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Ostertagiasis
Ostertagiasis in sheep, also called teladorsagiosis, is caused by a small brown worm that lives in the abomasum, the true stomach of ruminants. Unlike the red worm, which sucks blood and causes anemia, this worm disrupts digestion. Its larv...
What is it?
Ostertagiasis in sheep, also called teladorsagiosis, is caused by a small brown worm that lives in the abomasum, the true stomach of ruminants. Unlike the red worm, which sucks blood and causes anemia, this worm disrupts digestion. Its larvae develop in the glands of the abomasum wall, causing them to swell and destroy them. The abomasum then loses its acidity: it no longer digests proteins correctly and allows poorly prepared food to pass into the intestine. The result is watery diarrhea, a plummeting appetite, and rapid loss of condition, without the animal being anemic. This parasite is one of the best adapted to temperate regions and cool, humid seasons: it often dominates where the red worm, more fond of heat, retreats. In the northern Tunisian regions, the two meet depending on the season. It has another formidable characteristic: its larvae know how to go dormant in the wall of the abomasum and leave all together later, causing an attack without the animals having changed plot.
Commonly observed signs
These signs are neither exhaustive nor specific. Only a veterinarian can establish a diagnosis.
Related signs — each one links to its page:
Liquid diarrhea, often greenish, persistent, which soils the hindquarters and the wool of the tail.
Clear drop in appetite: the animals graze for less time, this is often the first change noticed at the scale of the lot.
Rapid weight loss or growth that stops abruptly among young people, with gaps widening within the same batch.
Dull, brittle, poorly established wool, sometimes coming loose.
Soft swelling under the jaw in prolonged forms, linked to protein leakage.
Dehydration and weakness when diarrhea lasts.
Slaughtered animals, which remain lying down and allow themselves to be approached.
The mucous membranes generally remain normal in color: looking for paleness, as with the red worm, misses the diagnosis.
In the delayed form, an attack occurs in older animals, often at the end of the cool season or around giving birth, even though they have not been returned to contaminated plots.
When to consult without delay
This list does not replace veterinary advice. It gathers situations that justify a prompt consultation.
Causes and risk factors
The adult worms live in the abomasum and lay eggs which leave with the droppings.
On the ground, the eggs produce larvae which climb onto the blades of grass with moisture and are swallowed by animals. These larvae tolerate cold and humidity well, and survive a long time on the plot.
Once swallowed, they enter the glands in the wall of the abomasum and develop there. The glands swell, transform and the wall takes on the appearance of small contiguous bumps, very recognizable at autopsy.
This transformation causes the acidity of the abomasum to drop. The proteins are no longer digested, the organ leaks proteins from the blood and diarrhea sets in: the disease is due to this disturbance, more than to the number of worms.
The larvae can also interrupt their development and remain dormant in the wall during the unfavorable season. They then leave all at the same time, often at the time of giving birth or when favorable conditions return, and the massive destruction of the glands then causes a sudden crisis, more difficult to treat.
Lambs and young animals in the first grazing season: they pay the heaviest price.
Ewes around birth and at the start of lactation, whose defenses naturally drop.
Cool and humid seasons, autumn and end of winter in the northern regions, periods following the rains.
Short grazing, high stocking rates, lack of rotation.
Insufficient diet, particularly in protein: the damaged abomasum already digests poorly, a poor ration makes everything worse.
Herds systematically dewormed on a fixed date for years: this parasite is among those in which resistance to antiparasitic drugs is most frequently observed.
Quarantine-free purchases, fairs and gatherings.
Transmission
Contamination occurs only through grass and contaminated water, without direct contact between animals, and without risk for humans.
Ewes at the end of gestation and at the beginning of lactation eliminate many more eggs than usual: they load the plots at the precise moment when their lambs begin to graze.
The larvae concentrate in the first centimeters above the ground: the shorter the grass, the more the animals swallow.
Plots grazed continuously by the same categories of animals become heavier from year to year.
An animal purchased without quarantine can introduce worms already resistant to antiparasitic drugs: this is particularly documented for this parasite.
Diagnosis and care
Diagnosis is the veterinarian's responsibility, based on clinical examination and laboratory tests. Care is decided case by case.
The veterinarian relies on the context, the age of the animals, the season and the condition of the lot.
Scat analysis with egg counting is the basic examination; it is done on several animals from the same batch, never on just one.
A culture of the larvae allows us to know which worm dominates, useful information because the behavior differs depending on whether it is mainly this brown worm or the red worm of the abomasum.
An important trap exists in the delayed form, where the sleeping larvae leave en masse: the worms are not yet adults and do not lay eggs, so the analysis of droppings can be light while the animals are doing very poorly. The result should not be wrongly reassuring.
Blood tests may show low protein levels, which explains the edema.
The autopsy of a dead animal is very telling: the wall of the abomasum has a lumpy appearance, in small bumps joined together.
A post-treatment dropping check is the most useful test to verify that the product used is still working on the farm.
Treatment
Several families of internal antiparasitics act on this worm. The choice is up to the veterinarian, depending on the age of the animals, milk production, the dominant worm species and above all what remains effective locally.
The delayed form, with larvae sleeping in the wall of the abomasum, is more difficult to treat than the ordinary form: not all the molecules reach these larvae. This is one more reason not to choose your product alone.
No dose or rhythm can be improvised: underdosing cleans poorly and directly selects resistant worms.
This parasite is one of those in which resistance is most widespread. Treating the entire herd on a fixed date, without analysis, is precisely the practice that established them. The recommended approach consists of relying on dung analyses, treating only batches or animals that really benefit from it, and voluntarily leaving a part of the herd untreated to preserve worms that are still sensitive to the products.
Changing bottles at random is not a strategy: alternating families can only be discussed with the veterinarian and on the basis of an effectiveness check.
Affected animals need a diet rich in good quality proteins, clean water and rest: the abomasum takes time to repair itself.
Waiting times for meat and milk vary depending on the product and some are prohibited for dairy females: ask for them before any treatment.
Treatment depends on the cause and the animal's condition: it must be determined by a veterinarian. No self-medication.
Prevention
Rotate plots and do not let animals shave the grass.
Reserve the less heavily loaded plots, for example after mowing or cultivation, for lambs and ewes at the end of gestation.
Avoid grazing young flocks behind ewes at the start of lactation, which have just loaded the plot.
Alternate with cattle or horses when the farm allows it.
Quarantine and treat, on veterinary advice, any animal purchased before releasing it to pasture: this is the action that avoids importing resistant worms.
Monitor the growth of lambs by regular weighing: stalling is often the first signal, even before diarrhea.
Ensure a sufficient diet of proteins and minerals.
Have it checked from time to time, by analyzing the droppings after treatment, that the products used are still working.
Keep for breeding animals that remain in good condition without treatment.
Possible complications
Long-term growth delay in young people, which does not completely catch up.
Weight loss in ewes, poor recovery after lactation, reduced fertility and weaker lambs at birth.
Dehydration and severe weakness during prolonged diarrhea.
Chronic protein leak, with edema under the jaw and under the abdomen.
Permanently soiled hindquarters, conducive to myiasis in the hot season.
Sudden attacks when sleeping larvae wake up, more difficult to treat and more deadly.
Installation of resistance to antiparasitics which deprives the exploitation of entire families of products.
When to see a veterinarian
Several animals in the same batch have persistent watery diarrhea.
The lot is visibly eating less and grazing for less time than before.
The lambs stop growing even though the grass and ration are correct.
Ewes lose weight after giving birth without explanation.
A soft swelling appears under the jaw.
A crisis occurs in animals which have not changed plot: this suggests the awakening of sleeping larvae, talk to the veterinarian.
Animals do not improve after deworming: have the effectiveness of the product checked rather than giving it again.
Prognosis
Animals treated early, with an effective product and a good diet, recover, but the abomasum takes weeks to return to normal functioning.
Delayed forms, due to the massive awakening of the larvae, have a more reserved prognosis: the lesions are extensive and treatment less easy.
Severely affected young people remain permanently stunted.
At the herd level, everything depends on grazing management, feeding and the state of resistance: where several families of products no longer work, control relies above all on management.
Frequently asked questions
My sheep have diarrhea but their mucous membranes are very pink: are they worms?
Yes, most likely. This brown abomasum worm does not suck blood: it disrupts digestion and causes diarrhea without anemia. Looking for pale mucous membranes, as for the red worm, misses the diagnosis here.
A crisis broke out when I did not change my plot animals: how is this possible?
This is the signature of this parasite. Its larvae can remain dormant in the wall of the abomasum during the bad season, then leave all together, often around births. The contamination is old, the crisis is recent. This form is more difficult to treat: talk to the veterinarian.
My dewormer no longer seems to be working, is this possible?
Yes, and it is common with this parasite, one of the most affected by resistance to antiparasitic drugs. The veterinarian simply checks it, comparing the number of eggs in the droppings before and some time after treatment. Continuing to use a product that has become ineffective is expensive and makes the situation worse.
What is the difference with the red abomasum worm?
Both live in the abomasum, but they do not have the same disease. The red worm sucks blood and kills through anemia, often without diarrhea. The brown worm damages the glands of the abomasum and causes diarrhea with loss of appetite, without marked anemia. An analysis of droppings with larvae culture allows you to know which one is dominant and to adapt your management.
References
FAO — Organisation des Nations unies pour l'alimentation et l'agriculture
ANSES — Agence nationale de sécurité sanitaire (France)
Content reviewed by the TunisieVet editorial team · Updated 11 August 2026
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