06b: Feed Toxins

Supplemental feed associated with gossypol poisoning

Cottonseed meal

Natural purpose for gossypol

Natural insecticide

Toxic effects of gossypol

• ROS formation (oxidative damage)

• Suppresses protective cellular redox cycling

• DNA damage (scission)

Most important toxic effect associated with gossypol

Heart failure

Secondary effects associated with gossypol toxicity

Decreased fertility and abortion

Cells most severely affected by gossypol poisoning

Rapidly dividing cells

Species that are less susceptible to gossypol poisoning and why

Adult ruminants; a full GIT is protective because gossypol reacts with proteins

Syndrome associated with acute gossypol toxicity

Heart failure

Syndrome associated with chronic gossypol toxicity

Different degrees of heart failure

• Exercise intolerance

• Ventral edema

• Poor doer

Characteristic postmortem sign associated with gossypol toxicity

Nutmeg liver from chronic passive congestion

Treatment for gossypol toxicity

Remove feed and treat symptomatically

Why is selenium toxicity such a present risk

There are benefits to giving excess selenium…up to a point

What determines how much selenium is in a plant

Form of selenium and soil characteristics

Soil pH that increases plant selenium uptake

Alkaline soil

Why are obligate Se accumulators useful

They are unpalatable, so not usually a risk, but they are an indicator of soil Se concentration

Plants that are the most risk for selenium toxicity

Normal grasses and grains that are palatable, but uptake just a little more Se than normal if the soil conditions are right

Mechanism of Se toxicity

Acts like and displaces sulfur in important proteins and systems

Proteins that are more susceptible to Se

Structural proteins (ex: keratin)

CS associated with acute Se toxicity

Generalized organ failure, especially heart failure

CS associated with subchronic Se toxicity

Progressive hindlimb ataxia from spinal column necrosis and hoof separation

CS associated with chronic Se toxicity

• Bilaterally symmetrical alopecia

• Hoof ridges → lameness

• Hair breakage

• Poor doer

Most common presentation of Se toxicity

Chronic

Legal limit of Se in feed

0.3 ppm

Se level in diet that is considered diagnostic for Se toxicity

>5 ppm

Postmortem samples to use for Se testing

Liver and kidney

Treatment for acute Se toxicity

Support the heart failure

Treatment for chronic Se toxicity

• Feed diet low in Se and high in S and protein

• Therapeutic shoeing

• NSAIDs

Primary use of ionophores

Coccidiostat

Mechanism of ionophore toxicity

Carries ions across membranes and messes with normal cell physiology and ion transport

Beneficial GIT effects of ionophores

Shifts microbial population to produce more propionic acid and increase energy efficiency

Specie that is very sensitive to ionophore toxicity

HORSES

Specie that is very resistant to ionophore toxicity

Poultry

Factors that increase risk of ionophore toxicity

• Repeat exposure

• Low quality diet

• Compromised liver health

CS associated with ionophores

Non specifically ADR, lots related to heart failure

Clin path abnormalities associated with ionophore toxicity

Increased muscle leakage enzymes

Postmortem lesions associated with ionophore toxicity

• Cardiac hemorrhage

• Cardiac necrosis

• Muscle degeneration in very active skeletal muscle

Decontamination method that is specifically helpful for ionophore toxicity

Activated charcoal → lots of enterohepatic recirculation, and AC interrupts that

Treatment for ionophore toxicity

• Support kidneys

• Supplement with antioxidants

• Treat colic in horses

Where does fluoride go when ingested

Teeth and bone mostly

CS associated with fluoride toxicity

Spongey bone deposition

When is fluoride toxicity a problem

Young animals when there is developing enamel

Diagnostics used for fluoride toxicity

Can test water or bone

Bone samples to take for fluoride testing

Coccygeal vertebra and ribs