Diseases & Solutions
Lungworm
Lungworm can affect cattle (Dictyocaulus viviparus) and sheep (Dictyocaulus filaria). However, for the most part, the parasite is only of commercial importance to cattle farmers. The symptoms of lungworm are commonly termed ‘husk’ or ‘hoose’. Classical hoose symptoms include:
- Coughing
- Laboured breathing
- Yield reduction
- Condition loss
- Pneumonia
- Death in dairy calves
While pneumonia is one of the most common causes of death in cattle currently, there is an acceptance among the veterinary profession that lungworm is a precursor for a lot of the pneumonia cases seen today. Given the additional costs on top of a lost animal, farmers can be reluctant to carry out the post mortems that would divulge this information (detection of heavy infestation of adult or larval lungworm in bronchi/lower trachea or inflammation/damage from previous infection).
Research published earlier this decade puts the cost of lungworm in a dairy herd between €159 and €167 per cow.
Lungworm can affect cattle (Dictyocaulus viviparus) and sheep (Dictyocaulus filaria). However, for the most part, the parasite is only of commercial importance to cattle farmers. The symptoms of lungworm are commonly termed ‘husk’ or ‘hoose’. Classical hoose symptoms include:
- Coughing
- Laboured breathing
- Yield reduction
- Condition loss
- Pneumonia
- Death in dairy calves
While pneumonia is one of the most common causes of death in cattle currently, there is an acceptance among the veterinary profession that lungworm is a precursor for a lot of the pneumonia cases seen today. Given the additional costs on top of a lost animal, farmers can be reluctant to carry out the post mortems that would divulge this information (detection of heavy infestation of adult lungworm in bronchi/lower trachea or inflammation/damage from previous infection).
Research published earlier this decade puts the cost of lungworm in a dairy herd between £140 and €£147 per cow.
In general, the animals most at risk of lungworm infection are first season dairy calves grazing permanent or semi-permanent pastures and we would expect to see infection from two months post-turnout. We also see it in suckler calves towards the end of their first season, when they are either weaned or still suckling but developed grazers.
However, growing stocking pressure coupled with Ireland's unpredictable weather extremes have led to an increased number of mature animals presenting with hoose. Unlike gastrointestinal worm immunity, elements of an animal’s natural immunity to lungworm will wane without regular exposure to small burdens.
Lungworm immunity has two components, immunity to maturation of adults and immunity to larval development (i.e. larvae reaching the lungs). While immunity to adult lungworm remains relatively constant once established, immunity to larval infection does not and this is what causes problems in adult cows. We now frequently see dropping milk yields and mature animals exhibiting hoose from two months post-turnout as a result of larval irritation of the respiratory tract. These larvae may not reach maturity, as this component of our animal’s immunity remains, but they still cause irritation in the respiratory tract. This is known as reinfection syndrome and is common in spring-calving dairy herds.
The lungworm lifecycle
Mature lungworm live in the bronchi (pipes that connect the windpipe to the lungs) and lay eggs which contain L1 stage larvae. These L1s are coughed up and swallowed. They then work their way through the digestive system and out onto pasture via the animal’s dung. In the dung an L1 will develop into an L2 and eventually an L3 – an infective larva. This process takes 5 to 7 days in ideal conditions but can take longer depending on weather. This L3 is what our animal eats to cause infection.
In order to find its way back into our animal, the L3 larvae must get from the dung pat out onto pasture. They do this in several ways:
- Their own movements
- Raindrops hitting dung pats act to spread larvae mechanically across pasture
- The larvae often migrate onto the orange fungus that is prevalent on dung pats (Pilobolus). When spores of this fungus explode, they can expel the larvae up to 3 metres away from the dung pat
- Animals themselves stepping on dung pats can act to spread L3 larvae
Once on pasture, the L3 are consumed by our animal as they graze. On reaching the intestine, they migrate into lymph glands and become L4 larvae. From here they use the blood stream to find their way into the capillaries – part of lungs responsible for transferring breathed-in oxygen into the blood stream. The L4 cross the capillary walls and into the lungs. Here they develop further into mature lungworm L5 and begin to lay eggs. Large numbers of mature lungworm cause inflammation and reduce the animal’s respiratory capacity, leading to hoose symptoms.
Relative to their body weight, the bovine lung capacity is small compared with other species. For example, a 600kg bullock could have a lung capacity of 12.5 litres, while a 90kg human could have up to 6 litres of lung capacity. This is why lungworm and other respiratory issues can be extremely detrimental to overall metabolism and performance.
The lungworm prepatent period (from ingestion to maturity) takes 21 to 28 days. Mature lungworm die naturally after two months in the animal. However, as with certain gastrointestinal worms, a portion of lungworm larvae will go into an arrested state in the animal, during which their development is stalled. This typically happens over winter and is one of the principle ways that pasture becomes re-infected in the spring, though some larvae survive the winter on pasture depending on weather conditions.
It typically takes at least two months post turnout before hoose symptoms will be seen in any animal groups. This delay is probably because it takes two life cycles to reach a high-enough burden to produce symptoms in our animal – i.e. it is the generation after the overwintered parasites that do the damage.
This coincides with the timing when farmers typically report hoose symptoms (May onwards). There are likely one of two things happening on these farms.
Firstly, we may have young or lungworm-naïve animals that have poorly-developed natural immunity, both from larvae and adult worm points of view. In these animals the parasite can complete its full life cycle.
Alternatively, and likely a feature on a lot of dairy farms, we could have older animals that have good immunity to adult lungworm but a reduction in immunity to larval infection. Immunity to reinfection with larvae begins to subside from three months post infection, unless further exposure happens. This may be the case where a dry period of weather has reduced L3 activity on pasture and/or a farmer has used a lot of long-acting anthelmintics. So, if a lactating cow’s reinfection immunity has reduced and they meet a sudden heavy worm burden, we can have trouble. Such an example would be a dry period followed heavy rainfall acting to accelerate the development and dispersal of L3 across pastures.
On the ground, we would see a performance reduction and coughing in this case. The larvae are causing significant immune responses as the cow battles the parasites. Her immunity is partially working, it is just causing pressure on the system. If no action is taken the animal is at risk of developing pneumonia.
There are three grades of hoose infection, based on the degree to which animals cough:
- Mild: animals cough when exercised
- Moderate: animals cough at rest
- Heavy: head down with tongue out, deep, gasping cough
In terms of controlling lungworm, advice is to monitor first-season calves and lactating cows from two months post turnout for first signs of coughing.
In terms of diagnostics around lungworm, ELISA tests can be used. However, lungworm antibodies will remain in the system for up to seven months post infections and so these can give a false positive reading.
Faecal analysis (Baermann test) can also be used but note that it will take up to four weeks post L3 ingestion before we will pick up L1 in dung. Also, if mature animals are suffering from reinfection syndrome, we may see few or no larvae in faeces as the parasite is not maturing enough to lay eggs. Suckler calves will typically not be consuming enough grass to ingest a lot of L3 larvae until late-summer/autumn-time.
There is a vaccination available against lungworm. It is given orally and contains irradiated lungworm larvae. Ideally, it is given to first season calves greater than eight weeks-of-age. The course is two treatments, four weeks apart with immunity achieved until two weeks after the second shot. It is important to note that the vaccination covers solely lungworm.
All classes of wormers work well against lungworm and there is currently no reported anthelmintic resistance among lungworm populations. The only current products with zero milk withdrawal in lactating dairy herds are Eprinomectin-based, which is a member of the clear wormer family.
Active ingredients belonging to the clear wormer (Macrocyclic Lactone) family have a licenced residual activity against lungworm in cattle. This means that parasites in the system on treatment day will be killed, as will any ingested larvae for a period following treatment.
Levamisole is often regarded as the treatment of choice for severely affected cattle, showing better post treatment survival rates relative to other actives. Levamisoles results in paralysis of the worms. This allows the worms to be removed by local physiological mechanisms, rather than the more severe immunological reactions generated with other products that kill parasites in the lungs. Note however, that levamisole products will have zero residual activity against lungworm following treatment.
Use the solutions below with our FAQ and Best Practice sections to make good decisions on lungworm control.
In general, the animals most at risk of lungworm infection are first season dairy calves grazing permanent or semi-permanent pastures and we would expect to see infection from two months post-turnout. We also see it in suckler calves towards the end of their first season, when they are either weaned or still suckling but developed grazers.
However, growing stocking pressure coupled with the UK's unpredictable weather extremes have led to an increased number of mature animals presenting with hoose. Unlike gastrointestinal worm immunity, elements of an animal’s natural immunity to lungworm will wane without regular exposure to small burdens.
Lungworm immunity has two components, immunity to maturation of adults and immunity to larval development (i.e. larvae reaching the lungs). While immunity to adult lungworm remains relatively constant once established, immunity to larval infection does not and this is what causes problems in adult cows. We now frequently see dropping milk yields and mature animals exhibiting hoose from two months post-turnout as a result of larval irritation of the respiratory tract. These larvae may not reach maturity, as this component of our animal’s immunity remains, but they still cause irritation in the respiratpry tract. This is known as reinfection syndrome and is common in spring-calving dairy herds.
The lungworm lifecycle
Mature lungworm live in the bronchi (pipes that connect the windpipe to the lungs) and lay eggs which contain L1 stage larvae. These L1s are coughed up and swallowed. They then work their way through the digestive system and out onto pasture via the animal’s dung. In the dung an L1 will develop into an L2 and eventually an L3 – an infective larva. This process takes 5 to 7 days in ideal conditions but can take longer depending on weather. This L3 is what our animal eats to cause infection.
In order to find its way back into our animal, the L3 larvae must get from the dung pat out onto pasture. They do this in several ways:
- Their own movements
- Raindrops hitting dung pats act to spread larvae mechanically across pasture
- The larvae often migrate onto the orange fungus that is prevalent on dung pats (Pilobolus). When spores of this fungus explode, they can expel the larvae up to 3 metres away from the dung pat
- Animals themselves stepping on dung pats can act to spread L3 larvae
Once on pasture, the L3 are consumed by our animal as they graze. On reaching the intestine, they migrate into lymph glands and become L4 larvae. From here they use the blood stream to find their way into the capillaries – part of lungs responsible for transferring breathed-in oxygen into the blood stream. The L4 cross the capillary walls and into the lungs. Here they develop further into mature lungworm L5 and begin to lay eggs. Large numbers of mature lungworm cause inflammation and reduce the animal’s respiratory capacity, leading to hoose symptoms.
Relative to their body weight, the bovine lung capacity is small compared with other species. For example, a 600kg bullock could have a lung capacity of 12.5 litres, while a 90kg human could have up to 6 litres of lung capacity. This is why lungworm and other respiratory issues can be extremely detrimental to overall metabolism and performance.
The lungworm prepatent period (from ingestion to maturity) takes 21 to 28 days. Mature lungworm die naturally after two months in the animal. However, as with certain gastrointestinal worms, a portion of lungworm larvae will go into an arrested state in the animal, during which their development is stalled. This typically happens over winter and is one of the principle ways that pasture becomes re-infected in the spring, though some larvae survive the winter on pasture depending on weather conditions.
It typically takes at least two months post turnout before hoose symptoms will be seen in any animal groups. This delay is probably because it takes two life cycles to reach a high-enough burden to produce symptoms in our animal – i.e. it is the generation after the overwintered parasites that do the damage.
This coincides with the timing when farmers typically report hoose symptoms (May onwards). There are likely one of two things happening on these farms.
Firstly, we may have young or lungworm-naïve animals that have poorly-developed natural immunity, both from larvae and adult worm points of view. In these animals the parasite can complete its full life cycle.
Alternatively, and likely a feature on a lot of dairy farms, we could have older animals that have good immunity to adult lungworm but a reduction in immunity to larval infection. Immunity to reinfection with larvae begins to subside from three months post infection, unless further exposure happens. This may be the case where a dry period of weather has reduced L3 activity on pasture and/or a farmer has used a lot of long-acting anthelmintics. So, if a lactating cow’s reinfection immunity has reduced and they meet a sudden heavy worm burden, we can have trouble. Such an example would be a dry period followed heavy rainfall acting to accelerate the development and dispersal of L3 across pastures.
On the ground, we would see a performance reduction and coughing in this case. The larvae are causing significant immune responses as the cow battles the parasites. Her immunity is partially working, it is just causing pressure on the system. If no action is taken the animal is at risk of developing pneumonia.
There are three grades of hoose infection, based on the degree to which animals cough:
- Mild: animals cough when exercised
- Moderate: animals cough at rest
- Heavy: head down with tongue out, deep, gasping cough
In terms of controlling lungworm, advice is to monitor first-season calves and lactating cows from two months post turnout for first signs of coughing.
In terms of diagnostics around lungworm, ELISA tests can be used. However, lungworm antibodies will remain in the system for up to seven months post infections and so these can give a false positive reading.
Faecal analysis (Baermann test) can also be used but note that it will take up to four weeks post L3 ingestion before we will pick up L1 in dung. Also, if mature animals are suffering from reinfection syndrome, we may see few or no larvae in faeces as the parasite is not maturing enough to lay eggs. Suckler calves will typically not be consuming enough grass to ingest a lot of L3 larvae until late-summer/autumn-time.
There is a vaccination available against lungworm. It is given orally and contains irradiated lungworm larvae. Ideally, it is given to first season calves greater than eight weeks-of-age. The course is two treatments, four weeks apart with immunity achieved until two weeks after the second shot. It is important to note that the vaccination covers solely lungworm.
All classes of wormers work well against lungworm and there is currently no reported anthelmintic resistance among lungworm populations. The only current products with zero milk withdrawal in lactating dairy herds are Eprinomectin-based, which is a member of the clear wormer family.
Active ingredients belonging to the clear wormer (Macrocyclic Lactone) family have a licenced residual activity against lungworm in cattle. This means that parasites in the system on treatment day will be killed, as will any ingested larvae for a period following treatment.
Levamisole is often regarded as the treatment of choice for severely affected cattle, showing better post treatment survival rates relative to other actives. Levamisoles results in paralysis of the worms. This allows the worms to be removed by local physiological mechanisms, rather than the more severe immunological reactions generated with other products that kill parasites in the lungs. Note however, that levamisole products will have zero residual activity against lungworm following treatment.
Use the solutions below with our FAQ and Best Practice sections to make good decisions on lungworm control.
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