Brown Stomach Worm
By Dr Mackie Hobson BSc(Agric),BVSc

Tuesday, 12th August 2014

The brown stomach worm (Teladorsagia circumcincta) has major health implications for Angora goats especially those grazing on lands and a common cause of hypoproteinaemia, weakness and ‘swelsiekte’ in Angora goats.

The natural and acquired immunity of weaned Angora kids under 9 -12 months is very poor and hence why they are particularly susceptible to Brown Stomach Worm (BSW) during autumn and early winter a few months after weaning.

In the spring when the risk of BSW is high, but the kids are now a year old so have a more developed immune system to deal with the challenge. Angora goats are generally much more susceptible than sheep to BSW. See immunity in the Angora goat

Clinical signs of Brown Stomach worm infection?

  • Poor appetite
  • Weak
  • Weight loss
  • Submandibular oedema as well as marked oedema of the abdomen and limbs ‘waterpens,’ ‘swelsiekte’
  • Diarrhoea
  • Anaemia may also occur although not always the case.




What causes the drop in blood protein (albumin) levels? (‘Swelsiekte’, ‘Waterpens’)

  • There is an inflammatory response and loss of protein through the mucosal wall of the abomasum caused by the penetrating brown stomach worm larvae.
  • Damage to the parietal cells of the abomasum by BSW causes an increase in the pH of the abomasum resulting in Pepsin and Trypsin not being formed and effecting protein digestion and absorption.
  • Loss of protein through diarrhoea and decreased protein uptake via the intestine.
  • The loss of appetite by the kid reduces protein intake
  • Adult worms also suck blood (3-4 weeks after initial infection) but the effect is not as pronounced as wireworm.
  • Inflammation of the intestinal tract causes the release of protein exudate and reduced the ability of the absorption of protein.

See Swelsiekte

How does the brown stomach worm cause diarrhoea?

Larvae are the most damaging stage burrowing into the stomach wall. The cells of the stomach proliferate trying to heal the injuries. 

The damaged parietal cells can't produce acid. The consequence is that the pH of the abomasum rises up from 2 to almost 7, with dramatic consequences. 

Secreted pepsinogen can't be transformed into active pepsin, which hinders protein denaturation and subsequent digestion of feed material in the intestine. The increased pH also leads to bacterial proliferation in the abomasum compounding the diarrhoea.

Undigested proteins in the gut hinder fluid absorption worsening the diarrhoea.

What time of the year is worse? 

The major impact of brown stomach worm is from February to June and again October to December. When sheep and goats graze together goats are always more heavily infected.

Larvae are common on pasture in the cooler months (April to September)

Life cycle

Eggs passed out in faeces  can hatch at temperatures even as low as 5C.The Larvae develop to stage 3 larvae 5-6 days after hatching ( at optimum temperatures of 22-27C and more slowly when cooler). The infective larvae can survive on pasture for up to 14 months and are capable of overwintering in cold conditions.

Infective larvae can actively move off the dung into pasture up to a distance of 50 cm.

The L3 stage larvae crawl up blades of grass and are taken in by the grazing goat. 

The larvae move through to the abomasum where they leave their protective sheath after 3 days and penetrate the lining of the abomasum. Adults can first be seen 9 days after infection and the adult females start producing eggs about 18-21 days after infection. 

The larvae in the abomasum can become arrested (hypobiotic, dormant) in the nodules for several months, especially in autumn and early winter, to emerge only during the next spring, when environmental conditions are more favourable.

 Post Mortem findings:

  • Anaemia,
  • Sub-mandibular and sternal oedema,
  • Diarrhoea.
  • Nodular gastritis covered by mucus.
  • Abomasitis with ‘ostrich leather’ appearance and ulceration of the mucosa.
  • The brown stomach worms are so small that they are hardly visibly with the naked eye.

Treatment and management of Brown stomach worm

It very important producers understand the concepts of ‘Roundworm management’

Various treatment (small field study n=6 per treatment group) to see if any treatment was of benefit in addition to the anthelmintic?




What are the possible reasons for the differences in the recovery rates of the treated groups?

Remember this is a very small sample (n=6) in each treatment group so must be taken in context.

F: No treatment

We can see from the graph that the protein levels continued to drop. For welfare reasons we treated these kids for BSW on day 7 after which they started to improve. It is quite obvious that the underlying the main underlying problem of Brown Stomach must be treated.

E: No additional treatment (apart from treating parasites)

It is clear from the graph that these kids were slower to recover after only receiving the parasite treatment. They recovered at a similar rate to Group D (ad lib pellets)

D: Add lib Pellets (feed)

It appears that up until day 14-28 the kids with ad lib pellets did not perform much better than the equivalent kids in the veld (E). The rate of improvement increased after day 21.

The damage to the parietal cells (acid secreting) lining the abomasum will result in a sub-optimum pH of the abomasum (more alkaline). The higher pH results in Trypsinogen and Pepsinogen not being converted to Pepsin and Trypsin so digestion of the pellets is ineffective? I would speculate that it takes about 2-3 weeks for the abomasum l to recover from the damage caused by the BSW. 

C: Antibiotic (Peni LA)

This was a surprise as I was not expecting much benefit from the use of antibiotics in these cases as is evident in the first 14 days. Due to the mucosal damage there could be a secondary bacterial invasion which the antibiotic may have eliminated resulting in a quicker healing process. The antibiotic may also have an influence on bacterial overgrowth following the altered digestive system.

B: Steroid (Dexamethasone)

The improvement in the kids injected with dexamethasone (steroid) may be due to the reduction of the inflammation of the abomasum wall.

A: Byboost ‘Kickstart’ (Bayer)

Byboost Kickstart is a concentrated liquid containing vitamins, trace elements, essential amino acids and essential fatty acids with added nucleotides. Byboost provides a nutritional and energy boost and hence the reason aided recovery.

The use of probiotics were not evaluated in this study.


Mohair SA conducted a field study to determine how long it took for severely affected young Angora goats (post weaning) to recover after anthelmintic treatment.

Graph of the group average Albumin levels (Goats that died were excluded from the average)




From this graph it can be extrapolated that it would take between 50-60 days for these kids to return to ‘normal’ after having had a severe brown stomach worm/coccidiosis infection.

The green line (red arrow) is the ‘normal’ level of Albumin.

Why do the goats keep dying post treatment for up to 2-3 weeks?

At what Albumin levels are Angora goats likely to die? Data collected (n=36) suggest the following outcomes:




Farmers often don’t understand why the goats continue to die after an initial diagnosis of hypoproteinaemia (following coccidiosis or brown stomach worm for example) is made- even after the underlying parasite problem has been treated?

  1. Albumin plays a vital role in survival as pointed out in the section below and hence goats continue to die. The Albumin levels may take up to 50 days to return to normal level.
  2. Immunoglobulins/antibodies are glycoproteins vital for a functioning and effective immune response. Their levels will be low until blood proteins return to normal. This is likely to be the reason that goats may die of many secondary causes such as pneumonia or septicaemia during the recovery period.

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