4, 5 - rumen acidosis, simple indigestion, rumen drinker

objectives

describe etiology, clinical signs, treatment, control and prevention of rumen acidosis, SARA

describe etiology, clinical signs, treatment, prevention, and control of rumen drinker and make a diagnosis

normal rumen

rumen epithelium villous to increase surface area → increased absorption

VFDs

acetate

highest amount

fat synthesis by adipose tissue/hepatic tissue

decreases with high carb diets

proprionate

gluconeogensis by liver

60% of glucose used by animal

butyrate

ketone bodies always used by extra hepatic tissues

rumen acidosis

high risk 28-60 days on new diet

acute

excessive consumption of readily fermentable carbs

increased production of lactic acid → rumenitis

decreased rumen pH

increased osmolality

microbes produce histamine → vasodilation → laminitis

D vs L lactate

D lactate = formed by microbes → lactate produced in rumen acidosis

L lactate = formed mammalian cells → measured on POC

subacute rumen acidosis

excessive carbs/low forage over long time

pH 5-5.5

high butryic/proprionic VFAs

risk for caudal vena cava syndrome

caudal vena cava syndrome

acidosis → lots of bacteria + vasodilation → penetrate protal vein → liver abscesses → septic thromboemboli → CVC rupture

diagnosis

pH <5.5

high D lacate

metabolic acidosis

acidic urine pH

tx of SARA and rumen acidosis

rumenotomy

MG hydroxide to neutralize

fluids

thamine (produced by microbes → dead microbes)

CD antitoxin

nsaids

abx

slow reintroduction to grain

transfaunate → from cow on same feed

    after pH is neutralized

simple indigestion

abrupt change in feed

doesn’t cause acidosis

imbalanced microflora and fermentation products

mild and self limitiing

rumen development

non funciton at birth

villi develop with feeding grain → from VFAs (microflora from environment)

rumen disorders in calves

fine-ground feed

chronic rumen acidosis

pot belly calf

hypomotility

poor PCS

excessive long stem forage

inadequate nutrition

poor rumen development

inability to digest fier

poor rumen microbes

esophageal groove

closes in response to milk succkling

diverts milk to abomasum

<12 weeks → use bucket or nipple

> 12 weeks → use nipple

oral tube feeding does not stimulate esophageal groove → feed goes to rumen → can spill to abomasum

rumen drinker syndrome

milk in rumen

failure of groove to close

calves on milk only for 3-4 mo

over-feeding (> 2L)

abomasal ulcers/inflammation

clinical signs

pot belly

depraved appetite

poor motility

poor PCS

poor haircoat

pasty feces

putrid rumen fluid

rumen bloat in calves

free gas (type 1 vaga)

extraluminal obstruction, irritation of vagal N

abomasal tympany