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)
How can Erysipelas be controlled or prevented?
-Vaccination of sows at weaning
-Quarantine incoming stock
-Good sanitation and hygiene- reduce infection pressure
-Cull animals with joint lesions (removing chronically infected animals)
-Treat affected animals with antibiotics/water medication
What is PRRSV? What are some other common names?
Porcine Reproductive & Respiratory Syndrome Virus (PRRSv)
-Previously referred to as:
-Mystery swine disease (USA)
-Blue ear disease (UK)
-Lelystad Virus (EU)
What disease is one of the most significant disease in the swine industry today?
PRRSv
-in ON aprox 80% or more inffected with PRRSv
What is the agent for PRRSv?
-Genus arteriveridae virus
Properties of genus
-Can cause asymptomatic persistent infections (very challenging)
-Can cause severe fatal disease (economic and welfare)
-Replicated in macrophages (has effect on immune system)
-Exhibit considerable genetic mutation and recombination
What is the Ethology for PRRSv?
-Considerable strain variation resulting from genetic mutation and recombination (considerable variation in virulence among strains)
-Distinct clusters which are antigenically & genetically distinct
-Antigenic drift within a herd
-Positive herds can become infected with a 2nd strain
-Heterologous strain are not fully cross-protective so if you have one can still get the other
What is the transmission of PRRSv?
-Highly infectious - low minimum infectious dose
-Persistent- prolonged carrier state (>200d)
-Shed virus for ~60 days in feces, urine, semen & nasal secretions
-Transplacental transmission to fetuses
-Passed in urine, feces, blood, saliva, semen
-Needles can transfer virus from one litter to another (1, for iron injection 2. NSAID time of castration)
-Pig-pig contact: especially if pigs fight (after mixing)
-Farm-farm via pigs, semen, trucks, fomites, (flies, mosquitoes) and aerosol
What is PRRSv susceptible to anything?
-Susceptible to drying, detergents, disinfectants (lysol)
-Susceptible at higher temps: Temperature dependant environmental survival: -20C-months to years, 20C - 6 days
What are clinical signs of PRRSv?
-2 main kinds are reproductive and respiratory
-Not all positive herds have clinical signs
What are the reproductive clinical signs of PRRSv?
-Infection of sow tonsil & URT, viremia
-Sow systemic effects - fever
-Crosses placental (>day 70)
-Fetal death due to vasculitis of umbilical vessels (inflammation of blood vessels results in fetus death)
-Vasculitis in neonates –> periorbital edema (eye swelling). PI
Infection of pregnant sows:
-Anorexia, fever
-Sow mortality- if virulent strain
-1st & 2nd trimester- minimal impact (bc have to be infected for around 70d)
3rd trimester- tranplacental infection (> 70 days gestation):
-Reproductive failure and infertility
What are the effects of transplacental infections for PRRSv?
later term abortions
-fetal infection and death
premature farrowing (<110d)
-Still booths, mummified piglets
Weak, liveborn piglets- viremic PI
-Neonatal diarrhea
-Elevated pre-weaning mortality (25-50%)
What are the respiratory pathogenesis of PRRSv?
-Infection of tonsil & URT, viremia, systemic effects –>
Destry alveolar (lung) macrophages & they decrease in function/number –> leading to pneumonia & decreased lymphocytes, monocytes, neutrophils and secondary infections ie neonatal diarrhea & secondary lung infections ie enzootic pneumonia
What are clinical signs of respiratory PRRSv?
-Any age, commonly pigs 4-10w
-Fever, depression, lethargy, stunted growth
-Pneumonia
-Dyspnea “thumping” most typical
-Cyanosis of extremities (“Blue-ear-disease”)
-Minimal coughing in pure PRRS pneumonia (coughing is more common following secondary bacterial invasion)
-Immunosuppressive- virus results in mixed infections (attacks white blood cells)
*important when trying to control enzootic pneumonia
How is PRRSv treated?
Treatment of affected animals:
-Supportive:anti-inflammatories (aspirin) in water
-Prevent secondary infections: strategic medication as required (or antimicrobials)
How can we control and eliminate PRRVs?
The following is breeding herd stabilization: mass exposure of breeding herd to homologues PRRSv to ensure development of immunity & cessation of ongoing vertical transmission from sow to piglet
-Herd closure
-Gilt acclimation (with virus to develop immunity)
-Mass exposure (vaccination, serum inoculation)
Implement McREBEL
Management Changes to Reduce the Exposure to Bacteria to Eliminate Losses from PRRSv
-Ex stop use of nurse sows, nursing pigs should be moved strict AIAO
-Off-site weaning
-Prevent re-infection ie biosecurity
Why is PRRSv not so simple?
-Many different strains of PRRS (thousands)
-Immunity to one strain may not provide protection against another strain
-Vax doesn’t always provide protection
-Vax can revert to virulence
How long does Immunity last
-Antibodies measurable 10-14d post infection, not detectable at 6months post infection
-Passive immunity lasts 30days
-Virus presists in tonsils for 6months- carrier pigs
