bvetmed3 pig reprod 2013 mn

8/12/2019 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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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


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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bvetmed3 pig reprod 2013 mn

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