Bovine GIT 3

Question 1

Drooling saliva.

Answer 1

Can be a physical thing e.g. unable to swallow.
Can be a physiological thing e.g. pain/lesions in the mouth.
Common presentation for FMD.
May possibilities.

Question 2

Differentials for saliva loss in cattle.

Answer 2

Malignant catarrhal fever.
FMD.
Vesicular stomatitis.
Listeria meningoencephalitis (facial nerve paralysis).
Actinobacillosis (tongue lesions).
Calf Diphtheria (infection of mouth soft tissues).
Abscess/lesion in mouth.
NOT A COMPLETE LIST!

Question 3

Differentials for saliva loss in cattle.
- physical and toxic causes.

Answer 3

Buttercups/Rhododendron.
Organophosphorus toxicity.
Botulism.
Oral FB.
Pharyngeal FB.
Oesophageal FB.
Teeth problems.
Jaw fracture.

Question 4

1. Causative agent of Actinobacillosis?
2. Why is the incidence of Actinobacillosis less now?
3. What may possibly initiate the lesion?
4. Clinical presentation?
5. Tx?

Answer 4

1. Actinobacillus lignieresii.
2. Silage diet.
3. “Rough” forage.
4. Pain and swelling at tongue base, the cheek, or anywhere in the mouth.
   Involvement of local draining LNs.
5. 5-7d IM streptomycin.
   Traditional IV sodium iodide now no longer available.

Question 5

1. What is choke?
2. What kinds of things cause it?
3. Common site?
4. Clinical presentation?
5. Tx?
6. What may increase risk of choke?

Answer 5

1. Oesophageal obstruction by a FB.
2. Potato, fodder beet pieces, turnips, apples.
3. Just behind mandible or by thoracic inlet.
4. Profuse salivation and then bloat.
5. Gag, examine, manipulate (sedate?), stomach tube.
   Smooth muscle relaxant if necessary.
6. Teeth problems - can’t chew properly.
   Facial nerve paralysis.
   Brain abscessation causing inability to swallow.

Question 6

1. Causative agent of actinomycosis?
2. Prevalence?
3. Clinical presentation of actinomycosis?
4. Tx?

Answer 6

1. Actinomyces bovis.
2. Not common - found in nature cattle.
3. Hard painless swelling on jaw, may lead to dysphagia and weight loss.
4. Tetracyclines.
   Traditionally sodium iodide IV (no longer available).
   Must treat early for favourable Px.

Question 7

1. What is pasture bloat?
2. When does pasture bloat occur?
3. Presentation.
4. Pasture bloat epidemiology.

Answer 7

1. Rumen distension due to normal gas of fermentation trapped in a foam (cannot be educated).
2. Occurs soon after moving cattle to lush (legume) pasture.
3. Animals may be found dead (sudden death).
4. Rapid intro of lush pastures.
   Increasing UK problems due to increased interest in legumes.
   Particular problem in spring after rapid plant growth.
   Breeds - jersey more than Holstein.
   Young more than adults.
   Animals in good condition seem to be at a particular risk.

Question 8

1. Pasture bloat clinical signs .
2. Pasture bloat PM pathology.
3. Pasture bloat dx.

Answer 8

1. Within hours or a few days of access to pasture.
   Animals uncomfortable with mild colic signs.
   Abdominal distension (upper left side).
   Rumen hypermotility first then hypomotility.
   Tachypnoea, tachycardia, progressive resp./CV compromise»_space; DEATH within minutes of animal assuming lateral recumbency.
   Mortality high in animals without tx.
2. Rumen contents depends on time of PM.
   Caudal carcass pale.
   Cranial carcass congested and haemorrhagic.
   Lungs congested.
   Oesophagus pale in thorax and congested in cervical portion.
3. Based on clinical signs and Hx in living animal.
   Difficult at PM - always consider other causes of sudden death e.g. Anthrax.

Question 9

1. Pasture bloat tx.
2. Pasture bloat prevention.

Answer 9

1. Anti foaming agents.
   - Poloxalene (Bloat Guard).
   - Simethicone emulsion (Birp).
   - Oils.
   - Detergents.
   Give meds via stomach tube, dilute or wash down into rumen as necessary, take care to avoid inhalation.
   May inject anti-foaming agents directly into rumen in emergency.
2. Pasture management.
   Regular administration of anti-foaming agents.

Question 10

1. Cause of grain bloat?
2. What does grain bloat lead to?

Answer 10

1. Feeding high quantities of rapidly fermentable carbohydrate, esp. finely milled cereals.
   Grain overload.
   Seen in feedlots, grain beef systems and after breaking into feed stores.
2. Ruminal acidosis, metabolic acidosis.

Question 11

1. Clinical signs of grain bloat.
2. How is grain bloat diagnosed?
3. Tx of grain bloat?

Answer 11

1. Bloat, anorexia, dehydration, collapse, severe metabolic acidosis (tachypnoea, hyperpnoea), diarrhoea, death.
2. Hx, clinical signs, rumen pH, plasma pH or TCO2.
3. Emergency - rumenotomy to remove contents.
   Correct ruminal and metabolic acidosis and dehydration - may require IV fluids.
   Encourage feeding on forage
   Rumen function stimulants e.g. Pro-rumen or Vetrumex.
   Transfer of rumen contents from healthy cattle.
   Consider on-farm emergency slaughter.

Question 12

Free-gas bloat causes.

Answer 12

Anything that interferes with normal eructation.
- oesophageal obstruction.
- external pressure on oesophagus.
- pathology of the oesophagus or reticulum.
- conditions affecting smooth muscle function.
- poor management at weaning — may result in chronic rumenal tympany.

Question 13

Clinical signs of free-gas bloat.

Answer 13

Increased intraruminal pressure resulting in bulging of left sub-lumbar fossa.
Additional signs follow from increased abdominal pressure as for pasture-bloat.
Additional specific signs related to underlying aetiology.

Question 14

Free-gas bloat Tx.

Answer 14

Relieve obstruction or allow escape of gas by some other means.
- stomach tube.
- Probang.
- trocar and cannula.
- treat metabolic disease (milk fever).
- treat underlying cause.

Question 15

Chronic ruminal distension.

Answer 15

Abdominal enlargement.
Weight loss.
+/- diarrhoea.
(Post-weaning diarrhoea syndrome).
Most common after weaning of artificially reared calves.
Syndrome not fully understood.
Multiple cases.
Diet.
Impaired eructation e.g. enlarged thoracic LNs.
May be seen in adults due to other conditions:
- chronic reticular adhesions.
- “Vagal indigestion”.
- sand impaction.
- alimentary tract carcinoma.
- rumeno-reticular Actinobacillosis.

Question 16

Tx of chronic ruminal distension.

Answer 16

None.
Diet change.
Semi-permanent rumen fistula.
Indwelling trocar and cannula (“Red Devil”).

Question 17

1. Traumatic reticulitis cause.
2. Preventing traumatic reticulitis.
3. Consequence of traumatic reticulitis.

Answer 17

1. Eating wire/ other metallic FB while grazing or eating food.
   Wire 7-8cm in length - shorter pass through, longer will not be eaten.
   FB gets into reticulum.
   Perforation of reticular wall - often at time of calving > raised abdominal pressure.
2. Bolus magnets which hold onto metallic FBs.
3. Could impale the heart.
   - abscessation gas filled, pus fluid and gas in pericardium.

Question 18

Clinical signs of traumatic reticulitis.

Answer 18

Dullness, anorexia, agalactia, fever, anterior abdominal +/- thoracic pain, abduction of elbows, alimentary stasis and mild bloat, grunt.
Other signs associated with different locations.

Question 19

1. Exam of cow with traumatic reticulitis.
2. Diagnosis of traumatic reticulitis.

Answer 19

1. Elevated rectal temperature.
   Ruminal tympany.
   Rumen stasis or weak contractions.
   Abdominal pain, withers test, pole test, Williams test positive.
2. May be aided by haematology, U/S exam.

Question 20

1. Indications for runenotomy.
2. Anaesthesia / surgical site of a rumenotomy.

Answer 20

1. Remove FB.
   Exploration.
   Some poisoning cases.
2. Left paralumbar fossa.
   Paravertebral - T13, L1, L2.
   Local infiltration line blocks.
   May also need to sedate animal.

Question 21

1. Why are cases of DA likely to have increased over the past 60years.
2. Cows that are usually affected by DA.

Answer 21

1. The anatomy of a bovine abdomen has changed as they have been bred differently in order to yield more milk.
2. Postpartum dairy cows within 6w of calving.
   Bulls.
   Heifers.
   Dairy calves.
   Beef cattle.

Question 22

DA as a multifactorial disease.

Answer 22

Age, breed, sex, body condition, stillbirths/twins, season?
Other conditions:
- hypocalcaemia.
- ketosis.
- acidosis.
- retained foetal membranes.
- metritis.
Familial or sire effect.

Question 23

Clinical signs and Dx and Px of LDA?

Answer 23

Reduced milk yield (30-50%).
Reduced appetite esp. concentrate feeds.
Full CE.
- auscultation and percussion over ribs 9-13 on left.
- rectal exam.
- biochem - ketosis, hypochloraemic, hypokalaemic, metabolic alkalosis.
Good Px with adequate Tx.

Question 24

Clinical signs, diagnosis and prognosis of RDA.

Answer 24

Severe and life threatening.
Full CE:
- auscultation and percussion over ribs 9-13 on right.
- rectal exam.
Severe dehydration.
- biochemistry — ketosis, severe hypochloraemia, hypokalaemia, metabolic alkalosis.
May have total abomasal outflow obstruction.
Very sick animal may become shocked and die.
Very poor Px.
(Usually postpartum dairy cattle but others incl. calves).

Question 25

Abomasum position / gas and DA.

Answer 25

At calving - abomasum relative high on left. As lactation progresses - moves back towards midline. Gas within abomasum originated in rumen. Outflow of rumen content containing gas and VFA in cows fed high concentrate diets may cause abomasal atony. Abomasal pH rises postpartum: - increased rumen outflow - bacterial fermentation and gas production.

Question 26

Dry matter intake and DA.

Answer 26

Dry matter intake negatively correlated with BCS. Fat cows at risk of DA. DMI may have physical effects via rumen fill. Mediated via metabolic status. Monitoring DMI and rumen fill postpartum may be a useful method of detecting cow at risk of DA. Diet changes at parturition need to be undertaken slowly to allow adaptation of rumen microflora and rumen papillae.

Question 27

DAs are associated with changes in metabolism.

Answer 27

Cows with high beta-hydroxybuturates after calving are associated with DA. Negative energy balance resulting in ketosis increased risk. Hypoglycaemia and low calcium increase risk.

Question 28

Ketosis and DA.

Answer 28

Prevention of sub-clinical ketosis very important if DA to be prevented. Manage body condition to maximise DMI. Optimise transition cow nutrition. Monitor situation (1:3 cost:benefit ratio shown in Canada) Use of monensin resulted in a 40% drop in both DA and clinical ketosis in one Canadian study undertaken on 45 farms.

Question 29

Feeding practices and DA.

Answer 29

Everything possible should be done to maximise DMI in periparturient cow. - palatable forage. - ad lib. - minimum competition. - may warrant a separate management group.

Question 30

Individual animal risk factors for DA.

Answer 30

Breed, sex, age. Milk yield - probably an indirect effect on nutrition. Over-fat body condition at calving. Reduced DMI in immediate postpartum period. High genetic merit cattle - poss familial effect. Dystocia / stillbirths. Twins. Intercurrent diseases: - ketosis. - excessive fat mobilisation. - hypocalcaemia. - retained foetal membranes. - periparturient infections including mastitis and metritis. - endotoxaemia. - acidosis leading to reduced DMI.

Question 31

Preventing DA in the individual.

Answer 31

Ensure cows dried off in optimum body condition and remain in condition until calving. Monitor rumen fill in cows around parturition. Monitor for signs of acidosis. Monitor for ketosis including subclinical ketosis and treat rapidly. Monitor for hypocalcaemia including subclinical. Prevent and/or treat hypocalcaemia. Prevent and/or treat RFM, metritis and mastitis around calving. Consider NSAIDs in Tx of periparturient cows. Consider not breeding replacement heifers from cow lines that appear to have a particular problem with DA.

Question 32

Preventing DA in herd.

Answer 32

Manage ration transition carefully from dry to lactation, introducing rapidly fermentable energy sources slowly. Feed some concentrates prior to calving to allow ruminal adaptation. Adequate fibre of sufficient length in diet. Maximise DMI in postpartum period. Palatable feed and water ad lib to periparturient cows. Supplement antioxidants in herds known to have a problem with vitamin E/Selenium deficiency. Metabolic profiles 7-10 days before and after calving to monitor nutritional status. Use faecal scores to assess ration. Select bulls to reduce dystocia problems.

Question 33

Other absomasal conditions.

Answer 33

Ulceration: - common. - adults. - calves. Impaction: - primary — straw, sand. - secondary — neurogenic or mechanical e.g. peritonitis.

Question 34

Other abdominal conditions.

Answer 34

Small intestinal obstruction: - intussusception. - “gut-tie”. Caecal dilatation and torsion: - aetiology similar to LDA/RDA. - gut stasis. - Sx Tx. Others: - fat necrosis. - neoplasia. - pneumoperitoneum. - peritonitis/abdominal abscesses.