Equine Intoxications Flashcards
1
Q
Obj: Familiarity with more common equine intoxications
A
2
Q
Obj: Understand risk and clinical manifestation for common toxins
A
3
Q
Obj: Establish diagnosis, treatment and prognosis
A
4
Q
What is Nigropallidal Encephalomalacia? Cause? symptoms? diagnostics? treatment? prognosis?
A
- Affects Equids
- Caused by 2,3-dihydro-3, 5-dihydroxy-6-methyl-4[H]-pyran-4-1
-
yellow star thistle (Centaurea melitensis)
- CA, OR, Western US
- Russian knapweed (Acroptilon repens)
-
yellow star thistle (Centaurea melitensis)
- Continuous ingestion at 80-200% BW for weeks to months
- Symptoms:
- Bilaterally symmetric lesions
- Non-progressive focal necrosis of globus pallidus or substantia nigra
- Facial hypertonicity increases w/ food being offered - inability to prehend
- Poor BCS
- Bilaterally symmetric lesions
- Dx - MRI for antemortem
- Tx - None
- Poor prognosis for recovery or survival
5
Q
What is Tremetol? sources?
A
- Fat soluble, high molecular weight alcohol
- toxic at 1-10% of BW and is cumulative!
- White snakeroot (Eupatorium rugosum)
- Rayless goldenrod (Isocoma wrightii)
5
Q
What damage does Tremetol cause in horses? signs/symptoms
A
- Affects Heart, Kidneys, gut, lungs
- Toxins concentrate in milk
- Do not give milk to offspring
- CBC/Chem/UA: (consistent w/ muscle necrosis)
- elevated CK, AST
- Hematuria
- Hemoglobinuria
- proteinuria
- acidosis
- hyperglycemia
- Signs/symptoms:
- Weight loss
- Tremors, ataxia
- Depression
- Cardiac arrhythmias
- Recumbency
- Skeletal muscle and myocardial streaking and necrosis
- Death
6
Q
What other toxin can cause similar signs to Tremetol poisoning, and needs to be ruled out for Dx?
A
Ionophore contamination
7
Q
How is Tremetol poisoning managed?
A
- Symptomatic treatment
- Supportive care
- Attempt to evacuate GIT
- Administer mineral oil or activated charcoal
- Diuresis
- Examine all herd mates
- prognosis is poor to grave
8
Q
What is Red Maple Toxicity? source? signs?
A
- Seasonal toxicity - Fall
- after trimming trees or storm
- Wilted Red Maple leaves
- Hematologic toxicity
- acute severe anemia (intravascular hemolysis)
- methemoglobinemia
- Signs: Tachypnea, Tachycardia
- Depressed
- anorexic
- Signs of Intravascular hemolysis (red/brown urine)
- Cyanotic
- Death
- CBC/Chem/Blood:
- hematacrit drops to 10%
- numerous Heinz bodies
9
Q
What are the differentials for Red Maple Toxicity?
A
- Phenothiazine toxicity
- Wild onion
- IMHA, EIA
- Drug hypersensitivity
- Ehrlichiosis, Piroplasmosis
- Endotoxemia
- Hepatic failure
10
Q
How is Red Maple Toxicity managed? prognosis?
A
- Stabilize
- Blood transfusion
- Anti-inflammatories
- Antibiotics
- Oxygen insufflation
- Environmental evaluation for affected herd mates
- Guarded prognosis
11
Q
What plants contain Cardiac Glycoside?
A
- Foxglove (Digitalis purpurea)
- Oleander (Nerium oleander)
- Azaleas (Rhododendron spp.)
12
Q
how much foxglove is lethal to horses?
A
~0.05% BW (~0.25kg)
13
Q
How is Cardiac Glycoside intoxication managed?
A
- Supportive:
- IV fluids
- Avoid calcium and potassium containing fluids
- Analgesics: NSAIDS (Flunixin meglumine or phenylbutazone)
- Antioxidants: Vit E, DMSO
- IV fluids
14
Q
What is the difference between primary and secondary photosensitization?
A
- Primary - Plant directly causes photosensitization
- Ex: St. John’s wort (Hypericum perforatum)
- Secondary -
- plant causes hepatic disease
- severe hepatic disease leads to phylloerythrin accumulation in skin → photosensitization
- Ex: Ragwort (Senecio spp)
- plant causes hepatic disease
15
Q
How are cases of photosensitization managed?
A
- Rule out significant hepatic disease
- if hepatic disease is present - treat as primary disorder
- Determine if/wat plants are in the pasture
- Remove patient from direct sunlight
- Lesions should heal in 2-3 weeks
- Topical silver sulfadiazine (SSD) - soothing and antimicrobial
16
Q
What is Pyrrolizidine alkaloid toxicity?
A
- Source: Senecio spp, crotalaria spp
- Ingestion of toxic plant causing hepatic damage
- alkaloid transformed to toxic pyrrole
- Reactive metabolites bind cell molecules and cross link DNA preventing mitosis
- Signs:
- Poor BCS
- Icterus
- Chem - consistent w/ primary hepatic disease
- Elevated GGT, AST, ALP
- reduced hepatic function: bile acids
- Histo:
- Megalocytosis
- Bridging Fibrosis
- Guarded prognosis
17
Q
What fungus may infect hay, forage, or grain? what do they cause?
A
- Rhizoctonia leguminicola - Slobber toxin
- Neotyphodium coenphialum - Fescue toxicosis
- Fusarium proliferatum - Leukoencephalomalacia (ELEM)
18
Q
what are the neurotoxins in Yellow Star thistle?
A
- aspartic acid
- glutamic acid
- sesquiterpene lactones:
- solstitialin A 13- acetate
- cynaropicrin
- dopaminergic neurotoxin (2,3 dihydro-3, 5 dihydroxy-6-methyl-4 (H) pyran-4-1) similar to the compound that induced Parkinson’s in People has been isolated
19
Q
What affect does yellow star thistle have on the nervous system?
A
- Destroys dopaminergic nigrostriatal pathway
- coordinates and inhibits the cerebral cortex pathways that control prehension and chewing of food (CN V, VII, IX)
20
Q
How is slobber toxin treated?
A
- removal of infected forage from the diet
21
Q
What toxin is found in tall fescue grass (Festuca arundinacea)
A
- Endophytic fungus - Neotyphodium coenophialum
- Produces ergopeptine alkaloids - primarily ergovaline
22
Q
What endocrine abnormalities are seen with Fescue Toxicosis?
A
- Depressed prolactin secretion
- Depressed fetal cortisol secretion
- Elevated circulating estradiol concentration
- suppressed final stages of gesation
23
Q
What are the clinical signs of Equine Fescue Toxicosis?
A
- Delayed gestation
- Thickened placenta
- impaired lactogenesis
- Poor fetal maturity
24
How is Fescue Toxicosis managed?
* Remove mares from pasture 90 days before foaling
* Treat with D2 antagonist - Domperidone 1mg/kg q24h
* during pregnancy until foaling
* after delivery if milk production is poor
25
What is the toxin responsible for Moldy Corn Toxicity?
* Mycotoxin - **Fumonisin B1**, B2, B3
* interferes with sphingolipid metabolism which disrupts endothelial cell walls and basement membranes
26
What lesions are seen with Moldy Corn Toxicosis?
* Long term, low dose
* Leukoencephalomalacia - liquefactive necrosis and degeneration of the cerebral white matter
* High dose
* liver toxicity
27
What are the signs of Moldy Corn Toxicosis?
* CNS signs predominate:
* blindness
* hypermetria
* depression
* disorientation
* Serum Chemistry for hepatic enzymes
28
What is the treatment for Moldy Corn Toxicosis
* Supportive care
* Prognosis is guarded to grave
29
What are the signs of Ionophore intoxication in horses?
* Anorexia
* Colic
* Acute death
* Weakness
* Myocarditis
* Congestive heart failure
* DCM
30
What is the MOA of Ionophore Intoxication?
* Lipid soluble transports monovalent cations preferentially across cell membranes
* Monensin is very potent in transporting Na+ across lipid membranes
* Proton exchange for sodium, leading to acidosis and potassium loss
* High intracellular sodium leads to secondary intracellular calcium overload
* This leads to mitochondrial swelling, catecholamine release, and increased myocardial cell and diaphragm cell contractility
* early positive ionotropyh
* later negative inotropy and contracture
* Results include skeletal muscle and cardiac muscle dysfunction with potential failure
31
How is Ionophore Toxicosis diagnosed
* History
* Feed evaluation (stomach contents)
* Liver and Muscle enzymes
* ALP, CK, AST
* Cardiac isoenzymes
* Troponin I
* CK-MB, LDH-HBD
* Cardiac evaluation
* ECG
* Echocardiogram
* Reduced fractional shortenting
* +/- thoracic radiographs
32
How are cases of Ionophore Toxicosis treated?
* Remove suspected feed
* Mineral oil or activated charcoal
* no digoxin or calcium
* Supportive
33
What would be the presentation of a horse with a low level of ionophore exposure
* Exercise intolerance
* cough
* weight loss
* congestive heart failure
34
What is the toxin in Blister Beetles?
Cantharidin
35
What issues does Cantharidin Toxicosis cause?
* Pseudomembranous inflammation of GIT
* hemorrhagic cystitis
* occult blood in urine
* Myocarditis and necrosis
36
How is Cantharidin toxicosis managed?
* Empty stomach, activated charcoal
* IV fluid for hypocalcemia
* Plasma transfusion for Hypoproteinemia
