performance and production Flashcards

Question

Erysipelas in layers

Answer 1

Erysipelothrix rhusiopathiae = causative agent Sources = pigs, sheep, rodents. Long survival in soil (1yr) Infection by skin lesions, consumption of infected material (cannibalism), red mite CS- acute death, congested extremities. Pm- liver lesions and splenic. Culture for definitive. Avoid- autogenous vaccine best or 2x commercial Treatment- amoxicillin will reduce mortality but often returns. Clear early.

Answer 2

Herpes virus which causes tumours to develop- Tumours in visceral organs Inflammation in peripheral nerves with paralysis Classic form usually starts between 12 and 24 weeks of age Not seen untill birds at least 8-10 weeks old Breeders and commercial layers protected by hatchery vaccination – Rispens vaccine Vaccine not effective for at least 8 days Infection from inhalation of skin and feather dust from other poultry. Vaccinated stock still replicate and shed the virus, but do not develop tumours- Provided sufficient time between vaccination and exposure to virus

Answer 3

Retroviruses- Avian Leucosis Reticuloendotheliosis virus (REV) Lyphoproliferative disease virus of turkeys (LPDV)

Answer 4

Intestinal worms. Ascarids, capillaria, heterakis. DX- FEC, postmortem physical presence. Location- capillaria scrapes from the crop. Acarids, present in gut. Heterakis- thread worm in caeca. Treatment- flubendazole, fenbendazole. (double dose capillaria) Heterakis can transmit blackhead (histomonas protozoan parasite)- no treatment. Red mite- very common, lice cycle as little as 10 days. Irritation causing immune suppression Nocturnal and feed on blood. Lice- common chicken louce, northern fowl mite. . Ecto parasite treatment- exxolt (fluralaner)- best but expensive, ivermectin, pyrethroid based spray on products for environments, diamatacious earth.

Answer 5

Stage 1 – Preliminary exam External examination Visual, palpation and manipulation Incisor teeth Eyes in a dark room Auscultate heart and lungs Stage 2: Walk and trot, in hand Walk and trot in hand Turned each way Backed for a few paces +/- flexion tests and trotting in a circle on a firm surface The purchaser must always sign to say they agree to a limited 2 stage examination. In this case the examination will be limited to these first 2 stages If the purchaser requests a limited (two-stage) examination, the examination will be limited in its scope and may not detect important clinical factors that could otherwise influence their decision to purchase the horse Stage 3: Exercise phase- The horse is given sufficient exercise to: Allow assessment of the horse when it has an increased breathing effort and an increased heart rate. 2. Allow assessment of the horse’s gait at walk, trot, canter and, if appropriate, gallop. Allow assessment of the horse for the purpose of stage five. If ridden exercise is not undertaken then this stage may be conducted by exercising the horse on a lunge. It should be made clear on the certificate what form of exercise was undertaken Stage 4: Period of rest and re-examination- The horse is allowed to stand quietly for a period. During this time the respiratory and cardiovascular systems may be monitored as they return to their resting levels. Stage 5: Second trot up- The animal is trotted in hand again to look for any signs of strains or injuries made evident by the exercise and rest stages Flexion tests? Trotting in a circle? Not mandatory! Can sometimes provide useful additional information about a horse. There may be circumstances when the examining veterinary surgeon concludes that it is unsafe or inappropriate to perform such tests. A mouth examination with a speculum is not included in the standard procedure and as such the examination of the mouth is limited. A blood sample may be taken for storage (usually for 6 months) for possible future analysis to detect substances present in the horse’s system at the time of the examination that might have masked any factors affecting the horse’s suitability for the purchaser’s intended use. If a blood sample is not taken, then the reason should be noted on the certificate. VDS system – blood sampling kit – no charge Report findings of the examination Provide the examining veterinary surgeons opinion on the horse’s suitability for purchase for its intended use “In my opinion, on the balance of probabilities, the conditions reported above do / do not prejudice this horse’s suitability for purchase to be used for …” This wording reflects the fact that there may be other reasonable interpretations of the findings, but it in no way reduces the responsibility of examining veterinary surgeons to examine and observe the horse carefully and to apply to the full their professional knowledge and experience. Negligence – failing to do what a similarly qualified person would be reasonably expected to do, or doing what a similarly qualified person would be reasonably expected not to do. Of the equine claims of negligence to the VDS – greatest percentage were associated with PPEs. At a PPE if a lesion is detected, it should be reported to the purchaser and recorded on the certificate considerations- Facilities – you need a suitable venue Environment – weather etc Re-examine – start again another day…from the beginning Purchaser present? Less claims if they are! Blood sample…not mandatory – permission from purchaser and seller (VDS scheme) Use the worksheet that’s available! You are in charge

Answer 6

Check the microchip Check passport Diagram can be omitted if the microchip is present and matches the horses passport – in this case the microchip and passport number must be recorded on the certificate. Do this at the beginning to save awkwardness!

Answer 7

The PPE report can affect how an insurance company views the horse in terms of risk. They may consider certain findings in the report to represent an increased risk for insurance, which could result in them placing exclusions on the policy. It is the purchaser's responsibility to ensure they can get the insurance they want prior to purchase

Answer 8

to give propper shape to handle weight during high stress periods- calvieng ect remove horn from toe and not sole to correct foot shape Dry off +/- 80-100 DIM Pregnant heifers Think ‘check’ rather than ‘trim’ Lame cows ASAP Things to avoid: Overtrimming Shaping the wall Removing the axial white line Chasing black marks Removing too much heel

Answer 9

Step 1- Start with weightbearing claw – inner claw of hind foot, outer claw of front foot Cut 1 – Toe length 8cm from hard horn to step (average Holstein cow) Cut 2 – Remove excess sole Do not over trim – measure from hard horn to step. Heifers Leave at least 5mm of sole Foot trimming - Step - Remove more from outer claw, ensure balance and do not remove axial white line step 3- Dishing' out the claws Model (dish) out the inner parts of both claws, behind the wall on the inner claw edge, to allow a flow of muck between the toes and to reduce weight-bearing on the typical sole ulcer site step 4- take weight odd of lesions remove horn from effecte claw to shift weight Check for any lesions Corrective trimming Provide appropriate treatment Check claws for problems (usually in the outer claw, back two thirds on hind feet) If the outer claw is damaged, make this claw lower towards the heel. So the weight is transferred partly to the sound claw Dutch five step technique – Step 5 remove loose horn from heel check for digital dermatitis beware fo removing too much for weight baring surface

Answer 10

trim block for 3 days nsiads- ketoprofen

Answer 11

Cattle: 3 weeks before to 3 weeks after calving Hypocalcaemia Ketosis/Fatty liver LDA RFM Metritis Sheep: 10 days before to 7 days after lambing Pregnancy toxaemia Hypocalcaemia Genital tract problems (tears, prolapse) Dystocia Acute clinical mastitis Respiratory disease

Answer 12

peripartuent problem in cows Average annual UK incidence - 5% Average cost of one case = £206 Simple case- £42 Downer cow - £137 Fatal case- £2,043 Only 3% of affected animals will die Can contribute to increased incidence of; “Downer cow” syndrome In uncalved cows Uterine inertia No voluntary straining – dystocia not detected Uterine prolapse RFM Risk of environmental mastitis Dietary absorption of calcium is ~70% Bone deposition and/or absorption (25g/day) Requirements of foetal skeleton (15g/day) Milk ~ 1.1g/l (20-50g/day) pregnacy puts strain on calcium homeostasos Clinical Signs: Loss of appetite, dullness and lethargy Afebrile / subnormal temperature Initial hypersensitivity / hyperaesthesia Stiff, straight hocks Reluctant to move Inco-ordination and ataxia Progresses to: Recumbency, head turned to side Increased heart rate (80-90 bpm) Dilated pupils, reduced PLR Gut stasis resulting in bloat and constipation Depression, unresponsive to stimuli can progress to - COMATOSE (lateral recumbency, HR>120bpm) -> DEATH Diagnosis: History Clinical signs Response to treatment Biochemistry- Calcium below 1.5mmol/l Phosphate below 1.0mmol/l Magnesium normal or slightly above 1.25mmol/l Treatment: Individual Full clinical examination Blood sample prior to treatment Intravenous calcium borogluconate (12g) Magnesium and/or phosphorous if required Removal of calf and/or restriction of milking TLC If no recovery in 5-6 hours, RE-ASSESS Treatment: Herd Changing the forage component of the diet Magnesium supplementation Prophylactic administration of calcium at calving Milk withdrawal- no pre-calving milking removal of calf at birth no milking for 3 - 4 days after calving (?Welfare) Dry cow nutrition (the basics)- correct body condition – not too fat supplement with forage ensure good dry matter intake in dry period DCAB/DACB diets

Answer 13

peripartuent pproblem in dairy cows Fatty infiltration of the liver Excessive fat mobilisation in early lactation as response to energy demands Excessive amounts deposited in hepatocytes as triglycerides- Affect liver function and causes cell injury Suggested that 1 in 3 dairy cows are affected ?Relatively normal in high yielding cows? No clinical signs, but may result in: Increased incidence of metabolic disease Poor fertility Depressed milk production one of the less severe energy disorders in cattle Can progress to Fat Cow Syndrome Above 34% fat → severely affected Excessively fat cows in the dry period B.C.S. > 4 Clinical signs: Rapid loss of body condition in early lactation Depressed appetite Cow clinically ill Metabolic disease Depressed milk production Poor response to treatment High mortality

Answer 14

Fatty liver syndrome-> Subclinical ketosis-> Clinical ketosis-> Chronic ketosis-> Fat cow syndrome

Answer 15

Impaired metabolism of carbohydrates and VFAs Incidence of: Clinical ketosis is approximately 1% Subclinical ketosis is approximately 30% Occurs in early lactation Large energy supply required by mammary gland in early lactation for milk production Inadequate energy supply to meet this demand Negative energy balance due to demands of udder Shortage of oxaloacetate for use in TCA cycle Mobilisation of fat reserves Metabolic pathways lead to the production of ketone bodies- Acetoacetate β-hydroxybutyrate (BHBA) Acetone Anything that causes inadequate energy supply -> ketosis Reduced appetite Starvation High production Clinical Signs: Usually occur within the first month after calving Subclinical - Loss of body condition Depressed milk yield Reduced fertility and milk protein long-term# One case of primary clinical ketosis represents the “tip of the iceberg” The other early lactation cows are likely to have subclinical ketosis Wasting form- Decreased milk yield Weight loss Dark firm “waxy” faeces Loss of appetite (refusal of concentrates) Sweet ketone smell on breath (“pear drops”) Remember to check for underlying cause (especially LDA) Nervous form- Excessive salivation Abnormal chewing Licking of any available object Inco-ordination, circling Head pressing, apparent blindness Signs intermittent Diagnosis: History and clinical signs Smell of ketone bodies on cow’s breath Rothera’s test- regent turns purple on pos result Clinical biochemistry- Lowered blood glucose levels Mobilisation of body fat (elevated NEFA) Ketone body formation (elevated BHBA) Remember to check for underlying cause (especially LDA)

Answer 16

Aims: Restore blood glucose levels Replenish oxaloacetate levels Increase dietary gluconeogenic precursors (propionate) Correct predisposing factors (eg. LDA) Restoration of blood glucose levels 400 ml of 40% glucose solution intravenously Oral administration of glucose precursors Propylene glycol (Ketol™) 115 – 225ml BID Propylene glycol + cobalt (Forketos™) Sodium propionate (digestive upset) Glycerol (but ketogenic) Glucocorticoids?

Answer 17

Typically occurs in the month following calving May reflect poor nutritional management prior to calving (?related to ketosis) Some association with high-concentrate/low-fibre rations Reported associated with previous hypocalcaemia, twins or (endo) metritis Occurs due to atony of the abomasum- Secondary to high VFA concentratons> Due to continued fermentation of high CHO rations> Accumulation of gas> Displacement> Clinical Signs: Variable Poor milk yield Reduced appetite Weight loss Gaunt appearance Sprung last lib Distended CrD abdomen Auscultation and percussion -> ping Can be complicated due to presence on concurrent disease Most severe in conjunction with metritis and toxaemia Pyrexia (>39.5) Anorexia Depression Reduced milk yield Can see profuse, foetid diarrhoea Diagnosis: Based on thorough clinical exam Don’t forget about ballotment – ping and tinkle Lots of ping differentials

Answer 18

Cast and Roll Toggle Surgical (omentopexy/abomasopexy) Surgical (laparoscopic) Follow all by oral fluid drenching

Answer 19

Energy deficiency due to increased demands at end of pregnancy Rapid growth of foetus(s) increases demand for glucose Predisposing factors- Last month of gestation 2+ lambs Prolonged period of energy shortage Ewes in poor condition Older ewes Stress Clinical signs: Isolation from flock Disinclined to move and easily caught Become dull and depressed Neurological signs- Apparent blindness Hyperaesthesia Head pressing Star gazing Teeth grinding Progresses to profound depression and recumbency Can lead to abortion Diagnosis: Based on clinical signs and history BHB > 3mmol/l

Answer 20

Treatment: Oral electrolyte and glucose solution or propylene glycol IV glucose Supportive care Induction of parturition/caesarean Euthanasia Control: Nutrition of ewe in late pregnancy

Answer 21

Usually seen in late pregnancy Sporadically occurs in lactation Affects older sheep Associated with stress Housing Weather changes Delay / change in feed Clinical Signs: Muscular paralysis Increased respiratory rate and reflux of rumen contents Diagnosis: History Clinical signs Response to treatment Serum calcium below 1.0mmol/l Concurrent pregnancy toxaemia

Answer 22

Treatment: 20 – 40mls of intravenous 40% calcium borogluconate 50 – 100mls of subcutaneous 40% calcium borogluconate Control and prevention Feed 5 – 10g calcium per day in late pregnancy Avoidance of stress

Answer 23

Common presentation in farm animal practice Cow has been recumbent for over 24 hours No specific cause for recumbency Cow is in sternal recumbency Usually related to calving Initial cause of recumbency; Traumatic: Related to calving injury, housing, bulling etc. Sacroilliac luxation / subluxation Dislocation of the hip Pelvic fracture Injury / fracture of limb Tendon / ligament rupture Neurological: Related to calving - Obturator nerve Sciatic nerve Related to trauma- Peroneal nerve Tibial nerve Metabolic: Hypocalcaemia Hypomagnesaemia Untreated ketosis Fat cow syndrome Toxaemia: Metritis Salmonella Peritonitis Acute coliform mastitis Secondary complications following recumbency very common (84% of cows) - nerve damage compartment syndrome skeletal damage Once cows were recumbent for more than 24 hours, the secondary damage was considered more important to prognosis than the primary cause. By day 7: 57% of cows with no evidence of secondary damage got back up Only 17% of those cows with some form of secondary damage got back up History How long has the cow been recumbent? When did she calve? Were there problems? Did she rise after calving? Has she received any treatment? Has the cow risen and/or moved? Where did the cow become recumbent? Provision of good TLC? Clinical Examination- General demeanour Position of cow and limbs Attempts to rise Creeper / Crawler cows Further clinical examination- Rectal examination Manipulation of hind-limbs Diagnostic tests- Muscle damage CK- Elevated for 1-2 days AST- Elevated for 1-2 weeks Diagnosis of primary cause- Calcium, magnesium, phosphorous Liver enzymes, β-hydroxybutyrate Myoglobin levels in serum / urine- Prognosis- Depends on: Clinical examination Attempts to rise Degree of ischaemic necrosis and damage Demeanour Quality of nursing on farm 50% of downer cows will rise in 4 – 7 days Prognosis poor after 10 days

Answer 24

Treatment- Correction of underlying disease Calcium borogluconate Phosphorous (“creeper cows”) Anti-inflammatory drugs (NSAIDs/Corticosteroids) Assistance in rising Hobbles or soft rope on hind legs, Bagshaw hoist, Inflatable bags, Cow nets / slings / harnesses Tender loving care- Critical for good prognosis (labour) Dry, clean, comfortable bed ?at grass (shelter) Turning of cow every ? hours Good quality food (accessible) Water (accessible) ‘Waters break’ Chorioallantois ruptures, releasing several litres of allantoic fluid END OF STAGE I

Answer 25

‘PREPARATORY PHASE’ 30 minutes - 4 hours Foal’s front end rotates – dorsopubic ---> dorsosacral Cervical relaxation Uterine contractions of increasing intensity Foal forefeet and muzzle pushed into cervix Mare is restless Flank watching Frequent urination Sweating Stretching Recumbency +/- rolling Tail swishing Similar to mild colic 1-12 HOURS

Answer 26

‘DELIVERY PHASE’ 20 – 30 minutes Quick and explosive Cervical dilation continues Presence of foal at pelvic inlet triggers powerful abdominal contractions Oxytocin released from pituitary gland ---> reinforced uterine contractions Mare usually in lateral recumbency, some mares foal standing up Amnion appears at vulva within 5 minutes of waters breaking Amnion ruptures Front feet and nose Mare will often rest for 10 – 15 minutes once foal’s hips are through the hips Umbilical cord remains attached until either mare stands or foal attempts to rise 30 MINS For every 10 minute increase in Stage II labour beyond 30 minutes, there is a 10% increase risk of the foal being born dead EARLY EFFECTIVE INTERVENTION CRITICAL TO FOAL HEALTH AND SURVIVAL

Answer 27

EXPULSION OF PLACENTA 10 minutes – 3 hours Expulsion of foetal membranes and uterine involution <3HOURS

Answer 28

= ABNORMAL FOALING May be maternal or fetal in origin More common in maiden mares EMERGENCY Potential loss of foal, mare or future fertility ABNORMAL ORIENTATION of the fetus in the birth canal by far the most common cause FETAL ABNORMALITY - Most commonly limb contracture Other anomalies eg hydrocephalus FETAL OVERSIZE- Rare. Not related to gestational age MARE PROBLEM- Uterine inertia, exhaustion Pre-existing orthopaedic condition (eg pelvic fracture resulting in distortion of birth canal) PRESENTATION - Describes orientation of fetal spine to that of the mare POSITION - Relationship of the fetal spine to the quadrants of the mare’s pelvis POSTURE- Describes the relationship of the extremities to the foal’s body Normal delivery is ANTERIOR presentation, DORSAL-SACRAL position, both forelimbs and head extended 98.9% OF FOALS DELIVERED IN CRANIAL PRESENTATION 1.0% IN CAUDAL 0.1% IN TRANSVERSE WHEN DO WE NEED TO INTERVENE?- Failure of progression of Stage II for >20 minutes Malpresentation Something at vulva that shouldn’t be there Severe colic

Answer 29

Examine mare in the box Avoid stocks – mares will often attempt to lie down Sedation if necessary - consider effects on foal Xylazine shorter duration of CVS depression vs detomidine Epidural normally too time consuming TOCOLYTICS (Clenbuterol, Isoxuprine) May be given by injection to relax the uterus Manual vaginal exam – plenty of obstetric lubricant Confirm waters have broken Assess dilation of cervix Identify orientation of fetus FRONT LEGS – fetlock and carpus flex in same direction HIND LEGS – fetlock and hock flex in opposite directions Any abnormality must be corrected prior to any attempt at delivery

Answer 30

Vaginal delivery with the mare awake Simple postural abnormalities can be corrected in this way For normal orientation or posterior presentation with both hindlimbs extended Pull in tandem with mare’s contractions Ropes/chains may be used No mechanical devices

Answer 31

Vaginal delivery under GA If significant progress is not made after 15 -20 minutes with mare awake GA eliminates uterine contractions and straining Elevation of hindquarters allows repulsion of fetus into abdominal cavity and repositioning Vaginal delivery under GA If significant progress is not made after 15 -20 minutes with mare awake GA eliminates uterine contractions and straining Elevation of hindquarters allows repulsion of fetus into abdominal cavity and repositioning

Answer 32

If no significant progress after 15 -20 minutes of controlled vaginal delivery Via ventral midline laparotomy under GA TERMINAL CAESAREAN if mare has fatal injury or disease FETOTOMY if foal is confirmed dead

Answer 33

PREMATURE PLACENTAL SEPARATION Caudal pole of placenta presents at vulva in Stage I without rupturing Foal is likely to be deprived of oxygen immediate intervention necessary CERVICAL STAR VISIBLE

Answer 34

HAEMORRHAGE RETAINED FOETAL MEMBRANES METRITIS UTERINE TEAR/RUPTURE PROLAPSE – UTERUS/GIT INVERSION OF UTERINE HORN TIP

Answer 35

Most frequent cause is rupture of the MIDDLE UTERINE ARTERY during foaling Rupture of utero-ovarian, vaginal or external iliac artery less common Degenerative changes in arterial wall with age and successive pregnancies Risk greater in older, multiparous mare Majority of bleeds are contained within the BROAD LIGAMENT resulting in a haematoma of variable size No blood visible externally Usually colic, sometimes violent due to stretching of the ligament often accompanied by flehmen response If haemorrhage escapes the confines of the broad ligament, uncontrolled bleeding into the abdomen Cardiovascular shock (predominates over signs of colic) Tachycardia, weak pulse Sweating Muscle fasciculations Pale mucous membranes Recumbency May be fatal diagnosis- Clinical signs usually enough Broad ligament haematoma palpable on rectal palpation BUT palpation can be very painful Care not to disrupt clot Blood sample in acute stage RBC parameters may be normal due to compensation Hypoproteinamia, high lactate treatment- Tranexamic Acid (antifibrinolytic) aids clot stabilization Shock therapy – Fluids (hypertonic followed by isotonic) NSAIDs Intranasal oxygen Whole blood transfusion Conservative treatment – permissive hypotension Haemorrhage may be subclinical and only picked up at subsequent reproductive exam

Answer 36

Inflammation of uterine wall allows passage of toxins/bacteria into circulation -> ENDOTOXAEMIA Usually follows traumatic delivery +/- retained fetal membranes Fever, anorexia, laminitis Laminitis potentially life threatening Foot support, icing Systemic broad spectrum antibiotics NSAIDs Intravenous fluids Large volume lavage to remove uterine contaminants

Answer 37

Clinical signs are dependent on the size of the tear and degree of contamination of the abdominal cavity The interval from occurrence of the tear to diagnosis and initiation of therapy has a marked impact on survival So early diagnosis essential Evisceration of gut through a tear in the uterus is a rare but usually fatal complication of the immediate post foaling period Diagnosis can be challenging as tears may be small and/or in inaccessible area The degree of contamination does not always correlate to the size of the tear Diagnosis often only made when mare develops peritonitis within 5 days of foaling (Colic, fever, depression) Abdominocentesis – peritonitis (usually serosanguinous, elevated WCC & TP) Examine the placenta carefully May reveal site of a uterine tear treatment of uterine tears Medical- Broad spectrum Antibiotics NSAIDs Oxytocin Surgical- Transvaginal, flank/ventral laparotomy, laparoscopy

Answer 38

Uncommon Most often following dystocia, but can occur after uneventful foaling Can be complicated by involvement of bladder or intestines, or concurrent haemorrhage Support prolapse at level of vulva to minimize tension and oedema Can be replaced with mare standing or in recumbency Standing sedation usually sufficient, but consider an epidural or even GA if mare strains too much or reacts violently Remove retained fetal membranes if still attached Gently clean and inspect endometrial surface of uterus for tears Uterus gently massaged back through vulva, avoiding using fingertips Ensure uterus is fully replaced - distension with fluid or the bottom end of a bottle may help Broad spectrum antibiotics NSAIDs Oxytocin to promote uterine involution +/- purse string suture Daily lavage to mitigate against metritis c. 80% survival

Answer 39

more common in mares post foaling than cows- speed of seond stage vaginal tears will heal by secondary intention 3rd egree tear- tear between rectum and vagina- examine extensivly, examine agin after inflamation has gone down trerepair several months on haemorage into vaginal wall-

Answer 40

Usually results from mare foaling without adequate cervical relaxation Prognosis depends on size and location of tear(s)- BIG THREAT TO FERTILITY Surgical repair is possible but injury may lead to a loss of cervical competency and cause permanent infertility DIAGNOSIS during diestrus- gentel digital palpation

Answer 41

Uncommon Usually follows excessive traction on retained fetal membranes May result in mild colic symptoms Tip of horn can suffer ischaemic necrosis if not corrected Manual reduction per vaginam +/- infusion of large volume of fluid

Answer 42

CONSTIPATION- common BRUISING OF VISCERA- Small colon, rectum or caecum May lead to ischaemic necrosis/peritonitis/colic RUPTURE OF VISCERA- Endotoxic shock. Invariably fatal

Answer 43

Each product has specific withdrawal instructions from the time of final administration. The legal minimum withdrawal period for drugs used 'off license' is as follows Statutory withdrawal periods: Meat from mammals and poultry (including offal): 28 days Milk: 7 days Eggs: 7 days Meat from fish: 500 degree days if normal withdrawl peiods longer, use those Bulk tank, test the individual cow's milk with a Delvotest to avoid bulk tank residue failure. Delvotest kits and consumables It should be remembered that 'off license' use of drugs includes situations where the specific licence use is breached, for example, combination therapy or alteration of the recommended dosage interval. In these situations, at least the statutory minimum withdrawal period will be applied by the prescribing vet. Organic-own rules (variable) using two preperations not licensed tohghter thoghtether even when on license indivisually yu must use statiuitory withdrawls

Answer 44

Veterinary Medicines and the Safety of Food From Animals | NOAH (National Office of Animal Health) Specific rules for food producing species: ‘Veterinary Medicines Regulations 2005’ lots guidance notes on VMD, annually refreshed. Licensed products: “in all species, if there is a product that is licensed for the particular condition being treated and the particular species, then this product should be used” Useful sources-VMD and NOAH licesnsed off license baned drugs cascade- If a licensed product does not exist or is not available in the UK the cascade provides options for use in order to prevent suffering. If no product exists, then a product licensed for use in that species for a different condition may be used or, a product licensed for that condition in another food producing animal may be used. If no products exist then a product available in another member state may be imported BUT only provided that the product is licensed for use in a food producing specified in that state.

Answer 45

If a licensed product does not exist or is not available in the UK the cascade provides options for use in order to prevent suffering. If no product exists, then a product licensed for use in that species for a different condition may be used or, a product licensed for that condition in another food producing animal may be used. If no products exist then a product available in another member state may be imported BUT only provided that the product is licensed for use in a food producing specified in that state. Specify a withdrawal period: 7days milk and eggs 28days meat 500 degree days for fish Keep records for 5 years, including: Name and address of owner ID of animal Date Diagnosis Drug details Treatment duration Applied withdrawals EU reg 37/2010: Lists drugs licenced and forbidden from use!!. eg metronidazole, chloramphenicol, metaclopromide, atipamazole

Answer 46

Differences in the cascade aim to protect the consumer. Whan an individual eats a product they have to be assure that levels of drugs in these products are within safe limits MRLS Maximum Residue Limits are created for certain drugs based on the calculated ADI (acceptable daily intake). Withdrawal periods take into account MRL and pharmacodynamics in the animal, allowing to calculate how long until the drugs fell below the MRL and so identifying a suitable withdrawal period . 4 annexes are related to this: Annexe 1: sufficient data for an MRL Annexe 2: sufficient data determining they are safe and no MRL is needed. Annexe 3: provisional MRL has been established, but more information is required Annexe 4: drug prohibited from use in food producing animals, either because they produce too much of a risk or they have not been sufficiently assessed to allow for a provisional MRL.

Answer 47

Legal requirement for the owner and the vet to keep records for 5 years Owner: At the time of purchase: Proof Name and address of supplier Name and batch number of drug Date of purchase Quantity Withdrawal period At time of administration: Name of product Amount of product Date of administration Withdrawal period Identification of animal treated If a vet administered the drug-vet can write in your records, or give you the information but it must have the name and address of the vet At time of disposal- Name of product Amount disposed of Method of disposal Legal requirement for the owner and the vet to keep records for 5 years Vet: Permitted to supply POM-Vs Keep records of in and out going transactions: Date and nature of transaction Identification of product Quantity Name and address of either the supplier or the recipient Copy of prescriptions, name and address of person who wrote the prescription Batch number ad date once product is in use. For drugs prescribed under the cascade: Date of examination of the animal Name and address of owner Identification of animals treated, diagnosis, trade name of the product Batch number Name and quantity of active ingredient Dose administered Duration of treatment Withdrawal periods

Answer 48

POM-V or POM-VPS (anthelmintics) Specific type of prescription - the name and address of the person prescribing the product; the qualifications enabling the person to prescribe the product; the name and address of the owner or keeper of the animal; the species of animal, identification and number of the animals; the premises at which the animals are kept if this is different from the address of the owner or keeper; the date of the prescription; the signature or other authentication of the person prescribing the product; the name and amount of the product prescribed; the dosage and administration instructions; any necessary warnings the withdrawal period if relevant; the manufacturer or the distributor of the feeding stuffs (who must be approved for the purpose); a statement that, if the validity exceeds one month, not more than 31 day’s supply may be provided at any time. It is the veterinarian’s responsibility to specify how much should be provided for each 31 day supply; the name, type and quantity of feeding stuffs to be used; the inclusion rate of the VMP and the resulting inclusion rate of the active substance; any special instructions for the stock farmer; and the percentage of the prescribed feeding stuffs to be added to the daily ration; If it is prescribed under the cascade, a statement to that effect.

Answer 49

Absorption of drugs: Ruminal microflora catalyse hydrolytic and reductive reactions. Readily inactivates orally administered drugs before they reach the circulation Conversely orally administered drugs may adversely affect gastrointestinal microflora and interfere with normal gastrointestinal processes (systemic drugs are not exempt from this) Oral boluses (modified drug release delivery systems) take advantage of the unique conditions in the rumen, sine the bolus stays in the rumen it allows time for the sustained or pulsatile release of drugs.

Answer 50

Significant changes in metabolic capability in preruminant vs ruminant animals, due to changes in the diet resulting in a change in nature and complexity of nutrient to which the liver is exposed. Differences in hepatic metabolism of certain anthelmintic drugs (benzimidazoles, clorsulon) probably explains the higher dose requirement seen in cattle and goats compared to sheep. For drugs that undergo hepatic metabolism, half lives are shorter in cattle and horses compared to SA. goats metabolise very quickly

Answer 51

Urinary pH. Herbivorous animals generally have an alkaline urine (pH 7-9), this may affect the elimination of certain drugs through the urinary tract Acidic drugs-are ionised in an alkaline pH and elimination should be enhanced since the drug remains in the urine. Alkaline drugs will be unionised and are more readily reabsorbed from the urine, reducing the rate of elimination. NB milk fed animals generally have acidic urine.

Answer 52

Receptor level differences- Eg xylazine. (alpha2 adrenoceptor agonist), a much smaller mg/kg dose is required compared to other species, due to an increased sensitivity of the receptor site.

Answer 53

Lesions in young calves often will not resolve and can enlarge as the animal grows S/C provides the least marking of the carcass I/M injections should ideally be given in the neck, away from expensive cuts of meat- especcialy dont use rears in pigs Maximum volume per injection site =10mls- reduces the pressure in the muscle allowing apropriate absorbton and preventing pressure necrosis Variety of needle bore sizes and lengths Keep injection sites 4 inches apart if possible

Answer 54

Amoxicillin Potentiated amoxicillin Tetracyclines Amphenicols: Florfenicols- use as little as possible 1st 2nd gen cephalosporinsuse as little as possible Penicillins TMPS Aminoglycosides (strep) Macrolides: Draxxin 3/4th gen cephalosporin Fluoroquinolones (enrofloxacin) lincosamides

Answer 55

Meloxicam Flunixin Kelaprofen Carprofen Tolfenamic acid- not common ion uk Corticosteroids

Answer 56

Prostaglandin (estrumate) GNrH (receptal) Progesterone releasing intravaginal device (PRID/CIDR)

Answer 57

Ketamine Butorphanol Isofluorane- hard to use outside of practice Thiopental sodium- not commonly in use lignocaine/lidocaine, mepivicaine, procaine

Answer 58

Xylazine detomidine, romifidine,

Answer 59

Pentobarbitone captive bolt gun

Answer 60

Phosphorus Vit B12 Vit B1 Propylene glycol Electrolytes

Answer 61

Wormer Coccidiostat/cidal in feed SCOPS technical manual- has table detailing these

Answer 62

Sprays: Copper and zinc based (CuSO4) Salicilic acid Tetracycline spray Aluminium based spray Foot baths: CuSO4 Formalin based.

Answer 63

Kexxtone bolus Coccidiosis treatment use ionophores abroad

Answer 64

Sheep CIDRs P4 devices PMSG (poor availability) need to use cascade often with sheep

Answer 65

Considerations: Food Producing Animal (regardless if O considers a pet) Licensed products Is the cascade available? Sedatives: Azaperone- (Pentobarbital) Anaesthetic(s): Ketamine Procaine Bupivicaine Lidocaine

Answer 66

Class: Butyrophenone Method of Action: Dopamine Antagonist (Binds to inhibit original reaction) Legal Category: POM-V only licensed sedative in pifd Licensing A neuroleptic sedative for pigs to be used for the treatment of: 1) Aggression 2) Stress (transport) in Boars Sows Weaners 3)Obstetrics 4) Premed Side Effects Peripheral Vasodilation Penile Prolapse ‘Boars exceeding 1mg/kg’ (Salivation & Panting) Penile prolapse can be replaced by hand once fully sedated, care with other pigs showing interest and physical damage Contra indications of peripheral vasodilation Dosing - Low Stress Environment Intramuscular Injection Wait… Peak Effect is 15-30minutes after injection Duration can be as long as 3 hours i.e. they’re still going to be asleep when you leave… consent?

Answer 67

Class: Dissociative Anaesthetic Method of Action: Non Competitive NMDA antagonist Legal Category: POM-V Legal Category Description: Controlled Drug (Schedule 2) Licensing- To be used to induce anaesthesia…in combination with azaperone in the pig (xylazine would make its use offlicense Why?- Ketamine causes neuromuscular excitement. We need to use a sedative first to reduce this effect Dosage and Administration - Intramuscular (15-20mg/kg) + Azaperone at 2mg/kg Off License: Intravascular (5mg/kg), Ear Vein **Pig must already be sedated (2mg/kg Azaperone)** Much quicker Onset Physiological effects- Sympathomimetic Increased muscle Tone (inhibition of extra pyramidal system) Salivation (brain stem stimulation) (tachycardia) (Hypertension) Increased sensibility especially against acoustic stimuli Nystagmus Pupil Dilation (mydriasis) Respiratory Depression Important in recovery

Answer 68

Licensed products - Cloprostenol d-cloprostenol Luprostiol Dinoprost Legal Category - POM-V CARE! Wear Gloves - Can be absorbed through skin Bronchospasm Miscarriage Prerequisites- Must have a very accurate farrowing date Do not give any earlier than 48hrs suspected farrowing date Do not repeat injection Will cause an abortion if used incorrectly or: ->Weak piglets ->Poor piglet birthweights ->poor lung development

Answer 69

Prerequisites- Must have a very accurate farrowing date Do not give any earlier than 48hrs suspected farrowing date Do not repeat injection Will cause an abortion if used incorrectly or: ->Weak piglets ->Poor piglet birthweights ->poor lung development CARE! Adverse affects in females

Answer 70

Action – Smooth muscle contraction Long Acting- Elimination time approx. 85-100 mins Licensed Use- Uterine atony during the puerperal period Supportive therapy of mastitis-metritis-agalactia (MMA-) syndrome Initiation of milk ejection Shortening of total parturition duration in sows: that have received PGF2a Dose - 1.5-3ml IM One injection in a 24hr period

Answer 71

GILTS! Why? Most farms work on a ‘three week batch’ system Each week in a three week cycle they: Wean Serve Farrow They need to maintain a replacement rate of between 40-50% Which means they need to serve a set number of gilts every three weeks Which menas they all need to be in oestrous at the same time as the sows come onto heat … Effects of Progesterone Maintain Corpus Luteum Dose 18 days consecutively Timing is very important Same time every day Dose Delivery Direct Oral Drench Mixed directly into feed - dosage not as good as every pig does not eat the same amount When will Oestrous begin? 5-7 days after cessation of treatment

Answer 72

Why? Fixed Time AI – Gilts Licensed Products -Busrelin acetate Dose- Fixed protocols Method of Action - Prevention of Oestrogen Secretion from ovaries

Answer 73

Why? Anoestrous sows post weaning (Desperation for anoestrous gilts) Small holder setting – Boar is being brought in Licensed Products - GnRH analogues Dose- Fixed protocols Method of Action - Surge of GnRH …

Answer 74

Anti GnRH Males - Immunological suppression of Testicular Function Alternative to surgical castration Removal of boar taint Females - Cessation of Ovarian Activity Prevents unwanted pregnancies

Answer 75

Meloxicam- Oral Injectable Ketoprofen- Injectable Flunixin - Injectable

Answer 76

viral- PRRSv SIA PCV2 Aujezkys Adenovirus Reo Virus parasites- Metastrongylosis Ascaris suum bacterial (mostly secondary)- Mycoplasma hyopneumonia Actinobacillus pleuropneumonia Actinobacillus suis Pasteurella multocida Glasserella parasuis Mycoplasma hyorhinis Bordatella Bronchisepta Atrophic Rhinits Chlamydia Salmonella Cholerasuis

Answer 77

PRDC? Porcine Respiratory Disease Complex primary- Mycoplasma hyopneumoniae secondary - PRRS SIA PCV2 APP Pasteurellosis Glasserella Environment Animal Immunity Complicated condition that incorporates multiple aetiologies both viral and bacterial. Secondary and primary pathogens play a role and this leads to a variety of pathology. PRDC is characterised by respiratory signs such as, coughing and dyspnoea. Growth rates are likely to slow and mortality increases

Answer 78

Pneumonia – Inflammation of the lung itself Suppurative Bronchopneumonia Fibrino Necrotizing Pleuropneumonia Interstitial Pneumonia Broncho-Interstitial Pneumonia

Answer 79

Acute inflammation (clotting cascade)

Answer 80

Chronic inflammation (organized)

Answer 81

commonly seen at slughter Cranioventral consolidation present, likely inhalational and therefore bacteria e.g. Mycoplasma hyopneumoniae

Answer 82

Fibrino-necrotizing pleuropneumonia

Answer 83

Patchwork type pattern often seen in viral disease in pigs e.g. Porcine Respiratory and Reproductive Disease

Answer 84

Both inhaled and further down, in more severe cases could be more diffuse e.g. Swine Influenza

Answer 85

Pathogenesis: Respiratory Pathogen inhaled from aerosol spread, Colonises lower respiratory tract Cilliostsasis, goblet cell downregulation and apoptosis of macrophages Epidemiology: Able to travel up to 9km as an aerosol ‘airborne pathogen’ (Otake et al, 2010) Slow Spreading and Shedding Clinical Signs: Coughing Laboured Breathing Poor Growth Rate (severe cases) - -Daily Live Weight Gain -Food Conversion Ratio Mortality? – from secondary bacterial disease not directly from Mycoplasma hyopneumonia Diagnosis: Clinical lesions Lung Scoring PCR -> Plain Swab (pretty much always for PCR!) - PCR will give you a definitive diagnosis Amies transport medium in a charcoal swab is likely to interfere with a PCR Post mortem: From Lower Respiratory Tract Not the lesion itself Ante mortem: Tracheal / Pharyngeal Swab (restrain & gag) BAL described (research) How many will you take???? – it Depends… Pathology: Cranioventral Suppurative Bronchopneumonia DDx: Swine Influenza A Virus, Inhalational No cell wall so must inhibit protein synthesis to create bacteriostatic effect In order of Pig Veterinary Society Prescribing Principles Tetracyclines -> Pleuromutilins -> Tylosin

Answer 86

Vaccination - Singular injection Normally given at weaning Often combined with PCV2 Inactivated Mycoplasma hyopneumonia Reduces shedding but does not prevent disease Environmental Management - Increase minimum ventilation rate Reduce dust levels in environment All in all out systems (separated age groups) Treatment - Tetracyclines, Pleuromutilins, (Tylosin) Group treatment likely in severe PRDC rather than individual treatment Elimination of Disease?- It’s possible Different methods available – Swiss Method Pre requisites: No animals under 240days ‘Reached Stability’ No back fostering of animals Isolated site Away from the road Strict Biosecurity Tetracyclines also useful as some of the secondary diseases in PRDC will also be sensitive such as Pasteurella and Actinobacillus pleuropneumoniae. The combination of Doxycycline and Tiamulinis synergistic and can be used where a response to doxyxycline alone isn’t seen. These are multifactorial diseases with many pathogens often involved simultaneously

Answer 87

Porcine Reproductive and Respiratory Syndrome (PRRS) Epidemiology 2 Genotypes Type 1 – Europe- Generally less virulent than type 2 Emerging Rosalia Strain – very virulent, Emerged in Spain 2020 Type 2 – North America - Accepted that is more virulent Passive Surveillance in the UK Pathogenesis- Respiratory pathogen -> Aerosol Reproductive pathogen ->Semen if Mycoplasma is the gateway disease … PRRS is the steam roller… It can be very severe especially in unstable herds in new outbreaks and unvaccinated herds Dysregulation of: Antigen Presenting Cells CD4 T helper Cells Interferon Gamma (viral) Neutralising antibodies (from B Cells) Macrophages Virus Transmission: Blood Nasal Secretions Saliva Semen Clinical Signs - It’s a Syndrome! -> A group of Clinical Signs Fertility ‘Issues’-Abortions, Early Farrowings, Weak Piglets, Still Borns, Mummified, Poor conception rates … Respiratory Issues -Coughing in all age groups, ‘Blue Ear’, Other respiratory outbreaks General-Wasting, Poor FCR and DLWG, Lethargy, Inappetence, Growing pig mortality increased N.b. Boar Studs are tested very regularly as their semen is used all over the country and could turn negative herds positive Diagnostics … Think about how the virus works Saliva Viral Secretion / Exposure -> ‘Rope Testing’ (saliva collected on ropes0 -> PCR/ELISA Blood Viraemia -> PCR Exposure -> Antibodies -> ELISA Tissue Tropism for lymphatic Tissue -> LN / Spleen / Tonsils Respiratory Pathogen -> Lungs -> PCR / Histopathology Management - Vaccination – Sows / Weaners DO NOT SWITCHBETWEEN Type of Vaccine – Modified Live, (Inactivated) Vaccine Delivery – Intramuscular, Intradermal Treatment? - Secondary bacterial disease as part of PRDC Interesting concept coming up …

Answer 88

4 Main subtypes in the UK [H1N2, H3N2, H1N1 avian, H1N1 pandemic] Reverse Zoonosis – Members of Staff should be vaccinated yearly, they should not enter the farm if they are ill/coughing Clinical signs – Cough that lasts for 7-10 days preceeded by temperature and runny nose (see also fertility signs), self limiting but may trigger secondary respiratory pathogens! Diagnostics - Viral Shedding does not last for very long -> PCR (nasal swabs) Sero-conversion takes time -> Require Paired Serology ELISA – Swine Influenza A (Screening) HAIT – Tells you which strain (definitive diagnosis) HAIT - Haemoglutinin inhibition test a paired serological titre should be taken, in the case of a rising titre, HAIT should be performed to confirm the types that are present Management -> Farrowing house is the reservoir for sow-piglet transmission Vaccination 2x Available, licensed in Sows/gilts Formuation 1 – H1N1 pandemic Strain Formulation 2 – H1N2, H3N2, H1N1 avian itersticial (someties brocho-intersticial pneumonia)

Answer 89

Actinobacillus pleuropneumoniae 15 Serotypes 4 Toxins- APX I, APX II, APX III, APX IV Determine ‘Pathogenecity’ from 1-4 where 1 is highest i.e. Apx 1 only: Isolate is serotype 10 or 14; Virulence Potential is 2 Primary and secondary role in PRDC depending on toxin make up Pathogenesis- Aerosol / Contact ->Tonsils ->Lower Respiratory Tract ->Toxin Release Cytotoxic effect on Macrophages Reduce Efficacy of Neutrophils … Rapid Onset (Acute lesions form in 3hrs (->Bacteraemia and Joints) pathogenisis- Aerosol / Contact ->Tonsils ->Lower Respiratory Tract ->Toxin Release Cytotoxic effect on Macrophages Reduce Efficacy of Neutrophils … Rapid Onset (Acute lesions form in 3hrs (->Bacteraemia and Joints) clinical signs- Aerosol / Contact ->Tonsils ->Lower Respiratory Tract ->Toxin Release Cytotoxic effect on Macrophages Reduce Efficacy of Neutrophils … Rapid Onset (Acute lesions form in 3hrs (->Bacteraemia and Joints) Diagnostics- Clinical signs – Thumping Breathing, Growers/Finishers Post Mortem - Fibrinous necro-haemorrhagic pleuropneumoniae lesions Pericarditis Culture and Sensitivity - Swab Lesion – Amies charcoal medium Swab Toxins typed on PCR and can be serotyped Live Pig- Tonsillar Scrapes (BAL) Growers ~over 25kg Finishers 40-50Kg and over May want to test the live pig in absence of disease for specific pathogen free or setting up a nucelus herd Picture to the right is an APP growing on Columbia blood agar with, satelism can be seen around the V Factors

Answer 90

Environmental- Min ventilation rate Draughts Vaccination- varied response depending on whether primary or secondary, animal immunity and environmental conditions Antimicrobials - High mortality so will need treating Amoxicillin/Tetracycline/Tiamulin

Answer 91

PGE Lungworm- one of the biggst production limiting disees, testing difficult, bearmans flotation not usefull. coughing in spring and autumn pathoneumonic Copper deficiency- ill thrift, ataxia, poor coat, repro problems, supliment by bolusing Pasteurella- can vaccinate, calved Yersiniosis- weaned calves, deaths Cryptosporidium- sudden death in calves at end of calving window Bovine tuberculosis Can undertake individual animal treatment Medicines recorded – prescribed and traceable Stress/ disruption of group handling? Stags deantlered – safety No remote injection necessary Oral drenches/ targeted treatments

Answer 92

Often related to stocking density PGE Lungworm Failure to thrive Clostridial disease Toxicities Dystocia Tangling/snaring injuries need license from natural island to catch wild deer- take 3-4 months to come through

Answer 93

PGE- poor tolerance for worms, threasholds for scuring low Nutritional scourin- flystrike issues MCF (ovine/caprine herpesvirus)- swelling and ulceration of mm around eyes, necrosis of ear tips, testing not sensitive, hard to treat, better to prevent Trace element deficiencies Lameness/ foot problems- designed for snow, difficult to trim- more like farriery Illthrift- nutrition? Clostridial disease Pasteurellosis routinly catrated for saftey- affects antler cycle. once castrated they will continue to grow antler that never hardens, usually manually deantler once a year around the time it would be cast naturallly classed as an act of veterinary surgery - Perruques Antler warts (antleroma) Broken antlers Pedicle infections Hormone therapy- injectable testosterone, dose very important can be hit and miss can get fly strike on antlers infection can track through

Answer 94

not common act of veterinary surgry Semen collection- Primarily imported from NZ Artificial Insemination- Transcervical Laparoscopic Act of veterinary surgery Embryo transfer- Not common in UK Conservation/biobanking

Answer 95

Species specific Releasing criteria Rehabilitation centres Castration or euthanasia of males- Behaviour during the rut Ewes’ milk or goats’ milk Consider colostrum status Co-morbidities Difficult fallow and reds straight froward sika harder Fly strike Colostrum management/status – supplementation Septicaemia Behaviour Socialisation

Answer 96

Deer can contract TB Deer can spread TB APHA spillover host- dont circulate and spread it but will get it when enviromental pressure high enough Deer establishments can be subject to statutory surveillance Skin testing Blood testing Post mortem identification Development of new protocols Raw pet food industry – cats + zoos

Answer 97

Bovine tuberculosis (TB) Foot and Mouth Disease Bluetongue Epizootic haemorrhagic virus (Chronic Wasting Disease)

Answer 98

TSE found in North American and Scandinavia Highly contagious – all secretions + tissue Fatal Non zoonotic Reason for import ban of Cervidae and strict controls on import of products of animal original from Scandinavia Not currently identified in the UK

Answer 99

Heavily controlled under firearms regulations – section 5 firearm Difficult skill – reading animal, dart placement and anaesthesia Risk to operator Risk to animal Legislative requirements Team job Further restraint Planning intramuscular injection of wild deer is technically an act of veterinary surgery legislation: Non vets may not legally dart ‘wild’ deer Must be under veterinary surgeon’s care ‘Stupefying drugs’ cannot be used to capture ‘wild’ deer without licence from Natural England Long turnaround Medicines used often have no MRL EU 2010/63 not requred in zoos tamper proof tags are put in darted deer so they dont go into food chain Many different protocols Species dependent Purpose dependent Anxiety levels dependent Time of year dependent Environment dependent Operator experience dependent Food producing animal status dependent Section 5 firearm- Rifle Pistol Blowpipe- technically fire arm in eyes of law different mechanism- CO2 compressed gas .22 blank cartridge Varying dart sizes and types Consider alternative delivery methods

Answer 100

magority of problems Anisognathia – maxillary teeth wider than mandibular Cingulae- the ridge round the base of a tooth, buccle aspect Normal vs. pathological Buccal aspect maxillary cheek teeth Lingual aspect mandibular cheek teeth Buccal (or lingual) ulceration Routine reduction with rasp- N.B. Dental eruption at 2-3mm per year

Answer 101

Aetiology: Absent teeth or defective opposing teeth Diastemata Displaced teeth Developmental disorders e.g. Mandibular brachygnathism (“Parrot mouth”) “Step mouth” and “wave mouth” Treatment- Sequential reduction Approximately 4mm q. 3 months

Answer 102

Rules when reducing equine teeth: Minimise time <7 seconds Flush often – cooling Clean burrs regularly Periodic examination of occlusal surface Limit removal to 3-4mm occlusal crown

Answer 103

Normal cheek teeth tight at interproximal margins Aetiology: Primary (Developmental) Secondary (Displacement) Senile Caudal mandibular cheek teeth commonly affected “Valve” or “open” Exaggerated transverse ridges (ETRs) on opposing teeth Compression and entrapment of food Gingival then periodontal disease Clinical signs: Quidding Weight loss Bitting problems treatment- Sedation and analgesia- N.B. Local anaesthesia Debridement and cleaning- Diastema forceps High-pressure lavage Complete clearance not always achievable Dietary management Odontoplasty- Diastema widening Contributing overgrowths ETRs N.B. Care adjacent pulp horns Repeated treatments often required Filling or bridging- Soft dental impression material Hard acrylic-based material

Answer 104

PAI more appropriate term than tooth root infection Pulpitis N.B. Occlusal pulpar exposure most often sequel to PAI not cause Aetiology- Anachoresis – i.e. haematogenous Vertical impaction of cheek teeth -> anachoresis Dental fracture Deep extension of periodontal disease Infundibular caries Iatrogenic pulpar exposure loss of tooth root definition on radiogreaph ct more sensitive- widening of periapicale space, fistulas, gas in pulp chamers

Answer 105

Maxillary cheek teeth Important disorder- Premature wear Fracture Apical infection Acidogenic bacteria- Impacted food material Concentrate feeding? Cemental defects

Answer 106

Odontoclastic resorption- Reserve crown Apical region Alveolar bone Proliferation of cementum in lytic region aetiology- Unknown age related?- 94% >20 years old sex predeliction for stallions Excessive strain on periodontal ligaments Inflammatory or immune-mediated? Husbandry? Cribbing? Bacterial? Presenting signs: Periodontal disease (17%) Decreased appetite Weight loss Oral ulceration Loose or fractured teeth Oral pain Advanced periodontal/dental disease: Gingival swelling and ulceration Periodontal pockets Bony swellings Abnormal dentition radiography- Osteomyelitis Loss of periodontal space Gingival swelling Bulbous enlargement of root Fracture- Teeth Alveolar Bone

Answer 107

Extraction not always required Consider extraction <18m.o- Protect developing 06 Consider radiography for: Unerupted (“blind”) wolf teeth Fractured teeth Mandibular wolf teeth – rare Displaced teeth “Molarised” or dysplastic teeth Local anaesthesia – infiltration: Palatal rugal fold Buccal reflection Periodontal elevation- Long handled elevators Careful and systematic Form a “friction bridge” with other hand N.B. Palatine artery

Answer 108

All goats classified as farmed animals Must be treated as such- Treatments - cascade Carcass disposal Legal requirements- Registered holding Ear tag Movement notification

Answer 109

History should give you an idea of where to focus Basic parameters- Temperature – 38.5 – 39.5o C Heart rate – very variable depending on age, size and metabolic work Resp rate – 10 – 30 breaths per min (20 – 40 for kids) Rumen turnover rate – 1 cycle per minute BCS – different to cattle and sheep- carry a lot of fat internally- check brisket

Answer 110

PGE- most common Fluke Johnes CLA CAE TB Chronic Illness Foreign body blood samples- Johnes CLA CAE fweg- PGE fluke post mortem

Answer 111

Goats don’t develop very good immunity to worms- natural browsers but often put to graze Can affect all ages Periparturient rise Weight loss, dull, reduced appetite, scurfy skin Not always scour FEC All classes of wormer effective- Care with levamisole if sick Use goat dose rates to avoid resistance Fluke and cocci

Answer 112

Mycobacterium avium paratuberculosis (MAP) Main transmission = faeco-oral MAP present in colostrum and milk Infected when very young Slow, progressing thickening of the ileum Immune suppression Weight loss +/- diarrhoea iceberg disease Little data available on prevalence in UK goat herds Recent study into OJD- 64% flocks infected Lower life expectancy in OJD positive flocks 17% survival beyond year 3 V 40% Many UK commercial herds vaccinate- Gudair Give early Snatch kidding testing- Post mortem :( Faecal culture- £££, Takes ages Serology - ELISA, AGID Milk ELISA Faecal PCR- Pool 10 indivduals Actiphage test – maybe one day

Answer 113

Also a big hitter Corynebacterium pseudotuberculosis Affects multiple lymph nodes Internal and external- Parotid, Submandibular, retropharangeal, supermammary, popliteal Diagnosis- Culture Serology No treatment Prevention- Stocking densities Snatch kidding

Answer 114

Lentivirus Similar to Maedi Visna in sheep- Cross-species transfer Transmission by direct or close contact- Dam – kid transmission is important Coughing and shared food troughs Milking machines Eradication is possible- Solid barriers Regular testing Serology

Answer 115

Behaves differently in goats- Large, thin walled abscesses Liquid pus Rapid spread No statutory testing Pre-movement recommended Biosecurity- AI to breed billies Wildlife proofing

Answer 116

signalment important- in kids: age?- cryto vs coxi in kids enviromental factors faecal sample very diagnostic in kids in adults- grazing history blood/faeces samples Young animals: Cryptosporidiosis Coccidiosis PGE- common in comercial herds Salmonella- common in comercial herds Adult animals- Clostridial scour Johnes PGE → Grazers Salmonella

Answer 117

Relatively common in kids Larger enterprises with higher stocking densities Sheds and pasture with long history of goats Causes scour in kids Cause of death Impairs normal growth and production Treat with Baycox at sheep rate Care with Deccox in feed Use appropriate disinfectant

Answer 118

Seen in young kids up to 5 weeks Profuse watery scour Up to 100% morbidity Deaths (up to 20%) Contamination of kidding area Poor colostral uptake Treat affected pen with Parofor powder in milk at 50mg/kg for 3-5 days Use an appropriate disinfectant

Answer 119

Clostridial overgrowth -> enterotoxaemia- C. perfringens D COMMON in milking goats Concentrate feeding Difficult to diagnose in the live animal Responds to B multi-vitamin injection Vaccine responsive scour Severe enterotoxaemia will require antibiotics, NSAIDs and fluid therapy vax- Lambivac 2ml s/c- Primary course as kids Boost at mating (5-6 mths) Adults vaccinated 3-4 times per year

Answer 120

Kids - Joint Ill White muscle disease Injuries Adults- Digital dermatitis Footrot CAE Bentleg Can have really high prevalence – up to approx. 70% Treat aggressively Treat early Cull hard- Chronic cases Horn changes Separate lame animals- Reduce spread of infection Makes new cases easier to spot Footbath healthy goats regularly with zinc sulphate Milk infected goats last Treat infected goats with amoxicillin (Betamox 150mg) at 7mg/kg Footbath infected goats after healthy goats

Answer 121

Joint Ill- T. pyogenes, E. coli, Streps and Staphs Mycoplasma Secondary to septicaemia Hygiene and colostrum Treat with Tulathromycin (Draxxin) at 1ml/40kg and Meloxicam (Metacam) at 1ml/40kg White muscle disease- Check milk replacer Concentrate to dam Vitesel at sheep dose…

Answer 122

Footrot- Dichelobacter nodosus Interdigital dermatitis → underrun horn Grey slimey discharge Sole horn separation No coronary band changes Treat – Oxytetracycline at 20mg/kg LA dose Digital dermatitis- Treponema spp Sole, wall and toe ulcers Coronary band swelling No interdigital involvement Sole horn separation Hyperkeratosis Bony changes within pedal bone Treat – Amoxycillin (Betamox) at 7mg/kg or LA at 15mg/kg

Answer 123

Very common Often found incidentally on PME Treat with Tulathromycin (Draxxin) at 1ml/40kg and Meloxicam (Metacam) at 1ml/40kg Amoxy clav (Synulox) at 1ml/20kg for milkers or oxytetracycline 20mg/kg LA dose Vaccine – Ovipast 2ml s/c- Primary course as kids Booster at weaning Very common Often found incidentally on PME Treat with Tulathromycin (Draxxin) at 1ml/40kg and Meloxicam (Metacam) at 1ml/40kg Amoxy clav (Synulox) at 1ml/20kg for milkers or oxytetracycline 20mg/kg LA dose Vaccine – Ovipast 2ml s/c- Primary course as kids Booster at weaning

Answer 124

Chorioptic mange- Really common Found on lower limbs, belly, scrotum (fertility issue, thickens skin and increases temp) Not itchy Injectable ivermectin or eprinomectin (0.4mg/kg)- need multple treatments Lice - Biting (D. caprae) and sucking (L. stenopsis) Can be really severe especially in kids and immunocompromised Itchy Eprinomectin (0.4mg/kg) differentaite with hair plucks and skin scrapes can send away to lab as they can clear up inconclusive samples cant also do punch biopsies if both inconclusive- give la, send to lab, look with histo

Answer 125

Why?- Control of kidding for smallholders AI Biosecurity In season manipulations Out of season manipulations CIDR synch Cloudburst- Pseudopregnancy Can ultrasound to diagnose 1ml PG IM – may need to repeat Discharge can be bloody in-season Day 0 – CIDR in + 2ml GnRH AM Day 6 – 200-250 IU PMSG (depending on yield) IM PM Day 7 – 1ml PG PM Day 8 – Pull CIDR + 1ml PG PM Day 10 – AI AM/ natural service out of season- short day breeders Lights protocol 200 lux at goat eye level Needs fairly dark sheds Take into account working hours (milking) Don’t forget the billies! Can use a CIDR synch 1 month after Regulin implant Cloudburst is more common 1st January -> 1st March: 16hrs light then- Natural light Regulin implant, 1 for nannies, 2 or 3 for billies 1st April – billies in

Answer 126

Necessary? Undertaken by a vet only- heat damage to brain and super sensitive to la, easirer procedure if GA Horn growth very rapid – disbud between 2 and 7 days Local anaesthetics not well tolerated (7mg/kg max) Anaesthetic Very thin skull Larger bore irons?

Answer 127

Do under sedation/anaesthesia WAIT if possible – why? Ring if under 7 days Surgical if over 7 days Open castrate, twist and pull NSAIDS and antibiotics (depending on cleanliness)- Metacam (1ml/40kg) LA amoxycillin (1ml/10kg)

Answer 128

Same procedure as in ewes Common in pygmy goats Care with local anaesthetic Do lying in right lateral recumbency OR standing NSAIDs and antibiotics- Metacam Synulox Oxytocin (after)

Answer 129

rimary: * Impinging (overriding) dorsal spinous processes – KISSING SPINES * Osteoarthritis of the articular process joints (APJs) * Spondylosis of the vertebral bodies * Enthesopathy of the supraspinous ligamen Secondary: * Muscle pain associated with hindlimb lameness * Incorrect saddle fit * Heavy or unbalanced rider

Answer 130

* Primary: * Osteoarthritis * Soft tissue (ligament) injury * Secondary: * Pain associated with hindlimb lamenes

Answer 131

* Diagnostic Imaging- * Radiographs * Ultrasound * Diagnostic Anaesthesia - * Local infiltration: * Dorsal spinous processes (DSP) * Sacroiliac joint (SIJ) * Intra-articular: * Articular process joints (APJ

Answer 132

* Ultrasound thoracolumbar spine * Curvilinear transducer * Patient preparation- clipping? * Start at T18-L1 * Move cranially – thoracic joints * Move caudally – lumbar joints

Answer 133

diagnostic Imaging- * Nuclear scintigraphy (bonescan) * Rectal ultrasound * Radiographs * Computed tomography * Diagnostic Anaesthesia- * Risks of desensitising nerves * Ridden assessment Trial medication- Corticosteroids * Methylprednisolone acetate * Triamcinolone acetonide

Answer 134

* Diagnostic Anaesthesia- * Required to help rule in/out significance of changing on clinical examination and diagnostic imaging * Ridden examination before/after

Answer 135

Medication: * Short term * Alleviate pain * Can help to better facilitate application of rehabilitation Corticosteroids- * Radiographic guided local infiltration around impinging DSPs * Ultrasound guided injection of articular process joints * Methylprednisolone acetate * Triamcinolone acetonide Rehabilitation exercise- * Long term * Physiotherapy treatmen Surgery: * After failed medical treatment * Interspinous ligament desmotom

Answer 136

Omeprazole- * Oral: * ‘Full Dose’ (4mg/kg PO SID) * ‘Maintenance dose’ (1-2mg/kg PO SID) * 4 weeks of treatment * Gastroguard® * Peptaleve®/Peptizole®/Ulcer Gold® * Injectable: * 2g/Horse IM q5-7days * 4 weeks of treatment * Sucralfate: * 12-20mg/kg PO BID-QID * Second line treatment

Answer 137

Misoprostol: * 5µg/kg PO BID * Tablets or paste * Care when handling * Administer 1 hour after omeprazole * Initial 4 week treatment course but often require longer Omeprazole- * Oral v injectable Corticosteroids- * ?Extension of IBD

Answer 138

Irregularly irregular heart rhythm- * Atrial fibrillation * Atrioventricular block- Normally regularly irregular Systolic heart murmurs: * Left side (grade 2/6) * Physiological flow murmur * Mitral valve regurgitation * Right side (grade 4/6)- * Tricuspid valve regurgitation * (Ventricular septal defect)

Answer 139

ECG * Irregularly irregular R-R intervals * No p waves preceding the QRS complexes * Fibrillating baseline/f waves between QRS complexes * Atrial fibrillation Echocardiography * Tricuspid valve regurgitation (right) * Flow murmur (left)

Answer 140

Muscle disorders: * Over-exertion * Recurrent Exertional Rhabdomyolysis (RER) * Polysaccharide storage myopathy (PSSM) * Quarter horses/Warmbloods * Type 1 * Type 2 Hyperkalaemia periodic paralysis (HYPP) * Quarter horses

Answer 141

Blood sample: * Aspartate aminotransferase (AST) * Creatine kinase (CK) * Rest * Post exercise- 4-6 hours Urine sample: * Urinalysis * Electrolyte clearance- Blood sample at the same time * Muscle biopsy: * Gluteal/semimembranous Genetic testing: * Hair pluck * Blood sample

Answer 142

* Acute episode * Pain relief: * Phenylbutazone, Flunixin meglumine * Fluid therapy Chronic management- * Dantrolene- * Limits calcium release from the sarcoplasmic reticulum * Administer orally a few hours before exercise * Long term effects uncertain prevention/ management-- Regular exercise program * Gradual changes * Daily pasture turnout Diet- * Low carbohydrate * High fat (>20%) * Alternative energy sources * Gradual introduction * Ensure balanced nutrient intake (vitamins and minerals) * Avoid stress

Answer 143

Irregular foot placement & circumduction * Grade 3/5 hindlimb deficits (ataxia) * Grade 1/5 forelimb deficits (ataxia) * Normal mentation/cranial nerves * Cervical spinal pathology- * Osteoarthritis * Cervical Vertebral Malformation (CVM) – Wobblers * Type 1: C3-5 (young horses) * Type 2: C5-T1 (older horses) * (Motor neuron disease)

Answer 144

Physical- Removes large particulate matter from the water. Usually involves different grades of ‘sieve’ from coarse to fine. Includes protein skimmers, which remove proteinaceous waste products from the water by trapping them as a stable foam which can then be skimmed from the surface of the water and removed. Biological- The bacterial element of the filter which removes nitrogenous waste products from the system. The bacteria require a surface to colonise, usually a sponge which also acts as a physical filtration medium. Chemical- Often only included in specific scenarios, e.g. to remove a known chemical from the water Activated carbon is the most common chemical filter used. Care must be taken to remove these filters when they are used up, or they may leach chemicals back into the tank. Ultraviolet- Often used in the sump of larger filtration systems. ‘Sterilises’ water – removes bacteria, parasites and some chemicals. Must not be in the same compartment as the biological filter as can affect beneficial bacteria levels.

Answer 145

diseases are often secondary to water qaulity issues High Ammonia High Nitrites High Nitrates Rapid pH changes Rapid temperature changes Extremes of temperature Low Oxygen Saturation Supersaturation

Answer 146

High environmental ammonia -> decreased concentration gradient between the gills and surrounding water -> failure of passive transport -> increased plasma ammonia -> : Increased plasma pH Destabilises proteins -> inhibition of enzymes required for energy generation. NH4 + substitutes for K+ in ion transporters, (e.g. Na+ -K+ -ATPases) -> disrupted electrochemical gradients. This results in osmoregulatory disturbance, increased tissue oxygen consumption, and decreased blood oxygen transport Clinical signs relate mainly to hypoxia i.e. sudden death, gasping at the water surface, gathering at aeration points. Chronic low grade exposure leads to stress related immunosuppression and secondary health issues such as bacterial and fungal disease. Options for management: Decreasing ammonia levels (50% Water change, Zeolite) Increasing oxygenation via an air stone Help filter mature via addition of filter start or a sponge from a mature tank Supportive care e.g. addition of sodium chloride at 1-5g/100L (not with zeolite)

Answer 147

High environmental nitrite levels -> absorption of nitrite across the gills -> oxidisation of haemoglobin to methaemoglobin. Methhaeboglobinaemia = brown blood disease; gills may appear pale tan or brown in colour. Methaemoglobin does not transport oxygen, -> hypoxia. Clinical signs as per ammonia Management options as for ammonia- Only exception = zeolite. Sodium chloride used instead - chloride ions competitively inhibit nitrite uptake across gills

Answer 148

Least toxic; eggs and fry show increased sensitivity. Clinical signs include poor growth, lethargy, anorexia, stress related immunosuppression with 2o infections. May -> increased plant growth, including algal blooms, which may -> decreased oxygen saturation (see later) Management: Reduce stocking density Decrease decomposing plant material Water change

Answer 149

Each fish species will have an ideal pH range. Goldfish and koi: 7.0-8.6 Malawi cichlid: 7.8-8 Discus: 6.0-7.0 Many marine species: 8.2-8.4 Fish can live with suboptimal pH if changes occur slowly. Rapid pH changes exceed the gills acid-base regulation capacity. Clinical signs are often non-specific and relate to immunosuppression and secondary opportunistic infections, and/or gill damage leading to decreased oxygen absorption and subsequent hypoxia.

Answer 150

Each fish species will have an ideal temperature range. Goldfish and koi -18oC-24oC ideal, 2oC – 30oC Malawi cichlid -24°C - 26°C Discus -28°C - 31oC Fish can live with suboptimal temperatures if changes occur slowly. Rapid temperature changes -> rapid changes in metabolic rate, metabolic stress and immunosuppression. Clinical signs are often non-specific.

Answer 151

Extreme cold -> decreased metabolism, lethargy and anorexia.- Over prolonged periods -> the immunosuppression and 2o infections. Extreme heat -> decreased oxygen saturation of water, increased toxicity of ammonia, and increased metabolic rates -> increased feeding and waste production.- Over prolonged periods ammonia toxicity and hypoxia due to low oxygen saturation will occur. Water heaters and chillers are available commercially to prevent extremes of temperature occurring, however these can be expensive.

Answer 152

Low oxygen saturation can occur for a variety of reasons: Insufficient water surface area (especially in bowls) Insufficient aeration Increased stocking density Increased water temperature Excessive planting Clinical signs: Hypoxia related: gasping behaviour (especially at points of aeration), sudden death (especially overnight) Chronic stress related: Non-specific signs of illness (skin ulcers, fungal infection etc.) Management: Increasing aeration Decreasing water temperature Decreasing planting Decreasing stocking

Answer 153

More common in large aquarium systems than home systems. May occur due to: High levels of plant material (photosynthesis during the day may  to oxygen saturation) Faulty pumps sucking in air at high pressure. Over-powerful submerged aerators Clinical signs: Gas bubbles (usually best visible in eyes and gills) Hyperinflation of the swim bladder Sudden death. Management primarily by addressing the underlying cause. Use of aerators which splash water into the air also allow for gases to devolve from water.

Answer 154

Skin scrapes- sample mucous with scalple Impression smears Gill clip- under sedation Blood sampling- lateral and caudal approch to caudal vein Swim bladder aspirate- undersedation, sterile saline injected and then aspirated Bacteriology- pm kidney samples reliable indicator Fine needle aspirate Decide on treatment or next steps as appropriate

Answer 155

There is currently no legislation regulating the slaughter of fish for food in the UK, apart from the Animal Welfare Act 2006. The Humane Killing of Animals under Schedule 1 of the Animals (Scientific Procedures) Act 1986 outlines the following methods as suitable for the humane killing of fish: Overdose of an anaesthetic agent Concussion of the brain by striking the cranium, with destruction of the brain before regaining consciousness (pithing – due to the extreme resilience of the fish brain to hypoxia) Euthanasia by the owner at home: Aquased (2-phenoxyethanol) Available OTC It has instructions on how to overdose fish in order to cause euthanasia. I recommend to owners that gill movement have stopped for a minimum of one hour prior to removal from the anaesthetic Anaesthetic protocols which can be considered for euthanasia of fish include: Use of 2- phenoxyethanol in water Use of buffered MS222 in water Use of buffered MS222 followed by IV or IP pentobarbital. IM ketamine followed by IV or IP pentobarbital. IV propofol followed by IV or IP pentobarbital. Doppler can be used to ensure cessation of heartbeat (though this can take several hours in fish) All fish should be pithed before disposal – IAAAM student study

Answer 156

pGE egg-> L3 pasture amanagement and rotation pasture selection cant remove f+ as with eqidae

Answer 157

for PGE L4 -> adult##anthelmintics vaccines breeding/ genetics nutritional

Answer 158

group 1 Benzimidazole active chemicals- lbendazole, Fenbendazole, Ricobendazole, Oxfendazole Extensive resistance

Answer 159

group 2 levimisole active ingredients- levimisole commonplace resistance

Answer 160

group 3 macrocyclic lactones vermectin, Moxidectin, Doramectin, Eprinomectin* Evident resistance

Answer 161

group 4 Amino acetonitrile derivatives active ingredient- Monepantel resistance Emerging?

Answer 162

group 5 spiroindoles derquantel (5) & abamectin (3) as a dual active Emerging resistance? hard to tell with dual formulation

Answer 163

10% of the flock reprisentecd cation against pooling sample on farm or even in practice to avoide samlpoe biase and ensure it is reprisentative in-house microscopy * In-house machine-based (ovocyte) * External lab * FECPAK on farm * On farm microscopy Results reported as epg (nematodes)/ opg (cocci) Advise on need to treat * Inform vet/farmer re: contamination risk of pasture Pooled is best! But beware farmer pooling! * < 1 hour old * Health sample bias * Expel air & refrigerate full aceess to pature, feed, water beforehand * AVOID FRIDAY

Answer 164

Idea that a proportion of population are not treated, therefore, we don’t only select for resistance alleles in the endoparasites * Theory is that it slows resistance developing

Answer 165

Abomasum: Haemonchus contortus* Teladorsagia circumcincta* Trichostrongylus axei

Answer 166

Small Intestinal: Nematodirus spp* Trichostrongylus spp* Cooperia spp

Answer 167

trichuris spp Oesophagostomum spp Chabertia spp

Answer 168

mass sudden death in ill thrft lambs bottle jaw anemia no dihors lethargy s low growth rates no age rrelated immunity l3 larve emerge mid spring-atumn so cause disease cold wether = hyperbiose l4 femacular testing- looking at ocular mucosa to asses colour to asses possibility of anemia with haemonchous contortus- treat those with poorest colour fec- needs speciation- penut aglutination test- very expensive and takes 8 days can treat on assumption for haemioncosus if fec very high- very prolific on pm- worms visible in abomasum lots of resistance good quarentine protocalls helpfull

Answer 169

larve hatch in grast and are eaten- l3 l3 stage causes disease one egg found = treat all sheep Dark, profuse watery d+ * Elevated dag score depression low bcs poor dlwg DEATH TX- The responsible product of choice is group 1- bz product The only indication for blanket treatment of lambs**. * OFT of the worst affected * Typically, late Spring * Survivors will have immunity fr

Answer 170

Presentation: Sudden death Weakness or dullness Abdominal pain (colic-esque) Anaemia Ascite Caused by large numbers of immature fluke migrating through the liver - no eggs seen at this point At PME haemorrhagic tracts, inflammation, fibrosis, liver enlargement can be observed There is a link between acute fasciolosis and clostridial disease causing sudden death from migratory larvae (Blacks disease) TREATMENT OF THE FLOCK: TRICLABENDAZOLE + MOVE TO CLEAN PASTUR

Answer 171

Presentation: Rapid weight loss Poor fleece Anaemia (some arguments now for the use of FAMACHA for diagnosing fasciolosis8 ) Reduced fertility in ewes Decreased growth rates Caused by 500-1000 immature & adult fluke ingestion of high numbers of metacercariae over a longer period of time, not quite severe enough for acute disease and sudden death eggs observed at fec <100 REATMENT OF THE FLOCK: TRICLABENDAZOLE + MOVE TO CLEAN PASTURE

Answer 172

Presentation: Progressive weight loss (BCS scoring!) Anaemia (some arguments now for the use of FAMACHA for diagnosing fasciolosis8 ) Oedematous third eyelid Submandibular oedema Ascites Poor milk production- decr lamb dlwtg used by 250-500 adult fluke through the liver and feeding on blood in bile ducts Notable liver pathology at pme- hyperplasia, cholangitis, calcified tracts, expressible adult fluke fLUKE EGGS OBSERVED AT FAECAL EGG COUNT (>100) TREATMENT OF THE FLOCK: Many options as adults causing the chronic disease*

Answer 173

fec- detects adult flukes- chrinic and subacute disease faecal coporoantigen- detects adult and older immature- detets it 2-3 weeks earlier than fec PM- detects any stage, fastest and most reliable serology- elisa- detects antibodies to fluke 2-4 weeks post infection. lebels may remian hih 8-10 weeks post infection

Answer 174

triclabendazole- all stages, best used in stumn, resistance detected closantel- good sucess form 6 weeks old, atumn, prevents egg laying in adults for 10 weeks. possibly developing resistance nitroxynil- 6 weeks and over, best used late summer to winter albendazole or oxycolozanide- adult fluke only, best used spring summer

Answer 175

G.truncatula feeds on algae and resistant to frost and drought consider likley areas for g.truncatula- wet but not underwater, including tyre ruts, cleared ditches and pond/stream banks can drainage or graveling or liming around pipes, troughs and gateways be used?

Answer 176

american foul brood european foul brood chalk brood- ascosphara apis defromed wing virus- spread by varroa chronic bee paralysis virus varoa common vector

Answer 177

Sea Lice Amoebic Gill Disease