UVEODERMATOLOGICAL SYNDROME IN A COCKER-POODLE MIXED-BREED DOG

The uveodermatological syndrome, an auto-immune disorder having ophthalmic and dermal signs, has been described frequently in Akita dogs, rarely in other purebred dogs but none description of this syndrome in mixed breed dogs has been reported. In this paper, we describe the syndrome in a Cocker-Poodle mixed breed dog.


Introduction
The Vogt-Koyanagi-Harada (VKH) syndrome is a well known disease in human beings.It was first described by Vogt in 1906, by Koyanagi in 1929and by Harada in 1926.The cause of this syndrome in human beings has been a mystery, but since 1969 there has been substantial evidence that it is an immune-mediated disease in which melanocytes are the target cells (MORGAN, 1989).
In man, the VKH syndrome has four recognized phases: (1) prodromal, characterized by neurologic and auditory manifestations; (2) acute uveitis, characterized by diffuse choroiditis, which may manifest as exudative retinal detachments and papillitis, with or without clinical signs of intraocular inflammation; (3) chronic, characterized by the variable development of depigmentation of the fundus (sunset glow fundus) and limbus (Sugiura sign), as well as poliosis, vitiligo and alopecia; and (4) chronic-recurrent, which may interrupt the chronic phase with iridociclitis, which can be recurrent, chronic or both (READ et al., 2001a).
In dogs, the disease lacks the systemic component, and is called uveodermatological syndrome (UDS).The ocular signs are usually the first abnormality noticed, which include bilateral anterior and posterior uveitis to severe panuveitis.Retinal detachment, optic neuritis, or changes in choroidal pigments may also be present.The dermatological signs include depigmentation of the eyelids, lips, nose and, less commonly of the scrotum, vulva, footpads, and anus.Neurological signs are rare, described only twice, in one Akita (COTTRELL and BARNETT, 1987) and in one Siberian Husky (DENEROLLE et al., 2000), but the suggestion of the neurological disease was made based only in behavioral changes, additional neurological evaluation was not performed.
Corticosteroids have been usually the treatment of choice for human beings and dogs.Other immunosupressive drugs can be associated when necessary.This syndrome is not a life threatening disease, however the prognosis for vision is poor, because severe complications often lead to visual loss.

Case Report
A 2 1 / 2 -year-old male mixed breed dog (English Cocker Spaniel x Poodle) was referred with a history of eye redness in the last 5 months.The owner reported visual impairment and the use of several systemic and topical medications with no success.Uveodermatological syndrome in a cocker-poodle mixed-breed dog The first ophthalmic examination revealed mild enlargement of the eyes, moderate mucous discharge, moderate to severe conjunctival hyperemia; opacity and vessels at the corneal surface.In the anterior chamber, there was an intense flare and rubeosis iridis.The pupillary light reflexes in both eyes were absent.The lens were cataractous, hence the ocular fundi could not be evaluated (FIGURA 1A).The IOP was 10 mmHg (TONOPEN) in both eyes.The dog had depigmentation of the lips, nasal planum, and scrotum (FIGURA 1B).Complete blood count has been performed.The treatment was prednisone 1mg/kg once a day; dexamethasone + neomycin + polymyxin four times a day; 1% atropine ophthalmic solution -twice a day for three days, and, once a day afterwards after one week, at the first examination, hyphema developed in the anterior chamber.The laboratory analysis (complete blood count, biochemistry) was normal, so a presumptive diagnosis of UDS was made.Skin samples were taken for hystological examination.One month later, the eyes were smaller, there was no conjunctival hyperemia, and the hyphema had disapeared, thereafter the medication was tapered and then discontinued.One month after the medication has been discontinued, the owner claimed that the dog eyes became red again, and at the ophthalmic examination, it has been observed that the ophthalmic signs had gotten worse.The medication (oral prednisone and topical dexamethasone + neomycin + polymyxin) was introduced again.Meanwhile, the result of the histological analysis had shown features compatible with the UDS.

Discussion
The VKH syndrome (VKHS) in human beings is considered a chronic, bilateral, granulomatous ocular and multisystemic inflammatory condition of unknown cause (READ et al., 2001a).It affects primarily Asians, Latinos, Native Americans or Asian Indians.Women appear to be affected more commonly than men.VKH disease may occur at all ages, including childhood (READ et al., 2000).Experimental data continue to support an autoimmune etiology for VKH disease, directed most probably against an melanocyte antigenic component, possibly tyrosinase or tyrosinase-related protein (YAMAKI et al., 2000), an identified 75kDa protein obtained from cultured human melanous cells (G-361) (KONDO et al., 1994) and the S-100 protein (GLODDEK et al., 1999).There are some evidence about the involvement of the Epstein-Barr virus in the pathogenesis of the VKHS (MINODA et al., 1999).In some cases, it is thought that the trigger is a cutaneous injury (RATHIMAN et al., 1999).There is likely a genetic predisposition, since specific HLA types have been associated with the disease (READ et al., 2001a).
There are no specific diagnostic tests for the VKH disease.The diagnosis is therefore based on a combination of suggestive clinical and ancillary test findings when other uveitic conditions have been excluded (READ et al., 2001b).
The features of the VKH syndrome may be shared by multiple other entities, such as sarcoidosis, sympathetic ophthalmia, syphilitic uveitis, tuberculosis uveitis, Lyme disease, posterior scleritis, intraocular lymphoma, central serous choroidopathy and uveal effusion syndrome (READ et al., 2001a).The most affected breed has been the Akita, althoug other breeds can be affected.
Depigmentation of the hair and skin usually follows the onset of ocular signs.Dermal depigmentation often involves the eyelids, nasal planum, lips, scrotum, and footpads (MORGAN, GODOY, C.A.L. et al.
Dermatohistopathologic findings include an interface dermatitis composed of large histiocytic cells, small mononuclear cells, and plasma cells.Other manifestations are irregular epidermal hyperplasia with hyperkeratosis and pigmentary incontinence with decreased numbers of epidermal melanocytes (BOLDY et al., 1989).There is one report about the association of anti-retinal antibodies with UDS (MURPHY et al., 1991).
The general guidelines in the therapy involve 1 to 2 mg/kg per day of oral prednisone (MORGAN, 1989).By analogy with human experience in VKH disease, systemic corticosteroids should be continued at relatively high doses for at least two or three months, and perhaps for as long as six months (ROMATOWSKI, 1985).Unfortunately, the prognosis for vision is often poor.
The macroscopic and microscopic lesions in the case presented in this paper were consistent with the uveodermatological syndrome described in dogs.
The veterinary practitioner should maintain a suspicion for this uveodermatological syndrome not only in the Akita dog, but in any dog displaying signals that remind those of this particular disease.
FIGURA 1 -A) CORNEAL OPACITY AND NEW VESSELS OF THE CORNEA OF RIGHT AND LEFT EYES.B) DERMAL DEPIGMENTATION OF THE NASAL PLANUM AND SCROTUM WITH EROSIONS AND CRUSTS.