Acidosis Flashcards
rumen temp
38-41 with decrease between meals
normal rumen pH range
5.5-6.9
rumen microbiota relative populations
most bacteria, then bacteriophages, then protozoa, then methanogens, then fungi,
3 types of microbe communities
particle associated: up to 75% high enzymatic activity
liquid associated: up to 50%, utilize soluble nutrients
epimural associated: more stable, urease activity
SCFA
major energy supply
production released ATP for microbial growth
difficult to measure production
major VFA, what changes between forage and concentrate diets
always mostly acetate
when on concentrate propionate increases
SCFA and lactic acid pKA
what does this mean
SCFA = 4.9
lactic acid = 3.9
at lower pH SCFA doesn’t grow as well and lactic grows better
predominant lactate isomer in the rumen
L lactate
absorption difference between L and D lactate
L lactate absorbs better. D is more predominant at lower pH and sticks around longer snowballing acidity
SARA pH
5.2-5.6 for atleast 3h in a day
acute acidosis pH
below 5.0 (5.2)
bacteria linked to liver abscess increase when pH
decrease
lactic acid utilizers trend for SARA and acute
lactic acid utilizers are increased in SARA and decreased in acute
cant deal with acute issues
main and other acid removal methods from rumen
main is absorption
others are bicarb and passage
relation between salvia and acidosis
more saliva does not prevent acidosis as more saliva comes from more intake which means more ferm to deal with
how does HCO3- get into rumen
antiport with VFA between rumen and blood stream
is bicarb higher in roughage or concentrate diets for salivary bicarb and rumen bicarb
salivary bicarb is higher in roughage
rumen bicarb is higher when on concentrate
main mechanisms for the removal of acid from ruminal contents (5)
saliva
passive diffusion of SCFA across rumen wall
SCFA absorption antiport with bicarb
carbonic anhydrase
passage of acid out of rumen
why consider ruminal acidosis
animal welfare
decreased performance
associated disorders
mortality
causes of acidosis
incr VFA production
excess grain
increase in dietary carb
insufficient fiber
insufficient buffering
sorting feed
SARA consequences
metabolic acidosis
death
poor performance
chronic SARA acidosis consequences
poor bunk management
cyclic intake pattern
reduced performance
types of bloat
free grass
frothy (can be feedlot due to microbial factors or pasture due to plant components)
consequences of acidosis
decr feed intake
decr absorptive capacity
incr liver abscesses
how do liver abscesses happen
low pH deteriorates rumen wall, bacteria invade systemic circulation, hepatic blood stream takes to liver where it becomes encapsulated
1-2 small abscesses is severe
laminitis
low pH degrades rumen wall allowing bacteria to enter systemic circulation and translocate causing infection
vascular seepage causes edema, hypoxia, degradation of corium and irreversible damage
cost to inflammation
induces glucose utilization that should be used for growth instead
increases liver amino acid uptake
decreased growth and feed efficiency
where does acidosis have a significantly different pH than normal
Rumen
Cecum
Proximal colon
distal colon
mucin cast
bandaid on LI to try and recover from pH damage
comes out in feces
what areas should you target when trying to mitigate ruminal acidosis
reduce fermentability
feeding management
how to reduce fermentability
increase fiber, byproducts, and fat
what to change in feeding management to reduce acidosis
frequency
bunk management
avoiding restriction
improve dietary adaptation
cascade of grain processing speed
wheat
barley
corn
sorghum
factors for variation in daily feed intake
weather
missed feedings
poor processing
stale feed
increasing too quickly
when would you feed the higher grain diet if you are having acidosis issues
in the afternoon feeding
