Verrucous pastern dermatopathy
This condition is also overrepresented in the Friesian breed as well as several other draught horse breeds. This chronic dermatitis
develops into thick, nodular, ulcerated skin on the caudal side of the pasterns. The long hair or feathering found in this
location is thought to accumulate moisture and debris, which may have some role in the development of skin irritation. This
condition has also been called chronic progressive lymphedema, grapes, greasy heel and granulomatous pastern dermatitis. These lesions are often frustratingly unresponsive to treatment. And although genetics is suspected of playing a role with
this skin condition in the Friesian, it hasn't been proven.1
Aortic artery rupture
Aortic rupture is an important and unique problem in the Friesian horse that again relates to a disorder in collagen tissue.1 Just about all equine aortic ruptures in non-Friesian breeds occur at the connection between the aorta and the heart in
an area called the aortic root. Rupture of the main blood vessel in the body at this level leads to rapid filling of the pericardial
sac and cardiac tapenade as the blood-filled sac around the heart does not allow the heart to expand and beat. This condition
leads to acute heart failure and death. Most horses suffering aortic rupture are either found dead with little to no sign
of struggle or discomfort before death or are stable one moment and die very rapidly once the aorta ruptures.
In Friesians, however, the site of aortic rupture is at the aortic arch near the ligamentum arteriosum. Because the rupture
occurs here in a more forgiving location in the heart, a number of scenarios can potentially develop that are unique to the
Friesian horse. Also, because aortic ruptures in Friesian horses only appear to occur in this unique location, a genetic or,
at the very least, breed-specific condition is considered likely.
If the aortic rupture is large, within seconds, the chest cavity is pumped full of blood, and the horse dies acutely. This
is rare in Friesians. More often the tear may be smaller, so the blood leaks into the tissue surrounding the aorta, forming
a perivascular pressure cuff. This pressure stops the bleeding, and these horses can remain stable for long periods. Because
the heart must still pump blood through an aorta that is under pressure from the tissue swelling around it, an increased heart
beat results even at rest. These horses often show poor performance, high heart rate and bounding pulses, intermittent lameness
and swelling through the chest and ventral abdomen. Eventually the pressure cuff will not hold and the aorta will rupture
completely, leading to death.
In some Friesians the rupture creates an aortopulmonary fistula, or an artificial connection between the damaged aorta and
the pulmonary blood vessels. In this scenario, the lungs slowly begin to receive a larger than normal volume of blood. This
can create a problem, as horses can go weeks to months before the lungs can no longer handle the increased blood flow from
the aorta. Affected horses will develop a dry, hacking cough; poor performance; swelling of the chest and legs; fluctuating
fever; pale mucous membranes; recurrent colic and intermittent lameness. Catherine Delesalle, DVM, PhD, DECEIM, of Ghent University
urges that "because Friesian horses show suspicious clinical signs sometimes weeks to months before fatal rupture, these 'predictive
signs' need to be put in the spotlight for the Friesian horse owners."5,6 Clinicians can also benefit by considering these signs and these breed-specific problems when dealing with Friesian horses.
The average age of horses with aortic rupture is 4 years old, so keep in mind that many of these horses will have been bred
before developing this problem. Increased awareness and better, earlier diagnosis might be the best way to remove these horses
from breeding consideration and the best way to eliminate these important conditions from the breed.
Dr. Ken Marcella is an equine practitioner in Canton, Ga.
1. Boerma S, Back W, Sloet van Oldruitenborgh-Oosterbaan MM. The Friesian horse breed: a clinical challenge to the equine veterinarian?
Equine Vet Educ 2012;24(2):66-71.
2. Gussekloo SWS, Lankester J, Kersten W, et al. Effect of differences in tendon properties on functionality of the passive stay
apparatus in horses. Am J Vet Res 2001;72:474-483.
3. Boerma S, Sloet van Oldruitenborgh-Oosterbaan MM. Megaoesophagus in the Friesian horse: a hereditary problem? in Proceedings. International Congress of World Equine Veterinary Association, 2008;484.
4. van Grevenhof EM, Ducro B, Heuven HCM, et al. Identification of environmental factors affecting the prevalence of insect
bite hypersensitivity in Shetland ponies and Friesian horses in The Netherlands. Equine Vet J 2007;39:69-73.
5. van Loon G, De Clercq D, de Bruijn CM, et al. Aortic rupture and aortopulmonary fistulation: increased prevalence in Friesian
horses and importance of early ante-mortem diagnosis, in Proceedings. Journées annuelles de l'Association Vétérinaire Equine Française, 2011;192-193.
6. Ploeg M, Saey V, de Bruijn CM, et al. Aortic rupture in Friesian horses: 3 scenarios revealed. Phyrso 2012.