BVetMed3 Pig Reprod 2013 MN
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Transcript of BVetMed3 Pig Reprod 2013 MN
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Reproduction of the Pig
Mandy Nevel
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Learning Outcomes 1
you should be able to . Describe how reproductive performance impacts farm economics and
sustainability
Discuss criteria for selection and rearing of breeding animals (sows and
boars)
Describe the key events in the sows reproductive life up to first insemination
(i.e. birth to puberty) and how these may be influenced e.g. bynutrition/hormones/genetics/environment
Outline the different mating regimes and comment on their
advantages/disadvantages
Describe the common methods of pregnancy diagnosis and comment on
their advantages/disadvantages Describe the normal events around parturition, lactation and weaning and
return to oestrus (insemination to farrowing to weaning back to
insemination)
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Learning Outcomes 2
You should be able to. Describe the common measures of sow fertility/infertility and how they
impact the overall farm performance (show farm production data)
Describe the normal and intervention levels of sow fertility/infertility
Describe and appreciate common causes of infertility in the sow
(management - including culling, infectious, physiological)
Describe the common problems encountered at parturition/farrowing
Describe the common causes of poor reproductive performance of boars
Describe a logical plan to investigate boar (or AI) failure
Outline options available for investigation of infertility problems in sows
On the farm
In the abattoir
In the laboratory
Describe possible strategies to improve reproductive performance in pigs.
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UK PRODUCTION
Low production generally
Poor investment
Poor buildings
Poor hygiene, cleaning etc
Shortage of finishing accommodation
Pollution control
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Pig production
/kg
-------------------------------------
Cost of prod p/s/y mortality
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Target / interference levels
Need to establish what we want our sows to doin reproductive terms before assessingperformance
What would the optimum sow be/give?
Gilt age at first mating, Litter size
Pre-weaning mortality
Weaning weight/ milk production
Weaning to oestrus interval Weaning to farrowing
(Food efficiency)
Longevity
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Pigs life cycle the sow
Reach puberty ~ days age, kg
Mated on oestrus
Gestation days Lactate weeks
Return to oestrus days later
Culled after
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Reproductive life cycle
Puberty E2 mating gestation lactation WOI mating p6 cull
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Gilts - selection
Age
Weight
Oestrus Disease status
Litter size
Vaccinal status
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OvaryOviduct
Pregnancy
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Pregnancy
PG
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Pregnancy Diagnosis
Non-return to oestrus
Ultrasound real time, A-mode, Doppler
Hormones Visual
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Farrowing - induction
Advantages Disadvantages
Management cost
Fostering risk of dates
Work out farm gestation length
Prostaglandin, oxytocin
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Litter size
Total born
Total born alive
Still births Mummies
Parity changes
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Litter Vs Parity
0
2
4
6
8
10
12
1 2 3 4 5 6 7 8
Parity
Litter
size
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Weaning to oestrus interval
Oestrus detection
Duration of oestrus
Insemination/mating timing Body weight loss
Cost of empty days
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OvaryOviduct
Optimum mating time
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E2
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Oestrus
ovulationweaning
LACTATION WOI OESTRUS
hours
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ovulationweaning
LACTATION
weeks
WOI
days
OESTRUS
hours
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Ability to increase productivity
p/s/y
Litter size number of litters pwm
Lactation gestation WOI
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Weaning to farrowing
Return rates
Regular returns
Irregular returns
Abortions
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Longevity
Culling rates
Age at culling
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Targets and interferenceParameter Target Interference
p/s/y 24 22
Litter size 11.5 11
Still births 10%
Mummies 2%
WOI 5 days 7 days
Regular returns 8% 10%
Irregular returns 42%
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Gestation: abortion, smedi, vaginal prolapse
Peri-parturient periodSow: uterine prolapse, Lactation. Agalactia,Mastistis
Piglet Mortality.chilling, crushing, starvation
Diseases of Reproduction.
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Investigating porcine
abortion/still birth.
Only 30-40% of abortions are infectiousin origin.
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Non-infectious causes of abortion.
Husbandry and management.
Stockmanship/hygiene
Management policies i.e. age structure of theherd
Environment.Season (heat stress)
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Infectious Causes.
Opportunists.Often ubiquitous microorganisms in theenvironment.
Risk Factors.
Poor health of the sow (immunocompromise)
Poor hygiene
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Specific Pathogens.
Swine influenza
Porcine reproductive and respiratorysyndrome,
leptospirosis
Erysipelas
Uncommon but when they do occur theycause severe reproductive disease.
****Aujeszkys, ASF, CSF****
Porcine Reproductive and Respiratory Syndrome
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Porcine Reproductive and Respiratory Syndrome.
blue-eared pig disease
Clinical signs:Reproductive losses
increased pre-weaning mortality
severe respiratory effort in neonates (thumps)Flu-like signs in older pigs
Blue extremities (
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Porcine Reproductive and Respiratory Syndrome.
blue-eared pig disease.
Diagnosis:>20% born dead
>25% die at 8% abortion/premature deaths
Suspect if have at least 2 of the above
Serology
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Economics:
Severe economic effects in acute phase (where mainlyreproductive losses occur).
**Chronic effects may include raised disease levels ingrower pigs (immunosuppresive effects) **
Porcine Reproductive and Respiratory Syndrome
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Vaccine available since 2001
Porcine Reproductive and Respiratory Syndrome.
blue-eared pig disease.
Treatment: Supportive, treat secondary pathogens
Control: Originally notifiable, now reported
throughout the UK.
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PRRS Vaccine available since 2001
*Vaccination against PRRS (when presenton farm) has decreased mortality seen
with PMWS.*
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Leptospirosis. (L.bratislava).
Clinical signs.
Most commonly abortion and reproductive failiure
Risk factors;
Rodent reservoirs
Outdoor herds (wallows)
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Diagnosis
Serology, dark ground microscopy, FAT
Treatment:
Antibiotic medication: Streptomycin, Tetracyclines. In
theory the whole herd should be treated at one time, thisrarely happens.
Recent moves towards the use of cattle lepto vaccines inpigs.
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Leptospirosis is a zoonosesnotifiable in man.
Urine is the most common source of infection.Leptospires gain entry via mucous membranes.
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Laboratory investigations.Sample at least three fetuses (andplacenta if poss).
Stomach contents and /or liver. If takenaseptically may indicate opportunisticinfections.
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Fetal fluid.
Transplacental transfer of antibodies does not occur:Fetus is immunocompetant after 70d
Antibodies in fetal fluids (pleural or abdominal fluid)
indicate in utero challenge and are significant.
Test for:
Parvovirus antibodyLeptospira bratislavaantibodySwine Influenza (new serotypes?)
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Also can do antigen detection tests.
Parvo, Lepto
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VLA Porcine Abortion Kit.
For a fixed fee will test sows serum for:
Swine influenza
ErysipelasParvovirus
PRRS
Leptospira
Oth f i t t i
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Other causes of intra-uterine
death
Not abortion!!
Think non-infectious as well as infectious
Variations in litters
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Variations in litters.
Small number born (
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Marker Stages of Gestation.
35days: mummifiedfetuses through to stillborn piglets.(aborted at any stage).
70d Fetus immunocompetant
Full Term 112-116 days.
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Genetic factors
Parental/progenyNutrition
Micronutrient deficiencies i.e. Vit E and AToxic agents
Misuse of hormonal drugs
Chemicals (eg. teratogens in hemlock).
Mycotoxins i.e Zearalenone.
SMEDI
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SMEDI
Stillbirth
Mummification
Embryonic Death
Infertility
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SMEDI -type problems.Majority caused by porcine parvovirus
porcine enterovirusesare less frequently implicated
Classic clinical signs:Full-term litter consisting of
small mummified fetuses
full grown stillborn
live weakly piglets
***Rarely see abortion***
P i (SMEDI)
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Parvovirus (SMEDI)
93%of UK herds infected.
Transmission:
oronasal/venereal
If non-pregnant become immune
If pregnant (depends on stage of gestation) smedi
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Highest Risk animals:
Nave animal enters infected herd.
Carrier animal enters nave herd (ALL sows at risk)
Piglets born to immune sows (seronegative = nave)
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Parvovirus (SMEDI)
Treatment: None
Control: Vaccinationis available and is widely practised
Vaccinate 8 weeks before service on first occasion and 2weeks before for subsequent boosters.
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investigations
Management observations/questions
Clinical signs
Laboratory investigations
Aborted material
Serology
Cull sow tracts
f llb h
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Causes of stillbirth
Examine fetus to determine when deathoccurred.
Pre partum-as for causes of abortion
Intrapartum usuallynon-infectious
Prolonged farrowing
Increased litter size (most deaths in lastthird).
Older sows, > 5 litters
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Causes of still birth
Overweight/emaciated sows
Elevated farrowing house temperatures
Mycotoxins
Environmental/stress I.e small farrowingcrates
Occasionally infectious causes get a rapidincrease in still births
Gross features of peri-partum
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Gross features of peri partumdeaths.
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Post partum deaths.
Mainly non-infectious:
Overlying and chilling
Weaker/smaller piglets most at risk
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Monitoring abortion/ still birth
Sow Examination
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Age
Condition scoreService date/ expected farrowing date
recent treatments
Concurrent illness
Management changes
Vaccination details (parvo, erysipelas)
Take paired blood samples 2-3 weeks apart
Estimation of approximate gestational age
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Estimation of approximate gestational age
Approx age (days) = 21 + (3xcrown/rump length(cm))
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Infection in-uterousually causes fetuses todie at different gestational ages.
Toxic/nutritional causes will result in deadfetuses of the same gestational age
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Economics:
Severe economic effects in acute phase (where mainlyreproductive losses occur).
**Chronic effects may include raised disease levels ingrower pigs (immunosuppresive effects) **
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Parturition
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Primary Uterine Inertia.
Early cessation of farrowing or failure to startfarrowing (end of first stage labour).
Behavioural signs of nesting and milk may bepresent.
No straining.
Causal Factors:
Lack of uterine contractility/tone.
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Diagnosis:
Absence of straining.
Cervix is dilated.
No obstruction present.Lack of uterine tone.
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DD: secondary uterine inertia
Treatment:
Assist at farrowing
Oxytocin 2-5iu given I/m at 30 min intervals
If toxaemia/ infection is present give antibiotics and /orNSAID.
Control:Allow acclimatisation to the farrowing house and staff
Secondary Uterine Inertia.
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Clinical signs:
2nd stage labour, sow is straining but no effect and may
become exhausted.
Cause:
Obstruction caused by:
malpresentation
two fetuses together
small pelvic inlet
distended bladder
vaginal prolapse
vulval haematoma
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Secondary Uterine Inertia
Diagnosis:
Vaginal examination, wear gloves, hygiene.
Treatment:
Correct malpresentation, manually deliver fetus.
Once obstruction is relieved give 1-5iu of oxytocin I/m.
Caesarean sections are performed ? Economically justified
Ut i l
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Uterine prolapse.
Seen post-farrowing. (Pig is often in shock).
Treatment.
Euthanase or immediate on-farm slaughter. Cross fosterpiglets
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Vaginal Prolapse.Seen pre-farrowing
Replace and hold in place with purse stringsutures or Buhner suture. Use antibiotics to
reduce swelling.
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Swollen/damaged vulva
May follow vulva biting, trauma related todystocia, farrowing crate injuries, zearelenonetoxicity.
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Downer Sow.
Failure to rise in the periparturient period.
Many possible causes:
Lactation osteoporosis- fracture of pelvis/femur
Muscle weakness
Apophysiolysis
Rupture of lesser trochanter
T tm nt:
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Treatment:
Cull if fractures present:
Move onto deep straw or put straw rubber matting undersow to prevent sores. Encourage movement a few times aday.
Control:
Improve floor surfaces
With the banning of sow stalls restricted exercise pre-partum will be reduced.
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Lactation
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Lactation.Non-functioning teats
Teat necrosisTraumaInverted nipples (inherited)Poor mammary development.
Ergot poisoningPoor water supplyPoor energy levelsChronic mastitis
Can protect nipples from necrosis using copydex or rubberglue
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Agalactia.
Failiure to let down milk:
Bright and alert, particularly in gilts, failure to let downmilk. Restless, will not let piglets suckle; especially giltsthat are unable to relax.
Treatment:
Inject oxytocin (10iu) once.
Control:
Quiet calm environment for gilts. House earlier than sowsto help acclimatise to the farrowing house.
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Agalactia
Hot painful immature glands with normal milk:
Can affect large numbers of the herd at one time.
May be nutritional/hormonal imbalances.
Treatment:
NSAIDs. Repeated injections (every 3 hours). Can take > 3days to resolve so will need to supplement affected litters.
Control:
Check diet and husbandry.
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Agalactia.Ergot poisoning.
Poor mammary development, no response to oxytoxin.
Control.
Remove ergot from ration, by diluting out with normalgrain.
Check storage facilities.
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Agalactia.Water deprivation.Empty looking dried up glands, dry chalky deposit on vulva.
Control.Ensure adequate water supply, sows need up to 25-40l perday should not need to expend too much effort to get it.
Coliform Mastitis.
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Anorexia, pyrexia,
Loss of milk production - unhappy noisy piglets!
Udder is hot and swollen and may be hard around affectedglands.
Causal agents
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Causal agents.
Coliform bacteria.
Pseudomonas, Enterobacter, Citrobacter and Morganella.Most commonly E.coli, Klebsiella
Environmental pathogens,
RISK FACTORS:
Sawdust or shaving bedding,
Poorly drained solid floorsDamp wet bedding
Damaged teats: poor flooring, damage from piglets teeth
Coliform Mastitis.
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Little gross pathology, culture from milk samples, oxytocin mayhelp let down to obtain a sample.
Treatment.
Antibiotic treatment (potentiated sulphonamides) are required
for at least 3-5 days.
NSAIDs
Oxytocin encourages milk flow.
**Supply supplementary feeding for the surviving litter.**
Coliform Mastitis
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Control:
Ensure clean and dry farrowing areas.
Repair floors.
Clip piglets teeth.
Control biting flies.
Check there are sufficient functioning glands forfuture litters
Mastitis (pyogenic)
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Mastitis (pyogenic).
Sow is generally well.
Usually a single gland is affected hard and pendulous not hot.Often at the end of lactation or soon after weaning.
Milk production is permanently lost.
Causal factors.
Staphylococci or Streptococci (also Actinomyces) are involve
Risk Factors.
Damaged floors, teat damage biting flies
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Pyogenic mastitis.
Treatment:
Early diagnosis may warrant penicillin injections butabscesses frequently become walled off.
Control:
Repair floors
Control flies
clip teeth
Cull sows with
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Urinary Tract Disease.
Pyelonephritis/cystitis.
Sudden death 3 weeks post-mating, mid pregnancy,postpartum,
Haematuria,
Pyrexia,Bloody vulval discharge,
Fibrin, pus and blood when urinating,
Inappetance,Depression,
Death.
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Pyelonephritis/ cystitis
Treatment:
Ineffective once signs are seenVery early cases. Potentiated sulphonamides.
P.M.ECystitis, ureteritis, nephritis.
Pre weaning mortality
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Pre-weaning mortality
Predisposing causes
Lack of colostrum
Non viable pigs
Diseases AIAO
Fostering
Management
Sow factors
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Piglet mortalityCrushing
Chilling
Hypothermia
Bleeding into umbilicus
congenital abnormalities
PIGLET MORTALITY
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PIGLET MORTALITY
CRUSHED PIGLETS: The most commonlyreported cause of death in piglets.
Sow factorssuch as lameness, lack of exerciseor deafness may influence death rates.
Environmental factorssuch as slippery floors,lack of a warm lighted creep area, lack of afarrowing crate or bars to protect piglets.
Piglet Factors: splayleg, starvation, chilling anyillness.
STARVATION
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STARVATION
Very common cause of mortality, pigletsshould suck every couple of hours.
Sow factors:Gilts may be unwilling to let
piglets suck, mastitis, sore teats,insufficient teat numbers (cross foster).
Piglet factors: Splayleg, any illness, weak
piglets. Birth weights of
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Uterine temperature is about 39C, piglets arebadly designed to cope with temperaturefluctuations outside the uterus. Farrowing housetemperature (for piglets) should be 30C.
If no heat lamps are used the body temperatureof the piglet can drop by as much as 20C inthe first 30 minutes after birth. If the pigletsurvives it can take up to 10 days to regain
normal temperature. These piglets are alwayslethargic, fail to suckle lie close to the sow andrisk being crushed.
CHILLING
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CHILLING.
Once piglets suck their demand forwarmth drops to about 24oC
Also linked to low birth weights andhypoglycaemia, insufficiently warm creepareas, poor insulation and draughtproofing.
Outdoor pigs may get trapped outside byhigh curbs etc.
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CARBON MONOXIDE POISONING.
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Faulty heaters in the farrowing house canproduce this odourless gas, can increase
numbers of still born and cause piglet
deaths.
CONGENITAL ABNORMALITIES
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1. SPLAY LEG Affected piglets do the splits with their back legs. It is considered a
muscle weakness problem in adductor muscles in heavy, malepiglets.
2. ATRESIA ANI
If a bulging mass is visible it may be possible to cut through a layerof skin and form an anus, passage of faeces maintains the opening.Many will be presented as poor pigs with large pot bellies and haveto be euthanased.
3. EPITHELIOGENESIS IMPERFECTA
Raw patches of flesh with skin curled up at the edges on new-born
piglets. Piglets may die or recover. Must be differentiated from otherpig wounds. Possibly inherited so use different boar on sow at nextmating.
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The Tale of a Pig Called Shorty
Investigations on farm
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Investigations on farm
Farm record analysis
Identify key areas of underperformance
Work out a plan for the visit
Target potential causes of
underperformance
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