Objective—To determine whether cyclosporine Ainduced
hyperplastic skin lesions of dogs were associated
with papillomavirus infections.
Animals—9 dogs that were treated with cyclosporine
A and developed hyperplastic skin lesions.
Procedure—History and clinical and histopathologic
data were collected. Paraffin-embedded skin biopsy
specimens from hyperplastic skin lesions were
immunostained for common papillomavirus genusspecific
structural antigens by use of a polyclonal rabbit
anti-bovine papillomavirus type 1 antiserum.
Sections from each tissue block underwent DNA
extraction, and polymerase chain reaction (PCR)
assays were performed with several sets of primers
to amplify a wide range of papillomavirus DNA from
humans and other animals.
Results—In 7 of 9 dogs, there were more than 10
hyperplastic skin lesions that microscopically resembled
those of psoriasiform lichenoid dermatosis. In
those dogs, results of testing for papillomavirus via
immunohistochemical analyses and PCR assays were
negative. In the other 2 dogs, there were only 1 and
3 verrucous lesions, and in those dogs, histologic
evaluation revealed koilocytes and nuclear viral inclusions
that were immunoreactive for papillomavirus
antigens. Papillomavirus DNA was amplified from
both dogs. One of the sequences was characteristic
for the canine oral papillomavirus, whereas the other
had similarities with the recently described canine
Conclusions and Clinical Relevance—In dogs,
hyperplastic skin lesions occasionally develop during
treatment with cyclosporine A. Most of the lesions
resemble those of psoriasiform lichenoid dermatosis,
although papillomavirus can be detected in some
instances. (Am J Vet Res 2005;66:1764–1769)
Objective—To evaluate efficacy of cyclosporine A,
administered at either of 2 dosages, in dogs with
atopic dermatitis (AD).
Design—Multicenter randomized controlled trial.
Animals—91 dogs with AD.
Procedure—Dogs were assigned to receive placebo
(30 dogs), cyclosporine at a low dosage (2.5 mg/kg
[1.1 mg/lb], PO, q 24 h for 6 weeks; 30 dogs), or
cyclosporine at a high dosage (5.0 mg/kg [2.3 mg/lb],
PO, q 24 h for 6 weeks; 31 dogs).
Results—After 6 weeks, mean percentage reductions,
compared with baseline scores, in scores of
lesion severity were 34, 41, and 67% for dogs treated
with the placebo, cyclosporine at the low dosage,
and cyclosporine at the high dosage, respectively.
Similarly, mean percentage reductions in pruritus
scores were 15, 31, and 45%, respectively.
Percentage reductions in skin lesion and pruritus
scores were significantly higher for dogs given
cyclosporine at the high dosage than for dogs given
the placebo. Treatment efficacy was significantly
associated with whether dogs had a history of seasonal
AD. Percentage reductions in skin lesion and
pruritus scores were high for dogs treated with
cyclosporine at the highest dosage that had a history
of nonseasonal AD. Dogs in all groups with seasonal
AD improved during the study period.
Conclusions and Clinical Relevance—Results suggest
that oral administration of cyclosporine at a
dosage of 5.0 mg/kg once daily is effective in reducing
severity of pruritus and skin lesions in dogs with
AD, especially those with nonseasonal disease. (J Am
Vet Med Assoc 2002;221:370–377)
Objective—To describe the immunopathologic characteristics of superficial stromal immune-mediated keratitis (IMMK) immunopathologically by characterizing cellular infiltrate in affected corneas of horses.
Animals—10 client-owned horses with IMMK.
Procedures—Immunohistochemical staining was performed on keratectomy samples with equine antibodies against the T-cell marker CD3 and B-cell marker CD79a (10 eyes) and the T-helper cytotoxic marker CD4 and T-cell cytotoxic marker CD8 (6 eyes). Percentage of positively stained cells was scored on a scale from 0 (no cells stained) to 4 (> 75% of cells stained). Equine IgG, IgM, and IgA antibodies were used to detect corneal immunoglobulin via direct immunofluorescence (10 eyes). Serum and aqueous humor (AH) samples from 3 horses with IMMK were used to detect circulating and intraocular IgG against corneal antigens via indirect immunofluorescence on unaffected equine cornea.
Results—Percentage scores (scale, 0 to 4) of cells expressing CD3 (median, 2.35 [range, 0.2 to 3.7]; mean ± SD, 2.36 ± 1.08) were significantly greater than scores of cells expressing CD79a (median, 0.55 [range, 0 to 1.5]; mean, 0.69 ± 0.72). All samples stained positively for CD4- and CD8-expressing cells, with no significant difference in scoring. All samples stained positively for IgG, IgM, and IgA. No serum or AH samples collected from horses with IMMK reacted with unaffected equine cornea.
Conclusions and Clinical Relevance—Pathogenesis of superficial stromal IMMK included cell-mediated inflammation governed by both cytotoxic and helper T cells. Local immunoglobulins were present in affected corneas; however, corneal-binding immunoglobulins were not detected in the serum or AH from horses with IMMK.