Cattle 5 Flashcards
Clinical signs for milk fever what divided into and how change/vary
Three (progressive non -discrete) stages described
- Stage 1
- stage 2
- stage 3
but:
1. They are overlapping
2. They are interfered with by farmer treatment - COMMON
- Most milk fever cows I have seen have already had some calcium
- Generally you tell farmers
3. Cows may have more than a single disease concurrently
4. Response to i/v calcium is often used as the basis for diagnosis!
What are the clinical signs in stage I and 2 of milk fever - EXAM
- Stage 1
○ Excitable
○ Hypersensitivity & tremors
○ Progressive ataxia
○ Rumen stasis
○ Cows acting strangely in the yard and rumen may have ‘pings’ (due to build-up of gas) - Stage 2
○ Sternal recumbency & depressed (S shaped neck)
○ Rumenal stasis & bloat (dry faeces)
○ Uterine inertia (if calving)
○ Dull and depressed and often won’t get up
What are the clinical signs in stage 3 of milk fever - EXAM
○ Lateral recumbency - EMERGENCY
○ Flaccid paresis
○ Tachycardia (heart very quiet)
○ Bloat (regurgitate contents)
○ Hypothermia
○ Often look dead and inhalation pneumonia is common
§ Therefore any cow in lateral recumbency - ANTIBIOTICS
What are 5 other differentials for a cow that is milk fever
1. Acute toxic mastitis ○ They have mastitis 2. Calving paralysis ○ Been up since calving, musculoskeletal exam 3. Grain overload ○ Smell of faeces, rumen pH 3. Other infections (uterine, peritonitis …) ○ History and clinical exam 4. Grass Tetany ○ Mentation - hyperactive 5. Fat cow syndrome ○ Ketones
Milk fever how what are the 6 steps in treatment and what recommend for different outcomes
1) Check to make sure no mastitis or other causes then quickly give:
2) Calcium borogluconate - IV
3) NSAIDS if the animal has been down or it’s very cold
§ Makes the more likely to try and get up THEREFORE MORE LIKELY TO LIVE
4) antibiotics if the cow has signs of other disease or if she has been in lateral recumbency
5) Then …Wait 5 -10 minutes (while you pack up your things)
6) Try to get the cow up. +/ -hip lifters.
§ If the cow does not get up, suggest re -treat/assess in 6 hours and treat as a “downer cow”.
§ If she does get up, recommend no or partial milking for 24 hours, and possibly a treatment of s/c or oral calcium at milking time to prevent relapse.
Calcium borogluconate when give, main types, properties and the 2 main ways to administer
- any down cow ○ Types - 4 in 1 or just calcium ○ Soluble in water - (relatively) non-irritant 1) Subcutaneous Calcium - most common farmer treatment 2) IV - do as the vet
Giving subcutaneous calcium to a down cow who generally does this, how to do and general advice
§ probably most common “farmer treatment” of milk fever
§ best to warm calcium to body temp (if cold vasoconstriction occurs) - just put in a hot bucket of water
§ ideally <125mls per site but most ignore this
§ over ribs is better than over shoulder
□ Tissue reaction won’t cause lameness
§ farmers expect vets to give calcium IV!
§ general advice “Give 2 packs, and 2 hours and call me if she is not up”
Giving IV calcium how give, requirement, how long over, safe rate and when reach point how give remainder
§ Give IV slowly, whilst listening to the heart - slows and gets louder
□ If hear ectopic beats -> stop for a minute
□ Do again until more ectopic beats -> STOP NOW FOR GOOD
§ Typical requirement is 1-1.5 mls per kg
§ Ideally give over 15 -20 minutes.
§ The “safe” rate of infusion is less than what flows through a 14g needle!
§ Give the remainder s/c
Individual level prevention for hypocalcaemia
- Supply calcium at or just before calving
○ s/c or oral
○ Labour intensive - Inject Vitamin D3 2-8 days before calving
○ 10 ml injection
○ Need to know when they will calve -> if doesn’t calve in this time then will produce cells that aren’t absorbing calcium - BAD so may need to give again - Correct transition feeding –DCAD (dietary cation anion difference)
○ [(Na+K)-(Cl+S)] or some other similar formula
○ In practical terms:
§ Avoid potassium
§ Provide chloride (Anionic Salts)
§ Add Mg
○ DCAD can be measured by feed testing companies –use lowest DCAD hay pre-calving
Non-parturient hypocalcaemia what also called, when occurs
Transit tetany”
- Cows on lush grass (oxalates, nitrates)
- Occasionally cows who have not recently calved become hypocalcaemic
How to transition feed appropriately to prevent metabolic conditions after parturition
○ Restrict green pasture in the 2 weeks before calving
○ Feed to appetite good quality hay low in K (lowers the DCAD)
○ Supplement with Mg
○ feed anionic salts/concentrate pellet combination for 10 days prior to calving
○ Anionic salts in water
○ Ensure that sufficient dietary calcium after calving
§ Grain is low in calcium
§ Most farmers who feed >4kg grain per day add 30g MgO and 1% to 2% limestone to the ration.
Grass tetany what is the issue, characterised by and pathogenesis/cause
HYPOMAGNASAEMIA
- Grass tetany, grass staggers
- Characterised by - hyperexcitable -> tetany & convulsions –death
○ Can occur in clumps -> come out one morning to 5 cows dead
- Combination of nutritional deficiency & metabolic factors ⇒reduced magnesium availability or increased loss
○ Fresh, rapidly growing pasture heavily fertilised N and/or K
○ Low Mg in CSF (not blood) causes convulsions
§ Blood brain barrier slows diffusion of Mg so CSF lags behind blood
○ Usually low Ca++ as well
○ Mg is not under hormonal control –bone resorption better in young animals
§ Cows very reliant on dietary absorption of Mg
What are the some common risk factors for grass tetany
- Grass dominant /low Mg pasture, heavily N & K
- Rapid growing after cold wet weather
- Cereal crop with high K
- Cold, wet weather –reduced intake (yarding & transport also)
- Common in older cattle (plus 4yo)
- Very fat cows or very thin cows
Grass tetany clinical signs what are the 3 main forms and signs within
- Sudden death may be first sign in herd
- May be evidence of struggling/convulsions
Sub-acute: - Staggers
- fall & tetanic spasms head, neck & legs
- Clonic convulsions (paddling legs)
- twitching of ears
- rolling of eyes & frothing –death in few minutes
- anxiety & ears may twitch
Acute - grinding of teeth
- salivation, frothing & muscle tremors
- animal aggressive –may charge
- progress to ataxia & tetanic muscle spasms (down)
- HR & RR markedly increased (heard externally)
- convulsions: opisthotonus, nystagmus, champing jaws, retraction of eyelids
- many recumbent animals die or remain recumbent
Grass tetany diagnosis what normally just do and what additional testing is available
Diagnosis
- Clinical signs (& history)
- Response to treatment
But also:
- Blood sample
- Serum levels Mg below 1.2mg/dl (Normal levels 1.8 –2.4 mg/dl)
○ Tetany generally only below 1.2mg/dl (some animals normal with levels this low)
○ Level of Mg in CSF critical to diagnosis (low CSF ⇒clinical -lasts 48 hrs. –use vitreous humour (in dead animals obviously!)
- Urine Mg levels used as herd guide 43
- Post mortem - look at evidence that they died after struggle
○ Moving around
Treatment for grass tetany
Restore serum Mg concentration ASAP (early)
- Slow IV of Ca & Mg solutions (“4 in 1”) although in extreme case give 50 to 100ml 20% Mg sulphate IV (Slowly & must monitor)
○ Must monitor for cardiac arrhythmias & slow or stop infusion if occurs
- Subcut Mg sulphate (500ml 20% solution) after IV
○ May need to sedate convulsing cow prior to IV
- Oral therapy (100g/cow/day) of MgOfor 2 days then 50g/day for 5 days
○ They respond slowly to treatment (raise CSF level)
prevention of grass tetany options, when start and what can also prevent
- Ensure receiving adequate daily amounts Mg during critical stress periods
- Options
○ Individual drench –60g MgO/day or 100g/day MgSO4 or MgCl2
○ Included in concentrates
○ Treat hay with 50g/day MgO
○ Dust pasture 75-100 g/cow/day (early in morning)
○ MgCl2 & MgSO4 added to water at 60g/cow/day
○ Intra-rumen Mg bullets given orally (release slowly over 9-12weeks)
○ Mg blocks –high cost & difficult to control intake - Must start at least 2 to 3 weeks before calving
- Also will reduce incidence of hypocalcaemia
Disorders of energy metabolism what are the 4 main ones and what are they essentially
- Pregnancy Toxaemia of Beef Cows
- “Starvation Ketosis” of Dairy Cows
- Fatty Liver Syndrome/ Fat Cow Syndrome
- Ketosis
Essentially different forms of hepatic lipidosis
What occurs with not enough propionate in the energy metabolism
Low oxaloacetate due to low propionate means the cow is unable to do krebs cycle -> more acetyl CoA that isn’t oxidised -> converted to ketones (Eventually)
- Ketones can be used and oxidised as energy for heart, kidney, skeletal muscle but if too much they can accumulate and excreted mainly in urine and milk
Hepatic lipidosis what are the 5 steps in the pathogenesis and the 3 main diagnostics used
- Requirement for energy leads to Hepatic uptake of lipids
- Insufficient Glucose to use up the lipids
- Liver overloaded
- Liver becomes less efficient (when it needs to be more efficient)
- Liver failure
Herd diagnosis
- Ketone bodies
- NEFA (non esterified fatty acids)
- Glucose
Pregnancy toxaemia what is it apart of and general presentation/history
part of hepatic lipidosis syndrome
- Fat late pregnant beef cows on sudden reduced plane of nutrition
- Often carrying twins
- Depression, anorexia, tachypnoea, condition loss
- Recumbency and Death
What is the treatment of pregnancy toxaemia
- Glucose IV - let liver metabolise the fat that is in there
- “ Ketol” –Propylene Glycol - combination of two glucose molecules stuck together
○ Splits into glucose in abomasum - Caesarian - help reduce the requirements - not always done
- Lift the cow
** check the whole herd nutrition! **
Protein energy malnutrition what is it apart of, presentation, cause and prognosis
part of hepatic lipidosis syndrome
- Late pregnant dairy cows being fed low quality feed (often carrying twins)
- “Thin late pregnant cows that can’t get up
○ Once you lift up though will stay up as take a lot of energy
- ” No other clinical signs to speak of
- “Starvation ketosis”
○ Commonly poor quality feeds rather than failure to provide feed
○ Imbalance between intake and requirement
○ Insidious weight loss then sudden recumbency
○ Serum metabolites often “normal” -insufficient to sustain defensible “starvation” diagnosis
- Prognosis depends on severity, time, treatment and nursing care
Protein energy malnutrition treatment
- Glucose IV
- “ Ketol” –Propylene Glycol
- Lifting
○ It’s a much slower onset disease than PregTox, and animals can often walk around but be unable to rise - Calving induction - maybe
- Caesarean
- “Nursing care” to avoid secondary muscle/nerve damage
Fatty liver/fat cow syndrome what part of, general cause and diagnosis
part of hepatic lipidosis syndrome
- “Fatty Liver” describes the increased risk of other disease due to increased fat mobilization
- Excessively fat dairy cows just after calving
- Something stops them eating
- Metabolic crisis and fatty liver
Diagnosis - hard as not really specific findings
- “lack of response to treatment of other diseases”
- Can do a liver biopsy
Fatty liver/fat cow syndrome presentation
- Fat cows are much more prone to other diseases because of secondary effects of ⇓liver function
- First 4 weeks after calving
- 30 -40% of cows have some degree of triglyceride accumulation in their liver
- Signs more directly due to liver dysfunction causing catastrophic failure of other systems
○ Dramatic weight loss, severe illness, often death
Ketosis what apart of, presentation, 2 main forms, treatment and prognosis
part of the hepatic lipidosis syndrome - Dairy Cows, early lactation - Demand for glucose greater than supply - Primary or secondary - Ketone bodies - “Nervous” and “Wasting” forms ○ Nervous -> lick at everything, pica Treatment - Glucose - Propylene Glycol - Treat concurrent disease - Corticosteroids Prognosis is usually good
What are the 4 main toxic causes of down cows
- Acute mastitis
- Salmonella
- Carbohydrate overload
- Peritonitis
What are 5 other causes of recumbency in cows
- Any severe toxaemia
- Dehydration
- Anaemia
- Neurological disease
- Terminal disease
Bovine ephemeral fever what is it known as, pathogen, transmission, location, presentation and treatment
- “3 day sickness”
- BEFV virus -arthropod borne –probably mosquitos
- Mostly NSW/Qld in Australia - Vaccines available
- Presentation
○ Recumbency for 2 -3 days followed by recovery
○ Biphasic Pyrexia -Very high temperatures in the early stages (41 degrees), then drops over 10 hours the up again for a day
○ Vasculitis, joint effusions, salivation - Most survive with or without treatment
- Hyperthermia is a common complication
Listeriosis leading to downer cows how often, associated with, what results in, main signs and treatment
- Sporadic
- usually associated with poor quality silage (high pH and water content)
- Encephalitis -probably due to local spread up trigeminal nerve
- Downer cow with unilateral facial signs - MAIN INDICATION
○ No corneal reflex
○ Droopy eye/ear
○ Tongue weakness - Often preceded by circling behaviour
- Treat with antibiotics –eg. Oxytet BID
Nitrate/nitrite poisoning what does it cause, how and sources of nitrites and when higher nitrate
- A serious cause of mass deaths in cattle
- Cattle eat plants containing nitrate/nitrite
- Nitrate -> Nitrite in rumen
- Normally Nitrite -> Ammonia and microbial protein
- In excess it oxidises Haemoglobin -> Methemoglobin ->Tissue anoxia and death
Sources of nitrites - Plants ( Capeweed, cereal oats, Brassicas toxic when below: - want to graze slowly if possible)
- Water sources
- Fertiliser
Higher
□ plant growth retarded by disease/herbicide/cold
□ esp after drought
□ with heavy use of N fertilisers
Nitrate/nitrite poisoning diagnosis, treatment and prognosis
Diagnosis
- Mucous membranes and blood is characteristic dark brown colour (that clots poorly)
- Nitrate levels in pasture -Squeeze the grass -> use it on special dipstick
Does vary from day to day
Treatment
- Methylene Blue (IV)
○ Off -label
○ Long meat withholds
○ Irritant
○ 4 to 6 mg/kg -about 3-4 grams per cow
○ Many vets carry vials with 3 -4g of powder
○ Add water just before use
Prognosis
- Generally well if treat
During outbreak need to move around and treat as many as possible
what is the minimum examination for a milk fever cow
○ Check Udder for mastitis
○ Check Uterus for a second calf (very embarrassing to miss this!)
○ Check Mucous membranes for pallor or chocolate colour (Nitrite)
In terms of clinical examination for down cow what are some special considerations
○ Rectal temp is often low –does not rule out infection - due to low perfusion
○ Systolic murmurs are common when cows are down
○ Pings are common when cows are down –may or may not be significant
○ Urine can be hard to obtain
○ Very important to examine both sides of the udder - generally the 2 quadrants under the cow are the ones with mastitis
○ Usually a 2 person job –tell the farmer you require assistance!
History taking during neurological diseases what is important to consider
- The affected animal
○ Age and breed (less popular breeds genetic neurological disorders are more common - inbreeding)
○ Onset, Duration and progression of signs… - Other animals on the farm
○ Relationship to affected animal by:
§ pedigree, time (same insult at the same time), exposure to environment (time within going into the paddock)… - The environment
○ Plants, toxins, feeds - wondering around should be able to identify certain plants
§ Local government -> identification of plants
○ Water ways -> draw a map and paddocks to determine the flow, possible relationship
Observation during neurological exam what observing
- Prior to disturbing the animal, assess its.... ○ Mental State ○ Behaviour ○ Stance ○ Gait
Clinical examination for neurology cases what need to remember and 7 species tests
- Remember…. The nervous system can be assessed at each of the five stations of the clinical examination
○ Anal tone, hyperesthesia (touching her skin), head
Specific Tests - Eyes:
- face and mouth
- other aspects of the head
- other neurological - gait and limb position
- tail and anal tone sensation
- urinary and faecal incontinence
- spinal reflexes
Examination of the eyes during neurology case what testing and looking at
○ Vision - tracking, are they bumping into things? - ADAPTION IS IMPORTANT THOUGH - can compensate
○ Menace Response
○ Pupillary Light Response - hard to do in the field
○ Eye position and movement
○ Eyelid position and movement
Examination of the face and mouth during neurology case what is involved
○ Sensation over face - but they don’t like you touching their face anyway
○ Jaw tone
○ Tongue movement and symmetry (licking on one side) - muscle tone
○ Swallowing and voice (voice change in rabies)
Examination of other aspects of the head during neurology case what involved
○ Ear, cheek, lip and nostril § position and movement ○ Response to sound - clap, behind the animal, no echoes (just sound not vibrations) ○ Head tilt and balance ○ Head nodding
