Lecture 20: Grow-Finish Pig Health Flashcards
What happens in the finishing phase?
-Housed in groups
-Remain here until reach market weight (110-120kg)
-Spend 100-120 days in finishing barn (pigs are ~6months old when reach market weight)
What is finisher pig health?
-Mortality should be <1% (spent lots of money and time caring and this is the final result)
-Respiratory disease most common &costly disease of finishers
-Gastro-intestinal disease also important
What is the etiological agent of enzootic pneumonia? What is transmission?
Mycoplasma hyopneumoniae
-Transmission: nasal secretions (nose-nose), coughing
-Sow-to-piglets: in crates
-Pig-to-pig: in grower/finisher
-Regional spread via aerosol (can travel in the air at least 4-5km) therefore makes keeping it out very difficult
What is the pathogenesis of enzootic pneumonia?
-MH colonizes trachea & bronchial epithelia cells
-Clumps cilia–> impairment of ciliary clearance (innate immunity rendering ineffective)
-Accumulation of secretary & cellular debris gravitate from bronchi to alveoli (deeper into the lung)
-Secondary invasion: in virtually all naturally occurring cases (mixed bacterial &viral infections) basically promotes or exelerates illness
What are clinical signs of enzootic pneumonia?
Clinical signs:
-Dry, hacking cough (chronic/persistent or spreads slowly)
-Rarely fatal (low mortality)
-Normal appetite, but reduced growth rate (1. Feed efficiency affected, 2. Return not as good)
-Typical expression in grower pigs (>12woa)
-HIGH MORBIDITY
-LOW MORTALITY- unless secondary infections, or lack of treatment/control interventions
What are prevention and control strategies for enzootic pneumonia?
-All-in/all-out pig flow (very important) ie horizontal transmission
-Maintain good air quality
-Buy mycoplasma- free pigs- difficult to find
What are vaccination and strategic medications for enzootic pneumonia?
Vaccination
-Vaccine reduces prevalence & severity of disease
-Vaccine does not prevent colonization or infection
-Vaccinate pigs 2-3 week poor to expected exposure (usually vaccinate in nursery phase)
Strategic medication with antibiotics
-Prior to or during peak exposure:
-Antimicrobials reduce infection pressure but do not eliminate M. hypo infection (similar to vaccines)
-Essential to control secondary bacterial infections
What is Ileitis? what is the agent and clinical signs?
Agent: Lawsonia intracellularis
Chronic disease:
-Poor growth rate
-Variation in piglet size
-Sporadic diarrhea
-Precipitated by stress- seasonal fluctuations, overcrowding, mixing
-Subclinical form
-Acute: sudden death with severe bloody diarrhea- adults, gilts
What is the pathogenesis of Ileitis?
-Bacteria invades crypt cells of intestine (intracellular)
-Cause thickening (hyperplastic) of the small intestinal wall
-“adenmastosis”
-Malabsorptive diarrhea (skippy peanut butter)
What are prevention and control strategies for Ileitis?
-Difficult to eliminate- some piglets likely infected by sow as young as 6doa
-Reduce stress- mixing, transport, crowing etc
-Vaccination is effective at controlling but not eliminating disease
-Strategic (mass) medicate with antibiotics when stressed or during outbreak
What are gastric ulcers?
Ethology: exact cause or causes not completely understood- multiple risk factors
-pH gradient and risk factors change pH gradient having an increase in acidity in an area where is usually not affected to protected
What are environmental factors of gastric ulcers?
Feed
-Particle size (avrge <700 um) balance: want small enough to promote digestion and increase SA but not too small that we cause ulcers
-Pelleted rations
-Disruption in feed delivery ex out-of-feed accidents, removing feed before shipping( increase fibre decrease ulcer)
Stressors
-Crowing, poor air quality, heat stress
What are host and agent factors of gastric ulcers?
Host factors:
-Anything that takes a pig go “off feed”
-Other underlying disease- especially respirator disease ***
-Peri-parturient sows are at high risk
Agent:
-A non-infectious condition
What is the pathogenesis of gastric ulcers?
-Increased fluidity of stomach contents, disruption of pH gradient of stomach areas
-Erosion of stomach lining near entrance of esophagus into stomach (pars esophagea)
-Damage to blood vessels (in stomach wall) which can cause bleeding into stomach- slow to acute
-Death can occur from acute blood loss or due to perforation of the stomach
What are clinical signs of gastric ulcers?
-Might contribute to slow growth +/-
-Pale (reflects degree of blood loss)
-Anorexic (off feed) pig
-Black tarry feces ( higher GI bleed and blood being digested with would lead to black blood), abdominal pain, bruxism (teeth grinding)
- +/- vomit and then eat again (healed, stricture)
-Found dead
