Reproduction of the pig Flashcards
optimum sow
Gilt – age at first mating, - 8 monthd Litter size - 14 Pre-weaning mortality <7 days Weaning to farrowing 115 + 5 days (Food efficiency) Longevity - 6
pigs life cycle
Reach puberty ~ 140 days age, 120 kg Mated on oestrus Gestation 115 days Lactate 4 weeks Return to oestrus 5 days later Culled after 6 parities 28 days until weanng
gilts - selection
Age Weight Oestrus Disease status Litter size Vaccinal status
pregnancy diagnosis
Non-return to oestrus
Ultrasound real time, A-mode, Doppler
hormones
Visual
farrowing induction
prostaglandin
oxytocin
farrowing induction - advantages
management
fostering
farrowing induction - disadvantages
cost
risk of dates
litter size
Total born Total born alive Still births Mummies Parity changes
Weaning to oestrus interval
Oestrus detection Duration of oestrus Insemination/mating timing Body weight loss Cost of empty days
optimum mating time
sperm needed in the oviduct before ovulation
oestrus
lactation - 3 weeks
weaning to oestrus interval (WOI) - 6 days
oestrus - 48h
shorter WOI gives longer oestrus period
weaning to farrowing
Return rates – Regular/irregular returns
Abortions
longevity
culling rates
age at culling
diseases of gestation
abortion
smedi
vaginal prolapse
disease of peri-parturient period
Sow: uterine prolapse, Lactation. Agalactia, mastistis
Piglet Mortality.chilling, crushing, starvation
Non-infectious causes of abortion
Stockmanship/hygiene
Management policies i.e. age structure of the herd
Season (heat stress)
abortion - Specific Pathogens
Swine influenza Porcine reproductive and respiratory syndrome, leptospirosis Erysipelas Uncommon but when they do occur they cause severe reproductive disease.
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 (25% die at 8% abortion/premature deaths
Economics - severe economic effects in acute phase, Chronic effects may include raised disease levels in grower pigs (immunosuppresive effects)
Porcine Reproductive and Respiratory Syndrome.
“blue-eared” pig disease - treatment
Supportive, treat secondary pathogens
Control: Originally notifiable, now reported
throughout the UK.
vaccinate
Leptospirosis. (L.bratislava)
Urine is the most common source of infection
Leptospires gain entry via mucous membranes
abortion and reproductive failiure
Risk factors; Rodents, Outdoor herds
Diagnosis - serology, dark ground microscopy, FAT
zoonotic
Leptospirosis. (L.bratislava) - 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
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
can also do antigen detection
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.
VLA Porcine Abortion Kit - tests for
Swine influenza Erysipelas Parvovirus PRRS Leptospira
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 forgetting……CSF etc)
Marker Stages of Gestation
35days: mummified fetuses through to stillborn piglets. (aborted at any stage).
70d Fetus immunocompetant
Full Term 112-116 days.
SMEDI
Stillbirth Mummification Embryonic Death Infertility porcine parvovirus most common cause
SMEDI - clinical signs
Full-term litter consisting of small mummified fetuses full grown stillborn live weakly piglets Rarely see abortion
parvovirus
93% of UK herds infected
Transmission - oronasal/venereal
If non-pregnant become immune
If pregnant (depends on stage of gestation) smedi
parvovirus - highest risk animals
Naïve animal enters infected herd.
Carrier animal enters naïve herd (ALL sows at risk)
Piglets born to immune sows (seronegative = naïve)
parvovirus - treatment + control
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.
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
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
sow exam
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
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.
primary uterine inertia - diagnosis
Absence of straining.
Cervix is dilated.
No obstruction present.
Lack of uterine tone.
primary 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.
secondary uterine inertia - causes
Obstruction caused by: malpresentation two fetuses together small pelvic inlet distended bladder vaginal prolapse vulval haematoma
secondary uterine inertia - diagnosis + treatment
Diagnosis - vaginal exam, wear gloves, hygiene.
Treatment - Correct malpresentation, manually deliver fetus, Once obstruction is relieved give 1-5iu of oxytocin I/m.
Caesarean? Economically justified?
uterine prolapse
post-farrowing
Treatment - Euthanase or immediate on-farm slaughter. Cross foster piglets
vaginal prolapse
pre-farrowing
Replace and hold in place with purse string sutures or Buhner suture. Use antibiotics to reduce swelling
swollen/damaged vulva
vulva biting, trauma with dystocia, farrowing crate injury, zearelenone toxicity
downer sow
Failure to rise in the periparturient period.
causes:
Lactation osteoporosis- fracture of pelvis/femur
Muscle weakness
Apophysiolysis
Rupture of lesser trochanter
downer sow - treatment + control
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.
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
hypocalcaemia - signs
Still births
Retained placenta
Uterine inertia
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.
agalactia - treatment
single oxytocin injection
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
agalactia - Hot painful immature glands with normal milk - treatment
NSAIDs. Repeated injections (every 3 hours). Can take > 3 days to resolve so will need to supplement affected litters.
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 - 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
coliform mastitis - cause
Coliform bacteria.
Pseudomonas, Enterobacter, Citrobacter and Morganella.
Most commonly E.coli, Klebsiella
Environmental pathogens
coliform mastitis - risk factors
Sawdust or shaving bedding,
Poorly drained solid floors
Damp wet bedding
Damaged teats: poor flooring, damage from piglets teeth
coliform mastitis - 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.
Staph. Strep. (also Actinomyces)
Damaged floors, teat damage biting flies
pyogenic mastitis - treatment + control
Early diagnosis may warrant penicillin injections but abscesses frequently become walled off. Repair floors Control flies clip teeth Cull sows with <10 functional teats
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.
actinobaculum suis found in most boar’s prepuce
Pyelonephritis/cystitis - risk factors
Indoor herds
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.
piglet mortality
Crushing
Chilling
Hypothermia
Bleeding into umbilicus
congenital abnormalities
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
piglets should suckle every 1-2h
Gilts may be unwilling to let piglets suck, mastitis, sore teats, insufficient teat numbers
Splayleg, any illness, weak piglets. Birth weights of <0.75kg are unlikely to live
chilling
Farrowing house temperature (for piglets) should be 30°C.
piglet body temp can drop rapidly and these piglets can take a long time to recover
linked to low birth weights and hypoglycaemia, insufficiently warm creep areas, poor insulation and draught proofing.
outdoor piglets may get trapped outside
umbilicus
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 - 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.
congenital abnormalities - 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.
congenital abnormalities - 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
investigations on farm
Farm record analysis
Identify key areas of underperformance
Work out a plan for the visit
Target potential causes of underperformance
