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Y4 FA - Pigs > Growing pigs > Flashcards

Growing pigs Flashcards

1
Q

What are the aims/challenges of the finishing period?

A
  • Maximise growth
  • Maximise efficiency
  • Huge balancing process based on: genetics, feed, housing, health
  • Needs monitoring in order to fine tune
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2
Q

What factors are finishing pigs assessed on?

A
  • Carcass weight
  • Grading – amount of back fat.
  • Condemnations
  • Growth rates
  • Feed consumption
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3
Q

What factors must pigs meet to be considered fit to travel?

A
  • Pigs must be able to load and unload themselves
  • Pigs must be able to support their weight on all four legs
  • Pigs must have no open wounds
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4
Q

Which 3 specific groups are excluded from travel

A

Piglets <3wks
Sows <1wk farrowed
Sows > 100d in pig

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5
Q

List the conditions assessed for in abattoir monitoring which determine if a carcass is fit for human consumption

A

Enzootic Pneumonia -like Lesions
Pleurisy
Pericarditis
Peritonitis
Milk Spot
Hepatic Scarring
Papular Dermatitis
Tail Damage
Viral-type Pneumonia
Pleuropneumonia-like
Abscess
Pyaemia

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6
Q

What is the most common cause of lung retention in the carcass

A

Pleurisy

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7
Q

Describe the presentation of Porcine Respiratory Disease Complex in the finishing period

A

Often starts in weaner period, but can be finishing only
Multiple triggers and pathogens involved
Classic clinical signs = Coughing, sneezing, dyspneoa, cyanosis, pyrexia

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8
Q

What are the impacts of Porcine Respiratory Disease Complex on production?

A

Decreased intake, reduced growth, loss of condition, low level mortality

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9
Q

Which 7 diseases are involved in the porcine respiratory disease complex?

A

Enzootic Pneumonia
Glasser’s Disease
PCV-2 +/- PMWS
PRRS
Actinobacillus pleuropneumonia (APP)
Pasteurella multocida
Swine Influenza

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10
Q

Describe the acute features of the porcine respiratory disease complex?

A
  • Lasts 2-15wks
  • Increased mortality 3-15% post weaning
  • Increased number of days to bacon
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11
Q

Describe the chronic features of the porcine respiratory disease complex?

A
  • Lasts forever
  • Increased mortality 2-10% post weaning
  • Increased number of days to bacon
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12
Q

Name the agent that causes enzootic pneumoniae

A

Mycoplasma hyopneumoniae

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13
Q

Describe the pathophysiology of Mycoplasma hyopneumoniae (Enzootic pneumonia)

A
  • 6-8 weeks incubation
  • Slow action of pathology interstitial pneumonia & bronchiolar cuffing
  • Mucocilliary escalator damage
  • Secondary infection often occurs
  • Decreased growth due to immune challenge and healing
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14
Q

Describe the changes seen on PME/slaughter of Mycoplasma hyopneumoniae (Enzootic pneumonia)

A
  • Dependent lobes end up consolidated with pneumonia - apical, cardiac, cranial region of diaphragmatic and the accessory lobes.
  • Lungs are dark purple, solid, loss of architecture
  • Dependent on secondary infection, overlying pleurisy can also be present
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15
Q

How is Mycoplasma hyopneumoniae (Enzootic pneumonia) diagnosed?

A

EP-like lesions grossly, histopathology, PCR (culture is possible, but difficult)

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16
Q

How is Mycoplasma hyopneumoniae (Enzootic pneumonia) treated/controlled?

A
  1. Treatment with antibiotics:
    - Individual, water and via the feed all work well
    - Tetracyclines – macrolides – pleuromutilins (TMPS has some effect)
  2. Vaccination strategy is important - various different programmes
  3. Full depop-repop – all animals off site and new herd brought in
  4. Partial medicated depop (move the most susceptible animals off site, vaccination, hygiene and medication - depends on planning it correctly!)
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17
Q

Porcine Reproductive & Respiratory Syndrome damaged which cells in the body?

A

Alveolar macrophages

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18
Q

Describe Actinobacillus pleuropneumoniae (APP) infections in a herd

A

Once in a herd it is persistent
Can give acute / peracute outbreaks, especially when on the back of PRRS or Influenza
Can also be chronic on its own, or part of PRDC

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19
Q

Describe the acute signs of Actinobacillus pleuropneumoniae (APP) infections

A

Acute – seen when they are close to death
- Big pigs suddenly dead – very little pathology
- Background cough
- Pyrexia & lethargy
- Bloody nares (often only seen once dead)

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20
Q

Describe the pathology of Actinobacillus pleuropneumoniae (APP) infections

A

Peracute – none!
Acute – haemorrhagic lesions
Chronic – solidified pneumonia with overlying pleurisy

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21
Q

Describe the treatment of Actinobacillus pleuropneumoniae (APP) infections

A

Treatment of individuals is often too late at an outbreak
Injectable, water or via feed
Penicillins – florfenicol – TMPS (- CIAs)

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22
Q

In an acute outbreak of Actinobacillus pleuropneumoniae (APP), which other conditions need to be ruled out?

A

CSF / ASF
Salt poisoning
Toxicities
Acute Glassers
Endocarditis

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23
Q

Name the causative agent of swine dysentery

A

Brachyspria hyodysenteriae

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24
Q

Describe the pathology of swine dysentery

A

Ulcerative colitis / typhylocolitis (caecum and colon)

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25
Q

Compare aggressive and milder strains of swine dysentery

A

Aggressive strains - Death, slow growth, poor feed efficiency
Milder strain - Slow growth, looseness, poor feed efficiency

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26
Q

Describe the clinical signs of swine dysentery

A

Characteristic smell
Mucohaemorrhagic scour
Lethargy
Reduced feed intake
Loss of condition – can be rapid
Death, dependent on strain

27
Q

Describe antibiotic use for swine dysentery

A

Antibiotic resistance is a problem
- Pleuromutilins
- Lincomycin
- Macrolides (not tylosin)

28
Q

How is swine dysentery controlled?

A

Hygiene is so important – spreads easily in muck
Often move towards elimination
Industry-led programme – now part of farm assurance
Not viable to control long term
No viable vaccine options currently

29
Q

Name the causative agent of spirochaetal colitis

A

Brachyspira pilosicoli

30
Q

Describe the main features of spirochaetal colitis

A
  • Mild colitis – common commensal
  • Often a mixed infection with Lawsonia and Salmonella
  • Has appearance of a grey cow pat in most cases, rarely has some blood present
  • Usually control through nutritional changes
31
Q

Name the porcine conditions caused by Lawsonia intracellularis

A

Ileitis – Porcine Haemorrhagic Enteropathy (PHE)
Also causes lower grade Porcine Intestinal Adenopathy (PIA)

32
Q

Describe the pathology and pathogenesis of porcine intestinal adenopathy

A

Thickened distal ileum can extend into proximal colon
Causes malabsorption of intestinal contents

33
Q

List the clinical presentation of porcine intestinal adenopathy

A

Low grade ‘food coloured’ scour
Poor growth – stunted pigs

34
Q

How is porcine intestinal adenopathy diagnosed?

A

Only differentiated from colitis by lab diagnostics
- PCR +/- culture

35
Q

Porcine haemorrhagic enteropathy can be hard to distinguish from which condition?

A

Swine dysentery

36
Q

Describe the clinical signs/findings of Porcine Haemorrhagic Enteropathy

A

Acute haemorrhage, rotten blood smell, sudden death
Usually more mature animals nearer bacon weight
Blood clot finding in intestinal lumen

37
Q

How is Porcine Haemorrhagic Enteropathy treated and controlled?

A
  • Treatment of ileitis is effective: Macrolides – intracellular penetration
    Vaccination is possible
  • Live oral vaccine – individual or via water
  • Injectable now licensed IM or ID
38
Q

What are the causes of nutritional scour?

A
  • More common than likely recognised
  • Low grade large intestinal colitis, often with disruption to the microbiome
  • Change of feed too abruptly (feed rations, raw materials (barley, whey))
  • Gorging suddenly
39
Q

Describe how Ascaris suum is involved in respiratory issues

A

Can cause some respiratory issues as part of PRDC
Migrating L3 – cause coughing. Coughed up, swallowed, passed out in faeces

40
Q

Which feature of an Ascaris suum infection is picked up at slaughter?

A

Milk spot liver

41
Q

What are the causes of the milk spots of the liver in an Ascaris suum infection?

A

Migrating L2

42
Q

How are Ascaris suum infections treated?

A

Pigs can be wormed individually or as a group
- Benzimidazoles & avermectins are effective
- Assume that eggs are indestructible - still viable 7y+ on paddocks

43
Q

Name the ‘whipworm’ of pigs

A

Trichuris suis

44
Q

Describe the disease caused by Trichuris suis

A

Clinically similar to Swine Dysentery
Irritative colitis – unresponsive to antibiotics

45
Q

Describe the treatment and control of Trichuris suis

A

Worming needs to be repeated at high doses
Hygiene really important - washing & lime wash

46
Q

Gastric ulceration is most commonly seen in which pigs?

A

Fast growing pigs

47
Q

List the possible triggers of GI ulceration in pigs

A

Stress
Grist size
High protein
High wheat

48
Q

List the clinical signs of GI ulceration in pigs

A

Melaena can be present, sudden death, pale carcass, clotted blood in GIT, ulcer can be found

49
Q

Describe gastro-intestinal volvulus in pigs

A
  • Half or full rotation around base of mesentery
  • Very quick progression to death
  • Complex aetiology: fresh grains, fermentation, high protein diets
  • Swollen carcass, pale, classic positioning of GIT on post mortem
50
Q

Describe the prevalence of rectal prolapse/strictures in pigs

A

Common finding – often linked to scour + increased abdominal pressure (coughing, huddling)
Often missed since they can be bitten off

51
Q

Describe treatment of rectal prolapse/strictures in pigs

A

Replace if fresh – gloves, pressure, purse string suture
Amputate if old – surgical, pipe and rubber band

52
Q

Describe the consequences of secondary strictures

A

Secondary stricture highly likely, leading to GIT blockage:
- Swollen abdomen, loss of condition, jaundice
- Can feel on digital palpation – ease open if possible
- Otherwise euthanasia is the only option

53
Q

Erysipelothrix rhusiopathiae is a very common disease leading to …?

A

Bacteraemia

54
Q

Describe the peracute, acute and chronic forms of Erysipelothrix rhusiopathiae

A

Peracute = found dead – septicaemic carcass
Acute = highly pyrexic, lethargy, raised skin lesions (typically diamonds, but not always!…)
Chronic = endocarditis, very stiff lameness

55
Q

How is Erysipelothrix rhusiopathiae control implemented on farms

A
  • Often environmental and carried by wildlife: more common in outdoor herds and small holdings
  • Commercial breeding herds are usually vaccinated: can cause abortions in gilts and sows
56
Q

How is Erysipelothrix rhusiopathiae treated?

A

Treatment with penicillin exceedingly effective
Can use water medication when a flare is occurring, but long term control should be via vaccination

57
Q

Describe vaccination of Erysipelothrix rhusiopathiae

A

Vaccination of growing pigs must be after MDA has decayed – therefore vaccinate after 6 weeks post weaning

58
Q

When are trauma lameness’s most prevalent?

A

Around puberty - fractures, dislocations, joint damage, OCD

59
Q

‘Stiff leg’ in older pigs is caused by?

A

Mycoplasma hyosynoviae

60
Q

Infection of Mycoplasma hyosynoviae is triggered by which factor?

A

Triggered by swinging temperatures, leading to acute synovitis – poor hygiene persists the infection

61
Q

Describe the clinical signs of Mycoplasma hyosynoviae infections

A

Swelling can be minimal – often hips and stifles affected
Off legs, difficulty rising, lameness
Early cases can apparently ‘walk it off’

62
Q

Describe the treatment of Mycoplasma hyosynoviae infections

A

Very speedy response to lincomycin / tiamulin & pain relief – need to complete the course
No vaccine available – no cross protection from EP vaccines

63
Q

How do vice problems manifest

A

Manifests as biting of: tail, flank, ear, leg, vulva, anus
Huge welfare issue
Local or tracking abscessation, death, need to euthanase

64
Q

What are the common causes of vice problems

A

Frustration, stress, ‘overstocking’, draughts, discontent, understocking, nutritional upset, disease

Y4 FA - Pigs (10 decks)

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