performance and production Flashcards
iceberg diseses in sheep
jhones disease
maedia-visna
ovine pulmonary adenomatosis (jaagsiekte)
causeas lymphadenitis
border disease
undetected disease causing profit losses
jhones disease in sheep
mycobaterium avium paratuberculosis
chronic dosease seen in sheep 4+ years of age (but can shed before clinically diagnosable)
An underestimated, underdiagnosed problem in sheep and goats globally
Bacterium infects macrophages of Peyer’s patches of small intestine – chronic granulomatous enteritis
Is it zoonotic? – Increasing volume of evidence from human medicine that it is
Adult sheep (and goats) – possibly prevalent in UK, but may be ignoredor pass unnoticed, and probably under-diagnosed
Rarely get diarrhoea until terminal stages – many sheep will be shedding MAP without obvious signs
Chronic weight loss is most obvious sign – thin ewes around 4 yrs old
Poor fleece quality also seen
Infertility - often culled as barren ewes before development of other signs
Diagnosis – group blood tests – hypoalbuminaemia (loss of albumin from damaged intestine), blood ELISA (low sensitivity, high specificity)
Faecal samples for bacteriology – poor diagnostic power
Post-mortem examination – emaciated carcass, thickening and ridging of the ileum, enlarged mesenteric lymph nodes – histopathology for confirmation
Vaccine available for sheep and goats (Gudair, Virbac: Clinical particulars - Gudair emulsion for injection for sheep and goats (noahcompendium.co.uk))
Vaccination offers the best long-term control prospect for Johne’s in sheep
Vaccination will prevent disease progression in most vaccinated animals, but does not entirely protect against infection
Injection site granulomas can be a common adverse effect (mineral oil adjuvant) in sheep
NB: Serious adverse reactions can also take place in humans accidentally self-injecting with the vaccine
Maedi-Visna in sheep
iceberg disease
Maedi-Visna virus (MVV) – lentivirus (‘slow’ virus) - long incubation period – c/s not seen until older
Maedi (‘short of breath’) – progressive pneumonia; Visna (‘wasting’) – brain/spinal cord pathology – neurological deficits
Persistent, lifelong infection
Highly infectious – easily spread – close contact and inhalation, milk/colostrum, contaminated needles
Closely related to Caprine Arthritis Encephalitis (CAE) virus in goats – interspecies transmission possible
Eventually fatal – but the damage to flock health and productivity goes on largely unseen over a long period unless diagnosis made
Slowly see more thin ewes (wasting) at > 4-5 yrs old, chronic mastitis, progressive weakness/toe dragging, arthritis, reduced fertility
No treatment or vaccination
Dependent on testing for identification and accredited schemes with high biosecurity to keep it out
Trade concerns after Northern Irish sheep tested positive for MV after export to Scotland in 2022
SRUC accreditation (and monitoring) scheme for MV (and other endemic diseases- need to follow the rules of membership – strict biosecurity!
Ovine pulmonary adenomatosis (OPA) (Jaagsiekte) in sheep
iceberg disease
Contagious tumour – respiratory transmission
Jaagsiekte sheep retrovirus (JSRV) – virus found in respiratory excretions
Causes the development of tumours in the lung
Lungs become filled with large quantities of fluid
Incubation period: up to 2 yrs
Secondary bacterial infection common in lungs - pneumonia
clinical signs-
Weight loss
Dyspnoea, especially when walking/running
Exercise intolerance – lagging behind flock when on the move
‘Wheel-barrow test’ – large quantities of fluid drain from the nose
Spread from animal to animal via infected expired air droplets and fluid
Caseous lymphadenitis (CLA) in seep
Corynebacterium pseudotuberculosis
Cutaneous form - Suppurative necrotising inflammation of superficial lymph nodes – esp. parotid, submandibular, popliteal, prescapular LNs
Visceral form – lesions in mediastinal and bronchial lymph nodes, also internal organs e.g. liver, spleen, lungs – could be seen at slaughter
First reported in UK in 1990 in goats that had contact with imported German goats
Then spread to UK sheep in 1991
Chronic infection, often subclinical
Transmission: close contact with infected sheep, contaminated shearing equipment, fighting leading to head injuries (rams)
No treatment or vaccine – culling and strict biosecurity
Differentials:
What else might cause superficial lymph node abscesses?
Here you might be thinking of tuberculosis or an infected injection site
Chronic, lifelong infections; will spread across the flock if left unchecked
Zoonotic
Border disease in sheep
iceberg disease
Pestiviruses (Genus Pestivirus)- like bvd in cattle and classic swine fever in pigs
First reported in Vet. Record in 1959, known to occur in the border region between England and Wales [Hughes et al., (1959) “B” or Border disease: an undescribed disease of sheep, 71, 313-316; 317]
Persistent infection possible (PIs) – infections of pregnant ewes before approx. 60-85 days (Remember 147 day gestation in sheep)
Pathogenesis of BD in sheep similar to that of BVD in cattle
Many of these infected ewes will abort – early embryonic death (barren ewes), aborted foetuses, stillbirths
If survive - lambs born immunotolerant – BDV virus positive, Ab negative – source of infection for others – cull (like the PI in BVD in cattle)
‘Hairy shakers’
- Tremors: hypomyelination of central nervous system
- Hairiness: changes in hair follicles causing coarse fleece
No treatment for Border disease; and no vaccine
Depends on identifying persistently infected lambs (PIs) – remove
Testing commercial flocks would be cost-prohibitive
Economic losses can be considerable in an infected flock
Buying in sheep might introduce the virus - biosecurity
Sheep could be infected by BVDV PI cattle – e.g. co-grazing at pasture
differantials-
Remember there could be various other causes of abortion in sheep apart from BDV (e.g. Toxoplasma) - need diagnostics from aborted material/serology
Swayback (lambs born from copper-deficient ewes) – congenital form – may be weak, poor limb co-ordination and fine head tremors
order disease virus infecting pigs!
what is the difference between a trace and a majour mineral
majour is measured in grams, trace is measured in mg
PROTECT ME ACRONYM
Prescribe only when necessary
Replace with non-antibiotic treatments
Optimise dosage protocols
Treat effectively
Employ narrow spectrum
Conduct cytology and culture
Tailor your practice policy
Monitor
Educate others
when does dihorea warrent antibiotics
reseved for severe disease- less than 1%
hospitalization/warrants IVFT
mental status:
moderately to severely depressed
systemic response to disease:
-> clinically detectable dehydration or hypovolaemia,
-> but no adequate improvement in response to appropriate fluid therapy
-> severe circulatory compromise
-> fever (T > 39.5°C)
Non-haemorrhagic/ Haemorrhagic
diseases in 0-5 day old chicks
Mortality targets less than 0.3% per day
Chick mortality peak at 3-4 days
Cause of the mortality can be parent flock issues, incubation/hatchery issues, transport, on farm issues
Diseases(common): omphalitis (unhealed navels), septicaemia, yolk sac infections.
Origin- flock code related (young/old, sick, dirty egg collection), hatchery related, farm related (poor brood, dirty water, not cleaned).
Medicate or leave? Antibiotics - linco-spectin, doxycycline, trimethoprim.
Uncommon- chicken anaemia virus (CAV), avian encephalomyelitis (AE). Dx- histopath, PCR. Prevention: vaccinate.
diseaes in 6-20 day old chickens
Mortality target less than 0.1% daily
Few issues
If using anticoccidials medication, tend to be around this age
If medicate before 20 days - need to consider salmonella swabs (only valid for 3 weeks)
Diseases- bacterial issues, IBH (adenovirus), gizzard erosion(viral or mechanical), metabolic disease (rickets, tibial dyschondroplasia- often feed related )
diseases in 21-27 day old chickens
Peak gut health challenge - usually do a routine visit
Coccidiosis: Coccidiostats routinely in feed.
e.acervulina- low effecton performance, high prevelance
e.maxima- high effect on performance, effect on health middling prevelance
e.tennela- high effect on performace, middling effect on health, can killl birds, low prevelance
Enteritis-on the back of a significant cocci challenge, can be caused by a disruption. Bacterial infiltration into the gut - often clostridium associated.
Dysbacteriosis in the caeca- overgrowth of pathogenic bacteria in the hindgut. Often acidity related (slight alkaline pH).
Treat- Amoxicillin, nutraceuticals, amprolium.
Focus on cleanout
Bacterial lameness- staphylococcis, Ecoli, Enterococcus caecourum.
APEC- avian pathogenic Ecoli. Generalised sick bird, uni/bilaterally lame. Risk factor- dirty water (90%) main, stress, environment. PM- colibacillosis, septicaemia, Purelant Arthritis, FHN, hepatomegaly, C+S.
E.caecorum. Risk factor- environment, flock code. Unilaterally lame or dog sitting (vertebral lesion) PM- Femoral head necrosis, pericarditis. C+S (anaerobic)
Treatment- amoxicillin, nutraceuticals.
Avoid- water sanitation, cleanout.
diseases in 27-38 day old chickens
31 days: Thin birds - take a proportion out - usually around 30%. Stress on birds
38 days: Clear - around 2.5kg on average. 850% increase in size from 30g at day old
Diseases: Occasional gut health issues but mostly bacterial lameness. Viral challenges- IBD (gumboro), IB.
IBD (infectious bursal disease)- gumboro.
Immunosuppresive disease. MDA cover initially, vaccinate with live vaccine in water 12-19d depending on strength of vaccine.
Clinical and subclinical disease due to vaccine failure or field challenge breaking through.
Clinical signs- enteritis, poor performance, spike in culls or mortality.
Broiler vaccines
Gumboro: Live vaccine. In-ovo an option but the majority in water around 14-17 days. Lots of options - mild, intermediate, hot. Strength used dependant on risk
IB: Vaccinated in the hatchery usually. Multiple field strains with different presentations. 4/91 and MA5 strains allow cross protection to cover most other strains including QX. Layers/breeders vaccinated every 6-8 weeks in water or spray
Cocci vaccines: Too expensive for standards. Used in organic and occasionally in slow growing broilers
layer vaccines
Comprehensive vaccination programme including Salmonella (T +E), IB, TRT, ILT, gumboro, AE.
Altered depending on challenges.
Eyrsipelas, pasturella if previous challenge or risk. Usually at transfer injected.
Hatchery vaccines- cocci, mareks, IB (live).
respiritory diseases in layers
IB
TRT (also called aMPV)
ILT
Mycoplasma
Newcastle disease (notifiable)
AI (notifiable)
Infectious Bronchitis (IB) in layers
Highly infectious coronavirus with many different variants. Defined by S protein.
Variants:
4/91 – common in UK
Qx – common in UK
Massachusetts (MAS)
D1466
Connecticut, Arkansas, Delaware
Starts in trachea, may reach blood stream. Depending on strain then can effect oviducts and kidneys. Possible secondary infections.
CS- drop in production, thin pale eggs, respiratory signs. QX- kidney damage. Dx- cs, pm, serology, PCR (mainstay)
Avoid- vaccine with 4/91 and MAS strains every 6wk in lay=cross protection
TRT in layers
Highly contagious metapneumonic virus.
Swollen head syndrome, decline in egg number, reduced shell quality (pale misshapen, thin)
. Dx- cs, pm, serology, PCR (mainstay- trahcel or cloacal swabs)
vaccine. One or two live in rear then killed at transfer.
ILT in layers
Highly contagious herpes virus.
Severe respiratory signs, reduced egg production,sudden death due to tracheal blockage.
. Dx- cs, pm, serology, PCR (mainstay- tracheal swabs.
Avoid- vaccine. Single in rear
mycoplasma in layers
Bacteria without cell walls
Can be transmitted vertically and horizontally
Establish a latent infection
Common on multi-age sites
Mycoplasma gallisepticum (Mg) – chickens, game birds, turkeys, most avian species. Chronic respiratory disease, sinsitis.
Mycoplasma synovia (Ms) - chickens, game birds, turkeys, most avian species. Lameness (swollen joints), egg shells powder topped.
Mycoplasma meleagridis (Mm) – turkeys
Mycoplasma iowae (Mi) – turkeys
Mycoplasma in chickens diagnostics
Serology – presence of antibodies diagnostic if no vaccine programme
PCR – very sensitive but requires DIVA if live vaccine has been used
Culture and MIC testing – gold standard but expensive
Multiage site issue
Control- biosecurity, antibiotics (tialmulin, doxycycline).
Vaccination- killed may reduce clinical signs but does not stop infection or vertical transmission.
Live vaccine- may prevent infections but limitations. Autogenous option.
Newcastle disease (notifiable) in layers
Highly contagious paramyxovirus.
Vaccine
Last confirmed in UK in 2006.
4 forms of the disease:Viscerotrophic velogenic -
Haemorrhages in intestinal tract
High mortality
Neurotrophic velogenic-
Respiratory and nervous signs
High mortality
Mesogenic -
Respiratory + nervous signs, low mortality
Lentogenic - Mild respiratory
Avian influenza (notifiable)
H5N1 strain in the UK last few years.
Transmitted faecal-oral route. Only need a microgram of infected droppings to infect thousands of birds
Migratory birds (pink footed geese, Canadian geese) spread it in droppings, often into rainwater or on fomites. Sea birds have been hit hard in the past 2 years.
Lots of different approaches in different countries
Vaccine available but not used in the UK
Clinical signs - bruising on legs, combs, wattles Neurological signs - twisted neck. Rapid death
Mortality rates - 95% in pheasants, chickens, turkeys
High path and low path. 3-5d incubation period
High path
CS- depressed quiet birds, neurological signs, bruised legs, rapid death.
Low path- Very variable from mild to severe disease. CS- drop in water and feed consumption. Respiratory signs
UK- emphasis on biosecurity-
3km protection zone and 10km surveillance zone. Require licence with vet visit 24 hours before movement from zone.
Biosecurity review before next placement of birds if in a zone.
Ducks PCR tested before movement
All birds testing positive on holding number are culled regardless.
First year without cases- virus less virulent
China- widespread H5N1 vaccination
France- Cull all turkeys and ducks within 20km of outbreak. Vaccinating ducks this year.
US- similar to UK
Variable approaches with varying success.
E.Coli peritonitis in layers
Caused by APEC, usually in compromised layer bird
Often immunosuppression or stress related.
Predisposing factors- stress, poor air quality, other respiratory pathogens, poor gut health, redmite.
Dx- postmortem, C+S.
Treatment- antibiotics (oxytetracycline) but original cause will need addressing.
Vaccine available every 20 weeks in lay. Autogenous vaccine if ongoing.
Erysipelas in layers
Erysipelothrix rhusiopathiae = causative agent
Sources = pigs, sheep, rodents. Long survival in soil (1yr)
Infection by skin lesions, consumption of infected material (cannibalism), red mite
CS- acute death, congested extremities. Pm- liver lesions and splenic. Culture for definitive.
Avoid- autogenous vaccine best or 2x commercial
Treatment- amoxicillin will reduce mortality but often returns. Clear early.
Mareks Disease in layers
Herpes virus which causes tumours to develop-
Tumours in visceral organs
Inflammation in peripheral nerves with paralysis
Classic form usually starts between 12 and 24 weeks of age
Not seen untill birds at least 8-10 weeks old
Breeders and commercial layers protected by hatchery vaccination – Rispens vaccine
Vaccine not effective for at least 8 days
Infection from inhalation of skin and feather dust from other poultry.
Vaccinated stock still replicate and shed the virus, but do not develop tumours-
Provided sufficient time between vaccination and exposure to virus
Leucosis and other viral causes of tumours in layers
Retroviruses-
Avian Leucosis
Reticuloendotheliosis virus (REV)
Lyphoproliferative disease virus of turkeys (LPDV)
parasites in layers
Intestinal worms. Ascarids, capillaria, heterakis. DX- FEC, postmortem physical presence.
Location- capillaria scrapes from the crop. Acarids, present in gut. Heterakis- thread worm in caeca.
Treatment- flubendazole, fenbendazole. (double dose capillaria)
Heterakis can transmit blackhead (histomonas protozoan parasite)- no treatment.
Red mite- very common, lice cycle as little as 10 days. Irritation causing immune suppression Nocturnal and feed on blood.
Lice- common chicken louce, northern fowl mite.
. Ecto parasite treatment- exxolt (fluralaner)- best but expensive, ivermectin, pyrethroid based spray on products for environments, diamatacious earth.
steps of a prepurchase exam
Stage 1 – Preliminary exam
External examination
Visual, palpation and manipulation
Incisor teeth
Eyes in a dark room
Auscultate heart and lungs
Stage 2: Walk and trot, in hand
Walk and trot in hand
Turned each way
Backed for a few paces
+/- flexion tests and trotting in a circle on a firm surface
The purchaser must always sign to say they agree to a limited 2 stage examination.
In this case the examination will be limited to these first 2 stages
If the purchaser requests a limited (two-stage) examination, the examination will be limited in its scope and may not detect important clinical factors that could otherwise influence their decision to purchase the horse
Stage 3: Exercise phase-
The horse is given sufficient exercise to:
Allow assessment of the horse when it has an increased breathing effort and an increased heart rate.
2. Allow assessment of the horse’s gait at walk, trot, canter and, if appropriate, gallop.
Allow assessment of the horse for the purpose of stage five.
If ridden exercise is not undertaken then this stage may be conducted by exercising the horse on a lunge. It should be made clear on the certificate what form of exercise was undertaken
Stage 4: Period of rest and re-examination-
The horse is allowed to stand quietly for a period. During this time the respiratory and cardiovascular systems may be monitored as they return to their resting levels.
Stage 5: Second trot up-
The animal is trotted in hand again to look for any signs of strains or injuries made evident by the exercise and rest stages
Flexion tests?
Trotting in a circle?
Not mandatory!
Can sometimes provide useful additional information about a horse.
There may be circumstances when the examining veterinary surgeon concludes that it is unsafe or inappropriate to perform such tests.
A mouth examination with a speculum is not included in the standard procedure and as such the examination of the mouth is limited.
A blood sample may be taken for storage (usually for 6 months) for possible future analysis to detect substances present in the horse’s system at the time of the examination that might have masked any factors affecting the horse’s suitability for the purchaser’s intended use. If a blood sample is not taken, then the reason should be noted on the certificate.
VDS system – blood sampling kit – no charge
Report findings of the examination
Provide the examining veterinary surgeons opinion on the horse’s suitability for purchase for its intended use
“In my opinion, on the balance of probabilities, the conditions reported above do / do not prejudice this horse’s suitability for purchase to be used for …”
This wording reflects the fact that there may be other reasonable interpretations of the findings, but it in no way reduces the responsibility of examining veterinary surgeons to examine and observe the horse carefully and to apply to the full their professional knowledge and experience.
Negligence – failing to do what a similarly qualified person would be reasonably expected to do, or doing what a similarly qualified person would be reasonably expected not to do.
Of the equine claims of negligence to the VDS – greatest percentage were associated with PPEs.
At a PPE if a lesion is detected, it should be reported to the purchaser and recorded on the certificate
considerations-
Facilities – you need a suitable venue
Environment – weather etc
Re-examine – start again another day…from the beginning
Purchaser present? Less claims if they are!
Blood sample…not mandatory – permission from purchaser and seller (VDS scheme)
Use the worksheet that’s available!
You are in charge
methods of identifying a horse for a pre-purchase examination
Check the microchip
Check passport
Diagram can be omitted if the microchip is present and matches the horses passport – in this case the microchip and passport number must be recorded on the certificate.
Do this at the beginning to save awkwardness!
Insurance considerations for pre-purchase exams
The PPE report can affect how an insurance company views the horse in terms of risk.
They may consider certain findings in the report to represent an increased risk for insurance, which could result in them placing exclusions on the policy.
It is the purchaser’s responsibility to ensure they can get the insurance they want prior to purchase
why are cow hooved trimmed
to give propper shape to handle weight during high stress periods- calvieng ect
remove horn from toe and not sole to correct foot shape
Dry off
+/- 80-100 DIM
Pregnant heifers
Think ‘check’ rather than ‘trim’
Lame cows ASAP
Things to avoid:
Overtrimming
Shaping the wall
Removing the axial white line
Chasing black marks
Removing too much heel
dutch 5 step method
Step 1- Start with weightbearing claw – inner claw of hind foot, outer claw of front foot
Cut 1 – Toe length 8cm from hard horn to step (average Holstein cow)
Cut 2 – Remove excess sole
Do not over trim – measure from hard horn to step. Heifers
Leave at least 5mm of sole
Foot trimming - Step -
Remove more from outer claw, ensure balance and do not remove axial white line
step 3- Dishing’ out the claws Model (dish) out the inner parts of both claws, behind the wall on the inner claw edge, to allow a flow of muck between the toes and to reduce weight-bearing on the typical sole ulcer site
step 4- take weight odd of lesions
remove horn from effecte claw to shift weight
Check for any lesions
Corrective trimming
Provide appropriate treatment
Check claws for problems (usually in the outer claw, back two thirds on hind feet)
If the outer claw is damaged, make this claw lower towards the heel. So the weight is transferred partly to the sound claw
Dutch five step technique – Step 5
remove loose horn from heel
check for digital dermatitis
beware fo removing too much for weight baring surface
Treatment of claw horn lesions
trim
block for 3 days
nsiads- ketoprofen
Peripaturient period common issues in farm animals
Cattle: 3 weeks before to 3 weeks after calving
Hypocalcaemia
Ketosis/Fatty liver
LDA
RFM
Metritis
Sheep: 10 days before to 7 days after lambing
Pregnancy toxaemia
Hypocalcaemia
Genital tract problems (tears, prolapse)
Dystocia
Acute clinical mastitis
Respiratory disease
Hypocalcaemia (Milk fever)
peripartuent problem in cows
Average annual UK incidence - 5%
Average cost of one case = £206
Simple case- £42
Downer cow - £137
Fatal case- £2,043
Only 3% of affected animals will die
Can contribute to increased incidence of;
“Downer cow” syndrome
In uncalved cows
Uterine inertia
No voluntary straining – dystocia not detected
Uterine prolapse
RFM
Risk of environmental mastitis
Dietary absorption of calcium is ~70%
Bone deposition and/or absorption (25g/day)
Requirements of foetal skeleton (15g/day)
Milk ~ 1.1g/l (20-50g/day)
pregnacy puts strain on calcium homeostasos
Clinical Signs:
Loss of appetite, dullness and lethargy
Afebrile / subnormal temperature
Initial hypersensitivity / hyperaesthesia
Stiff, straight hocks
Reluctant to move
Inco-ordination and ataxia
Progresses to:
Recumbency, head turned to side
Increased heart rate (80-90 bpm)
Dilated pupils, reduced PLR
Gut stasis resulting in bloat and constipation
Depression, unresponsive to stimuli
can progress to -
COMATOSE (lateral recumbency, HR>120bpm) -> DEATH
Diagnosis:
History
Clinical signs
Response to treatment
Biochemistry-
Calcium below 1.5mmol/l
Phosphate below 1.0mmol/l
Magnesium normal or slightly above 1.25mmol/l
Treatment: Individual
Full clinical examination
Blood sample prior to treatment
Intravenous calcium borogluconate (12g)
Magnesium and/or phosphorous if required
Removal of calf and/or restriction of milking
TLC
If no recovery in 5-6 hours, RE-ASSESS
Treatment: Herd
Changing the forage component of the diet
Magnesium supplementation
Prophylactic administration of calcium at calving
Milk withdrawal-
no pre-calving milking
removal of calf at birth
no milking for 3 - 4 days after calving (?Welfare)
Dry cow nutrition (the basics)-
correct body condition – not too fat
supplement with forage
ensure good dry matter intake in dry period
DCAB/DACB diets
Fatty Liver
peripartuent pproblem in dairy cows
Fatty infiltration of the liver
Excessive fat mobilisation in early lactation as response to energy demands
Excessive amounts deposited in hepatocytes as triglycerides- Affect liver function and causes cell injury
Suggested that 1 in 3 dairy cows are affected
?Relatively normal in high yielding cows?
No clinical signs, but may result in:
Increased incidence of metabolic disease
Poor fertility
Depressed milk production
one of the less severe energy disorders in cattle
Can progress to Fat Cow Syndrome
Above 34% fat → severely affected
Excessively fat cows in the dry period B.C.S. > 4
Clinical signs:
Rapid loss of body condition in early lactation
Depressed appetite
Cow clinically ill
Metabolic disease
Depressed milk production
Poor response to treatment
High mortality
Energy Disorders in Cattle
Fatty liver syndrome->
Subclinical ketosis->
Clinical ketosis->
Chronic ketosis->
Fat cow syndrome
Ketosis (Acetonaemia)
Impaired metabolism of carbohydrates and VFAs
Incidence of:
Clinical ketosis is approximately 1%
Subclinical ketosis is approximately 30%
Occurs in early lactation
Large energy supply required by mammary gland in early lactation for milk production
Inadequate energy supply to meet this demand
Negative energy balance due to demands of udder
Shortage of oxaloacetate for use in TCA cycle
Mobilisation of fat reserves
Metabolic pathways lead to the production of ketone bodies-
Acetoacetate
β-hydroxybutyrate (BHBA)
Acetone
Anything that causes inadequate energy supply -> ketosis
Reduced appetite
Starvation
High production
Clinical Signs:
Usually occur within the first month after calving
Subclinical -
Loss of body condition
Depressed milk yield
Reduced fertility and milk protein long-term#
One case of primary clinical ketosis represents the “tip of the iceberg”
The other early lactation cows are likely to have subclinical ketosis
Wasting form-
Decreased milk yield
Weight loss
Dark firm “waxy” faeces
Loss of appetite (refusal of concentrates)
Sweet ketone smell on breath (“pear drops”)
Remember to check for underlying cause (especially LDA)
Nervous form-
Excessive salivation
Abnormal chewing
Licking of any available object
Inco-ordination, circling
Head pressing, apparent blindness
Signs intermittent
Diagnosis:
History and clinical signs
Smell of ketone bodies on cow’s breath
Rothera’s test- regent turns purple on pos result
Clinical biochemistry-
Lowered blood glucose levels
Mobilisation of body fat (elevated NEFA)
Ketone body formation (elevated BHBA)
Remember to check for underlying cause (especially LDA)
treatment of ketosis
Aims:
Restore blood glucose levels
Replenish oxaloacetate levels
Increase dietary gluconeogenic precursors (propionate)
Correct predisposing factors (eg. LDA)
Restoration of blood glucose levels
400 ml of 40% glucose solution intravenously
Oral administration of glucose precursors
Propylene glycol (Ketol™) 115 – 225ml BID
Propylene glycol + cobalt (Forketos™)
Sodium propionate (digestive upset)
Glycerol (but ketogenic)
Glucocorticoids?
Left Displaced Abomasum
Typically occurs in the month following calving
May reflect poor nutritional management prior to calving (?related to ketosis)
Some association with high-concentrate/low-fibre rations
Reported associated with previous hypocalcaemia, twins or (endo) metritis
Occurs due to atony of the abomasum-
Secondary to high VFA concentratons>
Due to continued fermentation of high CHO rations>
Accumulation of gas>
Displacement>
Clinical Signs:
Variable
Poor milk yield
Reduced appetite
Weight loss
Gaunt appearance
Sprung last lib
Distended CrD abdomen
Auscultation and percussion -> ping
Can be complicated due to presence on concurrent disease
Most severe in conjunction with metritis and toxaemia
Pyrexia (>39.5)
Anorexia
Depression
Reduced milk yield
Can see profuse, foetid diarrhoea
Diagnosis:
Based on thorough clinical exam
Don’t forget about ballotment – ping and tinkle
Lots of ping differentials
Left Displaced Abomasum treatment
Cast and Roll
Toggle
Surgical (omentopexy/abomasopexy)
Surgical (laparoscopic)
Follow all by oral fluid drenching
Pregnancy Toxaemia in sheep
Energy deficiency due to increased demands at end of pregnancy
Rapid growth of foetus(s) increases demand for glucose
Predisposing factors-
Last month of gestation
2+ lambs
Prolonged period of energy shortage
Ewes in poor condition
Older ewes
Stress
Clinical signs:
Isolation from flock
Disinclined to move and easily caught
Become dull and depressed
Neurological signs-
Apparent blindness
Hyperaesthesia
Head pressing
Star gazing
Teeth grinding
Progresses to profound depression and recumbency
Can lead to abortion
Diagnosis:
Based on clinical signs and history
BHB > 3mmol/l
treatmentof pregnacy toxemia in sheep
Treatment:
Oral electrolyte and glucose solution or propylene glycol
IV glucose
Supportive care
Induction of parturition/caesarean
Euthanasia
Control:
Nutrition of ewe in late pregnancy
Ovine Hypocalcaemiaa
Usually seen in late pregnancy
Sporadically occurs in lactation
Affects older sheep
Associated with stress
Housing
Weather changes
Delay / change in feed
Clinical Signs:
Muscular paralysis
Increased respiratory rate and reflux of rumen contents
Diagnosis:
History
Clinical signs
Response to treatment
Serum calcium below 1.0mmol/l
Concurrent pregnancy toxaemia
treatment of ovine hypocalcemia
Treatment:
20 – 40mls of intravenous 40% calcium borogluconate
50 – 100mls of subcutaneous 40% calcium borogluconate
Control and prevention
Feed 5 – 10g calcium per day in late pregnancy
Avoidance of stress
Downer Cow Syndrome
Common presentation in farm animal practice
Cow has been recumbent for over 24 hours
No specific cause for recumbency
Cow is in sternal recumbency
Usually related to calving
Initial cause of recumbency;
Traumatic:
Related to calving injury, housing, bulling etc.
Sacroilliac luxation / subluxation
Dislocation of the hip
Pelvic fracture
Injury / fracture of limb
Tendon / ligament rupture
Neurological:
Related to calving -
Obturator nerve
Sciatic nerve
Related to trauma-
Peroneal nerve
Tibial nerve
Metabolic:
Hypocalcaemia
Hypomagnesaemia
Untreated ketosis
Fat cow syndrome
Toxaemia:
Metritis
Salmonella
Peritonitis
Acute coliform mastitis
Secondary complications following recumbency very common (84% of cows) -
nerve damage
compartment syndrome
skeletal damage
Once cows were recumbent for more than 24 hours, the secondary damage was considered more important to prognosis than the primary cause.
By day 7:
57% of cows with no evidence of secondary damage got back up
Only 17% of those cows with some form of secondary damage got back up
History
How long has the cow been recumbent?
When did she calve? Were there problems?
Did she rise after calving?
Has she received any treatment?
Has the cow risen and/or moved?
Where did the cow become recumbent?
Provision of good TLC?
Clinical Examination-
General demeanour
Position of cow and limbs
Attempts to rise
Creeper / Crawler cows
Further clinical examination-
Rectal examination
Manipulation of hind-limbs
Diagnostic tests-
Muscle damage
CK- Elevated for 1-2 days
AST- Elevated for 1-2 weeks
Diagnosis of primary cause-
Calcium, magnesium, phosphorous
Liver enzymes, β-hydroxybutyrate
Myoglobin levels in serum / urine-
Prognosis-
Depends on:
Clinical examination
Attempts to rise
Degree of ischaemic necrosis and damage
Demeanour
Quality of nursing on farm
50% of downer cows will rise in 4 – 7 days
Prognosis poor after 10 days
treatment of downer cow syndrome
Treatment-
Correction of underlying disease
Calcium borogluconate
Phosphorous (“creeper cows”)
Anti-inflammatory drugs (NSAIDs/Corticosteroids)
Assistance in rising
Hobbles or soft rope on hind legs, Bagshaw hoist, Inflatable bags, Cow nets / slings / harnesses
Tender loving care-
Critical for good prognosis (labour)
Dry, clean, comfortable bed ?at grass (shelter)
Turning of cow every ? hours
Good quality food (accessible)
Water (accessible)
‘Waters break’
Chorioallantois ruptures, releasing several litres of allantoic fluid
END OF STAGE I
stage 1 of partuition in the horse
‘PREPARATORY PHASE’
30 minutes - 4 hours
Foal’s front end rotates – dorsopubic —> dorsosacral
Cervical relaxation
Uterine contractions of increasing intensity
Foal forefeet and muzzle pushed into cervix
Mare is restless
Flank watching
Frequent urination
Sweating
Stretching
Recumbency +/- rolling
Tail swishing
Similar to mild colic
1-12 HOURS
stage 2 of partuition in the horse
‘DELIVERY PHASE’
20 – 30 minutes
Quick and explosive
Cervical dilation continues
Presence of foal at pelvic inlet triggers powerful abdominal contractions
Oxytocin released from pituitary gland —>
reinforced uterine contractions
Mare usually in lateral recumbency, some mares foal standing up
Amnion appears at vulva within 5 minutes of waters breaking
Amnion ruptures
Front feet and nose
Mare will often rest for 10 – 15 minutes once foal’s hips are through the hips
Umbilical cord remains attached until either mare stands or foal attempts to rise
30 MINS
For every 10 minute increase in Stage II labour beyond 30 minutes, there is a 10% increase risk of the foal being born dead
EARLY EFFECTIVE INTERVENTION CRITICAL TO FOAL HEALTH AND SURVIVAL
stage 2 of partuition in the horse
EXPULSION OF PLACENTA
10 minutes – 3 hours
Expulsion of foetal membranes and uterine involution
<3HOURS
dystocia in the mare
= ABNORMAL FOALING
May be maternal or fetal in origin
More common in maiden mares
EMERGENCY
Potential loss of foal, mare or future fertility
ABNORMAL ORIENTATION of the fetus in the birth canal by far the most common cause
FETAL ABNORMALITY -
Most commonly limb contracture
Other anomalies eg hydrocephalus
FETAL OVERSIZE-
Rare. Not related to gestational age
MARE PROBLEM-
Uterine inertia, exhaustion
Pre-existing orthopaedic condition (eg pelvic fracture resulting in distortion of birth canal)
PRESENTATION -
Describes orientation of fetal spine to that of the mare
POSITION -
Relationship of the fetal spine to the quadrants of the mare’s pelvis
POSTURE-
Describes the relationship of the extremities to the foal’s body
Normal delivery is
ANTERIOR presentation, DORSAL-SACRAL position, both forelimbs and head extended
98.9% OF FOALS DELIVERED IN CRANIAL PRESENTATION
1.0% IN CAUDAL
0.1% IN TRANSVERSE
WHEN DO WE NEED TO INTERVENE?-
Failure of progression of Stage II for >20 minutes
Malpresentation
Something at vulva that shouldn’t be there
Severe colic
APPROACH TO DYSTOCIA CASE in the mare- EXAMINE MARE -
Examine mare in the box
Avoid stocks – mares will often attempt to lie down
Sedation if necessary - consider effects on foal
Xylazine shorter duration of CVS depression vs detomidine
Epidural normally too time consuming
TOCOLYTICS (Clenbuterol, Isoxuprine)
May be given by injection to relax the uterus
Manual vaginal exam – plenty of obstetric lubricant
Confirm waters have broken
Assess dilation of cervix
Identify orientation of fetus
FRONT LEGS – fetlock and carpus flex in same direction
HIND LEGS – fetlock and hock flex in opposite directions
Any abnormality must be corrected prior to any attempt at delivery
APPROACH TO DYSTOCIA CASE in the mare- ASSISTED VAGINAL DELIVERY
Vaginal delivery with the mare awake
Simple postural abnormalities can be corrected in this way
For normal orientation or posterior presentation with both hindlimbs extended
Pull in tandem with mare’s contractions
Ropes/chains may be used
No mechanical devices
APPROACH TO DYSTOCIA CASE in the mare- CONTROLLED VAGINAL DELIVERY
Vaginal delivery under GA
If significant progress is not made after 15 -20 minutes with mare awake
GA eliminates uterine contractions and straining
Elevation of hindquarters allows repulsion of fetus into abdominal cavity and repositioning
Vaginal delivery under GA
If significant progress is not made after 15 -20 minutes with mare awake
GA eliminates uterine contractions and straining
Elevation of hindquarters allows repulsion of fetus into abdominal cavity and repositioning
APPROACH TO DYSTOCIA CASE in the mare- CAESAREAN/FETOTOMY
If no significant progress after 15 -20 minutes of controlled vaginal delivery
Via ventral midline laparotomy under GA
TERMINAL CAESAREAN if mare has fatal injury or disease
FETOTOMY if foal is confirmed dead
‘RED BAG’ IN MARES
PREMATURE PLACENTAL SEPARATION
Caudal pole of placenta presents at vulva in Stage I without rupturing
Foal is likely to be deprived of oxygen
immediate intervention necessary
CERVICAL STAR VISIBLE
COMMON COMPLICATIONS IN THE FOALING MARE
HAEMORRHAGE
RETAINED FOETAL MEMBRANES
METRITIS
UTERINE TEAR/RUPTURE
PROLAPSE – UTERUS/GIT
INVERSION OF UTERINE HORN TIP
HAEMORRHAGE after foaling
Most frequent cause is rupture of the MIDDLE UTERINE ARTERY
during foaling
Rupture of utero-ovarian, vaginal or external iliac artery less common
Degenerative changes in arterial wall with age and successive pregnancies
Risk greater in older, multiparous mare
Majority of bleeds are contained within the BROAD LIGAMENT
resulting in a haematoma of variable size
No blood visible externally
Usually colic, sometimes violent due to stretching of the ligament often accompanied by flehmen response
If haemorrhage escapes the confines of the broad ligament, uncontrolled bleeding into the abdomen
Cardiovascular shock (predominates over signs of colic)
Tachycardia, weak pulse
Sweating
Muscle fasciculations
Pale mucous membranes
Recumbency
May be fatal
diagnosis-
Clinical signs usually enough
Broad ligament haematoma palpable on rectal palpation BUT palpation can be very painful
Care not to disrupt clot
Blood sample in acute stage RBC parameters may be normal due to compensation
Hypoproteinamia, high lactate
treatment-
Tranexamic Acid (antifibrinolytic) aids clot stabilization
Shock therapy –
Fluids (hypertonic followed by isotonic)
NSAIDs
Intranasal oxygen
Whole blood transfusion
Conservative treatment – permissive hypotension
Haemorrhage may be subclinical and only picked up at subsequent reproductive exam
METRITIS in the mare
Inflammation of uterine wall allows passage of toxins/bacteria into circulation
-> ENDOTOXAEMIA
Usually follows traumatic delivery +/- retained fetal membranes
Fever, anorexia, laminitis
Laminitis potentially life threatening
Foot support, icing
Systemic broad spectrum antibiotics
NSAIDs
Intravenous fluids
Large volume lavage to remove uterine contaminants
UTERINE TEARS in the mare
Clinical signs are dependent on the size of the tear and degree of contamination of the abdominal cavity
The interval from occurrence of the tear to diagnosis and initiation of therapy has a marked impact on survival
So early diagnosis essential
Evisceration of gut through a tear in the uterus is a rare but usually fatal complication of the immediate post foaling period
Diagnosis can be challenging as tears may be small and/or in inaccessible area
The degree of contamination does not always correlate
to the size of the tear
Diagnosis often only made when mare develops peritonitis
within 5 days of foaling
(Colic, fever, depression)
Abdominocentesis – peritonitis (usually serosanguinous, elevated WCC & TP)
Examine the placenta carefully
May reveal site of a uterine tear
treatment of uterine tears
Medical-
Broad spectrum Antibiotics
NSAIDs
Oxytocin
Surgical-
Transvaginal, flank/ventral laparotomy, laparoscopy
UTERINE PROLAPSE- in the mare
Uncommon
Most often following dystocia, but can occur after uneventful foaling
Can be complicated by involvement of bladder or intestines, or concurrent haemorrhage
Support prolapse at level of vulva to minimize tension and oedema
Can be replaced with mare standing or in recumbency
Standing sedation usually sufficient, but consider an epidural or even GA if mare strains too much or reacts violently
Remove retained fetal membranes if still attached
Gently clean and inspect endometrial surface of uterus for tears
Uterus gently massaged back through vulva, avoiding using fingertips
Ensure uterus is fully replaced - distension with fluid or the bottom end of a bottle may help
Broad spectrum antibiotics
NSAIDs
Oxytocin to promote uterine involution
+/- purse string suture
Daily lavage to mitigate against metritis
c. 80% survival
PERINEAL INJURIES post foaling
more common in mares post foaling than cows- speed of seond stage
vaginal tears will heal by secondary intention
3rd egree tear- tear between rectum and vagina- examine extensivly, examine agin after inflamation has gone down
trerepair several months on
haemorage into vaginal wall-
CERVICAL TEARS post foaling
Usually results from mare foaling without adequate cervical relaxation
Prognosis depends on size and location of tear(s)- BIG THREAT TO FERTILITY
Surgical repair is possible but injury may lead to a loss of cervical competency and cause permanent infertility
DIAGNOSIS during diestrus- gentel digital palpation
INVERSION OF UTERINE HORN TIP POST FOALING
Uncommon
Usually follows excessive traction on retained fetal membranes
May result in mild colic symptoms
Tip of horn can suffer ischaemic necrosis if not corrected
Manual reduction per vaginam
+/- infusion of large volume of fluid
GASTROINTESTINAL COMPLICATIONS post foaling
CONSTIPATION- common
BRUISING OF VISCERA-
Small colon, rectum or caecum
May lead to ischaemic necrosis/peritonitis/colic
RUPTURE OF VISCERA-
Endotoxic shock. Invariably fatal
Withdrawals
Each product has specific withdrawal instructions from the time of final administration.
The legal minimum withdrawal period for drugs used ‘off license’ is as follows
Statutory withdrawal periods:
Meat from mammals and poultry (including offal): 28 days
Milk: 7 days
Eggs: 7 days
Meat from fish: 500 degree days
if normal withdrawl peiods longer, use those
Bulk tank,
test the individual cow’s milk with a Delvotest to avoid bulk tank residue failure. Delvotest kits and consumables
It should be remembered that ‘off license’ use of drugs includes situations where the specific licence use is breached, for example, combination therapy or alteration of the recommended dosage interval. In these situations, at least the statutory minimum withdrawal period will be applied by the prescribing vet.
Organic-own rules (variable)
using two preperations not licensed tohghter thoghtether even when on license indivisually yu must use statiuitory withdrawls
legislation for farm animal medication
Veterinary Medicines and the Safety of Food From Animals | NOAH (National Office of Animal Health)
Specific rules for food producing species:
‘Veterinary Medicines Regulations 2005’ lots guidance notes on VMD, annually refreshed.
Licensed products:
“in all species, if there is a product that is licensed for the particular condition being treated and the particular species, then this product should be used”
Useful sources-VMD and NOAH
licesnsed
off license
baned drugs
cascade-
If a licensed product does not exist or is not available in the UK the cascade provides options for use in order to prevent suffering.
If no product exists, then a product licensed for use in that species for a different condition may be used or, a product licensed for that condition in another food producing animal may be used.
If no products exist then a product available in another member state may be imported BUT only provided that the product is licensed for use in a food producing specified in that state.
cascade
If a licensed product does not exist or is not available in the UK the cascade provides options for use in order to prevent suffering.
If no product exists, then a product licensed for use in that species for a different condition may be used or, a product licensed for that condition in another food producing animal may be used.
If no products exist then a product available in another member state may be imported BUT only provided that the product is licensed for use in a food producing specified in that state.
Specify a withdrawal period:
7days milk and eggs
28days meat
500 degree days for fish
Keep records for 5 years, including:
Name and address of owner
ID of animal
Date
Diagnosis
Drug details
Treatment duration
Applied withdrawals
EU reg 37/2010:
Lists drugs licenced and forbidden from use!!.
eg metronidazole, chloramphenicol, metaclopromide, atipamazole
MRLs
Differences in the cascade aim to protect the consumer.
Whan an individual eats a product they have to be assure that levels of drugs in these products are within safe limits
MRLS Maximum Residue Limits are created for certain drugs based on the calculated ADI (acceptable daily intake).
Withdrawal periods take into account MRL and pharmacodynamics in the animal, allowing to calculate how long until the drugs fell below the MRL and so identifying a suitable withdrawal period
.
4 annexes are related to this:
Annexe 1: sufficient data for an MRL
Annexe 2: sufficient data determining they are safe and no MRL is needed.
Annexe 3: provisional MRL has been established, but more information is required
Annexe 4: drug prohibited from use in food producing animals, either because they produce too much of a risk or they have not been sufficiently assessed to allow for a provisional MRL.
Record keeping for production animals
Legal requirement for the owner and the vet to keep records for 5 years
Owner:
At the time of purchase:
Proof
Name and address of supplier
Name and batch number of drug
Date of purchase
Quantity
Withdrawal period
At time of administration:
Name of product
Amount of product
Date of administration
Withdrawal period
Identification of animal treated
If a vet administered the drug-vet can write in your records, or give you the information but it must have the name and address of the vet
At time of disposal-
Name of product
Amount disposed of
Method of disposal
Legal requirement for the owner and the vet to keep records for 5 years
Vet:
Permitted to supply POM-Vs
Keep records of in and out going transactions:
Date and nature of transaction
Identification of product
Quantity
Name and address of either the supplier or the recipient
Copy of prescriptions, name and address of person who wrote the prescription
Batch number ad date once product is in use.
For drugs prescribed under the cascade:
Date of examination of the animal
Name and address of owner
Identification of animals treated, diagnosis, trade name of the product
Batch number
Name and quantity of active ingredient
Dose administered
Duration of treatment
Withdrawal periods
Medicated feed Prescriptions in farm
POM-V or POM-VPS (anthelmintics)
Specific type of prescription -
the name and address of the person prescribing the product;
the qualifications enabling the person to prescribe the product;
the name and address of the owner or keeper of the animal;
the species of animal, identification and number of the animals;
the premises at which the animals are kept if this is different from the address of the owner or keeper;
the date of the prescription;
the signature or other authentication of the person prescribing the product;
the name and amount of the product prescribed;
the dosage and administration instructions;
any necessary warnings
the withdrawal period if relevant;
the manufacturer or the distributor of the feeding stuffs (who must be approved for the purpose);
a statement that, if the validity exceeds one month, not more than 31 day’s supply may be provided at any time. It is the veterinarian’s responsibility to specify how much should be provided for each 31 day supply;
the name, type and quantity of feeding stuffs to be used;
the inclusion rate of the VMP and the resulting inclusion rate of the active substance;
any special instructions for the stock farmer; and
the percentage of the prescribed feeding stuffs to be added to the daily ration;
If it is prescribed under the cascade, a statement to that effect.
abdorbtion of drugs in farm animals
Absorption of drugs:
Ruminal microflora catalyse hydrolytic and reductive reactions. Readily inactivates orally administered drugs before they reach the circulation
Conversely orally administered drugs may adversely affect gastrointestinal microflora and interfere with normal gastrointestinal processes (systemic drugs are not exempt from this)
Oral boluses (modified drug release delivery systems) take advantage of the unique conditions in the rumen, sine the bolus stays in the rumen it allows time for the sustained or pulsatile release of drugs.
metabolism of drugs in farm animals
Significant changes in metabolic capability in preruminant vs ruminant animals, due to changes in the diet resulting in a change in nature and complexity of nutrient to which the liver is exposed.
Differences in hepatic metabolism of certain anthelmintic drugs (benzimidazoles, clorsulon) probably explains the higher dose requirement seen in cattle and goats compared to sheep.
For drugs that undergo hepatic metabolism, half lives are shorter in cattle and horses compared to SA.
goats metabolise very quickly
excretion of drugs in farm animals
Urinary pH. Herbivorous animals generally have an alkaline urine (pH 7-9), this may affect the elimination of certain drugs through the urinary tract
Acidic drugs-are ionised in an alkaline pH and elimination should be enhanced since the drug remains in the urine.
Alkaline drugs will be unionised and are more readily reabsorbed from the urine, reducing the rate of elimination.
NB milk fed animals generally have acidic urine.
pharmaco dynamics in farm animals
Receptor level differences-
Eg xylazine. (alpha2 adrenoceptor agonist), a much smaller mg/kg dose is required compared to other species, due to an increased sensitivity of the receptor site.
Injection site lesions in meat produing animals
Lesions in young calves often will not resolve and can enlarge as the animal grows
S/C provides the least marking of the carcass
I/M injections should ideally be given in the neck, away from expensive cuts of meat- especcialy dont use rears in pigs
Maximum volume per injection site =10mls- reduces the pressure in the muscle allowing apropriate absorbton and preventing pressure necrosis
Variety of needle bore sizes and lengths
Keep injection sites 4 inches apart if possible
Common Antibiotics on farm
Amoxicillin
Potentiated amoxicillin
Tetracyclines
Amphenicols: Florfenicols- use as little as possible
1st 2nd gen cephalosporinsuse as little as possible
Penicillins
TMPS
Aminoglycosides (strep)
Macrolides: Draxxin
3/4th gen cephalosporin
Fluoroquinolones (enrofloxacin)
lincosamides
NSAIDs and steroids on farm
Meloxicam
Flunixin
Kelaprofen
Carprofen
Tolfenamic acid- not common ion uk
Corticosteroids
Fertility drugs on farm
Prostaglandin (estrumate)
GNrH (receptal)
Progesterone releasing intravaginal device (PRID/CIDR)
