Page 1318 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Skin 1293

VetBooks.ir Aetiology/pathophysiology 12.103
HERDA has worldwide distribution, with the
disease and/or causative allele being reported in
Europe and North and South America. HERDA
is attributable to an autosomal recessive mode of
inheritance of a mutation in equine cyclophilin B
(PPIB), resulting in a functional defect in this pro-
tein, which in turn causes less effective catalysis of
the rate-limiting step in collagen folding. The out-
come of the mutation is noted in the way the mid-
to deep collagen fibres are structurally disorganised Fig. 12.103 Cutaneous asthenia in a 3-year-old
and disoriented, with or without a decrease in the inbred Quarter horse filly (dam × own son). There is
ability of these fibres to repair themselves. Affected abscessation of loosened skin and the presence of old
horses have lower cutaneous tensile strength than scars from previous similar events. (Reprinted from
healthy horses. Pascoe RR and Knottenbelt DC (1999) Manual of
Equine Dermatology, WB Saunders, with permission)
Clinical presentation
Signs can appear at birth or may not be noticed
until the horse is being ridden for the first time Management
with tack. Foals may have loose, wrinkled skin, Affected horses should be removed from breeding
which is hyperextensible, hyperfragile, tears eas- programmes. There is no treatment, apart from
ily and repairs slowly. Older horses usually pres- minimising trauma, thus designating the horse a
ent with wounds and scarring in areas of friction pasture companion. Breeding stock genetics should
(often under the saddle, over the back and on the be investigated and all carriers should be culled.
sides of the neck). The condition may be gener- Inbreeding programmes should be avoided.
alised over the whole body or be sharply demar-
cated. Scar formation is common. Subcutaneous Prognosis
haematomas and abscesses occur (Fig. 12.103). The prognosis is guarded.
A defect in the elasticity and/or the tensile
strength of various tissues may also result in JUNCTIONAL EPIDERMOLYSIS BULLOSA
defects in the cornea, heart, tendons and great
vessels. Definition/overview
This refers to a group of hereditary mechanobullous
Diagnosis diseases characterised by blister formation following
This condition characteristically occurs in young mild trauma.
Quarter horses. The clinical appearance of loose,
hyperfragile skin is suggestive. Histopathological Aetiology/pathophysiology
findings are sometimes subtle, but ‘clumped’ or Junctional epidermolysis bullosa (JEB) is a hereditary
poorly organised collagen fibres below the level disease, occurring principally in Belgian draught
of the hair follicles may be seen. It is difficult to foals. JEB1 is found in Belgian draught horses, as well
distinguish affected from healthy horses with cer- as other related draught breeds including American
tainty on the basis of histopathology. Submission Cream, Breton and Comtois. In contrast, JEB2 is
of 20–30 hairs with roots to the Veterinary found in American Saddlebred horses. Phenotypic
Genetics Laboratory at UC Davis offers a diag- changes occur as a result of homozygous autosomal
nostic test to determine carrier or affected status recessive mutations in the laminin genes (LAMB3,
(www.vgl.ucdavis.edu/services/horse). LAMC2) responsible for skin attachment to the