Pig 2 Flashcards
Respiratory disease complex (RDC) what also called, what are the 3 main pathogens within
> Also called Enzootic pneumonia - Mixed infection with: ○ Mycoplasma hyopneumonia (hyo in front = pigs) ○ Pasturella multocida and maybe ○ Actinobacillus pleuropnemonia
Mycoplasma pneumonia what involved with, leads to, clinically characterized by
- Contagious pulmonary disease of pigs.
- Caused by Mycoplasma hyopneumonia.
- Characterised clinically by:
○ Coughing - severe, 14 day duration
○ Unthriftiness
○ Very low mortality
what is the incidence of respiratory disease complex and how is it transmitted
Incidence of RDC - Biggest health problem Worldwide ○ > 90% Australian herds affected ○ Cost approx. $70/ sow /yr. ○ Due effect on: § Medication, mortality, decrease in Feed conversion efficiency, decrease in average daily gain (ADG) How is it Transmitted - Inhalation from aerosol or direct contact with carrier pig. ( windborne 3 Km query 12k) -> farms within 3 km are a threat ○ Carrier pigs -> gilts are the most susceptible for carrying - Affects ciliated epithelium - Lesions seen 3-14 days post infection - Seroconvert 8 weeks post infection
Respiratory disease complex clinical signs in acute form
- Acute form uncommon.
- Occurs when a high health herd first becomes infected.
- Deaths all ages ie suckers through to sows
- After some months will become endemic when all animals infected -> want to become endemic to drop mortality
○ Increase spread of disease by exposing all pigs to infected pigs - Ideally get them all vaccinated and/ or infected ASAP
Respiratory disease complex clinical signs when endemic
- Chronic or enzootic ( endemic) form
○ Infected between 3-18 weeks of age -> generally gilts from mothers act as carriers and increase infection for later
○ Dry cough
○ Sneezing
○ Variation in growth rate in batch -> bad for selling the carcass, cannot sell as not large enough so need to keep feeding OR too large and will be penalised
○ Severe coughing and pneumonia with 2’ infection
○ death not uncommon from 2’ infection
Respiratory disease complex what are 4 main indications that we have it under control
- Few Clinical signs of coughing
- Good ADG (average daily gain - 650-660 range) and FCE (feed conversion efficacy - 3.5-3.6)
- Low mortality
- Few lesions at slaughter -> should be sold at week 22
Respiratory disease complex treatment and diagnosis
Treatment - Antibiotics -> hit both mycoplasma and Pasteurella (secondary bacterial infections is what is killing the animal) - In feed or in water - Based on sensitivities (cant culture) of ○ Tiamulin ○ Pulmotil ○ Amoxicillin ○ Lincomycin ○ Oxytet Diagnosis - Tracheal swab with PCR
What are 7 main ways to control respiratory disease complex
- Vaccination ( lung score 15% to 2%)
- SEW with multisite production
- AI/AO -> All-in/All-out
§ Average daily gain improved by 12%
§ Feed efficiency improved by 7% - Correct stocking density
- Strategic medication of weaners
- correct Ventilation-> insulate sheds, large ridge vents
- Good Housing -> clean between batches, effluent removal
What are the 2 main ways of eradication for respiratory disease complex, which better and what need to be careful of
1. Total Depopulation ○ Cost $700/ sow ○ Logistical nightmare 2. Swiss depopulation ○ cost $100/sow ○ still logistical nightmare - Beware of reintroduction ○ Exposure of gits between 8-10 weeks of age - VACCINE
Swiss depopulation what is it used for and how to perform
used to eradicate respiratory disease complex
○ Stop mating for 2 weeks, 14 weeks before day 0 (allow you to clean up and medicate before need sows farrow down)
§ At day -7 get rid of all animals less than 10 months of age.
§ Day -7 to -1 clean up farm
§ Day 0 commence medication at high level for 14 days
§ Day 15 + sows farrow down.
what age are sows mated, gestation length, weeks of weaning and average day of weaning
210d mated
Gestation is 115days
4 weeks weaning
Average day of weaning is 20 days
Actinobacillus pleuropneumonia (APP) what does it cause, compication of, age group affects, contagious status and results in
- Severe respiratory disease
- Most common complication of RDC
- Affects growers/ finishers/ weaners less common
- Highly contagious -> up to 500m distance
- Severe haemorrhagic pneumonia -> due to cytotoxins resulting in haemolysis
- Economically devastating and poor animal welfare
Lungs lesions for slaughter what are you checking for and the signs for each
IS IT APP OR PASTURELLA
APP -> pleusiy, pericarditis, abscesses
Pasturella -> same as APP but no areas of necrotic haemorrhage
Actinobacillus pleuropneumonia (APP) how are pigs infected
- Aerosol transmission from carriers
- Will travel on wind for 2 k
- Rapid onset of disease (4-12 hrs)
- Small dose lung lesions only
- Large dose blood poisoning
- (9 hrs post inf)
- Serovars 1, 5, 7 and 12
Actinobacillus pleuropneumonia (APP) clinical signs in the two types
- Acute ○ Sudden death ○ Fever ○ Reddened skin ○ Laboured breathing (thumping) ○ Blood stained frothy nasal discharge - Subacute ○ Reduced growth rate ○ Coughing ○ Variable mortality
Actinobacillus pleuropneumonia (APP) what are the 2 main other differential diagnosis that it looks like and how to differentiate
1) Glassers disease -> Haemophilus parasuis
○ Occurs earlier (usually weaners)
○ Presents as fading pigs -> leads to septicaemia
○ No haemorrahgic infarcts in lung
○ Fibrin formation, pleuritis 2) Pasturella pneumonia ( see later)
○ No haemorrahgic infarcts in lung
Actinobacillus pleuropneumonia (APP) what are the main risk factors
- Respiratory transmission from carrier or recovered pigs
- Multisourcing pigs in SEW / MS
- Predisposing factors
○ Overcrowding
○ Ventilation/ temperature fluctuations
○ Stress
§ Movement
§ PST - growth hormone - NO LONGER USED IN AUSTRALIA
§ Feed changes
Actinobacillus pleuropneumonia (APP) treatment and prevention
Treatment - injection of individual pigs - Water medication of at risk group ○ Tetracyclines, Amoxycillin, Tiamulin - Based on Lab culture and sensitivities Prevention - Vaccination of weaners - Multisite rearing plus AI/AO by site (deniliquin) - Strategic medication ○ Cough index ○ Seroconversion pattern ○ Water intake
Actinobacillus pleuropneumonia (APP) eradication options and how to perform
- Swiss depop does not work
- Total depopulation or Vaccination of sow and MEW (medicated early weaning)
○ Medicated early weaning; medicate sow for 2 weeks before and while pigs suckling.
○ Wean at 10 days to a new site and medicate weaner diet
Pasturellosis what does it cause, main clinical signs and primary or secondary
- A respiratory disease caused by Pasturella multocida. Very simliar to APP
- May be sub clinical or associated with:
○ Pneumonia
○ Septicaemia
○ Mortality
○ Depressed growth rate - Often 2’ to M.hyo and usually seen in growers or finishers. Can be a primary pathogen
Pasturellosis cliical signs and treatment and prevention
- Acute ○ Sudden death ○ Laboured breathing, cough, cyanosis. - Subacute. ○ Pneumonia ○ Coughing, Fever Treatment - Same as for APP - Treat individual pigs -> not drinking so won't take medicated water - Water medicate at risk group - Prevention see RDC
Streptococcal infection in pigs what generally lead to, prevention and lesions
- Sudden death or nervous signs in suckers, weaners and growers.
- Prevention: Pulse medicate at strategic times, Control environment
Lesions - lungs are wet and heavy (pulmonary oedema), vegetative endocarditis
Mycoplasma hyosynovia what mainly lead to
- respiratory infection
- invades joints
- increased in times of stress such as transport
Causes of sneezing list 6
- Mycoplasma hyopneumonia
- Atrophic rhinitis
- Bordetella bronchiseptica
- Cytomegalovirus
- Dust
- Ammonia
What are 5 main ways to determine whether respiratory disease complex is causing an issue and the main one
- What is growth rate
- Do post mortem on dead pigs
- Check coughing index - MAIN
- When do they seroconvert
- Abattoir check of lung score
coughin index what used for and 5 steps wtihin, what mean intervention
To detect whether respiratory disease complex is an issue 1. Select about 50 pigs 2. Wake them and count coughs for 3 min. 3. Repeat * 3 lots 4. Repeat next day 5. Repeat every 2/4 weeks ○ 3-5 coughs 3 min. borderline ○ > 5 coughs intervene ○ > 10 coughs = trouble
What are the 4 main causing of caughin in weaners
- Mycoplasma pneumonia
- Pasteurella pneumonia
- Pleuropneumonia (APP)
- GLASSERS DISEASE - most common
Glassers disease what caused by and main effects
- Caused by Haemophilus parasuis
- An infectious respiratory disease
- Effects
○ Fibrinous bronchopneumonia is a common finding in animals weaned 7-14 days
○ Empty stomach is typical finding
○ Following invasion of the blood stream, multiplication at multiple serosal surfaces produces the typical, Polyserositis, polyarthritis (and sometimes meningitis) seen in pigs from 14-21 days post weaning
○ Puss in hock joint can also occur -> carpal and tarsal joints
Glassers disease what result in and clinical signs
- Results ○ Sometimes fatal ○ arthritis ○ Bronchopneumonia ○ Polyserositis ○ Meningitis - Clinical signs ○ Suckers or weaners ○ Cough, laboured breathing, fever ○ Fading pigs ○ Rough hair coat ○ Sometimes swollen, painful joints ○ Sometimes, meningitis ○ May be found dead ○ Usually euthanased as poor doers
Glassers disease treatment and prevention
- Treatment ○ Penicillin treatment of individual pigs ○ Group medicate in contact pigs ○ Amoxycillin soluble - Prevention ○ Vaccinate sows- Booster shot at 13 weeks of gestation ( when is colostrum formed???) ○ strategic medication § LA penicillin § Water medication § Feed medication Check housing/ environment
Differentiate between Glassers and PCVAD (porcine circovirus associated disease)
- Glassers usually occurs within 2 weeks of weaning (5-6 weeks of age)
- PCVAD usually not seen till about 8-10 weeks of age with peak occurence/ viraemia @ 10- 13 weeks of age
Sow mortality rates common and what farms lower in and why
- 10% die
○ Half are destroyed on farm for welfare reasons -> mostly lameness - Mortality rates are lower in outdoor farms
○ In smaller groups there is no escape areas for fighting sows
○ Stalls -> can only move forward and backwards and therefore not much room for separation of faeces and laying down -> increased opportunity for ascending infection
§ Not an issue with group housing
Common cause of death in sows what are the 9 main ones
- Hyperthermia at point of farrowing (Heart failure)
- Post farrowing infection
- Oesophago-gastric ulcer
- Gastric accident - torsion of stomach intestine or organ
- Retained pig
- Cystitis
- Clostridium novyi
- Lameness/downer/destruction
- Infectious disease is unusual
What is the major problem with mortality in sows, when generally occur and how to fix
HEAT
- At point of farrowing or within ten days
○ Often in Nov - why?
- Daily temp > 35 degrees
- RR > 100 bpm (resting between 12-18 bpm) -> panting -> like dogs how they remove heat
- Fix
○ Immediate cooling (water) -> not done as much as worried about chilling the piglets
○ Cooling system long term
§ Drip cooling applied to sows in farrowing crates very effectively reduces respiration rate and increases comfort
○ Wallows management for outdoor sows
Post farrowing infection when and how generally occur, what associated with, signs and treatment
- Ascending infection within 24 hours of farrowing
- Often associated with retained pigs -> generally when a manual exam is done without antibiotics afterwards
- Signs
○ Discharge
○ Feed intake decreased -> drops 24 hours before temperature spikes
○ Temperature increased
○ Poor milk production - Treatment
Antibiotics (Amoxycillin, OTC), Meloxicam -> label recommendations
Post farrowing disease what is the most common one, main signs, cause
mastitis - Agalactia (failure of secretion of milk)
○ Usually isolated gland
○ Ascending infection
○ May involve several glands
○ May be a consequence of asynchronous lactation and engorgement
○ Linked to constipation?
○ Mycotoxins can be involved (Ergot) -> powerful vasoconstrictor
Mastitis what need to check to help prevent and treatment
- Always check hygiene and feeding to excess in the last week of gestation or early lactation
- Treatment
○ Amoxycillin
○ Flunixin, meloxicam good
○ Lasix when oedema is excessive
○ Oxytocin to assist let down (need 2-4ml) –> contraindicated in farrowing sows????
Ulcers in sows main causes and clinical signs
- Causes ○ Pelleted feed and low fibre diets § Variable and small particle size ○ Reduced intake or out of feed events? - Clinical signs ○ Vomiting blood and poor condition score
Gastric accidents in sows what occurs, associated with, highest risk period
- Torsion of stomach and/or abdominal organs
- Associated with rapid intake of water and feed
○ Possible pellet feeding, poor grain quality -> fermentation and gas production -> gastric dilation -> pressure on diaphragm -> dyspnoea -> death - Highest risk period in the farrowing house
- Gastric dilation as a consequence of fermentation and gas production
Erysipelas how common in sows, results from
Erysipelas is very common in sows
- Incomplete protection provided by the vaccines
- Large number of cases over periods of weeks are uncommon but this can occur in naïve growing pigs
Clostridial infections what result in, when see, what need to differentaite from and how
- Acute deaths
- See in mid lactation when feed intakes are suddenly high
- Differentiate from gastric accidents
- Rapid decomposition, gas bubbles soon after death
- Response to zinc bacitracin (200ppm) good
Rectal prolapse in sows what is the treatment and what involved
- Sedate the sow, local anaesthetic around the perineal skin
- Reduce and stabilise with an anal purse string suture
- Or, if the tissue is necrotic, suture and amputate
Mycotoxins leading to sow mortality what found in, main types and what do they cause
- Fusarium spp
- Zearalenone: reproductive impact
- Vomitoxin (deoxynivalenol): feed refusal
- Ochratoxin: nephropathy
- Aflatoxin: immunosuppression
- Ergot (sorghum): agalactia following vasoconstriction
- Fumonisin: liver dysfunction
Myxotoxins leading to sow mortality how to control
- To bind the toxin
- Neutralise the activity chemically
- Enzymatically degrade the mycotoxin
- efficacy unsupported
Cystitis what age of sows occur, where generally seen, link with, pathogens involved and treatment
- Older sows
- Stalled sows but also pens
- Link between frequency of feeding and urination, urinary stasis, contamination
- Actinomyces/Eubacterium/Coryneb (now Actinobaculum) sinus +++ others
- Treatment
○ Antibiotics 10-14 days (long acting tetracyclines)
for all sick sows what are the main things need to do
- Recovery area is needed
- Cover, access to water, feed and straw
what are the 10 external signs of impending farrowing and at what day
- Dropped hip muscles (gluteus and biceps femoris group) (F-3d)
- If outside this sow would be nesting (F-3d)
- Swollen vulva (F-2d)
- Restless (F-12 hrs to 2 d)
Mammary glands swell and feel firm and distended - Clear fluid expressed (F1-10d)
- Secrete milk F12-24 hours -> need this before give oxytocin
- Abundant milk F-8 hours
- Resting quietly about 30-90mins before farrowing
- Increased respiration rate (>30br/min F 15-60mins)
- Straining: passing blood tinged oily fluids/meconium F0
- Tail wagging -> very close within minutes
Farrowing what endocrine events occur at what day
- 112 days foetal pituitary releases ACTH,
- Foetal adrenals produce glucocorticoids
- Release of maternal PCF2alpha and foetal placental oestrogen followed by
○ Luteolysis, a fall in progesterone, a rise in relaxin (luteal cells) and uterine contractions in response to oxytocin
How long does farrowing take for sows and gilts and intervals for piglets
- Takes about 3 hours sows, 2 hours gilts
- Pigs appear at about 12-25 minute intervals
What are some risk factors for stillbirths
○ Older sows
§ Want to keep sows as old as possible without sacrificing stillborn rate
○ Last to be born piglets
○ Larger litters
○ Summer or in hot (>21 degrees) farrowing houses
○ Very thin and very fat sows
○ Multiple still births in one litter -> more in the next one
○ After long farrowing >4 hours
○ After long interpig interval >40mins (generally about 30mins)
○ With gas heaters and increased CO levels -> foetus will concentrate that CO born anorexic (blood colour is cherry red) leading to stillbirth
○ After induced farrowing and oxytocin
○ Premature rupture of the cord and foetal anoxia - the main reason for stillborns
Stillbirth prevention strategies
○ Farrowing house should be clean
○ Be clean, use lube, be gentle -> where gloves NEED TO USE NEW ONE EACH TIME
○ Don’t push against the sow
○ Broad spectrum antibiotic cover
At what parity do you get the highest % born dead and what occurs after this
Parity 7
- Ones that have the issues at parity 7 will then be culled or possibly this large number has been identified by the farming staff and put in interventions
- Therefore the ones above parity 7 have been selected for their low born dead percentage
First aid for farrowing sows what are the 3 main things to help, one that isn’t required and the main rule
- Manual examination
- Oxytocin 5-10IU -> if haven’t got milk ejection response and give then increase chance of stillbirths -> late in the intervention
○ Manual interventions FIRST - Caesars are not required
- A walk can be helpful
- RULE: manual examination after 45 mins after pig #7 then oxytocin, antimicrobial cover
○ Most problems occur after pig #7
Lactation what hormone changes, from what day do you produce milk and what occurs with milk let down at birth
- As progesterone drops and oestrogen rises there is major metabolic activity in the mammary gland
-> Relaxin increases growth of mammary gland parenchyma - Gland capable of producing milk from day 105
- At birth there is copious “milk” -> comes from gland secretion (epithelium) and serum transudation from between the epithelial cells
- For the first 24 hours the sow lets down continuously
- After that she lets down about every hour -> only let down for 20-30seconds, sow lets the piglets know it is coming and piglets need to attach to the teat
○ If miss the let-down for some reason (sick, small, weak, lame) then need to wait - The stimulus for milk production is milk removal
What are the 3 main things that lead to piglet mortality
- Need colostrum
- Warm environment
- Birth weight
what age is a weaner, grower and finisher
Weaner: removal from sow to 20Kg
Grower: 20-50kg liveweight
Finisher: 50-100+ kg
Grower and finisher pigs what are the 3 main causes of death
1) Infectious
○ Respiratory disease - APP, Pasteurella, streptococcus
○ Enteric disease - Swine dysentery, ileitis
2) Non-infectious
○ Gastric ulcers
○ Twisted bowel - liver is very pale (congestion of blood)
3) SCOURS - IMPORTANT
Scours in grower and finisher pigs what are the 6 main causes and which is rare
1) Ileitis
2) Swine dysentery (SD)
3) Salmonella - rare - notifiable (just the disease)
4) PCVAD (porcine circovirus associated disease)- granulomatous enteritis -> IMMUNOSUPPRESSIVE -> predispose to the other disease especially salmonella
§ No lesions just hyperaemic mucosa, caecum and colon large watery contents
5) Whip worms - more common in free range systems
6) Excess salt >5000 ppm - RARE
What are the 3 main control strategies for scours and the 2 main treatment options
Control strategies for scours
- Don’t contaminate other pens
- Stop floor feeding
- Clean pens (scrape and hose out)
Treatment
- Inject individually affected animals with appropriate antibiotic
- Water medicate affected pens and at risk pigs
Swine dysentery what is it, manifests as, characteristic and transmission
- An infectious disease of the large intestine - brachyspira hyodysenteriae
- Manifested as wasting, diarrhoea and death
- Characteristic foul smell
- Transmission
○ Infection by oral route from sow to her litter - faecal-oral route
○ From infected weaner to pen mates
○ Organism invades the wall of the bowel
§ Interferes with absorption of fluid and electrolytes
§ Death from dehydration and ion imbalance
Swine dysentery clinical signs
○ Diarrhoea containing blood, mucus and necrotic material
○ May only present as “grey scour”
○ Pigs fall back in condition
○ Paper test-mucus sticks paper together
○ Death - dehydration, electrolytes imbalance
Swine dysentery post mortem lesions and diagnosis
- Post mortem lesions
○ Lesion confined to large intestine (salmonella and ileitis is small intestine as well)
○ Red and swollen
○ Spiral Colon most affected
○ Colonic contents
§ Fluid, mucus, necrotic material, flecks of blood - Diagnosis
○ Submit large intestine or manure to Lab - scrap part of the wall
§ Spirochetes seen on dark field exam
§ Culture organism and PCR
Swine dysentery treatment and prevention
- Treatment
○ Scouring pigs -> injection for 3 days, lincomycin or Tylosin (also good for ileitis)
○ In contact pigs -> water medicate for 6 days, lincomycin or Tylosin - Prevention
○ Strategic medication of weaners to eliminate organism (Tiamulin 200ppm)
○ Clean pens, don’t floor feed
○ Minimise stress
○ Strategic water medication
○ In feed medication; salimomycin (30 day withhold period)
§ Withdraw at 16 weeks so can sell at 20 weeks - when most susceptible
Swine dysentery eradication what are the 2 main ones, how perform and how long does it stay in the environment
a. Depopulation if have respiratory disease
b. Medicated eradication - tiamulin
i. High level for 7 days and then clean (400ppm = 10-12mg/kg) THEN
ii. Medium level for 14 days during clean (200ppm-6mg/kg) THEN
iii. 25 ppm tiamulin for 6motnhs until all infected growers have left property
○ How long does it survive in the environment -> 3-4 days
Ileitis what also called, what is it, main cause and where generally occur (how to tell)
(porcine proliferative enteropathy)
- Collective name for different manifestation of same disease complex
- Lawsonia intracellularis invades cells of the small intestine
○ Cells fail to mature and become hyperplastic
○ intestinal wall becomes thickened and invaded by other bacteria
- Not usually large intestine, tarry faeces (digested blood - different to swine dysentery)
What are the 3 main manifestation of ileitis and what leads to in terms of clinical signs
a. Proliferative intestinal adenomatosis: ileum and proximal colon
§ Scouring in early stages
b. Necrotic enteritis - if infected before 12 weeks of age
c. Haemorrhagic form/PHE (proliferative haemorrhagic enteritis) - if infected after 12 weeks of age
i. Sudden death, pale, anaemic pigs or carcasses, black and tarry faeces
Porcine proliferative enteropathy transmission and presentation
- Transmission
○ Organism excreted in the manure of infected pigs
○ Infected by faecal-oral route - scour in 18-21 days - Presentation
○ Animals fall back - slab sided
○ Poor weight gain
○ Pigs cranky - tail and flank biting
○ Sudden death in older pigs (12 weeks +) or replacement
Porcine proliferative enteropathy effect on production and treatment
- Effect on production
○ Can reduce ADG and FCE by 6-20%
○ Causes large variation in batch of pigs which causes grid penalties
○ FCE from 3.8 to 4.56 = 4.56 $1.52 to $1.82 or 30c/kg which is about their profit margin - Treatment
○ Inject any clinically obvious pigs
○ Water medication 3 days with tylosin or lincomycin
Porcine proliferative enteropathy prevention
○ Weaners covered by routine medication
○ Growers -> water pulse for 2 days every 14 days 0r medicate in feed continuously
§ Allows exposure and hence immunity
○ Replacement breeders - 2 treatments 14 days apart
○ Try enterisol vaccine as sucker and discontinue medication in growers - HIGHLY EFFECTIVE THUS FAR
Salmonella what seen as, is it common, due to what found with what animals
- Seen as outbreak of scours and wasting pigs
- Used to rare in Australia now more common due to circovirus 2 (PCVAD)
- Due to S. typhimurium in rodents, birds, feed and by-products
Salmonella transmission and clinical signs
- Transmission ○ Oral ingestion from feed, environment (rodents, birds) or manure of carrier animal § Animals may die or develop scour - Clinical signs ○ All ages - usually weaner/grower ○ Sudden death ○ Chronic poor does - looks like PCVAD ○ Scour - no mucus or blood
Salmonella treatment and prevention
○ Inject affected animal ○ Water and feed medicate at risk group ○ Oral vaccination of suckers Vavsafe ST ○ QA program - biological standards § Rodents, cleaning, by-products, approved suppliers, is it due to circovirus 2??
Whipworm what does the diarrhoea look like and the main worm involved with lifecycle and treatment
- May be mucous diarrhoea BUT NOT BLOOD
Ascaris suum
If swallow L1 - nothing
Swallow L2 -> burrow into small intestinal wall -> migrate to liver -> migrate to lung -> coughed up and back into small intestines -> 30days from L3-L5 -> lay eggs -> eggs in faeces and beyond - Leads to white spot liver
- PPP -> 42 days
THEREFORE CONTROL -> worm once a month - fenbendazole - total of 10mg/kg over 7-10 day period
Gastric ulcers leading to diarrhoea generally secondary to, what lead to with clinical signs and what can cause in oesophagus
- Generally secondary to other diseases
- Go off feed, inappetence, weight loss
- Can cause a crater where oesophagus enter pars oesophagus (opening of the pigs oesophagus)
causes of reduced feed intake resulting in poor average daily gain
- Stocking density
- Temperature
- Air quality
- Water volume and quality
- Disease
what are the 5 main causes of growth rate issues and causes within
- Respiratory disease
- Enteric disease
- Mange
- Nutritional
○ Diet formulation/ingredients
○ Water - poor quality, too hot, frozen - Housing and management
○ Overstocking
○ Poor temperature control
○ Poor air quality
○ Poor effluent control
○ Poor hygiene
When investigating growth rate issues what issues do you need to check off the list for causes
- Stocking rate and density
- temperatures ( data loggers / max/min therm
- diets ( source and specs)
- Air quality ( Dust / gas)
- Clinical signs ( cough, scour, rubbing)
- feed intake ( how?)
- Growth rate (how)
- Abattoir
Weaner diarrhoea what risk factors at weaning lead to stress and factors that affect weaner health
Stress factors at weaning - Change from liquid to solid diet - Removed from sow - Mixed with unfamiliar pigs - New environment Factors affecting weaner health - Age and weight at weaning - Environment and housing - Nutrition - disease
Requirement for weaners to help reduce scours
- temperature constant
- Eliminate draughts
- All in all out
- Stocking rate avoid overcrowding - generally when just wean not an issue
- Sort on size
- Dust
- Nutrition
Transmission of disease and immunity for weaners what is the 2 ways this occurs
1) Sow passes immunity and bacteria through milk to offspring
○ Infected sows will give immunity to offspring BUT NON-INFECTED SOW will not give immunity to offspring -> PROBLEM WHEN MIXED AT WEANING
2) Sow passes bacteria through faces
What are the 5 main causes of scour in weaners and the main way to diagnose
- Excess salt in water
- Post weaning scours ( E.coli)
○ usually in first 2 weeks - Ileitis
○ Usually in last 3 weeks - NOT IN THE 1ST 3 WEEKS - Salmonella
○ Rare but occurs at any stage - Granulomatous enteritis - PCV2
Diagnosis -> autopsy dead or typically affected pigs
Granulomatous enteritis - PCV2 how presents, what associated with and how grossly presents
- Diarrhoea associated with fading pigs 8-12 weeks of age
- Diarrhoea associated with a granulomatous enteritis
- Grossly seen only as reddened/ congested mucosa of distal ileum and large intestine.
What are the other disease in weaners that lead to scours
- Twisted bowel
- Mulberry heart disease
- Starvation syndrome
- greasy pig,
- arthritis
- Worms - rare
Greasy pig diseasewhat caused by, when occur and how to treat
- Caused when staph bacteria invade skin abrasions in immune deficient animal
○ Ie after fighting - Treat with antibitoic, amoxil, trisoprim - only if very red
- If severe use flunixil as well
E.coli what leads to in weaners and pathogenesis
post weaning scours -> enteric colibacillosis
- Pathogenesis
○ Ingestion of bacteria -> bacterial colonization of ileum and jejunum -> too much fluid through large intestine
§ E. coli attach to the intestine with pili and fimbriae
§ Produce a enterotoxin and destroy villi -> lead to hypersecretion of water and electrolytes
§ Animal dies from shock of dehydration
Enteric colibacillosis clinical signs
○ Occurs within first 7-10days ○ Scouring pigs ○ Or sudden death - good sized pigs ○ Post mortem findings § Sunken eyes § Fluid filled, reddened small intestine
Enteric colibacillosis predisposing factors
○ Lack of gut immunity ○ Wet, dirty pens ○ Draughts,Too cold ○ Overcrowding etc, ○ See essential requirements, earlier
Enteric colibacillosis treatment
○ Short terms
§ Inject affected pigs with antibiotic - neomycin
§ Water medicate at risk pigs
§ Electrolytes and antibiotic in troughs
§ Inspect 3-4 times a day
○ Long term
§ Correct the environment
§ Vaccinate if the problem persists
§ Antibiotics in feed for first 14 days OR pulse antibiotic in water 48-72 hours prior to anticipated onset
What are the 4 main causes of sudden death in weaners
- Mulberry heart disease
- Strep septicaemia - meningitis
- Twisted intestine
- E. coli
Muberry heart disease what does it manifest as and 3 main causes
- Manifest as sudden death in good sized pigs 15-30kg in size
- Causes
○ Vitamin E deficiency
○ High levels of polyunsaturated fats
○ Fast growing pigs
Mulberry heart disease autopsy findings and prevention
- Autopsy findings are characteristic and include
○ Large amount of fluid around heart and lungs
○ Haemorrhagic and pale areas in heart muscle
○ Fluid in abdomen with fibrin strains
○ There is often haemorrhage in abdominal cavity due to rupture of the liver (congestion due to heart failure) - Prevention
○ Check vitamin E and fat levels in diet
○ Ignore if mortalities <1%
Strep infection in weaners what lead to, how and other results
- sudden death in weaners Meningitis ○ Most commonly caused by strep infection ○ Can be caused by glassers ○ Animals lies on the side and cannot stand ○ Differential - talfan disease (polio) - Other results ○ Arthritis ○ Pneumonia ○ Heart valve lesions
What are the 9 main causes of sucker diarrhoea
- NHEC (non-haemolytic E.coli)
- Coccidia
- HEC (haemolytic E.coli)
- Rotavirus
- Strongyloides ransomi
- Clostridial perfringens type A
- Clostridial perfringens type C
- salmonella
- Cryptosporidium
Non-haemolytic E.coli age of occurance, clinical signs, neoscopy and histology.smears
- Age of occurrence -> 2 hours - 5 days
- Clinical signs -> mild to severe scour, dehydration and/or death
- Necropsy -> fluid filled intestines, chyle in mesenteric lymphatics
- Histology/smears -> no blunting of villi, gram negative bacilli > 10per/1000 magnification
Non-haemolytic E.coli diagnosis, treatment, prevention and vaccine
- Diagnosis -> sample rectal swab, culture of enterotocigenic E. coli, alkaline intestinal contents, response to treatment
- Treatment -> pigs respond to antibiotic therapy -> should show results within 6 hours
- Prevention -> pay attention to warmth, hygiene and immunity, colostrum of cows specifically vaccinated against porcine colibacillosis strains is useful
- Vaccination -> commercial E.coli vaccines are very effective, if you vaccinate you do not have E.coli in the first week of life
What coccidia causing sucker diarrhoea age of occurrence, clinical signs, necropsy, histology, treatment, prevention and vaccine
Isospora suis
- Age of occurrence - 5-15 days.
- Clinical signs - Scour; death uncommon.
- Necropsy - Ranges from no visible change to necrotic enteritis affecting distal ileum. Probably no chyle present in mesenteric lymphatics.
- Histology/smears - Necrosis and blunting of villi, sexual and asexual stages visible on histology and smears.
Isospora suis treatment, prevention and vaccine
- Treatment - Treatment with Baycox, even though efficacious, may not show dramatic results until intestinal necrosis heals.
- Prevention - Toltrazuril (BaycoxR) given at day 4 is highly effective. Attention to hygiene of farrowing pens is important.
- Vaccination - No vaccines commercially available.
Haemolytic E.coli what does it cause, age of occurrence, clinical signs and diagnosis
diarrhoea in suckers
- Age of occurrence - +10 days through to postweaning period.
- Clinical signs - Sudden death from endotoxic shock, or severe scour with dehydration.
- Diagnosis - Can invariably isolate heavy to pure cultures of K88 positive haemolytic E.coli from the ileum and colon of dead pigs.
Haemolytic E.coli treatment, prevention and vaccination
- Treatment - Antibiotics, however limited efficacy as resistance is common and pigs may be too ill to absorb a parenteral injection due to hypovolaemic shock.
- Prevention - Commence antibiotic in water 2-3 days before expected onset of problem. Stopgap only
- Vaccination - Oral Vaccination of breeders 4-5 weeks prior to farrowing has proven to be highly effective.
○ Top-dress feed with 200mL of an overnight milk culture of a tame K88 E. coli daily for 4 days at week 11 of gestation.
Prevention of post weaning scours what is the most important thing with short and long term
- Fix the environment
- Short term - Antibiotics administered in water commencing 2-3 days before expected onset of problem
- Long term . Orally vaccinate with the troublesome strain for 3 days commencing 10 days before weaning.
- Beware of the emergence of the virulent O149 strain during vaccination
Rotavirus age of occurrence, clinical signs and diagnosis
sucker diarrhoea
- Age of occurrence 4- 7+ days,
- Clinical signs - scour.
- Diagnosis. Absence of any other agent/ cause. Acidic faeces, demonstration of rotavirus in scour material
○ Microscopic evidence of blunting of villi
Rotavirus treatment, prevention and vaccination
- Treatment - Secondary bacterial infections may complicate the problem so antibiotics may be of benefit. Warmth and glucose/electrolyte indrinkers useful.
- Prevention - Pay attention to warmth, hygiene and immunity. Colostrum of cows is useful, as we rarely see rotavirus in calves before 14 days of age.
- Vaccination - Feedback is the only option as no commercial vaccines available
Clostridial perfringens type A age of occurrence, clinical signs and necropsy findings
sucker diarrhoea
- Age of occurrence - 1-21 days.
- Clinical signs - Mild to moderate scour.
- Necropsy - Fluid filled intestines. Neutral to alkaline faeces.
Clostridial perfringens type A histology.smears and diagnosis
- Histology/smears - Necrosis of villi due to enterotoxins. Large numbers of gram positive rods.
- Diagnosis - Culture of organisms in large numbers from faeces. Demonstration of enterotoxin in faeces or intestinal contents.
Clostridial perfringens type C what does it cause, age of occurence, clinical signs and necropsy
sucker diarrhoea
- Age of occurrence - 2+ days. ( usually only outdoor herds)
- Clinical signs - Severe dysentery.
- Necropsy - Severe haemorrhagic enteritis.
Clostridial perfringens type C histology and diagnosis
- Histology/smears_ Ghosts of villi left with large numbers of gram positive rods adhering.
- Diagnosis- Haemorrhagic diarrhoea. Culture of organisms in large numbers from faeces. Demonstration of enterotoxin in faeces or intestinal contents.
Clostridial perfringens what are the 2 types, what cause, treatmetn, prevention and vaccination
Type A and C
- sucker diarrhoea - BUT NEVER BEEN ABLE TO DEMONSTRATE AS A MAJOR CAUSE
- Treatment - Antibiotics effective but will not show immediate benefits due to intestinal necrosis.
- Prevention - Pay attention to hygiene of sow and farrowing pen. Addition of antibiotic to lactating sow ration has been used in some countries. No benefit here
- Vaccination - Toxoid vaccine for sows available in some countries. We have never been able to isolate a toxin producing strain to use as a vaccine.
Salmonella what is the age of occurrence in suckers, clinical signs, necropsy, histology and diagnosis
- Age of occurrence - 5+ days through to postweaning period.
- Clinical signs - Scour and respiratory disease.
- Necropsy - Bronchopneumonia in 50% of animals and a necrotic enteritis affecting distal ileum and colon.
- Histology/smears - Necrotic enteritis.
- Diagnosis - Isolation of salmonella from intestine and lung.
