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Case Reports in Veterinary Medicine
Volume 2015, Article ID 469317, 5 pages
Case Report

Regressing Multiple Viral Plaques and Skin Fragility Syndrome in a Cat Coinfected with FcaPV2 and FcaPV3

1Department of Veterinary Medicine, University of Sassari, Via Vienna 2, 07100 Sassari, Italy
2Department of Veterinary Medical Sciences, University of Bologna, Via Zamboni 33, 40126 Bologna, Italy
3Private Practitioner, Via Giovanni da Verrazzano 19, 52100 Arezzo, Italy
4Department of Veterinary Sciences, University of Pisa, Viale delle Piagge 2, 56124 Pisa, Italy

Received 28 September 2015; Accepted 1 December 2015

Academic Editor: Katerina K. Adamama-Moraitou

Copyright © 2015 Alberto Alberti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Feline viral plaques are uncommon skin lesions clinically characterized by multiple, often pigmented, and slightly raised lesions. Numerous reports suggest that papillomaviruses (PVs) are involved in their development. Immunosuppressed and immunocompetent cats are both affected, the biological behavior is variable, and the regression is possible but rarely documented. Here we report a case of a FIV-positive cat with skin fragility syndrome and regressing multiple viral plaques in which the contemporary presence of two PV types (FcaPV2 and FcaPV3) was demonstrated by combining a quantitative molecular approach to histopathology. The cat, under glucocorticoid therapy for stomatitis and pruritus, developed skin fragility and numerous grouped slightly raised nonulcerated pigmented macules and plaques with histological features of epidermal thickness, mild dysplasia, and presence of koilocytes. Absolute quantification of the viral DNA copies (4555 copies/microliter of FcaPV2 and 8655 copies/microliter of FcaPV3) was obtained. Eighteen months after discontinuation of glucocorticoid therapy skin fragility and viral plaques had resolved. The role of the two viruses cannot be established and it remains undetermined how each of the viruses has contributed to the onset of VP; the spontaneous remission of skin lesions might have been induced by FIV status change over time due to glucocorticoid withdraw and by glucocorticoids withdraw itself.