Equine Med- Infectious and Neuro Diseases 3

wilsbach's version from 2016-04-30 23:10


Question Answer
Etiological agent of botulism? how do they get it/pathogenesis?Clostridium botulinum- gram + anaerobic bacteria. Spore forming and exotoxin forming. Found in soil and decaying carcasses. A,B,C toxins effect horses- B most common. Infection occurs after ingesting spores in contaminated feed or through wound entry. Toxin prevents release of Ach @ neuromuscular end plate. (can only grow more motor end plates to get around this)
what are the toxins with C. botulinum?7 types of toxins, most common - A, B and C. Type B >85% of cases in Europe and North America. West USA - type A. Type C though processed forages (B for botulism-- convenient)
CSs of botulism?Flaccid paralysis, ataxia, dysphagia, mm tremors, flaccid tail and anal tone, facial hypotonia and facial edema. ↓ menace and palpebral. Ptyalism, ↓ tongue tone, weakness, dyspnea, difficulty urinating/defecating, weight loss, death from cardiac or resp paralysis. Bloods usually normal. Shaker Foal Syndrome: stilted gait, mm tremors, inability to stand > 5 min. (then can leads to other signs above)
what is Shaker Foal Syndrome/ what causes it?C. BOTULINUM: (INFECTIOUS FORM) stilted gait, mm tremors, inability to stand > 5 min
how to dx botulism? Gold standard?CS is mouse bioassay but is not practical, also horses WAY more sensitive than mice so can get false negs. Can do RT-PCR. If it's a toxico-infection, it can be cultured from tissues.
tongue test is, and is for? Grain test?both for botulism- pull tongue out, see if they can pull it back in. Grain test- take too long to eat grain and it falls from mouth and nose.
tx of botulism?Polyvalent antitoxin, Plasma w/ antitoxin B, trivalent serum. Anti-toxin not effective once toxin bound to receptor. Supportive care: gastric lavage and act. charcoal. IV fluids, parenteral nutrition, GI protectants, ventilation support. Penicillin and metronidazole for toxico-infections
prog of botulism?Prognosis is worse for recumbent horses. Mortality rate is high for Adults, foals given anti-toxin have better survival rates. Usually die from resp or cardiac
Prevention of botulism?have good haylage that has pH < 6- have higher moisture or acid preservatives. Make sure no carcasses in feed. Cut hay grass > 10cm to prevent soil contamination.Vx-not licensed in US
is the core vx tetanus toxoid or antitoxin?TOXOID- antitoxin is for exposure
etiology of tetanus? how do they get it/pathogenesis?Clostridium tetani- gram + anaerobic spore forming bacteria. Potent neurotoxin. Found in GI and feces of horses and in soil. Transmission via wound-esp punctures-wound needs to be necrotic*** to lyse bacteria in order to release toxin. Cleaves synaptobrevin –preventing release of neurotransmitters. Leads to ascending paralysis from site of infection.
synaptobrevinToxin that tetanus releases, stops release of NTs
CSs of tetanus? Spasticity, stiff gait, extended head, sawhorse stance, elevated tail, clamped jaw, spasms elicited by noise and sudden movements, dilated nares, sweating, tachycardia, prolapse third eyelid, tachypnea, congested MM, ptyalism
dx tetanus?Anaerobic culture, Gram stain, Presumptive Dx based on Hx and CS
Tx of tetanus?Anti-toxin ASAP and toxoid vx, if Not previously vx. If previously vx-toxoid vx. Risk of Theiler’s w/ anti-toxin. Keep away from external stimuli. Sedatives and mm relaxants-diazepam/phenobarb. Dark quiet room. Tx any wounds/abscesses as needed. Parenteral nutrition, IV fluids. Open and drain wounds (anaerobic organism wont like it)
Theiler's dz associated with?Tetanus ANTITOXIN (so if already vx and then exposed, just vx again and leave the anti toxin to unvx horses bc there is this risk) Theiler's= acute hepatic necrosis
prog of tetanus?Prognosis depends on vx status and severity of CS. Good prognosis if vx prior to inf and poor prognosis if recumbent. Prevention- VX annually!! Can give anti-toxin to foals right after birth if in high risk areas
Cervical Stenotic Myeloencephalopathy- etiology and pathogenesis?Aka Wobblers Syndrome. Malformed cervical vertebrae cause neuro deficits due to spinal cord compression. Causes linked to genetics, high nutrition, imbalances of nutrients, trauma, rapid growth
CSs of Wobblers (cervical stenotic myeloencephalopathy)Abnormal Gait, lacerations on heel bulbs, chipped hooves, squared toe, thin neck mm, cervical pain. CNs are normal. Circumduction of limbs, varying stride lengths, exacerbated limb movements, stumbling, striking one foot with other foot. Neuro tests to do are walking in straight line, circling (most sensitive), backing, tail pull, stepping.
Dx of Cervical stenotic myeloencephalopathy?CSF electrophoresis. Lateral radiographs-bony malformations, malalignment, DJD. Myelography to confirm dx-compression of spinal cord.
who is prone to wobblers?TBs, males, esp tall ones
Tx of wobblers?Surgery- ventral stabilization-fuse bodies in extension with baskets. Or dorsal laminectomy- not done mostly bc more post-op complications. Dietary management (if less than a year): restrict energy and protein, balanced vits and minerals. NSAIDs or joint injections of steroids for temporary relief.
Prog of cervical stenotic myeloencephalopathy?Prognosis: Ventral stabilization- good prognosis for dynamic over static compressions. C3-C5 compressions better prognosis than C6-C7. Good prognosis if improved neuro status post-op. Prevention- don’t breed, dietary management to slow bone growth!
location of best prog for wobblers?C3-C5. (better than C6-C7)
is ventral stabilization better for static or dynamic wobblers?dynamic (it....needs to be stabilized)
Equine Degenerative Myeloencephalopathy: etiology? how do they get it?Unknown etiology: Suggested: Vit E deficiency-probs with metabolism or diet, Hereditary-higher incidence in Arabians or foals from affected Stallions (male linked?), insecticide exposure causing oxidative stress. (how did EDM music start? the world may never know)
CSs of equine degenerative myeloencephalopathy? Age affected?Young horses 6mos-3yrs. Signs stabilize by 2-3 yrs. Symmetric proprioceptive ataxia. All limbs can be affected or only hind limbs: knuckling, circumduction, abduction, hypermetria, spasticity, wide or narrow base stance, may have dull mentation. Do dynamic neuro test: circling, backing, curbs/hills.
EPM and equine degenerative myeloencephalopathy: both cause ataxia in young horses. how will you know which is which?EPM is usually unilateral, EDM is usually bilateral
Dx equine degenerative myeloencephalopathy? which is definitive? DDX from wobblers, herpes, EPM. Check Vit E levels. Histopath only def dx: dorsal******(D in the word for dorsal) spinocerebellar tracts of white and grey matter have diffuse axonal degeneration: myelin loss and can have accumulation of lipofuscin, vacuolization or astrogliosis.
tx for equine degenerative myeloencephalopathy?No effective tx: Supplement vit E is controversial- can reduce CS but not reverse changes. Dz is non-progressive or slowly progressive- neuro deficits remain unchanged for life.
equine degenerative myeloencephalopathy-- hind or forelimbs more affected?hind (WNV and pigeon fever also hindlimb tropism)
how can you prevent equine degenerative myeloencephalopathy?Prevention: supplement brood mares and foals w/ Vit E (alpha tocopherol). Shd do genetic testing before breeding- suspected autosomal dominant.
which is TRULY caused by vit e deficiency?Equine Motor Neuron Disease (need E oil for the motor to run!!), WMD (equine degenerative myeloencephalopathy is implicated to)
Equine Motor Neuron Disease: etiology? pathogenesis?True Vit E deficiency! Absence of green grass for 18 mos, high grain diets, poor quality grass or hay, older horses in paddocks. Bc no antioxidant effects- free radicals damage neurons and denervation of type 1 mm fibers= neurodegenerative dz in LMNs and neurogenic atrophy of skeletal mm.
which mm fibers are denerved/affected in equine motor neuron dz?TYPE 1 MM FIBERS (always seems to be these ones...)
horse looks like it is standing on a ballequine motor neuron dz
neuron problem with NO ATAXIAequine motor neuron disease
CSs of equine motor neuron disease?Weight loss, mm fasciculations, shifting weight, narrow base stance-“horse on ball”. Flaccid lower lip, low head and neck carriage, short stride gait, hyperesthesia, resp distress, weak palpebral tone and other CN abnormalities. ATAXIA is NOT SEEN.
what does biochem look like with equine motor neuron dz? mm bx? CSF?elevated CK and AST. ↓ Vit E conc. MM bx: atrophy of mm fibers. Electromyography abnormalities. CSF inc TP
abnormal glucose absorption tests in...equine motor neuron dz
what will nerve bx look like with equine motor neuron dz?Wallerian degeneration of axons and proliferation of schwann cells.
tx for equine motor neuron dz?No specific tx. Supplement Vit E if cannot give green forage. Some can improve after 2-3 mos
prog of equine motor neuron dz?Grave prognosis. Deterioration occurs rapidly after CS start. Survivors have permanent mm damage. No return to work. Prevent w/ good quality hay or pasture. Supplement Vit E.
arabians seem predisposedEquine degenerative meyloencephalopathy (arabic EDM music)