Sudden death in Angora Goats
By Dr Mackie Hobson BSc(Agric),BVSc

Monday, 15th April 2019

An Angora farmer when checking his goats may occasionally find a goat that has died suddenly. “The goats all appeared well yesterday and when checking the flock today a goat has been found dead”


These sudden (acute) deaths may be due to a number of possible causes and hence it is a good idea to contact your vet with a good history and when possible get a Post Mortem done.

These causes are usually either infection or poisonings and may include:

  1. Enterotoxeamia

Enterotoxeamia is the most common cause of acute Angora goat death under intensive conditions (feeding, pasture) but do still occur extensively on the veld due to the common predisposing factors. These predisposing factors may include

  • Changes in diet
  • Stasis of the intestinal tract (insufficient roughage)
  • Grazing on fodder crops,
  • High protein and energy diets
  • Deworming,
  • Coccidiosis, roundworms burdens
  • Sudden changes in the weather
  • Wilting of pasture.

The interval between predisposing factor and disease may be 2-14 days (usually 7-14). Ruminal flora adapt to a diet over several days. When a feed is changed to one with a high starch content the flora has not adapted to some of the starch which would normally be converted to fatty acids in the rumen. This carbohydrate then passes into the intestine where it results in the proliferation of Clostridium perfringens types of bacteria and production of toxins including epsilon toxin (Clostridium perfringens D) being the most common.

The different types of C perfringens produce different combinations of the four major lethal toxins — alpha, beta, epsilon and iota

For more information on Clostridium perfringens D (Pulpy Kidney, ‘Bloednier’) see

Clostridium perfringens type A has been associated with Angora kids that die from an enterotoxeamic condition and a may have a haemorrhagic enteritis. C.perfringens type A occurs naturally in the intestinal tract.

Similar predisposing factors exist with excessive amounts of protein and carbohydrate reaching the small intestine leading to an overgrowth of Clostridium perfringens  Type A and production of the alpha toxin.

  • Young goats grazing on lush pastures
  • Fed carbohydrate and protein rich diets,
  • Can occur sporadically after weaning,
  • After deworming
  • After a stress event.

For more info on ‘Rooiderm’ see


Clostridium perfringens type B  ‘Lamb dysentery’,’ Bloedpens’, ‘Bloodgut’  ‘Enterotoxeamia’ ‘Rooiderm’  usually affects very young kids (usually less than 2 weeks old) causing acute haemorrhagic to muco-haemorrhagic enteritis resulting in death. The kids may die within a few hours or 1-4 days.  It occurs more in winter and spring and is often with associated with cold weather. It is seldom seen in summer. The Clostridium perfringens B produces alpha, beta and epsilon toxins. The reason young kids are more susceptible to the Beta toxin is that trypsin is not secreted in sufficient amounts by the kids to inactivate the toxin. It is interesting to note that goats with a high levels of brown stomach worm causes the pH of the abomasum to rise which has the same result in that Trypsinogen is not converted o Trypsin.

For more info on ‘Bloedpens’ see

  1. Other Clostridia diseases that cause sudden death:

Clostridium septicum can cause uterine gas gangrene (also called ‘baarmoeder sponssiekte’) in Angora goat ewes. This malignant oedema is highly fatal and farmers may find an Angora ewe having died within 4 days of kidding – usually on the lands. Ewes with twins are more susceptible than those with single kids. The bacteria usually enter through lacerations contracted while giving birth. The bacteria produce toxins which causes tissue necrosis.

Deaths may also occur after a wound such as at shearing or castration.

For more info see

Gas gangrene, Blackquarter, ‘sponsiekte’  (Clostridium chauvoei)  is a very rare clostridium infection following wound infection in Angora goats (usually cattle). Goats are more resistant than sheep to infection. The infection causes gangrenous myositis, localised cellulitis and is usually fatal. Death is caused by the systemic effect of the toxins. There has been difficulty differentiating C. chauvoei from C. septicum (’Baarmoeder sponsiekte’). Outbreaks are usually seen in summer and autumn after heavy rains.

The areas of infection are related to the area of trauma such as injury to the vaginal mucosa during kidding or open castration. Dipping after shearing when goats have shearing wounds. Vaccinating with unhygienic needles or Umbilical cord infection.

Clostridium novyi Type A ( ‘Dikkop’ Swollen head ) is a very rare condition that can effect young rams and causes a swelling of the head and neck. The infection usually occurs through wounds occurring during fighting and usually the summer months. Death usually occurs within 48-72 hours. Similar swelling of the head can be confused with ‘Geeldikkop’ (photosensitivity), snake bite or oedema through hypoproteinaemia caused by roundworms in Angora goats.

  1. Heartwater


Angora goats are very susceptible to Heartwater (Ehrlichia). The time from the tick bite (The ‘Bont’ tick Amblyomma hebraeum) to a rise in temperature (>40C) is usually 7-35 days (average of 14 in the Angora goat). The disease in Angoras usually progresses so quickly that they often collapse, go into convulsions and die without the farmer seeing other clinical signs. The first signs are a poor appetite, lethargy, fever, lagging behind the flock and as the condition deteriorates the goat can have difficulty breathing and may stand with its tongue protruding, bleat, the tail and eyelids can twitch and usually lies down. Chewing movements can sometimes be seen. The goat starts paddling with its leg and its head pulls back before dying.

For more info on Heartwater see


  1. Pneumonia


Goats may just be found dead, deaths can occur within 12-24 hours of infection and  may occur for further 4-6 weeks

Pasteurellosis is often used to describe the disease ‘pneumonia’ or ‘bontlong’ and occurs more commonly in late autumn and early winter.  Losses are usually 2-8% but 10-50% can show signs of the disease.

Pneumonia is a disease of complex aetiology, involving interactions between a range of micro-organisms and the immunological and physiological responses of the host. Pasteurella (Manneheimia) haemolytica is ofyten considered to be the main bacteria.

For more info see



  1. Rift Valley Fever (RVF)


Angora goats are thought to be slightly less severely affected than sheep. The disease can be classified into 4 grades depending on severity.

  • Hyperacute RVF:

80-100% kids under 10 days old may die

Kid deaths occur within 12 hours after the fever reaction starts, others may survive longer and die within 12-24 hrs.

  • Acute RVF:

10-60% of kids older than 2 weeks may die.

Deaths 24-48 hours after start fever reaction

  • Subacute RVF

More adult goats

Death rate (5-20%)

For more information see

  1. Wesselbron disease


Wesselsbron disease is usually associated with Rift Valley Fever (RVF) as the conditions and vectors (mosquitos) are similar.

New-born Angora kids are most susceptible and deaths are seen whereas in adult goats cases are usually subclinical, although abortions may occur.

Wesselsbron disease is caused by a flavivirus and transmitted by mosquitoes. Aedes are thought to be the major vectors, but it has also been detected in other mosquitoes including Culex, Anopheles and Mansonia.


After an incubation period of 1–3 days deaths may occur in up to 30% of kids.

Non-specific signs of fever, anorexia, listlessness, weakness, and increased respiration.

Icterus (jaundice). For more info see


  1. Twisted gut ‘Rooiderm’’Draaiderm’


‘Rooiderm’ is a term that is used for a number of different conditions in the Angora goat. In this case the ‘Twisted gut’ or ‘Draaiderm’ leads to the bloody red colouring of the intestine, and hence the name ‘rooiderm’. This must not to be confused with ‘Rooiderm’ caused by the Clostridium perfringens group of bacteria.

Twisted gut is rare but may occur in Angora goats when:

  • Grazing on young fresh lush pastures. The high volume intake of lush pasture, such as lucerne or wilted pasture, can cause the rumen and intestine to swell and become displaced.
  • Physical movement such as at shearing, dipping, handling in the ‘kraal’ or when the goat’s position is rapidly changed. If a goat is rapidly turned to a seated position the movement can lead to the heavy and distended intestines twisting.

For more info see

  1. Bloat

Goats may just be found dead with a distended rumen (blown up like a drum). Usually they are more distended on the left hand side. Effected goats will be uncomfortable, have difficulty breathing and the tongue may protrude. The goat may die within a matter of hours.

Bloat in Angora goats can occur particularly when Lucerne lands are grazed but also when certain toxic plants have been eaten.

There are basically 2 types of bloat, both of which can be fatal.

  • Free gas bloat may be caused by certain plant poisons which cause rumen stasis such as in cases of tulp, krimpsiekte (cardiac glycosides) and prussic acid poisoning.
  • Frothy bloat occurs when the gas gets trapped in the foam and can’t be released. Frothy bloat is seen especially in green, wilted or frost damaged grazing pastures such as lucerne and clover.

For more info on bloat see


  1. Poisoning


  1. Prussic acid Poisoning ‘Geilsiekte’


Farmers speak about ‘prussic acid’, ‘geilsiekte’, ‘droë geilsiekte’, ‘opblaasgeilsiekte’, ‘blousuurvergiftiging’ and ‘opblaaskrimpsiekte’ relating to cyanide (HCN) poisoning

Prussic acid poisoning must be considered a possibility in any acute death in Angora goats (sheep and cattle).

Prussic acid poisoning is most likely to occur when grazing occurs:

  • After plant wilting (berg winds, frost)
  • Soon after a drought is broken by rain.
  • Plants that have regrown following tissue damage from livestock trampling or mowing.
  • Following high temperatures or water stress

The limp, green or partially wilted yellowed leaves are the most dangerous as they can also be sweet and more palatable. Once the plant material regains the moisture or dries out it loses its toxicity.

For more info on prussic acid poisoning see

  1. Cardiac Glycoside Poisoning (‘Nenta’, ‘Krimpsiekte’)

Although Nenta poisoning probably has a higher incidence in goats (more common in kids), other animals like sheep, cattle and horses are also susceptible. Angoras reportedly are more prone to “krimpsiekte” than boer goats. Cardiac glycoside-containing plants, collectively, is the single most important plant poisoning in South Africa.

Although symptoms mostly involve the nervous system, affected animals may also show signs of acute abdominal pain. These symptoms may also be features of other diseases. Sudden death, which may occur especially in young goats, is quite a common in a large number of diseases other than plant poisoning.

Members of three genera of the Crassulaceae (Cotyledon, Tylecodon and Kalanchoe), generally referred to as “plakkies”, contain cumulative, neurotoxic bufadienolides and may cause either acute or chronic poisoning.  The chronic form of the poisoning is colloquially referred to as “krimpsiekte” and is primarily a disease of small stock.

“Tulp” poisoning (induced by various Moraea species) and “slangkop” poisoning (caused by various Drimia species) induce only acute intoxication as these species contain non-cumulative bufadienolides.

'Witstorm’ ‘Vaalstorm’ Thesium spp also cause a cardiovascular syndrome Bufadienolide (cardiac glycoside)

For more info see

  1. Urea poisoning


Urea poisoning can occur when Angora goats take in excess amounts through a lick or if a lick gets wet (urea dissolves easily in water).

The maximum levels of urea tolerated by an adult Angora goat is 15g/day.

Goats should be adapted over 2-3 weeks by increasing the urea level slowly.

If they do not receive urea for a gap of 2-3 days then again an adaption period is needed.


An intake of 25-45g could potentially kill a goat within an hour. Clinical signs and death can occur from 30 minutes to 2 hours after ingesting excess urea


Due to the brain being affected we can see neurological signs:

For more info on urea poisoning see

Dr Mackie Hobson BSc Agric BVSc


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