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3. Food Animal > Swine 8 > Flashcards

Swine 8 Flashcards

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1
Q

Actinobacillus pleuropneumoniae (APP) - traditional aissue, and more recent situation in canada

A

n Traditionally a devastating respiratory disease
n Less severe in Canada in last 2 decades

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2
Q

Actinobacillus pleuropneumoniae; biotypes

A

I: Typical > NAD dependent
II: Atypical > NAD-independent

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3
Q

Actinobacillus pleuropneumoniae differential diagnosis

A

Actinobacillus suis

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4
Q

what does the virulence of Actinobacillus pleuropneumoniae vary with? what are the most virulent types?

A

15 APP serotypes
* Virulence varies with serotype
* 1, 3, 5, & 7 most virulent and common in Canada

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5
Q

APP transmission and incubation period? most common source of infection? environmental survival?

A
  • Primarily horizontal (pig-to-pig) transmission
  • Aerosol transmission unlikely between herds but maybe short distances
    > Doesn’t survive in environment for a long time
    > Carrier pigs most common source of infection
  • Short incubation period (6-12 hours)
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6
Q

APP severity in herd depends on?

A

§ Serotype
§ Exposure dose
§ Immune status of herd
§ Concurrent disease

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7
Q

APP – Pathogenesis, toxins

A
  • Colonization of tonsils & alveolar epithelium facilitated by fimbrial adhesion
  • Adhere to or phagocytosed by alveolar macrophages
  • Produce 4 RTX exotoxins (Apx I, II, III, IV) which are hemolytic & cytotoxic
  • Inflammatory cytokine production
  • Exotoxins & cytokines result in:
    > septic shock (peracute death)
    > arteriolar thrombosis & alveolar necrosis (acute lung lesions)
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8
Q

APP – Clinical signs; peracute

A
  • May be found dead (3-36 hrs PI)
  • Sporadic pigs
  • Increase respiratory and heart rates
  • Sternal recumbency
  • Cyanosis (extremities > generalized)
  • Foamy bloody nasal discharge
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9
Q

APP – Clinical signs; acute

A
  • Depression, anorexia, fever >40 C
  • Dyspnea, coughing & agonal breathing
  • Outcome varies with animal
  • May be fatal - due to CV &
    circulatory collapse
  • May survive and demonstrate chronic form
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10
Q

APP - clinical signs: chronic

A
  • Survivors
  • Chronic cough resulting from chronic pleuritis??
  • No fever
  • Reduced appetite & growth rates
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11
Q

APP – Pathology; Peracute & acute:

A

n Severe, acute necrotizing & hemorrhagic pneumonia
n Well demarcated, generally caudal lobes
n Focal pleuritis
n Blood-tinged froth in trachea

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12
Q

APP – Pathology; chronic

A
  • Chronic pleuritis and adhesions
  • Focal areas of consolidation & necrosis
  • Pulmonary abscesses in survivors
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13
Q

APP – Diagnosis

A
  1. Pathology: necrotizing haemorrhagic pneumonia with focal pleuritis
  2. Slaughter check: high % pleural adhesions
  3. Culture & serotyping of lung lesions
  4. Serology: ELISA’s
    a) APP-Multi ELISA: screens for all serotypes § If positive, request ELISA for individual
    serotypes (ie 1,5,7)
    § Some serotypes cross react
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14
Q

APP – Treatment & Control

A
  1. Environmental control:
    § Same as Enzootic Pneumonia
  2. Strategic medication:
    § Peracute & acute stages only
    -Inject antibiotics to ALL pigs in barn
    > ceftiofur, penicillin (only works for 25% of cases) or tulathromycin (Draxxin)
    § Mass meds: water, feed (amoxicillin, tiamulin, tilmicosin)
  3. Vaccination (breeding herd):
    § Vaccination may protect against clinical
    disease, but not against infection
    § Vaccination of variable value – rarely used
    except in pre-entry acclimation
    § Subunit and killed products available
    § Serotype specific
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15
Q

actinobacillus suis compared to actinobacillus pleuropneumoniae; diffrence in disease caused, how infection occurs, body parts affected and lesions

A
  • Causes more diverse clinical disease
  • Healthy pigs can be carriers
  • Infection occurs through respiratory tract or invasion through abrasions in the skin
  • Infection spreads to multiple organs**
  • Bacteria causes hemorrhage and necrosis due to the production of toxins**
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16
Q

A. Suis - Clinical signs; Suckling and weaned pigs

A
  • Sudden death in one or more litters
  • Cyanosis, petechial hemorrhage
  • Swollen joints, necrosis of feet, tail, ears
  • Anorexia, fever, persistent cough and respiratory distress
17
Q

A. Suis - Clinical signs; older pigs and sows? could be confused with what?

A
  • Fever, skin lesions resembling erysipelas, inappatence and sudden death. Usually low mortality
  • Could be confused with erysipelas or pleuropmeumonia
18
Q

Porcine Respiratory Disease Complex (PRDC)
Pathogens (Component Causes)

A
  • Mycoplasma hyoneumoniae
  • PRRS virus +/- PCV-2 +/- SIV
  • Actinobacilus pleuropneumoniae
  • Pasteurella pneumoniae
  • Actinobacillus suis
  • Other pathogenic bacteria and viruses
    > Farm-specific
19
Q

PRDC – Typical History

A
  • Pigs in multi-site systems
  • Growing pigs enter finisher barn with low immunity
  • Carrier pigs
  • Slow spread in early phase – followed by epidemic spread
20
Q

PRRS, SIV, PCV2; how they come together to cause issues

A
  • PRRS Destroys alveolar macrophages
  • PCV2 + SIV – reduces immune function
  • Lungs - interstitial pneumonia
21
Q

PRDC - Clinical signs

A
  • Slow growth
  • Decreased feed efficiency nAnorexia, Fever
  • Cough, dyspnea
  • Increased mortality, culls
  • May die of gastric ulcers ??
  • 16 to 22 weeks of age
22
Q

PRDC - Control

A
  • Determine pathogens involved
  • Establish vaccination protocols (SIV, PCV2 or Mycoplasma hyopneumonia
  • Farm-specific treatment
  • Implement Good Production Practices
    ()
  • Short term – culling of severely affected
  • Treat secondary bacterial infections with antimicrobials
  • +/- Vaccination against PRRS after other vaccines have been tried
23
Q

good production practices that can be implemented to control PRDC

A
  • Less mixing of pigs
  • Strict all-in-all-out movement
  • Proper stocking density
  • Adequate air & environment quality
  • Sanitation
  • Single source pigs
24
Q

types of atrophic rhiniitis

A
  1. non-progressive
  2. Progressive
25
Q

Non-Progressive atrophic rhinitis (NPAR) pathogens

A
  • Bordetella bronchiseptica (Bb)
  • Cytomegalovirus (Inclusion Body Rhinitis)
26
Q

Progressive atrophic Rhinitis (PAR) pathogens

A
  • Toxigenic Pasturella multocida (TPm)
  • typesA&D
  • +/- other agents including Bb & PCMV which enhance colonization on nasal mucosa, ammonia, irritants
27
Q

Atrophic Rhinitis; commonality of toxigenic Bb, Pm

A
  • Toxigenic Bb & Non-toxigenic Pm are widespread
  • Toxigenic Pm (TPm) is limited to herds with PAR
    >Typically absent in high health herds
    > May be present but subclinical in older farms, unless a recent depopulation has been performed
28
Q

atrophic rhinitis transmission, and when in life infection occurs

A
  • Horizontal transmission
    > Sow to piglet during suckling
    > Pig-to-pig in nurseries
  • Infection generally occurs early in life (before 8 wks of age)
29
Q

Pathogenesis - Progressive AR

A
  • Infection with a toxigenic strain of Pm
  • TPm by itself is a non-aggressive colonizer
  • Usually follows pre-existing damage to nasal mucosa (mixed infections, Bb, NH3 etc) which assists colonization of TPm
  • Production of dermonecrotic toxin by TPm * Reduced osteogenesis
  • Increased osteolysis
  • Permanent turbinate destruction
  • Severity varies
30
Q

Non-Progressive AR clinical signs:

A

n Sneezing and sniffling in piglets
n As young as 1 wk age, generally 3-4 weeks n serous or mucopurulent nasal discharge

31
Q

Progressive AR clinical signs in an endemic or vaccinated herd:

A

ENDEMIC OR VACCINATED HERD
* Sneezing similar to NPAR
* Few if any epistaxis or snout deviations
* Subclinical turbinate atrophy – which is progressive

32
Q

prograssive AR acute infection clinical signs

A
  • May be explosive sneezing in naïve herds (any age)
  • Nasal hemorrhage (any age)
    > pathognomonic if epistaxis noted on a herd basis
  • Lacrimation: tearing & dark lines under the eyes
  • Facial deformities in advanced stages (grower & finisher)
    – twisted, shortened, deviated snouts
  • Grow retardation & reduced feed efficiency (grower & finisher)
    – Metabolic impact of TPm toxin
    – Reduced feed intake due to facial deformities
33
Q

Treatment & Control - Progressive AR; broad methods

A

1) Environmental control

2) Control concurrent colonizers of upper respiratory tract with feed meds or vaccination

3) Antimicrobials

4) Vaccination of sow herd

34
Q

environmental controls for progressive AR

A
  • Improve indoor air quality (dust, NH3, humidity) to minimize nasal mucosa irritation
  • Separate age groups (AIAO) to reduce infection pressure, horizontal transmission potential
35
Q

which concurrent colonizers should be controlled to alleviate pre=ogressive AR? how?

A

Control concurrent colonizers of upper respiratory tract with feed meds or vaccination:
* Bordetella,S trepsuis, H.parasuis

36
Q

how to use antimicrobials to control progressive AR

A
  • Treatment of piglets prior to & after weaning is indicated in clinical herds (not if subclinical)
  • Parenteral long acting oxytetracycline (LA-OTC) administered at birth, day 7-10, and weaning
  • Medication of nursery and grower diets
37
Q

how to use vaccine to control progressive AR

A
  • Must contain TPM, Bb, toxoids
  • Pre-farrowing Vx to enhances passive & mucosal immunity which delays infection to about weaning
  • Sows (2 wk pre-farrow); Gilts (2&5 wks pre- farrow)

3. Food Animal (22 decks)

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