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117 Cards in this Set

  • Front
  • Back
what is the overall aim of GIT nematode control in cattle?
"the main aim is to avoid [L3] ingestion. If treating clinically affected cattle is it too late.
- mainly ML-resistant cooperia
describe the preventive drenching system in spring-born dairy calves
"- similar approach to sheep
- aim to avoid autumn/early winter peak
- prevent the early season contamination
- treat regularly from weaning (5-6 months)
- interval varies depending on product and its persistent activity
- ML kills Ostertagia for 5-6months, but must give every month for Cooperia (no refugee of ostertagia)
- if using short acting anthelmintic such as BZ or BZ+Lev combo then every 4w
what are the (dis)advantages of preventive drenching system?
- minimises subclinical effects
- increase growth before winter
- relatively low cost and reliable outcome
- benefits > cost
- independent of management
- reduces parasite challenge for older cattle

- total reliance on anthelmintics
- neglect of other factors e.g. good nutrition
how does protective drenching compare to protective drenching?
"protective drenching occurs later to animals considered to “need a drench”

the peak of larvae count on grass is higher

it is better to use preventative drench until immune response kicks in, then use protective drenching strategically when you need to.
describe and explain the different systems of rotational grazing to manage parasites in dairy calves:
"“Ruakura system”
- aim: avoid drenching cattle
- shifts calves every 1-2 days over the whole farm
- not always possible
- effective: frequent moving avoids reinfection from shed eggs —> L3

Irregular system
- shifts at varying intervals
- probably creates hotspots
- parasite problems
- need drenching programme. excessive challenge to cows.
describe and explain other grazing systems in cattle to manage parasites:
"set stocked 2-4 calves per paddock
- cows move through leaving calves
- usually from when vaccination complete
- minimal drenching required (drench before dividing)
- need to keep adequate feed but usually not a problem

- grazing area away from main farm
- most commonly used to take calves in May (9months) and return in-calf heifers at about 21months
- many variations
- sometimes used for dry cows and to conserve feed on main farm
- potential problems
- usually young stock only: can get heavily contaminated so may be dangerous all year
- out of sight, out of mind
- good drenching programme required + good nutrition

Spelling pasture
- timing: how long is enough?
- dung pat excellent reservoir of [L3]
- moist inside
- usually not feasible in NZ as grass will get out of control
- hay/silage aftermath is the best option
- safe but not worm free
- risk of overgrazing
what are the main issues with and how can parasites be managed in bull/beef contract-rearing dairy heifers?
"- bringing in successive groups of young stock
- heavy reliance on drenching: need regular programme
- preventive scheme
- endeavour to utilise other classes of stock but often none available
- widespread ML-resistant C.oncophora
- use BZ+Lev combination: less convenient than pour-on ML
- important to drench calves/older cattle on arrival
- quarantine drench, then triple drench and put on “dirty” pasture to dilute/compete resistant worms
- transportation, diet change may trigger Type 2 ostertagiosis
describe and explain the cow-calf system to manage parasites in cattle:
"- calves weaned at 4-8 months (Feb-May)
- not normally drenched until weaning
- can be significant parasitism before
- while on mum, cows help keep down [larvae] on pasture. should still do regular treatments.
- 3-4 treatments after weaning advised
- interval affected by drug and formulaton
what is some evidence supporting worm treatment impacting production?
"MSD field trial:

treated with 1x ivermectin injection: 0.2kg/day
treated with 4x ivermectin injection:
treated with 6x ivermectin injection: 0.5kg/day
what factors need to be considered when choosing a drench?
"- consider anthelmintic resistance status on that farm
- early drenches: effective against Cooper
- late winter: effective against Ostertagia
what is the current situation of anthelmintic resistance in cattle?
"- beef certainly. Dairy possibly worse
- Cooperia oncophora main problem
- BZ and ML resistance
- so far LEV is working
- Ostertagia
- BZ resistance
- ML resistance first few reports
- LEV dose limiting species. Poor, especially against inhibited L4
- T.axei and T.longispicularis
- some resistance
mode of delivery (anthelmintics): pour on vs oral or injectable?
"- MLs and LEV
- available as pour-ons
- ML dose rates:
- pour on: 0.5mg/kg
- injectable: 0.2mg/kg
- pour ons:
- farmers favour
- issue: cattle licking product off back; penetrating into skin
what is the management protocol against Type 2 Ostertagiosis?
"- prevention
- good parasite control to limit (L3) on pasture
- late winter/early spring: preventative Rx to kill EL4
- MLs best anthelmintic
- pour-ons no WHT for milk
- most problems: younger animals, 12 months
- can still see in older, but less common
- routine treatment older dairy: small response
- Eprinomectin and Moxidectin: increase milk volume, MS (fat, protein); 2yo in calf sooner
- 0.03kgMS/day ~7.5kg MS —> 10 fold return
- anti-ostertagia Ab levels in milk suggests we are losing production to worms.
- overall: no significant effect.
main causes of poor growth in lambs:
"- poor nutrition
- quality and or quantity
- internal parasites
- trace element deficiencies
- cobalt, selenium
- disease; pneumonia
- enzooitc pneumonia in sheep common in NZ esp warmer regions
- December-May

"- chronic “non-progressive” pneumonia

- >20% lung affected - decreased growth are - pleurisy: inflammation of pleurae - would normally only affect growth rates of smallish proportion of the mob
pneumonia: microorganisms associated with ovine pneumonia
- Manneheimia haemolytica
- Pasteurella multocida
- Pasteurella trehalosi
- Bordetella parapertussis

- Mycoplasma ovipneumoniae
- Mycoplasma arginini

- Parainfluenza Virus Type 3
- Respiratory Syncytial Virus
- Ovine adenovirus type 6
- Bovine adenovirus type 7
- unidentified cell associated agent
pneumonia: Suggested pathogenesis
"Pasteurella?Manneheimia commensals in upper respiratory tract

lung defences compromised by viruses, Mycoplasma

heat stress induced open mouth panting

combination of young sheep, open mouth panting, dust lung damage from viruses/Mycoplasma allows Pasteurella/Mannheimia to colonise
what might cause stress and open mouthed panting in young sheep?
- drenching, vaccinations

pneumonia: Risk factors ID’d at slaughter
"difficult to define as the condition is only identified at slaughter
- shearing lambs on day of weaning
- shearing lambs twice
- frequent yarding post-weaning
- motorised mustering
- increased age of lambs at slaughter
pneumonia: Diagnosis
"- history esp management
- range of clinical expression
- mild: nothing seen
- moderate: coughing, ill thrift, some deaths
- severe: sudden deaths
- observation at a distance
- coughing
- clinical examination of affected lambs
- auscultation
- necropsy
- slaughter-house surveillance
- report pleurisy
pneumonia: treatment
"- antibiotics may suppress development and give partial recovery
- generally unsatisfactory
- chronic lung abscesses may result
Pneumonia: prevention
"- yard in the morning: cooler
- wet yards: reduce dust
- cull bad animals: more likely to pick it up and spread through the flock
- reduce yarding frequency: multiple procedures at one time
- enough labour to minimise animals’ time in yards
Pinkeye: proper term, cause, morbidity
"- Ovine infectious keratoconjunctivitis
- bacterial cause
- Chlamydophilia
- associated with dust, wind, flies
- more common in summer and autumn
- Mycoplasma
- probably carrier sheep
- not seasonal
- transmission: direct contact and fomites
- can be severe, can get recurrence
- 10-20% morbidity,
pinkeye treatment
- may resolve spontaneously

- oxytetracyclin SC/IM
- oxytet in solution: in eyes
- may recur
"inversion of the eyelid
common in new-born lambs
thought to be inherited
entropion: treatment
"evert eyelid
- mild: manually
- inject antibiotic in lower eyelid
- remove elliptical section of skin under lower eyelid
- Michele clip under lower eyelid
- cull carrier ran (if identifiable)
what are the health challenges facing NZ pastoral livestock?
"- Primary food source is pasture, so it is at risk of:
- under nutrition
- trace element deficiencies
- internal parasites and soil bacteria
- toxic plants
- management: rotational grazing and strip-grazing. Meaning there are high stocking densities
- potential rapid transmission of infectious diseases
- large flock/herd sizes
- easy for problems in individuals to go un-noticed
- periods of acute severe stress
- mustering, yarding, shearing, trucking
- other than that, a “relaxed” lifestyle
- Outdoors all year round: exposed to extremes of weather
- mortality of new-born lambs during storms
- warm, moist, climate
- fungal diseases in pasture
- rapid development and good survival of parasites
- fleece provides a warm moist micro-climate
- flies, bacterial conditions
- generally fed monoculture, often exposed to sudden ∆
- subject to wounds and abrasions which may predispose to infection/disease
- deliberate: tail-docking. deep anaerobic wound where ring is placed —> increased susc. to tetanus
- accidental: sharp object
where should the focus be when dealing with flock/herds?
"Big flocks/herds mean low’ish profitability

- focus on flock/herd health rather than individual
- focus on prevention of poor production/disease rather than treatment
- focus on subclinical as well as clinical
- integrate animal health with husbandry and consideration of the farm business
where is usually the issue in a production/poor health pastoral livestock system?
most production or poor health issues in a pastoral livestock have a large management or husbandry component
define the 7 steps in the herd/flock investigation
"- Define the problem
- History taking
- a.) environmental examination
b.) distance exam 4. a.) Individual animal exam
b.) +/- post mortem exam
5. ancillary aids/further diagnostic tests
6. Data analysis and decision making
- short and long term

7. reporting back and future monitoring
explain the 1st step to the herd/flock investigation
"1. define the problem

What what where when why
use data if available, be specific
explain the 2nd step to the herd/flock investigation
"2. History taking

on-going throughout investigation
most important part!!
Asks “How” for the 5 w’s
differential diagnoses
explain the 3rd step to the herd/flock investigation
"3. a) Environment examination

observational skills v.v imp
begins as soon as you drive onto the farm

3. b) distance examination
RR, hunger, BCS, behaviour, scouring, discharge, coughing, obvious cuts/injuries/swellings, variation in size
explain the 4th step to the herd/flock investigation
"4. a) individual animal exam

- individuals that are clearly sick or badly affected
- can undertake some procedures on large number relatively quick

- eg MM, BCS, weighing

4. b) +/- PME

- read animals +/- euthanasia of severely affected
- large numbers, low individual value
- consider sample size
- “on the spot” diagnoses for many diseases
- collect samples for further analysis
explain the 5th step to the herd/flock investigation
"5. ancillary aids/further diagnostic tests

- collect correct, appropriate number of samples
- compromise between cost and quality information

Note: “i’ll do bloods” insufficient answer
explain the 6th step to the herd/flock investigation
"6. Data analysis and decision making

- is an abnormality present?
- if so, what?

- is treatment possible or warranted?
- may be better to focus the attention/funds on control and prevention

- how can the problem be prevented/minimised?
- short/long term
- many production problems related t management:
- intervention or change to management required for long term prevention
explain the 7th step to the herd/flock investigation
"Reports are useful:
- clarify thoughts (for you and farmer)
- written document that can be referred back to
- poor record keeping often a problem in LA practice

Future monitoring
- correct course of action in many cases
- on-going contact with farmer
- may lead to further work/greater involvement
what issues can arise in the mating area that affect reproduction?
"- long WOI (interval from weaning to service) due to:
- poor nutrition during lactation
- cycling before weaning
- mycotoxins
- Poor farrowing rate due to:
- EED —> infertility, delayed returns
- disease: parvovirus
- small litter size, infertility
- poor timing of matings
- overusing boars
- poor semen handling
- post-service discharge syndrome
- mating late
what issues can arise in the dry sow area that affect reproduction?
"- poor FR due to:
- early pregnancy stress
- (embryo loss —> small litters, delayed return)
- later pregnancy stress
- (abortion)
- disease (—> abortion)
- eg lepto
- long farrowing interval
- failure to detect returns —> high NPDs, NIPs
- low weaning weight
- poor nutrition —> poor lactation
- high stillborn
- overfeeding sows —> fat sows —> farrowing problems
what issues can arise in the farrowing area that affect reproduction?
"- low weaning weights
- farrow in poor condition
- poor nutrition (lactation)
- disease
- high PWM (—> low numbers weaned —> loose $$)
- starving piglets
- mastitis
- overfeeding sows
- poor fostering
- scours
- poor hygiene and management
- disease
- high stillborns
- farrowing difficulties
summarise the reproductive disorders of pigs into 5 failures:
"- failure of sows and gilts to show heat
- failure of sows and gilts to be bred
- failure to conceive when bred
- failure to maintain pregnancy
- failure to produce good litters
common health issues in pigs that affect reproduction?
"- parvovirus
- enterovirus
- original cause of SMEDI
- no vaccines available
- leptospirosis
- encephalomyocarditis
- toxoplasmosis
- mycotoxicosis
- seasonal infertility
- Discharge:
- vulvar discharge
- cystitis
- uterine infection discharge
- vaginal infection
parvovirus in pigs: transmission, clinical signs, diagnosis, prevention/control
"- Oral-nasal infection
- clinical signs:
- males + non-pregnant females = none
- SMEDI (stillbirth, Mummification, Embryonic Death, Infertility): spreads slowly from foetus to foetus
- <30d = I, ED
- 30-70d = M, ED
- >70d = S, WP
- Diagnosis:
- clinical signs
- detection of viral Ag’s in foetus
- sow serology = little value
- Immune sows pass on high levels of Abs to piglets that last for 3-6m
- prevents infection and seroconversion of young pigs
- interferes with vaccine in young pigs
- prevention/control
- natural infection (= lifelong protection)
- vaccination (protection only 1-2y)
leptospirosis in pigs: transmission, clinical signs, diagnosis, treatment
"- spread in urine (long term shedding), reproductive discharges
- infection via MM or broken skin
- Clinical signs
- reproductive disease:
- abortions (+2-4w), stillbirths, weak piglets
- sow: usually sub-clinical, sometime pyrexia and anorexia
- diagnosis:
- serology (MAT)
- titres 1:1600+ (diff from vaccine titre)
- culture not routinely done
- Treatment:
- Antibiotics, isolation
- streptomycin , oxytetracycline
"- effect depends upon stage of exposure, toxin level
- Zearalenone
- “reproductive failure syndrome”
- M, irregular returns to service, reduced litter size, deaths
- rectal prolapse, swollen vulvas on newborn gilts, splay-legged piglets
Mycoplasma suis: transmission, clinical signs, treatment
"- spread by direct exposure, blood components and blood sucking parasites
- clinical signs:
- causes anaemia
- associated with illness in periparturient sows
- hyperaemia, oedema, swelling of vulva around farrowing
- sub-optimal reproductive performance
- treatment:
- oxytetracycline
Discharge: types, differentiating, treatments
"most common bug: E.coli

- cystitis:
- discharge at end of urination
- small volume (<20mL)
- no systemic illness (unless ascends to kidneys)
- urine pH >8
- blood and pus in urine
- treat:
- amoxicillin
- clean living conditions
- uterine infection:
- discharge unrelated to urination
- large volume (>100ml)
- w/i 6d of oestrus
- no systemic illness
- treatment:
- cull
- vaginal
- moderate volume ~50ml
- unrelated to oestrus and reproduction
- common in gilts
why do breeding soundness in bulls?
- reducing the risk of having fertilisation failure
- risk of exacerbating infertility with poor quality sires
what does a breeding sounds examination entail?
"- ID
- service testin/ observation of coitus and penis
- scrotal circumference
- palpation of genitalia
- semen examination
which is more favourable: service testing or clinical/semen evaluation?
"depends on aim of farmer.

service testing:
- usually more appropriate for beef industry
- most concerned whether bull can serve

clinical/semen evaulation
- usually most appropriate for dairy industry
- most concerned about conception rates opposed to breeding bahaviour
list the steps of completing a bull soundness examination:
"- general inspection, feet, legs, BCS
- scrotal circumference
- clinical examination of genital
- scrotal contents, accessory sex glands (vesicular glands)
- behaviour, locomotor system
- service test
- semen examination
- final assesments
what are some abnormalities of the locomotor system leading to “unsound” BSE?
"impaired mounting or service behaviour
- foot
- temporary: abscess, overgrown
- permanent or congenital: malformed claws
- back:
- spondylitis: excess Ca2+ leads to increase bone deposition across vertebral bodies
- upper limb:
- less common
what are the penile lesions affecting service due to impaired mounting?
"- ruptured penis
- oedema and pre-scrotal swelling
- compromised vascular drainage
- pain in genitalia BoHV-1, orchitis, seminal vesiculitis
- temporarily unsound
- inability to achieve intromission
what are the penile lesions affecting service due to mounting without intromission?
"- Vascular defects:
- abnormal venous drainage
- bv’s drain to corpus cavernosum
- age: occlude. drain via root of penis
- can’t get erect
- blockage of longitudinal canals
- penile deviations
- frendulum fails to break down, pulls penis down
- temporarily unsound
- spiral deviations of the penis
- corkscrew upon ejaculation = normal
- corkscrew upon touching cow = abnormal
- adhesions:
- post BoHV-1, post trauma, penile neoplasia (fibropappilomata)
- papillomas (can be temporary —> unsound)
what are issues that affect service by achieving intromission but failure to ejaculate
"- neural damage: sensory nerves of the penis, spinal sensory nerve roots
- seminal vesiculitis (acute stages)
- back pain (spondylitis) in mature bulls. usually progressively worsens, with acute episodes
what are the major syndromes causing lowered semen quality?
"- testicular degeneration
- immaturity and overuse
- young bulls: small production capability. immature sperm ejaculated
- sperm defects
- knobbed, dags, diadem, tail stump
what characteristics are attributed to a “sound ram”?
"the ability to:
- successfully locate ewes
- perform the act of mating
- fertilise the ova with a net result of achieving pregnancy in the ewe

actual mating behaviour rarely a problem
- exception: young rams raised away from ewes
How do soundness exams test for fertility
"they don’t.

eg monorchids are fertile but permanently unsound
what does a ram breeding soundness exam involve?
"- palpate with both hands from behind the ram

check for:
- anatomy of all structures within the scrotal sac
- testis, epididymis (head, body, tail), spermatic cord
- testicular symmetry
- testicular tone
- 29-35cm
- testicular freedom from scrotal adhesions/ abscesses
- spermatic cord
- scrotal skin
- heat releaser: should be think skin and small wool length
- chorioptic mange
- presence of abscesses or shearing cuts
when are ram soundness exams performed?
"- pre-mating (Feb). 8w prior to PSM
- Pre-Sale (Oct)
- Ram lambs at weaning to detect genetic trends from sires + can cyll non-suitable stud rams at premium abs prices rather than as 2t
- Pre-purchase examination of a single sire = full individual fertility check
- Failure of a ram(s) detected at next seasons lambing
- detection of ram epididymitis lesions by client or by yourself following a fertility investigation
what is the aim of a ram soundness exam?
"to determine the rams Category of Soundness and whether it should be used for this seasons mating

A genitally sound ram:
- one that has no congenital, physical or genital abnormalities or any condition that will lead to this ram becoming incapable of service

A fertile ram:
- Is a ram that is capable of service and able to impregnate ewes mated to him

can only be classed “At time of examination""
what are the categories of soundness?
- free from all defects of the genitalia and can be judged at time of clinical examination as fit for mating and able to be sold

Temporarily unsound:
- has a defect that can be treated returning the ram to full soundness for mating and sale

- has an untreatable defect that will impair his mating performance
what are the cases of testis degeneration (testis atrophy)?
"- Seasonal atrophy
- out of season can be 1/3rd size due to decreased testosterone and decreased spermatogenesis
- malnutrition
- stocking rates/feet/teeth
- Parasitism
- —> poor BCS and atrophy
- Heat
- decreases spermatogenesis —> atrophy
- excess wool length (>10mm)
- dags
- environmental temp: over yarding/transportation in summer
- Chorioptic Mange causes exudative dermatitis of scrotal wall
- diseases: fly strike, pnuemonia - fever
- Disease of scrotal contents
- Epididymitis
- Anatomical
- segmental aplasia
- short scrotum lambs
- vasectomised rams
what are examples of anatomical irregularities?
"- asymmetry
- segmental aplasia
- hypospadia
- incomplete closure of the urethra: scrotal, mid-penis, end-penis
- high riding scrotum
- inguinal hernia
- monorchid
- micro-orchis
- cryptorchid
what are the main 4 diseases of testis?
- Brucella ovis
- Gram -ve Pleomorphs

Chorioptic Mange
- Chorioptes bovis

CLA Abscesses
- Corynebacterium pseudotuberculosis

Trauma to scrotum
- shearing cuts
what are the further examinations that can be done to investigate ram soundness?
"- penis and prepuce examination
- for individual animals for sale or purchase
- or animals with question to performance history

NOT routine

- sigmoid flexure, body of penis, glans penis, urethral process,
- smooth and even
- prepuce entire with no ulceration/wound preventing penile extrusion
what are some prepucial conditions that should be documented?
- infection limited to exterior of prepuce

- Infection penetrated deep into prepuce

(lay term = puzzle rot)

- From Corynebacterium renale
- transmitted by direct contact
- ulcerated prepuce orifice becomes scabbed over and ultimately blocked
- treament:
- acidify urine by removing access to high protein diets or Ammunium Chloride TID
how would you categorise a ram affected with mange?
"most often temporary unsoundness as the lesions disappear after treatment.

Severe infestations can result in permanent unsoundness if >50% scrotum affected
- results in scrotal wall thickening which affects heat loss and is detrimental to spermatogenesis
what are the 3 methods of semen collection?


Collection from ewes vagina post service (morphology only)
What can semen be used for?
"fertility indicator and culture for disease diagnosis

look at:
semen density
total volume (variable)
wave motion
what is the sperm quality?
"normal sperm
why is epididymitis always classified as permanently unsound?
"infection causes inflammation of the seminiferous tubules in the epididymis resulting in obstruction and occlusion

the buildup of sperm results in rupture and spermatozoa flow out into the surrounding interstitial space

sperm are haploid so are immunogenic resulting in a sperm granuloma

sperm antibodies are produced further decreasing the viability of any semen produced
how is Brucella ovis diagnosed?
"blood test (after 6 weeks)

semen (after 3w)
how is Brucella vis treated?
"palpate ALL rams
any with lesions isolate and CFT blood test
cull all positives

repeat palpations at monthly intervals
once celar test wait 60 days and repeat palpation
2x clear tests 60d apart = Brucella ovis free flock
how is gram -ve epididymitis transmitted? what are the clinical signs? how is it diagnosed?
- retrograde infection up the urethra into the accessory sex glands and epididymis from the environment

clinical signs:
- usually young rams
- may become systemically ill
- abscess may burst and thick pus drain outside
- remnant epididymitis lesion, atrophied testis

- can carry bacteria is sex glands for up to 2y
- pus and inflammatory cells in semen samples
- palpation and semen culture
- BT no use
what are the factors that affect lambing percentage that we cannot influence? what impact do these factors have
"- Weather and topography
- topography: can influence to a degree
- choose where to mate ewes, lambing paddock, fertilisers
- impact:
- topography: ram tupping capacity, ewe feeding level via quantity and quality of pasture, neonate survival immediately post-birth
what (11) factors influencing lambing percentage can be altered by good management?
"- Oestrus
- mature ewes stay in oestrus for 12-36hr
- 2t 1-24hr
- breeding season in ewes
- ovulation rates
- mating
- fertilisation
- embryo development and survival
- foetal development and survival
- birth
- ewe survival rates
- perinatal survival
- growth of lamb
what effects do delaying the ewe joining mate have?
"- high first cycle submission rate
- less ewes returning
- shorter mating period
- shorter lambing period
- lambs born later = more grass for ewes = better lactation = faster lamb growth and survival rate

advancing the mating date does NOT guarantee an advancement of mean lambing date due to lower ovulation rates earlier on (ewes are seasonal breeders)
why is the mating not delayed?
"- premium lamb prices
- set lambing date that matches grass growth rate
what are the factors affecting the ewes breeding season?
"- breed of sheep
- all short day breeders (Romneys < merinos)
- latitude
- closer to equator = sooner PSM
- altitude
- higher altitude = shorter breeding season
- age of ewe
- younger ewes are more difficult to get pregnant
- ram effect
- photoperiod control and melatonin
- stress
- eg shearing. should not be done 3 weeks before, during or after mating
- hormonal induction of oestrus
- CIDR/sponges (12-14d)
- PMSG: injection. oestrus 24-72hr later
what impact does age have on ewe breeding season and why?
"younger ewes are more difficult to get pregnant
(hoggets and maiden 2t)

- cycle later
- have shorter heats
- have less cycles with lower ovulation rates
- have lower conception rates
- have higher EED rates
how can young ewes’ conception rate be increased?
"- mate separately to main mob of ewes
- mate on easy rolling to flat paddocks so rams can find them
- use more rams per 100 ewes - 1:50
- use experienced rams not young rams

target hogged weight PSM = 39-42kg
write up a plan to synchronise ewe hoggets:
"- ewes must not have contact with rams for at least 3w prior to PSM
- flush hoggets on good quality feed on a rising plane of diet >1250kgDM/ha (5cm)
- Mate hoggets in small flat paddock so rams can find them
- Put teasers out for 17 prior to PSM (tease hoggets for a long time = better response).
- rams go out at day 17 at 1:50 ratio
- hoggets should have 70% pregnancy rate post synchrony
what is the sequence of hormonal events occurring when between the teasers and rams being put out?
"- within 10mins after teasers in: LH pulses. main pulse 27-36hr after.
- within 3d most ewes have silent ovulation (no ∆behaviour)
- 60% of these ewes develop CL which maintains the cycle with a repeat ovulation occurring 18-20d after initial ram introduction
- in 40% the CL regresses and at 6-8 days after ram introduction these ewes have a 2nd silent heat which is then maintained for a normal cycle length
what are the factors (11) affecting ovulation rates?
"- bodyweight and nutrition level at mating
- aim: 55-60kg . draft out light ewes and priorities feed.
- flushing 3w prior PSM >1250kgDM/ha
- time of mating (early season vs Late)
- ewe age
- older ewes = more ovulations
- genetics
- finish landrace very fecund
- Booroola gene : additive effect ( Merinos )
- Inverdale gene : very small increase. Rams —> daughters. ewes —> 50% offspring
- homozygous = ovarian hypoplasia = infertile
- diet : mating on lucerne and phyto-oestrogens in clovers
- high OE —> inhibit LH —> inhibit ovulation
- mycotoxins
- reproductive depression
- Pithomyces chartarum (FE)
- liver damage —> low BCS —> low fertility
- Zearalenone
- level of feeding when younger
- pre mating shearing
- immunisation against ovarian steroids: Androvax
- Androvax: immunisation against ovarian androgen Androstenedione (OE precursor)
- 2x dose before PSM (8w, >4w prior) + annual booster >4w prior PSM
- trace elements: Selenium
what effect does Oestrogen have on ovulation?
"non breeding season:
- low level estradiol released from ovaries has negative feedback , inhibiting LH

breeding season:
- hypothalamus loses sensitivity to low dose OE, releases GnRH
- stimulates pituitary to release LH and FSH
- FSH stim’s follicles to mature
- high OE —> LH surge —> ovulation

oestradiol controls the number of follicles selected for ovulation
what factors affect fertilisation?
"- length of mating
- ram harness + coloured crayon
- detect mating patterns. aids in feed budgeting
- embryonic mortality
- fertilisation - 30d pregnant
- >12d, affects cycle (CL doesn’t regress as fast)
what are the common causes of Abortion in NZ?
"Camplyobacter fetus fetus
Toxoplasma gondii
Salmonella brandenberg (South Island)
what part of gestation are Campy losses associated with?
"ONLY associated with late gestation losses
what is the epidemiology of Campy?
"- introduced by carrier sheep to naive flock
- transmitted by
- ingestion in feed or water
- direct contact with aborted foetuses/membranes
- scavengers eatting aborted foetuses
- NO veneral transmission
- can survive in envt for ~20d
what is the pathogenesis of Campy?
"- bacteraemia
- bacteria invades and localises in the placenta and foetus
- bacterial growth enhanced by placental blood supply and nutrients
- placentitis: areas of necrosis in placenta and foetal tissues
- foetal liver, lungs
- Foetal death
- infected ewes may become carriers
- ewe post infection become immune
what are the clinical features of Campy infection?
"- abortion storm
- last 6w pregnancy
- may see ewes with blood on perineum or membranes protruding
- most often in maiden ewes
- ewes healthy (rarely metritis)
- early neonatal loss
- birth of weak lambs, reduced lamb viability
- often outbreaks after ewes have been stressed
- high stocking rate (high density winter grazing)
- ewes remain immune for years afterwards
how would you diagnose Campy?
"look at placenta:
- gross lesions
- +/- oedematous, opaque placentae
- +/- foteal liver lesions
- foetus usually fresh
- PM= microscopy of foetal stomach contents
- culture
how do you control a campy outbreak?
"- prevent/reduce exposure to infected pasture
- decrease stock density
- shift u’s
- remove/dispose of aborted material
- quarantine affected cows
- personal hygiene: fomites
- antibiotics
- not practical, but can be used
- Streptomycin, penicillin, tetracycline
- vaccinate for prevention, too late once broken out (3w prior. takes 10 days for effect)
how is toxoplasma gondii transmitted?
"- reservoir: mice —> cats
- young cats shed > older cats
- resistant oocytes contaminate hay , bedding , concentrate feeds where the faecal oral route occurs in the ewe
- ram semen
- Once infected immunity is lifelong so see abortions in completely naive flocks (rare) or mostly maiden ewes
what is the time from infection to abortion for T. gondii?
"40 days
what are the clinical signs of T. gondii?
"EED (early embryonic death)
- resorption
- late return to oestrus or increased Dry/Dry at end of scanning

Mid-pregnancy (60-120d)
- undeveloped foetal immune system
- foetal death/ mummification/ abortion

120+ gestation
- immune competency in lambs
- born normal

no systemic signs in ewes
how would you diagnose T. gondii?
"- gross lesions +/- mummified foetus
- “strawberry cotyledons”
- cotyledons with white/grey areas of necrosis
- clear intercotyledon area
- histopathology or cotyledons, foetal lungs, liver, brain
- sera from ewe: too late
how do you control T. gondii?
"limit breeding cat population, especially litters in hay barns

vaccination: Toxovax
- fragile
- single dose to maiden ewes
- ≥4w prior PSM
how is salmonella brandenburg transmitted
"- introduced by:
- carrier sheep (up to 6m)
- mechanical vectors: gulls
- dust fomites
- environmental survival ~ >4m
- high stock density —> increased stress —> increased shedding of carriers
- both MA ewes and 2t susceptible and often multiple bearing ewes
what are the clinical features of salmonella?
"- abortion in late pregnancy
- foetus autolysed, smelly (dead>1d)
- ewe often has difficulty expelling lambs
- ewe sick.
- necrotising metritis
- ~50% aborting ewes die
how do you diagnose salmonella?
"- location: south island
- history
- clinical features
- samples
- culture of foetal stomach contents or liver, placenta, vaginal swabs
- histopathology of placenta
how do you treat salmonella?
"- guarded prognosis
- early and aggressive treatment of placentitis may prevent ewe death but not abortion
- LA oxytetracycline
- potentiated sulphonamides
- fluid therapy: not practical

- spread ewes out to decrease stocking rate and drop faecal/oral contamination
- ensure plenty of clean, fresh water and adequate feed
- avoid stressing ewes
how do you control salmonella?
"vaccination “salvexin”
- incomplete protection, but pre-tup vax in face of outbreak recommended

- avoid high stocking rate late pregnancy
- minimise pre-lamb yarding and other stressors
- purchasing
- hygiene
- disposal, quarantine, control gulls, personal/vehicle hygiene
- Zoonotic
how is Hairy shaker disease/ Border disease transmitted?
"via MM
introduced to flock by clinically normal sheep
- persistently infected are source of infection
what are the clinical signs of hairy shaker/ border disease?
"depends on when infection occurred:
- early gestation:
- EED —> late return to oestrus, increased dry/dry at scanning
- 60-120d:
- mummies/abortion
- +120d:
- birth of hairy shakers
- hairy, stunted lambs
how do you diagnose hairy shakers?
"the presence of the lambs
- hairy, stunted, discoloured path of hair on back of neck
how do you control hairy shaker/border disease?
"- avoid exposure of pregnant ewes to infection
- especially young naive ewes
- mix new stock months before tupping ≥4w
- cull affected lambs
- call infected ewes who drop HS lambs
what are some other causes for abortion?
- Bacillus spp
- Fusobacterium spp
- Brucella ovis (rare)
- Listeria (silage)
- Yersinia

non-infectious: rare
- high nitrate
in a PM on an aborted lamb, what samples should be taken?
"take all samples as can have duel infections:
- foetal stomach contents
- culture + microscopy
- foetal liver/ lungs/ heart blood
- culture/IFAT
- foetal brain/ heart/ liver/ lungs
- histology
- placenta
- fixed and fresh for culture and histology
what determines value of production animals:
"how much output you can generate from a given set of inputs

inputs (costs)
- feed/pasture
- vet care
- farm labour
- housing/utilities

Outputs (market value)
- milk
- meat
- eggs
- offspring
- fibre
- labour
your role as a farm consultant includes:
"correcting problems
- developing treatment protocols

identifying opportunities
- reproduction, nutrition, management
- improve herd performance

preventing problems
- vaccination, biosecurity
interventions that can be used to address health issues:
"diagnostic tests

decisions should be made that takes into account:
- knowledge about disease
- epidemiological consqeuences, available interventions, effects on production
- knowledge about farm
- cost of intervention, farmer objective, available resources
- knowledge about externalities
- animal welfare, environmental, and public health consequences
"“road map"""
"- define the problem
- list alternative interventions
- enumerate the costs and benefits
- select a decision framework
- decision tree analysis
- partial budget analysis
- cost-benefit analysis
- choose course of action
- monitor response
What are the main 3 species of concern regarding GIT parasites in cattle?
"- Ostertagia ostertagi
- Trichostrongylus axei
- Cooperia oncophora

2º importance
- intestinal Trichostronglyus spp
- other Ostertagia app
- Oesophagostomum radiatum
- Nematodirus
how quickly does immunity develop in cattle and sheep?
- most disease in stock <18months
- especially <12mnths

development of immunity similar to sheep
- apparent by 6mnths
- starts to have impact
- fully mature by 18mnths
- still recognising parasite as foreign: will have protein losing enteropathy

note: no PPR in cattle
describe the seasonal pattern of FEC and larvae in cattle:
"- Winter/spring:
- larvae population declines
- spring flush (grass growth) provides dilution factor
- neglible FEC
- Aug—> Nov
- FEC increases before larvae
- Oct—> Dec
- conditions for larval development improves
- increase population
- calves reinfect calves
- summer:
- dry period limits FEC and larvae survival
- dungpats: eggs survive more than in sheep pellets
- peak larvae end of summer/spring
- Autumn
- conditions for good larval development: peak (partially winter)
- immune response kicks in: FEC peaks and begins decline
- Autumn/Winter
- FEC dropped (immune response)
- last wave of eggs develop into larvae
- lag behind FEC in larval drop