Lecture 3: Diseases of the nervous system Flashcards
What is the mechanism of action for clostridium tetani
- Tetanospasmin binds to renshaw cells within the central nervous system
- Irreversible blockade of GABA/glycine
- Leads to continued stimulation of the action potential
What are some clinical signs of tetanus
Third eyelid prolapse, lockjaw, sawhorse stance, elevated tail head, hyperesthesia, muscular spasms, recumbency, convulsions, death by respiratory failure
How do you dx tetanus
Clinical signs and finding anaerobic site of infection
How long does it take to develop and replace new synapses with tetanus infection
6-8 weeks
What is treatment for tetanus
- Antibiotics- metro, penicillin
- Drain abscess
- Antitoxin- Colorado serum company
- Sedatives/ muscle relaxants
- Vaccinate
How long is passive immunity from tetanus antitoxin
7-14 days
What is a rare side effect of tetanus antitoxin that could contain parvovirus
Acute fatal hepatic necrosis (Theiler’s disease)
What symptoms is more common in non-survivors of tetanus
Dysphasia, dyspnea and recumbency
Survivors of tetanus will stabilize in __-__ days
5-7 days
What are the 3 ways horses can get exposed to clostridium botulinum
- Preformed toxin eaten
- type B- decomposing vegetation
- type C- decomposing carcasses in feed - Grows in intestine- type B- shaker foal
- Grows in anaerobic wound- type B
What is the pathogenesis/ MOA of botulinum
Blocks acetylcholine release at NMJ resulting in descending symmetrical progressively flaccid paralysis
How can you dx botulinum
- Identify toxin in feed, serum, GI contents, feces, debris
- Grain test- should consume 8oz grain in under 2 minutes
What are some clinical signs of botulism
Dysphasia, poor tongue and lip tone, weakness, lethargy, head carriage, muscle tremors, recumbency, death from respiratory failure
What is tx for botulism
- Antitoxin
- Supportive care
Botulism antitoxin is not effective after botulinum toxin has been ___
Translocated into the cells
What is the prognosis for botulinum
70-99% mortality, 48% survival
T or F: horses with botulinum in which treatment is started after they are already down usually die
True
How do you prevent botulinum
Type B vaccine
What is the pathogenesis/ MOA of rabies
Virus travels to CNS via neurons and reaches salivary glands via associated cranial nerves
What are the reservoir hosts for rabies
Skunks, raccoons, bats, and red fox
What is the incubation period for rabies
9 days- 1year
What is the most common clinical sign of rabies in horses
Colic
What is the furious form of rabies
Aggressive behavior, photophobia, hydrophobia, tremors, hyperesthesia, convulsions
What is the dumb form of rabies
Depression, anorexia, head tilt, salivation, circling, ataxia, dementia
What is the paralytic form of rabies
Ascending paralysis, ataxia
How do you dx rabies and what is standard
- Immunofluorescence of brain- standard
- Histo of Negri bodies
- CSF may be normal or pleocytosis
What is the first thing you do for suspected rabies case
Contact state vet
After contacting state vet what are the next steps in rabies treatment/biosecurity
- Quarantine 6 months
- Aggressive wound care- scrub and clean for 15 mins
- Unvaccinated can’t be vaccinated for 6 months
- Vaccinated horses should be boostered immediately
What is prognosis for rabies
100% fatal
What is metabolic encephalopathy characterized by
Abnormal mental status and elevation of ammonia in blood
What is the pathogenesis of metabolic encephalopathy
- Glutamine and urea broken down to ammonia
- Ammonia overwhelms hepatocytes and crosses into circulation and crosses BBB
- Ammonia is converted to glutamine which has an osmotic effect resulting in cerebral edema
What cell is indicative of metabolic encephalopathy
Type II astrocytes
What are some clinical signs of metabolic encephalopathy
Behavior changes, depression, head pressing, circling, mild ataxia
What can cause hyperammonemia
- Hepatic dysfunction: liver failure or PSS
- Excessive ammonia produced in intestinal tract
What can cause renal (uremic) encephalopathy
Accumulation of metabolic wastes in the brain
How do you dx metabolic encephalopathy
- Blood-ammonia levels
- Liver enzymes may or may not be elevated
What is tx for metabolic encephalopathy
Lactulose
What does a true seizure look like
Repetitive and rhythmic muscle movements, premonitory signs and aura, postictal signs, not aware or responsive, rapid eye movement
What is affected in partial seizure
Discrete area of cerebrum affected
What is affected in generalized seizure
Arises from both cerebral hemispheres simultaneously
What is a status epilepticus
Succession of seizures without regaining consciousness or continual seizures for 5 minutes
What cardiovascular events mimic seizures
Syncopal episode from arrhythmia, ruptured chordae tendinae, myocardial infarction
What circulatory shock events mimic seizures
Hemorrhage, volume depletion
What electrolyte disorders mimic seizures
Hypocalcemia, hypo magnesium
What muscle diseases mimic seizures
HYPP, recumbency myopathy, exertional rhabdomylosis
What development abnormality can be a differential for seizures
Hydrocephalus
What metabolic abnormalities are differentials for seizures
Hyperammonemia, hypo/hyperosmolality, electrolyte disorders
What neoplasms can be differentials for seizures
Cholesterol granuloma, PPID
What are some iatrogenic differentials for seizures
Air embolism, intracarotid injection, fluphenazine
What is a differential dx for idiopathic seizures
Epilepsy
What are some differential dx for infectious seizures
Encephalitis, meningitis
What are some toxic differential dx for toxic
Locoism, moldy corn
What is used for immediate control of seizures
Diazepam- increase GABA
What drugs can be used for prevention of seizures
Phenobarbital, potassium bromide, phenytoin
