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Respiratory LA > Equine respiratory > Flashcards

Equine respiratory Flashcards

1
Q

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?

A
  • Presence of D. arnfieldi larvae in BAL or TTW
  • Increase eosinophils in TTW or BAL

Baerman usually false

Peripheral eosinophilia does not correlate.

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2
Q

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

A

Clinical presentation:

  • any age but more common in young horses
  • clinical signs include poor performance (non-respiratory causes should be ruled out if this is only clinical sign) and chronic (>3 weeks), occasional coughing.

Diagnostic confirmation:

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

Rule out other causes of poor perfromance OR

  • BAL cytology characterised by mild increases in neutrophils, eosinophils and/or metachromatic cells
  • further confirmed for research purposes by documenting pulmonary dysfunction based on evidence of lower airway obstruction, airway hyperresponsiveness or impaired blood gas exchange

Exclusion criteria:

  • evidenced of systemic signs of infection (anorexia, lethargy, haematologic abnormalities compatible with infection)
  • increased respiratory effort at rest (heaves)
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3
Q

Action of macrophages in R. equi ©

A

Activation of IFNg by CD4+

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4
Q

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?

a) The fraction Pa02/Fi02 is >300mm Hg in cases of ALI (which is the less severe form) and >200mm Hg for ARDS.
b) It is related to pulmonary surfactant deficiency in neonatal foals
c) The pathophysiology includes dysregulation of pulmonary inflammation and coagulation
d) It is not related to an infectious etiology

A

c) The pathophysiology includes dysregulation of pulmonary inflammation and coagulation

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.

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5
Q

Advantages of ultrasound for R. equi

A

Evaluation of severity of pneumonia and response to therapy

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6
Q

Best measure for eradication of EAV from herd ©

A
  • Manage carrier stallions
  • Vaccinate mares that are bred to the carrier stallion
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7
Q

What is the most effective treatment for M. capillaris?

A

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

*Resistant to levamisole

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

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.

Smith, Bradford P.. Large Animal Internal Medicine, Elsevier, 2014, page 628.

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8
Q

Mention some primary pathogenic fungi.

A

Primary pathogenic fungi such as Blastomyces dermatitidis, Histoplasma capsulatum, Coccidioides immitis, Cryptococcus neoformans, and Conidiobolus coronatus usually infect immunologically normal horses.

Smith, Bradford P.. Large Animal Internal Medicine, Elsevier, 2014, page 495.

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9
Q

Best way to determine the carrier status in strangles

A
  • Endoscopic examination of the GP
  • Culture + PCR of GP lavage
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10
Q

Best way to increase detection of R. equi

A

Culture + PCR (90% detection)

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11
Q

Characteristic pulmonary lesion of EIPH

A

Bilateral and caudo-dorsally

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12
Q

Cytology of a normal BAL, in horses and llamas?

A
  • Neutrophils: < 5%
  • Mast cells: < 2%
  • Eosinophils: <1%
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13
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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14
Q

Describe herpesviruses.

A
  • Family: Herpesviridae. - Double-stranded DNA viruses. - Two subfamilies: alpha and gamma.
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15
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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16
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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17
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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18
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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19
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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20
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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21
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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22
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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23
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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24
Q

Describe the equine adenovirus (EAdV).

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

Describe the equine influenza virus (EIV).

A
  • Family: Orthomyxoviridae. - Genera: Influenza A virus. - Segmented, single-stranded RNA virus.
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27
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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28
Q

Describe the features of Acute respiratory distress syndrome (ARDS)

A

A syndrome of lung injury characterised by:

  • alveolar damage
  • high-permeability pulmonary oedema
  • respiratory failure
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29
Q

Describe the findings on BAL fluid cytology on horses with IAD

A
  • mild to moderate increase in neutrophil, eosinophil and /or mast cell percentages
  • > 10% neutrophils, > 5% mast cells, > 5% eosinophils
  • importance of BAL cytology should be interpreted in light of history, clinical exam and endoscopic findings
  • NB. TW cytology not considered an appropriate alternative to BAL cytology for diagnostic confirmation or characterisation of IAD
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30
Q

Describe the Hendra virus.

A
  • Family: paramyxoviridae. - Genus: henipavirus. - Enveloped RNA virus.
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31
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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32
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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33
Q

Describe the mucus scoring system used to quantify mucus accumulation in the trachea

A

Grade 0 - no visible mucus

Grade 1 - single to multiple small blobs of mucus

Grade 2 - larger but nonconfluent blobs

Grade 3 - confluent or stream forming mucus

Grade 4 - pool forming mucus

Grade 5 - profuse amounts of mucus

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34
Q

Describe the pathophysiological mechanisms leading to increased pleural fluid production.

A

Fluid production in the pleural space increases if any of the following occurs:

1) elevation of the hydrostatic pressure gradient (CHF, portal hypertension)
2) a decrease in the colloid osmotic pressures (hypoproteinaemia)
3) an increased permeability of the capillary vessels (infection, malignancy, inflammation)
4) decreased removal of fluid because of impaired lymphatic drainage or obstruction (neoplasia) or infiltration of the pleura or parenchyma (neoplasia).

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

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35
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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36
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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37
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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38
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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39
Q

Diagnosis of Chronic carrier state for S. equi

A

Guttural pouch fluid/swab PCR

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40
Q

Diagnosis of P. carinii pneumonia

A
  • Trophozoites in histology
  • Interstitial, miliary pattern
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41
Q

Diagnosis of R. equi pneumonia

A

Bacterial culture and PCR for VapA gene from TBA

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42
Q

Diseases cause by EHV-1

A
  1. Respiratory
  2. Abortion/Neonatal death
  3. EHVM
  4. Chorioretinopathy –> shotgun lesions
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43
Q

Does furosemide affect performance in cases of EIPH?

A

Administration 4 hrs before is associated with improved racing outcomes

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44
Q

Drug of choice of Pneumocystis carinii

A

TMS

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45
Q

EIPH, what is associated with?

A

Histology changes

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46
Q

Elimination of EIV Australia

A

canary pox 14 days

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47
Q

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

A

EHV-5

PCR or IHC in lung biopsy or BALF

Is this a definitive diagnosis?

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48
Q

For glanders (farcy), why would you do a IDT?

A

To certify negative horses

Is zoonotic and cases have to be reported to OIE

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49
Q

Fungi that most commonly causes pneumonia in horses

A

Coccidiomicosis

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50
Q

Fungi that most commonly causes pneumonia in horses

A

Coccidiomicosis

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51
Q

Gene associated with virulence in R. equi, and where is it located?

A

Vap A gene, located in the pathogenicity island (PAI)

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52
Q

Gene implicated in heritability of RAO

A

IL-4 receptor gene

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53
Q

Gold standard for diagnosis of strangles

A

Culture

  • Nasopharynx, GP wash*
  • Preferred method on aspirate of masses
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54
Q

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

A

Condidiobolus coronatus

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 appearance is 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.

Smith, Bradford P.. Large Animal Internal Medicine, Elsevier, 2014, page 498

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55
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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56
Q

How can you differentiate between mild and severe equine asthma?

A
  • Poor performance –> mild
  • H2 challenge test –> mild
  • Bronchoconstriction at rest –> severe
  • Hay challenge test –> severe
  • BALF cytology
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57
Q

How could you differentiate between some of the causes of pleural effusion?

A

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

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

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

infectious and intraabdominal diseases - can distinguish septic effusions from nonseptic effusions by biochemical analysis of pleural fluid –

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

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58
Q

How does EHV-1 evade the immune system?

A
  • Downregulationof MHC-1
  • Alteration of NK cells
  • Modulation of cytokine response
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59
Q

How does furosemide help RAO affected horses, and which drug blocks this effect?

a. Removes pulmonary edema from negative-pressure pulmonary edema, blocked by diphenhydramine
b. Causes a prostaglandin E2 mediated bronchodilation, blocked by diphenhydramine
c. Removes pulmonary edema from negative-pressure pulmonary edema, blocked by flunixin
d. Causes a prostaglandin E2 mediated bronchodilation, blocked by flunixin

A
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60
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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61
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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62
Q

How is equine adenovirus infection prevented?

A

No vaccine available.

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63
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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64
Q

How is equine rhinitis virus infection prevented?

A

No vaccine available.

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65
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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66
Q

How is Hendra virus prevented/controlled?

A
  • Vaccine. - Strict biosecurity.
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5
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67
Q

How is IAD diagnosed?

A

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

2) documentation of lower airway inflammation based on excess mucus on endoscopy, BAL cytology or abnormal lung function
3) exclusion of severe equine asthma (RAO/heaves) as well as infectious and other respiratory diseases

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68
Q

How is pleural fluid formed?

A

Pleural fluid is the interstitial fluid of the parietal pleura.

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.

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69
Q

How long is the isolation for cases of EHV-1?

A

28 days!

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70
Q

How long is the nasal shedding in strangles

A

2-3 weeks

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71
Q

How long is the quarantine for strangles?

A

2-3 weeks

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72
Q

How long is the shedding for EIV?

A

~ 7 days

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73
Q

How long is the shedding of EHV-1?

A

4-7 days

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74
Q

How to determine strangles titer?

A

SeM protein

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75
Q

If you want to diagnose pneumocystosis, what sample would you submit?

A

BAL for cytology

  • Can NOT be cultured
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76
Q

Immune response in R. equi pneumonia

A

IFN-g –> macrophages

77
Q

In cases of strangles, how long does the nasal shedding last?

A

2-3 weeks

78
Q

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

A

Increase in pneumocytes type II

79
Q

In strangles, what is a positive nasal PCR

A

Actively shedding

80
Q

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

Lymphocytes: 19%

Macrophages: 10.2

Neutrophils: 71.4%

Mast cells: 0.32% %

Eosinophils: 0.03%

a. RAO
b. IAD
c. Exercise induced pulmonary hemorrhage
d. Pneumonia

A

a. RAO

81
Q

Interpretation of a SeM ELISA for strangles where the titer is ≥ 1:3200

A

High antibody → predispose to develop purpura when vaccinated

  • Do NOT vaccinate
82
Q

Is furosemide effective prophylaxis for EIPH?

A

4 hours before extrenous exercise decreases the severity and incidence of EIPH

  • Furosemide decreases pulmonary capillary and transmural pressure
83
Q

It is believed that there is a genetic component in severe equine asthma.

Which gene could be implicated?

A
  • IL-4 receptor gene
    • IL-4 enhances IL-8
84
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.
85
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.
86
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.
87
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.
88
Q

List important diagnostic tests to consider in horses with pleural effusion.

A

1) physical and rectal examination
2) CBC & Biochemistry
3) Cardiac evaluation
4) thoracic and abdo u/s
5) abdominocentesis
6) transtracheal aspirate (if infectious agents suspected) +/- (depending on nature of effusion and geographic location of horse)
7) Coggins test (AGID)
8) titers against Coccidioides immitis, Cryptococcus neoformans, Mycoplasma felis

89
Q

List necropsy findings in foals that die following EAV infection.

A
  • Interstitial pneumonia. - Lymphocytic arteritis. - Renal tubular necrosis. - Tunica media necrosis.
90
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.
91
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.
92
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.
93
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.
94
Q

List the differential diagnoses for bilateral epistaxis

A

■ Trauma (iatrogenic/external head trauma)

■ Guttural pouch mycosis
■ Progressive ethmoidal haematoma (unilateral or bilateral)
■ Exercise-induced pulmonary haemorrhage

■ Neoplasia (unilateral or bilateral)

■ Clotting/bleeding disorders
■ Pneumonia/pulmonary abscess

■ Rhinitis/sinusitis (unilateral or bilateral)

Unilateral:

Foreign body

Nasal amyloidosis/polyps (unilateral)
Infected nasolacrimal duct (unilateral)

95
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.
96
Q

Lung lesions in EIPH ©

A

Bilateral and more in caudo-dorsal region

Pleural and septal fibrosis and angiogenesis

Venous remodeling

97
Q

Lung mechanism of IAD

A

?

98
Q

Measures to prevent EAV

A
  • Vaccinate colts in the first year and annually thereafter
  • Vaccinate mares that will be bred
  • Manage carrier stallions separate, or castrate
  • MLV
99
Q

Most common age for R. equi pneumonia

A

3 weeks - 5 months

100
Q

Most common cell in RAO BAL

A

Neutrophils

101
Q

Most common presentatio of R. equi

A

Subclinical, might recover without therapy

102
Q

Most important cell for immunity against EHV-1?

A
  • CTLs –> MHC class I restricted
  • Mediated by CD8+
103
Q

What are some of the most important cells for R. equi immunity?

A

T lymphotytes - Cytotoxic T lymphocytes (CTL) and T-helper type 2 (Th2)

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 the hypothesis that an IFNγ deficiency and T-helper type 2 (Th2) cells might be at the basis of their peculiar susceptibility to R. equi infections.

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.

Smith, Bradford P.. Large Animal Internal Medicine, Elsevier, 2014, page 485-486.

104
Q

Mucus scoring for equine asthma

A
  • Grade 0 = no mucus
  • Grade 1 = single to multiple small blobs
  • Grade 2 = larger but non confluent blobs
  • Grade 3 = confluent or stream forming
  • Grade 4 = pool forming
  • Grade 5 = profuse amounts
105
Q

Necropsy finding in vena caval thrombosis

A

Thrombus between the liver and right atrium at the caudal vena cava

106
Q

Negative prognostic indicator in R. equi pneumonia

A

Intra-abdominal abscess

Osteomyelitis

107
Q

Negative prognostic indicator in R. equi pneumonia

A
  • Intra-abdominal abscess
  • Osteomyelitis
108
Q

OIE recommendations for influenza vaccine

A

Florida clades 1 and 2

109
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
110
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.
111
Q

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

a) It’s frequently followed within a few days by opportunistic bacterial pneumonia
b) Can produce interstitial pneumonia and alveolar type II cell proliferation
c) Can result in lysis of the macrophage, chronic alveolitis, and fibrosis
d) Can result in bronchopneumonia and alveolar type I cell proliferation

A

b) Can produce interstitial pneumonia and alveolar type II cell proliferation

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.

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.

Smith, Bradford P.. Large Animal Internal Medicine, Elsevier, 2014, page 511.

112
Q

Pathogenensis R. equi and decreased immune (macrophage) response

A

Lipoarabinominam on bacterium surface and Macrophage phagocytosis of R. equi

113
Q

Pathophysiology of EIPH

A

Rupture of alveolar capillaries secondary to increase in intramural pressure (increase in both capillary and alveolar pressure)

114
Q

Pneumocytes II

A

Lush pastures

115
Q

Purpura hemorrhagica is a type ____ hypersensitivity reaction

A

III

116
Q

RAO is characterized by?

  1. Excessive mucus production, intraluminal macrophage accumulation, bronchiolar hyperreactivity, and bronchospasm
  2. Excessive mucus production, intraluminal neutrophil accumulation, bronchial hyperreactivity, and reversible bronchospasm
  3. Excessive surfactant production, intraluminal macrophage accumulation, bronchiolar hyperreactivity, and bronchospasm
  4. Excessive surfactant production, alveolar neutrophil accumulation, bronchial hyperreactivity, and reversible bronchospasm.
A

b. Excessive mucus production, intraluminal neutrophil accumulation, bronchial hyperreactivity, and reversible bronchospasm

117
Q

Receptor used by macrophages to engulf opsonized R. equi

A

Complement receptor 3 = CR3 or Mac-1

118
Q

Receptor used by macrophages to engulf opsonized R. equi

A

Complement receptor 3 = CR3 or Mac-1

119
Q

Response that mediates ocurrence of RAO

A

Th-2 mediated pathway

120
Q

Rhodococcus equi is a ….

A

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.

121
Q

Status of bronchi in IAD ©

A

No bronchoconstriction

122
Q

Summarise the pathogenesis of IAD and reported risk factors

A
  • dysregulation of the inflammatory cell homeostasis in the airway lumen leading to clinical signs of variable severity
  • variety of aetiological agents might be involved
  • relative contribution to the development of IAD varies among different populations of horses based on:

– environmental conditions they are exposed to during and after training

– feeding – housing

– season – preventive medicine practices

– differences in distribution of infectious agents

– varying genetic influences

  • activation of innate immune system and Th-1 polarization often involved in pathogenesis of IAD and most likely drive the luminal neutrophilia
  • implication of adaptive immune response, including Th-2 type polarization in some IAD phenotypes
  • non-infectious agents central to development of IAD
  • high burdens of aerosolised particles and gases eg stabling is a risk factor
  • exposure to cold, dry environments may predispose to pathogenesis of BAL neutrophilia in some horses with IAD
  • contribution of infectious agents uncertain
  • difficult to determine if bacterial infections contribute to increased mucus or if bacterial colonization occurs as a consequence of impaired mucus clearance
  • role of viral infection in IAD is controversial
123
Q

T/F

For EIV, serum antibody concentrations correlates with protection

A

True

124
Q

T/F

For EIV, serum antibody concentrations correlates with protection

A

True

125
Q

T/F

Oestrus ovis only infects sheep, and less commonly, goats.

A

F- other animals and humans can become accidentally infected

126
Q

Test to diagnose airway responsiveness in cases of IAD ©

A

Histamine aerosol –> elevated levels of leukotriene C4

127
Q

Test with highest Se and Sp for diagnosis of respiratory viruses in horses

A

RT-PCR

128
Q

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

  1. Inhaled chemicals (oxygen or smoke)- Acute
  2. Adverse drug reactions- Acute
  3. Inhaled inorganic dust (pneumonoconises- silicosis)- Chronic
  4. Endogenous metabolic/toxic conditions (ARDS, DIC) Uremia)- Chronic
A

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

129
Q

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?

A

VirR and Orf

Each of them encondes a regulatory protein

130
Q

Treatment for D. viviparus

A

Ivermectin -> 3, 8, 13 weeks Doramectin -> 0, 8 weeks If treatment during PPP -> larvae never shed in feces

131
Q

Treatment of horse with strangles

A

Horses with early clinical signs • ATB on early stage, before abscessation (3-5 days) • May prevent local abscess and shedding Horses 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

132
Q

Types of equine adenoviruses

A
  • EAdV-1 → respiratory disease, conjunctivitis
  • EAdV-2 → diarrhea in foals
133
Q

Vaccination of EIV

A

Canary q14d

134
Q

Vaccine recommendation for EIV by OIE

A

Florida clades 1 and 2

135
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.
136
Q

What are some other diagnoses associated with the development of pleural effusion?

A

1) thoracic neoplasia eg. lymphoma (most common), fibrosarcoma, gastric or oesophageal SCC, hepatoblastoma, haemangiosarcoma, melanoma, mesothelioma, metastatic mammary or ovarian adenocarcinoma
2) thoracic trauma
3) pericarditis
4) peritonitis
5) viral, mycoplasmal, fungal infections
6) CHF
7) liver disease
8) diaphragmatic herniation
9) hypoproteinaemia
10) EIA
11) pulmonary granulomata
12) damage of the thoracic duct

137
Q

What are the different phenotypes of IAD?

A
  • some associated with specific inflammatory cells in BAL:

– metachromatic cells - associated with airway hyperreactivity and subclinical pulmonary obstruction

– neutrophilic IAD

  • more often associated with cough and presence of tracheal mucus
  • BAL eosinophilia more common in younger horses (< 5yo)
  • BAL neutrophilia more frequently diagnosed in older horses (> 7yo)
138
Q

What are the main differences between RAO and IAD?

A
  • lack of laboured breathing at rest permits differentiation of IAD from RAO
  • severe exercise intolerance in RAO
  • combination of pronounced BAL neutrophilia (> 25%) and tracheal mucus accumulation (grades >2/5) in RAO
139
Q

What are the most common diagnoses associated with the development of pleural effusion?

A

Bacterial pneumonia or lung abscesses

140
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.
141
Q

What breed is most prone to rhinitis/enzootic nasal granulomas?

a. Hereford + Angus
b. Limousin
c. Friesian + Guernsey
d. Belted Galloway

A
142
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).
143
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.
144
Q

What complications can occur following EIV infection?

A
  • Secondary bacterial pneumonia. - Myositis. - Myocarditis. - Limb oedema. - Potentially may predispose to IAD, RAO, EIPH.
145
Q

What is known about the use of furosemide for EIPH? ©

A

Decrease severity and incidence

(reduces pulmonary vascular pressure)

146
Q

What is necessary in a cytology to diagnose a fungal pneumonia?

A

Large number of fungi in degenerated neutrophils in a speedily processed sample

147
Q

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

A

CBC, monitoring for fever, cough

148
Q

What is the best immune response against R. equi:

A

IFN-y

149
Q

What is the detection rate for strangles when both culture + PCR are used?

A

~ 90%

150
Q

What is the effect of antibodies against EHV-1?

A

Decrease virus shedding, but fail in preventing infection, abortion and EHM

151
Q

What is the effect of vaccination of mares against R. equi?

A

Does not increase protection

152
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.
153
Q

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

A

Equine influenza.

154
Q

What is the pathogenesis of R. equi?

A

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.

155
Q

What is the prognosis for horses with EMPF?

A

Guarded to poor.

156
Q

What is the purpose of the lymphocyte-associated viremia of EHV-1?

A
  • Virus reaches other tissues, targets the endothelial cells and causes vasculitis
  • Viremia can persist for 21 days! FFS!
157
Q

What is the reason for vaccine failure in EIV?

A

Antigenic drift

158
Q

What is your interpretation of high titers for aspergillosis?

A

Is common from environmental exposure

  • Definitive diagnosis is by culture*, IHC, IF
159
Q

What kind of immunologic response occurs in severe equine asthma?

A

Th2 response, IgE mediated

160
Q

What stage of D. arnfieldi is in the bronchi?

A

L5, is retained in non-patent infection

But remember, horse also patent infection

161
Q

What test should be used to certify a horse negative for Glanders?

A

IDT

162
Q

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

A

SeM ELISA? Nasal PCR?

163
Q

What three countries are free of EIV?

A

Australia, New Zealand and Iceland.

164
Q

What virulence factor is requiered for R. equi to grow within the macrophages?

A

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.

165
Q

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

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

A

d. Titer < 1:3200

166
Q

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?

A

ipratropium bromide

167
Q

Where are the places for latency of EHV-1?

A
  • Trigeminal ganglion
  • Lymphoreticular system
168
Q

Which animals are at higher risk for infection with equine adenovirus

A
  • Arabian foals with SCID
  • Immunocompromised animals
169
Q

Which bronchodilator can be used in a case of RAO? ©

A

Ipratropium

170
Q

Which cell is required for complete pulmonary clearance of R. equi

A

T lymphocytes (> CD4+)

171
Q

Which diagnosis with high Se and Sp can be used for Conidiobolomycosis?

A

Serum antibodies

172
Q

Which disease is difficult to erradicate with vaccination and isolation? ©

A

Equine Influenza Virus

173
Q

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

A

VapA

174
Q

Which immunological response is detrimental for foals infected with R. equi?

A

Th 2 response:

Predicted to develop potentially life-threatening pulmonary lesions

175
Q

Which infectious agents can cause lung infections in utero?

A
  • EVA
  • EHV-1, 4
176
Q

Which inflammatory mediators are upregulated in cases of severe equine asthma?

A
  • IL-8
  • IL-1b
  • TNF-a
177
Q

Which is the desired immunological response in cases of R. equi pneumonia?

A

Type 1 response:

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.

178
Q

Which is the desired immunological response in cases of R. equi pneumonia?

A

Type 1 response:

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.

179
Q

Which lineage of EIV is currently circulating?

A

H3N8

180
Q

Which receptor does R. equi use for entry in the macrophage

A

Mannose receptor in the macrophage that recognized lipoarabinomannan (LAM) in the bacterium

181
Q

Which receptor does R. equi use for entry in the macrophage

A

Mannose receptor in the macrophage that recognized lipoarabinomannan (LAM) in the bacterium

182
Q

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

A

IL-4 receptors –> enhances IL-8 production

183
Q

Which test is more sensitive than culture for diagnosis of strangles?

A

PCR → SeM protein, the gene for the antiphagocytic M protein

  • Guttural pouch sampling is the most reliable
  • > Se than culture, always use in combination

What is the detection rate? ~90%

184
Q

Which toxicity causes congenital tracheal stenosis in lambs?

a. perilla ketones
b. pyrrolizodine alkaloids
c. Californicum veratrum
d. Perennial ryegrass

A

c. Californicum veratrum

185
Q

Why antifungals like azoles or amphotericin B are not effective against pneumocystosis?

A

Pneumocystis carinii lacks ergosterol! FML!

186
Q

Why are adult horses more resistent to R. equi pneumonia?

A

Developement of R. equi-specific CTLs

187
Q

Why are foals more susceptible to R. equi pneumonia?

A
  • Deficient in CTL
  • Ag presenting cells have decrease CD1, MHC II expression
  • IFN-g deficiency and Th2 bias
188
Q

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

A

No! It can worsen the V/Q mismatch

Use low tidal volumes

189
Q

Zoonotic in dog and horse?

A

Blastomycosis?

Respiratory LA (5 decks)

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