Horses 5 Flashcards
High cervical (C1-C5) lesions what clinical signs seen, which limbs more affected
- Hemiparesis/plegia or tetraparesis/plegia
- Clinically dominated by signs of proprioceptive ataxia
○ Disruption of descending UMN tracts cause paresis
○ Paresis can be (very) difficult to appreciate in mildly affected animals - Pelvic limbs (more severely affected)»_space;» thoracic limbs
○ Longer tracts in the pelvic limbs so metabolically affected
○ Neural tracts pelvic are more superficial in the spinal cord - more susceptible to damage
High cervical (C1-C5) lesions what if severe lesions, what results with muscle tone, spinal reflexes and bladder
- If severe lesions
○ Recumbent
○ Die suddenly following respiratory paralysis
○ Can raise the head and neck only when lying with the lesion side facing down (with unilateral lesions) - Muscle tone? - HYPERTONIC
- Spinal reflexes? - HYPER-REFLEXIA
- Distended bladder, difficult to express
Cervicothoracic (C6-T2) lesions what clinical signs seen, what occurs in terms of muscle tone, spinal reflexes with fore and hindlimbs and bladder
- Lesions also result in tetraparesis/plegia
○ BUT nature of deficits differs between front and hind limbs - Forelimbs - damaged the cell bodies (LMN)
○ Muscle tone - hypotonia
○ Spinal reflexes - hypo-reflexia
○ Thoracic limb muscle atrophy - rapid, can occur over 3 weeks - Hindlimbs - damaged the neural tracts (UMN)
○ Muscle tone - hypertonia
○ Spinal reflexes - hyper-reflexia
○ Distended bladder, difficult to express
Thoracolumbar (T3-L2) what clinical signs seen with incomplete and complete lesions
- Incomplete lesions
○ Normal activity of the forelimbs
○ Proprioceptive ataxia in the hindlimbs - Complete lesions
○ Recumbent
○ May assume a “dog sitting” position - paralysis
○ Hindlimbs may show hypertonia and hyper-reflexia - difficult to assess
Lumbosacral (L3 - S2) what does it contain, clinical signs in forelimbs and hindlimbs for incomplete and complete lesions
- Contains the LMN Efferents for pelvic limbs
- Normal forelimbs
- Incomplete lesions
○ Appear unable to support weight
○ Stride length is shortened
○ Hypometria
○ Joints might be overly flexes (crouches stance and gait) - Complete
○ Flaccid paraplegia
○ Hyporeflexia or areflexia (no reflexes)
○ Hypotonia
Sacrococcygeal (S3 - C5) what clinical signs seen with lesions
- Flaccidity of the tail and anus
- Paraphimosis in males
- Desensitization of the tail, penis, vulva, anus and perineum
- Urethral sphincter is dilated
○ Urinary incontinence - Unable to defecate
Neuromuscular disease what are the 2 main ones and how common
Tetanus and botulism -> not that common
How does the tetanus and botulism toxin work (mechanism of action)
- Cell binding: toxin circulate in bloodstream
○ Both BoNT and TeNT bind receptors on the pre-synaptic membranes of the NMJ
○ Specific receptors for each toxin -> different intracellular routing - Internalization: neurotoxins internalised within vesicles (pinocytosis) in the neuron
○ Tetanus neurotoxin -> transported to spinal cord
○ Botulinum neurotoxin -> mostly remains at NMJ - Blockade of neurotransmitter release: both toxins have proteolytic activity
○ Disrupt specific components of the neuroexocytosis apparatus -> prevents release of neurotransmitters into the synaptic cleft
Tetanus what does it lead to and pathogenesis
Tetanospasmin -> spastic paresis
○ Toxin diffuses from production site (wound) into bloodstream
○ Distributed to the pre-synaptic membrane of the motor end-plate (of the alpha motor neuron)
○ Travels centripetally toward spinal cord and enters inhibitory interneurons (Renshaw cells)
○ Blocks release of inhibitory neurotransmitters by the interneuron:
§ Glycine and gamma-aminobutyric acid (GABA)
○ Dis-inhibition of the gamma-motor neuron
Tetanus epidemiology when generally occur and sites of growth
- Horse -> puncture wounds to the foot or soft tissues
○ ENSURE THAT IT HAS BEEN VACCINATED AGAINST BEFORE SURGERY OR WHEN SEE WOUNDS - Other sites for growth of C. tetani include:
○ Uterine infections
○ Castration wounds (especially when using elastrator bands)
○ Tail docking
○ Dehorning
○ Bull rings
○ Infected umbilical stalks
Tetanus clinical signs and what result in
- Vague stiffness and lameness initially
○ Reflect local effects of the absorbed toxins - Generalised stiffness
○ Hypertonia most evidence in anti-gravity muscles
○ Sawhorse stance
○ Excessive facial muscle tone -> lock jaw
○ Eyeball retracted into orbit with menace -> 3rd eyelid flashes across the cornea
○ Lips retracted -> sardonic grin
○ Ears pulled slightly downward and caudally
○ Tailhead elevated - Tetanic spasm elicited by auditory, visual or tactile stimulation
○ Severely affected animals become recumbent with opisthotonus (totally rigid)
○ Increased muscle activity -> pyrexia (sweating in horse) - Aspiration pneumonia develops in some cases -> contributes to mortality
- Death due to respiratory muscle paralysis and heart failure
Tetanus what are the 6 main things need to do
1) provide muscular relaxation
2) ensure good footing
3) elimination of infection
4) neutralise unbound toxin
5) maintain hydration adn nutritional status
6) establish active anti-toxic immunity - if unsure on vaccination history
in terms of treating tetanus what is involved in providing muscular relation and ensuring good footing
1. Provide muscular relaxation ○ Quiet darkened stall ○ Pack ear with cotton wool ○ Acetylpromazine - long acting mild sedation 2. Ensure good footing ○ Sling support - may not tolerate
in terms of treating tetanus what is involved in eliminating infection and neutralising unbound toxin
- Elimination of infection
○ Surgical debridement
○ Systemic and local penicillin - Neutralize unbound toxin
○ Infiltration area around wound with TAT (tetanus anti-toxin)
○ Systemic TAT ( 2 to 5000 IU/kg slow IV - broad dose range)
§ Not particularly expensive -> generally pick in the middle
○ Theiler’s disease (acute hepatic necrosis or serum hepatitis) - concern when give TAT
in terms of treating tetanus what is involved in establishing active anti-toxin immunity
○ TAT and tetanus toxoid can be administered simultaneously but must not be mixed and should be given at different sites
§ Opposite side of the neck
How do you diagnose tetanus
- Clinical signs and history
- No reliable diagnostic test
- Attempt to culture C. tetani
Hypocalcaemia clinical signs
- Clinical signs very similar to tetanus
○ Clinically quite different to hypocalcaemic in cattle
○ Synchronous diaphragmatic flutter - thumps
§ Diaphragm contracts in time with the heart (due to phrenic nerve being close to the heart)
□ Hypocalcaemia leads to hyperexcitable nerves
Hypocalcaemia in horses what associated with
○ Lactating mares
○ GIT disease
○ Renal disease
○ Prolonged transport with food deprivation
○ Endurance events (esp during hot weather) - sweat a lot which contains a lot of calcium
○ Cantharidin (blister beetle) toxicity (oxalate, cadmium)
○ Idiopathic
Botulism what lead to, caused by and the 3 ways to become infected and how common
- BoTN block the release of acetylcholine at the NMJ -> flaccid paralysis
- Caused by toxins produced by clostridium botulinum
○ Soil organisms
○ Most common risk factor is horse being fed with round bail hay
1. Ingestion of the preformed toxin
○ Most common form in cattle and adult horses
2. Ingestion of spores and toxins production within the GIT:
○ Toxico infectious botulism (shaker foal syndrome)
3. Contamination of wounds with Cl. Botulinum spores:
○ Subsequent production and absorption of toxins
○ Rare in horses (not uncommon in cattle)
In terms of types of toxins within botulism what is the most common one and why shouldn’t fee cattle chicken poo
○ Type B: 85% of cases of botulism in horses, associated with forage - MOST COMMON - just learn this one
§ Commonly associated with round bale hay
○ Type D: associated with poultry litter -> sporadic disease in cattle - SHOULDN’T FEED CATTLE CHICKEN POO
What are common clinical signs in foals with botulism
- Lie down more often than normal
○ When forced to rise, stands for a few moments, then develops generalised muscle tremors (shaker foal) and drops to the ground - Typically well- nourished, bright and alert
○ Normal heart rate, respiratory rate and rectal temperature - Clinical pathology findings are often normally
- Progressive symmetric myasthenia -> recumbency
what are some additional clinical signs of botulism in foals and 2 main complications
- Additional clinical signs include: ○ Drooling milk ○ Tongue easy to pull from the mouth ○ Mild mydriasis and weak eyelid tone ○ Constipation and ileus consistent - As disease progresses… increase HR and RR - Complications include ○ Aspiration pneumonia ○ Decubital ulceration
Botulism what are the early clinical signs in adults
- Clinical signs are always symmetric and progressive
- Early clinical signs include:
○ Decreased exercise tolerance
○ Dysphagia -> slow to eat, diminished ability to swallow
○ Mild depression
○ Colic -> gastrointestinal ileus and gas accumulation - Decreased tongue, eyelid and tail strength
○ Typically occur before obvious skeletal muscle weakness - Vital signs usually normal initially
Botulism what are the moderately affected and late clinical signs in adults
- Moderately affected -> shuffling gait, evidence of muscle weakness:
○ Elephant on a ball stance - shuffling gait
○ Muscle tremors begin in triceps -> extend to involve other muscle groups
○ Some horses have difficult lifting their head -> oedema of the muzzle and face - Can progress to difficult rising and recumbency
○ HR and RR increase
○ Increase abdominal component to respiration
○ Decreased borborygmi - Death -> respiratory paralysis
How to diagnose botulism
- Often diagnosis of exclusion
○ Clinical signs can be very suggestive and response to treatment
○ Might be supported by history (round bale hay) - Haematology and serum biochemistry usually normal
- Definitive diagnosis can be difficult - NOT DONE COMMONLY
○ Demonstration performed toxins in the serum or intestinal contents
○ Presence of botulinum spores and toxin in recently consumed feedstuff - suggestive
What are the 4 main parts of therapy for botulism
1) anti-toxin administration
2) excercise restriction
3) antimicrobial therapy
4) supportive care
in terms of botulism therapy what is involved with anti-toxin administration and excercise restriction
- Anti-toxin administration
○ Antitoxin has no effect on the toxin after it has bound to the cell receptor
○ Single dose of antitoxin should provide passive protection for more than 60 days -> only single dose needed - Exercise restriction
○ Confined to a stall or limit muscular activity
○ Frequent attempts to force animals to rise or move are contraindicated -> depletes acetylcholine stores
○ Can use slings to keep horse up (don’t want compartment syndrome)
In terms of botulism therapy what is involved with antimicrobial therapy and supportive care and prognosis
3. Antimicrobial therapy ○ Aspiration pneumonia ○ Infected pressure sores ○ Avoid drugs that might potentiate neuromuscular weakness (procaine, penicillin, aminoglycosides, and the tetracycline) 4. Supportive care ○ Fluids, analgesia ○ Ventilator Good prognosis if have the money
Snake and tick bites clinical signs and the 3 main types of vectors
- Common clinical signs to botulism ○ Anti-toxins available and effective - Types ○ Notechis scutatus (tiger snake) ○ Demansia textilis (common brown snake) ○ Ixodes holocyclus
Stringhalt what is it, how generally occurs, when worse
- Involuntary flexion of one or both hindlimbs (occasionally forelimbs)
○ Pasture derived neurotoxin (flatweed) -> not sure on the exact toxin
○ Injury to the hock - Generally gets worse when cold or nervous and excited
Stringhalt treatment and what can be confused for
- Treatment
○ Many of the pasture associated cases will resolve eventually with removal
○ Phenyoin - not sure how works
○ Resection of the lateral extensor tendon
Can be confused for shivers (where you pick up the hindlimb and it hoovers and shivers before being placed back down) - Possible cross-over with the diseases
in horses what is a common cause of polyphagia and anorexia
Polyphagia - Equine metabolic syndrome Don't eat - Hyperlipemia and hepatic lipidosis - Re-feeding syndrome
Equine metabolic syndrome what is it, associated with is it related to PPID and certain breds
- Endocrine and metabolic abnormalities associated with development of laminitis
- Hyperinsulinemia, insulin resistance, insulin dysregulation
- Genetic predisposition + exposure to environmental factors = EMS
- Some similarities, but DIFFERENT from PPID
○ Both have lameness as an issue
○ May have both
○ One can influence the other - Why certain breeds
○ Evolution within different environments
§ Ponies - harsh mountain areas, donkeys - Arad areas -> metabolism made to get most out of the feed
Equine metabolic syndrome pathophysiology and what is the most important clinical consequence
- Incompletely understood
- Thought genetic predisposition in combination with environmental factors (overfeeding, high CHO pastures/diets) leads to EMS phenotype & disease
- High CHO diet → insulin dysregulation
○ Similar to metabolic syndrome/type II diabetes in humans - Inflammatory role of excess adipose tissue
○ Production of inflammatory cytokines - Hyperinsulinemia linked to laminitis
- Laminitis most important clinical consequence
Equine metabolic syndrome clinical picture
- Generalised obesity –BCS 7/9 or greater
○ Regional adiposity - neck, ribs, rump - or just generally
○ Crestyneck - Laminitis - multiple founder lines (repeated subclinical)
- Pony breeds, some horse breeds
○ Morgans, paso fino
Equine metabolic syndrome what is important to consider
- Client education
○ Lots of owners underestimate the obesity of their animal
○ Or just think that is normal
○ Laminitis is NOT NORMAL
In terms of equine metabolic syndrome what are the 6 main tests for diagnostics and what is important
- BCS, crestyneck score, midneck circumference, girth circumference at withers and umbilicus
- Basal plasma insulin concentration
- Oral glucose tolerance test/oral sugar test
- Oral sugar test
- Insulin tolerance test
- Combined glucose-insulin test
- Minimise stress
Basal plasma insulin concentration what used for how to perform and when highly likely
Diagnosis of equine metabolic syndrome
○ Fasting no longer recommended - just low sugar hay
§ (can induce ID)
○ Try to limit dietary influences (no grain 4-5 hours prior)
○ Reference range will vary depending on lab and type of assay used
§ Generally ID suspected if 20-50 μIU/ml
§ Highly likely if >50 μIU/ml
Oral glucose tolerance test/oral sugar test what used for, what does it measure, how to perform
Diagnosis of equine metabolic syndrome - most common
○ Bodies insulin response to glucose - different to glucose absorption in gut test
○ Overnight fasting
○ Baseline blood sample in morning
○ Horse given small meal (low sugar feed e.g. chaff) with 1 g/kg dextrose powder
○ Blood collected again 2 hours later for insulin concentration
Oral sugar test what used for and how to perform
Diagnosis of equine metabolic syndrome
○ Fast at least 3 hours, not >12 hours
a. Baseline blood sample
b. Karo light syrup 0.15 ml/kg PO (dosing syringe) - not as commonly found in AUS
c. Blood sample again at 60 and 90 minutes
○ Insulin > 45 μIU/ml at 60 or 90 minutes suggests ID
