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3. Food Animal > Swine 7 > Flashcards

Swine 7 Flashcards

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1
Q

main respiratory diseases of swine

A
  • Mycoplasma hyopneumoniae
  • Swine Influenza Virus
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2
Q

Mycoplasma hyopneumoniae; other names

A
  • MH, M. hyo
  • Enzootic pneumonia
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3
Q

geographical distribution of Mycoplasmal Pneumonia of Swine? prevalence?

A
  • Widely distributed
    > worldwide, but maybe not Switzerland
  • COMMON
    > high prevalence
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4
Q

typcal type of disease caused by Mycoplasmal Pneumonia of Swine, and less common presentation? general symptoms? what type of operation is it common in and what time of year?

A
  • Chronic respiratory disease
    > there is a less common acute presentation
  • Coughing, reduced growth, reduced feed efficiency
  • Common in continuous-flow production
  • Occurs year round
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5
Q

significance of MPS? (3 things)

A
  • A major swine respiratory pathogen in N.A.
  • $$$$ very costly disease
  • Contributor to Porcine Respiratory Disease Complex (PRDC) along with other pathogenic respiratory bacteria & viruses
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6
Q

Features of M. hyopneumoniae: growth, sensitivity, survival?

A
  • Slow growth in culture: 4 to 8 wks
  • Poor antibiotic sensitivity
  • Poor survival in the environment
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7
Q

most common source of MPS?

A

n Carrier pigs most common source

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8
Q

MPS incubation time

A

Incubation 2-3 weeks

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9
Q

MPS transmission

A

Horizontal transmission:
- Sow-to-piglet: in crates
- Pig-to-pig: in nursery & grower

  • Regional spread via aerosol at least up to 3.2 km
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10
Q

at what life stage is MPS a problem generally

A

Typical expression in grower pigs (>10 wks old)
> Grower – Finisher Phase

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11
Q

MPS acute herd presentation;
-severity, ages affected, symptoms and signs

A
  • Uncommon
  • Acute outbreaks in naïve farms can be severe
  • All ages of pigs affected**
  • Pyrexia (40-41.5C), anorexia, depression
  • Severe respiratory signs:
    > dyspnea, coughing, extensive lung involvement
  • Some peracute deaths
  • Some abortions in pregnant sows due to pyrexia
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12
Q

MPS Endemic Herd Presentation;
- how it becomes a problem, signs and symptoms

A

(most common***)

  • Chronically infected herds
  • Susceptible (naïve) pigs exposed to M. hyopneumoniae upon entry to grower barn associated with:
    > Waning passive antibody
    > Shedding from older animals
  • Coughing develops 2-3 wks post-exposure, in the early grower period
  • High morbidity
  • Usually low mortality (unless complications arise)
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13
Q

MH/MPS clinical signs

A

Coughing:
- Uncomplicated: non-productive, dry raspy
- Productive coughing associated with concurrent infections (bacterial or viral)

Other signs:
- Tachypnea, dyspnea
- Uneven growth rates

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14
Q

Severity of MPS influenced by

A
  • MH strain
  • Pig flow
  • Overcrowding (vicious circle)
  • Poor air quality
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15
Q

MPS pathogenesis?
what increases severity?

A
  • MH colonizes trachea and bronchial epithelial cells
  • Clumps cilia > impairment of ciliary clearance
  • Accumulation of secretory & cellular debris gravitate from bronchi to alveoli
  • Secondary invasion: in virtually all naturally occurring MPS cases (mixed bacterial & viral infections)
  • Resolution in uncomplicated cases
  • Increased severity if infected concurrently with other respiratory pathogens à PRDC
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16
Q

MPS pathology

A

Bronchopneumonia (anteroventral (AV) consolidation)
- Cranial, middle & accessory lobes
- +/- cranial portion of caudal lobes
- Firm to touch (meaty)
- Deep red to dark purple colour
()
* Catarrhal exudate in airways on cut surface
* Enlarged, edematous mediastinal lymph nodes
* Characteristic (non-pathognomonic) histopathology
> Peri-bronchial lymphoid peribronchiolar hyperplasia “cuffing” - characteristic of M. hyopneumoniae
> Alveoli filled with debris and inflammatory cells
> Atelectasis

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17
Q

diagnostic methods for MPS (broadly)

A

A) Tissues (individual pigs):
B) Serology:
> herd testing – not helpful at at individual level
C) Slaughter check (herd testing)

18
Q

how to diagnose MPS in swine using tissues

A

A) Tissues (individual pigs):
* Gross: AV bronchopneumonia (suggestive)
* Histopathology: peri-bronchiolar lymphoid hyperplasia “cuffing” (suggestive)

Confirmation
* Culture: not feasible (slow growth)
* Demonstration of antigen:
§ **PCR – lung (including airway), bronchial fluid, trachea, nasal mucosa
§ Fluorescent antibody test (FAT) on lung (sample should include airway with ciliated epithelium)
§ IHC – rarely and not widely available **PLUS demonstration of histo lesions

19
Q

how to use serology to diagnose MPS? pros and cons?

A

Serology:
herd testing – not helpful at at individual level:
- IgG ELISA’s –DAKO, IDEXX
- Measures exposure but interpretation can be difficult:
§ Seroconversion highly variable (dose dependent)
§ May require up to 6 wks to induce IgG response following
natural infection
§ Cannot differentiate vaccine titres & natural infection
§ No correlation between vaccine titres and protection
§ Excellent specificity, but a few false positives occur
§ Sensitivity low

20
Q

diagnosis of MPS via slaughter check - how to do it, what info you can gain? what samples are not reliable and why?

A

Slaughter check (herd testing):
- Lung lesion scoring at slaughter to determine severity and prevalence of disease
- Likelihood of MH herd infection increases if:
§ Individual lesions score >5%
§ Prevalence of infected lungs >15-20%

  • PCR/FAT is unreliable on samples collected at slaughter
  • due to comingling of positive and negative pigs at the assembly yard and scalding tank
21
Q

4 methods for treatment and control of MPS

A
  1. vaccination
  2. strategic medication
  3. Environmental control
  4. Control other respiratory pathogens & ascarids
22
Q

how to use vaccines to prevent MPS? what can the vaccine do? when to vaccinate? how many doses? is this a common strategy? what to keep in mind about sows and vaccination timeline?

A

Vaccination of sow, nursery or grower herds:
§ Vaccine reduces prevalence & severity of lesions
§ Vaccine does not prevent colonization or infection
§ Vaccinate pigs 2-3 wks prior to expected exposure
§ One and two dose products available – selection depends on severity, infection pressure & cost
§ COMMON

  • If sows are vaccinated pre-farrowing, piglet vaccination must be delayed until after 6-8
    wks of age due to maternal antibody interference
23
Q

how to use strategic medication to treat MPS? when? how do they work and when are they useful?

A

Strategic medication prior to or during peak exposure:
- Antimicrobials reduce infection pressure but do not eliminate M. hyo infection
- Essential to control secondary bacterial infections
- Cost effective in grower, less so in finisher

24
Q

Antimicrobial programs for MPS

A

Chlortetracycline in feed, also tiamulin, tylosin
§ Feed (mass medication of population):
> Continuous during periods of infection/transmission
> Pulsed (ie 1 week on/1 week off)
§ Parenteral (treatment of individual animals)

25
Q

environmental control for MPS

A
  • Improve indoor air quality (NH3, dust, humidity)
  • Segregate age groups (AI/AO mgmt)
26
Q

Control other respiratory pathogens & ascarids: what to focus on to reduce problems with MPS

A

PRRS, PCV2, swine influenza, Strep suis, H parasuis, etc.

especially PRRS!

27
Q

influenza type A viruses of swine: type of virus, genome structure, genetic change over time mechanisms, and surface glycoprotein antigens

A
  • Type A influenza virus; Family Orthomyxoviridae
  • Enveloped with 8 segments SS RNA
  • Subject to genetic/antigenic evolution:
  • DRIFT: point mutations following dual infection
  • SHIFT: reassortment
  • Surface glycoprotein antigens:
    – “HA” – hemagglutinin
    – “NA”- neuraminidase
28
Q

historical swine influenza outbreaks - what is the suspected cause of the 1918 outbreak? what occurred from 1930-98?

A
  • “SIV”-like illness killed thousands of pigs in 1918
    > Suspected that HUMANS infected PIGS
  • 1930-98: Classic swine H1N1 exclusive strain in NA
    – Stable genotype due to abundant naïve pigs
    – Unique to highly pathogenic European H1N1
29
Q

what type of swine influenza is most common after 1998 and why?

A

After 1998: (USA & EU)
* Double and triple reassorted
* Genes from human, swine & avian viruses
* H3N2 genotypes most common
* pH1N1 (2009)

30
Q

infectivity and seasonality of SIV? transmission mechanism?

A
  • Highly infectious common respiratory disease
  • Seasonal: most outbreaks occur in late fall and winter
  • Horizontal transmission:
    § Direct contact (pig-to-pig) nasopharyngeal secretions
    § Airborne spread in hog dense regions
31
Q

host protection against SIV

A
  • Passive Ab protect against disease
32
Q

SIV incubation time

A
  • Short incubation: 1-3 days
33
Q

SIV survival ability outside of host

A

Does not survive long outside of the host (estimate 2 weeks) and inactivated by many disinfectants

34
Q

IAV-S (SIV) – Clinical Signs - ACUTE

A
  • All finisher pigs are suddenly ill
    ***NOTE: Now see commonly in nursery pigs as well
  • high fevers, anorexia, depressed
  • look like they will all die – but don’t
  • barking cough
  • Prostration
  • MORBIDITY HIGH
  • MORTALITY LOW
35
Q

IAV-S (SIV) – Clinical Signs - CHRONIC

A

SIV is part of the Porcine Respiratory Disease Complex that may include:
* Mycoplasma hyopneumoniae, PRRSv, Circovirus, and Pasteurella multocida
* Mortality in the grower-finisher pigs increases (5-8%) and 20% of finishers have respiratory problems

36
Q

Lesions seen with SIV PM? what often causes death?

A

-Bronchointerstitial pneumonia: anteroventral distribution: purple consolidated and meaty (right), sharp line of demarcation between normal & diseased tissue (bottom).
- excess fluid and mucus in airways is very typical
Often secondary bacterial infections are the cause of death.

37
Q

IAV-S (SIV) - Histopathology

A
  • Necrotizing bronchitis/bronchiolitis
    > Degeneration & necrosis of airway epithelium
    > Lumen of bronchi, bronchioli, alveoli filled with exudate, desquamated cells, neutrophils
  • Atelectasis and bronchointerstitial pneumonia
38
Q

IAV-S (SIV) - Diagnosis via histo? how to confirm? when may we see a flase negative and how to avoid this?

A
  • Histo: Necrotizing bronchiolitis and bronchitis
  • Confirmation: nucleic acid (PCR), or antigen detection
    (IHC)
    – Lung tissue, nasal swabs
    – False negative may occur if > 8 days post infection
    – CHOOSE ACUTELY INFECTED (febrile) PIGS
39
Q

IAV-S (SIV) - Diagnosis from live pigs

A

1) Serology (HI, ELISA):
- Paired samples recommended (HI)
- Sensitivity varies depending on the specific strain used in the assay
- Titres higher if homologous strains used in the assay (can develop strain specific assays)

2) Virus Isolation (rarely performed):
– nasal/pharyngeal swabs, chicken eggs

3) ***PCR and genomic analysis (sequencing) – NASAL SWABS

40
Q

IAV-S (SIV) Infection Timeline

A

exposure
- 24h peak fever
- 48h peak excretion
>best time for sample collection
- 192h (6-8d) viral clearance
- 240-336h (10-14d) seroconversion

> coughing starts at 24h and lasts ~2wks

41
Q

IAV-S (SIV) - Treatment

A

1) Supportiveonly–viral disease

2) Antimicrobials to control concurrent diseases or secondary bacterial infections in complicated cases
- Individual
- Mass feed medication

3) Improve indoor air quality & sanitation (NH3, dust free etc)

42
Q

IAV-S (SIV) - Vaccination; what types, which are effective, how are they administered?

A

Vaccination: H1N1, H3N2, ±pH1N1
> Monovalent and multivalent, killed
- Vaccines are generally effective for classic H1N1; variable for H3N2
> Efficacy of commercial H3N2 vaccines have been variable because of rapid drift/shift in the H3N2 genome
- Autogenous vaccines are effective
- Vaccines administered to sows (pre- farrowing) or piglets (at or after weaning)

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