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Grouse Diseases

Coccidiosis

Some people question the significance of coccidiosis in grouse but we do know of their effect in other species. In both red-legged partridges and pheasants we see mortality in reared birds every year caused by coccidiosis. Usually coccidiosis is regarded as a disease of intensification and the recent increase in observed levels of grouse coccidiosis corresponds to several years of high grouse numbers on the moors.

The life-cycle of coccidiosis starts with an infected birds excreting what are known as oocysts in their faeces. These undergo a period of development before they become infective and they will then infect another bird when they are eaten. The oocysts are very hardy and survive easily from one season to the next. Once swallowed the oocyst divides and the parasites released invade the gut lining. Each type of coccidia is both species specific and also area specific within the bird’s gut. Once in the cells of the gut lining the parasites divide and these are then released to invade more gut lining cells and divide again. This can be repeated several times. A single ingested oocyst can result in hundreds of thousands of oocysts being available to be excreted in due course in the faeces so numbers can increase rapidly. As the number of wild birds in an area increases this has the effect of increasing the contamination of the land.

Death in a grouse due to coccidiosis has been seen at the practice but the effects of sub-lethal levels are harder to quantify. Poor development of young birds due to damage to the gut lining is likely but less obvious is the effect the parasite will have at lower levels on a bird’s performance.

If we take the example of racing pigeons where levels are closely monitored and where the birds performance is also well known, we believe that levels of less than 3,000 oocysts per gram of faeces has no clinical effect, between 3,000 and 20,000 affect performance without the birds looking ill, between 20,000 and 50,000 clinical disease is likely with birds being scoured and depressed and above 50,000 deaths may start to occur. In grouse it is possible that moderate levels will affect performance and make the birds more available to predators.

In other livestock coccidiosis is a disease of intensification.

In dry years such a concentration could occur around areas of available water where contamination levels will be higher. The other area that birds are attracted to is the grit boxes and contamination of the ground around the boxes may help increase the incidence of the disease.

Cryptosporidiosis (‘BULGY HEAD’)

Cryptosporidiosis is caused by a protozoan parasite with some similarities to Coccidiosis but it also has some noticeable differences. The Cryptosporidiosis we are seeing in grouse is the respiratory form caused by Cryptosporidium baileyi. Cryptosporidiosis can also affect mammals but mammalian types rarely affect birds and avian types rarely affect mammals.

Cryptosporidiosis

Unlike coccidiosis the Cryptosporidium does not have rigid host specificity so it can spread between different species of birds. The parasite affects epithelial cells – those are cells that line the respiratory tract. Here they multiply like the coccidia in the gut damaging the tissues and causing the swelling we see as bulgy head. The parasite can then be spread by being coughed up and in nasal discharges and in severe cases will kill affected birds. The oocyst, which is the infective stage of the parasite, spreads in the discharges and is environmentally resistant. So once land is infected it can remain so for a long period of time – certainly many months and possibly years if conditions are right. Sunlight is the best natural disinfectant for killing oocysts. Once another bird comes into contact with infective oocysts it also may become infected and the process is repeated. From this it can be deduced that the spread of the disease is more likely with higher stocking levels and as with coccidiosis areas where birds congregate are areas where spread is particularly likely to happen.

Trichostrongylus

Adult Trichostrongylus tenuis worms live in the caecae of grouse and they can live there for long periods as the birds’ immune system is often not able to expel them. The adult female worms lay eggs throughout their lives. These are voided in the caecal pats and the eggs develop into infective larvae in and around these pats. The time taken for the eggs to hatch and the larvae to become infective varies depending upon humidity and environmental temperature.  In typical winter conditions between November and mid-February the larvae are all likely to die before reaching the infective stage. A peak of infective larvae usually become available in late May and can infect chicks as well as adults. In hot dry summer conditions both the worm eggs and any developing larvae are likely to be killed by desiccation but in mild, moist weather worm burdens can rise rapidly.

Trichostrongylus

High levels of worms can result in worm-induced crashes in grouse numbers as seen in 2005. Less dramatic but of real concern are the detrimental effects on the breeding performance of grouse caused by non-lethal levels of worms.

The worms cause damage to the lining of the caecal wall allowing protein to leach into the caecae and be voided in the faeces. The natural diet of grouse is not particularly protein rich so birds can rapidly go into negative protein balance if they carry significant levels of Trichostrongylus worms. This leads to loss of condition, a reduced ability of the birds to rear young and the possible death of birds in severe cases.

Levels of worms are monitored by worm counts. The following are standard interpretations of numbers:

Young Birds:   
<650 worms per bird                  Normal
650 –2000 worms per bird          Action advised
2000+ worms per bird                Clinical problem likely

Old Birds:       
<2000 worms per bird                Normal
2000 –5000 worms per bird        Action advised
5000+ worms per bird                Clinical problem likely

Treatments – types of grit and how they work

Types of Grit:
There are two available medicated grit treatments both using the drug Flubendazole as the active ingredient.

Low strength or standard products consist of grit of a variety of sizes suitable for both young and adult birds with a fat coating binding the Flubendazole to the grit at levels giving a final concentration of 1mg / gram to 2mg / gram of finished product. Using the 5% flubendazole licensed for use in the UK this is as high a level of drug as can be practicably added to the grit.
Low strength grit had given good control of worms on many moors since 2005 but after a number of years, some moors using this product finished seasons with worm counts so high that they suggested the likelihood of a very poor subsequent breeding season.

High strength product consists of graded Cornish quartz grit with particles primarily between 2.0 -2.5mm in diameter. These are coated with a fat coating and using a 100% flubendazole give a final concentration of 10mg / gram of finished product – up to ten times higher than the standard product. This may seem ideal but the objective in using any product should not be to try to eliminate all the worms because if levels are kept too low this may well result in drug resistant strains of worms becoming dominant relatively quickly. If this happened the medicated grit now available would no longer be effective.

The objective with any worming programme is to maintain a parasite population at a level below which the grouse will not suffer but high enough for there to be high levels of non-resistant worms in the population. On this basis, if autumn worm burdens are very low (possibly less than 200 worms in old and 50 worms in young birds at the end of September) the decision may be taken not to treat. This will reduce the likelihood of the development of resistant worms on the moor.

How the different products work
It is suggested that low strength or standard grit acts by blocking new infections occurring. The amount of drug available to the birds from low strength grit is unlikely to be sufficient to kill adult worms or to stop them from laying eggs. The suggested mechanism for this control is that drug in the faeces will be of sufficient concentration to prevent eggs developing into larvae.

It is therefore most likely that low strength grit it has its greatest effect from mid-February onwards (before that eggs and larvae are naturally killed in most years) by preventing new infections occurring in adult birds and preventing infection in the young birds. Once the product is withdrawn then new infections will be possible. With use in subsequent seasons low levels of worms should be achieved.

The high strength grit works by killing adult worms. Hence this is the product to use if there are high worm counts in autumn that are clinically significant. High strength grit should be withdrawn by mid-March to allow modest numbers of parasites that have never experienced the drug to survive from over wintered larvae and so reduce the likelihood of resistance developing.

Legal requirements and prevention of resistance

It is important that drugs are used as recommended in the treatment regimes.
Failure to withdraw all low strength grit by mid-July is both ill-advised as it will hasten the onset of a population of resistant worms on the moor and it would also be illegal if treated birds were to be presented to guns within 28 days of the grit being removed. This is to avoid the drug entering the human food chain. The Food Standard’s Agency randomly test game birds each year for residues and the presence of illegal residues would have economic implications far beyond any moor on which such birds were to be found and would destroy the image of grouse being a healthy meat to eat. In addition moors may be visited and grit boxes examined. The removal of all medicated grit at least 28 days before the shooting season is therefore essential. Failure to withdraw all high strength grit by mid-March may seem beneficial as it will keep worm levels very low. This is a fallacy and will encourage early onset of drug resistance. As with the low strength grit there is a legal requirement for the removal of all medicated grit at least 28 days before the shooting season but if used correctly high strength grit will have been removed well in advance of shooting.

Best practice

Not everyone agrees with the analysis of how wormers work simply because the research that has been done has not been able to give definitive answers.
However if the mechanisms of how they work are as outlined above then for best practice:

  1. Medicated grit should not be used without first determining the parasite status of old and young birds at the end of the shooting season.
  2. If counts are very low then the birds should not be wormed as this will encourage drug resistance to develop which will cause long-term problems.
  3. If worm burdens are high then the use of high strength grit is indicated as low strength grit may not give the worm control required.
  4. Low strength grit will be used most effectively between mid-February and July.
  5. High strength grit can be used over winter and removed by mid-March.
  6. All grit must be removed at least 28 days before shooting.

SUBMITTING GROUSE SAMPLES TO THE LABORATORY

We carry out Trichostrongylus worm counts on grouse intestines to monitor worm levels. In order to carry out the count, we need the whole gut of each grouse with both the caecae attached if they are submitted in bulk.

If we receive a bag of intestines with caecae detached, we cannot be sure we are testing different birds; we may be sampling two caecae from one bird. If intestines cannot be sent in immediately they can be frozen and sent or brought to us when convenient.

Please ensure all samples are clearly marked with your name, contact number, approximate age of birds (where appropriate) and the area the sample was taken.

If sending by carrier, please wrap securely in leak-proof plastic bags, then send in a box with ice packs to keep them cool.


  Sandhill Veterinary Services 14 Long Street, Topcliffe YO7 3RW telephone 01845 578710 fax 01845 577685 email rtb@sandhillvet.co.uk