DVM 3 - 2 > Cattle 5 > Flashcards

Cattle 5 Flashcards

(103 cards)

Study These Flashcards
1
Q

Clinical signs for milk fever what divided into and how change/vary

A

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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the clinical signs in stage I and 2 of milk fever - EXAM

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the clinical signs in stage 3 of milk fever - EXAM

A

○ 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are 5 other differentials for a cow that is milk fever

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Milk fever how what are the 6 steps in treatment and what recommend for different outcomes

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Calcium borogluconate when give, main types, properties and the 2 main ways to administer

A 
- 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Giving subcutaneous calcium to a down cow who generally does this, how to do and general advice

A

§ 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”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Giving IV calcium how give, requirement, how long over, safe rate and when reach point how give remainder

A

§ 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Individual level prevention for hypocalcaemia

A
  1. Supply calcium at or just before calving
    ○ s/c or oral
    ○ Labour intensive
  2. 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
  3. 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Non-parturient hypocalcaemia what also called, when occurs

A

Transit tetany”

  • Cows on lush grass (oxalates, nitrates)
  • Occasionally cows who have not recently calved become hypocalcaemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How to transition feed appropriately to prevent metabolic conditions after parturition

A

○ 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Grass tetany what is the issue, characterised by and pathogenesis/cause

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the some common risk factors for grass tetany

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Grass tetany clinical signs what are the 3 main forms and signs within

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Grass tetany diagnosis what normally just do and what additional testing is available

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment for grass tetany

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

prevention of grass tetany options, when start and what can also prevent

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Disorders of energy metabolism what are the 4 main ones and what are they essentially

A
  1. Pregnancy Toxaemia of Beef Cows
  2. “Starvation Ketosis” of Dairy Cows
  3. Fatty Liver Syndrome/ Fat Cow Syndrome
  4. Ketosis
    Essentially different forms of hepatic lipidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What occurs with not enough propionate in the energy metabolism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hepatic lipidosis what are the 5 steps in the pathogenesis and the 3 main diagnostics used

A
  1. Requirement for energy leads to Hepatic uptake of lipids
  2. Insufficient Glucose to use up the lipids
  3. Liver overloaded
  4. Liver becomes less efficient (when it needs to be more efficient)
  5. Liver failure
    Herd diagnosis
    - Ketone bodies
    - NEFA (non esterified fatty acids)
    - Glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pregnancy toxaemia what is it apart of and general presentation/history

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the treatment of pregnancy toxaemia

A
  • 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! **
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Protein energy malnutrition what is it apart of, presentation, cause and prognosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Protein energy malnutrition treatment

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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
26
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
27
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 ```
28
What are the 4 main toxic causes of down cows
1. Acute mastitis 2. Salmonella 3. Carbohydrate overload 4. Peritonitis
29
What are 5 other causes of recumbency in cows
1. Any severe toxaemia 2. Dehydration 3. Anaemia 4. Neurological disease 5. Terminal disease
30
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
31
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
32
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
33
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
34
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)
35
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!
36
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
37
Observation during neurological exam what observing
``` - Prior to disturbing the animal, assess its.... ○ Mental State ○ Behaviour ○ Stance ○ Gait ```
38
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
39
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
40
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)
41
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 ```
42
What are 2 special examination procedures for neurology cases that aren't used often and how done/who performed on
1. Cerebrospinal Fluid Collection - not commonly done ○ EDTA and Smear ○ Lumbosacral - wings of ilium ○ Cisterna magna - more in a calf - sternal and tilt head forward to expose 2. Radiography - only done in calves ○ Plain - feasible in calf ○ Contrast - not common
43
What are the 5 manifestations of neurology disease in cattle
1. Changes in Mental State 2. Involuntary Muscle Movements 3. Paralysis 4. Incoordination 5. Abnormality of Sensation
44
in terms of changes in mental state for neurology case what can occur
- Mania ○ “excitement… bizarre… unaware of surroundings (more subjective) - Frenzy - want to kill you ○ "violent… uncontrolled… dangerous…may be aggressive…” - Aggression and other ‘personality’ changes - especially if a jersey cow - Depressive mental states - maybe used to be in the front now always at the back ○ may lead to coma - Syncope (fainting) - not common - Narcolepsy (with flaccid paralysis) - Compulsive walking (just keep walking in straight line) or head pressing - Aimless wandering (not necessarily in a straight line)
45
in terms of involuntary muscle movement for neurology cases what are the 6 main ones and define
- Tremor ○ “A continuous repetitive twitching of skeletal muscle, usually palpable and visible” - Tics ○ "A spasmodic twitching movement made involuntarily by muscles that are ordinarily under voluntary control” - Myoclonus ○ “Repetitive rhythmic contractions of a group of skeletal muscles, persisting in sleep” - Tetany ○ “Continuous tonic spasm of a muscle” - Convulsions ○ Intracranial (encephalitis, meningitis, brain oedema...) ○ Extracranial (hypoxia, hepatic encephalopathy...) - Involuntary spastic paresis
46
Paralysis as a manifestation of neurological issues define and the 2 types with characteristics within
- Loss of voluntary movement - Spastic paralysis ○ loss of voluntary movement ○ Increased tone of muscles ○ increased spinal reflexes - Flaccid paralysis ○ loss of voluntary movement ○ decreased muscle tone ○ absence of spinal reflexes ○ muscle wasting - can occur quickly in flaccid paralysis
47
Incoordination and abnormalities of sensation as manifestations of neurological issues what is involved
4. Incoordination - Posture ○ Vestibular disease - head tilts - Gait ○ Ataxia ○ Cerebellar disease - if makes you laugh then probably this ○ Spinal cord disease - not sure where the feet area - swinging of the hips 5. Abnormalities of Sensation - Can be hard to assess in animals ○ Blindness - incomplete blindness and night blindness can complicate ○ Skin sensitivity (hypo- or hyper- aesthesia) ○ Deafness (or hypersensitivity to sound) ○ Taste / Smell
48
What are the main 11 nervous diseases of cattle
1) lead poisoning 2) polioencephalomalacia (vitamin B1 (thiamine) deficiency) 3) nervous coccidiosis 4) Meningoencephalitis 5) Hypovitaminosis A 6) tetanus 7) listeriosis 8) brain abscess 9) rabies 10) bovine sponioform encephopathy 11) botulism
49
Lead poisoning how occurs, how common, types and significance
- Ingestion from environmental sources - Common in Australia - Can be either acute (death sudden) or chronic - nervous disease - Significance -> if in cattle then could be effecting other mammals including humans
50
Acute lead poisoning age common in, signs and result generally
- More common in calves (possible more susceptible or more curious) than adults - Signs: ○ head tremor and staggery gait ○ jaw champing and frothy saliva (due to the jaw champing) ○ pupils dilated, palpebral reflex absent - important ○ Calves § convulsions separated by opisthotonus and hyperaesthesia ○ Adults - blindness, mania, head pressing - Death after 12 - 24 hours
51
Subacute lead poisoning signs and result
``` - Signs: ○ depression and anorexia - head pressing ○ blindness with absent palpebral reflex ○ complete ruminal atony ○ constipation followed by dark scour - Become recumbent and die a quiet death ```
52
Diagnosis of lead poisoning what are the main ways
- Elevated blood lead (>~0.30ppm) ○ Use whole blood. Pb assoc with RBCs. LH better than EDTA - Elevated blood and urine dALA ? - Necropsy may show lead in GI tract -> lead is soft metal so if think you found in stomach then see if you can scratch - if so lead - Liver & Kidney [Pb] - samples of tissue - Investigate environment to demonstrate access to lead (Pb) - car battery, old shed with metal within the paint - main
53
Treatment of lead poisoning 4 main things and what need to consider
``` 1. Remove source of lead ○ gastric lavage or rumenotomy 2. Sedation to relieve convulsions ○ eg Xylazine 3. CaEDTA (calcium versenate) ○ chelates absorbed lead ○ iv or sc (30mg/kg tid for 3 days) 4. Thiamine (Vit B1) - unsure why it works ○ 2 to 4mg/kg/day sc - WHP (with-holding period) may be prolonged. Test prior to slaughter? ```
54
Polioencephalomalacia what is it, occurs in, why and fatality
- Inadequate supply of thiamine (Vit B1) ○ not completely understood (multiple causes?) - Occurs in well fed (esp. young) cattle - Low fibre diets - Thiaminases produced by gut flora (reason?) - High sulphate intake (possible on boar water with high sulphate) - Case fatality 50%
55
Polioencephalomalacia presentation
``` Presentation - Very similar to Lead Poisoning ○ but palpebral reflex is normal (“pol pal per” - polio palpebral persists) - important EXAM - Blind - Acute animals more severely affected ○ Subacute animals may remain standing - CSF pressure is increased - Some older animals recover as imbeciles (complete morons) -> won't eat, just stands there ```
56
Polioencephalomalacia diagnosis
Diagnosis - History and Epidemiology - Blood tests sometimes hard to interpret ○ Blood thiamine may be decreased, but not always - Autopsy ○ Yellow discolouration of cortical gyri ○ Autofluoresence under ultraviolet light in many cases ○ Low brain and liver thiamine content
57
Polioencephalomalacia treatment
- Early and aggressive treatment gives best response - Injectable thiamine 10-15 mg/kg iv, repeated im ○ oral thiamine is degraded - Increase roughage in diet - Rumen liquor transplantation of some help?
58
Nervous coccidiosis what is it, caused by, age, following with presentation and mortality
- A sequel to infection with coccidia ○ occurs in some affected animals (up to 50% ?) - Eimeria zuernii, E. bovis - > 5000 faecal oocysts/g is significant - Young animals (calves and yearlings) generally <12months old - Usually follows signs of scouring etc - Tremor, hyperaesthesia and convulsions - some if get to this point poor prognosis - High case mortality (80 – 90%)
59
Nervous coccidiosis treatment
- Sedation - Calcium + Magnesium subcutaneous - unsure if it does anything - Sulphadimidine or Amprolium used - may kill coccidia ○ little hard evidence to support either - Warmth, fluids and nursing - supportive care
60
Meningoencephalitis what caused by, what group mainly in, mortality and main issues
- Caused by Histophilus somni (nee Haemophilus somnus) - Mainly in young, feedlot cattle (esp USA) - Low morbidity, but high mortality - Originally was seen as primary meningoencephalitis ○ Stumbling gait, recumbency, tremor, opisthotonus, depression, droopy eyelids - Now more a disease of respiratory tract. [TEME 2°] - not as common as neurological disease
61
Meningoencephalitis treatment, prevention and is it in aus
- Good response to early antibiotics ○ Penicillin, Oxytet… Tilmicosin, Florfenicol… ○ Prognosis poor if recumbent - Component of feedlot vaccination in USA - Reported in Australia
62
Hypovitaminosis A what is it caused by, main case seen, how long need to be deficient for, what more prone, presentation, treatment and prevention
- Lack of carotene in diet - Occurs in animals with a lack of green feed ○ e.g. housed on poor rations, pastured during drought - Liver stores last 6 - 18 months - need to be lacking for 6 months plus - Calves have no stores so more prone - Staggery, Convulsions - Blindness (esp night blindness) - bumping into things at night - hard to diagnose - Treat with parenteral Vitamin A (lipid soluble, need to give good quality calf milk replaces otherwise will absorb vitamin A) - Prevent with dietary supplementation but Vit A is fat soluble, so long term ingestion of indigestible fats may decrease Vit A stores ○ Management issue
63
Tetanus what caused by, generally when occurs/cause, how susceptible are cattle and 3 main clinical signs
- Clostridium tetani, from soil contamination ○ Poor vaccination (uncommon), dehorning, ear tagging, castration - Wound often not evident - Cattle least susceptible of domestic animals - uncommon Clinical signs - Spasticity, ‘saw horse’ stance (rigid) - Stiff gait, passive flexion not possible - 3rd eyelid prolapse, locked jaw and bloat
64
Tetanus treatment and prevention
Treatment - High doses of antibiotics (eg penicillin) - Antitoxin? - probably not on you anyway - Sedation as hyperactive - Keep quiet, in a dark place - lock in shed -> avoid the tetanic spasm Prevention - Best to prevent with vaccination program ○ Cases may indicate vaccination failure? - Hygienic management practices
65
Listeriosis how common in what climates, where generally infected from and main clinical signs
- Most common in colder, wet climates - Listeria monocytogenes found in gut ○ Accesses Trigeminal n. via mouth abrasions ○ high challenge in poor quality silage - Signs suggestive of cranial nerve dysfunction ○ head tilt, circling (only wants to go one way -> try to go the other way will fall off) ○ unilateral ear, eyelid, lip and/or jaw paralysis - Also causes abortion, but not together ○ Last trimester with RFM, morbidity <10%
66
Listeriosis treatment and zoonosis?
- Aggressive, early treatment with antibiotics ○ penicillin (or tetracycline?) - Protect from misadventure -> don't put in a paddock near water, roads -> incapable of controlling where she goes - Control by feed management ○ Silage -> the better you remove the air the better it will be, once open cannot reseal -> need to finish opening it - What to do if cases occur and there is still lots of silage to be eaten?! ○ Tricky situation -> risk?, giving at lower amount with other things??? No zoonotic
67
Brain abscess general cause, signs and treatment
- Localisation of haematogenous infection - post ear tagging and dehorning common ○ Nasal granuloma -> stick up the nose -> penetrate cribriform plate - Signs related to site and size of abscessation ○ Initially discrete signs ○ Progress to generalised signs of cerebral dysfunction - Treatment pointless if signs severe
68
Rabies importance, transmission, 3 phases, death time and diagnosis
- Exotic and Zoonotic (100% fatality!) - Spread and maintained in specific ecologies - Saliva most infectious fluid - Three phases of variable duration ○ Prodromal - change in temperament, 1-3 days can be subtle enough not to notice ○ Furious - aggressive - lash out on objects and people (charge at anything that moves), restless, paralysis of the jaw ○ Dumb (paralytic) - can go from prodromal to this and skip furious, flaccid paralysis, muscle tremors and convulsions - Death 7-10 days after infection ○ Most times the post-mortem has no abnormal findings - Diagnosis -> clinical signs
69
Bovine spongiofrom encephopathy importance, incubation, clinical signs and what can no longer do and other form
- Exotic, related to scrapie of sheep - Zoonotic potential (?) - Major new disease in the UK in 1985 ○ Loss of cattle ○ Loss of domestic and export markets ○ Public hysteria - main issue -> thinking mad human disease would occur - Prolonged incubation (generally seen at 3-6 years of age), no viva test available, abattoir testing expensive - Clinical signs -> Loss of condition, hyperaesthesia, temperate change, tremors, ataxia, abnormal head carriage - No longer allowed to feed ruminal protein to ruminants - Sporadic form as well -> need to be able to differentiate and ensure you don't have BSE in that country
70
Botulism pathogen, how acquire, when most important, clinical signs, diagnosis, treatment and prevention
- Clostridium botulinum - Cattle infected by ingestion ○ Contaminated feedstuffs (eg poultry litter) ○ Consumption of cadavers - Important cause of losses in Nth Australia due to scavenging by roaming stock Signs of Botulism - May present as sudden death - Flaccid paralysis - progressive ○ initially of jaw, head and neck ○ progresses to wider paralysis of limbs ○ Sensation and consciousness maintained - Often die in sternal recumbency -> respiratory failure and aspiration - No simple diagnostic test - No effective treatment - Vaccine needs to be serotype specific - generally not done in VIC but is in QLDS and some NSW farms
71
List the 4 main plant toxicities leading to neurological dysfunction
1) paspalum staggers 2) perennial ryegrass staggers 3) phalaris staggers 4) Xanthorrhoea poisoning
72
Paspalum staggers what caused by, conditions, age and clinical signs/treatment
- Claviceps paspali ergot infects paspalum grasses - (eg P. distichum... “distichum staggers”) ○ Ergots look like sticky dew or black tar ○ Pasture infection mostly after wet, humid summers ○ Often seen in autumn when feed restricted - More often seen in calves Clinical signs: - hypermetric gait - rigid gait - hypersensitive to sound but not touch - appear normal when relaxed, but will eventually show persistent signs - Death can occur via misadventure - no treatment, but animals recover once removed from source
73
Perennial ryegrass staggers what caused by, more common in which species and clinical signs
- Acremonium lolii endophyte infection of ryegrass dominant pastures ○ Mainly in lower outer leaf sheaths, so disease seen when animals grazing short pasture, usually in autumn ○ More common in sheep ○ Not seen simultaneously with facial eczema Clinical signs - Fine tremors with muscle fasciculations - mainly around the head - Followed by coarse tremor - Signs induced by forced movement - Abnormal postural reflexes, so show a bounding gait and falling into lateral or ‘frog leg’ recumbency - Left alone, animals will regain composure and rise unassisted
74
Xanthorrhoea poisoning what caused by, where generally located, clinical signs and recovery
- Flower spikes of Xanthorrhoea (“grasstree”) - Mainly one found in peoples gardens -> when cattle get into neighbours - Cattle show: ○ urinary incontinence ○ Erect tail ○ Posterior incoordination so that they fall always to one side.... wamp! - Onset may be delayed, but recover if nursed
75
Periodic spasticity what also called, how common, age occurs with clinical signs and outcome
- aka “Stall cramp” - rare - Seen in Holsteins, Guernseys... - Occurs in adults: ○ difficulty rising ○ extensor rigidity of hind limbs (hindlimb spasm) ○ attacks become more severe, longer and frequent - Once occur will just get worse and have to get euthanised
76
Elso heel what also called, how common, age, clinical signs and possible treatment
- aka “Inherited spastic paresis” - more common - Seen in many breeds - Usually appears in calves to 6 months old - Spasticity of one or both hind limbs, with a swinging, ‘can’t touch the ground’ gait -> if one leg can look like patella or hip dislocation - No resistance to passive flexion (if put in sternal recumbency - different to rabies (cannot flex), but hock joint may become distorted - Respond to partial tibial neurectomy (??)
77
Cranial and spinal trauma main causes and signs of facial nerve paralysis
``` - Fractures of the skull occur with: ○ misadventure (esp during transport) ○ malicious injury - Spinal fractures occur secondarily to: ○ falls due to paresis or paralysis ○ mating behaviour - Facial nerve paralysis relatively common ○ drooping of ear, eyelid, lip ○ asymmetry of face and drooling ```
78
What are the 7 main neurology diseases of calves
1) meningitis 2) citrullinaemia 3) inherited congenital myoclonus 4) maple syrup urine disease 5) cerebellar defects 6) vertebral body abscess 7) alpha-mannosidosis
79
Meningitis at what age, cause, clinical signs and accompanied with
- In calves, usually secondary to navel infection - Often accompanied by other signs of generalised infection: - joints, lungs, nervous tissue ○ scouring, arthritis, omphalophlebitis - Exacerbated by failure of passive immunity - Contamination of CSF leads to irritation of central and peripheral nerve systems Clinical signs: - muscular spasm, rigidity, hyperaesthesia - tremor and convulsions - toxaemia and pyrexia - opthalmitis and hypopyon - depression, recumbency and coma
80
Meningitis diagnosis and treatment and prevention
Diagnosis and treatment - Dx difficult without CSF premortem ○ Increase protein, increase WCC - Needs aggressive antibiotics, but often unrewarding ○ Penicillin, Tri/Sulph, oxytetracycline, or 3rd gen cephalosporins Prevention - Good calf hygiene and colostrum management
81
Citrullinaemia what is it, seen in what breeds, clinical signs and diagnosis
Neurological disease of calves - Seen in Holstein Friesians in Australia - autosomal recessive - Arginosuccinate synthetase deficiency - Normal at birth ○ develop signs in first week of life ○ die within 12-24 hours - Depression, compulsive walking, blindness, head pressing, hyperthermia, recumbency, opisthotonus and convulsions - look like meningitis differentiate via below ○ Blood citrulline levels very high ○ PCR for heterozygotes -> bulls with these issues use properly (not onto cows that are daughters of these bulls)
82
Inherited congenital myoclonus what also called, breeds, age, clinical signs, outcome
- aka “Neuraxial oedema” - Poll Herefords and their crossbreeds ○ autosomal recessive - Affected calves: ○ unable to rise and hyperaesthetic to touch ○ extreme extensor spasm - try to stand but rigid and then fall ○ consciousness, intellect and vision not impaired - Can survive temporarily if nursed vigilantly - SHIT QUALITY OF LIFE - No histological lesions, only functional
83
Maple syrup urine disease breeds, type of disease, clinical signs
- Poll Herefords, Herefords etc - Autosomal recessive - genetic disorder of metabolism - Some stillbirths, but others born normal but develop signs at 1 -3 days old ○ Dullness, recumbency, tremor, blindness, hyperthermia ○ When held upright, some tetanic, some flaccid ○ Urine smells of burnt sugar, due to accumulation of branched chain amino acids
84
Cerebellar defects types/causes
- Several inherited diseases of cerebellum ○ cerebellar hypoplasia and ataxia - can stand but doesn't know where the legs are ○ familial convulsions and ataxia ○ inherited congenital spasms - Most common is secondary to pestivirus (BVD) infection in utero (125-180 days) ○ cerebellar hypoplasia and ocular abnormalities
85
Vertebral body abscess what breed more common, secondary to, location, onset and clinical signs, diagnosis and prognosis
- More common in dairy calves than beef - Secondary to chronic suppurative focus - Usually in caudal thoracic or cranial lumbar vertebrae - Slow progression... ○ ataxia and proprioceptive defects - unable to remain standing - Pathological fracture... ○ sudden onset of ataxia or paralysis - Diagnosis - radiograph of the spinal cord - Prognosis ○ If large not worth treating If smaller maybe worth treating with antibiotics and supportive care
86
Alpha-mannosidosis breeds, is it in aus, what occurs, clinical signs and outcome
- Angus, Murray Grey and Galloways - BREED PROBLEM - Controlled in Australia 1980s (auto. recess.) - Lysosomal storage disease, with build-up of mannose and glucosamine in neural tissue - Show signs from immediately after birth to several months old - Ataxia, intention tremor, aggression (can in mental status) - Ill-thrifty and tend to die, or euthanised
87
What are the main important diagnostic things that need to be done to investigate a sudden death case
- Get a good history ○ Animal & Environment ○ Which animals in which paddocks, diet, treatment, bloodlines - Keep good records ○ Record all findings - Examine the environment - Examine the animals (both dead and alive) ○ Struggle? Discharges? Blood? Mucosa? Trauma? etc - Collect samples - important with insurance and if leads to suing - takes pictures ○ Water, Plants, Toxins, Necropsy ○ Sealed and labelled! Duplicated - good if issue with first lot of send to different areas)
88
Sudden death in individual animals what are the 4 main causes
1. Haemorrhage 2. Peracute toxaemia ○ Endogenous & Exogenous 3. Trauma ○ Self-inflicted ○ Malicious 4. Iatrogenic
89
Haemorrhage leading to individual sudden death what are the 2 main types and causes within
1) External ○ Not hard to diagnose § Caudal Vena Caval Syndrome - bleeding out of respiratory tract (bright red arterial blood) □ Caudal vena cava thrombi -> lungs -> bleed out § Laceration 2) Internal ○ Usually obvious at necropsy § Cardiac § Pulmonary § Uterine arteries -> uterine prolapse or internally after calving § Abomasal
90
Peracute toxaemia leading to individual sudden death what are the 2 main sources and causes within
``` - Endogenous ○ Not hard to diagnose at necropsy § Rupture of abomasum - spillage of GI contents § Rupture of rumen etc. - Exogenous ○ Usually not very obvious § Snakebite? (It’d need to be a very poisonous snake!) □ Cows have very thick skin unlikely ```
91
Trauma and iatrogenic causes of sudden death in individual animals list the main ones
3. Trauma - Car accidents, falling in hole - Internal haemorrhage - Damage to CNS ○ Brain trauma ○ Gunshot ○ Aggravated assault - uncommon 4. Iatrogenic - Improper treatment ○ Calcium - MUST ALWAYS LISTEN TO THE HEART WHEN PUT IN CALCIUM § Rapid fluid infusion - Other drugs/preparations
92
What are the 6 main causes of sudden death in groups
1. Electrocution 2. Anaphylaxis 3. Nutritional poisoning 4. Potent poisons 5. Nutritional deficiency 6. Septicaemia or Toxaemia
93
Electrocution leading to sudden death in a group what are the 2 main sources when/where generally occur, clinical signs and what need to be careful of
1) Lightning strike ○ History of electrical storm (usually) ○ Cows around tree with tree crack within ○ Clinical signs § Extensive bleeding subcutaneously § Scorch marks of burned hair 2) Mains electricity ○ Especially around sheds, pole and water ○ Electricity kills people too. Be careful!! - if cows drop dead in shed -> turns of electrical power to shed
94
Anaphylaxis leading to sudden death in groups general causes and signs
- Soon after injection of biological materials ○ Vaccines & sera ○ Signs include: § anxiety, distress, salivation, tachycardia, collapse, dyspnoea, convulsions, nasal discharge, nystagmus, rapid death. - Usually reasonably obvious!
95
Nutritional poisoning that lead to sudden death in groups what are the
1) bloat eally digestible feed, cannot eructate fast enough -> can die in minutes ○ Post mortem -> congested at front and not in back 2) Grain overload 3) Nitrite - common 4) cyanide 5) lead 6) blue green algae
96
Cyanide poisoning cause, sources, man risk, clinical signs and treatment (if not dead)
○ Ingestion of cyanogenetic glycosides ○ Many plant sources § Gums, sorghums, acacia (wattle) - generally don't eat ○ Rapid growth after stunting; Frost damaged. § Only graze well grown ‘mature’ plants ○ Greatest risk when animals hungry ○ Clinical signs: § Dyspnoea.. Restlessness.. Recumbency.. Death § Bright red blood - DIFFERENTIATE FROM NITRITE POSIONING § Depressed, staggery, tremors, dyspnoea § Weak pulse and dilated pupils ○ Treatment: - IF BEFORE DEATH § Na thiosulphate (660 mg/kg iv) § Na thiosulphate (30g/cow orally) ‘preventative
97
Blue-green algae poisoning leading to group sudden death when generally occur, clinical signs with different toxins and treatment/prevention
``` ○ Algal blooms in dams § N and P fertiliser (high concentrations) § shallow water & high water temp § wind concentration ○ Fast death factor (neurotoxins) § Staggering, muscle tremor, weakness, diarrhoea & dyspnoea ○ Slow death factor (heptotoxicosis) ○ Many species affected ○ Activated charcoal ? ○ Restrict access. ○ Treat dams with copper sulphate ```
98
What are the 3 other potent poisoning that lead to sudden death in groups, source, clinical signs and treatment
1) Monensin - bloat preventive ○ Usually errors in feed formulation ○ Acute (or chronic) cardiomyopathy 2) Organophosphates ○ Accidental or overdose toxicity. Increased salivation, dyspnoea, diarrhoea and muscle twitching ○ Tx: Remove source of OP, and give increase atropine 3) Urea ○ On pastured cattle, usually due to accidental exposure (eg access to spilt fertiliser) ○ Urea > Ammonia in rumen. If excess urea is ingested it overwhelms microflora capacity to utilise ammonia and results in high blood ammonia > CNS signs ○ Salivation, abdominal pain, muscle tremors, incoordination, convulsions, collapse… death
99
What are the 3 main nutritional deficiencies that lead to sudden death in a group and how characterised
1) Hypomagnesaemia ○ Grass tetany 2) Vit E / Se Deficiency ○ Usually characterised by ill-thrift and poor growth ○ White muscle disease, especially in calves 3) Chronic, severe copper deficiency ○ aka ‘Falling disease’ ○ Atrophy of myocardial cells ○ “Adult cattle that are apparently clinically normal may die suddenly”
100
What are the 3 main infectious agents that lead to septicaemia or toxaemia resulting in sudden death of a large group
1) blackleg 2) black disease 3) anthrax
101
Blackleg what caused by, age, clinical signs, diagnosis, treatment and prevention
- Cl. chauvoei - Good condition cattle 6 months to 2 years - ?? Inciting cause ○ Anything that causes anoxia in muscles - fighting, exercise - Severe lameness, fever & tachycardia - Death in 12 - 36 hours - PM - bloat, decomposition, blood stained fluid - muscle bruising - Massive parental antibiotics - penicillin High losses unless vaccinate (7 in 1) - uncommon due to the vaccination
102
Black disease pathogen, associated with, when occurs, clinical signs, treatment and prevention
- Cl. novyi - Associated with Fascioliasis - Sporadic in cattle & seasonal (fluke) - Depression, reluctance to move, fever - Rapid putrefaction of carcass/ liver damage - Tx: Penicillin - Vaccination & liver fluke control
103
anthrax pathogen, location, clinical signs, transmission and diagnosis
- Bacillus anthracis - Enzootic areas - QLDS, NSW, VIC (northern vic) - Rapid putrefaction of carcass - Bloody discharge from orifices - ASSUME ANTHRAX AND DON'T POST MORTEM (OR MOVE) - CALL UP LOCAL DEPARTMENT ○ Dark, tarry, does not clot - Transmission by inhalation. Incubation: 1-3 wks - Peripheral blood smear ○ Gram +ve, capsulated, ‘square’ -> bacillus anthracis -> die from septicaemia ○ Rapid ICT (detects toxin)
DVM 3 - 2
flashcards
Decks in class (40)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions