The impact of Brown Stomach Worm (and Coccidiosis) on Angora Kids

Wednesday, 29th August 2018

Dr Mackie Hobson

Brown Stomach worm (BSW) (Teladorsagia circumcincta) can have a significant impact on weaned Angora goat kids especially in the autumn and early winter (March-June).

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

 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.

The infective stage 3 larvae develop 5-6 days after the eggs hatch. These infective larvae are relatively tough and are capable of overwintering in cold conditions. Once the L3 larvae are taken in by the grazing goat they leave their protective sheath after 3 days and penetrate the lining of the abomasum. Brown stomach worm larvae do not feed on blood, but damage the lining of the stomach as they mature to adult worms. For this reason pale mucous membranes (anaemia) are not such a significant feature compared to ‘wireworm’ infestations.

Adults (about 10mm in length) develop after about 9 days and the adult females start producing eggs (50-100 eggs a day) at about 18-21 days after infection. The larvae can become ‘hypobiotic’ and remain dormant for several months in the abomasum to emerge the following spring.

What damage does the BSW larvae do?

  • After exiting their protective sheath the larvae penetrate the lining of the abomasum. This causes an inflammatory response by the wall of the abomasum.
  • Parietal cells are penetrated and damaged. The parietal cells are responsible for secreting acid and maintaining a low pH environment of the abomasum. The result is that the pH of the abomasum rises (becomes more alkaline) which results in Trypsinogen and Pepsinogen not being converted to Pepsin and Trypsin. The enzymes Trypsin and Pepsin are vital for the digestion and breakdown of protein into a useable form.
  • The increased pH may also lead to bacterial proliferation and resulting diarrhoea. That is why the abomasal content may appear and smell unfavourably different on PM.

Photo of the Abomasum showing severe inflammation and the ‘ostrich’ skin ulcerated and nodular appearance following Brown Stomach worm (Photo www.wormboss.com Source: Dr R Woodgate, Department of Agriculture Western Australia)

What damage does Coccidiosis do?

There are many stages in the development of the coccidia, and at each stage intestinal cells are invaded and then destroyed – causing repeated damage to the intestine. The intestinal damage can release blood and cause inflammation of the lining of the gut. The animal loses blood, water and protein and cannot absorb nutrients as efficiently. If enough damage is done, it becomes extremely ill and may die. Angora goats are less prone to haemorrhage (bleeding) than sheep as a clinical sign.

 

What causes the blood protein levels of the goats to drop?

  • 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 with both coccidiosis and BSW.
  • 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 by coccidiosis causes the release of protein exudate and reduced the ability of the absorption of protein.

Photo: An Angora kid with heavy Brown Stomach Worm and Coccidiosis showing ‘swelling disease’. Note there is no significant diarrhoea.

The Recovery of Albumin levels in Angora kids following Brown Stomach Worm and Coccidiosis

A case study involved 9 month old Angora kids which had been dosed with a levamisole containing product 10 days earlier. The kids were weak, showed a loss in condition, some had diarrhoea and a few kids showed swelling ‘swelsiekte’ and deaths were reported.

A post mortem was conducted to determine the cause of deaths.

On Post Mortem the following was found:

  • Subcutaneous oedema, ascites. (‘Swelsiekte’)
  • Brown stomach worm (and a few wire worm) in abomasum.
  • Inflamed abomasal wall
  • Faecal egg count of 36 kids averaged 8600 epg roundworm (Brown stomach worm) and 22 900 epg Cocciodiosis.
  • The mesenteric lymph nodes were enlarged

Mesenteric Lymph nodes enlarged

Mesenteric Lymph nodes enlarged

Ascites (fluid in abdomen)

Ascites (fluid in abdomen)

 

36 of kids showing clinical signs of weakness, oedema (swelling) and diarrhoea were:

  • blood sampled on day 0, 3, 7, 14, 21. 28, 38 (albumin levels)
  • all dewormed (First Drench) and treated for coccidiosis (vecoxan)

 

Blood samples were taken on days 0, 3, 7, 21, 28, 38 after treatment for BSW and Coccidiosis.

 

 The Albumin levels were checked arranged highest to lowest in the table below.

 

day o

day 3

day 7

day 14

day 21

day 28

day 38

22

21

20

22

23

22

25

20

21

22

25

28

31

30

19

20

22

25

28

29

29

19

19

21

24

28

28

29

18

19

21

24

25

27

29

18

18

20

24

25

26

28

17

18

19

24

25

26

27

20

17

18

21

23

25

27

15

16

17

21

23

25

27

15

15

16

20

23

24

27

13

15

16

20

22

23

27

18

14

16

19

21

23

27

14

14

15

18

21

22

26

16

13

14

17

21

21

26

15

13

14

17

21

21

26

13

13

13

17

20

21

26

15

12

13

17

20

21

26

15

12

13

16

19

21

25

14

12

13

16

18

21

25

14

12

12

16

18

20

23

13

12

12

16

17

20

23

12

12

11

16

17

20

22

14

11

11

15

17

19

21

14

11

10

13

13

16

21

13

11

10

 

 

 

 

12

11

 

 

 

 

 

11

11

 

 

 

 

 

11

9

 

 

 

 

 

11

7

 

 

 

 

 

12

6

 

 

 

 

 

10

 

 

 

 

 

 

9

 

 

 

 

 

 

 

The RED (table above) indicated kids that died post treatment. It is interesting to note that:

  • If the Albumin level dropped below a critical level of
  • ALL the kids died- no exceptions.
  • If the Albumin level was between or equal to 10-11 the survival rate was 50% (3/6)
  • If the kids maintained a blood Albumin level of >12 g/l they recovered post treatment

Faecal samples were checked on day 14 to ensure no parasites remained.

What are ‘normal’ Albumen levels in Angora goat kids?

  • 6 ‘normal kids’ were blood sampled and the Alumen levels ranged between 30-38 g/l (average 33 g/l).
  • From previous studies on ‘swelling disease’ goats which did not swell the albumin levels averaged 30g/l.

For kids recovering with the albumin levels returning to normal the target would be for the Albumin levels to return to > 30g/l (target- marked green on the graph below)

 

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.

This study highlights a few important points for the Angora farmer to keep in mind in order to ensure the health and wellbeing of their Angora kids

  1. Taking a faecal sample and getting it check 10-14 days after dosing is important to ensure there is no anthelmintic (dose) resistance on his farm.
  2. The anthelmintic (dose) treatment in Angora goats should be 1,5x that of sheep
  3. Combination doses are better and slower to develop resistance.
  4. From the end of March to June it is vital that Faecal egg counts are monitored to prevent the kids getting into this position

 

A study field study of different treatments has was also done to determine if any treatment protocol resulted in a quicker recovery to normal albumen levels. SAMGA Website

Dr Mackie Hobson (SAMGA vet)

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