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FARM ANIMAL > 11.3.4: Brisket oedema in cattle > Flashcards

11.3.4: Brisket oedema in cattle Flashcards

1
Q

Differential diagnoses for oedema in cattle

A
  • High altitude disease
  • Malignant oedema
  • Liver fluke
  • Johne’s disease
  • PGE
  • Other clostridial disease e.g. struck
  • Heart disease
  • Reduced venous return e.g. in udder oedema
  • Non-parasitic liver disease
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2
Q

Broad causes of oedema

A
  • Reduced venous return
  • Loss of protein
  • Leaky capillaries
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3
Q

Describe the pathogenesis and clinical signs of high altitude disease

A
  • Low oxygen saturation in the air
  • Pulmonary hypertension -> pleural effusion
  • Oedema in the ventral tissues of the chest
  • Ascites
  • Jugular pulses noted
  • Exophthlamos due to oedema behind the eyes

Not seen in the UK - threshold for clinical disease is 5000ft above sea level

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4
Q

Treatment and prevention of high altitude disease

A
  • Move animals to lower area
  • Administer diuretics, and appetite stimulants (B vitamins)
  • Thoracocentesis is helpful
  • Do not breed from affected animals -> breed for more resistant stock
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5
Q

What is the cause of malignant oedema?

A

Malignant oedema is clostridial driven (most commonly = Cl. Chauveoi)

Any clostridial infection into an open wound can lead to malignant oedema

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6
Q

How might we introduce clostridial disease into animals? How can this be prevented?

A
  • By injection using contaminated needles
  • Ideall sterilise needle between uses e.g. use Steri-caps
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7
Q

Clinical signs of malignant oedema

A
  • Clostridia multiply rapidly in low oxygen environment (e.g. under skin)
  • There is oedema everywhere
  • Depression
  • Anorexia
  • Pyrexia
  • Sometimes local swelling around the point of infection
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8
Q
A

Malignant oedema
In this case the pressure has forced the rectum out

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9
Q

Describe the immunity to malignant oedema and which animals are most susceptible

A
  • Animals do not naturally build up immunity or resistance to clostridial species (although we can vaccinate!)
  • There is no age susceptibility
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10
Q

Describe how malignant oedema could develop in a group of animals

A
  • Spores have entered the animal at some point
  • Then bruising has occurred (perhaps when the animals were moving against one another when being gathered) and this releases the spores into a low oxygen environment in the body
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11
Q

Describe the pathological findings associated with clostridial infection/malignant oedema

A
  • Muscles are dry and friable, sometimes black
  • There is myocardial necrosis and sometimes haemorrhage
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12
Q

Treatment of malignant oedema

A
  • “White drugs” i.e. straight penicillin in good high doses to allow it to cross BBB etc. if required
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13
Q

Prevention of malignant oedema

A
  • Vaccinate!
  • Multi-valent clostridial vaccines are not very expensive (£1 per cow, £0.50 per sheep)
  • Initial course: 2 injections 6 weeks apart
  • Thereafter yearly booster
  • Good investment!
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14
Q

Aetiology of reduced venous return with udder oedema

A

Aetiology and sequence of events not entirely clear
* Correlation with reduced DMI
* Probably some transient liver dysfunction (hence low total protein in these cows) probably linked to a ration deficient in dry matter
* Seen in heavily pregnant animal - calf may put pressure on caudal vena cava

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15
Q

Treatment and prevention of reduced venous return with udder oedema

A

Treatment
* Massage and hot compress to stimulate circulation
* Diuretics: frusemide 1mg/kg 2x daily IV
* Corticosteroids once calved 1mg/12.5kg IV or IM

Prevention
* Diet during dry period = most effective form of prevention

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16
Q
A

Udder oedema and reduced venous return
This cow will be painful!

17
Q

Differential diagnoses for non-parasitic liver disease in cattle

A
  • Copper toxicity
  • Neoplasia
  • Liver abscess
  • Hepatic necrosis
  • Cholecystitis
  • Cirrhosis
  • TB
  • Fatty liver syndrome
18
Q

What is almost always the cause of cirrhosis in cattle?

A

Fluke!
Cirrhosis = chronic subacute liver fluke infestation unless otherwise specified

19
Q

Possible causes of cirrhosis in cattle

A
  • Fluke infestation
  • Ragwort toxicity
20
Q

When does cirrhosis tend to show itself?

A

When metabolic demands on the liver are highest e.g. early in lactation

21
Q

True/false: liver fluke damage can be associated with other syndromes including endocarditis and salmonellosis.

A

True.
Damage to the liver by the fluke can allow in other bacteria that cause disease.

22
Q

How does an animal with copper toxicity present?

A
  • Anorexic
  • Depressed
  • Diarrhoea
  • Abdominal pain
  • Weakness
  • Jaundice of sclera and skin
  • Urine is black in colour
  • Found dead
23
Q

What PM findings might be observed in an animal that dies of copper toxicity?

A
  • Liver is bronze-coloured
  • Kidneys have gunmetal appearance
24
Q

Which is a more common cause of death in sheep: copper deficiency or copper toxicity?

A

Copper toxicity
* May occur as chronic problem, then become acute after storage capacity of liver is exceeded
* Or may be genuine acute problem after inadvertant over-administration

25
Q

True/false: cattle will readily eat ragwort when pasture is lush.

A

False
Cattle will usually self-select to avoid ragwort unless pasture is barren.
May eat it if it is gathered in hay/silage etc.

26
Q

Clinical signs of ragwort toxicity

A
  • Weight loss
  • Mild to moderate jaundice
  • Photosensitisation - peeling of white areas
  • Diarrhoea
  • Low grade colic
  • Hypoalbuminaemia (+oedema) due to impaired liver function
  • Hepatic encephalopathy as liver struggles and ammonia levels rise
27
Q

Treatment and prevention of ragwort poisoning

A
  • Treatment of clinically sick animals often unrewarding as they have overcome their hepatic threshold
  • Adjust diet
  • Pull ragwort plants before they flower and seed
  • Do not make hay or silage from affected fields
28
Q

Which species from cows and sheep is less susceptible to ragwort poisoning?

A

Sheep
They may even be able to tolerate ragwort at pasture in low doses

29
Q

Clinical signs of liver abscesses

A
  • Cranial abdominal pain - grunting every time they ruminate/stand up/lie down
  • Generally looking uncomfortable/painful
30
Q

Describe the pathogenesis of liver abscesses (as related to diet)

A
  • Damage to rumen occurs through grain overload (e.g. cow breaks into feed store)
  • There is ruminal acidosis
  • This leads to ruminitis
  • Bacteria move out of the rumen and bacterial emboli pass into portal blood
  • Portal blood reaches the liver and bacteria settle here. Abscesses form.
31
Q

Describe the possible complications of liver abscesses

A

Complications can be very serious and even more damaging than the original abscess itself!
* Rupture into the abdominal cavity -> massive peritonitis
* Rupture into a major vessel -> major haemorrhage, shock and sudden death
* Vena cava thrombosis: usually occurs where the vena cava passes through the diaphragm (this results in decreased venous return and ascites, cough). May result in pulmonary thromboembolism with pulmonary abscessation -> painful cough and dyspnoea, probably + haemorrhage.

32
Q

True/false: liver abscesses produce non-specific signs and it is therefore a good go-to diagnosis because it’s hard to ever be proved wrong.

A

True.

*According to James Russell

33
Q

Treatment and prevention of liver abscesses

A
  • Treatment is unrewarding. If grain overload is seen, try to restore rumen pH and get the cows cudding so saliva helps buffer the rumen
  • Prevention: avoid acidotic ruminal conditions
34
Q

How do you prevent acidotic ruminal conditions?

A
  • Feed enough roughage
  • Do not overfeed grain
  • Stimulate the rumen to ruminate, cudding to happen and therefore the buffering effect of saliva to be maximised
  • If you see grain overload, try to restore rumen pH and get them cudding

FARM ANIMAL (56 decks)

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