As in sheep, an infestation of gastrointestinal roundworms has the potential for a 30% performance (growth rate) reduction in cattle, particularly in young animals such as first-season calves.
Common signs of clinical disease include the classic scouring, inappetence and a loss in condition. However, the disease can also affect mature animals in a sub-clinical nature – in adult dairy cows a significant gastrointestinal worm burden can reduce milk production by >2kg daily. This is generally due to a ‘cost of immunity’ as energy is diverted away from production and towards the necessary immune response which prevents clinical symptoms from manifesting.
Adult worms lay eggs within the animal which are dispersed onto pasture via dung. Eggs hatch into L1 larvae in the dung, which then molt in L2. Subsequent development into L3 infective larvae – the stage ingested by the animal to cause an infection – is heavily temperature-dependent.
As in sheep, an infestation of gastrointestinal roundworms has the potential for a 30% performance (growth rate) reduction in cattle, particularly in young animals such as first-season calves.
Common signs of clinical disease include the classic scouring, inappetence and a loss in condition. However, the disease can also affect mature animals in a sub-clinical nature – in adult dairy cows a significant gastrointestinal worm burden can reduce milk production by >2kg daily. This is generally due to a ‘cost of immunity’ as energy is diverted away from production and towards the necessary immune response which prevents clinical symptoms from manifesting.
Adult worms lay eggs within the animal which are dispersed onto pasture via dung. Eggs hatch into L1 larvae in the dung, which then molt in L2. Subsequent development into L3 infective larvae – the stage ingested by the animal to cause an infection – is heavily temperature-dependent.
In temperatures between 15°C and 23°C, L3 larvae can be present in dung within a week. Down at 10°C, the process can take up to three weeks. The role of moisture and rainfall is to facilitate the movement of infective L3 larvae off the dung pat and onto pasture, where it can be ingested by the animal.
Generally, L3 levels on pasture will peak in July if no previous action is taken to reduce build-up. Such action could include strategic dosing of animals early in the season to prevent proliferation of gastrointestinal worms and larvae on pasture. For example, if animals are dosed at turnout with a product that has residual activity (or within three weeks post-turnout when using non-residual activity products) and again shortly after that residual activity ends, no over-wintered larvae on pasture will have been afforded a chance to develop and no overwintered worms in the animal itself will have laid eggs onto pasture.
Infective L3 larvae can survive on pasture for over 12 months and the temperature conditions of the UK and Ireland are ideal for facilitating this. During warm spells, the larvae’s metabolism will increase, and energy stores will be used up more rapidly. Hence, a drought spell will act to kill off a lot of L3 on pasture. A long warm winter will have the same effect and mortality rates will be lowest in a cold, snowy winter. Contrary to belief, the survivability of gastrointestinal worms in conserved forages is very poor.
Once ingested, the L3 develops into L4 within the glands and a parasite will reach adulthood (eggs detectable in faeces) within three weeks.
While there are four in sheep, two species of gastrointestinal worm are of commercial importance to cattle farmers in Ireland and the UK – Cooperia oncophora, which affects the small intestine and Ostertagia ortertagi, which acts in the abomasum (stomach).
Cooperia
Cooperia is less obvious than Ostertagia in terms the prevalence and severity of symptoms during an infection. Its action involves damage to the lining of the intestine, reducing the animal’s capacity to digest and absorb nutrients. Animals will generally become naturally immune to Cooperia after one full grazing season.
In cattle, initial reports of anthelmintic resistance appear to be mainly among Cooperia populations and predominantly to ivermectin-based wormers. It is worth noting that differences in rates at which resistance develops to actives within the macrocyclic lactone wormer class has been noted in studies to date – e.g. moxidectin resistance is slower to develop than ivermectin resistance.
Ostertagia
Ostertagiosis affects the glands in the lining of the abomasum (stomach) and causes a thickening of the lining and associated glands. A heavy infestation causes a reduction in the acidity of the stomach, leads to poorer protein ingestion and sees the proliferation of unwanted bacteria and appetite-suppressant compounds. Ostertagiosis can be divided into two forms, Type I which occurs during the summer when the larvae development progresses as outlined above, and Type II when the larvae effectively ‘hibernate’ in the glands of the animal. This hibernation, or arrested development, can last for up to six months and during the period L4 stage larvae remain in the gastric glands. There is no definitive answer as to what triggers their development into adults and emergence, but it typically occurs late in the winter, while animals are housed.
Natural immunity to Ostertagia may take up to two full grazing seasons to develop and older animals are still at risk if burdens are high enough. Research shows that immunity to both Cooperia and Ostertagia will develop in cattle irrespective of the type and frequency of previous anthelmintic treatments. As in sheep, immunity can recede around calving time, particularly in heifers.
Dual infection of cattle with both Cooperia and Ostertagia is common and much worse than either of the parasites on their own. Both parasites are species specific, meaning for example that sheep Ostertagia worms (Teladorsagia) will not be of any detriment to cattle grazing the same pasture. Indeed, alternating between cattle and sheep groups on a given pasture is one strategy for reducing gastrointestinal worm risk on farms. However, it must be noted that on a farm with liver fluke, such a strategy would exacerbate the problem as the same species of parasite affects both cattle and sheep. Also, cattle can become infected by Nematodirus battus, which can be a big problem for lambs in late-spring/early-autumn.
In terms of diagnostics around gastrointestinal worms in cattle, common methods include faecal egg analysis, milk tank antibody tests and weight gain monitoring.
In recent years, progress has been made around using milk antibody tests as part of a control strategy. Milk ODR (observed density ratio) for Ostertagia o. antibodies has demonstrated use as a metric for determining whether anthelmintic treatment is required/would be advantageous. Research has shown that once ODR surpasses 0.5, potential yield is reduced. At ODR values of 0.8 and 1.1, yield is reduced by 1 and 2 litres/day, respectively.
Visually, scour caused by Ostertagia will have a green tinge and a heavily-infected animal can lose 20% of bodyweight within 10 days.
Research has shown that regular weighing of animals is a better indicator of worm burden than faecal egg analysis, from a gastrointestinal worm point of view. Indeed, targeted anthelmintic treatment of individual animals seen to be performing below group averages can be rewarding.
Use the solutions below with our FAQ and Best Practice sections to make good decisions on gastrointestinal worm control in cattle.
In temperatures between 15°C and 23°C, L3 larvae can be present in dung within a week. Down at 10°C, the process can take up to three weeks. The role of moisture and rainfall is to facilitate the movement of infective L3 larvae off the dung pat and onto pasture, where it can be ingested by the animal.
Generally, L3 levels on pasture will peak in July if no previous action is taken to reduce build-up. Such action could include strategic dosing of animals early in the season to prevent proliferation of gastrointestinal worms and larvae on pasture. For example, if animals are dosed at turnout with a product that has residual activity (or within three weeks post-turnout when using non-residual activity products) and again shortly after that residual activity ends, no over-wintered larvae on pasture will have been afforded a chance to develop and no overwintered worms in the animal itself will have laid eggs onto pasture.
Infective L3 larvae can survive on pasture for over 12 months and the temperature conditions of the UK and Ireland are ideal for facilitating this. During warm spells, the larvae’s metabolism will increase, and energy stores will be used up more rapidly. Hence, a drought spell will act to kill off a lot of L3 on pasture. A long warm winter will have the same effect and mortality rates will be lowest in a cold, snowy winter. Contrary to belief, the survivability of gastrointestinal worms in conserved forages is very poor.
Once ingested, the L3 develops into L4 within the glands and a parasite will reach adulthood (eggs detectable in faeces) within three weeks.
While there are four in sheep, two species of gastrointestinal worm are of commercial importance to cattle farmers in Ireland and the UK – Cooperia oncophora, which affects the small intestine and Ostertagia ortertagi, which acts in the abomasum (stomach).
Cooperia
Cooperia is less obvious than Ostertagia in terms the prevalence and severity of symptoms during an infection. Its action involves damage to the lining of the intestine, reducing the animal’s capacity to digest and absorb nutrients. Animals will generally become naturally immune to Cooperia after one full grazing season.
In cattle, initial reports of anthelmintic resistance appear to be mainly among Cooperia populations and predominantly to ivermectin-based wormers. It is worth noting that differences in rates at which resistance develops to actives within the macrocyclic lactone wormer class has been noted in studies to date – e.g. moxidectin resistance is slower to develop than ivermectin resistance.
Ostertagia
Ostertagiosis affects the glands in the lining of the abomasum (stomach) and causes a thickening of the lining and associated glands. A heavy infestation causes a reduction in the acidity of the stomach, leads to poorer protein ingestion and sees the proliferation of unwanted bacteria and appetite-suppressant compounds. Ostertagiosis can be divided into two forms, Type I which occurs during the summer when the larvae development progresses as outlined above, and Type II when the larvae effectively ‘hibernate’ in the glands of the animal. This hibernation, or arrested development, can last for up to six months and during the period L4 stage larvae remain in the gastric glands. There is no definitive answer as to what triggers their development into adults and emergence, but it typically occurs late in the winter, while animals are housed.
Natural immunity to Ostertagia may take up to two full grazing seasons to develop and older animals are still at risk if burdens are high enough. Research shows that immunity to both Cooperia and Ostertagia will develop in cattle irrespective of the type and frequency of previous anthelmintic treatments. As in sheep, immunity can recede around calving time, particularly in heifers.
Dual infection of cattle with both Cooperia and Ostertagia is common and much worse than either of the parasites on their own. Both parasites are species specific, meaning for example that sheep Ostertagia worms (Teladorsagia) will not be of any detriment to cattle grazing the same pasture. Indeed, alternating between cattle and sheep groups on a given pasture is one strategy for reducing gastrointestinal worm risk on farms. However, it must be noted that on a farm with liver fluke, such a strategy would exacerbate the problem as the same species of parasite affects both cattle and sheep. Also, cattle can become infected by Nematodirus battus, which can be a big problem for lambs in late-spring/early-autumn.
In terms of diagnostics around gastrointestinal worms in cattle, common methods include faecal egg analysis, milk tank antibody tests and weight gain monitoring.
In recent years, progress has been made around using milk antibody tests as part of a control strategy. Milk ODR (observed density ratio) for Ostertagia o. antibodies has demonstrated use as a metric for determining whether anthelmintic treatment is required/would be advantageous. Research has shown that once ODR surpasses 0.5, potential yield is reduced. At ODR values of 0.8 and 1.1, yield is reduced by 1 and 2 litres/day, respectively.
Visually, scour caused by Ostertagia will have a green tinge and a heavily-infected animal can lose 20% of bodyweight within 10 days.
Research has shown that regular weighing of animals is a better indicator of worm burden than faecal egg analysis, from a gastrointestinal worm point of view. Indeed, targeted anthelmintic treatment of individual animals seen to be performing below group averages can be rewarding.
Use the solutions below with our FAQ and Best Practice sections to make good decisions on gastrointestinal worm control in cattle.