7. CNS - ...Dr. Stockler, what are we doing here?

clostridium botulinum

What is the toxin that causes botulism?

ingestion of preformed toxin/forage poisoning, toxico-infectious/shaker foal syndrome, wound botulism

What are the three types of botulism? (full name and common name)

horses

Who gets toxico infectious botulism that germinates in the GIT more often?

cattle

who gets wound botulism more often?

AcH, motor endplate

botulism toxins inhibit the release of __________ at the ____________

false; binding is permanent

true/false: binding of botulism toxin to motor endplates is reversible

nerve terminal must regenerate

Because the binding of botulism toxin is permanent, what must happen in order to reverse it?

afebrile, progressive muscular paralysis, dysphagia, muscular weakness, shaking, recumbency, decreased tone in tail/eye/tongue

What are the initial clinical signs of botulism?

respiratory paralysis

What eventually kills an animal with botulism?

grain test, tongue test (pull it out... does it stay?), clinical signs, qPCR on feces or wound

how can you diagnose botulism?

neutralize toxin, eliminate active infection, supportive care

What are the three main goals of botulism treatment?

multivalent antiserum, type B antiserum

What is used to neutralize the circulating toxin in botulism cases?

penicillin (clostridial gram +), metronidazole (NOT IN FOOD ANIMAL)

what is used to eliminate active infection in botulism cases?

mechanical ventilation, vaccination against type B (clostridial 8 way vax)

What is done specifically in foals to combat botulism?

carbomates and organophosphates

What is the large group of pesticides for use on plants and animals that can expose livestock via overdose or accidental ingestion?

acetylcholinesterase inhibitors, leads to overstimulated Ach receptors (if you inhibit the 'ase' then Ach will build up)

How do carbamates and organophosphates work?

reversible, irreversible

carbomates action is [reversible/irreversible]

Organophosphates action is [reversible/irreversible]

muscarinic, nicotinic, central receptors

What three types of receptors do carbamates and organophosphates affect by building up Ach?

increased salivation, lacrimation, urination, defecation/diarrhea (SLUD), constriction of pupils, congestion of eyes and nose, coughing, sweating

What signs does accumulating AcH cause via the muscarinic receptors

pallor, dyspnea, muscle tremors, fasciculations

What signs does accumulating AcH cause via the nicotinic receptors

incoordination, convulsions

What signs does accumulating AcH cause via the central receptors

stropine, reduction of absorption, pralidoxime chloride (2PAM)

What are the three treatments of carbamates and organophosphates?

receptor blocking

What does Atropine do to help with carbamate/organophosphate toxicity?

Reactivates acetylcholinesterase

What does pralidoxime chloride do to help with carbamate/organophosphate toxicity?

false; only OP poisoning

true/false: pralidoxime chloride (2PAM) is highly effective in carbamate poisoning cases, but not in organophosphate cases

rumenocentesis, emetics (dogs), activated charcoal

What are three ways to reduce the absorption of carbamate/organophosphates?

cyanobacteria

Blue-green algae contains what that is toxic?

late summer, stagnant warm water with high nutrient content (nitrogen/phospherous)

When and where do cyanobacteria survive?

microcystin = hepatotoxic; anatoxins = neurotoxic

What are the two toxins from cyanobacteria and what types of toxins are they?

dogs, no specific treatment... atropine?

Who is most affected by cyanobacteria and what treatment can you give them?

muscle tremors, rigidity, respiratory failure, convulsions, death in 30 minutes

What are the clinical signs that set in rapidly after ingestion of cyanobacteria?

thiamine deficiency, salt toxicity, sulfur toxicity, lead toxicity,

What are the four causes of polioencephalomalacia in ruminants?

rumen acidosis, bacterial, plant thiaminases, thiamine inhibition

What can cause a ruminant to have a thiamine deficiency?

bracken fern, horsetail

What two plants are phytothiaminases? (destroy thiamine in the ruminant)

central blindness, dorsoedial strabismus

What are the TWO clinical signs of polioencephalomalacia that he said you NEED to know?

incoordination, depression, Opisthotonos, convulsions, :)

For completeness sake, what are the other four clinical signs of polioencephalomalacia?

(for those who wanna skip, I ended this term with ":)" so multiple choice people know which it is)

dehydrated, brain shrinks, add water too fast, brain swells and you get cerebral edema

What, in the MOST BASIC terms, is the mechanism of action for salt toxicity?

seizures

If you give an animal with cerebral edema and salt toxicity fluids too quickly, what will happen?

thiamine, diuretics, dexamethasone, fluid therapy

What is the therapy for polioencephalomalacia cases?

give mannitol, no furosemide

Which diuretics should and shouldnt you give?

make sure animal not pregnant, will abort

What do you need to be careful of when giving an animal dexamethasone?

hyper tonic saline

Which type of fluid therapy should NOT be used in salt toxicity cases

CHO, fat, protein, clotting, acid base

sulfur is necessary for _____a dn _______ metabolism, ______ synthesis and metabolism, and blood ______ and _________ balance

water, feed

What are the sources of sulfur for a cow?

water source, forages/weeds

If a cow gets sulfur toxicosis in the pasture, where should you look?

depress consumption, inhibits absorption of Cu

What does high water sulfur cause in cattle?

dry dairy cattle

Who will often get sulfur ADDED to their diets?

lung damage, cell damage in the brain, polioencephalomalacia

Sulfur is reduced in the rumen and inhaled by the cow causing _________. It also is absorbed into the blood and causes ___________. This leads to ____________ specifically

blindness, bilateral cranial nerve deficits, stargazing, ataxia, seizures, headpressing

What are the clinical signs of polioencephalomalacia with sulfur origins?

necrosis of cerebrocortical neurons

What is the CLASSIC lesion found on necropsy after sulfur causes polioencephalomalacia?

ruminants, rumen catabolizes urea to ammonia

Who is at greatest risk of urea toxicity? Why?

feedstuff containing urea or amonia salts, contaminated water source, ingestion of fertilizer

What three ways are cattle most often exposed to toxic doses of urea?

GIT

Too much ammonia in cattle will overwhelm the assimilation and hepatic urea cycle leading to _______ damage and absorption

lack of adaptation, high rumen pH, lack of fermentable carbs

What are three risk factors for urea toxicity?

abdominal pain, bloat, frothing, ruminal stasis, ataxia, incoordination, hyperesthesia, violent struggling, convulsions

What are clinical signs of urea toxicity?

Rumen pH of 8.0-9.2, history, blood or rumen ammonia, chemical analysis of feed

What are some ways to diagnose urea toxicity?

6.2-7 ish

What is a normal rumen pH (noting that is varies based on feeds, higher with forage diets, lower with concentrate diets)

relieve bloat, infuse rumen with water or vinegar, IV fluids, rumenotomy

What are some ways to treat urea toxicity?

lowering rumen pH

Vinegar is great in ruminants for doing what?

slow inrtoduction of urea to diets

What is the only real preventative of urea toxicity?

grayanotoxins

What is the toxin found in azaleas?

voltage gated sodium channels, cardiac/GI/neuro signs

Grayanotoxins will interfere with ______________ causing ___/_____/_____ signs in the body

false; its not (he had that on his slide... I dunno why he felt it so important)

true/false:a buckeye is related to a chestnut

spring, fall, shoots, bark, flowers

Buckeyes are not typically cnosumed... but when they are, the most common time of year is _______ or _______ and the ______, _____ and ______ are the most toxic parts of the plant

1, 20

The seeds of buckeyes are also very toxic... how many seeds does it take to cause toxicity in a dog? How about a horse?

GI irritation and neuro signs

What are the general clinical signs from buckeye toxicity?

colic, diarrhea, depression, sawhorse stance, ataxia, hypermetria, muscle trembling, excitement, paralysis, seizures, convulsions

Okay, get more specific with it. What are some specific clinical signs of buckeye toxicity?

grass staggers

_____________: another name for Grass Tetany... although he said he 'doesn't think we need to know the grasses exactly"

trembling, stiff gait, hypermetria

what are three clinical signs of grass staggers?

worsens with excitement

What is an important concept to remember about the clinical signs seen in grass staggers?

cardiovascular disease; dyspnea, cyanosis, tachy/bradycardia

In addition to the other grass tetany signs, canary grass will also cause ___________________

calm removal from pasture, testing of grasses and seed heads, mowing seed heads, raking, burning or spraying and reseeding

What is the treatment and prevention listed for grass staggers?

months

spontaneous recovery from grass tetany may take _________

lupines

If you get a neonatal calf presented to you after about 40-70 days of gestation with a cleft palate and skeletal defects.... what should you be worried the mother ate?

western US, young plants and seeds, yes

Lupines are not all toxic, but the toxic types are mostly where?

Which parts are most toxic?

Are they still toxic in hay?

neuro signs, crooked calf syndrome

What are the general signs of lupine toxicity?

excessive salivation, ataxia, acute respiratory failure, convulsions, coma and death

What re the specific neuro signs of lupine toxicity?

clinical signs, test for lupine alkaloid, remove access to lupines, supplemental feeding

What are the four things listed as diagnosis and control of lupine toxicity?

cool

whatever this means.

Cool?