Calcinosis circumscripta following an injection of proligestone in a Burmese cat.

A 9-month-old speyed Burmese cat was presented with a cutaneous lesion in the dorsal thoracolumbar region. The lesion was characterised by alopecia and whitish deposits within the subcutis and had occurred at the site of a previous progestogen injection (Covinan; Intervet). Excisional biopsy confirmed the diagnosis of calcinosis circumscripta. Recovery of the cat following surgical excision was excellent, with no recurrence of the lesion detected 12 months later. The classification of tissue calcification and the proposed aetiology of calcinosis circumscripta is reviewed. It is concluded that further work is required to determine any link between subcutaneous injections, especially of progestogens, and calcinosis circumscripta.

Disseminated haemangiosarcoma in an eastern barred bandicoot (Perameles gunnii).

A captive adult male Eastern barred bandicoot (Perameles gunnii) presented with three palpable subcutaneous masses in November 1998. A diagnosis of haemangiosarcoma was made based on histological examination of one excised mass. Euthanasia of the animal was performed 11 days postsurgery and a proliferative lesion in the paralumbar musculature and similar, smaller proliferative lesions surrounding the right popliteal lymph node and in the ventricular wall of the heart were found. Metastatic lesions were found in the liver and lung. The histological features of the neoplastic tissues supported the diagnosis of a poorly differentiated, disseminated haemangiosarcoma. This is the first reported case of haemangiosarcoma in the Eastern barred bandicoot.

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.

Altered spontaneous and histamine-induced in vitro suppressor-cell function in dogs with atopic dermatitis.

Spontaneous, histamine-induced and Concanavalin A (Con A)-induced suppression of Con A mitogenesis of autologous responder cells was studied in normal dogs and in dogs with atopic dermatitis. Histamine-induced suppression was significantly decreased in the atopic dogs, as was the Con A-induced suppression, at supraoptimal concentration of Con A, to a lesser extent. Total numbers of histamine type 1 or type 2 receptors were not different for cells from atopic or normal dogs. The spontaneous suppression was significantly greater for the atopic dogs and this was not accounted for by the effect of non-specific dermatitis, increased macrophage-induced suppression or increased induction by mitogenic factors in the culture medium. Some possible mechanisms for these results are discussed, and the similarities to suppressor cell function in humans with atopic disease are noted.

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.

In vitro lymphocyte stimulation by concanavalin A and with histamine as a co-mitogen in dogs with atopic dermatitis.

Cell-mediated immune function was assessed in a group of dogs with atopic dermatitis by measuring the responses of peripheral-blood lymphocytes (PBL) to various concentrations of Concanavalin A (Con A) and comparing them to those of normal dogs. No difference from normal was found in any of the stimulation indices neither was spontaneous tritium uptake of unstimulated cells different between the groups. We also measured the response to Con A stimulation in vitro of PBL preincubated for 24 h, either in cell-culture medium at 37 degrees C, or in whole blood containing EDTA at room temperature, as an indirect measure of function of a subgroup of suppressor cells. Preincubation caused enhancement of mitogenesis for normal dog lymphocytes but not for the atopic dog cells, particularly for suboptimal concentrations of Con A. No differences were found in the responsiveness following incubation in cell-culture medium between normal and atopic dog cells but for both groups the cells preincubated in whole blood were generally more responsive. Histamine, which is one of the mediators of type 1 hypersensitivities such as atopy, can modulate lymphocyte function. At 10(-4) and 10(-8) M histamine, when added simultaneously with Con A, enhanced mitogenesis of normal dog PBL but suppressed mitogenesis of atopic dog PBL. By using histamine H1 and H2 antagonists, we concluded that histamine enhanced mitogenesis via H1, receptors and suppressed it via H2 receptors. Our results suggest that there are abnormalities in lymphocyte function in dogs with atopic dermatitis which may be important in the pathogenesis of 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)

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.

Accidental sulfur poisoning in a group of holstein heifers.

Fourteen animals died or were euthanized after toxic levels of elemental sulfur were accidentally fed to a group of 120 Holstein heifers. Dehydration, rumen stasis, tachycardia, and diarrhea were seen along with metabolic acidosis, hypokalemia, and hypochloremia. The majority of deaths occurred from 3 to 10 days after the sulfur was fed to the heifers. Postmortem examination showed rumenitis, acute alveolitis, and renal tubular necrosis. The toxicity of ingested sulfur was attributed to the conversion of sulfur to hydrogen sulfide in the rumen.

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.

Necrotic colitis in two cats - a description of the lesions.

The lesions in two cases of necrotic colitis in old cats are described. Both had gross lesions of a necrotic, hemorrhagic colitis without gross lesions in the small intestine. Histologically the lesions resembled those of feline panleukopenia virus infection, namely: necrosis and loss of crypt epithelium, dilation of crypts and lining of crypts by flattened epithelium, subsequent collapse of the lamina propria and hemorrhage from subepithelial capillaries. Both grossly and histologically these lesions were restricted to the colon without similar involvement of the small intestine.The histories and clinical signs, the virological and hematological studies suggest that feline panleukopenia virus was not the etiological agent in these cases. No other causal agent was identified.

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.

In vitro metabolism of possible ecdysone precursors by the prothoracic glands of the tobacco hornworm, Manduca sexta.

3 beta, 14 alpha-Dihydroxy-5 alpha-7-en-6-one (5 alpha-ketodiol) (1) is metabolized by the prothoracic glands to 2,22-dideoxy-5 alpha-ecdysone (4) and 2-deoxy-5 alpha-ecdysone (3) but not to ecdysone (5) or any other 5 beta-metabolites. Similarly, 3 beta,5 alpha,14 alpha-trihydroxy-cholest-7-en-6-one (5 alpha-ketotriol) (8) is hydroxylated at C-22 and C-25 (9,10) of the side chain. However, 3 beta,14 alhpa-dihydroxy-cholesta-4,7-diene-6-one (ketodienediol) (11) is not metabolized. The absence of 2 beta-hydroxymetabolites for substrates (1) and (8) implies that hydroxylation at C-2 can occur only when the A-B rings are cis fused (5 beta-configuration). By contrast, the enzyme complexes that introduce hydroxyls at C-22 and C-25 do not exhibit a preference for cis over trans fusion and appraently cannot recognize the planar A-B ring configuration.