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96 Cards in this Set
- Front
- Back
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Disease Diagnosis
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Lecture 1
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Why do you do a PM?
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- To inspect the stock
- To keep records of growth rates, treatments, death rates - To understand why pigs die randomly - To inspect pigs at the abattoir |
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When should you do a PM?
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1. When you notice something different
2. When there is a drop in growth rates 3. When mortality rates are abnormally high |
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What are the normal mortality rates?
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Pre-weaning deaths < 12%
Weaner deaths < 3% Grower/finisher deaths < 2% Breeder deaths < 5% Breeder euthanasia < 4% |
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When do you use the penetrating captive bolt gun (on which pigs?)
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Pigs that are more than 10kg
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How do you use the penetrating captive bolt
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1. Stun the animal
2. Wait until major seizures are done (30secs - 1min) 3. Check if concious (righting reflex, vocalisation etc.) 4. Bleed out 5. Check for vital signs (lack of corneal reflex, pupils fixed and dilated, no signs of breathing) |
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Where do you aim?
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Right between the eyes
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What is another method you could use for big pigs?
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- Gun shot
- Do it outside - Stand at lest 5m away from pig - Can shoot via frontal or temporal methods |
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What are the steps to doing a PM?
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1. External assessment (BCS)
- Assess whether chronic or acute - Skin lesions - Sunken eyes - Purple extremities (septicaemia) - Swollen joints 2. Open up the carcass - Lay pig on LHS - Cut under R front and back legs - reflect away - Cut through the skin from neck to end of belly along underside of pig - Make sure you don't puncture any organs - Cut through ribs at soft spot in cartilage, and reflect Confirm lab tests - Culture (bacteria) - Serotyping (subclasses of bacteria) - Histology (to work out pathology in tissue) - PCR (genetic material for bacteria or viruses) Record your findings - Photos, label samples, notes etc |
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What is normal?
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Lungs
- Feel spongy - Light pink - Small amount of froth (no pus) - Should collapse - Should not be solid Intestines - Should not be thick, should not contain blood or other material, should not be black Heart - Freely floating in cardiac sac - No blood spots on surface - Nothing on valves |
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Do we normally PM suckers?
What are the clinical signs we see that determine cause of death? |
No - clinical signs usually give it away
No walking = still birth Sunken eyes = dehydration/scours Obvious abnormality = defect Swollen joints = Arthritis Good condition = overlay of acute disease Less than 800g = small/non-viable Bite wounds = trauma Pale = anaemia Abrasions on innerlegs = splayleg Poor condition = chronic disease/starvation |
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What are some common causes of death for weaners (3-8 weeks)
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- Failure to thrive
- Trauma - Strep suis - Glassers disease (Haemophilus parasuis) - E. coli (blood poisoning, diarrhoea, oedema disease) - Pleurpneumonia - Pasteurella - Mulberry heart |
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What are some common causes of death in growers (8weeks +)
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- Trauma
- APP - Pasteurella - Step suis - Glassers disease - Porcine circovirus - Ileitis/prolif enteropathy - Swine dystenery - Intestine spirochetosis - Stomach ulcer - Twisted bowels - Erysipelas |
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What are some common causes of death in sows and boars?
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- Farrowing difficulties
- Retained placenta/piglets - Erysipelas - Urinary/uterine infections - Over-heating/heart failure - Bleeding stomach ulcer - Twisted bowels |
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If pigs all have the same findings in a PM, what does this mean?
If PM shows 3 different signs in 3 different pigs, what does this indicate? |
Something new
Multi-factorial, longer standing problem |
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What are some rules about culturing?
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- Only send clean samples
- One sample per jar ONLY - Samples should be at least 3-4cm in diameter - Keep in fridge, no freezing - Send within 24hrs |
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What are some rules about histology?
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- Handle samples gently
- Make them about 1cm thick - Use 10% formalin - Send normal and abnormal tissues - Send via courrier overnight - Don't freeze samples |
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What is the one rule you should be aware of with PCR?
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Send DRY swabs
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Enteric Diseases
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Lecture 2
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What are some signs of enteric disease?
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- Diarrhoea
- Death - Dehydration - Reduced growth - Poor FCE - Reduced feed intake |
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If a pig is less than 5 days, what is likely cause of diarrhoea?
> 5 days? |
Non-haemolytic E coli
Scour only = coccidiosis, rotavirus Scour + death = haemolytic E. coli |
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E. coli
Pathogenesis? Diagnosis? Risk factors? Prevention? |
Pathogenesis
- E. coli attach to receptors lining intestine - Toxins are produced - Salts are lost out of the intestine and fluid moves in = diarrhoea Diagnosis - Serotyping - PCR Risk factors; - Genetically susceptible - Cold piglets <30-35 - Bad hygiene (spread from sows to piglets) - Poor immunity Prevention - Vaccinate sow - Hygiene - Warmth |
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Coccidiosis
Organism? Pathogenesis? Diagnosis? Treatment? Prevention |
Organism = isospora suis
Pathogenesis - Toothpaste white diarrhoea + dehydration at 10 days - Source = faeco-oral oocysts from sows faeces or floor Diagnosis - Gross path (mucosal necrosis of ileum) - Histo (see villous atrophy, thickened walls) - Faecal smears - pool 3 samples from 5 affected litters. You will see coccidial oocysts and fat in faeces indicating malabsorption Treatment - Toltrazuril (baycox) - Hygiene Prevention - No vaccine - Farrowing pen hygiene and Baycox |
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Rotavirus
Organism/pathogenesis Diagnosis |
Significant in Australia?
Organisms/pathogenesis - Organism is ubiquitous - Concurrent infections are common - Group A is most common in pigs Diagnosis - Villous atrophy - ELISA for Ag detection |
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Haemolytic E. coli
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Serotype most involved = K88:O149
Clinical signs (at 10days and post weaning) - Sudden death - Scouring May be due to an incline in mAb Prevention - Not easy - Highly resistant |
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How do you treat baby pig scours?
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- Oral electrolytes & glucose
- Antibiotic injections (broad spectrum) - Group in water medication - TLC (warm, colostrum, dry) |
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What are some causes of old pig scours?
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- Swine dysentery
- Intestinal spirochaetosis - Proliferative enteropathy - Salmonella - Internal parasites |
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Brachyspira spirochaetes
What does it cause? Organisms in each disease? What organ do they affect? Features of organism? Faecal appearance Treatment |
Causes:
- Swine dysentery: B. hyodysenteriae - Intestinal spirochaetosis: B pilosicoli (hairy colon) What organ do they affect? - LI Organism - Hard to culture - Anaerobic - Survive in faeces, but not dessication Faecal appearance in swine dysentery - Faeces contain mucus, blood and necrotic material - Foul smell Faecal appearance for intestinal spirochaetosis - No mucus or blood Treatment - Tiamulin and lincomycin |
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Proliferative enteropathy
Organism involved? Where is it? Pathogenesis Types Diagnosis Treatment |
Organism involved = Lawsonia intracellularis
Where is it? - SI Pathogenesis - Bacteria enters cells - Cells fail to mature and become hyperplastic - Mucosa becomes thickened - Other bugs invade Types: - Non-haemorrhagic (6-20 weeks) - Haemorrhagic (16 weeks +) Haemorrhagic clinical findings - Sudden death - Pale, anaemic pigs - Black, tarry faeces Diagnosis - Cell culture to grow at lab - Gold standard = histo Treatment - Chlortetracycline, tylosin and lincomycin |
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Salmonella
Food concern Organism most concerning Acute form Chronic form Treatment |
- Food issue
- Organism most worried about = S typhirium Acute form - Enlarged intestine - Fluid contents - Obvious lymphatics Chronic - Emaciated - Thickened intestine - Necrotic Treatment - Sulphonamide/trimethoprim |
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Whipworm
Clinical signs Necropsy findings Control PPP and LC |
Clinical signs
- Mucoid, bloody scour - Weight loss Necropsy - Colon grossly enlarged - Masses of worms Control - Clean up enviro - Avermectin or fenbendazole PPP = 6 weeks, direct LC |
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Ascaris suum
Other name? Found where? Eggs features? LC features? Liver gross pathological lesions? |
Roundowrm!!
Found in SI Eggs - Long term survival in enviro - Readily transmitted by birds, insects boots etc cause sticky - Hard to eradicate LC - Eggs out in faeces - Develop on pasture for 3-5 weeks - Ingest eggs, hatch in intestine - Larvae migrate through liver to lung within 1 week of ingestion - Larvae are coughed up and swallowed and get back into SI - Shed eggs etc. Liver pathology - White spots |
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In general, how do you daignose these older, squirting pigs?
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- Consider age
- Look at nature of faeces (mucus for SI vs LI) - Necropsy - Subdmit dung section of small and large to look for Culture = Salmonella Histo = prolif enteropathy, dysentery PCR = simple, multiplex Egg counts = worms |
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In general, how do you treat diarrhoea?
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- Inject individual animals
- Water medicate pens - Prevention in feed medication - Don't contaminate other pens (biosecurity) - Clean and disinfect - Control rodents |
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What vaccines are available?
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E. coli
- IM for sows - Oral for piglets and sows PE - Live oral (enterisol ileitis) |
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What are some non-infectious GIT causes of death in pigs?
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Oesophago-gastric ulcers
Porcine intestinal distension syndrome - Round belly |
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Respiratory disease
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Lecture 3
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What are some of the manifestations of respiratory disease in the pig?
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- Coughing
- Sneezing - Poor growth - Increased variation - Increased susceptibility to other diseases - Nasal discharge - Ocular discharge |
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What are some ways we can assess the impact of resp disease?
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- Coughing index
- Carcass weight/time to slaughter - Increased variation - FCE (feed conversion efficiency) - Mortality rates - Necropsy of dead pigs - Carcass penalties - Serology - Abattoir health check - Medication/vaccination costs |
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What are some infectious causes of resp disease in Australia?
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- Mycoplasma hyopneumoniae
- Actinobacillus pleuropneumoniae - Pasteurella multocida - Haemophilus parasuis - Strep suis - Porcine circovirus type 2 |
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Describe what the coughing index is
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1. Select 50 pigs
2. Wake them and count coughs for 3 mins 3. Repeat x 3 lots that night 4. Repeat next day 5. Repeat every 2-4 weeks 3-5 coughs in 3 mins is borderline > 5 coughs required intervention > 10 cough = trouble |
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What do some of the clinical signs indicate?
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Coughing and ill-thrift
- Enzootic pneumonia (M hyopneumoniae complex) Coughing, ill-thrift and arthritis - Glassers disease Short incubation period and sudden death - Pleuropneumonia - Pasteurellosis Dysnpea and ill-thrift - PCV2 Sneezing - Non-progressive atrophic rhinitis - Dust Sneezing and nasal distortion - Atrophic rhinitis |
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Enzootic pneumonia
Organism involved Clinical signs |
Organism = mycoplasma hyopneumoniae
Transmission - Aerosol - Direct contact Clinical signs - Coughing - Ill-thrift - Very low mortality |
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Actinobacillus pleuropneumonia (APP)
General info Transmission |
- Different serovars (1 and 15 most important)
- Severe disease - Highly contagious - Rapid onset of disease Transmission - Aerosol |
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Glassers disease
Organism? What is it? |
- Organism = haemophilus parasuis
- 15 strains different strains - Sometimes fatal - Causes bronchopneumonia and polyserositis |
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Pasteurella
Organism? Associated with? |
- Organism = P. multocida
- May be subclinical May be associated with: - pneumonia - septicaemia - mortality - depressed growth rate |
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What are some causes of sneezing in the pig?
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- Dust
- Poor air quality - M hyopneumonia (enzootic pneumonia) - Atrophic rhinitis - Bordetella bronchiseptica - Cytomegalovirus/IBR |
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Atrophic rhinitis
Organism? Clinical signs? Common in Aus? |
- Organism = bordetella bronchiseptica and toxicgenic pasteurella multocida (type D)
Clinical signs - Growth depression - Sneezing - Nasal discharge - Bleeding - Deformities - Turbinate hypoplasia Uncommon in Aus |
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Bordetella bronchiseptica
Organisms normal enviro? Other organisms that get involved? |
- This organism is a common inhabitant of the nose in pigs
- It is an opportunistic invader if management is poor - Can cause non-progressive atrophic rhinitis - Non-toxigenic P multocida is involved with this - Can also cause bronchopneumonia (but uncommon) |
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What lab tests can confirm the diagnosis of resp disease?
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Culture and sens = APP, Pasteurella adn H parasuis
Cultural nasal swab = AR and P multocida Serotyping = APP and H parasuis PCR = M hypopneumonia, APP, H parasuis, PCV2 Histopath Immunohistochem = PCV2 Serology - ELISA (MH, APP and PCV2) |
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What should you do on the day when you are presented with resp illness?
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Antibiotics
- Penicillin/draxxin injections of individual pigs Anti-inflamms - Flunixin Water med of at risk groups Antibiotic sensitivity pattern needed TLC for affected pigs |
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What should you do in longer term for resp disease?
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Vaccinate pigs
Improve air quality (ventilation, housing, all in all out etc.) Minimise vertical transmission (age segregated rearing) Minimise horizontal transmission (stocking densities) Strategic medication |
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What vaccines are available for resp diseases?
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MH
APP H parasuis PCV2 |
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Diseases of the Nervous System
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Lecture 4
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What are some clinical signs of NS conditions?
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- Ill thrift
- Dull - Blind - Head pressing - Ataxia - Loss of balance - Lateral recumbency - Padding - Coma - Squeeky voice - Death |
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What are some common NS diseases in aus?
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- Hypoglycaemia
- Congenital tremors - Strep suis - Haemophilus parasuis - Oedema disease - Salt poisoning - Vit A deficiency - Vita B deficiency |
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Hypoglycaemia
What is it? Clinical signs DDx? |
- Weak newborns who fail to nurse regularly
Clinical signs - Tremors - Nervous - Vocalisation - Irritable - Hypothermia - Mental dulness - Seizures DDx - Congen tremors |
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Congenital tremors
What is it Clinical signs Treatment |
What is it
- Hypo/de-meylination of brain and spinal cord Clinical signs - Generalised tremor - especially in head and limbs - Worsen when pigs are aroused and stops when they sleep Treatment - Supportive |
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Strep suis
Discuss the organism (serotypes etc.) How is it transmitted? Zoonotic? |
Organism
- 35+ serotypes - Type 2 most common in pigs - opportunistic lung pathogen after mycoplasma hyopneumoniae Transmission - Transmitted at farrowing and later horizontally as weaners Zoonotic!! |
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Oedema disease
Organism? Pathogenesis? What is it? Clinical signs? |
Organism
- E. coli (producing shiga - like - toxin) Pathogenesis - Colonises SI and releases toxin systemically What is it? Degen angiopathy Clinical signs - Oedema of face and eyelids (and other organs) |
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Salt poisoning/water deprivation
What is it/pathogenesis? Clinical signs |
Brain tissues dehydrated --> Na increases --> water moves out of cells due to hyperosmalarity of the extracellular fluid
Clinical signs - Observed after water has been restored - Acute repeated seizures at 3-7min intervals - Twitching face and ears - Dog sitting - Head up and back - Falling over - Violent paddling - Salivation - Then recovery, and walk away - Apparent blindness - Wandering aimlessly |
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Vit A deficiency
What are the 2 different scenarios? What are the lesions due to? |
2 different scenarios
1. Impaired repro in sows (death of dead or weak piglets) 2. Posterior paresis in growing pigs Lesions due to - Osteodystrophy of skull and vertebral column - Increased CSF pressure from increased production by choroid plexus and decreased absorption by arachnoid villi - Epithelial degeneration leads to increased susceptibility to resp and/on enteric disease and skin lesions |
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How do you diagnose CNS disease?
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Signalment (age, history of water deprivation? feed)
Check for other clinical signs - Arthritis - Scouring with oedema disease - Sudden death with H. para and S. suis - Squeaky voice with oedema disease - Regular convulsions - salt poisoning - Swaying gaite - posterior paresis of hindlimbs, lean against fences for support, blindness - vit A deficiency - Goose stepping - vit B deficiency |
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How do you confirm the diagnosis?
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Culture
Sensitivity Serotyping (H parasuis and E. coli) PCR (H parasuis) Plasma and liver samples (Vit A deficiency) Histopath of brain |
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Discuss histopath findings of nervous system disease
- Vit A deficiency - Salt poisoning - S suis and H parasuis - Oedema disease |
Vit A = wallerian degen with myelin macros
Salt poisoning = eosinophils around vessels S suis and H parasuis = meningitis Oedema disease - Brain = necrosis, oedema, perivascular cuffing, occasional thromboses - Encephalomalacia and cyst formation |
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What will you do on the day?
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- Correct enviro issues
- Isolate sick pigs to recovery pen - Salt poisoning (gradual water provision, sedate, dexamethasone injections) Medication - Supportive - Antibiotic injections - Anti-inflamms - Water med at risk groups |
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What will you do long term?
(2 things) |
Fix enviro and diet
Use vaccines - Nothing for S suis - H parasuis - Oedema disease |
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Skin Conditions
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Lecture 5
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How can skin conditions be grouped?
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- Sores
- Lumps - Different colour - Thickening - Alopecia |
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What type of skin conditions will result in sores?
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- Bite wounds
- Sharp objects - Fly strike - Greasy pig - Mange - Lice - Ringworm/pigpox.pityriasis rosea - FMD |
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Bite wounds
Control/prevention Treatment |
Control
- Clip needle teeth - Minimise fostering - Milk supply (crucial, so not fighting each other) Treatment - Antibiotics (penicillin) - Anti-inflamms - Antiseptic - Udder cream |
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Flystrike
Treatment Control |
Treatment
- Remove maggots - Clean wound using insecticidal cream or powder Control - Traps - Fly papers - Improve hygiene |
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Greasy pig disease
Organism |
Organism = staphy hyicus
Transmission - From sows to piglets during lactation - More common in gilt litters - Can occur pre and post weaning - More likely to occur if fighting - Can be transmitted by biting flies Control/prevention - Beware gilt litters - Rough floors/equipment - Reduce fighting - Liquid feed weaners Treatment - Antibiotics (penicillin etc) - Anit-inflamms - Antiseptics - Udder cream |
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Pityriasis/Ringworm/Pig pox
Control Treatment |
Control
- Improve hygiene - Control biting insects Treatment - Usually not needed - Iodine maybe - Antibiotics for secondary infections |
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Mange
Organism involved? What is the disease? Diagnosis? Control |
Organism = sarcoptes scabei var suis
What is it - An encrustation in ear - Ear skin thickens - Dermatitis results - Mites burrow into skin inside the ear, lay eggs which hatch and turn into larvae - Do not survive off host Diagnosis - Examine ear wax - Skin scraping may be negative Control - Products (e.g. injections, pour ons and sprays) - Treat sows pre-farrowing and piglets at weaning - Aim for eradication |
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Lice
Diagnosis Clinical signs Treatment |
Diagnosis
- Large and easy to see - Usually on head and neck and b/w legs Clinical signs - Skin irritation - Scratching Treatment - Insecticidal sprays |
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What skin conditions result in lumps?
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- Abscesses
- Mosquitos and fly bites |
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Abscesses
Treatment? |
Treatment
- Treat them quickly - Antibiotics - If soft, cut and clean with water and disinfectant - Fly repellant |
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What skin conditions cause different coloured skin?
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- Erysipelas (diamond skin disease)
- Fever - Sunburn - Ergot poisoning |
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Erysipelas
Organism Clinical signs for per-acute, acute and chronic Diagnosis Is it zoonotic? Predisposing causes Control/prevention Treatment |
Organism = eysipelothrix rhusiopathiae
Per-acute disease - Sudden death Acute - Septicaemia - Fever - Diamond skin lesions - Abortions Chronic - Arthritis Pathogenesis - 30-50% of pigs carry the organism in their tonsils - They survive in dirt floors for a long time - Enters via the GIT or tonsils Diagnosis - Signs and culture ZOONOTIC Predisposing causes - Fatigue - Enviro stress - Nutrition changes - Temp - Failure to vaccinate Control/prevention - Always vaccinate - Consider vaccinating progeny - Strategically use in-feed meds Treatment - Penicillin injection for sick pigs - Anti-inflamms for arthritic patients - Amoxy, tlosin and tetra in water for 3 days (may need to increase dose to compensate for poor consumption) |
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Ergot poisoning
What is it caused by Clinical signs Control |
Caused by fungal contam of food
Clinical signs - Dead skin on feet, tips of ears and tail Control - Fresh food, non-moldy |
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What skin conditions cause thickening/alopecia?
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- Mange
- Zinc deficiency - Scald |
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Zinc deficiency
Common or not? Clinical signs? DDx? Diagnosis? Treatment? |
Uncommon
Clinical signs - Thickened skin - Subacute inflamm change - Incomplete keratinsation DDx - Mange Diagnosis - Serum Zn - Histopath - Response to Zn Treatment - Zn |
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So how do you know what the skin disease is?
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Previous experience
Response to treatment - Antibiotics - Increase Zn - Replaced feed (ergot/Zn) - Remove antibiotics (scald) Lab tests - Skin biopsy - Skin swab for culture (greasy pig, erysipelas) - Examine ear wax (mange) |
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Locomotor disease
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Lecture 6
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What are some common locomotor disorders of baby pigs, weaners and older pigs?
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Babies
- Splayleg - Neonatal polyarthritis Weaners - H parasuis - S. suis Older - Superficial injury - Arconbacter pyogenes - Mycoplasma hyosynoviae - Erysipelas - Degen joint disease PSS Vit E/selenium deficiency |
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Splayleg
Cause Treatment |
Causes
- Breed most affected = landrace - Slippery surfaces - Induction of farrowing < 112 days Treatment - Tape legs together - Crib and heater to prevent overlays - Massage - Use non-slip creep surface - Poor prognosis if front AND back legs affected |
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Neonatal polyarthritis
Major pathogens? How do they infect? Prevention? |
Look this up...
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Superficial injury
Possible results Clinical signs Bushfoot? What role does arconbacter pyogness play? |
Possible results
- Can result in cellulitis or osteomyelitis Clinical signs - Lameness involving one or more limbs - Unwilling to stand Bushfoot a problem with sows A pyogenes - Infects joints secondary to soft tissue damage and infection Diagnosis - Culture Prevention - Repair sharp edges - Re-surface rough concrete - Stop tail biting Treatment - Topical - Parenteral antibiotics - Anti-inflamms |
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Infectious arthritis
Organisms involved? |
Organisms
- Mycoplasma hyorhinus - Mycoplasma hyosynoviae - Erysipelas - H parasuis - S suis |
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Mycoplasma hyorhinis
Transmission? Clinical signs? Pathogenesis? Diagnosis Treatment |
Uncommon in Aus
Transmission - From oro-nasopharynx Clinical signs - Fever - Lameness - Abdominal discomfort with polyserositis Pathogenesis - Local damage to resp epithelium --> septicaemia --> polyserositis/polyarthritis Diagnosis - Necropsy (polyserositis, fibrinous exudate), PCR, response to treatment Treatment - Tylosin/linomycin/tiamulin - Anti-inflamms |
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Mycoplasma hyosynoviae
Morbidity and mortality? Transmission? Clinical signs? |
Low-mod morbidity, v. low mortality
Transmission = vertical (Carrier sows in tonsils) or horizontal (at weaning) Clinical signs - Painful - Swollen joints - Usually afebrile - Excess synovial fluid may distend joint Diagnosis - Age of onset (most common in weaners and growers) - Afebrile and lacking polyserositis - Lesions restricted to synovium at necropsy - PCR - Response to treatment Treatment - Tylosin/lincomycin/tiamulin + corticosteroid/flunixin IM |
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DJD
Main manifestation? Predilection sites? Clinical signs onset? Aetiology? Pathogenesis? Clinical signs Diagnosis Treatment Prognosis Prevention |
Main manifestation = OCD
Predilection sites - Medial humeral and femoral condyles - Growth plates of costocondral junctions - Distal ulna - Ischial tuberosities Clinical signs from 4mo Aetiology unknown/multifactorial - Genetics - Nutrition - Enviro Pathogenesis - Disturbed endochondral ossification in the growth cartilages - Osteochondrosis (cartilage flaps or areas with loss of cartilage result in exposure of the subchondral bone to the joint cavity --> results in pain and lameness) Clinical signs - Mod-severe lameness in 1 or more legs - Kneeling walk or on tip toes - Onset may be insidious, progressive lameness - Involvement of synovial joints of vertebrae --> kyphosis Diagnosis - Clinical signs - PM lesions (joint cartilage has folds and flaps, craters expose bone, excess synovial fluid, villous proliferation, joint mice ossified, osteophytes Treatment - Rest - Anti-inflamms Poor prognosis... Prevention - None |
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Rickets and osteomalacia
Prevention? Clinical signs for both? Lesions for both? |
Rare
Prevention - Ensure you diets are well formulated (Ca and P) Rickets clinical signs - Pigs unwilling or unable to stand - Enlarged joints, skull disproportionately large - Bowed, truncated limbs - Fractured long bones, ribs or vertebrae - Paresis or paralysis Osteomalacia clinical signs - Lameness or inability to stand late in pregnancy/lactation/weaning Ricket lesions - Enlarged costochondral junctions and pliable ribs - Thickened haemorrhagic growth cartilages at ends of long bones - Bones poorly mineralised, fractures and/or calluses Osteomalacia lesions - Poorly mineralised bones - Fractures (femoral neck and shaft, humerus or vertebrae) - Secondary osteomyelitis at fracture site |
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Porcine stress syndrome (PSS)
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What is it
- A side effect of the halothane gene (used in the past to increase lean yield) Lesions - Rapid development of rigor mortis - Pale, soft, watery musculature Pathogenesis - Stress --> increased adrenaline --> muscle glycogenolysis and increased lactic acid --> high metabolic rate --> increase muscle temp --> death Clinical signs - Tremor - Acute lameness and collapse - Muscle rigidity - Reddened skin - Hyperthermia - Shock - Death Diagnosis - Clinical signs - Blood test for stress gene Prevention and treatment - Rest (reduce temp rapidly, tranquiliser) - Avoid mixing stress susceptible animals - Market animals on dry cool days and withdraw feed for 12-24 hrs before - Genetic selections (test for gene) |
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Vit E/Selenium deficiency
Causes what? What do we see in weaners? What do Se and Vit E do normally? What deficiencies do we see? Diagnosis? Prevention? |
Causes
- Mulberry heart disease/ hepatosis dietetica Weaners - good pigs found dead Se and Vit E prevent excessive lipid peroxidation of cell membranes... Deficiencies - Absolute - Vit oxidation in rancid food - Rapidly growing pigs exceed avge requirements in diet Diagnosis - History - Clinical signs - Characteristic lesions - Unexpected deaths in best pigs - Heparinized blood for glutathione peroxidase - Histology (coag necrosis of muscle fibres) Prevention - Good feed management - Sodium selenite supplement in diet |
