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Nutritional Disorders in Beef Cattle . Rumen acidosis liver abscess Polioencephalomalasia , or Polio, or PEM, or “Brainer” Nitrate poisoning. Acute Laminitis, founder Hopelessly off-feed Sell immediately Chronic or subacute A little off feed, poor performers. Long term effect
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Nutritional Disorders in Beef Cattle • Rumen acidosis liver abscess • Polioencephalomalasia, or Polio, or PEM, or “Brainer” • Nitrate poisoning
Acute Laminitis, founder Hopelessly off-feed Sell immediately Chronic or subacute A little off feed, poor performers Long term effect Rumenitis: more problems as we have longer fed cattle – calf-feds, Holsteins, Japanese Probably bigger problem in the PNW with barley, wheat and potato feeding Best symptom is liver abscesses (Fusobacteriumnecrophorum; Actinomycespyogenes) Feedlot: Acidosis and other “digestives” Its all about bunk management!!
Ruminant system of carbohydrate digestion and absorption: Effect of feeding grain • Acidosis symptoms • variable feed intake (symptom and cause) • feces: loose – splattering, less than 1” high, no dimpling/concentric rings • lack of cud chewing • hoof lines, abnormal hoof growth • dairy: milk fat inversion • beef: liver abscesses
Acidosis • Indicates rumen insult • Grows .25 inch (6 mm) / month
Liver Abscess Classification A - O A A +
Total Abscesses by Month, 1990 - 1999Tylan Fed Steers, All Districts sbl 00
EFFECT OF RUMENSIN PLUS TYLAN ON LIVER ABSCESS INCIDENCE CONTROL RUMENSIN +TYLAN NO. HEAD 976 1937 % A- 7.7 5.4 % A 8.4a 3.5b % A+ 20.1a 3.5b TOTAL 36.2a 12.4b LAUDERT, 1990, 4 TRIAL SUMMARYab(P<0.02)
Polioencephalomalasia, or Polio, or PEM, or “Brainer” • Classically associated with periods of rumen digestive upset • irregular feed intake • Consumption of moldy feed • Lush highly fermentable forages – rapeseed forage • Classically considered to be thiamine deficiency • Usually from presence of thiaminases • Administer thiamine – oral or injectible
Polioencephalomalasia, or Polio, or PEM, or “Brainer” • Symptoms: • Laminar cortical necrosis (brain damage) • Blindness • Staggering • Down • Seizures • Recent understanding is that high dietary sulfur is a predisposing factor: rumen bacteria convert sulfur to hydrogen sulfide, enters the blood, interferes with energy metabolism, “starves” the CNS
Polioencephalomalasia, or Polio, or PEM, or “Brainer” • Current issue is with corn byproducts – wet milling involves softening the grain with sulfuric acid • Inclusion of high levels of corn gluten feed or corn distillers grain can increase risk of PEM • Low rumen pH increases production and absorption of sulfide • My thought is no amount of dietary thiamine can eliminate the risk – may reduce the incidence • Formulate diets to have 0.4% Sulfur (or less)
Nitrate poisoning • Ruminal conversion of nitrates in plants to nitrites (instead of ammonia to microbial protein), enters blood, binds with hemoglobin to form methemoglobin, reduces oxygen transport to cells. • Formation of methemoglobin is normally reduced (via electron donation) by protective enzyme systems: • e.g., NADH methemoglobinreductase (cytochrome-b5 reductase)
Nitrate poisoning, cont • Symptoms: • Respiratory distress • Incoordination • Weakness • muscle tremors • Collapse - dead • Don’t stress affected cattle!
Nitrate poisoning, cont • Common feeds: • Stressed crops (drought, frost, hail) • Cool, overcast climate • Lower portion of stem/stalks of certain plants: pigweed, sorghum, corn, sudan grass, barley and oats • High N fertilizer • Immature more than mature forages
15 to 45 g of Nitrate per 100 pounds body weight – from feed and water • 1% nitrate in forage dry matter • 1,500 mg/ml nitrate (ppm) in water • Younger cattle are more susceptible