Ostertagia and Teladorsagia are two genera of parasitic roundworms that infect cattle, sheep and goats and other wild ruminants. Worms of these genera are also called brown stomach worms. In the past most species were considered as belonging to the genus Ostertagia. They have very similar features and life cycles.
They are found worldwide, depending on the species, but are more abundant in regions with temperate and cool climate. They are the most damaging gastrointestinal worms of ruminants in regions with moderate and cool climate, particularly for cattle.
The most relevant species for livestock are:
- Ostertagia lyrata infects mainly cattle.
- Ostertagia ostertagii infects mainly cattle, but also sheep, goats and other domestic and wild ruminants.
- Teladorsagia circumcincta (=Ostertagia circumcincta) infects sheep and goats worldwide.
- Teladorsagia pinnata (= Ostertagia pinnata) infects sheep and goats worldwide.
- Teladorsagia trifurcata (= Ostertagia trifurcata) infects sheep and goats worldwide.
These worms do not affect dogs, cats or swine.
The disease caused by Ostertagia or Teladorsagia worms is called ostertagiasis or ostertagiosis.
Is livestock infected with Ostertagia or Teladorsagia worms contagious for humans?
- NO: The reason is that these worms are not human parasites.
Final location of Ostertagia and Teladorsagia worms
Predilection sites of adult Ostertagia and Teladorsagia worms are the stomach (abomasum) and the upper small intestine.
Anatomy of Ostertagia and Teladorsagia worms
Adult worms of these two genera are very similar, up to 12 mm long and rather thin. They have a brownish color. As for other roundworms, the body of these worms is covered with a cuticle, which is flexible but rather tough and in these worms has several longitudinal ridges. The worms have a tubular digestive system with two openings, the mouth and the anus. They also have a nervous system but no excretory organs and no circulatory system, i.e. neither a heart nor blood vessels. The female ovaries are large and the uteri end in an opening called the vulva. Males have a copulatory bursa with two short and thin spicules for attaching to the female during copulation.
The eggs are ovoid, about 45x85 micrometers, often slightly asymmetric, have a thin shell and contain 16 to 32 cells (blastomeres).
These worms have a direct life cycle, i.e. there are no intermediate hosts involved. Adult females lay eggs in the stomach or intestine of the host that are shed with the feces. Once in the environment the eggs release the L1-larvae that complete development to infective L3-larvae in a few weeks depending on temperature and humidity. These infective larvae can survive on pasture for up to 14 months and are capable of overwintering in cold regions such as Northern Europe. Eggs and infective larvae can survive also in manure or slurry for months. Infective larvae can actively move off the dung into pasture up to a distance of 50 cm, or are spread passively when the dung is trampled.
Livestock becomes infected after ingesting infective larvae on pasture. Housed stock can also become infected through contaminated hay or bedding.
Ingested larvae reach the stomach and burrow into its wall, where they cause the appearance of characteristic nodules. About 2 weeks later they leave the nodules and complete development to adults in the lumen. The adults attach to the stomach or the guts wall and star producing eggs that are shed with the feces. Or the larvae 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 favorable.
The prepatent period (time between infection and first eggs shed) is 2 to 4 weeks (without dormancy) depending on the species and the host.
Harm caused by Ostertagia and Teladorsagia worms, symptoms and diagnosis
As already mentioned, Ostertagia and Teladorsagia are the most damaging worms of cattle in regions with temperate and cool climate.
There are two major clinical developments, type I ostertagiasis (also called summer ostertagiasis), and type II ostertagiasis (also called winter ostertagiasis).
- Type I ostertagiasis affects calves and young stock during their first grazing season when they become infected with these worms for the first time.
- Type II ostertagiasis affects adult stock that becomes sick when arrested larvae resume development during winter and early spring. Outbreaks can happen any time during winter and spring before the next grazing season.
Larvae are the most damaging stage. The cells of the stomach proliferate trying to heal the injuries caused by the burrowing and feeding larvae. But such cells can't produce acid. The consequence is that the pH of the abomasum rises up to almost 7, with dramatic consequences. Secreted pepsinogen can't be transformed into active pepsin, which hinders protein denaturation and subsequent digestion in the intestine. Blood gets undigested into the gut and bacteria proliferate in the abomasum. Undigested proteins in the gut hinder fluid absorption, which causes diarrhea. Incomplete protein digestion decreases albumin absorption to blood, which has to be compensated with increased food intake, which is very difficult because the affected animals lose appetite.
Typical clinical signs and symptons are gastroenteritis (inflammation of the stomach and/or the gut), anemia, diarrhea (mucous or watery, often putrid), dehydration, loss of appetite and weight (up to 20% in 1 week after outbreak!), all more or less severe depending on the number of larvae that cause the infection and the condition of the animals. Other effects are also edema, i.e. accumulation of liquid in the abdomen (ascites) and also in the submandibular tissue, which is know as "bottle jaw" and is characteristic of infections with these and other gastrointestinal worms.
Fatalities are frequent both in young and old stock. Type II ostertagiasis can be particularly dramatic if the animals had been previously weakened or stressed due to poor food during winter or pregnancy.
Most infections are mixed with other gastrointestinal roundworms (e.g. Cooperia spp, Haemonchus spp, Nematodirus spp, Trichostrongylus spp, etc.) which worsen the damage caused by Ostertagia and/or Teladorsagia worms.
Diagnosis is based on the clinical signs and confirmed after detection of characteristic eggs in the feces. However, as already mentioned, outbreaks of type I ostertagiasis occur before larvae have completed development to adults, i.e. before the onset of egg production and shedding. And outbreaks of type II ostertagiasis are due to arrested larvae resuming development, also before they have started shedding eggs in the feces.
Prevention and control of Ostertagia and Teladorsagia infections
Preventative measures that reduce the contamination of pastures with infective larvae (e.g. pasture rotation) and reduce the risk the animals become infected are essential to prevent infections.
Such preventative measures are the same for all gastrointestinal roundworms and are explained in a specific article in this site (click here). Such measures must be applied for both young and adult livestock, because infections with these worms can be fatal for animals of any age.
When designing specific preventative measures for a given property it must be taken into account that infective larvae can remain infective on pasture for up to 14 months, even through very cold winters. It is also very important to avoid progressive pasture contamination with larvae along the summer (avoid overstocking!) because infections with these larvae in autumn will cause the type II winter outbreaks: the more infected the pastures in autumn, the more likely and threatening the winter outbreaks will be.
Systematic and thorough removal of all manure, keeping the facilities dry and additional hygienic measures of animal facilities will reduce the risk of infection of housed livestock.
Livestock exposed to these worms may develop natural resistance progressively and may recover spontaneously, but only well fed healthy animals, not already weakened animals. Such resistant animals do not become sick if re-infected, but continue shedding eggs that contaminate their environment.
A lot of research has been carried out on vaccines, but so far no really effective one is available against Ostertagia and/or Teladorsagia worms. To learn more about vaccines against parasites of livestock and pets click here.
Biological control of Ostertagia and/or Teladorsagia worms (i.e. using its natural enemies) is so far not feasible. Learn more about biological control of worms.
You may be interested in an article in this site on medicinal plants against external and internal parasites.
Numerous broad spectrum anthelmintics are effective against adult worms and larvae, e.g. several benzimidazoles (albendazole, febantel, fenbendazole, oxfendazole, etc.), levamisole, as well as several macrocyclic lactones (e.g. abamectin, doramectin, eprinomectin, ivermectin, moxidectin). But not all of them are effective against arrested larvae of Ostertagia and/or Teladorsagia. Read the product label carefully to find it out.
A few other narrow-spectrum anthelmintics such as closantel and tetrahydropyrimidines (e.g. morantel, pyrantel) are effective against adult worms but may not control larvae and other roundworm species that often infect livestock simultaneously with these worms.
In some countries (e.g. Australia, Argentina, EU, New Zealand, Uruguay) monepantel, an anthelmintic of a new chemical class, has become available as a drench for use on sheep (in some countries also on goats). It is effective against Teladorsagia strains that have developed resistance to other anthelmintics. It controls adult worms, immature L4 larvae, and also inhibited larvae. Unfortunately it is not yet available in many countries and it is not approved for cattle.
Numerous commercial products contain mixtures of two or even more active ingredients of different chemical classes. This is done to increase the chance that at least one active ingredient is effective against gastrointestinal worms that have become resistant, or to delay resistance development by those worms that are still susceptible.
Depending on the country most of these anthelmintics are available for oral administration as drenches, feed additives and/or tablets. Levamisole and most macrocyclic lactones are usually also available as injectables. A few active ingredients are also available for livestock as pour-ons and slow-release boluses.
Excepting slow-release boluses, most wormers containing benzimidazoles (e.g. albendazole, febantel, fenbendazole, oxfendazole, etc.), levamisole, tetrahydropyrimidines (e.g. morantel, pyrantel) and other classic anthelmintics kill the worms shortly after treatment and are quickly metabolized and/or excreted within a few hours or days. This means that they have a short residual effect, or no residual effect at all. As a consequence treated animals are cured from worms but do not remain protected against new infections. To ensure that they remain worm-free the animals have to be dewormed periodically, depending on the local epidemiological, ecological and climatic conditions. An exception to this are macrocyclic lactones (e.g. abamectin, doramectin, eprinomectin, ivermectin, moxidectin), that offer several weeks protection against re-infestation, depending on the delivery form and the specific parasite.
There are reports on confirmed resistance of Ostertagia and/or Teladorsagia to the most common anthelmintics (e.g. benzimidazoles, macrocyclic lactones, levamisole). The problem is not as acute as for Haemonchus spp, but it is worsening and spreading.
This means that if an anthelmintic fails to achieve the expected efficacy against Ostertagia and/or Teladorsagia worms, there is a considerable risk that it is due to anthelmintic resistance.
Ask your veterinary doctor! If available, follow more specific national or regional recommendations for Ostertagia and/or Teladorsagia control.