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Discuss indigestion
- Due to sudden dietary changes causing rumen microflora changes and stasis
- Present with anorexia, reduced milk production, reduced rumen contractions and diarrhoea
- Diagnose with history and exclusion of forestomach dysfunction with rumen fluid sampling (normal pH with decreased protozoa)
- Spontaneous recovery with good-quality hay and vitamin B supplementation
Discuss bloat
- Excess accumulation of gas in rumen, causing severe distension of rumen and subsequent left paralumbar fossa
- Primary/frothy (pasture) or secondary/gaseous (free gas) bloat
Describe primary/pasture bloat
- Excessive production of gases and raising of rumen fluid viscosity, causing stable and persistent foam (i.e. cannot be relieved by stomach tube)
- Associated with feeding of lush, immature, rapidly growing legumes, such as clovers and lucerne (pasture bloat), or finely ground grain (feedlot bloat)
- Present with bellowing, frequently lying down and getting up, kicking at ventral abdomen, respiratory distress, excessive salivation, tongue protrusion and death
- PM = bloat-line in oesophagus
- Perform emergency rumenotomy or drench with antifoaming agent (e.g. pluronic/alcohol ethoxylate-based bloat drench and paraffin, mineral or vegetable oil) and remove from source
Describe secondary/gaseous bloat
- Chronic or recurrent accumulation of free gas in dorsal sac of rumen due to physical or functional defect in eructation of free gas
e.g. enlarged lymph nodes, tetanus, milk fever or prolonged lateral recumbency
Distinguish diagnosis of primary and secondary bloat
- Pass tube easily, but no gas → frothy bloat
- Tube does not pass → oesophageal obstruction
- Tube passes with resistance and releases gas → oesophageal compression or distortion of cardia
- Tube passes easily and releases gas → hypocalcaemia, ruminal stasis, failure to clear cardia, tetanus, rumenitis or weakened contractions due to over-distension of rumen
Discuss rumen acidosis
- Sudden unaccustomed ingestion of large quantities of carbohydrate-rich feeds (e.g. grain, concentrates, potatoes or bread)
Describe the pathogenesis of peracute rumen acidosis
Rumen pH = < 5.0 and lactic acid upto 300mmol/L;
1. Rapid fermentation of carbohydrates and less saliva buffering
2. Excess VFA production → rumen pH drops
3. Streptococcus bovis and Lactobacillus produce lactic acid → severe ruminal acidosis
4. Rumen becomes hypertonic → fluid shifts into rumen → dehydration
5. Low pH reduces rumen motility → stasis and mild bloat
6. Lactate absorbed into blood → metabolic acidosis
7. Severe acidosis and dehydration can lead to death
8. Chemical rumenitis allows Fusobacterium necrophorum invasion → liver abscesses
9. Abnormal fermentation products cause vasoconstriction → laminitis
List clinical signs of peracute rumen acidosis
- Present within 8hr of excess carbohydrates ingestion
- Anorexic, dull, weak and ataxic
- Signs of colic and tooth grinding (bruxism)
- Increased HR (120 bpm)
- Rumen motility decreased • and distended
- Fluid-splashing or tinkling sounds on ballottement/auscultation of distended rumen
- Profuse foul-smelling diarrhoea (sweet-sour odour), which may contain whole grains
- Dehydration (enophthalmos, congested mucous membranes)
- Nervous signs of staggering, head pressing, posterior paresis and recumbency
Discuss treatment of peracute rumen acidosis
- Administer alkalinising agents via stomach tube with procaine penicillin
- Provide free access to good-quality grass hay
- Perform rumen transfaunation to re-populate rumen
- Rumenotomy and rumen lavage (severe cases)
Describe subacute rumen acidosis (SARA)
- Rumen pH 5.0-5.5
- Due to increased concentrate to forage ratio, causing increased propionate and butyrate with reduced acetate
- Present with intermittent diarrhoea with undigested food particles, reduced milk fat, reduced cud chewing (< 50%) and increased lameness
- Perform rumenocentesis
- Ensure carbohydrate-rich diet with adequate effective fibre (eNDF) and additives (e.g. buffers, neutralising agents, oral antibiotics or rumen modifiers)
Discuss traumatic reticulo-peritonitis (hardware disease)
- Penetration of reticular wall by sharp foreign body
- Present with anorexia, sudden reduced milk production, rumen tympany, reluctant to move, high fever, shallow respiration, inappetence and constipation
- Perform exploratory laparotomy and rumenotomy or give oral magnet with antibiotics
Discuss vagus indigestion
- Chronic in adult cattle
- Due to vagus nerve damage, mechanical impairment of motility or oesophageal groove dysfunction
- Left abdomen distension (palpable per rectum L-shaped/'ten-to-four') with reduced appetite, weight loss, reduced faecal output or diarrhoea and bradycardia (pathognomic)
- Relieve distension with stomach tube, perform rumenotomy or rumen fistulisation (chronic cases)
Classify vagus indigestion
1. Obstruction of the oesophagus or cardia with accumulation of free gas in rumen
2. Failure of omasal transport
3. Failure of abomasal outflow with reflux of abomasal secretions (HCl) into rumen