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DVM 3 - 2 > Small ruminants 1 > Flashcards

Small ruminants 1 Flashcards

1
Q

Deer what are the important parts of the husbandry

A
  • Fences, yards, crushes
  • Common injuries
  • Velvet harvesting
  • Deer nutritional preferences
  • Seasonal food intake variation
  • Importance Of winter energy reserves
  • Nutrition And pregnancy
  • Effects of overfeeding
  • Key trace mineral deficiencies
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2
Q

Temperate and subtropical deer species

A 
Temperate
- Fallow deer
- Red deer 
- Elk/Wapiti 
- Red/Wapitis hybrids
- Fallow/Meso hybrids 
Subtropical 
- Rusa deer 
- Chital 
- Hog deer 
- Sambar
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3
Q

deer fences and yards what are important factors to consider

A
  • Deer tend to crash into fully see through mesh when put under pressure to escape (especially into gates)
    ○ Could be too close together - not far enough away
  • Causes fractured incisors, jaws, necks
  • Always yard as a group
  • Fully closed walls can encourage jumping
  • Partial see through fences work best in lanes approaching yards
  • Important to allow deer to become familiar with lanes and yards by feeding them into these
  • Rounded corners are important
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4
Q

getting deer into confined spaces what shouldn’t and should do

A
  • Like to escape around corners
  • Can’t force deer into place they balk at as a group. Will jump back over you
  • Collectively behave like a school of fish
    ○ Want to move like a group, if scatter put too much pressure on it
  • Don’t try to stop them. Once one goes the rest will follow no matter what
  • Follow up quickly and shut gates # once deer go into any yard or they will come out again. Let farmer do all this for you
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5
Q

Trauma to head for deer what are the 2 main ones

A

1) Antler pedicle fractures (antler grows from the pedicle so will impair the future growth of that antler, will decrease the value of that antler and therefore the deer)
2) Fractured jaw

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6
Q

Capture myopathy in deer what is it,, caused by and clinical signs

A
  • White muscle disease
  • Anaerobic muscle activity ++ lactic acid
    Clinical signs
  • Peracute - death in 24hours
  • Acute - later collapse, nephrosis myoglobinuria
  • Subacute - ataxic, myoglobinuria, wry neck
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7
Q

Capture myopathy in deer treatment

A
  • Difficult to treat. Damage is often too severe
  • If mild leave alone and watch
  • RX - control pH, fluids, flunixin (anti-inflammatory), Vit E
  • Consider kangaroos and horses trying up
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8
Q

Capture myopathy in deer mechanism of action and what organs affected

A
  • When the muscle is exerted (used) its metabolism changes from aerobic (uses oxygen) to anaerobic (uses stored energy in the muscle)
  • This leads to the build-up of lactic acid causes acidosis
  • Lactic acid in the bloodstream drop the pH in the body, affecting cardiac output
  • This affects oxygenation to muscle tissue in turn leading to myositis and release of myoglobin
  • Myoglobin damages the excretion part of the kidney (the renal tubule)
  • Other organs are affected: the lungs become congested and bleed
  • The liver becomes swollen and pale
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9
Q

What are some common yarding injuries for deer

A
  • Loss of incisors - weight loss
  • Fractures of mandible - death from starvation
  • Fractured atlas - instant death
  • Fight punctures - minimal etx. Signs
  • High limb fractures
  • Ruptured gastrocnemius tendon
  • Low limb fractures - severe contamination
  • Antler pedicle fractures
  • Velvet antler injuries/fractures
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10
Q

What is involved in the velvet growth and harvest

A

○ At beginning of growth get spike called velvet antler then eventually goes into a hard antler
○ Want to sell at the velvet (soft) antler stage, at this stage not high in testosterone
§ When cut at this point will get a button when meant to shed the hard antler (pedicle)

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11
Q

Red deer crushes what is the main type, what is involved

A
  • Padded mattress type
  • Expensive but required - drug immobilisation NOT a substitute
    ○ Crushes have very significant OHS benefits
  • Sliding door front and back with side curtains
  • Pads operated using fitted hydraulic rams
  • Can be lowered/raised to mid body height
  • Deer compressed, then bodily lifted off the ground to reduce capacity for struggling
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12
Q

fallow drop floor crush for deer why for fallow and features

A
  • Works best with fallow deer, not good for reds
    ○ They are too “jumpy” for padded hydraulic type
    Features
  • Pre-adjust to correct width
  • Deep leaps into Y shaped ply race extended
  • Drop floor hinges open along far side
  • Deer wedged down into Y shaped space
  • Deer released by releasing the near side at its bottom and via sliding door at front
  • TRAPS - can struggle forward - so strap down
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13
Q

Hard antlers on deer farms do they belong and what do they result in

A
  • No place for hard antlers on farms
  • Are deadly weapons - very dangerous -> high on testosterone
  • Stag/buck fight injuries and deaths -> if leave one with hard antler - BAD
  • PM finding: severe subcut, trauma, few external punctures
  • Fence and tree damage - fighting through fences, thrashing trees, shrubs
  • Attacks on other deer in yards
  • Risk to handlers, stockpersons
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14
Q

Antler growth who grows, where grow on, when shed and what occurs

A
  • Antlers are unique to the deer family
  • Only found on males except reindeer/caribou
  • Grow from solid pedicles on temporal bones
  • Antler shed annually - where find buttons if harvested
  • Antlers increase in size and complexity with age
  • Each deer species has its own characteristic antler configurations. Specific terminology for parts
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15
Q

growth cycle of the antler and the seasons

A
  • Summer - velvet shed
  • Autumn - hardened antler used for fighting
  • Winter - harden start to prepare to shed -
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16
Q

Danger of captive stags what occurs with behaviour and hormones for male deer

A
  • Docile and sometimes friendly when seasonal testosterone levels are low
  • Dramatic changes in behaviour when testosterone levels peak with high levels of aggression and loss of fear in humans
  • There are more people killed by capture antlered deer than by captive large cats
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17
Q

What risk factors for hand rearing male deers and prevention

A

Particular dangers of hand reared male farm animals
- Socialised to humans
- Confusion re own species identity
- Lack of fear of humans (beware “quiet” bulls)
- Particularly marked in species with seasonal rut cycles
Prevention
- Early castration: fawn- lamb elastrator rings - no cycling of antler without testis
- Minimum handling if artificially reared

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18
Q

Stag antler Ca and P demand what is needed, what relies on, what occurs if bad, what use to increase

A
  • Massive short term skeletal Ca and P mobilisation
  • Antlers are the product of last year’s nutrition (hypocalcaemia not seen in hind/does)
  • Ricketts (Vit D deficiency) rare even on high grain and Lucerne rations in deer
  • Most deer farms use superphosphate
  • Bone chewing for mineral recycling
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19
Q

Velvet antler what used for, when cut, price and what need to do

A
  • Is a valuable by-product used in traditional oriental medicine
  • General tonic and arthritis treatment
  • Crushed and ground to a powder
  • Various active substances isolated
  • Cut November- December (Red), Dec-Jan (Fallow)
  • Price peak $200 (1990) - approx. $25/Kg today
  • Need to freeze the antler so management is important otherwise will rot
  • Different grading on velvet
  • Accreditation scheme
  • Nerve supply to the pedicle and growing velvet -> supraorbital, auriculopalpebral, zygomaticotemporal
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20
Q

What are the 2 main blocks used in removal of velvet antler and the blocks within - EXAM

A

1) Single blocks
○ Supraorbital (infratrochlear), 1mL lignocaine injected on the nerve midway between the medial canthus of the eye and the base of the pedicle
○ Zygomaticotemporal; 2mls into trough of soft tissue behind the ridge ascending fromt eh orbit to the pedicle
○ Auriculopalpebral, 5mls under the skin behind and the outside (caudolateral aspect) of the pedicle
2) Ring -> MOST USED

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21
Q

Velvet antler what are the 12 steps within the removal

A
  1. Strap down deer hand firmly in crush
  2. Place regional blocks - xylocaine 2ml
  3. Test effect, wear gloves
  4. Apply rubber figure of eight tourniquet
  5. Saw off antler 10mm above coronet
    ○ Do not tear skin, finish cut with scalpel
  6. Invert cut velvet antler and stand in rack to allow clotting
  7. Clean saw in disinfectant
  8. Cover stumps with cotton wool, release stag but hold in pen
  9. Record data to stag ear tag ID
  10. Remove tourniquet in 15min and release stage into yard
  11. Bag, tag and freeze velvet after weighing
  12. Check in yard 30mins later and release into paddock
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22
Q

What is important thing about nutrition for stags and deer and the capacity of deer to digest fibre and when this becomes an issue

A
  • Stag/bucks eat little during rut-marked weight loss
  • All deer must have adequate fat reserve put on by end autumn in order to survive winter
    Capacity of deer to digest fibre
  • Temperate species better at this, although still poor
  • Deer rumen smaller, lighter, drier - cannot just bulk up like cows
  • This becomes a problem when coupled with normal reduced winter feed intake hence “winter death syndrome”
  • Becomes critical in sub-adults which have lower fat reserves (4% lambs 18%)
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23
Q

What are some hazardous material on deer farms diagnosis and treatment

A
  • Plastic bags, silage wrap, nylon rope
  • Loose ends on shade cloth wall covers
  • Polythene bale string
  • Dx. Palpate rumen, weight loss
  • Rx. Rumenotomy - G.A
  • Loose wires or mesh
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24
Q

deer nutrition how relate to pregnancy and neonate survival and what maintenance is needed mid to late pregnancy and lactation

A
  • Lowered energy intake in pregnancy leads to lowered foetal bird weights, results in higher mortality rate
  • Drop in neonate survival rates - hypoglycaemia
  • At mid to late pregnancy = 2x maint
  • Lactation = 3 x maintenance energy requirement
    ○ Lactation fallow dose = 12MJ and red hinds = 47MJME/day
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25
Q

trace element deficiencies in deer what are the main ones and what result in

A
  • Iodine (NZ) - stillbirths
  • Copper - swayback - pale coat
  • Selenium - WMD sudden death
  • Cobalt - not seen - no response to B12 trails
  • Magnesium - rare - transport stress
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26
Q

sick deer behaviour and what should examination involve

A
  • Deer aware when being observed
  • Programmed predation avoidance
    ○ Will disguise effects of injury/illness
  • Required trained eye to pick - need to educate owners
  • Observe from long distance
    Examination
  • Check the lone animal
  • Check sitters among standing group
  • Check tail enders when moving off
  • Check those not feeding in group
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27
Q

What are the 2 main ways to euthanise a deer and details within

A
  1. Downers - IV green dream
  2. Or head kill zone shot
    ○ Captive bolt pistol
    ○ Rifle - minimum .22 LR RF
    § Close range standing - head KZ .22 Magnum
    □ Neck shot
    § Medium range standing. Chest KZ shot
    □ Fallow, chital, hog deer - Min .243 Win
    □ Rusa, Reds Elk Sambar - Min .270 Win
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28
Q

What to do with the body of a dead deer

A 
- Make full use of ALL bodies for diagnoses and further learning 
○ Histopathology confirms gross finding 
- Allows spot on checks on:
○ Past health events 
○ Current parasite status 
○ Response to recent treatments 
○ Current nutritional/trace elements 
○ DON'T WASTE SUCH IMPORTANT DATA
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29
Q

Female deer reproduction how often cycle, synchronise with, AI or embryo transfer, gestation time for different species

A
  • 17-21 days, varies with species
  • Synchronise with goat CIDRs
  • Red deer AI as per bovines
  • Embryo transfer per laparoscope + GA
  • Gestation time variers with species
    ○ Fallow 7.5 months
    ○ Reds, elk, sambar 8.5m
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30
Q

Deer obstetrics how common is dystocia, what risk factors can lead to this

A
  • Dystocia rare in fallow and subtropical
  • Foetal oversize/reds/red hybrids
  • Maternal obesity
  • Pelvic fat necrosis - rusa deer
  • Posterior with stifle flexion
  • Anterior with retained foreleg
  • Anterior with lateral head deviation
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31
Q

Hind/fawn bonding what interferes with it and how to prevent bad bonding

A
  • Improper handling and over handling will result in inappropriate mothering
  • High adrenalin interferes with bonding
  • Low level of success after obstetrics’
    Minimize
  • Use epirdural (2ml) to minimise pain
  • Left hind/doe smell neonate
  • Collect colostrum (2ml oxytracycline IV)
  • Lightly sedate hind with xylazine
  • Feed fawn with tube and syringe
  • Leave together in darkened room
  • Check quietly to confirm if bonding
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32
Q

General anaesthesia for deer premed, induction, stabilisaton and what not to use

A
  • Xylazine sedation premed IM
  • Valium/ketamin induction IV
  • Intubate and put on isoflurane and stabilise
  • Can slowly give calcium IV dose
  • Insert IV drip into cephalic vein
  • Halothane can cause cardiac arrests in deer
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33
Q

What are the 4 main parasites of deer, clinical signs and diagnosis

A

1) lungworms
2) ostertagia
3) spiculageroptera
4) trichostrongylus in weaners
Clinical signs - Illthift, scour
Diagnosis - FEC

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34
Q

Lugnworms in red and fallow deer what lead to, mortality, diagnosis and treatment

A

leads to
○ Cough, bronchopenumonia - adult worm
○ Unthritfy
○ Possible secondary bacterial pneumonia
○ Verminous pneumonia
- Occansional high mortalities in fallow deer
- Diagnosis -> faecal larvae, PM - adult with histopathology larvae
- Treatment -> worm immediately after first heavy autumn rain, strategic worming

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35
Q

Lungworms in deer what are important worming options

A
  • Fenbendazole; okay for intestinal worms and lungworms
  • Cydectin (moxidection); v-effective dewormer (pour-on)
  • Levamisole; seems to be less effective
  • Ivermectin
  • Remember to rotate pastures
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36
Q

List the 8 main important deer diseases and the most common one

A
  1. Yersinia pseudotuberculosis - COMMON
  2. Leptospirosis
  3. Clostridia
  4. Listeria monocytogenes
  5. Malignant catarrhal fever
  6. Tuberculosis
  7. JD not seen in Australia as yet
  8. Campylobacter - rusa in queensland
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37
Q

Yersinia pseudotuberculosis what is it, assocaited with and leads to

A

in deer
○ Is a bacterial zoonoses
○ Associated with enterocolitis and diarrhoea
○ Leads to clostridial disease especially perfingens type D (enterotoxaemia) pulpy kidney… which is seen a lot in colder weather especially in lambs

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38
Q

what are the 6 main miscellaneous conditions in deer and the important one to look for

A

1) Ryegrass staggers - occasional
2) Polio-encephalomalacia - occasional
3) Grain overload - max 1Kg fallow 2Kg reds
4) Footrot - occasional
5) Inhalation pneumonia
6) Botulism - bone chewing - IMPORTANT TO LOOK FOR

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39
Q

botulism in deer what results in and clinical signs

A
  • bone chewing - IMPORTANT TO LOOK FOR
    ○ Muscle weakness - very poor jaw tone
    ○ Weight loss - down but can get up
    ○ Unable to chew or swallow
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40
Q

Deer and FMD is it a threat

A
  • UK experience indicates that wild deer in Australia are low threat as FMD reservoir
  • No cross infection in UK due to limited exposure to livestock under normal farming methods
  • Disease was self-limiting and acquired from livestock and not vice versa
  • Pattern indicates there is no point in trying to exterminate susceptible wildlife during an outbreak
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41
Q

what are important factors in deep transport vehicles

A
  • Fully enclosed - conv. Bus or semi
  • Shaded air vents
  • Wood shaving on non-slip floor
  • Or bare slatted floors
  • Multiple compartments
  • Provision from drinkers
  • Air conditioning in case of breakdown
  • Alternate power source for A/C
  • Provision for feeding in emergency
  • CAUTION WITH AIR TRANSPORT
42
Q

how to assess live weights in deer and what needed for

A
  • Electronic scales
  • Mature male approx. 2X of female weight
  • Important for drug dosage calculations
  • Critical for sedatives etc.
43
Q

Sedation of deer what is the main drug used and combination with, where inject

A
  • Main drug is xylazine 100mg/ml
  • Reverse with yohimbine IV
  • Xylazine/ketamine combo better
  • All sedative dose rates are IM
44
Q

deer intramuscular drug administration what are the routes

A
  • By hand syringe in deer crush
  • By pole syringe
  • By blow pipe and dart
  • By short range dart pistol
  • Be medium range dart gun
  • By long range dart gun
45
Q

Dart drug administration what use and the drug used

A
  • By blow pipe
  • By dart gun or pistol
  • By arrow fitted with terminal dart
  • Possession or use of any device capable of delivering drug bearing darts required category C shooter’s license
  • Require high security storage in gun safe
    Draxone -> use for darting cattle -
46
Q

What is important for goat dairy breeds and therefore diseases common and things need to consider

A

energy -> highly productive
○ Common to see metabolic disease -> pregnancy toxaemic and hypocalcaemia -> another lecture
§ Also more fussy with their feed -> need to encourage them to eat more and get the energy needed
□ Apple trees -> browse -> chopped up the best way
○ Need to graze on higher quality food -> longer grass better for energy AND decrease risk of parasitism

47
Q

What are 2 main nutritional conditions of goats, what makes more susceptible and therefore what need to do

A

1) Goats need iodine more than sheep -> GOITER IS COMMON
○ Routine supplementation with iodine (potassium iodine - can add into drenching solutions) is appropriate in iodine deficient pastures
§ Kids are the main issue so give to mothers prior to kidding
○ Clinical signs -> enlarged thyroids, less hair cover
2) Hypothermia
○ As body condition score goes down due to higher stocking rate more susceptible to hypothermia
§ And if co-grazing with other species - cannot compete as well with other species
○ Prevention
§ Good and feed shelter
□ Preferential daytime feeders (3pm finish)
□ Shearing increase feed required 40%
® DON’T shear in cool months of the year
□ Good body condition

48
Q

Goat reproduction type of breeders, puberty, cycling and 2 main conditions that are important in goats,

A

• Seasonally polyoestrous
• Early puberty
• Strong ‘buck effect’ - > same as in sheep
○ Introduce them to induce cycling in does
1. Cloudburst/Pseudopregnancy
2. Abortion is common in goats
○ Anything that causes regression of CL and therefore progesterone will result in embryonic loss ANY POINT OF PREGNANCY

49
Q

Cloudburst/pseudopregnancy what species occur in, signs, what results in and how to treat

A 
GOAT
○ Signs 
§ Doe overdue 
§ Abdo enlargement 
§ Fluid accumulation and the burst once the uterus opens and uterine fluid is released "cloudburst"
○ Persistent CL +/- embryonic loss 
○ Prostaglandin to treat 
§ WHOLE PREGNANCY IS CL DEPENDENT -> be careful make sure NOT PREGNANT -> need to ultrasound
50
Q

What are 5 main zoonotic causes of abortion in goats

A

1) toxoplasma gondii
2) coxiella burnettii (Q fever)
3) campylobacter (C. feotus, foetus)
4) chlamydia abortus
5) listeria

51
Q

Toxoplasma gondii what is different about infections in goats

A

still zoonotic and causes abortion BUT there is a risk of this causing abortion in the future
○ Risk is low -> just monitor through next pregnancy and if loss the second time then cull
§ Serology -> cannot know with the second case if that is occurring due to toxoplasma
§ CHECK THE FOETUS -> like for toxo titres or histopathology of foetal brain

52
Q

Coxiella burnettii what disease does it cause, results in what in goats, transmission, treatment and immunity

A 
Q - fever - abortion in goats 
transmission 
- carrier does
- contact with abortus
- biting insects 
treatment 
- tetracyclines may control outbreak 
immunity 
- healthy carrier exist but most goats develop long-lasting immunity post-abortion
53
Q

Campyobacter in goats what lead to, transmission, treatment and prevention

A

abortion in goats
transmission
- contact with abortus
- carrier does
treatment
- separate herd - prophylactic tetracyclines
- consider culling kids (potential carriers)
prevention - VACCINE - give protective immunity

54
Q

what is the most important thing with kid management, how to measure, how important

A

Good colostrum management is VERY IMPORTANT

  • Qualitative measure of passive transfer: low-IgG kid serum has prolonged coagulation time (>10 mins) with glutaraldehyde (3 samples are poor-acceptable-good)
  • Kids with low IgG died at 1.9 times the rate of high IgG kids
  • 41% of all deaths were ‘attributable’ to a kid having low IgG -> IMPORTANT
  • Needs to be stored well
55
Q

dehorning kids when best done, 2 ways mainly done when young and how done as adults

A
  • Best done when young
    ○ Gas dehorning -> quaraterise the horn bud (kill the cells)
    ○ In clinic -> gas down then remove gas (don’t want oxygen) then quaraterise)
    § SUSCEPTIBLE TO LIGNOCAINE TOXICITY -> be careful with local anaesthetic - max 6mg/kg
  • Adults -> need GA + cornual block + excellent analgesia
    ○ Bleeding is excessive and the amount of horn and cornual sinus removes give appearance of complete decapitation
56
Q

Goats what are the main infectious disease within GIT, 2 main other ones, 3 vaccinatbles and 2 others

A 
- With GIT signs 
		○ Worms
		○ Coccidiosis 
		○ Yersinia 
	- Johne's disease 
	- CAEV - Caprine Arthritis Encephalitis Virus 
	- Vaccinatable's 
		○ Enterotoxaemia 
		○ Tetanaus 
		○ CLA - caseous lymphadenitis 
	- Others
		○ Footrot 
		○ Lice
57
Q

Goat internal parasites how susceptible, why and which level do you drench for which worms and when different

A
  • Very susceptible to parasites -> evolutionary are not grazers so not exposed to parasites like cattle have been historically (graze long grass)
    1) >500eggs/gram -> DRENCH - clinically important
  • For trichomonas and coccidia
  • Different for sheep (250eggs/gram - will be the same worm burden generally)
    2) Haemonchus -> drench at 800eggs/gram -> causes clinically significant disease
    For strategic management for pastures -> will be lower than this
58
Q

Internal parasite issue in goats what are the 2 main ways to diagnose and treatment options (how differ from sheep)

A

Diagnosis
- Worm egg count -> IF DIARRHOEA DO THIS
- Blood -> ANAEMIA -> Haemonchus important
Treatment
○ Not all drenches registered in goats: beware WHPs
○ Fast metabolism
§ BZ (2x sheep dose), MLs (2x sheep dose), monepantel (2x sheep dose), LEV (narrow safety margin 1.5 time sheep dose), Ops (at sheep dose and follow all precautions)

59
Q

Internal parasites in sheep what are the main ways to control (in general)

A

○ Nutrition and SR
○ Exposure - which are contaminated paddocks -> cross-over, grazing other species
○ Grazing management -> horses and cattle grazing
○ Monitoring
○ Suppressive/strategic -> reduce stocking rate and proper pasture management to ensure the grass remains long to reduce worm burden in the goats

60
Q

Eimeria in goats what environment occur, when infected what can co-contribute

A
  • Disease of confinement -> cycle of infected oocytes within the pens
  • Signs variable
  • Usually late-born kids: infected → shedder → reinfected (exposed to large worm burdens at a younger age)
  • Adults usually good immunity
  • Cryptosporidium can contribute to neonatal diarrhoea too
61
Q

Eimeria goat diagnosis what are the 2 main ways and what to do if high and well or low and unwell

A
  • Faecal float to see oocysts -> number of excreted oocysts may not represent the infection rate
    ○ High number of oocyst but well -> probably not the issue
    ○ Low number of oocyst but clinically unwell and high infection
    § Young kids, scouring, not responding to other treatments but low number then possible this an issue
    □ In this case post mortem and histopath to confirm
  • Dead animal -> histopathology -> invasion of Eimeria within the epithelium -> needed to confirm diagnosis
62
Q

Eimeria treatment in goats what are the 2 main options and what situations good for

A
  • Neither are registered -> not specified
  • Sulphadimidine 1–3+ days (oral/injectable) -> good for general infections
  • Baycox (toltatrazuril) 20 mg/ kg once PO -> better for more severe
    ○ off-label cattle drug, recommended 90 d. withhold
63
Q

Eimeria in goats 2 main ways to control and things within

A

1) Coccidiostats: amprolium & monensin to does prekidding as preventive
2) Address risk factors:
○ hygiene -> reared on hay and stored and completely cleaned between batches of kids
○ Transmission -> reduce multiple ages within the shed, separate in two week intervals
○ Immunity -> snatch rearing -> failure of passive immunity is a risk factor

64
Q

Yersinia in goats what also cold, 2 pathogens, what condtiions and main alert

A

“winter scours”
- Yersinia enterocolitica, Y. pseudotuberculosis
○ Cold and wet weather conditions -> Due to nutritional and environmental stressed -> disease
○ Diarrhoea doesn’t respond to drenching

65
Q

Yersinia in goats main issues, diagnosis and treatment

A
  • Severity/disease course can be more severe than in sheep -> can lead to death
  • Other problems
    ○ Abortion
    ○ Milk -> risk for contaminating milk
  • Diagnosis
    ○ Faecal culture -> very easy to grow, large number of growths from large number of animals
    ○ Post mortem -> run histopathology and microbiology to confirm and while waiting treat otherwise more will die
  • Treatment
    ○ Oxytetracyclines
66
Q

Caprine arthritis encephalitis virus (CAEV) importance, cause, what important about immunity

A

Importance - notifiable (govenment won’t do anything just want to get rid of disease) and costly
cause - lentivirus
immunity - Low circulating Ab when finally seroconverts:
○ levels essentially provide no immunity
○ not indicative of presence/absence of infection -> generally clinical signs only present in adults

67
Q

Caprine arthritis encephalitis virus (CAEV) what characterised by andt eh 5 main clinical syndromes

A
  • Characteristic non-suppurative (mononuclear cell) inflammation:
    1. Arthritis (‘big knee’)
    2. Hard udder
    3. Chronic interstitial pneumonia
    4. Chronic weight loss
    5. Leukoencephalomyelitis-> ascending paralysis
    Often more in kids than adults, likes like spinal lesion
68
Q

Caprine arthritis encephalitis virus (CAEV) what occurs during infection, seroconversion, after infection and clinical outcomes

A
  1. Infection -> vertical (colostrum or milk) OR horizontal
  2. seroconversion -> kids may be seropositive from Ab in pasteurised milk for 2-3months
  3. after infection -> seroconversion may take months after becoming infected, some goats revert to seronegative, Ab NOT PROTECTIVE
  4. clinical outcomes -> many affected animals have no clinical signs BUT
    - Are source of infection for others, may have sub-clinical lower production -> many infected animals still culled/euthanised
69
Q

Caprine arthritis encephalitis virus (CAEV) diagnosis what are the 4 main ways and what need to be careful of

A
  • Clinical signs -> waxing and waning
  • Cytology (e.g. joint fluid) -> non-suppurative inflammation
  • Histopath
  • Serology
    ○ Beware potential poor sensitivity & late seroconversion
    ○ Need to repeat testing
    ○ If positive on one animal positive for the whole herd
70
Q

Caprine arthritis encephalitis virus (CAEV) when considered herd free

A

○ 5 yr q. 6–12 months -> now don’t have to do as much as serology is more sensitive
○ Ongoing surveillance & biosecurity

71
Q

Caprine arthritis encephalitis virus (CAEV) control considerations what are the 2 main ones and what involved

A

1) Try to maintain production but stop disease spread
○ Late seroconverters can keep infecting offspring if only doing ‘test &cull’
○ Likely many animals infected when finally detected → pure culling program would be costly
2) Only moderate test sensitivity
○ Seroprevalence may appear to ‘rise’ with age because of late seroconversion

72
Q

Caprine arthritis encephalitis virus (CAEV) what are the 2 main control strategies, what is involved in surveillance

A

1) test and cull whole herd
2) prevent further transmission with a 2-herd system
Surveillance
○ Test all snatched kids > 6 mo to check control is working
○ Quarantine all new goats 2 months then test

73
Q

Test and cull whole herd as control strategy for Caprine arthritis encephalitis virus (CAEV) what need to consider and what need to do

A

○ Can you afford to cull all seropositive -> high change over cost and need to repeat testing anyway to catch later seroconverters
§ Then need to buy from an accredited negative CAE herd
○ If not then run a 2-herd system

74
Q

Caprine arthritis encephalitis virus (CAEV) 2-herd system for control and eradication what are the 3 steps involved

A

Step 1
§ Cull clinical signs
§ Keep other positive animals that aren’t showing clinical signs in another herd -> as culled for age will then remove CAE from herd
step 2
○ Vertical: Snatch rearing on pasteurised colostrum & milk
§ Don’t batch feed colostrum to limit damage if virus still present
○ Horizontal: no direct contact between groups (especially old to young) -> hard on the same property
§ Need double fencing to prevent nose to nose contact
Step 3 - ensure biosecruity
○ Laneways between clean & dirty (not just a fence)
○ Milk seropositives last (or don’t share milking facilities!) -> this will happen for years
§ Disinfect all equipment between herds

75
Q

Enterotoxaemia/pulpy kidney in goats, what usually associated with and the 3 main clinical presentations

A
  • Goats particularly sensitive
  • Usually associated with feed change to soluble CHOs (like sheep)
  • Clinical:
    ○ Peracute: sudden death in neonatal kids
    ○ Acute: abdo pain, diarrhoea (yellow/green progressing to bloody/ watery), death
    ○ Chronic(?): D+, wasting
76
Q

Enterotoxaemia/pulpy kidney in gaots diagnosis, treatment and vaccine

A 
- Diagnosis (as per sheep)
○ Normal gut inhabitant
○ Presence of ε toxin
○ Clin signs, glycosuria
- Treatment
○ Antitoxin, tetracyclines, pain relief, fluids
- Vaccination v. important
○ 3-, 5-, 8-, 6-in-1
○ 2–3 times annually/ pre-kidding
77
Q

Tetanus in goats how susceptible and preventions

A
  • Important part of general clostridial vacc program
  • Goats quite susceptible!
    ○ Routine use of anti-toxin + toxoid for all surgery & obstetrical interventions
78
Q

Cheesy gland what also called, main species within, treatment and prevention

A

Caesous lymphadenitis
- Economically important in dairy goats (cf. sheep)
- Treatment
○ Isolate cases; excellent hygiene
○ Drain & flush abscesses
○ Dispose of all contaminated material (infectious)
○ Maintain isolation until fully healed
- Vaccinate! (cf. sheep) -> 6 in 1 vaccine

79
Q

Lice in goats what is the main one, importance and treatment

A
  • B. ovis will cross-infect & multiply on goats
    ○ i.e., goats pose a biosecurity risk for sheep!
  • Backline treatments probably effective without shearing
80
Q

footrot in goats what important to consider

A
  • Different expression of virulent and benign ovine strains

- Will cross-infect sheep - include in treatment and eradications

81
Q

Mastitis in goats what important to consider as how different to other species

A
  • False +ves possible with automated mastitis counters
  • Beware damage with cow preparations!
    ○ Use just the very end of the intra-mammary syringe (smaller teat canal) and use a smaller quantity
  • Can be caused by zoonotic organisms (Klebsiella, Campylobacter, Listeria
82
Q

Other udder conditions in goats what are the 2 main ones and what to do

A

1) Precocious lactation -> spontaneous milking
○ Not always associated with pseudopregnancy
○ DO NOT MILK, just reduce nutritional value of feed and not milk so dry up
2) Hard udder (CAEV)

83
Q

AUSVETPLAN who coordinated by, what is within and what eradicated in australia

A
  • Coordinated by Animal Health Australia
  • Industry agreement
    ○ EADRA – cost-sharing agreement
  • Disease manuals
  • Proud Hx of eradicating EADs
    ○ Equine influenza
    ○ 20th century
    § TB & Brucellosis
  • Classical swine fever
    § Scrapie
    ○ 19th century
    § Sheep scab, FMD
84
Q

What are 7 factors that result in an emergency animal disease

A
  1. • Likely to enter and spread
  2. • Difficulty to control
  3. • Severity of damage
    ○ Trade impacts
    ○ Human health
    ○ Industry disruption
  4. • Disease
  5. • Host range
  6. • Transmission
  7. • Zoonosis
85
Q

FMD how does the disease affect sheep, what does AUSVETPLAN mean and cost of the outbreak

A 
- Likelihood of detecting in Australia 
○ Always a delay in notification 
- a ‘silent’ disease in sheep
○ Sheep express clinical signs poorly
○ Sheep movements caused spread in UK in 2001 -> efficient as sheep -> motivation for effective traceability in sheep
- AUSTVETPLAN
○ Use of DIVA vaccines
- Victorian FMD plan
- Cost to Australia of an outbreak is about $50 billion
86
Q

FMD UK 2001 outbreak what are the 4 main transmission routes

A

○ Swill feeding illegally imported meat
○ Aerosol spread from pigs
○ Silent spread by sheep
○ Local spread by close contact and fomites

87
Q

Bluetongue what is it, where found, transmission, motality and morbidity and main importance

A
  • Arbovirus endemic in northern Australia
  • Spread by Culicoides midges -> Australia culicoides austropalpalis
    ○ Enter by ‘vector dumping’
    ○ Unlikely to persist in Vic
  • Likely high:
    ○ morbidity 20-50%
    ○ Mortality 5-20%
  • Severe trade disruptions when detected in Aust. in 197
88
Q

Bluetongue vector what is the most common one, what environment found in, where does disease occur and epidemic

A 
Culicoides vector -> most common is Culicoides austropalpalis
- Moist, humid environment
○ Wet season activity
- Incubates in vector
○ No other means
- Species variation in efficacy
- Disease occurrence where both:
○ vector distribution and
○ susceptible hosts
- Epidemic requires a reservoir of viraemic hosts
89
Q

Bluetongue virus what type of virus, serotupes and the 2 things that affect expression of disease and what result in cattle

A
  • Orbivirus
  • 26 serotypes
    ○ Strain variation in virulence
    ○ 12 now known in Australia
  • Expression of disease
    ○ Breed of sheep
    ○ Immunity (exposure/vaccination)
  • Cattle mild/subclinical
90
Q

Bluetongue what occurs after midge bite in cattle and sheep and gross lesions

A 
- Viraemia of:
○ < 50 days in cattle
○ < 20 days in sheep
- Incubation of 4-7 days, fever
- Systemic vasculitis resulting in
- gross lesions of
○ ischaemic necrosis
○ oedema
○ haemorrhage
91
Q

Bluetongue clinical signs

A
  • Salivation
  • Initial serous nasal discharge
  • Oedema of the face, swollen tongue
    ○ **‘Blue’ tongue an infrequent finding
  • Erosions about gingiva and nares
  • Coronitis
  • Wool break and weight loss in convalescent
  • Abortion
92
Q

Bluetongue diagnosis what are the 3 main ways

A 
- Combination of signs with
○ High morbidity &amp; mortality
- Petechiae
○ Oral cavity
○ Base of pulmonary artery**
○ Intestinal
○ Muscle and myocardium
- Serology (ELISA &amp; AGID)
- PCR &amp; virus culture
93
Q

National arbovirus monitoring program what is it, what does it do and the 3 main diseases it monitors

A 
- Justifying OIE zoning
○ No clinical disease in Australia -> all tested negative for export in 2017 
- Sentinel flocks
○ NT
○ Throughout free zone
- Insect trapping
○ C. brevitarsis
- Effective surveillance to satisfy trading partners
1. Murrary Valey encephalitis 
2.Ross river virus 
3. Bluetongue
94
Q

Anthrax what also called, differential, clinical signs and importance

A
  • Wool-sorters disease
  • Differential -> looks like Malignant oedema
  • Clinical signs
    ○ Bloody discharge from orifices
    ○ SUDDEN UNEXPLAINED DEATHS
  • Killed thousands of sheep in 1885 in NSW riverina
    ○ Imported in bone meal from India
    ○ Follows stock routes -> 4-12 day incubation
  • Spores survive decades -> deep sol disturbance may lead to outbreaks
95
Q

Anthrax what are the 4 main things in the control strategy and diagnosis

A 
Anthrax control strategy
1. • Quarantine
2. • Decontamination
3. • Disposal - incineration
4. • Vaccination of at-risk animals
Diagnosis 
- ICT test for anthrax (snap test)
96
Q

Scrapie what is it, importance, incubation period and what are differents

A
  • A TSE (prion disease)
  • Not a zoonosis
  • Long incubation period
    ○ Disease in adult sheep
  • Introduced in 1956
    ○ Quickly eradicated
  • Atypical scrapie
  • Variation in genome
    ○ Determines
    § Susceptibility
    § Incubation period
    § PrP gene -> mutations at 3 codon
97
Q

Scrapie transmission how occur, what not in, species within

A 
sheep
- Horizontal, maternally
- Placenta to all lambs in flock
- Not in
○ Excretions
○ Semen or embryos
- Goats can be infected
- Prions resistant to disinfection
98
Q

Scrapie clinical signs and the clinical course

A
  • Behavioural changes
  • Tremor & hyperaesthesia
  • Pruritis
  • Gait abnormalities
  • Trotting forelimbs
  • ‘Bunny-hop’ rear legs
  • Weight loss
  • Clinical course of 2-6 weeks
99
Q

Freedom assurance program for scrapie what are the 3 main things involved and what has australia done

A
  1. Ruminant Feed Ban
  2. Imported Cattle Monitoring
  3. NTSESP: neuro signs
    ○ Adult sheep or cattle
    ○ Fixed entire brain
    ○ Fresh/frozen spinal cord and dorsal cerebellum
    ○ Samples to prove DDx
    - Australia will no longer import second generation embryos via NZ
    ○ from 20 October 2016
100
Q

What are 6 main differentials for scrapie like symptoms

A
  1. Flystrike
    1. Perennial ryegrass staggers
    2. Hypocalcaemia
    3. Pregnancy toxaemia
    4. Listeriosis
    5. Ojd

DVM 3 - 2 (40 decks)

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