Inferring diet, feeding behaviour and causes of mortality from prey-induced injuries in a New Zealand fur seal.

New Zealand fur seals Arctocephalus forsteri are the most abundant of the 4 otariid (eared seal) species distributed across Australasia. Analyses of stomach contents, scats and regurgitates suggest a diet dominated by bony fish and squid, with cartilaginous species (e.g. sharks and rays) either absent or underrepresented because of a lack of preservable hard parts. Here we report on a subadult specimen from south-eastern Australia, which was found ashore emaciated and with numerous puncture wounds across its lips, cheeks, throat and the inside of its oral cavity. Fish spines embedded in the carcass revealed that these injuries were inflicted by chimaeras and myliobatiform rays (stingrays and relatives), which matches reports on the diet of A. forsteri from New Zealand, but not South Australia. Shaking and tearing of prey at the surface may help to avoid ingestion of the venomous spines, perhaps contributing to their absence from scats and regurgitates. Nevertheless, the number and severity of the facial stab wounds, some of which led to local necrosis, likely affected the animal's ability to feed, and may account for its death. Despite their detrimental effects, fish spine-related injuries are difficult to spot, and may be a common, albeit cryptic, type of trauma. We therefore recommend that stranded seals be systematically examined for this potentially life-threatening pathology.

Trichophyton dermatophytosis--a disease easily confused with pemphigus erythematosus.

Trichophytosis is a rare diagnosis in dogs in Ontario, but recently 4 dogs with a scaling and crusting, alopecic, facial dermatitis have been so diagnosed. In all cases, the histopathological findings of severe epidermal and follicular interface dermatitis, accompanied by an acantholytic intraepidermal pustular dermatitis suggested an immune-mediated disease.

A prospective study of the immunophenotype and temporal changes in the histologic lesions of canine demodicosis.

Mural folliculitis is a consistent histologic lesion of canine demodicosis. The objective of this study was to describe the immunophenotype and to evaluate temporal changes in histologic lesions of demodicosis during the course of therapy. Five dogs with demodicosis were examined and biopsied biweekly for up to 14 weeks; three dogs were evaluated once only. Lymphocyte subsets infiltrating the lesions were quantified using immunohistochemistry to detect CD3, CD21, CD4, and CD8 antigens. Lymphocyte subsets in blood were analyzed from four dogs using flow cytometry. Mural folliculitis was always present during clinically active disease. In contrast, following resolution of clinical lesions, perifolliculitis and/or perifollicular granulomas were present but mural folliculitis was absent. Most lymphocytes infiltrating the follicular epithelium in lesions of mural folliculitis were CD3+ and CD8+; the ratio of CD4+ :CD8+ cells in this epithelium was 0.032. In contrast, the perifollicular dermis contained approximately equal numbers of CD4+ cells and CD8+ cells, with slightly fewer CD21+B cells. In peripheral blood, the ratio of CD4+:CD8+ lymphocytes was reduced and the percentage of CD8+ cells was increased in three of four dogs. These results indicate that mural folliculitis is a consistent lesion of clinically active canine demodicosis and is characterized by infiltration of the follicular epithelium by CD3+ CD8+ T lymphocytes. These lymphocytes are cytotoxic T cells, which may mediate the injury to the follicular epithelium in demodicosis. Alternatively, CD8+ T cells may play a role in resistance to Demodex canis infection or may represent a deleterious immune response in dogs that develop demodicosis.

Familial cutaneous vasculopathy of German shepherds: clinical, genetic and preliminary pathological and immunological studies.

A genodermatosis affecting the German shepherd breed has been recognized in 26 dogs in Ontario since 1991. Clinical signs, first noted in young puppies,are manifested as pyrexia and lethargy. The main cutaneous lesions are footpad swelling and depigmentation,but there is also crusting and ulceration of ear tips and tail tips, and focal depigmentation of the nasal planum. Affected puppies show no consistent abnormalities in hematological or biochemical parameters, and immunological tests (antinuclear antibody and rheumatoid factor titer,immunoglobulin levels, and CD4+ and CD8+T-lymphocyte percentages) are normal. Bone marrow analysis has shown myeloid hyperplasia in 5 of 7 cases and myelofibrosis has been detected in 1 case. All but 3 of the 19 clinical cases have been strongly positive for platelet factor-3; however, normal puppies routinely develop positive platelet factor-3 tests. Furthermore, affected pups all had normal numbers of platelets on repeat complete blood counts.Light microscopic examination of footpad biopsies reveals a multifocal nodular dermatitis in which neutrophils and mononuclear inflammatory cells surround foci of dermal collagenolysis, and degenerative and inflammatory vessel lesions. Depigmented lesions have a mild, cell-poor, interface dermatitis,characterized by single cell necrosis of the basal cells, in addition to the nodular dermatitis. Similarities and differences between this disease,a condition known as collagen disorder of the footpads of German shepherds and other forms of cutaneous vasculitis in the dog are discussed. The cause and the pathogenesis of the disease are yet to be elucidated;however, pedigree analysis indicates an autosomal recessive inheritance pattern. Hypersensitivity reactions, directed against normal or damaged self-collagen, may be involved. The role of cell-mediated immunity against native or altered collagen is an area worthy of further investigation.

Abnormal cutaneous response to mitogens and a contact allergen in dogs with atopic dermatitis.

Antigen specific and nonspecific T-lymphocyte activity was evaluated in normal dogs and in dogs with atopic dermatitis by measuring the increase in skin thickness after application of the contact allergen dinitrochlorobenzene and after intradermal injection of the mitogens phytohemagglutinin and concanavalin A. The atopic dogs had a significantly reduced response to the contact allergen (P less than or equal to 0.001) but a significantly increased response to the mitogens (P less than or equal to 0.001). The atopic and normal dogs responded similarly to intradermally injected histamine. The response of dogs with non-atopic skin conditions to the cutaneous mitogen test was like that of normal dogs. Pre-existing dermatitis does not apparently influence cutaneous response to mitogens in dogs. The cutaneous response of atopics during treatment with corticosteroids is not different from normal controls. These results suggest a role for altered cell-mediated immunity in the pathogenesis of canine atopy and that the cutaneous mitogen test may have value as a rapid screening test for the disease.

Morphometric analyses of the skin of dogs with atopic dermatitis and correlations with cutaneous and plasma histamine and total serum IgE.

In order to improve the diagnostic value of histopathologic examination of skin biopsy samples from dogs with atopic dermatitis and, perhaps, to identify any differences from the normal state that may predispose to this skin condition, we compared the anatomic and cellular morphology of skin from three standard sites in 21 normal and 15 atopic dogs. The standard sites were lateral neck, dorsal rump, and craniolateral abdomen. No differences between the two groups were found in the means of area or thickness of the stratum corneum or the remainder of the epidermis at any site. The area of sebaceous glands, but not apocrine sweat glands, was larger in the atopic group (P less than or equal to 0.05 for the lateral neck skin and P less than or equal to 0.1 for the dorsal rump skin). The mean number of non-metachromatic mononuclear cells in combined skin samples (126 microns 2) in atopic dogs (91.0 +/- 28.7) was significantly greater (P less than or equal to 0.01) than for the control normal dogs (65.3 +/- 19.3); the mean number of mast cells in atopic dogs (12.39 +/- 6.44) was similarly greater than in the controls (8.48 +/- 5.14; P less than or equal to 0.1). Eosinophils were significantly increased in atopic dog skin (P less than or equal to 0.01). with the mean for all three sites combined of 0.81 +/- 0.90 compared with a mean of 0.06 +/- 0.15 for normal dogs. Numbers of circulating blood eosinophils were not significantly different in the atopic and normal group.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoimmune skin diseases in the dog.

Diagnoses of autoimmune skin diseases require very careful observation of the skin lesions, and selection of an intact vesicle for histopathological examination. If available, immunofluorescent studies can be very useful in confirming the diagnosis of autoimmune skin disease. Seven autoimmune skin diseases are briefly reviewed. Therapy must be aggressive and owner warned of the guarded prognosis.