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Reproduction > Reproduction of the pig > Flashcards

Reproduction of the pig Flashcards

1
Q

optimum sow

A 
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
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2
Q

pigs life cycle

A 
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
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3
Q

gilts - selection

A 
Age 
Weight 
Oestrus 
Disease status 
Litter size 
Vaccinal status
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4
Q

pregnancy diagnosis

A

Non-return to oestrus
Ultrasound real time, A-mode, Doppler
hormones
Visual

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5
Q

farrowing induction

A

prostaglandin

oxytocin

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6
Q

farrowing induction - advantages

A

management

fostering

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7
Q

farrowing induction - disadvantages

A

cost

risk of dates

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8
Q

litter size

A 
Total born 
Total born alive 
Still births 
Mummies 
Parity changes
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9
Q

Weaning to oestrus interval

A 
Oestrus detection 
Duration of oestrus 
Insemination/mating timing 
Body weight loss 
Cost of empty days
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10
Q

optimum mating time

A

sperm needed in the oviduct before ovulation

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11
Q

oestrus

A

lactation - 3 weeks
weaning to oestrus interval (WOI) - 6 days
oestrus - 48h
shorter WOI gives longer oestrus period

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12
Q

weaning to farrowing

A

Return rates – Regular/irregular returns

Abortions

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13
Q

longevity

A

culling rates

age at culling

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14
Q

diseases of gestation

A

abortion
smedi
vaginal prolapse

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15
Q

disease of peri-parturient period

A

Sow: uterine prolapse, Lactation. Agalactia, mastistis

Piglet Mortality.chilling, crushing, starvation

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16
Q

Non-infectious causes of abortion

A

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

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17
Q

abortion - Specific Pathogens

A 
Swine influenza 
Porcine reproductive and respiratory 
syndrome, 
leptospirosis 
Erysipelas 
Uncommon but when they do occur they 
cause severe reproductive disease.
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18
Q

Porcine Reproductive and Respiratory Syndrome.

“blue-eared” pig disease

A

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)

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19
Q

Porcine Reproductive and Respiratory Syndrome.

“blue-eared” pig disease - treatment

A

Supportive, treat secondary pathogens
Control: Originally notifiable, now reported
throughout the UK.
vaccinate

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20
Q

Leptospirosis. (L.bratislava)

A

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

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21
Q

Leptospirosis. (L.bratislava) - treatment

A

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

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22
Q

Laboratory investigations.

A

Sample at least three fetuses (and placenta if poss).

Stomach contents and /or liver. If taken aseptically may indicate opportunistic infections.

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23
Q

fetal fluid

A

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

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24
Q

sow sampling

A

Positive titres.
May indicate the presence of disease within a
herd.
A significant rise in titre on paired serology may
indicate a recent infection.

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25
Q

VLA Porcine Abortion Kit - tests for

A 
Swine influenza 
Erysipelas 
Parvovirus 
PRRS 
Leptospira
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26
Q

Variations in litters

A

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)

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27
Q

Marker Stages of Gestation

A

35days: mummified fetuses through to stillborn piglets. (aborted at any stage).
70d Fetus immunocompetant
Full Term 112-116 days.

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28
Q

SMEDI

A 
Stillbirth 
Mummification 
Embryonic Death 
Infertility
porcine parvovirus most common cause
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29
Q

SMEDI - clinical signs

A 
Full-term litter consisting of 
small mummified fetuses 
full grown stillborn 
live weakly piglets 
Rarely see abortion
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30
Q

parvovirus

A

93% of UK herds infected
Transmission - oronasal/venereal
If non-pregnant become immune
If pregnant (depends on stage of gestation) smedi

31
Q

parvovirus - highest risk animals

A

Naïve animal enters infected herd.
Carrier animal enters naïve herd (ALL sows at risk)
Piglets born to immune sows (seronegative = naïve)

32
Q

parvovirus - treatment + control

A

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.

33
Q

causes of stillbirth

A

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

34
Q

sow exam

A 
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
35
Q

primary uterine inertia

A

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.

36
Q

primary uterine inertia - diagnosis

A

Absence of straining.
Cervix is dilated.
No obstruction present.
Lack of uterine tone.

37
Q

primary uterine inertia - treatment

A

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

38
Q

secondary uterine inertia - clinical signs

A

2nd stage labour, sow is straining but no effect and may become exhausted.

39
Q

secondary uterine inertia - causes

A 
Obstruction caused by: 
malpresentation 
two fetuses together 
small pelvic inlet 
distended bladder 
vaginal prolapse 
vulval haematoma
40
Q

secondary uterine inertia - diagnosis + treatment

A

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?

41
Q

uterine prolapse

A

post-farrowing

Treatment - Euthanase or immediate on-farm slaughter. Cross foster piglets

42
Q

vaginal prolapse

A

pre-farrowing

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

43
Q

swollen/damaged vulva

A

vulva biting, trauma with dystocia, farrowing crate injury, zearelenone toxicity

44
Q

downer sow

A

Failure to rise in the periparturient period.
causes:
Lactation osteoporosis- fracture of pelvis/femur
Muscle weakness
Apophysiolysis
Rupture of lesser trochanter

45
Q

downer sow - treatment + control

A

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.

46
Q

hypocalcaemia

A

Occurs post farrowing:
Recumbency, coma, death.
Eclampsic form with convulsions.
Rapid Response to calcium boroglutanate IV/SC

47
Q

hypocalcaemia - signs

A

Still births
Retained placenta
Uterine inertia

48
Q

non-functioning teats

A 
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
49
Q

agalactia

A

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.

50
Q

agalactia - treatment

A

single oxytocin injection
calm environment for gilts.
House earlier than sows to help acclimatise to the farrowing house.

51
Q

agalactia - Hot painful immature glands with normal milk

A

Can affect large numbers of the herd at one time.

May be nutritional/hormonal imbalances

52
Q

agalactia - Hot painful immature glands with normal milk - treatment

A

NSAIDs. Repeated injections (every 3 hours). Can take > 3 days to resolve so will need to supplement affected litters.
Check diet and husbandry

53
Q

agalactia - ergot poisoning

A

Poor mammary development, no response to oxytoxin.

Control - Remove ergot from ration, by diluting out with normal grain, check storage facilities.

54
Q

agalactia - water deprivation

A

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.

55
Q

coliform mastitis

A

Anorexia, pyrexia,
Loss of milk production - unhappy noisy piglets
Udder is hot and swollen and may be hard around affected glands

56
Q

coliform mastitis - cause

A

Coliform bacteria.
Pseudomonas, Enterobacter, Citrobacter and Morganella.
Most commonly E.coli, Klebsiella
Environmental pathogens

57
Q

coliform mastitis - risk factors

A

Sawdust or shaving bedding,
Poorly drained solid floors
Damp wet bedding
Damaged teats: poor flooring, damage from piglets teeth

58
Q

coliform mastitis - treatment

A

Antibiotic treatment (potentiated sulphonamides) are required for at least 3-5 days.
NSAIDs
Oxytocin encourages milk flow.
Supply supplementary feeding for the surviving litter

59
Q

coliform mastitis - control

A 
Ensure clean and dry farrowing areas. 
Repair floors. 
Clip piglets teeth. 
Control biting flies. 
Check there are sufficient functioning glands for future litters
60
Q

mastitis (pyogenic)

A

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

61
Q

pyogenic mastitis - treatment + control

A 
Early diagnosis may warrant penicillin injections but abscesses frequently become walled off.  
Repair floors 
Control flies 
clip teeth 
Cull sows with <10 functional teats
62
Q

Pyelonephritis/cystitis

A

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

63
Q

Pyelonephritis/cystitis - risk factors

A

Indoor herds
Higher environmental contamination.
Faecal organisms.(E.coli, proteus, pseudomonas)

64
Q

Pyelonephritis/cystitis - treatment

A

Ineffective once signs are seen
Very early cases. Potentiated sulphonamides.
P.M.E
Cystitis, ureteritis, nephritis.

65
Q

piglet mortality

A

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.

66
Q

starvation

A

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

67
Q

chilling

A

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

68
Q

umbilicus

A

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

69
Q

carbon monoxide poisoning

A

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

70
Q

congenital abnormalities - splay leg

A

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

71
Q

congenital abnormalities - atresia ani

A

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.

72
Q

congenital abnormalities - epitheliogenesis imperfecta

A

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

73
Q

investigations on farm

A

Farm record analysis
Identify key areas of underperformance
Work out a plan for the visit
Target potential causes of underperformance

Reproduction (25 decks)

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