Review Note

Be able to describe the physiology, prevention, symptoms, and treatments of each of the different conditions discussed in lecture.

Mineral Deficiency: common for cow/calf operations Negative impact on production, immunity and enzyme function, Maximum growth/fertility, Normal growth/fertility
Treatment: Depends on mineral.
Diagnosis: liver biopsy
Prevention: best strategy is to provide mineral packs/supplementation.
Bloat: Feedlot bloat: increase in concentrates to fast, and microbes cat adjust. Gas production increases and can’t get rid of. Frothy bloat: Gas gets trapped in froth bubbles and prevent normal gas escape. Caused by legumes.
Prevention: ionophores (rumensin), improve microbial health, surfactants (bloat bocks), reduce froth.
Treatment: Concentrated poloxalene, surfactant to break forth apart to release gas, Diet takes time, Remove gas manually with trocars or tube
Ruminal Acidosis: caused by high concentrate dietsà decrease rumen PH à harmful to microbial population
Clinical signs: Off feed
Prevention: gradual increase of grains (step up rations), Ionophores at least 10% forage in final ration
Treatment: diet changes, antibiotics, Similar to prevention, we need to re-establish rumen pH and microbial population.
Grass tetany: Grazing lush green pastures, low blood levels of Mg or Ca. soil/plant deficiency
clinical signs: nervousness, twitching, staggers, down cattle.
Prevention: Supplementation, treatment of pasture can be hard to do depending on moisture and terrain.
Treatment: IV calcium borogluconate with 5% magnesium hypophosphate, CMPK gel orally (Ca, P, Mg, K).
Range plants toxicities: Larkspur, Mountain summer range, death occurs with 5 h of a toxic dose. Graze early in season prior to plant flowering. flowered plant = most toxic. Ponderosa pine and broom snakeweed. Late term abortions in cattle, Decrease fetal blood flow.
Ammonia toxicity: Ammonia toxicity occurs when ruminants get more that 1/3 of total protein as urea and the microbes don't have time to adjust. Urea will rapidly hydrolyze to ammonia and build up in blood.
Clinical sings: Uneasiness, staggering, kicking at flank, down animals, slobbering, labored breathing, incoordination, bloat. Reaction typical all or none: animal dies or recovers with little to no side effects.
Prevention: do not feed more than 1/3 of total protein in diet as NPN.  Treatment: Catch early, give vinegar and other acids,1 gal on vinegar and 1 gal of water per 100lbs of body weight
Hardware disease: Metal items “fall” into reticulum and puncture, die of peritonitis. 55-75% of slaughtered cattle have hardware in their reticulum. 
Clinical signs: decrease appetite, lethargic, fluid around heart, pain,
Prevention: magnets, clean up. 
Treatment: surgical if worth it.
Urinary Calculi (small ruminants): 
Hard mineral deposit in urinary tract
Clinical signs: Difficulty urinary, blood in urine, dribbling, stomping feed or kicking feet, Rupture of bladder or urethra – toxemia within 48 hrs , Phosphate calcui – high grain diets, Silicate calcui – rangelands
Prevention: decrease P in diet. Acidifying urine and increase urine volume.
Treatment: not very successful surgery, Consider value of animal
Polio encephalomalacia: Disturbed thiamine (Vitamin B1) metabolism. more grain and more thiaminase producing bacteria that will consume thiamine. Some plants produce thiaminase: kochia, bracken fern, equisetum. High sulfate diet (DDG) will inhibit thiamine)
Clinical signs: Generalized neurological symptoms. Death
Prevention: Watch diet. Can supplement thiamine.
Treatment: early treatment is necessary. Give thiamine. May have neurological deficits forever.