Women's eating disorder origins as responses to childhood trauma and negative social self: a qualitative study exploring lived experience perspectives.

The cutaneous leishmaniases, caused by infection with several different species of , are some of the most important neglected tropical diseases affecting the skin with approximately one million new cases annually, across more than 70 countries (). For example, in the Ethiopian highlands, up to 29 million people are at risk with an estimated 20,000-50,000 annual cases (), predominantly affecting young adults and children (). Facial lesions represent 45 - 97.6% of Ethiopian cases () and active lesions or disfiguring scars can lead to stigma, social exclusion, and poor mental health (). Current treatments remain inadequate, with 32-38% failure rates (, ) and treatment-related morbidity that further compromises quality of life (). In Ethiopia, is the dominant causative agent of cutaneous leishmaniasis (CL) producing an unusually broad range of clinical presentations (), from self-healing localized lesions to chronic disfiguring disease. CL due to , (, ) and () infections has also been reported (). Localized CL (LCL) is most prevalent, but mucosal and mucocutaneous disease is also frequent (, ), while diffuse cutaneous leishmaniasis (DCL) is rare and presents as non-ulcerating nodules (–). Clinical as well as preclinical studies in rodent and primate models of and LCL have indicated that protective immunity involves highly regulated Th1-polarized CD4 T cell responses and nitric oxide and reactive oxygen species-producing macrophages (). In contrast, exaggerated inflammatory responses observed in mucosal and disseminated American tegumentary disease caused by are driven by cytolytic/senescent CD4 and CD8 T cells, NK cells and local environmental cues, including hypoxia and inflammasome activation (–). Conversely, immunosuppressive cytokines (IL-10, TGF-β) (–) and “anergy” are associated with DCL in and infections (). Despite being first reported in the 1930s (, ), the immunopathogenesis of Ethiopian CL remains poorly characterised at the tissue level. Histologically, Ethiopian CL lesions show predominantly dermal lymphohistiocytic inflammation with variable presence of granulomas (), neutrophil-mediated tissue damage via death ligands (FasL, TRAIL) () and elevated arginase in lesions (). A recent analysis of plasma chemokines and cytokines and parasite sequencing failed to identify systemic immune signatures or parasite genetic factors associated with different clinical presentations () suggesting that pathological mechanisms may be localized to lesional tissue. These studies have provided only a glimpse at the complexity underlying the immune response during human CL, limited by the number of analytes/cell types that are studied in any individual patient (). More recently, bulk (, –) and spatial (–) transcriptomics have been used to provide a more holistic picture of the immune landscape associated with CL lesions, with the latter best suited to the identification of specialised niches within complex tissues. To date, similar studies have not been conducted in the context of CL in Ethiopia or elsewhere in East Africa.