title: Experimentally induced Vogt-Koyanagi-Harada disease in two Akita dogs.
abstract: We have investigated whether a Vogt-Koyanagi-Harada (VKH)-like disease can be induced in Akita dogs by immunizing them with tyrosinase related protein 1 (TRP1), and compared the alterations induced to those of Akita dogs with a spontaneously occurring disease that resembles human VKH disease. Two Akita dogs were immunized with a peptide mixture of human TRP1. The changes in the eyes were followed by slit-lamp biomicroscopy, ophthalmoscopy, and fluorescein angiography (FA). The eyes, skin, and brains were studied by standard histological methods at about 20 months after the first immunization in one dog (dog 1), and at 3 weeks after the second immunization in the second dog (dog 2). Both dogs developed chorioretinal disease 3-4 weeks after the first immunization. Many inflammatory cells infiltrated into the anterior chamber and anterior vitreous. The fundus showed geographic, multifocal exudative retinal detachments. Multifocal leakages of fluorescein were detected from the choroid. Histologically, exudative retinal detachment was present, and inflammatory cells were seen in the subretinal space in the eyes of dog 2 taken three weeks after the second immunization. The choroid was thickened by the infiltration of inflammatory cells in some lesions. Dalen-Fuchs nodules were seen in the eye of dog 2. Depigmentation, pigment dispersion, and infiltration of many inflammatory cells around hair follicles and vessels were seen in the skin taken three weeks post-immunization. The clinical course and changes in the eyes and skin were very similar to those seen in the Akita dogs with spontaneously occurring VKH disease. We concluded that a VKH-like disease had been induced in these dogs, and this supports the tentative conclusion that the spontaneously occurring chorioretinal disease in Akita dogs is VKH disease.
authors.affiliation: Department of Ophthalmology, Akita University School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan. kunihiko@oph.med.akita-u.ac.jp
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Yamaki
authors.forename: Naoaki
authors.initials: N
authors.lastname: Takiyama
authors.forename: Norihiko
authors.initials: N
authors.lastname: Itho
authors.forename: Nobuhisa
authors.initials: N
authors.lastname: Mizuki
authors.forename: Maehara
authors.initials: M
authors.lastname: Seiya
authors.forename: Wakaiki
authors.initials: W
authors.lastname: Sinsuke
authors.forename: Kouichi
authors.initials: K
authors.lastname: Hayakawa
authors.forename: Tadao
authors.initials: T
authors.lastname: Kotani
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology* / Q000473:pathology / Q000662:veterinary*; D004195:Disease Models, Animal; D004283:Dog Diseases / Q000209:etiology* / Q000473:pathology; D004285:Dogs; D005123:Eye / Q000473:pathology; D005260:Female; D007114:Immunization; D008297:Male; D010446:Peptide Fragments / Q000276:immunology; D012867:Skin / Q000473:pathology; D014357:Trypsin / Q000276:immunology; D014362:Trypsinogen / Q000276:immunology; D014607:Uveomeningoencephalitic Syndrome / Q000209:etiology* / Q000473:pathology / Q000662:veterinary*
chemical_list: D010446:Peptide Fragments; D014362:Trypsinogen; C489303:PRSS1 protein, human; D014357:Trypsin