. Which of the following statements is correct?</span></b></p>

<p><span>a) The fraction Pa02/Fi02 is >300mm Hg in cases of ALI (which is the less severe form) and >200mm Hg for ARDS. </span></p>

<p><span> b) It is related to pulmonary surfactant deficiency in neonatal foals</span></p>

<p><span> c) The pathophysiology includes dysregulation of pulmonary inflammation and coagulation</span></p>

<p> <span>d) It is not related to an infectious etiology</span></p>

<p></p>

<p></p>

<p></p>

<p></p>

A

<p>c) The pathophysiology includes dysregulation of pulmonary inflammation and coagulation</p>

<p></p>

<p>ALI or ARDS arises as a complication after major infectious or noninfectious bodily injury. When this occurs, a protective response starts that involves controlled activation of the inflammatory and coagulation system. In ALIARDS an imbalance of pro inflammatory and anti-inflammatory factors produce an uncontrolled pulmonary inflammatory response and pro coagulation environment in alveoli and the pulmonary microcirculation.</p>

221
Q

<p>Advantages of ultrasound for R. equi</p>

A

<p>Evaluation of severity of pneumonia and response to therapy</p>

222
Q

<p>Best measure for eradication of EAV from herd©</p>

A

<ul> <li>Manage carrier stallions</li> <li>Vaccinate mares that are bred to the carrier stallion</li></ul>

223
Q

<p>What is the most effectivetreatment for M. capillaris?</p>

A

<p>A regimen of fenbendazole (1.25 to 5 mg/kg) 1 week on/ 1 week off/ 1 week onappeared to provide the most effective treatment.</p>

<p>*Resistant to levamisole</p>

<p></p>

<p>Muellerius Capillaris is probably the most common of the lungworms of sheep and goats. Infection is more pathogenic in goats than in sheep.</p>

<p>Several anthelmintics have been used in the treatment. Moxidectin (0.2 mg/kg oral or injectable) is effective in sheep and may be equally effective in goats. Although larvae may initially disappear in the feces after treatment, they often reappear in fecal samples again after 1 to 2 months, either because anthelmintics are ineffective against immature worms and/or because of resumption of development by inhibited larvae. Treatments that appear to eliminate adult parasites in goats include fenbendazole (15 to 30 mg/kg), albendazole (10 mg/kg),oxfendazole (7.5 to 10 mg/kg),and ivermectin (0.3 mg/kg). Better control of immature or inhibited larvae with fenbendazole was achieved by administering the drug (1.25 to 5 mg/kg) for 7 to 14 days.</p>

<p><br></br><span>Smith, Bradford P..Large Animal Internal Medicine, Elsevier, 2014, page 628.</span></p>

224
Q

<p>Mention some primary pathogenic fungi.</p>

A

<p>Primary pathogenic fungi such as Blastomyces dermatitidis, Histoplasma capsulatum, Coccidioides immitis, Cryptococcus neoformans, and Conidiobolus coronatususually infect immunologically normal horses.</p>

<p><span>Smith, Bradford P..Large Animal Internal Medicine, Elsevier, 2014, page 495.</span></p>

225
Q

<p>Best way to determine the carrier status in strangles</p>

A

<ul> <li>Endoscopic examination of the GP</li> <li>Culture + PCR of GP lavage</li></ul>

226
Q

<p>Best way to increase detection of R. equi</p>

A

<p>Culture + PCR (90% detection)</p>

227
Q

<p>Characteristic pulmonary lesion of EIPH</p>

A

<p>Bilateral and caudo-dorsally</p>

228
Q

<p>Cytology of a normal BAL, in horses and llamas?</p>

A

<ul> <li>Neutrophils: < 5%</li> <li>Mast cells: < 2%</li> <li>Eosinophils: <1%</li></ul>

229
Q

<p>Describe gross findings in the lungs of horses with EMPF on post mortem exams.</p>

A

<p>- 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.</p>

230
Q

<p>Describe herpesviruses.</p>

A

<p>- Family: Herpesviridae.- Double-stranded DNA viruses.- Two subfamilies: alpha and gamma.</p>

231
Q

<p>Describe histopathologic findings in the lungs of horses with EMPF.</p>

A

<p>- 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.</p>

232
Q

<p>Describe the clinical signs and necropsy findings of EAdV infections in immunocompetent yearlings and foals.</p>

A

<p>- 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.</p>

233
Q

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

A

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

234
Q

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

A

<p>- 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.</p>

235
Q

<p>Describe the epidemiology and pathophysiology of Hendra virus infection.</p>

A

<p>- 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.</p>

236
Q

<p>Describe the epidemiology of EAdV infection.</p>

A

<p>- 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).</p>

237
Q

<p>Describe the epidemiology of EAV infection.</p>

A

<p>- 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.</p>

238
Q

<p>Describe the epidemiology of EHV-1 and EHV-4 infections.</p>

A

<p>- 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. </p>

239
Q

<p>Describe the epidemiology of equine rhinitis virus.</p>

A

<p>- 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.</p>

240
Q

<p>Describe the equine adenovirus (EAdV).</p>

A

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

241
Q

<p>Describe the equine arteritis virus (EAV).</p>

A

<p>- 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.</p>

242
Q

<p>Describe the equine influenza virus (EIV).</p>

A

<p>- Family: Orthomyxoviridae.- Genera: Influenza A virus.- Segmented, single-stranded RNA virus.</p>

243
Q

<p>Describe the equine rhinitis virus.</p>

A

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

244
Q

<p>Describe the features of Acute respiratory distress syndrome (ARDS)</p>

A

<p>A syndrome of lung injury characterised by:</p>

<p>- alveolar damage</p>

<p>- high-permeability pulmonary oedema</p>

<p>- respiratory failure</p>

245
Q

<p>Describe the findings on BAL fluid cytology on horses with IAD</p>

A

<p>- mild to moderate increase in neutrophil, eosinophil and /or mast cell percentages</p>

<p>- > 10% neutrophils,> 5% mast cells,> 5% eosinophils</p>

<p>- importance of BAL cytology should be interpreted in light of history, clinical exam and endoscopic findings</p>

<p>- NB. TW cytology not considered an appropriate alternative to BAL cytology for diagnostic confirmation or characterisation of IAD</p>

246
Q

<p>Describe the Hendra virus.</p>

A

<p>- Family: paramyxoviridae.- Genus: henipavirus.- Enveloped RNA virus.</p>

247
Q

<p>Describe the immune response in horses infected with EIV and defences of the virus to the immune response.</p>

A

<p>- 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.</p>

248
Q

<p>Describe the immune response to EHV-1 and EHV-4 infection in horses.</p>

A

<p>- 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.</p>

249
Q

<p>Describe the mucus scoring system used to quantify mucus accumulation in the trachea</p>

A

<p>Grade 0 - no visible mucus</p>

<p>Grade 1 - single to multiple small blobs of mucus</p>

<p>Grade 2 - larger but nonconfluent blobs</p>

<p>Grade 3 - confluent or stream forming mucus</p>

<p>Grade 4 - pool forming mucus</p>

<p>Grade 5 - profuse amounts of mucus</p>

250
Q

<p>Describe the pathophysiological mechanisms leading to increased pleural fluid production.</p>

A

<p>Fluid production in the pleural space increases if any of the following occurs:</p>

<p>1) elevation of the hydrostatic pressure gradient (CHF, portal hypertension)</p>

<p>2) a decrease in the colloid osmotic pressures (hypoproteinaemia)</p>

<p>3) an increased permeability of the capillary vessels (infection, malignancy, inflammation)</p>

<p>4) decreased removal of fluid because of impaired lymphatic drainage or obstruction (neoplasia) or infiltration of the pleura or parenchyma (neoplasia).</p>

<p>Also, excessive amounts of peritoneal fluid may accumulate in the pleural cavity as the fluid moves through diaphragmatic defects or through diaphragmatic lymphatics.</p>

251
Q

<p>Describe the pathophysiology of EAV infection.</p>

A

<p>- 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.</p>

252
Q

<p>Describe the pathophysiology of EHV-1 and EHV-4 respiratory disease in horses.</p>

A

<p>- 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.</p>

253
Q

<p>Describe the pathophysiology of EIV infection.</p>

A

<p>- 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.</p>

254
Q

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

A

<p>- 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.</p>

255
Q

<p>Diagnosis of Chronic carrier state for S. equi</p>

A

<p>Guttural pouch fluid/swab PCR</p>

256
Q

<p>Diagnosis of P. carinii pneumonia</p>

A

<ul> <li>Trophozoites in histology</li> <li>Interstitial, miliary pattern</li></ul>

257
Q

<p>Diagnosis of R. equi pneumonia</p>

A

<p>Bacterial culture and PCR for VapA gene from TBA</p>

258
Q

<p>Diseases cause by EHV-1</p>

A

<ol> <li>Respiratory</li> <li>Abortion/Neonatal death</li> <li>EHVM</li> <li>Chorioretinopathy --> shotgun lesions</li></ol>

259
Q

<p>Does furosemide affect performance in cases of EIPH?</p>

A

<p>Administration 4 hrs before is associated with improved racing outcomes</p>

260
Q

<p>Drug of choice of Pneumocystis carinii</p>

A

<p>TMS</p>

261
Q

<p>EIPH, what is associated with?</p>

A

<p>Histology changes</p>

262
Q

<p>Elimination of EIV Australia</p>

A

<p>canary pox 14 days</p>

263
Q

<p>Equine multinodular pulmonary fibrosis is thought to be caused by which infectious agent? How would you diagnose?</p>

A

<p>EHV-5</p>

<p>PCR or IHC in lung biopsy or BALF</p>

<p>Is this a definitive diagnosis?</p>

264
Q

<p>For glanders (farcy), why would you do a IDT?</p>

A

<p>To certify negative horses</p>

<p>Is zoonotic and cases have to be reported to OIE</p>

265
Q

<p>Fungi that most commonly causes pneumonia in horses</p>

A

<p>Coccidiomicosis</p>

266
Q

<p>Fungi that most commonly causes pneumonia in horses</p>

A

<p>Coccidiomicosis</p>

267
Q

<p>Gene associated with virulence in R. equi, and where is it located?</p>

A

<p>Vap A gene, located in the pathogenicity island (PAI)</p>

268
Q

<p>Gene implicated in heritability of RAO</p>

A

<p>IL-4 receptor gene</p>

269
Q

<p>Gold standard for diagnosis of strangles</p>

A

<p>Culture</p>

<ul> <li>Nasopharynx, GP wash*</li> <li>Preferred method on aspirate of masses</li></ul>

270
Q

<p>Horse with a nasal granuloma (mass), histopathology revealed large amounts of eosinophils around the lesions.</p>

A

<p>Condidiobolus coronatus</p>

<p></p>

<p>Condidiobolus is a saprophytic fungus that causes granulomatous lessions in the upper respiratory tract in horses. Single to multiple granulomatous lesions in the nasal passages, trachea, or soft palate can be observed endoscopically.Histologic appearanceis similar to that of pythiosis and of basidiobolomycosis. Hyphae are thin-walled, highly septate, and irregularly branched. The lesions typically have large numbers of eosinophils and fewer macrophages, neutrophils, plasma cells, and lymphocytes sur­rounding hyphae. Definitive diagnosis is based on microbiological culture, immunodiffusion, or PCR.<br></br></p>

<p><span>Smith, Bradford P..Large Animal Internal Medicine, Elsevier, 2014, page 498</span></p>

271
Q

<p>How can EHV respiratory disease be prevented?</p>

A

<p>- 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.</p>

272
Q

<p>How can you differentiate between mild and severe equine asthma?</p>

A

<ul> <li>Poor performance --> mild</li> <li>H2 challenge test --> mild</li> <li>Bronchoconstriction at rest --> severe</li> <li>Hay challenge test --> severe</li> <li>BALF cytology</li></ul>

273
Q

<p>How could you differentiate between some of the causes of pleural effusion?</p>

A

<p>Cytologic and microbiological evaluation of pleural fluid - identify neoplastic cells or fungal elements - transudate (protein <25g/L; few cells):</p>

<p>CHF, liver fibrosis, hypoalbuminaemia, early neoplastic processes - modified transudate (low NCC; moderate to high protein >25g/L):</p>

<p>neoplasia + many other disorders - exudate (high NCC; protein > 30g/L):</p>

<p>infectious and intraabdominal diseases - can distinguish septic effusions from nonseptic effusions by biochemical analysis of pleural fluid --</p>

<p>septic: pH <7.2, glucose < 40mg/dL, lactate dehydrogenase > 1000IU/L -- chylous: milky white-pale pink, TG > simultaneously measured serum</p>

274
Q

<p>How does EHV-1 evade the immune system?</p>

A

<ul> <li>Downregulationof MHC-1</li> <li>Alteration of NK cells</li> <li>Modulation of cytokine response</li></ul>

275
Q

<p>How is EAV infection diagnosed in horses?</p>

A

<p>- 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. </p>

276
Q

<p>How is equine adenovirus infection diagnosed?</p>

A

<p>- 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.</p>

277
Q

<p>How is equine adenovirus infection prevented?</p>

A

<p>No vaccine available. </p>

278
Q

<p>How is equine rhinitis virus infection diagnosed?</p>

A

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

279
Q

<p>How is equine rhinitis virus infection prevented?</p>

A

<p>No vaccine available.</p>

280
Q

<p>How is Hendra virus diagnosed?</p>

A

<p>- 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. </p>

281
Q

<p>How is Hendra virus prevented/controlled?</p>

A

<p>- Vaccine.- Strict biosecurity.</p>

282
Q

<p>How is IAD diagnosed?</p>

A

<p>The diagnosis of IAD (mild-moderate equine asthma) is based on: 1) presence of clinical signs of lower airway disease (poor performance, cough)</p>

<p>2) documentation of lower airway inflammation based on excess mucus on endoscopy, BAL cytology or abnormal lung function</p>

<p>3) exclusion of severe equine asthma (RAO/heaves) as well as infectious and other respiratory diseases</p>

283
Q

<p>How is pleural fluid formed?</p>

A

<p>Pleural fluid is the interstitial fluid of the parietal pleura.</p>

<p>A pressure gradient driving its formation exists because the parietal pleura is supplied by the systemic circulation and because the pressure of the pleural space is more negative than that of the subpleural interstitium.</p>

284
Q

<p>How long is the isolation for cases of EHV-1?</p>

A

<p>28 days!</p>

285
Q

<p>How long is the nasal shedding in strangles</p>

A

<p>2-3 weeks</p>

286
Q

<p>How long is the quarantine for strangles?</p>

A

<p>2-3 weeks</p>

287
Q

<p>How long is the shedding for EIV?</p>

A

<p>~ 7 days</p>

288
Q

<p>How long is the shedding of EHV-1?</p>

A

<p>4-7 days</p>

289
Q

<p>How to determine strangles titer?</p>

A

<p>SeM protein</p>

290
Q

<p>If you want to diagnose pneumocystosis, what sample would you submit?</p>

A

<p>BAL for cytology</p>

<ul> <li>Can NOT be cultured</li></ul>

291
Q

<p>Immune response in R. equi pneumonia</p>

A

<p>IFN-g --> macrophages</p>

292
Q

<p>In cases of strangles, how long does the nasal shedding last?</p>

A

<p>2-3 weeks</p>

293
Q

<p>In interstitial pneumonia, what are the changes in the proliferative phase that leads to fibrosis and decrease in lung capacities?</p>

A

<p>Increase in pneumocytes type II</p>

294
Q

<p>In strangles, what is a positive nasal PCR</p>

A

<p>Actively shedding</p>

295
Q

<p>Interpret the following BAL result in this 10-year-old Tennessee Walking gelding with chronic cough and poor performance.</p>

<p>Lymphocytes: 19%</p>

<p>Macrophages: 10.2</p>

<p>Neutrophils: 71.4%</p>

<p>Mast cells: 0.32% %</p>

<p>Eosinophils: 0.03%</p>

<p></p>

<p>a. RAO</p>

<p>b. IAD</p>

<p>c. Exercise induced pulmonary hemorrhage</p>

<p>d. Pneumonia</p>

A

<p>a. RAO</p>

296
Q

<p>Interpretation of a SeM ELISA for strangles where thetiter is ≥ 1:3200</p>

A

<p>High antibody → predispose to develop purpura when vaccinated</p>

<ul> <li>Do NOT vaccinate</li></ul>

297
Q

<p>Is furosemide effective prophylaxis for EIPH?</p>

A

<p>4 hours before extrenous exercise decreases the severity and incidence of EIPH</p>

<ul> <li>Furosemide decreases pulmonary capillary and transmural pressure</li></ul>

298
Q

<p>It is believed that there is a genetic component in severe equine asthma.</p>

<p>Which gene could be implicated?</p>

A

<ul> <li>IL-4 receptor gene <ul> <li>IL-4 enhances IL-8</li> </ul> </li></ul>

299
Q

<p>List causes of interstitial lung disease in horses.</p>

A

<p>- 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.</p>

300
Q

<p>List clinicopathologic findings in horses with EMPF.</p>

A

<p>- 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.</p>

301
Q

<p>List components of treatment in horses with EMPF.</p>

A

<p>- Corticosteroids.- Broad-spectrum antibiotics.- Anti-virals (valacyclovir better bioavail than acyclovir).- NSAIDs.- InO2.- Fluid and nutritional support.</p>

302
Q

<p>List diagnostic imaging findings in horses with EMPF.</p>

A

<p>- 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.</p>

303
Q

<p>List important diagnostic tests to consider in horses with pleural effusion.</p>

A

<p>1) physical and rectal examination</p>

<p>2) CBC &amp;amp; Biochemistry</p>

<p>3) Cardiac evaluation</p>

<p>4) thoracic and abdo u/s</p>

<p>5) abdominocentesis</p>

<p>6) transtracheal aspirate (if infectious agents suspected) +/- (depending on nature of effusion and geographic location of horse)</p>

<p>7) Coggins test (AGID)</p>

<p>8) titers against Coccidioides immitis, Cryptococcus neoformans, Mycoplasma felis</p>

304
Q

<p>List necropsy findings in foals that die following EAV infection.</p>

A

<p>- Interstitial pneumonia.- Lymphocytic arteritis.- Renal tubular necrosis.- Tunica media necrosis.</p>

305
Q

<p>List the alpha herpesviruses that infect equids and the diseases they cause.</p>

A

<p>- 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.</p>

306
Q

<p>List the clinical signs associated with EAV infection.</p>

A

<p>- Majority of infections are subclinical.</p>

<p>- Occasional outbreaks of resp dz and abortions.</p>

<p>- Incubation period: 2-14d (resp), 6-8d (venereal).</p>

<p>- Mild (fever, leukopaenia) to severe (death).</p>

<p>- Fever (1-5d), anorexia, nasal discharge (serous to mucoid), conjunctivitis +/- cough, +/- urticaria, oedema.</p>

<p>- Stallions: transient dec in sperm quality (16wk).</p>

<p>- Mare: abortions, 2-10mo gestation, no premonitory signs.</p>

<p>- Foals: severe resp signs, high mortality.</p>

307
Q

<p>List the clinical signs associated with equine rhinitis virus infections.</p>

A

<p>- Subclinical infection can occur; horses may shed for a long time in urine and faeces.</p>

<p>- Fever, anorexia, nasal discharge, pharyngitis, lymphadenitis.</p>

<p>- Rarely laryngitis or mild bronchitis.</p>

<p>- Viraemia 4-5d --> long lasting antibodies.</p>

308
Q

<p>List the clinical signs of EMPF.</p>

A

<p>- 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.</p>

309
Q

<p>List the differential diagnoses for bilateral epistaxis</p>

<p></p>

A

<p>■Trauma (iatrogenic/external head trauma)</p>

<p>■Guttural pouch mycosis<br></br>■Progressive ethmoidal haematoma (unilateralor bilateral)<br></br>■Exercise-induced pulmonary haemorrhage</p>

<p>■Neoplasia (unilateral or bilateral)</p>

<p>■Clotting/bleeding disorders<br></br>■Pneumonia/pulmonary abscess</p>

<p>■Rhinitis/sinusitis (unilateral or bilateral)</p>

<p></p>

<p>Unilateral:</p>

<p>Foreign body</p>

<p>Nasal amyloidosis/polyps (unilateral)<br></br>Infected nasolacrimal duct (unilateral)</p>

<p></p>

310
Q

<p>List the gamma herpesviruses that infect equids and the diseases they cause.</p>

A

<p>- 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.</p>

311
Q

<p>Lung lesions in EIPH©</p>

A

<p>Bilateral and more in caudo-dorsal region</p>

<p>Pleural and septal fibrosis and angiogenesis</p>

<p>Venous remodeling</p>

312
Q

<p>Lung mechanism of IAD</p>

313
Q

<p>Measures to prevent EAV</p>

A

<ul> <li>Vaccinate colts in the first year and annually thereafter</li> <li>Vaccinate mares that will be bred</li> <li>Manage carrier stallions separate, or castrate</li> <li>MLV</li></ul>

314
Q

<p>Most common age for R. equi pneumonia</p>

A

<p>3 weeks - 5 months</p>

315
Q

<p>Most common cell in RAO BAL</p>

A

<p>Neutrophils</p>

316
Q

<p>Most common presentatio of R. equi</p>

A

<p>Subclinical, might recover without therapy</p>

317
Q

<p>Most important cell for immunity against EHV-1?</p>

A

<ul> <li>CTLs --> MHC class I restricted</li> <li>Mediated by CD8+</li></ul>

318
Q

<p>What are someof the most important cells for R. equiimmunity?</p>

A

<p>T lymphotytes - Cytotoxic T lymphocytes (CTL) and T-helper type 2 (Th2)</p>

<p></p>

<p>Antigen-presenting cells from foals have signifi­cantly lower CD1 and MHC class II expression compared with adult horses. Young foals are deficient in their ability to produce IFNγ in response to mitogens, leading to thehypothesis that an IFNγ deficiency and T-helper type 2 (Th2) cellsmight be at the basis of their peculiar susceptibility to R. equi infections.</p>

<p>In general, neo­nates and perinates have diminished innate immune responses and decreased antigen-presenting cell function and are less able to mount type I immune responses, which gives them an increased susceptibility to certain infections.In addition, the ability of equine lymphocytes and neutrophils to produce and/or upregulate various cytokines is strongly influenced by age.</p>

<p><span>Smith, Bradford P..Large Animal Internal Medicine, Elsevier, 2014, page 485-486.</span></p>

319
Q

<p>Mucus scoring for equine asthma</p>

A

<ul> <li>Grade 0 = no mucus</li> <li>Grade 1 = single to multiple small blobs</li> <li>Grade 2 = larger but non confluent blobs</li> <li>Grade 3 = confluent or stream forming</li> <li>Grade 4 = pool forming</li> <li>Grade 5 = profuse amounts</li></ul>

320
Q

<p>Necropsy finding in vena caval thrombosis</p>

A

<p>Thrombus between the liver and right atrium at the caudal vena cava</p>

321
Q

<p>Negative prognostic indicator in R. equi pneumonia</p>

A

<p>Intra-abdominal abscess</p>

<p>Osteomyelitis</p>

322
Q

<p>Negative prognostic indicator in R. equi pneumonia</p>

A

<ul> <li>Intra-abdominal abscess</li> <li>Osteomyelitis</li></ul>

323
Q

<p>OIE recommendations for influenza vaccine</p>

A

<p>Florida clades 1 and 2</p>

<p></p>

324
Q

<p>Outline recommended strategies to prevent/control EAV infection.</p>

A

<p>- 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 </p>

325
Q

<p>Outline recommended strategies to prevent/control EIV infection.</p>

A

<p>- 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.</p>

326
Q

<p><b><span>Oxygen toxicity is more likely to be seen in neonatal foals mechanically ventilated with increased levels of 02 (Fi02>50%) for several days. Which statements is correct</span></b></p>

<p><span>a) It's frequently followed within a few days by opportunistic bacterial pneumonia</span></p>

<p><span>b) Can produce interstitial pneumonia and alveolar type II cell proliferation</span></p>

<p><span>c) Can result in lysis of the macrophage, chronic alveolitis, and fibrosis</span></p>

<p><span>d) Can result in bronchopneumonia and alveolar type I cell proliferation</span></p>

A

<p>b) Can produce interstitial pneumonia and alveolar type II cell proliferation</p>

<p></p>

<p>Damage is thought to be due to production of reactive oxygen metab­olites, which attack a lung that may already have been injured by barotrauma resulting from a ventilator-driven increase in airway pressure.<br></br></p>

<p>Type II cells are spherical pneumocytes which comprise only 4% of the alveolar surface area, they constitute 60% of alveolar epithelial cells and 10-15% of all lung cells. Four major functions: (1) synthesis and secretion of surfactant; (2) xenobiotic metabolism; (3) transepithelial movement of water; and (4) regeneration of the alveolar epithelium following lung injury.</p>

<p><span>Smith, Bradford P..Large Animal Internal Medicine, Elsevier, 2014, page 511.</span></p>

327
Q

<p>Pathogenensis R. equi and decreased immune (macrophage) response</p>

A

<p>Lipoarabinominam on bacterium surface and Macrophage phagocytosis of R. equi</p>

328
Q

<p>Pathophysiology of EIPH</p>

A

<p>Rupture of alveolar capillaries secondary to increase in intramural pressure (increase in both capillary and alveolar pressure)</p>

329
Q

<p>Pneumocytes II</p>

A

<p>Lush pastures</p>

330
Q

<p>Purpura hemorrhagica is a type \_\_\_\_ hypersensitivity reaction</p>

A

<p>III</p>

331
Q

<p>RAO is characterized by?</p>

<ol> <li>Excessive mucus production, intraluminal macrophage accumulation, bronchiolar hyperreactivity, and bronchospasm</li> <li>Excessive mucus production, intraluminal neutrophil accumulation, bronchial hyperreactivity, and reversible bronchospasm</li> <li>Excessive surfactant production, intraluminal macrophage accumulation, bronchiolar hyperreactivity, and bronchospasm</li> <li>Excessive surfactant production, alveolar neutrophil accumulation, bronchial hyperreactivity, and reversible bronchospasm.</li></ol>

A

<p>b. Excessive mucus production, intraluminal neutrophil accumulation, bronchial hyperreactivity, and reversible bronchospasm</p>

332
Q

<p>Receptor used by macrophages to engulf opsonized R. equi</p>

A

<p>Complement receptor 3 = CR3 or Mac-1</p>

333
Q

<p>Receptor used by macrophages to engulf opsonized R. equi</p>

A

<p>Complement receptor 3 = CR3 or Mac-1</p>

334
Q

<p>Response that mediates ocurrence of RAO</p>

A

<p>Th-2 mediated pathway</p>

335
Q

<p>Rhodococcus equi is a ....</p>

A

<p>Gram-positive facultative intracellular bacterium. It is one of the most common causes of pneumonia in foals between 3 weeks and 5 months of age. </p>

336
Q

<p>Status of bronchi in IAD©</p>

A

<p>No bronchoconstriction</p>

337
Q

<p>Summarise the pathogenesis of IAD and reported risk factors</p>

A

<p>- dysregulation of the inflammatory cell homeostasis in the airway lumen leading to clinical signs of variable severity</p>

<p>- variety of aetiological agents might be involved</p>

<p>- relative contribution to the development of IAD varies among different populations of horses based on:</p>

<p>-- environmental conditions they are exposed to during and after training</p>

<p>-- feeding -- housing</p>

<p>-- season -- preventive medicine practices</p>

<p>-- differences in distribution of infectious agents</p>

<p>-- varying genetic influences</p>

<p>- activation of innate immune system and Th-1 polarization often involved in pathogenesis of IAD and most likely drive the luminal neutrophilia</p>

<p>- implication of adaptive immune response, including Th-2 type polarization in some IAD phenotypes</p>

<p>- non-infectious agents central to development of IAD</p>

<p>- high burdens of aerosolised particles and gases eg stabling is a risk factor</p>

<p>- exposure to cold, dry environments may predispose to pathogenesis of BAL neutrophilia in some horses with IAD</p>

<p>- contribution of infectious agents uncertain</p>

<p>- difficult to determine if bacterial infections contribute to increased mucus or if bacterial colonization occurs as a consequence of impaired mucus clearance</p>

<p>- role of viral infection in IAD is controversial</p>

338
Q

<p>T/F</p>

<p>For EIV, serum antibody concentrations correlates with protection</p>

A

<p>True</p>

339
Q

<p>T/F</p>

<p>For EIV, serum antibody concentrations correlates with protection</p>

A

<p>True</p>

340
Q

<p>T/F</p>

<p>Oestrus ovis only infects sheep, and less commonly, goats.</p>

A

<p>F- other animals and humans can become accidentally infected</p>

341
Q

<p>Test to diagnose airway responsiveness in cases of IAD©</p>

A

<p>Histamine aerosol --> elevated levels of leukotriene C4</p>

342
Q

<p>Test with highest Se and Sp for diagnosis of respiratory viruses in horses</p>

A

<p>RT-PCR</p>

343
Q

<p>There are many causes of Equine Interstitial Pneumonia. Which pair do not match with etiology and acute/chronic?</p>

<ol> <li>Inhaled chemicals (oxygen or smoke)- Acute</li> <li>Adverse drug reactions- Acute</li> <li>Inhaled inorganic dust (pneumonoconises- silicosis)- Chronic</li> <li>Endogenous metabolic/toxic conditions (ARDS, DIC) Uremia)- Chronic</li></ol>

A

<p>d. Endogenous metabolic/toxic conditions (ARDS, DIC) Uremia)- Chronic</p>

344
Q

<p>These genes are necessary for the correct functioning of the main virulence factor of R. equi, so the bacteria can replicate and survive in the macrophages. Y'all know what I'm talking about?</p>

A

<p><em>VirR</em>and <em>Orf</em></p>

<p></p>

<p>Each of them encondes a regulatory protein</p>

345
Q

<p>Treatment for D. viviparus</p>

A

<p>Ivermectin -> 3, 8, 13 weeksDoramectin -> 0, 8 weeksIf treatment during PPP -> larvae never shed in feces</p>

346
Q

<p>Treatment of horse with strangles</p>

A

<p>Horses with early clinical signs • ATB on early stage, before abscessation (3-5 days) • May prevent local abscess and sheddingHorses with lymph node abscessation • Supportive care • Soft food • NSAIDs, hot compress, drainage, lavage • ATB recommended if horse is depressed, anorectic, dyspneic • Penicillin → drug of choice • Cephalosporins, macrolides • ATBs may prevent development of lasting immunity</p>

347
Q

<p>Types of equine adenoviruses</p>

A

<ul> <li>EAdV-1→ respiratory disease, conjunctivitis</li> <li>EAdV-2→ diarrhea in foals</li></ul>

348
Q

<p>Vaccination of EIV</p>

A

<p>Canary q14d</p>

349
Q

<p>Vaccine recommendation for EIV by OIE</p>

A

<p>Florida clades 1 and 2</p>

350
Q

<p>What are risk factors for development of EIV infection?</p>

A

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

351
Q

<p>What are some other diagnoses associated with the development of pleural effusion?</p>

A

<p>1) thoracic neoplasia eg. lymphoma (most common), fibrosarcoma, gastric or oesophageal SCC, hepatoblastoma, haemangiosarcoma, melanoma, mesothelioma, metastatic mammary or ovarian adenocarcinoma</p>

<p>2) thoracic trauma</p>

<p>3) pericarditis</p>

<p>4) peritonitis</p>

<p>5) viral, mycoplasmal, fungal infections</p>

<p>6) CHF</p>

<p>7) liver disease</p>

<p>8) diaphragmatic herniation</p>

<p>9) hypoproteinaemia</p>

<p>10) EIA</p>

<p>11) pulmonary granulomata</p>

<p>12) damage of the thoracic duct</p>

352
Q

<p>What are the different phenotypes of IAD?</p>

A

<p>- some associated with specific inflammatory cells in BAL:</p>

<p>-- metachromatic cells - associated with airway hyperreactivity and subclinical pulmonary obstruction</p>

<p>-- neutrophilic IAD</p>

<p>- more often associated with cough and presence of tracheal mucus</p>

<p>- BAL eosinophilia more common in younger horses (< 5yo)</p>

<p>- BAL neutrophilia more frequently diagnosed in older horses (> 7yo)</p>

353
Q

<p>What are the main differences between RAO and IAD?</p>

A

<p>- lack of laboured breathing at rest permits differentiation of IAD from RAO</p>

<p>- severe exercise intolerance in RAO</p>

<p>- combination of pronounced BAL neutrophilia (> 25%) and tracheal mucus accumulation (grades >2/5) in RAO</p>

354
Q

<p>What are the most common diagnoses associated with the development of pleural effusion?</p>

A

<p>Bacterial pneumonia or lung abscesses</p>

355
Q

<p>What are the two subtypes of EIV and what is the basis of this subdivision.</p>

A

<p>- 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.</p>

356
Q

<p>What clinical signs are demonstrated by horses infected with EIV?</p>

A

<p>- 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).</p>

357
Q

<p>What clinical signs are seen in horses with HeV infection?</p>

A

<p>- 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.</p>

358
Q

<p>What complications can occur following EIV infection?</p>

A

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

359
Q

<p>What is known about the use offurosemide for EIPH?©</p>

A

<p>Decrease severity and incidence</p>

<p>(reduces pulmonary vascular pressure)</p>

360
Q

<p>What is necessary in a cytology to diagnose a fungal pneumonia?</p>

A

<p>Large number of fungi in degenerated neutrophils in a speedily processed sample</p>

361
Q

<p>What is the best for monitoring and early diagnosis of R. equi pneumonia in endemic farms:</p>

A

<p>CBC, monitoring for fever, cough</p>

362
Q

<p>What is the best immune response against R. equi:</p>

A

<p>IFN-y</p>

363
Q

<p>What is the detection rate for strangles when both culture + PCR are used?</p>

A

<p>~ 90%</p>

364
Q

<p>What is the effect of antibodies against EHV-1?</p>

A

<p>Decrease virus shedding, but fail in preventing infection, abortion and EHM</p>

365
Q

<p>What is the effect of vaccination of mares against R. equi?</p>

A

<p>Does not increase protection</p>

366
Q

<p>What is the mode of transmission, incubation period and duration of shedding of EIV?</p>

A

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

367
Q

<p>What is the most frequently reported viral respiratory disease in horses?</p>

A

<p>Equine influenza.</p>

368
Q

<p>What is the pathogenesis of R. equi?</p>

A

<p>The ability of R. equi to persist in, and eventually destroy, alveolar macrophages seems to be the basis of its pathogenicity and inhalation the major route of pulmonary infection in foals. Incubation period in experimental intrabronchial challenge (9 days to 2 - 4 weeks when a lower inoculum is administered). Incubation period under field conditions is unknown and varies depending several factors (number of virulent bacteria, age, host defense mechanisms). Lung consolida­tion can be detected as early as 3 days following heavy intrabronchial challenge. </p>

369
Q

<p>What is the prognosis for horses with EMPF?</p>

A

<p>Guarded to poor.</p>

370
Q

<p>What is the purpose of the lymphocyte-associated viremia of EHV-1?</p>

A

<ul> <li>Virus reaches other tissues, targets the endothelial cells and causesvasculitis</li> <li>Viremia can persist for 21 days! FFS!</li></ul>

371
Q

<p>What is the reason for vaccine failure in EIV?</p>

A

<p>Antigenic drift</p>

372
Q

<p>What is your interpretation of high titers for aspergillosis?</p>

A

<p>Is common from environmental exposure</p>

<ul> <li>Definitive diagnosis is by culture*, IHC, IF</li></ul>

373
Q

<p>What kind of immunologic response occurs in severe equine asthma?</p>

A

<p>Th2 response, IgE mediated</p>

374
Q

<p>What stage of D. arnfieldi is in the bronchi?</p>

A

<p>L5, is retained in non-patent infection</p>

<p>But remember, horse also patent infection</p>

375
Q

<p>What test should be used to certify a horse negative for Glanders?</p>

A

<p>IDT</p>

376
Q

<p>What test to run in a horse that had been exposed to S. equi 3 weeks before</p>

A

<p>SeM ELISA? Nasal PCR?</p>

377
Q

<p>What three countries are free of EIV?</p>

A

<p>Australia, New Zealand and Iceland.</p>

378
Q

<p>What virulence factor is requiered for R. equi to grow within the macrophages?</p>

A

<p>Vap A, which encodes an immunodominant, temperature-inducible, and surface-expressed lipoprotein (it is the only vap gene with a demonstrated role in viru­lence).VapA is required for intracellular growth in macrophages, once in the macrophage, it prevents maturation of the phagosome to the stage of fusion of R. equi –containing vacuoles with lysosomes.</p>

379
Q

<p>When is it appropriate to vaccinate a horse for strangles after recovering from clinical disease?</p>

<p><br></br>a. Never- immunity is lifelong<br></br>b. Titer > 1:3200<br></br>c. 3-5 years<br></br>d. Titer < 1:3200</p>

A

<p>d. Titer < 1:3200</p>

380
Q

<p>When treating equine asthma, bronchodilation is often times necessary. For rapid relief of bronchospasm, atropine is an anticholinergic that can be given, but the owner is worried about colic. Which other drug from the same family might be safer?</p>

A

<p>ipratropium bromide</p>

381
Q

<p>Where are the places for latency of EHV-1?</p>

A

<ul> <li>Trigeminal ganglion</li> <li>Lymphoreticular system</li></ul>

382
Q

<p>Which animals are at higher risk for infection with equine adenovirus</p>

A

<ul> <li>Arabian foals with SCID</li> <li>Immunocompromised animals</li></ul>

383
Q

<p>Which bronchodilator can be used in a case of RAO?©</p>

A

<p>Ipratropium</p>

384
Q

<p>Which cell is required for complete pulmonary clearance of R. equi</p>

A

<p>T lymphocytes (> CD4+)</p>

385
Q

<p>Which diagnosis with high Se and Sp can be used for Conidiobolomycosis?</p>

A

<p>Serum antibodies</p>

386
Q

<p>Which disease is difficult to erradicate with vaccination and isolation?©</p>

A

<p>Equine Influenza Virus</p>

387
Q

<p>Which gene in R. equi encodes a immunodominant, temperature-inducible, surface expressed lipoprotein?</p>

A

<p>VapA</p>

388
Q

<p>Which immunological response is detrimental for foals infected with R. equi?</p>

A

<p>Th 2 response:</p>

<p>Predicted to develop potentially life-threatening pulmonary lesions</p>

389
Q

<p>Which infectious agents can cause lung infections in utero?</p>

A

<ul> <li>EVA</li> <li>EHV-1, 4</li></ul>

390
Q

<p>Which inflammatory mediators are upregulated in cases of severe equine asthma?</p>

A

<ul> <li>IL-8</li> <li>IL-1b</li> <li>TNF-a</li></ul>

391
Q

<p>Which is the desired immunological response in cases of R. equi pneumonia?</p>

A

<p>Type 1 response:</p>

<p>This is characterized by the production of antigen-specific Th1 lymphocytes, which allow for clearance of intracellular R. equi via the production of IFN-g and the activation of macrophages, and by antigen specific cytotoxic T lymphocytes which recognize and kill R. equi infected cells.</p>

392
Q

<p>Which is the desired immunological response in cases of R. equi pneumonia?</p>

A

<p>Type 1 response:</p>

<p></p>

<p>This is characterized by the production of antigen-specific <u>Th1 lymphocytes</u>, which allow for clearance of intracellular R. equi via the production of IFN-g and the activation of macrophages, and by antigen specific cytotoxic T lymphocytes which recognize and kill R. equi infected cells.</p>

393
Q

<p>Which lineageof EIV iscurrently circulating?</p>

A

<p>H3N8</p>

394
Q

<p>Which receptor does R. equi use for entry in the macrophage</p>

A

<p>Mannose receptor in the macrophage that recognized lipoarabinomannan (LAM) in the bacterium</p>

395
Q

<p>Which receptor does R. equi use for entry in the macrophage</p>

A

<p>Mannose receptor in the macrophage that recognized lipoarabinomannan (LAM) in the bacterium</p>

396
Q

<p>Which receptors are upregulated in cases of severe equine asthma and may be a tool for genetic testing?</p>

A

<p>IL-4 receptors --> enhances IL-8 production</p>

397
Q

<p>Which test is more sensitive than culture for diagnosis of strangles?</p>

A

<p>PCR → SeM protein, the gene for the antiphagocytic M protein</p>

<ul> <li>Guttural pouch sampling is the most reliable</li> <li>> Se than culture, always use in combination</li></ul>

<p>What is the detection rate? ~90%</p>

398
Q

<p>Which toxicity causes congenital tracheal stenosis in lambs?</p>

<p><br></br>a. perilla ketones<br></br>b. pyrrolizodine alkaloids<br></br>c. Californicum veratrum<br></br>d. Perennialryegrass</p>

A

<p>c. Californicum veratrum</p>

399
Q

<p>Why antifungals like azoles or amphotericin B are not effective against pneumocystosis?</p>

A

<p>Pneumocystis carinii lacks ergosterol! FML!</p>

400
Q

<p>Why are adult horses more resistent to R. equi pneumonia?</p>

A

<p>Developement of R. equi-specific CTLs</p>

401
Q

<p>Why are foals more susceptible to R. equi pneumonia?</p>

A

<ul> <li>Deficient in CTL</li> <li>Ag presenting cells have decrease CD1, MHC II expression</li> <li>IFN-g deficiency and Th2 bias</li></ul>

402
Q

<p>Would you use bronchodilators to treat a case of ALI/ARDS?</p>

A

<p>No! It can worsen the V/Q mismatch</p>

<p>Use low tidal volumes</p>

403
Q

<p>Zoonotic in dog and horse?</p>

A

<p>Blastomycosis?</p>

404
Q

<p>Describe the epidemiology of fungal rhinitis in cattle and common fungi implicated.</p>

A

<p>- Rare. - No age/breed/sex predisposition. - More common in warm, wet climates. - Rhinosporidium, helminthosporidium, dreschslera rostrata, aspergillus, phycomycetes, stachybotrys, bipolaris; also nocardia bacteria.</p>

405
Q

<p>List the clinical signs of fungal rhinitis in cattle. </p>

A

<p>- Stridor.- Dyspnoea.- Mucopurulent nasal discharge.- +/- epistaxis.- +/- open-mouth breathing.</p>

406
Q

<p>How is fungal rhinitis diagnosed in cattle?</p>

A

<p>Histo: granulation tissue with eosinophils, mononuclear cells, sporangia, hyphae, filamentous bacteria.</p>

407
Q

<p>How is fungal rhinitis treated in cattle?</p>

A

<p>- Surgical debulking.- Sodium iodide (NB overdose --> cough, scaly skin, excessive lacrimation).</p>

408
Q

<p>Describe the pathophysiology of allergic rhinitis/Enzootic Nasal Granuloma of cattle and sheep.</p>

A

<p>Type I (IgE) hypersensitivity to pollen/fungi etc --> ongoing reaction exposure --> tissue damage by mast cell factors --> chronic epithelial, duct, goblet cell hyperplasia, mucus hypersecretion and granulomatous inflammation (type IV hypersensitivity).</p>

409
Q

<p>Is there a breed or age predisposition for Enzootic Nasal Granuloma in cattle?</p>

A

<p>- Channel island breeds (Guernsey, Jersey, Alderney) and Friesians. - 6mo to 2yo.</p>

410
Q

<p>Describe the clinical signs of Enzootic Nasal Granuloma in cattle and sheep.</p>

A

<p>- Sneezing.- Nasal pruritis.- Dyspnoea.- Stertor.- Profuse bilateral nasal discharge.- +/- facial swelling, tachypnoea, hyperpnoea, ulceration of nasal mucosa, lacrimation, chemosis.- Granulomas: multiple, firm, white, raised, 1-2mm.</p>

411
Q

<p>How is Enzootic Nasal Granuloma in cattle and sheep diagnosed?</p>

A

<p>- Endoscopy.- Biopsy.- Culture.- Antigen detection/serology to rule out bacterial, viral or fungal infection.- Inc eosinophils in nasal secretions. </p>

412
Q

<p>Describe the treatment of Enzootic Nasal Granuloma in cattle and sheep.</p>

A

<p>- Remove allergens.- Anti-histamines.- Meclofenamic acid.- Steroids.</p>

413
Q

<p>List the neoplasias that have been reported to occur in the nasal passages of cattle.</p>

A

<p>- Osteomas. - Osteosarcomas. - Squamous cell carcinomas. - Neuroblastomas. - Haemangiosarcomas. -</p>

<p>Ethmoid adenocarcinoma: endemic pattern, 6-9yo, unilateral, viral origin? Mets in LN and lung.</p>

414
Q

<p>List clinical signs of nasal neoplasia in cattle.</p>

A

<p>- Inspiratory dyspnoea.- Stridor.- Nasal discharge.- Epistaxis.- Halitosis.- Decreased airflow through nares.- Open-mouth breathing.- Distortion of facial bones.- NB not typically treated.</p>

415
Q

<p>Describe the lesion seen in congenital cystic nasal turbinate disease of cattle.</p>

A

<p>Nasal conchae lack communication with nasal cavity and fill with fluid.</p>

416
Q

<p>Describe the clinical signs and diagnosis of congenital cystic nasal turbinates in cattle.</p>

A

<p>- Stridor.- Tachypnoea.- Decreased air flow.- Exercise intolerance.- Open-mouth breathing.- Palpation.- Endoscopy.- Rads --> large, smooth, cystic ventral conchae. </p>

417
Q

<p>Describe the treatment of congenital cystic nasal turbinates in cattle.</p>

A

<p>- Sx: bilateral dorsal lateral nasal bone flaps.- Sx: transnasal removal with gigli wire.</p>

418
Q

<p>Describe the signalment and aetiology of sinusitis in ruminants.</p>

A

<p>- Cattle > sheep or goats.- Usually frontal (dehorning) or maxillary (tooth).- Other causes: injury, extension of actinomyces or nasal neoplasia, resp viruses (MCF, IBR, PI3), sinus cysts, lymphoma, oestrus ovis.</p>

419
Q

<p>Describe the clinical signs of sinusitis in cattle.</p>

A

<p>- Acute or chronic.- Anorexia.- Lethargy.- +/- fever.- Dehorning site discharging pus.- Unilateral or bilateral nasal discharge.- Stridor.- Foul breath.- Head held at an angle.- +/- frontal bone distortion, exophthalmus, neuro signs.</p>

420
Q

<p>Describe the diagnosis of sinusitis in cattle.</p>

A

<p>- Clinical signs and history.- Percussion (dull sounds or pain).- Radiographs.- Sinus centesis (Steinmann pin).</p>

421
Q

<p>Describe treatment of sinusitis in cattle.</p>

A

<p>- Sinus trephination (1 or 2 sites).- Lavage.- +/- remove tooth.- If systemic signs: NSAIDs, ABs (penicillin for Trueperella - dehorning, oxytet for pastuerella - not dehorning). </p>

422
Q

<p>Describe the aetiology of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.</p>

A

<p>- Trauma: balling gun, dose syringe, specula, stomach tube, rough stemmy feeds, grass awns, brias, FBs.- T. pyogenes, Actinobacillus, Pastuerella, Bordatella. Fusobacterium necrophorum, Streptococcus.</p>

423
Q

<p>List the clinical signs of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.</p>

A

<p>- Inspiratory dyspnoea with stertor.- Extended head and neck.- Ptyalism.- Quidding.- Pain or swelling.- Regurgitation through nostrils.- Mucopurulent to blood nasal discharge with fetid odour.- Cough.- Bloat.- Palpable swelling in the pharyngeal area.- If severe dz: depression, fever, anorexia, dehydration, forestomach stasis.</p>

424
Q

<p>Describe the diagnosis of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.</p>

A

<p>- Oral exam.- Endoscopy.- Rads.- CBC: neutrophilia, +/- metabolic acidosis due to saliva loss.</p>

425
Q

<p>List the treatment of pharyngeal trauma, abscesses, cellulitis and granulomas in cattle.</p>

A

<p>- Drain abscess into pharynx and lavage.- Drain externally.- ABs.- NSAIDs.- Tracheotomy.- IVFT.- Feed through rumenostomy.- Good Px.</p>

426
Q

<p>Describe the epidemiology and pathophysiology of Necrotic Laryngitis (aka Calf Diphtheria).</p>

A

<p>- Feedlot cattle.- Young (3-18mo); >30 days on feed.- URT infection --> laryngeal contact ulcers or H. somni infection --> damage to laryngeal mucosa --> invasion of F. necrophorum --> acute to chronic infection of laryngeal mucosa and cartilages.- Worldwide distribution, occur year-round but more common in Autumn and Winter.</p>

427
Q

<p>Describe the clinical signs of Necrotic Laryngitis in cattle.</p>

A

<p>- Acute onset moist, painful cough.- Severe inspiratory dyspnoea, stertor, head and neck extended.- Salivation/frequent swallowing or sipping water.- Anorexia, fever, hyperaemic MMs.- Bilateral fetid nasal discharge.- Un-treated die in 2-7d.- Recovered may become roarers, get aspiration pneumonia or be poor doers.</p>

428
Q

<p>Describe the treatment and prognosis of Necrotic Laryngitis. </p>

A

<p>- ABs: oxytetracycline, penicillin, TMPS.- NSAIDs (1 dose steroid if severe swelling).- +/- tracheotomy.- Nursing care.- Px good if dx early and aggressive tx, otherwise poor.</p>

429
Q

<p>Describe lesions found at necropsy of cattle that have died from Necrotic Laryngitis.</p>

A

<p>- Vocal processes and medial angles of arytenoids.- Acute: oedema, hyperaemia, swelling, discharge around necrotic ulcer.- Chronic: focus of necrotic cartilage surrounded by purulent exudate with tract to mucosal surface; arytenoid rotated into lumen or cavities.</p>

430
Q

<p>Describe laryngeal papillomatosis of feedlot cattle.</p>

A

<p>- Common disease.- Papovavirus enters via laryngeal ulcers.- CSx: sterterous respiration, cough.- Lesion: sessile to pedunculated, yellow, frond-like, 1-10mm growths on vocal processes or arytenoids.- Tx: usually not indicated; may remove surgically.</p>

431
Q

<p>Describe the aetiology of tracheal collapse and stenosis in cattle.</p>

A

<p>- Infrequently reported.- Unknown aetiology; potential causes incl trauma (roping, dystocia), tracheostomies, congenital defects.</p>

432
Q

<p>Describe the clinical signs of tracheal collapse and stenosis in cattle.</p>

A

<p>- BAR --> tachypnoea, tachycardia, mucosal hyperaemia, dyspnoea exacerbated by exercise/excitement, stertor, 'honking' cough.- Lack of response to tracheostomy, NSAIDs, ABs.</p>

433
Q

<p>Describe the diagnosis of tracheal collapse and stenosis in cattle.</p>

A

<p>- Endoscopy.- Rads: dorsoventral flattening in caudal cervical or cranial thoracic trachea most common; can be lateral.- Necropsy: dorsally or laterally flattened trachea. </p>

434
Q

<p>Describe the treatment and prognosis of tracheal collapse and stenosis in cattle.</p>

A

<p>- Px poor.- Surgery reported to enable survival to slaughter.</p>

435
Q

<p>Describe the aetiology and pathogenesis of tracheal oedema syndrome (aka Honker Cattle) of feedlot cattle.</p>

A

<p>- Extensive oedema and haemorrhage of dorsal wall of trachea.- Acute and chronic form; unknown if related.- Proposed aetiologies: URT viruses, bacteria e.g. P. multocida or H. somni, feedbunk trauma, fat, mycotoxins, hypersensitivity reaction.</p>

436
Q

<p>Describe the clinical presentation of the acute form of tracheal oedema syndrome in cattle.</p>

A

<p>- Heavy feedlot cattle in last 2/3 feeding period.- Summer.- Subclinical: sudden death.- Dyspnoea, guttural inspiratory sounds, open mouth breathing, extending head and neck, cyanosis, recumbency, death.</p>

437
Q

<p>Describe the clinical presentation of the chronic form of tracheal oedema syndrome in cattle.</p>

A

<p>- Lighter cattle (130-400kg).- +/- Hx of IBR/pneumonia.- Continuous deep, hacking cough.- +/- unthrifty.</p>

438
Q

<p>Describe treatment and prognosis of tracheal oedema syndrome in cattle.</p>

A

<p>- Acute: steroids, oxygen, decrease stress.- Chronic: no tx.- Px: poor.</p>

439
Q

<p>Describe necropsy findings in cattle that have died from tracheal oedema syndrome.</p>

A

<p>- Acute: dorsal oedema up to 5cm thick, caudal half of trachea; mucosal, submucosal and peritracheal oedema +/- haemorrhage.- Chronic: hyperaemia of mucosa in caudal third of trachea; +/- thin layer mucopurulent exudate; +/- fibre-like projections and polyps.</p>

440
Q

<p>List the infectious pathogens which contribute to he Bovine Respiratory Disease Complex.</p>

A

<p>- Bovine Herpesvirus-1 (BHV-1).- Bovine Respiratory Syncytial Virus (BRSV).- Bovine Viral Diarrhoea Virus (BVDV).- Bovine Parainfluenza 3 Virus (PI3).- Bovine Coronavirus (BCoV).- Adenovirus.- Viruses of unknown clinical sig: Bovine Rhinitis Virus, Bovine Reovirus, Calicivirus, Influenza.- Mannheimia haemolytica.- Pastuerella multicodia.- Histophilus somni.- Mycoplasma bovis.- Biberstenia trehalosi.- Trueperella pyogenes.- Bacteria w unknown clinical sig: Chlamydial organisms.</p>

441
Q

<p>Describe the Bovine Herpesvirus-1 (BHV-1).</p>

A

<p>- Family: Herpesviridae.- Subfamily: alpha.- Enveloped DNA virus.</p>

442
Q

<p>List the diseases caused by BHV-1.</p>

A

<p>- Infectious Bovine Rhinotracheitis (IBR).- Conjunctivitis.- Infectious pustular vulvovaginitis.- Balanoposthitis.- Encephalomyelitis.- Mastitis.</p>

443
Q

<p>List the clinical signs of IBR in cattle.</p>

A

<p>- Can be mild to severe (influence of type-1 interferon genotype??)- 'Red nose': hyperaemic muzzle.- Pustules on nasal mucosa --> diphtheritic membranes.- Conjunctivitis +/- corneal opacity.- Pyrexia.- Anorexia.- Dec milk prod.- Tachypnoea.- Ptyalism.- Cough.- Nasal discharge (serous to mucopurulent).- Harsh bronchovesicular sounds; referred tracheal noise.- +/- secondary bacterial pneumonia.- +/- abortion.</p>

444
Q

<p>Describe the pathophysiology of IBR.</p>

A

<p>- Transmitted via aerosol and direct contact.- BHV-1 surface glycoproteins interact w heparin sulfate proteoglycans and other host cell proteins --> enter resp epi cells and neighbouring epi cells via intracellular bridges.- Invade lymphocytes and monocytes --> extra-respiratory infections.- Latency in trigeminal ganglia and tonsils mediated by latency-related transcript (prevents apoptosis, re-activates shedding).- Disease mechanisms:i) Direct injury of infected URT/bronchial epi cells --> inflammation and susceptibility to secondary infection.ii) Immunosuppression: dysfunction of neuts, lymphs, macro incl dec neut chemotaxis, dec mitogen-induced blastogenesis of lymphocytes, dec expression of MHC-1 molecules, inc apoptosis of lymphs, mono.</p>

445
Q

<p>Describe the epidemiology of IBR.</p>

A

<p>- Widespread.- Adult cattle are reservoir.- Increased attack rate and fatality in feedlot cattle.- Historically first few weeks after entry, now seeing late outbreaks (mutation not covered by current vacc?).- Not important in epizootic pneumonia of calves.</p>

446
Q

<p>Describe necropsy findings in animals that have died from IBR.</p>

A

<p>- Rhinitis, laryngitis, tracheobronchitis.- Mucosa congested or haemorrhagic.- Pustular lesions --> plaques on resp. ocular, repro mucosa.- +/- oesophageal lesions.- Neonates: systemic dz w necrotic foci in all organs.- NB intranuclear inclusion bodies NOT common feature of BHV-1 infections.</p>

447
Q

<p>How is IBR diagnosed in cattle?</p>

A

<p>- Virus isolation, IFA, PCR from nasal and conj swabs.- Paired serology (Ab titre).</p>

448
Q

<p>Describe treatment and prevention of IBR in cattle.</p>

A

<p>- Decrease stress.- Ensure access to food and water.- +/- NSAIDs.- +/- ABs (if evidence of secondary infection).- +/- vaccination (outbreak).- IN/IM vaccines are widely available; protect from infection in challenge studies but few field trials; inactivated for preg cows and neonates, MLV others --> immunity in 2-3d therefore must induce CMI.- Management essential in prevention e.g. dec co-mingling, dec stress.</p>

449
Q

<p>Describe the Bovine Respiratory Syncytial Virus (BRSV).</p>

A

<p>- Family: Paramyxoviridae.- Subfamily: Pneumovirina.- Enveloped RNA virus.- Recent change in BRSV G glycoprotein reported in Europe, likely secondary to antigenic pressure from vaccination.</p>

450
Q

<p>List the clinical signs of BRSV infection in cattle.</p>

A

<p>- Inapparent to severe; CSx limited to resp tract.- Fever, depression, inappetence.- Tachypnoea.- Ptyalism.- Cough.- Nasal/lacrimal discharge.- Inc bronchovesicular sounds +/- wheezes/crackles in mid- to dorsocaudal lungfields.- +/- absent dorsal BV sounds (ruptured bullae).- Late infection: pronounced dyspnoea, inc expr effort, open-mouth breathing, +/- s/c emphysema.</p>

451
Q

<p>Describe the epidemiology of BRSV infection in cattle.</p>

A

<p>- 60-80% US cattle have Abs assoc w seroconversion.- High morbidity, low mortality (0-20%).- Adult cattle believed to be reservoir.- Tranmission: aerosol, direct contact, fomites.- Incubation period: 3-5 days.</p>

452
Q

<p>Describe the pathogenesis of BRSV infection in cattle.</p>

A

<p>- Infects cells of nasal, tracheal, bronchial epi +/- alveolar and circulating macrophages.- Epi cells fuse --> multinucleated cells (syncytia) --> slough into lumen --> phagocytosed by neut/alv macro.- Bronchitis, bronchiolitis, alveolitis +/- AIP.- Infected macro have dec function, dec phagocytosis, dec prod chemotactic factors.</p>

453
Q

<p>Describe the role of the immune response in BRSV infection in cattle.</p>

A

<p>- Severity of dz is related to humoral and CM immunity.- CSx most notable mast cell degran --> bronchoconstriction, pulmonary oedema.- Vaccine-enhanced dz is rare but is reported w inactivated and MLV vaccines (vacc is still recommended as rare).</p>

454
Q

<p>Describe necropsy findings in cattle that have died from BRSV infection.</p>

A

<p>- Neutrophilic to mononuclear bronchitis, broncheolitis, alveolitis +/- syncytial cells.- AIP --> dorsocaudal lungs heavy, rubbery, emphysema.- Histo: alveolar epi hyperplasia, hyaline membranes, interstitial inflamm cells, haemorrhage, oedema.</p>

455
Q

<p>Outline diagnosis of BRSV in cattle.</p>

A

<p>- Virus does not survive well, therefore not virus iso.- PCR, IHC, IFA of nasal swabs, TTW or BALF, lung tissue; less likely to be found 10-15d post-infection.- Seroconversion: ELISA or VN Abs.</p>

456
Q

<p>Describe treatment and prevention of BRSV infection in cattle.</p>

A

<p>- Goal: decrease resp inflamm and prevent secondary bacterial infection.- NSAIDs; steroids if severe resp distress/AIP.- Antibiotics.- InO2, furosemide if required.- IN/IM vaccines available.</p>

457
Q

<p>Describe the Bovine Viral Diarrhoea Virus (BVDV).</p>

A

<p>- Family: Flaviviridae.- Genus: Pestivirus.- Enveloped RNA virus.</p>

458
Q

<p>Describe the respiratory disease causes by BVDV infection in cattle.</p>

A

<p>- Some strains cause mild pneumonia.- Importance is as a co-infector in BRDC e.g. w M. haemolytica, M. bovis, BHV-1, BRSV.</p>

459
Q

<p>Describe the pathogenesis of BVDV in BRDC infections.</p>

A

<p>- Suppresses immune resp to co-infecting agents.- Suppresses immune resp to vacc against other BRDC pathogens.- Infects the resp tract and enhances pathogenicity of co-infectors.</p>

460
Q

<p>Describe the Bovine Parainfluenza-3 Virus (PI3).</p>

A

<p>- Family: Paramyxoviridae.- Subfamily: Paramyxovirinae.- Enveloped RNA virus.</p>

461
Q

<p>List the clinical signs of PI3 infection in cattle.</p>

A

<p>- Range from subclinical to mild.- Fever.- Cough.- Nasal and ocular discharge.- Tachypnoea.- Inc bronchovesicular sounds, wheezes.</p>

462
Q

<p>Describe the epidemiology of PI3 infection in cattle.</p>

A

<p>- Very widespread.- Often no clinical signs.- Important initiator of BRDC.- Incubation period 2d.</p>

463
Q

<p>Describe the pathophysiology of PI3 infection in cattle.</p>

A

<p>- CSx of URT and LRT infection.- Virus found in nasal, tracheal, broncheolar, alveolar epi cells.- Damages mucociliary apparatus, dec alveolar macro function (Fc receptor expression, phagocytosis, microbicidal action) --> predisposes to secondary infection.</p>

464
Q

<p>Describe necropsy findings in cattle that have died from PI3 infection.</p>

A

<p>- Rarely seen.- Experimental infection --> necropsy --> changes like mild BRSV.</p>

465
Q

<p>Outline the diagnosis of PI3 infection in cattle.</p>

A

<p>- Virus isolation.- PCR of nasal swabs.- Paired serology to demonstrate rising titre.</p>

466
Q

<p>Describe methods for prevention of PI3 infection.</p>

A

<p>- Inactivated and ML vaccines.- Registered for cattle only; off-label in sheep and goats.</p>

467
Q

<p>Describe the Bovine Coronavirus (BoCV).</p>

A

<p>- Family: Coronaviridae.- Group 2 Coronavirus.- Enveloped, single-stranded RNA virus.</p>

468
Q

<p>List diseases caused by Bovine Coronavirus.</p>

A

<p>- Calf diarrhoea.- Winter dysentary of adult cattle.- Respiratory disease (recent evidence).</p>

469
Q

<p>Describe the contribute of BoCV to BRDC in cattle.</p>

A

<p>- Important role identified in two Shipping Fever outbreaks.- Evidence vaccination --> less resp dz in feedlot cattle.- Other evidence suggests no role in BRDC.</p>

470
Q

<p>Describe the Bovine Herpesvirus-4 Virus.</p>

A

<p>- Family: Herpesviridae.- Subfamily: Gamma herpesviridae.- Enveloped DNA virus.</p>

471
Q

<p>List the diseases caused by BHV-4.</p>

A

<p>- Abortions.- Metritis.- Mammilitis.- Enteric dz.- Conflicting data whether or not causes respiratory dz.</p>

472
Q

<p>Describe adenoviruses of ruminants.</p>

A

<p>- Family: Adenoviridae.- Serotypes: Cattle - at least 10, sheep - at least 6, goats - 2.- Non-enveloped, double-stranded DNA viruses.</p>

473
Q

<p>Describe presentation of Bovine Adenovirus infections.</p>

A

<p>- Widespread.- Frequently subclinical, often assoc w other pathogens.- Assoc w pneumonia, enteritis, keratoconjunctivitis; weak calf syndrome?</p>

474
Q

<p>Describe the bacteria Mannheimia haemolytica.</p>

A

<p>- Family: Pasteurellaceae.- Gram negative aerobe, small rod.- At least 12 serotypes.- Cattle: A1, A6 most common pneumonic lungs, A2 normal flora in nasopharynx.- Sheep and goats: A2 most common pneumonic lungs; A7, A9 pathogenic.</p>

475
Q

<p>Describe the epidemiology of Mannheimia haemolytica infection in cattle.</p>

A

<p>- Most common bacterial isolate from feedlot cattle w fatal fibrinous pleuropneumonia.- Not commonly associated with outbreaks of pneumonia in dairy calves.</p>

476
Q

<p>Describe the pathophysiology of Mannheimia haemolytica infection in cattle.</p>

A

<p>- Infected v early in life -> n commensal org in nasopharynx.- Numbers inc w transport/URT viral infection --> opportunistic pathogen of LRT --> multiply in lungs --> severe, necrotising, fibrinous pleuropneumonia.- Virulence factors:-- Leukotoxin: binds to cells via CD18, beta subunit of beta 2 integrins --> inc expression of LFA-1 by leukocytes --> apoptosis/cell lysis of platelets, lympho, macro, neut.-- LPS: works synergistically w leukotoxin; v rapid resp --> initiation of complement and coag cascades, activation of endo cells, recruitments of neuts, activation of neuts and macro --> inc pro-inflam cytokines (IL-1b, IL-8, TNF-a); death of massive influx of neuts --> elastase, collagenase, reactive O2 --> necrosis/fibrinous exudation.-- Polysaccharide capsule: aids attachment, prevents phagocytosis by neutrophils.-- Iron-regulated outer membrane proteins: bind transferrin, alter neutrophil function.-- Adhesins: mediate attachment to host cells.-- Neuraminidase: dec viscosity of mucus, dec repellant negative charge on host cells. </p>

477
Q

<p>List clinical signs of Mannheimia haemolytica infection in cattle.</p>

A

<p>- Fever.- Tachypnoea.- Depression.- Dec appetite.- NB no cough during early disease.- +/- thoracic pain.- +/- endotoxaemia.- Harsh BV sounds over cranioventral lungs.- +/- death/chronic infection.- Usually secondary to viral dz.</p>

478
Q

<p>Describe necropsy findings in cattle infected with Mannheimia haemolytica.</p>

A

<p>- Fibrinopurulent bronchopneumonia or pleuropneumonia OR pulmonary consolidation w/out fibrin (dairy calves, sheep, goats).- Cranioventral lobes to whole lung.- May see infarcts, coagulative necrosis, swollen red LNs.</p>

479
Q

<p>Outline diagnosis of Mannheimia haemolytica infection in cattle.</p>

A

<p>- Culture and cytology.- TTW, BAL, thoracocentesis or lung tissue.</p>

480
Q

<p>Outline treatment of Mannheimia haemolytica infection in cattle.</p>

A

<p>- Many labelled antibiotics.- NSAIDs in cattle with SIRS.</p>

481
Q

<p>Outline methods for prevention of Mannheimia haemolytica infection in cattle.</p>

A

<p>- Antibiotic metaphylaxis e.g. tilmicosin, florfenicol just pre- or post-shipping.- Ensure no FPT.- Vaccination.- Minimise stressors: viral infection, co-mingling, long distance shipping, pre-conditioning. </p>

482
Q

<p>Describe the bacteria Pasteurella multocida. </p>

A

<p>- Family: Pasteurellaceae.- Gram negative aerobe.- 5 serogroups: A - most common resp infection, B+E - haemorrhagic septicaemia (Asia and Africa), D+F - resp infection in some regions (esp in sheep).</p>

483
Q

<p>Describe the epidemiology of Pasteurella multocida infection in cattle.</p>

A

<p>- Normal URT commensal in cattle, sheep and goats.- Debate if primary or only secondary lung pathogen.</p>

484
Q

<p>Describe the pathophysiology of Pasteurella multocida infection in cattle.</p>

A

<p>- Little known.- LPS.- Capsule: resists phagocytosis.- Iron-regulated outer membrane proteins: inc ability to proliferate in host.- Damage to resp epi (viruses, poor ventilation etc) --> chronic inhalation of small numbers of bacteria --> bronchopneumonia.- Possible cause of enzootic pneumonia of calves.</p>

485
Q

<p>List clinical signs of Pasteurella multocida infection in cattle.</p>

A

<p>- Fever.- Tachypnoea.- Depression.- Coughing.- Mucoid to mucopurulent nasal discharge.- Harsh BV sounds cranioventrally; crackles (fluid in large airways).- +/- endotoxaemia.- Generally milder CSx than M. haemolytica.- Calves > feedlot cattle.</p>

486
Q

<p>Describe necropsy findings in cattle infected with Pasteurella multocida.</p>

A

<p>- Purulent bronchopneumonia w plum-coloured CV consolidation and purulent exudate on cut section.- Fibrin possible.</p>

487
Q

<p>Outline diagnosis of Pasteurella multocida infection in cattle.</p>

A

<p>- Culture and cytology.- TTW, BAL or lung tissue.</p>

488
Q

<p>Outline methods for treatment and prevention of Pasteurella multocida infection in cattle.</p>

A

<p>- Many labelled antibiotics; as infections usually chronic may require 3-5d at labelled dose.- Dec exposure to viruses and environmental contributors.- Vaccines available but questionable efficacy.</p>

489
Q

<p>Describe the bacteria Histophilus somni. </p>

A

<p>- Family: Pasteurellaceae.- Gram negative aerobe.- NF of URT and genital mucosa of cattle, goats, sheep.- Different strains have different virulence.</p>

490
Q

<p>Describe the epidemiology of Histophilus somni infection in cattle.</p>

A

<p>- Exposure common.- Dz of feedlot cattle > calves.</p>

491
Q

<p>Describe the pathophysiology of Histophilus somni infection in cattle.</p>

A

<p>- Primary viral dz --> secondary bacterial infect of resp tr.- Virulence factors:-- Outer membrane proteins: bind Fc region of Ab --> escape opsonisation, resist killing following phagocytosis.-- Lipooligosaccharide: like LPS; interacts w P2X7 receptor on endo cells --> apoptosis --> vasculitis and thrombosis; induces IgE prod --> hypersens post-vacc/more severe dz.</p>

492
Q

<p>List clinical signs of Histophilus somni respiratory infection in cattle.</p>

A

<p>- Causes dz in multiple body systems: septicaemia, TEME, endometritis, abortion, infertility, pneumonia, pleuritis, laryngitis, otitis, conjunctivitis, myocarditis, mastitis, polyarthritis.- Mild to severe respiratory infections.- Fever.- Tachypnoea.- Cough.- Nasal discharge.- Depression.- Harsh BV sounds cranioventrally.- Pain (pleuritis).- +/- SIRS.</p>

493
Q

<p>Describe necropsy findings in cattle infected with Histophilus somni.</p>

A

<p>- Plum and brown consolidation CV lungs.- +/- abscesses.- Purulent material on cut section of lung tissue.- +/- fibrinous pleuritis.- +/- haemorrhage.</p>

494
Q

<p>Outline diagnosis of Histophilus somni infection in cattle.</p>

A

<p>- Culture: TTW, BAL, pleurocentesis, lung tissue; NB hard to grow in culture therefore trans immediately, pre-tx samples.- IHC lung tissue.- Paired titres.</p>

495
Q

<p>Outline methods for treatment and prevention of Histophilus somni infection in cattle.</p>

A

<p>- Several antibiotics.- Prophylaxis w oxytet does not result in improvement.- Killed whole bacterins --> IgE prod --> risk of anaphylaxis on subsequenc vacc therefore only vacc high risk cattle.- Enviro/stress management, dec viral infections.</p>

496
Q

<p>Describe the bacteria Mycoplasma bovis. </p>

A

<p>- Family: mycoplasma.- Small, pleomorphic organisms w/out cell wall.</p>

497
Q

<p>Describe the epidemiology of Mycoplasma bovis infection in cattle.</p>

A

<p>- Cattle; rare in sheep and goats.- Found in healthy and diseased cattle.- Spread by aerosol, direct contact, in milk.- Spreads rapidly in feedlots.- Found in dairy calves and feedlot cattle, partic w chronic resp dz.</p>

498
Q

<p>Describe the pathophysiology of Mycoplasma bovis infection in cattle.</p>

A

<p>- Little known.- General mycoplasma characteristics:-- Variable surface proteins allow attachment to host cells.-- Invasion of tissues e.g. can move b/w resp epi cells.-- Evade host IR, impair neut activity, kill lymphocytes, induce inflammatory response.</p>

ACVIM (11 decks)

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