Clostridium Perfringens Type A
By Dr Mackie Hobson BSc(Agric),BVSc

Friday, 8th August 2014

Enterotoxeamia, ’Rooiderm’, Haemorrhagic enteritis

Clostridium perfringens type A is associated with Angora kid deaths, which die from ‘enterotoxaemia’ and a form of haemorrhagic enteritis.

Clostridium perfringens Type A produces enteric diseases, generically called enterotoxemia.


This microorganism can be a normal inhabitant of the intestine, but when the intestinal environment is altered by sudden changes in diet or other factors, it leads to the proliferation of the bacteria and the production of alpha-toxin. It has a generation time of 8-10 minutes which is one of the fastest known for bacteria.

The alpha-toxin acts locally or is absorbed into the general circulation with usually devastating effects.

Young goats are particularly susceptible to haemorrhagic enteritis, and we tend to see most cases in kids when first introduced onto concentrate feeds and after weaning.

It is probably best to refer to the group of Clostridium Type A and Type D as enterotoxaemia due to the similarity in clinical signs.


How does the alpha-toxin kill the goat?

The toxin binds to the surface of the host cell, whereby a series of pathways result in increased permeability in blood vessels.


What are the main predisposing factors to cause the overgrowth of the bacteria?

  • Young goats (often pre-weaning to 18 months)
  • Grazing on lush pastures
  • Fed carbohydrate and protein-rich diets,
  • It can occur sporadically after weaning,
  • After deworming
  • After a stressful event.
  • Often the biggest, best kids as they tend to dominate at feed troughs.


What are the clinical signs?

Goats are usually found dead without evidence of disease. ‘They were fine yesterday and dead today’. Those goats that are alive may show signs of abdominal pain. The deaths usually occur within two weeks of the predisposing cause.


What signs can be seen on Post Mortem?

  • Rapid decomposition occurs in the carcasses.
  • Bloodstained fluid may ooze from the nostrils and anus.
  • Characteristic lesions are severe congestion and haemorrhage of the small intestine.


  • Some blood-stained fluid in the thorax and abdomen may be present.


  • Because the lesions are not specific, diagnosis is confirmed by isolation and detection of the toxin. Brain samples are the best way to check if the cause is Clostridium perfringens Type D (pulpy Kidney) than Type A due to the similarity in clinical signs and history.

How can we prevent the condition?

Vaccines are available which provide partial protection.

  1. Vaccinate the mother 4-6 weeks before kidding
  2. Make sure kids are fully vaccinated (have had both injections 4 weeks apart) at least 2 weeks before concentrate feed is introduced, or predisposing factors are expected to occur.
  3. Make sure fibre makes up the bulk of the diet (for example, Lucerne hay)
  4. Always slowly adapt young goats onto a different diet.
  5. Prevent stronger kids from dominating the feeding space.


What to do when you have deaths due to ‘Rooiderm’?

It is seldom effective to treat sick goats - the time from normal to death is very short (Per-acute- hours). Goats are usually just found dead. So preventing other goats from dying is the main goal.

If a sick goat is treated, then

  • pain relief (anti-inflammatory)
  • antibiotic (penicillin or tetracycline)
  • anti-toxin if available
  • Tube or dose activated charcoal 2mg/kg
  • Tube probiotic rumen stimulant such as ‘Rumix.’


What to do with the other goats?

  • Remove concentrate feed
  • If it is suspected it was caused by a change in diet, return to the previous camp or diet immediately.
  • Provide dry fibre (example, dry lucerne hay and no concentrate)
  • Vaccinate as soon as possible
  • Treating goats with long-acting tetracyclines between vaccination and immunity may help.


Which vaccines cover Clostridium perfringens Type A?

See the website

Also, see what age the different vaccines can be given to ensure cover 2 weeks before predisposing factors are encountered,


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