Peer-reviewed veterinary case report
Immune cells in dogs with leishmaniosis skin peeling
By Papadogiannakis, E I et al.·Published in Veterinary immunology and immunopathology·2005·Clinic of Companion Animal Medicine·View original on PubMed →
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Original publication title: Cellular immunophenotyping of exfoliative dermatitis in canine leishmaniosis (Leishmania infantum).
- Species:
- dog
Plain-English summary
A group of 48 dogs with leishmaniosis (a disease caused by a parasite) was studied to understand skin issues, particularly exfoliative dermatitis (ED), which causes severe skin shedding. Skin samples were taken from dogs with ED, those with normal skin, and dogs without any skin issues. The results showed that dogs with ED had more immune cells in their skin, indicating a strong immune response, and also had higher levels of the parasite in their skin compared to those without ED. This suggests that dogs with ED may have a more severe form of the disease, and understanding these immune responses can help in managing their treatment.
People also search for: dog leishmaniosis skin problems · canine exfoliative dermatitis treatment · leishmaniasis immune response in dogs
Abstract
Lymphocyte subsets, major histocompatibility complex (MHC)-II expressing cells and number of amastigotes in the epidermis and dermis were investigated immunohistochemically in 48 dogs with patent leishmaniosis, with or without exfoliative dermatitis (ED) to study the immunopathogenesis of this common cutaneous form of the disease. Skin biopsies were obtained and compared for ED sites (group A, n = 26), normal-appearing skin from the same animals (group B, n = 24), and leishmanial dogs not exhibiting ED (group C, n = 22), and normal controls (group D, n = 22). The CD3+, CD45RA+, CD4+, CD8+ (CD8a+), CD21+, and MHC-II+ cells and leishmania amastigotes were identified immunohistochemically and counted with the aid of an image analysis system. Pyogranulomatous to granulomatous dermatitis, expressed in various histopathological patterns, was noticed in all groups A and B and in half of group C dogs. In the epidermis, the low number of T-cells and their subsets did not differ significantly between groups A and B, but CD8+ outnumbered CD4+ lymphocytes in both groups. MHC-II+ expression on epidermal keratinocytes was intense in the skin with and without lesions from dogs with ED but not in group C dogs. CD3+, CD8+ and MHC-II+ cells were fewer in group C compared to group A and B dogs. In the dermis, CD3+ cells in group A animals were mainly represented by the CD8+. CD45RA+ and CD21+ cells were also seen in high numbers. MHC-II expression, potentially in lymphocytes, fibroblasts, dendritic cells, and macrophages was intense. The numbers of all cellular subpopulations in the dermis were significantly different between the groups, being highest in group A and lowest in group D. In sebaceous adenitis sites, CD4+ outnumbered CD8+ cells in contrast to the neighbouring dermis and the epidermis. The number of CD21+ and CD45RA+ cells was much lower in the inflamed sebaceous glands compared to the dermis. Finally, the number of amastigotes in the normal-appearing skin was significantly higher in the ED dogs (group B) than in those not exhibiting this cutaneous form of the disease (group C).
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/15734543/