Toxicants Affecting the Nervous System II (7) Flashcards
How can an animal get salt toxicity?
- by being dehydrated then all of a sudden not
- high salt diet
What species is salt toxicity common in?
pigs and poultry
What is direct salt toxicity?
Direct: excessive dehydration → increased Na+ levels (hypernatremia) → ingest water → Na+ back into tissues → water follows → edema | cattle
What is indirect salt toxicity?
high salt diet → hypertonic blood → outward fluid movement from brain → dehydration → ingest water → inward movement from hypotonic blood to hypertonic brain → osmotic edema | pig
What are the effects of salt toxicity (indirect) with a pig?
edema, laminar cortical necrosis, and eosinophilic meningoencephalitis, zone of vacuolation
What are the effects of salt toxicity (direct) with a cattle?
pressure buildup —> instability or seizures
death
What are symptoms of botulism?
weak, reluctant to move, difficulty swallowing / moving tongue (hanging out)
weakness in legs
What are common sources of botulism?
improperly ensiled small-grain forage - ryelage, wheatlage
rotting anything - forage, carcasses, etc
What does botulism cause in waterfowl?
“limberneck”
What are the properties of clostridium botulinum?
anaerobic, gram-positive rod
metabolizes in anaerobic conditions and reproduces via spores that can survive in aerobic conditions
What is the common mode of transmission for clostridium botulinum?
spores - most often ingestion
How does clostridium botulinum cause paralysis?
- interferes with proteins
- ends up inside the vesicle
- blocks fusion of the vesicle holding all of the NT
- no release = no contraction
What is the ultimate affect of botulism?
flaccid paralysis - respiratory paralysis
Death due to botulism is due to _______
respiratory paralysis (diaphragm)
What does botulism prevent?
the release of acetylcholine at
- motor endplates (NM junction)
- autonomic ganglia
- postganglionic parasympathetic nerves
- postganglionic sympathetic nerves (w/ Ach)
What are early manifestations of tetanus?
rigidity of the massater muscles and facial muscles with a distinct straightening of the upper lip causing a grimacing posture to the face
What are other frequent clinical signs associated with tetanus at the site of the penetrating wound?
rigidity of the axial muscles involving the neck, back muscles (opisthotonos), and abdomen
How bad can tetanus spasms be?
can be significant enough to break long bones of the extremities
spasms affecting the larynx, diaphragm, and intercostal muscles = respiratory failure
cardiac arrhythmias, tachycardia, hypertension
What are characteristics of clostridium tetani?
anaerobic, gram-positive rod
metabolizes in anaerobic conditions and reproduces via spores that can survive in aerobic conditions
What is the common mode of transmission for tetanus?
spores
How does tetanus enter the body?
the bacterium survives in soil and in the intestines and feces of animals from which the spore invaded the body through seemingly insignificant wounds and subsequently multiplies
Who are the most susceptible species to tetanus? Least?
horses, lambs, people
birds
[Botulinum/Tetanus] is the deadliest toxin
botulinum - tetanus is a close second
What is the pathogenesis of tetanus?
Tetanus is transported to the spinal cord from the neuromuscular junction and then transported by transcytosis to the inhibitory Renshaw cell and to the upper motor neurons
retrograde transport from LMN —> spinal cord —> blocks the release of glycine and GABA from inhibitory neurons, leading to spastic paralysis -> no relaxation of the antagonistic muscle during normal contraction
How do you treat tetanus?
elimination of the source of toxin, toxin neutralization, control of muscle rigidity and spasms, ventilatory support
tetanus antitoxin
What is a toxoid regarding tetanus?
taking the tetanus toxin and modifying it
stimulate the immune system to make antibodies
What is the toxin in locoweed?
swainsonine
When is locoweed toxic?
all times, even when dried
What does swainsonine do?
inhibits the enzymes alpha-mannosidase I & II which are there to clean up fats, lipids
What are the clinical signs of locoweed?
sudden changes in temperament, aggressiveness, ataxia
Which species especially shows more severe neurological effects of locoweed poisoning?
horses
What is the toxicant in Larkspur (delphinium spp.)?
diterpene alkaloids
What is the toxicokinetics of Larkspur?
readily absorbed by the GI tract and not degraded in the rumen → compete with ACh binding to the nicotinic receptors at the NM junction (reversible blockade)
What are the clinical signs of Larkspur toxicity?
curare-like, reversible blockage causing muscle weakness and paralysis
What is the toxic principle for monkshood (aconitum spp)?
polycyclic diterpenoid alkaloids
aconitine tetrodotoxin
What is the toxicokinetics of monkshood (aconitum spp)?
interferes with Na+ channel function in excitable tissues - prolonged activation
What are the clinical signs of monkshood (aconitum spp)?
usually begin with paresthesia, vomiting, diarrhea, muscle paralysis
life-threatening arrhythmias incleading ventricular tachycardia & fibrillation, followed by cardiac arrest
What is the mechanism of action with bromethalin?
uncoupling oxidative phosphorylation in the brain & liver mitochondria → intramyelin fluid accumulation → long nerve demyelination (paralysis) and intramyelin cerebral edema
What is the main effect of bromethalin?
long nerve paralysis
What are the three most common genuses in cyanobacteria?
anabaena
aphanizomenon
microcystis
“Annie - Phanny - Mike”
What are the types of toxins in cyanobacteria?
hepatotoxins
neurotoxins
dermotoxins
endotoxins
What are the hepatotoxins and their effects in cyanobacteria?
microcystins - hepatotoxic, tumor promoter
nodularins - carcinogenic
chronic
What are the neurotoxins and their effects in cyanobacteria?
anatoxin-a: AChE inhibitor, neuromuscular blocker
saxitoxin: Na+ channel blocker
acute
