Ruminants Flashcards
Acute lactate acidosis: local Consequences
a, decreased rumino-reticular (forestomach) motility b, increased ruminal osmotic pressure (osmolality)
physiological: 200-250 mOsm
pathological: > 400 mOsm
c, mucosal injury (ruminitis)
d, decreased activity (even death) of microorganisms,
especially protozoa. Overgrowth of Clostridia/coliforms, later funghi
Acute lactate acidosis: general Consequences
a, dehydration (hypovolaemic shock): PCV↑
b, metabolic acidosis (lactate acidosis, lactacidaemia)
c, increased production and absorption of endotoxins (death of Gram negative bacteria)
d, increased biogen amine (histamine etc.) production:
1. in the ruminoreticulum ↓bacterial effect 2. in the wall of reticulorumen inflammatory
effect
e, ethanol, methanol production : depression of CNS
Clinical symptoms of SARA(sub-acute(chronic) rumen acidosis)
- Low or fluctuating dry matter intake
- Decreased milk production
- Poor milk quality (low milk fat)
- Episodes of lameness (laminitis, sole abcesess, ulcers) •Episodes of diarrhea
- Unexplained high culling rate due to vague health problems
None of these are specific symptoms for sara!
EFFECT OF MODERATE NH3 EXCESS (before toxicosis) in RU: local and general
Local consequences -disorders in ruminoreticular motility - pH increases - Decreased microbial activity (especially protozoa) - Ruminal mucosa damage Alkalosis: pH alkalitic, ammonic smell
General consequences
➡️protein deficiency
➡️threatening NH3-toxicosis
- Increased urea synthesis and excretion
NH3 POISONING (TOXICOSIS) Causes:
- sudden high protein or NPN (non - protein nitrogen, ie. urea) ingestion (without adaptation)
Ruminal NH3 concentration > 60-100 mmol/l
(300-500% fold increase, as normal value < 20-30 mmol/L)
NH3 POISONING (TOXICOSIS) consequences: local and general
Local
- motility decreases
- gas production increases tympany
- absorption of inorganic compounds (ie. Ca2+) decreases
General
-first: compensated metabolic alkalosis
- second: incompensated respiratory acidosis
- tetany (decreased Ca2+, increased Na+, increased K+)
- hypersalivation, CNS symptoms, incoordination
- increased lipid mobilization (increased FFA in the blood) - ketone production
RUMINAL PUTREFACTION causes
-death of useful bacteria following acute acidosis, survival
and owergrowth of putrefactive bacteria (E. coli, Pasteurella)
– starvation
– protein (NPN-) overload (absolute)
– energy- (CHO-) deficiency (relatíve protein-overload)
– consumption of putrefactive food
– non accomodated rumen for the type of protein given
RUMINAL PUTREFACTION Consequences:
– alkalosis (local and general)
– decreased production (meat, milk)
– mucosal damage, potential bacterial invasion
– dyspepsia(indigestion)
Putrefaction: ruminal content is dark brown, stenchy,
ammonic or fecal smell, watery consitency
Simple Indigestion (Mild dietary indigestion)
Almost any dietary factor that can alter the intraruminal environment can cause simple indigestion.
Causes:
– Hand-fed dairy and beef cattle - variability in the quality and
quantity
– Sudden change in the pH
decreased: rapid fermentation,
increased: forestomach hypomotility and putrefaction
– Sudden excess to highly palatable feeds (corn or grass silage), relatively indigestible (poor-quality roughage, poor- quality straw, grain, spoiled or frozen feeds), introducing urea to a ration, turning cattle onto a lush cereal grain pasture
Simple Indigestion (mild dietary indigestion) consequences
-Anorexia, drop in milk production
– Rumen is full, firm, and doughy
– Primary contractions: decreased or absent, secondary contractions: decreased in strength
– Normal temp., heart rate, breathing rate, normal feces, but reduced in quantity
– Recovery usually is spontaneous within 24–48 hr
Lipid supplementation in ru
- Fat of animal origin ( tallow) up to 2% of DM is accepted (fat of fish origin - mammalian source is not allowed
anymore (BSE) 2. Lipid of plant origin (oils and seeds)
Consequences of lipid overload in ru
- protein, carbohydrate maldigestion
- ruminal C3 and C4 increases, C2decreases - abnormal motility
- milk protein decreases
Protected or “bypass” fat
types: fat treated with formaldehyde, microcrystalline, soya flour, Ca- soaps
Important: rate of protection shows negative correlation with the
utilization
PUFA-rich fat mammary gland TG uptake : LMF syndrome
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INHIBITING FACTORS OF FORESTOMACH MOTILITY
- Neurogen effects
a) central (sympathetic) effects decrease while parasympathetic effects increase the motility
b) peripherial (reflex) - Changes in the content of reticulorumen
a, physical/mechanical factors (fiber, sand, gas, temperature, strech – sympathetic effectes)
b, chemical factors
- pH<5.5 or pH>7.8 decreases motility
- toxic metabolites (ie. Amines, histamin derivates) - Other factors
a, blood constituents (NH3, VFA, glucose etc.) b, omasal obstruction
c, inflammatory processes (reticulo-peritonitis) d, decrease of the abomasal and duodenal pH
DISORDERS OF ERUCTATION causes
a, Generally: impaired forestomach motility (local inflammation, adhesion, stress)
b, Oesophageal spasm, obstruction, compression
c, Injury of the eructation reflex arc
DISORDERS OF RUMINATION
(regurgitation, remastication, reinsalivation, redeglutition)
Causes:
a, central (excitement, stress, fever, intoxication)
b, peripherial
- changes in the ruminal content - impaired forestomach motility
- organic causes (local inflammation, adhesion, stress)
