Sheep

7 Step Process of Herd Investigative Approach

1. Define the problem

2. History taking

3. Environment and distance exam

   • Not realistic to perform “full farm walk”

4. Individual exam ± PM exam

5. ± Additional tests (eg. faecal or blood samples)

   • Must be justified

6. Data analysis and decision-making

7. Implement plan and monitor response

ONE: Define The Problem

Farmer Joe asks you to have a look at his flock of sheep as he is “a bit disappointed with the ewe hoggets at the moment”

Question: What additional information do you require to better define the problem?

1. What does “disappointed” mean?

   • Death? Poor growth rates?

2. Number of ewe hoggets and number affected

3. Signalment of ewe hoggets: Breed, age

4. Weight of ewe hoggets (when where they last weighed?)

5. What does “at the moment” mean?

   • Yesterday? Progressive? Since summer?

Example: Problem = Poor average growth rates of Romney ewe hoggets between December - April (average 27kg and 32kg respectively = ~5kg growth in 5 months) in a herd of 800.

→ Use data where available to define problem clearly

• +ve: Helps formulate DDx list to guide investigation

THREE: Distance and Environmental Exam

• Importance

• 11 Features to assess on distance exam

Importance: Usually called out to examine MOB vs. individual → Impossible to conduct individual exam on every animal (unless lifestyle block or prize ram)

• Important to assess paddock which animals have been grazing but not always feasible (lack of transport or distance away)

Features:

1. Signalment and variation in mob

2. Behaviour, posture and mentation

3. Swelling or oedema (eg. bottle jaw)

4. External skin lesions, defects and wool condition (eg. flystrike or FE)

5. Nasal, ocular or oral discharge

6. Faeces on ground (consistency and variation)

7. Sick individuals (depressed, separated from group)

8. Coughing or dyspnoea

9. Soft grunting

10. Bruxism (hunger or pain)

11. Flystrike or footrot smell

12. Gut fill

List 3 features to assess on individual examination of a sheep

1. MM

2. BCS = Palpate lumbar dorsal and transverse processes

3. Weight

→ Can perform quickly on large number of animals (50 - 100)

Which sheep should be selected for physical exam?

• Disease of entire mob → Assess worst affected and some not so badly affected

• Disease of individuals → Examine small number of diseased animals

Random selection is rarely rewarded, but may be justified

7 Differences between sheep and cow PE

1. MM = 3rd eyelid (vs. vulva of cows) ± gums

   • Gums in black-faced breeds (eg. Suffolk) are pigmented

   • Normal: Pale pink

2. RR and HR = ALWAYS elevated due to stress from handling

3. Lung Auscultation = Poor correlation between auscultation and pathology

   • Part fleece so stethoscope contacts skin

4. Pulse = Femoral artery

5. GI sounds = GI accidents rare in sheep (pinging uncommonly performed)

6. Hydration = Pinch upper eyelid

7. Oral Examination = Tight cheek muscles → Examine incisors and dental pad ONLY

   • Sharp molars → Do NOT put fingers in mouth

   • Palpate ventral mandible for osteomyelitis due to tooth root abscess

   • Age of sheep ≤4yr assessed by number of permanent incisors erupted

     • 1yr = 1 pair of incisors

Normal TPR and rumination rate of sheep

Temperature = 39.5 ± 0.5˚C (sheep are HOT)

HR = 70 - 90bpm

RR = 20 - 30brpm

Rumination Rate = 1 - 3/min

2 Indications for field necropsy

1. Animals found dead

2. Alive animals BUT unlikely to recover and/or low value

   • Necropsy must have high likelihood of helping to achieve diagnosis (i.e. benefit rest of flock to prevent further death)

   • eg. Ill-thrift ewe

   • Avoid ill-thrift lambs (treatable disease in high-value stock class)

Ideally ≥3 animals

7 Health and safety recommendations for field necropsy

1. Care with walking while holding a knife

2. ONE person cutting at a time

3. Cut AWAY from yourself and others

4. Do NOT hand knife to another person (place on ground)

5. Wear appropriate PPE (overalls, gumboots, waterproofs and gloves)

6. Hold body part up so skin is cut under tension

7. Easier to cut UNDER skin vs. on top

Describe the field necropsy technique (+ features to assess)

Field Necropsy = Quick technique assuming limited DDx → Carefully examine few specific organs to rule in/out diseases

• More thorough necropsy technique for single animal or many possible DDx

1. EXTERNAL EXAMINATION

   • AM: BCS, tag and PE

   • Assess for paddling (scuff marks in dirt), position of head (opisthotonus), discharge, signs of injury, predation or damage

2. REFLECT LEGS AND SKIN

   • Lie in LEFT lateral recumbency (rumen on dependent side)

   • Reflect cheek tissue to expose molars and assess dentition

   • Reflect front leg → hindleg (cut ligament to dislocate hip)

   • Remove skin

     

3. OPEN ABDOMEN (+ quick inspection of abdominal organs)

   • Start caudal to last rib (near spine) and extend cut caudoventrally

   • ID ileocaecal junction and roll caecum to assess for Johne’s disease

     

4. OPEN THORAX

   • Cut through soft tissue over sternum and ventral to spine → Cut ribs with loppers

   • Remove pluck by cutting through:

     1. Mediastinum (ventrally)

     2. Oesophagus and CdVC (caudally)

     3. Ao, oesophagus and trachea (cranially)

   • Care with interpretation:

     • M. capillaris cysts are NORMAL = Small and gritty lesions over dorsal lung surface

     • Firm = Abnormal

   • Cut down trachea into bronchi and bronchioles to ID lungworms

   • Heart not normally examined in field necropsy unless indicated

     

5. CAREFUL EXAMINATION OF ABDOMINAL ORGANS

   • Liver: Assess shape, fibrosis and train track lesions for FE and liver fluke

     • Cut into bile ducts for liver fluke

   • GI: Normal for slight variation in colour

     • Intestinal adenocarcinoma

     • Can cut into abomasum for Haemonchus (not routine) → Tie for worm count or assess top for wriggling worms

       

List 5 zoonotic agents of sheep

1. Leptospirosis → Flu-like symptoms ± severe illness and death

   • Almost all NZ sheep have serological evidence of exposure

   • Commonly localised in kidneys and shed in urine

   • Most dairy herds vaccinated to protect humans but does NOT eliminate shedding

2. Listeria → Abortion

   • GI of sheep

3. Salmonella spp. → GI disease

   • Normal GI commensal of sheep and cattle

4. Yersinia spp. → GI disease

   • Normal GI commensal of sheep and cattle (rare clinical disease)

5. Campylobacter jejuni → GI disease

   • Normal GI commensal of sheep and cattle

NOT Zoonotic:

1. Brucella ovis = ONLY Brucella spp. in NZ AND not zoonotic

2. BVDV

3. Rotavirus

4. Coronavirus

Methods of Sheep Euthanasia

• Advantages

• Disadvantages

1. Overdose of Pentobarbitone IV

   • +ve:

     1. Humane (rapid loss of consciousness)

     2. Minimal distress to owner (eg. lifestyle block)

   • -ve:

     1. Requires vet (controlled substance)

     2. Residues in carcass (cannot be used in food chain)

     3. $$$

     4. Technically challenging (stick vein)

2. Throat cut ± Pre-Stunning

   • +ve:

     1. Simple equipment

     2. Culturally/religiously required in some context

   • -ve: Animal remains conscious → Pain for some time during exsanguination (major welfare concern)

3. Stunning with Mallet → Throat Cut

   • +ve:

     1. Cheap

     2. Superior welfare over non-stunning slaughter

   • -ve:

     1. Requires skill to ensure effective stun

     2. Aesthetic concerns (cannot use for brain necropsy)

4. Shoot with Captive Bolt Gun (CBG)

   • +ve:

     1. Humane (instantaneous unconsciousness)

     2. Does not require firearms license

   • -ve:

     1. Requires restraint and good aim

     2. Equipment maintenance required

     3. Cannot use brain for necropsy

5. Shoot with Free Bullet (Rifle)

   • +ve:

     1. Done from distance

     2. Good for field euthanasia of large animals

   • -ve:

     1. Safety concerns of free bullet

     2. Requires firearms license and training

     3. Risk of poor aim

     4. Cannot use brain for necropsy

Captive Bolt Gun

• Structure and MoA

• 3 Normal post-CBG responses

• Positioning

  • Sheep (polled)

  • Sheep and goats (horns)

  • Cattle

  • Pigs

• Restraint technique

• 4 Signs of effective shot

• 5 Signs on ineffective shot

• Method of exsanguination

MoA: Steel bolt inside gun powered by small grain bullet

• When fired, bolt shoots out to penetrate brain → Concussive forces and damage to brain from bolt (and skull fragments)

  • No recoil (low-grain cartridge)

• → Immediate and irreversible concussion → Exsanguination or pithing immediately after CBG

Normal Responses:

1. Sheep to kick after being shot with CBG (after short delay) = Normal post-death neurological reflex

2. Heart continues to beat (~2 minutes an dup to 10 minutes) after CBG

3. Occasional agonal gasping (uncommon)

Positioning: Must go through mid-brain down into pons

• Different species have different shaped heads → Different species CBG position

• Sheep (polled) = Highest point on top of head → Aim directly towards back of throat

• Sheep and goats (horns) = Back of head → Aim towards base of tongue (cannot place at highest point of head due to horns)

• Cattle = Middle of forehead at crossing point of two imaginary lines between eyes and centre of base of opposite horn

• Pigs = 3/4 inches (20mm) above eyes and halfway across forehead → Aim slightly up

Restraint: Adequate restrain sheep ensuring handler out of way (hands down neck and not directly under chin)

• Can have 1/both hands on gun (care with hand placement over vent hole)

Effective Ahot:

1. Dilated pupils

2. Absent corneal reflex

3. No jaw tone

4. No breathing

Exsanguination: Place head around gumboot → Place knife perpendicular just below cervical vertebra (caudal to angle of mandible) and cut outwards/ventrally (check BOTH carotids are cut through)

4 Example ancillary tests

1. FEC

2. TE analysis

3. Liver fluke testing

4. Serology for specific disease (eg. Johne’s)

CBC, biochemistry and histology rarely indicated

4 Advantages of creating reports for farmers

1. Clarify thought for you and the farmer

2. Legal requirement

3. Allows future monitoring

4. Builds rapport with farmer

List 7 causes of low reproductive performance (+ 3 common times of callout for the veterinarian)

1. Low conception = Ram factors

2. Poor ovulation = Ewe factors

3. Embryonic death

→ Low scanning/pregnancy%

4. Abortion

5. Metabolic disease → Adult mortality

→ Low lambing/calving%

6. Perinatal death

7. Lamb/calf death

→ Low tailing or weaning%

Scanning important to determine when lamb loss occurred

3 Types of factors to ask the farmer about which contribute to poor reproductive performance (+ examples)

1. HUSBANDRY FACTORS

   1. Date rams join ewes

   2. Length of mating period/return to service

   3. Lambing period (does it match the length of time rams were with the ewes?)

   4. Ram soundness

   5. Ram:ewe ratio

   6. Teaser ram used?

2. FARM FACTORS

   1. Geography

      • South Island → Mate ewes later so lambs miss poor weather events

      • North Island → Mate ewes earlier so lambs have enough feed when born

      • Hill country ewes cycle LATER with SHORTER mating period

   2. Age structure of farm

      • Younger ewes cycle LATER with SHORTER overt oestrus AND lower ovulation rate → Affects management

   3. Vaccination records (eg. Campylobacter, Toxoplasma and Salmonella)

   4. Pregnancy scanning data

      • Determine where the problem occurred

      • Make decision about preferential feeding

3. ANIMAL FACTORS

   1. Nutrition

   2. BWT and BCS

   3. Genetics

   4. Age

   5. Reproductive diseases

   6. Other diseases

   7. Stress

Why are reproductive problems so difficult to investigate? Why are they so important to investigate?

Difficultly: Usually retrospective → Aim to determine cause to prevent problem occurring NEXT YEAR

Importance: Good reproductive performance is fundamental for profitability of a sheep farm

• Number of lambs at DOCKING ÷ Number of ewes mated

What is the difference between fertility and fecundity?

Fertility = Ability of animal to get pregnant (affected by ovulation) → Proportion of ewes in lamb

Fecundity = # of offspring produced (number of ovulations per oestrus cycle) → Lambing%

• + Scanning% for timing of loss

Increased lambing% in NZ

• 5 Reasons why lambing% has increased in NZ

• 4 Reasons why it is becoming an issue

Causes:

1. Genetic improvement (incorporated highly fecund breeds as twinning is NOT a highly heritable trait)

2. Superior nutrition

3. Superior vaccinations

4. Hogget mating

5. Better management (scanning to improve lamb survivability and timing of the breeding season to match weather)

-ve:

1. Ewe only has two teats

2. Lower birth weight of individual lambs

3. Dystocia

4. Ewe carrying multiples requires more feed

Describe the THREE major ewe factors affecting reproductive performance

1. NUTRITION = Vital from weaning to mating (3m to get ewe in good BCS for mating)

   • Flushing/Dynamic Effect = Increase feeding in 3 - 6w pre-mating to increase fecundity

     • Larger response observed in thinner ewes (BCS 2 - 2.5) but no effect in BCS 3.5 ewes as they already benefit from the static effect

   • Recommendation: BCS ewes 3 - 6w pre-mating to preferentially feed thinner ewes to utilise flushing effect → Ensure good BCS for mating

2. BWT and BCS = #1 effect on fecundity

   • Compromise between reproductive performance and efficiency (higher BWT = higher maintenance requirements)

   • Reduced fertility if BCS <2 and big -ve impact on fecundity if BCS <2.5

   • Recommendation:

     1. BCS flock q1m between weaning and mating to preferentially feed

     2. BCS at scanning to preferentially feed

     3. Ensure light ewes meet target weights of ≥55kg AND BCS 3 - 3.5 at mating (effect on fecundity plateaus at 65kg → Decreased ovulation rate when >65kg)

3. GENETICS = Big impact on fecundity

   • Introduction of Finnish Landrace = Highly fecund breed into traditional breeds to produce the maternal breed

   • Ram has less impact on fecundity (lowly heritable trait)

Describe the FIVE minor ewe factors affecting reproductive performance

4. AGE

   • Younger sheep = Lower fertility and fecundity

   • Romney lambs reach puberty at 5 - 8m (~35kg)

     • Aim ≥40 - 42kg for hoggets at mating → Mate later to ensure they reach these target weights

   • Commercial ewes culled at 5 - 7yr → Old-age poor fertility is no issue on-farm

5. REPRODUCTIVE DISEASES

   1. Phytoestrogens = Lucerne and clover (more issue with pure swards or older varieties)

      • Recommendation: Do NOT graze ewes on lucerne/clover pastures ≥3w pre-mating + during mating

   2. Zearalenone = Fungal mycotoxin that decreases fertility and fecundity

      • Can test in urine (rare)

   3. Abortive Diseases

6. AUTUMN DISEASES (breeding season)

   1. Facial eczema → Decreased feed intake

   2. Parasites

   3. Trace element deficiency (eg. selenium)

7. STRESS → Decreased fecundity and delayed ovulation

   • eg. Yarding, shearing, transport, dogs, bikes, poor weather events

EXAMPLE: In July, a farmer contacts you because the scanning % of the MA ewe flock is only 142% and they would normally expect ~180%

Based on the scanning data, the issue is reduced fecundity – only 1.6% of the ewes are non-pregnant (normal for this farm) but a higher proportion of ewes are carrying single lambs compared with previous years

Questions:

1. What ewe factors may have contributed to this problem?

2. What history questions would you ask?

1. What ewe factors may have contributed to this problem?

   1. Conception, ovulation rate, embryonic loss

   2. Nutrition prior to mating (BCS)

   3. Stress (events prior to mating)

   4. Age structure of flock (similar effect in 2-tooths?)

   5. Mating length

   6. Phytoestrogens or zearalenone

2. What history questions would you ask?

Overview of Ovine Abortion

• Prevalence

• 3 Most common DDx

Prevalence: Common (1 - 2% = ~800,000)

• Outbreaks most common due to introduction of new disease to unexposed flock

DDx:

1. Toxoplasmosis

2. Campylobacter fetus fetus

3. Salmonella Brandenburg

Toxoplasmosis

• Agent

• Lifecycle

• IP

• 4 Outcomes of infection

• Clinical signs of ewe

• PM examination

• 5 Methods of diagnosis

• 3 Methods of control/prevention

Agent: Protozoan parasite Toxoplasma gondii

• IH = Sheep (ALL mammals, birds and reptiles)

  • Mouse + cat = Maintenance cycle

  • ZOONOTIC!!!

• DH = Cat (tissue cysts can spillover from GI infection)

Lifecycle:

1. Cat (DH) infected via:

   1. Bradyzoites within tissue of IH (sheep/mouse)

   2. Sporozoites from sporulated oocysts in environment

2. Toxoplasma undergoes schizogony and gametogony → Unsporulated oocysts which are shed in faeces

3. Environment = Unsporulated oocysts undergo sporogony to produce an oocyst with 2 sporocysts each with 4 sporozoites (2 - 3d)

4. Sporulated oocyst within cat faeces ingested by IH sheep which liberates sporozoites

5. Sporozoites invade GI cells and transform into tachyzoites which can disseminate to brain, heart, lung, eye, muscle, placenta via monocytes

   • Clinical signs reflect organs infected by tachyzoites

6. Rate of division slows due to host immunity (2 - 3w) and switches to bradyzoite formation (100s of bradyzoites within a tissue cyst of ANY tissue)

7. Tissue cyst ingested by IH/DH which releases tachyzoites

IP: Long (up to 40d from infection to abortion)

Outcomes: Tachyzoites cross placenta to infect foetus

1. Non-pregnant = Lifelong immunity

   • Once infected, IH is immune to reinfection as tissue cysts with bradyzoites can periodically breakdown ⇔ tachyzoite which refreshes the parasite population and reinforces immune response

2. Early pregnancy = Embryonic death → Not pregnant at scanning

3. Mid - late pregnancy = Abortion

4. Late pregnancy = Weak lambs (immunity develops)

   • Stillbirth uncommon

Ewes: Healthy

PM:

• Strawberry cotyledons = Necrotic placental lesions with dystrophic mineralisation

• Variable appearance of foetus

  • One twin may be affected, but other appears okay (both die) as one horn affected more than the other

  • ± Mummified

Diagnosis:

1. History

   • Naive ewes (hoggets or 2-tooths) ONLY

   • Presence of ferrel cats (contamination of hay barns)

   • Low scanning% (EED)

2. Clinical signs = Overt abortion with mummified lambs and strawberry cotyledons

3. Placenta/foetal brain for histopathology → ID tachyzoites

4. PCR of aborted materials

5. Foetal heart blood OR serum titres from ewe for Ab

Control/Prevention: Farmer PPE important as zoonotic disease

1. Dispose of aborted tissue and lambs (consumed by cats to continue lifecycle)

   • No need to isolate as no sheep-to-sheep transmission

2. Vaccination with Toxovax = Live attenuated vaccine containing tachyzoites passaged through mice for many years

   • Single dose ≥4w pre-mating to maiden ewes = Lifelong immunity

   • May NOT prevent abortion if high environmental challenge with oocysts (20% may still abort)

3. Control ferrel cats

Campylobacteriosis

• Agent

  • Transmission

  • 3 Sources of infection

  • IP

• Pathogenesis

• 2 Outcomes of infection

• Clinical signs of ewe

• PM examination

• 4 Methods of diagnosis

• 3 Methods of control/prevention

Agent: Campylobacter fetus fetus = Vibrio bacterium carried in the reproductive tract of sheep

• Transmission: Spread via vaginal secretions and aborted materials (unclear what triggers this commensal organism to cause disease)

• Sources:

  1. Sheep-to-sheep transmission (high stocking density)

  2. Indirect contact (eg. gumboots)

  3. Carrier birds

• IP: 2 - 3 weeks

• NOT zoonotic

Pathogenesis:

1. Ingestion of bacterium

2. Bacteraemia and spread to the placenta

3. Necrosuppurative placentitis

4. Foetal death OR reduced neonatal viability

5. Lifelong immunity after exposure

Outcomes:

1. Abortion in last 6w of gestation (abortion storms ≤50% of flock possible)

2. Late gestation = Stillbirth or weak lambs

   • More common than toxoplasmosis

Ewe: Clinical healthy ± vaginal discharge

PM:

1. Foetus with fresh appearance

2. Necrotic target liver lesions in ¼ of aborted lambs

3. Placenta oedematous and opaque

Diagnosis:

1. History

   • High stocking density

   • Naive hoggets or 2-tooths affected

2. Clinical findings

   • Stillbirth (NOT mummified like Toxoplasmosis)

   • Necrotic liver of foetus

3. Foetal liver for histology

4. Culture of foetal stomach contents

Control/Prevention: NOT zoonotic

1. Hygiene and reduce stocking density

2. Antibiotics to manage abortion storm

3. Vaccination with killed vaccine

   • Sensitiser + booster 4 - 6w later by mid-pregnancy

   • Annual booster (most farmers ONLY give to 2-tooth ewes)

   • Can give early gestation BUT stressful for pregnancy

Salmonella Brandenburg

• Signalment

• 3 Sources of infection

• Environmental resistance

• Outcome of infection

• Clinical signs of ewe

• PM examination

• 3 Methods of diagnosis

• 4 Methods of control/prevention

Signalment: South Island sheep ONLY

• Adult ewes more likely than young ewes

• Multiples have higher incidence

• Can re-abort in subsequent years

Sources:

1. Carrier sheep in naive flock (excreted in faeces)

2. Aborted material (risk with high stocking density)

3. Vectors: Farmer, vet, vehicles, BBG, dust

Resistance: Survives 4 - 6m in environment

Outcome: Abortion storms in last 6w of gestation

• 3 - 4% of flock over 30d → Up to 50% with no treatment

Ewe: 50% aborted ewes die from necrotising metritis = Ill, dull ± enteritis

PM: Necrotic, macerated or autolysed foetus

Diagnosis:

1. History = Sick ewe (mature) with septicaemia prior to abortion

2. Tips of cotyledons to ID organism

3. Culture of foetal stomach contents

Control/Prevention: Farmer PPE important as zoonotic disease

1. Antibiotics during outbreak (prevent ewe death NOT abortion)

2. Vaccination (reduce disease, but small number of abortions still occur)

   • Salvexin+B in winter

   • Do NOT vaccinate ewes in the face of outbreak (yarding)

3. Dispose of aborted material and prevent access to BBG

4. Lower stocking density and isolate affected ewes to prevent further spread

EXAMPLE: In July a sheep farmer rings to say that they have had some abortions occur in the ewe flock

Questions:

1. What further data could you gather to help define the problem?

2. What history questions would you ask?

3. Assuming you visit the farm, what distance and clinical exams would you do?

4. What would you specifically look for in/on aborted foetuses and placenta?

5. What samples would you submit to the laboratory for further diagnostic testing?

6. What recommendations would you make for management of this problem right now (before getting lab results back)?

…

3 Reasons to examine rams for breeding soundness

1. Ensure healthy rams for sale and fit for breeding

   • Important in NZ when ram : ewe ratio is ≥1 : 100 → Must be very fit to complete task

2. Pedigree breeders require it to be accredited-free from Brucella ovis

3. Excellent opportunity for vet input on farm

3 Times when ram breeding soundness exams should be performed

1. Pre-Sale (2-tooth rams) = October - November

2. Pre-Mating = January - February

   • ≥1m pre-mating → Enough time for farmer to replace unsound ram OR make temporarily unsound ram sound (~6w for sperm to develop)

   • Only stud farms conduct single-sire mating to control genetics (vs. commercial farms with team of rams)

3. In response to a problem = Low scanning%

List 4 differences between ram vs. bull breeding soundness

1. Smaller = Examination is easier, faster and safer (more common for vets to check rams)

2. Main problems = Epididymitis, congenital defects and poor health

3. Penis/prepuce abnormalities are rare in rams (do NOT need routine checking)

4. Pedigree rams must be vet-checked pre-sale and accredited free from Brucella ovis

Describe 3 (6) steps of the ram breeding soundness examination

FOUR T’s

TEETH and TOES

1. Clinical history = Signalment, health, reproductive history and future use

2. Physical examination = Lameness (ability to mount), BCS and free from disease (eg. flystrike, FE, parasites)

   • Pre-breeding ram aim BCS 3.5 - 4/5

TESTICLES

3. Genital examination = Systematic evaluation of scrotum and its contents (scrotum → head of epididymis → testicles → tail of epididymis)

   1. Size

   2. Tone/consistency

   3. Symmetry

   4. Lesions (scrotal skin and wool)

TESTOSTERONE

4. ± Semen evaluation

   • Not routine for rams as there is goof correlation between appropriately sized, firm testicles, free of defects AND good sperm production

5. Mating ability (bulls)

6. Other tests eg. B. ovis

ONE: Testicle Size

• Importance

• Pre-sale diameter aim

• Pre-breeding diameter aim

Importance: Directly proportional to amount of sperm produced (1g testes = 20M sperm)

• Judgement call (unsure → recheck several weeks later) as highly variable due to seasonal atrophy

Pre-Sale (15m): ≥28cm diameter

Pre-Breeding (MA): > 32cm

TWO: Testicle Tone

• Importance

• Normal

• 4 Causes of soft testes

Importance: Good indicator of sperm production

• Sperm takes 6 - 8w to develop and mature → Soft testes in January (unsound) may not recover in the breeding season

Normal: Flexed bicep

Causes of Soft Testes:

1. Out of season

2. Over-heating (eg. long wool over scrotum)

3. Poor health (infection → febrile)

4. Malnutrition and low BCS (eg. parasites)

FOUR: Lesions

• 3 DDx for epididymitis

• 6 Congenital reproductive defects

• 2 scrotal DDx

• Main penis/prepuce DDx

Epididymitis: Enlarged and hardened epididymis (head/tail)

1. Brucella ovis

2. G- pleomorphs

3. Vasectomy (surgical disruption of tubes → sperm leakage)

Congenital: 1 - 5% of rams at pre-sale

1. Monorchid = ONE testicle develops

2. Cryptorchid = Partially descended testis

3. Asymmetrical testis size = Hypoplasia of ONE testicle

4. Segmental aplasia = Missing bits, usually epididymes)

5. Micro-orchid = Tiny testis

6. Hypospadia = Urethral NOT at the tip of the penis

Scrotal:

1. Scrotal mange (Chorioptes bovis)

2. Scrotal abscess following shearing cuts

Penis/Prepuce: Balano-posthitis = Pizzle rot (feed → highly alkaline urine → inflammation of penis

Pathogenesis of epididymitis

1. Disruption of tubular epithelium by pathogen

2. Inflammatory reaction causes leakage of sperm into interstitium

3. Sperm outside the testes = Foreign body reaction (haploid cells)

4. Chronic granulomatous inflammation with fibrosis → Obstructed tubules

5. 2˚ testicular atrophy (orchitis rare)

Brucella ovis

• Transmission

• 4 Sources of infection

• Diagnosis

• Treatment

Transmission: Bacterium shed in semen and spread via direct contact between rams

• Ram → Ewe → Ram

Sources: Infected ram

1. Newly purchase ram

2. Leased ram contracted to another farm

3. Neighbouring farms

4. Transport of rams from different locations → Ram from accredited free farm can still carry brucella ovis)

Diagnosis: Serology to detect Ab (CFT)

• Rams with epididymitis require separation and screening with blood test to rule out B. ovis

• Pedigree breeders must be accredited free from B. ovis (tested annually) and commercial farms should aim to be free → Reduced ram wastage and superior reproductive performance

Treatment: Cull and eradication programme (ram with B. ovis continues to secrete organism for up to 2yr)

Gram Negative Pleomorphs

• 2 Agents

• Source of infection

• Transmission

• Diagnosis

• Treatment

Agents:

1. Actinobacillus seminitis

2. Histophilus ovis

Sources: Widespread in environment

Transmission: Gain entry into urogenital tract by retrograde urethral infection around puberty

• Unknown risk factor

Diagnosis: Identified in rams pre-sale (1 - 10%)

• Diagnosis of exclusion (must test for B. ovis)

Treatment: Cull, but no eradication programme required

Scrotal Mange

• Agent

• Pathogenesis

• Clinical appearance

• Treatment

Agent: Chorioptes bovis mite

Pathogenesis:

1. ALL rams carry small proportion, but some develop an allergic hypersensitivity reaction

2. Inflammation and heat → Reduced sperm output

3. 1/3 of testicle must be affected to reduce fertility

4. → Temporarily unsound

Clinical Appearance: Scrotum with crusty lesions

Treatment: Ectoparasiticides (OP or ML)

Pizzle Rot

• Signalment

• Agent

• Pathogenesis

• 4 Sequelae

Species: Balanoposthitis most commonly in wethers (occasionally in rams and bulls)

Agent: Urease-producing Corynebacterium renale

Pathogenesis:

1. High-protein diet (eg. clover-dominant pasture)

2. → High urinary urea is broken down by C. renale to cytotoxic ammonia

3. Preputial ulceration and 2˚ bacterial infection

Sequelae:

1. ± Extensive balanoposthitis with ulceration and necrosis of head of penis due to obstruction of the preputial orifice

2. Phimosis

3. Inability to serve

4. ± Death from urinary obstruction (post-renal azotaemia)

How to classify rams during a breeding soundness exam

NEVER certify as fertile (use sound/temporarily unsound/unsound)

• Unsound rams can still be fertile

  • eg. lesion in ONE testicle with SECOND normal testicle (still get ewe pregnant)

  • Unsound from commercial perspective (pedigree breeders should never sell and unsound ram)

Classification:

• Sound = Ram with no physical or genital defects who is considered sound for breeding or sale

• Temporarily Unsound = Ram with physical or genital defects which can be completely resolved BUT currently unsound for breeding or sale

• Unsound = Ram with permanent physical or genital defect who is not sound for breeding or sale

Classify the following rams as sound, temporarily unsound or unsound

1. Scrotum with crusty lesions on bottom half

2. Soft testes with small scrotal circumference

3. Right testicle significantly smaller than left testicle

4. BCS 2/5

5. Testes with lots of wool on scrotum

1. Scrotum with crusty lesions on bottom half = Temporarily unsound (scrotal mange)

2. Soft testes with small scrotal circumference

   • Temporarily unsound (out of season)

   • Unsound if at pre-mating (not enough time for recovery)

3. Right testicle significantly smaller than left testicle = Unsound (but fertile)

4. BCS 2/5 = Unsound (insufficient time to gain BCS for mating)

5. Testes with lots of wool on scrotum = Temporarily unsound

Define “ill-thrift” for lambs vs. adults

Lambs = Poor growth rates

Adults = Poor BCS and/or weight loss

6 Benefits of reaching target liveweights for lambs

Reach slaughter weights faster → Fewer days on-farm

1. Superior schedule prices

2. Less cost associated with dagging, feeding and treatments

3. Reduces parasite burden on-farm

4. More feed partitioned to breeding ewes or other livestock classes

Replacement ewe lambs mature earlier

5. Opportunity to breed as ewe hoggets (≥42kg)

6. Superior growth as 2-tooths → Lifelong reproductive performance

Lamb Growth Rates

Time	Ill-Thrift	Target	Maximum
Pre-weaning
Post-weaning
Average GR throughout life

Time	Ill-Thrift	Target	Maximum
Pre-weaning	<250g/d	300g/d	400g/d
Post-weaning	<50g/d	250g/d on crops (realistic = 150g/d on pasture)
Average GR throughout life	100g/d

3 Times when a farmer will identify ill-thrift in lambs

1. Routine weighing (begins at weaning)

   • Frequency varies between farmers

2. Observation #1

3. Slaughter records (eg. % slaughtered at weaning in March)

→ Retrospective and vague data

List 7 DDx for ill-thrift in young livestock

1. Inadequate nutrition (quality and/or quantity)

2. Internal parasites

3. Trace element deficiencies (Co and Se)

4. Pneumonia

5. Facial eczema

6. Flystrike

7. Ryegrass staggers

*Whole mob issues

3 Methods of diagnosis of undernutrition

1. History

2. Pre- and post-grazing covers (sward sticks)

3. Feed quality by eye or lab testing

Difficult to diagnose → Diagnosis of exclusion

Pneumonia

• Seasonality

• Geographical distribution

• Infectious agents

  • 3 Bacteria

  • 2 Viruses

• Pathogenesis

• 2 Forms

  • Clinical signs

  • PM lesions

• 5 Risk factors

• 4 Methods of diagnosis

• Treatment

• 8 Methods of prevention

Seasonality: Summer/autumn (December - May)

Distribution: Increasing prevalence in Northern regions

Agents: Complex with many pathogens

• Bacteria = Mannheimia haemolytica, Pasteurella multocida and Mycoplasma ovipneumoniae

• Viruses = Parainfluenza virus-3 and respiratory syncytial virus

Pathogenesis: Requires respiratory defence mechanisms to be overwhelmed with inciting damage for some pathogens to invade

1. Young sheep have reduce immunity which is further exacerbated by stressors associated with yarding = Long distance from paddocks → Crowded into dusty yards

2. Heat stress induces open-mouth breathing and dust inhalation → Air bypasses defence mechanisms (nasal turbinates and mucociliary apparatus)

3. Viruses and Mycoplasma invade which compromise lung defences

4. Allows Pasteurella and Mannheimia to colonise lung = Commensal URT species

   • Cannot diagnose disease with nasal swab

Forms:

Chronic Non-Progressive Pneumonia (CNPP)

Clinical Signs: Slowly progressive and mild

1. Reduced GR when >20% lung affected

2. Cough

PM:

1. Consolidation of cranioventral lung lobes

2. Pleuritis/pleurisy which can persist as adults = Adhesions between lung and thorax → Reported at meatworks

3. Occasional chronic lung abscess

Acute Fibrinous

Clinical Signs: Severe and acute

1. Outbreaks of coughing

2. SICK animals

3. Sudden death

PM:

1. Severe fibrinous pleuritis

2. Dark red, solid lung lobes

Risks: Stress and yarding

1. Shearing and weaning on SAME day (running up and down fence lines)

2. Shearing lambs twice (shed overnight)

3. Frequent yarding post-weaning (eg. drenching)

4. Motorised mustering

5. Increased age of lambs at slaughter

Diagnosis:

1. History (esp. management)

2. Clinical signs

   • Mild

   • Moderate = Coughing and ill-thrift

   • Severe = Sudden death

3. Necropsy (esp. for poor BCS lambs)

4. Slaughter records for pleurisy

Treatment: NONE for CNPP

• Antibiotics useful for early stage acute fibrinous form to prevent lamb death

Prevention: NO vaccination (commensal bacteria)

1. Allow time post-weaning before shearing

2. Minimise number of shearing times

3. Muster in early morning

4. Slower and calmer yarding (minimise use of dogs)

5. Minimise time in yards

6. Keep dogs tied up while in the yards

7. Sprinkler system to dampen dust

8. Scrape concrete base of faeces and dust

Define “Wastage”

• Natural lifespan of sheep

• Age at culling

• 2 Causes of early death

Wastage = Loss of ewes from flock BEFORE the end of their productive lifetime

Natural Lifespan: 10 - 13yr

Age at Culling: 5 - 7yr

• Only 10 - 30% of ewes make it to 6yrs

Causes: Low BCS associated with increased wastage

1. Premature culling

2. ~7% mortality (most risky period = lambing)

4 Reasons why BCS is superior to BWT

Minimises issues of:

1. Skeletal size between and within breeds

2. Physiological status (pregnancy = ewe weight + foetal weight)

3. Gut fill

4. Fleece length and wetness

4 Times to BCS sheep

Must encourage farmers to BCS ewes

1. Post-shearing (accurate by eye at the drafting gate)

2. Weaning = Lowest BCS

3. 6w Pre-mating (mid-Feb) → Influences fecundity and fertility

4. Pregnancy scanning (6w pre-lambing)

ID during yarding and may have progressed for some time (4 - 5 yardings/yr)

What does the animal welfare code say about sheep BCS?

Vague = All sheep should be BCS 3 - 4 and any sheep BCS ≤ 1 requires urgent remedial action (euthanasia OR feeding)

• Minimum Standard No. 5 on the Code of Welfare for Sheep and Beef Cattle

Describe the typical BCS distribution of NZ sheep

Normal distribution

• ~50% optimal (BCS 3 - 4)

• 30% borderline (BCS 2.5)

• Tail-end = BCS 2

Event well-managed farms will have ewes with low BCS

List 4 times when a vet will intervene with BCS

1. Farmer concerned about ewes with extremely low BCS

2. More ewes at tail-end (BCS 2)

3. Flock average BCS is lower than expected

4. Investigation of welfare complainy by MPI

DDx for Ill-Thrift in Ewes = Low BCS

• 4 Treatable DDx

• 2 Fatal DDx

• 3 DDx where they do okay if fed well

Treatable:

1. Undernutrition

2. Parasitism = Likely symptom of low BCS rather than cause

3. Liver fluke

4. Foot disease/lameness

Fatal:

1. Johne’s disease

2. Intestinal carcinoma

Okay if Fed:

1. Dental disorders

2. Chronic FE?

3. Lung disease/abscess

Dental Disorders

• Importance

• Function of incisors vs. molars

• Diagnosis

• Treatment

Importance: Major reason for culling as important cause of ill-thrift

Function:

• Incisors = Cut grass with dental pad

• Molars = Flat surface for grinding

Diagnosis: Easy to examine incisors

• Impossible to examine molars due to sharp cheek teeth, narrow dental arcade and tight cheek muscles

• Severe → Palpable osteomyelitis and tooth root abscess

Treatment: Revise culling policy

Johne’s Disease

• Agent

• Signalment

• Clinical signs

• Pathogenesis

• PM lesions

• Prevention

Agent: Mycobacterium paratuberculosis

Signalment: >18m (long IP)

Clinical Signs: Poor BCS and generalised oedema

• Otherwise normal temperature, hydration and rumination rate

• Usually over winter and spring due to poorer nutrition and added stressors of pregnancy and lactation

Pathogenesis: Chronic granulomatous enteritis → Intestinal malabsorption

PM: Assess ileocaecal junction for thick and corrugated ileal mucosa + enlarged mesenteric lymph nodes

• Collect terminal ileum, liver and mesenteric lymph nodes for histology when in doubt

Prevention: Vaccination available to reduce shedding ONLY

DDx?

Small intestinal adenocarcinoma (1% of old ewes)

• Variable appearance, but usually jejunal area

• Fatal

DDx? Significance?

Chronic facial eczema = Fibrosis and end-stage liver disease

• May not have a big impact on ill-thrift (often incidental at PM)

Significance of lung abscesses on ill-thrift

Consequence of lamb pneumonia but no data on effects on ill-thrift (presumed)

• May rupture → Sudden death

Significance of nematode parasites on ill-thrift

Thin ewes have high FEC likely a CONSEQUENCE of ill-thrift (i.e. reduced immunity) rather than a case

• Low BCS → Poor health and immunity → Reduced immunity → Increased worm burden

• Recommend drenching thin ewes with high FEC

DDx for Sudden Death

• Young sheep (13)

• Adult sheep (14)

YOUNG SHEEP

Infectious:

1. Clostridial

2. Acute fibrinous pneumonia

3. Leptospirosis

4. Haemophilus

Parasites:

5. Haemonchosis

6. Other nematodes

7. Acute liver fluke

Nutritional/Metabolic:

8. Intestinal torsion (redgut)

9. Acidosis

10. PEM

Other:

11. Toxicity

12. Climatic/misadventure (eg. hypothermia, lightening strike, drowning, stuck in fence, dog attack)

13. Anthrax (exotic)

ADULT SHEEP

Infectious:

1. Salmonellosis

2. Clostridial

3. Listeriosis

Parasites:

4. Haemonchosis

5. Other nematodes

6. Acute liver fluke

Nutritional/Metabolic:

7. Ketosis

8. Hypocalcaemia

9. Hypomagnesaemia

10. Acidosis

11. PEM

Other:

12. Toxicity

13. Climatic/misadventure (eg. hypothermia, lightening strike, drowning, stuck in fence, dog attack)

14. Anthrax (exotic)

MANY DDx → Requires thorough investigation and PM highly recommended

• MUST put short-term plan in place BEFORE leaving farm and often before DDx confirmed

4 Signs indicating a carcass is too autolysed for necropsy

1. Extremely bloated (bubbles of gas from anus)

2. Skin sloughing

3. Blue/green colour (esp. groin)

4. Smell

Enteric Salmonellosis

• Agents

• Source of infection

• Transmission

• Signalment

• Seasonality

• Prevalence

• 2 Risk factors

• 6 Clinical signs

• 5 PM features

• 2 Methods of diagnosis

• 3 Treatments

• Prognosis

• 3 Recommendations when dealing with an outbreak

• 2 Methods of prevention

Agents: Salmonella Hindmarsh, Typhimurium, Bovismorbificans

• Brandenburg → Abortive

Source: Carrier sheep (commensal in intestines)

Transmission: Faecal-oral

Signalment: Adult ewes (often well-fed with good BCS)

• Extremely rare in ewe hoggets

Seasonality: December - July (intensive grazing)

Prevalence: 1 - 2%/yr?

Risks:

1. Stress → Shedding (eg. shearing, yarding, transport)

2. High stocking density (eg. break-feeding or set-stocking)

Clinical Signs: Progression over 2 - 3d

1. Lethargy (lagging behind mob)

2. ± Fever (≥40.2˚C) but may be hypothermic due to recumbency

3. Khaki green and watery diarrhoea with mucus

4. Dehydration

5. Injected MM

PM:

1. Fatty liver (mobilisation of fat due to anorexia)

2. Large gallbladder (anorexia → not excreting bile)

3. Enteritis = Inflammation of intestine and abomasum with watery contents

4. Petechial haemorrhage of serosal surfaces

Diagnosis:

1. Culture after 24 - 48hr (growth ≠ diagnosis)

2. Histopathology up to 1w later

Treatment:

1. Antimicrobials (if not too sick and well-monitored)

2. Supportive care (PO fluids)

3. Euthanasia

Prognosis: 50%

Outbreak Management:

1. Reduce faecal-oral transmission = Move to new paddock and reduce stocking density

2. Vaccination = Death stops in 10d

   • Do NOT vaccinate sick sheep (immunity develops slower than disease progression)

3. Warn farmer of zoonosis

Prevention:

1. Reduce risk factors

2. Vaccinate ewes BEFORE risk period (weaning in November - December)

   • Sensitiser and booster 4w apart → Annual booster

Enterotoxaemia (“Pulpy Kidney”)

• Signalment

• Seasonality

• Pathogenesis

• 2 Clinical signs

• 6 PM lesions

• 2 Methods of diagnosis

• 2 Recommendations when dealing with an outbreak

• Long-term preventative method

• Recommendation if dam is not vaccinated

Signalment: Well-fed lambs ≤6 - 8m (largest of the mob)

• Uncommon in cattle and deer

• Vaccinated dam → MDA in lambs for 8 - 16w

• Most common in unvaccinated weaned lambs (dams ARE vaccinated)

Seasonality: Summer and early autumn (may coincide with weaning or change in feeding for finishing)

Pathogenesis:

1. Good nutrition/excess CHO → Additional nutrition for bacterial

2. Proliferation of Cl. perfringens Type D in gut which produces epsilon toxins

3. Toxins absorbed into bloodstream

4. Vascular endothelial damage and generalised vasculitis throughout body

   • Most damage in organs with highest blood flow = Kidneys and brain

Clinical Signs:

1. Sudden death of unvaccinated lambs on good quality feed

2. Signs of agonal struggle (pain = Struggle marks from feet, foam from nostrils and head thrown back)

PM:

1. Rapid carcass decomposition and bloating

2. Excess pericardial fluid and fibrin clots

3. Petechial and ecchymotic haemorrhage over serosal surfaces of intestine and heart

4. Pulpy kidney 1 - 2hr PM (NOT pathognomonic)

5. Glucosuria

6. Focal symmetrical encephalomalacia = Pathognomonic

Diagnosis: History and clinical signs →

1. Necropsy of several lambs

2. ± Confirmatory test ($) = Histology of brain and kidney

   • Detection of epsilon toxin from ileal contents (BUT also found in 20% of healthy animals)

Outbreak Management:

1. Reduce feed quality short-term

2. Vaccination in face of outbreak (deaths stop within 2d)

Prevention: Routine vaccination with toxoid (5in1, 7in1 or 10in1)

• Ewes: Sensitiser + booster 4 - 6 weeks later

  • Booster 3 - 4 weeks pre-lambing (peak at colostrogenesis)

  • Take average of mob due to difference in lambing date

  • NOT recommend at set-stocking (1 - 2 weeks pre-lambing)

• Young lamb: Maternal Ab lasts ~8 - 12 weeks (depends on vaccine) until weaning

  • Weaned replacement lambs: Sensitiser at docking or weaning then booster 4 - 6 weeks later

  • Weaned non-replacement lambs: Decide whether to vaccinate, depending on length of time to sale/slaughter

    • Disease often observed as farmers do not vaccinate lambs destined for slaughter in a few months

ALTERNATIVE if Dam NOT Vaccinated:

1. Lambs given tetanus anti-toxin and pulpy kidney toxoid at docking (”Lamb vaccine” or “PK-Anti-tet”)

   • Tetanus #1 risk after docking

2. Lambs then given 5in1 at weaning and booster 4 - 6 weeks later

List 3 essential vaccines on sheep farms

1. Toxoplasma

2. Campylobacter

3. Clostridia (cheap)

4. ± Scabby mouth (if on farm)

Other vaccines (eg. Salmonella) depends on risk-benefit analysis

Prevalence of metabolic diseases in sheep

1. High-producing commercial farms (esp. crops)

2. Lifestyle farmers due to overfeeding

Risk: Underfeeding OR overfeeding

• Associated with major physiological challenge to animal (eg. ewes with triplets or high-producing cows pushed to max)

• Body good at deal with challenge due to homeostasis UNLESS acute/extreme (livestock at risk but not everyone affected)

• Sheep will NOT abort in the face of a metabolic disease (prioritise growth of foetus)

Describe the 2 differences between cattle and sheep metabolic disease

1. Hypomagnesaemia uncommon in sheep

2. Ketosis = Pregnancy toxaemia, sleepy sickness or twin lamb disease in sheep

   • Cattle = At calving or peak lactation

   • Sheep = Late pregnancy → x2 energy requirements and lower feed intake

     • BUT further risk factors required to precipitate metabolic disorders (homeostatic mechanisms prevent disease)

List 6 risk factors for metabolic disease in ewes

1. Old = More foetuses (fecund) and reduced skeletal supply of Ca due to multiple lambings

2. Multiple foetuses

3. Sudden feed restriction or diet change (eg. yarding for set-stocking)

   • eg. Triplet ewes set-stocked on high-quality pasture (eg. Italian ryegrass) from annual ryegrass

4. Falling plane of nutrition

5. Concurrent disease (eg. poor dentition or lame)

6. Inclement weather and inadequate shelter (seek shelter → reduced feeding)

Pathogenesis of ketosis vs. hypocalcaemia

KETOSIS

1. Hypoglycaemia

2. Catabolise fat reserves for gluconeogenesis

3. FFA enters circulation resulting in fatty liver

4. FFA also used for acetyl-CoA production BUT shortage of oxaloacetate

5. → Ketone production and hyperketonaemia

HYPOCALCAEMIA

• Ca2+ metabolism complex

• Late gestation ewes cannot meet Ca2+ requirements from diet

  • Up to 20% bone Ca2+ mobilised during pregnancy

  • When foetal demand exceeds diet and bone Ca2+ → Hypocalcaemia

Clinical signs of ketosis vs. hypocalcaemia

Similar Presentation: Time period = 24 - 48hr depending on severity

1. Separation from flock, reluctance to move and weak

   • Paresis and will not running away from farmer

2. Neurological signs

   • Depressed and apparent blindness

   • Recumbent, comatose, die

Differences:

• Hypocalcaemia = Ruminal tympany

• Ketosis = Wool plucks easily

Biochemistry features of ketosis vs. hypocalcaemia

KETOSIS

1. Hyperketonaemia = Increased BOH (handheld ketometer)

2. Ketonuria (dipstick)

3. Decreased BUN

4. Increased cortisol

5. ± Hypoglycaemia

6. ± Hypocalcaemia

HYPOCALCAEMIA

1. Hypocalcaemia (cannot measure on-farm)

2. ± Hyperketonaemia

Often ewes with ketosis ALSO have low Ca2+ and visa-versa

4 Ways to differentiate ketosis from hypocalcaemia

1. Blood test BEFORE treatment

2. Ketostix, handheld ketometer and wool pluck → Ketosis

3. Supplement with calcium regardless

   • Rapid response = Hypocalcaemia

   • No response = Ketosis (± euthanasia and necropsy)

4. Necropsy

   • Ketosis = Fatty liver and large adrenal glands with dark cortex

Treatment of ketosis (5) vs. hypocalcaemia (2)

KETOSIS

1. IV dextrose ± PO propylene glycol

2. PO rehydration (or IV if high-value sheep)

3. SC Ca2+

4. Flunixin

5. ± Caesarean section (lifestyle block)

Do NOT place in nursing situation (reduces grazing as no grass and way from flock)

HYPOCALCAEMIA

1. IV Ca2+ with care ± SC or PO

2. PO propylene glycol

Prognosis of ketosis vs. hypocalcaemia

KETOSIS

Irreversible if not treated early

• Recumbent, neurological signs or renal failure = Poor prognosis

HYPOCALCAEMIA

Excellent prognosis if uncomplicated

List 3 most important sheep skin conditions

1. Facial eczema (see “Systemic Diseases”)

2. Scabby mouth

3. Flystrike (see “Parasitology”)

Effects of acute vs. chronic facial eczema

Acute: Major reduction in growth and reproductive performance (eg. ewes in mating season)

Chronic: Unknown effects of liver fibrosis

Scabby Mouth (Orf)

• Agent (+ environmental resistance)

• Transmission

• 3 Clinical signs

• Treatment

• Prevention

Agent: Parapox virus

• Highly resistant in environment (persists for 1yr)

• ZOONOTIC!

Transmission: Penetrates skin through abrasions

• Mainly lambs (soft mouths) eating thistles or other rough feed

Clinical Signs:

1. Proliferative, solid lesions around mouth ± feet

2. Reduced GR due to reduced eating

3. ± 2˚ bacterial infection in wet conditions

Treatment: Self-limiting

Prevention: Vaccination with live vaccine scratched into axilla or groin → Cause disease at site that is NOT going to affect production

• Recommend ONLY if farmer had disease (otherwise introducing virus onto naive farm)

• SINGLE dose to lambs at docking

• Check lambs 1w after to assess for scabs

Importance of lameness (2) + 4 times of vet involvement

Importance:

1. Transport limitations (>10% sheep lame at works → Fine)

2. $ to treat and control (early treatment important for quick resolution)

Vet Involvement:

1. Ram soundness exams

2. Pet sheep and goats

3. Bad flock problems (10 - 15% flock influenced)

4. Transport (NO certificates for sheep)

7 DDx for ovine lameness

ALL ovine lameness in the foot:

1. Ovine interdigital dermatitis (OID)

2. Footrot

3. Foot abscess

4. Toe granuloma

5. (Arthritis - esp. old pet sheep)

   • NOT commercial sheep

6. (White line disease)

7. (Shelly hoof)

Describe the pathogenesis/progression of ovine foot disease

1. Moisture/predisposing factors (eg. trauma to skin)

   • Autumn and spring (wet)

2. Invasion of interdigital skin by Dichelobacter nodosus

   • Hoof damage rare as light weight (vs. cattle)

3. Ovine interdigital dermatitis (OID) = Mild to moderate dermatitis which is easy to treat as a superficial bacterial infection

4. →

Foot Abscess via infection with Trueperella pyogenes

• Initial bacterial infection allows T. pyogenes to invade and penetrate the interdigital skin → JOINTS

Footrot via deeper infection by Dichelobacter nodosus

• Bacteria erodes hoof wall

Dichelobacter nodosus

• Source

• Environmental resistance

• 3 Risk factors

Source: Anaerobic an present on most NZ farms

Environment: ONLY survives in ruminant feet (environmental survival of 5 - 7d)

Risks:

1. Virulence of D. nodosus strains (some farms never see footrot as only have benign strains)

2. Susceptibility of host

   • Coarse-wool sheep (90%): Usually OID, but footrot uncommon

   • Fine-wool sheep eg. Merinos (and goats): Footrot can be major problem

   • Farmers deal with footrot via culling → Indirect selection for high footrot tolerance

3. Wet conditions

Diagnosis of ovine foot disease

History and clinical findings

• Vets rarely involved but should be (improper treatment or ID of cause)

• Lab diagnosis NOT useful as culture commensal bacteria

Ovine Interdigital Dermatitis (OID)

• 2 Clinical signs

• Treatment

Clinical Signs: MAY resolve spontaneously in dry conditions

1. Superficial and mild infection = Erythema and moisture of interdigital space

2. Mild - moderate lameness

Necessary precursor for foot abscess/footrot

Treatment: Topical antibiotics (blue spray = oxytetracycline) OR footbath

• Ideally place in drier environment BUT typically indoors → Reduced grazing

• Ideally multiple treatments of blue spray but not feasible on large farm

Footrot

• Pathogenesis

• 4 Clinical signs

• 3 Treatments

• 4 Methods of prevention

Pathogenesis: Deeper penetration of D. nodosus which produces keratolytic proteases to dissolve the hoof wall → Hoof destruction and under-running

• Severity depends on virulent and chronicity (i.e. mild footrot = OID → Continuum of disease)

Clinical Signs:

1. Moderate - severe lameness

2. Obvious hoof under-run on examination

   • Broken skin horn junction which extends under the horn tissue of the heel

   • Soft horn is separated from underlying sensitive tissue

   • Hard horn in anterior part of sole under-run

   • Untreated cases can become chronic and severe with deformation of the hoof horn

     • ± Flystrike

     • Never grows back normally

3. Small amount of black necrotic tissue (no pus) = Degraded hoof wall

4. Foul smell

Treatment:

1. Antibiotics (topical AND injectable) = Injectable penicillin/oxytetracycline and blue spray

   • Past: Footbath of formalin BUT Lame foot never touches bath

   • 80 -90% recover with SINGLE dose of antibiotics

2. Trim hoof exposing anaerobic bacteria to air and kill (1 week after antibiotic treatment)

   • Difficult follow-up on commercial farm

3. Analgesia

4. Keep in dry environment

Prevention: Eradication feasible BUT difficult in NZ conditions

1. Foot bath with zinc sulphate

   • Useful for superficial infection (OID) → Preventing footrot

   • Difficult to do well (footrot = hold up lame foot)

   • “Cure rates” for footrot 30 - 50% with foot bathing ONLY (not effective treatment)

2. Keep in dry paddock where possible

3. Vaccine: Footrot ~14w protection

4. Culling (tolerance for footrot is heritable)

Foot Abscess

• Agent

• Signalment

• 3 Treatments

Agent: Trueperella pyogenes infection 2˚ to OID which allows breach of skin integrity of the interdigital space

Signalment: Heavy ewes and rams

• Small number of severely lame animals (non-weight bearing)

Treatment: Difficult as most cases are advanced

• Cannot insert scalpel to drain as vital structures around foot

1. Do nothing → recovery in 1 - 2m (ankylosis and bone fusing BUT very painful and welfare concern)

2. Consider culling as single dose of antibiotics not effective

3. Amputation of affected digit if appropriate

Toe Granuloma

• Cause

• 2 Clinical signs

• Treatment

Cause: Toe damage when haemorrhage occurs at trimming (overzealous)

• Common for goats and lifestyle sheep

Clinical Signs:

1. Proud flesh (excessive granulation tissue) with hoof growing around → Pinching

2. Moderate to severe lameness

Treatment: Difficult

• Ideally trim horn, amputate, cauterise, aftercare (regular bandaging)

Describe the role of foot trimming

• Past: Frequently used to treat footrot BUT inappropriate

  • Use antibiotics

  • Over-zealous trimming = Toe granuloma

• Useful when:

  1. Hoof is so over-grown it is causing lameness

  2. Hoof shape accumulating debris (white line accumulating pockets of debris)

• Common trimming in goats but less common now in sheep farms (culling main treatment option)

9 DDx for neurological disorders of sheep

1. Listeriosis

2. Brain and spine abscess

3. Polioencephalomalacia (PEM)

4. Tetanus

5. Ryegrass staggers

6. Congenital disorders (eg. Border disease)

7. Metabolic disease (eg. hypocalcaemia, ketosis, hypomagnesaemia)

8. Scrapie*

9. Maedi-visna*

*Exotic

List 7 neurological features to assess on distance and physical exam

Symmetrical vs. asymmetrical neurological changes → Drive DDx list

1. Head carriage (tilting, asymmetrical drooping of lips, ears, nose)

2. Tremours

3. Gait, circling, recumbency

4. Response to humans (lack of awareness of humans = ketosis)

5. Nystagmus

6. Cranial nerve reflexes (eg. response to pinching both nostrils and menace response)

7. Withdrawal reflex (pinch interdigital skin)

History features of:

1. Listeriosis

2. Brain abscess

3. Spinal abscess

4. PEM

5. Ryegrass staggers

6. Scrapie

	Signalment	Additional History	Number affected	Clinical Signs
Listeriosis	Adult sheep	Fed poor quality silage	Small number	Unilateral CNS deficits
Brain Abscess	Adult ram	Head-butting wounds	ONE	Unilateral CNS deficits but BAR
Spinal Abscess	Young pet lamb (2 - 3w)	No colostrum	Small number	Progressive bilateral HL paralysis but BAR
PEM	Post-weaning	Change in fibre content OR high sulphur	Several	Bilateral and generalise neurological signs
Ryegrass Staggers	Grazing animals	Hard grazing in summer/autumn	Individuals	Head tremours and staggering with stimulated
Scrapie	Adult sheep	Exotic	Sporadic	Slow and progressive neurological signs

Listeriosis

• 4 Clinical signs

• Treatment

• Prognosis

• Prevention

See “Systemic Disease” for aetiopathogenesis

Clinical Signs: Slowly progressive (BUT often not observed by sheep farmer)

1. Found dead

2. Depression and anorexia

3. Excessive salivation

4. Unilateral neurological deficits

   • Facial paralysis (ear drooping and less movement in one nostril)

   • Circling in ONE direction

Treatment: High dose penicillin EARLY in disease process

• Monitor flock to observe early signs of disease (outbreak unlikely)

Prognosis: Poor (micro-abscesses in brain → euthanasia)

Prevention: Prevent remaining flock from eating poor quality silage

Brain Abscess

• Pathogenesis

• 2 Clinical signs

• Treatment

• Prevention

Pathogenesis: Bacteria gain entry from head wounds via fighting → Large unilateral brain abscess

Clinical Signs:

1. Unilateral neurological deficits

   • Circling

   • Facial paralysis

2. Otherwise BAR (± depression)

Treatment: Euthanasia

• Once showing clinical signs, treatment NOT effective (cannot use antibiotics to clear abscess)

Prevention: Difficult to prevent rams from fighting

Spinal Abscess

• Pathogenesis

• 2 Clinical signs

• Treatment

Pathogenesis:

1. Poor colostrum intake → Failure of passive transfer of immunity

2. Infection via umbilicus

3. Bacteraemia

4. Spinal abscess and compression of spinal cord

5. Abscesses throughout body (eg. liver, lung, kidneys)

Clinical Signs:

1. Progressive bilateral HL paralysis ± FL (depending on location of lesion)

   • No withdrawal reflex of HL

2. Otherwise BAR

Treatment: Euthanasia (poor prognosis)

PEM

• 4 Clinical signs

• Treatment

For aetiopathogenesis, see “ Systemic Diseases”

Clinical Signs:

1. INITIAL: Apparent blindness and isolation (no response to humans)

2. Nystagmus

3. ± Dog-sitting with head back (“star gazing”) to relieve pressure from cerebral oedema

4. → Lateral recumbency, opisthotonos, seizures and death (3d progression)

Treatment: Rapid response to IV vitB1 → IM

Prognosis: Excellent (if treated before irreversible cerebral necrosis)

• Response to treatment aids diagnosis

Transmissible Spongiform Encephalopathy (“Scrapie”)

• Agent

• 2 Clinical signs

• 2 Methods of surveillance

Agent: Prion protein (exotic to NZ)

• Long IP

Clinical Signs: Slowly progressive

1. Pruritic and nibbling form

2. Incoordination form

Surveillance: Prove to trading partners we are free from scrapie

1. Active = Random histology of brains at meatworks

2. Passive = Vet submits brain to lab when suspicious of disease

   • Monetary incentives for vet and farmer

Ovine Infectious Keratoconjunctivitis (“Pinkeye”)

• 2 Agents

  • Severity

  • Source

• Morbidity

• 4 Progressive clinical signs

• 3 Treatments

• Prevention

Agent: NO cell wall → Different AB requires to cattle

1. Chlamydia = Self-resolving when mild

   • Source: Dust, wind and flies → Irritation to eye

   • More common in summer/autumn (yarding and dry/stalky grass)

2. Mycoplasma = More severe ± recurrence

   • Source: Carrier sheep, transmitted by direct contact and fomites (dry/stalky grass)

Morbidity: 10 - 20% (highly contagious)

Clinical Signs: Unilateral OR bilateral

1. Red sclera with mild tear-staining

   • → Spontaneous resolution OR

2. Progression to corneal oedema and severely red sclera

3. Apparent blindness

4. Pus in eye → Rupture

Treatment: Cattle penicillin-based pinkeye treatments are NOT effective in sheep

1. Spontaneous resolution (eg. mild Chlamydia)

2. Oxytetracycline diluted in spray bottle (Chlamydia and Mycoplasma)

3. Oxytetracycline SC/IM (Mycoplasma)

Prevention: Isolate affected animals (yarding increases transmission)

Entropion

• Signalment

• Clinical signs

• 2 Treatments

• Prevention

Signalment: Recently born lambs

Clinical Signs: Eyelashes rub against cornea = Corneal ulcer

• Risk of misadventure and mismothering

Treatments: Do NOT prescribe eye ointment to pet lambs without seeing them

1. Manually evert eyelid for 30s (mild cases)

2. SC injection of AB into lower eyelid (bleb evert eyelid)

Prevention: Cull carrier ram (inherited)

Vaginal Prolapse (“Bearings”)

• Signalment

• Prevalence

• 4 Risk factors

• 3 Protective factors

• 6 Treatments

Signalment: Late-gestation, multiple-bearing ewes

Prevalence: 1% (#1 welfare concern to farmer at lambing)

• Risks are poorly understood as prevalence is highly variable between farms and years

Risks: Increased intra-abdominal pressure

1. High fecundity

2. Hill country (ewes sit with rump down to relieve weight from diaphragm)

3. Gain in weight pre-tup to scanning → Increased weight of placenta and conceptus

4. Feeding swede late pregnancy (high water content and bulky feed in rumen)

Protective:

1. Culling policy of bearing ewes and their offspring

2. Mid-pregnancy shearing

3. VitD injections during pregnancy? (Increase Ca2+ metabolism and muscle strength)

Treatment:

1. Assess viability of ewe and prolapse

   • Fresh prolapse vs. damaged/gangrenous

   • Herniation of intestines = Bad prognosis

2. Reduce vaginal prolapse

   1. Epidural (1.8mL local + 0.2mL 2% xylazine) → Reduce straining and pain

   2. Lift prolapse to allow urination (avoid bladder rupture)

   3. Clean prolapse

   4. Lubricate prolapse and use flats of hands to reduce

3. Place retaining suture/device (recurrence of prolapse possible as pre-lambing vs. post-calving)

   1. Umbilical tape with purse-string suture around vulva = Vet insertion and farmer removal

   2. Bearing harness #1 for farmer (reduce hunching during straining and enables lambing through harness)

   3. Some farmers use ear tags and safety pins

4. Antibiotics (penicillin)

5. Analgesia (NSAIDs)

6. Monitor for lambing to remove retaining device