Ocular pathology in the minimally depigmented subline of the vitiliginous Smyth chicken

Choroidal melanocytes and the retinal pigmented epithelium (RPE) were studied morphologically and histochemically in the Smyth chicken, an avian model for human vitiligo. The sequence of cytological events occurring in the ocular tissue of minimally depigmented Smyth birds was determined. Abnormalities of melanocytes and the associated inflammation was least severe in peripheral areas of the choroid and most pronounced in the back of the eye at the base of the optic nerve head. In the peripheral choroid, morphologically normal melanocytes and an occasional mononuclear leukocyte were observed. However, some of these morphologically normal melanocytes histochemically demonstrated atypical tyrosinase activity at the trans area of the Golgi apparatus. Toward the back of the eye, the melanocytes first appeared swollen and had retracting dendrites. Ultrastructurally these melanocytes demonstrated an increase in extramelanosomal cytoplasm. Later, melanocytes became spherical and had membrane bound, autophagosome-like compartments of pigment granules. As the melanocyte injury progressed, macrophages invaded the tissue and phagocytized melanocytic dendrites. These were followed by numerous plasma cells. Eventually, the back of the eye contained no pigment and was infiltrated with numerous mononuclear inflammatory cells. The retinal pigment epithelium also demonstrated a gradient in the degree of destruction, related to its topography. These cytological features consisted of the retraction of apical RPE processes, the disappearance of the basal plasma membrane infoldings, and the replacement of Bruch's membrane by collagen-like fibrils. These results demonstrate that the uveitis which develops in vitiligo appears to be a consequence of an inherent choroidal melanocyte defect.     

Herpesvirus connection in the expression of autoimmune vitiligo in Smyth line chickens

The Smyth line (SL) chicken is an animal model for human vitiligo, a common acquired depigmentary disorder affecting about 1-2% of people worldwide. The vitiligo-like depigmentation in SL chickens typically develops when the birds are between 6 and 14 weeks of age and may affect 70-95% of hatch mates. The development of SL vitiligo is considered to depend on two interacting components, namely an inherent melanocyte defect and an autoimmune reaction to melanocytes. Recently, a role for an environmental factor in the expression of vitiligo was suggested by the observation that only 10% of SL chicks imported from the University of Massachusetts (UM) and reared in isolation at biosecurity level 2 (BSL 2) at the University of Arkansas (UA) exhibited vitiligo. Following further assessment of environmental differences between UA and UM SL chickens, three environmental factors that may have influenced the expression of SL vitiligo were identified. Included were housing condition, status of Mycoplasma synoviae infection, and turkey herpesvirus (HVT) vaccination status. Studies were subsequently conducted at UA and UM to assess the role of these environmental factors in the expression of SL vitiligo. M. synoviae infection was not found necessary for vitiligo expression in SL chickens. However, HVT emerged as a strong candidate for an important environmental factor in SL vitiligo. The connection between HVT and SL vitiligo was confirmed for both BSL 2 and conventional housing. Therefore, the observations reported here suggest a strong causative link between HVT infection and SL vitiligo.