end of life and slaughter Flashcards

Question

Animal By-Product: Categories 2

Answer 1

High risk Staining required?- Sometimes – stained black Material potentially infectious to humans or other animals e.g. bTB lesions. Products containing residues of authorized vet medicines. Manure and digestive tract contents. Carcasses of dead livestock not containing SRM. Dead on arrivals.

Answer 2

Lowest risk material no staining required Can go for pet food. e.g. Carcasses or parts which have passed ante- and post-mortem inspection but not intended for human consumption. Heads and feathers of poultry. Incised pig offal. Bovine udders. Poultry intestines. Animal hides and skins. Horns and feet

Answer 3

the tonsils, mesentary, caecum and last 4 meters of smal intestine of cattle o all ages the sull excluding the mandible, the spinal cord, the brain and the eyes of cattle ovfr 12 months old the vertebral colum of cattle over 30 mnths the sull, brain , eys and spinal cor of sheep and goats more than 12 months old stated in Regulation (EC) 999/2001- Annex V made in respnse to BSE FBO (Food Business Operator) is responsible for removal of spinal cord No trace of spinal cord can remain in the spinal canal – major infringement if found The FBO must be meticulous about removing spinal cord The meat inspector/OV will check that everything has been removed as part of the meat inspection procedure A designated tool or knife must be used to remove the meninges, fat and debris Removed from slaughter hall with no contact with fresh meat or floor – stained 100% with blue dye (patent blue)

Answer 4

Before processing any ABP material it must be crushed into smaller pieces – dimensions set by legislation – mincers, crushers 6 approved methods to process ABPs Category 1 and 2 ABP must be pressure sterilized Pressure sterilization means that the pieces must be a maximum size of 50mm, heated to 133C for 20 minutes without interruption at core temp, under a minimum pressure of 3 bars (three times normal atmospheric pressure, under steam rather than air) where- An ABP processing facility Biodiesel factory Pet food manufacturer ABP combustion site Organic fertilizer manufacturer Incinerator site Compost or biogas/anaerobic digestion site

Answer 5

Rendering is the cooking and drying process that destroys pathogens, removes moisture and separates the fat (tallow) and protein (MBM from Cat 1 and 2, PAP from Cat 3) components of ABP into marketable products It’s big business! Turning ABP into useful products that can be used elsewhere The products of rendering can be used for pet food, animal feed, pharmaceuticals, organic fertilizers, biofuels and oleochemicals (animal oils and fats) Category 1 ABP are rendered to produce biodiesel or are combusted as fuel

Answer 6

Livestock dying on farm must be collected, identified and transported from a farm ‘without undue delay’ Must arrange for the animal (incl. stillbirths and afterbirths) to be collected by an approved transporter and taken for disposal to one of the following: Knacker Renderer Hunt kennel Maggot farm Incinerator The burial or burning of fallen stock in the open is illegal Prevents the risk of disease spread from residues in the soil, groundwater or air pollution Exemptions to this ban include: Burial of dead pet animals (e.g. dog or cat) and horses (any horse in England; only pet horses in Scotland and Wales) (authorisation C2) Remote areas – Isles of Scilly, Lundy Island and Coquet Island (authorisation C3) After a natural disaster (authorisation C4) The burning of fallen stock in the open is illegal But licensed and approved on-farm incinerators may be used The disposal of carcasses of livestock during the Foot and Mouth Disease outbreak in 2001 provoked huge controversy On-farm pyres, mass burial sites, rendering as ABP Concerns around aerosolisation of FMDv, soil contamination, water pollution, SRM in mass burial sites, psychological impacts on local communities, and health impacts of pyre smoke

Answer 7

need for wider consideration of public and environmental health aspects of carcass disposal Nutrient pollution – N, P – excesses in soil, water, air Pathogen survival in leachate – E. coli, Salmonella, prions from TSEs Veterinary drugs – antibiotics Chemicals and elements – Na, Cl, VOCs Lessons learned from the disposal of carcasses of livestock during the Foot and Mouth Disease outbreak in 2001 Use of on-farm pyres and on-farm burial was superseded by mass burial sites (Army involved) and rendering as ABP as outbreak wore on

Answer 8

Scrapie Another Transmissible Spongiform Encephalopathy (TSE) Notifiable disease – prions are the infectious agent (as with BSE) Two forms – Classical and Atypical Classical – animals between 2 and 5 yrs old; Atypical - > 5 yrs old Highly contagious – colostrum, milk, contamination in the environment (for years) – bedding, feed troughs, pastures contaminated by birthing fluids from infected sheep Sheep can have genetic resistance – genotyping and selection to breed it out No known link to human illness – removed as precaution linked to BSE controls

Answer 9

leading to eventual death Excitability – acting nervously or aggressively Depression, vacant stare Trembling of the head, drooping ears High stepping trot, incoordination of limbs Unable to stand Skin irritation – repeated scratching against posts, gates Nibble reflex when rubbed on their back Excessive wool loss, skin damage

Answer 10

Equine Metabolic Syndrome is not a disease per se “Collection of risk factors for endocrinopathic laminitis” Insulin Dysregulation- Obesity or regional adiposity “Easy Keeper” +/- hypoadiponectinemia +/- hyperleptinemia which leads to - Laminitis! Hypertension Pro inflammatory state Diagnostic tests: Basal Insulin Oral glucose/ Karo test IV tests: CGIT / insulin tolerance test / others.

Answer 11

Age related degenerative condition in horses Loss of dopaminergic inhibition Hypothalamus unable to regulate pars intermedia of pituitary gland Hypertrophy / hyperplasia of PI Increase production of many hormones from PI which have wide array of effects on body Clinical Signs- Pathognomonic hypertrichosis Hair Colour Changes & Patchy Shedding Lethargy / Poor performance Skeletal muscle atrophy Rounded abdomen Abnormal sweating (↑ or ↓) Polyuria/polydipsia (↑ urinating/drinking) Regional adiposity Absent reproductive cycle/Infertility Laminitis ( 1/3 od PPID cases will have ID) Susceptible to other infections *** NOT ALL SIGNS MAY BE PRESENT ESPECIALLY IN EARLY CASES*** Diagnostic tests: Basal ACTH TRH stimulation test

Answer 12

There is no cure. Treatment is intended to reduce clinical signs and should be lifelong Treatment: Pergolide mesylate (Prascend, Boehringer Ingelheim) – dopamine agonist Initial dose of 2 mcg/kg (0.5 mg for a 250 kg pony and 1.0 mg for a 500 kg horse). Rarely some horses may require doses as high as 10 µg /kg body weight per day Side effects: decreased appetite 33% lethargy 9.8% Reduce or stop treatment for a few days and restart with gradual dose increase Controlled drug under FEI rules. After initiation of treatment (2 mcg/kg ) Re check clinical signs and basal ACTH +/-insulin at 1-2 months If there is an improvement in c.s and laboratory parameters maintain on current dose: 6 Monthly evaluation ( clinical signs + ACTH+ insulin) Ensure at least one evaluation in Autumn? (natural dynamic test) Currently no evidence that treatment with pergolide improves insulin sensitivity but studies have suggested that increases in alpha-MSH and CLIP can increase insulin secretion and severe cases of PPID might be more likely to have ID If not improved ***Increase the dose*** Expect one or more clinical signs to improve and/or the basal ACTH to have returned to normal or close to normal range Re‐evaluate baseline endocrine and clinical values every 1‐2 months until improvement is seen Owner to document clinical examination findings monthly. Individually tailored diet and exercise program (may be overweight/ underweight/ +/-insulin dysregulation/ PPID associated muscle atrophy) Good preventative veterinary care: Regular dental and endoparasite checks Regular farriery ( particularly if laminitic) Clipping / skin health Geriatric health checks ( concurrent issues)

Answer 13

(Prascend, Boehringer Ingelheim) used to manage PPID dopamine agonist Initial dose of 2 mcg/kg (0.5 mg for a 250 kg pony and 1.0 mg for a 500 kg horse). Rarely some horses may require doses as high as 10 µg /kg body weight per day Side effects: decreased appetite 33% lethargy 9.8% Reduce or stop treatment for a few days and restart with gradual dose increase Controlled drug under FEI rules. After initiation of treatment (2 mcg/kg ) Re check clinical signs and basal ACTH +/-insulin at 1-2 months If there is an improvement in c.s and laboratory parameters maintain on current dose: 6 Monthly evaluation ( clinical signs + ACTH+ insulin) Ensure at least one evaluation in Autumn? (natural dynamic test) ** Currently no evidence that treatment with pergolide improves insulin sensitivity but studies have suggested that increases in alpha-MSH and CLIP can increase insulin secretion and severe cases of PPID might be more likely to have ID ** If not improved ***Increase the dose*** Expect one or more clinical signs to improve and/or the basal ACTH to have returned to normal or close to normal range Re‐evaluate baseline endocrine and clinical values every 1‐2 months until improvement is seen Owner to document clinical examination findings monthly.

Answer 14

ID is a central feature of EMS and at least 33% of horses with PPID Laminitis associated with insulin dysregulation (ID) hyperinsulinaemic laminitis (HAL) is a significant welfare concern Management of Hyperinsulinaemia is achieved using: Dietary management Exercise +/- pharmaceuticals (severe cases/ non responders) Dietary management is critical Aim: to reduce post prandial hyperinsulinaemia Remove feeds high in non-structural carbohydrates (NSC) e.g. grain feeds /pasture. In obese animals restrict intake and increase exercise if possible (often not possible if laminitic) Hay should form the bulk of ration ideally hay with a low (<10%) water soluble carbohydrate (WSC) content or non‐structural carbohydrate (NSC) ≈ 10-12% DM. %NSC = %WSC + %Starch Feed little and often to avoid insulin “spikes” Feeding lean horses with ID: Maintain BCS- Low glycaemic diet Use low insulinaemic calories Oil Unmolassed sugar beet pulp Balancer Exercise Soaking Hay - Reduces WSC content but also DM and minerals. (balancer essential) Temperature of the water, soak time and volume of water affect amount of sugars leeched from the hay. But long soaks in warm water can lead to microbial growth. Typically soak for 6-8 hours in ambient temperatures. In warmer conditions soak time can be reduced Overnight soaking probably acceptable in cool conditions. Steaming hay is not effective in reducing WSC Feeding a 50:50 mixture of hay and straw possible alternative? exersise- Only in horses with ID without signs of lameness Improves insulin sensitivity when compared to dietary restriction alone. But moderate exercise without dietary restriction has minimal effect on ID. Increase gradually monitoring for lameness. Build up to a min of 15-20 min trot/canter / day (moderate intensity) Use a soft conforming surface in cases with previous laminitis

Answer 15

In severe cases or cases which are unresponsive in the first 4 – 6 weeks consider medication. No licensed treatment for HAL in horses. 3 drugs/ drug classes that are used in clinical practice. Gliflozins/ SGLT2i (Sodium-glucose co-transporter-2 inhibitors) Levothyroxine Metformin

Answer 16

Velagliflozin, canagliflozin and ertugliflozin (doses vary with drug) Appear to be rapidly effective in reducing insulin concentrations Long term safety studies lacking Used in human medicine for last decade for tx of type 2 diabetes In humans SGLT2 receptor in the proximal convoluted tubule is responsible for 90% of glucose reabsorption, and the SGLT1 receptor is responsible for the remaining 10% SGLT2i block glucose reabsorption > reduction in insulin production. Side effects> Hypertriglyceridaemia /PUPD & UTI (glucosuria) Tapering doses when discontinue **Assess and monitor hepatic and renal function and triglyceride concentrations **

Answer 17

In severe cases or cases which are unresponsive in the first 4 – 6 weeks consider medication. No licensed treatment for HAL in horses. 3 drugs/ drug classes that are used in clinical practice. Gliflozins/ SGLT2i (Sodium-glucose co-transporter-2 inhibitors) Levothyroxine Metformin

Answer 18

Synthetic thyroid hormone Increases basal metabolic rate and results in both weight loss and improved insulin sensitivity in obese horses. (not used in lean horses with ID) Must control diet as increases appetite Typically administered at 0.1 mg/kg PO SID for 3–6 months Taper at discontinuation to allow restoration of thyroid axis

Answer 19

Anti-glycaemic medication used to improve insulin sensitivity in humans with diabetes. Use in horses is controversial Limited bioavailability Effective in a small percentage of horses Short duration of action Administer 30 min before turnout or feeding to reduce post-prandial insulinaemic response. Dose 15–30 mg/kg PO BID

Answer 20

Essential in the care of horses and ponies with laminitis. Acute laminitis should be treated as an emergency (covered by Jenny) Once pain and lameness is present cellular damage has already occurred. If the horse is shod or if the horse stands on a hard surface, weight bearing is concentrated around the perimeter of the hoof onto the compromised lamellae. May be appropriate to remove shoes Apply some type of deformable material to the solar surface of the foot such that the sole, bars, and frog in the palmar/plantar section of the foot become load sharing with the hoof wall. Or place on a soft conforming surface/ strict box rest. Baseline radiographs

Answer 21

Essential in the care of horses and ponies with laminitis. In chronic laminitis treatment aimed at improving morphology and function of a foot or feet where there has been structural change Radiography (Lateral +/- DP views) used to assess: Degree of dorsal rotation of P3. <5.5 ° good, 6-11° fair, > 11° poor Sinking/ Founder or Coronary band : extensor process distance (CE) 2-8mm, >15 mm poor prognosis. Thickness of the sole Thickness of the dorsal hoof wall Angle of the solar surface of the distal phalanx relative to the ground Distance between the dorsal margin of the distal phalanx and the ground Horizontal position of the distal phalanx in the frontal plane (DP view) In chronic laminitis, trimming and farriery should aim to: Decrease the stress on the most damaged lamellae Recruit all available ground surface that is capable of bearing weight Position breakover appropriately Restore the alignment of the pedal bone to the dorsal hoof wall and sole There are a large number of methods / shoeing options available Work closely with your farrier Problems: Diseased, weak laminar growth Tension in the DDFT (DDFT tenotomy?) Chronic pain Tearing of laminae Sensitisation of tissues Chronic infections Seedy toe Abscesses

Answer 22

ACP and ketamine subcutaneously - good for spicy cats as everything else needs to be given im medetomadine- makes them vomit and vasodilation gabapentin and trazadone are oral

Answer 23

Reliably causes a quick loss of consciousness and death with the minimum amount of pain and distress for the animal. Barbiturates depress the central nervous system (CNS) in descending order beginning with the cerebral cortex and resulting in inducing a loss of consciousness, progressing to general anaesthesia. With an overdose, apnea due to depression of the respiratory centre is followed by cardiac arrest. Sedate or not to sedate- often delays death How predictable is it? How healthy is the horse?- good option for young otherwise health horses but not for old or chronically ill horses Alpha 2 – avoid xylazine (exitable reaction) and use low doses 2. Catheter- 12g or 14g Three-way tap – ensure you know which way!!! Place local anaesthetic TIE IT IN!!!! Extension set? 3. Set up Leave plenty of space around you and the horse. Clearly communicate AGAIN what is going to happen, what you want the owner to do… ‘Are you happy to hold Fred? What I will do it start injecting the somulose once you are happy, when I have administered it all please hand the lead rope to me and step backwards away from Fred. I will tell you when its safe to return to him. As soon as the somulose has been administered he wont feel anything, so don’t worry if doesn’t lie down as expected. When he is down he may move or twitch which is completely normal, he cant feel anything’. 4. Injection Administered the first 10ml over 15seconds, and then administer the remainder as quickly as the catheter allows. Disconnect and close the 3way tap 5. Going down Sometimes this will be perfect, sometimes it wont be. They will often take 2 agonal breaths before they go down Hold the horse rope and place you hand on its shoulder The horse will sway forwards and as it does so put some pressure on its shoulder to guide it down. 6. Confirming death Remind owners they may move/twitch which is completely normal. When safe, and the owners want to, get them to approach the horse at the neck on the mane side. DO NOT RUSH THIS BIT!! It can take a while for some horses to die. Once the owners are away from the horse I will go to the car and get my stethoscope – this gives time to ensure the horse has died CONFIRM WITH NEGATIVE CORNEAL REFLEX

Answer 24

Single shot – barrel in contact with the animal Must be accurate Association of Racecourse Veterinary Surgeons- firearms training Must have firearms certificate Must be stored in a locked gun cabinet Locked metal box in car for transport Ammunition must be stored separately Death is instantaneous After death the horse’s reflex actions in its muscles will twitch or spasm and their legs may kick. Your horse’s heart may continue to beat for a short time, however this is normal and the horse is not suffering during these reflex actions. Death is instant There can be blood Owners cannot hold during the procedure Horse drop the floor immediately. Can be more shocking for some owners Reflexes including heartbeat Advise you always sedate Be critical of your location for euthanasia You can learn more at ARVS courses Very useful for needle shy horses

Answer 25

As a guide, BEVA considers that an affected horse will need to meet the following requirements to satisfy a claim under a mortality insurance policy: “That the insured horse sustains an injury or manifests an illness or disease that is so severe as to warrant immediate destruction to relieve incurable and excessive pain and that no other options of treatment are available to that horse at that time.” It is the responsibility of the attending veterinary surgeon Regardless of whether the horse is insured or not. Primary responsibility is the welfare of the horse When a veterinary surgeon is presented with an insured horse where the owner or agent feels that it should be euthanased, the veterinary surgeon should remember the following points: The horse should be positively identified - either from a passport or by taking separate markings. Check for the presence of a microchip. The race card number will aid identification at the racecourse. A full or complete as possible clinical examination of the horse should be made and all details recorded. Once the horse is euthanased, an independent post mortem examination should be carried out. There will be a number of situations encountered requiring different approaches A) Definitive Grounds for Immediate Euthanasia- Clear-cut case for immediate euthanasia on humane grounds delay should be avoided. PM findings may be needed to corroborate any decision made B) Suspected but not definite grounds for immediate euthanasia- Must seek 2nd opinion. Contact insurance company Transport horse to appropriate premises Provide first aid treatment until 2nd opinion is obtained C) No grounds for Immediate Euthanasia in the Opinion of the Attending Veterinary Surgeon- Inform owner to contact insurance company for guidance In case of difficulties obtain a 2nd opinion If the owner insists on euthanasia request they sign ‘request for euthanasia’ stating it may invalidate their insurance claim Document findings D) Cases where injured or ill animals require urgent surgical or specialised medical intervention to save the horses life- Its important to keep the insurance company notified. Difficult OOH E) Where an owner requests euthanasia of a horse for other reasons- Doesn’t meet the requirements but owner still requests euthanasia Inform owner they have no recourse to the insurance company subsequent to euthanasia. Document findings and request owner signs ‘request for euthanasia’ form. Chronic disease and lameness- Significant pain and suffering Chronic severe permanent lameness + evidence of significant suffering e.g. chronic weight loss, prolonged recumbency, persistently raised pulse, unwillingness to move AND no recognised alternative treatment and routine analgesia does not alleviate the pain OR B) Where the horse is likely to die within the period of insurance because of an insured condition

Answer 26

Porcine circovirus type 2 (PCV-2) Identified in 1998 30% post weaning mortality 3-4 weeks post weaning Pigs weaned in good condition start to loose weight, then yellow scour, then death. No useful treatment yellow watery intestinal contents on pm- could also be salmonella or rotavirus inguinal lympnoed congestion- lymphid depeltion in lymphonode pathoneumonic lung congesion- intersitial pneumoia- can do immuniohistochem Diagnosis: Clinical Signs Gross Pathology Histopathology Lymphoid Depletion is Pathognomonic Immunohistochemistry of affected Tissue: Heart Muscle, Lung, Kidney PCR Oral Fluids (Ropes) Blood: Care when vaccinated

Answer 27

Porcine Circovirus Type II / PMWS - Complication Older than in PMWS – Growing/Finishing pig Raised Erythematous macules and papules Extremities – Ears, Scrotum multifocal haemoragic nephritis- could also be ASF! CSF! so be aware

Answer 28

Post-weaning Multisystemic Wasting Syndrome (PMWS) Porcine Dermatitis and Nephropathy Syndrome (PDNS) Now endemic - most herds are infected PCV2 vaccination of piglet - At Weaning Circoflex (most successful vaccine ever!) PCV2 vaccine so successful that we have seen a shift and emergence in PCV2 strains Vaccination of sow – circovac Vaccination of breeding gilts

Answer 29

E.coli Salmonella

Answer 30

Review: Virulence Factors Classification Enteritis Timing: Immediately Post Weaning -> 2 weeks post weaning Clinical signs: Diarrhoea –Watery Grey/Brown Diarrhoea, No Blood, No Mucous Pig – Peri Anal Staining, Dehydrated, Poor Body Condition Diagnosis- Clinical Signs Faecal Sampling – in the best order! Small Intestinal Contents - Charcoal Swab / Pot Rectal Swabs - Charcoal Swab(Amies Transport Medium) Pooled Faecal Samples - Pot – care with environmental contamination Virulence gene PCR!!! Preventative Health Measures: Weaning age- The immune function of the gut increases as the pig gets older Weaning is Associated with Villus Atrophy and Crypt Hyperplasia Weaning Process significantly increases levels of pathogenic Coliforms and reduces levels of favourable lactobacilli Developing a healthy gut - Crumb/Creep Feeding in the Farrowing House (not possible outdoors)- Develops Lactobacilli – Develop gut barrier function Increasing fibre content pre weaning i.e. Corn Cob Maize - Develops Lactobacilli – Develop gut barrier function Avoiding prophylactic antimicrobial use - Reduces Lactobacilli and lactate production Increases protein fermentaion Hygiene! – i.e. reduce pathogen load - In the farrowing accommodation (harder outdoors) Weaning Accommodation Weaning onto the correct feed and following the programme Example: 2-2.5kg ‘1st Stage’ followed by 6-7Kg ‘2nd Stage’ Pro – Biotics - Competitive Exclusion – i.e. TopGut = Clostridum butyricum More claims in preventing Salmonella (Zinc Oxide) Reduce environmental stressors - Avoid Cold temperatures/Draughts - 28 degrees Provide thermal comfort – Straw, Micro environments Reduce Pathogen Load - Hygiene Have seen creep feed before Stocking - Group by Size Do not overstock Vaccination- F4/F18 Combination- Oral via water / Individually dosed From 18 days of age Onset of immunity is 7 days – When is Disease Occurring? Duration of immunity is 21 days – When is disease Occurring? (Shigatoxin – Two vaccines commercially available) - They are for Bowel Oedema – not Post Weaning Diarrhoea N.B Bowel Oedema E.coli must have an F18 and Stx2e gene therefore potential to prevent with the F4/F18 combo vaccine

Answer 31

Apply Similar Principles to Post Weaning E.coli Zoonotic Classification / nomenclature Genus: Salmonella Species x2: Bongori, Enterica Sub-Species x6 for Enterica Species: enterica … Serotypes (Serovars) (x2500): typhimurium, dublin, newport, montevideo, I 4,[5],12:i:-... = Salmonella enterica subsp enterica serotype Typhimurium Typhimurium = Group B Salmonella Characterised by antigens. Somatic Antigens (O) and Flagella antigens (H) O – 4, 5, 12 H – i:1, 2 I 4,[5],12:i:- - Monophasic Variant of Salmonella Typhimurium So why is this one important? One of the most common (Human & Animals) Characterised by it’s multi drug resistance (H Sun et al., 2019) Clinical Signs – can be any age post weaning Faecal oral Transmission Pig – Poor Body Condition, Dehydrated, Lethargic, can appear neurological, Found Dead (Septicaemic form) Poop – Yellow Watery Diarrhoea, Sometimes haemorrhagic, Sometimes Mucous, Very smelly! Forms (D.J. Taylor, Pig Diseases) Septicaemic Enteritis Colonisation Septicaemia comes from damage to tight junctions and salmonella can infiltrate the blood Neurological signs may appear due to Salmonella crossing Blood Brain Barrier Differentials for Button Ulcers are important – particularly Swine Fevers and potentially Swine Dysentery septicaemic- High Mortality Fever Neurological signs Found dead Good Condition Pathology – Minimal Acute- Fever Neurological signs Yellow Watery Diarrhoea Lead to Septicaemia – Found Dead Enlarged Lymph Nodes Necrotic Intestinal wall Watery GI contents Chronic - Fever Neurological signs Yellow Watery Diarrhoea Wasting, Emaciated, Dehydrated Enlarged Lymph nodes Button Ulcers Thickened intestinal wall Apply Similar Principles to Post Weaning E.coli Diagnosis Clinical Signs Faecal Sampling – in the best order! Small Intestinal Contents -Charcoal Swab / Pot Rectal Swabs -Charcoal Swab(Amies Transport Medium) Pooled Faecal Samples -Pot – care with environmental contamination ** ZOONOTIC POTENTIAL** Diagnosis Faeces - Salmonella Culture Direct Indirect – Enrichment via selenite broth Histopathology - Will show necrosis different variants can be very resistant to treatment. In the acute setting options are generally – Water soluble Neomycin, Apramycin or TMPS. This must be combined with an injectable approach. Treatment must start empirically to prevent high levels of mortality Control - Salmonella Control Plan Vaccination - Sow - Piglet at Weaning Live Attenuated available Feed – Reducing Wheat content and increasing barley content, increasing grist size Visitors – Have a visitor policy, provide with own overalls and PPE Pig Movements – Run all in all out systems to allow for cleaning and disinfection Salmonella cholerasuis- Not in the UK Prominent in America Low morbidity High Mortality Apply similar principles for control

Answer 32

Spirochaete – gram negative Brachyspira hyodysenteriae Colon Faecal Oral Transmission Severe Economic impacts – Morbidity Clinical Signs- Diarrhoea - Profuse Watery Brown/grey with BLOOD and MUCOUS (Colitis) followed by Necrotic Material Wasting - Pigs become pinched, Spines become prominent Morbidity up to 75% (D.J. Taylor) Mortality – 5-25% (D.J. Taylor) Diagnosis- History Faeces -> BLOOD and MUCOUS - Brachyspira PCR & culture Post Mortem -> Gross Pathology - Morphological Diagnosis: Severe Chronic Diffuse Fibrinonecrotizing Colitis Colon ->Histopathology Treatment – In Water and Individual Treatment Tiamulin Lincomycin (Macrolides) **NO Vaccines Available** Depopulate Disinfect – EVERYTHING!! Remove muck from Site Dry Repopulate

Answer 33

Two Disease Presentations Porcine Intestinal Adenopathy (Ileitis) ->Necrotic Enteritis Proliferative Enteropathy Two Disease Presentations Porcine Intestinal Adenopathy (Ileitis)  Necrotic Enteritis Proliferative Enteropathy Diagnosis Clinical Signs Faeces -> PCR -> qPCR Histopathology -> Ileocaecal Junction -> Silver Staining Control Live attenuated oral vaccine available All other techniques we have already described qPCR- Allows us to see time point when most shedding odf disease to target management decisions

Answer 34

6 weeks post weaning onwards Sub Clinical to clinical Grey Pasty Faeces Distal Ileum (ileocaecal junction) and Proximal Colon thickened Morbidity but pigs recover Two further conditions associated with PIA Can lead too: Necrotic Enteritis – Necrotic Luminal Surface Hospipe Gut – Smoothed luminal surface

Answer 35

Older Pigs (further post weaning) Blood Rope Appearance Ileum Found Dead Pale Pigs Can lead too: Necrotic Enteritis – Necrotic Luminal Surface Hospipe Gut – Smoothed luminal surface

Answer 36

Legislation to consider Animal Welfare Act Section 4 and 9 The Fraud Act 2006 – in particular conspiracy to commit fraud and fraud by false representation The Animal Welfare (licensing of activities involving animals) (England) regulations 2018 Lucy’s Law -The Animal Welfare (licensing of activities involving animals) (England)(Amendment) regulations 2019

Answer 37

Any age of cattle but especially young cattle due to curious nature Access to old car batteries, engine oil, old lead paint, asphalt roofing, environmental pollution from industrial works Acute encephalopathy (as opposed to horses). Cerebral and GI signs Clinical signs: First stages: stand alone and depressed; hyperaesthesia, muscular fasciculations Progresses to ataxia, blindness (pupillary reflexes present), head pressing, episodic manic behaviour, convulsions, coma Also abdominal pain, rumen atony (bloat), diarrhoea, frothing at the mouth Severe will die 12-24 hrs; sudden death may also occur

Answer 38

Control fits with I.v pentobarbitone (dose to effect) Chelate lead CaEDTA slow drip 110mg/kg I.v every 2nd day for 3 treatments Thiamine 20-100mg/kg subcut daily (mobilises intracellular lead into blood) Oral magnesium sulphate 500-100g to precipitate lead from GI tract Prognosis poor!! Consider whether meat or milk is suitable for human consumption estimated 6-7 months for blood and milk levels to return to normal – Get APHA involved

Answer 39

Senecio jacobea Occurs in many countries Extensive grazing conditions Aetiology: Senecio spp. contain pyrrolizidine alkaloids. Ingested in hay / silage Presentation: Chronic weight loss Diarrhoea Jaundice Peripheral oedema -Ascites Dull / depressed demeanour Differential Diagnosis: Liver Fluke Lead poisoning Management: No effective treatment Remove contaminated feed Control ragwort on pasture

Answer 40

Aetiology: Photodynamic substance enters the skin and reacts with UV light ->Inflammation / photochemical reaction Two common types: Primary (most common) Ingestion of plants such as St. John’s Wort Agent/metabolite reaches skin through circulation and reacts with UV Secondary- Hepatogenous origin Liver function severely impaired leading to ↑ phylloerythrin levels in blood- Normally metabolised in liver and excreted in bile Phylloerythrin builds up in the skin and acts as photodynamic agent Pyrrolizidine alkaloids (e.g. ragwort) can cause hepatic damage and therefore secondary photosensitisation Presentation: Oedema, erythema, vesicles, dermal effusions, skin necrosis Progresses to crusting, ulceration and skin sloughing Most commonly occurs in white/ lighter patches of skin and over the ears and muzzle Painful/sensitive over affected areas Pruritis? Concurrent hepatic signs? Diagnosis: Clinical signs Establishing cause often difficult Serum biochemistry ↑ GGT, AST Liver biopsy Management: Remove animals from sunlight! ?systemic antibiotics (Broad spectrum e.g. penicillin) Debride necrotic skin Control / manage flies Primary: Remove causative agent Prognosis is fair/good unless extensive skin Loss Secondary: Manage hepatobiliary disease Prognosis poor

Answer 41

Yew (Taxus spp.) common ornamental trees, esp. churchyards Aetiology: Accidental exposure + ingestion leads to rapid death Presentation: Sudden death DDX: Common causes of sudden death at pasture inc. anthrax, blackleg and lightning strike Diagnosis: History of exposure Remains of leaves/twigs in rumen on PM Management: No treatment Prevent access to yew (good fencing)

Answer 42

Quercus spp. Deposited on pasture after autumn storms Aetiology: Tannins in acorns are nephrotoxic Presentation: Anorexia Depression Bloat (rumen stasis) Initial constipation + tenesmus ->fetid tarry diarrhoea Occasionally sudden death Death within 4-7d despite treatment DDX: Severe type 1 ostertagiosis Mucosal disease (BVD) Diagnosis: Clinical signs Exposure to Acorns Acorns in rumen on PM Management No specific treatment Supportive therapy inc, large volumes of IV fluids (£££) Remove cattle from pasture with oaks (fence off area under trees?)

Answer 43

Ingestion over several weeks Usually in sparse pasture Aetiology: Bone marrow suppression (Thrombocytopaenia + leucopenia) Carcinogenic (Ingestion over months/years ->bladder tumours / SCC in oesophagus/rumen) Presentation: Anorexia Retinal atrophy (bright blindness) in sheep Pyrexia (2ndry bacterial infection) Petechial haemorrhages (+/-) blood in nasal passages/vagina Occasionally sudden death HR + RR marked increase Weakness -> Recumbency -> Death Bladder tumours -> haematuria in older cattle Chronic weight loss DDX: Check sudden deaths for anthrax Bladder tumours: Cystitis / pyelonephritis Redwater fever (Babesiosis) (Geographic area dependant) Diagnosis: Clinical signs, esp widespread petechiation Exposure to bracken in pasture Management: Treatment with dl-batyl alcohol and broad-spectrum antibiotics generally unsuccessful. Adequate feeding regimes to reduce ingestion

Answer 44

Accidental access to gardens Usually in sparse pasture / temporary starvation (winter snows) Aetiology: Grayanotoxins in leaves, nectar and stems Partial agonists of Na+ channels +ve inotropic effects, causing severe weakness + depression Presentation: Weak / recumbent Abdominal pain (bruxism + vocalising) Rumen atony + bloat ‘Vomiting’/ Ruminal regurgitation May have rumen contents around muzzle Death within hours (goats) DDX: Hypocalcaemia Diagnosis: Clinical signs, esp vomiting Exposure to rhododendron (inc garden cuttings) Management: Treatment with 3mg/kg pethidine q 12hrs + NSAIDs Supportive therapy Adequate feeding regimes to reduce ingestion

Answer 45

Inadvertent dietary supplementation / feedstuff with high Cu content (contamination?) Much more common in sheep than cattle! Aetiology: Ingestion of high Cu content in ration over weeks/months -.>high liver copper. Sudden release of Cu ->acute intravascular haemolytic crisis Presentation: Acute: Severe gastroenteritis Colic signs Diarrhoea Dehydration Severe depression Death within 3 days Chronic (haemolytic crisis): Weakness Depression Isolated from group Poor appetite Fetid diarrhoea ( Mucus ++) Dehyrdration Jaundice (check MM) HR + RR Increased (abdominal effort) No rumen turnover Recumbency -> Death DDX: Other causes of haemolytic anaemia Babesia PP haemoglobinuria Kale Poisoning Diagnosis: History of excess copper Clinical signs (Jaundice in chronic cases) Lab results (↑ serum Cu, ↑++ serum AST and GGT) Post mortem: Acute Severe gastroenteritis Erosion of abomasal mucosa Chronic: Diffuse jaundice (esp. omentum) Swollen dark grey (‘Gun Metal’) kidneys Cu conc ↑++ (>3000 µmol/kg DM (normal <314 µ mol/kg DM) Dark red urine in bladder Hepatomegaly Friable Liver Cu are usually elevated but kidney Cu are more reliabl e Management: Remove source of Cu!! Select animals most at risk by determining AST levels Treat with Ammonium tatrethiomolybdate IV/SC 2/3 times (2 days apart) IV = 1.7mg/kg SC = 3.4mg/kg No licenced preparation Poorly defined regulations Copper supplementation must be managed carefully after diagnosing a deficiency

Answer 46

Over ingestion of brassica plants (Kale, turnips, cabbage etc) or fertiliser Aetiology: Nitrates -> Nitrites by rumen microflora -> Methaemoglobinaemia Presentation: Acute poisoning (within hours) Cyanosis Weak rapid pulse Dyspnoea Rapid recumbency -> Death Abortion is common DDX: Causes of sudden death Hypomagnesaemia Lightning Diagnosis: Clinical signs + Exposure Management: Treat with IV Methylene blue (2%) @ 4mg/kg Carefully introduce brassica crops to herd/flock (never more than 70% of diet, always supplement with good quality forage) (https://forage.msu.edu/wp-content/uploads/2014/07/ID223-BrassicasBeAwareOfTheAnimalHealthRisks-ArnoldLehmkuhler-2014-UKy.pdf) for more information on feeding brassica crops

Answer 47

Overdosage / accidental exposure Aetiology: OPs block cholinesterase  continual action of acetylcholine Presentation: Profuse salivation Colic Diarrhoea Muscle fasciculations -> Stiffness -> Paralysis Depression -> Dyspnoea + Sweating -> Death DDX: Other poisonings Diagnosis: Clinical signs + exposure / treatment Cholinesterase levels in whole blood (certain labs) Management: Atropine sulphate (0.1mg/kg slow IV followed by 0.4 mg/kg SC) repeated as necessary Correct storage and disposal of OPs

Answer 48

Urea is a source of non-protein nitrogen used in feed Nitrogen from urea is released into the rumen as ammonia Can cause severe losses if overdosed Aetiology: Sudden access to urea (or withdrawal then free access) Highly soluble (can wash out of diet/feed blocks after heavy rain) Cattle drinking from puddles / accidental contamination with urea fertiliser to water supply Presentation: RAPID! 15m – hours after ingestion Ear and facial muscle twitching Bruxism Frothy salivation Bloat Severe abdominal pain Frequent urination Forced tachypnoea Staggering Vocalisation Terminal seizures Often found dead at source of urea DDX: Other causes of sudden death Botulism Hypomagnasaemia Anthrax Clostridial disease e.g. blackleg Diagnosis: History of sudden urea access Clinical signs Blood ammonia PM (rapidly after death): Bloat, Congested MM Pulmonary oedema Haemorrhages on heart Management: Pass stomach tube to relieve bloat 50L cold water followed by several litres of 6% vinegar Supportive therapy (isotonic saline?) Thorough mixing of the ration Gradual Introduction to urea feeding Do not interrupt supply- If interrupted restrict access for a short period Consider salt limited feeding of 100% natural protein supplements that do NOT contain urea or ammonium salts

Answer 49

Wales Animal Boarding Establishments Act 1963 Riding Establishments Acts 1964 and 1970 The Animal Welfare (Breeding of Dogs) (Wales) Regulations 2014 The Animal Welfare (Licensing of Activities Involving Animals) (Wales) Regulations 2021 – selling pets Scotland: The Animal Welfare (Licensing of Activities Involving Animals) (Scotland) Regulations 2021 Riding Establishments Acts 1964 and 1970 Northen Ireland: Welfare of Animals Act (Northern Ireland) 1972 (dog boarding) – being looked at The Welfare of Animals (Dog Breeding Establishments and Miscellaneous Amendments) Regulations (Northern Ireland) 2013 Petshops Regulations (Northern Ireland) 2000 Riding Establishment Regulations (Northern Ireland) 1980

Answer 50

Licenses the keeping of dangerous species. Covers a wide range of mammals, birds, reptiles and invertebrates. F1 hybrids are also covered with some felidae exceptions. A 2020 survey showed that approximately 4000 animals were being held under DWA licenses by private collectors in the UK

Answer 51

What species/how many will be kept? Will the animal’s welfare needs be met according to conditions set out in the Animal Welfare Act 2006? Is the enclosure constructed in such a way to prevent escape? What biosecurity measures are in place? What emergency plans are in place? Are appropriate records kept?

Answer 52

Activities covered under these regulations: Selling animals as pets Providing or arranging for the provision of boarding for cats or dogs (including day care) Hiring out horses Breeding dogs Keeping or training animals for exhibition (not including zoos or circuses) Do they need a license?- Business Test – what makes a business? (a) makes any sale by, or otherwise carries on, the activity with a view to making a profit, or (b) earns any commission or fee from the activity. Trading allowance = a tax exemption of up to £1,000 a year for individuals with trading income from: Self-employment (including sale of goods) Casual services e.g. babysitting or gardening Hiring personal equipment e.g. tools If income does not exceed the trading allowance, a license is not required. When does a vet have to do an inspection? Hiring of horses – specific list of suitable people Breeding dogs – new applications only When might a vet be asked to do an inspection? Selling of pets (especially NTCAs) Where a complaint has been made e.g. welfare concern, noise complaint etc. Where the LA think the conditions of the license are not met Preparation is key! Pre-inspection : Ask the LA to forward the application and any relevant documentation Read the guidance notes Research husbandry guidelines if necessary Generally less prep than a DWA license Inspection key points: Go through the checklist to ensure all general and specific conditions are met for the type of license being applied for. Determine if any of the higher standards are being met – this feeds into risk scoring and star ratings Use the statutory guidance – personal opinions can be expressed but must not influence decision making. Risk scores are determined by the local authority, but they may request your input. Based on: History of meeting licensing conditions History of complaints received Understanding of relevant environmental enrichment Understanding of potential risks/hazards and role under relevant legislation Welfare management procedures

Answer 53

take from low in the nec- c5/c6 CANNOT INJECT IN SAME PLACE- take dro higher up- dotn want to jiht artery

Answer 54

only consider glucose fluids if glucose can be monitered * Care with >5% of BW/24 hours * Care with glucose * Youngsters & Adults: use alkaline fluids use right side jugular or cephalic in cria blood colour does not indicate arterial blood Prone to hypoproteinaemia Goal: ▪ Albumin > 20 g/l ▪ TP > 40 g/l plasma can be good option stress important- mouth breathing bad sign, stress fold below eye

Answer 55

Upper left neck Care with angle (30-45)

Answer 56

Clostridial = a MUST Others = as required ▪ Bluetongue ▪ Orf, leptospirosis, salmonellosis ▪ Rota & Coronavirus, E.coli ▪ Abortion agents Care Enzootic abortion vaccine: systemic & local ADR possible

Answer 57

Soft faeces (Diarrhoea) Ill thrift Anaemia- can result in death after birth, heamonchus contortus Malaise & death Cut-off for FEC (Eggs per gram)- when to treat- Trichostrongyle-type = 300-400 Fluke, Nematodirus = 1 Haemonchus, Lungworm = any are noteworthy Dung-piles and poo-picking = aid reducing pasture contamination

Answer 58

Benzimidazoles * 10 mg/kg (= 2x sheep dose) * Albendazole: NEVER in pregnant NEVER > 10mg/kg Levamisol * Only if able to weigh * 6 mg/kg injection, 8 mg/kg by mouth MCLs * Generally 1 – 1.5x cattle / sheep dose * Moxidectin for haemonchus: 0.4 mg/kg oral or injection- no pour ons, absorbtion poor nitroxynil and clorsulon not sutible Monepantel * 3x sheep dose antifluke drugs-- High forecast: dose 6 weeks later * Typical (sheep): Oct & Jan (+/- Nov, May, Jun Triclabendazole Closantel Albendazole

Answer 59

Eimeria lamae * E. alpacae * E. Punoensis * E. macusaniensis = species-specific ↓ Immunity with age & stress severe damage to lining of intestine, marked weight loss, long healing phase treatment- Early-born crias @ weaning ▪ Late-born crias @ 2-3 mo ▪ Adults after stress ▪ Incoming animals Move troughs

Answer 60

treatment- vermectins * Injectable for Sarcoptic mange * Pour-on for Chorioptic mange Typically 3 - 4 treatments 7 – 10 days apart treat whole group- 1/2 animals will carry mites regardless of clinical signs keep away from watercourses – highly toxic to aquatic life! In addition: * Shampoo (keratolytic) * Topical acaricide (Deosect, Frontline) * Skin conditioner * Antibiotics (systemic)

Answer 61

mange nausance flys- black anials blowfly strike orf- not outbreaks though,2-3 animals

Answer 62

orf? autoimune disease? chemical burn? photosensitisation rule out with skin scrapes and bloods treatment- symptomatic- debridment, skin conditioner, antibiotics and antiinflamitories

Answer 63

Rule out CLA! Caseous Lymphadenitis = Corynebacterium pseudotuberculosis in the lymphnodes- fna, dont lance- be careful when sheering

Answer 64

* 5% of deaths 20% contributory / incidental * All age groups * Non-specific clinical signs * Cause?? * Tx: systemic! (ranitidine, pantoprazole)

Answer 65

wide veriety of lesion- liver, spleen, casuus abseesses in lungs, trachea report!- culling intradermal skin test not very sentistive

Answer 66

white musouse membranes rule out = cardio-vascular compromise → Pulse deficit, heart murmur, cold extremities, CRT anemia will not affect these but may get murmer is sever anemia Correct measurement? * Chronic disease * Haemonchosis, fluke * Gastric ulceration- ultrasound, occult blood not useful * Haemolysis- red mape leaf toxicity * Ivermectin toxicity * Mycoplasma haemollamae blod tranfusion very safe- rations rare so use them if possible

Answer 67

> 18 mo Preparation: ▪ Tetanus cover ▪ Withhold concentrates 24 hours Immediate pre-op: ▪ AB & NSAIDs ▪ 2x testicles? withold concentrats for 24 hours anasthesia- * Local infiltration * Max. 6 mg lidocaine/kg BW * Along median raphe +/- intra-testicular * Triple stun (+/- local)- xylozine, ketamine, butorphanol- may negate need for extra local * Caudal epidural * 1ml/45 kg BW closed technique

Answer 68

xylozine, ketamine, butorphanol Recumbent: * Tie out like horse * Nose below larynx * Blindfold Llama * Duct tape useful for longer fleace

Answer 69

Only if poor BCS, quidding etc * Care not to expose pulp cavity- darker bit on tooth dremel or embryotomy wire retained incisiors- decidous whiter and taper towards gumline only remove if struggling with mastication unter anestehrsia

Answer 70

swelling most in mandible

Answer 71

) Triple stun: 0.3 mg/kg xylazine + 0.3 mg/kg ketamine + 0.1 mg/kg butorphanol, iv 2) Abrahamson mix: 1000 mg ketamine + 100 mg xylazine + 10 mg butorphanol  1ml/18 kg alpaca / 1ml/22.5 kg llama plus 1ml, im 3) Cria: 0.1 mg/kg butorphanol + 0.2 mg/kg diazepam Cuffed ET tube size: * Adults 9-12 * Weanling 5.5-7 2-3 litre flowrate on closed cir induction- Xylazine 0.3 mg/kg i/v; 0.4-0.5 mg/kg i/m or Detomidine 0.02-0.04 mg/kg i/v +/- Butorphanol 0.05-0.2 mg/kg i/v plus Ketamine 2-5 mg/kg [Alfaxan 2 mg/kg; premedicate!!] [Propofol 3-6mg/kg] Maintain on gas or double-drip

Answer 72

Fentanyl patch 2 - 5 μg/kg/hr [5 mg patch = 50 g/h] q72 hrs, 12 hrs to peak Butorphanol- <0.2 mg/kg iv, im, only 60 mins effect? Buprenorphine- 0.002-0.01mg/kg iv, im; q6-8hrs? Meloxicam- 0.5 -1 mg/kg q48-72 hrs po, 22 hrs to peak

Answer 73

Common malpresentations- * Foot / lower limb caught on pelvic brim * Carpal flexion * Head deviation, neck flexion * Breech (posterior presentation with hip / hock flexion) * Twins small pelvis- 1-2 cm gain by rotating foetus 30-45 Clean- * Tail-wrap, vet, perineum * Gentle * Good restraint + Epidural +/- Sedation * Lubricant = plenty! * Clenbuterol? 15 Minute Rule- if cant solve issue after 15 min, c section

Answer 74

Local >> GA 45 – lateral recumbency Left flank Incision: * Angled, 15 cm * Thin layers! * Layer ID less obvious * Spleen! Gentle tissue handling * Generous incision * Lavage, not swabbing

Answer 75

Normally passed 1-3 hrs Weight: 800-1000 grams = retained > 6 hours * Gentle pull * Oxytocin (5 IU i/m q2h, 2-4x) * Systemic check (T) avoid antibiotics unless clinical signs

Answer 76

last 2-3 months of pregancy * Uterine torsion- dxx for colic signs * Vaginal prolapse- rare, treat like sheep * Uterine prolapse- rare, tret like coe or ewe * Mastitis- mastitis rare but need to be agressive when it happens * Endometritis- common, too agrsive intervention or overbreeding

end of life and slaughter Flashcards

(100 cards)