Small ruminants 3 Flashcards
(104 cards)
1
Q
Clinical signs of redgut and post-mortem changes
A
- Clinical signs -> dead and dying animals with abdominal crisis: abdominal pain, tympany/distention, recumbency
○ Post mortem changes - Most cases 180-360 clockwise torsion of intestines
- Devitalisation of blood vessels supplying the gut - cranial mesenteric artery is the one that is blocked
○ Generally the devitalised section of GIT is distinct from the vitalised area - Bright -> dark red intestinal discolouration from after 1st meter of small intestine through to rectum
2
Q
Redgut what are the 2 other main differentials and why
A
○ Other causes of sudden death following feed change
§ Pulpy kidney (unvaccinated lambs)/enterotoxaemia
§ Plant positioning -> nitrate, cyanide, phalaris
3
Q
Redgut treatment and prevention
A
○ Immediately removing affected mob from high-risk pastures stop outbreaks
○ Address risk factors by reducing digestibility of diet
§ Providing source of higher fibre of feed amongst the higher digestible pasture -> hay
§ Gradually introduce the animals to the higher digestible pasture
4
Q
Where is a place that you see a lot of abdominal problem, why and the 3 main abdominal issues
A
FEEDLOT DISEASES
- SUDDEN DIETARY CHANGES
○ Intensive feeding - from paddock feeding to grain feeding
Main Health Issues
- Abdomen-related:
1. Ruminal acidosis
2. Shy feeders
3. Entertoxaemia/pulpy kidney (overgrowth of C perfringens - IN SUDDEN DEATH LECTURE)
§ Vaccine preventable disease - BOOSTER BEFORE INTENSIVE SYSTEM INTRODUCTION
5
Q
Ruminal acidosis in sheep pathophysiology and presentation/diagnosis
A
- Same pathophysiology as in cattle
- Presentation
○ Intermittent inappetence, dullness, recumbency and deaths in late-pregnancy ewes
○ History of: Receiving “on and off” grain ration in paddock
○ Doughy rumen with undigested grain
○ Ruminitis -> painful abdomen
○ Flystrike - diarrhoea leading to flystrike
Diagnosis
○ Rumen pH about 5 -> if >25% have rumen pH <5.5
○ need to consider history and clinical signs
6
Q
What are some important mob management/prevention strategies for grain overload
A
§ Reintroduce grain…slowly! - 50g/h/d to build to final ration over 3 weeks (2-3 feeds per week)
® Sheep in feedlot need full ration of 3.5 kg/h/week
□ But these ewes need extra feed to prevent pregnancy toxaemia
□ Add virginiamycin to help protect as feed reintroduced faster?
□ OR use alternate feed -> high fibrous feed
§ Mix batches of feed when changing over
§ When on full ration feed only 2-3 times per week gives all animals time to access feed, avoiding unpredictable, intermittent access by sky feeders
7
Q
What are some individual management/prevention strategies for grain overload
A
§ Oral drench several times daily
□ sodium bicarb. 20 g
□ magnesium hydroxide 40 g
§ Penicillin, fluids and supportive care
8
Q
Entertoxaemia/pulpy kidney what caused by, presentation, differentiation from redgut and prevention
A
- Clostridium perfringens type D overgrowth due to diets high in soluble carbohydrates
- Presentation
○ Sudden death
○ Abdominal pain
○ Bloating
○ (Diarrhoea in goats)
○ But pathology in intestines, body cavities & brain - HOW DIFFERENTIATE FROM REDGUT
§ Hyperaemia due to general vasculitis - Prevention - Vaccinate in the face of an outbreak & try to reduce concentrate feeding
9
Q
Shy feeders in feedlot situations what are the 4 main reasons this occurs
A
- Poor adaptation to feed ○ Behavioural § Not imprinted on feed (or infrastructure) § Small size/Low in social hierarchy ○ Dietary § Not accustomed to diet § Low-grade digestive problems reducing VFI ○ Physical § Insufficient trough or pen space ○ Concurrent disease e.g. § Vitamin E defic, scabby mouth
10
Q
Shy feeders in feedlot situations diagnosis, management/prevention and what is important to consider
A
- Diagnosis
○ Poor weight gain/weight loss
○ Atrophic rumen papillae - animal has not eaten for many weeks - Management & Prevention
○ Regularly identify & remove for paddock feeding - important
○ Draft pens by size/age
○ Sufficient space
○ Imprinting!
○ Make sure enough roughage (≥10% w/w of concentrates)
SHY FEEDERS AND ACIDOSIS CAN OCCUR IN THE SAME MOB
11
Q
What are the 10 general guidelines for inducing animals into feedlots
A
- Site: good drainage, enough space (pens, troughs, water supply)
○ Water: 10% BW/day (5+ L) - Draft into weight groups
- Pre-treatments:
○ 5 in 1 vaccine, Drench
○ Treat external parasites if needed - Good quality hay if must enter immediately
- Introducing concentrates
○ 2-3 weeks BEFORE entering feedlot
○ Familiarise with feeding equipment
○ Only ad-lib once introduction complete (production) - Roughage: 10-20% of conc. ration
- Remove any sick or diseased sheep or other problems (lame)
- Weigh and redraft to remove lambs not growing
- Follow WHP and ESI of treatments and keep records
- Removal onto pasture
○ Ensure adequate pasture and let out after feeding to avoid gorging
12
Q
PSI what is it, what situations generally found within and what occurs
A
LIVE EXPORT - PSI (persistent inappetence, salmonellosis and inanition syndrome)
- Syndrome of sheep on live-export ships leading to increased mortality
- Inappetence increases the risk of sheep being infected by salmonella resulting in clinical salmonellosis or starting to shed the organism
○ Additionally ruminal acidosis can also favour salmonella problems
§ Low pH disrupts normal rumen microflora, allowing salmonella overgrowth
13
Q
PSI (persistent inappetence, salmonellosis and inanition syndrome) risk factors and management/prevention
A
- Epidemiology/risk factors
○ Poor adjustment to total ration during pre-export feedlotting
§ If sheep remain inappetant as they start voyage are 3-14 times more likely to develop
○ Dietary upsets and poor adjustment increase inappetence therefore increase risk - Management - BEFORE EMBARKATION
○ Not mixing groups
○ Gradual introduction of feed
○ Managing high risk groups
○ ONCE ON SHIP - move to hospital pen with higher fibre feed
14
Q
What are the 3 main production areas in terms of weather and what worms are found there
A
- summer dominant
- Haemonchus contortus
- Tr. Colubriformis - uniform rainfall - heading south (Gippsland)
- Haemonchus contortus - winter rainfall
- Ostertagia (teladorsagia circumcincta), Trichostrongyles
15
Q
Roundworms of sheep what is the main points of the lifecycle
A
- Pre-patent period is 17-21 days
- Eggs, LI and L2 susceptible to desiccation, L3 more resilient
- Population ecology - variation in fecundity and rate of development
○ Haemonchus contortus > Trichostrongyles colubriformis > Trichostrongyles vitrinus > Teladorsagia circumcincta - Delay in translation of infection from eggs in faeces to L3 on pasture (>8 weeks), hence infection of sheep
○ Impact of PPR variable
○ Weaning of lambs - getting off before this point at 8 weeks
16
Q
Winter rainfall area in terms of internal parasites what are 4 main things that occur with L3, contamination and strategic drenches
A
- Highest availability of L3 in winter - June, July, August
- Late summer/autumn contamination important source of winter peak in availability of L3 - reduce with drench
- Significant over-summer survival of L3 developing from eggs-deposited in spring and early summer (adequate ‘refugia’)
- Strategic summer drenches generally works well (less reliable in wet summers)
17
Q
In terms of infection and L3 in winter rainfall areas for internal parasites what occurs in summer, autumn, winter and spring
A
- Summer generally too hot and dry for development of eggs to L3
- Dews and autumn break provide moisture
- Low winter temperature slows development but long survival and short pasture -> max L3/kg herbage
- Spring ideal for development, but longer grass dilutes L3/kg - drop off in numbers
- Rising temp in late spring/summer limits survival of eggs/L1/L2 BUT also locks L3 in faecal pat (can survive)
18
Q
Internal parasite control programs list 7 things can use concurrently to get the best result
A
1) test for drench resistance (every 3-4 years)
2) 1 or 2 stragic summer treatments in winter/winter rainfall areas
- > highly effective - SD1 in DEC, SD2 in FEB
3) WEC monitoring to avoid unnecessary treatments
4) quarantine and treatment for introduced sheep - not generally done
5) nutrition
6) grazing management (wet years, high rainfall) - lower risk pastures for weaners
7) breeding for increased immunity - rams selected for low WEC
19
Q
testing for drench resistance how often done, how
A
(every 3-4 years)
○ WECRT - worm egg count reduction trail
○ 10 (15) samples per group, 5-8 groups (each drench + control group), best to get lambs at weaning as exposure but not drench yet - IMPORTANT (If used adult sheep -> Change in egg count could be about the ewe’s immune
Lambs -> Closest correlation between egg count and worm burden)
○ Single pre and post drench WEC -> 10-14 days (before PPP - 3 weeks)
20
Q
WEC monitoring to avoid unnecessary treatments what need to do, when and how often
A
○ Bulk WEC, 10-20 sheep/mob
○ Before SD1
○ All mobs before SD2 (cut off is 25-50 eggs)
§ Do larval culture/PCR if Haemonchus present
○ Weaners - after autumn break (every 4-6 weeks)
○ Ewes - before lambing (need to pre-lamb drench)
21
Q
Nutrition for reducing internal parasites what is needed
A
○ Feed availability and CS target for ewes
○ Growth targets for weaners
○ Feeding protected protein
○ Pasture containing condensed tannis
22
Q
Grazing management to reduce internal parasite burden what are the 2 main things can do
A
1) sheep-cattle interchange - sheep benefit the most
2) smart -grazing - low-risk pastures
23
Q
Sheep-cattle interchange for grazing management with internal parasites how effective, what cattle needed, how often rotate, who benefits the most and why
A
○ Very effective grazing management strategy
○ Needs cattle to be at least 20% of DSEs
○ Avoid young cattle (T. axei and H. contortus)
○ Initially suggested a 6-monthly rotation in Jan-Jul, but this can be varied (6 weeks min >12 weeks better)
○ Sheep benefit the most
§ Reduces teladorsagia (Ostertagia), haemonchus, trichL3 by >90%
§ Increase GFW by 25% (0.7kg) and Wt gain by 65% (7kg)
§ Decrease TWC by 85% (2160 vs 14800)
○ Can move sheep first and delay moving cattle for 2-3 weeks if sheep pastures too short for cattle
24
Q
Smart-grazing for grazing management to reduce internal parasites what are the 2 steps within
A
a. Prepare paddock (nov-mar)
- Graze at 2.5 times stocking rate for 30 days post drench then rotate to another paddock
- After second drench same stocking rate place again onto that paddock for 30 days (PPP)
b. Graze after autumn break on this pasture that should have low worm burden
- Graze the weaners that are most susceptible
25
Breeding for increased immunity to internal parasites what is involved and which worms work best on
- Selection for low WEC
○ Sheep (rams) are selected using one WEC at 12 months heritability 0.25
○ Worm resistance increases significantly after - 7-10 years
○ Resistance to Trichostrongyles and Haemonchus > teladorsagia (Ostertagia)
○ Decreased contamination gives significant production advantages
26
Vaccines for internal parasites, what one use, where and why and the intervals for the V1-V6 in lambs
- Barbervax program
- Spring-born lambs in summer rainfall areas (NSW) -> where Haemonchus is common
- V1: 1st vaccination at lamb marking
- V2: 2nd 3-4 weeks later
- V3: 3rd vaccination + drench 3-4 weeks later at weaning (move lambs to a prepared low worm-risk paddock, ideally one not grazes by sheep for 3 months) -> significant advantages found here
○ Need to also do smart grazing technique
-V4: 6 weeks later
- V5: 6 weeks later
- V6: 6 weeks later
27
Ewes vaccine for internal parasites what areas and when give V1-V4
```
again in the summer rainfall areas
V1: 8-9 weeks pre-lambing
V2: 4-5 weeks pre-lambing
V3 - 1-2 weeks pre-lambing effective drench to control scour worm and early barbers pole
V4 lamb marking
```
28
Nematophagous fungi what is it 2 main ones, what used for, what is needed and results
```
fungi that attack nematodes
1) Duddingtonia flagrans
○ Known about since 1930s
○ Decrease larvae on pasture by 50-70%
○ L3 need to be active
○ Need to get fungal spores into the dung at the best time:
§ Feed 1.5 million spores/50kg sheep daily for 8-12 weeks -> when already feeding supplementary feed
§ Controlled release capsules
2) BioWorma - new product
○ Just released
○ Not cost-effective for sheep
```
29
Efficacy of ML on internal parasites in VIC, QLD/NSW and which best
- VIC -> less resistance found here
- NSW/QLD -> higher resistance to MLs due to worms present in these areas
- Ivermectin -> abamectin -> moxidectin (higher potency and less resistance than ivermectin)
30
what is the resistance like with BZ and OPS
- BZ - high resistance, combination of BZ/LEV -> less resistance
- Combinations wit OPS are effective (>95% reduction in WEC) on 60-70% farms tested
31
Anthelmintic Resistance what are the 5 main principles
a. Late detection of the resistance in the population
b. Very slow/negligible 'reversion'
§ Levamisole generally greater reversion then others
c. Side resistance (within group) is universal
d. Cross-resistance (between groups) is rare
e. Short-acting vs persistent drugs
§ 'head selection' (potency) and 'tail selection' (persistency - long acting moxidectin, Closantel)
§ Long-acting preparations tend to have a longer tail ( closantel, LA, Mox injection, Mox oral)
32
Anthelmintic Resistance impacts on the farm what does it depend on
has resistance reduced farm productivity and profitability
○ Generally business as usual for resistance on farms -> effective strategies to prevent this can be profitable
○ Depends on:
§ Region/location (much worse with Haemonchus)
§ Genetics of resistance
§ How well farmer adopts 'best practice' - both for worm control and other determinants of farm profitability
33
Anthelmintic Resistance risk factors what are the 4 main ones
a. Frequent treatments
§ First report in sheep on research farms (Haemonchus)
b. Under-dosing
§ Dosing strategy (average vs heaviest)
§ Under-estimating BWts
§ Low volume drenches - cheaper to ship
§ Goats (rapid metabolism of anthelmintics)
c. Movement of animals
d. Proportion of worm population 'in refugia'
§ Rapid increase in ML resistance by teladorsagia (Ostertagia) in WA and kangaroo island
□ Assumed to be significantly lower proportion of over-summering larvae
WANT HIGHER REFUGIA
34
What are the 3 main options to combat low refugia populations
1. Crop stubbles and fodder crops
○ Graze with contaminator mobs of known WEC
○ 'move then treat'
2. Delay summer drenches
○ Now suggested for ewes in WA
○ Weaners still get 2-summer drenches
3. Targeted selective treatments
○ Based on higher body weight/CS, growth rate or lack of anaemia (resilient sheep)
○ For tactical drenches (Haemonchus)
○ Problem with higher labour costs
○ Strategic drenches - what proportion treated
§ Target WEC
§ Set percentage - generally doesn't work as well
35
What 3 things need to consider when trying to combat low refugia populations
1. Worm ecology and control programs differ markedly between regions
○ Amount and distribution of rainfall
○ Length of growth season
2. Importance of summer/autumn contamination in winter rainfall areas
3. Difference between wool and prime lamb flocks
36
What population of refugia is needed to delay resistance
○ Need 30% of population to escape treatment to delay resistance
37
In south east Australia what refugia is present, should you increase contamination and what is important to look for with refugia
- Already ample over-summering (refugia) populations of infective larvae in Victoria
- Deliberately increasing contamination is not appropriate as a general recommendation
○ Needs A LOT more monitoring
○ Increases risk of unacceptable production losses
○ Unlikely to make a big difference if genes for Rx are dominant/semi-dominant
- Identify risks of extremely low refugia
○ Drought, crops and previously de-stocked farms
○ Devise and monitor a strategy
38
Live fluke what losses occurm what drives life cycle and the 2 main types of diseases
- Similar production loss to scour worms
- Breeding season of lymnaeid snail intermediate host drives the life cycle
- Types of disease
○ Acute fluke disease (immatures Dec, Jan) - blood feeders - pale and jaundice - MOST COMMON IN SHEEP
○ Chronic disease (May-Jul) -> bile ducts blockage -> anaemia and bottle jaw - MOST COMMON IN COW
39
Live fluke what is involved in the control
○ Extent of infestation - most of the farm (irrigated farms or just isolated areas)
1. Isolated areas
□ Fence or don't graze with young stock
□ WEC before graze area (treat if +ve) and/or treat when remove (max 9 weeks = PPP)
2. If more widespread - treat
□ Feb and Aug (before autumn and spring breeding of snail)
□ Triclabendazole - activity vs 2-4 weeks old
□ Combinations of Closantel with OFZ or ABZ (8w.o)
□ ABZ (14w.o)
40
Goat and internal parasites what is different
- Few products registered
- Different pharmacokinetics in goats
- Less immune/resilient - frequent treatments
- Rapid selection for resistance in high rainfall areas (Haemonchus)
- FAMACHA can work well in smaller flocks
41
What are the 5 main causes of diarrhoea in sheep
```
1. Worm related
○ High WEC/TWC or high larval challenge
○ Hypersensitivity scouring
2. Weaner colitis/enteritis
○ Coccidiosis
○ Campylobacter
○ Yersinosis
○ Often made worse by nematodes, SE/Vitamin E deficiency, M.ovis
3. Adult sheep
○ Yersinosis
○ Salmonellosis
○ OJD
4. Nutritional scouring
○ Lush feed, PRG endophyte, phalaris
5. Neonatal scouring
○ Cryptosporidium, giardia
○ E. coli, rota- and coronavirus
```
42
what is the pathophysiology of diarrhoea
- Increased intestinal motility
- Altered permeability:
○ Leakage of plasma protein (30-50g/d)
○ Loss of water and electrolytes (esp Na+)
- Increased secretion
- Decreased absorption
-Increase osmotic gradient in lower bowel
- Dehydration and acid-base imbalance
43
Cost of diarrhoea/scours what are the direct and indirect costs
- Direct costs
○ Decrease money per head due to high dag score -> crutch cost, clean wool in crutching, foregone wool, dag-weight loss
- Indirect costs
○ Decreased production
○ Increase susceptibility to other diseases such as fly strike
○ Treatment of sick sheep
○ Prevention of disease and parasites leading to diarrhoea
§ Crutching, anthelmintics
44
worm infections what TWC and WEC is considered high worm budens (pathogenic) in sheep and what is a high larval challenge
- High worm burdens (pathogenic burden)
○ TWC > 10-20,000 (deaths when over 20,000) ○ WEC > 300-500 egg
- High larval challenge
○ >5-10,000 L3/week (teladorsagia and trichostronglus spp)
○ Nematodirus spp
45
What are hte 3 main effects on sheep from worm infections
○ Loss of appetite - MAIN PRODUCTION LOSS
○ Gut damage and hypersecretion
§ Decrease digestion and decrease absorption
§ Increase protein loss
○ Altered gut motility
46
Hypersensitiviy scouring where occur, what occurs and presentation
winter and uniform rainfall areas
- A relatively low dose of worm larvae will induce scouring in susceptible sheep
- Persistent diarrhoea/breech soiling on lush pastures during winter-spring
§ Typically affects 10-40% of sheep that are >10 months
§ Usually low WECs
§ Has substantial financial penalties
§ Scouring not stopped by short-acting anthelmintic
47
Hypersensitivity scouring effects, treatment and diagnosis
- Effects
§ Enhanced inflammatory response in the gut:
§ 50-80% more eosinophils, increased CD4/CD8 T-cell ratios
§ NOT associated with measures of protective immunity (WEC, TWC, Mast cells, blood eosinophils, response to larval mitogen)
- Treatment
○ With a controlled-release anthelmintic capsule prevents most dag
- Diagnosis
○ Rule out other causes of diarrhoea (faecal egg count or total worm count (if post mortem samples))
○ Flock history
§ Winter or uniform rainfall areas
§ Good worm control and low/moderate WECs
§ Affected sheep >10-15 months
48
Hypersensitivity scouring what will not control with and what can control with
○ WILL NOT CONTROL WITH
§ Traditional control programs (summer treatments + grazing management)
§ Selection for low WECs/increased immunity (nemesis)
○ CAN CONTROL WITH
§ Long-acting treatments (drench capsules)
□ Economics and sustainability questionable
§ Culling and genetic selection (repeatability)
□ Dag score (some ASBV data becoming available)
□ Age of selection (not too young)
49
Weaner enteritis/colitis what are the main causes and other causes
```
- Illthrift, diarrhoea and deaths
○ Coccidiosis (terminal ileum/caecum/colon) rarely a primary problem
§ Secondary to drought
○ Yersinia (ileum onwards) and campylobacter (caecum/colon)
- Other Causes
○ Sub-optimal management
○ Nematodes
○ Under-nutrition
○ Se/vitamin E
```
50
Weaner enteritis/colitis treatment and diagnosis
- Treatment
○ Sulphadimidine (1g/7kg)
○ Sulphatrim (sulfadiazine and trimethoprim) (1mL/30kg)
○ 1-2 x with L/A (long-acting) Oxytetracycline
- Diagnosis
○ High worm counts or heavy larval challenge
○ WECs (+/- oocysts)
○ Faecal smears and culture
○ Post mortem (ileum, caecum, colon): TWC, gut smears and culture, histo
○ Response to treatment
51
Bacterial enteritis what are the 2 main ones, at what age and general history of
- Epidemiology of bacterial enteritis not completely understood and diagnosis can be difficult
○ Campylobacter 12-20 weeks old - often cured with antibiotics
○ Yersinosis: 5-10months with more deaths
○ History of
§ Nutritional and environmental stress
□ Recent weaning
□ Drought (aggregation, trough feeding)
□ Cold, wet weather
Recent drenching and/or worm control problems
52
Yersiniosis what does it cause, most common species and risk factors
○ Outbreaks in weaners (and sporadic cases in later pregnancy ewes)
§ Diarrhoea, illthift and deaths in late autumn/winter
○ Y. pseudotuberculosis (mostly serotype III - generally more serious disease) and Y. enterocolitica (generally subclinical)
§ Differ from wildlife serotypes
○ Risk factors
§ Previous outbreaks - seems to be more a problem with high input system
§ Stress (nutrition, worms, environmental) on carriers
□ Oro-faecal cycling
53
Yersiniosis diagnosis and treatment
```
○ Diagnosis
§ History and clinical signs (2-20% deaths)
§ Gross PM - diptheretic enteritis
§ Histo and culture
○ Treatment
§ 1-2 x with L/A oxytetracycline
§ (sulphadimidine variable)
§ Sulphatrim (sulfadiazine and trimethoprim)
```
54
Salmonellosis leading to enteritis when generally occur and diagnosis
```
○ Sporadic - stress and crowding
§ Drought-lots
§ Transport
§ Ewes at lambing (abortion)
○ Variable serotypes
○ Diagnosis
§ PM (acute vs chronic)
§ Bacto (SI, MLN (mesenteric lymph nodes), gall bladder, heart blood)
```
55
Salmonellosis treatment and control
```
§ Isolate and treat clinical cases
§ Raise feed off the ground
§ Provide roughage
§ Decontamination after an outbreak
§ Antibiotics to whole group? - NOT GOOD FOR RESISTANCE
§ Bacterin?
```
56
Nutritional scouring what crop associated with and other risk factors
- Lush feed eg: phalaris, capeweed
- Rotational grazing (cereal crops)
- Ryegrass endophyte
- Excess water/minerals
○ K+ in potash
○ Mg++ in water
- Excess soluble CHO (fructans) or dietary soluble fibre (non-starch polysaccharides) in LI -> hind-gut fermentation/acidosis
- Excess protein in hindgut
57
Neonatal diarrhoea what leads to, 4 main causes, how common, treatment and importance
- Afebrile, anorectic lambs/kids
○ Cryptosporidia (C. parvum); 5-10 days old
○ Giardia; 2-4 weeks old
○ E. coli; 1-5 days old
○ Viruses
- All occur but rarely confirmed
- Fluid and electrolyte therapy for affected lambs as for calves
- Can be zoonoses
○ Orphan lambs or kids
○ Petting zoos
○ Grazing of water catchments -> secretion of cryptosporidium and giardia
58
Wasting only how common an what leads to
○ Large inflammatory reaction -> fairly uncommon to have JUST wasting WITHOUT diarrhoea
○ Ovine Johne's disease -> would lead to wasting WIHTOUT diarrhoea
59
How to determine whether egg burden is pathological
```
Pathological burden in:
• Adult sheep: ≥ 4 severity points
• Weaners: ≥ 2 severity points
Haemonchus - 500 = 1 severeity point
Trichostrongylus/ostertagia - 4000 = 1 severity point
Immature - 4000 = 1 severity point
```
60
WECRT how to calculate % reduction, what is considered not to be resistant and what is important to ensure can compare treatment and control group
% reduction -> 1 - (Drench average WEC/control average WEC)
No resistance parameters
- % reduction -> >95%
- Confidence intervals -> LOWER NEEDS TO BE ABOVE 90% to be no resistance
Collect all the faeces at the same time from treatment and control group
61
What can do after the WECRT to increase information and possible strategic management
PCR test to identify species that are the main clinical concern
62
If having issues with parasite control what need to consider changing
- Change the summer drenching (if noT DEC, feb)
- Ensure not under-dosing
- Make sure staff know what they are doing
- Smart grazing - use cattle to prepare low-risk paddocks too
○ Weaners and maiden ewes are the vulnerable groups
- WEC monitoring on different mobs - every 6-8 weeks
○ Help to work out is it just one paddock or mob or whole herd issue
- CHANGE THE DRENCH - rotate - WECRT to determine resistance
63
What are the 2 alternative to the WECRT
– single post-treatment WEC
| – post-treatment TWC
64
What is the best option for drench resistance in a small flock and what couldn't do
- A full WECRT- NOT ENOUGH ANIMALS - 90 animals needed
BEST - Pre- and post drenching WEC (‘Drenchcheck’)
○ Just do a bulk on them
○ Only tells efficacy of CURRENT GROUP -> don't know what the something else to go to is if the result is resistance
65
In a farm with small angora goats (40 does) and 2 cows on 5 Ha what is the winter stocking rate for the herd, is this over or under stocking
1.2DSE late pregnant doe (40x1.5)
10-15DSE -> depending on lactation (2x15)
60+30 = 90/5 = 18DSE
13DSE/ha - overstocking
66
What occurs with copper storage and liver disease in small ruminants
In small ruminants the liver is an important storage organ for copper -> copper directly damaging to RBCs
- If liver accumulates too much copper due to liver damage or increased consumption -> build-up of copper -> jaundice (due to hepatopathy ALSO could be due to copper destroying the RBC - haemolysis -> SEVERE ANAEMIA)
67
Mycoplasma (Eperythrozoon) ovis what is it, results in and epidemiology
- Intracellular parasite
- Increase RBC destruction - haemolytic anaemia
- Epidemiology
○ Particularly affects young animals
§ Lamb marking increase susceptibility
○ Blood-blood / insect transmission
§ Is this present in history?
○ Carriers?
68
Mycoplasma (Eperythrozoon) ovis clinical signs, diagnosis and treatment
- Clinical signs:
○ Anaemia, jaundice & illthrift
○ Occasional haemoglobinuria
- Diagnosis
○ Only real cause of haemolytic anaemia that leads to the salmon pink kidneys
○ HARD TO DETERMINE ON BLOOD SMEAR - if don't detect mycoplasma doesn't rule out the disease
- Treatment
○ Improve hygiene
○ ↓ stress (mark earlier, better nutrition) -> help reduce the susceptibility and severity of the disease
○ LA oxytetracycline - but how much of the mob needs treating?
§ affected/at risk
§ all in severe outbreak
69
What are the 3 main causes of haemolytic anaemia in sheep
1) Brassica toxicity
○ kale, turnip, rape
2) Tick-borne Babesia & Theileria infections
3) Mycoplasma ovis
70
Brassica toxicity what plants caused by, what occurs, how does risk vary and treatment
- e.g. kale, rape, turnip, swede, winifred, canola
- SMCO converted to dimethyl disulfide in rumen
○ Haemolysis
○ ± photosensitisation, nitrate poisoning, goitre, diarrhoea, respiratory distress
- Risk very variable: maturity, variety, frost, etc – NEED TO KNOW WHICH BRASSICA YOU’RE DEALING WITH
- Treatment
○ No cure - same treatment as for PA poisoning -> REMOVAL FROM PASTURE
71
Pyrrolizidine alkaloid poisoning what occurs/clinical signs and main presentation
PAs are Hepatotoxic
- Permanent & cumulative
○ Acute toxicosis: jaundice, death within two weeks - DEAD
○ Chronic liver damage
§ 2º ill-thrift & photosensitisation - PEELING
§ predispose to/precipitate Cu release & haemolytic anaemia - YELLOW OR PALE
Presentation
- Placed onto these plants, see deaths, weakness
- Find jaundice and pale in PM
72
Pyrrolizidine Alkaloid Poisoning diagnosis and main plants involved
- Dead/pale/yellow + hx of exposure
- Southern Aust.:
○ Paterson’s Curse (Echium)
○ Heliotrope (potato weed)
○ Ragwort (Senecio)
- Serum biochemistry
- Gross PM & liver histology
PLANTS - patterns curse, reagwot
73
Pyrrolizidine Alkaloid Poisoning post mortem changes and main presentation
- photosensitisation and hypoproteinarmia - subcutaneous oedema of the head
- micronodular cirrhosis - chronic poisoning
REMEMBER -> PA poisoning doesn't always cause JAUNDICE - but MORTALITY is the most common presentation
74
Pyrrolizidine Alkaloid Poisoning treatment options
- No direct effective treatment
- Remove from source
- Supportive care - can save some animals - need to re-evaluate on a daily or weekly basis
○ Low protein, high energy feeds
§ Good access to feed and water
○ Subcutaneous (or IV!) fluids
○ Avoid sunlight: put in shearing shed, shaded paddocks - DUE TO RISK OF PHOTOSENSITISATION
○ Antihistamines
○ Antibiotics & flystrike prevention for secondary skin infections
- Salvage slaughter? - generally once recover do want to sell then
75
Copper what are sheep good at, 2 ways chronic copper toxicity can occur and bred variation in susceptibility
- Sheep are very good at absorbing copper & storing copper (compared to cattle)
CHRONIC
1. damaged liver - excess storage
2. Diet low in MO - Mo antagonises the Cu so when low INCREASE availability of Cu to the sheep - Liver is normal but still getting the toxicity
BREEDS
- Certain breeds are better absorbers
Big breed variation in susceptibility:
- Many continental breeds (e.g. Texel) good absorbers (& easily poisoned)
- North Ronaldsay breed eats only seaweed: absorbs Cu so well can suffer toxicity on diets that cause Cu deficiency in other breeds
- Merinos absorb less well so less at risk of toxicity
76
Copper toxicity in sheep treatment
- Need to bind copper - need to give the Mo
- Drench/inject with ammonium tetrathiomolybdate (contains the Mo that binds)
○ Acute cases: 3.4 mg/kg IV q 48 h for 3 treatments
- At-risk pre-haemolytic cases: Excellent results by providing loose lick to bind copper:
○ 90% salt
○ 9.8% gypsum
○ 0.2% sodium molybdate
○ 50 g/head/day
77
Target for pregnancy rate, conception rate and lamb marking rate
- Pregnancy rate ≳ 95%
- Conception rate: as high as possible! - realistically 90–150+%)
- Lamb marking rate must be> ~60–70% to remain self-replacing
78
In reality what occurs for lamb marking rate for merinos, prime lamb and mortality leading to what
- Lamb Marking Rates
○ Merinos 60 – 100%
○ Prime Lambs 100 – 160%
- Mortality in Pasture Lambing Systems
○ e.g. Hamilton: 13% (singles) – 30% (twins)
- Potential for increased production and better animal welfare
79
Lambing systems what are the 3 main aims and the challenges
- Efficiently use feed (lactating ewes need more)
○ Also if twins and triplets need better nutrition
- Improve supervising labour efficiency
○ Too much interference may increase mismothering
- Good animal welfare (ewes and lambs)
Challenges
- Disturbances causes, MISMOTHERING and lamb deaths (especially merinos)
80
what is the current recommendation for lambing systems and the 3 main types
Current recommendations
§ Lambs in smaller mobs (<100-150 maidens) -> easier for lambs to find mothers and ewes won't interfere with mothering interaction
§ Avoid excessively high stocking rate (try <7-10 ewes/ha)
Types
1. Paddock lambing - tight lambing period important - 6 weeks
2. Indoor lambing
3. Drift lambing - within smaller paddocks outside
81
Vaginal prolapse how similar to cattle, high risk and what is important to advise clients on
- Principles same as cattle BUT can see as a sporadic outbreak in a flock in
- over-fat ewes / twinstriplets / hilly paddocks! (NZ)
- Less likely for farmer to call vet and can be important welfare problem
Correcting vaginal prolapse in small ruminants
- Client education: recognition, seeking help
○ Case selection is important -> fresh uterine prolapse easier to replace, chronic ones may be better to euthanise
82
What is involved in correcting vaginal prolapse in small ruminants
- Lignocaine + xylazine low epidural very helpful to reduce straining
○ 0.07 mg/kg xylazine mixed with 0.5 mg/kg lignocaine injected into sacrococcygeal space
○ e.g. 0.2 mL xylazine & 1.5 mL lignocaine (both 20 mg/mL)
○ lasts ~24 hours
- Retain with umbilical tape -> Buhner stitch
○ Leave 2-finger space
○ Long tape ends to untie easily at lambing
83
Perinatal lamb mortality what is the average, main risk period, other risks and what needs to be done to determine cause of death (most common)
- Average 15%, twins > singles -> FIRST 3 DAYS OF LIFE IS THE RISK PERIOD
○ Twins -> lightweight, less stores -> hypothermia more at risk
- Do a series of necropsies in the field, determine major cause of death and then form a management plan
Multiple causes - SEM (starvation, exposure, mismothering)
84
What are the 5 main causes of perinatal lamb mortality
1) starvation
2) mismothering
3) exposure
4) predation
5) dystocia - more common in single larger lambs
85
Starvation causing perinatal lamb mortality why generally results, risk factors and risk factor for
○ Dystocia makes bonding and suckling less successful
-> weaker and less able to establish maternal bond
○ Risk factors due to poor fat reserves in neonates
○ Starvation is a risk factor for exposure
86
Mismothering causing lamb mortality what leads to, possible causes
○ Leads to Poor milk and colostrum intake
○ Possible causes
§ Foetal anorexia if a twin -> decreased mothering interactions
§ Disturbance of the ewes and the lambs -> use binoculars for observation
□ Critical time is the ewe needs to stay with the lamb >5 hours after birth
® If moves away and stays away at this point more likely to have mismothering
87
Exposure causing lamb mortality risk factors and prevention
```
○ Risk factors
§ Low birthweight
§ Poor brown fat reserves
§ Cold, wet and windy weather
§ Poor shelter
○ Prevention
§ Need lots of shelter across paddocks to be effective (<50m apart)
§ Shearing doesn't help overall
§ Care not to compromise ewe nutrition
□ Ensure ewe CS -> to provide adequate milk, birthweight and fat reserves
® Target is CS3 at lambing
□ ALSO -> ensure enough nutrition in the paddock -> to maintain energy requirements for lactation
```
88
What are the 9 main ways to diagnose perinatal mortality cause
1) weight - expect 8% of mother
2) mothered - has been cleaned
3) walked - slippers (crow also possible)
4) predation
5) dystocia - subcutaneous oedema head and legs, meconium staining
6) breathes - lungs - partially inflated? dystocia
7) drunk - milk in abomasum
8) metabolised brown fat - not live long enough to be exposed to cold conditions
9) hemorrhages or signs of infection - viscera
89
Predation what signs indicate and foxes vs crows
○ Prior to death-> lots of haemorrhage around wounds indicate heart still beating while being predated -> may need to look under the skin to find this
○ Foxes -> more likely to puncture wounds around neck and remove viscera
○ Crows -> pecked out eyes, anus, mouth
90
In summary what is the 3 main solutions to perinatal mortality
```
1) Ewe CS & nutrition!
○ Targets:
§ CS 3, 900 kg DM/ha (late gest.) rising to
§ 1200–1500 kg DM/ha (lact.)
○ Better birthweight
○ Better fat stores
○ Better cold resistance
○ Better bonding
2) Shelter
○ Needs lots of it across paddock
○ Costly
○ Don’t compromise ewe feed quality
○ IS A LONGER TERM OPTION -> not a thing that can be done 2 weeks out from lambing
3) (Coordinated) predator management
○ Needs to be done across farms -> baiting
```
91
Iodine deficiency what can it lead to, what does iodine result in, what varies intake
can be a specific cause of perinatal mortality and hypothermia
- Iodine → T4:
○ foetal growth
○ CNS development
○ neonatal survival
- Great Div. Range soils deficient
- Seasons intake varies with soil ingestion
○ low in winter/spring
○ high in summer
- Goitrogens in white clover, Brassica spp
- ‘Big springs’ – seasons/years with very abundant pasture growth
92
Iodine deficiency risk factors and clinical signs
- > 80 mm rain/month ≥ 3 months before pregnancy/lambing
○ High rain dilutes the amount of iodine available in the grass
○ Also increases the grass length which decreases soil grazing (where get iodine
- Goitre in lambs/kids
- Weak lambs/kids
- High neonatal mortality
93
Iodine deficiency diagnosis
- Thyroid > 0.4 g per kg bodyweight (0.04%)
- Histology of thyroid
- Response to iodine treatment
- Lamb T4 < ewe T4
94
Iodine deficiency treatment and prevention
- Response to treatment is good -> can be used to confirm diagnosis
- 280 mg KI to ewes in last trimester
- 20 mg KI to lambs
- Lipidol 1 mL
- Check for/treat concurrent Se deficiency
- Overdosing can cause iodism
95
Principles for what is needed to artificially rear kids
- Good colostrum management essential
- Avoid overfeedings
- Vit A/D/E at birth
- Vaccinate
- Excellent hygiene
- Solid feeds -> introduce as soon as possible
○ >11MJ/ME/kg DM
○ >18% CP
- Dehorn
96
Colostrum management in sheep how much need to supply, how to test
- Supply IgG 3 g/kg (volume ≈ 10-20% of BWT)
- Can’t use bovine colostrometers
- Can test kid serum afterwards with general assays (e.g. gluteraldehyde coagulation test)
97
Neonatal diarrhoea in sheep what are the main pathogens, prevention and treatment
```
Similar to other ruminants
- Rotavirus
- Coronavirus
- Cryptosporidium
- E. coli (enterotoxic) strains
- + coccidia?
- Kids can succumb quickly (light bodyweight, poor colostrum intake, potential poor milk access)
Prevention
- Same as calves -> generally due to failure of passive transfer of colostrum -> correct this
- Also hygiene and contamination of the environment
Treatment
- Like calves
○ Electrolytes, fluids nutrition vital
- Supportive
```
98
Rearing orphan lambs and kids when need o be done and inital treatment
- Usually a lost twin or the ewe has died
- Often found cold and weak
- Initial treatment
○ Warm up – warm air, hot water bottles etc
○ Colostrum before 12 hours
○ If very weak give 20–50 mL warm 20% dextrose IP
○ Then may foster onto ewe or bottle feed
- Hand feeding is a big job – train onto teat & bucket asap
99
Rearing orphan lambs and kids feeding what is the aim, main thing need to give
- Aim to get suckling and introduce milk
○ Stomach tube at start if necessary
- COLOSTRUM COLOSTRUM COLOSTRUM
○ From ewe: lambed or freshly dead ewe (beware diseases)
○ Cow colostrum acceptable
○ Fresh or thawed
- Sheep milk has higher fat and protein than cow’s milk -> don't use cows milk or just add below
○ Make ‘egg nog’:
§ 4 eggs in 500 ml of full cream supermarket milk
§ Junket tablet aids curd formation in stomach
- Feed little and often to start
○ 4 x 200 mL/day
○ progress to 1.5–2 L/day by 3-4 weeks
100
hand-rearing what need to train with, introduce to and monitor success, what also need to provide
- Train onto commercial milk replacer (e.g. Veanavite®, Divetalac, Wombaroo)
- Introduce to lamb feeder when expecting next feed (i.e., hungry but NOT starving)
- Train with warm milk; cold thereafter
- Monitor success by regular weighing
○ Target: ≥ 150 g/day
• Also provide:
- Clean drinking water
- Access to lamb pellets & hay/straw from week 2
- Access to short pasture (but beware worm, etc contamination!!)
101
Hand rearing problems at what age and treatment
```
- Bloat
○ Age 3–4 weeks old, guzzling milk → Sarcina overgrowth
○ Tx: slow drinking rate
§ Add formalin 1 ml / litre
§ Feed milk replacer cold ad lib
§ Reduce orifice size in teat
```
102
Fostering lambs what type of lamb, what from and foster ewes
- Only foster strong, healthy lambs
- Lambs may be from
○ ewes w. too many lamb
○ Poor condition ewe with Twins
○ lamb from AR group
- Foster ewes:
○ lamb died or stillborn (but disease risk?)
○ in good condition,
○ plenty of milk,
○ healthy
○ NOT young or old
103
Fostering strategies what are the 5 main ones
- Smell: Rub fostering lamb in birthing fluids from adopter ewe soon after lambing
○ Can tie afterbirth around lamb’s neck too
○ OR skin dead lamb & tie pelt over fostering lamb (NOT if lamb died of disease)
- Behaviour: Confine lamb (e.g. in a clean rubbish bin) or temporarily tie front legs together so behaviour mimics newborn lamb that isn’t walking yet
- Confinement: Afterwards confine ewe & lamb in small pen for several days so lamb can suckle easier
- Checking: Monitor closely to ensure ewe not harming lamb
- Alternatively, confine lamb with adopter ewe in head bail so lamb can suckle several times daily – after several days ewe may accept lamb
104
Weaning lambs when to introduce pellets, when to wean, why and what need to ensure
- Introduce to pellets & roughage from d. 7
○ Encourages rumen development
- Wean > 30 days old (pref. 40–60) d.o. & 10 kg
○ Rumen function starts @ 3 weeks
○ Fully functional @ 6 weeks
- Ensure eating solids well
- Wean abruptly (avoids big bullies taking all milk)
