Pigs Flashcards
What is porcine malignant hyperthermia syndrome (4 marks)? Which anaesthetic drugs may trigger this syndrome (4 marks) and which breeds are susceptible (2 marks)?
Can be apart of the porcine stress syndrome however it has been reported to occur without this defect. It is an Inherited defect caused by an autosomal recessive gene which codes for the ryanodine receptor resulting in instability of the calcium channel and hyperaesthesic muscle. Results in rapid onset anaerobic glycolysis and loss of control of skeletal muscle metabolism. Results in increased muscle rigidity, rising temperature and high lactate causing an increased heart rate, dysrhythmias and death.
Halothane, succinylcholine, isoflourane and sevoflourane.
Landrace and large white, also Duroc and pietrain and Poland China.
Initial investigations of high pre-weaning mortality on a 500 sow breeding unit indicate insufficient milk intake by the piglets.
a) List 8 possible factors that could underlie insufficient milk intake. (8 marks)
b) List 4 signs of insufficient milk intake by piglets (2 marks).
Sow unwell - MMA, mastitis, general illness.
Dehydration or insufficient feed to the sow.
Litter savaging by the sow - puerperal psychosis.
Piglets biting teats and discouraging the sow from milk let down.
Poor crate or creep design - sow uncomfortable and doesn’t want to lie down.
Cold environment discourages sow from milk let down.
Piglets unwell and not trying hard enough to stimulate let down.
Problems with the mammary gland such as mammary aplasia, inversion of the nipples, nipple necrosis or mastitis.
Signs in piglets - hypothermia, vocalising more, ataxia/incoordination/reduced movement, increased signs off illness like diarrhoea and enteritis.
You are asked to investigate an outbreak of suspected Salmonellosis in finisher pigs on a large all-in all-out batch finisher unit holding 1200 pigs aged 16 weeks.
a) List 3 common differential diagnoses for diarrhoea in this age group of pigs, in addition to Salmonella, giving the full names for any infectious agents. (3 marks)
b) How might you confirm a diagnosis of Salmonellosis? (2 marks)
c) Give a total of 5 recommendations for the control or prevention of Salmonellosis in finisher pigs. (5 marks)
Classical swine fever - pestivirus, acute swine erysipelas - erysipelothrix rhusiopathiae, swine dysentery - brachyspira hyodysenteriae.
Post mortem - septicaemia - multiple haemorrhages including petechiation in the kidneys, enteritis - severe bowel inflammation with infarcts and ulcers, mesenteric lymph nodes enlarged, chronic - necrotic enteritis with destruction of mucosal surface.
Culture organism to confirm, may need to be several as excreted intermittently.
Control and prevention - identify and eliminate source, improve hygiene (vehicle hygiene, staff training, source of stock, bedding, water and food, aiao, bio security between batches, cleaning and disinfection) closed herd, avoid stress, vaccines not very effective, acidification of food and water, inclusion of sodium chlorite into water reduces shedding, wet feeding or wet meal, barley instead of wheat.
One of your pig farm clients has reported an outbreak of tail-biting in a pen of finisher pigs aged 18 weeks. Why is tail biting a problem (5 marks)? How would you investigate this problem (10 marks)? What advice would you give on management of this outbreak and prevention of future outbreaks (15 marks)?
Entry point for infections, especially t pyogenes and s aureus to cause spinal cord abscesses and vertebral fractures. Sign of poor welfare as it is a stereotypy and is done to alleviate boredom and environmental stress due to poor husbandry, inadequate accommodation and poor feeding.
History - diet change, environmental change, mixed pigs up, happened before, any other problems.
Clinical examination - look at environment, look at food, cleanliness, stocking densities, water supply, behaviour of pigs together, signs of bullying, hazards in environment. Look at pigs themselves, clinical examinations, systemic parameters, condition of pigs, cleanliness of pigs. Observe when they do not know of your presence if possible and at feeding.
Metabolic profile to assess systemic parameters of pigs, assess tails for signs of infection and signs of the pig that started it all.
Management - good hygiene, remove pig that started it all if possible, par enteral and local antibiotics if signs for infection but leave minor injuries, isolate batch, euthanise any severely injured ones on humane grounds. Improve hygiene, improve diet, remove change that has led to the start of this, add enrichment to the pens such as tyres or chains, decrease stocking density, increase cleanliness, don’t mix batches, feed enough for all, enough trough space, enough lying down space. Only once managemental correction has not worked and the problem is not solved you can introduce tail docking. Before the age of 7d otherwise anaesthesia required. Welfare farmed animal regulations 2003.
Describe five problems associated with porcine general anaesthesia (5 marks). What steps would you take to minimise these problems when anaesthetising a pet Vietnamese Pot-Bellied pig for an ovariohysterectomy (5 marks)?
Malignant hyperthermia - don’t use halothane or succinylcholine, monitor temperature closely, take immediate actions if suspected.
Restricted drug use due to cascade and licensing laws - use the drugs available on the food producing cascade and follow meat withdrawal periods (even if it is a pet).
IV access is difficult and IM injections are hard due to the layer of fat - inject sedation into the neck with a long needle as smallest amount of fat here, use an extension line as the pig may not be used to being handled so will move when the needle goes in.
Variation in bodyweight and not knowing the weight to begin with - as it is a pet pig it may be easier to get it into a pair of scales.
Under sedated or under anaesthetised pigs become easily overheated - with an accurate weight and good IM injection technique can get a good premedication of sedation and can be quick to monitor the temperature, take cooling actions as needed.
Pigs are not used to being handled so can be dangerous - a pet pig may be more amenable to handling but take care, use the extension lead as above, use pig boards to move it about and use appropriate restraint.
Write short notes on the cause and clinical signs of porcine proliferative enteropathy complex (2 marks). In addition to the clinical signs and history, how would you confirm your diagnosis (3marks)? Briefly outline ways to prevent the disease (5 marks).
Cause is an intra cellular bacteria called Lawsonia intracellularis. Usually in pigs aged ten weeks onwards, with the incidence increasing since the ban of growth promotors in feed. Two main syndromes seen, proliferative enteropathy where pigs are dull, poor appetite and poor FCE, may see pale diarrhoea, chronic signs. Other syndrome is the proliferative haemorrhagic enteropathy usually in young adults resulting in sudden death and sometimes the passage of haemorrhagic faeces, can be pale due to heavy blood loss into bowel.
Identify organism in faeces or gut wall, PCR on faeces, post mortem reveals inflammation of the bowel, possible terminal thickening and some necrosis of the wall of the terminal ileum. Necrotic enteritis and terminal ileitis. Blood in bowel lumen.
Prevention: vaccination for 17 weeks protection after in water addition of live attenuated organism, strategic antibiotic therapy with oxytetracycline of clinically affected animals, in contacts and even vitamins to help blood levels. Improve hygiene to prevent spread etc. AIAO, with disinfection and removing all stock, care with incoming potential carrier pigs, have good sourcing or have a closed herd.
- Name 5 common aetiological agents that result in septic arthritis of newly weaned pigs (5 marks). For one of these agents briefly state how you would reach a diagnosis (1 mark) and how you would attempt to prevent the problem (4 marks).
T pyogenes, Erysipelothrix rhusiopathiae, Staphlococcus aureus, Streptoccoccus suis type 1, Haemophilus parasuis, actinobacillus suis.
Erysipelas - clinical signs and progression of untreated disease, pm the joints are thickened, granulation tissue, culture organism from the joint.
Prevention - vaccinate sows and ensure colostrum intake with piglets who then get active immunity with partial exposure. Can vaccinate growing pigs as may be necessary. Good biosecurity, aiao, cleaning and disinfection, closed herd, monitor with bloods, monitor at post mortem.
A wean to finisher pig unit reports an increase in mortality of pigs at 6 weeks of age. He describe neurological lesions amongst a significant number of pigs including blindness, recumbency, opisthotonus and paddling. Give 3 differential diagnoses including one of non-infectious origin. 4 For each of these possible causes, what samples and investigations would be required to reach your diagnosis? 8
Salt Poisoning - Cause is either water deprivation or salt too high in the diet. Diagnosis - Clinical signs, history of water deprivation, high NaCl in diet, eosinopaenia. PM shows eosinophilic meningitis and possibly gastroenteritis.
Streptococcus meningitis - Strep suis type 2, 14. Diagnosis - Clinical signs, culture organism form the post mortem, either from the joints, the meninges. Care as zoonotic.
Classical swine fever - History, clinical signs, post mortem has petechial haemorrhages in kidney, larynx and bladder. Enlarged haemorrhagic LDs, splenic infarcts, button ulcers in caecum. Detect virus with FAT, agar gel precipitation, pcr, serology and ELISA.
State 10 simple guidelines to help your pig farming clients maximise colostral antibody protection in their suckling piglets. 12
1) Sow in ideal body condition before parturition so will want to eat post partem.
2) Sows must be healthy systemically before parturition and does not have defunct teats.
3) Shorten parturition time as much as possible
4) Once each pig has stopped suckling for the first time, tie it to the creep area.
5) Split suckling increases availability and intake of colostrum.
6) Withdraw colostrum from sow and give to weaker piglets via a syringe.
7) Assist weaker piglets to a teat.
8) Provide adequate water to the sow.
9) Farrowing crate should be comfortable for the sow to lie down on.
10) Ensure farrowing pen is warm so piglets do not get hypothermic.
- Discuss the signs which would lead you to suspect an outbreak of Leptospirosis in a pig herd.
How are these signs different from those associated with other possible specific infectious causes of reduced fertility?
Outline the action you would advise the producer to take.
(30)
Host adapted and non host adapted serovars. L Pomona in pigs is host adapted but not in the uk. Non host adapted include L icterohaemorrhagica, muenchen, bratislava, canicola.
Icterohaemorrhagica is the brown rat.
Clinical signs:
Acute infection - canicola and icterohaemorrhagica - pyrexic, dull and anorexic, diarrhoea and jaundice (rare, associated with haemolysis).
Subclinical infection - widespread, serological evidence of infection but no clinical signs.
Reproductive - abortion and neonatal mortality of unthrifty pigs, sows can show agalactia and jaundice, aborted fetuses may be autolysed (bratislava and muenchen).
Differentials include other causes of abortion such as swine erysipelas, parvovirus, PRRS; pyrexic pigs other acute infections either bacterial or viral.
Swine erysipelas differentiation - usually more severe, and affects sows in late pregnancy, commonly get characteristic diamond shaped and elevated skin lesions (necrotic vasculitis) in 24hrs of the disease, start on dorsal surface of neck and shoulders. Abortion is the least common sign, chronic infections lead to chronic arthritis and endocarditis. Also per acute version resulting in sudden spdeath and purplish discolouration of the skin and bloating.
Parvovirus differentiation - small litters associated with early embryonic loss, mummified pigs, stillbirths, abortions uncommon, neonatal deaths not affected, no other signs of systemic illness in the sow unlike lepto, can take a long time to go through the herd (4 months).
PRRS differentiation - virus belonging to arteriviridae, closely related to equine arteritis virus, enters via semen, faeces and wind possible, immunity short lived. Signs very variable, get late abortion, stillbirth, weak piglets for many months, get good immunity following abortion, can get early stage damage and increased numbers of irregular returns. Respiratory signs of pyrexia, anorexia, cough, dyspnoea, skin discolouration and ill thrift - can die with secondary infection with Haemophilus parasuis, can precede abortion in gilts, anaemia, predisposes to resp disease.
Aujeszkys - vomiting and diarrhoea in piglets less than four weeks leading to neurological signs like incoordination, convulsions, recumbency and death. Older animals can get anorexia then respiratory signs. Sows have repro failure with abortion, early embryonic death and vaginal discharge.
Bacterial causes - klebsiella, E. coli, streps, pseudomonas.
Parasite burdens, cystitis and nephritis.
Can be non infectious causes - seasonal infertility, decreasing day light length, low temps, chilling, draughts, poor nutrition, no boar contact, vaccine reaction, lameness, poor hygiene.
Find the cause - demonstrate organism or culture from body fluids and tissues, serology, agglutination tests, Elisa DNA probes.
Control - usual biosecurity, vermin control, no vaccines but can be imported under special treatment authorisation from veterinary medicines directorate.
- Porcine Malignant Hyperthermia is a potential complication of general anaesthesia in pigs. Describe in note form what it is, and how it may be avoided or prevented. (10)
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- An inexperienced pig client is concerned about high mortality in piglets. Most of them die in the first 3 days of life and many litters have diarrhoea.
a) List the two most likely causes
b) What could you advise for immediate help.
c) How could you confirm your diagnosis
d) What preventative measures could be taken to avoid this problem in future?
(10)
Enterotoxigenic E. coli; rotavirus
Give oral antibiotics to all susceptible for full five day course, keep piglets warm and hydrated, supplement with electrolyte or glucose solutions but do not take off the sow. Steroids and NSAIDS to very ill piglets may reduce mortality.
Diagnosis - clinical signs, post mortem, history of poor colostrum intake, stomach has very little fluid or even empty, intestines thin walled and fluid filled, confirm by isolating organism.
Prevention - maximise colostrum intake; strict cleanliness; wash sows before moving into farrowing crates; boost piglet immunity through sow vaccination during pregnancy, killed vaccines.
- In note form, describe how would you provide anaesthesia /analgesia for a piglet requiring umbilical hernia repair, indicating which products are licensed for the pig.(10)
Azaperone licensed, ketamine. Ketamine induce. IV access, stress, malignant hyperthermia dantrolene for five days prior, weight, hyperthermia, IM injection, handling. Intubation due to laryngeal spasm. Analgesia butorphanol and tolfenamic acid.
Licensed - tolfenamic acid, meloxicam, flunixin, ketoprofen, atropine and Azaperone.
- Outline the post-mortem signs you would expect to see in cases of PDNS (Porcine Dermatitis & Nephropathy Syndrome), and explain how you would differentiate this from CSF (Classical Swine Fever).(10)
Post mortem - kidneys mottled with numerous small haemorrhages, free fluid in abdomen and enlarged, oedematous and red black lymph nodes of the caudal abdomen. Extensive dermatitis of the chest, abdomen, thighs and forelegs, purplish red bumps of various signs, some may not have skin signs.
Differentiation - usually small number of pigs affected unlike CSF and other signs if CSF, lab tests done which take seven days, includes virus isolation by FAT for CSF, agar gel precipitation, PCR, serology FA neutralisation test and Elisa.
Clinical signs CSF - acute - sudden deaths, depressed with high temps, anorexic and bury themselves in straw, reluctant to move and walk with swaying gait, constipated then diarrhoea and vomiting, ocular discharge with eyes shut together, purely blotchy discolouration of the skin esp ventral abdomen and necrosis of ear tips. Get muscle tremors and convulsions.
Chronic - dull anorexic, fail to thrive, skin discolouration and dermatitis, glomerulonephritis, decreased repro efficiency.
Congenital - mild pyrexia, abort or small litters with mummified piglets, cerebellar hypoplasia and type a1 congenital tremor - myoclonia congenita.
- Outline clinical signs, diagnosis and control of Streptococcus suis type 2 infection in pigs. (10)
Occurs 3-7 days after environmental stress inc mixing and moving pigs. Clinical signs - weaners, growers and finishers normally, sudden death may be the first sign, anorexia and pyrexic, glassy stare, acute arthritis with warm, swollen and painful joints, others show meningitis and become recumbent, convulsing and nystagmus.
Diagnosis - history of farm and pigs, clinical signs, culture from post mortem material.
Control - treatment starts with aggressive antibiotic therapy, NSAIDS may help, nursing care including food and encouraging exercise.
Strategic meds at stressful times, husbandry improvement, aiao, good c and d, eradicate strep suis, depopulation and restock with hysterectomy derived stock, then a closed herd with strict hygiene. No vaccine commercially available.
