Ulcerative dermatitis of the nasal planum or haired skin of the face, associated with intranuclear inclusion bodies compatible with herpesvirus, was identified in nine cats. Clinically, lesions were ulcerative and crusted, and often persistent. A tenth cat had focal proliferative ulcerative stomatitis, also associated with intranuclear inclusion bodies. Microscopically, there was necrosis and ulceration associated with prominent eosinophilic inflammation. Intranuclear inclusion bodies were noted in all cases, within the surface or adnexal epithelium. Ultrastructural examination of skin from two cats revealed virions morphologically compatible with a herpesvirus. Polymerase chain reaction (PCR) specific for feline herpesvirus 1 on DNA extracted from fresh‐frozen or formalin‐fixed paraffin‐embedded biopsy samples and/or consensus primer PCR with DNA sequencing performed on DNA extracted from formalin‐fixed paraffin‐embedded biopsy samples from seven cats revealed that the virus was indistinguishable from feline herpesvirus 1. PCR was negative in one of eight cats tested.
The clinical, biochemical, histological, or ultrastructural abnormalities of ®ve related female Rottweiler dogs with a hereditary disorder of corni®cation are reported. Three of the ®ve dogs also had multiple noncutaneous congenital defects. Cutaneous abnormalities included generalized, hyperkeratotic, variably pigmented plaques, which in one dog were distributed along Blaschko's lines. Moderate to severe parakeratosis involving the follicular infundibula and ostia and focal orthokeratosis with variable vacuolation of spinous cells was observed on histopathologic examination of all skin specimens. Supplementation with oral zinc in two dogs and vitamin A alcohol and calcitriol in one dog did not result in clinical or histological improvement of the hyperkeratotic lesions. This disorder of corni®cation in dogs is similar to human disorders of corni®cation that follow the lines of Blaschko. Blaschko's lines follow a V-shape over the spine, an S-shape on the abdomen, and an axial distribution on the limbs. No related male dogs were aected, suggesting an Xlinked dominant mode of inheritance. Many features of this hereditary DOC correspond to the human condition CHILD syndrome.
Seven cats diagnosed as¯ea allergic by speci®c criteria and seven normal control cats were exposed to¯ea bites in a controlled manner and were given intradermal injections of 1:1000 w/v¯ea antigen. Subjective evaluation of gross lesions and documentation of histological changes at¯ea antigen intradermal skin test (IDST) and¯ea bite sites were performed at 15 min, 24 h and 48 h after IDST or¯ea exposure. Control cats did not develop an immediate gross reaction to either¯ea bites or the intradermal injection of¯ea antigen. All seven¯ea-allergic cats had an immediate gross reaction at the site of IDST with¯ea antigen; ®ve of these cats also developed immediate gross reactions to¯ea bites. Three of seven¯ea-allergic cats developed a gross 24 h and/or 48 h delayed reaction at the¯ea antigen IDST sites. These three and one other cat had both an immediate and delayed gross reaction to¯ea bites. Histological examination of 15 min skin specimens from IDST and¯ea bite sites of¯ea-allergic cats were similar with a mild lymphocytic, histiocytic and mastocytic super®cial perivascular dermatitis. Histological examination of 24 h and 48 h skin specimens from IDST and ea bite sites of¯ea-allergic cats showed that they were often indistinguishable. Histological features of IDST and¯ea bite sites of¯ea-allergic cats at 24 h consisted of a perivascular to diuse predominately eosinophilic dermatitis and mural folliculitis with variable epidermal necrosis and ulceration.
A 1‐day‐old Appaloosa colt developed vesicles/bullae involving the skin of the lips and prepuce and multiple mucous membranes. Histopathology revealed subepidermal vesicles/bullae that were clear or contained variable numbers of neutrophils and erythrocytes. The separated epidermis appeared viable. The denuded dermal papillae were often disrupted by microabscesses or coated with fibrinosuppurative debris. Fragmented basement membrane components were attached to exposed dermal papillae. Immunoperoxidase staining of sections for deposition of IgG, IgM, IgA, and C3 were positive for IgG at the basement membrane and intercellular bridges. Complete recovery ensued. The characteristics of the subepidermal bullous lesions and clinical course of lesion resolution in this foal suggested a drug‐induced pathogenesis. The only known drug exposure of the foal or mare was topical application of 7% iodine to the umbilicus at the time of foaling. Similar reactions to iodine administration have been reported in humans.
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