Swine 8 Flashcards
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
2
Q
Actinobacillus pleuropneumoniae; biotypes
A
I: Typical > NAD dependent
II: Atypical > NAD-independent
3
Q
Actinobacillus pleuropneumoniae differential diagnosis
A
Actinobacillus suis
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
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)
6
Q
APP severity in herd depends on?
A
§ Serotype
§ Exposure dose
§ Immune status of herd
§ Concurrent disease
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)
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
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
10
Q
APP - clinical signs: chronic
A
- Survivors
- Chronic cough resulting from chronic pleuritis??
- No fever
- Reduced appetite & growth rates
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
12
Q
APP – Pathology; chronic
A
- Chronic pleuritis and adhesions
- Focal areas of consolidation & necrosis
- Pulmonary abscesses in survivors
13
Q
APP – Diagnosis
A
- Pathology: necrotizing haemorrhagic pneumonia with focal pleuritis
- Slaughter check: high % pleural adhesions
- Culture & serotyping of lung lesions
- 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
14
Q
APP – Treatment & Control
A
- Environmental control:
§ Same as Enzootic Pneumonia - 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) - 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
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**
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
- non-progressive
- Progressive
25
Non-Progressive atrophic rhinitis (NPAR) pathogens
* Bordetella bronchiseptica (Bb)
* Cytomegalovirus (Inclusion Body Rhinitis)
26
Progressive atrophic Rhinitis (PAR) pathogens
* Toxigenic Pasturella multocida (TPm)
* typesA&D
* +/- other agents including Bb & PCMV which enhance colonization on nasal mucosa, ammonia, irritants
27
Atrophic Rhinitis; commonality of toxigenic Bb, Pm
- 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
atrophic rhinitis transmission, and when in life infection occurs
* Horizontal transmission
> Sow to piglet during suckling
> Pig-to-pig in nurseries
* Infection generally occurs early in life (before 8 wks of age)
29
Pathogenesis - Progressive AR
- 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
Non-Progressive AR clinical signs:
n Sneezing and sniffling in piglets
n As young as 1 wk age, generally 3-4 weeks n serous or mucopurulent nasal discharge
31
Progressive AR clinical signs in an endemic or vaccinated herd:
ENDEMIC OR VACCINATED HERD
* Sneezing similar to NPAR
* Few if any epistaxis or snout deviations
* Subclinical turbinate atrophy – which is progressive
32
prograssive AR acute infection clinical signs
- 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
Treatment & Control - Progressive AR; broad methods
1) Environmental control
2) Control concurrent colonizers of upper respiratory tract with feed meds or vaccination
3) Antimicrobials
4) Vaccination of sow herd
34
environmental controls for progressive AR
* Improve indoor air quality (dust, NH3, humidity) to minimize nasal mucosa irritation
* Separate age groups (AIAO) to reduce infection pressure, horizontal transmission potential
35
which concurrent colonizers should be controlled to alleviate pre=ogressive AR? how?
Control concurrent colonizers of upper respiratory tract with feed meds or vaccination:
* Bordetella,S trepsuis, H.parasuis
36
how to use antimicrobials to control progressive AR
* 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
how to use vaccine to control progressive AR
* 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)
