Cattle 2 Flashcards
RDA what is it, 2 main types with typical history
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
What are the typical clinical signs and duration of onset for right displaced abomasum
- 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.
Right displaced abomasum cause and prognosis
- 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
Right displaced abomasum correction what are the steps within
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
Dietary abomasal impaction typical history and clinical signs
- 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
Dietary abomasal impaction treatment and prognosis
○ move impacted material with paraffin oil
○ surgery right paramediam approach
○ results often poor
Physical obstruction of the pylorus what generally due to and typical history
- 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
Physical obstruction of the pylorus typical clinical signs and treatment
- 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
Intestinal phytobezoars what size, what can result in, where harder to find
- 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
Intestinal phytobezoars common physical examination findings
○ 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
Intestinal phytobezoars treatment and prognosis
- 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
Intussusception signs and findings
- 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
Intussusception diagnosis and surgery what involved
- 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
Intestinal torsion what generally involve and findings
- 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.
Intestinal torsion diagnosis/treatment and prognosis
- 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
Dilation, volvulus and torsion of the caecum what occurs and what can look like
- 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
Dilation, volvulus and torsion of the caecum signs, treatment and prognosis
- 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
Definition of abdominal distension, bloat and drench
- “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
Principles in diagnosing abdominal distention
- 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
Left abdominal distention how common, what is most likely cause and the 3 main mechanisms
- 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
Left abdominal distention what causes bilateral and trilateral and does LDA cause
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
What are the 3 main diseases that cause abdominal distention and causes within
- Primary (Frothy) Bloat
- Secondary (Free Gas) Bloat
○ Acute
§ Recumbency
§ (Hypocalcaemia)
§ Oesophagealobstruction
○ Chronic
§ Simple Indigestion
§ Vagus Indigestion - Right sided distension (fluid)
○ Ascites
Bloat what type of problem, 3 main types and causes within
- 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!
Frothy bloat/pasture bloat which side distention and pathophysiology and things can do
○ 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
Frothy bloat/pasture bloat treatment 3 main types and when does bloat generally occur
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
Drenching cows with bloat what use, how much give and when see relief
□ “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
Stabbing cows with bloat (rumenotomy) when do, how perform and then what do
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
Pasture bloat prevention what are the 4 ways
1) diet - restrict pasture intake, fill animals on hay before putting on high risk pasture
2) oils
3) detergents
4) monensin
Oils to prevent pasture bloat how long work for, how give and what do in outbreak situation
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
Detergents to prevent pasture bloat what use, how give and how long give protection
□ Teric -> not as common ® Drench ® Bail ® May provide up to 12 hours protection ® Used to be common, but not so much any more
Monensin to prevent pasture bloat what is it, what does it do and types
□ 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
Monensin to prevent pasture bloat how used, what feed put in and do you use on horses
□ 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
Secondary bloat what need to do first and causes of acute secondary bloat and how to stop from dying
○ 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
Chronic secondary bloat how severe and the 5 main mechanisms
§ generally not severe
1) Dysfunction of oesophageal groove and eructation
2) Compression of oesophagus
3) Simple indigestion
4) vagus indigestion
5) tetanus
Chronic secondary bloat resulting from simple indigestion clinical findings, diagnosis and treatment
® 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
Chronic secondary bloat resulting from simple indigestion causes
® Causes ◊ Sudden change to diet ◊ Indigestible roughange; very wet grass; overheated, frosty or sour feeds ◊ Oral antibiotics ◊ Temporary disruption to fermentation ◊ Often self -limiting
Chronic secondary bloat resulting vagus indigestion what type of problem, distention of what structures, what occurs and causes
® 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
Secondary free gas bloat diagnosis/presentation
§ 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
Secondary free gas bloat treatment what are the 3 things needed and what do
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
Sykes drench what does it do and the ingredients within
- appetite stimulant -> drink more -> pass more
- Magnesium sulphate
- Ammonium sulphate
- Calcium hydroxide
- Cobalt sulphate
Post mortem bloat when occurs, why, and main thing to see
○ 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
Right abdominal distention without left, what is it, problems with what structures and differentials
- 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)
Ascites leading to right abdominal distention what part of, diagnosis how common and causes
○ 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
Abomasal volvulus what is it and presentation seen
○ Fluid, not gas ○ Right lower distension ○ Cow systemically sick § Off milk § Sunken eyes
Hydrops amnion and allantois what is it, how forms, what is the issue, presentation, treatment and prognosis
○ 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
What are the 4 other differentials for right abdominal distention
○ Oedema
§ Especially udder oedema- pitying oedema
○ Uroperitoneum (“waterbelly”)
§ Different profile and urea smell when tapped
○ Pneumoperitoneum
§ Palpably different, history
○ Subcutaneous swellings
Besides abdominal distention what are 3 other condition affecting the abdomen
- Abomasal ulceration
- Peritonitis
- Traumatic Reticuloperitonitis(TRP)
Abomasal ulceration incidence and the 4 types with cause
- 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
Abomasal ulceration typical history and clinical signs with main differentials
- 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
Abomasal ulceration how to differentaite that and intussusception
- 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
Abomasal diagnosis and treatment
- 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
Peritonitis how common, types, where lead from and treatment
- 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
Traumatic reticuloperitonitis pathogenesis
○ 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
Traumatic reticuloperitonitis presentation and treatment
- 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
Traumatic reticuloperitonitis prevention
○ Nonspecific
§ Maintain clean environment, avoid use of wire
§ Use only ‘clean’ feed
§ Feed from troughs rather than off ground
○ Specific
§ Magnets
Secondary rumen atony what occurs due to
- 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
Cows fever, neurtrophils, PCV and calcium levels
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
carbohydrate overload what are the 2 different conditions
1. “Rumenal acidosis” ○ “Grain Overload” ○ “Grain Poisoning” ○ “Lactic Acidosis” ○ Not always Grain ! 2. “SARA” – Sub acute rumen acidosis ○ Different condition
acute rumen acidosis history and when can occur
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
Concentrate feeding how much fed, sudden increases from and what is the main issue
- 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%)
Besides concentrate what are other rapidly fermentable carbohydrates
- Summer crops -> ○ Turnips ○ Canola ○ Stop from overdosing by using temporary fencing or limiting time on the feed - By Products ○ Brewers grain ○ Citrus pulp
Acute rumen acidosis pathogensis and the 6 steps within
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
What occurs in mild and severe cases of acute rumen acidosis and the 4 secondary effects
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
what secondary effects of acute ruminal acidosis in liver and lungs
- 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
acute rumen acidosis diagnosis the 4 main ways and how perform
- 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 - Rumen pH < 5
○ Can’t use dipstick as not low enough Ph detected - Smell of faeces “like a brewery”
- 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
What are the 4 stages of ruminal acidosis - EXAM
- Cow observed getting into grain
- Cow has diarrhoea/low rumen pH
○ Hasn’t progressed beyond the rumen yet - Cow has above + some systemic effects
- Cow is down
Stage 1 of acidosis treatment
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
Stage 2 and 3 of acidosis treatment
- 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 - Cow has above + some systemic effects
○ As above plus antibiotics
§ Broad-spectrum due to likely bacteraemia (Oxytetracycline for 5 days)
Stage 4 of acidosis treatment and what are 3 ancillary treatments
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
Rumen buffers what are the 3 main ones, how work and how often give
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)
Subacute rumen acidosis how different from grain overload and what present
- 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
Sub acute rumen acidosis presentation/clinical signs
- 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
What are the 3 indirect indictors of ruminal acidosis
- Chewing activity - probably not accurate
- Faces scoring
○ Score faecal pats - score 1-4, score 3 is perfect - Increase laminitis or lameness -> predisposed due to subclinical infection
Treatment for sub acute ruminal acidosis
- 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
What are the 5 ways to prevent rumen acidosis (both forms)
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!!
Virginiamycin
what is it, how to get and when used
- 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
Other rumen upsets besides ruminal acidosis
- Excessive roughage, very wet grass, mouldy, stale, sour feeds
- > Simple Indigestion
- Excessive protein
- > Nitrate or Nitrite toxicity
Treatment abdominal conditions what are the 4 things within
- 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
What decisions need to made in terms of fluid therapy with cows
1) what are we treating
- dehydration, acidosis or alkalosis
2) with what type
- isotonic, hypertonic
3) what route
- IV, oral
Fluid therapy what use to determine amount of dehydration, how precise, how much blood in cows and what is the aim
- 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
Acidosis or alkalosis for fluid therapy cows
- 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
Fluid therapy in older cows, how much can give over what period, often in combination with what and how given
- 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)
Parasitic gastroenteritis in cattle what are the 3 main parasites
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
What are the 7 main mechanisms of parasites in cattle and the examples of parasites that cause this
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
Parasites what are the main effects
- “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
Nematodes in what climates are what types present and where found
- Temperate climatic regions AU/NZ ○ Ostertagiaostertagi ○ T. axei ○ Cooperia spp - Northern coastal/tablelands NSW/QLD ○ Haemonchus spp HOT - abomasum - Haemonchus - Ostertagia - Trichostrongyles (and intestine)
Ostertagia (teladorsagia) how pathogenic, size, 2 main outbreaks and
- 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
Trichostrongylus axei size and look, where found, species, pathogenicity, main issue and what cause
- 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
Cooperia species where found, location, effect, how prolific and infective state
- 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
Nematode length of lifecycle what influenced by, which undergo hypobiosis
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
Dung pat environment for parasites why within, what is consistent and what occurs with ostertagia
○ 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
Laval migration out of dung pat, how large is this population, what is needed and what occurs
○ 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
parasite Syndromes what are the 4 main things they vary with
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
Sucking beef calves what is their relationship with parasites, do they need drench
○ 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
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
○ 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”
Yearling and older beef cattle when high risk for parasites and what shift in relationship with parasites
○ 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
In odlder beef cattle what is the main nematode disease, what occurs, trigger, presentation and time
§ 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
Drenching beef cattle when given
○ 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
Dairy calves how different from beef, what get instead and how controlled
- 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
What are the 4 main ways to diagnose nematodiasis
1) post mortem
2) faecal egg counts (larval culture) - EXAM
3) plasma pepsinogen
4) bulk milk ostertagia ELISA
