Reproduction of the Pig

Mandy Nevel


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. by
nutrition/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)
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.
UK PRODUCTION
Low production generally
Poor investment
Poor buildings
Poor hygiene, cleaning etc
Shortage of finishing accommodation
Pollution control
Pig production
/kg

-------------------------------------

Cost of prod p/s/y mortality

Target / interference levels
Need to establish what we want our sows to do
in reproductive terms before assessing
performance
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

Pigs life cycle the sow
Reach puberty ~ days age, kg
Mated on oestrus
Gestation days
Lactate weeks
Return to oestrus days later
Culled after


Reproductive life cycle
Puberty E2 mating gestation lactation WOI mating p6 cull
Gilts - selection
Age
Weight
Oestrus
Disease status
Litter size
Vaccinal status
Ovary
Oviduct
Pregnancy
Pregnancy
PG
Pregnancy Diagnosis
Non-return to oestrus
Ultrasound real time, A-mode, Doppler
Hormones
Visual

Farrowing - induction
Advantages Disadvantages
Management cost
Fostering risk of dates

Work out farm gestation length
Prostaglandin, oxytocin
Litter size
Total born
Total born alive
Still births
Mummies
Parity changes

Litter Vs Parity
0
2
4
6
8
10
12
1 2 3 4 5 6 7 8
Parity
L
i
t
t
e
r

s
i
z
e

Weaning to oestrus interval
Oestrus detection
Duration of oestrus
Insemination/mating timing
Body weight loss
Cost of empty days

Ovary
Oviduct
Optimum mating time
E2
Oestrus
ovulation
weaning
LACTATION WOI OESTRUS
hours
ovulation
weaning
LACTATION
weeks
WOI
days
OESTRUS
hours
Ability to increase productivity
p/s/y
Litter size number of litters pwm
Lactation gestation WOI
Weaning to farrowing
Return rates
Regular returns
Irregular returns
Abortions


Longevity
Culling rates
Age at culling

Targets and interference
Parameter Target Interference
p/s/y 24 22
Litter size 11.5 11
Still births <7% >10%
Mummies <1% >2%
WOI 5 days 7 days
Regular returns 8% 10%
Irregular returns <3% 4%
Abortions <1% >1%
Farrowing rate 87 85
Culling rate 35% >42%
Gestation: abortion, smedi, vaginal prolapse

Peri-parturient period
Sow: uterine prolapse, Lactation. Agalactia,
Mastistis
Piglet Mortality.chilling, crushing, starvation


Diseases of Reproduction.
Investigating porcine
abortion/still birth.


Only 30-40% of abortions are infectious
in origin.
Non-infectious causes of abortion.

Husbandry and management.
Stockmanship/hygiene
Management policies i.e. age structure of the
herd
Environment.
Season (heat stress)

Infectious Causes.
Opportunists.
Often ubiquitous microorganisms in the
environment.

Risk Factors.
Poor health of the sow (immunocompromise)
Poor hygiene
Specific Pathogens.
Swine influenza
Porcine reproductive and respiratory
syndrome,
leptospirosis
Erysipelas
Uncommon but when they do occur they
cause severe reproductive disease.
****Aujeszkys, ASF, CSF****
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 (<1% of cases)

**Immunosuppression animals are more vulnerable to
many secondary pathogens**
Porcine Reproductive and Respiratory Syndrome.
blue-eared pig disease.
Diagnosis:
>20% born dead
>25% die at <7days
>8% abortion/premature deaths
Suspect if have at least 2 of the above

Serology

Economics:
Severe economic effects in acute phase (where mainly
reproductive losses occur).

**Chronic effects may include raised disease levels in
grower pigs (immunosuppresive effects) **
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.
PRRS Vaccine available since 2001
*Vaccination against PRRS (when present
on farm) has decreased mortality seen
with PMWS.*
Leptospirosis. (L.bratislava).

Clinical signs.
Most commonly abortion and reproductive failiure

Risk factors;
Rodent reservoirs
Outdoor herds (wallows)
Diagnosis
Serology, dark ground microscopy, FAT

Treatment:
Antibiotic medication: Streptomycin, Tetracyclines. In
theory the whole herd should be treated at one time, this
rarely happens.
Recent moves towards the use of cattle lepto vaccines in
pigs.
Leptospirosis is a zoonoses notifiable in man.

Urine is the most common source of infection.
Leptospires gain entry via mucous membranes.
Laboratory investigations.
Sample at least three fetuses (and
placenta if poss).
Stomach contents and /or liver. If taken
aseptically may indicate opportunistic
infections.

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 antibody
Leptospira bratislava antibody
Swine Influenza (new serotypes?)
Also can do antigen detection tests.
Parvo, Lepto
Sow sampling.
Positive titres.
May indicate the presence of disease within a
herd.

A significant rise in titre on paired serology may
indicate a recent infection.
(not conclusive evidence of cause of abortion)

VLA Porcine Abortion Kit.
For a fixed fee will test sows serum for:

Swine influenza
Erysipelas
Parvovirus
PRRS
Leptospira
Other causes of intra-uterine
death
Not abortion!!

Think non-infectious as well as infectious
Variations in litters.
Small number born (<6), embryos lost pre-ossification.

Mummified foetuses/stillbirths/weak pigs of all
one size. = uterine environment affected at one time
(stress, fever).

Mummified foetuses/stillbirths/weak pigs of differing
sizes = prolonged damage to foetuses. Think infectious
causes (commonly viral - parvo, PRRS, not forgettingCSF
etc)


Marker Stages of Gestation.
<35days : most absorbed
35-40 days ossification begins
Fetuses dying >35days: mummified
fetuses through to stillborn piglets.
(aborted at any stage).
70d Fetus immunocompetant
Full Term 112-116 days.
Genetic factors
Parental/progeny
Nutrition
Micronutrient deficiencies i.e. Vit E and A
Toxic agents
Misuse of hormonal drugs
Chemicals (eg. teratogens in hemlock).
Mycotoxins i.e Zearalenone.
SMEDI
Stillbirth
Mummification
Embryonic Death
Infertility

SMEDI -type problems.
Majority caused by porcine parvovirus
porcine enteroviruses are less frequently implicated

Classic clinical signs:
Full-term litter consisting of
small mummified fetuses
full grown stillborn
live weakly piglets

***Rarely see abortion***
Parvovirus (SMEDI)
93% of UK herds infected.
Transmission:
oronasal/venereal

If non-pregnant become immune
If pregnant (depends on stage of gestation) smedi
Highest Risk animals:

Nave animal enters infected herd.

Carrier animal enters nave herd (ALL sows at risk)

Piglets born to immune sows (seronegative = nave)
Parvovirus (SMEDI)

Treatment: None

Control: Vaccination is available and is widely practised

Vaccinate 8 weeks before service on first occasion and 2
weeks before for subsequent boosters.

investigations
Management observations/questions
Clinical signs
Laboratory investigations
Aborted material
Serology

Cull sow tracts

Causes of stillbirth
Examine fetus to determine when death
occurred.
Pre partum-as for causes of abortion
Intrapartum usually non-infectious
Prolonged farrowing
Increased litter size (most deaths in last
third).
Older sows, > 5 litters
Causes of still birth
Overweight/emaciated sows
Elevated farrowing house temperatures
Mycotoxins
Environmental/stress I.e small farrowing
crates
Occasionally infectious causes get a rapid
increase in still births
Gross features of peri-partum
deaths.
Post partum deaths.

Mainly non-infectious:

Overlying and chilling
Weaker/smaller piglets most at risk


Monitoring abortion/ still birth
Sow Examination
Age
Condition score
Service 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
Approx age (days) = 21 + (3xcrown/rump length(cm))
Infection in-utero usually causes fetuses to
die at different gestational ages.

Toxic/nutritional causes will result in dead
fetuses of the same gestational age

Economics:
Severe economic effects in acute phase (where mainly
reproductive losses occur).

**Chronic effects may include raised disease levels in
grower pigs (immunosuppresive effects) **
Parturition
Primary Uterine Inertia.
Early cessation of farrowing or failure to start
farrowing (end of first stage labour).
Behavioural signs of nesting and milk may be
present.
No straining.
Causal Factors:
Lack of uterine contractility/tone.

Diagnosis:
Absence of straining.
Cervix is dilated.
No obstruction present.
Lack of uterine tone.
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 /or
NSAID.

Control:
Allow acclimatisation to the farrowing house and staff
Secondary Uterine Inertia.
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
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
Uterine prolapse.

Seen post-farrowing. (Pig is often in shock).


Treatment.
Euthanase or immediate on-farm slaughter. Cross foster
piglets
Vaginal Prolapse.
Seen pre-farrowing

Replace and hold in place with purse string
sutures or Buhner suture. Use antibiotics to
reduce swelling.

Swollen/damaged vulva
May follow vulva biting, trauma related to
dystocia, farrowing crate injuries, zearelenone
toxicity.
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


Treatment:
Cull if fractures present:
Move onto deep straw or put straw rubber matting under
sow to prevent sores. Encourage movement a few times a
day.

Control:
Improve floor surfaces
With the banning of sow stalls restricted exercise pre-
partum will be reduced.
Hypocalcaemia.
Occurs post farrowing:
Recumbency, coma, death.
Eclampsic form with convulsions.
Rapid Response to calcium boroglutanate IV/SC
Control:
Suspect on farms if see:
Still births
Retained placenta
Uterine inertia

Increase calcium levels in feed.

Lactation.
Non-functioning teats

Teat necrosis
Trauma
Inverted nipples (inherited)
Poor mammary development.
Ergot poisoning
Poor water supply
Poor energy levels
Chronic mastitis

Can protect nipples from necrosis using copydex or rubber
glue
Agalactia.
Failiure to let down milk:
Bright and alert, particularly in gilts, failure to let down
milk. Restless, will not let piglets suckle; especially gilts
that are unable to relax.
Treatment:
Inject oxytocin (10iu) once.
Control:
Quiet calm environment for gilts. House earlier than sows
to help acclimatise to the farrowing house.


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 > 3
days to resolve so will need to supplement affected litters.
Control:
Check diet and husbandry.
Agalactia.
Ergot poisoning.
Poor mammary development, no response to oxytoxin.
Control.
Remove ergot from ration, by diluting out with normal
grain.
Check storage facilities.
Agalactia.

Water deprivation.
Empty looking dried up glands, dry chalky deposit on vulva.

Control.
Ensure adequate water supply, sows need up to 25-40l per
day should not need to expend too much effort to get it.
Coliform Mastitis.

Anorexia, pyrexia,

Loss of milk production - unhappy noisy piglets!

Udder is hot and swollen and may be hard around affected
glands.
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 floors
Damp wet bedding
Damaged teats: poor flooring, damage from piglets teeth
Coliform Mastitis.
Little gross pathology, culture from milk samples, oxytocin may
help 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

Control:
Ensure clean and dry farrowing areas.
Repair floors.
Clip piglets teeth.
Control biting flies.
Check there are sufficient functioning glands for
future litters

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 involved

Risk Factors.
Damaged floors, teat damage biting flies
Pyogenic mastitis.
Treatment:
Early diagnosis may warrant penicillin injections but
abscesses frequently become walled off.
Control:
Repair floors
Control flies
clip teeth
Cull sows with <10 functional teats.
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.
The bacterium Actinobaculum suis is found in the prepuce of
most boars >10 weeks old.
(Previous names = Eubacterium suis, Actinomyces suis,
Corynebacterium suis.)

Risk Factors:
Indoor herds
The condition (and all vulval discharges) is more common
Higher environmental contamination.
Faecal organisms.(E.coli, proteus, pseudomonas)
Pyelonephritis/ cystitis

Treatment:
Ineffective once signs are seen
Very early cases. Potentiated sulphonamides.

P.M.E
Cystitis, ureteritis, nephritis.
Pre-weaning mortality
Predisposing causes
Lack of colostrum
Non viable pigs
Diseases AIAO
Fostering
Management
Sow factors

Piglet mortality
Crushing
Chilling
Hypothermia
Bleeding into umbilicus
congenital abnormalities
PIGLET MORTALITY

CRUSHED PIGLETS: The most commonly
reported cause of death in piglets.
Sow factors such as lameness, lack of exercise
or deafness may influence death rates.
Environmental factors such as slippery floors,
lack of a warm lighted creep area, lack of a
farrowing crate or bars to protect piglets.
Piglet Factors: splayleg, starvation, chilling any
illness.

STARVATION
Very common cause of mortality, piglets
should 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 <1kg need help,
<0.75kg are unlikely to live.

CHILLING.

Uterine temperature is about 39C, piglets are
badly designed to cope with temperature
fluctuations outside the uterus. Farrowing house
temperature (for piglets) should be 30C.
If no heat lamps are used the body temperature
of the piglet can drop by as much as 20C in
the first 30 minutes after birth. If the piglet
survives it can take up to 10 days to regain
normal temperature. These piglets are always
lethargic, fail to suckle lie close to the sow and
risk being crushed.

CHILLING.

Once piglets suck their demand for
warmth drops to about 24
o
C
Also linked to low birth weights and
hypoglycaemia, insufficiently warm creep
areas, poor insulation and draught
proofing.
Outdoor pigs may get trapped outside by
high curbs etc.

UMBILICUS
About 1 in 5 have umbilicus broken before
birth resulting in bleeding from the
umbilical stub. These tend to take longer
to suck, piglets can die from blood loss.
CARBON MONOXIDE POISONING.

Faulty heaters in the farrowing house can
produce this odourless gas, can increase
numbers of still born and cause piglet
deaths.


CONGENITAL ABNORMALITIES

1. SPLAY LEG
Affected piglets do the splits with their back legs. It is considered a
muscle weakness problem in adductor muscles in heavy, male
piglets.

2. ATRESIA ANI
If a bulging mass is visible it may be possible to cut through a layer
of skin and form an anus, passage of faeces maintains the opening.
Many will be presented as poor pigs with large pot bellies and have
to 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 other
pig wounds. Possibly inherited so use different boar on sow at next
mating.
The Tale of a Pig Called Shorty
Investigations on farm
Farm record analysis
Identify key areas of underperformance
Work out a plan for the visit
Target potential causes of
underperformance
p/s/y

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litter size woi pwm