Milk production in sows

Question 1

Describe the sow’s mammary gland.

Answer 1

The actual number of glands varies between 12 and 18, pigs of the Meishan breed can have up to 22 mammary glands.

The thoracic glands produce the most milk.

There are usually two complete gland systems within each mammary gland of the pig.

Image of teats: 1-3 are functional, 4-inverted and 5-non-functional are not desirable.

Question 2

Ideal teat placement for replacement sows.

Answer 2

Boars and gilts retained for breeding purposes should have more then 14 well-placed normal nipples with the rows of teats properly parallel for proper teat presentation.

Question 3

Why are the last-born piglets typically weaker?

Answer 3

Prolonged farrowing time contributes to hypoxia.
They may also get less colostrum.

Question 4

The mammary glands of the lactating sow are composed of

Answer 4

a compound tubuloalveolar tissue with the secretory units arranged in lobules.

The lobules are lined by epithelial cells (lactocytes) that synthesize milk. These secreting units are connected by a non-secreting duct system to an ostium found in the teat.

There are usually two complete gland systems within each mammary gland of the pig.

There is no muscular sphincter around the teat orifice, therefore, intramammary treatment by way of the teat opening is not possible.

Question 5

Age of puberty in sows.

Answer 5

5-7 months old

Question 6

Nutrition in the two periods of rapid mammary development impacts the extent of development. When are the 2 periods?

Answer 6

from 90 days of age until puberty and during the last third of gestation

Either a 20% or a 26% feed restriction from 90 days of age until puberty drastically reduces mammary tissue mass.

Gilts fed 2.3 g/day of phytoestrogen genistein from 3 months of age until puberty had a 44% increase in the number of mammary cells at 183 days.

Question 7

How might feeding high energy feeds during gestation affect mammary gland development of the sow before farrowing?

Answer 7

During gestation, feeding very high energy levels (44 vs. 24 MJ ME/day) may have detrimental effects on mammary development and subsequent milk production whereas increasing the amount of dietary protein (16 vs. 4 g lysine/day) did not affect mammary development but may increase subsequent milk production.

Overly fat gilts (36 mm backfat at the end of gestation) on a high energy-low protein diet had reduced mammary development and produced less milk than leaner gilts (25 mm backfat) at the same body weight.

Question 8

Lactogenesis is the ability of mammary glands to synthesize milk components (lactose, casein, lipids).

Involves 2 phases:

Answer 8

I phase – preparation for lactation phase 90(105) - 115 gd

II phase: colostral phase and lactation
- Colostral (12-24 h), ascending (10-14 days), plateau and descending.

Question 9

Physiological process of preparation to lactate within the sow’s body.

Answer 9

Prostaglandin is carried from the uterus to the ovary, where it stops the production of progesterone (luteolysis) and stimulates the release of relaxin for dilating the cervix.

At the same time, prostaglandin is carried to the sow’s pituitary glands and causes release of oxytocin into the bloodstream. Oxytocin causes contractions of smooth muscles in the milk glands (milk letdown) and in the uterus (expulsion of piglets).

Stimulation of the sow’s udder by nursing pigs or through rubbing by hand can stimulate release of oxytocin further, causing more contractions for piglet delivery.

“Relaxin increases
Progesterone decreases
Relaxin then decreases
Prolactin increases”

Question 10

Physiological process of Lactation: colostral phase. 4 points to remember:

Answer 10

High concentration of lactose (>200mmol/L) in blood plasma.

Blood plasma immunoglobulins migrate to mammary glands.

Cervix swelling and sow moving before farrowing - colostrum ejection.

Colostrum is ejected from alveoli every 10-20 minutes.

2.5-5 kg of colostrum is produced

Question 11

Sow colostrum contains a lot of protein, what protein and how much?

Answer 11

Mainly immunoglobulins – 60-80 g/l, less fat and less sugar than cow milk.

It contains 157, 130, 9 and 6 grams of protein per liter at 0, 6, 12 and more than 12 h after the first suckling so it clearly decreases acutely the more time goes on from farrowing.

Colostral phase ends completely 24 h after the start of farrowing.

2.5-5 kg of colostrum is produced

Question 12

Physiological process of Lactation: II phase, lactation. 4 points to remember:

Answer 12

Low concentration of lactose (>100mmol/L) in blood plasma at this point.

Secretion of immunoglobulins in mammary glands.

Cyclic secretion of milk, synchronous with the sow’s grunting.

Stimulation of the udder (massage or piglets) induces oxytocin which induces the myoepithelial bascket cells in the mammary glands to contract.

Question 13

How frequently do the piglets nurse?

Answer 13

Up to > 24 times per 24 hours, for 4-5 minutes at a time.

Minimum nursing interval of 35 minutes is required for proper refill of the mammary glands.

Piglets choose ‘their’ gland 48-72 h post-partum.

Question 14

How much milk do sows produce per day?

Answer 14

5-11 kg of milk per day

Minimum nursing interval of 35 minutes is required for proper refill of the mammary glands.

Piglets are weaned mostly at the plateau lactation phase.

Question 15

Inadequate milk production in sows leads to (2)

Answer 15

Leads to reduced piglet growth and to increased mortality in the litter.

Question 16

There are numerous factors affecting sow milk production, what are 3 “built-in” physiological factors?

Answer 16

The number of lactocytes (of epithelial cells) producing the milk.

The intensity of milk synthesis by lactocytes.

The capacity of the other organs and systems to supply the nutrients needs by the mammary gland.

Question 17

Manipulation of milk production. Lactation feeding strategies? (2)

g/day of crude lysine required?

Answer 17

Body reserves might be sufficient in early lactation but not in late lactation.

The impact of lactating sows’ feed intake on litter-weight becomes larger as lactation progresses.

The intake of protein/amino acids is critical for lactation performance.

45-55 g/day of crude lysine are required for normal and high-yielding sows.

Sows can mobilize amino acids from muscle to support mammary growth and milk production.

Question 18

Main 4 diseases of the sow mammary gland.

Answer 18

Mastitis

PPDS - postpartum dysgalactia syndrome

Actinomycosis

MMA syndrome - mastitis-metritis-agalactia syndrome

Question 19

Describe mastitis in sows. (4+)

Answer 19

May affect only one or a few mammary glands. Post-weaning or dry-sow mastitis usually affects one or a few glands as well. A non-suckled mammary gland is a candidate for infection.

Acute mastitis is usually accompanied by systemic and local signs.

Mainly occurs within the first 3 days post-partum.

Chronic mastitis is characterized by the formation of abscesses and granulomas.

Redness, heat, keeping the piglets from suckling, hungry noisy piglets.

The cranial teats appear to be more at risk of trauma which predisposes to mastitis.

Question 20

Bacteria involved in sow mastitis. (3+2)

Answer 20

Gram-negative: E. Coli, Enterobacter, Klebsiella

Gram-positive : streptococci, staphylococci

Tx: no intramammary possible in sows, can use topical liniments, oxytocin inj. to clear out infection with more milk.

Question 21

Describe PPDS - postpartum dysgalactia syndrome in sows. (4+)

Answer 21

Insufficient colostrum and milk production during the first days post-partum. You can identify this based on the piglets; the piglets will be at the udder nuzzling constantly but their body condition will decrease.

Pathways of pathophysiology:
- Sow eating and drinking inadequately
- Endotoxins
- Stress (heat stress, 1st timers)
- „Body building syndrome“ („fat sow syndrome“ and „over-muscled sow syndrome“)

Try to decrease the sows’ stress, give more fiber too.

Minimum 2L/min water flow required for lactating sows.
Tip: beer can be given to first-time farrowing sows in order to destress them.

Question 22

Describe actinomycosis in sows. (4)

Answer 22

Bacterial infection caused by anaerobic Actinomyces suis. Same family of bact. that causes actinomycosis/lumpy jaw in cattle (A.bovis).

Is normal flora of the oral and nasopharyngeal membranes but when it gets in the mammary glands is causes pyogranulomatous porcine mastitis = hardened lumps (abscesses) in the udder tissue.

Chronic, deep-seated abscesses may fistulate through the skin, draining tracts.

Occasionally pyogranulomatous infections develop in lungs, spleen, kidneys, and other organs.

Slow progression differentiates it from acute mastitis.

Palpate all sow udders when they are in the 2nd gestation of pregnancy (when the udder is smallest) in order to feel for the actinomycosis lumps easiest.
Tx: penicillin, erythromycin

Question 23

Describe the etiology of MMA syndrome - mastitis-metritis-agalactia syndrome in sows. (4+)

Answer 23

Mastitis–metritis–agalactia syndrome is caused by bacteria and their toxins.
- E. Coli
- ß hemolytic streptococci

Hormonal factors influence this as well (insulin, cortisone, prolactin, oxytocin, estrogen, progesterone).

Question 24

Clinical signs of MMA syndrome. (6)

Answer 24

mastitis-metritis-agalactia syndrome

Anorexia
Sternal recumbency
Piglets lean, weak, have diarrhea
Sow’s udder is hard
Milk production disturbed
Vaginal discharge

Question 25

Tx of MMA syndrome. (4)

Answer 25

mastitis-metritis-agalactia syndrome AB Oxytocin NSAIDs Milk substitutes for piglets

Question 26

Describe vaginal discharge syndrome in sows.

Answer 26

Etiology: - Post-farrowing; β-hemolytic Streptococcus, Arcanobacterium pyogenes, Actinobacillus suis, Bacteroides spp. Clostridium spp. - Post-mating; E. coli and Staph. hyicus Diagnose with vaginoscopy, endoscopy. NB Some vaginal discharge is normal a couple of days after farrowing and mating. ## Footnote Signs: vag discharge, increase in recurrent estrus

Question 27

Tx of vaginal discharge syndrome. (3)

Answer 27

definitely AB Hygiene (spread of infection) Boars: examination, tests, treatment (can be carriers of bacteria)

Question 28

Describe PPV in swine. (5)

Answer 28

Porcine parvovirus, DNA virus, causes cell lysis. Endemic throughout the world. Normal inhabitant of pig GI tract. Virus is thermostable, resistant to many common disinfectants. Some strains of porcine parvo are completely non-pathogenic, others can cause disease even in immunocompetent fetuses (after day 70 of gestation). Pig fetuses are sensitive to parvovirus before day 70 of gestation. Parvo causes various sized fetal mummies. ## Footnote Immunotolerant carriers of porcine parvo are a result of early in-utero infection.

Question 29

Describe PPV vaccination in swine. (5)

Answer 29

Porcine parvovirus Once a pig is exposed, there is a lifelong immunity. But due to replacing stock - cyclicity of disease resurgence occurs: Reproductive problems may appear every 3-4 years in a herd if vaccination is not carried out. Pig fetuses are sensitive to parvovirus before day 70 of gestation. Vaccination is the only way to protect fetuses, and does not protect the sow herself. Vaccination of sows only protects their fetuses for approx. 4 months. Gilts: Usually vaccinated twice before their first breeding, with the second dose given 2-3 weeks before insemination. Sows: Sows are typically vaccinated before insemination, during the pre-breeding period. Typically receive a booster before each breeding cycle, often at weaning.

Question 30

Routes of infection of porcine parvo virus.

Answer 30

horizontal oronasal, seminal fluid vertical transplacental But every piggery in the world likely has porcine parvo in it.

Question 31

Clinical signs of porcine parvovirus. (4)

Answer 31

- fetal mummification - fetal time of death differing (various sized mummies) - maternal reproductive failure: recurrent or delayed estrus - abortions can happen but is not typical ## Footnote acute infection in sows is usually subclinical. transient leukopenia within 10 days after initial exposure but you won't see this if you're not running bloods

Question 32

Affect of porcine parvo virus on sow pregnancies. (4)

Answer 32

Up till day 35 of gestation: embryonic death. Between day 35-70 of gestation: embryonic death followed by mummification. After day 70 of gestation: infection is subclinical. NB! Typical: there can be mummified pigs of different sizes, stillborn and live piglets with reduced neonatal vitality in the same litter.

Question 33

Diagnosis of porcine parvo virus by: (4)

Answer 33

Must send several mummified fetuses (smaller then ≤16 cm in length) to the laboratory. - Identification of viral antigen by IF microscopy (in the absence of a fetal antibody). - PCR - Detection of viral hemagglutinin And/or Serologic assays

Question 34

TX of porcine parvo.

Answer 34

No treatment. Infection or vaccination of gilts before they are bred (rather than during gestation). The use of vaccine is the only way to ensure that gilts develop active immunity before conception.

Question 35

Various alt. names for leptospirosis in swine. Reservoir of infection for pigs?

Answer 35

Weil’s Syndrome Swamp Fever, Mud Fever Autumn Fever (Akiyami), Swineherd’s Disease Rice-Field Fever Cane-Cutter’s Fever Hemorrhagic Jaundice Stuttgart Disease Canicola Fever Redwater of Calves - Rodents spread it.

Question 36

Describe leptospirosis in swine. (3)

Answer 36

Most common zoonosis in the world. Endemic infection, may produce little evidence of clinical disease. However, Can cause very appreciable losses through abortion or birth of dead or weak piglets, if it is first introduced, or during periods of waning herd immunity.

Question 37

Lepto in swine is caused by the following species: (5)

Answer 37

Caused by a variety of morphologically similar, but genetically distinct small gram-negative motile aerobic spirochetes. L. pomona L. tarassovi L. bratislava L. Muenchen L. icterohaemorrhagiae

Question 38

Routes of infection for lepto in pigs. (4)

Answer 38

Via the mucous membranes of the eye, mouth, nose, vagina Transmission through milk Is excreted in urine and genital fluids Frequently, swine do not show signs of infection but shed large amounts of leptospires in their urine for periods of up to one year following infection.

Question 39

Signs of acute lepto in swine herds. (5)

Answer 39

anorexia, pyrexia, jaundice (High proportion of these undergo spontaneous recovery.) hemoglobinuria, death can occur

Question 40

Signs of chronic lepto in swine herds. (5)

Answer 40

abortions in the last third of pregnancy, reduced conception rate, vulvar discharge, stillborn or weak piglets, reduced litter size

Question 41

Lepto lesions in organs. (7)

Answer 41

Multifocal haemorrhages Petechial and ecchymotic hemorrhages in the lungs Minor renal tubular damage Focal liver necrosis Meningoencephalitis Scattered small gray foci in the kidneys , often surrounded by a ring of hyperemia, fibrosis. Jaundice in some aborted piglets.

Question 42

Diagnosis of lepto in pigs. (3)

Answer 42

Late-term abortions are typical to lepto in pigs. Detection of antibodies (at least 10 animals or 10% of the herd should be tested). Demonstration of leptospires (liver, lungs, brain, blood, fetal organs, placenta after abortion, urine). (isolation is difficult) - PCR is the most sensitive method of detecting leptospires.

Question 43

Tx of lepto in pigs. (3)

Answer 43

Antibiotic therapy only of acute lepto (streptomycin, oxytetracycline, tylosine, erythromycin). Vaccination (relatively short duration) during gestation to protect fetuses. Management to limit spread of infection.

Question 44

Brucellosis in pigs is caused by: (3)

Answer 44

gram-negative coccobacilli (short rods) Brucella suis (biovars 1, 2, 3) B. abortus B. melitensis All of the above are zoonoses except for biovar 2 of B.suis! | Found worldwide but eradicated in most places like Estonia. ## Footnote Wildboar reservoir.

Question 45

Brucellosis in pigs is characterized by

Answer 45

Characterized by granulomatous inflammation in a variety of organs including the reproductive tract organs. Severity of disease depends on the virulence and dose of the infecting strain and resistance of the host.

Question 46

Transmission and routes of entry for Brucella bacteria.

Answer 46

Direct contact, aerosol, ingestion of infected materials. Contaminated feed, water, premises. Via mucosa - oral, conjunctival or penetration through breaks in the skin. Insemination with semen from infected boars. Vertical through milk. The main risk – introduction of infected live animals that have been in contact with infected wildlife reservoirs, Indirect transmission through mechanical vectors such as dogs, cats, wild carnivores has been suspected. Has also been shown to persist in some arthropods such as the tick. ## Footnote At the time of abortion; fetuses, placentas and vaginal discharge contain myriad B. suis bacteria.

Question 47

Uterine and vaginal shedding of brucellosis usually ends by

Answer 47

40 days (3-36 months) after abortion.

Question 48

B. suis differ from most other brucellae by its propensity for

Answer 48

venereal transmission, as well as vertical transmission.

Question 49

The majority of congenitally infected pigs clear the brucella infection by

Answer 49

6 months of age, but some of pigs are still tissue positive at 2 years of age. Soe Congenitally infected pigs may become latent carriers.

Question 50

Clinical signs of brucellosis in sows. (7)

Answer 50

Abortions (at any stage of gestation, but mostly early-stage, 21-27 days of gestation). Stillbirths Increased perinatal mortality Metritis Placental retention (very rare in pigs!) Infertility Persistence of uterine infection 30-40 days after abortion (4-36 months).. ## Footnote Can go undetected completely.

Question 51

Clinical signs of brucellosis in boars. (3)

Answer 51

Chronic infection is more often in males (up to 42 months old): Granulomatous orchitis is typical to brucellosis. atrophic nodular testicles and epididymides. ## Footnote Can go undetected completely.

Question 52

Brucellosis signs In case of congenital infection? (2)

Answer 52

In case of congenital infection - swollen joints and lameness. Paralysis, spondylitis and abscess formation in various organs are less common.

Question 53

Lesions of brucellosis. (2+)

Answer 53

B. suis incites granulomas with caseous central forms: mammary glands, placentas, synovial tissues, seminal vesicles, prostate, epididymides, testes, uterus, oviduct, liver, spleen, bones, tendons, bursae, brain, lymph nodes. Catarrhal endometritis

Question 54

Diagnosis of brucellosis. (3)

Answer 54

Bacteriological assays from: lymph nodes, swabs, milk, semen, fetal membranes, spleen and lungs of aborted fetuses. Serological assays PCR

Question 55

Tx of brucellosis in pigs.

Answer 55

Its treated with AB, oxytetracycline with aminoglycosides in people but NOT in pigs. No suitable vaccine so must Test-and-slaughter to stamp out. Prevent by: Prevention of contact with infected wildlife reservoirs Biosecurity Whole-herd depopulation

Question 56

Describe the types of PCV.

Answer 56

Porcine circovirosis, family circoviridae. 3 types: - PCV1 - newborn piglet tremor - PCV2 - is the main problematic one and causes a bunch of diff diseases (see attached image) - PCV3 - arthrogryposis and pre-weaning nervous disease

Question 57

Describe the problematic PCV-2 specifically.

Answer 57

3 genotypes of PCV2 (a, b, and c) Discovered In the late 1990s but PCV2 has probably circulated in pigs during the past 100 years. Virus preferentially targets the lymphoid tissues. Accumulation of virus in macrophages and dendritic cells. Epithelial and endothelial cells seem to be the main target for PCV2 replication. PCV2 is able to replicate in fetuses as well as in zona pellucida–free embryos. Abortion-associated strains have different replication kinetics compared with PMWS (postweaning multisystemic wasting syndrome) or PDNS-associated PCV2 isolates (Porcine dermatitis nephropathy syndrome). ## Footnote PCV2 infection is usually associated with multiple pathogenic agents (PPV, PRRS, M. hyopneumoniae, A. pleuropneumoniae, P. multocida, H. parasuis, Staphylococcus spp, and Streptococcus spp.

Question 58

Effect of Porcine circovirus-2 on the cellular and tissue level: (5)

Answer 58

Lymphoid depletion and histiocytic replacement of follicles in lymphoid tissues. Impaired adaptive immune response that may compromise vaccine efficacy. Lymphoid depletion, immunosuppression and lymphopenia in peripheral blood. Significantly lower red blood cells counts and hematocrit values (gastric ulcerations). Upregulation of IL-10 and proinflammatory cytokines.

Question 59

Porcine circovirus-2 is secreted via

Answer 59

nasal, ocular, and bronchial secretions; saliva; urine; feces and semen

Question 60

Porcine circovirus-2 affect on pregnancy.

Answer 60

Infection of embryos and fetuses during dam viremia in PCV2 negative or naïve pregnant dams. Affects all stages of gestation The heart is the primary site of PCV2 replication in fetuses thus causes early emrbyonic death, abortions, Increased numbers of mummified fetuses and Stillbirths etc.

Question 61

Clinical signs of porcine circovirus-2. (7)

Answer 61

Early embryonic death Abortion Increased numbers of mummified fetuses Stillbirths Increased pre-weaning mortalities Decreased reproductive performances Decreased litter sizes

Question 62

Based on clinical signs, How do you differentiate porcine parvo virus infection from porcine circo virus infection since they both cause fetal mummification?

Answer 62

Parvo fetal mummies will be differently sized and no signs of illness in the sow. In parvo, Abortions are uncommon; instead, infected fetuses are retained until farrowing. Circovirus fetal mummies should be more uniform and the mummies remain small. More frequent abortions compared to PPV. More severe systemic illness in sows (in some cases) compared to PPV.

Question 63

How do you differentiate lepto infection from porcine circo virus infection if they both cause abortions?

Answer 63

Lepto causes late-term abortions and systemic illness in sows. PCV2 causes more mummified fetuses and weak piglets, WITHOUT systemic illness in sows. Circo has endocarditis of fetuses (you must investigate the fetuses at a lab)

Question 64

How do you differentiate brucellosis from porcine circo virus infection if they both cause abortions?

Answer 64

PCV2 causes Mid- to late-gestation abortions., mummification, and sows appear clinically normal. circo has endocarditis of fetuses (you must investigate the fetuses at a lab) in brucella: Abortions occur at any stage of gestation, but mostly in late pregnancy. brucella causes granulomatous infections, and orchitis in boars. + infertility, arthritis, and systemic illness in both sows and boars.

Question 65

Post-mortem lesions in porcine circovirus. (3)

Answer 65

Myocarditis and myocardial fibrosis of fetuses. NB As only individual fetuses may be affected, samples (especially heart) need to be collected from several piglets or fetuses within a litter. The thymus is atrophied, and the tonsils are thinner than normal.