Resp2- Equine Resp

  1. What are the major equine respiratory viruses?
    EHV-1, EHV-4, EIV
  2. What are the 3 syndromes associated with EHV1/4?
    equine rhinopneumonitis, equine herpesviral myeloencephalopathy, equine herpetic abortion
  3. What are the slight differences b/w EHV-1 and -4?
    • EHV-1: URT infection, abortion, severely compromised foals (fatal), neurologic disease
    • EHV-4: primarily associated with MILD URT disease (but can also cause all the stuff listed above)
  4. What horses usually get disease caused by EHV-1 and -4?
    weanling-aged foals (2-6months old)
  5. What's usually the source of rhinopneumonitis in weanling foals?
    mom- clinically silent reactivation of latent EHV at foaling; foals develop clinical signs when maternal antibody wanes
  6. What are clinical signs of rhinopneumonitis? (6)
    [MILD] fever, serous nasal d/c, cough, inappetence, submandibular lymphadenopathy, +/- secondary bacterial infection
  7. EHV-4 rhinopneumonitis is usually limited to _____(2)_____.
    URT epithelium, regional lymph nodes
  8. EHV-1 rhinopneumonitis commonly causes... (4)
    URT infection in weanlings, death in neonates, abortion, myeloencephalopathy [last 3 are VERY rare with EHV-4 but can happen]
  9. Neuropathogenecity is associated with a(n) __________; the associated clinical syndrome is...
    mutation in viral DNA polymerase gene; cauda equine syndrome/ ascending myelitis
  10. Is EHV-1 myeloencephalopathy infectious?
    YES can be spread from affected horses to in-contact animals
  11. How is EHV-1 diagnosed? (4)
    virus isolation (nasal swab, whole blood), PCR (nasal swab, whole blood, fetal tissue), fluorescent antibody (nasal swab, fetal tissue), serology (serum)
  12. How is rhinopneumonitis caused by EHV-1 and -4 treated? (2)
    [supportive] NSAIDs, ventilation, +/- antiviral drugs
  13. What is the prognosis for recovery for EHV-1?
    • respiratory disease: uncomplicated
    • abortion: good prognosis for future fertility
    • neurologic disease: fair to good if not recumbant, guarded is recumbant
  14. What is important to remember about vaccination for EHV-1?
  15. Equine influenza viruses are ____________ that undergo __(2)__ frequently.
    orthomyxoviruses; antigenic drift and shift
  16. What are the 2 subtypes of influenza virus that are pertinent in horses?
    H3N8, H7N7 (not documented in 20 years)
  17. How is EIV transmitted?
    inhalation of aerosols, fomites- HIGHLY contagious
  18. What population of horses are most affected by EIV?
    2 year olds at a racetrack
  19. What is often sequelae to EIV infection?
    serious secondary bacterial infection (ciliated respiratory epithelium denuded)
  20. In what populations is EIV fatal? (3)
    naive populations, donkeys, neonates born to unvaccinated dams
  21. EIV initiates the _________, which leads to rapid spread throughout the __________.
    lytic replication cycle; respiratory tree (LRT)
  22. EIV has a(n) _________ incubation period; clinical signs include... (4)
    short; fever, dry hacking cough, serous oculonasal d/c, regional lymphadenopathy
  23. What secondary bacterial infections occur with EIV?
    bronchopneumonia most serious, but all levels of respiratory tree can be affected
  24. How do you diagnose EIV?
    clinical signs, outbreak/multiple horses affected, [acute] nasal swab for PCR
  25. Treatment for EIV. (6)
    rest/3-4 weeks off even if they look fine, ventilation, NSAIDs, soft diet, monitor/treat secondary bacterial infections, +/- amantadine/rimantadine (antivirals)
  26. How can you prevent EIV outbreaks?
    vaccination!- modified live intranasal
  27. Unique to EIV, when should first vaccination occur?
    6-9 months old b/c vaccinating too early might make them anergic against future vaccinations (hyporesponders)
  28. What is the main primary respiratory bacterial pathogen in adult horses?
    Strep equi
  29. What is the result secondary (opportunistic) respiratory bacterial pathogen in adult horses?
    septic pleuropneumonia
  30. What is the main respiratory bacterial pathogen in weanling foals?
    Rhodococcus equi
  31. What animals are susceptible to Strep equi?
    any equids who haven't already had it (protective immunity)
  32. In an outbreak of Strep equi, what role to immune horses play?
    do not develop infection but can serve as asymptomatic carriers/ transmit disease
  33. Why "should" strangles be easy to eradicate? (3)
    only colonizes equids, fever occurs ~48 hrs before they nasally shed organism (can isolate infected animals prior to transmission), easy to kill in environment
  34. Even though strangles should be easy to eradicate, why isn't it? (3)
    asymptomatic carriers, organism shed 3-4 weeks post-recovery, intermittent shedding may persist for months to years
  35. How do you ID an asymptomatic carrier of strangles?
    gutteral pouch lavage with saline, catch it as it flows out of the horse's nose (through eustachian tube) [endoscopy]-->bacterial culture and PCR
  36. What populations are at low, medium, and high risk populations for strangles?
    • Low: closed populations that do not travel
    • Medium: closed populations that travel
    • High: open populations (frequent mixing/new arrivals)
  37. Describe the pathogenesis of strangles. (4)
    adhesion to respiratory epithelium--> invasion of lamina propria--> entry into lymphatic--> evasion of phagocytosis
  38. What lymph node chains are most likely to be affected with strangles? (2)
    submandibular lymph nodes, retropharyngeal lymph nodes
  39. How does strangles lead to gutteral pouch empyema?
    rupture of retropharyngeal ln dorsally into gutteral pouch
  40. What surface protein is measured as a titer in some non-typical cases of strangles?
    M protein
  41. How do we diagnose acute strangles? (3)
    bacterial culture (nasal swab, nasopharyngeal lavage, ln aspirate), PCR, serology- serum M protein titer (most sensitive)
  42. What should you do before vaccinating a horse for strangles and why?
    test M protein titers; vaccination is contraindicated in animals with high M protein titers because it can lead to immune reaction/ purpura hemorrhagica
  43. How do you treat strangles? (3)
    supportive care, quarantine, +/- penicillin (if severe, tracheostomy if can't breathe, metastatic abscessation, purpura hemorrhagica)
  44. What are potential complications of strangles? (5)
    URT obstruction (tracheostomy asap!), gutteral pouch empyema, immune-mediated purpura hemorrhagica/ myositis, metastatic abscessation (bastard strangles), membranous glomerulonephropathy
  45. What is purpura hemorrhagica?
    immune-mediated vasculitis, type III hypersensitivity a few weeks after recovering from strangles or post-vaccination (high serum M protein titer)
  46. How do you treat purpura hemorrhagica? (3)
    penicillin, immunosuppressive doses of dexamethasone, supportive care
  47. How can you deem a carrier "clean"?
    three negative gutteral pouch lavages at weekly intervals [expensive]
  48. How can you prevent strangles? (2)
    inactivated M protein derivative vaccine, modified live intranasal strangles vaccine
  49. When are foals infected with Rhodococcus?
    EARLY- within the first 7-10 days of life
  50. What is the most important virulence factor of Rhodococcus?
    VapA gene
  51. What disease is most commonly caused by Rhodococcus in weanling foals?
    pyogranulomatous bronchopneumonia
  52. What disease is most commonly caused by Rhodococcus in adult horses?
    immune compromise
  53. What is a public health concern associated with Rhodococcus equi?
    people with AIDS can get severe disease caused by R. equi
  54. Clinical signs of R. equi in foals.
    fever, +/- cough, +/- nasal d/c
  55. How do you diagnose R. equi in foals?
    trans-tracheal wash for bacterial culture [definitive], radiographs are suggestive
  56. What is the classic radiographic lesion in foals with R. equi?
    cotton ball abscesses- pyogranulomas- consolidations
  57. How do you treat R. equi in foals? (2)
    macrolide antimicrobial (erythromycin, Clarithromycin, Azithromycin) in combination with Rifampin [continue until normal thoracic rads, normal bloodworm, normal foal]
  58. Foals do not ________ when they are on a macrolide; therefore...
    sweat; can lead to hyperthermia (do not exercise, house in cool, shaded area)
  59. How can you prevent R. equi? (6)
    lower stocking density, avoid dirt lots for neonates, hyperimmune plasma for prophylaxis, screening, prophylactic macrolides (yikes.....not recommended)
  60. Equine shipping fever is _____________.
    septic bacterial pleuropneumonia
  61. What are risk factors for pleuropneumonia? (8)
    distance travel, heads tied up during transport,  insufficient time with head lowered during breaks (mucociliary elevator), viral disease (esp. influenza), stress/immunosuppression, racehorses, poor dentition/choke, general anesthesia
  62. What organisms are associated with equine pleuropneumonia? (4)
    Strep equi subsp zooepidemicus, Actinbacillus equuli, Anaerobes, +/- coliforms
  63. Clinical signs of pleuropneumonia. (5)
    fever, tachypnea, purulent hemorrhagic nasal d/c, anorexia, injected MMs
  64. How do you diagnose pleuropnemonia? (3)
    trans-tracheal wash for culture, +/- thoracocentesis for culture [TTW more important], US chest
  65. How do you treat pleuropneumonia? (6)
    thoracic drainage (thoracocentesis), broad spectrum antibiotics (penicillin, gentamicin, metronidazole), fluids, NSAIDs, laminitis prophylaxis, respiratory support
  66. Complications associated with pleuropneumonia. (6)
    laminitis, thrombophlebitis, pleural adhesions, thoracic abscess, cachexia, cellulitis near chest tube
  67. The most common non-infectious lower airway disease of horses.
    recurrent airway obstruction (Heaves, RAO)
  68. In what horses does RAO occur?
    10-15 year old horses in the northern hemisphere with moist, cool climates
  69. Describe the pathophysiology of RAO.
    inhale particulates--> inflammation of airway d/t hypersensitivity to inhaled molds/organic dusts--> elaboration of cytokines in airways--> neutrophil chemoattraction and influx
  70. What are the 3 most important pathologies associated with RAO?
    neutrophilic airway inflammation, bronchoconstriction/increased airway reactivity, mucus production
  71. What are the end pathophysiologic results of RAO? (4)
    small airway obstruction, expiratory small airway collapse, peripheral air trapping, hypoxemia
  72. What are clinical signs of RAO? (5)
    [episodic and progressive] cough at work and when fed, expiratory effort, nostril flaring at rest, nasal d/c, exercise intolerance
  73. How do you definitively diagnose RAO?
    bronchoalveolar lavage for fluid cytology >20% non-degenerate neutrophils
  74. How do you environmentally manage RAO? (6)
    put the horse outside all the time, stalls near end of barn/away from hay storage (if can't be outside all the time), low particulate bedding options/wet down bedding, low particular forage, wet down feed/ hay steamer, DON'T feed round bale hay/moldy shit
  75. What drugs are used to manage RAO? (4)
    corticosteroids (prednisolone, dexamethasone), [bronchodilators] beta 2 agonists (albuterol, clenbuterol), muscarinic antagonists (atropine, glycopyrrolate); topical (inhaled) corticosteroids and bronchodilators
  76. Exercise-induced pulmonary hemorrhage (EIPH) usually affects...
    young athletes/ racehorses
  77. Risk factors for EIPH.
    breed (Tbs and STBs) and speed
  78. What causes EIPH?
    alveolar capillary rupture with consequent extravasation of blood into the pulmonary alveoli and interstitium
  79. How do you diagnose EIPH? (3)
    visual inspection, tracheobronchoscopy within an hour or 2 of work, bronchoalveolar lavage shows RBCs, Erythrophages, hemosiderophages
  80. What drug is used to manage EIPH?
    furosemide (also performance enhancing in horses that are not bleeders...)
  81. Clinical findings with URT obstruction. (4)
    inspiratory stridor, tachypnea, sweating, anxiety
  82. What is the treatment for URT obstruction?
    tracheostomy tube!!!!!!! ASAP, treat underlying condition
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Resp2- Equine Resp
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