Lecture 21: Breeding Herd Health Swine 5 Flashcards
How can breeding herd health manifest into other issues? ie what are the 2 types if reproductive problems?
Management-related problem
-Chronic losses (>3months)
Disease-related problem
-Rapid change from good to poor production
-Reductions in multiple areas affected (increased still births, decreased litter size, low pregnancy rate etc)
What are the breeding herd health reproductive targets?
Targets
-Farrowing rate >&_ 85% (determined by # of sows that farrow/ # of sows bred)
-Total born/litter: > 14
-Born alive/ litter: >12
-Stillborn pigs/litter: 6-8% (~1 pig per litter)
-Mummified pigs: 1-2% (<0.5 pigs per litter)
What are stillbirth piglets (still borns)?
-Full term fetuses that are alive until term, but die of hypoxia during farrowing
What are risk factors to stillborns?
Risk factors
-Higher parity
-Over-conditioned (high BCS)
-Season (Summer, heat)
-Higher birth order (farrowing fatigue)
How can we tell a difference between a piglet that was crushed (no physical signs) vs a piglet that was still born?
Lungs
-Never have taken a breathe so can take biopsy of lungs and put into water, if lost then died after birth if sink was still born
What is fetal mummification? What are some causes?
-Fetuses that die prior to term, but after the skeletal calcification (begins ~D30) unable to be absorbed after
-Inspissated remains of fetal tissues
-Age determined by crown-rump length
Causes:
-Infectious (ie PPV,PRRS)
-Non-infectious (ie low or high parity, large litter size)
What is the agent for parvovirus? How Is it transmitted?
Agent: Porcine Parvovirus (PPV)
-Very stable virus, virtually impossible to eliminate
-Ubiquitous virus, endemic infection in most herds- worldwide
-Oronasal transmission- shed in secretions + excretions (feces, fluids, like placental and mummies)
-Transplacental infection
-Usually subclinical infections, outbreaks rare (cause of embryonic and fetal death)
What is the pathogenesis of parvovirus?
Pathogenesis: viral crosses placenta (transplacental) and travels from fetus to fetus along the uterine horn- replicates in cells undergoing mitosis
-Will kill piglets and continue to replicate
What are clinical signs of parvovirus?
SMEDI (Stillbirth, Mummification, embryonic, Death, infertility)
-Increased in number of sows returning to estrus post-breeding
-Decrease in number of piglets born alive (some affected litters only have 2-3 live/litter
-Increase in number if mummified piglets
-Mainly gilt litters affected- naive dams (less developed immunity)
-DONT SEE IN FECES/DIARRHEA
Hoe do you control parvovirus?
-Virtually impossible to eliminate (so dont bother eradication)
-Continued vaccination- many effective killed vaccines available (administer prior to conception before breeding)
What is the recommended vaccination program for Parvo?
Gilts: twice- 5-2w pre-breeding
Sows: revaccinated 2 w pre-breeding
What is the agent for Erysipelas or Dimond skin Dz?
agent: Erysipelothrix rhusiopathiae
-Bacteria- resistant to drying, susceptible to common disinfectants (can be killed)
-All age groups susceptible (piglets nursing protected by lactogenic immunity)
-Infected swine shed the bacteria profusely & contribute to contaminating environment (ingestion of feed and water contaminated with bacteria)
What is the pathogenesis of Erysipelas?
-Bacteremia and sepsis
-Systemic vasculitis- toxins circulate in the blood stream then become localized in skin, joints, heart
What are clinical signs of Erysipelas?
-Resist getting up - squeal
-High fever- can cause abortion
-Purplish skin on snout, abdomen, ears, Dimond skin lesions- raised, red
-Chronic: Arthritis and vegetative endocarditis (inflammation of the heart)
Is Erysipelas zoonotic?
-yes potential zoonosis
-Causes “erysipeloid” skin lesion
-High risk populations - rendering plant workers, vets (usually in hands)
