Small ruminants 4 Flashcards
Urinary tract problems main clinical signs
- 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
What are the 3 major urinary tract problems
- Urolithiasis (goats, wethers and rams)
- Pizzle rot (wethers)
- Knob rot/balanoposthitis (rams)
General approach for urinary tract problems
- 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
Urolithiasis how common, where generally occur and rate of recurrence
- 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
Urolithiasis what are the 3 main risk factors
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)
risk factors for urolithiasis diets and stones what are the 4 main ones and plants come from
○ 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
Urolithiasis clinical signs and therefore what is needed
- 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
Urolithiasis what occurs with lesions localisation/progression
- 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
Urolithiasis what are the 4 main ways to diagnose
- 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
Urolithiasis treatment considerations
- 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
What are the 5 main procedures for urolithasis when done, what need to use and what result in
- 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
Retrograde catheterisation in ruminants for urolithasis is it used, why or why not
○ 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
If find sludge in urethrea with urethrotomy what is the future breeding value
likely more sluge sitting up the bladder - future breeding value not good
Urolithiasis prevention what is involved
- 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
Pizzle rot what is it, caused by, when and result
- ‘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
Pizzle rot treatment for individual level
- 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
Pizzle rot treatment at the mob level
- 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
Knob rot/balanoposthitis what is it also called, what sex affects, cause, major effect and treatment
- 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
what is the role of perineal urethrostomy surgery
To restore urine flow to prevent worsening of azotaemia - JUST A SHORT TERM OPTION
□ Mainly in beef cattle that have more individual worth
Sudden death what are the 4 main steps in the diagnostic method
1) history and signalment
2) is it really sudden death
3) further investigation
4) working differentials and hypothesis
In terms of sudden death diagnostic method what is involved with the history and signalment
○ Shock class affected ○ Spatial (map) and temporal (history) patterns § Identifies the importance of a good history taking ○ Management, animal and environmental risk factors
In terms of sudden death diagnostic method what is involved in questioning if it is a really sudden death
○ 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
In terms of sudden death diagnostic method what is needed in the further investigation
○ 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
In terms of sudden death diagnostic method what are the factors for working differentials and hypothesis
○ 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
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
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
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)
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)
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
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
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)
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,
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
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)
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
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
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
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)
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
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)!
