Resp2- Swine Resp Dz

  1. What are the most common viral agents involved with PRDC? (3)
    porcine reproductive and respiratory syndrome virus (PRRSv), porcine circovirus type II (PCV2), influenza A virus (IAV)
  2. What bacterial agents are most commonly associated with PRDC? (8)
    Mycoplasma hypopneumoniae, pasteurella multocida, Actinbacillus pleuropneumonia (APP), Bordatella bronchispecitica, Strep suis, Haemophilus parasuis, Actinobacillus suis, Salmonella choleraesuis
  3. Clinical signs of PRDC? (6)
    fever, anorexia, lethargy, coughing, gauntness, labored breathing ("thumping")
  4. Acute outbreak of fever and a barking cough leads you to think of _________.
  5. Thin, fuzzy, thumping nursery pigs leads you to think of _________.
  6. Wasting pigs in finisher with respiratory disease and loose stools leads you to think of _________.
  7. Anteroventral consolidation (bronchopneumonia) is a result of... (5)
    Mycoplasma hyo, IAV, Bacterial [P. multocida, Strep suis, Haemophilus parasuis]
  8. Interstitial pneumonia is a result of... (5)
    PRRSV, PCV2, bacterial septicemia (Salmonella cholerasuis, Strep suis), ascarid larval migration
  9. PRRSV is a(n) __________ virus; therefore, it should be _________.
    enveloped; easy to kill
  10. What makes PRRSV so hard to prevent and treat?
    mutates at an unusually rapid rate
  11. PRRSv is _______ infectious; it is transmitted by... (6)
    highly; direct contact, aerosol, fomites (on your boots!), semen from boar studs, needles, +/- biting insects
  12. Does immunity to one strain of PRRSv protect against other strains?
  13. What is the most significant (dollar-wise) disease in the swine industry?
    PRRSv [widespread cause of abortion and respiratory disease]
  14. ________ is an important trigger for clinical PCV2 infection.
  15. Clinical signs associated with PRRSv infection? (7)
    dyspnea, tachypnea, ill-thrift, poor growth, grower/feeder pigs, rarely fatal in adults; subclinical infections common
  16. PRRSv targets ________ [cell type]; primary sites in acute disease include... (2)
    macrophages; lung, lymphoid tissue [chronic--> kidney, spleen, spleen, heart, thymus, lymph nodes, tonsils]
  17. What gross lesions are seen with PRRSv? (2)
    diffuse interstitial pneumonia (red, rubbery, non-collapsing), diffuse lymph node enlargement
  18. All strains of PRRSv induce __(2)__.
    lymphadenopathy and hyperplasia of lymphoid follicles
  19. How do you diagnose PRRSv? (4)
    PCR, virus sequencing (to determine what strain), ELISA, immunohistochemistry
  20. Are vaccines effective at controlling PRRSv?
    No- lack of protection b/w strains
  21. When trying to control PRRSv, the focus should be on...
    stopping PRRSV transmission from sow to pig
  22. PCV2 causes __________, which is...
    porcine circovirus associated diseases (PCVAD); a slew of diseases that may be a result of initial viral infection.
  23. PCV2 is found in ___________; it does/does not always cause disease when present.
    healthy pigs; does not
  24. How can you attribute disease to PCV2? (3 criteria)
    clinical signs (wasting), lymphoid depletion, isolate PCV2 virus
  25. Lesions associated with PCV2? (4)
    interstitial pneumonia, ulcerative bronchiolitis, peribronchiolar inflammation and fibroplasia, granulomatous inflammation in septae
  26. What tissues need to be addressed/ sent out when diagnosing PCV2? (5)
    tonsil, lymph nodes, spleen, peyer's patch (ileum), lung
  27. Clinical signs of PCV2? (2)
    wasting/ ill thrift, marked lymphadenopathy
  28. What is the focus when trying to control PCV2? (4)
    decreasing stress, improving pig comfort (stocking density, minimize regrouping pigs- all in, all out), vaccinate, ID and control concurrent diseases
  29. Influenza A virus is a(n) _________ virus; it is hard to vaccinate for because... (2)
    enveloped; lots of antigenic drift (point mutations) and antigentic shift (genetic reassortment)
  30. Clinical signs of IAV. (7)
    coughing/ sneezing, nasal d/c, fever, lethargy, decreased appetite, ill thrift, abortions
  31. Why does IAV cause abortions in sow units?
    the sow gets a fever--> abortion; does NOT directly attack fetus/repro tract
  32. Recovery from IAV is _______ if it is a(n) _________ infection.
    rapid; uncomplicated
  33. The 2009 flu pandemic was caused by _______.
    H1N1 (IAV)
  34. After the 2009 flu pandemic, the USDA began a surveillance program to monitor... (4)
    trends in virus prevalence, emergence of new subtypes, interspecies transmission events, baseline to develop intervention strategies
  35. With acute flu in pigs, there is ________ morbidity and ________ mortality; recovery occurs within _________.
    high; low; 2-6 days [if uncomplicated]
  36. With chronic flu in pigs, it is difficult to distinguish from ___________; chronic flu is more common in ___________ operations.
    Mycoplasma; continuous flow (not all in, all out)
  37. IAV is usually seen in pigs __________ of age.
    over 12 weeks
  38. What are gross lesions of IAV?
    patchy consolidation in anteroventral lung lobes
  39. What are antemortem diagnostics for IAV in pigs? (3)
    nasal swabs, oral fluids, snout wipes--> PCR, ELISA, serology
  40. What are post-mortem diagnostic for IAV in pigs? (2 tissues you must send out)
    lung tissue and nasal swab- send out
  41. How do you prevent IAV on pig operations? (2)
    prevent new introductions (all in, all out- biosecurity), vaccine gilts as they come in and pre-farrowing [vaccine isn't great...can do without this]
  42. Infection with Mycoplasma hyo is also known as ____________; characteristics of this bacterium include... (3)
    enzootic pneumonia; lacks cell wall, gram-neg, survives up to 27d in wet environment.
  43. One of the most common and economically important diseases of swine.
    Mycoplasma hyo [decreased growth, lower feed efficiency]
  44. What age animal are usually affected by Mycoplasma hyo?
    >6 weeks of age because very long incubation period (21 days)--> stress of weaning aids in establishment of active infection
  45. Describe the pathogenesis of Mycoplasma hyo infection.
    attached to ciliated cells of upper airways--> damage cilia/decrease motility--> impaired mucociliary clearance--> secondary infections
  46. What are the clinical signs of the acute and chronic phases of infection with Mycoplasma hyo? (acute 3, chronic 3)
    • Acute: moderate fever, decreased feed intake, +/- diarrhea
    • Chronic: chronic dry hacking cough, increase in severity of cough over time, +/- dyspnea with secondary infection
  47. Chronic Mycoplasma hyo infection has ________ morbidity and ________ mortality.
    high; low
  48. Describe the gross necropsy findings with Mycoplasma hyo infection.
    well-demarcated, tan, anteroventral consolidation
  49. What is a characteristic finding on histopath of animals infected with Myoplasmal pneumonia?
    peribronchiolar lymphoid hyperplasia
  50. How is Mycoplasma hyo diagnosed ante mortem? (3)
    immunohistochemistry, PCR, serology (ELISA)
  51. Describe Myoplasma hyo control in swine herd. (4)
    • All in, All out (AIAO)
    • Medicated Early Weaning (MEW)
    • Vaccination (these vaccines actually work!)
    • Medication for txt/control: Lincomycin, tetracycline, tiamulin, pulmotil
  52. Both IAV and Mycoplasma hyo have _________ lesions associated with disease; tell them apart by....
    anteroventral; patchy AV consolidation (IAV) versus consolidation of entire AV lobe (Mycoplasma)
  53. What are the 2 primary differentials for hemorrhagic and necrotizing pleuropneumonia?
    Actinobacillus pleuropneumonia (APP) and Actinobacillus suis
  54. How is APP transmitted?
    moderately resistant in environment, direct contact, droplets over a short distance [pigs that survive remain carriers]
  55. What are the clinical signs of acute outbreaks of APP? (6) Signs of chronic infection? (2)
    • Acute outbreak: sudden death of finisher hogs, high fever, prostration, dyspnea, bloody d/c, no eating/DRINKING
    • Chronic: chronic cough, slow growth
  56. APP causes __________; many pigs harbor the organism and _________ causes clinical disease.
    contagious pleuropneumonia; environmental stresses (temperature fluctuations, etc)
  57. What lesions are associated with APP? (4)
    [dorso-caudal lungs] blood tinged fluid in thorax, bloody froth in airways, fibrinous pleuritis, large areas of hemorrhage
  58. What are ante mortem tests for APP? (4)
    culture followed by serotyping, serology (complement fixation, ELISA, hemolysin neutralization)
  59. How do you control APP? (6)
    ANTIBIOTICS ASAP- Penicillin, Ceftiofur, Tulathromycin, improved ventilation, difference source for pigs in the future, +/- vaccines (not that great)
  60. Describe Actinbacillus suis in healthy pigs.
    resides in tonsils, nostrils, vaginas--> subclinical infection is widespread, clinical infection is sporadic
  61. What is the most commonly affected group with A. suis infections?
    suckling and recently wean pigs (2-4 wks old)--> found dead
  62. What clinical signs are associated with active A. suis infection in the following groups:
    Nursery pigs (6)
    Grow/Finish pigs (4)
    Adults (4)
    • Nursery pigs: sudden death, fever, anorexia, polyserositis, arthritis, pneumonia
    • Grow/Finish pigs: sudden death, pneumonia, fever, coughing
    • Adults: lethargy, anorexia, reproductive infections in sows, red rhomboid skin lesions
  63. What diseases must you be sure to rule out when diagnosing A. suis in the following groups:
    Nursery pigs (2)
    Grow/Finish pigs (1)
    Adults (1)
    • Nursery pigs: Strep suis, Haemophilus parasuis
    • Grow/Finish pigs: APP
    • Adults: Erysipelas
  64. How is definitive determination b/w A. suis and APP currently performed?
    culture [CANNOT be reliably differentiated based on gross or microscopic lesions]
  65. How do you control A. suis infections? (6)
    • Antibiotics ASAP- Ceftiofur and Ampicillin (+/- penicillin and tetracycline)
    • Sanitation, ventilation, temperature control, stocking density
  66. What bacteria is strictly secondary, ie. is NOT  a primary cause of pneumonia?
    Pasteurella multocida
  67. How do you diagnose P. multocida ante mortem? (2)
    culture and sensitivity- FIND PRIMARY CAUSE
  68. What are etiologies of atrophic rhinitis? (2)
    • Bordatella bronchiseptic - atrophic rhinitis [reversible, mild]
    • Pasteurella multocida- progressive atrophic rhinitis [permanent turbinate atrophy]
  69. What are clinical signs of atrophic rhinitis? (4)
    deviated snout, tear staining, sneezing (esp in nursery), bleeding/crusting of nostrils/snout
  70. Atrophic rhinitis causes _________ morbidity and _________ mortality.
    high; low
  71. What is the most costly aspect of atrophic rhinitis?
    retardation of growth
  72. What is the predominant gross lesion associated with atrophic rhinitis?
    atrophy of the turbinate bones
  73. How is atrophic rhinitis diagnosed? (4)
    deviation/shortening of snout, culture, PCR, probes
  74. The severity of atrophic rhinitis is influenced by... (4)
    air quality, genetics (yorkshires), immunity of dams, weaning age (<14d elliminated transmission)
  75. How do you control atrophic rhinitis? (3)
    vaccination (esp. of sows), medication (oxytetracycline, ceftiofur), environmental management
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Resp2- Swine Resp Dz
vetmed resp2