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Food animal production > Respiratory diseases of pigs > Flashcards

Respiratory diseases of pigs Flashcards

1
Q

What is an upper respiratory disease of pigs caused by toxigenic pasturella multocida?

A

progressive atrophic rhintis

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2
Q

What is an upper respiratory disease of pigs caused by toxigenic pasturella multocida?

A

progressive atrophic rhintis

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3
Q

What causes non-progressive rhinitis in pigs?

A
  1. bordetella bronchiseptica

2. procine cytomegalovirus (inclusion body rhinitis)

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4
Q

What causes progressive rhintis?

A
  1. toxogenic pasturella multcida +/- 2. other agents which enhance colonization (bordetella, cytomegalovirus),
  2. environmental (high ammonia, dust)
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5
Q

What is the epidemiology of progressive rhinitis?

A
  1. agents causing rhinitis wide-spread
  2. toxigenic PM limited to herds with progressive atrophic rhinitis
  3. horizontal transmission (sow piglet, piglet-piglet)
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6
Q

What age of pig gets INFECTED with progressive atophic rhinitis?

A
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7
Q

What is the pathogenesis of progressive atrophic rhintis?

A
  1. pre-existing damage to mucosa assists colonization of TPM (infections, environmental)
  2. infection with TPM
  3. dermonecrotic toxin production
  4. permanent turbinate destruction
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8
Q

What does toxogenic pasturella multocida produce and what does it do?

A 
Dermonecrotic toxin
causes
1. decreased osteogenesis
2. increased osteolysis
==>turbinate damage
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9
Q

What are the clinical signs of progressive atrophic rhinitis in an ENDEMICALLY INFECTED FARM

A

sneezing (SUCKING AND NURSERY PIGS)
little or no epistaxis
little or no snout deviations
SUBCLINICAL TURBINATE ATROPHY

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10
Q

What are the clinical signs of progressive atrophic rhinitis in an ENDEMICALLY INFECTED FARM

A

sneezing
little or no epistaxis
little or no snout deviations
SUBCLINICAL TURBINATE ATROPHY

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11
Q

What causes non-progressive rhinitis in pigs?

A
  1. bordetella bronchiseptica

2. procine cytomegalovirus (inclusion body rhinitis)

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12
Q

What causes progressive rhintis?

A
  1. toxogenic pasturella multcida +/- 2. other agents which enhance colonization (bordetella, cytomegalovirus),
  2. environmental (high ammonia, dust)
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13
Q

What is the epidemiology of progressive rhinitis?

A
  1. agents causing rhinitis wide-spread
  2. toxigenic PM limited to herds with progressive atrophic rhinitis
  3. horizontal transmission (sow piglet, piglet-piglet)
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14
Q

What space is used to check for turbinate atrophy in progressive atrophic rhinitis?

A

the space between the nasal septum and the vental scroll (plus check septal deviation, dorsal space)

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15
Q

What is the pathogenesis of progressive atrophic rhintis?

A
  1. pre-existing damage to mucosa assists colonization of TPM (infections, environmental)
  2. infection with TPM
  3. dermonecrotic toxin production
  4. permanent turbinate destruction
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16
Q

What does toxogenic pasturella multocida produce and what does it do?

A 
Dermonecrotic toxin
causes
1. decreased osteogenesis
2. increased osteolysis
==>turbinate damage
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17
Q

What are the clinical signs of rhintis?

A 
sneezing
nasal discharge (no blood)
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18
Q

What are the clinical signs of progressive atrophic rhinitis in an ENDEMICALLY INFECTED FARM

A

sneezing
little or no epistaxis
little or no snout deviations
SUBCLINICAL TURBINATE ATROPHY

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19
Q

What are the clinical signs of progressive atrophic rhinitis in a NAIVE FARM (epizootic)

A
  1. severe sneezing (ANY AGE)
  2. NASAL HEMORRHAGE (any age)
  3. lacrimation
  4. facial deformities (chronic)
  5. growth retardation (grow finish)
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20
Q

How does toxigenic pasturella multocida cause growth retardation

A
  1. metabolic impact of toxin

2. reduced feed intake due to facial deformities

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21
Q

How is progressive atrophic rhinitis diagnosed?

A
  1. facial deformities, epistaxis (herd basis)
  2. sneezing (NOT pathopneumonic)
  3. tubinate atrophy @slaughter
  4. deep nasal swab–culture, ID toxin–ELISA, PCR
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22
Q

Where is the snout sectioned to look at progressive atrophic rhinitis?

A

at the level of the first/second premolar

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23
Q

What is the epidemiology of mycoplasma hyopneumoniae?

A
  1. two to three weeks
  2. horizontal transmission (sow-piglet, pig-pig)
  3. expression in GROWER PIGS >10WEEKS
  4. REGIONAL spread via aerosol-water droplets (although poor environmetnal survival)
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24
Q

What are two snout score thresholds that indicate PAR requiring intervention

A

multiple individual scores >3.5

average score >1

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25
Q

What are the principles of progressive atrophic rhinitis control

A
  1. decrease concurrent colonization (improve air quallity, separate age groups, feed medication)
  2. antimicrobials targeted at TPM (prior and after weaning)–oxytet parenteral and feed Ab
  3. vaccination of sow herd–pre-farrowing (passive immunity)
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26
Q

What must a vaccine for progressive atrophic rhinitis contain?

A

TPM, Bb, toxoids

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27
Q

Why should you do a pre-farrowing vaccination of breeding herd for PAR

A

to enhance passive and mucosal immunity

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28
Q

What causes enzootic penumonia?

A

mycoplasma hyopneumoniae

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29
Q

What is a contributor to procine respiratory disease complex

A

mycoplasma hyopneumoniae

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30
Q

What is severity of enzootic penumoniae influenced by?

A
  1. MH strain
  2. pig flow
  3. animals per air space
  4. pen density
  5. air quality
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31
Q

Should you use culture to diagnose mycoplasma hyopneumoniae?

A

NO!

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32
Q

What is the epidemiology of mycoplasma hyopneumoniae?

A
  1. two to three weeks
  2. horizontal transmission (sow-piglet, pig-pig)
  3. expression in GROWER PIGS >10WEEKS
  4. regional spread via aerosol
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33
Q

Is the epizootic herd presentation of mycoplasma hypneumoniae common or uncommon?

A

uncommon

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34
Q

What are the issues with using serology to diagnose mycoplasma hyopneumoniae at the herd level?

A

No correlation between vaccine titre and protection
seroconversion HIGHLY VARIABLE and may require 6wks in natural infection
LOW SENSITIVITY–not for individual pig (but specificity high)

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35
Q

Does toxogenic pasteurella multocida spread regionally?

A

no

36
Q

What is the endemic herd presentation of mycoplasma hyopneumoniae?

A
  1. chronically infected herds
  2. exposed in GROWER BARN
  3. coughing in early grower period
  4. high morbidity, low mortality
37
Q

What is the treatment and control for mycoplasma hyopneumoniae?

A
  1. vaccination of sow, nursery, grower
  2. strategic medication
  3. environmental control
  4. control other resp pathogens and ascarids (PRDC)
38
Q

What are the clinical signs of Mycoplasma hyopneumoniae?

A
  1. non-productive, dry raspy cough (uncomplicated)
  2. productive coughing if concurrent infections
  3. tacypnea, dyspnea
  4. uneven growth rates
39
Q

What is severity of enzootic penumoniae influenced by?

A
  1. MH strain
  2. pig flow
  3. animals per air space
  4. pen density
  5. air quality
40
Q

What environmental control can be done to prevent m. hyo pneumoniae infection?

A

improve indoor air quality

segregate age groups

41
Q

How is mycoplasma hyopneumoniae diagnosed on an individual basis?

A

FAT-antigen

PCR-DNA

42
Q

How is mycoplasma hyopneumoniae diagnosed on a population basis?

A
  1. Serology
  2. slaughter check scoring
  3. confirmatory testing (PCR, FAT on slaughter lungs)
43
Q

What are the issues with using serology to diagnose mycoplasma hyopneumoniae at the herd level?

A

No correlation between vaccine titre and protection
seroconversion HIGHLY VARIABLE and may require 6wks in natural infection
LOW SENSITIVITY–not for individual pig (but specificity high)

44
Q

What are lungs score intervention levels for mycoplasma hyopneumoniae

A

individual lesions scores >5%

prevalence of infected lung >15-20%

45
Q

Why might confirmatory testing of lungs at slaughter for myccoplasma hyopneumoniae be unreliable?

A
  1. comingling of positive and negative pigs at assembly yard

2. scalding tank

46
Q

What is the treatment and control for mycoplasma hyopneumoniae?

A
  1. vaccination of sow, nursery, grower
  2. strategic medication
  3. environmental control
  4. control other resp pathogens and ascarids (PRDC)
47
Q

What are different vaccination strategies that can be used to control mycoplasma hyopneumoniae?

A
  1. vaccinate sows, then delay piglet vaccination until maternal antibodies dropped
  2. vaccinate progeny (suckling or nursery)
48
Q

Does antimicrobial medication eliminate m. hyo infection?

A

NO. reduce infection pressure and control bacteiral infections

49
Q

What environmental control can be done to prevent m. hyo pneumoniae infection?

A

improve indoor air quality

segregate age groups

50
Q

What are three diseases that cause coughing and dyspnea?

A
  1. mycoplasma hyopneumonia (enzootic pneumonia)
  2. swine influenza virus
  3. actinobacillus pleuropneumoniae
51
Q

What type of virus is the swine influenza virus?

A

type A influenza virus (orthomyxoviridae)

52
Q

What are the two ways swine influenza can evolve?

A

drift–point mutations

shift–reassortment

53
Q

What was the original source of swine influenza virus?

A

humans

54
Q

What type of swine influenza was seen from 1930-1998?

A

classic swine H1N1

55
Q

What type of swine influenza emerged in 1998?

A

H3N2

56
Q

How did the H3N2 virus originate?

A

from triple reassortment from human, swine and avian

57
Q

What is the epidemiology of swine influenza?

A
  1. highly infectious
  2. most often late fall and winter
  3. direct contact (nasopharyngeal secretions)
  4. airborne spread in hog dense regions
58
Q

What is the pathogenesis of swine influenza?

A
  1. short incubation 1-3d
  2. rapid replication
  3. tropism for bronchiolar epithelium
  4. cytokine secretion
  5. epithelial cell necrosis
  6. exudate accumulation
  7. rapid virus clearance
59
Q

What are the signs of classic H1N1?

A
  1. explosive coughing (sudden onset)
  2. paroxysms “seal bark”
  3. high morbidity, low mortality
  4. rapid recovery 5-7d
60
Q

What are the clinical signs of modern swine fever?

A
  1. variable and potentially subtle resp signs
  2. all ages
  3. herd presentation varies
61
Q

What is the gross pathology of swine influenza?

A
  1. conjunctivitis and nasal discharge
  2. consolidation of cranial and middle lobes
  3. enlarged and edematous bronchial/mediastinal LN
  4. blood tinged fibrinous exudate
  5. interlobular edema
  6. gross lesions similar to mycoplasma hyopneumoniae
62
Q

What is the distribution of swine influenza in lung pathology?

A

anteroventral
consolidation
checkerboard appaerance

63
Q

What is the histopathology of swine influenza?

A

necrotizing bronchitis/bronchiolitis
airways/alveoli filled with exudate
bronchointerstitial pneumonia

64
Q

How is swine influenza diagnosed?

A
  1. histopathology (necrotizing bronchiolitis and bronchitis)

2. confirmation via PCR, IHC

65
Q

Why might a false negative occur with swine influenza?

A

lesions come and go very quickly

may get false negative >8 days post infection

66
Q

What kind of antibody is used with SIV IHC?

A

type A antibody

works in all species

67
Q

How is diagnosis of SIV done on a population level?

A
  1. serology–serotypes specific or generic
  2. PCR–nasal swabs
  3. genomic analysis
68
Q

When is the best time to collect a sample for SIV?

A

48 hr post exposure (24hr of showing signs)

69
Q

What are 4 aspects of treatment and control of SIV?

A
  1. anti-inflammatories
  2. antimicrobials (2ndry infection)
  3. improve indoor air quality
  4. vaccination–commercial vs autogenous
70
Q

What are the most virulent serotypes of actinobacillus pleuropneumoniae?

A

1
5
7

71
Q

What is the epidemiology of actinobacillus pleuropneumoniae?

A
  1. primarily horizontal transmission
  2. not likely to transmit between herds
  3. short incubation periods (6-12hrs)
72
Q

Which resp disease is likely to transmit between herds in hog dense areas: SIV or actinobacillus pleuropneumoniae?

A

SIV

73
Q

Severity of actinobacillus pleuropneumoniae depends on what?

A
  1. serotype
  2. exposure dose
  3. immune status of herd
  4. concurrent dz
74
Q

Which resp disease has an incubation period of 6-12hrs?

A

actinobacillus pleuropneumoniae

75
Q

What is the pathogenesis of actinobacillus pleuropneumoniae?

A
  1. colonize tonsils, alveolar epithelium
  2. phagocytosed by macrophages
  3. produce 4RTX exotoxins
  4. inflammatory cytokine production
  5. septic shock
  6. arteriolar thrombosis and alveolar necrosis
76
Q

What exotoxins does actinobacillus pleurpneumoniae produce?

A

4 RTX exotoxins (Apo I, II, III, IV)

77
Q

What do the exotoxins and the cytokines involved in actinobacillus pleuropneumoniae infection cause?

A
  1. septic shock (peracute death)

2. arteriolar thrombosis and alveolar necrosis

78
Q

What are the clinical signs of actinobacillus pleuropneumoniae?

A
  1. peracute: cyanosis, foamy bloody nasal discharge, found dead
  2. acute: dyspnea, coughing, agonal breathing
  3. chronic: chronic pleuritis–>chronic cough; reduced appetite/growth
79
Q

What is the pathology of peracute and acute actinobacillus pleuropneumoniae?

A

necrotizing and hemorrhagic pneumoniae
well demarcated, usually CAUDAL LOBES
focal pleuritis

80
Q

What is the pathology of chronic actinobacillus pleuropneumoniae

A
  1. chronic pleuritis and adhesions
  2. consolidation and necrosis
  3. pulmonary abscesses
81
Q

Why is pleuritis an important feature to look for when looking for actinobacillus pleuropneumoniae

A

because carcasses going through a scalding tank can look like they have hemorrhagic pneumoniae but they wont have pleuritis

82
Q

How is actinobacillus pleuropneumoniae diagnosed at the individual level?

A
  1. necrotizing hemorrhagic pneumoniae with focal pleuritis

2. culture and serology

83
Q

What types of serology is there for actinobacillus pleuropneumoniae?

A
  1. generic ELISA
  2. specific for individual serotype
    (remember some cross react)
84
Q

How is actinobacillus pleuropneumoniae controlled?

A
  1. environmental control
  2. strategic medication
  3. vaccination (serotype specific, autogenous)
85
Q

Does actinobacillus pleuropneumoniae vaccine protect against infection? are they used much in canada?

A

no and no

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