Cattle 2

Question 1

RDA what is it, 2 main types with typical history

Answer 1

Abomasal dilation and torsion - generally dilation then torsion
- “RDA” = right displaced abomasum
- “RTA” = right torsion of the abomasum
- Many vets use them synonymously because dilations become torsed, and then the cow is sick
○ Blood supply to abomasum is occluded
- Typical History
○ A recently calved cow that is suddenly “off her milk” - pathognomonic
○ Looks sick, abdominal pain

Question 2

What are the typical clinical signs and duration of onset for right displaced abomasum

Answer 2

• Typical Clinical Signs
  ○ Vary with severity – the blood supply is compromised
  ○ A high-pitch ping, high up on the right side
  ○ Little or no milk in udder
  ○ Sometimes palpate abomasum per rectum
  ○ Sometimes melena (bad prognosis) - BAD
  ○ Sometimes heart rate high heart rate - over 120-150bpm - BAD
  PROGNOSTIC
• a very acute condition
  ○ the heart rate rapidly increasing up to 160 per minute.
  ○ peripheral circulatory failure ‐ the animal feels cold, mucus membranes pale.

Question 3

Right displaced abomasum cause and prognosis

Answer 3

• Cause
  ○ Probably similar to that of LDA (but it’s less common)
  ○ Abomasal atony results in a distended abomasum.
  ○ The distended abomasum can become displaced in a dorsal direction
  ○ The displaced abomasum and attached structures may rotate – compromising the blood supply
• Prognosis -> uncomplicated displacement surgically is good if volvulus prognosis is guarded at best

Question 4

Right displaced abomasum correction what are the steps within

Answer 4

a. Assess prognosis - >melena and HR >100 are bad signs when corrected - euthanasia
b. IV fluids if very shock
c. If fairly early, can correct torsion by “rocking” ‐ sweeping action
§ if very distended, may need to drain via large needle with rubber tube attached - need to be careful
§ Know when fixed, when untwist then gas leaves and disappears
d. Standard closure
e. Antibiotics and NSAIDS

Question 5

Dietary abomasal impaction typical history and clinical signs

Answer 5

• Typical History:
  ○ Cows fed large amounts of poor quality roughage
  ○ complete anorexia
  ○ very scant faeces
  ○ and a distended abdomen
• Typical Clinical Signs:
  ○ heart rate, respiratory rate commonly rise
  ○ expiratory grunt due to abdominal distension.
  ○ the impacted abomasum palpated in the right lower quadrant of the abdomen

Question 6

Dietary abomasal impaction treatment and prognosis

Answer 6

○ move impacted material with paraffin oil
○ surgery right paramediam approach
○ results often poor

Question 7

Physical obstruction of the pylorus what generally due to and typical history

Answer 7

• Due to intestinal phytobezoars from plants such as onion weed
• Typical History:
  ○ cattle which are grazing on country which contains large amounts of onion weed
  ○ sudden depression in milk yield
  ○ Mild distended abdomen

Question 8

Physical obstruction of the pylorus typical clinical signs and treatment

Answer 8

• Typical clinical signs
  ○ a gradual distension of the abdomen
  ○ fluid splashing detected in the lower right flank
  ○ in many cases a solid lump can be detected on ballottement on the lower right abdomen ‐ this is usually a phytobezoar.
  ○ faeces scant and pasty.
• treatment
  ○ surgical approach ‐ low right flank incision
  ○ standing or cast
  ○ open over phytobezoar and remove
  ○ suture mucous membrane lining of abomasum separately from muscle layer

Question 9

Intestinal phytobezoars what size, what can result in, where harder to find

Answer 9

• smaller phytobezoars pass into the small intestine.
• may cause obstruction at any site along the small intestine
• Harder to find as hidden within omentum
• Less severe unless cause volvulus or intussusception

Question 10

Intestinal phytobezoars common physical examination findings

Answer 10

○ sudden severe depression in milk yield.
○ dehydration.
○ commonly a very small amount of greenish rumen discharge observed at nares of affected animals
§ GREEN NASAL DISCHARGE INDICATION FOR LAPORAOTOMY -> intestinal blockage
○ ballottement/auscultation right abdomen ‐ may detect fluid splashing sounds.
○ rectal examination ‐
§ early stages the amount of faeces is reduced and somewhat pasty
§ Later, grey yellow faeces ‐ extremely pasty, very foul smell ‐ pathognomonic
○ as condition progresses
§ dehydration increases
§ heart rate increases

Question 11

Intestinal phytobezoars treatment and prognosis

Answer 11

• Treatment - removal
  ○ Right paralumbar approach as cranial as possible
  ○ Careful search of intestines - palpation
  § duodenum a common site, but can be anywhere.
  ○ Incise over phytobezoar, remove and close intestine ‐ double layer inturning suture using O Dexon.
• Prognosis -> good in early case but worsen the longer the condition is left untreated

Question 12

Intussusception signs and findings

Answer 12

• signs with an intussusception more severe and more acute in onset than those seen with a phytobezoar.
• Findings
  ○ initially, colic may be observed by farmer
  ○ completely off milk, complete anorexia.
  ○ the pulse becomes increasingly fast and weak.
  ○ as condition progresses, dehydration increases.
  ○ faeces reduced in amount ‐
  § animals start to pass blood and mucus with the faeces - MELENA
  § soon only small quantities of tenacious blood stained faeces
  on rectal examination may be possible (20% of cases) to palpate lesion per rectum ‐ banana shaped

Question 13

Intussusception diagnosis and surgery what involved

Answer 13

• Diagnosis -> presence of pings in the right caudal abdomen and the presence of distended loops of bowel on rectal palpation
• Surgery
  ○ Usually need fluid and supportive therapy
  ○ right paralumbar approach, paravertebral
  a. identify intussusception
  b. try and gently pull it apart
  c. alternatively, resect affected area
  d. end to end anastomosis, using simple interrupted
  e. crushing sutures 0 Dexon (long acting absorbable) -> longer functional life than catgut

Question 14

Intestinal torsion what generally involve and findings

Answer 14

• Generally involved volvulus of the small intestines (+ large intestine) around the root of the mesentery
• Finding
  ○ abdominal pain ‐ the colic soon disappears
  ○ the heart rate becomes elevated, respiration is laboured and the mucus membranes are pale.
  ○ auscultation ballottement right abdomen elicits splashing sounds
  ○ distended loops of bowel may be detected on a rectal examination.

Question 15

Intestinal torsion diagnosis/treatment and prognosis

Answer 15

• Diagnosis/treatment -> exploratory laparotomy
  ○ identify twist at root of mesentery, or may involve only part of intestine. attempt to correct twist
• Prognosis
  ○ Good if no dying tissue and catch early, generally by the time they are presented it is poor

Question 16

Dilation, volvulus and torsion of the caecum what occurs and what can look like

Answer 16

• dilation of the caecum usually precedes caecal torsion.
  ○ simple caecal dilation is not a surgical problem.
• In volvulus, the apex of the cecum is rotated cranially and caecal body becomes distended
• Rotation of the caecum along its long axis is caecal torsion – which may occur around the base of the caecum and may involve the distal ileum, caecum and colon.
• Can look like LDA -> prognostic factors the same

Question 17

Dilation, volvulus and torsion of the caecum signs, treatment and prognosis

Answer 17

• Signs
  ○ anorexia and abdominal pain.
  ○ right flank becomes distended - USUALLY DISTEND ON THE LEFT (rumen)
  ○ very scanty faeces. auscultation percussion right abdomen ‐ a high pitched resonant “ping” high in the right paralumbar fossa.
  ○ rectal ‐ dilated apex of the caecum detected in pelvic cavity.
• treatment
  ○ Right paralumbar fossa laparotomy exteriorise apex of caecum, drain (small incision), then exteriorise until get to the twist
  § May need to get whole caecum out to get to base where twist is but easier if deflated at this point
  ○ correct torsion or volvulus
• Prognosis
  ○ If twist easily then generally do well otherwise risk of secondary complications

Question 18

Definition of abdominal distension, bloat and drench

Answer 18

• “Abdominal distension”
  ○ The term usually reversed for abdominal enlargement due to causes other than simple obesity
• “Bloat”
  ○ What farmers call abdominal distension, but also the name of a specific condition
• “Drench”
  ○ give something orally
  ○ give an anthelmintic by any means

Question 19

Principles in diagnosing abdominal distention

Answer 19

• What is distended
  a. left, right or both sides?
  b. Is it acute or chronic
  c. Is it air or fluid ?
  d. Infectious, traumatic or metabolic ?
• Air or fluid ?
• a “ping” means trapped air

Question 20

Left abdominal distention how common, what is most likely cause and the 3 main mechanisms

Answer 20

• Most common
• Likely the rumen (possibly a displaced abomasum)
• Mechanisms:
  a. Cannot belch gas
  § Free Gas Bloat
  § Obstruction of oesophagus -> if any fluid over cardia it WILL NOT OPEN -> will die of bloat before it opens
  § Recumbency -> lateral recumbency is an emergency -> the cardia is in liquid at this point
  b. Rumen not contracting
  § Actinobacillosis of rumen/reticulum
  § Simple Indigestion
  § (Acidosis)
  c. Reduced outflow from rumen
  § Vagus indigestion
  § (Dietary Abomasal Impaction -already covered)
  § (Intestinal Phytobezoars-already covered

Question 21

Left abdominal distention what causes bilateral and trilateral and does LDA cause

Answer 21

Bilateral
- Bilateral abdominal distension is generally just a progression from left sided distension
Trilateral
- Left, right and cranial
- Problem is that once the rumen can go no further laterally -> It expands cranially and squashes the lungs -> death
LDA -> DOES NOT CAUSE BLOAT
- Cranial so behind ribs and therefore do need distend, increase pressure result in bing

Question 22

What are the 3 main diseases that cause abdominal distention and causes within

Answer 22

1. Primary (Frothy) Bloat
2. Secondary (Free Gas) Bloat
   ○ Acute
   § Recumbency
   § (Hypocalcaemia)
   § Oesophagealobstruction
   ○ Chronic
   § Simple Indigestion
   § Vagus Indigestion
3. Right sided distension (fluid)
   ○ Ascites

Question 23

Bloat what type of problem, 3 main types and causes within

Answer 23

• Is a ‘herd problem’, if one cow has it, others are at risk
  1) Primary Rumen Tympany
  ○ “Frothy Bloat”, “Pasture Bloat”
  ○ Foam covers cardia so gas cannot escape
  2) Secondary Rumen Tympany
  ○ “gaseous bloat”
  ○ Acute
  § Recumbency
  § (Hypocalcaemia)
  § Oesophagealobstruction
  ○ Chronic
  § Simple Indigestion
  § Vagus Indigestion
  3) Post Mortem Tympany
  ○ Cows stop eructating at death!

Question 24

Frothy bloat/pasture bloat which side distention and pathophysiology and things can do

Answer 24

○ Starts on the left side but eventually extends to the right side 
○ Pathophysiology 
§ Cow eats a large amount of Grass
§ Reaction in the rumen causes foam production
§ Foam blocks entrance of oesophagus to rumen
- prevention 
§ Cow can’t Belch
§ Gas keeps being produced
§ Cow Bloats
- Bloat oil, stomach tube 
§ Rumen squashes lungs
Cow dies of respiratory failure
- Emergency - STAB

Question 25

Frothy bloat/pasture bloat treatment 3 main types and when does bloat generally occur

Answer 25

1) drenching cows with bloat 2) tubing cows with bloat - stomach tube - can also treat for obstruction 3) stabbing cows with bloat (rumenotomy) ○ When does bloat occur § “ruins a nice day” § Within 20 mins of access to bloaty pasture § Especially if they haven’t been fed for a while (ie after milking) § High moisture content, high clover content pasture

Question 26

Drenching cows with bloat what use, how much give and when see relief

Answer 26

□ “oil calms water” and disperses the bubbles. □ Any (mineral) oil (paraffin oil), and most detergents. (Registered products preferably!) □ Give about 100 - 200mls oil. □ Detergent dose varies - start with 40mls □ Relief in about 10 minutes

Question 27

Stabbing cows with bloat (rumenotomy) when do, how perform and then what do

Answer 27

when in respiratory distress □ Farmer advice ® A life saving measure - not a treatment ® Left side middle of the flank ◊ There are intestines on the right side ® Use trochar and canula (tube) if possible ◊ If need to stab with pocket knives -> stand to the side and don't want the hole to be too large (hard to stitch up) -> stitch rumen to abdominal wall which will heal eventually and leave hole ◊ Likely to cause peritoneal infection -> DRAINAGE IS IMPORTANT ® Antibiotics ® Vet possibly (depending on hole size) □ Remember ® The hole can block up but only need enough gas out so that the cow can breathe again ® Drench her with bloat oil then

Question 28

Pasture bloat prevention what are the 4 ways

Answer 28

1) diet - restrict pasture intake, fill animals on hay before putting on high risk pasture 2) oils 3) detergents 4) monensin

Question 29

Oils to prevent pasture bloat how long work for, how give and what do in outbreak situation

Answer 29

``` Work for 2- 4 hours □ Drench the cow □ Add to water □ Flank application (they lick it off) □ Spray on paddock - in outbreak situation ® Use 100mls Bloat oil per cow ® Use 1 part Bloat oil to 40 parts water ® Spray the paddock starting at one end ® Put the fence up when the tank runs dry □ Tympanyl (can be used) - mix practice ```

Question 30

Detergents to prevent pasture bloat what use, how give and how long give protection

Answer 30

``` □ Teric -> not as common ® Drench ® Bail ® May provide up to 12 hours protection ® Used to be common, but not so much any more ```

Question 31

Monensin to prevent pasture bloat what is it, what does it do and types

Answer 31

□ Ionophore antibiotic (no withholding periods but 7d ESI) □ changes the ratio of volatile fatty acids produced in the rumen □ main use is to improve feed efficiency (also prevention of coccidiosis) □ it also decreases rumen methane gas production and reduces the amount of stable foam produced during fermentation □ Types ® Powder -Mixed in with the feed ◊ Short lasting effect ® Bloat Capsules ◊ Last 100 days ◊ 80% effective ◊ Need to remove plastic cap otherwise won't work ◊ Have a number on the capsule so you know if eructate then can know what number cow come from to replace

Question 32

Monensin to prevent pasture bloat how used, what feed put in and do you use on horses

Answer 32

□ Often added to the grain ration fed to dairy cattle ® Increases propionic acid production ® Prevents coccidiosis in young stock □ Typically occurs in feed at 11-18mg/kg (dairy) or 25-33mg/kg (beef) □ Very Very toxic for horses ® Horses 20 times more sensitive than cattle (200x more than chooks!) ® Heart and skeletal muscle death from mitochondrial dysfunction

Question 33

Secondary bloat what need to do first and causes of acute secondary bloat and how to stop from dying

Answer 33

``` ○ Need to find primary cause AND TREAT THAT -> stop dying from ○ Acute § can be mild or severe § Causes □ ANY recumbency □ Oesophageal obstruction ® Turnips (when too small often swallow whole - obstruction, if large will chew) ® applies, gold balls, potatoes ® Often stuck near base of heart □ Hypocalcaemia Treatment § Treat underlying condition □ Buscopan - off label ® Hyoscine ◊ N-butyl bromide 4 mg/mL, dipyrone500 mg/mL ◊ Smooth muscle relaxant ◊ Use in cattle is off label ```

Question 34

Chronic secondary bloat how severe and the 5 main mechanisms

Answer 34

§ generally not severe 1) Dysfunction of oesophageal groove and eructation 2) Compression of oesophagus 3) Simple indigestion 4) vagus indigestion 5) tetanus

Question 35

Chronic secondary bloat resulting from simple indigestion clinical findings, diagnosis and treatment

Answer 35

® Clinical findings ◊ Off milk (chronic indicator), Off feed, Reduced rumination but cardinal signs normal ◊ Abdominal discomfort, Faecalchanges, mild bloat ® Diagnosis ◊ Based on history and clinical signs ◊ Differentiate from serious conditions ◊ History & Examination, Revisit if necessary ® Treatment ◊ Epsom salts (MgSO4) several times a day to encourage rumen emptying ◊ Alkalizing agents if excessive grain involved ◊ Vinegar if excess protein involved ◊ Cud transfer ? ◊ Palatable, quality feed

Question 36

Chronic secondary bloat resulting from simple indigestion causes

Answer 36

``` ® Causes ◊ Sudden change to diet ◊ Indigestible roughange; very wet grass; overheated, frosty or sour feeds ◊ Oral antibiotics ◊ Temporary disruption to fermentation ◊ Often self -limiting ```

Question 37

Chronic secondary bloat resulting vagus indigestion what type of problem, distention of what structures, what occurs and causes

Answer 37

® An OUTFLOW problem ◊ At either end of the abomasum ® Progressive distension of Rumen/Reticulum ® Vagal nerve dysfunction - often secondary ◊ Runs along both sides of the oesophagus and terminates in branches that innervate the forestomach and abomasum -> many areas for disruption ◊ Causes } Rumenitis and Peritonitis (impact vagal nerve) } DECREASE OUTFLOW TO ABOMASUM

Question 38

Secondary free gas bloat diagnosis/presentation

Answer 38

§ Gradual onset of disease § Abdominal distension, often with large rumen gas cap § Hypermotility of rumen (3-6 contractions per minute, but weak and ineffective) -> ONLY ONE IF BLOATY AS WELL □ Often funny sounding -> ineffective contraction □ DIFFERENTIATE FROM SIMPLE INDIGESTION § Ventral rumen sac enlarges –L shape, can feel per rectum § Sometimes, bradycardia (40bpm) § Small quantities of pasty or runny faeces -> simple indigestion -> normal faeces

Question 39

Secondary free gas bloat treatment what are the 3 things needed and what do

Answer 39

``` 1) Address Primary cause □ Peritonitis, obstruction, rumenitis □ Antibiotics / anti-inflammatories ® Antibiotics - oxytetracycline, TMS ® Anti-inflammatories ◊ Useful because they } Reduce inflammation (!) } Act as painkillers –which may increase appetite and exercise - short acting - flunixin, long acting - meloxicam ◊ NOT PHENYLBUTAZONE! - FORBIDDEN 2) Stimulate rumen contractions □ Feed, appetite stimulants, drugs - skyes drench 3) Rumenotomy □ Emptying and cud transfer ```

Question 40

Sykes drench what does it do and the ingredients within

Answer 40

- appetite stimulant -> drink more -> pass more - Magnesium sulphate - Ammonium sulphate - Calcium hydroxide - Cobalt sulphate

Question 41

Post mortem bloat when occurs, why, and main thing to see

Answer 41

○ Cows will bloat after death ○ They generally stop eructating ○ Bloat line on the oesophagus (line where rumen has prevented blood flow in the distal part of the oesophagus) § If present then had bloat premortem

Question 42

Right abdominal distention without left, what is it, problems with what structures and differentials

Answer 42

- Looks different because it’s fluid, not gas - ASCITES - Generally problems with caecum, abomasum or uterus a. Abomasal impaction or volvulus (already covered) b. RDA /cecaltorsion (already covered) c. Other obstructions (phytobezoars) (already covered) d. Ascites e. Hydrops amnion or allantois f. Uroperitoneum g. Extra abdominal swellings (eg Udder Oedema)

Question 43

Ascites leading to right abdominal distention what part of, diagnosis how common and causes

Answer 43

○ Generally part of an oedema/pleural effusion/ascites complex ○ Diagnosis -> Fluid thrill on percussion; fluid on abdominocentesis ○ Less common in cattle than dependent oedema (submandibular, ventral) ○ Causes -> Liver disease, cardiac disease, abdominal mesothelioma

Question 44

Abomasal volvulus what is it and presentation seen

Answer 44

``` ○ Fluid, not gas ○ Right lower distension ○ Cow systemically sick § Off milk § Sunken eyes ```

Question 45

Hydrops amnion and allantois what is it, how forms, what is the issue, presentation, treatment and prognosis

Answer 45

``` ○ Fluid in the uterus “Dropsy” ○ Hydrallantois § Rapidly forms in last trimester § A uterus problem § Cannot feel placentomes - rectal diagnosis ○ Hydrops amnion § Gradual accumulation over months § A fetal problem § Can usually feel placentomes - rectal diagnosis ○ Tx = Calving induction or surgery ○ Often poor prognosis ```

Question 46

What are the 4 other differentials for right abdominal distention

Answer 46

○ Oedema § Especially udder oedema- pitying oedema ○ Uroperitoneum (“waterbelly”) § Different profile and urea smell when tapped ○ Pneumoperitoneum § Palpably different, history ○ Subcutaneous swellings

Question 47

Besides abdominal distention what are 3 other condition affecting the abdomen

Answer 47

1. Abomasal ulceration 2. Peritonitis 3. Traumatic Reticuloperitonitis(TRP)

Question 48

Abomasal ulceration incidence and the 4 types with cause

Answer 48

- Incidence -> as high as 97% in dairy cows at slaughter, 1% asymptomatic dairy cows, 3% feedlot cattle - not common - 4 types: ○ Type 1: Erosions and non-perforating ulcers ○ Type 2: Ulcers with profuse intraluminal bleeding ○ Type 3: Perforated with local peritonitis ○ Type 4: Perforated with diffuse peritonitis - Uncertain aetiology - Common

Question 49

Abomasal ulceration typical history and clinical signs with main differentials

Answer 49

- Typical history: ○ Sick/depressed (anaemia -> look like they don't have the energy) ○ Decreased milk yield ○ Loss of condition - Typical clinical signs ○ Internal haemorrhage -> melaena § variable anaemia, increased HR, RR ○ Signs associated with blood loss and bleeding and -peritonitis - main differential -abomasal ulcer or intussusception

Question 50

Abomasal ulceration how to differentaite that and intussusception

Answer 50

- more severe ulceration ○ impaired appetite and ruminal function, ○ decreased milk yield and loss of condition. ○ ulcer may erode into a blood vessel -variable haemorrhage occurs. ○ Perforation of the abomasal ulcer may occur and lead to an acute diffuse peritonitis

Question 51

Abomasal diagnosis and treatment

Answer 51

- Diagnosis: Pallor of mucous membranes; malaena; colic - Treatment: Poor prognosis–advise immediate slaughter if no concurrent peritonitis (otherwise carcass condemned - bad - NEED TO DETEMRINE); knackery if there is ○ Cannot give proton pump inhibitors (like small animal or horse)-> no research on if it works

Question 52

Peritonitis how common, types, where lead from and treatment

Answer 52

- Commonly diagnosed in cattle - Possibly common in cattle! - Peracute, acute or chronic - Local or diffuse - Contamination of abdomen from ○ Uterus ○ GI tract ○ Surgery ○ Urinary tract ○ Liver abscesses - Treatment ○ antibiotics and anti-inflammatories

Question 53

Traumatic reticuloperitonitis pathogenesis

Answer 53

○ Intake § Twist their tongues around grass and eat it whole, with minimal chewing § Regurgitate and chew § THEREFORE -> since ruminant don't chew food when taken in -> foreign materials like rocks, nails and wires can be swallowed -> ALSO DON'T SPIT (hard to remove foreign body) □ Generally then sink into reticulum and can stay there for life ® If reticulum squeeze a piece of wire may penetrate through the chest/heart -> Localised peritonitis ◊ Vomiting indicates forestomach dysfunction ◊ Wire often corrodes away and is not found -> generalised peritonitis (serous fibrin tags - red generally) -> pleuritis/pericarditis -> pitting oedema -> failure of venous return

Question 54

Traumatic reticuloperitonitis presentation and treatment

Answer 54

``` - Presentation ○ Anorexia and fall in milk production ○ Acute abdominal pain may be suspected if... § Abdominal guarding & thoracic respiration § Immobility and shuffling gait § Positive Grunt test - Treatment ○ Conservative § Antibiotics (oxytetracycline) § Restricted movement § Magnets § Symptomatic Tx with fluids and diet ○ Aggressive § Rumenotomy to remove wire and break adhesions § Lavage and drain pericardium/pleura ```

Question 55

Traumatic reticuloperitonitis prevention

Answer 55

○ Nonspecific § Maintain clean environment, avoid use of wire § Use only ‘clean’ feed § Feed from troughs rather than off ground ○ Specific § Magnets

Question 56

Secondary rumen atony what occurs due to

Answer 56

``` - can also occur when it is not the main problem Endotoxin -> dehydration, tachycardia - forestomach hypo-motility or atony - fever - decrease systemic O2 delivery - weakness, diarrhoea - leukopenia (neutropenia) - decrease cardiac output and hypotension - hypoxaemia ```

Question 57

Cows fever, neurtrophils, PCV and calcium levels

Answer 57

Cows generally cannot hold a high temperature for long Neutrophils -> not ideal due to low reserve, will generally decrease after acute PCV -> 0.12 should get blood transfusion, 0.07 can still be standing Calcium - <2 BAD -> low albumin leading to low calcium (most calcium bound to albumin but cannot be used in this form) Haemorrhage as PCV and protein low

Question 58

carbohydrate overload what are the 2 different conditions

Answer 58

``` 1. “Rumenal acidosis” ○ “Grain Overload” ○ “Grain Poisoning” ○ “Lactic Acidosis” ○ Not always Grain ! 2. “SARA” – Sub acute rumen acidosis ○ Different condition ```

Question 59

acute rumen acidosis history and when can occur

Answer 59

History - sudden introduction (intentional or not) of CHO - sudden increase in intake of CHO - Sudden decrease in fibre - Increase can be relative rather than absolute When can occur - Cow gets into feed where she shouldn't have, cow doesn't eat so cow afterwards get double in the dairy

Question 60

Concentrate feeding how much fed, sudden increases from and what is the main issue

Answer 60

- Australian dairy cows are commonly fed 5-15kg concentrates per day ○ Production of saliva is important to lubricate for the large amount of concentrates - Half that as a bolus during milking twice a day - Facilities vary – individual vs trough feeding - Additives help reduce the risk of acidosis - Sudden increases from ○ errors in feeding ○ introduction of cows into a herd where individual feeding not possible ○ previous cow did not eat - BUT -> main grazing/diet is uncontrolled in the paddock (65-80%)

Question 61

Besides concentrate what are other rapidly fermentable carbohydrates

Answer 61

``` - Summer crops -> ○ Turnips ○ Canola ○ Stop from overdosing by using temporary fencing or limiting time on the feed - By Products ○ Brewers grain ○ Citrus pulp ```

Question 62

Acute rumen acidosis pathogensis and the 6 steps within

Answer 62

Pathogenesis - Readily fermentable CHO -> lactic acid ○ Rumen pH normally 5.5 – 7.0 (diet dependent) - Local rumen effect ○ Microflora and ruminitis ○ Kills the bacteria that removes the lactic acid due to the low pH ○ The bacteria that produce more lactic acid remain -> cycle increase lactic acid - Systemic effect ○ Dehydration, Acidosis, Laminitis ○ Water drawn into gut lumen due to increase solids (lactic acid) Steps 1. Access to soluble carbohydrate ○ Relative – not absolute amount matters 2. Soluble CHO causes growth of Strep bovis 3. Strep bovis produces lactic acid 4. pH drops to below 5 5. Bacteria/protozoa that use lactate die 6. Secondary problems due to acidosis and dehydration - Mild -> Severe

Question 63

What occurs in mild and severe cases of acute rumen acidosis and the 4 secondary effects

Answer 63

``` Mild cases - Chemical Ruminitis -> meant to be higher pH ○ Don't have the protection that the abomasum has Severe cases - Increase in decrease in pH - Favours strep bovis - Increase lactate ○ Further decrease pH § Severe rumenitis and acidosis ○ ALSO increase osmotic pressure Diarrhoea -> fluid accumulation in gut Secondary effects 1) liver 2) lungs 3) rumen - fungal ruminitis, common cause of LDA 4) bacteraemia - embolic miliary hepatitis ```

Question 64

what secondary effects of acute ruminal acidosis in liver and lungs

Answer 64

- Liver ○ Haematogenesises spread of bacteria and fungi to liver ○ Meant to filter blood -> grab bacteria by macrophages ○ Abscesses - Lungs ○ Thrombus of CaVC ○ Haematogenous spread to lungs ○ Lung abscesses ○ Erode into pulmonary blood vessels Haemorrhage, epistaxis -> death -> VENA CAVAL SYNDROME

Question 65

acute rumen acidosis diagnosis the 4 main ways and how perform

Answer 65

1. Rumen tap ○ To collect rumen contents to test pH ○ Need to use long needle and aspirate via syringe ○ Landmarks § Paralumbar fossa (left) § Not too far back - legs § Not too far forward - ribs 2. Rumen pH < 5 ○ Can't use dipstick as not low enough Ph detected 3. Smell of faeces “like a brewery” 4. Undigested grain in faeces (if it was grain) ○ Cow is not eructating it and chewing it properly ○ Even when this does occur -> bacteria not digesting properly

Question 66

What are the 4 stages of ruminal acidosis - EXAM

Answer 66

1. Cow observed getting into grain 2. Cow has diarrhoea/low rumen pH ○ Hasn't progressed beyond the rumen yet 3. Cow has above + some systemic effects 4. Cow is down

Question 67

Stage 1 of acidosis treatment

Answer 67

Observe and give rumen buffer drench ○ Types § MgO MgCO3 - Alkalinizer – powder vs granulated □ Continues to increase pH -> goes beyond neutral pH □ BAD -> Flows to the abomasum -> meant to be low pH now will increase ® Meant to kill bacteria -> kill salmonella before flow through □ GOOD -> Works more quickly than below § NaHCO3 - Buffer □ If add to solution to acidic environment will make more alkaline -> etc □ May not act as quickly as needed as get closure to neutral slows down § Possibly use 50:50

Question 68

Stage 2 and 3 of acidosis treatment

Answer 68

2. Cow has diarrhoea/low rumen pH ○ Drench with MgO/ MgCO3 / NaHCO3 ○ 1-2 cups in some water bid ○ Twice per day for 3-4 days - ONCE HAS CLINICAL SIGNS 3. Cow has above + some systemic effects ○ As above plus antibiotics § Broad-spectrum due to likely bacteraemia (Oxytetracycline for 5 days)

Question 69

Stage 4 of acidosis treatment and what are 3 ancillary treatments

Answer 69

``` 4. Cow is down ○ As above plus NSAIDs (Tolfenamic acid - long duration of action) , Fluids ○ ? how much fluids and what type ? -> 2L hypertonic fluids + 20L water oral with or without NaHCO3 - IF NOT DEHYDRATED, if dehydrates isotonic fluids ○ Consider rumenotomy ○ Careful of water Ancillary treatments - Penicillin into the rumen - Thiamine - Calcium - downer cows need calcium ```

Question 70

Rumen buffers what are the 3 main ones, how work and how often give

Answer 70

1) Sodium Bicarbonate ○ “Buffer” ○ A normal component of bovine saliva ○ Add about a cup to some water and drench several times per day 2) Magnesuim Oxide, Magnesium Hydroxide, Magnesium Carbonate ○ Similar treatment regimes ○ “Alkalising agents” rather than buffers – don’t overdo it 3) Hay ○ If the cow will eat, hay is a great buffer - it adds fibre and Bicarbonate (via saliva)

Question 71

Subacute rumen acidosis how different from grain overload and what present

Answer 71

- Different condition from “Grain Overload” ○ A herd problem rather than an individual problem - just caused by diet not being ideal ○ Rumen pH 5-5.5 ○ Acetate/propionate/butyrate -> toward butyrate ○ Dominance of G-ve bacteria ○ Protozoa still present

Question 72

Sub acute rumen acidosis presentation/clinical signs

Answer 72

- Herd problem due to diet - Reduced rumenation (cud chewing) - Mild diarrhoea - Foamy faeces containing gas bubbles ○ Decreased contraction of the rumen - Undigested grain in faeces - Reduced Milk Fat (<3%) - often how presented

Question 73

What are the 3 indirect indictors of ruminal acidosis

Answer 73

1. Chewing activity - probably not accurate 2. Faces scoring ○ Score faecal pats - score 1-4, score 3 is perfect 3. Increase laminitis or lameness -> predisposed due to subclinical infection

Question 74

Treatment for sub acute ruminal acidosis

Answer 74

- Fibre in Diet - Particle Length - Bolus feeding of grain - Eskalin (Virginiamycin) - SARA is a subclinical herd problem – treatment and prevention are essentialy the same thing

Question 75

What are the 5 ways to prevent rumen acidosis (both forms)

Answer 75

``` 1. Change the feed slowly ○ Start at less than 4kg/day if possible § 2kg twice per day ○ Change by less than 20% every few days 2. Buffers in feed ○ NaHCO3 / MgO in grain ○ May predispose to milk fever in preparturient cows 3. Eskalin in feed (Virginiamycin) ○ Need vet prescription ○ Takes 2 weeks to work ○ Kills S. bovis selectively 4. Tylosin in feed ○ Prevents secondary hepatic abscessation ○ Became a prescription animal remedy in 2014 5. Get the diet right!! ```

Question 76

Virginiamycin | what is it, how to get and when used

Answer 76

- Trade name Eskalin® - A streptogramin antibiotic (same “family” as macrolides and lincosamides) - A prescription only remedy ○ Need a “Medicated Feed Order” from a veterinarian § Different to prescription and drug label ○ Vets still have prescribing responsibilities! - Concern about inducing antibiotic resistant bacteria in human medicine

Question 77

Other rumen upsets besides ruminal acidosis

Answer 77

- Excessive roughage, very wet grass, mouldy, stale, sour feeds - > Simple Indigestion - Excessive protein - > Nitrate or Nitrite toxicity

Question 78

Treatment abdominal conditions what are the 4 things within

Answer 78

- Some ancillary treatments in common ise: 1) Sykes Drench - appetite stimulant 2) ketol § Bypasses rumen into abomasum splitted into glucose 3) Tympanyl § Likely in the cow to treat horses - good to treat bloat 4) Fluid Therapy

Question 79

What decisions need to made in terms of fluid therapy with cows

Answer 79

1) what are we treating - dehydration, acidosis or alkalosis 2) with what type - isotonic, hypertonic 3) what route - IV, oral

Question 80

Fluid therapy what use to determine amount of dehydration, how precise, how much blood in cows and what is the aim

Answer 80

- Eye position - most commonly the only one used - Assessment is not precise in adult cattle - Cattle are ~8% blood = 40 litres - Maximum IV rate is about 40mL/kg/Hr (half blood volume per hour) - Often use oral fluids as well as IV in ruminants - Often the aim is “improvement” rather than “cure

Question 81

Acidosis or alkalosis for fluid therapy cows

Answer 81

- Unlike calves, most dehydrated adult cows have a normal or alkaline blood pH - If not lactic acidosis or severe diarrhoea, then likely alkalosis - Need to avoid oral fluids containing bicarbonate

Question 82

Fluid therapy in older cows, how much can give over what period, often in combination with what and how given

Answer 82

- Cows are often treated “on farm” - Can only give 5-8 litres of fluids in 20 minutes ○ This can be enough to get a cow to a point where they stand and drink - Often in combination with “hypertonic” fluids How done - A practical method of treatment is 2 - 3 L of hypertonic saline (4 ml/kg BW) intravenously (over at about four minutes) plus 20 L of water administered by stomach tube (use a aggers pump) - Can add some bicarbonate in grain overload cows - Be careful of hypertonic fluids in very dehydrated cows (as distinct from endotoxic shock) - don't use - MUST follow up with oral fluids (water is ok)

Question 83

Parasitic gastroenteritis in cattle what are the 3 main parasites

Answer 83

``` 1. Nematodes ( roundowms) ○ abomasum, intestines, lungs ○ most important type in cattle 2. Cestodes (tapeworms) ○ Intestines - Little importance 3. Trematodes (flukes) ○ liver and rumen ○ Important in limited areas ```

Question 84

What are the 7 main mechanisms of parasites in cattle and the examples of parasites that cause this

Answer 84

``` 1. Reside in gut lumen absorbing nutrients ○ Eg. Tapeworms 2. Penetrating and destroying mucosal cells ○ Eg. Ostertagia 3. Feeding on mucosa ○ Eg. Trichostrongylus 4. Sucking Blood ○ Eg. Haemonchus 5. Physical obstruction ○ Eg. tapeworms, large roundworms 6. Other organs 7. Hypersensitivity ```

Question 85

Parasites what are the main effects

Answer 85

- “Clinical” and “Sub- clinical” effects - Weight loss, diarrhoea, dehydration, death - Loss of productivity ○ Growth rate, milk production, feed intake/conversion, reproductive performance, immune responses ○ Appetite suppression at low levels of larval challenge

Question 86

Nematodes in what climates are what types present and where found

Answer 86

``` - Temperate climatic regions AU/NZ ○ Ostertagiaostertagi ○ T. axei ○ Cooperia spp - Northern coastal/tablelands NSW/QLD ○ Haemonchus spp HOT - abomasum - Haemonchus - Ostertagia - Trichostrongyles (and intestine) ```

Question 87

Ostertagia (teladorsagia) how pathogenic, size, 2 main outbreaks and

Answer 87

- Most pathogenic nematode per worm - Small –up to 9mm - Outbreaks ○ Type I ○ Type II - Abomasum Effects - Ostertagia in the abomasum: a. Worms emerge from gland◦ b. Large nodular lesions c. Reduced parietal cells d. Reduced acid e. Increased abomasal pH f. -> Incoming bacteria and protozoa not killed g. -> pepsinogen ⇏pepsin -> protein not digested h. protein loss into abomasum

Question 88

Trichostrongylus axei size and look, where found, species, pathogenicity, main issue and what cause

Answer 88

- Small thin reddish brown (up to 5.5mm) - Abomasum - Affect sheep also - Highly prolific - Moderate pathogenicity - Infective larvae may develop in 4-6 days and can live 4-6 months ○ Quick infection rate - Feed on mucosa –ulcers and infections

Question 89

Cooperia species where found, location, effect, how prolific and infective state

Answer 89

- Species variation ○ C. punctata; C. pectinatain Australia ○ C. oncophera; C. punctatain NZ - Small intestine without adhering to wall - just sit and ingest the ingesta ○ Act like tapeworm -> do very little damage - Do not suck blood ○ Less pathogenicity ○ More “resistance” to anthelmintics ○ Increasing importance - Most prolific egg producers - faecal egg count in placed with this - useless - Infective larvae within 4 days

Question 90

Nematode length of lifecycle what influenced by, which undergo hypobiosis

Answer 90

``` Length of life cycle - Delay between parasites on pasture and clinical disease - Dung pats hold high numbers of larvae - Not all released at once ○ Rainfall ○ Temperature ○ Oxygenation Reliant on 2 main things 1) dung pat 2) larval migration - Hypobiosis - ostertagia ```

Question 91

Dung pat environment for parasites why within, what is consistent and what occurs with ostertagia

Answer 91

○ Most nematodes are in dung -> anoxic environment and moist ○ Contamination of a paddock with eggs/larvae may be consistent through a year § emergence from dung pats is not -> has to be the right environmental conditions ○ Eg - Ostertagia: § Delay in hatching 4-12 days in summer; 34-68 in winter § Drying out and temp critical for survival □ 21-47% larvae in May-October dung □ 2-5% December -March Desiccation and dying of dung pats in summer -> DECREASE AVAILABILITY OF LARVAE ON PASTURE

Question 92

Laval migration out of dung pat, how large is this population, what is needed and what occurs

Answer 92

○ Free living stages is next largest population of nematodes ○ Migration needs contiguous water films and T ○ 50 -100mm rain over >2 days ○ Eggs deposited over time may emerge together ○ Disease syndromes vary with climate and management Mild weather in north - worms available for longer time during the year

Question 93

parasite Syndromes what are the 4 main things they vary with

Answer 93

``` 1) Age ○ Young vs sold 2) Management ○ Beef Cattle - stays within the same paddock longer ○ Dairy Cattle - rotational grazing often - reinfection rate is lower 3) Climate ○ Tropical/temperate 4) Species ```

Question 94

Sucking beef calves what is their relationship with parasites, do they need drench

Answer 94

○ Most calves have eggs in faeces by weaning ○ Little evidence that anthelmintics increase weight gain ○ Establishment and effects are reduced on milk diet ○ Most beef calves are first drenched at weaning

Question 95

Weaned beef cows when is high risk for parasites, what is the main nematode disease occuring, how occur and what leads to in the body

Answer 95

○ their first spring is a high risk time ○ (age will depend on calving and weaning times) ○ “Type I Ostertagaisis” § Rapid infection large numbers of larvae over 4-8w □ Larvae enter gastric glands and undergo growth -L4 □ They emerge 3-4w later as adults § Worm burdens of ½ million § Damage to parietal cells -> pH rise, decreased pepsinogen, epithelial damage, mucosal permeability □ Plasma protein leaks into lumen; pepsinogen leaks in to blood □ Leakage of plasma proteins -> hypoalbuminemia; peripheral oedema □ Damage to abomasal wall -> diarrhoea and “morocco leather gut”

Question 96

Yearling and older beef cattle when high risk for parasites and what shift in relationship with parasites

Answer 96

○ Toward end of spring (13 -20 months old)\ ○ Immunity increases and environmental signals § Egg counts drop (<10epg) § Not much change in total worm numbers § Shift toward hypobiosis □ (hypobiosis= inhibited or arrested development) § Hypobioticlarvae mostly non-pathogenic § Can be 80-90% of total population

Question 97

In odlder beef cattle what is the main nematode disease, what occurs, trigger, presentation and time

Answer 97

§ Type II Ostertagiasis □ Synchronous resumed development of hypobioticlarvae □ Mechanism/trigger not well understood □ Individual predisposition □ Small % of a mob □ Older animals: 2 -4 yo - generally quite sick □ Late Summer onwards

Question 98

Drenching beef cattle when given

Answer 98

○ January drenches are common - most of the worms on farm at this point are IN THE COWS (desiccation on the paddock) ○ Pre -calving drenches are common - better for management as harder to get in once calved ○ Always drench the bulls ○ Drenching adult cattle is a good idea

Question 99

Dairy calves how different from beef, what get instead and how controlled

Answer 99

- Different syndromes from beef - Calves weaned typically 8-12 weeks old - Calves reared on the same pastures every year (why?) ○ May get carry over of worms and coccidia - Reinfection from calves –“calf pat” - Exposure to pasture = exposure to worms - Parasitic gastroenteritis is common - Controlled with anthelmintics - generally deworm once per year - don't die from parasites

Question 100

What are the 4 main ways to diagnose nematodiasis

Answer 100

1) post mortem 2) faecal egg counts (larval culture) - EXAM 3) plasma pepsinogen 4) bulk milk ostertagia ELISA