Eosinophilic Plaque Research Articles

Molecular cloning of the feline thymus and activation-regulated chemokine cDNA and its expression in lesional skin of cats with eosinophilic plaque.

Thymus and activation-regulated chemokine (TARC) is a member of CC chemokine and plays an essential role in recruitment of CC chemokine receptor 4 positive Th2 cells to allergic lesion. To investigate the association of TARC in allergic inflammation of cats, a TARC cDNA was cloned from feline thymus by RT-PCR with 3' rapid amplification of cDNA ends (RACE) method. The feline TARC clone contained a full length open reading frame encoding 99 amino acids which shared 80.8%, 72.5%, 65.6% and 67.8% homology with dog, human, mouse and rat homologues, respectively. Expression of TARC mRNA was detected not only in thymus but also in spleen, lung, lymph node, kidney, small intestine, colon and skin of the normal cat tissues examined. Furthermore, it was found that TARC mRNA was strongly expressed in lesional skin of cats with eosinophilic plaque. The present results demonstrated that TARC might be involved in the pathogenesis of eosinophilic plaque in cats.

Ultrastructural findings of feline eosinophilic dermatoses

Despite the increasing evidence that degeneration of collagen is not involved in the histogenesis of the eosinophilic debris observed with light microscopy in feline eosinophilic dermatoses (FED), flame figures and foci of ‘collagen degeneration’ are still reported as degenerated collagen mixed with degranulated eosinophils. The purpose of this study was to investigate ultrastructurally eosinophil degranulation pathways and dermal collagen morphology in FED. Four patients with histopathological diagnosis of FED, three clinically diagnosed with eosinophilic granulomas and one with an eosinophilic plaque, and one healthy control were studied. Areas that contained eosinophils, collagen, flame figures and ‘collagen degeneration’ were ultrasectioned and examined with transmission electron microscope. Eosinophils (48 to 123 per cat) were classified into resting (intact cells), undergoing piecemeal degranulation (PMD) (viable cells with partially empty granules) and cytolytic [disrupted cells with clusters of free eosinphil granules (Cfegs)]. Longitudinal and transverse sections of collagen fibrils were also evaluated. 9.01% of eosinophils examined were resting, whereas 90.98% had released their content, 70.14% by cytolysis and 20.84% by PMD. Collagen fibrils showed no ultrastructural abnormalities and appeared identical to those observed in the control. Flame figures and foci of ‘collagen degeneration’ appeared constituted by collagen fibrils–fibers interspersed with cytolytic eosinophils. Based on these findings we conclude that eosinophils play an active role in the pathogenesis of FED through their granule content release, by cytolysis and PMD. Moreover, based on the normal collagen ultrastructure, the use of the term ‘collagen degeneration’ to describe the eosinophilic debris observed with light microscopy in FED should be definitely avoided. The study was funded by a grant of the European Society of Veterinary Dermatology.

Clinical and histological evaluation of an analogue of palmitoylethanolamide, PLR 120 (comicronized Palmidrol INN) in cats with eosinophilic granuloma and eosinophilic plaque: a pilot study.

Fifteen cats with eosinophilic granuloma or eosinophilic plaque were given PLR 120 at the dosage of 10 mg kg-1 twice daily for one month. PLR-120 down-modulates mast cell degranulation via a receptor-mediated mechanism. No other drugs were permitted and cats were kept free of parasites throughout the study. A clinical evaluation and skin biopsies were performed before and after the treatment. Clinical improvement was assessed at 15 and 30 days. Mast cell numbers were counted and their granular content was assessed by densitometric analysis on toluidine blue-stained sections before and after the treatment. Ten of 15 (67%) cats showed clinical improvement of signs and lesions. There was no significant difference between mast cell numbers in skin biopsies taken before and after the trial, whereas the number of granules was significantly increased (P < 0.009). This pilot study suggests that PLR-120 might be a useful drug for the treatment of eosinophilic granuloma and eosinophilic plaque.

Selected Feline Eosinophilic Skin Diseases

The eosinophilic skin diseases: eosinophilic plaque, mosquito bite hypersensitivity, eosinophilic granuloma, and indolent ulcer are discussed. The importance of identification of which syndrome is present in an individual cat is emphasized as there are differences in clinical course. Recommendations for diagnostic evaluation and therapeutic menagement are made.

Cytophilic antibodies in cats with miliary dermatitis and eosinophilic plaques: Passive transfer of immediate‐type hypersensitivity

Passive cutaneous anaphylaxis test and Praunitz-Küstner tests were performed in healthy recipient cats with heated and unheated sera of 17 cats suspected of having allergic dermatitis and of 12 healthy control cats. Positive reactions occurred with heated and unheated sera. It was therefore hypothesized that a heat-stabile cytophilic antibody is involved in the pathogenesis of eosinophilic plaques and miliary dermatitis in some cats.

Focal Proliferative Eosinophilic Dermatitis of the External Ear Canal in Four Dogs

Dermatitides with marked tissue eosinophilia are commonly occurring lesions in the cat, and two distinct entities are described: feline eosinophilic plaque characterized histologically by a hyperplastic superficial and deep perivascular to diffuse eosinophilic dermatitis with intraepidermal eosinophilic microabscesses, and feline eosinophilic granuloma, which is a granulomatous eosinophilic dermatitis with multifocal flame figure^.^ A similar granulomatous lesion occurs in hor~es .~ Eosinophilic granuloma has been reported in the dog as a rare lesion of the skin and oral Although it has been described in dogs of all ages, breeds, and sexes, dogs under 3 years of age, Siberian Huskies, and males appear to be at risk. The most common site of canine eosinophilic granuloma is the oral cavity, and the lesions are characterized by vegetative and ulcerated lingual or palatine masse~.~.~.~. l l Multiple cutaneous nodules and raised plaques on the ventral abdomen, prepuce, flanks, and limbs have also been reported.5.8Jo One case involved the nasal skin.' The cutaneous lesions are non-pruritic and non-painful. Peripheral blood eosinophilia is occasionally observed. Although the blood and tissue eosinophilia and the response to corticosteroid therapy suggest that cutaneous hypersensitivity may be inv o l ~ e d , ~ the cause of canine eosinophilic granuloma is still not clear. In this report, we describe an unusual location of focal,

Lack of autologous tissue transmission of eosinophilic plaques in cats

SUMMARY Autologous tissue transmission of spontaneously developing feline eosinophilic plaques was attempted in 5 cats. Macerated tissue from the plaque was vigorously rubbed onto 2 scarified skin sites in each cat. The inoculated areas were observed daily for 30 days. During that time, no clinical or histologic evidence of transmission was found.

Familial neurological disease associated with spongiform encephalopathy.

In a family in whom susceptibility to neurological diseases was transmitted in autosomal dominant fashion, the diseases affecting different family members ranged from subacute and chronic dementias to various motor system abnormalities without dementia. The propositus suffered a typical clinical course of Creutzfeldt-Jakob disease. Neuropathological observations revealed spongiform encephalopathy. A first cousin had a chronic dementia; no spongiform changes were present at autopsy. Both patients had PAS-positive, eosinophilic plaques throughout the brain. Muscle biopsy of the propositus revealed some changes suggestive of "ragged-red" myopathy. The heterogeneity of disease and the inheritance pattern in this family suggests that general susceptibility to neurological disease is a genetic trait.

Progressive ataxia of Charolais cattle associated with disordered myelin.

The pathology of a recently recognised progressive disorder of myelin in mature Charolais cattle is described. Clinical signs are first noticed at 8–24 months of age and progress from slight ataxia to recumbency over a period of 1–2 years. Lesions are microscopic and restricted to the white matter of the central nervous system. They are most marked in the internal capsule, cerebellar white matter and spinal cord and consist of multiple eosinophilic plaques. Ultrastructurally the lesions are associated with the nodal region of the myelin sheath. They are composed of disordered myelin, hypertrophied and hyperplastic oligodendrocytic tongues and many small processes which originate from these. There is evidence of myelin breakdown, but this does not elicit a phagocytic response. The aetiology of this condition is not known but the nature of the pathological process suggests a basic derangement of the myelin bearing cell.