Help us fight disease and injury in animals

Foal Immunodeficiency Syndrome

Foal Immunodeficiency Syndrome (FIS) is an inherited fatal disease that affects Fell and Dales ponies and potentially any mixed breed ponies which are closely related to either of these breeds. Affected foals appear ‘normal’ at birth but at around two-four weeks of age, they show signs associated with immunodeficiency and progressive anaemia. Eventually affected foals fail to thrive and succumb to persistent infections and die or are euthanized before they reach sixteen weeks.

FIS is inherited as an autosomal recessive trait. An affected foal will have two copies of the defective gene, one copy inherited from each parent. Ponies with one copy of the defective gene and one copy of the normal gene - known as “carriers” - will not show any clinical signs of the disease, but will be able to pass on the defective gene to their offspring. Carriers exist in both the Fell and Dales population; when two carriers are bred, their offspring have a 25% risk of disease, a 50% risk of being carriers themselves, and 25% chance of being clear.

Funding from The Horse Trust has enabled scientists at the Animal Health Trust, in collaboration with the University of Liverpool, to identify a mutation that is associated with the development of FIS.  A test has now been developed and can be used to examine the DNA from each pony for the presence or absence of this mutation. With careful breeding, the disease gene may eventually be eradicated from the population.

Breeders will be sent results identifying their pony as belonging to one of three categories:

Clear: The pony has two copies of the normal gene. It will neither develop FIS, nor pass the mutation to its offspring.
Carrier: The pony has one copy of the normal gene and one copy of the defective gene. It will not develop FIS but will pass the mutation to (on average) 50% of its offspring which will therefore also be carriers.
Affected: The foal has two copies of the defective gene and has FIS, a lethal disease.

We advise that all breeding stock should be retained for breeding to avoid the loss of desirable breed traits and prevent a loss of genetic diversity in the population. Carriers can still be bred to tested clear ponies; on average 50% of the offspring will be clear and 50% carriers - there are no affected animals produced from a carrier-clear mating. Youngsters which will go on to breed themselves can be DNA tested to determine whether they are clear or a carrier.

Previously there has been no definitive test for an early FIS foal, so diagnosis was made on clinical history and signs as they appeared. In 2010, the test will act as a diagnostic aid to confirm suspected syndrome foals and will be particularly useful before any clinical signs appear. Foal samples submitted will be processed as urgent and the result available in three working days from receipt of sample.

Clinical signs of FIS include scouring, nasal discharge, breathing with abdominal effort, pale mucous membranes, failing to suckle, frequent chewing movements, dull coat, hunched stance and dull demeanour. If your foal is showing signs consistent with those listed and is of Dales or Fell origin then you should contact your veterinarian for FIS testing. He will test for anaemia and confirm a clinical diagnosis.

Samples should be collected by your veterinarian in the form of a pulled (NOT cut) mane or tail hair sample and submitted to our genetic services lab. Sample collection bags, which are provided with a submission form, are available on request from the Fell and Dales Pony Societies, or on application by your vet to the Animal Health Trust.

For further information about the submission of samples for equine DNA testing please click here, and to view frequently asked questions click here.

For further information please contact the Fell or Dales Pony Society, or Angie Stagg at the Animal Health Trust on 01638 555645 or via e-mail at FIStesting@aht.org.uk.

We would like to acknowledge The Horse Trust for funding the work which has led to the development of this test. We would also like to thank the breeders and vets who helped our investigations, in particular Paul May MRCVS.