Biochemical disorders of the rumen Flashcards
(39 cards)
Physiology of rumen function
Rumen juice
• Contents: o 80-90% water ▪ Feed, water and plasma ▪ Saliva daily is 90-160 L Chewing, swallowing, rumen homeostasis pH is 8.2-8.7 (and contains Na+, HCO3 and HPO4) Recirculation of N material Contains fibre o pH: 6.3-7.1 Can degrade VFA and NH3 o Temperature 39-40 ̊C o Anaerobic conditions o Rumen homeostasis
Regulation of acid-base household in the rumen
• Natural feeding: rumen pH: 6,3-7,1
• Too much carbohydrates: many organic acid– pH decreases
• pH influences life of microbials, species content, activity
• Carbohydrate (grain) feeding pH 2.8-3.0 would be metabolic acidosis but
o Compensatory mechanism
o Saliva production: 60-180 1/day (pH:8.1), NaHCO3 1-1.2 kg/day, Na2HPO4 0.2-0.25
kg/day
o = buffering 5-6 kg volatile fatty acid daily
• NPN feeding or protein overload leads to formation of NH3 which results in metabolic alkalosis
Examination of ruminal content
- Tubing
- Transcutaneous punction, rumenocentesis
- Fecal lipopolysaccharides measurement
- Ruminal fistula
- Milk Fatty Acid Pattern
- Blood Gas Analysis, Urine Netto Acid base Excretion
- Intraruminal bolus: Indwelling pH Data Logging
Forestomach disorders
Classification
• Localization
o diseases affecting more forestomach compartment (rumen)
o diseases affecting one forestomach
Forestomach disorders
Course
- Peracute: a few hours – 2 days
- Acute: 3-14 days
- Subacute: 2-4 weeks
- Chronic: > 4 weeks
Forestomach disorders
Pathological process
• Primary
o Biochemical disorders
o Motoric disorders
• Secondary
Forestomach disorders
Diseases of the forestomach
• Biochemical disorders
- Rumen overload and dilatation
- Simple indigestion
- Ruminal alkalosis
- Ruminal acidosis
- Ruminal tympany (bloat)
- Ruminal putrefaction
Rumen overload and dilatation
Aetiology
- Suddenly much rough fodder (too tasty, much fibre or unusual)
- Running away, hunger, lack of drinking, frozen or mouldy feed
Rumen overload and dilatation
Pathogenesis
• too much feed leads to ruminal dilatation and overload, obturated cardia and smooth muscle spasm and pain
• improper digestion, mixing leads to biochemical disorder
• lack of belching, rumination leads to gas accumulation which will compress the diaphragm
vena cava
• respiratory and circulatory failure occurs and then asphyxia
• prolonged biochemical disorder leads to shock
Rumen overload and dilatation
Clinical signs
- Restlessness, colic
- Salivation, retching
- Dyspnea (labial) breathing, cyanosis, tachycardia
- Tense, overfilled abdomen (left flank)
- Ruminal statis, compact (thick), sedimented ruminal content
Rumen overload and dilatation
Diagnosis
- History and clinical signs
* Probing shows only few gas and thick content
Rumen overload and dilatation
Differentials
1. Other biochemical disorders o triad: feeding history o typical clinical signs o examination of the ruminal fluid 2. Diseases with sudden death o Cyanide poisoning, “fog fever”, methemoglobinemia 3. Diseases with abdominal distension
Rumen overload and dilatation
Treatment
- Analgesics, spasmolytics
- Emptying the rumen with tube and lavage with rumenotomy (Götze technique)
- Follow-up care includes dietetic feeding (see: simple indigestion)
Simple indigestion of the rumen (indigestion simplex ingestae ruminis)
Etiology and Pathogenesis
• Feeding abnormalities leads to
a) quantitative-qualitative b) change of the feed→disorder of adaptation c) technological problems (e.g. lack of cribs or water) d) trace elements: (--Co; ++ Mn and ++Cu)
Leads to
• Dysfunction of ruminal microorganisms
• Slow-down of biochemical processes
• Lack of ruminal protein and vitamin synthesis and VFA
Later metabolic products (NH3 and lactic acids)
Simple indigestion of the rumen (indigestion simplex ingestae ruminis)
Clinical signs
• Not remarkable, but often appear as a herd problem:
o Milk: (–) amount, (–) fat content
o Anorexia; weight loss; mild, but long-lasting deterioration
o Mild digestive disorders: (–) rumination, (–) rumen motility
▪ Moderate ruminal tympany
▪ Small, firm, doughy rumen
o Inactive ruminal fluid
Simple indigestion of the rumen (indigestion simplex ingestae ruminis)
Diagnosis
• Rather by exclusion of other diseases « triad
Differentials
• According to the triad (from biochemical disorders)
• Secondary forestomach disorders
• Primary motoric disorders
Other organic symptoms
Simple indigestion of the rumen (indigestion simplex ingestae ruminis)
Treatment and Prevention
- Good quality food: molasses, sugar beet, hay, grass
- Ruminal digestive: yeast, rumen juice, Ruminogen pulv. A.U.V., Diernhofer mixture, rumen extract (Simulex A.U.V.), probiotics (Probios por A.U.V)
- Loosening of the rumen content: water, mineral oil, salt laxatives
- Elimination of feeding abnormalities
Ruminal alkalosis / putrefaction
Etiology
RA:
(++)NH3
RP:
(++)NH3, toxic amines
Ruminal alkalosis / putrefaction
Pathogenesis
RA: Feeding failures (too much protein NPN substance)→ alkalic ruminal content, NH3 gets into circulation
RP: Putrid bacteria (E.coli, Proteus) from surroundings or overgrowth in the rumen leads to alkalic ruminal content and NH3 and biogenic amines get into circulation and damages other organs
Ruminal alkalosis / putrefaction
Clinical signs
RA:
General and digestive signs
RP:
Same general and digestive signs but + nervous signs
Ruminal alkalosis / putrefaction
Ruminal fluid analysis
RA:
Moderate abnormalities
RP:
Expressed abnormalities
Ruminal alkalosis / putrefaction
Diagnosis and differential diagnosis
According to the triad (from biochemical disorders)
Ruminal alkalosis / putrefaction
Treatment
- Controlling ruminal pH (carbohydrate) vinegar, lactic acid 2. Antihistamines and flunixin meglumine maybe
- Antibiotics (neomycin, oxytetracycline) po.
- Sol. contra alkalosi/putrefaction FoNoVet
- parenteral fluid/electrolyte replacement
- Evacuation of the rumen
AFTER-CARE: fresh rumen juice, hay, fermentable carbohydrates, probiotics, Ruminogen pulvis A.U.V. (sugar beet, molasses)
(Acute) Ruminal acidosis (acidosis ruminis acuta)
Etiology and Pathogenesis
• High carbohydrate (Streptococcus bovis and Lactobacillus) and D-lactic acid (butyric acid) and shift in microflora
• Local changes
o (–) rumen pH (butyric acid)
o Mucosal damage
o (++) osmotic concentration
o (++) carbon dioxide concentration
• Systemic changes
o Metabolic acidosis
o (–) saliva production (buffer)
o Parenchymal organ degeneration o Paralysis of medullar centre
• Other consequences
o Bacterial toxins→parenchymal organ degeneration
o Biogenic amines→(++) permeability of vessels, laminitis
o Ethylene alcohol → toxic sings