Toxic range plants 2.5 Flashcards
Selenium
-antioxidant
-varies in soils
-more commonly, deficiency=poisoning , but excess as well
-exposure= grazing pastures with selenium accumulating plants, iatrogenic over supplementation
Selenium accumulating plant categories
- Se hyperaccumulators
-non palatable
-in high soil areas - Facultative Se accumulators
-soils can be normal or seleniferous
-eg. Brassica spp - Passive Se accumulators
Target and mechanism of selenium
Target:
-acute=heart
-chronic= keratinized tissues
-pigs=spinal cord
Mechanism:
-spinal cord is unknown
-chronic= replace sulfur with selenium in amino acids =weaker
-Acute= ROS accumulation leading to myocardial necrosis
Acute Selenium tox clinical signs
Acute selenosis
-sudden death
-onset within hours to days= lethargy, diarrhea, dyspnea, tachycardia, weak gait, tetany
-similar to white muscle disease lesions
Chronic selenium
Alkali disease or bob tail disease
-from chronic consumption of high selenium feed
Dystrophic keratinization (horses, cattle, pigs)
-hair loss, claw deformaties, hook cracks
-swelling of coronary band
-heart failure (brisket edema and jug distension)
Clinical signs of Selenium tox in pigs
Poliomyelomalacia
-acute= ascending paralysis progressing up limbs
-chronic= skin changes and hindlimb prop deficits
Selenium tox management
Acute= no antidote. Supportive care. no treatment for poliomyelomalacia
Chronic= remove from pasture, give high quality diet, supportive care for hooves
Diagnosis of selenium tox
-presence of plants on pasture
-plants in stomach/rumen
-liver Se concentration
-chronic=clinical signs with ID in blood
**poor for acute, guarded for chronic
Selenium tox deficiency
-acute myocardial necrosis (ionophores, cardiotoxic plants)
-Poliomyelomalacia= botulism, salt poisoning
-Chronic selenosis= gangrenous ergot
Sweet clover species and toxin
-affects cattle > sheep»_space; horses
-Toxin= dicoumarol from aspergillus or pericillum conversion
Target of sweet clover
Blood
-inhibits vit K epoxide reductase= depretion of 1972 clotting factors
Moldy sweet clover
-chronic consumption (weeks)
-disease progresses over 24-48hrs
-severely affects young calves with normal dams
Moldy sweet clover clinical signs
-pale MM, weak
-hemorrhage, hematomas
-increased PT, PTT
Management of sweet clover
-antidote: Vit K for several weeks
-remove suspected feed
-blood transfusion
**generally poor prognosis with significant blood loss
Diagnosis of sweet clover
-Bleeding in herd
-dicoumarol detected in feed
DDx for sweet clover
-bracken fern
-anticoagulant rodenticides
-liver failure
Bracken Fern in cattle
-Ptalquiloside toxin causing carcinogenicity and bone marrow suppression
-ACUTE= small petechial hemorrhage then bleeding, dull, fever, sudden death, pancytopenia
Bovine enzootic hematuria
-bracken fern toxicity
-CHRONIC- mths of ingestion
-bladder tumors with bleeding, anemia, weight loss
Bracken fern in horses
Bracken staggers= CHRONIC
-incoordination, ataxia, recumbency, odd arched back stance, clonic seizures
Management of bracken fern
Acute= no treatment or antidote, give blood, supportive care
Bovine enzootic hematuria= no antidote
Bracken staggers= give thiamine, supportive care
Diagnosis of bracken fern tox
-presence of bracken fern near pastures, multiple animals affected
-clinical signs
-response to thiamine for horses
Soluble oxalates
Na and K salts of oxalic acid present in plants (rhubarb, shamrock)
-highest in leaves and mature plants
-livestock problem; lack of other feed
Soluble oxalates mechanism
High oxalic acid ingestion leads to the binding and sequestration of Ca and Mg = hypocalcemia and calcium oxalate crystals in kidneys
Clinical signs of soluble oxalates
Acute; few hrs
-hypocalcemia= weakness, muscle tremors, collapse
-renal failure= vomiting, PU/PD, crystals;
