Case Study: Brown Stomach Worm

CASE STUDY: 1

BROWN STOMACH WORM

February through to June is often the time when we see the most problems associated with brown stomach worm (Teladorsagia circumcincta) and problems often arise again in early summer.

In this case study on a very progressive Angora farm, kids were being run on the lands.

The weaker kids started dying more so after shearing towards the end of January when cooler weather was experienced for a few days. The condition of the majority of kids was very good but the odd kid kept dying.

Previous preventative health management included:

  • The kids had their second Coglavax vaccination during the last week of January
  • The kids had been dosed for roundworms (Zolvix) during the 2nd week of  February.
  • The kids were dosed for tapeworm (Conifluke + Tape). One group during the last week of February and the other the first week in March.
  • The SAMGA vet visited the farm in mid-March, under 2 months since the colstridial vaccination, just over a month since the kids were dosed for roundworms and just over a week since the tapeworm dose.

Symptoms  

The majority of the kids were in good condition with signs amongst some of weaker kids of:

•          Poor appetite

•          Weak

•          Weight loss

•          A few kids had submandibular as well as oedema of the abdomen and   

            limbs so called ‘waterpens’ ‘swelsiekte’

•          Diarrhoea

•          A few kids had pale eye mucous membranes but the majority were 3 on

           FAMACHA.

The likely cause of the symptoms:

The diarrhoea can be caused by brown stomach worm larvae which burrow and feed in the lining of the abomasum damaging the cells. These damaged cells then can’t produce acid which results in the pH of the abomasum rising from 2 to almost 7. The increased pH has dramatic consequences as the enzyme pepsinogen can’t be converted to active pepsin which prevents subsequent digestion of feed material. This changed pH also results in the proliferation of bacteria so together result in diarrhoea. Undigested protein also hinder fluid absorption worsening the diarrhoea.

 

The well-known signs of ‘swelsiekte’ where tissue fluid (oedema) collects under the skin and  gravitates to areas under the belly, down the legs and under the jaw.

 

The brown stomach worm results in a decrease in protein and especially albumin levels in the blood. The loss of proteins caused by the diarrhoea, reduced uptake from the intestine and the loss of appetite results in further declining protein levels.

This decrease in albumin decreases the oncotic pressure within the blood vessels leading to oedema and ‘swelsiekte’.

Faecal samples were taken from all the different groups of kids on the lands to be analysed later back at the practice.


A post Mortem
 was then done on 2 dead kids as well as a kid about to die to make a diagnosis.

During the post mortem we saw the following.

  • Fluid ‘oedema’ under the skin

 

  • Fluid in the abdomen (ascites) and thorax

  • Enlarged mesenteric lymph nodes (the lymph nodes through which the blood from the digestive tract drains)

  • Inflammation of the abomasal wall (abomasitis) with ulceration. The photo is after a section of the abomasum has been washed. The brown stomach worms are so small that they are hardly visibly with the naked eye. We took samples from the abomasal wall to examine under a microscope back at the vet clinic. 

  • Intestines were filled with watery diarrhoea  and gas 

Presumptive diagnosis:(made on the farm)

Brown stomach worm

 

Samples for Histopathology:
Because of the diarrhoea, fluid and gas in the intestines we took tissue samples and sections of the intestine to check to see if there was any indication of a colostridial bacterial overgrowth also playing a role in the deaths of the kids.

This is a possibility due to undigested material passing through to the small intestine due to the effects of the brown stomach worm leading to an overgrowth of clostridial bacteria and production of toxins.

We also wanted to evaluate the intestinal walls to determine if coccidiosis was playing a role in the diarrhoea.

 

Faecal samples were taken back to the vet clinic and analysed:

  • Smears from the contents of the abomasum reflected a heavy brown stomach worm burden.
  • The faecal egg counts  (FEC) confirmed our initial diagnosis.

            The FEC in the different kid groups ranged

1)    1 800  to 10 800 eggs per gram (epg) brown stomach worm

2)    400- 11 200 epg coccidian

The Post mortem kids:

1)    10 000 – 32 000 epg brown stomach worm

2)    600- 1000 epg Coccidia

  • he coccidian counts indicated a presence but along with the clinical signs did not suggest a cause of the deaths.

The pathology report confirmed the diagnosis. It also ruled out any clostridial involvement and indicated that the coccidia had not caused any significant pathological damage to the intestinal walls.

  • The farmer dosed the kids with Zolvix
  • A faecal egg count reduction test (FECRT) was carried out 10 days after dosing. The egg counts in all 6 groups of kids on the lands were zero. The coccidian counts also declined due to the likely improvement of the immune status of the kids after being dosed again.

Discussion points:

  • Infected larvae on the land can survive on pasture for up to 14 months and are capable of overwintering in cold conditions. The L3 stage larvae crawl up blades of grass up to 50cm from where they were passed in the faeces 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.
  • It is important to do regular FEC to monitor the situation on the pasture.
  • 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.
  • Do FECRT (faecal egg count reduction tests) to determine the efficacy of the different active ingredients of the doses you use on the farm.
  • Check all the different dose groups and their active ingredients on the SAMGA web site to ensure you maintain efficacy of the different doses. Also see the ‘ Roundworm Resistance to Anthelmintics in Angora Goats’ on the web site.

CASE STUDY: 2

The importance of a Faecal Egg Count Reduction Test (FECRT) is demonstrated in another case study in April also involving Brown Stomach Worm.

A farmer was experiencing kid deaths.

He had a post Mortem done by the SAMGA vet which again indicated brown stomach worm the cause of the deaths.

  • The farmer dosed all the kids with an ivermectin product
  • As advised the farmer took faecal samples from kids at the time of dosing (which he marked) and again 7-10 days later.
  • The kids continued to die.
  • When the faecal samples were analysed after 10 days the faecal egg counts in one group remained 1000 epg and the other dropped from 1000 to 800.
  • The farmer then dosed 90% of the flock with Zolvix and re-dosed the other 10% of the flock with the Ivermectin at 1.5x the dose of sheep.
  • 10 days later the FECRT was done on another sample.

The Zolvix group had Zero eggs (100% FECRT) while the Ivermecting  egg count only dropped by 20%.

This demonstrates that on this particular farm there was a resistance to ivermectin.

Every farm differs in terms of the resistance status to different drug groups. Ivermectin is still effective on most farms.

Most resistance has occurred in the following active ingredients:

  • Benzimidazoles (Group 2 on the drug label- Febendazole, Oxfendazole, Albendazole)
  • Imidazoles ( Group 3 -Levamizole)
  • Macrolytic lactones (Group 1- ivermectin)

Find out what is happening on your farm regarding the resistance status of your drugs.

 See ‘ Roundworm Resistance to Anthelmintics in Angora Goats’ on the web site as well at the different Anthelmintic drug groups listed on the web site.

Dr Mackie Hobson

Photo courtesy of: The Genome Institute Washington

 

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