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what tends to fall within the rumen and what tends to fall within the reticulum

rumen - lighter materials - grass and hay
reticulum - heavier material like nails, grains, rocks


volatile fatty acids, can they move across mucosa, how much energy do they provide why transport important

can be directly absorbed across the mucosa into blood
provide more than 70% of dietary energy
continuous removal of VFA prevents acidification of the ruminal pH


what receptors in rumen involved with contractions and via what innervation

stretch receptors and chemoreceptors modulate contractions via vagul axons that reply signals to brainstem


what papillae found in newborns, what does exposure to roughage do to the papillae
what compounds stimulate papillary growth

rudimentary in newborn and suckling ruminants - exposure to roughage promotes development of papillae
proprionate, butyrate - produced by fermentation and possibly insulin-like growth factor-1


what does a high plane of nutrition, poor plane of nutrition and adequate fibre do to the ruminal papillae

high plane - production of abundant VFA - larger papillae to promote absorption
poor plane - small blunt papillae
fibre - 15% of diet - long slender papillae


High concentration rations with inadequate roughage what is the result for papillae and why, what else causes this

tumpy, club-shaped papillae that tend to form clumps, nodules and rosettes, especially in the ventral sac of the rumen
1) mucosa undergoes hyperplasia, hyperkeratosis and often hyperpigmentation
2) clumping is encouraged by hyperplasia of secondary papillae
Vitamin A deficiency in calvs can also cause hyperkeratosis of the forestomach mucosa.


what occurs when plant fibre or animal hairs adhere to forestomach mucosa - what is the disease called

contribute to mattered appearance may penetrate mucosa and cause inflammation - barley beef rumenitis in feedlot cattle


what is an appropriate pH for the ruminal fluid

5.5 - 7.5


what does overly dry ruminal content, excessively watery ruminal content, voluminous frothy content and acidic pH

1) dehydration
2) vagal indigestion or grain overload
3) primary bloat
4) grain overload (lactic acidosis)


what does ammoniacal odour and alkaline pH, ordour of cooked turnips or pugent insecticida smell, rancid odour and puterfied milk say about the animal during post mortem

1) urea toxicity
2) organophosphate poisoning
3) failure of the oesophageal groove reflex


what does lead flakes or motor oil, aromatic ordour and pine needles mean for the animal during post mortem and what other plant poisonings are there

1) lead poisoning
2) yew posioning - toxic alkaloids
runus spp. (plums, cherries, peaches, apricots, almonds) all contain hydrogen cyanide)


other things to look at during post mortem

the papillae, if any erosin, ulceration or scarring and how well the mucosa can be peeled away - adherence of the mucosa is abnormal and may reflec rumenitis or ruminal fibrosis


Bloat what is it, what are the types, mortality rate, what does it occur

dilation of the rumen, ruminal tympany
primary (acute) or secondary (chronic)
up to 50% mortality rate
rumen generates high amount of gas 30-50L per hour cows 5L per hour sheep and goat and if anything interferes with eructation can cause bloat


primary bloat what other name, what occurs, what most often associated with and what is the mechanisms

frothy bloat
acute condition of rumen in which stable foam forms preventing the eructation of gas - generally only small volume of unstable foam forms
often associated with succulent legumes (e.g. alfalfa and clover) (pasture bloat) -bloat within 1-3 days
1) succulents stimulate less saliva production
]2) increased viscosity of ruminal fluid -promotion of foam formation
3) soluble proteins released from legume chloroplasts are degraded by ruminal flora
4) rise to the surface of the ruminal fluid and become denatured and insoluble - stabilisation of the foam
5) legume acids also drop the ruminal pH to 5.4-6 (optimal for formation of stable foam)
6) failure of eructation
7) distension of the rumen
8) massive increase in intra-abdominal pressure 9) pressure on the diaphragm and lungs - dyspnoea - hypoxaemia
10) high intra-abdominal pressure +/- direct compression of the intra-abdominal caudal vena cava by the rumen also causes impaired venous return to the heart
11) circulatory failure with congestion of the distal hindlimbs


what other causes for primary bloat and mechanism

1) genetically predisposed because produce less saliva
2) in feedlot cattle feed on high concentrate and low roughage diets - onset of feedlot bloat is usually more gradual than that of pasture bloat
1) high concentrate/low roughage diets
2) decreased saliva production
3) a gradual change in the ruminal flora
4) increased bacterial production of polysaccharides
5) increased viscosity of the fluid - stable foam formation
6) as said before - failure of eructation etc.


post mortem findings of animals with primary bloat

1) sudden death - laying on back sawhorse posture
2) abdomen markedly distended by gas
3) dark, poorly clotted blood from orifices
4) pale muscles of proximal hindlimbs
5) bloat line in the oesophagus at the level of thoracic inlet
6) bulging diaphragm
7) lungs pale and compressed
8) bulky forthy contents in rumen however may disappear more than 10-12 hours after death


secondary bloat what is it why occurs and causes

usually chronic condition - episodes of acute - physical or functional obstruction preventing eructation of gas
1) physical obstruction of oesophagus by tumour, foreign body, stricture
2) fibrous adhesions, tumours, abseceses or peritonitis interfering with contraction rumem and reticulum
3) functional obstruction of oesophagus due to vagal nerve injury or organophosphate poisoning
4) excess indigestible roughage
5) failure of oesophageal groove reflex in bucket-feed calves


what are the post mortem findings for secondary bloat and what are the mechanisms behind the cause of excess indigestible roughage and failure of the oesophageal groove reflex for second what clinical signs and where may else see

as per primary but without stable foam formation and possible presence of physical obstruction
1) if digestible nutrients (starch, sugars) in the diet are inadequate, excess roughage cannot be digested and accumulates in the rumen and reticulum - distension - inhibition of contractions - failure of eructation
2) ruminal drinkers”) milk or milk replacer flows into the rumen - putrefaction - mild rumenitis and hyperkeratosis
- clinical signs include inappetence, recurrent bloat, abdominal pain and passage of clay-like faeces
- may see a similar problem in calves fed by stomach tube


what are the 3 main groups of foreign bodies that get lodges in rumen or reticulum, why- what species most common in

cows due to non-selective eating habits
1) trichobezoars = spherical masses largely composed of hair or wool
- more common in younger animals
- may be associated with inadequate dietary fibre, boredom, pica or skin disease (e.g. lice)
- may become impregnated with mineral
- usually incidental
2) phytobezoars = spherical masses largely composed of plant fibres
- may be due to rough feed or oral or dental disease that impairs mastication
- may become impregnated with mineral
- usually incidental
3) bezoars are only of importance if they are regurgitated to obstruct the oesophagus or if they obstruct the reticulo-omasal orifice, the abomasal pylorus or the intestines


what can foreign bodies, sharp objects and wood shavings or straw lead to

1) lead poisoning when dissolved
2) traumatic reticuloperitonitis
3) may cause diffuse mixed bacterial cellulitits


traumatic reticuloperitontitis what occurs what if incomplete perforation and penetration through the wall

sharp bodies may move into reticulum during contractions generally cranioventral direction, bacteria extend alon perforation track from reticulum
incomplete - often inconsequential but may cause focal suppurative or granulomatous inflammation in the wall of reticulum with minor overlying peritonitis
complete - acute local peritonitis - chronic local fibrosis - sometimes can be drawn back into reticulum


traumatic reticuloperitontitis what occurs if penetrate diaphragm, pericardial sac and what are some other sequels

diaphragm - pleuritis and pneumonia
heart - florid suppurative pericarditis and eventual right sided congestive heart failure
1) pentration of myocardium or artery - haemorrhage
2) penetration liver or spleen - abscessation
3) penetration reticulum wall - chronic suppurative inflammation in grooves resulting in vagus indigestion


Vagus indigestion what is it and what are the clinical signs

a clinical syndrome resulting from a physical or functional outflow obstruction of the forestomach or abomasum - distension of the rumen and reticulum
- characterised by persistent ruminal atony or irregular motility, gradual bilateral abdominal distension, inappetence and decreased milk production


List 6 causes of vagus indigestion

1) traumatic reticuloperitonitis
2) physical obstruction of outflow from the rumen/reticulum, omasum or abomasum
- e.g. foreign bodies, neoplasms, abscesses adjacent to the reticulo-omasal orifice
3) damage to the vagus nerve anywhere along its length (neck, pharynx, intra-thoracic, intra-abdominal)
4) degeneration of muscle in the wall of the oesophageal groove - flaccidity
5) pregnancy
- possibly due to displacement of the abomasum by the uterus
6) idiopathic


what are the post mortem findings of vagus indigestion and what is rumenitis

- rumen distended with watery fluid lacking odour; unmacerated food particles float on the surface of the fluid
- omasum can be very large and impacted with dry feed
- abomasum may be distended and impacted with dry feed
inflammation of the rumen


lactic acidosis what is it, where does it occur, what may it trigger, what what are survivors predisposed to

ruminal acidosis, grain overload, rumen overload, carbohydrate engorgement
most common cause of rumenitis
occurs in dairy and feedlot cattle, sheep and goats
- due to dietary overload with rapidly fermentable carbohydrate (e.g. grain, bread, root crops) or a sudden increase in the amount of carbohydrate in the diet - the amount of carbohydrate consumed is less important than the rapidity of the dietary change
- may trigger a severe acute metabolic disease - high morbidity and mortality
- survivors have chemical rumenitis and are predisposed to development of secondary infections with Fusobacterium necrophorum and/or fungi


what is the mechanism behind lactic acidosis

1) fermentation of the carbohydrate
2) increased VFA production
3) decreased ruminal pH
○ at a pH of ≤ 5.0, ruminal Gram-negative bacteria (which predominate in health) and protozoa die
○ streptococci (especially Streptococcus bovis) begin to proliferate and produce lactic acid - further decrease in the pH
○ at a pH of 4.5-5.0, streptococci then decline and lactobacilli proliferate
4) low pH  ruminal atony and reduced secretion of saliva ( decreased buffering of ruminal acid by salivary bicarbonate)
5) lactic acid acts osmotically
6) fluid moves from circulation into the ruminal lumen
7) ruminal distension and then diarrhoea
8) profound dehydration and hypovolaemic shock 9) death


post mortem findings of lactic acidosis what is diagnostic

1) a rumen pH


Secondary Bacterial Rumenitis (Necrobacillary Rumenitis)
when does it occur what occurs

- ruminants that survive a mild episode of lactic acidosis may develop secondary bacterial infection of the damaged ruminal mucosa
1) the necrotic lesions slough - ulcers
2) healing by granulation tissue - white stellate scars lacking papillae
3) embolism of infection via portal vein branches to the liver
4) multiple foci of coagulative necrosis that ultimately liquefy to form conventional hepatic abscesses (= hepatic necrobacillosis)


Secondary Fungal Rumenitis
what is it, how severe is it, what occurs, when to suspect

- mycotic infection of the rumen is most often a complication of lactic acidosis
- much more severe than necrobacillary rumenitis and often fatal
- fungal hyphae invade blood vessels of the ruminal wall - vasculitis, thrombosis and infarction, lesions are typically circular
- always suspect fungal infection if fibrinohaemorrhagic lesions extend from the ruminal mucosa to the serosal surface
- in fatal cases, most of the ventral sac of the rumen and parts of the reticulum and omasum are involved