Accumulated overtime and incorporated into RBC

Placed in bone

Neurologic signs due to a decrease in energy metabolism 

Peripheral neuropathy due to demylination

Differentials: polioencephalomalacia, cerebrocortical necrosis, Vit A deficiency

Cauda equina neuritis, yellow star thistle poisoning, hepatic encephalopathy

Interferes with cytochrome oxidase →no electron transport →cells become anoxic

brain and cardiac have the greatest concentration of cytochrome oxidase and are rapidly affected

High in colostrum, not milk

High in hay and silage, not fresh veggies

Coarse perennial found in Southeast USA

Endophytic fungus produces ergot toxins

Endophytic fungus

SS: agalactia, hyperthermia, fat necrosis, decrease feed intake

Damp weather predisposes infection of plant

>25 degrees decreases production of toxin

Central mediated vomiting

Gastric irritation, refusing to eat, diarrhea, reduced weight gain

Sows: reduced fetal body weight/length

Gilts are most susceptible

Preputial gilt: swollen vulva, edema, vaginal/rectal prolapse, uterine enlargement, atrophy of ovaries, exudate from vulva, enlarged mammary gland

Males: enlarge mamary gland, prepuces

Sows: Anestrous, nymphomania

Cattle are "resistance" due to rumen detoxification 

Mild udder development, reduced fertility

Blue-green fluoresensce (B1, B2, G1, G2)

Milk (M1)

Liver toxins: Increased bilirubin, PT, AST, ALT, ALP, SDH, ICD, PCV, OCT

Reduced BUN, TPP, globulins, C', lipase

Reduced productivity, increase feed costs

Reproductive problems, increased disease incidence, staggers, nasal discharge, laminitis, blindness, circling, photosensitization

Acute: acute liver failure

Peripheral vasoconstriction, decreased prolactin release, oxytocic on uterus, reduced feed intake, lameness, sloughing claws, tips of ear, tail;

gangrene, hyperthermia

Flaccid paralysis

circulatory and respiratory collapse

Progressive muscle weakness, drooping head, carriage tongue, paralysis, increased respiratory difficulty

7 days

Differential: milk fever

much slower onset and many animals sick (and timing of birth) is how you tell the difference

Tx: ultrahigh dose of penicillin; artificial ventilation

Do NOT use aminoglycosides

Soybean meal enhances toxicity

Gradual increases in concentrations in feeed can be tolerated, but tolerance is rapidly lost in 3 days

Alkaline rumen pH > 8

Metabolic acidosis (lactic acidosis)

hyperkalemia

Tx: 2-5% acetic acid

cool rumen 10-30L of cold water

rumen lavage/rumenotomy

Sodium bicarb

NH₃ added to feed → ammoniated feed → 2- and 4- methylimidazole

treated cereal straw is a common exposure

Suckling calves can become intoxicated from mom

Signs of toxicity seen when animal does not have access to unlimited water

When followed by access to unlimited water, neurological signs develop

Alters balance of Na⁺, K⁺, Cl^-, Ca²⁺ in cells and organelles

Muscle cell pathology

Acute increase in RR, dyspnea, inability to stand, muscle tremors, legs stretched out behind body, death

Chronic: decrease egg production, anorexia, limb paralysis, cyanosis of comb and wattle

Acute: anorexia, sweating, depression, colic like signs, posterior paresis (w/ w/o paralysis), death

Subacute: ill-thrift, heart failure, atrialfibrillation, tachycardia

Acute: diarrhea, depression, anorexia, dyspnea, rear limb ataxia, death

Sublethal/ Chronic: decrease appetitie, heart failure

Ruminants have greatest susceptibility due to microorganism conversion of nutrient to toxin

Ruminants can adopt to toxic levels overtime