Small ruminants 4 Flashcards
1
Q
Urinary tract problems main clinical signs
A
- Kicking at belly -> colic -> can be diagnosed as GIT disease
- Signs of straining -> can then kick out as trying to urinate -> look like neurological cause
- Reduced flow/dribbling urine
- Haematuria
- Lingering death
- Dull and depressed - generally advanced at this point
- Pretty normal then slowly dying
○ Disease course often over several days - Reluctance to serve (rams) - mainly with knob rot
2
Q
What are the 3 major urinary tract problems
A
- Urolithiasis (goats, wethers and rams)
- Pizzle rot (wethers)
- Knob rot/balanoposthitis (rams)
3
Q
General approach for urinary tract problems
A
- History - diet and management are key factors for crystals present
- Clinical exam
○ Looking at prepuce, extend penis and urethral process, looking for crystals around prepuce - Imaging
○ Ultrasound and radiography
§ With obstruction enlargement of -> Urethra, bladder, ureters, enlargement of renal pelvis, hydronephrosis - Samples
○ Blood - biochemistry
§ Creatinine is good
§ Electrolytes and PCV for anaesthesia
○ Urine - dipstick and cytology
§ Alkaline urine is normal and so is trace protein
○ Abdominocentesis
○ Stones
§ Send away from investigation
4
Q
Urolithiasis how common, where generally occur and rate of recurrence
A
- Most common cause of urinary tract issues
- Most common sites for obstruction are urethral process and distal sigmoid flexure
- Generally when there is one stone there will be more upstream
○ Rate of recurrence VERY HIGH
5
Q
Urolithiasis what are the 3 main risk factors
A
1) diet and stones - IMPORTANT FOR MANAGEMENT STRATEGY
- phosphates, silica, calcium carbonate and oxalates
2) Male animals, especially wethers - castrated
○ Without testosterone urethral process is narrowed so increase risk for obstruction
3) Feedlots
○ Grain feeding
○ ?poorer water access - also test electrolyte in water - magnesium can be high in boar water
○ Low roughage diet (P excreted through urine instead of saliva & GIT)
6
Q
risk factors for urolithiasis diets and stones what are the 4 main ones and plants come from
A
○ Phosphates:
§ feeding cereal grains (Ca:P ≈ 1:8 in these feeds but need < 2:1)
§ precipitation of Ca & Mg phosphates (e.g. magnesium ammonium phosphate – struvite)
○ Silica
§ cereal stubbles (wheat/sheep zone)
○ Calcium carbonate
§ plants in semiarid zones: high Ca or oxalate
§ lucerne (‘alfalfa’)
§ alkaline urine (normal for ruminants)
○ Oxalates
§ Rare but can come from toxic plants, cause tubular nephrosis
7
Q
Urolithiasis clinical signs and therefore what is needed
A
- Teeth grinding, increase HR, abnormal urination - others listed above
- Large amount of animals don’t show pain - PAIN RELIEF IS ADVISIBLE IN ALL CASES
○ But want to be careful with using NSAIDS
8
Q
Urolithiasis what occurs with lesions localisation/progression
A
- Obstruction, no rupture:
○ gradually increasing uraemia
○ dullness, depression, uraemic coma & death - Bladder rupture
○ immediate relief then uraemia, coma, death - Urethra rupture
○ ventral abdo swelling (water belly) -> can be hard to determine when in full wool - need to palpate
○ subcut urine, necrosis & sloughing of tissue, sinus formation, secondary infection
○ some survive but most die
9
Q
Urolithiasis what are the 4 main ways to diagnose
A
- Urinalysis/dipstick
○ Classic red coloured urine
§ Blood OR haemoglobin OR myoglobin
□ If can spin down then red blood cells - HAEMATURIA - Blood work
○ Target to creatinine or urea if low on money - Abdominal ultrasound - cranial to pubic symphysis
○ Full, distended bladder
○ Echogenic dots floating throughout bladder
§ Uroliths or sediment
○ If chronic check kidney for hydronephrosis - Post-mortem - uroperitoneum, nephrosis, fibrin tags on peritoneum
10
Q
Urolithiasis treatment considerations
A
- Individual or mob?
○ Individual -> Are more cases on the way? - Cost?
- High risk of recurrence without medical intervention or temporary/permanent surgical diversion
- More conservative treatments probably more successful with lower obstructions
○ Can you locate urolith with palpation? catheter?
○ Amputating urethral process only help for a temporary time - What preventive therapy will you use to stop more cases?
Need to know type of urolith present (may be able to analyse crystals found on hairs at end of prepuce
11
Q
What are the 5 main procedures for urolithasis when done, what need to use and what result in
A
- Amputate the urethral process
- Common place to lodge so always try -> should do WITH tube cystostomy
- Need to use sedation (NOT XYZALINE - diuretic) and local anaesthetic (lumbosacral epidural)
- Extrude penis and milk out or amputate urethral process
- Recurrence likely - urethrotomy
- Must use local anaesthesia
- If rupture then DON’T DO - long term prognosis is poor - permanent
- penectomy - removal of penis
- Urethrostomy - hole into urethra
- Allow them to be sold for slaughter later on - SALVAGE - tube cystostomy
- GA, examine bladder wall and divert urine away with catheter to allow bladder to heal, after 10 days and start clamping catheter off and seeing if can urinate properly
- Individual animal treatment
12
Q
Retrograde catheterisation in ruminants for urolithasis is it used, why or why not
A
○ Difficult in ruminants - NOT USED
- Risk is causing more damage resulting in more stricture formation
Sigmoid flexure and urethral diverticulum makes is nearly impossible
VERY HARD DON’T TRY
13
Q
If find sludge in urethrea with urethrotomy what is the future breeding value
A
likely more sluge sitting up the bladder - future breeding value not good
14
Q
Urolithiasis prevention what is involved
A
- Sufficient & easy water access
○ 1–4% salt in ration to increase water intake- - Check water mineral content (esp Mg)
- Dietary Ca:P = 2:1
○ P usually high → avoid these diets - cannot avoid in feedlot so do below
○ OR add 1.5% CaCO3 if prolonged cereal grain feeding - Dietary urinary acidifiers
○ Ammonium chloride 7–10 g/d (≈ 0.5–1% of daily DM)
§ Unpalatable—can reduce feed intake if excessive
15
Q
Pizzle rot what is it, caused by, when and result
A
- ‘Ulcerative posthitis’, ‘sheath rot’
- Corynebacterium renale overgrowth in high-urea urine (spring pasture) & chemical ulceration
○ Ammonium production increase -> destruction of preputial membrane - Inflammation & potential obstruction
- Can get secondary pizzle strike
16
Q
Pizzle rot treatment for individual level
A
- Dependent on severity and duration of disease
Individual - Mild - antibiotic flush into prepuce
- Surgery - incising the ventral surface of prepuce and allowing necrotic material to drain
○ Not too large as mucosa shouldn’t dry out
17
Q
Pizzle rot treatment at the mob level
A
- Shaving around the pizzle area
- Administer testosterone to whole mob in face of an outbreak
○ Ropel -> can use for prevention and double dose for treatment during outbreak
§ Prevention in high risk time - Pizzle dropping procedure
○ NOT PERMITTED NOW
18
Q
Knob rot/balanoposthitis what is it also called, what sex affects, cause, major effect and treatment
A
- aka ulcerative dermatosis, venereal orf
- Can affect ewes
- Multiple organisms, aetiology poorly understood
- Major effect is stopping rams serving ewes - MAIN INFERTILITY ISSUE
Treatment - sexual rest, topical antiseptic/parenteral antibiotic (e.g. longacting oxytet)
- isolate affected rams because it is infectious
19
Q
what is the role of perineal urethrostomy surgery
A
To restore urine flow to prevent worsening of azotaemia - JUST A SHORT TERM OPTION
□ Mainly in beef cattle that have more individual worth
20
Q
Sudden death what are the 4 main steps in the diagnostic method
A
1) history and signalment
2) is it really sudden death
3) further investigation
4) working differentials and hypothesis
21
Q
In terms of sudden death diagnostic method what is involved with the history and signalment
A
○ Shock class affected ○ Spatial (map) and temporal (history) patterns § Identifies the importance of a good history taking ○ Management, animal and environmental risk factors
22
Q
In terms of sudden death diagnostic method what is involved in questioning if it is a really sudden death
A
○ History of observation/checking of mob
○ Struggle/recumbency/other pre-mortem signs
○ Careful clinical exam of mob for early signs -> possibly able to identify high risk and prevent the deaths
23
Q
In terms of sudden death diagnostic method what is needed in the further investigation
A
○ Describe neuro signs”: typical of one syndrome
○ Clinical pathology (facial eczema: GGT)
○ Response to treatment (vit B1, calcium) -> classic is the downer animals with hypocalcaemia (4 in 1 treatment)
○ Necropsy: system, aetiologic agent
§ Bacteriology, histology, body fluids? (important - ocular fluids can be better than submitting bloods)
§ Ensure sending in the right tissues
24
Q
In terms of sudden death diagnostic method what are the factors for working differentials and hypothesis
A
○ Start treatments (who to? All? Affected/sick?)
○ Reduce exposure?
○ How will you monitor for response to treatment
○ Communication skills important for the farmer -> supporting them through the practicalities of the next few steps
25
General cause of sudden death in small ruminants what occurs and the 4 main causes
- No/few proceeding signs = failure of cardiorespiratory system (or cerebrum)
○ If you have signs of struggle may be moving away from the following differentials
1. Bacterial toxin
2. metabolic failure (HypoCa or HypoMg)
3. mechanical circulatory failure
4. environmental toxin
26
in terms of sudden death what bacterial toxin and environmental toxin can result in
```
Bacterial toxin
○ Commensal (pulpy kidney) -> change in management, animal or pathogen factors that lead to disease
○ Environmental (anthrax) -> exposure
Environmental toxin
○ Plant-derived
○ Accidental or deliberate exposure
```
27
in terms of sudden death what mechanical circulatory failure results in
○ Cardiovascular collapse
○ Electrocution
○ Exsanguination (caudal vena cava syndrome)
○ EG -> shock from
§ Poor venous return (bloat)
§ Venous pooling (endotoxic shock of salmonellosis
§ Electrolyte disturbances (acidosis)
28
What are the 7 main diseases causing sudden death in sheep
```
1. Clostridial!
○ pulpy kidney - very common in sheep - more susceptible
○ Blackleg - more common in cows
○ (malignant oedema)
○ black disease (infxs nec. hepatitis)
2. Anthrax
3. Phalaris toxicities
4. Blue green algae psg
5. Cyanide psg - plant poisoning
6. Nitrate/nitrite psg - plant poisoning
7. (Redgut) - circulatory failure
○ Obvious demarcation between devitalised (Caudal) and vitalised GIT (cranial) -> due to dilation and torsion (abdominal lecture)
```
29
What are 4 less common diseases resulting in sudden death in sheep
○ salmonellosis
○ drenching dz (respiratory diseasE) - organophosphate toxicity - LARGE MANAGEMENT FACTOR (time factor within the race after anthelmintic)
○ acute liver fluke infection - possible grazing swampy areas from mid-spring onwards (snails are around then)
○ Tetanus - any wounds - castration, tail docking, dehorning -> a couple of weeks after lambing marking
30
Pulpy kidney what results from, what looks like, diagnosis and treatment
- Lambs placed on highly digestible (grain) diet
○ Looks like redgut
- diagnosis
-> submitting brain for histopath, confirm diagnosis but takes awhile as needs to be fixed in formalin for a few days - also need pathological changes (as commercial)
-> ELISA on gut contents for epsilon toxin
- Give clostridial booster to any sheep before give lots of grain - drought stock containment area or feedlot
○ Short lasting immunity
31
Pulpy kidney clinical signs and postmortems lesions
1) FSE (focal symmetrical encephalomalacia) cerebral damage - due to cerebral oedema - leading to seizure stance in dead sheep (could be another neurological disease)
2) autolysis of kidney - hard to diagnose
3) haemorrhagic enteritis - serosanguinous fluid in abdomen and thorax - differentiate from red gut (caudal intestines)
32
Black leg when occurs
- Typically spores ingested and lodge somewhere in the animal -> only when create anaerobic conditions around the spores does the spores germinate (also for malignant oedema and black disease)
○ Sit in the muscle and risk factor is bruising of muscles
§ Could be recently in the yards, worse if animals have horns possibly,
33
Black leg presentation - clinical signs and necropsy findings
- Clinical signs
○ Sudden death
- Necropsy findings
○ Necrotising gangrene - leg generally - DEATH
○ Crinkling sensation as rub hands over the legs - gas bubbles under the skin
34
Malignant oedema and black disease what result in, when seen
Malignant oedema
- Big head -> sometimes see in rams where wound in in the polls after fighting
- Necrotising gangrene as well
Black disease
- Anerobic conditions occurs in the liver
○ Necrotising hepatitis usually secondary to liver fluke migration
- Focal hepatic necrosis
- Haemorrhage Peritonitis - possibly looks like pulpy kidney (if originate from liver more likely black disease)
35
diagnosis of clostridial disease what is the signalment of affected animals and post-mortem/clinical signs
○ Signalment of affected animals e.g.
§ After transport… black leg, tetanus
§ Young sheep put onto lush lucerne paddock…redgut, pulpy kidney
○ Post-mortem or clinical signs e.g.
§ Gangrenous necrosis of muscle and subcutaneous emphysema
§ Abdominal pain - redgut, pulpy kidney
§ Extensor muscle rigidity- tetanus
§ Multifocal hepatic necrosis - black disease, campylobacter (different signalment - pregnant)
§ Clostridium …… cultured from gut at necropsy - NOT CONFIRMATION
36
Clostridial disease what are the 5 main treatment/control diseases
1) vaccination - when done correctly normally effective
2) control exposure to spores - tetanus
3) control or vaccinate in face of risk factors - pulpy kidney booster before grain feeding
4) pencillin - remember toxins can survive/activate long after bacteria gone
5) symptomatic therapy - ACP, nursing care, quite and anti-toxin for tetanus
37
Clostridial vaccination which vaccine, when, booster and when else
○ 5 or 6-in-1 (or 8- or 10-in-1!)
○ At marking and weaning, well protected for ~12 m.o. - NEED TWO SHOTS
§ 2 weeks after lamb marking -> oldest 7 weeks (maternal immunity decreasing), youngest 3 weeks (able to handle marking procedures)
§ Weaning - fully functioning rumen at 6 weeks
○ If then give another booster at 12 months -> years of protection (tetanus, black leg, black disease and malignant oedema) - not necessary pulpy kidney (high risk situations need a booster then - below)
○ Prior to ‘high risk’ (e.g. to ewes pre-lambing)
Stock containment area
38
Clostridial treatment control exposure to spores (tetanus) what are the 3 main things involved
○ Hygiene
§ Temporary yards (marking) -> to move the area for marking to decrease the spore accumulation
§ Marking equipment -> dipping into disinfectant between each animal
§ Also help control mycoplasma spread (insect transmission around marking high risk)
○ Control dust
○ Dispose of necrotic material (e.g. tails)
39
Anthrax in sheep where common, when differential, what is the role of vets
- Common only in areas where been diagnosed before
- ANY DIFFERENTIAL FOR PERACUTE DEATH - bloody orifices not always observed
○ Main role is to identify the possible case -> tell farmer not to move, will get paid not to move the carcase
○ Second role is notification of the distinct veterinarian
§ Government will step in and vaccinate the exposed herd and ring vaccinate around the farm
40
Anthrax epidemiology
- Usually in a ‘known’ anthrax area
- Environmental history leading to spore dispersal
○ soil disturbance
○ dry conditions
○ flooding can distribute spores & lead to exposure
- Long environmental persistence (Gruinard Island, Scotland)!
41
Anthrax clinical signs and which species most susceptible
- Cattle & sheep most susceptible (horses & goats less)
- ***Peracute
○ Found dead after clinical course of 1–2 hours
○ May observe fever, congested MMs, dyspnoea
- Acute
○ Clinical course 48 hours of severe septicaemia:
§ Congested MMs
§ High HR & RR
§ Inappetence
§ Congestion, oedema
§ Coagulopathy
No rigor mortis in carcase and rapid gaseous decomposition
42
Anthrax diagnosis and what NOT TO DO
- Polychrome methylene blue stain: Blue, short, square ended rods with pinkish-red capsule (not always; definitely no capsule on Gram stain)
- Look for bacteria in
○ Blood (esp sheep, cattle) OR
○ Swollen organs (but don’t open carcase!!)
- Snap test
○ Ensure that you don't expose yourself, use blood
- What not to do
○ DO NOT MOVE OR DO POST-MORTEM IN THE FIELD
§ Opening carcase leads to vegetative bacteria producing spores +++ environmental contamination and risk of infection
43
Phalaris toxicities why is pharalis used, what are the 3 main acute-death syndromes and what else causes
- Very useful pasture plant
- BUT acute-death syndromes:
○ “Polioencephalomalcia (PE)-like sudden death syndrome”
○ Cardiac death
○ Cyanide poisoning
- Also staggers (not directly fatal) - can treat this with staggers
44
Phalaris toxicities when generally occur, what leads to death and prevention
- Late summer, early august, highly fertilised area (highly available nitrogen due to increased urea)
- Certain species but not every year?
Ammonia poisoning leads to death
Prevention
- Avoid sudden changes in feed availability
- Rotational grazing riskiest: self-stocking safest
- Don't put hungry animals onto risky pastures
45
Phalaris toxicites diagnosis and what occurs in the cardiac form
```
Diagnosis
- Post mortem diagnosis
○ Measure ammonia levels in ocular fluid (double every 24 hours after death - should be able to determine the level at death)
§ Generally quite high
- Cardiac form
○ Different toxin causing peracute heart failure
○ Even more rapid than PE-like toxicity
○ Much rarer than PE like syndrome
```
46
Phalaris toxicites treatment
- REMOVE FROM exposed paddock and move onto area without highly fertilised area
○ If cannot leave and reduce intake via supplementary feeding
- Drench with
○ 0.5 (sheep)-2l/2-8 (cattle)L vinegar - reduce the alkaline
○ 4 (sheep)/40 (cattle)L iced water - changes solubility of ammonia - reduce entering of bloodstream
- Supportive care: IV fluids if dehydrated
47
Blue-green algae poisoning when occur and the 2 main toxins involved and what they lead to (clinical signs)
- Stagnant dams with lots of sunlight -> allow algae to overgrow (bloom)
○ Nutrients + anerobic conditions + sunlight
- Blooms produce 2 toxins: (toxins contained within the algae)
a. Neurotoxins
§ Neuromuscular Cholinesterase blockers
§ Paralytic toxins
§ Cholinesterase inhibitors
§ → peracute deaths with few clinical signs (maybe tremors, recumbency, salivation, hyperaesthesia)
b. Hepatoxins
§ Massive hepatic necrosis
→ deaths days-weeks later with jaundice, weight loss, photosensitisation
48
Blue green algae poisoning do blooms always lead to toxicity and prevention
Just because see bloom doesn't mean toxicity will occur - IF HAVE ACCESS to the whole dam can choose an area upwind from the bloom (able to get non-toxic area)
Prevention
- Avoid nutrient contamination of water or aerate the water
- Pump out into troughs and fence off the dam
49
Blue green algae poisoning diagnosis and treatment
Diagnosis
- Jar of water with some air at the top and submit to local water authority lab
○ Or commensal labs
○ Wear gloves - can be directly irritant to the skin
- ELISA test to detect the toxin within
Treatment
- Exclude stock from the area and generally toxic for a few weeks after
- Don't treat with copper sulphate - results in release of toxins
50
Cyanide poisoning what does it do, 2 main sources and when highest risk
- Inhibit cellular respiration
○ Bright red blood & MMs (saturated oxyhaemoglobin)
- Sources
○ Eucalyptus spp. (esp. manna & sugar gums in Vic)
○ Sorghum in northern Aust.
- Highest risk
○ Wilting/frost damage increases risk
○ New growth/regrowth (don't graze if <50cm high)
51
Cyanide poisoning clinical signs and treatment/prevention
- Clinical signs
○ Peracute deaths
§ Open up rumen - belly full of eucalyptus leaves, smells of almonds
○ Respiratory distress followed by death
- Treatment/prevention
○ Sodium nitrite/sodium thiosulphate
§ IV for immediate effect & PO to detoxify ongoing HCN release in GIT
○ Prevent exposure - REMOVE FROM PASTURE and don't graze hungry stock
○ Also providing salt + sulphur lick reduces cyanide availability to stock
52
Nitrate poisoning how occurs (pathogenesis) and diagnossi
```
Pathogenesis
- Nitrates in soils -> drought (low plant uptake) -> urea application -> rapid uptake post-drought (first thing to grow after over-grazing) -> concentrating plant species -> capeweed, oats, canola -> nitrate not converted to plant proteins -> moisture stress - > cloudy days -> nitrate -> nitrite -> creates methaemoglobin (low O2 carrying capacity) -> SUDDEN DEATH FROM CELLULAR ANOXIA
Diagnosis
- Brown blood & mucous membranes
- History of likely exposure
- Positive nitrate
○ Aqueous humour
○ In feed source
```
53
Nitrate poisoning treatment and when can start re-grazing
```
- Methylene blue IV (binds to nitrate and preventing methaemoglobin production)
○ 1-2 (up to 20) mg/kg IV PRN
○ Off-label: specify WHP of 180 days
- Remove from source
- Can re-start grazing
○ Gradual reintroduction - rumens can adapt and learn to detoxify
○ Sunny afternoon, after rain(?)
○ Not hungry!!
```
54
What are 8 other causes of sudden death in sheep that aren't as common
1) Salmonella
○ Many animals die before developing diarrhoea
2) Acute intoxication e.g.
○ Wrong route: e.g. naphthalphos drenched down trachea
○ Wrong dose: e.g. selenium
3) Acute liver fluke
○ Sheep less resistant to fluke than cattle
○ Acute disease occurs from juvenile adult migration (no eggs on WEC)
○ Ingestion of 1000 larvae can cause subsequent sudden death
4) Grain Overload/Acidosis
5) Bloat
○ Common < cattle
6) Hypomagnesaemia
○ Pure form is rare; usually concurrent hypoCa in sheep (see recumbency lectures)
7) Braxy
○ Cold climate clostridial disease, uncommon
8) Anaphylaxis post vaccine
○ from lung worm following injectable levamisole
55
Lingering deaths resulting from neurological signs what are the 3 main common diseases and the 3 others
```
Common diseases
1. Polioencephalomalacia
2. FSE - focal symmetrical encephalomalacia
3. Listeriosis
Other important diseases covered in other blocks
1. Ovine Johne's disease
2. PA poisoning
3. Urolithiasis
```
56
In terms of investigating lingering deaths what are the 2 important things
- Describing the neuro signs via doing a detail neurologically focussed neurological examination
- NECROPSY sample of the brain and some peripheral nerves (sciatic nerves)
○ In some cases need to get spinal cord as well
57
What are the general clinical signs of lingering death from neurological causes
- Central dysfunction
○ Convulsions
○ Opisthotonus
○ Head-pressing
○ Blindness OR
- Circling/unilateral motor dysfunction - listeria is commonly unilateral
- c.f staggers; principally bilateral ataxia/incoordination, which may/not progress to central signs
58
Polioencephalomalacia what is it, the main cause, why occurs, what associated with
- ‘PEM’, cerebrocortical necrosis (CCN), polio
- Principal cause is thiamine (vit B1) deficiency
○ decreased production, antagonism OR increased destruction
§ Thiaminases found in some bacteria & plants
- Frequently associated with rumen upsets
○ e.g. after a change in feed in the last 1-2 weeks
- Same pathological changes from other substances
○ e.g. sulfur/sulfates (sulfur possible antagonism of vit B1)
59
Polioencephalomalacia clinical signs
- Sporadically affected individuals or ‘outbreak’
- 12–24 hour progression
○ Separate from mob
○ Appear blind
○ Star gaze
○ Head lowered to ground/pressing
○ Recumbency
○ Convulsions
- Death 2–3 days - lingering death
VERY VARIABLE
60
Polioencephalomalacia diagnosis and treatment
- Diagnosis - brain Fluro (will see fluorescence on the cut surface of the brain) - only 50% fluoresces so if doesn't, doesn't rule out
- Treatment - increase fibre can also help, IV vitamin B1 (will not save every animal)
61
What is the diagnostic approach in the investigation of lingering deaths
- Suggestive risk factors in history and environment
- Careful clinical and neurological assessment
- Evaluate response to thiamine
- Collect CSF sample (lumbosacral puncture) for cytology (1ml)
- If necropsy available: collect CSF, swab brain for culture (listeria), submit whole brain for histo
62
Listeriosis how to get infected and the 3 main forms
```
- Associated with moisture - WHENEVER HAVE WATER INFESTED VEGETATION
○ Waterlogged vegetation
○ Silage
§ Risky silage
□ pH > 5, DM (dry matter) < 40%, exposure to air (near the outer layers)
- Also other organic sources
Forms
- Abortion
- Meningoencephalitis
- Septicaemia
```
63
Listeria clinical signs, clinical course, diagnosis and treatment
- UNILATERAL NEUROLOGICAL - Facial nerve paralysis -> drooping of the ear, drooling
○ Depression and abortion, variable deaths
- Clinical course - 1-8 weeks
- Diagnosis - history, culture, CSF tap (neutrophils), brain abscess
- Treatment - single dose corticosteroids - reducing inflammation as well as antibiotics
○ If treat long enough likely to get better
64
Focal symmetrical encephalomalacia (FSE) what is it, when occurs and clinical signs
- Neurological, subacute presentation of pulpy kidney
○ In presence of partial immunity
○ Following lower exposure in more susceptible, vaccinated animals (e.g. goats)
- Very similar signs to polioencephalomalacia:
○ Blindness, aimless wandering, circling, head-pressing
- Deaths tend to occur after 3- 10 days
65
Focal symmetrical encephalomalacia (FSE) diagnosis and prevention
Diagnosis:
- pre-mortem as for pulpy kidney (which is…?)
- Necropsy: brain changes of FSE resemble early changes seen with pulpy kidney / enterotoxaemia -> cerebrocortical necrosis
Prevention
- Correct deficiencies in vaccination program!
66
The recumbent ewe what are the 7 main differentials and 4 other causes
1. Pregnancy toxaemia
2. Hypocalcaemia
3. Dystocia
4. Mastitis
5. Ruptured uterus
6. Vaginal prolapse
7. Uterine prolapse
other causes
1. Parasitism - suppress the appetite of sheep (possibly leave to pregnancy toxaemia)
2. Hypomagnesaemia (grass tetany)
○ Loss common, risk factors same as hypocalcaemia
3. Botulism - generally carcase of dead animals
4. Spinal abscess - mentally fine but caudally paralysed
67
What should ALWAYS give recumbent ewe and what will this help
- GIVE 4 IN 1 even if not hypocalcaemia
- will help hypocalacemia, hypomagnesaemia and hypoglycaemia
Treat as many sheep as possible in an outbreak situation
68
Pregnancy toxaemia what are the 2 main factors that lead to this
- Hypoglycaemia and hyperketonaemia
○ Increase in energy requirements in last 6 weeks of ewes pregnancy
○ Specific need for glucose for foetal growth, udder development, colostrum and lactose production
- Dietary energy intake < requirements and utilisation of glucogenic precursors from maternal body fat reserves cannot compensate
○ Low blood glucose, fat mobilisation procedures excess ketones -> acidotic, dehydration (osmotic active ketones), starving -> cannot produce glucose
69
Pregnancy toxaemia what are the 3 main risk factors
1) Anything that decreases feed intake
○ Dental problems, foot abscess, cold weather, low feed, yarding overnight
2) Anything that increases energy requirements
○ Twins (twin lamb disease) -> high metabolic demand from foetus AND lower area within rumen due to large gravid uterus for decreased feed and therefore energy intake)
○ cold weather, shearing, stressful handling
3) Over-fat ewes (CS > 4)
○ Decrease feed intake = increased abdominal fat + gravid uterus
○ High rate of fat metabolism - prone to ketonaemia
70
What type of sheep is pregnancy toxaemia more common in
○ Mature ewes - bigger lambs, more colostrum, more twins, more body fate
○ British breeds and crossbred over merinos - more twins, bigger body frame
71
Pregnancy toxaemia clinical signs on the individual and herd level
- Mainly affects the brain
- Individual level
○ Dull, poor appetite, falling behind mob
○ Becomes recumbent and prolonged inappetence, coma
- Herd level
○ Lower lamb birth weight
○ More deaths from mismothering, starvation and exposure
○ Poorer milk supplies and lamb growth rates
72
What are the 3 treatments/prevention for pregnancy toxaemia
1) correct metabolic demands
2) correct hypoglycaemia
3) correct dehydration and acidosis (vytrate)
73
For pregnancy toxaemia what is involved in correcting metabolic demands
○ Induce parturition (unless induce on term unlikely to save lambs) using long-acting glucocorticoids
§ Also gluconeogenic
○ Emergency caesareans -> case selection is very important -> high risk of death
§ Due to fluid and electrolyte imbalances enough to tip the patient over the edge
74
For pregnancy toxaemia what is involved in correcting the hypoglycaemia
○ IV dextrose (could be in 4 in 1) and large bolus dosage as well
§ Hypotonic (will lyse red blood cells) - don't give as massive bolus dose
○ Oral propylene glycol - not readily metabolised by rumen microflora BUT feeds into gluconeogenesis (forms glucose)
○ Good supplementary feed
○ Anabolic steroids to encourage feeding (stimulate appetite)
75
Hypocalcaemia causes/pathogenesis
○ Due to failure of calcium homeostasis (not deficiency in calcium) when need to use calcium for foetal calcification
§ Extracellular calcium + plasma calcium (maintain within a tight range)
□ Drain serum calcium with foetal bone growth - try to maintain the plasma via extracellular calcium supplementation
® Extracellular pool supplemented by calcium being pooled from the bone marrow (something that stops this process from occurring in bone resulting in hypocalcaemia - process needs low pH)
76
Hypocalcaemia risk factors and treatment
Risk factors
- Increase in pH -> lack of eating -> stop salivation -> stop alkaline buffering -> increase pH -> reduced bone calcium resorption
-> Lush pastures, feeding short pastures, keeping locked in yards overnight, alkalinizing diets (potassium)
- Light weight undergrown ewes or weaners after drought - low bone density
Treatment
- Oral calcium to get through subacute phase
- Give roughage -> promote salivation
- Supplement Vitamin D3 drench
77
Hypocalcaemia what is the prevention mechanisms
- NOT withholding feed at late pregnancy
} Unimix (Ca + P drench) if NEED to withhold feed
- Avoiding risk pastures - low calcium or short pastures, with lots of potassium or ammonia
- Ensure ewe weaners are well grown (good bone density)
- Add 1.5% CaCO3 to prolonged grain feeding to balance P:Ca and avoid bone depletion
- DON'T GIVE PREGNANT EWES TOO MUCH CALCIUM LATE PREGNANCY
-> Reduce calcium late pregnancy to turn on the regulatory system
78
what are the steps in the diagnosis of staggers
- Careful neuro exam to characterise signs
- Look for environmental clues
○ Pasture type/toxin exposure
○ Time of year/weather
- Response to therapy?
○ e.g. thiamine - NEVER GOING TO CAUSE DAMAGE BY GIVING THIAMINE
§ If have Polioencephalomalacia then will respond
- Necropsy
○ Remember possibly only biochemical ‘lesions’
79
What are the 3 important plant staggers and what does it cause
1. Phalaris staggers - ataxia (rather an convulsions - but will be terminal feature)
2. Perennial ryegrass staggers - ataxia - but hyperexcitability (rather than convulsions - but will be a terminal feature)
3. Annual ryegrass toxicity
80
What are the 3 other diseases that cause staggers
- Other plant-associated neurological disorders
- PEM (thiamine deficiency)
- Border disease / hairy shakers -> Pestivirus (similar to bovine viral diarrhoea virus in cattle)
○ In utero infection will get neurological disorders - cerebellar hypoplasia (ataxia) or abortion
§ Also called hairy shakers due to damage to the hair follicle growth - hairy not woolly
81
Phalaris staggers what can phalaris also cause, when cause and pathogenesis
- Also can cause PE like sudden death (phalaris staggers)
- Variety, environmental and soil dependent to whether cause this
Aetiology/Pathogenesis
- Tryptamine alkaloid neurotoxins in plant affect midbrain function
- Deficient/marginal cobalt areas
- All ages affected
- n.b. different syndrome to acute toxicity
82
Phalaris staggers epidemiology
- Autumn–winter
- Onset
○ Weeks–months grazing
○ Can be delayed - therefore may not be grazing that pasture when you arrive - HISTORY IS IMPORTANT
- Variable morbidity, low direct mortality
- May recover or signs persist - salvage slaughter if can still be transported
○ If fast to occur more likely to resolve, slow damage more likely to have longer neurological damage
83
Phalaris staggers presentation on farm and what to do
- THEREFORE when arrive on farm
○ Likely to have some showing mild clinical signs -> okay to be keep if can still function well - will not be 100%
○ Some showing severe clinical signs -> salvage slaughter
○ Those that aren't showing clinical signs -> move into their own paddock as could develop clinical signs
○ IN THE FUTURE - give cobalt supplementation
84
Phalaris staggers clinical signs
- ‘Falling with tremors’ similar to PRG staggers
- INCOORDINATION - wide based stance, ataxia
- Worsened by stimulation - movement in paddock
- Often an intention tremor - as cerebellar and brainstem issue
- Only convulsive in terminal stages
85
Phalaris staggers diagnosis
- Clinical signs and history - first half of the year
- Necropsy: - choose the more clinical cases for the necropsy
○ Yellow-brown pigment in midbrain and medulla
86
Phalaris staggers treatment and prevention
Treatment
- No effective treatment
- May or may not recover (cf. PRG staggers)
- Quick onset more likely to resolve
Prevention
- Cobalt bullets (x 2) - binds the toxins within the rumen (unlike phalaris toxicity where no prevention)
○ NEED TO GIVE 2
- Low alkaloid cultivars may have greater levels of other staggers-inducing toxins
87
Perennial ryegrass stagger where found and how to differentiate from annual
```
- Found in higher rainfall areas
Dark green with waxy underside of the leaf
Annual looks similar
- If rainy environment - perennial
- If drier environment - annual
```
88
Perennial ryegrass staggers pathogenesis - what are the two types and what do they lead to and what is important
- Toxins from plant endophyte (helper fungus)
○ Promotes insect resistance
○ But toxic to livestock! - damage the purkinje fibres within the cerebellum
- Two types
a. Lolitrem B
§ neurotoxic, diarrhoea
b. Ergovaline
§ hyperthermia, illthrift, ?infertility
- Different PRG cultivars have different endophytes & toxicities
○ Trying to balance the insect resistance with the toxicity
89
Perennial ryegrass staggers epidemiology where is the endophyte found, therefore when does staggers occur as well as ill-thrift
- Endophyte especially in
○ crown (base) & leaf sheath (i.e., short feed) - SHORT GREEN RYEGRASS
○ flowering stem & seed
- Staggers: especially end of summer/atumn rain then plant heat stress:
○ short green plant with concentrated toxin
○ animals forced to graze most toxic parts & high ingestion of toxin - as green feed after being on dried paddock
- Illthrift - different season - ‘Big’ springs with abundant pastures bolting to seed (endophyte also found in seed)
90
Perennial ryegrass staggers clinical signs and what can look like
- Stimulation -> Hyperexcitability incoordination (ataxia)
○ High gait
○ Rigid falling down
- Hyperthermia -> cattle stand in water
- Scours and diarrhoea
Can look like cervical lesions or cerebeller disase
91
Perennial ryegrass staggers recovery
- TEND TO RECOVER IF LEAVE THEM ALONE - difficult to muster (cut fencing or walk along feed trail to another paddock)
- Remove affected sheep from toxin source
○ Minimal handling, drift mobs
○ Expect slow recovery over 2-3 weeks
92
Perennial ryegrass staggers management and prevention
- Know & take preventive measures in risky seasons
○ Know ‘danger’ pastures - pasture improvement - replace with lower risk pasture
○ Beware short, stressed ryegrass pastures in late summer– autumn
§ Test graze
§ Avoid altogether
○ (Remember risky pastures with good growth & bolted to seed in spring can be cause of other aspects of PRGT)
- Feed additives becoming available that bind endophyte toxins to prevent absorption from diet
○ Should be used with supplementary feed
- New low-/safe-endophyte cultivars becoming available that seem to persist OK
93
Annual ryegrass toxicity where found compared to perennial and what causes the toxicity
- Found in drier environments - WA, SA, NT - more common in the West
Epi/Aetiology
- Annual ryegrass paddocks
○ WA SA wheat/sheep belts 350-500mm rainfall
- Anguina nematode
○ Invades seed head forms gall - generally spring time issue
○ Can carry Claviceps bacteria which produces toxin
- Toxins very stable in hay (esp.) and paddock
94
annual ryegrass toxicity clinical signs
- Usually 4-6 days after going into a toxic paddock
- Worse by stimulation
- Generally more severe incoordination and hyperexcitability than perennial
- Mild
○ Unable to keep up with mob and has a high stepping gait.
- Severe
○ Generalised convulsions (cf. PRG, phalaris) in response to stimulus
§ If really hot days then can lead to hyperthermia -> death
○ Variable tremors, opisthotonus, fasciculations
95
annual ryegrass toxicity diagnosis and treatment
```
Diagnosis
- Clinical signs
- Pasture - need to ryegrass seed heads
○ Bacterial slime
○ Nematodes
○ Lab test
§ Preflowering test
§ Mature ryegrass test
- Pathology subtle/absent
○ (Perivascular oedema & necrosis)
Treatment
- No effective treatment
- Remove from pasture
- Avoid stimulus
```
96
Annual ryegrass toxicity prevention and some future options
- Pasture management - safer species that are more resistant to the nematode
- Crash graze late winter - getting rid of seed heads
- Spray topping - getting rid of seed heads
- Burn paddocks
- Establish safe nonryegrass paddock
- Future
○ TWIST FUNGUS
○ Safe cultivars
§ “Guard”
§ “Safeguard”
○ Safe bacteria
97
What plant posioning cause the following CNS signs 1) falling with tremors 2) generalised cnvulsions 3) hindlimb paresis, knuckling
1) Paspalum staggers (nervous ergotism)
2) Thiamine antagonists or thiaminases: e.g. nardoo fern, common bracken
3) Coonabarabran staggers: often irreversible
Romulosis due to onion grass (Romulea): bunny hopping
98
If suspect hypocalcamia what would you do to investigate further
1. Further clinical examination of the ewes - to ensure not missing anything else
2. Collect blood samples of 10 animals that seem well - indication of the risk
3. Perform necropsies - looking a bone structure - trabecular bone
4. Sample aqueous or vitreous humour - confirm cause of death hypocalcaemia
5. Collect soil samples - if had suspicions?
99
Weaner illthrift what is it and what are the 3 main ways it presents
- Failure of weaners to grow/thrive when other sheep are doing well
○ Increased mortality - reduced numbers is generally what is measured at different time points
○ Poor production - will also be low - should also measure
§ Reduced fertility (conception rate), growth rate, wool production
○ Poor animal welfare
Very insidious - dead weaners 'disappear' and mortality may be much greater than farmer thinks
100
Illthirthy weaner what also called, percentage of mob, what result in individual sheep and what is important to remember
Tail of the mob -> the illthrifty weaners
- Could be up to 30% of the mob
- Over-represented in other diseases
○ High risk of mortality and health problems (pneumonia, mycoplasma ovis, salmonella)
§ More stressed, lighter in weight (fewer bodyweight stores)
- Direct interventions TO THIS PROPORTION will give the best economic value
○ Placing into separate paddock - give better pasture, supplementary feed
