11.3.4: Brisket oedema in cattle Flashcards
Differential diagnoses for oedema in cattle
- 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
Broad causes of oedema
- Reduced venous return
- Loss of protein
- Leaky capillaries
Describe the pathogenesis and clinical signs of high altitude disease
- 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
Treatment and prevention of high altitude disease
- 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
What is the cause of malignant oedema?
Malignant oedema is clostridial driven (most commonly = Cl. Chauveoi)
Any clostridial infection into an open wound can lead to malignant oedema
How might we introduce clostridial disease into animals? How can this be prevented?
- By injection using contaminated needles
- Ideall sterilise needle between uses e.g. use Steri-caps
Clinical signs of malignant oedema
- 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
Malignant oedema
In this case the pressure has forced the rectum out
Describe the immunity to malignant oedema and which animals are most susceptible
- Animals do not naturally build up immunity or resistance to clostridial species (although we can vaccinate!)
- There is no age susceptibility
Describe how malignant oedema could develop in a group of animals
- 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
Describe the pathological findings associated with clostridial infection/malignant oedema
- Muscles are dry and friable, sometimes black
- There is myocardial necrosis and sometimes haemorrhage
Treatment of malignant oedema
- “White drugs” i.e. straight penicillin in good high doses to allow it to cross BBB etc. if required
Prevention of malignant oedema
- 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!
Aetiology of reduced venous return with udder oedema
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
Treatment and prevention of reduced venous return with udder oedema
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
Udder oedema and reduced venous return
This cow will be painful!
Differential diagnoses for non-parasitic liver disease in cattle
- Copper toxicity
- Neoplasia
- Liver abscess
- Hepatic necrosis
- Cholecystitis
- Cirrhosis
- TB
- Fatty liver syndrome
What is almost always the cause of cirrhosis in cattle?
Fluke!
Cirrhosis = chronic subacute liver fluke infestation unless otherwise specified
Possible causes of cirrhosis in cattle
- Fluke infestation
- Ragwort toxicity
When does cirrhosis tend to show itself?
When metabolic demands on the liver are highest e.g. early in lactation
True/false: liver fluke damage can be associated with other syndromes including endocarditis and salmonellosis.
True.
Damage to the liver by the fluke can allow in other bacteria that cause disease.
How does an animal with copper toxicity present?
- Anorexic
- Depressed
- Diarrhoea
- Abdominal pain
- Weakness
- Jaundice of sclera and skin
- Urine is black in colour
- Found dead
What PM findings might be observed in an animal that dies of copper toxicity?
- Liver is bronze-coloured
- Kidneys have gunmetal appearance
Which is a more common cause of death in sheep: copper deficiency or copper toxicity?
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
True/false: cattle will readily eat ragwort when pasture is lush.
False
Cattle will usually self-select to avoid ragwort unless pasture is barren.
May eat it if it is gathered in hay/silage etc.
Clinical signs of ragwort toxicity
- 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
Treatment and prevention of ragwort poisoning
- 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
Which species from cows and sheep is less susceptible to ragwort poisoning?
Sheep
They may even be able to tolerate ragwort at pasture in low doses
Clinical signs of liver abscesses
- Cranial abdominal pain - grunting every time they ruminate/stand up/lie down
- Generally looking uncomfortable/painful
Describe the pathogenesis of liver abscesses (as related to diet)
- 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.
Describe the possible complications of liver abscesses
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.
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.
True.
*According to James Russell
Treatment and prevention of liver abscesses
- 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
How do you prevent acidotic ruminal conditions?
- 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
