Bilateral osteoma cutis in a Peach-Faced Lovebird (Agapornis roseicollis).

An osteoma is an infrequent tumor documented in avian species. An adult female Peach-Faced Lovebird (Agapornis roseicollis) with a history of previous trauma was examined due to the presence of bilateral hard and yellowish-white masses in the radio-cubital humerus junction. Histopathological dermal examination revealed a non-neoplastic process of mesenchymal origin, characterized by the formation of well-differentiated trabecular bone, multiple areas of medullary bone and loose connective tissue and coagulation of the necrosis foci. Based on the histological findings and the medical history, the masses were diagnosed as bilateral secondary osteoma cutis. To our knowledge, this is the first report of this pathology with an acute course in this exotic pet bird. The previous trauma could be the initiating cause.

Primary Osteoma Cutis in the Interscapular Region of a Dog.

A 9-year-old neutered male Shih Tzu was presented with three contiguous firm nodules in the subcutaneous tissue of the interscapular region. Histopathological examination revealed that the nodules consisted of mature lamellar bone with a Haversian system, with no apparent lesion around the bone. Clinical examination revealed that the dog had no underlying disease and no history of trauma at the lesion site. Based on these findings and on the medical history, a diagnosis of primary osteoma cutis was made. Osteoma cutis is rare in both human and veterinary medicine, and most dogs reported to have secondary osteoma cutis. To our knowledge, this case is only the second report of primary osteoma cutis in a dog.

Localized parakeratotic hyperkeratosis in sixteen Boston terrier dogs.

BACKGROUND: Although zinc responsive dermatosis is typically a disorder of Arctic breed dogs, this study identifies similar cutaneous lesions on the face and pressure points of Boston terrier dogs. HYPOTHESIS/OBJECTIVES: To document the clinical and histological features of localized parakeratotic hyperkeratosis of Boston terrier dogs, to determine if the lesions respond to zinc supplementation and to determine whether tissue zinc levels were decreased in affected versus unaffected dogs. MATERIAL AND METHODS: Sixteen Boston terrier dogs with similar gross and histological findings were identified retrospectively from two institutions. Follow-up information for nine dogs from one institution was obtained from referring veterinarians using a questionnaire. Tissue zinc levels were measured from formalin-fixed paraffin-embedded skin biopsy samples of affected and unaffected dogs using inductively coupled plasma mass spectrometry. RESULTS: Mild to severe parakeratotic hyperkeratosis with follicular involvement was present in all 16 cases. Of the nine dogs for which follow-up information was available, five dogs received oral zinc supplementation and four dogs had documented clinical improvement or resolution of dermatological lesions. The median skin zinc levels were not significantly different between affected and unaffected dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: To the best of the authors' knowledge this is the first report of localized parakeratotic hyperkeratosis in Boston terrier dogs, some of which improved with oral zinc supplementation. Prospective studies in Boston terrier dogs are warranted to document potential zinc deficiency (serum and/or tissue levels, pre- and post-treatment) and to objectively assess response to zinc supplementation and other therapies.

Primary isolated osteoma cutis causing eyelid deformation and strabismus in a dog.

Osteoma cutis describes bone formation in skin and is well documented in the medical literature, but veterinary reports are few. We report a single case of a juvenile samoyed that was referred for assessment of a superior eyelid anomaly. Exploratory surgery and histopathology revealed the presence of mature, lamellar bone within the superior eyelid. The histologic appearance was consistent with primary osteoma cutis. The presence of the ossification within the deep dermis of the eyelid was associated with an abnormal conformation causing trichiasis, keratitis and dorsal strabismus. Identification of the osseous lesion during surgery and its removal was curative with no recurrence of disease during the 32 month follow-up period.

Dermatological and morphological findings in quarter horses with hereditary equine regional dermal asthenia.

BACKGROUND: Hereditary equine regional dermal asthenia (HERDA) is an autosomal recessive disorder affecting quarter horses (QHs); affected horses exhibit characteristic skin abnormalities related to abnormal collagen biosynthesis. HYPOTHESIS/OBJECTIVES: To characterize the thickness and morphological abnormalities of the skin of HERDA-affected horses and to determine the interobserver agreement and the diagnostic accuracy of histopathological examination of skin biopsies from horses with HERDA. ANIMALS: Six affected QHs, confirmed by DNA testing, from a research herd and five unaffected QHs from a stud farm. METHODS: The skin thickness in 25 distinct body regions was measured on both sides in all affected and unaffected horses. Histopathological and ultrastructural evaluation of skin biopsies was performed. RESULTS: The average skin thickness in all of the evaluated regions was thinner in the affected horses. A statistically significant difference between skin thickness of the affected and unaffected animals was observed only when the average magnitude of difference was ≥38.7% (P = 0.038). The interobserver agreement for the histopathological evaluation was fair to substantial. The histopathological sensitivity for the diagnosis of HERDA was dependent on the evaluator and ranged from 73 to 88%, whereas the specificity was affected by the region sampled and ranged from 35 to 75%. CONCLUSIONS AND CLINICAL IMPORTANCE: Despite the regional pattern of the cutaneous signs, skin with decreased thickness was not regionally distributed in the HERDA-affected horses. Histopathological evaluation is informative but not conclusive for establishing the diagnosis. Samples of skin from the neck, croup or back are useful for diagnosis of HERDA. However, the final diagnosis must be confirmed using molecular testing.

Aspectos clínicos, histopatológicos e moleculares da dermatosparaxia em ovinos White Dorper / Clinical, histopathological and molecular aspects of the dermatosparaxis in White Dorper sheep

Dermatosparaxia em animais é uma doença autossômica recessiva do tecido conjuntivo caracterizada por fragilidade e hiperextensibilidade cutânea. A doença em ovinos White Dorper é provocada pela mutação c.421G>T no gene ADAMmetalopeptidase com trombospondina tipo 1 motif, 2 (ADAMTS2). O objetivo deste estudo foi descrever os achados clínicos, moleculares e histopatológicos da dermatosparaxia em ovinos White Dorper de um rebanho localizado no Centro-Oeste Paulista. [...] Dos nove animais examinados, dois apresentavam sinais clínicos compatíveis com dermatosparaxia. O exame histopatológico de amostras cutâneas das lesões destes dois animais revelou também achados compatíveis com dermatosparaxia, sendo caracterizados por epiderme e anexos cutâneos preservados e sem características atípicas; colágeno displásico arranjado em feixes pequenos, fragmentados e com focos de degeneração, anexos cutâneos proeminentes e na região da derme foco hemorrágico intenso associado a moderado infiltrado neutrofílico na derme profunda. Com o objetivo de realizar o diagnóstico molecular da enfermidade, uma PCR foi padronizada utilizando primers específicos desenhados para amplificar a região do gene ADAMTS2 que continha a mutação c.421G>T e o DNA obtido de amostras de sangue de todos os animais do rebanho. O sequenciamento direto dos produtos da PCR, comprovou que os dois animais clinicamente afetados possuíam a mutação responsável pela dermatosparaxia. A metodologia descrita neste estudo possibilitou o diagnóstico definitivo da doença. Segundo a literatura consultada, esta é a primeira vez que a dermatosparaxia é descrita em ovinos White Dorper no Brasil. A metodologia aqui descrita poderá ser empregada em estudos futuros que avaliem a prevalência desta mutação no Brasil, possibilitando a adoção de medidas que previnam a disseminação dessa mutação no rebanho brasileiro de ovinos White Dorper.

Dermatosparaxis in animals is an autosomal recessive disorder of the connective-tissue clinically characterized by skin fragility and hiperextensibility. The disease in White Dorper sheep is caused by mutation (c.421G>T) in the ADAM metalloproteinase with thrombospondin type 1 motif, 2 (ADAMTS2) gene. This study describes the dermatological, histological and the molecular findings of the dermatosparaxis in White Dorper sheep from a herd located in the center-west of São Paulo State. [...] The herd consisted of one ram, four ewe and their lambs. In this herd two lambs had clinical signs consistent with dermatosparaxis. Histopathological evaluation of the affected skin of these two animals also revealed consistent findings with dermatosparaxis, characterized by dysplasia of the collagen, which were arranged in small and fragmented collagen bundles and with foci of degeneration of collagen. Prominent cutaneous appendages and severe hemorrhagic focus in dermis region associated with mild neutrophilic infiltrate in the deep dermis. PCR using DNA blood and specific primers to amplify the mutation region c.421G>T was optimized in order to perform molecular diagnosis of the disease. The direct sequencing of the PCR products proved that the two clinically affected animals had the mutation responsible for dermatosparaxis, previously described for this breed and allowed the definitive diagnosis of the disease. This is the first report of the dermatosparaxis in White Dorper sheep in Brazil and the methodology used to confirm the diagnosis could be used in future studies to assess the prevalence of this mutation in Brazil, allowing the adoption of measures to prevent the spread of this mutation in the Brazilian White Dorper herd.

Preservation of phenotype in an organotypic cell culture model of a recessive keratinization defect of Norfolk terrier dogs.

The purpose of this study is to reproduce in vitro a recessive keratinization defect of Norfolk terrier dogs characterized by a lack of keratin 10 (K10) production. Keratinocytes from skin biopsy samples of four normal dogs and two affected dogs were cultured organotypically with growth factor-supplemented media in order to stimulate cornification. The cultured epidermis from the normal dogs closely resembled the normal epidermis in vivo and cornified. The cultured epidermis from the affected dogs displayed many phenotypic alterations identified in skin biopsies from dogs with this heritable defect. Immunohistochemistry and immunoblotting showed a marked decrease in K10 from the cultures of the affected keratinocytes, compared to that in K10 from the cultures of the normal keratinocytes. Real-time reverse transcription polymerase chain reaction quantitation showed a 31-fold decrease in K10, a 1.75-fold increase in K1 and a 136-fold increase in K2e between the affected and the normal epidermis. Organotypic keratinocytes showed a 241-fold decrease in K10, a 31-fold decrease in K1 and a 1467-fold decrease in K2e between the affected and normal cultures. Although in vitro keratin expression did not precisely simulate in vivo, the morphology of the normal and the affected epidermis was largely preserved; thus, this culture system may provide an alternative to in vivo investigations for cutaneous research involving cornification.