1
Q
Nasal bot flies lifecycle, size and lifecycle
A
- Similar life cycle to blowflies but uses the nasal passages and sinuses for larval development instead of skin
- Adult is grey in colour, size of a bee
- Grubs are 3cm long with distinctive black banding
Lifecycle - Larvae deposited in nasal passages, sometimes orbits
- Larvae take 1-9 months (longest in winter) to develop then are sneezed out and pupate in the soil
- Adult fly emerges after a month
- 1-2 generations per year
- Over-wintering as 1st instar larvae in sheep
2
Q
Nasal bot flies clinical signs and treatment
A
Clinical signs - Irritation and head tossing - Mild discharge - Snoring - Incidental finding in post-mortems - Not economically significant Treatment not warranted – ML drenches and closantel give good control
3
Q
Pesticide residues what occurs with pesticides, what are the 3 main things they have implications for
A
- All pesticides break down gradually after application and are diluted as wool grows
○ but all except Mg fluorosilicate and spinosad leave some residue at shearing - These residues have implications for:
○ Environment
○ Trade
○ OHS
4
Q
Pesticides residues what are the 4 important things to observe
A
○ Meat and milk withholding periods (WHP)
○ Export slaughter interval (ESI)
○ Wool harvesting interval (WHI)
○ Wool rehandling period
5
Q
Fleece rot cause pathogenesis and clinical signs
A
Cause - Pseudomonas aeruginosa, but other bacteria can be involved
Pathogenesis
- Prolonged wetting of the skin and warm temperatures cause bacterial proliferation and production of pyocyanin
Clinical signs
- Small crusts seen but mainly discolouration: blue-green to brown over time, also green, purple, brown, grey
- Shoulder, back, loin most affected
- Self-limiting - last for a week or two and then heals and grows away from the body
6
Q
Fleece rot significance, which sheep most suceptible, risk period, predisposing factors and what can do to prevent
A
Significance
- Some stain does not scour (cleaning the wool) and therefore devalues the wool
- BUT MOST IMPORTANTLY
○ Fleece rot is very important predisposing factor in body blowfly strike
- Sheep are most susceptible with 4-6 months’ wool
○ Can penetrate easily but doesn’t dry out as easily
- Risk period is late spring to early autumn – so late summer/autumn shorn sheep most susceptible
- Predisposing factors
○ Merinos more susceptible than British breeds and strong wool > fine wool strains
○ High colour, FD variability, shaggy tip, high suint (like sweat) are associated with fleece rot
- High heritability of susceptibility within flocks (h2 ~ 0.4) -> can cull successfully
7
Q
Fleece rot treatment/prevention and the 4 key points
A
Treatment/Prevention
- No treatment, but consider fly prophylaxis
- Look for bloodlines with active policy to select against fleece rot – difficult to do in low rainfall areas
- Cull on fleece rot and undesirable fleece characteristics
- Choose a low-risk time of shearing – but many other factors must be taken into account
KEY POINTS
1. Prolonged wetting in warm conditions
2. Sheep in 4-6 months’ wool
3. Predisposition to flystrike
4. Highly heritable, but must show itself
8
Q
Dermatophilosis what also called, caused by and clinical signs
A
- Dermo, lumpy wool, mycotic dermatitis
Cause - by Dermatophilus congolensis
Clinical signs - Ulceration then sloughing and repeat
- Active lesions on wool-producing skin show inflammation leading to exudate which forms a crust and mats the wool fibres, initially at skin level
- Chronic lesions present as scabs or mats of dried exudate grow out with the fleece, few mm to several cm across
- Lesions on non-wooled areas are small plaques <1cm -> ears and face -> important source of infection
- Severe generalised dermo may be seen in young sheep
- Derangement of fleece - matted
9
Q
Dermatophilosis how common, resistence, what are the 3 things dermo requires to infect
A
- Very common
- Sheep develop some resistance on exposure -> why dip older sheep last
- Dermo requires:
○ Susceptible sheep + A wetting event + Suitable contact
1. Wetting is needed to release zoospores on carrier animals – events include jetting, dipping, rain
2. Mechanical transfer can commence by ~30 minutes after wetting
3, Close contact is likely to occur at yarding, transport in the rain or dipping
□ DON’T YARD ANIMALS WHEN WET, RAINING OR AFTER DIPPING
10
Q
Dermatophilosis significance and treatment
A
Significance
- Can reduce fleece weight by 5% and cause downgrading of cotted wool – weaners / hoggets produce the most valuable wool
- Difficult to shear cleanly
- Unsuitable for pour-on lice control
- Active lesions predispose to fly strike
- Deaths, especially young animals
Treatment
- One dose of long-acting oxytetracycline may be effective in resolving more lesions than would self-cure
- May be useful to stop active lesions in advance of shearing (at least 6 weeks) or in severely affected young animals - otherwise not done as will generally self-cure
11
Q
Dermatophilosis prevention and 5 key points
A
Prevention
- Avoid prolonged contact events when sheep are wet – especially young sheep
- Use zinc sulphate (heptahydrate) in dip or jet fluid
- Breeding for resistance is not very useful (h2 ~ 0.1-0.15)
Key points
1. Effects on FW, $/kg and ability to be shorn
2. Mainly young sheep
3. Susceptibility + wet sheep + close contact
4. Avoid letting these things happen together!
5. ZnS04 in the dip or jet
12
Q
Strawberry footrot what is it, when common, what age most susceptible and clinical signs
A
- Dermatophilosis of the legs
- Common in winter with persistent wetting
- Weaners and hoggets most susceptible
Clinical signs - Exudative dermatitis extending from the pasterns dorsally
- Confined generally to haired regions
- Scabs are easily knocked off when walking revealing raw granulating tissue - source of infection
- Lameness
13
Q
Diagnosis and treatment of strawberry footrot
A
- Clinical signs and confirmation by Gram stain
- May be able to move sheep to a drier paddock or one with shorter pasture
- Antibiotics may help, but are rarely justified - only if very severe
- Clinical course is 4-6 weeks, prolonged if lesions are continually wet or secondary bacterial infections occur
- Looks like scabby leg - similar pathogenesis and treatment -> prevent excessive wetting
14
Q
Scabby leg location and what common
A
- Scabby leg is seen around the pastern, coronet and between the bulbs of the heel
- Secondary infection by Dermatophilus is common, as is flystrike
15
Q
Scabby mouth what also called, cause, pathogenesis
A
- Contagious ecthyma, contagious pustular dermatitis, orf, scabby leg
Cause - Caused by a Parapoxvirus
Pathogenesis - Infection requires a break in the epithelium
- Small hyperaemic foci develop within 7 days, vesicle forms and bursts, scabs left in areas other than the oral mucosa
- Lesions and disease usually resolve within 3 weeks
16
Q
Scabby mouth clinical signs, where present, which month most common, spread of disease and immunity
A
Clinical signs
- Lesions are seen mostly at the commissures of the lips but also anywhere on the oral mucosa, nasal membranes, ears and teats
- Almost ubiquitous and exists on most farms in Victoria
- Occurs most commonly in summer months, with virus entering through cuts and abrasions associated with dry feed
- Scabby leg is usually seen in winter with persistent wetting and softening of the skin
- Disease can spread quickly when there is a large number of naïve sheep feeding from troughs
- Large quantities of virus are produced in the lesions, which remains infective on pasture and in feed for very long periods
- Immunity following infection (or vaccination) is long lasting (2-3 years)
17
Q
Scabby mouth/leg diagnosis and significance
A
Diagnosis
- Via clinical signs
- Looks like strawberry footrot but treated the same - both self-limiting just dry
Significance
- Usually of little consequence with outbreaks in weaners which resolve over several weeks
- May be decreased grazing and therefore weight loss due to painful mouths
- Ewes with teat lesions are reluctant to allow lambs to drink - transmission
18
Q
Scabby mouth/leg treatment, control and zoonosis
A
Treatment, control
- There is no treatment and the disease is self-limiting
- Live virulent vaccine
○ Scratched onto skin of axilla
○ The vaccination site of a few sheep should be checked for ‘take’ (reaction)
○ Some shipments require vaccination
Zoonosis
- People can be infected on the hands or leg
- Handling infected sheep and accidental inoculation with vaccine are the most common sources
19
Q
Actinobacillosis what also called, cause, when main issue, prevalence in herd and clinical signs
A
- Leather lips
- Actinobacillus lignieresii (causes woody tongue in cows)
- Occasionally causes problems when sheep are on coarse dry feed in late autumn and summer
- <10% affected but occasionally large outbreaks with up to 30% of animals - rare
Clinical signs - Areas affected include the lips, face, nose, lower jaw and lower neck, and rarely the tongue
- Lesions may be superficial or a deep honeycomb of small abscesses beneath the skin, often discharging sinuses with yellow-green pus
20
Q
Actinobacillosis diagnosis and treatment
A
- Clinical signs are diagnostic, swabs to confirm
- Most sheep recover
- Can treat with antibiotic (iodides, tetracyclines, erythromycin), provide soft feed
21
Q
Squamous cell carcinoma how common, location, prevalence and what can be associated with
A
- Very common on older sheep
- Occur on 2 major exposed areas: vulva, anus, tail and bare mulesed skin (‘rear end’ cancer) and face, planum, lips, and especially the ears
- Prevalence influenced by age: 1% typical but can be >20% SCC in sheep older than 5 years
- SCCs of the perineal region are usually associated with mulesing – trauma to the skin may be a risk factor
22
Q
Squamous cell carcinoma pathogenesis how grow, what prove to, predisposes to and diagnosis and treatment
A
Pathogenesis
- Usually start as one of two forms: a hyperkeratotic nodule or a column (cutaneous horn)
- Tumours grow relatively slowly – around 6 months to get to around 5cm – and rarely metastasise remotely
○ Treat if high valuable animal is possible -> removal of tumor
- Very vascular and prone to damage and bleeding
- Predispose to secondary bacterial infection and flystrike
Diagnosis, treatment
- Diagnosis based on clinical signs – most farmers are very familiar with them
- Treatment is seldom worthwhile but some farmers will trim ears to remove tumours (chargeable offense)
○ EUTHANASIA
23
Q
Squamous cell carcinoma what are options for prevention
A
- Lower the culling age
- Cut tails at the 3rd coccygeal joint (cover the tip of the vulva) -> don’t cut too short
- Use ‘modified V’ mulesing pattern to leave wool on the tail - better still - DON’T MUSEL
- Provide shade in all paddocks
- Minimise the number of eartag notches etc
24
Q
Facial ecezma what is it caused by, when present, what prefer, when have outbreaks and where
A
- Hepatogenous photosensitisation caused by ingestion of the fungal toxin sporodesmin, produced by Pithomyces chartarum
- Fungus is present all year round but requires moist warm conditions to multiply sufficiently – late summer/autumn
○ minimum temps >15oC for 72 hours - predictable -> warnings about storms - annual pastures are less dangerous
- outbreaks in summer/autumn (gippsland)
25
Facial ecezma clinical signs and how long take to develop
- Signs develop within about 1-3 weeks of toxic insult
- Initially photophobia and pruritis, restlessness, shadeseeking, twitching, shaking of head and ears
- Affected areas rapidly become erythemic and oedematous – swelling of the ears, eyes, intermandibular space, nose
- Nasal discharge and lacrimation
- Serous weeping of the skin as it becomes necrotic and progresses from crusty to black and eventually sloughs leaving areas of raw skin
- Jaundice in more severely affected animals
- Many animals slowly recover but many have permanent liver damage
26
Facial eczema treatment and prevention
Treatment
- Move animals from source of toxin to safer areas with access to shade
- Put severely affect sheep in sheds and feed low protein diet (give the liver a break)
- After recovery cull all affected sheep
Prevention
- Do spores counts after high risk weather
○ When spore counts are high move sheep to tallest pasture to minimise grazing of lower sward, feed hay
- In NZ, pastures may be treated with fungicides such as thiabendazole
- Zinc can be useful if given before exposure – ZnSO4 in drinking water not as effective as in cattle but ZnO as a slurry every 2 weeks has helped
- Controlled-release capsule (Time Capsule®) available in NZ: 6 weeks’ protection
- In NZ, selection for resistance to facial eczema
○ High heritability: h2 = 0.42
27
Lupinosis cause, where located, what conditions, what most susceptible
Cause - Hepatic disease caused by the fungus Diaporthe toxica (ex Phomopsis leptostromiformis) which grows on lupin stubbles - MAINLY IN WA AND SA
- Under moist warm conditions the fungus proliferates and produces a stable hepatotoxin
- Affected paddocks are dangerous until fresh growth is treated
- Weaners most susceptible because they eat more stem
28
Lupinosis clinical signs and diagnosis for the two types
Clinical signs
- Two syndromes
○ Acute: inappetence, depression, lethargy, jaundice, deaths
○ Chronic: weakness, lethargy, loss of condition, stifflegged gait, disorientation
- Abortions, reduced lambing percentage, reduced wool production and tender wool with both syndromes
- Sheep that recover often fail to thrive
Diagnosis
- Diagnosis based on clinical signs, history and PM findings of acute to chronic liver damage
○ Differential diagnosis for acute: caltrop, other plant toxins e.g. Paterson’s Curse, eperythrozoonosis
○ Differential diagnosis for chronic: protein/energy deficiency, parasites, OJD, trace elements
29
Lupinosis treatment
- Move animals from source of toxin to safer areas with access to shade
- Put severely affected sheep in sheds or paddocks with good shade and feed low-protein diet (e.g. oaten hay)
- Euthanase severely affected sheep
- After recovery cull all affected sheep
30
Lupinosis prevention 6 options
1. Use lupin stubbles efficiently and quickly after harvesting
2. Provide two watering points to promote even grazing
3. Train sheep with lupin seed
4. Once grain falls below 40/sqm remove sheep
5. Observe sheep on lupin stubbles as closely as possible
6. Check lupin seed before feeding – avoid using if >10% discoloured
31
Dermal necrosis when most susceptible, location, clinical signs and treatment/prevention
- Recently shorn, fat sheep (<2 weeks), in very hot weather and lack of shade
- Subcutaneous fat on backline heats up
- Hard, black skin after a few days, sloughs, heals over several weeks
- Antibiotics and a fly preventive may be useful
32
Grass seeds how common an issue, main involved, what affect and mostly problem in which sheep
- Grass seeds are a major problem on some farms - depends on the pasture used
○ Barley grass, spear grass and corkscrew are the major offenders in southern Australia
- Can affect lamb growth rates
- Seeds are unsightly and publicly unacceptable in meat cuts – heavy carcase contamination can cause downgrading due to heavy trimming
- Mostly a problem in sheep with long wool
33
Grass seeds prevention
- Shear before problem grasses set seed
- Young sheep are at greatest risk so keep them out of affected paddocks
- Spray graze
- Renovate pastures to displace problem species - ryegrass, phalaris, clover
34
List 10 causes of damage to sheep skins
1. Over-crutching
2. Trucking stain
3. Raddle marks
4. Grass seeds in the wool and pelt
5. Burrs in the wool
6. Vaccination puncture sites
7. Shearing cuts
8. Wool diseases – dermo, fleece rot, lice
9. Dog bites
10. Handling injuries
35
Over crutching what is the main affect, raddle (large cradle used to mark sheep) marks how occurs, how to prevent
Over crutching
- Meat buyers often like a wide crutch, but skin is more valuable with a keyhole crutch
- Crutching over a larger area reduces the area of woolly skin and destroys the natural shape of wool on the skin, which may necessitate further trimming
Raddle (large cradle used to mark sheep) marks
- Woolly skins are scoured at body temperature (37°C) and raddle marks may not be removed
- Raddles and stock markers should be kept to an absolute minimum on sheep destined for sale
- Marks should be restricted to the head or top knot only, with the central panel of the skin kept clean
36
Trucking stains what regulations in place to prevent this and what does it increase the risk of
- Sheep should be yarded for at least 12 hours before transportation, and:
○ Offered only dry feed
○ Offered water, then none for 12 hours (journeys <24 hours)
○ Offered water to at least 4 hours pre-loading for journeys >24 hours
§ But refer to the Standards
- This ‘curfew’ minimises soiling of wool on the belly, flanks and/or hind legs
- Trucking stain significantly increases the risk of carcase contamination with Salmonella and E. coli bacteria at slaughter
37
Burrs on sheep skin how to remove, when cause issue and prevention
- Skins can be deburred, but this involves additional costs and causes damage to some skins
- Hard burrs such as Bathurst and Noogoora burrs cause problems during fleshing
- Prevention involves shearing or selling lambs before burrs appear, and pasture management to eradicate burrs from paddocks where sale sheep are run
38
Vaccination sites causing skin issues what result in and how to prevent
- Vaccination punctures can leave a small fibrous scar which is a visible blemish in the processed leather, or at worst, subcutaneous adhesions and abscesses
- Sheep should not be vaccinated on the back or shoulder
○ the easiest and most commonly used sites! – better to use the brisket, neck, cheeks or axilla
39
Sheep and goat mastitis how common and causes
Sheep
How common
- Terminal sires -> up to 5% normal
- First cross - about 2%
- Merino - 1 or 2%
- All breeds - outbreak with up to 20-30% of ewes affected
- Dairy breeds - depends on hygiene/environment
Causes
1. Mannheimia (pasteurella) spp. - most common (not seen in dairy cows)
2. Staphylococcus aureus
- Both can lead to black or blue mastitis
Goats
- Relatively uncommon but same causes
40
Sheep and goat mastitis what is the worse mastitis type, clinical signs and what does other clinical mastitis lead to
Black mastitis
- Can lead to death quite rapidly
- Almost all ewes culled at end of current lactation
- If retained, half udder non-functional - problem with twins and triplets
- Lambs generally die or are fostered
○ Quality and quantity of milk declines
- Lame, lose weight
Other clinical mastitis
- Less severe, may not result in loss of udder
- Milk quality impact
- Lamb death rate
- Reduced production
41
Subclinical mastitis in goats and sheep, what is the most common pathogenis, how tested and what can predispose
Sub-clinical
- Most common pathogens = staphylococcus and streptococcus
- Not as well tested for as sheep generally not as used to being milked -> not routinely done
- Higher cell count in ewes with twins -> more milk produced and more nursing events leading to larger infection rates
Predispose = Genetics
Udder confirmation -> teat placement
42
Treatment for goat and sheep mastitis
- Antibiotics
○ Intramuscular - most common
○ Intramammary - not as common as NOT REGISTERED PRODUCTS - off-label use
§ Need to use cattle intramammary -> need to give smaller dose than cattle, half tube but don’t use tube again for other sheep -> need to give specific instructions for
○ Penicillin and tetracycline
○ NEED TO GET IN EARLY -> otherwise likely to die
- Give anti-inflammatory
43
If have a long wool and in joining with lice what should you advise the farmer to do for treatment
- Not in short wool so likelihood of eradication is low -> therefore maybe shouldn't treat everything as expensive and won't be able to eradicate
- As now in joining -> shouldn’t shear and movement of rams
- If want eradication -> need to shear everything and treat everything on the farm
○ Premature shearing has a bad cost
○ At 11 months okay but NOT 8 MONTHS
- TREAT just this mob of ewes now with a long-wool lice product
○ Should treat as if leave for another 4 months then more wool damage - cost associated
44
List 3 reasons that a farmer may fail to eradicate lice in the previous year treatment
1. The farmer was not careful to muster and treat all sheep last year
2. The lice on this farm are resistant to the class of chemicals used last year
3. The ewes lambed within the "quarantine period" of the chemicals used last year
○ If ewes were still infected than the lambs become infected and when the chemicals finally kills the lice on the ewes will get reinfested from the lice on the lambs
45
in terms of medication for lice which is the best and which wouldn't use in terms of resistance
Imidacloprid -> Avenge - BEST
Diflubenzuron - Magnum -> resistance - WOULDN'T USE
Cypermethrin - synthetic pyrethroid -> resistance - WOULDN'T USE
46
alpaca puberty what is important with reproduction, what indicates puberty, ideal joining weight at what age
- Induced ovulators
- Urinary hormones indicate ovarian activity from 6 months of age
- Ideal joining weight
○ Aim for 65% of mature body weight
§ 45kg @ 1 year -> 70kg mature body weight
Australian conditions achievable at 1 year of age
47
Alpaca ovaries what size how important are corpus luteum and what is important to remember about passing a caetheter
- When only small ovarian structures present: PEANUT-sized - KNOW
○ Corpus luteum
§ Produces progesterone
§ Induced ovulators so CL only seen after mating
§ Required for duration of pregnancy
Generally if present WILL SEE THEM ON U/S as bulge out
PASSING CATHETER -> need to stable uterus with hand in rectum
48
What are the 3 stages of reproduction for female alpacas
```
1. The unmated, non-ovulatory female
○ Unstimulated, non-pregnant
2. The mated, ovulatory but non-pregnant female
○ Female mated but fails to conceive
3. The pregnant female
○ Mated, ovulated and pregnant
```
49
The unmated, non-ovulatory female alpaca what is occuring at this stage with ovary and is this seasonal
- Ovarian follicular waves ever 12-22 days
○ Synchronous emergence of group of follicles on both ovaries
○ One follicle becomes dominant (5-6mm)
§ Growth phase 4-6 days (4-6mm)
§ Mature phase 4-8days (7-12mm)
§ Regression phase 4-6
- Interval between emergence of new group of follicles 12-22days
- Waves overlap by 1-4
- Ovarian follicular activity alternates between ovaries randomly
- Non-seasonal
○ Follicle activity occurs all year
50
The unmated, non-ovulatory female alpaca what is the ideal mating time and how does ovarian function tie in with sexual behaviour and therefore when present
- Ideal mating time appears to be later growing/early mature phases of follicular growth
How does ovarian function tie in with sexual behaviour
- Follicles produce oestrogen -> sexual receptivity - all the time
51
Alpaca male scrotum what is the main issue, the average testicular length for fertility, how does test hang and type of penis with characteristics
scrotum - Thermoregulatory problems -> issues here -> generally in high heat environment
- Tests are small
○ 4-5cm x 2.5 - 3.5cm - mean testicular length for fertility
- Testes
○ Cranioventral/caudodorsal axis
- Fibroelastic penis
○ Pre-scrotal sigmoid flexure retracts penis into prepuce
○ Tapering tip ends in curved fibro-cartilagenous projection
○ Urethra at base of process
○ Dorsal urethral recess at pelvic flexure
§ DON'T TRY TO PASS A URETHERAL CATHETER
52
Puberty in the male alpaca what is neonatal addition, mating behaviour from, testosterone production and detachment therefore male fertile from
- Neonatal adhesion of penis of prepuce
- Mating behaviour from 1 month old
- Testosterone production 12 months
○ Peno-preputial detachment
§ 10% at 1 yo
§ 60-80% at 2 yo
§ All males should be fertile by 3yo -> sub-fertile if not by this point
53
alpaca semen characteristics spermatogenesis time, influenced by, what increases spern number, average, is production seasonal, high or low sperm volume, what is bulbourethral glands function
```
Spermatogenesis 12-18months
- Influenced by:
○ Genetics
○ Body weight (nutrition)
- Small testes = low sperm numbers - much lower than cattle
○ Average 30-300million sperm/mL
○ Sperm produced all year - non-seasonal
○ Low sperm volume
- Bulbourethral glands x 2 (G)
○ Provides highly viscous mucin
○ Viscosity hindering development of AI
```
54
Alpaca testicular size, how many mating per day and the 3 phases of courting
- Testes should be >4cm long - IMPORTANT - mean average length
- 2 matings/day
Courting phase
1. Male chases female
○ Libido indicator
○ Phlemen
2. Mounts
○ Pressure on pelvis encourages female to sit
3. Intromission followed by full erection of penis
No correlation between time it takes for female to sit, and pregnancy rate
55
Alpaca copulation phase what position, what occurs with male and is there correlation between mating time and conception rate
- Copulation in sitting position
- Intracornual deposition of semen
○ Rotation of tup of penis to penetrate cervix -> uterine tubular junction - maintain fertility
○ Adaptation to overcome low sperm concentrations
- Multiple ejaculations over 15-20mins duration - up in each horn
○ Range 5-50mins
- No correlation between mating time and conception rate
56
What are the 3 functions of copulation in alpacas
```
1. Induction of ovulation
○ Release of egg from ovarian follicle
2. Sensory inputs
a. Ovulation inducing factor in semen
§ OIF = beta-NGF
§ Absorption of OIF after intrauterine deposition is facilitated by the transient inflammation of endometrium caused by copulation
b. Penetration of cervix
c. Orgling - male mating sounds
3. Fertilisation of egg
```
57
Alpaca ovulation after coaputation what size follicle, time for egg to be released from follicle and then what occurs and percentage of mating resulting in conception
- Dominant follicle > 6mm present on ovary at the time of mating
○ Producing oestrogen, sexually receptive
- Egg released from follicle 26 hours after mating - consistent
○ Mating 26 +/- 3h
○ No relation between follicle size and time of ovulation post-mating
- Formation of corpus luteum (CL) at site of ovulated follicle
○ Conversion of residual follicle into CL
Rule of thumb - 50% of mating result in conception
58
Alpaca corpus luteum when develop, what when conception fails and if so when receptive afterwards
- Corpus luteum (CL) develops on ovary at site of ovulation - 3 days post-mating
○ Maximum diameter 10-15mm approx. 8-9days after mating
- When conception fails, PG release from uterus induces CL regression 9-11 days after mating - MATED BUT DOESN'T CONCEIVE
○ P4 declines soon after PG release -> once low enough will become sexually receptive and will have large follicle!!
- Female receptive approx. 12-14 d after mating
- Follicular activity continues during luteal phase
59
What is the alpaca test to determine whether conceived after mating how perform and how accurate
SPIT-OFF TEST
- When placed in a yard with a male, females with elevated plasma progesterone
○ Spit at the male
○ Try to escape from yard
○ Kick, squeal, ears back
- Definition of elevated plasma progesterone
○ P4 >2ng/ml
- Accurate 90-95% of the time, but note sometimes
○ Pregnant females that "stress-sit" - sub-ordinate
○ Non-pregnant females that "spit-off" - dominant
60
The pregnant female what day does hatched blastocyst, embryo elongation, implantation and therefore how many days for maternal recognition, what horn pregnancies generally occur in and average gestation length
○ Hatched blastocyst enters uterus 6-7d after mating - different to other animals
○ Embryo elongation day 10-12
○ Implantation day 18-20
- Embryo has only 8-10 days to send signal to uterus - for maternal recognition
- 98% pregnancies in left uterine horn
- Average gestation length 342 days (range 300-380 days) - 342 days +/- 2 months -> VARIABLE
○ Longer in spring, shorter in autumn
61
Alpaca twins how common, are freemartins present and what type of membrane present
Twins
- Rare despite
○ Multiple ovulation frequency 5-10%
○ Singleton pregnancies can have multiple CLs
- Dizygotic
- Mechanism to reduce twin conceptions
- Freemartinism reported in female-male camelid twin pairs
Membranes
- Epitheliochorial, diffuse placentation - microcotyledonary
62
Pregnancy test indirect method and direct method from what timeframe
- Indirect methods
○ Sexual behaviour - spit-off test - most common
- Direct methods identify foetus - gold standard -> certify pregnancy after 6-days
a. Ultrasound - foetal heart beat 25d+
b. Manual rectal palpation - 35d+
c. Transabdominal ballottement - 8m+
63
Alpaca estimating day of delivery what varies with and therefore what variation give
○ Average gestation length about 342 days
○ Range 300-380 days
- Dependent of season
○ Tends to be longer in spring (348d)
○ Tends to be shorter in autumn (340d)
- When foetal aging, warm owners that date could vary +/- 6 weeks from your estimate
64
Alpaca parturition clinical signs, when occur, how long does each stage last and uterine involution takes how many days
Parturition
- Do not use same paddocks as maternity paddock long-terms
- Alpacas do not often show external signs of impending delivery
- Time of parturition under photoperiodic control
○ Most births occur between 7am and 2pm
○ Never let the sun set on an alpaca trying to give birth
- Stage I: 1.5-4 hours
- Stage II: 30-45 mins
- Stage III: 1-4 hours, RFM >6 hours
- Foetus covered in epidermal membrane
- Dam does not lick newborn nor eat placenta
Receptivity after unpacking
- Ovarian activity resumes 5-7 days after unpacking
- Uterine involution takes 20 days
Rapid because of diffuse (microcotyledonary) nature of placentatio
65
Breeding recommendations for alpacas at what age and BW and the things to do to check after breeding
- First breeding
○ 12+ months of age if reached 65% of mature BW
○ 15-20 days after unpacking is unassisted birth
- Breed ONCE when receptive
○ Spit off at 7 days to check for conception
○ Spit off at 14 day to check for pregnancy
○ Spit off regularly (every 2-4 weeks) until ultrasound pregnancy test at (30 and) 60 days post-joining
○ Spit off intermittently throughout gestation
○ REPEAT 3 TIMES BEFORE SEEKING HELP
66
Alpaca paddock mating what percentage joining, how long for and when/how to determine pregnancy rate
- Join males at 3-4% (1 per 25-33 females)
○ Except 50% conception rate/mating if fertile
- Join for 4 weeks. Most matings will occur
○ Days 0-4
○ Days 12-16
○ Days 24-28
- Ultrasound females 30 days after male/s removed
○ Foetal aging accurate at this stage: 30,35 or 60d gestation
○ Expect 90% pregnancy rate
○ Treat/cull those that FTC
67
What are the 5 most common causes of lameness
1. Individual trauma - dislocated hip, broken pelvis
2. Hoof problems
○ Physical abnormalities +/- infection entering through the defect
○ Often compounded by foot/limp conformation
§ Eg - white line disease, sole ulcer, foot abscess
3. Foot abscess - (+/- extending to septic pedal arthritis)
4. Infections
○ Foot: footrot (fusobacterium, dichelobacter)
○ Joints: septic arthritis eg. Chlamydia
5. Nutritional disorders affecting
○ Skeletal: general nutriton, calcium, phosphorus, trace minerals, vit D/sunlight
○ Muscles: myositis
68
What are 2 uncommon causes of lameness
1. Neurological disorders -> cause gait abnormalities
2. Digital disease -> ulcers, pustules
○ IBR, scabby mouth, strawberry footrot
○ Exotic disease as well
69
What are the 3 important investigation techniques for lameness
```
1. Clinical examination of individual sheep
○ Localise and characterise the lesions
○ Systemic signs
○ Samples collected possible imaging if economically viable
2. Environmental factors contributing
○ What animals are affected most
○ What risk factors are they exposed to
3. Management factors
```
70
What are some important management and animal factors that affect lameness investigation
Management
- Do yards, tracks, animal handling contribute to trauma
- Nutrition -> particularly for growing and pregnant animals
- Dose the management system predispose to disease transmission
○ Intensive, rearing, quarantine, yarding
Animal
- Confirmation - affected by genetics, nutrition, environment
- Physiological status: weight (Gestation), activity level
- Age
○ Susceptibility to nutritional deficits
○ Immune status
○ Opportunities for infection
71
What are the 4 things in the environment that are important for a lameness investigation
- Increased exposure to environmental infections (mud, wet)
- Increased susceptibility to infection (maceration)
- Facilitate transmission (warmth and moisture for footrot)
- Nutrient availability - macro, micro and sunlight (vit D)
72
In terms of energy and protein what is important and what are the 2 problems that occur and the main problem from this
○ Correct amount of ME and CP from pasture, supplements, human-formulated diets
§ Enzyme activity to cross-link collagen in matrix
§ Cu for enzyme activity
1. Problems occur with Over-nutrition (excess ME)
§ Osteoarticular disorders
2. Problems with Under-nutrition (low energy and protein)
§ Osteoporosis - not enough bone
73
Over-nutrition (excess ME) what disorders does it lead to and prevention
§ Osteoarticular disorders
□ Osteochondrosis, osteochonritis, dissecans
□ Canine hip dysplasia
® MORE oesteoarticular disorders when feed ad lib rather than restricted
® Larger breeds have higher genetic potential to overgrow with over-nutrition
§ Prevention
□ Growing puppies should be lean (CS4/9) - feel animals ribs but don't see them
□ Beware of unrestricted feeding of growing dogs
□ Don't restrict protein - high protein is restrictive
□ Cat much less susceptible to over-feeding
74
Under-nutrition (low energy and protein) what diseases does it lead to and what situations does this occur
□ Stunting, pathological fractures, subsequent hypocalcaemic crises
® Milk deficiency - autumn born lambs on malnourished ewes
® Copper deficiency - weakened/reduced osteoid in lambs, calves, piglets
® Weaner sheep grazing poor summer pastures
◊ Normal shape of bone but reduced trabecular bone and thin cortices
® Drought-affected calves
® Gastrointestinal parasitism
75
What is the main way to prevent under-nutrition (low energy and protein) and ways within
□ Ensuring adequate energy and protein nutrition
® Mother: monitor CS, correct for time of lambing
® Progeny: energy and protein (appropriate pasture and supplements)
® Good worm management - lambing and weaning paddock, weaning drench
® Copper supplementation
◊ Need to be careful due to different species susceptibility to Cu overdose
76
Problems with Low Dietary Ca or Ca:P ratio what is it caused by in dogs/cat, horses and growing cattle/sheep, what does this lead to and then 2 diseases it causes in different species
§ Caused by
□ Dogs or cats: all meat diets □ Horses: diets high in cereal grains (including bread), tropical grasses containing oxalates
□ Growing cattle, sheep: diets high in cereal grains
§ ALL LEAD TO -> high serum phosphate antagonises serum Ca2+ -> low Ca2+ stimulates PTH -> Ca2+ resorbed from bine
□ TENDS TO CAUSE
® osteoporosis in sheep and cattle
® Nutritional secondary hyperparathyroidism in dogs, cats, horses, pigs, reptiles and eventually osteodystrophia fibrosa
77
Low Dietary Ca or Ca:P ratio how to assess
□ Serum calcium tightly regulated
□ No commercial assay for PTH
□ BUT increased PTH activity will also release P from bones
□ So indirectly assess PTH activity by measuring urinary P excretion via fractional clearance rate:
® Sample blood and urine
® Compare urine:serum % of phosphorus and creatinine
□ Increased urinary fractional excretion of P suggests excessive parathyroid activity
® Nutritional
® PTH analogue from neoplasia (lymphoma)
Parathyroid tumour?
78
Low Dietary Ca or Ca:P ratio prevention in dogs and cats
□ Avoid or restore imbalanced Ca:P diets
® Dogs and cats
◊ Don't feed all-meat diets try to provide >50% commercial diet
◊ Need dietary Ca = 1.2% of DM P = 0.6-1.2%
◊ Don't add extra supplements (Ca) - over-supplement BAD
} Excess calcium can also STUNT growth
– High serum Ca inhibits calcium resorption and necessary bone remodelling
79
Low Dietary Ca or Ca:P ratio prevention in ruminants
□ Avoid or restore imbalanced Ca:P diets
® Ruminants
◊ Add calcium carbonate (limestone) to high grain diets to rebalance high P:CaCO3 at 1.5% w/w (15kg CaCo3 per tonne of cereal)
} Immediately for growing ruminants
} If >8 weeks full feeding for adults
® Horses: Lucerne hay or maloasses is good Ca source if horses also consuming grain
80
Low phosphorus or vitamin D what caused by in cats/dogs, sheep and cattle and what leads to and the 2 main diseases
§ Caused by
□ Cats and dogs: low dietary vitamin D
□ Growing alpaca, sheep, piglets: low vitamin D activity if poor exposure to sunlight
□ Cattle: low dietary phosphorus (northern australia)
§ ALL LEAD TO -> vitamin D needed for active Ca and P absorption from gut -> low Ca or P means bone can't be mineralised
§ RESULTS IN - what you can diagnose
□ Rickets in growing animals
® Shifting lameness, hypocalcaemic crises, degenerative joint disease following articular collapse
□ Osteomalacia in adults (remodelled bone is soft)
81
Low phosphorus or vitamin D prevention
□ Ensure adequate vitamin D
® Good levels in organ meats, fish, fish oils, dairy
® Avoid rachitogenic factors (anti-vitamin D) and high Nh4+ in oat vrops
® Oral or injectable supplements
◊ Preventively to all growing alpaca in autumn
◊ Therapeutically to young sheep if signs are developing or to help in situations of Ca deficiency
◊ Vitamin D toxicity causes abnormal tissue mineralisation
82
What are 3 other nutritional causes that affect lameness besides nutrient deficiencies ,
1. Ruminants and horses: grain overload -> dietary lactic acidosis can cause laminitis
○ Introduce over days-weeks
§ Sheep/cattle 50/500g/d
§ Horses <50% total diet
2. Nutritional myopathies: selenium, vitamin E deficiency
3. Fluorosis in northern cattle, macropods, abnormal bone matrix and mineralisation
83
Even if there are no clinical bone abnormalities, poor skeletal growth can lead to what 3 things
1. Prolong time to reach sale weight or puberty
2. Increase risk of dystocia (due to small frame size)
3. Increase risk of hypocalcaemia at lambing
84
Footrot what type of disease, what caused by, variation and how long live off sheep
- Contagious disease
- Caused by bacteria Dichelobacter nodosus
- Numerous strains can affect sheep at any time
- The bacteria lives no more than seven days off sheep
○ In all conditions
85
What are the 3 things that affect the expression of the disease and factors within
```
1. The strain of bacteria: virulence
○ Benign
○ Intermediate
○ virulent
2. Sheep susceptibility
○ Breeds merino>crossbred>British breed
○ Age - no natural immunity - DOESN'T AFFECT
○ Sheep immunity - genetics
3. Environmental factors
○ Rainfall - high rainfall important
○ Temperature - generally spring
○ Pasture - higher longer grass
○ Length of growing season - longer more footrot
```
86
What are the 3 important facts about footrot and environment
1. Footrot spreads when wet
2. Footrot lesions can progress when dry
3. But there is a lot of self-cure when dry
87
What are the 3 ways footrot is transmitted
1. Infected livestock carriers
○ Sheep § All strains
○ Goats § All strains but benign looks virulent and virulent benign
○ Cattle § Benign long term
§ Virulent short term in wet conditions?
○ Cats, dogs and native animals etc – no!
2. Interdigital skin must be disrupted - IMPORTANT
○ Wet conditions water maceration
○ Mixed bacterial flora
○ Ovine interdigital dermatitis (OID)
○ Unlikely to spread in dry conditions
3. Environmental conditions
○ Wet
○ Temp > 100C
○ Observed underrun in lambs when conditions are frosty (superficial damage?)
88
List 7 direct costs of footrot
1. Increase mortalities 1-4.5%
2. Clean fleece wt
○ 3% virulent
○ 2% intermediate
○ 0.5% benign
3. 0.5 micron reduction in fibre diameter?
4. 10% reduction in staple strength
5. 4-5% loss of fleece value
6. Body weight
○ 5% virulent
○ 2.5% intermediate
○ 0.5% benign
7. Fertility
○ 1.5% lower per 1 kg body weight
89
What are the 4 secondary costs of footrot and describe
1. Supplementary feeding
○ Due to lower bodyweight
○ Lower ewe fertility
2. Poorer quality lambs
○ Weaner ill-thrift higher mortality rate
○ Higher death rate
○ Prime lambs lower body weight at sale
3. Metabolic diseases
○ Preg tox - not eating as much so cannot get energy needed
4. Flystrike susceptibility
○ Direct cost due to feet and sitting down
○ Increased risk due to high fly population
90
Describe 4 indirect effects off footrot
```
1. Less sale opportunities
○ Less options as cannot go to sale yards - notifiable disease
○ Sell on property or direct to abattoir
2. Harder management
○ Time taken on management
○ Weaner ill-thrift
3. Farmer stress
○ Inappropriate decisions
4. Lower stocking rate
○ Very common and a huge costs
```
91
How important is footrot diagnosis and how to determine benign, virulent or intermediate footrot
```
Footrot diagnosis how important
- Fundamental to making a rational decision on footrot management
- May take 5 minutes to make a diagnosis
- May take > 12 months to confirm a diagnosis
Diagnostic choices
- Benign footrot
○ <1% of sheep with score 4 lesions
○ No serious damage to feet
○ Benign strains
- Virulent footrot
○ >1% with score 4 lesions (other states GG/underrun – big issue)
○ Serious damage to feet
§ Intermediate or virulent strains
- Intermediate footrot
○ Can be difficult making a diagnosis
```
92
Footrot investigation what are the 4 main techniques and one most used for diagnosis
1) history
2) clinical expression - MOST OF THE TIME
3) smear to show presence of bacteria? Of no real value - doesn't tell you anything about severity - benign or malignant
4) laboratory tests
93
important history for footrot investigation
○ Age, Breed etc
○ Previous footrot history
○ Recent introductions (last 3 years)
○ Recent treatment (may mask clinical expression)
○ Pasture conditions (especially last 6 weeks)
94
how to investigate the clinical expression of footrot in a herd to determine what type of footrot
○ Inspect individual sheep
○ Inspect 20-30 sheep - if not sure then
○ Inspect 100 plus sheep at random and foot score
○ Progression test inspect and re-inspect at intervals of 2-4 weeks during spring
95
Laboratory test for footrot how important, what are the 3 tests, what do they tell you and what sheep take from
○ Should not be used alone although in Western Australia & NSW it is considered as part of regulatory diagnosis
○ Tests
1. Gelatin Gel - lots of false negatives or positives
□ Unstable vs stable protease thermostability
□ Unstable - benign
□ Stable - virulent
2. Elastase - best but expensive
□ How long bacteria take to get elastin
3. PCR
§ Virulence
§ Serogrouping/Serotypes - used for to create a vaccine
□ Each serotypes has benign and virulent strains
○ Collect full history
○ Take from at least 5 sheep with suitable lesions to allow spectrum of isolates to be examined
96
Benign footrot clinical signs, treatment/eradication and control options
```
- Clinical signs
○ Mild signs most years
○ Few signs in dry years
○ Very few score 4
○ Lots of score 1-2 lesions
- Self-cure in dry period
- Back next wet period
- Not obliged to eradicate
○ Eradication not cost effective or likely
○ True carrier state more likely?
- Big decision with borderline strains
- Control options
○ Simple footbathing as necessary
```
97
Virulent footrot what conditions are needed, clinical signs, what need to do with this outbreak
- Needs suitable weather - wet
- Initially signs similar to benign
- Keeps progressing
- Some self-cure
- Severe disease
- Obliged to eradicate
- Can be eradicated
- Cost effective to eradicate
98
What are the legal issues with managing footrot and what management needed for benign and virulent
- Legal issues
○ Sale of sheep
§ Virulent footrot
§ Benign footrot
○ Notifiable disease in VIC not NSW
○ Infected sheep must be treated
- Benign footrot - don't need to eradicate
○ Only issue is when in sale yards and confusing lesions with early virulent footrot
- Virulent Footrot - needs to be eradicated
99
What are the 2 periods of footrot weather, what occurs, the season and control or eradication at this time
```
1) The spread period
○ Warm moist weather
○ Mostly spring/autumn
○ Less in winter except i north
○ Summer requires summer rain
This is when footrot should be controlled
2) The non-spread period
○ Hot and dry
○ Usually summer
○ Can be at other times when dry
This is the time to eradicate footrot
```
100
What are the 5 steps in the eradication of footrot
1) planning
2) control - footbath, vaccination, do nothing
3) eradication
4) surveillance
5) prevention
DVM 3 - 1
flashcards
Decks in class (33)
# Cards
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ECP 1100
-
ECP 292
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ECP 3106
-
ECP 4100
-
ECP 5100
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ECP 669
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Dog and Cat 1100
-
Dog and Cat 2101
-
Dog and Cat 399
-
Dogs and Cats 4112
-
Birds 198
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Birds 2101
-
Bird 3101
-
Horses 1100
-
Horses 2101
-
Horses 394
-
Bird 426
-
Horses 4103
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Cattle 1101
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Cattle 2103
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Cattle 3100
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Cattle 447
-
Dog and Cat 5100
-
Dogs and Cat 6101
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Dog and Cat 7101
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Horses 589
-
Dog and Cat 8101
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Dog and Cat 9100
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Dog and Cat 10100
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Dog and Cat 1188
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Small Rum 1101
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Small Rum 2100
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Small Rum 339
