Changes in cell-mediated immune responses after experimentally-induced anaphylaxis in dogs.

Experimentally-induced type 1 hypersensitivities were induced in normal dogs to either ovalbumin or Ascaris antigen. In vitro and in vivo cell-mediated immune responses were measured before sensitization and again at 1 and 6 days after induction of anaphylaxis by intravenous challenge with antigen. Histamine-modulated lymphocyte functions, such as histamine-induced suppression, histamine co-mitogen induced blastogenesis and the in vivo cutaneous responses to intradermally injected mitogens decreased post anaphylaxis. Spontaneous suppression of the autologous mixed-lymphocyte reaction increased post anaphylaxis. Lymphocyte blastogenic response to Concanavalin A (Con A) decreased at 6 (but not at 1) days post anaphylaxis probably due to a mediator other than histamine. Blastogenesis of 24 h preincubated cells by suboptimal concentration of Con A, declined post anaphylaxis, but Con A-induced suppression was not significantly altered. Dogs with atopic dermatitis have some altered cell-mediated immune responses. Altered histamine-induced and spontaneous suppression, histamine suppression of mitogenesis and decreased contact sensitivity observed in this experimental type 1 hypersensitivity mimicked that of atopic dogs. Increased cutaneous response to mitogens observed in atopic dogs was not reproduced in the type 1 hypersensitive dogs. These findings suggest some of the altered cell-mediated immune functions observed in dogs with atopic dermatitis result from type 1 hypersensitivity. The other abnormalities may be intrinsic to the atopic state.

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.

An inherited connective tissue disease in the horse.

The hyperextensible, fragile skin of two related horses was compared with the skin of eight normal horses. Skin sections were examined by light microscopy and transmission electron microscopy. The deep dermal layer of the dorsal abdomen was much thinner in the affected horses, and contained bundles of collagen fibers which were more loosely packed. Within individual fibers, the fibrils were frequently curved and nonparallel rather than straight and parallel. Both of the affected animals had a greater range of fibril diameters than a normal horse. They had some unusually thick fibrils with very irregular outlines in cross-sections, not observed in the normal animal. Other skin samples were subjected to acetic acid extraction, pepsin digestion, amino acid analysis and polyacrylamide gel electrophoresis. In the skin of the two affected horses, the proportion of total extracted collagen which was acid-soluble was twice as high as in two normal horses. Collagen types I and III were present in similar proportions in normal and affected horses, and the collagen chains were of normal molecular weights. The disorder resembles the group described by Minor (Minor RR: Am J Pathol 98: 226, 1980) as 'dominant collagen packing defect I' which has been reported in dogs, mink, and cats, and which shares features with Ehlers Danlos Syndrome I, II, and III in man. The pedigree data available for these horses suggest an autosomal recessive mutation, but are also consistent with autosomal dominant inheritance.

Confronting cisternae complexes in Purkinje cells of a dog.

During the course of our studies on the cerebellum of a dog we found large eosinophilic inclusions in Purkinje cells. Ultrastructural studies revealed that these inclusion bodies are composed of aggregates of stacks of confronting cisternae or modified confronting cisternae. The nature and significance of these unusual inclusions is obscure.

Chronic eosinophilic dermatitis: a manifestation of a multisystemic, eosinophilic, epitheliotropic disease in five horses.

A generalized, chronic, progressive, exfoliative dermatitis in five horses is described. Histologically, the lesion is characterized by a superficial and deep perivascular dermatitis which is eosinophil-rich with a marked lymphocytic and plasmacytic component, accompanied by marked acanthosis and hyperkeratosis. More severe cases progress to a lichenoid pattern with the same cellular composition with focal eosinophilic spongiosis and eosinophilic subcorneal pustules. Clinically, the disease is associated with chronic, severe weight loss and is fulminating. The skin lesions are accompanied by lymphoplasmacytic and eosinophilic infiltrates and formation of eosinophilic granulomas in other epithelial organs, most noticeably the pancreas, in which a chronic, fibrosing pancreatitis develops. Other epithelial organs involved to various degrees are salivary glands, the gastrointestinal system, including the oral cavity and esophagus, biliary epithelium and bronchial epithelium. The etiology of this disease is unknown.

Fusobacteremia in a calf with necrotic stomatitis, enteritis and granulocytopenia.

This case of fusobacteremia appears to be identical to an interesting and unusual syndrome previously reported. We wish to bring the syndrome to the attention of others who may be able to elucidate the etiology further. Because hematological examinations are frequently not done on calves, this condition may be more common than reports suggest. Perhaps others who observe this syndrome in calves may be able to investigate the role of other agents such as viruses or mycotoxins. Experimental work may be able to establish whether or not the exotoxins of Fusobacterium necrophorum can suppress granulopoiesis.