Pig 2 Flashcards

1
Q

Respiratory disease complex (RDC) what also called, what are the 3 main pathogens within

A
> Also called Enzootic pneumonia
- Mixed infection with:
○ Mycoplasma hyopneumonia (hyo in front = pigs) 
○ Pasturella multocida and maybe
○ Actinobacillus pleuropnemonia
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2
Q

Mycoplasma pneumonia what involved with, leads to, clinically characterized by

A
  • Contagious pulmonary disease of pigs.
  • Caused by Mycoplasma hyopneumonia.
  • Characterised clinically by:
    ○ Coughing - severe, 14 day duration
    ○ Unthriftiness
    ○ Very low mortality
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3
Q

what is the incidence of respiratory disease complex and how is it transmitted

A
Incidence of RDC
- Biggest health problem Worldwide
○ > 90% Australian herds affected
○ Cost approx. $70/ sow /yr.
○ Due effect on:
§ Medication, mortality, decrease in Feed conversion efficiency, decrease in average daily gain (ADG)  
How is it Transmitted
- Inhalation from aerosol or direct contact with carrier pig. ( windborne 3 Km query 12k) -> farms within 3 km are a threat 
○ Carrier pigs -> gilts are the most susceptible for carrying 
- Affects ciliated epithelium
- Lesions seen 3-14 days post infection
- Seroconvert 8 weeks post infection
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4
Q

Respiratory disease complex clinical signs in acute form

A
  • Acute form uncommon.
  • Occurs when a high health herd first becomes infected.
  • Deaths all ages ie suckers through to sows
  • After some months will become endemic when all animals infected -> want to become endemic to drop mortality
    ○ Increase spread of disease by exposing all pigs to infected pigs
  • Ideally get them all vaccinated and/ or infected ASAP
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5
Q

Respiratory disease complex clinical signs when endemic

A
  • Chronic or enzootic ( endemic) form
    ○ Infected between 3-18 weeks of age -> generally gilts from mothers act as carriers and increase infection for later
    ○ Dry cough
    ○ Sneezing
    ○ Variation in growth rate in batch -> bad for selling the carcass, cannot sell as not large enough so need to keep feeding OR too large and will be penalised
    ○ Severe coughing and pneumonia with 2’ infection
    ○ death not uncommon from 2’ infection
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6
Q

Respiratory disease complex what are 4 main indications that we have it under control

A
  • Few Clinical signs of coughing
  • Good ADG (average daily gain - 650-660 range) and FCE (feed conversion efficacy - 3.5-3.6)
  • Low mortality
  • Few lesions at slaughter -> should be sold at week 22
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7
Q

Respiratory disease complex treatment and diagnosis

A
Treatment
- Antibiotics -> hit both mycoplasma and Pasteurella (secondary bacterial infections is what is killing the animal)
- In feed or in water
- Based on sensitivities (cant culture) of
○ Tiamulin
○ Pulmotil
○ Amoxicillin 
○ Lincomycin
○ Oxytet
Diagnosis 
- Tracheal swab with PCR
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8
Q

What are 7 main ways to control respiratory disease complex

A
  1. Vaccination ( lung score 15% to 2%)
  2. SEW with multisite production
  3. AI/AO -> All-in/All-out
    § Average daily gain improved by 12%
    § Feed efficiency improved by 7%
  4. Correct stocking density
  5. Strategic medication of weaners
  6. correct Ventilation-> insulate sheds, large ridge vents
  7. Good Housing -> clean between batches, effluent removal
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9
Q

What are the 2 main ways of eradication for respiratory disease complex, which better and what need to be careful of

A
1. Total Depopulation
○ Cost $700/ sow
○ Logistical nightmare
2. Swiss depopulation
○ cost $100/sow
○ still logistical nightmare
- Beware of reintroduction
○ Exposure of gits between 8-10 weeks of age - VACCINE
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10
Q

Swiss depopulation what is it used for and how to perform

A

used to eradicate respiratory disease complex
○ Stop mating for 2 weeks, 14 weeks before day 0 (allow you to clean up and medicate before need sows farrow down)
§ At day -7 get rid of all animals less than 10 months of age.
§ Day -7 to -1 clean up farm
§ Day 0 commence medication at high level for 14 days
§ Day 15 + sows farrow down.

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11
Q

what age are sows mated, gestation length, weeks of weaning and average day of weaning

A

210d mated
Gestation is 115days
4 weeks weaning
Average day of weaning is 20 days

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12
Q

Actinobacillus pleuropneumonia (APP) what does it cause, compication of, age group affects, contagious status and results in

A
  • Severe respiratory disease
  • Most common complication of RDC
  • Affects growers/ finishers/ weaners less common
  • Highly contagious -> up to 500m distance
  • Severe haemorrhagic pneumonia -> due to cytotoxins resulting in haemolysis
  • Economically devastating and poor animal welfare
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13
Q

Lungs lesions for slaughter what are you checking for and the signs for each

A

IS IT APP OR PASTURELLA
APP -> pleusiy, pericarditis, abscesses
Pasturella -> same as APP but no areas of necrotic haemorrhage

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14
Q

Actinobacillus pleuropneumonia (APP) how are pigs infected

A
  • Aerosol transmission from carriers
  • Will travel on wind for 2 k
  • Rapid onset of disease (4-12 hrs)
  • Small dose lung lesions only
  • Large dose blood poisoning
  • (9 hrs post inf)
  • Serovars 1, 5, 7 and 12
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15
Q

Actinobacillus pleuropneumonia (APP) clinical signs in the two types

A
- Acute 
○ Sudden death 
○ Fever 
○ Reddened skin 
○ Laboured breathing (thumping) 
○ Blood stained frothy nasal discharge 
- Subacute 
○ Reduced growth rate 
○ Coughing 
○ Variable mortality
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16
Q

Actinobacillus pleuropneumonia (APP) what are the 2 main other differential diagnosis that it looks like and how to differentiate

A

1) Glassers disease -> Haemophilus parasuis
○ Occurs earlier (usually weaners)
○ Presents as fading pigs -> leads to septicaemia
○ No haemorrahgic infarcts in lung
○ Fibrin formation, pleuritis 2) Pasturella pneumonia ( see later)
○ No haemorrahgic infarcts in lung

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17
Q

Actinobacillus pleuropneumonia (APP) what are the main risk factors

A
  • Respiratory transmission from carrier or recovered pigs
  • Multisourcing pigs in SEW / MS
  • Predisposing factors
    ○ Overcrowding
    ○ Ventilation/ temperature fluctuations
    ○ Stress
    § Movement
    § PST - growth hormone - NO LONGER USED IN AUSTRALIA
    § Feed changes
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18
Q

Actinobacillus pleuropneumonia (APP) treatment and prevention

A
Treatment
- injection of individual pigs
- Water medication of at risk group
○ Tetracyclines, Amoxycillin, Tiamulin
- Based on Lab culture and sensitivities
Prevention
- Vaccination of weaners
- Multisite rearing plus AI/AO by site (deniliquin)
- Strategic medication
○ Cough index
○ Seroconversion pattern
○ Water intake
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19
Q

Actinobacillus pleuropneumonia (APP) eradication options and how to perform

A
  • Swiss depop does not work
  • Total depopulation or Vaccination of sow and MEW (medicated early weaning)
    ○ Medicated early weaning; medicate sow for 2 weeks before and while pigs suckling.
    ○ Wean at 10 days to a new site and medicate weaner diet
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20
Q

Pasturellosis what does it cause, main clinical signs and primary or secondary

A
  • A respiratory disease caused by Pasturella multocida. Very simliar to APP
  • May be sub clinical or associated with:
    ○ Pneumonia
    ○ Septicaemia
    ○ Mortality
    ○ Depressed growth rate
  • Often 2’ to M.hyo and usually seen in growers or finishers. Can be a primary pathogen
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21
Q

Pasturellosis cliical signs and treatment and prevention

A
- Acute
○ Sudden death
○ Laboured breathing, cough, cyanosis.
- Subacute.
○ Pneumonia
○ Coughing, Fever
Treatment 
- Same as for APP 
- Treat individual pigs -> not drinking so won't take medicated water 
- Water medicate at risk group 
- Prevention see RDC
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22
Q

Streptococcal infection in pigs what generally lead to, prevention and lesions

A
  • Sudden death or nervous signs in suckers, weaners and growers.
  • Prevention: Pulse medicate at strategic times, Control environment
    Lesions
  • lungs are wet and heavy (pulmonary oedema), vegetative endocarditis
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23
Q

Mycoplasma hyosynovia what mainly lead to

A
  • respiratory infection
  • invades joints
  • increased in times of stress such as transport
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24
Q

Causes of sneezing list 6

A
  1. Mycoplasma hyopneumonia
  2. Atrophic rhinitis
  3. Bordetella bronchiseptica
  4. Cytomegalovirus
  5. Dust
  6. Ammonia
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25
Q

What are 5 main ways to determine whether respiratory disease complex is causing an issue and the main one

A
  • What is growth rate
  • Do post mortem on dead pigs
  • Check coughing index - MAIN
  • When do they seroconvert
  • Abattoir check of lung score
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26
Q

coughin index what used for and 5 steps wtihin, what mean intervention

A
To detect whether respiratory disease complex is an issue 
1. Select about 50 pigs
2. Wake them and count coughs for 3 min.
3. Repeat * 3 lots
4. Repeat next day
5. Repeat every 2/4 weeks
○ 3-5 coughs 3 min. borderline
○ > 5 coughs intervene
○ > 10 coughs = trouble
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27
Q

What are the 4 main causing of caughin in weaners

A
  1. Mycoplasma pneumonia
  2. Pasteurella pneumonia
  3. Pleuropneumonia (APP)
  4. GLASSERS DISEASE - most common
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28
Q

Glassers disease what caused by and main effects

A
  • Caused by Haemophilus parasuis
  • An infectious respiratory disease
  • Effects
    ○ Fibrinous bronchopneumonia is a common finding in animals weaned 7-14 days
    ○ Empty stomach is typical finding
    ○ Following invasion of the blood stream, multiplication at multiple serosal surfaces produces the typical, Polyserositis, polyarthritis (and sometimes meningitis) seen in pigs from 14-21 days post weaning
    ○ Puss in hock joint can also occur -> carpal and tarsal joints
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29
Q

Glassers disease what result in and clinical signs

A
- Results 
○ Sometimes fatal
○ arthritis
○ Bronchopneumonia
○ Polyserositis
○ Meningitis
- Clinical signs
○ Suckers or weaners
○ Cough, laboured breathing, fever
○ Fading pigs
○ Rough hair coat
○ Sometimes swollen, painful joints
○ Sometimes, meningitis
○ May be found dead
○ Usually euthanased as poor doers
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30
Q

Glassers disease treatment and prevention

A
- Treatment 
○ Penicillin treatment of individual pigs 
○ Group medicate in contact pigs 
○ Amoxycillin soluble 
- Prevention
○ Vaccinate sows- Booster shot at 13 weeks of gestation ( when is colostrum formed???)
○ strategic medication
§ LA penicillin
§ Water medication
§ Feed medication
Check housing/ environment
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31
Q

Differentiate between Glassers and PCVAD (porcine circovirus associated disease)

A
  • Glassers usually occurs within 2 weeks of weaning (5-6 weeks of age)
  • PCVAD usually not seen till about 8-10 weeks of age with peak occurence/ viraemia @ 10- 13 weeks of age
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32
Q

Sow mortality rates common and what farms lower in and why

A
  • 10% die
    ○ Half are destroyed on farm for welfare reasons -> mostly lameness
  • Mortality rates are lower in outdoor farms
    ○ In smaller groups there is no escape areas for fighting sows
    ○ Stalls -> can only move forward and backwards and therefore not much room for separation of faeces and laying down -> increased opportunity for ascending infection
    § Not an issue with group housing
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33
Q

Common cause of death in sows what are the 9 main ones

A
  1. Hyperthermia at point of farrowing (Heart failure)
  2. Post farrowing infection
  3. Oesophago-gastric ulcer
  4. Gastric accident - torsion of stomach intestine or organ
  5. Retained pig
  6. Cystitis
  7. Clostridium novyi
  8. Lameness/downer/destruction
  9. Infectious disease is unusual
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34
Q

What is the major problem with mortality in sows, when generally occur and how to fix

A

HEAT
- At point of farrowing or within ten days
○ Often in Nov - why?
- Daily temp > 35 degrees
- RR > 100 bpm (resting between 12-18 bpm) -> panting -> like dogs how they remove heat
- Fix
○ Immediate cooling (water) -> not done as much as worried about chilling the piglets
○ Cooling system long term
§ Drip cooling applied to sows in farrowing crates very effectively reduces respiration rate and increases comfort
○ Wallows management for outdoor sows

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35
Q

Post farrowing infection when and how generally occur, what associated with, signs and treatment

A
  • Ascending infection within 24 hours of farrowing
  • Often associated with retained pigs -> generally when a manual exam is done without antibiotics afterwards
  • Signs
    ○ Discharge
    ○ Feed intake decreased -> drops 24 hours before temperature spikes
    ○ Temperature increased
    ○ Poor milk production
  • Treatment
    Antibiotics (Amoxycillin, OTC), Meloxicam -> label recommendations
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36
Q

Post farrowing disease what is the most common one, main signs, cause

A

mastitis - Agalactia (failure of secretion of milk)
○ Usually isolated gland
○ Ascending infection
○ May involve several glands
○ May be a consequence of asynchronous lactation and engorgement
○ Linked to constipation?
○ Mycotoxins can be involved (Ergot) -> powerful vasoconstrictor

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37
Q

Mastitis what need to check to help prevent and treatment

A
  • Always check hygiene and feeding to excess in the last week of gestation or early lactation
  • Treatment
    ○ Amoxycillin
    ○ Flunixin, meloxicam good
    ○ Lasix when oedema is excessive
    ○ Oxytocin to assist let down (need 2-4ml) –> contraindicated in farrowing sows????
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38
Q

Ulcers in sows main causes and clinical signs

A
- Causes 
○ Pelleted feed and low fibre diets 
§ Variable and small particle size 
○ Reduced intake or out of feed events?
- Clinical signs 
○ Vomiting blood and poor condition score
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39
Q

Gastric accidents in sows what occurs, associated with, highest risk period

A
  • Torsion of stomach and/or abdominal organs
  • Associated with rapid intake of water and feed
    ○ Possible pellet feeding, poor grain quality -> fermentation and gas production -> gastric dilation -> pressure on diaphragm -> dyspnoea -> death
  • Highest risk period in the farrowing house
  • Gastric dilation as a consequence of fermentation and gas production
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40
Q

Erysipelas how common in sows, results from

A

Erysipelas is very common in sows

  • Incomplete protection provided by the vaccines
  • Large number of cases over periods of weeks are uncommon but this can occur in naïve growing pigs
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41
Q

Clostridial infections what result in, when see, what need to differentaite from and how

A
  • Acute deaths
  • See in mid lactation when feed intakes are suddenly high
  • Differentiate from gastric accidents
  • Rapid decomposition, gas bubbles soon after death
  • Response to zinc bacitracin (200ppm) good
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42
Q

Rectal prolapse in sows what is the treatment and what involved

A
  1. Sedate the sow, local anaesthetic around the perineal skin
  2. Reduce and stabilise with an anal purse string suture
  3. Or, if the tissue is necrotic, suture and amputate
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43
Q

Mycotoxins leading to sow mortality what found in, main types and what do they cause

A
  • Fusarium spp
  • Zearalenone: reproductive impact
  • Vomitoxin (deoxynivalenol): feed refusal
  • Ochratoxin: nephropathy
  • Aflatoxin: immunosuppression
  • Ergot (sorghum): agalactia following vasoconstriction
  • Fumonisin: liver dysfunction
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44
Q

Myxotoxins leading to sow mortality how to control

A
  • To bind the toxin
  • Neutralise the activity chemically
  • Enzymatically degrade the mycotoxin
  • efficacy unsupported
45
Q

Cystitis what age of sows occur, where generally seen, link with, pathogens involved and treatment

A
  • Older sows
  • Stalled sows but also pens
  • Link between frequency of feeding and urination, urinary stasis, contamination
  • Actinomyces/Eubacterium/Coryneb (now Actinobaculum) sinus +++ others
  • Treatment
    ○ Antibiotics 10-14 days (long acting tetracyclines)
46
Q

for all sick sows what are the main things need to do

A
  • Recovery area is needed

- Cover, access to water, feed and straw

47
Q

what are the 10 external signs of impending farrowing and at what day

A
  1. Dropped hip muscles (gluteus and biceps femoris group) (F-3d)
  2. If outside this sow would be nesting (F-3d)
  3. Swollen vulva (F-2d)
  4. Restless (F-12 hrs to 2 d)
    Mammary glands swell and feel firm and distended
  5. Clear fluid expressed (F1-10d)
  6. Secrete milk F12-24 hours -> need this before give oxytocin
  7. Abundant milk F-8 hours
  8. Resting quietly about 30-90mins before farrowing
  9. Increased respiration rate (>30br/min F 15-60mins)
  10. Straining: passing blood tinged oily fluids/meconium F0
  11. Tail wagging -> very close within minutes
48
Q

Farrowing what endocrine events occur at what day

A
  • 112 days foetal pituitary releases ACTH,
  • Foetal adrenals produce glucocorticoids
  • Release of maternal PCF2alpha and foetal placental oestrogen followed by
    ○ Luteolysis, a fall in progesterone, a rise in relaxin (luteal cells) and uterine contractions in response to oxytocin
49
Q

How long does farrowing take for sows and gilts and intervals for piglets

A
  • Takes about 3 hours sows, 2 hours gilts

- Pigs appear at about 12-25 minute intervals

50
Q

What are some risk factors for stillbirths

A

○ Older sows
§ Want to keep sows as old as possible without sacrificing stillborn rate
○ Last to be born piglets
○ Larger litters
○ Summer or in hot (>21 degrees) farrowing houses
○ Very thin and very fat sows
○ Multiple still births in one litter -> more in the next one
○ After long farrowing >4 hours
○ After long interpig interval >40mins (generally about 30mins)
○ With gas heaters and increased CO levels -> foetus will concentrate that CO born anorexic (blood colour is cherry red) leading to stillbirth
○ After induced farrowing and oxytocin
○ Premature rupture of the cord and foetal anoxia - the main reason for stillborns

51
Q

Stillbirth prevention strategies

A

○ Farrowing house should be clean
○ Be clean, use lube, be gentle -> where gloves NEED TO USE NEW ONE EACH TIME
○ Don’t push against the sow
○ Broad spectrum antibiotic cover

52
Q

At what parity do you get the highest % born dead and what occurs after this

A

Parity 7

  • Ones that have the issues at parity 7 will then be culled or possibly this large number has been identified by the farming staff and put in interventions
  • Therefore the ones above parity 7 have been selected for their low born dead percentage
53
Q

First aid for farrowing sows what are the 3 main things to help, one that isn’t required and the main rule

A
  • Manual examination
  • Oxytocin 5-10IU -> if haven’t got milk ejection response and give then increase chance of stillbirths -> late in the intervention
    ○ Manual interventions FIRST
  • Caesars are not required
  • A walk can be helpful
  • RULE: manual examination after 45 mins after pig #7 then oxytocin, antimicrobial cover
    ○ Most problems occur after pig #7
54
Q

Lactation what hormone changes, from what day do you produce milk and what occurs with milk let down at birth

A
  • As progesterone drops and oestrogen rises there is major metabolic activity in the mammary gland
    -> Relaxin increases growth of mammary gland parenchyma
  • Gland capable of producing milk from day 105
  • At birth there is copious “milk” -> comes from gland secretion (epithelium) and serum transudation from between the epithelial cells
  • For the first 24 hours the sow lets down continuously
  • After that she lets down about every hour -> only let down for 20-30seconds, sow lets the piglets know it is coming and piglets need to attach to the teat
    ○ If miss the let-down for some reason (sick, small, weak, lame) then need to wait
  • The stimulus for milk production is milk removal
55
Q

What are the 3 main things that lead to piglet mortality

A
  • Need colostrum
    • Warm environment
    • Birth weight
56
Q

what age is a weaner, grower and finisher

A

Weaner: removal from sow to 20Kg
Grower: 20-50kg liveweight
Finisher: 50-100+ kg

57
Q

Grower and finisher pigs what are the 3 main causes of death

A

1) Infectious
○ Respiratory disease - APP, Pasteurella, streptococcus
○ Enteric disease - Swine dysentery, ileitis
2) Non-infectious
○ Gastric ulcers
○ Twisted bowel - liver is very pale (congestion of blood)
3) SCOURS - IMPORTANT

58
Q

Scours in grower and finisher pigs what are the 6 main causes and which is rare

A

1) Ileitis
2) Swine dysentery (SD)
3) Salmonella - rare - notifiable (just the disease)
4) PCVAD (porcine circovirus associated disease)- granulomatous enteritis -> IMMUNOSUPPRESSIVE -> predispose to the other disease especially salmonella
§ No lesions just hyperaemic mucosa, caecum and colon large watery contents
5) Whip worms - more common in free range systems
6) Excess salt >5000 ppm - RARE

59
Q

What are the 3 main control strategies for scours and the 2 main treatment options

A

Control strategies for scours
- Don’t contaminate other pens
- Stop floor feeding
- Clean pens (scrape and hose out)
Treatment
- Inject individually affected animals with appropriate antibiotic
- Water medicate affected pens and at risk pigs

60
Q

Swine dysentery what is it, manifests as, characteristic and transmission

A
  • An infectious disease of the large intestine - brachyspira hyodysenteriae
  • Manifested as wasting, diarrhoea and death
  • Characteristic foul smell
  • Transmission
    ○ Infection by oral route from sow to her litter - faecal-oral route
    ○ From infected weaner to pen mates
    ○ Organism invades the wall of the bowel
    § Interferes with absorption of fluid and electrolytes
    § Death from dehydration and ion imbalance
61
Q

Swine dysentery clinical signs

A

○ Diarrhoea containing blood, mucus and necrotic material
○ May only present as “grey scour”
○ Pigs fall back in condition
○ Paper test-mucus sticks paper together
○ Death - dehydration, electrolytes imbalance

62
Q

Swine dysentery post mortem lesions and diagnosis

A
  • Post mortem lesions
    ○ Lesion confined to large intestine (salmonella and ileitis is small intestine as well)
    ○ Red and swollen
    ○ Spiral Colon most affected
    ○ Colonic contents
    § Fluid, mucus, necrotic material, flecks of blood
  • Diagnosis
    ○ Submit large intestine or manure to Lab - scrap part of the wall
    § Spirochetes seen on dark field exam
    § Culture organism and PCR
63
Q

Swine dysentery treatment and prevention

A
  • Treatment
    ○ Scouring pigs -> injection for 3 days, lincomycin or Tylosin (also good for ileitis)
    ○ In contact pigs -> water medicate for 6 days, lincomycin or Tylosin
  • Prevention
    ○ Strategic medication of weaners to eliminate organism (Tiamulin 200ppm)
    ○ Clean pens, don’t floor feed
    ○ Minimise stress
    ○ Strategic water medication
    ○ In feed medication; salimomycin (30 day withhold period)
    § Withdraw at 16 weeks so can sell at 20 weeks - when most susceptible
64
Q

Swine dysentery eradication what are the 2 main ones, how perform and how long does it stay in the environment

A

a. Depopulation if have respiratory disease
b. Medicated eradication - tiamulin
i. High level for 7 days and then clean (400ppm = 10-12mg/kg) THEN
ii. Medium level for 14 days during clean (200ppm-6mg/kg) THEN
iii. 25 ppm tiamulin for 6motnhs until all infected growers have left property
○ How long does it survive in the environment -> 3-4 days

65
Q

Ileitis what also called, what is it, main cause and where generally occur (how to tell)

A

(porcine proliferative enteropathy)
- Collective name for different manifestation of same disease complex
- Lawsonia intracellularis invades cells of the small intestine
○ Cells fail to mature and become hyperplastic
○ intestinal wall becomes thickened and invaded by other bacteria
- Not usually large intestine, tarry faeces (digested blood - different to swine dysentery)

66
Q

What are the 3 main manifestation of ileitis and what leads to in terms of clinical signs

A

a. Proliferative intestinal adenomatosis: ileum and proximal colon
§ Scouring in early stages
b. Necrotic enteritis - if infected before 12 weeks of age
c. Haemorrhagic form/PHE (proliferative haemorrhagic enteritis) - if infected after 12 weeks of age
i. Sudden death, pale, anaemic pigs or carcasses, black and tarry faeces

67
Q

Porcine proliferative enteropathy transmission and presentation

A
  • Transmission
    ○ Organism excreted in the manure of infected pigs
    ○ Infected by faecal-oral route - scour in 18-21 days
  • Presentation
    ○ Animals fall back - slab sided
    ○ Poor weight gain
    ○ Pigs cranky - tail and flank biting
    ○ Sudden death in older pigs (12 weeks +) or replacement
68
Q

Porcine proliferative enteropathy effect on production and treatment

A
  • Effect on production
    ○ Can reduce ADG and FCE by 6-20%
    ○ Causes large variation in batch of pigs which causes grid penalties
    ○ FCE from 3.8 to 4.56 = 4.56 $1.52 to $1.82 or 30c/kg which is about their profit margin
  • Treatment
    ○ Inject any clinically obvious pigs
    ○ Water medication 3 days with tylosin or lincomycin
69
Q

Porcine proliferative enteropathy prevention

A

○ Weaners covered by routine medication
○ Growers -> water pulse for 2 days every 14 days 0r medicate in feed continuously
§ Allows exposure and hence immunity
○ Replacement breeders - 2 treatments 14 days apart
○ Try enterisol vaccine as sucker and discontinue medication in growers - HIGHLY EFFECTIVE THUS FAR

70
Q

Salmonella what seen as, is it common, due to what found with what animals

A
  • Seen as outbreak of scours and wasting pigs
  • Used to rare in Australia now more common due to circovirus 2 (PCVAD)
  • Due to S. typhimurium in rodents, birds, feed and by-products
71
Q

Salmonella transmission and clinical signs

A
- Transmission
○ Oral ingestion from feed, environment (rodents, birds) or manure of carrier animal 
§ Animals may die or develop scour  
- Clinical signs 
○ All ages - usually weaner/grower 
○ Sudden death 
○ Chronic poor does - looks like PCVAD
○ Scour - no mucus or blood
72
Q

Salmonella treatment and prevention

A
○ Inject affected animal
○ Water and feed medicate at risk group 
○ Oral vaccination of suckers Vavsafe ST
○ QA program - biological standards 
§ Rodents, cleaning, by-products, approved suppliers, is it due to circovirus 2??
73
Q

Whipworm what does the diarrhoea look like and the main worm involved with lifecycle and treatment

A
  • May be mucous diarrhoea BUT NOT BLOOD
    Ascaris suum
    If swallow L1 - nothing
    Swallow L2 -> burrow into small intestinal wall -> migrate to liver -> migrate to lung -> coughed up and back into small intestines -> 30days from L3-L5 -> lay eggs -> eggs in faeces and beyond
  • Leads to white spot liver
  • PPP -> 42 days
    THEREFORE CONTROL -> worm once a month - fenbendazole - total of 10mg/kg over 7-10 day period
74
Q

Gastric ulcers leading to diarrhoea generally secondary to, what lead to with clinical signs and what can cause in oesophagus

A
  • Generally secondary to other diseases
  • Go off feed, inappetence, weight loss
  • Can cause a crater where oesophagus enter pars oesophagus (opening of the pigs oesophagus)
75
Q

causes of reduced feed intake resulting in poor average daily gain

A
  • Stocking density
  • Temperature
  • Air quality
  • Water volume and quality
  • Disease
76
Q

what are the 5 main causes of growth rate issues and causes within

A
  • Respiratory disease
  • Enteric disease
  • Mange
  • Nutritional
    ○ Diet formulation/ingredients
    ○ Water - poor quality, too hot, frozen
  • Housing and management
    ○ Overstocking
    ○ Poor temperature control
    ○ Poor air quality
    ○ Poor effluent control
    ○ Poor hygiene
77
Q

When investigating growth rate issues what issues do you need to check off the list for causes

A
  • Stocking rate and density
  • temperatures ( data loggers / max/min therm
  • diets ( source and specs)
  • Air quality ( Dust / gas)
  • Clinical signs ( cough, scour, rubbing)
  • feed intake ( how?)
  • Growth rate (how)
  • Abattoir
78
Q

Weaner diarrhoea what risk factors at weaning lead to stress and factors that affect weaner health

A
Stress factors at weaning 
- Change from liquid to solid diet 
- Removed from sow
- Mixed with unfamiliar pigs
- New environment 
Factors affecting weaner health 
- Age and weight at weaning 
- Environment and housing 
- Nutrition 
- disease
79
Q

Requirement for weaners to help reduce scours

A
  • temperature constant
  • Eliminate draughts
  • All in all out
  • Stocking rate avoid overcrowding - generally when just wean not an issue
  • Sort on size
  • Dust
  • Nutrition
80
Q

Transmission of disease and immunity for weaners what is the 2 ways this occurs

A

1) Sow passes immunity and bacteria through milk to offspring
○ Infected sows will give immunity to offspring BUT NON-INFECTED SOW will not give immunity to offspring -> PROBLEM WHEN MIXED AT WEANING
2) Sow passes bacteria through faces

81
Q

What are the 5 main causes of scour in weaners and the main way to diagnose

A
  1. Excess salt in water
  2. Post weaning scours ( E.coli)
    ○ usually in first 2 weeks
  3. Ileitis
    ○ Usually in last 3 weeks - NOT IN THE 1ST 3 WEEKS
  4. Salmonella
    ○ Rare but occurs at any stage
  5. Granulomatous enteritis - PCV2
    Diagnosis -> autopsy dead or typically affected pigs
82
Q

Granulomatous enteritis - PCV2 how presents, what associated with and how grossly presents

A
  • Diarrhoea associated with fading pigs 8-12 weeks of age
  • Diarrhoea associated with a granulomatous enteritis
  • Grossly seen only as reddened/ congested mucosa of distal ileum and large intestine.
83
Q

What are the other disease in weaners that lead to scours

A
  • Twisted bowel
    • Mulberry heart disease
    • Starvation syndrome
    • greasy pig,
    • arthritis
    • Worms - rare
84
Q

Greasy pig diseasewhat caused by, when occur and how to treat

A
  • Caused when staph bacteria invade skin abrasions in immune deficient animal
    ○ Ie after fighting
  • Treat with antibitoic, amoxil, trisoprim - only if very red
  • If severe use flunixil as well
85
Q

E.coli what leads to in weaners and pathogenesis

A

post weaning scours -> enteric colibacillosis
- Pathogenesis
○ Ingestion of bacteria -> bacterial colonization of ileum and jejunum -> too much fluid through large intestine
§ E. coli attach to the intestine with pili and fimbriae
§ Produce a enterotoxin and destroy villi -> lead to hypersecretion of water and electrolytes
§ Animal dies from shock of dehydration

86
Q

Enteric colibacillosis clinical signs

A
○ Occurs within first 7-10days 
○ Scouring pigs 
○ Or sudden death - good sized pigs 
○ Post mortem findings 
§ Sunken eyes
§ Fluid filled, reddened small intestine
87
Q

Enteric colibacillosis predisposing factors

A
○ Lack of gut immunity
○ Wet, dirty pens
○ Draughts,Too cold
○ Overcrowding etc,
○ See essential requirements, earlier
88
Q

Enteric colibacillosis treatment

A

○ Short terms
§ Inject affected pigs with antibiotic - neomycin
§ Water medicate at risk pigs
§ Electrolytes and antibiotic in troughs
§ Inspect 3-4 times a day
○ Long term
§ Correct the environment
§ Vaccinate if the problem persists
§ Antibiotics in feed for first 14 days OR pulse antibiotic in water 48-72 hours prior to anticipated onset

89
Q

What are the 4 main causes of sudden death in weaners

A
  • Mulberry heart disease
  • Strep septicaemia - meningitis
  • Twisted intestine
  • E. coli
90
Q

Muberry heart disease what does it manifest as and 3 main causes

A
  • Manifest as sudden death in good sized pigs 15-30kg in size
  • Causes
    ○ Vitamin E deficiency
    ○ High levels of polyunsaturated fats
    ○ Fast growing pigs
91
Q

Mulberry heart disease autopsy findings and prevention

A
  • Autopsy findings are characteristic and include
    ○ Large amount of fluid around heart and lungs
    ○ Haemorrhagic and pale areas in heart muscle
    ○ Fluid in abdomen with fibrin strains
    ○ There is often haemorrhage in abdominal cavity due to rupture of the liver (congestion due to heart failure)
  • Prevention
    ○ Check vitamin E and fat levels in diet
    ○ Ignore if mortalities <1%
92
Q

Strep infection in weaners what lead to, how and other results

A
- sudden death in weaners
Meningitis 
○ Most commonly caused by strep infection 
○ Can be caused by glassers 
○ Animals lies on the side and cannot stand
○ Differential - talfan disease (polio) 
- Other results 
○ Arthritis 
○ Pneumonia
○ Heart valve lesions
93
Q

What are the 9 main causes of sucker diarrhoea

A
  1. NHEC (non-haemolytic E.coli)
  2. Coccidia
  3. HEC (haemolytic E.coli)
  4. Rotavirus
  5. Strongyloides ransomi
  6. Clostridial perfringens type A
  7. Clostridial perfringens type C
  8. salmonella
  9. Cryptosporidium
94
Q

Non-haemolytic E.coli age of occurance, clinical signs, neoscopy and histology.smears

A
  • Age of occurrence -> 2 hours - 5 days
  • Clinical signs -> mild to severe scour, dehydration and/or death
  • Necropsy -> fluid filled intestines, chyle in mesenteric lymphatics
  • Histology/smears -> no blunting of villi, gram negative bacilli > 10per/1000 magnification
95
Q

Non-haemolytic E.coli diagnosis, treatment, prevention and vaccine

A
  • Diagnosis -> sample rectal swab, culture of enterotocigenic E. coli, alkaline intestinal contents, response to treatment
  • Treatment -> pigs respond to antibiotic therapy -> should show results within 6 hours
  • Prevention -> pay attention to warmth, hygiene and immunity, colostrum of cows specifically vaccinated against porcine colibacillosis strains is useful
  • Vaccination -> commercial E.coli vaccines are very effective, if you vaccinate you do not have E.coli in the first week of life
96
Q

What coccidia causing sucker diarrhoea age of occurrence, clinical signs, necropsy, histology, treatment, prevention and vaccine

A

Isospora suis

  • Age of occurrence - 5-15 days.
  • Clinical signs - Scour; death uncommon.
  • Necropsy - Ranges from no visible change to necrotic enteritis affecting distal ileum. Probably no chyle present in mesenteric lymphatics.
  • Histology/smears - Necrosis and blunting of villi, sexual and asexual stages visible on histology and smears.
97
Q

Isospora suis treatment, prevention and vaccine

A
  • Treatment - Treatment with Baycox, even though efficacious, may not show dramatic results until intestinal necrosis heals.
  • Prevention - Toltrazuril (BaycoxR) given at day 4 is highly effective. Attention to hygiene of farrowing pens is important.
  • Vaccination - No vaccines commercially available.
98
Q

Haemolytic E.coli what does it cause, age of occurrence, clinical signs and diagnosis

A

diarrhoea in suckers

  • Age of occurrence - +10 days through to postweaning period.
  • Clinical signs - Sudden death from endotoxic shock, or severe scour with dehydration.
  • Diagnosis - Can invariably isolate heavy to pure cultures of K88 positive haemolytic E.coli from the ileum and colon of dead pigs.
99
Q

Haemolytic E.coli treatment, prevention and vaccination

A
  • Treatment - Antibiotics, however limited efficacy as resistance is common and pigs may be too ill to absorb a parenteral injection due to hypovolaemic shock.
  • Prevention - Commence antibiotic in water 2-3 days before expected onset of problem. Stopgap only
  • Vaccination - Oral Vaccination of breeders 4-5 weeks prior to farrowing has proven to be highly effective.
    ○ Top-dress feed with 200mL of an overnight milk culture of a tame K88 E. coli daily for 4 days at week 11 of gestation.
100
Q

Prevention of post weaning scours what is the most important thing with short and long term

A
  • Fix the environment
  • Short term - Antibiotics administered in water commencing 2-3 days before expected onset of problem
  • Long term . Orally vaccinate with the troublesome strain for 3 days commencing 10 days before weaning.
  • Beware of the emergence of the virulent O149 strain during vaccination
101
Q

Rotavirus age of occurrence, clinical signs and diagnosis

A

sucker diarrhoea
- Age of occurrence 4- 7+ days,
- Clinical signs - scour.
- Diagnosis. Absence of any other agent/ cause. Acidic faeces, demonstration of rotavirus in scour material
○ Microscopic evidence of blunting of villi

102
Q

Rotavirus treatment, prevention and vaccination

A
  • Treatment - Secondary bacterial infections may complicate the problem so antibiotics may be of benefit. Warmth and glucose/electrolyte indrinkers useful.
  • Prevention - Pay attention to warmth, hygiene and immunity. Colostrum of cows is useful, as we rarely see rotavirus in calves before 14 days of age.
  • Vaccination - Feedback is the only option as no commercial vaccines available
103
Q

Clostridial perfringens type A age of occurrence, clinical signs and necropsy findings

A

sucker diarrhoea

  • Age of occurrence - 1-21 days.
  • Clinical signs - Mild to moderate scour.
  • Necropsy - Fluid filled intestines. Neutral to alkaline faeces.
104
Q

Clostridial perfringens type A histology.smears and diagnosis

A
  • Histology/smears - Necrosis of villi due to enterotoxins. Large numbers of gram positive rods.
  • Diagnosis - Culture of organisms in large numbers from faeces. Demonstration of enterotoxin in faeces or intestinal contents.
105
Q

Clostridial perfringens type C what does it cause, age of occurence, clinical signs and necropsy

A

sucker diarrhoea

  • Age of occurrence - 2+ days. ( usually only outdoor herds)
  • Clinical signs - Severe dysentery.
  • Necropsy - Severe haemorrhagic enteritis.
106
Q

Clostridial perfringens type C histology and diagnosis

A
  • Histology/smears_ Ghosts of villi left with large numbers of gram positive rods adhering.
  • Diagnosis- Haemorrhagic diarrhoea. Culture of organisms in large numbers from faeces. Demonstration of enterotoxin in faeces or intestinal contents.
107
Q

Clostridial perfringens what are the 2 types, what cause, treatmetn, prevention and vaccination

A

Type A and C

  • sucker diarrhoea - BUT NEVER BEEN ABLE TO DEMONSTRATE AS A MAJOR CAUSE
  • Treatment - Antibiotics effective but will not show immediate benefits due to intestinal necrosis.
  • Prevention - Pay attention to hygiene of sow and farrowing pen. Addition of antibiotic to lactating sow ration has been used in some countries. No benefit here
  • Vaccination - Toxoid vaccine for sows available in some countries. We have never been able to isolate a toxin producing strain to use as a vaccine.
108
Q

Salmonella what is the age of occurrence in suckers, clinical signs, necropsy, histology and diagnosis

A
  • Age of occurrence - 5+ days through to postweaning period.
  • Clinical signs - Scour and respiratory disease.
  • Necropsy - Bronchopneumonia in 50% of animals and a necrotic enteritis affecting distal ileum and colon.
  • Histology/smears - Necrotic enteritis.
  • Diagnosis - Isolation of salmonella from intestine and lung.