What is this plant and its characteristics?
fiddleneck; Amsinckia spp.
-erect, sparsely branching, hairy, 2-3 foot tall weed
-lanceolate leaves
-5-parted orange-yellow flowers in distinctive, terminal grouping on one side of the axis
-fruits contain 2 to 4 black-ridged seeds
-common in dry cultivated soils and waste areas
-all parts of plant are toxic; fresh or dry
What is the mechanism of toxicity for fiddleneck?
-cattle > horses > sheep and goats
-pyrrolizidine alkaloids cause chronic, progressive intoxication
-PA toxin is absorbed from the GI tract and transported to liver
-hepatocytes metabolize PA to pyrroles
-pyrroles cross-link with DNA and prohibit mitosis
-cross-linking causes formation of hepatic megalocytes
-results in hepatocyte and periportal necrosis followed by fibrous connective tissue replacement
-full liver failure after several months
-secondary photosensitization
What are the non-specific signs of liver disease seen with fiddleneck toxicity?
-weight loss or ill-thrift
-icterus
-ascites
-ventral edema
-hemoglobinuria
-diarrhea
-photosensitization
What are the neurologic signs caused by hyperammonemia secondary to liver disease with fiddleneck toxicity?
-head-pressing/walking forward despite obstacles
-depression
-obtundation
-seizure
-coma
-death
How is fiddleneck toxicity diagnosed?
-historical consumption of PA plants with clinical signs
-elevated liver enzymes
-histologic findings including small, hard, fibrotic liver, hepatocyte megalocytosis, and bile duct perforation
What is the treatment for fiddleneck toxicity?
-remove animal from PA plants
-supportive care based on clinical signs
-poor prognosis due to irreversible liver damage
What is this plant and its characteristics?
Lantana camara
-shrubs with square stems
-oval, serrated leaves
-flat-topped clusters of tubular flowers
-very common in southeast
-all parts of plant are toxic
What is the mechanism of toxicity for Lantana camara?
-affects ruminants
-1% bodyweight ingestion causes toxicity
-lantadene A and B cause intrahepatic cholestasis
-leads to periportal parenchymal necrosis due to lack of biliary excretion
-liver damage leads to ruminal stasis and increased toxin absorption
-liver injury leads to secondary photosensitization
What are the clinical signs of Lantana camara toxicity?
-vomiting/regurgitation
-ruminal atony
-jaundice/liver failure
-weakness
-labored breathing
-emaciation
-death
-photosensitization
-conjunctivitis
How is Lantana camara toxicity diagnosed?
-presumptive based on proximity, clinical signs, and elevated serum levels of liver enzymes and bilirubin
-post-mortem evidence of periportal parenchymal necrosis, hyperplasia of bile ducts, and yellow color of liver and kidneys
What is this plant and its characteristics?
pigweed; Amaranthus spp.
-stout, erect, hairy, many-branched stems reaching 30 to 150 cm tall
-greenish flowers in densely crowded spikes 8 to 20 cm wide
-many small, shiny, black seeds
-toxic fresh or dried
What is the prevention for Lantana camara toxicity?
remove plants via herbicides or grubbing
What is the treatment for Lantana camara toxicity?
-supportive care based on clinical signs
-gastric lavage/rumenotomy
-activated charcoal
What is the mechanism of toxicity for pigweed as it pertains to the renal system?
-oxalates enter blood stream and bind to calcium to produce calcium oxalate
-calcium oxalate is filtered by kidneys
-results in oxalate renal tubular nephrosis and renal failure
What are the clinical signs of pigweed toxicity?
-renal tubular necrosis
-perirenal edema
-accumulation of peritoneal and pleural free fluid
-muscle weakness
-ataxia
-recumbency
-cardiac arrest due to hyperkalemia
How is pigweed toxicity diagnosed?
-elevated serum potassium, creatinine, and BUN in animals with known exposure or proximity
-oxalate crystals (but not produced by all animals)
-hemorrhagic fluid in retroperitoneal space post-mortem
What is the treatment for pigweed toxicity?
supportive care for diuretic needs and hyperkalemia
What is the prevention for pigweed toxicity?
cut, gather, and burn/remove plant material
What is this plant and its characteristics?
St John’s wort; Hypericum perforatum
-erect, branching plant with rhizomatous root system
-elliptical to triangular leaves with translucent or black dots
-yellow, 5-petal flowers on terminal ends of stems
-seeds in capsules
-roadside weed and wildflower
What is the mechanism of toxicity for St John’s wort?
-common in cattle, horses, sheep, goats
-hypericin is a photodynamic pigment that causes primary photosensitization
-pigment is absorbed from GI tract
-when pigment is exposed to UV light, it causes acute inflammation and necrosis of endothelial cells of the skin capillaries
-also causes free radical production
-effect is most commonly seen on white-skinned or non-pigmented and non-haired areas that receive sunlight
What are the clinical signs of St John’s wort toxicity?
-erythema
-edema of the skin
-pruritus
-exudation
-sloughing of skin
-hypersensitivity to touch
-blindness (if sclera affected)
-mastitis (with udder ulceration)
How is St John’s wort toxicity diagnosed?
clinical signs of photosensitization with normal serum liver enzymes
How is St John’s wort toxicity treated?
-remove animal from sunlight and maintain in darkened stall/barn
-remove plant from diet
-anti-inflammatory and anti-histamine drugs
-topical medications to sooth skin
What are the characteristics of secondary photosensitization?
-caused by plants that cause liver failure
-impaired hepatic function reduces excretion of plant pigments that cause photosensitization
-similar signs and treatment to primary photosensitization (St John’s wort)
-diagnosed based on clinical signs + elevated serum liver enzymes
