end of life and slaughter Flashcards
Notifiable diseases in companion animals
Equine viral arteritis (EVA) – notifiable in stallions and in mares mated/inseminated within 14 days of suspicion – last occurred in UK in Shropshire in 2019: Info: Equine viral arteritis (publishing.service.gov.uk)
Rabies – affects all mammals (including livestock) – eradicated from all UK animals except bats in 1922. Most recent detected case of bat rabies in GB was 2022 (disease still very rare in British bats, but ongoing risk of rabies entry across borders in mammals). See Vet Record editorial: Rabies risk is very real - Loeb - 2022 - Veterinary Record - Wiley Online Library
West Nile fever – particularly horses, birds, humans – mosquitoes are vectors – disease not present in UK, but the vector mosquito spp. are present – increasing WNV incidence in Europe - potential for future infections in UK?
Important notifiable diseases (Farm species)
Anthrax - mammals and some species of bird - (last in GB 2015 – Wiltshire) - zoonotic
Bovine TB (endemic – ongoing problem)
Bovine Spongiform Encephalopathy (BSE) – peak >37,000 reported cases in 1992 – last confirmed GB in 2021 (1 case of classical BSE in a cow in Somerset: Report on the epidemiological investigation of a single BSE case in Somerset (publishing.service.gov.uk) )
Bluetongue (significant outbreak in GB in 2007-2008): See: https://www.nature.com/articles/s41598-018-35941-z and new isolation Nov 2023 in Kent: Bluetongue: how to spot and report the disease - GOV.UK (www.gov.uk) – see latest situation
Foot and Mouth Disease (cloven-hoofed species) (last in GB in 2007)
Classical Swine Fever (CSF) (pigs) (last in GB in 2000)
African Swine Fever (ASF) (pigs) – never in UK – ongoing in EU
Newcastle Disease (poultry) (last in GB in 2006 – game birds)
Avian Influenza (poultry) (ongoing in 2023 – still circulating in wild birds)
Bluetongue virus
Family Reoviridae
Genus Orbivirus
Double-stranded RNA virus
29 recognized serotypes: Bluetongue virus | Virus | The Pirbright Institute
Very stable in presence of protein (eg. survives years in stored blood)
Viraemia in infected animal can persist for up to 60 days
Virus infects and replicates in endothelial cells – hemorrhage
First discovered in South Africa 1902
Disease of ruminants and camels/camelids - sheep, cattle, goats, deer, camels, camelids (alpaca, llama)
Vector-borne - spread primarily by biting midges – single bite enough to cause infection
Non-contagious between animals – essentially needs an insect bite to become infected
Previously a disease of the Tropics – has been widespread in Europe since 1998, and especially since 2006 – now making a very significant return in northern Europe (BTV-3)
Trade losses – live animals and germplasm (semen, embryos) - export restrictions, regionalisation, cost of testing and certification
Production losses – morbidity and mortality, vaccine costs (if used), reduced value of livestock in restricted zones
Welfare issue – clinical signs in affected animals
Difficulty in control – insect vector widespread, vaccines only protect against particular serotypes
Vector-borne - certain spp. Culiciodes biting midges
Female midges feed on viraemic ruminant hosts; replication of virus in salivary glands of midge
Limited to times of midge activity – vector-free periods in winter, early spring – temp. dependent – but climactic conditions may favour midge survival in winter
Non-contagious
Sexual transmission possible
Transplacental and oral infection possible in the field (Menzies et al. 2008; van Wuijckhuise et al., 2008; Backx et al., 2009)
Introduction of BT into new areas-
Movement of infected ruminants (domestic and wild)
Germplasm (infected semen, embryos)
Active flight of Culicoides (few kms - local)
Passive flight of Culicoides – carried by wind – (many kms possible – long distance – crossing Channel from mainland Europe)
Carriage of infected vectors in transport vehicles – important?
Sheep – clinical signs of BTV-8
Usually more severe than cattle
Swelling around mouth, head
Oral erosions – drooling saliva
Conjunctivitis, lacrimation
Nasal discharge - crusty
Tongue may be swollen (cyanotic)
Lameness - coronitis
Depression – pyrexia
Pneumonic lung sounds, mouth breathing
Mortality
Cattle – clinical signs BTV-8
Mucopurulent nasal discharge
Conjunctivitis, lacrimation
Oral ulceration, swelling around muzzle
Coronary band swelling
Teat lesions and pain
Pyrexia
Decreased milk yields
Abortions, reproductive failure
Clinical outcomes of bluetongue
Can be fatal – esp. in sheep; lower mortality rates in cattle
Supportive treatment – antibiotics and NSAIDs
Production and therefore economic losses can be very significant at a farm and national scale – e.g. see Gethmann et al. (2020)
Newcastle disease
Caused by a group of closely-related viruses that form the avian paramyxovirus type 1 (APMV-1) serotype
Considerable antigenic variation between different Newcastle Disease virus strains – therefore arrange of different clinical features of infection
Over 250 species of bird have been demonstrated to be susceptible to infection with NDV
Live and inactivated vaccines are widely used worldwide to prevent
Newcastle disease – clinical signs
Depression, lack of appetite, dead birds
Respiratory signs - gaping beak, coughing, sneezing
Nervous signs – tremors, paralysis, twisting of the neck (torticollis)
Diarrhoea – watery yellow-green colour
Egg drop, or soft-shelled eggs – farm records and observations important here
many other diseases present simiar clinical signs-
Avian influenza
Fowl cholera
Infectious laryngotracheitis
Infectious bronchitis
Salmonellosis
Egg drop syndrome
Avian influenza
HPAI and LPAI – highly and low pathogenic
(HPAI) H5N1 - first case in UK in Whooper swan (Cygnus cygnus) found dead in Fife, Scotland
Picked up and tested as part of AI surveillance
Initial APHA tests confirmed H5N1 on 5th April 2006
Whooper swans migrate between Britain and Iceland – spend winter in Britain
Estimated UK wintering of 11,000 birds (RSPB)
Subtype H5N1 Tends to present as:
Increased mortality - sudden (peracute) deaths
Reduced egg production
Respiratory signs
Excessive lacrimation
Sinusitis
Oedema of head and face
Subcutaneous haemorrhage
Diarrhoea
Sometimes nervous signs
Classical Swine Fever
Highly contagious, easily spread between farms
High morbidity and mortality
Fever – dull pigs, huddling, anorexic
Conjunctivitis
Reddening of the skin
Nervous signs – convulsions, swaying gait, leaning
Constipation, then diarrhoea
East Anglia 2000 – 16 farms affected with CSF
Initial source? Probably an infected pork product of unknown origin fed to outdoor pigs
Porcine epidemic diarrhoea (PED)
Caused by PED virus (PEDv) – a coronavirus
Only affects pigs – biosecurity key to disease freedom
Watery diarrhoea that spreads quickly over a few days/weeks
At least 50% of a group/herd will have diarrhoea – high morbidity
Causes death in 30-100% of young piglets (if the virus is a severe strain)
Diarrhoea in older pigs temporary and they recover
Reduced appetite, lethargy, temp. can be normal
Diarrhoea, (vomiting) - dehydration
Highly contagious and notifiable in England & Scotland – but no restrictions or culling will be instituted – only industry-led response – rapidly tighten biosecurity
AHDB have developed useful information resources about the disease:
Porcine epidemic diarrhoea virus (PEDv) | AHDB
PEDv is one of the two diseases covered by the Significant Diseases Charter in the GB pig industry along with swine dysentery (Brachyspira hyodysenteriae)
The SDC provides early warning of outbreaks because of a notification system for producers – text and email alerts – pig producers are encouraged to sign up through the AHDB Pig Hub
Camelpox
Listed as a camel-specific notifiable disease by WOAH (with MERS-CoV)
Extremely contagious skin disease
Most common infectious viral disease of camels
Also a zoonosis – but mild in humans
Economic loss – loss of production (milk), weight loss, mortality in young camels
Middle East, north and eastern Africa, Asia, (not seen in Australia)
Incubation period 9-13 days
Pyrexia – may cause abortion if in calf
Localised or general pox lesions on skin – esp. head, neck, near the tail
Also pox lesions on oral and respiratory tract mucous membranes seen at PM
Enlarged lymph nodes, swelling of head possible
More frequent and more severe in young and pregnant animals – may cause death due to secondary infection and septicaemia
transmission-
Contact – skin abrasions
Contaminated environment – scabs, water
Inhalation of aerosolized virus
Camelpox virus secreted in milk, saliva, nasal discharge
Can be controlled/prevented by vaccination
Routine biannual vaccination recommended for young animals 6-9 months old
Live attenuated and inactivated vaccines are commercially available
Isolation and treatment of affected camels from the herd and other herds
Separate water troughs – biosecurity measures
Appropriate carcass disposal of dead animals – incineration best in developing world context
Camelpox – diagnosis
Transmission electron microscopy (TEM) to demonstrate camelpox virus in scabs or tissue samples
Virus isolation – cell cultures
PCR/Real-time PCR
Serology
ELISA
Camelpox virus is part of the Orthopoxvirus family
Equine notifiable diseases in the UK
Equine Infectious Anaemia (EIA)
Equine Viral Arteritis (EVA)
Contagious Equine Metritis (CEM)
African Horse Sickness
Equine Viral Encephalomyelitis
Glanders and Farcy
Rabies
Vesicular stomatitis
West Nile Virus
Dourine
Epizootic Lymphangitis
Equine Infectious Anaemia (EIA)
– “Swamp Fever”
Caused by bloodborne lentivirus – causes lifelong infection
If suspect must notify APHA
Any horse testing positive will be slaughtered
Most horses subclinical therefore routine testing paramount
Coggins test needed for international movement and all travel in the US
ELISA available which is quicker but produces false positives
On studs, yearly blood test prior to breeding – requirements of visiting mares vary so check!
Equine Viral Arteritis (EVA
Equine arteritis virus which targets vascular endothelial cells and macrophages
Shedder stallion important source of the virus – can shed in semen for weeks, months or years.
May not show clinical signs and fertility unaffected but infect mares at mating.
These mares can then infect other horses via the respiratory route (handler, tack, equipment etc can be a source).
Testing: seropositive = active infection or previous infection or vaccination.
Vaccination is recommended for all teasers and stallions (not mares!).
MUST BE ABLE TO DEMONSTRATE VACCINATION STATUS
Contagious Equine Metritis (CEM)
Taylorella equigenitalis
Contagious equine venereal disease
Laboratories that have a suspect isolation are required to send the swab or sample to APHA for PCR testing – official confirmation.
APHA will then inform the owner
Code of Practice protocol which owners should comply – approved veterinary surgeon appointed to inspect the premises.
Transmitted during natural mating, teasing, semen from AI, staff/equipment who have handled genitalia of infected horses.
Testing pre breeding – culture or PCR of swabs
See HBLB Code of Practice for further details
Rabies in the Horse
Presents differently than in SA’s – wider range of symptoms
Rabies is a differential for ANY unexplained neurological signs in a horse from an endemic region:
Looks like “everything, but nothing”
“Dumb” rabies more common – depression, hyper-responsive, self-mutilation
100% fatal
Incubation highly variable – 10 days to 6 months
Check vaccination status
Track all who have had contact – will need post-exposure prophylaxis (PEX)
Handle animal with care, even after death and do not post-mortem without safety measures
Rabies can only be diagnosed post-mortem – direct fluorescent antibody (DFA) of fresh brain tissue
Differentials for rabies in the United States:
West Nile Virus (WNV)*
Eastern Equine Encephalomyelitis (EEE)*
Western Equine Encephalitis (WEE)*
(Venezualan Equine Encephalitis)*
Equine Herpesvirus-1
Equine Protozoal Myelitis
(Equine Infectious Anaemia)*
Non-infectious neurological diseases (e.g. trauma or congenital conditions)
West Nile Virus
Originally identified in humans West Nile delta in 1937
More virulent strain started to kill birds (natural host) in 1997
Spread to New York, causing an outbreak in humans in 1999
Also affected horses – higher fatality rate than in humans
Spread by mosquitoes – no evidence of direct infection between horses, humans and birds
Recently spread to Europe - new strain
Related to urbanisation, climate change and new agricultural practices which affect migratory patterns
Risk for spread to UK?
Flavivirus, related to Japanese Encephalitis (JE), Kunjin virus (KV) and Murray Valley encephalitis virus (MVEV) -> all cause similar encephalitides
Likely widespread subclinical infection in humans and horses in endemic areas
Pyrexia, anorexia and depression initially, followed by gait abnormalities due to loss of proprioception
Flaccid paralysis with muscle fasiculations common
Diagnosis – serologic testing for IgM antibody response
BUT vaccinated horses will be seropositive, so need to observe a 4x increase in paired titers
Spontaneous death rate ~35% but often euthanised due to long-lasting effects
Rabies
Multispecies, including humans
Caused by viruses in the genus Lyssavirus, rabies virus being the most important
Bats carry European Bat Lyssaviruses, which can cause rabies-like disease
Pathogenesis:
Transmitted via saliva, usually via a bite
Local replication in non-nervous tissue -> peripheral nerves -> spine -> brain
Three phases of clinical signs
Phase 1:
Behaviour changes
Hypersensitivity to noise or light
Phase 2:
Increased aggression
“Staring expression”
Hypersalivation and drooping lower jaw
Pruritus
Polydipsia
Phase 3:
Muscle weakness
Difficulty swallowing
Ptosis
Hypersalivation and dysphagia
General paralysis, convulsions and coma.
Diagnosis:
No definitive antemortem test; serology used to confirm vaccination status
Post mortem testing on fresh brain tissue - fluorescent antibody test (FAT) or RT-PCR/qPCR most common.
Prevention:
UK is rabies free.
NB: EBLV has been found in some UK bats, but does not affect our rabies free status.
Import regulations vary according to species and country – usually some combination of vaccination, serology testing, and quarantine.
Pet passport scheme replaced with animal health certificates – rabies vaccination is still a requirement.
Anthrax
Affects mammals and some species of birds
Cattle, sheep, pigs, horses, humans
Last outbreak in GB in livestock was 2015 in Wiltshire: Anthrax tests after second cow dies on Westbury farm - BBC News
The last case before 2015 had been in cattle in Wales in 2006
Anthrax spread when spores of Bacillus anthracis are inhaled, ingested or contact skin lesions (Skin lesions most common manifestation in humans)
Spores survive for decades buried in soil – dug up to surface
Global distribution – endemic in Central Africa, Iran, Russia, South America – meat consumption from anthrax carcass often the source
Legislation: The Anthrax Order 1991 (legislation.gov.uk)
Cattle & sheep quickly die from anthrax – Sudden death
If see clinical signs before death:
- Dull, stop eating - pyrexia
- Harsh cough, blood in dung or from nostrils
- Drop/loss milk production
- Fits, staring eyes, colicky pains
Pigs and horses:
- Take longer to die than ruminants
- Hot painful swellings in throat
- Colic in horses
- Loss appetite in pigs
ACTION ON SUSPICION: Report to APHA – they will collect a blood smear
Animal By-Products
An animal by-product (ABP) is the entire body, part of an animal or a product of animal origin which is not intended for human consumption
Animal By-Products Legislation in England
The Animal By-Products (Enforcement) (England) Regulations 2013:
Regulation (EC) No 1069/2009 of the European Parliament and of the Council:
Animal By-Product: Categories 1
Highest risk material – for rendering and incineration
Staining required?- Yes – patent blue
All SRM and bodies containing SRM. Animal suspected of being infected with a TSE.
Carcasses of animals used in experiments.
Carcasses from zoo and circus animals.
Animal By-Product: Categories 2
High risk
Staining required?- Sometimes – stained black
Material potentially infectious to humans or other animals e.g. bTB lesions. Products containing residues of authorized vet medicines. Manure and digestive tract contents. Carcasses of dead livestock not containing SRM. Dead on arrivals.
Animal By-Product: Categories 3
Lowest risk material
no staining required
Can go for pet food. e.g. Carcasses or parts which have passed ante- and post-mortem inspection but not intended for human consumption. Heads and feathers of poultry. Incised pig offal. Bovine udders. Poultry intestines. Animal hides and skins. Horns and feet
Specified Risk Material (SRM)
the tonsils, mesentary, caecum and last 4 meters of smal intestine of cattle o all ages
the sull excluding the mandible, the spinal cord, the brain and the eyes of cattle ovfr 12 months old
the vertebral colum of cattle over 30 mnths
the sull, brain , eys and spinal cor of sheep and goats more than 12 months old
stated in Regulation (EC) 999/2001- Annex V
made in respnse to BSE
FBO (Food Business Operator) is responsible for removal of spinal cord
No trace of spinal cord can remain in the spinal canal – major infringement if found
The FBO must be meticulous about removing spinal cord
The meat inspector/OV will check that everything has been removed as part of the meat inspection procedure
A designated tool or knife must be used to remove the meninges, fat and debris
Removed from slaughter hall with no contact with fresh meat or floor – stained 100% with blue dye (patent blue)
Animal By-Product Processing
Before processing any ABP material it must be crushed into smaller pieces – dimensions set by legislation – mincers, crushers
6 approved methods to process ABPs
Category 1 and 2 ABP must be pressure sterilized
Pressure sterilization means that the pieces must be a maximum size of 50mm, heated to 133C for 20 minutes without interruption at core temp, under a minimum pressure of 3 bars (three times normal atmospheric pressure, under steam rather than air)
where-
An ABP processing facility
Biodiesel factory
Pet food manufacturer
ABP combustion site
Organic fertilizer manufacturer
Incinerator site
Compost or biogas/anaerobic digestion site
Rendering animal by-products
Rendering is the cooking and drying process that destroys pathogens, removes moisture and separates the fat (tallow) and protein (MBM from Cat 1 and 2, PAP from Cat 3) components of ABP into marketable products
It’s big business! Turning ABP into useful products that can be used elsewhere
The products of rendering can be used for pet food, animal feed, pharmaceuticals, organic fertilizers, biofuels and oleochemicals (animal oils and fats)
Category 1 ABP are rendered to produce biodiesel or are combusted as fuel
Dead animals at farm level: ‘fallen stock
Livestock dying on farm must be collected, identified and transported from a farm ‘without undue delay’
Must arrange for the animal (incl. stillbirths and afterbirths) to be collected by an approved transporter and taken for disposal to one of the following:
Knacker
Renderer
Hunt kennel
Maggot farm
Incinerator
The burial or burning of fallen stock in the open is illegal
Prevents the risk of disease spread from residues in the soil, groundwater or air pollution
Exemptions to this ban include:
Burial of dead pet animals (e.g. dog or cat) and horses (any horse in England; only pet horses in Scotland and Wales) (authorisation C2)
Remote areas – Isles of Scilly, Lundy Island and Coquet Island (authorisation C3)
After a natural disaster (authorisation C4)
The burning of fallen stock in the open is illegal
But licensed and approved on-farm incinerators may be used
The disposal of carcasses of livestock during the Foot and Mouth Disease outbreak in 2001 provoked huge controversy
On-farm pyres, mass burial sites, rendering as ABP
Concerns around aerosolisation of FMDv, soil contamination, water pollution, SRM in mass burial sites, psychological impacts on local communities, and health impacts of pyre smoke
Carcass disposal after mass culling for disease control
need for wider consideration of public and environmental health aspects of carcass disposal
Nutrient pollution – N, P – excesses in soil, water, air
Pathogen survival in leachate – E. coli, Salmonella, prions from TSEs
Veterinary drugs – antibiotics
Chemicals and elements – Na, Cl, VOCs
Lessons learned from the disposal of carcasses of livestock during the Foot and Mouth Disease outbreak in 2001
Use of on-farm pyres and on-farm burial was superseded by mass burial sites (Army involved) and rendering as ABP as outbreak wore on
Why the removal of SRM from sheep and goats?:
Scrapie
Another Transmissible Spongiform Encephalopathy (TSE)
Notifiable disease – prions are the infectious agent (as with BSE)
Two forms – Classical and Atypical
Classical – animals between 2 and 5 yrs old; Atypical - > 5 yrs old
Highly contagious – colostrum, milk, contamination in the environment (for years) – bedding, feed troughs, pastures contaminated by birthing fluids from infected sheep
Sheep can have genetic resistance – genotyping and selection to breed it out
No known link to human illness – removed as precaution linked to BSE controls
Scrapie: clinical signs
leading to eventual death
Excitability – acting nervously or aggressively
Depression, vacant stare
Trembling of the head, drooping ears
High stepping trot, incoordination of limbs
Unable to stand
Skin irritation – repeated scratching against posts, gates
Nibble reflex when rubbed on their back
Excessive wool loss, skin damage
Equine Metabolic Syndrome
Equine Metabolic Syndrome is not a disease per se
“Collection of risk factors for endocrinopathic laminitis”
Insulin Dysregulation-
Obesity or regional adiposity
“Easy Keeper”
+/- hypoadiponectinemia
+/- hyperleptinemia
which leads to -
Laminitis!
Hypertension
Pro inflammatory state
Diagnostic tests:
Basal Insulin
Oral glucose/ Karo test
IVtests:CGIT/insulintolerancetest/others.
PPID
Age related degenerative condition in horses
Loss of dopaminergic inhibition
Hypothalamus unable to regulate pars intermedia of pituitary gland
Hypertrophy / hyperplasia of PI
Increase production of many hormones from PI which have wide array of effects on body
Clinical Signs-
Pathognomonic hypertrichosis
Hair Colour Changes & Patchy Shedding
Lethargy / Poor performance
Skeletal muscle atrophy
Rounded abdomen
Abnormal sweating (↑ or ↓)
Polyuria/polydipsia (↑ urinating/drinking)
Regional adiposity
Absent reproductive cycle/Infertility
Laminitis ( 1/3 od PPID cases will have ID)
Susceptible to other infections
* NOT ALL SIGNS MAY BE PRESENT ESPECIALLY IN EARLY CASES*
Diagnostic tests:
Basal ACTH
TRH stimulation test
Management and monitoring of PPID
There is no cure. Treatment is intended to reduce clinical signs and should be lifelong
Treatment: Pergolide mesylate (Prascend, Boehringer Ingelheim) – dopamine agonist
Initial dose of 2 mcg/kg (0.5 mg for a 250 kg pony and 1.0 mg for a 500 kg horse).
Rarely some horses may require doses as high as 10 µg /kg body weight per day
Side effects:
decreased appetite 33%
lethargy 9.8%
Reduceorstoptreatmentforafewdaysandrestartwith gradualdoseincrease
Controlled drugunderFEIrules.
After initiation of treatment (2 mcg/kg )
Re check clinical signs and basal ACTH +/-insulin at 1-2 months
If there is an improvement in c.s and laboratory parameters maintain on current dose:
6 Monthly evaluation ( clinical signs + ACTH+ insulin)
Ensure at least one evaluation in Autumn? (natural dynamic test)
Currently no evidence that treatment with pergolide improves insulin sensitivity but studies have suggested that increases in alpha-MSH and CLIP can increase insulin secretion and severe cases of PPID might be more likely to have ID
If not improved Increase the dose
Expect one or more clinical signs to improve and/or the basal ACTH to have returned to normal or close to normal range
Re‐evaluate baseline endocrine and clinical values every 1‐2 months until improvement is seen
Owner to document clinical examination findings monthly.
Individually tailored diet and exercise program (may be overweight/ underweight/ +/-insulin dysregulation/ PPID associated muscle atrophy)
Good preventative veterinary care:
Regular dental and endoparasite checks
Regular farriery ( particularly if laminitic)
Clipping / skin health
Geriatric health checks ( concurrent issues)
Pergolide mesylate
(Prascend, Boehringer Ingelheim)
used to manage PPID
dopamine agonist
Initial dose of 2 mcg/kg (0.5 mg for a 250 kg pony and 1.0 mg for a 500 kg horse).
Rarely some horses may require doses as high as 10 µg /kg body weight per day
Side effects:
decreased appetite 33%
lethargy 9.8%
Reduceorstoptreatmentforafewdaysandrestartwith gradualdoseincrease
Controlled drugunderFEIrules.
After initiation of treatment (2 mcg/kg )
Re check clinical signs and basal ACTH +/-insulin at 1-2 months
If there is an improvement in c.s and laboratory parameters maintain on current dose:
6 Monthly evaluation ( clinical signs + ACTH+ insulin)
Ensure at least one evaluation in Autumn? (natural dynamic test)
** Currently no evidence that treatment with pergolide improves insulin sensitivity but studies have suggested that increases in alpha-MSH and CLIP can increase insulin secretion and severe cases of PPID might be more likely to have ID **
If not improved Increase the dose
Expect one or more clinical signs to improve and/or the basal ACTH to have returned to normal or close to normal range
Re‐evaluate baseline endocrine and clinical values every 1‐2 months until improvement is seen
Owner to document clinical examination findings monthly.
approach to ID/ Hyperinsulinaemia
ID is a central feature of EMS and at least 33% of horses with PPID
Laminitis associated with insulin dysregulation (ID) hyperinsulinaemic laminitis (HAL) is a significant welfare concern
Management of Hyperinsulinaemia is achieved using:
Dietary management
Exercise
+/- pharmaceuticals (severe cases/ non responders)
Dietary management is critical
Aim: to reduce post prandial hyperinsulinaemia
Remove feeds high in non-structural carbohydrates (NSC) e.g. grain feeds /pasture.
In obese animals restrict intake and increase exercise if possible (often not possible if laminitic)
Hay should form the bulk of ration ideally hay with a low (<10%) water soluble carbohydrate (WSC) content or non‐structural carbohydrate (NSC) ≈ 10-12% DM.
%NSC = %WSC + %Starch
Feed little and often to avoid insulin “spikes”
Feeding lean horses with ID:
Maintain BCS-
Low glycaemic diet
Use low insulinaemic calories
Oil
Unmolassed sugar beet pulp
Balancer
Exercise
Soaking Hay -
Reduces WSC content but also DM and minerals. (balancer essential)
Temperature of the water, soak time and volume of water affect amount of sugars leeched from the hay.
But long soaks in warm water can lead to microbial growth.
Typically soak for 6-8 hours in ambient temperatures.
In warmer conditions soak time can be reduced
Overnight soaking probably acceptable in cool conditions.
Steaming hay is not effective in reducing WSC
Feeding a 50:50 mixture of hay and straw possible alternative?
exersise-
Only in horses with ID without signs of lameness
Improves insulin sensitivity when compared to dietary restriction alone.
But moderate exercise without dietary restriction has minimal effect on ID.
Increase gradually monitoring for lameness.
Build up to a min of 15-20 min trot/canter / day (moderate intensity)
Use a soft conforming surface in cases with previous laminitis
Pharmaceutical adjuncts for HYPERINSULINAEMIA Assosiated laminitis
In severe cases or cases which are unresponsive in the first 4 – 6 weeks consider medication.
No licensed treatment for HAL in horses.
3 drugs/ drug classes that are used in clinical practice.
Gliflozins/ SGLT2i (Sodium-glucose co-transporter-2 inhibitors)
Levothyroxine
Metformin
Gliflozins/ SGLT2i
Velagliflozin, canagliflozin and ertugliflozin (doses vary with drug)
Appear to be rapidly effective in reducing insulin concentrations
Long term safety studies lacking
Used in human medicine for last decade for tx of type 2 diabetes
In humans SGLT2 receptor in the proximal convoluted tubule is responsible for 90% of glucose reabsorption, and the SGLT1 receptor is responsible for the remaining 10%
SGLT2i block glucose reabsorption > reduction in insulin production.
Side effects> Hypertriglyceridaemia /PUPD & UTI (glucosuria)
Tapering doses when discontinue
**Assess and monitor hepatic and renal function and triglyceride concentrations **
