Small Ruminants Past Exams Flashcards
Describe the equipment, drugs and the procedures for harvesting velvet antlers in Fallow deer and Red deer. Describe suitable restraint facilities for each species, the consequences of the lack of such facilities, and an outline of the correct handling of the velvet after harvesting.
* Antler casting initiated by falling testosterone with increasing photoperiod– spring.
Velvet harvesting:
*Restraint in a crush
* Regional nerve blocks of the supraorbital and zygomatico-temporal nerves
* Place tourniquet
* Fine tooth saw parallel to and above the coronet leaving about 15 mm of antler remaining otherwise permanent damage to subsequent growth
* Invert antler to retain its blood content and hence weight and place on a clean rack in a dust free environment
* Tourniquet is left on for 10- 15 minutes
* Spray with antiseptic
* Antler is tagged, wrapped in plastic film and frozen
You have a client with a 250 doe Saanen herd in south Gippsland, where you have recently identified both Caprine Arthritis and Encephalitis (CAE) virus, and Johne’s disease (JD). A whole herd blood test reveals an overall seroprevalence of 33% for CAE and 13% for JD. A careful analysis of the results shows that the seroprevalence of both diseases increases with age. There are no other ruminants on the property except for a 6-month-old steer, which they plan on killing for home consumption. The owner wishes to control both diseases and minimise losses.
a) How do you interpret the results of the blood tests?
b) Design a control program which will control both CAE and JD in the herd.
a) with serology potential poor sensitivity and late seroconversion. Occasionally goats have a very low tier that is not detectable, common in late pregnancy. Definitive diagnosis of clinical CAE requires demonstration of chracteristic lesions in biospy specimen or necropsy or PCR for viral antigen in tissues may be helpful.
b) prevent vertical transmission by snatch rearing to prevent colostral transmission and pasteurized goat/cow milk and artificial colostrum only
- prevent horizontal transfer with a 2 herd system– separating clean and infected adults– milking infected last (or don’t share facilities)
** Surveillance: ongoing test & cull program
* Excellent biosecurity and hygiene
Discuss the two most common non-traumatic causes of lameness in growing alpacas.
a) Clinical presentation
b) Diagnostic procedures
c) Treatment and prevention
Metabolic or Infectious. e.g. Angular limb deformities- congenital +/- vitamin D deficiency as young have lower levels, infectious examples include bone sequestra
a) Clinical presentation
- Vit D deficiency: recumbent, reluctant to stand
- Bone sequestra: unilateral limb lameness, pain on palpation of the affected bone in the early stages, often progresses to a purulent sinus tract
b) Diagnostic procedures
- How many animals affected, how many limbs, which group, signs of infection? Radiographs likely necessary. Multiple limb problems or shifting lameness– better to have a blood phosphorous performed as a screening test
c) Treatment and prevention
- avoid breeding with undesirable limb angulations or deformities
- supplement young with vit D
- angular limb deformity- consider splinting or surgery such as wedge transection or HCP
- infectious causes– remove sequestra surgically, if septicaemic or bacteraemic or infection elsewhere– systemic antimicrobials
Write a control program for a 200 doe milking herd in the Yarra Valley for endemic CAE
* monitor for signs and symptoms: arthritis, hard udder, chronic interstitial pneumonia, chronic weight loss, leukoencephalo-myelitis
* Serology- poor sensitivity and late seroconversion, some may have too low antibodies to show up as positive (false negative)
* BUT herd free testing every 6-12 months serology for 5 years
** Ongoing surveillance and biosecurity
Plan
* Source goats from CAE accredited free herd, especially dairy goats
* Emphasis on providing disease free colostrum and milk for kids & separating virus infected from virus free kids
* Diagnostic testing followed by removal of infected animals; disinfection and temporary removal of animals from premises and separation of newborn kids from their does; feeding cows colostrum, milk and milk replacer; establishing separate pastures for rearing young goats
A client of your practice has had benign footrot diagnosed in their Merino sheep by the local Department of Agriculture veterinarian. They seek your advice about management of benign footrot.
a) Describe the key features that affect the expression of footrot
b) Describe the key features that determine the diagnosis of benign footrot
c) Briefly outline the management of benign footrot
a) Describe the key features that affect the expression of footrot
* foot rot is caused by Dichelobacter nodosus- many different strains of D. nodosus that vary in virulence and pathogenecity. benign strains can never cause severe disease.
* some breeds of sheep are more resistant e.g. british breeds are more resistant compared to merinos
* moisture and temperature affect transmission and expression of footrot
b) Describe the key features that determine the diagnosis of benign footrot
* < 1% of sheep with score 4 lesions = benign footrot
* interdigital skin (webbing)- look for hair loss and reddening of the skin
* Inside of skin and toes and the soft horn of the heel- look for reddening, erosion of the skina nd white (dead) tissue
* skin/horn junction- look for separation of the horny layer from the skin
* Sole of the heel- progressive separation.
c) Briefly outline the management of benign footrot
* not cost effective to eradicate and probably cannot be anyway
* you would first make sure it was benign footrot by looking at 100 sheep to ensure < 1% score 4 lesions
* sheep with any footrot lesions must not be presented for sale in the saleyard
* no action- but regularly monitor …
* eradication– if you have to– Isolate suspect mobs from clean sheep until diagnosis is made, plan–> destock, retained stock: control in wet and eradicate in dry… surveillance–> prevention & quarantine
You are in a practice in the western district of VIC. It is mid-August and you have discovered virulent footrot on the property of one of your practice clients. The property has a self replacing fine-wool merino flock with 3,000 ewes and a similar number of wethers. The property is a family farm, run by a couple in their late 60s, who are not in particularly good health. A son who works in Melb helps out on the farm most weekends.
Footrot is present in all mobs, with many severely affected sheep.
Design a footrot control and eradication program for the property. Justify your recommendations for the property owners.
* sale for slaughter of all sheep in the infected mob and spelling the property for at least 7 days then restocking with clean sheep is the best method of eradicating.. may need this because old
* Cost is the change over price of sheep involved
The cost of selling and buying stock must be weighed up against
the cost of a control/eradication program. Selling infected sheep
and restocking may be cheaper than an eradication program which
fails.
Before making a decision about destocking it is important to
consider the farm resources and budget.
Eradicating footrot by destocking is worth considering when:
• A farmer is unwilling or unable, to commit the labour or
resources required to set up a proper eradication program.
- Only one or two mobs on the farm are infected.
- The footrot-infected sheep are at the end of their productive life.
- Sheep prices are low, for example during a drought, so the
changeover costs are reduced
The type of farm operation and the number and size of mobs
involved has a big influence on the decision to destock. Part-time
farmers with relatively small flocks may find destocking effective if
they can are unable to commit the time required to implement a
footrot eradication program.
You are in a practice in the western district of VIC. It is the middle of May and you are called to visit a client’s property. You discover virulent footrot is present in many mobs, with many severely affected sheep on the property. The property has 1500 first cross ewes which are due to begin lambing in August.
Design a footrot control and eradication program for the property. Justify your recommendations to the property owners.
* eradication– if you have to– Isolate suspect mobs from clean sheep until diagnosis is made, plan–> destock, retained stock: control in wet and eradicate in dry… surveillance–> prevention & quarantine
* Important point: eliminate any source of reinfection, so first mend fences and set up a system where you can separate infected from clean
* Control- footrot spreads during warm, wet periods typically in spring– so control during dry periods (summer)
* Footbathing- 10% zinc sulphate walk through at least 8 meters long as long as lesions 2-3a.
* vaccine not currently available in Australia
* sheep with four normal feet can stay separated– all sheep who don’t– culled (make sure inspectors are trained, part of planning)
* First inspection– as soon as dry conditions
* Second inspection- four weeks after the first
* third and any subsequent- four weeks after second
** Surveillance and monitoring– including isolation of new sheep brought in
** Also routine handling msut be done in the paddock so they aren’t brought through the same yard or at least consider bringing clean sheep through first and then dirty– and then not bringing clean sheep for 7 days over that part
** Final audit to ensure footrot eradication
A farmer from Seymour in the north central Victoria, who runs 3000 fine wool merinos, seeks your opinion as to the cause of lameness in a mob of 200 ewes. He and his wife purchased them 5 months ago, in April, from a dispersal sale at the local sale yards. It is now September and the sheep have been grazing lush pasture for the last 10 weeks. Prior to this, before the seasonal winter rains arrived, the sheep were grazing dry hill country.
a) Outline your approach to investigate and diagnose the problem in the sheep.
b) If you find that 10% of sheep have score 2 lesions, 10% have score 3a lesions and the remainder appear to be normal, what is your advice to the farmer and his wife about how to manage this problem?
* moist and warm conditions- prime footrot!! But looking at feet to search for signs of scald, severe footrot, grossly swollen claws or discharging sinuses
** DDX of large numbers of sheep lameness:
- scald, soil balling (impaction of the interdigital space with dried mud, grass or manure), footrot, contagious ovine digital dermatitis (CODD), FMD
(scald- F. necrophorum- common in growing lambs but also older sheep)
b) Benign footrot– would advise that it would not be economical to eradicate
a) Discuss the important diagnostic features that differentiate benign and virulent footrot.
b) You are asked to investigate the cause of lameness in a mob of 500 merino wethers of Ballarat in Western VIC in early Sept. Outline the steps required to differentiate between benign and virulent footrot in the mob which on initial examination has 10% of sheep affected with score 1 lesions, 10% score 2 lesions, 5% score 3a lesions and 5% score 3b lesions. All other sheep have normal feet.
a) Score 1- limited to mild interdigital dermatitis, slight to moderate inflammation confined to interdigital skin (surface layers), red, moist, shedding hair
Score 2- more extensive interdigital dermatitis; severe inflammation of the interdigital skin which involves all or part of the soft horn of the inside walll of the toe
Score 3a - separation at the skin horn junction, with under-running extending no more than 5 mm
Score 3b- Under-running extends half way across the heel
Score 3c, 4- Under running continues across heel or sole
b) Inspect 100 plus sheep at random and foot score– keeping a record sheet.. laboratory tests should not be used alone. Take from at least 5 sheep with suitable lesions to allow spectrum of isolates to be examined.
* chronic infestation with sheep lice- frustrated as can’t eradicate, ewes lamb in July- lambs are sold off their mothers in Nov and Jan– shorn in Oct and treated with Zapp off shears. Replacement ewes purchased in January. Lice eradication plan:
Weigh up the losses of premature shearing against cost and inconvenience. Apply suitable off shears/ short wool treatment after shearing.
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Eradication is only possible in short wool (< 6 weeks)
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An unchecked infestation will reduce fleece weight and
increase
cotting
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Chemical and labour incur a cost
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Short (
prem
) wool may incur a price penalty
}
Shearers may not
be
available
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Pesticide residues may incur a price
penalty
** I would recommend saturation (dipping and jetting) as opposed to back-liner as chronic problem.
** Consider withholding periods of wool– so I wouldn’t recommend treating with long wool
**dipping hygiene important because of cheesy gland, fleece rot, etc.
* Dip between 10 days and 4 weeks off shears, use Hibitane disinfectant, dip young sheep first (most susceptible), vaccinate with 6-in-1
** All sheep must be treated… Neonicotin– Thiacloprid not overly expensive– check local resistance
Main epi features of
a) fleece rot– Pseudomonas aeruginosa- possibly other bacteria– prolonged wetting of skin and warm temperatures are usually required. P. aeruginosa multiplies rapidly in most conditions. Self limiting but can stain fleece. Young sheep more susceptible, most susceptible with 4-6 months wool growth– long enough to trap moisture but not to repel it. High rainfall areas with warm weather, stronger wool merinos more susceptible than finer wool. British breeds more resistant. High fibre diameter and high greasy wool more susceptible.
b) scrotal mange in rams- Chorioptes bovis (transmission via direct contact– joining, suckling), pick up from pasture. C. bovis 3 week life cycle.
c) rear end cancer in ewes- SCC common in older sheep occur on exposed areas such as vulva, anus, tail or bare mulesed skin (rear end cancer) (face, planum, lips, ears especially). animals over 5 years old, trauma to the skin risk factor (mulesing)
d) perennial ryegrass staggers- fungus growing on dead pasture during late summer and autumn. Requires warm and moist conditions to multiply. Pithomyces chartarum– produces a toxin– causes staggers, facial eczema, etc. Fungus prefers dead perennial rye grass pasture
Apparent failure to control Bovicola ovis. Lice in several mobs. Client applied IGR pour on back liner after shearing. 3 months since shearing and client discovered some lice on 6 month old weaners when brought in for drenching.
Approach to investigate and most likely reasons for apparent breakdown
* Direct life cycle lasting 35 days, eggs take 10 days to hatch, host specific, sensitive to environment so limited survival off the sheep, reduced in number by shearing, transmitted by direct contact, almost always introduced to flock by the intro of lousy sheep
* Easily killed by direct sunlight, water, extremes of temperature or humidity
* degree of wrinkle can allow lice to survive, also one or two lousy sheep from a neighbor’s flock can cause a new infestation which may not be noticed until after the next shearing. Good fences important.
** To confirm the diagnosis- yard one or more suspect mobs– catch sheep that rub or show signs of fleece derrangement to look for lice– make 5 partings on the neck, shoulders, and flanks of at least 10 sheep. Best done in direct sunlight as the lice move when the wool is opened. Only one louse needs to be found to confirm.
* Protection period of most products is 3-4 months
Rules for eradication
- ALl sheep must be treated- treating for lice during lambing is not usually recommended except perhaps with some long-acting IGR backliners.– possible resistance IGRs– if previous tx failed use a different product)
- sheep must be treated at the same time (avoid split shearing) or quarantine with good fences
- Apply chemicals properly according to the labels
Epi features and control
- Acute phalaris toxicity
- Phalaris aquatica with its numerous cultivars is a much-valued perennial grass species widely used in improved pastures across south-eastern Australia. However in certain circumstances, it does have the potential to become a toxic pasture plant, producing a variety of unrelated syndromes which manifest either as neurological or cardiac disturbances, presumably involving different toxins. The poisonous potential of Phalaris aquatica is dynamic and is a function of interacting plant, animal, environmental and management factors. Currently it is generally accepted that there are three distinct syndromes: chronic phalaris staggers, cardiac sudden death and ‘PE (polioencephalomalacia)-like’ sudden death, although recent evidence suggests that PE is not involved in the latter syndrome and a urea cycle disorder has been proposed.
- Avoid hungry stock on freshly-shooting phalaris dominant pastures, especially following periods of frost or moisture stress… phytotoxins are yet to be identified so no way to neutralize
- Itch Mite (Psoregates ovis)
- 5-6 week life cycle on the sheep
- Problem in older sheep and under nutritional stress
- Sensitive to hot weather and desiccation
- Transmission most effective when sheep are newly shorn, transmission from ewe to lamb important
- Can cause HS rxn and result in pulled wool and cotting, excessive scurf
- skin scrapings for diagnosis
- Macrocyclic Lactones– more than one treatment required… can also add rotenone or amitraz to plunge or shower dip
- Facial eczema
- Hepatogenous photosensitisation caused by the ingestion of sporodesmin, a fungal toxin produced by the fungus Pithomyces chartarum
- Fungus grows on dead pasture litter during late summer and autumn. Present year round but requires moist warm conditions to multiply enough to cause disease (>15 C for 72 hours)
- Prefers freshly dead perennial rye grass pasture – most spores on the bottom 25 mm of pasture (annual pasture is less dangerous because less freshly dead annual pasture)
- Have spore counts done after high risk weather
- Move sheeps to paddock with tallest pasture
- Avoid paddocks that have been cut for hay because the litter increases toxicity
- Fungicides in NZ
- Zinc salts can prevent development of clinical signs as zinc binds the toxin
Oct- Nov jetted with Vetrazin
mid Dec after another problem- Vetrazin and Diazinon
February- same as Dec
** Prevention relies mainly on reducing the susceptibility of the sheep, using a range of breeding, surgical and husbandry and chemical measures
* Breeding, surgical
* Time of shearing- shearing in the spring just before fly season helps to reduce body strike and cleans up breach area… crutching in late autumn or in early spring if sheep are daggy
** Good worm control
* long wool– jetting and long back liners
* Diazinon is now banned but only protective for 2 weeks
* Cyromazine (IGR) and dicyclanil
- Scabby mouth
- Parapoxvirus
- requires break in the epithelium
- Small hyperaemic foci develop within 7 days into a vesicle
- Ubiquitous on farms in VIC
- Large amounts of virus in the scab and the virus remains infective on pasture and in feed for very long periods
- Immunity following infection is long lasting (2-3 years)
- Live virulent vaccine available– scratch lamb at marking
- Hypocalcaemia in ewes
- Ewes in their last six weeks of pregnancy most at risk
- Grazing weeds that contain high levels of toxaemia increases the risk
- Good nutrition and careful management are the keys to avoiding hypocalcaemia e.g. good quality hay and grain to stock about to lamb and avoiding sudden changes in their feed or any sudden periods of starving such as yarding
- Adding limestome to grain rations or loose lick with calcium
- Pinkeye
- Mycoplasma conjunctivae but a variety of organisms
- Non-clinical carriers source of infection
- Dust irritation increases susceptibility
- Mechanical spread with flies, midges, etc.
- Late summer and autumn when paddocks are dry and flies are active
- Most clinical cases resolve over 2-3 weeks… only severely affected mobs worth treating with injectable oxytet
- Severely affected sheep in wool shed out of the sun and dust
Hydatids in sheep
- Echinococcus granulosus
- dog carries adult tapeworm, eggs passed in dung, sheep swallows the egg and cysts form in tissues such as liver or lungs
- no ill effects
- prevent dogs from eating sheep offal
- regular treatment of working dogs and pets in sheep areas with praziquantel
Sheep scab (Psoroptes ovis)- mite
- can survive off the sheep for up to 3 weeks
- cool, moist environment
- Direct contact
- eradicated through dipping OPs or MLs
Urolithiasis in wethers
- can cause obstruction of the urethra or anywhere in the urinary tract
- common in male goats
- Ruminants fed high grain diets with a low calcium to phosphorous ratio
Dermatophilus congolensis- invades the skin aka Dermatophilosis, dermo, mycotic dermatitis, and lumpy wool
Motile zoospores
To establish infection, the infective zoospores must reach a skin site where the normal protective barriers are reduced or deficient. The respiratory efflux of low concentrations of carbon dioxide from the skin attracts the motile zoospores to susceptible areas on the skin surface. Zoospores germinate to produce hyphae, which penetrate into the living epidermis and subsequently spread in all directions from the initial focus. Hyphal penetration causes an acute inflammatory reaction. Natural resistance to the acute infection is due to phagocytosis of the infective zoospores, but once infection is established, there is little or no immunity.
Actinobacillosis lignieresii (wooden tongue in cattle)
* coarse dry feed in late autumn and summer, adults more affected than young animals
* Lesions may be superficial or deep honeycomb of small abscesses beneath the skin… yellow green pus– lips, face, nose, jaw, and lower neck
Tetracyclines and erythromycin– most sheep recover anyway
* Placing animals on soft feed also helps
D) introduce blood lines with pigmented skin on face
A) because it is banned– Diazinon
F) dicyclanil
False- low heritability of resistance
FINISH
CLA Vaccine Merino flock
a) epi and control of CLA
- Corynebacterium pseudotuberculosis
- contagious disease
- test and cull or erdication programs can control it
- start during shearing or dipping– infected sheep cough up from lung lesions or from ruptured, draining abscesses
- survives weeks to months in the environment
- prevalence increases with age
- largest single cost is reduced wool production– 5% less wool in the year cheesy gland first gets established… then no reduction in subsequent years- limits importance of disease in wool flocks
- vaccination– good against new infection but does nto cure existing abscesses
- two doses four weeks apart are required to establish high level of immunity… and annual booster required to maintain adequate protection
- reduces prevalence from 31% to 3% if vaccination is used every year
– production cost only felt through one year of decreased wool production and currently no financial incentive to reduce abscess prevalence at abattoir
b) Cost benefit analysis
* 4kg of wool per wew 4500 ewes, avg of 18 micron… worth around 1000c/kg
5 in 1 - 12 c
6 in 1- 20 c
avg prevalence of CLA is 30% in cull for age ewes in unvaccinated merino flocks in VIC
1 ram, 10 wethers, 18 ewes and lambs and weaners
ram runs with ewes all year round, ewes lamb from april to november. No sheep handling facilities
* flock is normally shorn in October when all sheep and lambs with more than 6 months of wool are shorn
* May– lice on the sheep
Control & eradication
* Eradication only possible in short wool
* Treating all sheep at the same time
* Treat sheep now with spray on back liner Spinosad since shearing is more than 3 months away. Temporary control of lice infestation is the goal.
Then treat at shearing with Triflumuron or spinosad using a backliner (due to lack of facilities)
** quarantine new sheep, stock proof fences are vital, check sheep for lice every time they are in the yards
Epi and control of
a) Damalinia caprae (body lice) in goats
b) Malignant catarrhal fever in farmed deerMalignant catarrhal fever (MCF) is an infectious systemic disease that presents as a variable complex of lesions affecting mainly ruminants and rarely swine.
MCF results from infection by one of several members of a group of closely related ruminant gammaherpesviruses of the Rhadinovirus genus.
- stress disease, sudden death with severe haemorrhagic signs on PM
- lab samples and histology
The only other effective control strategy is separation of carriers from susceptible species
Disease control… virulent footrot, lice, and worm control in small sheep flocks
* Maintain good fences
* Monitor purchased sheep and kept in quarantine
* Footbathing all introduced sheep
* Realize the role of cattle in spreading footrot or goats
* controlling lice and flies on hobby farms
* Lice- host specific, sensitive to the environment– short survival off the host, hugely reduced in number by shearing, transmitted by direct contact between sheep, almost always by introduction of lousy sheep
* quarantine and treat new sheep added to the flock
* Protection period for most products 3-4 months, do not have to treat unless you have found lice.
* If you do have lice and have to treat, ensure you treat with the appropriate product based on length of wool and leaving appropriate time off shears
* Only try to eradice when sheep have short wool, can treat for temporary relief when sheep have long wool so that you can then try to eradicate after the next shearing– this way you can still have long wool at shearing– caveat if the sheep are severely affected
Controlling FLIES:
* Not a realistic aim to decrease fly numbers on the property
* Aim to make sheep less susceptible
* Sheep carrying long wool during fly season are more prone to strike– so can change management calendar
* Flies seek moisture and protein which are provided by excreta, exudate and/or rainfall– providing sheep shelter may help– such as shearing in the spring prior to fly season helps reduce body strike and clean up breech area
*with a small herd very possible to perform ringing, crutching
* Good worm control is important to reduce dag
* Control foot rot or foot abscesses as they are prone to harbouring covert strikes
** Chemicals– backline methods for fly prevention– IGR Dicyclanil offers 20 weeks protection
- April infestation of lice Merino ewes—300/ 3000
- Ewes due to be shorn in August and lamb in September
- Treated all sheep within 24 hours of shearing with an off shears pour on treatment—Magnum (diflubensuron) after shearing last August, 4 weeks before lambing
- DDX: Itchmite, grass seeds, dermo, fleece rot and photosensitisation and exotic diseases which should be ruled out (scrapie, sheep pox, Aujeszky’s)
- Describe the options the farmer has to control the problem prior to shearing
- Do nothing for now then treat shearing.
- Apply a chemical treatment– since shearing is more than 3 months away. Eradication is rarely achieved with long wool. Residue problems must be considered as well.
- Shear prematurely and treat. Shearing the sheep immediately stops ongoing fleece damage and allows short wool treatment and therefore chance of lice eradication. Anything less than 9 months growth is likely to incure price pentalities. Throws future years out of line as well.
- Describe the most likely reasons for the failure to eradicate lice from the sheep last August
- All sheep must be treated, sheep must be treated at the same time (no split shearing/ split shearing), Apply chemicals properly– equip in good working order
- Try a different chemical group and possibly different treatment method
- What are your recommendations to eradicate lice after shearing this year?
- Quarantine and good fences are very important
- Eradication only possible with short wool
Alpacas appropriate time of mating
* 12 months of age or 65% of mature body weight or 15-20 days after unpacking if parturition unassissted and straightforward
* Evidence of oestrus is when they submit to a macho for mating
Brief physiological basis regarding use of the spit off test
* Behavioral oestrous associated with lack of progesterone, as oppposed to the presence of oestrogen
* Most alpaca are receptive if non-pregnant except for a brief period of non-receptivity lasting 1-2 days as a new follicle wave develops… non-seasonal breeders so ovarian follicular activity occurs all year
* Induced ovulators so ovulation occurs approximately 26 hours after mating
* Spit off test– strongly reject male by spitting, kicking, squealing if they have a CL and elevated plasma progesterone
* spit off at 7 days to check for ovulation, at 14 days to check for pregnancy
How many matings to achieve conception would be expected in a female with normal fertility
90% of females will conceive in the first 3 mating attempts
Expected number of females to conceive in this herd if the farmer follows your advice
90% of females will be pregnant when scanned 30 days after removal of males–3 matings each 14 days apart if not pregnant
Methods and timing of examination for pregnancy
* detection of CL/ elevated plasma protein
* transrectal or transabdominal ultrasound– foetal heart beat from 25 days of gestation
* spit off every 2-4 weeks until U/S test at 30 days and 60 days post joining
Describe the epi and control of:
a) Polioencephalomalacia: animals may be recumbent, often apparently blind. Deficiency in vitatmin B1– usually identified with management change e.g. change of feed
b) Vit D deficiency: in the winter when daylight hours are relatively short– alpacas have very few lightly wooled areas– mainly their ears so are more susceptible. Can cause ill thrift and shifting lameness. Measure blood phosphorous level as an indirect screening test. It will drop when vit D drops. Rickets…
At risk– young animals, actively gorwing
- Fallow deer as an alternative to his current Chital deer
- Hog deer
- Fallow are a temperate species– orderly seasonal breeding cycles. Rut occurs in autumn and fawns are dropped in late spring
- nervous and flighty, reds are less aggressive
- Chital are sub tropical species– less defined breeding cycle
- Require good winter shelter in cold conditions as they lack subcutaneous fat deposits, winter coats and under fur
- rather fallow deer-like in their behavior. Stags are very aggressive towards each other. Herds are difficult to manage because of all year round stag antler cycles.
- Difficulty coping with our southern climate and winter deaths and stress diseases are common.
- Not successful in Victoria as a farmed species.
- Factors that impact on the management and profitability of the enterprise, in relation to the choice of the two deer species
- Year round stag antler cycles– so won’t all be ready to remove antlers at the same time
- susceptible to illness, poor growth, lower meat yield
- e.g. Winter Death Syndrome– failure of energy metabolism in sub tropical deer in a cold climate
Normal birth between 7am and 2pm- never let the sun set on a camelid trying to give birth
- Female 345 days gestation from last mating date which has been intermittently recumbent and visiting the dung pile frequently since 10 am. No foetus or placenta visible.
- DDX
- Torsion of the uterus
- Dystocia from foetal malpositioning
- poor cervical dilation
- Pelvic canal problem such as fractures
- Describe the treatment of conditions
- Detorse by rotating the mother under xylazine sedation and applying external abdominal pressure to create intertia of the uterus OR caesarean
- Breech- caesarean
- Alpaca caesarean 4 months ago and has failed to conceive after a few mating
- When should the female have been mated post-partum and why?
- females can be ready to ovulate by 10 days post-partum
- Uterus takes 20 days to involute probably because of the diffuse (microcotyledonary) nature of placentation
- May be difficult to get female pregant again if they wait 3 to 4 weeks post partum… probably lactation hormones and metabolic needs of lactation
- How many matings to achieve conception would be expected in a female alpaca with normal fertility?
- 3 matings, 90% conception rate
- What simple mating management program can the farmer try in the coming weeks to establish what ovarian/uterine capability the female has before you embark on blood tests, uterine cultures, biopsies and other ancillary tests and pharmacological intervetions?
- Spit off at day 7 to check for ovulation, if receptive ovulation occurred and female should be mated
- If non-receptive, elevated progesterone and presence of a CL
- Spit off at 14 days to check for pregnancy– every 2-4 weeks until U/S at day 30 and 60
- Spit-off intermittently through gestation as up to 5% foetal loss occurs after 60 days gestation
- Describe the epi, clinical signs, diagnostic procedures, control and treatment of Vit D def in alpacas in VIC?
- At risk Jun-Aug
- Clinical signs: proppy gait, failure to keep up with the group, arched back, walking on eggshells, multiple limbs affected or shifting lameness
- Measure P
- Our r
ecommendation to clients is that all alpaca under two years of age or older animals that are
pregnant be given 1500 IU/kg cholecalciferol (Vitamin D) by subcutaneous or intramuscular injection in
May. Cria born between May and September receive a vitamin D injection at 4 weeks of age and then
with the next herd dose. Adults suspected of having deficiencies should
have blood phosphorous levels
performed and be treated on a needs basis.
- Physiological aspects of temperate and tropical species of deer that would influence the suitability of a deer enterprise in Gippsland.
- Temperate (Red, Fallow, Wapiti)
- Orderly seasonal breeding cycles based on survival of winter snowfalls
- Rut in the autumn
- Fawning in late spring/ early summer
- Antler growth and casting in stags/buck synchronized with these cycles
- Show marked seasonal hari coat changes and subcutaneous fat deposition
- Possess a thick fine insulating under-fur in winter
- Sub Tropical (Sambar, Rusa, Chital, Hog)
- Less defined breeding cycles except for Rusa and hog
- Lack subcutaneous fat deposits
- Lack winter coats and under fur
- Fat reserves are scant and mainly found on the mesentery, omentum and around the kidneys and pelvic area
- Temperate (Red, Fallow, Wapiti)
- List diseases and disease syndromes in deer that would be important in Gippsland
- Winter Death Syndrome
- Mineral deficiency- selenium seen in VIC in fallow weaners
- Copper deficiency
- Rye Grass Staggers
- Polio encephalo Malacia
- JD
- Yersenia pseudotuberculosis
- Clostridia
- Leptospirosis
*
- Epidemiology, gross pathology and control, of the common causes of abortion in sheep in the UK
- Onion grass poisoning- early pregnancy- fertiliser helps avoid
- Campylobacteriosis (C. fetus fetus or C. jejuni)- maiden ewes- oral infection- multiply in ewes gut- invade fetus- placentitis and foetal infection- abortion within 3 weeks- mid to late pregnancy- reddish brown vaginal discharge- yellow/white patches 1-3 cm on liver- vaccine
- Toxoplasmosis gondii- oral infection when grazing pasture contaminated with oocysts from cat faeces-1-2 mm white necrotic foci in cotyledons-vaccine
- Listeria monocytogenes- sporadic abortion- ewe stress and weakened immunity- bacteraemia- grazing wet or flood pastures- reddish brown vaginal discharge- beware feeding spoilt silage/ grazing water affected, rotting vegetation
- Alpaca is pregnant on behalf of prospective purchaser. U/S—what features would you look for on the ultrasound image and what stage of gestation would you be happy to certify pregnancy?
- Foetal heart beat from 25 days of gestation
- Look for embryo in amniotic cavity
- The classic “signet” appearance on the scan at about day 45 of gestation can be taken as a sure sign of twin
- Early embryonic loss is common in camelids in the first 60 days so I would warn them but happily certify pregnancy at day 30
- Advice so the owner can check that the pregnancy is maintained to term
- spit offs every 2-4 weeks through to 60 days gestation
- Epi of
- Pregnancy toxaemia in ewes (aka Hypocalcaemia)
- Late pregnancy- anorexia and depression–> recumbency and death
- More common with multiple foetuses
- Inadequate nutrition during late gestation
- Vibriosis in ewes (Campylobacteriosis)
- Most common cause of abortion outbreaks in VIC
- Mostly in maiden ewes especially in prime lamb flocks where replacement ewes are brought in rather than bred on the property–> ie lack of acquired immunity, which is otherwise protective
- Oral infection–> bacteria multiply in ewe’s gut–> invade foetus, membranes, and fluids–> placentitis and foetal infection–> abortion within 3 weeks
- Aborting ewes discharge a lot of bacteria which contaminates the pasture–> contagious
- Small nubmer become carriers.. may lamb normally the next year but shed bacteria when they lamb
- Brucella ovis infection during routine accreditation testing on a poll dorset stud. 80 rams more than 12 months of age on the property. Seventeen were serologically positive and six of these plust two other rams were serologically negative had palpable epididymal lesions.
- 200 6-7 month old ram lambs prepared for sale in 6 months time. Joining is about to start. Brucellosis accreditation is important to the stud and the owners are keen to eradicate.
- Prepare a Brucellosis eradication for the property. Explain and justify recommendations.
- Rams are permanently infected where as ewes do not carry B. ovis for long
- Diagnosis
- testicular palpation for granulomas in the epididymal tail
- Be suspicious of brucellosis in a flock with > 5% of rams with abnormal testes
- Serology– Complement Fixation Test (CFT) or ELISA; takes 14-60 days to seroconvert
- Semen culture- not routinely done
- Eradication
- Recommended due to on going wastage of rams. 3 strategies
- Sell or slaughter all rams and replace with brucellosis free rams– small flocks where most rams are infected– eradication is immediate and assured but high cost
- Two flock system–buy new clean rams and keep them separate– infected flock gets smaller and eventually disappear as rams are culled–testing costs eliminated and not a large capital outlay… main disadvantage there is a big risk infection will spread to clean rams
- test and slaughter infected and suspect rams
- Palpate testicles and test
- Break the group into small herds to avoid spread
- Testing can get expensive
- Best strategy in large ram flocks and in small flocks were rams are too valuable to consider culling thema ll
- Eradication testing must be 14-21 day intervals.. if > 3 week infection can keep spreading fast
- Recommended due to on going wastage of rams. 3 strategies
- *
*
- Epi
- Dermatophilosis in weaner sheep
- Mycotic dermatitis, lumpy wool, dermo
- D. congolensis– motile zoospore which invades skin
- Requires: susceptible sheep, a wetting event, suitable contact– common
- Strong wool sheep are more susceptible
- Pizzle rot in wethers
- Caused by Corynebacterium renale overgrowth in the presence of high urea concentration urine
- Inflammation of the prepuce which can extend to the penis
- Urinary concentration of urea raised when sheep graze high protein pastures such as lush, legume dominated pastures
- Cheesy gland
- Start after shearing or dipping– sheep infected with bacteria cough up lung lesions or from ruptured, draining abscesses
- C. pseudotuberculosis can survive for weeks to months in the environment
- More prevalent in older sheep
Penicillin
Shearing
- Reproductive management procedures for 50 ha alpaca stud near Geelong
- Male management to maximise fertility in the herd
Check scrotum for testes at birth.
Measure testicular length every 6 months and record findings.
Check for scrotal oedema during hot/humid conditions.
Complete breeding soundness exam
ination, vaccinations, drenches
, shearing 2 months before breeding
season.
Adopt early pregnancy diagnosis to observe early infertility pr
oblems.
- Breeding recommendations
First breeding at 12 months of ag
e (maiden) when reached 65% of
estimated mature body weight OR 15-20
days after unpacking if parturition was straightforward and una
ssisted.
Breed once when receptive. Multiple
matings may lead to metriti
s as male penetrates cervix with penis and
traumatises the endometrium to assist with OIF absorption.
Spit-off at 7 days to check for
ovulation. If receptive, ovulat
ion did not occur and female should be mated
again (to coincide with a diffe
rent stage of the ovarian follic
ular wave). If non-receptive at 7 days, her
behavior indicates presence of elevated plasma progesterone and
presence of a CL ….
Spit-off at 14 days to check for
pregnancy. If receptive, conce
ption did not occur and female should be
mated again, at a time when the newly emerged dominant follicle
will be an optimal diameter and the
oocyte contained within, at an optimal age. Non-receptivity ind
icates presence of elevated plasma
progesterone and a corpus luteum
…. And probably pregnancy.
Spit-off regularly (every 2-4 weeks) until ultrasound pregnancy
test at (30 and) 60 days post-joining to
observe foetus and therefore
confirm pregnancy status.
Spit-off intermittently throughout gestation as up to 5% foetal
loss occurs after 60-days gestation.
- Deer on 20 Ha Mornington Peninsula
- Species of deer recommend
- Red deer because they are cow like to handle. May kick but most hinds are not aggressive. Stags also easy to handle except for rut period
- Routine management procedures you would recommend
- Remove antlers annually, even if not interested in m aking money, for safety
- Grazing feeding habits similar to goats– browsers– so require more supplementation when farmed and higher quality feed
- Mineral deficiencies common– ensure Selenium, Copper, Iodine is sufficient in the diet
- Parasite control– lice, ticks, lungworms, nematodes
- Facilities required
- High fences as they can jump
- Hydraulic mattress padded crush
- Blindfolds
D because PGF2alph before day 50 when placenta makes own progesterone… and after day 144 for live birth if giving corticosteroids to induce parturition
Brucella ovis is not zoonotic
Anaemia and ill thrift
D
Set stocking over autumn- Continuous set stocking refers to the situation where livestock numbers in a paddock vary little from month to month, or from year to year
Part A
Parts A and B
Parts C & D
Part B
(cont after picture)
* Low ovulation rate
* Major imp in AUS- strong positive correctlation between BW/CS and avg. number of ovulations
* ewes in light BWT have fewer ovulations and hence conceive fewer lambs because of poor nutritional management overall
* Light CS after drought
* prolonged lactation (no early weaning)
* The flushin effect– good nutrition for a few weeks pre-joinging seems to improve ovulation rate but the effect is very variable and only a boost to reproductive efficiency; not flushing is an unlikely cause of low conception rate
Part B continued
(cont from picture)
* Border disease: pregnancy loss usually following infection in 1st half of pregnancy; later infections usually result in birth of lambs with congenital defects
* Border disease, Campy, Toxo: disease usually only seen in ewes that haven’t been exposed to the infectious agent of vaccinated before pregnancy so havent’ acquired immunity which tends to be protective
(cont from pic)
* Toxo: avoid young cats (who are the worst shedders) around farm/avoid cat faeces contaminating feed (more of an issue in more intensive systems)
* Vaccs available - not all in AUS
* Listeria: often from rotting vegetation/ silage or chicken litter: avoid exposure
* Border disease
- diagnosed on histopathology of congenitally affected lamb or abortus, or detection of viral antigen in persistently infected lambs
- Prevention: want ewes to acquire protective immunity before becoming pregnant, so mix age groups of ewes pre-joining; (pestivirus vaccine available in cattle but not registered for use in sheep)
Question 4.
15 minutes
A client has
asked
you to investigate an apparen
t failure to control body lice in their
September
-‐
lambing Merino flock
. Lice
were present in several mobs, and the client
applied an ‘IGR pour
-‐
on back liner’ product immediately after shearing
in August
. It is
now
7
months since shearing and the client has discovered lice on 6
-‐
month
-‐
old weaner
sheep when they were brought in for dr
enching.
List your main differential diagnoses for the problems described
in this mob.
Briefly
explain why you
have
included each one.
[the problems are
(
1) diarrhoea, (2) mortality
, although I haven’t specifically asked for
these to be written down
]
•
major differentials
1.
worms
(
main species of concern
Oster
tagia
&
Trichostronglyus
)
worms
can cause both diarrhoea & morta
lity if burdens high enough
rainfall over summer is conducive to worm
pickup
from pasture
weaners particularly susceptible to worm infestation
2.
bacterial enteritis:
another major cause of diarrhoea & mortality
especially
common in weaners
Campylobacter
ent
eritis
reasonably common in summer
•
other
possibili
ties
:
o
malnutrition
is a
common contributing cause of death but won
’t cause
diarrhoea on its own
o
coccidiosis can cause diarrhoea and mortality but more likely in younger
animals than these
in more confined/
unsanitary conditions
o
perennial ryegrass
toxicosis (PRGT)
will cause diarrhoea & may be
associated with mortality, although would expect neuro signs to be very
prominent if lots of deaths
; right seasonal epidemiology for disease
o
hypersensitivity scouring
f
ollowing ingestion of worm larvae
occurs but
is less
likely in sheep of this age (normally > 12 mo, when they’ve developed good
immunity to nematodes)
& shouldn’t cause death
o
other nutritional causes of diarrhoea
possible
but most wouldn’t cause
mortality
unless something like
widespread
breech
fly
strike was
a
complication
in the scouring animals
(10 minutes)
How will you diagnose the cause of the problems in these
weaners? List
two
procedures you will perform to help obtain a diagnosis
and, for each proce
dure, explain
the reason for performing
it
and the way you
would interpret
its results
.
need to at least
mention
WEC/faecal exam & necropsy
!
•
worm egg count
(
‘WEC’ or ‘FEC’;
some
may say “
faecal exam
” but really we want to
know about
presence of
worm eggs
&
hence adult worms by
specifically
doing a
WEC
)
:
o
why:
to
identify
& quantify
presence of worms
o
interpretation:
would expect weaners dying of parasitism to have
high
WEC;
generally concerned if WEC >
~
250
*
epg
but would probably be higher if
significant de
aths are occurring
[ *
Prof
Ian Beveridge says 150 epg
but
Mackinnon has a different opinion here! Either was marked correct, so don’t
get your knickers in a knot.
]
o
other comments
:
faecal
exam
also lets us
check for other
less common
causes of
diarrhoea, in
cl coccidia
, large numbers of bacteria
if the
WEC
is done
10
-
14 days after drenching
then it’s
particularly
helpful because we can
check whether drench was effective
(WEC
should be 0 if drench was effective)
faecal culture may help with bacterial enteritis
but beware
interpreting results (see point below)
•
necropsy
:
o
why
:
usually very helpful for identifying
causes of disease & death in groups
of animals (& we have dead animals available!)
o
interpretation:
we are looking for
presence of nematodes with a
total
worm count
(
TWC
)
and
(& this
quantifies level of parasitism
gut histopath
to identify bacteria colonising
GIT
mucosa
if bacterial
enteritis
is present
•
this is the
diagnostic method of choice for bacterial enteritis,
as faecal culture can give false +
ve
(b
ug
s may be
present
but
not
causing disease
e.g. if we happen to sample a
healthy carrier
)
•
it’s also an
effective way of diagnosing other causes of
enteritis
(including coccid
i
a: see above)
;
may
be able rule
out PRGT (
absence of axonal torpedoes in
brain hi
stopath
but lack of characteristic neurological clinical signs will be
most important here
)
•
Minor points:
o
measure
bodyweight
: poor nutrition in mob may predispose to other death,
although not scouring;
40
–
80
weights will give reasonable estimate of mob
ave
rage; is there a visual ‘tail’
of illthrifty animals in
mob indicating chronic
undernutrition?
o
history:
of pastures/plants grazed (nutritional causes of scouring)
drenching history (likelihood of worms pres
e
nt now; efficacy of
current control program; lik
elihood of drench resistance)
(5 minutes)
The farmer tells you that the weaners last received a
benzimidazole/levamisole treatment at marking.
Briefly describe why this
information might be relevant to your diagnosis and
how you would
investigate whether
or not
it
has contributed to the problems in the weaners.
Obviously identifying appropriate causes is the most important thing, even if you conceptually
list them at different points in the reproductive process.
•
before mating:
any of these reasons are OK
(
I’ve grouped them under different
topics but
you didn’
t
have to)
:
o
ewe anoestrus
poor bwt (mainly maidens): lightweight ewes don’t come into or
display oestrus
coumestans in white clover: hormonal effects to suppress oestrus
behaviour
stress (shearing): these ewes still ovulate but do not display oestrus
behav
iour
due to photoperiod effects in seasonal breeds (less important in
Merinos) where the ‘ram effect’ (teasing) hasn’t been used properly
[young ewes won’t reaching puberty if they are poorly grown ewes:
this won’t be a cause of poor repro across the whol
e of this particular
flock because it is presumably composed mainly of adult ewes]
o
low ovulation rate
(major importance in Australian flocks): strong positive correlation
between bwt/
CS
& average no. of ovulations
ewes in light bwt have fewer ovulations an
d hence conceive fewer
lambs because of e.g.
•
poor nutritional management overall
•
having light CS after a drought
•
prolonged lactation (no early weaning)
[the ‘flushing effect’ (= good nutrition for a few weeks pre
-
joining)
seems to improve ovulation rate b
ut the effect is very variable & only
a boost to reproductive efficiency; not flushing is an unlikely cause of
low conception rate]
o
at fertilisation
o
brucellosis
(ram):
Brucella ovis
infection of epididymis causing granuloma &
reduced sperm output and thus
reduced rates of fertilisation; quite
widespread in Australia, spread ram
-
to
-
ram
o
other infectious causes
of ram infertility include
Actinobacillus seminis
infection:
similar pathophysiology to brucellosis but epidemiology not clearly
understood; probably
much less common
o
ewe causes: [may be hard to distinguish from embryonic death]
infertility caused by grazing
oestrogenic clover
cultivars
•
older clovers contain oestrogen
-
like compounds that affect
sheep reproductive tract & impair sperm transport/embryo
implantation
•
‘temporary’ clover infertility due to changes in cervical mucus
& uterine fluid that impairs sperm transport & reduces
likelihood of fertilisation; disappears when grazing stops
•
‘permanent’ infertility from years of grazing is both
fertilisati
on failure (as above) + embryonic loss [cystic
endometrial hyperplasia that’s present impairs implantation]
nutritional stress
may impair fertilisation/cause early embryonic
death
out of season breeding
: if ewe shows oestrus but doesn’t
ovulate/ovulates un
reliably then this could be considered failure of
fertilisation
•
gestation:
loss could occur early (embryonic loss ± return to service) or later in
gestation
o
onion grass poisoning
: fungal toxin (can also cause staggers but usually
not concurrent) infecting
plant causes early embryonic loss w/o return to
service;
o
ewe infections:
Campylobacter fetus fetus, Listeria spp., Toxoplasma
gondii
, Border Disease Virus (hairy shaker disease, pestivirus)
infections
all
cause embryonic/foetal death (the 1st three tend t
o be last trimester but
theoretically
can cause losses early in gestation)
all cause infection of placenta (esp. toxo) and/or foetus (others),
leading to foetal death: observed as pregnancy loss if early or
abortion if late & abortuses detected
border dise
ase: pregnancy loss usually following infection in 1st half
of pregnancy; later infections usually result in birth of lambs with
congenital defects
border disease,
Campy
,
Toxo
: disease usually only seen in ewes
that haven’t been exposed
to
the infectious a
gent or vaccinated
before pregnancy and so haven’t acquired immunity, which tends to
be protective
How should individually struck sheep be treated now?
